1 STAGERS NOTES

STAGERS
NOTES
CLINICAL SURGERY

CLINICAL MEDICINE

CLINICAL PEDIATRICS

Edited by

Abdulbasit rashed
MB.Ch.B
2 STAGERS NOTES

Special thanx to :
Dr. marwa Mohamed K.
Dr.zainab jumaa J.
‫‪3‬‬ ‫‪STAGERS NOTES‬‬

‫مالحضة‪ /‬هذا الكتاب غير كامل وغير منقح لغويا ‪..‬‬

4 STAGERS NOTES

STAGERS NOTES
CLINICAL SURGERY

Acute appendicitis 5
Breast 15
Thyroid gland 29
Abdominal exam 43
Hernia 63
jaundice 81
IO 89
Acute cholycystitis 100
Assessment of pulse 111
scrotum 116
Penail conditions 127
stoma 131
mass 134
Surgical incisions 136
Preparation for surgery 142
Diabetic foot and amputations 147
Fluid therapy 155
anatomy 169
5 STAGERS NOTES

Acute appendicitis
Q1/ Take short history from this patient ?
Peri-umbilical colic ,Pain shifts to the right iliac
fossa,associated with Anorexia and Nausea and
usually one or two episodes of vomiting that
follow the onset of pain

Q2/ what are the anatomical site of appendix ? according to the

frequency?

Q3/how can you detect the site of the appendix at the operation ?
The position of the base of the appendix is constant, being found at the
confluence of the three taeniae coli of the caecum, which fuse to form the outer
longitudinal muscle coat of the appendix. At operation, use can be made of this to
find an elusive appendix, as gentle traction on the taeniae coli, particularly the
anterior taenia, will lead the operator to the base of the appendix

Q/what are the condition that needs urgent surgical intervention?

or what are the conditions that associated with high risk of rapture ?
1- Extremes of age
2- Immunosuppression
6 STAGERS NOTES

3- Diabetes mellitus
4- Faecolith obstruction
5- Pelvic appendix
6- Previous abdominal surgery

Q/ define the silent appendix?

Retrocaecal appendix
Rigidity is often absent, and even application of
deep pressure may fail to elicit tenderness (silent
appendix), the reason being that the caecum,
distended with gas, prevents the pressure exerted
by the hand from reaching the inflamed structure.
However, deep tenderness is often present in the
loin, and rigidity of the quadratus lumborum may be
in evidence

Q/ At any age group the appendicitis is more dangerous ?

 in infants and young children this because :
1. the patient is unable to give a history. Because of this, diagnosis is often
delayed, and thus the incidence of perforation and postoperative
morbidity is considerably higher than in older children.
2. Diffuse peritonitis can develop rapidly because of the underdeveloped
greater omentum, which is unable to give much assistance in localising
the infection.
 in elderly this because of :
1. lderly patients with lax abdominal walls or obesity may harbour a
gangrenous appendix with little evidence of it, and the clinical picture
may simulate subacute intestinal obstruction.
2. coincident medical conditions

Q/what are the DDX of acute appendicitis?

IN CHILDREN:
1) GE
7 STAGERS NOTES

2) Mesnt. Adenitis
3) Meckel’s diverticulum
4) Intussus
5) Henoch-schole
6) Lobar pneumonia

IN ADULT
1) Regional enteritis
2) Ureteric colic
3) Perforated Peptic ulcer
4) Torsion testis
5) Pancreatitis
6) Rectus sheath haematoma

IN FEMALE
1) Mittelschmerz
2) Pid
3) Pyloneph
4) Ectopic
5) Torsion/rapture of ovarian cyste
6) Endometeriosis

IN ELDERLY
1) Divrticulitis
2) IO
3) CA
4) Mesteric infaction
5) Torsion appendix epiploica
6) Mesenteric infection
7) Leaking aortic aneurysm
Q/ how can you differentiate between acute appendicitis and ruptured
ectopic pregnancy ?
In ruptured ectopic pregnancy :

1. the pain commences on the right side and stays there.

2. there is a history of a missed menstrual period.
8 STAGERS NOTES

3. urinary pregnancy test may be positive.

4. Severe pain is felt when the cervix is moved on vaginal examination.
5. Pelvic ultrasonography.
6. There are well-defined signs of haemoperitoneum.

Q/ how can you diagnose patient with suspected acute appendicitis?

A/according to The Alvarado (MANTRELS) score:

 score of 7 or more is strongly predictive of acute appendicitis.

In patients with an equivocal score (5–6), abdominal ultrasound or contrast-
enhanced CT examination further reduces the rate of negative appendicectomy

Q/ What is the most dangerous type of appendicitis ? why ?

 Post-ileal type is considered the most dangerous type because :
1. No shift of pain which is misdiagnosed as gastroenteritis
2. No omental localization …Peritonitis
3. Affection of iliocaecal vein ….. Portal pyemia
4. Affection of appendicular artery ….gangrene
9 STAGERS NOTES

Q/ what are the signs elicited on physical examination?

1. Rovsing sign

Pressure on left iliac fossa : pain on right iliac fossa due to:
Shifting of gases from the pelvic colon to the caecum.

2. obturator sign (in pelvic appendicitis )

Pain on internal rotation and flexion of the right thigh

due to irritation of obturator internus muscle by pelvic
appendicitis.

3. Psoas sign :in retrocecal type)

Pain on extension of the right thigh due to psoas spasm as a resurl of
irritation by retrocaecal appendicitis.

Q/ why the pain starts around the umbilicus then shift to the Rt. Iliac
fossa ?
Initially the inflamation of the appendix causes irritation of the visceral peritonuem
(layer in the abdomen) which leads to reffered pain to the umbilical area(boath are
11 STAGERS NOTES

supplyied by T 10). As the disease progresses it then causes irritation of the parietal
peritoneum which then localises the pain to the right lower abdominal
area(McBurneys point) where the appendix lies

The origin of psoas M.

in the lumber vertebra …

the insertion in the lesser

trochanter on the femur

Q/how to deffrentiaate between sub-hepatic acute appendicitis and acute

cholycycstis?
1-type of the patient

In acute appendicitis : the patient is young , slim

In acute cholycysstis: female , fatey , fertile, fortie, fair

2- hyperesthesia

in appendicitis: hyperesthesia in the tringle of shirine

In cholycytisits : hyperesthesia in the on the back( boass sign)

3- US

Q/what are the investigations that you want to do ?

A/ Routine Pelvic appendix …the patient
1) FBC present with diarrohea( false
2) GUE diarrohea)
Selected
11 STAGERS NOTES

1) PT
2) Urea and electrolyte
3) Supine abdominal x ray
4) US
5) CT scan
Q/ you are in the ER dep. how can you manage this patient ?
1. short history with rapid abdominal examination
2. vital signs
3. large bore I.V. line
4. fluied according to the patient need and his vital signs
5. In cases of diagnostic doubt a period of 'active observation' is useful
6. when the diagnosis is established give opiate analgesics
7. Antibiotics should not be given until a decision to operate has been made
8. Diagnostic laparoscopy should be considered particularly in young women
9. appendicectomy: open or laproscopic

Q/what are the types of the incisions for appendicectomy ?

1- grid iron incision
2- Lanz incision In pregnant patient with acute
3- Rutherford-morrison incision appendicitis….. the incison should be higher
4- laproscopic incisions
12 STAGERS NOTES

Q/what are the indications , advantage and disadvantage of Lap.

Appendicectomy?
Indication:

• management suspected appendicitis

• Childbearing age female

• Diagnostic tool
In acute appendicitis …thers no
Advantage: great increament in body temp…it
1) Less postoperative pain relatively reach 38 -38.5
2) Early recovery
If greater think of complication or
3) Less wound infection other Ddx
Disadvantage:
1) Facility
2) Special training

Q/ what are the post-operative complications ?

Early:
1. Wound infection
2. Ileus
3. Resp. cx
4. Portal pyemia
5. DVT & pulmonary embolism
Late
1. Intra-abdominal abscess
2. Frozen pelvic
3. IO
4. RIH
5. Faecal fistulae

 Appendicular abscess

If the signs and symptoms of appendicular mass increases with the

deterioration of the clinical condition with hectic tempreture ….think of
appendcullar abscess…. Treated by aspiration under US
13 STAGERS NOTES

Q/ how to differentiate between acute appendicitis and mesenteric lymph

adenitis ?
in mesenteric lymph adenitis the patient has
shifting tenderness ( the patient has Pain localize to
the RIF…. When he tern to the other side … the pain
shift with the direction of the movement) also the
patient has tonsillitis

Q/ define appendicular mass? How could it occur ?

When the inflammatory process is slow (> 48 hours),
the body defense mechanism has enough time to
surround the inflamed appendix by adhesions to the
nearby intestine and omentum. Thus, forming
appendicular mass within 3-5 days after starting of pain.
lt is suspected by history of pain 3 days ago and
temperature 39 c .the patient develops repeated
vomiting , with increase the constipation , gradually mass in the right iliac fossa
beguns to increase…

Q/ how do you know that the appendix has been raptured ?

1. The patient develops generliaised abdominal pain
2. Temperature increases ( 39-40 c)
3. Gardening and rigidity all over the abdomen
4. Shifting dullness ( due to fluid)
5. Diminished the liver dullness on percussion
6. US : fluied around the appendix and peritoneal cavity
7. CXR: air under diaphragm
14 STAGERS NOTES

Q/ how to treate reptured appendix?

1. Rescetaion
2. Laparotomy + appendectomy
3. Peritoneal toilet
4. Put drain
5. Follow up

Q/ how to differentiate between acute appendicitis and renal colic?

 Acute appendicitis : the patient loathy to move, ask him to cough he
develops pain
 Renal colic: rolling on the bed , coughing doesn’t elicit pain

Q/Where dose appendicular mass doesn't occur?

1. Children not > 10 years of age as the omentum is not well developed.

2. Elderly as there is atherosclerosis of the appendicular artery & perforation is

easier.

3. Pregnancy as the omentum is shifted upward

Q/How to know improvement in appendicular mass ? when does you

discontinue conservative treatment ?
1. clinical picture :
Symptoms: no pain, no vomiting, no constipation.
Signs: reduce abdominal signs, reduce the size of mass, reduce fever &
tachycardia.
2. investigations:
reduce Leukocytosis in acute appendicitis

Discontinue if

1. Patient presented with abscess.

2. Doubtful diagnosis.
3. Dangerous group (children >10 yrs ,elderly, pregnancy, DM)
15 STAGERS NOTES

Thyroid gland

Q/ What do you know about thyroid embryology?

 From the floor of the pharynx at the Foramen caecum
which descends in the neck to form both lobes & isthmus.
 From the 4th branchial arch which gives the superior parathyroid and para-
follicular C cells (neural crest).

Q/what is the blood supply to the thyroid gland ?

A/ 1-arterial blood supply:
1. superior thyroid artery …first branch of external
caroted a.
2. inferior thyroid artery : Arises from the thyro-
cervical trunk which is branch of the first part of
the sub-clavian artery

3. thyroidea ima a… may be arise from the arch of

aorta
accessory tracheal and bronchial vessels

b-venous drainage
1. Superior and middle thyroid v….. To the internal iugular vein
2. Middle thyroid v.: drain to the IJV
3. inferior thyroid vein…..drain into left innominate vein
16 STAGERS NOTES

Q/ what is the lymphatic drainage from thyroid gland?

Peripheral part:. To the upper & lower deep cervical lymph nodes.
Medial parts of both lobes:
1) Pre-laryngeal LNs over cricothyroid membrane (gland of Poirier).
2) Pre-tracheal LNs (Delphi).
3) Deep cervical LNs : para-tracheal LNs (mediastinal).

Q/ what is the result of complete injury to the

RLN ?
If its unilateral : hoarseness of the voice

If its bilateral : aphonia

Q/ what is the result of partial injury to the RLN?

If its unilateral : dyspnoia on exertion

If its bilateral : stridor

Q/ what are the importance of US scan in the

investigation for thyroid gland?
1- deffrentiated solid from cyctic structure
2- adjunct to FNAC
3- the assessment of malignant lymphadenopathy.
4- domenstrate subclinical nodularity
17 STAGERS NOTES

Q/what are the signs and symptoms of hypothyroidism?

The signs of thyroid deficiency are:

1. bradycardia;
2. cold extremities;
3. dry skin and hair;
4. periorbital puffiness;
5. hoarse voice;
6. bradykinesis, slow movements;
7. delayed relaxation phase of ankle jerks.

The symptoms are:

1. • tiredness;
2. • mental lethargy;
3. • cold intolerance;
4. • weight gain;
5. • constipation;
6. • menstrual disturbance;
7. • carpal tunnel syndrome

Q/how can you treate myxedema coma?

1. thyroid replacement, either a bolus of 500 mg of T4 or 10 μg of T3 either
intravenously or orally every 4–6 hours
2. If the body temperature is less than 30∞C the patient must be warmed
slowly.
3. Intravenous broad-spectrum antibiotics and hydrocortisone (in divided
doses) are recommended.
18 STAGERS NOTES

Q/ why thyroid moves with the swelling and thyroglossal cyst with the
protrusion of the tongue ?

Thyroid invested with pri-tracheal fascia

Thyroglossal cyst attach to the base of the tongue

Q/classification of thyroid swelling ? (final 2015)

1. Simple goitre (euthyroid)
 Diffuse hyperplastic
Physiological
Pubertal
Pregnancy
Multinodular goiter
2. Toxic
 Diffuse
Graves’ disease
Multinodular
Toxic adenoma
3. Neoplastic
 Benign
Malignant
4. Inflammatory
 Autoimmune
Chronic lymphocytic
thyroiditis
Hashimoto’s disease
Granulomatous
De Quervain’s thyroiditis
Fibrosing
Riedel’s thyroiditis
5. Infective
19 STAGERS NOTES


Acute (bacterial thyroiditis, viral thyroiditis, ‘subacute thyroiditis’)
Chronic (tuberculous, syphilitic)
6. Other
 Amyloid
Q/what are the uses of FNAC?

FNAC can be use to diagnose :

1- colloid nodule
2- thyroditis
3- papillary Ca
4- medullary Ca
5- anaplastic Ca
6- lymphoma

Q/ what are the Indications for operation in thyroid swellings?

1- aisalNoeN
 FNAC positive
 Clinical suspicion, including:
 Age
 Male sex
 Hard texture
 Fixity
 Recurrent laryngeal nerve palsy
 Lymphadenopathy

2- tiucttieRrucoR
21 STAGERS NOTES

3- asoeurN iesoN
4- Pressure symptoms
5- Cosmesis
6- Patient’s wishes

Q/ how can you diagnose the retrosternal goiter ?

A/ 1- clinically :
- Dyspnoea, particularly at night, cough
and stridor
- Dysphagia
- Engorgement of facial, neck and
superficial chest wall veins
- Recurrent nerve paralysis is rare; the
goitre may also be malignant or toxic
-
2-radiologically:
- Chest and thoracic inlet radiographs show a soft-
tissue shadow in
the superior mediastinum, sometimes with
calcification and often
causing deviation and compression of the trachea.
- A CT scan
gives the most accurate and often
dramatic anatomical visualization

Q/ what are the causes/types of hyperthyroidism ?

1. diffuse toxic goitre (Graves’ disease);
2. toxic nodular goitre;
3. toxic nodule;
4. hyperthyroidism due to rarer causes
21 STAGERS NOTES

5. Post-partum hyperthyroidism
6. Thyrotoxicosis factitia
7. Jod–Basedow thyrotoxicosis
8. Subacute/acute forms of autoimmune thyroiditis or of
de Quervain’s thyroiditis

Q/ what are the clinical features of hyperthyroidism?

Thyrotoxicosis should always be considered

The symptoms are: in:
• children with a growth spurt, behaviour problems or


myopathy;
• tachycardia or arrhythmia in the elderly;
• tiredness; • unexplained diarrhoea;
• loss of weight.
• emotional lability;
• heat intolerance;
• weight loss;
• excessive appetite;
• palpitations.

The signs of thyrotoxicosis are:
• tachycardia;
• hot, moist palms;
• exophthalmos;
• lid lag/retraction;
• agitation;
• thyroid goitre and bruit..

Q/what is the deference of AF due to hyperthyroidism from other

causes?

persistent atrial fibrillation, not responsive to digoxin.

Q/what are the pre-operative preparations for thyroid surgery and How
to know that the patient is ready for surgery?
22 STAGERS NOTES

1. 1-Carbimazole 30–40 mg day–1 is the drug of choice for preparation.

When euthyroid (after 8–12 weeks), the dose may be reduced to 5 mg 8-
hourly or a ‘block and replace’ regime used The last dose of carbimazole
may be given on the evening before surgery.
2. B-blockers: act on the target organs and not on the gland itself.
Propranolol inhibits the peripheral conversion of T4 to T3. This results in
very rapid control and operation may be arranged within 1 week

The app -blocker is

increased to achieve the required, clinical response and quite often larger
doses (propranolol 80 mg t.d.s. or nadolol 320 mg once daily) are necessary
B-Blockers do not interfere with synthesis of thyroid hormones, and
hormone levels remain high during treatment and for
some days after thyroidectomy. It is therefore important to continue to give
the drug for 7 days postoperatively.

3. Iodine -blocker for the 10

days before operation. Iodide alone produces a transient remission and
may reduce vascularity, thereby marginally improving
safety.
Q/How to know that the patient is ready for surgery?
1. Symptomatic relief.
2. Gaining weight.
3. Sleeping pulse.(pulse alone is not an indicator of euthyroid as lnderal
will normalize pulse even before action of Neomercazol)
4. Serum T3 ,T4 level.
23 STAGERS NOTES

Q/ what are the pre-op investigations ?

1. Thyroid function tests.
2. Laryngoscopy : to assess RLN function
3. Thyroid antibodies.
4. Serum calcium estimation.
5. An isotope scan before preoperative preparation in toxic
nodular goitre if total thyroidectomy is not planned.

Q/ what are the post-operative complications of thyroid surgery ?

1- Haemorrhage
2- Respiratory obstruction
3- Recurrent laryngeal nerve paralysis
and voice change
4- Thyroid insufficiency
5- Parathyroid insufficiency
6- Thyrotoxic crisis (storm)
7- Wound infection
8- Hypertrophic or keloid scar
9- Stitch granuloma

Q/ What are swellings which move up and down with deglutition?

o Thyroid : thyroglossal cyst, ectopic thyroid gland, parathyroid gland tumors.
o Larynx: pre-laryngeal L.N ., laryngocoele, cold abscess of the larynx.
o Trachea :pretracheal L.N., tracheocoele.
o Subhyoid bursitis.

Q/ How is the thyroidgland descend down after deglutition ?

By the contraction of strap muscles (sternohyoid, sternothyroid, omohyoid)
Q/ When does the goiter lose the up and down with deglutition?
ln the following conditions:
a. Huge goiter,
24 STAGERS NOTES

b. Malignant goiter
c. Retrosternal goiter.

Q/ What do you know about thyroglossl fistula?

 it is one of the complications of thyroglossal cyst. It is acquired never
congenital.
Occurs either due to:
1. lnfection and spontaneous rupture
2. Drainage of infected cyst
3. inadequate excision of the cyst
Clinically:
- it is an opening in the midline of the neck or near to the midline.
- Moves upward with deglutition.
- it may discharge viscid fluid or pus
Q/how can you differentiate rapid radial pulse due to hyper thyroidism
from tachycardia due to anxiety ?
 tachycardia due to hyperthyroidism persist during sleep …

Q/ What do you know Pendred's syndrome ?

It is inborn error of iodine metabolism due to peioxiade
enzyme deficiency within the gland and in which there is
goiter , deafness , dwarfism mental deterioration

Q/ Mention the complications of simple nodular goiter?

1. Pressure on surrounding structures (dyspnea and dysphagia)
2. Disfigurement
3. 2ry toxic goiter
4. malignant transformation
5. Hemorrhage in a cyst
6. infection
7. Retrosternal extension
25 STAGERS NOTES

Q/ What are the pressure symptoms of goiter?

1. Pressure on trachea : dyspnea .
2. Pressure on the esophagus : dysphagia
3. Pressure on recurrent laryngeal N : hoarseness of voice
4. Pressure on carotids : fainting attacks
5. Pressure on internal jugular : black outs which increase on
leaning forward
6. Pressure on sympathetic chain : Horner syndrome

Q/ what are the causes of dyspnea after thyroidectomy ?

1. tension hematoma
2. Laryngeal edema due to trauma by endotracheal tube or secondary
extensive manipulation of larynx during surgery .
3. bilateral recurrent laryngeal N palsy
4. trachiomalacia

Q/ what are the investigations of simple nodular goiter?

1. T3 , T4 , TSH
2. US
3. Isotops scan
4. FNAC

Q/ what are the causes of weight loss despite good appetite?

1. Thyrotoxicosis
2. Diabetes Mellitus
3. Parasitic infestation
4. Mal-absorption syndrome
26 STAGERS NOTES

Q/ What is the deffrence between exopharhamos and proptosis?

 Exophthalmos-* protrusion of the eyeball due to thyroid disease.
 Proptosis :protrusion of the eyeball due to diseases other than
thyroid disease

Q/ Ddx of Solitary Nodule Thyroid

1. Dominant nodule MNG
2. Adenoma
3. Carcinoma
4. Thyroid cyst
5. Localized Hashimoto’s disease

Q/Isotope studying in solitary nodule?

Cold nodule - Mostly malignancy
Warm - Euthyroid
Hot nodule - Hyperthyroid
Mainly done in cases of toxicity in association with Nodularity.

Q/ what are the general examination findingsin of patient with

thyrotoxicosis?

1. Upper limb:
 Nail changes :
 Brittle.
 Spooning
 Pitting.
 Fissuring.
 Thin.
27 STAGERS NOTES

 Exaggerated capillary pulsations.

 Onycholysis ) Separation of nail from
its bed.
 8. Plummer's nail ) distal end of nall is
covered by skin.
 Acropachy.
 Fine tremors.
 Palmer erythema.
 Moist warm sweaty skin.

2. Lower limb:
 Pretibial myxedema (non pitting edema)
 Pitting edema if heart failure
 Myopathy of proximal muscles

3. Gardiac examination:
 Accentuated heart sounds-s3

4. Abdomen
 Hepatosplenomegaly

Q/ why diarrhea could occcure in patient with thyrotoxicosis?

Due to increased c-AMP which increases permeability of cells of the mucous
membrane.

Q/ why polyuria could occcure in patient with thyrotoxicosis?

due to:
1. Increase in COP which causes increses renal blood flow leads to increase GFR.
2. Secondary DM ( Glucosuria)
3 .Increase in metabolic water.
4. Increase in water intake secondary to polyphagia.

Q/Define thyroid auopachy:

Acral changes associated with thyrotoxicosis:
28 STAGERS NOTES

o Tremors.
o Pretibial myxedema. (due to deposition of hyaluronic acid in the dermis and
subcutis usually in the areas of trauma ccc by thickening of the skin)
o Nail changes

Q/what are the causes of dysphagia with thyroid disese ?

1) Retrosternal goitre riddles thyroiditis
3) malinancy (infiltration of the esophagus.
4) Myopathy of striated muscle of the
esophagus in toxic patients

Q/What are the DDx of shadow in superior mediastinum

1- Retrosternal goitre.
2- Thymoma
3- Lymphoma
4- Enlarged LN.
5- Aortic aneurysm

Q/which thyroid swelling does not move up and down with deglutition?
1. Carcinoma thyroid with local infiltration
2. Riedel's thyroiditis
3. Huge goiter
4. Retrosternal goiter with intrathoracic impaction.

Q/Where do you palpate the normal carotid artery?

At the level of upper border of thyroid cartilage along the anterior border of
sternocleidomastoid

Q/What is Berry’s sign?

When carotid pulse is impalpable due to infiltration of carotid sheath by a
malignant thyroid swelling then it is called positive Berry’s sign.
29 STAGERS NOTES

The Breast

Q/ What is the embryology of the breast?

It arises from the milk line which extends from the axilla to the mid- inguinal point.
it is considered to be modified sweat gland
Lt is formed of:
o Epithelia, element from ectoderm
o The connective tissue from mesoderm

Q/How will you demonstrate skin tethering?

As the malignant breast lump grows it may infiltrate the Cooper’s ligament and
make these strands inelastic and pulls the skin inwards
rendering puckering of the skin. At this stage the lump
can be movedforlimiteddistanceindependantlyoftheskin.
Thetetheringcanbedemonstratedbymovingthe lump
from side to side and observing if skin dimples appear
at the extremes of movement . Tethering may also be
demonstrated by asking the patient to lift her hands
above the head or pressing the waist with both hands .
when the skin dimple will appear.

Q/How will you demonstrate skin fixity?

Skin fixity implies direct infiltration of the skin by the underlying malignant tumor.
When the ump is fixed to the skin, the lump and the skin cannot be moved
independently.
The skin fixity is demonstrated by trying to lift the skin from the underlying lump in
between fingers. If the skin is fixed to the underlying lump, the overlying skin
cannot be lifted up from the underlying lump .
31 STAGERS NOTES

Q/What is a sentinel lymph node?

Sentinel lymph node is the lymph node which is in a direct drainage pathway
from the primary tumor„ Sentinel lymph node is the first node encountered by the
tumor cells and its histological status predicts distant lymph basin status with
regard to metastasis

Q/ what do you know about ligament of cooper?

 Suspensory ligament of the breast
 Bands of connective tissue called Ligaments of Copper.
 it's between the overlying skin and the pectoral fascia.

Q/ what is the blood supply of the breast ?

 Arterial blood supply
1. . The lateral thoracic artery :From 2nd part
of the axillary artery
2. The medial perforators:
- From the internal mammary artery
- The interna[mammary artery arises
from subclavian artery.
3. . Lateral perforators
- From the 2nd 3rd and 4th intercostal
arteries
 Venous Drainage
1. . Superficial. Veins: Cross midline.
2. o Deep veins: accompany the arteries.
3. intercostal veins
- Drain into azygus system on the rt.
side &-hemyazygus on the left Side.
- They are communicating with the para-vertebral veins.
31 STAGERS NOTES

Q7/ What is the anatomy of the breast? 

 it extends from the 2nd to the 6th rib.
 it extends from the sternum to the mid axillary line.
 it lies superficial to deep fascia.

 Axillary tail passes deep to the deep fascia.

 the nipple protrude forward ,downward, and lateral , at the Level of 4'h
intercostal space ,it gets lower by age
 Areola ; dark area of skin . becomes mote pigmented with pregnancy

Q8/ what are the lymphatic drainage of the breast?

The lymphatics of the breast drain predominantly into the axillary and internal
mammary lymph nodes. The axillary nodes receive approximately 85% of the
drainage and are arranged in the following groups:

• lateral, along the axillary

vein;
• anterior, along the lateral
thoracic vessels;
• posterior, along the
subscapular vessels;
• central, embedded in fat in
the centre of the axilla;
• interpectoral, a few nodes
lying between the pectoralis
major
and minor muscles;
• apical, which lie above the level of the pectoralis minor tendon
in continuity with the lateral nodes and which receive the
efferents of all the other groups.
32 STAGERS NOTES

Q/what are the uses of Magnetic resonance imaging (MRI) in the

diagnoses of breast pathologies?
1• It can be useful to distinguish scar from recurrence in women who have had
previous breast conservation therapy for cancer(although it is not accurate within 9
months of radiotherapy because of abnormal enhancement)
2• It is the best imaging modality for the breasts of women with implants.
3• It has proven to be useful as a screening tool in high-risk
women (because of family history).
4• It is less useful than ultrasound in the management of the
axilla in both primary breast cancer and recurrent disease

Q7/ what do you know about Triple assessment ?

A/ In any patient who presents with a breast lump or other symptoms
suspicious of carcinoma, the diagnosis should be made by a combination of

1-clinical assessment

2- radiological imaging

3-and a tissue sample taken for either cytological or histological analysis the so
called triple assessment. The positive predictive value (PPV) of this combination
should exceed 99.9%.

Q8. What are the indications, benefit and disadvantage of mammography

in the diagnosis of the breast Ca ?
Indications are:
1. Screening of high risk patient.
33 STAGERS NOTES

z. When there is pain, nipple discharge or axillary L.N which no palpable mass.
3. To identify contralateral breast lesion or other multifocal lesion in the same
breast after +ve biopsy.

The benefit in diagnosis of breast cancer:

Mammography may show some radiological findings in the breast cancer e.g.
microcifications, masses, swelling larger than the surroundings.

The disadvantages of mammography.

1. Exposure to irradiation
2. false –ve results
3. false +ve results
4. it is less sensitive in young Ladies due to increase breast density

Q/ what are the causes of nipple retraction ?

a. simple nipple inversion, is of unknown aetiology (benign horizontal
inversion) , occur at puberty
b. A slit-like retraction of the nipple may be caused by duct ectasia and
chronic periductal mastitis
c. circumferential retraction, with or without an underlying lump, may well
indicate an underlying carcinoma
34 STAGERS NOTES

Q/ what are the causes of nipple discharge?

Discharge from the surface
■ Paget’s disease
■ Skin diseases (eczema, psoriasis)
■ Rare causes (e.g. chancre)
Discharge from a single duct
Blood-stained:
■ Intraduct papilloma
■ Intraduct carcinoma
■ Duct ectasia
Serous (any colour):
■ Fibrocystic disease
■ Duct ectasia
■ Carcinoma
Discharge from more than one duct
Blood-stained:
■ Carcinoma
■ Ectasia
■ Fibrocystic disease
Black or green:
■ Duct ectasia
Purulent:
■ Infection
Serous:
■ Fibrocystic disease
■ Duct ectasia
■ Carcinoma
Milk:
■ Lactation
■ Rare causes (hypothyroidism, pituitary tumour)
35 STAGERS NOTES

Q/ what are the congenital abnormalities of the breast ?

1. Amazia: Congenital absence of the breast
2. Polymazia: Accessory breasts
3. Diffuse hypertrophy (virginal hypertrophy)
4. Abnormality of the nipple:
 Athelia: absence of the nipple
 Polythelia: multiple nipples
 Retrated nipple

Q/Cutaneous Manifestations of Carcinoma Breast?

1. Dimpling or Tethering involvement of ligament of Cooper.
2. Infiltration
3. Peau de’orange (orange peel appearance) Subcuticular lymphoedema with
pitting at the sites of hair follicles.
4. Cancer—encuirasse—armor chest
5. Ulceration
6. Paget’s disease of nipple with excoriation

Q/ what do you know about Mondor’s disease?

 Mondor’s disease is thrombophlebitis of the
superficial veins of
the breast and anterior chest wall
 cause : injury ., infection or idiopathic
 The pathognomonic feature is a thrombosed
subcutaneous cord, usually attached to the
skin.
 The only treatment required is restricted arm
movements and, in any case, the condition subsides within a few months
without recurrence, complications or deformity.
36 STAGERS NOTES

Q/ duct ectasia ?
1. defention:
this is a dilatation of the breast ducts,
which is often associated with periductal
inflammation.
2. the pathogenesis of duct ectasia:
dilatation in one or. more of the larger
lactiferous ducts, which fill with a
stagnant brown or green secretion. This
may discharge. These fluids then set up
an irritant reaction in surrounding tissue
leading to periductal mastitis or even
abscess and fistula formation In some
cases, a chronic indurated mass forms beneath the areola, which mimics a
carcinoma.

3. Risk factors:

A marked association between recurrent periductal inflammation and smoking has

been demonstrated.

arteriopathy

4. Ttt:
 carcinoma must be excluded
 Antibiotic therapy may be tried, the most appropriate agents being co-
amoxiclav or flucloxacillin and metronidazole

Q/ what are the risk factor for breast Ca?

1. Geoghrafical : developed > developing
2. Age: rare before 20, increase with the age
3. Gender : F>M
4. Genetic: increses with + family hx
5. Diet; alcohol and diet low with phytoestrogen increses the risk
37 STAGERS NOTES

6. Endocrine: more in nillpara , having a first child at an early age. late menarche
and early menopause and obese patients
7. Previous radiation

Q/ what do you know about paget disese of the nipple ?

Paget’s disease of the nipple is a superficial
manifestation of an underlying breast carcinoma. It
presents as an eczema-like condition of the nipple and
areola, which persists despite local treatment.
The nipple is eroded slowly and eventually disappears. If
left, the underlying carcinoma will sooner or later
become clinically evident.
Nipple eczema should be biopsied if there is any doubt about its cause

Q/ what are the routs of the sepread of the breast Ca ?

1. Local spread : to the skin or the chest wall
2. Lymphatic spread: primarily to the axillary and the
internal mammary lymph nodes.
3. Spread by the bloodstream In order of frequency:

 the lumbar vertebrae

 femur
 thoracic vertebrae
 rib and
 skull
 Metastases may also commonly occur in the liver, lungs and brain
and, occasionally, the adrenal glands and ovaries; they have, in
fact, been described in most body sites.
38 STAGERS NOTES

Q/ what is the most common

site for breast Ca?
A/ upper outer quadrant .(60%)

Q18. How to know that abreast

lump is fixed to the breast tissue.

By holding the breast by one hand

and trying to move the lump within the breast by the other hand in two
perpendicular directions

Q/ How to know that abreast lump is fixed to the pectoral muscles?

By moving the [ump while the patient pressing with her hands against her
waist. if the mobility of the lump becomes restricted, then it is attached to the
muscle.

Q/ What are the differences between Paget's disease of the nipple and
eczema in the nipple?
Eczema Paget's disease
1.Bilateral 1.Unilateral
2.Young lactating female 2.old non-lactating
3.itchinq 3. No itchins
4. lntact nipple 4.Eroded nipple
5. No lumps 5.May be on under[ying [urnp
6.Responds to short term steroids 6.Not respondinc to treacment
7.Present at other sits of the body ex: 7.Only in the breast
anticubital fossa

Q/ what are the indications of mastectomy in the breast Ca?

 large tumours (in relation to the size of the breast)
central tumours beneath or involving the nipple,
 multifocal disease
 local recurrence
 patient preference.
39 STAGERS NOTES

Q/ what are the indications for radiotherapy in breast Ca?

1. large tumours
2. those with large numbers of positive nodes
3. extensive lymphovascular invasion.

Q/ what are the role of hormonal therapy in breast Ca?

1. nefixomaT
 reduce the annual rate of recurrence by 25%,
 17% reduction in the annual rate of death.
 The beneficial effects of tamoxifen in reducing the risk of tumours in the
contralateral breast have also been
observed,
 has its role as a preventative agent
 5 years of treatment is preferable to 2 years.

2. tnin eaiToHL
 These include the LHRH agonists, which induce a reversible ovarian suppression
have the same beneficial effects as surgical or radiation-induced ovarian ablation
in pre-menopausal receptor-positive women, and the oral aromatase inhibitors
for post-menopausal women.
3. the oral aromatase inhibitors:
 treatment of recurrent disease, in which they have been shown to be
superior to tamoxifen
 here is an additional reduction in contralateral disease, which makes this
drug suitable for a
study of prevention

Q/What are the side effects of chemotherapy?

1. Nausea and vomiting
2. Alopecia
3. Myelosuppression
41 STAGERS NOTES

4. Cardiac toxicity (Adriamycin)

5. Premature menopause
6. Second malignancy

Q/ what do you know about Peau d’orange?

Peau d’orange is caused by cutaneous lymphatic oedema. Where
the infiltrated skin is tethered by the sweat ducts it cannot swell,
leading to an appearance like orange skin. Occasionally, the same
phenomenon is seen over a chronic abscess

Q/ what do you know about Cancer-en-cuirasse?

The skin of the chest is infiltrated with carcinoma and has been
likened to a coat. It may be associated with a grossly swollen arm.
This usually occurs in cases with local recurrence after mastectomy
and is occasionally seen to follow the distribution of irradiation to
the chest wall. The condition may respond to
palliative systemic treatment but prognosis in terms of survival is
poor.

Q26/ what are the causes of gynecomastia?

1. ldiopathic. (the most common cause)
2. physiological
neonatal : from exposure to high maternaL estrogen.
Pubertal
OId age: decreases testicular function.
3. Patholosical:
 increase Estrogren:
E secreting tumor (Sertoli cell tumor).
Feminizing tumors of adrenals.
Para malignant syndrome as bronchogenic carcinoma.
41 STAGERS NOTES

 decreases Testosterone:
Orchiectomy.
Testicular atrophy: mumps/ Leprosy and heat exposure.
 decrease metabolism of E ex: liver failure.
4. iatrogenic:
Digitalis.
Cimitidnine.
Estrogen therapy as in cancet ptostate.
5. genetic : klinefilter syndrome.

In any brest examination you have to examine the follwoing

Q/Abdomenal examination findings in patient with breast CA?

1. Liver enlargement
2. Presence of free fluid
3. In pre-menopausal women for any ovarian lump(Krukenberg tumor)
4. PR—for evidence of ‘Blummer Shelf’—malignant
deposit in the pouch of Douglas.
Q/Respiratory System examination findings in patient with breast CA?
For pleural effusion, metastatic
deposits—in case of bone pain, examine region of pain
particularly:
1. Spine,
2. Ribs,
3. Upper end of femur and humerus.

Q/Causes of massive swellings of the breast include:

1- Cystosarcoma phylloides.
2- Diffuse hypertrophy.
3- Giant fibroadenoma
42 STAGERS NOTES

Q /What are the risk factors for development of male breast cancer?
1. Gynecomastia
2. Klinfelter’s syndrome—associated with testicular atrophy
3. Mutation in BRCA 2 gene is associated with increased risk of breast cancer in
males.

Q/What is fibroadenoma?
This is a benign breast disease containing both fibrous and glandular tissue. This is
not a true tumor and has been regarded as one spectra of aberrations of normal
development and
involution (ANDI).

Q/When you will consider surgical treatment?

Excision of the fibroadenoma is indicated:

1. fibroadenoma larger than 4 cm in size

2. When the tumor is increasing in size at follow-up
3. Patient is apprehensive and wants to get the tumor removed
4. In patient with age more than 30 years
5. When there is suspicion of malignancy.
43 STAGERS NOTES

Abdominal examination

a) general look:

middle/old age male/F ,lying flat ,conscious ,confortable , responding

to me body weight(obese/weight loss),looks well/ill, cyanosis , pallor ,
dyspnea ,jaundice, any cannula and its site ,drain OR I.V. fluid
concioussnes assessment according to GCS

b) general examination:

1. the hand: -clubbing,koilonechia(spoon shape

nails) , leukonechia(white nails),palmer
erethema, dupuytrens contracture flapping tremor ,prphral cyanosis
,muscle weasting
2. forearm: scratching mark (ex: in obstructive jaundice and CRF)
3. the head: yellow sclera, conjucntival pallor,xantholasma,spider naevi,
parotid swelling, angular stomatitis, glossitis, oral hygiene, dental
carries
4. the neck: LAP
5. the chest: gynecomastea (in male) and breast atrophy (in female),
spider naevi

c) abdominal examination:

1. 1)exposure : from the nipple to mid-thight

44 STAGERS NOTES

2. 2)stand at the end of the bed and look to :

1- Shape of abdomen
o a-distention:
 symmetrical:
6F…..fat,,fuied,,,fetus,,,faeces…flatus…functional
 asymmetrical : organomegally and IO
o b-scaphoid abdomen …..CA..Starvation…old age

2-pattern of movement:

 Abdominothoracic : in male and children

 Thoraco-abdominal: females
 No movement :occurs in peritonitis
 Visible peristalsis : occurs in IO and normally in thin patient

3) kneel at the right side of the patient and ask him to hold his breath:

look for visible pulsation :

 1-normally in thin patient
 2-abnormal in abdominal aortic aneurism
 3-liver pulsation in tricuspid valve
 4-regurgitation

5)stand to the right of the abdomen with your eye perpendicular to the
patient abdomen (birds eye position)

 scar & scratching marks

 visible dilated veins & spider naevi
45 STAGERS NOTES

 masses
 hernial orifices (aske him to turn his head and cough)
 site of incision or straia , tattoo
 discoloration,, bruises,
 hair distribution
 umbilicus ….
 Normally situated midway between xiphisternum and pubic
symphysis
 downward displacement of umbilicus due to ascites
 Umbilicus may be displaced upwards by swelling from pelvis
Swelling (ovarian cycst )
 from one side of abdomen may push umbilicus to the opposite
side
 Normally inverted and slightly retracted
o Everted in ascites
o Tucked in obesity
o Sister Joseph’s nodule (malignant deposits in visceral
carcinoma).

6) palpation:

1. superfecial palpation:

To detect tenderness.

To palpate superficial mass.

46 STAGERS NOTES

To get confidence of the patient

To detect rigidity and guarding.

2. deep palpation: for deep masses and tenderness

3. organ palpation: liver and spleen and the kidney

When liver is enlarqed we have to comment on:

o Edge: sharp &well defined

Surface: Smooth, nodular, or granular
Consistency: firm Cm below costal margin: (....) cm
4. palpation and percussion of the organ at the same time
5. palpation of left supraclavicular lymphnode is part of abdominal
examination

7) percussion : with the palpation at the same time

 -examination for ascites include shifting dullness and

transmitted Thrill
 -examination for urinary bladder

8)auscultation :

 1-at the mcburney point: bowel sound

 2-at right hypochondrium : hepatoma
 3-renal vessels : 2.5 cm above and lateral to the
 4- below and lateral to the umbilicus for iliac a. bruit
47 STAGERS NOTES

 umbilicus…renal artery stenosis

D) examination of the genetalia ,inguinal LAP ,hernia orifices

and PR

1-gentelia :

1. inspection
 any mass ,skin lesion, discoloration ,ulcerative lesion,
 Hypospadias

2. Palpation

 tenderness ,secrotal swelling ,cord …assess the mass according

to SECTOR-MG
 Spermatic cord….
*Beaded - T.B
*Matted- filarasis
 Scrotum
Scrotum (ant, post aspect)Shape, symmetry and swelling

ln all cases both sides of the scrotum should be palpated

Back of the scrotum for T.B sinus
48 STAGERS NOTES

Starting with the healthy side, first with the patient

standing & then in the recumbent position
 Palpation of the epididymis(size, consistency, presence of sulcus, between
it and the testis)
tunica vaginalis (early hydrocele detected by pinching test.
i.e. you feel double layers)

 The testes
*Size
*Consistency
*Testicular sensation

Penis for ulcer or scar of chancre external meatus

(site, discharge by pressing the glans)

2-PR:

1. -greet the patient and introduce your self

- privet room
2. -explain to the patient what you have to do and the perpous from doing
this
3. procedure
- the position: sims, knee-elbow or lithotomy
- wash your hand and wear gloves
4. -use lubricant
49 STAGERS NOTES

5. -seperat the buttock and look for: skine lesion ,pilonisal sinus m fistula ,
anal fissure
- Haemmorrhois , discoloration , discharge .
6. -place the pulp of your finger not the tip on the anal opening , aske the
patient to
7. Tacke breath in and out then press gently into the anal opening
8. -assess the content of the anal canal , then rotate your finger 360 degrees
feel any
9. Irregularity of the wall of the canal

assss the rectal wall in relation to its anterior wall where the
anatomy from bellowUpward is that :

In men:the membranous urthral,prostate,and the base of

the bladder

In women: the vagina and the cervix

The prostate and the cervix should be assessed in the form of size,
shape, consistency And any tenderness

Normally the prostate has smoth surface ,regular surface, rubbery

consistency

Wirh two lobes and smoth median sulcus

10. finally withdrow your finger and look for any discharge ,blood
11. tthank the patien
51 STAGERS NOTES

Q/what are the abnormality in the shape of the umbilicus ?

deep : obesity

Everted: Everted (chronic f in intra-abdominal pr.) = umbilical

hernia.

Nodule : sister Joseph.

Q/what are the causes of discharge from the umbilicus?

A/ pus: from pilonidal sinus. Or ompohlitis

Urine: frorn patent urachus.

Stool: from patent vetello-intestinal duct.

Q/what are the causes of the stria in the

abdominal wall?
A/ Ascites, pregnancy, obesity, Cushing

Q/how can you differentiate between Gaput medusa and IVC

obstruction ?
A/ Gaput medusa: 1-By milking: Direction of blood Away from the umbilicus

2- Site Around the umbilicus

IVC obstruction: 1- By milking: Direction of blood From below upwards

2- site : Mainlv at flanks

51 STAGERS NOTES

Q/ what are the differences between gardening and rigidity?

Risiditv Guardinq
Definition Reflex spasm of abdominal Voluntary contraction of
muscles abdominal muscles on
attempting to palpate over a
tender area

During Does not disappear Disappear

exoiration
Site Accordino to the cause Usuallv bilateral

Q/how to do Murphy's sign?

Ask the patient to take deep breath while exerting pressure on
surface anatomy of gall G.B (junction between Rt. Costal margin
& linea semilunaris) ) sudden catch in breath with a gasp.

Q/What is the etiology of gynaecomastia in liver cell

failure?
Defective metabolism of estrogen by the Liver & decrease the activation of
testosterone.

Q/ What is the etiology of bleeding tendency in liver cell failure?

1. Defective synthesis of prothrombin by the liver
2-. Diminished factor V / Vii/ X
3. Thrombocytopenia due to hypersplenism
4. Thromboasthenia due to coating of platelets by abnormal globulins formed by
RES

Q/ What is hepatic encephalopathy?

-lt is a chronic fluctuating neuropsychiatric disorder.
- lt occurs when Toxic products as (Ammonia,aminobutyric acid, methionine
and mercapan) which are normally detoxified by the Liver; bypasses the Liver
to the systemic circulation in large amounts and hence can reach the brain and
can affect it.
This can occurs by;
52 STAGERS NOTES

Liver decompensation and collaterals

surgically created portosystemc shunt operation

Q/ ddx of acute upper abdominal pain ?

Oesphagitis

Boerhaave's syndrorne
Perforated peptic ulcer
Acute cholecystitis
gall stone and biliary colic

Acute pancreaticis

Q/what are the causes of colicky abdominal pain?

Contraction of the smoth muscle in hallow organs Ex:

1. ureter
2. Gallbladder
3. Fallbian tube
4. Intestine
5. Biliary system

Q/ defferntila diagnosis of abdominal pain in DM?

DKA

Mesenteric infarctiom

Vague

Other causes

Q/ What are the regions of the abdomen ?

1. Two vertical lines are drawn from midinguinal point
towards mid clavicular line.
2. Two horizontal lines are drawn
– Transpyloric plane: Midway between xiphisternum and umbilicus—lower border of
53 STAGERS NOTES

L1 vertebra.
– Transtubercular plane: Connecting the tubercles of iliac crest on each side—upper
border of L5 vertebra.

Nine Regions
1. Right hypochondrium
2. Epigastrium
3. Left hypochondrium
4. Umbilical
5. Right lumbar
6. Left lumbar
7. Right iliac fossa

8.Hypogastrium
9. Left iliac fossa

Q/What are the different abdominal

incisions?

1. Midline incision:
• Upper (above the umbilicus).
• Lower (below the umbilicus).
• Mid-midline (midline incision centreing the umbilicus).
54 STAGERS NOTES

Indicated in:

 emergency exploratory laparotomy

 gastric operations
 colonic resection
 abdominoperineal resection

2. Paramedian incision:

• Right paramedian incision— Vertical incision 2.5 cm to the right of midline.

Indicated in:
 gall bladder
 surgery, right hemicolectomy.

• Left paramedian incision—Same incision to the left of midline.

Indicated in:

 Gastric operations
 left hemicolectomy
 splenectomy.

3. Mayo Robson’s incision: Right upper paramedian incision extended like a

hockey stick to the midline.
Indicated in cholecystectomy.

4. Subcostal incision:

• Right subcostal incision (Kocher's subcostal incision)—Oblique incision 2 cm

below and parallel to the right costal margin, extending from midline to
beyond the tip of the costal cartilage.
Indicated in:

 Cholecystectomy
55 STAGERS NOTES

 CBD exploration
 biliary enteric bypass.

• Left subcostal incision—Same incision on the left subcostal region.

Indicated for
splenectomy.
• Roof top or chevron incision—Bilateral subcostal incision joined in the
midline. Indicated for :
 pancreatic surgery—Whipples’ operation
 pancreaticojejunostomy
 liver resection.

5. Transverse incision:
• Upper abdominal transverse incision. Indicated for:

 gallbladder surgery
 gastric operations.

• Infraumbilical transverse incision. Indicated for exploratory

laparotomy in children.
• Suprapubic transverse incision (Pfannensteil incision).
Indicated in :
 pelvic operations
 prostatectomy.

6. McBurneys’ gridiron incision: Indicated for appendicectomy.

7. Lanzs’ incision: Used for appendicectomy.
8. Inguinal incision: Incision at the inguinal canal running parallel to the
inguinal ligament. Used for hernia operations.

9. Loin incision or lumbar incision:

Incision from the lateral border of erector spinae downward and forward midway
56 STAGERS NOTES

between the 12th rib and the iliac crest upto the lateral border of rectus
abdominis. Used for operations in kidney.

10. Mercedez Benz incision: Bilateral subcostal incision with vertical incision
extending from
center of the ∧-shaped cut to the xiphoid process

Q/When normal liver is palpable?

In infants below 3 years of age liver may be palpable 2–3 fingers breadth below the
right costal
margin.
In healthy thin adult liver may be palpable just below the costal margin.

Hyperinflated lung

Interposition of loop of largeintistine

Q/What are the important causes of palpable gallbladder?

- Acute cholecystitis
- Mucocele
- Empyema
- Carcinoma gallbladder
- Carcinoma of head of pancreas (Courvoisier’s law)

Q/How will you elicit Murphy’s sign?

In Moynihan’s method for elicitation of Murphy’s sign, the patient lies supine. Place
the left hand on the right costal margin so that the thumb lies over the region of
the fundus of gallbladder(area just lateral to the junction of the
lateral border of right rectus abdominis and the tip of the right
9th costal cartilage). Exert moderate pressure with the thumb
and ask the patient to take deep breaths.
At the height of inspiration when the inflamed gallbladder
impinges on the thumb there will be a catch in breath and
patient will wince with pain. The Murphy’s sign is said to be
57 STAGERS NOTES

positive
This sign may also be elicited with the patient in sitting position keeping hand in
the right costal margin as described above .
This is found in acute cholecystitis. Not found in chronic cholecystitis or
uncomplicated gallstone disease.

Q/When an abdominal mass is palpable how to decide that the lump is

parietal or intra-abdominal?

This can be done by head rising or leg rising test (Carnett’s test).
Ask the patient to keep his hands over his chest and ask him to lift his head and
shoulder
off the pillow. If the swelling disappears or becomes less prominent then the
swelling is intraabdominal. If the swelling becomes more prominent or remains the
same then the swelling is parietal. For lower abdominal swelling this can be
ascertained by leg rising test. Patient lies supine and is asked to lift both the legs
from the bed. The interpretation is same as for head rising test

Q/What are the consequences of gastric outlet obstruction?

- Anatomical effect: because of obstruction there is hyperperistalsis of the stomach
leading to hypertrophy of the musculature of the stomach and later on there is
huge dilatation of the stomach.
- Metabolic effect: because of vomiting there is chronic dehydration, prerenal
azotemia and there is loss of H+, Cl– and K+ ion leading to hypochloremic,
hypokalemic metabolic alkalosis.
- In early stage: Loss of H+ and Cl– ion leading to
hypochloremic alkalosis. Sodium may be normal
and hypokalemia may not be obvious.
Kidney tries to compensate metabolic alkalosis by
excreting low chloride and more
bicarbonate. While excreting bicarbonate sodium is
also lost in urine.
- If vomiting continues patient becomes more
58 STAGERS NOTES

dehydrated and hyponatremia develops.

- To conserve circulatory volume kidney reabsorbs water and sodium due to
aldosterone effect.
Sodium is retained by the distal renal tubule in exchange of H+, K+ ions. To
conserve Na+ ions H+ and K+ ions are excreted in urine.
- At this late stage of metabolic alkalosis, the kidney passes acidic urine due to
passage of H+ ion in urine in exchange of sodium ion. This is called paradoxical
aciduria as on the background of metabolic alkalosis kidney should have excreted
alkaline urine.

Q/ causes of abdominal pain according to the regions ?

A. Epigastric
Peptic ulcer
Pancreatitis
Reflux oesophagitis
Acute gastritis
Malignancy: gastric, pancreatic
Pain from adjacent areas: See RUQ, central abdominal pain,
cardiac/pulmonary/pleural
pathology, e.g. MI, pericarditis, pneumonia
Functional disorders: non-ulcer dyspepsia, irritable bowel syndrome
B. Right upper quadrant (RUQ)
Gall bladder pathology: cholecystitis (usually related to gallstones,
occasionally may be
acalculous), biliary colic, cholangitis
Liver pathology: hepatitis, hepatomegaly (congestive, e.g. in congestive
cardiac failure,
Budd–Chiari syndrome), hepatic tumours, hepatic/subphrenic abscess
Pain from adjacent areas: See Epigastric (e.g. pancreatitis, peptic ulcer), RIF,
Loin pain,
pulmonary/pleural pathology, e.g. pneumonia, empyema, pulmonary
infarction
59 STAGERS NOTES

Appendicitis, e.g. in a pregnant woman

Colonic cancer (hepatic flexure)
Herpes zoster
Fitz–Hugh–Curtis syndromerare (rare complication of pelvic inflammatory
disease)
C. Right iliac fossa (RIF)
Gastrointestinal: appendicitis, mesenteric adenitis (Yersinia, in children),
’Meckel’s diverticulum (in children), inflammatory bowel disease, colonic
cancer, constipation, irritable
bowel syndrome
Reproductive: Females: Mittelschmerz (ovulation), ovarian cyst
tortion/rupture/haemorrhage, ectopic pregnancy, salpingitis/pelvic
inflammatory disease, endometriosis. Males:
seminal vesiculitis, cancer in undescended testis
Renal: UTI, ureteric colic (renal stones)
Pain from adjacent areas: See RUQ, suprapubic, central abdominal pain, groin
pain, hip
pathology, psoas abscess, rectus sheath haematoma, right-sided lobar
pneumonia
D. Suprapubic
Urinary retention
Cystitis
Pain from adjacent areas: See RIF, LIF
E. Left iliac fossa (LIF)
Gastrointestinal: diverticulitis, inflammatory bowel disease, colonic cancer,
constipation,
irritable bowel syndrome
Reproductive: See RIF
Renal pain: See RIF
Pain from adjacent areas: See LUQ, suprapubic, central abdominal, hip
pathology, psoas abscess, rectus sheath haematoma, left-sided lobar
pneumonia
61 STAGERS NOTES

F. Left upper quadrant (LUQ)

Splenic rupture, splenic infarction (e.g. sickle cell disease), splenomegaly
Subphrenic abscess
Pain from adjacent areas: See epigastric (e.g. pancreatitis, peptic ulcer), LIF,
loin pain, cardiac/
pulmonary/pleural pathology, e.g. MI, pericarditis, pneumonia, empyema,
pulmonary
infarction
Colonic cancer (splenic flexure)
Herpes zoster
G. Central abdominal (periumbilical)
Gastrointestinal: intestinal obstruction, early appendicitis, gastroenteritis
Vascular: abdominal aortic aneurysm (leaking, ruptured), mesenteric
ischaemia (thrombosis, embolism, vasculitis, e.g. polyarteritis nodosa)
Medical causes, e.g. diabetic ketoacidosis, uraemia
Pain from adjacent areas, e.g. epigastric, iliac fossae
H. Loin pain
Infection: UTI (pyelonephritis), perinephric abscess/pyonephrosis
Obstruction e.g. renal stones (See Urinary tract obstruction)
Renal disease: Tubulointerstitial nephritis, IgA nephropathy, renal vein
thrombosis, renal
carcinoma, polycystic kidney disease
Haemorrhagic adrenal infarction
Aortic dissection (type B)
Pain from vertebral column
I. Groin pain
Renal stones (pain radiating from loin to groin)
Testicular pain, e.g. torsion, epididymo-orchitis (pain radiating from scrotum
to groin)
Hernia (inguinal)
Hip pathology
Pelvic fractures
61 STAGERS NOTES

J. Diffuse abdominal pain

Gastroenteritis
Peritonitis
Intestinal obstruction
Inflammatory bowel disease
Mesenteric ischaemia
Medical causes e.g. diabetic ketoacidosis (see Medical causes)
Irritable bowel syndrome

Q/causes of abdominal distension

1. Fat (obesity)
2. Fluid (ascites, fluid in the obstructed intestine)
3. Flatus (intestinal obstruction), perforated viscus
4. Faeces
5. Fetus
6. Giant organomegaly (e.g. an ovarian cystadenoma, lymphoma)

Other Qs:

Q/ what are the causes of upper GIT bleeding

How can you investigate it
What are the causes of lower git bleeding
Wht are the causes of abdominal destention
What are the causes of hepatomegaly
What are the causes of spleeenomegally
What are the causes of massive solenomegally
What are the causes of enlarge kidney
Whata re the causes of abdominal masses according to ther regions
What are the causes of abdominal pain according to the regions
62 STAGERS NOTES

What do you know about sister josef nodules

What do you know about culline and gry turner sign
How can you detect the renal angle
63 STAGERS NOTES

Hernia
Q/ what is hernia?
A hernia is a protrusion of a viscus or part of a viscus
through an
abnormal opening in the walls of its containing cavity.

Q/ what are the risk fctors of hernia ?

1. Coughing
2. Straining
3. Obesity
4. Intra-abdominal malignancy

Q/ What are the anatomical classicfcation of the hernia?

64 STAGERS NOTES

Q/ what are the composition of hernia ?

1. The sac
The sac is a diverticulum of peritoneum,
consisting of mouth, neck, body and fundus.
The diameter of the neck is important because
strangulation of bowel is a likely complication
when the neck is narrow, as in femoral and
paraumbilical hernias.
2. The covering
Coverings are derived from the layers of the
abdominal wall through which the sac passes.
3. Contents: These can be:
• omentum = omentocele (synonym: epiplocele);
• intestine = enterocele; more commonly small bowel but may be large
intestine or appendix;
• a portion of the circumference of the intestine = Richter’s hernia;
• a portion of the bladder (or a diverticulum) may constitute part of or
be the sole content of a direct inguinal, a sliding inguinal or a femoral
hernia;
• ovary with or without the corresponding fallopian tube;
• a Meckel’s diverticulum = a Littre’s hernia;
• fluid, as part of ascites or as a residuum thereof.

Q/ what are the surgical classification of the hernia?

1. Reducible – contents can be returned to abdomen
 The intestine : usually gurgles on reduction and the first
portion is more difficult to reduce than the last.
 The Omentum : in contrast, is described as doughy and the
last portion is more difficult to reduce than the first

2. Irreducible – contents cannot be returned but there are no

other complications, It is usually due to adhesions between the sac and
65 STAGERS NOTES

its contents or overcrowding within the sac.

3. Obstructed – bowel in the hernia has good blood supply

but bowel is obstructed, he symptoms (colicky abdominal
pain and tenderness over the hernia site) are less severe and the
onset more gradual than in strangulated hernias
4. Strangulated – blood supply of bowel is obstructed
Gangrene may occur as early as 5–6 hours after the onset of the
first symptoms. Although inguinal hernia may be 10 times more
common than femoral hernia, a femoral hernia is more likely to
strangulate because of the narrowness of the neck and its rigid
surrounds
5. Inflamed – contents of sac have become inflamed e.g. acute
appendicitis or salpingitis ,The hernia is usually tender but not tense
and the overlying skin red and oedematous. Treatment is based on
treatment of the underlying cause.
6. Other types:
Incarcerated hernia: it is considered that the lumen of that portion of
the colon occupying a hernial sac is blocked with faeces.it can be
indented

Q/What are the defrences between direct and indirect inguinal hernia?
66 STAGERS NOTES

Q/ how to know that the hernia becomes strangulated?

Present with local then sever general abdominal pain of sudden onset and
vomiting, the patient generally unwell

Q/ what are the surgical anatomy of the inguinal hernia?

The superficial inguinal ring is a triangular aperture in the aponeurosis of the

external oblique muscle and lies 1.25 cm above the pubic tubercle.
The deep inguinal ring is a U-shaped condensation of the transversalis fascia and
it lies 1.25 cm above the inguinal (Poupart’s) ligament, midway between the
symphysis pubis and the anterior superior iliac spine

The inguinal canal

In infants, the superficial and deep inguinal rings are almost superimposed and the
obliquity of the canal is slight. In adults, the inguinal canal, which is about 3.75 cm
67 STAGERS NOTES

long, is directed downwards and medially from the deep to the superficial inguinal
ring.
An indirect hernia travels down the canal on the outer(lateral and anterior) side of
the spermatic cord. A direct hernia comes out directly forwards through the
posterior wall of the inguinal canal.
Inguinal canal
Boundaries:

anterior wall : skin , superficial fascia , external oblique [ for whole length] , internal
oblique for lateral 1/3.

posterior wall : transversalis fascia [ for whole length] , conjoint tendon & pectineal
ligament [ Cooperʾs ] medially

floor : inguinal [Poupartʾs] ligament.

roof : arching fibers of internal oblique & transversus abdominis which fuse to form
the conjoint tendon on the posteromedial aspect of the canal.

The deep ring is a hole in the transversalis fascia & lies a finger breadth above the
mid inguinal ligament [ half way between the anterior superior iliac spine & pubic
tubercle .

The superficial ring lies above & medial to the pubic tubercle , while a femoral
hernia lies below & lateral to the pubic tubercle.

Content of the spermatic cord

Apply the rule of 3

- 3 constituents :- vas deferens [ the round ligament is the female equivalent] ,

lymphatics & obliterated processus vaginalis.

- 3 nerves :- genital branch of the genitofemoral nerve [ motor to cremaster with

sensory to cord] , ilioinguinal nerve [ within the inguinal canal but outside the
spermatic cord] , autonomics .
68 STAGERS NOTES

- 3 arteries :- testicular artery , artery to the vas [ from superior or inferior vesical
artery ] , cremasteric artery [ from the inferior epigastric artery] .

- 3 veins :- pumpiniform piexus , vein from vas , cremasteric vein

- 3 fascial covering :- external spermatic fascia [ derived from external oblique] ,

crematseric muscle & fascia [ derived from internal oblique & transversus
abdominis ] , internal spermatic fascia [derived fromtrasversalis fascia].

Q/ What are the cause of inguinal hernia after appendicectomy?

injury to the ileoinguinal nerve ( supplying the conjoint tendon)

Q/ what are the types of indirect inguinal hernia?

1 Bubonocele. The hernia is limited to the inguinal canal.
2 Funicular. The processus vaginalis is closed just above the epididymis. The
contents of the sac can be felt separately from the testis, which lies below the
hernia.
3 Complete (synonym: scrotal). A complete inguinal hernia is rarely present at
birth but is commonly encountered in infancy. It also occurs in adolescence or in
adulthood. The testis appears to lie within the lower part of the hernia.

Q/ what are the DDx of inguinal hernia?

In males the differential diagnosis includes the following:

1. vaginal hydrocele
2. encysted hydrocele of the cord;
3. spermatocele;
4. femoral hernia;
5. incompletely descended testis in the inguinal canal
– an
inguinal hernia is often associated with this
condition;
6. lipoma of the cord – this is often a difficult but
unimportant
69 STAGERS NOTES

diagnosis and it is usually not settled until the parts are displayed by
operation.

Differential diagnosis in the female

1. • hydrocele of the canal of Nuck – this is the most common differential

diagnostic problem;
2. • femoral hernia.

Q/ what is taxis? What are its complications?

 Defention: it is manual reduction of complicated hernia.
 ls done by flexion, internal rotation of the thigh to relax the external
oblique.
 sedation ex: bezodiazpens
 Cold compresses
 Trial of reduction after 30 min
 it is more useful in children with early
strangulation.

Complications:

• contusion or rupture of the intestinal wall

 reduction-en-masse: ‘The sac together with its contents is pushed forcibly
back into the abdomen; as the bowel will still be strangulated by the neck of
the sac, the symptoms are in no way relieved
 reduction into the a loculus of the sac
 the sac may rupture at its neck and the contents are reduced,
not into the peritoneal cavity but extraperitoneally
71 STAGERS NOTES

Q/ what are the boundaries of femoral ring?

• anteriorly by the inguinal ligament;
• posteriorly by Astley Cooper’s (iliopectineal)
ligament, the pubic bone and the fascia over the
pectineus muscle;
• medially by the concave knife-like edge of
Gimbernat’s (lacunar) ligament, which is also
prolonged along the iliopectineal line, as Astley
Cooper’s ligament;
• laterally by a thin septum separating it from the femoral vein.

Q/ what are the differential diagnosis of femoral hernia.

1. Inguinal hernia.
2. Lipoma.
3. Saphena varix. Fluid thrill, venous hum, other of varicose vein.
4. Enlarged lymph node.
5. Psoas abscess.
6. Femoral artery aneurysm.
7. Distended psoas bursa.
8. Hydrocele of the femoral sac.

Q/ what do you know about Hasselbachʾs triangle?

A/ Its weak area in the anterior abdominal wall since it is not reinforced by the
conjoint tendon . It is responsible
for causing direct inguinal hernia.

Itʾs boundaries are :-

- medial half of the inguinal

ligament

- linea semilunaris [lateral border

of rectus abdominis]

- inferior epigastric artery

71 STAGERS NOTES

Q/ What are the content of spermatic cord?

Rule of 3

1. 3 covering:
 External spermatic fascia
 Internal spermatic fascia
 Cremastric fascia
2. 3 vessels
 Vas deference
 Testicular artery
 Testicular vein
3. 3 structures
 Lymph vessels
 Autonomic nerves
 Processes vaginalis

Q/What are the differential diagnosis of groin lump?

1) Skin: sebaceous cyst.
2) Subcutaneous tissue: lipoma, fibroma.
3) Lymphatic: inguinal lymphadenopathy.
4) Vein: saphena varix.
5) Nerve: neuroma, neurofibroma.
6) Artery: femoral artery aneurysm.
7) Spermatic cord: lipoma, encysted hydrocele.
8) Bowel: inguinal or femoral hernia.
9) Testis: undescended testis.
10) Psoas abscess, psoas bursae and rupture adductor longus muscle.
11) Muscle: benign and malignant tumours.

Q/ what are the complications of Inguinal Hemiorrhaphy?

1. Post-herniorrhaphy groin pain: usually as a consequence of :
scarring reaction to prosthetic material
incorporation of a nerve in staples or suture material during the repair
Treatment:
72 STAGERS NOTES

 Ruled out recurrent hernia.

 Reassurance and conservative treatment (e.g. NSAID and local nerve
blocks)
 Immediate reexploration: only indicated in severe pain immediately after
operation, (i.e., in the recovery room).
2. Ischemic orchitis & testicular atrophy: (if the testicular blood supply is
compromised during herniorrhaphy).
3. Hemorrhage: from the cremasteric artery, the internal spermatic artery
4. Osteitis pubis
5. Prosthetic related complications: Erosion of mesh can result in intestinal
obstruction or fistulization
6. Infection: Usually due to prostheses used for inguinal herniorrhaphies, they
can occasionally be successfully treated with drainage and prolonged
antibiotic therapy; more often, however, the prosthesis must be removed

When the case is inguinal hernia and you asked why this not
femoral hernia ?
It is inguinal because
1) The hernia is above inguinal ligament,
2) The neck of the hernia is above & medial to pubic tubercle and
3) Because the hernia descends into the scrotum (if so).

Q. How to reach pubic tubercle?

1. By asking the patient to put the thigh in
flexion ,adduction and. internal
rotation against resistance. And following
the tendon of the adductor longus muscle
(the most medial, muscle) the first bony
prominence that meet your finger is the
pubic tubercle.
2. By following the inguinal ligament to its
insertion
73 STAGERS NOTES

Q/Wheres the defect in direct and indirect inguinal hernia ?

 indirect inguinal hernia the defect is the incernal ring.
 diect inguinal hernia the defect is the posterior wall of the inguinal canal
(Hasselbachs triangle)

Q/how to know that this hernia contains bowel?

 soft in consistency Up to 4 years the external
 Reducibility first difficult then easy, and internal inguinal rings
are axactly lies opposet
 auscultation reveals bowel sound
others
 gurgle during reduction

Q/ how do you know that this hernia contains omentum ?

 No gurgle
 Doughy in consistency.
 Reducibility first easy then. difficult.

Q/ what is the organ than didn't herniate through the abdominal wall ?
 A/ any organ can be herniate through the abdominal wall except the pancreas
because its retroperitoneal organ

Q/ What is Richter's hernia

 the content of the hernia is part of the circumference of
an intestinal loop.

Q/ What is Maydl's hernia?

 lt is the W shaped hernia., its importance is: if this hernia is
strangulated, the gangrenous loop might not be within the
sac, it may be within the abdomen
74 STAGERS NOTES

Q/What is pantaloon hernia?

 It is a combination of indirect and direct inguinal
hernias

Q/ What is a sliding hernia?

 It's a hernia in which a viscous (usually an extra
peritoneal structure) "slides" to form part of the wall of
the hernial sac. The commonest sliding structure on
both sides is the urinary bladdet.
The caecum can descend on the right side, sigmoid
colon can descend on the
left side.

Q/What is Littre’s hernia?

Hernial sac containing Meckel’s diverticulum as the content is
called Littre’s hernia.

Q/ What is herniotomy ? heniorhaphy and hernioplasty

 Herniotomy: Excision of the hernial sac
 Herniorrhaphy: Excision of the hernial sac + repair of the defect using the
Local tissues
 Hernioplasty: Excision of the hernial sac and repair of the defect using tissues
other than the local ones or synthetic graft.

Q/ What are the indications of hernioplasty?

1. Recurrent hernias
2. Wide defects
3. Weak muscles as in old age
75 STAGERS NOTES

Q/ if the patient has bilateral inguinal hernias ,how would you

proceed? And which side to operat first?
 we will repair one side only and then the other side after 6 months. This is
to
avoid over stretching the abdominal muscles if both sides were repaired in
the same time.
 We usually started by:

a. The bigger hernia.

b. That with narrower neck.
c. The more painful side.

Q/ What are the causes of recurrence of hernia?.

1-preoperative condition: chronic straining (asthmatic bronchitis, prostatic
enlargement . . . etc.), debility, obesity
2-. intra-operative causes: improper hemostasis, tense repair, lax repair, repair
with absorbable suture material
3. Postoperative causes: hematoma, infection

Q/ define the internal hernia with examples?

Herniacion of intestine through peritoneal fossae or defect in the
messentry.examples are:

 All diaphragmatic hernias

 Hernia through foramen of Winslow
 Retrocecal hernia through rettoceca| tecess.
 Paraduodenal hernia (through peritoneal fossae near
the duodenum
 Detect in (transverse mesocolon , meserntry of small intestine or broad
ligament of the uterus)
76 STAGERS NOTES

Q/ what are the surgical option for patient with inguinal hernia ?
Herniotomy
Herniorrhaphy
Hernioplasty

Q/Why do you say this is an enterocele?

By definition, enterocele is one which contains intestine.
From history, patient says that while he lies down the hernial content reduces with a
gurgling
sound.
-On inspection there is visible peristalsis over the swelling.
- On palpation the swelling is soft and elastic in feel. While attempting reduction,
the first part
was difficult to reduce, but the last part reduces easily with a gurgling sound.
- On percussion the swelling is resonant
- On auscultation bowel sounds are audible over the swelling.
So this is an enterocele.

Q/How will you differentiate inguinal and femoral

hernia?
* Relation with pubic tubercle: Inguinal hernia lies above and
medial and the femoral hernia lies below and lateral to the
pubic tubercle

Q/How will you differentiate direct and indirect inguinal hernia?

-Direct hernia comes out through the Hesselbach’s triangle, whereas the indirect
inguinal hernia comes out through the deep inguinal ring
-Direct hernia is more commonly incomplete whereas indirect hernias are
commonly complete
- Direct herniae are commonly bilateral whereas indirect herniae are commonly
77 STAGERS NOTES

unilateral
- On cough the direct hernia appears as a direct forward bulge, whereas the indirect
hernia comes out downward and forward
- On invagination test, the palpating finger goes directly backward in direct hernia,
whereas in indirect hernia the finger goes upward and backward. The cough
impulse will touch the tip or dorsum of the finger in indirect hernia and pulp of the
finger in direct hernia
- Deep ring occulsion test is positive in indirect inguinal hernia

Q/What are the important complications of herniorrhaphy/hernioplasty?

General complications:
1- Pulmonary: Atelactasis, pneumonia and pulmonary embolism.
2- Cardiac: Particularly in patient with overt cardiac diseases.
3- Urinary retention: Usually caused by overzealous fluid administration leading to
diuresis and atony of the overfilled bladder.

Local complications:
1-Hemorrhage
2-Urinary bladder or bowel injury during dissection and ligation of the sac
3-Injury to testicular vessels during dissection, leading to:
• Testicular swelling
• Testicular atrophy
4-Closing the superficial inguinal ring tightly may cause testicular swelling and
subsequent atrophy

5- Injury to vas deferens

6- Injury to nerve like iliohypogastric, ilioinguinal and genital branch of
genitofemoral nerve
7- Wound infection
8- Recurrence of hernia
9- Hydrocele or lymphocele
10-Edema of the penis due to injury to superficial external pudendal vein.
78 STAGERS NOTES

Q/ What would you tell patients about their recovery from inguinal
hernia repair?'

1. Early mobilization is important

2. They should keep the area clean and wash carefully, especially after the
clips/sutures have been removed
3. They are able to bathe immediately
4. They may need to be off work for 6 weeks if their job involves heavy lifting
5. They should avoid prolonged coughing(control chronic obstructive
pulmonary disease preoperatively)
6. They should take laxatives if they get constipated postoperatively.

Q/What are the complications of hernia?

Untreated the hernias may lead to a number of complications.These includes:
-Irreducible hernia
-Obstructed hernia
- Incarcerated hernia
-Strangulated hernia
- Inflamed hernia due to inflammation of the contents of hernia
- Hydrocoele of the hernial sac.

Q/What do you mean by obstructed hernia?

Hernia containing intestine may lead to acute intestinal
obstruction due to obstruction of the lumen of the gut
inside the hernia.
In addition to irreducibility patient complains of colicky
pain initially over the hernia and later on colicky abdominal
pain. The hernia becomes tense and tender and there may be visible peristalsis over
the hernia. Unrelieved the patient may present with cardinal features of acute
intestinal obstruction—pain abdomen, vomiting, abdominal distension and absolute
constipation.
Unrelieved the obstruction may lead to impairment of blood supply to the gut
79 STAGERS NOTES

causing strangulation of the hernial contents.

Q/What are the characteristics of strangulated hernia?

Due to impairment of blood supply there is ischaemic necrosis of the hernial
contents.
The hernial swelling becomes irreducible, no cough impulse, tense, tender and
there may be rebound tenderness.
In strangulated omentocoele the symptoms and signs may be mild and if not
relieved ischemic necrosis of omentum may lead to bacterial invasion leading to a
localised abscess.
In strangulated enterocoele symptoms and signs are more severe with features of
acute intestinal obstruction and if not treated patient condition will deteriorate
rapidly. The ischemic gut may perorate leading to initially localised and then
generalised peritonitis and septicemia.

Q/What do you mean by inflamed hernia?

When the contents of the hernial sac get inflamed, this is known as inflamed hernia.
Patient complains of pain over the swelling and may be febrile. The hernia may
become irreducible, there may be localised tenderness over the hernia.

Q/What do you mean by incarcerated hernia?

This is a type of obstructed hernia where the lumen of the colon is blocked with
faecal matter.
The hernial contents may be indented with the finger.
The term incarcerated hernia is often used as an alternative to obstructed or
strangulated hernia.

Q/What are the important causes for development of incisional hernias?

Many factors singly or in combination are responsible for development of incisional
hernia.
1. Poor surgical technique:
a. Non-anatomic incision:
81 STAGERS NOTES

b. Method of closure.
c. Inappropriate suture material:

d. Suturing technique:

e. Drainage tube

2. Preoperative straining factors: Chronic cough,

chronic constipation and urinary obstruction.
3. Postoperative complications: Abdominal
distension, cough, respiratory distress due to pneumonia or lung collapse, and
postoperative wound infection.
4. General factors: Age (elderly patients), malnutrition, hypoproteinemia, jaundice,
malignancy, diabetes, chronic renal failure, steroid or immunosuppressive therapy
and alcoholism.
5. Tissue failure: Late development of hernia after 5, 10 or more years after
operation is usually associated with tissue failure. Abnormal collagen production
and maintenance has been shown to be associated with increased incidence of
incisional hernia.

Q/How will you manage patient with incisional hernia ?

1. The patient has incisional hernia through lower midline incision. Patient does
not have any medical disease and there are no straining factors, I will prepare
this patient for surgery
2. Associated cardiovascular disease, if any or hypertension needs to be treated
3. Associated respiratory disease, if any, needs treatment
4. If diabetic, needs good control before surgery
5. If obese, weight reduction before surgery is helpful
6. Intertrigo or any infected skin lesion overlying the hernia needs attention
7. Investigation for any intra-abdominal pathology—USG / Upper GI endoscopy.
81 STAGERS NOTES

jaundice

Q/Define jaundice ?
It is yellowish discoloration of the skin, sclera & mucous
membrane resulting from increase bilirubin
concentration in the body fluids

Q/At which level it detect clinically ?

 it is detected clinically when the plasma bilirubin more than 3mg/dl.

Q/What are the casue of yellowish discoloration of the skin with normal
color sclera ?
Carotenaemia

Q/Where you can examine the jaundice ?

 sclera below the upper eye lid ear lobule, nasal tip, nail bed, lip, hard palate,
under surface of the tongue, tympanic membrane & the skin.

The sclera color remains about 3 months after normalize the level of bilirubin in
the blood because bilirubin has more affinity to elastic tissues, blood vessels &
nervous tissues

Q / Prepare this patient with obstructive jaundice to surgery …

1. History
2. Physical examination
3. Investigations
 CBC
 Liver function
 Renal function
 Coagulation profile
82 STAGERS NOTES

 Virology screen
 CXR
4. Treat any infection with antibiotic
5. Vit. K before 3 days before the operation or FFP if emergent
6. Rehydration and give MANITOL to this patient …

Q/Why does you give vit, K to those patient ?

 Vit . k is fat soluble vitamin required bile for its metabolism , this patient has
obstructive jaundice so no metabolism for vit k which case coagulopathy
(dangerous in operation )

Q/What are the other fat soluble vitamins ?

 AKED

Q/Why does you give manitol to this patient ?

To avoid hepato-renal syndrome

Q/What is the hepato - renal syndrome

Hepatorenal syndrome is a condition in which there is progressive kidney failure. It

occurs in a person with chronic liver disease. It is a serious complication that can
lead to death.

Hepatorenal syndrome occurs when the kidneys stop working well in people with
serious liver problems. Less urine is removed from the body, so waste products that
contain nitrogen build up in the bloodstream (azotemia).

Q/What do you mean by liver function test ?

7. Enzymes that reflect liver cell damage
 They include aspartate aminotransferase (AST) present in the liver , the
skeletal muscle, cardiac muscle, RBC and other organs
 alanine aminotransferase (ALT). ALT is specific to the Liver.

8. Enzymes that reflect cholestasis

 5-nucleotidase
 gamma-glutamyl transferase (GGT)
83 STAGERS NOTES

 alkaline phosphatase.
9. Excretory Function
 Bilirubin

10. Biosynthetic Function

 Serum albumin:
 Has long half-life(18—20) days and ~4% degraded per day. Because of
this slow turn over, the serum albumin is not a good indicator of
acute or mild hepatic dysfunction.In hepatitis ,serum albumin level <
3 g/dl should raise the possibility of chronic liver disease, and in liver
disease it may be useful as aprognostic factor.
 Coagulation factors
 With the exception of factor VIII, the blood clotting factors are made
exclusively in hepatocytes. Their serum half lives are much shorter
than albumin ranging from 6 h for factor VII to 5 days for fibrinogen.
Because of their rapid turnover, measurement of the clotting factors is
the single best acute measure of hepatic synthetic function and
helpful in both the diagnosis and assessing the prognosis of acute
parenchymal liver disease. Useful for this purpose is the prothrombine
time which measures factors II, V, VII, X.

Q/wha are the fucntios of the liver ?

— Metabolism – Carbohydrate, Fat & Protein

— Secretory – bile, Bile acids, salts & pigments

— Excretory – Bilirubin, drugs, toxins

— Synthesis – Albumin, coagulation factors

— Storage – Vitamins, carbohydrates etc.

— Detoxification – toxins, ammonia, etc.

84 STAGERS NOTES

Q/Which is more specific for liver cell damage ALT or AST ?

ALT

Q/ What are the characteristic features of malignant obstructive

jaundice. differentiating it from calcular obstructive jaundice?

1. History
 - Age: Usually old
 - Sex: more in males
 - Onset :Gradual
 - Course :Steadily progressive
 - Duration :Not more than 2 years
 - Pain :My be present epigastric pain radiating to the back
 - Pruritus Severe
 - Past history negative

2. General examination
 - Depth of jaundice: Deep olive green.
- Weight loss: Progressive
- Lower limb edema a: May be due to:
o o LVC obstruction
o Lowq Limb Phlebothrombosis
o Trousseau's sign
3. Abdominal Examination
- Liver May be nodular
- Palpable gallbladder Common
- ascites only in metastases

Q/ What is the value of plain X-ray in obstructive

jaundice

it may show radiopaque gallstones calcification of the

gallbladder.
85 STAGERS NOTES

Q/Causes of enlarged tender liver

1. Viral hepatitis.
2. Amoebic hepatitis.
3. Hepatoma.
4. Congested liver (CHF).

Q/what are the features of obstructive jaundice?

Patient complains of gradually progressive increase in yellowish discoloration of
eyes and urine.
Patient is having itching all over the body and he is passing clay colored stool since
the onset of jaundice. So, this is a case of obstructive jaundice.
Q/what are the features of obstructive jaundice due to periampullary
carcinoma in this patient?
Patient is elderly and presented with history of painless progressive jaundice for last
6 months. Jaundice is associated with itching all over the body and passage of clay
colored stool. Patient had melena 2 months back which was followed by diminution
in intensity of jaundice. Patient also complains of anorexia and weight loss for last 6
months. Patient also complained of a lump in his right side of upper abdomen for
last 3 months. No history of biliary colic.
On examination, patient is deeply jaundiced, malnourished and abdominal
examination gallbladder is palpable, which is tense cystic in feel and is nontender.
Liver and spleen is not palpable.
So, obstructive jaundice in this patient is likely to be due to periampullary
carcinoma in this patient.

Q/Why spleen palpation is important in patient with obstructive

jaundice?
Associated splenomegaly may suggest associated portal hypertension. Portal
hypertension may be due to extrahepatic portal venous obstruction due to splenic
vein thrombosis or secondary biliary cirrhosis.

Q/What is Courvoisier’s law?

If in a jaundice patient, the gallbladder is palpable, then it is not due to
choledocholithiasis as the gallbladder would have been fibrosed by previous
86 STAGERS NOTES

cholecystitis
Q/Why prothrombin time is prolonged in obstructive jaundice?
In obstructive jaundice there is defect in absorption of fat soluble vitamins like
vitamin A, D, E and K from the gut. Vitamin K is required for synthesis of
prothrombin in the liver. Deficiency of Vitamin K dependent coagulation factors
may cause prolongation of prothrombin time.
Q/What preoperative preparation will you do for this patient?
1. Patient is usually anemic. If Hb level is less than 10 gm%—correction of anemia by
preoperative blood transfusion.
2. because of associated hepatocellular dysfunction glycogen reserve is reduced in
these patients. Glycogen store may be replenished by administration of plenty of
glucose by mouth.
3. Patients with obstructive jaundice usually have chronic dehydration and impaired
renal function. Correct dehydration by oral and intravenous fluid before operation.
Adequate rehydration is indicated by good urinary output.
4. Prothrombin time may be prolonged due to decreased synthesis of prothrombin
consequent to vitamin K deficiency—may be corrected with injection of vitamin K
for 5–7 days before operation.
5. Renal function may be impaired in obstructive jaundice and may be complicated
by postoperative renal failure. One mechanism for postoperative renal failure has
been said to be due to blockage of renal tubules by deposition of bile salts. Gram-
negative septicemia has been said to be the other mechanism for development of
renal failure in patients with obstructive jaundice. Needs treatment with adequate
IV fluid and intravenous turosemide or mannitol to ensure adequate diuresis.
6. There is increased chance of infection in patients with obstructive jaundice and
are prone to develop Gram-negative septicemia. Patient is started on a broad
spectrum antibiotics
like second generation cephalosporin and aminoglycoside combination 1–2 days
before surgery.
7. If patient is malnourished enteral or parenteral nutrition may be given
preoperatively.
8. Evaluation of pulmonary function by chest X-ray and pulmonary function test.
Pulmonary physiotheray is to be started from the preoperative period.
87 STAGERS NOTES

Q/What is Trousseau’s sign of malignancy?

Migratory thrombophlebitis in patients with an underlying
abdomi nal malignancy is known as Trousseau’s sign. This may
be found in pancreatic malignancy and in other gastrointestinal
malignancy.

Q/What is Trousseau’s sign of hypocalcemia ?

Trousseau sign of latent tetany is a medical sign

observed in patients with low calcium. This sign
may be positive before other manifestations of
hypocalcemia such as hyperreflexia and tetany, as
such it is generally believed to be more sensitive
(94%) than the Chvostek sign (29%) for
hypocalcemia.

To elicit the sign, a blood pressure cuff is placed

around the arm and inflated to a pressure greater
than the systolic blood pressure and held in place
for 3 minutes. This will occlude the brachial artery.
In the absence of blood flow, the patient's
hypocalcemia and subsequent neuromuscular
irritability will induce spasm of the muscles of the hand and forearm. The wrist and
metacarpophalangeal joints flex, the DIP and PIP joints extend, and the fingers
adduct.

Q/What is Troisier’s sign?

Left supraclavicular lymph node enlargement due to metastasis
from an intra-abdominal malignancy is known as Troisier’s
sign.

Q/What is Charcot’s triad?

- Intermittent pain.
- Intermittent jaundice.
- Intermittent fever.
This triad of symptoms suggest cholangitis.
88 STAGERS NOTES

Q/ causes of post-operative jaundice ?

89 STAGERS NOTES

Intestinal
Obstruction(IO)

Q/What are the causes of IO ?

Strangulated hernia is a common cause in different age groups.
1- Neonates:

. Congenital atresia, volvulus neonatorum, anorectal malformation, meconium ileus

and Hirschsprung's disease.
2- lnfants:
. lleocecal intussusception, Hirschsprung's disease and
strangulated hernia
(commonest cause).
3- Adults:

 . Post surgical adhesions (commonest cause).

 . Strangulated hernia
4- Elderlv:
 Strangulated hernia
 Cancer colon 'Sigmoid volvolus.
 Diverticular disease.
 Pseudo obstruction.(Ogilvie syndrome)

Q/ Causes of abdominal destention in IO?

1. Gasses
 Swallowed air (68%): Patients with lO may swallow excessive amounts of air
due to acute pain and anxiety.
 Diffusion from congesfed vessels (22%).
91 STAGERS NOTES

 Bacterial formation (10%)

2. Fluid
 GIT secretion 10 L / day

Symtoms of IO

Pain,Distention,Vomiting,Absoluteconstipation

Q/ what are the symptoms of IO?

1.
Pain: (due to hyperactive peristalsis) usually the 1st tsymptom
 Onset:
 in high small lO) within a day
 ln low small lO ) within 2-3 days
 Character: colicky.
 Site:
 ln high small lO : above the umbilicus.
 ln low small lO : around and below the umbilicus.
 ln large lO : lower & peripheral parts of the abdomen.

Painless : if paralytic ileus.

Severe stabbing pain : in case of ischemia

2. Distension:
 Marked in: colonic obstruction "flanks",
 Mild or absent in: high small lO.
 Central abdominal in: low small lO.
3. Vomitinq: (caused by anti-peristaltic wave)

Onset:
 High small lO :early with the onset of pain.
91 STAGERS NOTES

 Low small lO: after few hours from the onset of pain.
 Colonic obstruction : it may be delayed for 1-2 days.
 Content:

 First: gastric juice (whitish mucoid).

 Then: bile stained (greenish).
 Finally: feculent (brown and offensive).

Q/ What are the findings on examinations in patient with IO?

a) General:
. Dehydration: Dry tongue, tachycardia, oliguria and hypotension may be present.
B- Local:
b) local
lnspection:
1. Distension of the abdomen:
 High small lO ) may be absent.
 Low lO ) mainly central (Step-Ladder pattern
 Colonic obstruction ) mainly in the flanks.
2. Visible peristalsis: may be observed (absent in paralytic ileus).
3. evidences of the cause:

 Hernialorifices: Commonest cause of obstruction is

external strangulated hernia

 Scars of previous operations: Obstruction by bands &

adhesions
Palpation (Empty Rt. iliac fossa)
 Sausage shaped mass (intussusception)
 Volvulus mass.
 Might be palpated as in malignancy.
92 STAGERS NOTES

Percussion: Tympanic abdomen.

Auscultation :for intestinal sou nds:

 Frequent, loud in simple obstruction
 Silent in paralytic ileus, except for tinkling sound.

DRE (normally empty):

 Red current jelly stool or head of intussusception.
 Carcinoma of the rectum
 lmpacted feces in the rectum (elderly bed-ridden pt).

Q/ When to suspect strangulation ?

1. Pain not relifed by by NG section
2. Fever ,toxic or shocked patient
3. Abdominal exam: tenderness , rigidity and rebound tenderness
4. CBC and leckocytosis

Q/ what are the X ray features of IO?

Erect : multiple air fluied level

Supine :

 Jejunal loop : mucosal folds (Valvulae conniventes)

crossing from one side of the lumen to the other &
regular interval.
 Colon : hausterations do not reach the other side of the
lumen.
93 STAGERS NOTES

Q/How to differentiate between small and large bowel on X ray?

SI LI
Centrally located Prephrally loated
Volvuli convnvnintis haustra
Small caliber Larger caliber

Q/ how can you treate this case ?

A. Correction of the general condition
1. IV line

 correct Fluids and electrolytes disturbance

 Blood and plasma in case of shock.
 Antibiotics if there is suspicion of strangulation.

2. NG tube ( decompression of the bowel )

 Relieve the pain.
 Relieve the pressure on the intestinal wall to preserves intestinal viability.
 reduces the risk of inhalation during the induction of ansthesia

3. Catheter : Urine output.(at least 0.5m1/Kg/hour) .

4. moniter of the fluied status by

1. Puls
2. BP
3. UOP
B. Conservative treatment : indications are :

1. Adhesive intestinal obstruction, may be relieved by lV drip and NG

suction.

2. lleocecal intussusception may be relieved by hydrostatic effect of barium

enema.
3. Sigmoid volvulus may be reduced by rectaltube.
94 STAGERS NOTES

4. Fecal impaction : treated by enema.

C. Operation

Q/ what are the compostion of the intussception portion?

Intussusceptum(inner layer)

Intussuscipiens (outer sheath)

Q/ what is the most common site for intussuccption ?

Ileocecal (75%)

Any infant having colicky abdominal pain with passage of blood-stained mucus per rectum
should be suspecfed of having infussusception until proved otherwise

Q/ What are the abdominal examination findings in patient with

intuscessuption?
A. General
 Dehydration: sunken eyes, depressed fontanelles & inelastic skin.
B. Abdominal
 lnspection:
1. Visible peristalsis may be observed.
2. Distension of the abdomen
 Palpation:
95 STAGERS NOTES

1. Sausage-shaped mass : may be felt concave towards umbilicus. lt hardens

during the attack & softens in between attacks.
2. Signe de Dances : right iliac fossa feels empty.

 Percussion: Tympanic abdomen.

 Auscultation: Exaggerated bowel sounds
 DRE
 The finger is stained with mucous & blood.
 Apex of the intussusception may be felt.
 rarely, intussusception may protrude through the anus.

Q/How many fluid levels in abdomen X-ray may be regarded as normal?

In adults two inconstant fluid levels—one at duodenal cap another at terminal ileum
may be regarded as normal.
In infants few fluid levels (2–4) in small gut may be regarded as normal.

Q/What is the commonest cause of small bowel obstruction?

Adhesion and bands are the commonest cause of small bowel obstruction.
Q/How will you prevent intra-abdominal adhesions?
- Good surgical technique: Minimize peritoneal injury by gentle handling, use of
atraumatic instruments and achieve good hemostasis.
- Pharmacological agents: Various agents has
been used—Ringer’s solution, hyaluronidase,
dextran, anticoagulants, streptokinase.
However, the exact role of these substances
has not been substantiated.

Q/What are the usual presentation of patient with acute intestinal

obstruction?
The cardinal symptom of acute intestinal obstruction are:
96 STAGERS NOTES

-Abdominal pain: colicky abdominal pain, coinciding with the waves of peristalsis.
-Vomiting: More marked with proximal obstruction,less frequent but feculent in
distal obstruction.
-Abdominal distension: The distension is more marked in distal obstruction than in
proximal obstruction.
- Absolute constipation: no passage of flatus and feces.

-Some patients may pass flatus or feces at the onset of obstruction due to
evacuation of the contents of the bowel distal to the point of obstruction.
However, constipation may not be a feature in following situations—
1-Richter's hernia
2-Gallstone ileus
3-Intestinal obstrucion associated with pelvic abscess
4-Subacute intestinal obstruction.44

Q/How the fluid and electrolyte deficits are caused?

The fluid and electrolyte deficits are caused by:
1-Vomiting.
2- Reduced oral intake.
3-Defective absorption.
4- Sequestration of fluid in the lumen of gut.
Q/What are the volumes of different GI secretions?
-Saliva—1–1.5 liters.
-Gastric njuice—1.5–2.5 liters.
-Bile—1 liter.
-Pancreatic juice—1.5 liters.
-Small intestinal juice—3 liters.

Q/What do you mean by strangulation

obstruction?
Intestinal obstruction with compromise of blood supply
to the gut results in strangulating obstruction.
The impairment of blood supply may be due to:
97 STAGERS NOTES

1-Twisting of mesentery (volvulus).

2-By massive distension of the bowel, which initially results in impairment of venous
drainage causing venous congestion and subsequent impairment of arterial supply
resulting in gut infarction.
3- External compression of the vessels due to hernia or adhesion bands.
4-Primary obstruction of the mesenteric circulation (mesenteric vascular
thrombosis).

Q/What are the features of strangulation obstruction?

1-The pain which was colicky becomes continuous.
2-Fever and toxemia.
3-Features of shock—tachycardia and hypotension.
4-Abdominal tenderness, muscle guard and rebound tenderness.
5-A strangulated hernia is suggested by:
• Irreduciblility
• Tense and tender swelling
• no impulse on cough
• There may be rebound tenderness
• Leukocytosis.

Q/What do you mean by closed loop obstruction?

A short segment of bowel is obstructed at a proximal
and a distal point usually due to internal volvulus or
by a tight ring at the hernial neck. The obstructed
segment of the gut becomes hugely dilated and may
result in strangulation or perforation before the
proximal gut distension occurs.

Q/What are the indications of surgery in acute intestinal obstruction?

-Strangulation obstruction.
-Failure of conservative treatment in simple obstruction.
- When diagnosis is in doubt.
98 STAGERS NOTES

Q/How will you differentiate a viable and non-viable segment of gut?

An obviously black, flaccid segment of gut is gangrenous and there will be no
pulsation in the vessels in the mesentery.

When the gut is having doubtful viability with

slight color change with very poor peristaltic
wave and doubtful arterial pulsation, then this
segment of gut is covered with a hot moist
packand anesthetist is asked to give the patient
100% oxygen for about 10 minutes and the gut
is reviewed. If the color becomes pink, the
peristalsis returns and the arterial pulsation returns
then that segment will be viable.
In doubtful cases, color Doppler study may demonstrate the blood flow and
injection of intravenous fluorescent dye may help. The viable segment of the gut
will fluoresces purple.

Q/What are the sites where volvulus may occur in the gastrointestinal
tract?
1-Sigmoid colon
2-cecum
3-Transverse colon
4-Small intestine
5-Stomach.

Q/What are the important causes of large gut obstruction?

The important causes of large gut obstruction are:
1-carcinoma colon
2-Volvulus
3-Stricture-tuberculosis, crohn’s disease, ischemic colitis, anastomotic and radiation
induced
4-Hernias
5-Fecal impaction
6-Pseudo-obstruction (ogilvie syndrome).
99 STAGERS NOTES

Q/What may be the findings in a plain supine film of abdomen in large

bowel
obstruction ?
- Gas distended colon up to the point of obstruction.
- Little or no gas in colon or rectum distal to the point of obstruction.
- In closed loop obstruction cecum may appear as large gas filled gut in the right
lower quadrant.
111 STAGERS NOTES

Acute cholecystits

This patient is 4o years old , presented with right subcostal pain radiating to the
back and to the shoulder. The pain is usually severe and may last several hours.
the pain started during the night and wakes the patient.from the sleep, associated
with dyspepsia

Q/What is your possible diagnosis

 Acute Calculous Cholecystitis

Q/What are your deferential diagnosis

1) Acute Appendecitis.
2) Perforated peptic ulcer.
3) Acute pancreatitis.
4) Occasionally acute pyelonephritis of the right kidney.
5) Mocardial infarction
6) Right lower lobe pneumonia.
Q/ how to approach such patient ?
1. History
2. Physical examination (general + abdominal exam)
3. Investigations :
 ultrasonography which should show the
presence of stones in an inflamed gall
bladder with oedema around the gall
bladder wall.
 A serum amylase estimation should be
performed to exclude pancreatitis
 liver functions tests to exclude liver disease or hyperbilrubinemia
 A chest X-ray will exclude pneumonia
 ECG (IHD)
111 STAGERS NOTES

 urine for microscopy and culture.

4. treatment
 Nill by mouth and nasogastric aspiration and intravenous fluid
administration.
 administration of analgesics.

 administration of antibiotics A broad-spectrum antibiotic effective

against Gram-negative aerobes is most appropriate (e.g. Cephazolin,
Cefuroxime or Gentamycin).

 When patient improve (pain and temperature subsided ) ,Ultrasonography

is performed to ensure that :
 no local complications have developed
 the bile duct is of a normal size
 no stones are contained in the bile duct.
 Cholecystectomy may either be performed on the next available list, or the
patient is allowed home to return later when the inflammation has
completely resolved.

Q/ what are the indications to discontinue conservative treatment ?

1) there is uncertainty about the diagnosis .
2) the possibility of a high retrocaecal appendix
3) a perforated peptic ulcer cannot be excluded.

Q/What are the casues of elevated S. bilirubin in patient with acute

cholycytitis ?
mild elevation of the bilirubin can be due to oedema around the porta hepatis or
obstruction of the biliary tree by a stone escaping into the common bile duct

Q/ define Acalculous Cholecystitis , how can you treat it ?

Acute and chronic inflammation of the gall bladder can occur in the absence of
stones and give rise to a clinical picture similar to calculous cholecystitis. Acute
112 STAGERS NOTES

acalculous cholecystitis is particularly seen in patients recovering from major

surgery, trauma and burns

Diagnosis by Oral cholecystography is more useful than ultrasonography in the

diagnosis of those patients presenting with chronic symptoms, and
radioisotope scanning in those presenting acutely

Q/Patient with asymptomatic gall stone finde incedently on abdominal

US, WHAT WOULD YOU DO ?
We have to explain the possible ccomplications of gall stone , she will decide either
to remove it or to keep it … but there are certain indications to remove
asymptomatic gall stone include :

1. DM
2. Gig stone > 2cm
3. Young patient
4. Male patient

Q/ What are the types of gall stone ? which is more common

1-Cholesterol stones consist almost entirely of cholesterol and are often solitary
(cholesterol solitaire).

2- Mixed stones account for 90 % of gallstones.(the most

common)

Cholesterol is the major component. Other components

include calcium bilirubinate, calcium phosphate, calcium
carbonate, calcium palmitate and proteins. Usually they are
multiple, and they are often faceted.

3-Pigment stones are most common in the Far East and are
composed almost entirely of calcium bilirubinate. They are mostly small and
multiple.They are either black or brown in colour.
113 STAGERS NOTES

Q/What are the patient that have hight risk to develop gallstone ?
Female Fatty, Fertile, Flatulent, of Fifty’

Q/What are the drugs that cause gallstone ?

1. OCP
2. clofibrate , a drug used in the treatment of certain-hyperlipoproteinaemias.
3. Oestrogens,

Q/Where the pigmented stones could occure ?

(1) haemolysis in which bilirubin production is increased. Examples are hereditary
spherocytosis, sickle cell anaemia, thalassaemia
(2) patients with benign and malignant bile duct strictures
(3) infestations of the biliary tree by Clonorchis sinensis and Ascaris lumbricoides.

Q/What are the complications of gallstone ?

I- In the gall bladderr:

A) Asymptomatic Silent stones

B) Symptomatic:
 Acute & chronic cholecystities
 Gangrene
 Perforation
 Empyema
 Mucocele
 Carcinoma

rIIr-rIn the bile ducts:

 Obstructive jaundice
 Cholangitis
 Acute pancreatitis

III-In the intestiner:

 Acute intestinal obstruction (gallstone ileus(

114 STAGERS NOTES

Q/DD of radio-opacity in Rt. hvpochondrium:

1. Stone in the Rt. kidney.
2. Fecolith in intestine.
3. Calcified LN.
4. Phlebolith.

Q/whay are the parts of CBD?

The common bile duct is about 7.5cm long and formed by the junction of the
cystic and common hepatic ducts. It is divided into four parts,

1) The supraduodenal portion, about 2.5 cm long, running in the free edge of
the lesser omentum.
2) The retroduodenal portionr
3) The infraduodenal portion lies in a groove, but at times in a tunnel, on the
posterior surface of the pancreas.
4) The intraduodenal portion passes obliquely through the wall of the second
part of the duodenum where it is surrounded by the sphincter of Oddi. It
terminates by opening on the summit of the papilla (ampulla) of Vater.

Q/What are the functions of the gall bladder

1) Reservoir for bile
2) Concentration of bile
3) Secretion of mucus

Q/Preparation for cholecystectomy ?

1. Appropriate history taking.
2. Assessment of the patient’s fitness for the procedure, which will include
investigations of the cardiovascular and respiratory systems (ECG &CXR) if
history suggests these to be risk factors, a full blood count and biochemical
profile are done to exclude abnormal liver function tests or anaemia. Blood
coagulation is checked if there is a history of jaundice (PT &PTT).
3. For inpatients, fluid depletion and electrolyte imbalance must also be corrected.
115 STAGERS NOTES

4. The patient is given prophylactic antibiotics either with the premedication

intramuscularly or intravenously at the time of induction of anaesthesia. A

second-generation cephalosporin is appropriate.
5. Heparin (5000 units subcutaneously twice a day) and antiembolus stockings are
prescribed for all patients.
6. Aconsent form is signed ensuring that the patient is fully aware of the procedure
being undertaken, the risks involved and complications that may occur.
7. Patients are asked to empty their bladder before coming to theatre and are not
normally catheterized.
8. Elective female patients should stop the contraceptive pill 1 month before
admission.

Q/This ptient presented to you after 4 days from cholycytectomy with

obstructive jaundice, how can you mange him ?
The first step in management is to undertake an immediate
ultrasound scan. If there is evidence of fluid in the subhepatic
space or obstruction of the biliary tree as shown by bile-duct
dilatation then an immediate ERCP should be performed to
ascertain whether a stone is present or there is obstruction of
the common bile duct due to damage at the time of surgery .If
116 STAGERS NOTES

a stone is present immediate removal endoscopically is indicated. If the common

bile duct is obstructed by clips or there is leakage from the biliary tree due to a
cystic duct leak then a drain should be placed in the subhepatic space
percutaneously and a stent placed in the bile duct when possible. Small leaks will
usually resolve spontaneously. Should the common bile duct be damaged, the
patient should be referred to an appropriate expert for reconstruction of the duct

Transection of theCBD,CHD and RHDor LHD are treated by Roux-en-Y

Choledochojejunostomy. Bengin strictures of the bile ducts are treated with ballon
dilatation.

Q/Define the Courvoisier’s law

Courvoisier’s law — ‘in obstruction of the common bile duct due to a stone,
distension of the gall bladder occurs rarely,because the organ usually is already
fibrosed and contracted due to chronic inflamation. However, if there is no disease
in the gall bladder and the obstruction is due to a cancer of the ampulla, pancreas
or bile duct, then the gall bladder may well be distended.

Q/what are the Indications for choledochotomy?

(1) palpable duct stones.
(2) there is jaundice or a history of jaundice or cholangitis.
(3) the common bile duct is dilated.
(4) the liver function tests are abnormal, in particular, the alkaline phosphatase is
raised.

Q/When do you find Murphy’s sign is positive?

Murphy’s sign is positive in acute cholecystitis. In chronic
cholecystitis Murphy’s sign is not positive
Q/Why do you prefer laparoscopic cholecystectomy?
„ Laparoscopic cholecystectomy has been established as
gold standard for the treatment of
gallstone diseases
117 STAGERS NOTES

• Surgery is safe in the hands of a trained surgeon

• Less pain, less hospital stays
• Cosmetic
• Early return to work is possible
• More acceptance by the patient.

Q/What is the boundary of Calot’s triangle?

Calot’s triangle is bounded below by the
cystic duct, medially by the common
hepatic duct and above by the inferior
surface of the liver. The triangle is crossed
by the cystic artery

Q/What is postcholecystectomy syndrome?

In 15% cases cholecystectomy fails to relieve the symptoms for which the
operation was done.
This is called postcholecystectomy syndrome.
The important causes of postcholecystectomy syndrome are:
- Missed stone in common bile duct
- A stone in cystic duct stump
- Operative damage to biliary tree
-Peptic ulcer
- Hiatus hernia
- Gastroesophageal reflux disease.
Q/How will you manage a patient with postcholecystectomy syndrome?
1- Clinical evaluation by detailed history and physical examination and
relevant examination
2-Liver function test
3- Ultrasonography of upper abdomen
4- Upper gastrointestinal (GI) endoscopy
5-barium meal X-ray of esophagus, stomach and duodenum
6- Appropriate treatment depending on the cause.
118 STAGERS NOTES

Q/What are the different types of gallstone?

1- Cholesterol stone
2- Pigment stone
3- Mixed stone.

Q/Describe a classical attack of biliary colic?

Acute onset of pain in right upper quadrant of abdomen,
severe spasmodic in nature, may radiate to back of chest
or shoulder. Pain may last for few minutes to several
hours. Pain is often precipitated by a fatty meal. Attacks
of pain are usually self-limiting, but recur in an
unpredictable manner. Fever and leukocytosis are
uncommon. Pain may occur in the epigastrium or rarely
in the left upper quadrant of the abdomen (in 4% cases).

Q/What are the features of acute cholecystitis?

1- History
• Acute onset pain in right upper quadrant of abdomen. Severe spasmodic
in nature with radiation to back or the right shoulder. Later on pain
becomes dull aching and constant and usually lasts longer than 24 hours.
• Marked nausea and vomiting.
• Fever.
2-Examination.
• Tachycardia and jaundice may be present.
• Abdominal examination may reveal marked tenderness in right upper
quadrant of abdomen.
• Murphy’s sign will be positive.
• A vague mass may be palpable.
3-Investigation
• Leukocytosis is usually a feature.
• Liver function test: There may be mild rise of serum bilirubin.
• USG examination may diagnose acute cholecystitis, wall thickening,
pericholecystic fluid collection.
119 STAGERS NOTES

Q/What is mucocele of gallbladder?

When there is obstruction to the cystic duct or the neck of the gallbladder
by a stone or a growth then the contained bile in the
gallbladder is absorbed by the gallbladder epithelium
and is replaced by mucus secreted by the gallbladder
epithelium. The content is usually a clear sterile fluid.

Q/What is empyema of gallbladder?

Gallbladder is filled with pus and may follow as a

consequence of acute cholecystitis or as result of
infection of a mucocele. In 50% cases the contained pus
is sterile.

Q/What is acalculous cholecystitis?

Acute or chronic inflammation of the gallbladder in absence of gallstone is

known as acalculous cholecystitis.

Q/What are the predisposing factors for development of acalculous

cholecystitis?

-Critically ill patients in intensive therapy unit

- Following major surgery, trauma or burns.

Q/What is strawberry gallbladder?

There is deposition of cholesterol crystals in the submucosa
and they may appear as yellow specks and the interior of the
gallbladder looks like a strawberry. This may be associated
111 STAGERS NOTES

with cholesterol stones in gallbladder.

Q/What is lithogenic bile?

In normal bile the cholesterol, phospholipids and bile salts remain in optimum
concentration.
This keeps the cholesterol in solution. bile supersaturated with cholesterol is known
as lithogenic bile as this predisposes to gallstone formation .

Q/What do you mean by silent gallstone?

Incidentally found gallstones during examination for other pathology or in
routine health check-up that does not produce symptoms are called silent
gallstones.

Q/When do you consider prophylactic cholecystectomy in silent

gallstones?
Prophylactic cholecystectomy is not indicated in all patients with silent
gallstones. Prophylactic cholecystectomy is indicated in population at high
risk of developing
complications. This includes:
-Diabetic patients
-Patients on immunosuppressive therapy
-Candidates for renal transplant
-Large gallstones (>2.5 cm)
-Multiple small gallstones
-Patients living in high risk areas where there is increased incidence of
gallbladder carcinoma
-Porcelain gallbladder in view of increased risk of carcinoma of gallbladder.
111 STAGERS NOTES

Assessment of pulse

Important anatomy :

1. Dorsalis Pedis
Lateral to extensor hallucis longus tendon at the
proximal end of first web space against medial
cuneiform bone.

2. Posterior Tibial
Midway between medial malleolus and tendoachilles, against calcaneum.
112 STAGERS NOTES

3. Popliteal
Supine position - Knee flexed; felt against tibial condyle
Prone position - Knee flexed; felt against femoral condyle.

4. Femoral Artery
Below mid inguinal point against head of femur with
hip joint flexed, abducted and externally rotated.
113 STAGERS NOTES

5. Radial Pulse
Proximal to the wrist against lower end of radius.

6. Brachial Pulse
Medial to the biceps tendon against medial humeral
condyle.

7. Axillary
Against humerus head in the axilla.
114 STAGERS NOTES

8. Subclavian
Supraclavicular fossa in the midclavicular line
against first rib.

9. Common Carotid

At the level of upper border of thyroid cartilage against trans

vese process of C6 vertebra.

10. Superficial Temporal

Anterior to the tragus against temporal bone.

Q/What do you know about Buerger’s Test?

Elevation of the ischemic limb causes
marked pallor of limb. (normal limb—no change even on elevation to 90°)

Q/what are the symptoms of peripheral arterial disease

Intermittent claudication Pain in calf, thigh or buttocks when walking; typically
relieved with rest.

Nocturnal pain Wakes patient and relieved by hanging legs out of bed or walking;
suggestive of severe disease.
Erectile dysfunction Often an early sign of peripheral arterial disease (ask in history).
Ulceration Signs of severely ischaemic limbs and poor wound healing is also
common.
115 STAGERS NOTES

Examination of the peripheral arterial system

Introduction
• Gain permission to examine patient and explain what you are about to do.
• Clean your hands prior to beginning.
Inspection
• Start with hands—look for tobacco staining.
• Face—look for xanthelasma.
• Scars—look for scars on the abdomen (aortic aneurysm repair), groin
(angiography)
or medial aspect of thighs (bypass grafting).
• Ulcers—comment on arterial ulcers (punched out, usually over medial malleoli) or
venous (anterior aspect of shin, associated with venous eczema and skin changes).
• Skin changes—loss of hair and skin thinning.
• Feet—examine dorsum and plantar aspects and between toes for ulcers.
• Feel for the skin temperature in the feet.
Palpation
• Measure (or say you would) the blood pressure in both arms.
• Palpate the major pulses—radial, carotid, aortic, femoral, popliteal and
dorsalis pedis.
• Check for radio-femoral delay after palpating radial pulse—explain this to the
patient.
• Check for capillary refill time over big toe.
Auscultation
• Listen over the aorta, carotid and femoral arteries for bruits.
Special tests
Buerger’s test—With patient lying on their back, raise their feet to 45 for 2 minutes.
Then sit the patient on the edge of the bed with legs down. A positive test
(peripheral arterial disease) occurs when legs initially go pale when raised then
hyperaemic (red) when down.
116 STAGERS NOTES

Scrotum
Examination of the scrotum and groin

Introduction
• Introduce yourself, and explain briefly what you plan to do.
• Ask for consent and offer a chaperone.
• Clean your hands and put on a pair of gloves.
• Examination of the scrotum is best performed with the patient standing. You will
also need to examine the groin so this must be visible—explain that you will need
to examine the lower abdomen to the upper thigh. Allow the patient privacy
to undress.
• Check with the patient whether there is any pain or tenderness before you start.
Inspection
• Look at the scrotum and groin. Are there any obvious areas of swelling? Are there
any previous surgical scars? Is there any redness?
Palpation
• Palpate the scrotum gently, using both hands (thumb and forefingers). Check that
both testes are present in the scrotum; if not, examine the inguinal canals.
• With each testis in turn, immobilise one side by placing one hand behind it, and
use the index finger and thumb to palpate the entire body of the testis, and then
the cord structures and epididymis at the top of each testis.
• If you palpate a swelling, try to ascertain whether it is separate to the testis or part
of it, or part of the epididymis. If you cannot get ‘above’ the swelling, it may be an
inguinal hernia.
• Finally, palpate both groins for any swelling and for inguinal lymph nodes which
may be present in epididymitis (but remember that testicular tumours spread to the
para-aortic nodes).
Auscultation
• You should auscultate any scrotal swelling for bowel sounds as it may be an
inguinal hernia.
117 STAGERS NOTES

Special tests
Using a torch, shine the light through any scrotal swellings. Hydrocoeles and larger
epididymal cysts will transmit the light and transilluminate, whereas other
swellings will not
• If you suspect an inguinal hernia, ask the patient if they can reduce (push back or
move) the swelling, and if not, try and reduce it yourself. If it is reducible, then once
reduced place your fingers over the deep inguinal ring and ask the patient to cough
to see if it is contained.

Q/Differential Diagnosis of Scrotal Swelling:

A. Scrotal swelling with pain:
1. Epididymitis
2. Orchitis
3. Testicular trauma
4. Testicular torsion
5. Incarcerated scrotal hernia
6. Testicular tumor
B. Scrotal Swelling without pain:
1. Hydrocele
2. Spermatocele
3. Varicocele
4. Hematocele
5. Scrotal hernia
6. Testicular tumor

Q/What is hydrocele?
Hydrocele is a condition of collection of fluid in the tunica
vaginalis sac.

Q/What is primary hydrocele?

When there is no obvious cause to explain collection of fluid
in tunica vaginalis sac.
118 STAGERS NOTES

Q/How primary hydrocele develops?

There may be collection of fluid in the tunica vaginalis due to:

1. Excessive secretion of fluid within the tunica vaginalis sac—as in secondary

hydrocele
2. Defective absorption of the secreted fluid—most primary hydrocele is due to
this
3. Due to defective lymphatic drainage of the scrotal strucutres
4. Peritoneal fluid may reach the patent processus vaginalis leading to a
congenital hydrocele.

Q/What is secondary hydrocele?

When there is collection of fluid in tunica vaginalis sac secondary to some disease
of testis or the epididymis. Secondary hydrocele are usually small and lax.
Secondary hydrocele may be secondary to epididymo-orchitis, testicular tumor,
torsion or trauma.

Q/What is the explanation for development of hydrocele following

inguinal herniorrhaphy?
One of the explanation is probably due to interruption of lymphatics draining the
scrotal contents following herniorrhaphy.
Q/What is hydrocele of the hernial sac?
This is one of the complication of an inguinal hernia. If the neck of the hernial sac is
plugged with omentum then there may be collection of fluid in the distal part of
the sac resulting in hydrocele of the hernial sac.

Q/What are the complications of hydrocele?

The hydrocele if untreated, may treated:

1. Infection—pyocele
2. Trauma—hematocele
3. Atrophy of testis
4. Rupture
5. Calcification of the sac
119 STAGERS NOTES

6. Hernia of the sac.

Q/What is spermatocele?
Spermatocele is an unilocular retention cyst
developing from some portion of the epididymis
usually the head of the epididymis.

Q/What is varicocele?
This is a condition of dilatation and tortuosity of pampiniform
plexus of veins of the spermatic cord.

Q/What are the types of varicocele?

There are two types of varicocele:
1. Primary
2. Secondary.

Q/What is primary varicocele?

In 95% cases no cause for varicocele could be found. This is called primary
varicoccle.

Q/What is secondary varicocele?

When the varicocele is secondary to obstruction of testicular vein then it is called
secondary varicocele. The obstruction of the testicular vein may be due to
retroperitoneal tumor or kidney tumor.

Q/Why varicocele is common on left side?

Ninty percent cases of varicocele is found on the left side. The important cause for
this left preponderance are:

1. The left testicular vein joins the left renal vein at right angle.
2. The left testicular vein joins the left renal vein which drains into the inferior
vena cava 8–10 cm more cranial than the right testicular vein, as a result the
left testicular vein has a 8–10 cm greater pressure head than the right
testicular vein.
121 STAGERS NOTES

3. Left testicular vein is longer as left testis lies at a lower level and left renal vein
lie at a higher level. Hence, longer column of blood in left testicular vein
exerting more pressure in left pampiniform plexus.
4. Left testicular vein is liable to be compressed by loaded pelvic colon as it
ascends behind the left colon.
5. The left renal vein may be sandwiched between the abdominal aorta and
superior mesenteric artery and compression of the left renal vein may lead to
varicocele.
6. Left testicular artery may arch over the left renal vein and may cause
compression of the renal vein and testicular vein leading to varicocele.
7. In carcinoma of left kidney the tumor may grow along the renal vein causing
obstruction of left testicular vein leading to varicocele.

Q/Which factors are responsible for development of primary varicocele?

Varicocele formation usually is caused by:

1. Increased venous pressure in the left renal vein.

2. Incompetent valves of the testicular vein.

Q/What are the effects of varicocele on testicular function?

Varicocele is one important cause of male infertility. There is adverse effect on
spermatogenesis.
The pathopyhsiology of testicular dysfunction due to following mechanisms:

1. Hyperthermia: Presence of varicosities impedes the countercurrent heat

exchange
mechanism. Increased scrotal temperature inhibits spermatogenesis.
2. Intratesticular hyperperfusion injury: Abnormal elevation of microvascular
blood flow and increased intratesticular temperature increases the metabolic
activity and depletes the intracellular glycogen store and induces testicular
parenchymal injury.
3. Hypoxia.
121 STAGERS NOTES

4. Local testicular hormonal imbalance: Leydig cell dysfunction in patients with

varicocele may be caused by diminished intratesticular testosterone.

5. Unilateral varicocele may show bilateral finding of decreased

spermatogenesis, maturation arrest and tubular thickening.

Q/What operation will you do in this patient?

I will do Palomo’s operation in this patient.

Q/What are the complications of varicocele operation?

1. Hydrocele: This is due to lymphatic obstruction.
2. Testicular artery injury: There is 10–20% chance of testicular atrophy. In
children the incidence of testicular atrophy is less than in adults.
3. Recurrence of varicocele.

Q/ take short history from patientwith Undescended testes?

1. Absence of testis in the scrotum—one side or both
side.
2. Duration—whether since birth or it was present in
the scrotum at birth and subsequently not present
in the scrotum (retractile testis or atrophic testis).

3. Any swelling present in the line of normal descent

of testis—in the loin, right iliac fossa or inguinal
canal.
4. Any swelling present at the sites of location of
ectopic testis—in thigh, root of penis, perineum and in subinguinal pouch.
5. Any pain over the swelling (pain may due to trauma or torsion of an
undescended testis)
6. Any swelling in the groin which comes up on straining and disappears on
lying down
122 STAGERS NOTES

(suggestive of an associated inguinal hernia—which may be present with

undescended testis).
7. „ In patient with bilateral undescended testes—enquire about appearance of
secondary sex
characters and infertility (in aged patients).

Examine patient with undesendent patient ?

1. Look at the scrotum—whether well developed or ill developed on one or both
sides (in undescended and ectopic testis the scrotum is ill developed, whereas
in retractile testis the scrotum is well developed).

2. Palpate along the normal line of descent—from lumbar region to the region of
deep inguinal ring, inguinal canal, superficial inguinal ring and root of the
scrotum to ascertain the presence of undescended testis at these sites.

3. Palpate at the sites of ectopic location of testis for any swelling at—root of
penis, thigh, perineum and inguinal canal at subinguinal pouch.

4. Examine inguinal canal for any swelling—any expansile impulse on cough over
that swelling, whether the swelling is reducible or not (reducible swelling with
expansile on cough suggest associated inguinal hernia).
123 STAGERS NOTES

5. If testis is palpable at the inguinal canal try to manipulate the testis into the
scrotum—in retractile testis it can be brought down to the bottom of the
scrotum. If the testis cannot be brought down to the scrotum—this is likely to
be ectopic or undescended testis.

6. Look for any other congenital anomalies.

Q/Intrepretate the result of the examination or What is your diagnosis?

When you asked about the diagnosis , you have to mention 3 things :

1. Unilateral or bilateral undescended testis.

2. „ Whether testis is palpable or impalpable, if palpable at what site?
3. „ Presence of any associated inguinal hernia.
For example :
This is a case of left sided undescended testis, testis is impalpable in the inguinal
canal and there is an associated left sided inginal hernia.

Q/How will you proceed to manage this patient?

1-In this child as the testis is impalpable I would suggest ultrasonography (USG)
of groin, pelvis and retroperitoneal area to localize the testis.

2-I will advise baseline investigations to assess patient fitness for general
anesthesia and surgery.
Q/How else impalpable testis may be localized?
-Computed tomography (CT) scan and magnetic resonance imaging (MRI) are
not very reliable investigation for localization of impalpable testis.
-Diagnostic laparoscopy is now the standard method of localization of
impalpable testis.
Q/How will you treat this patient?
- If the testis is localized by ultrasonography then I will do orchidopexy.
-If the testis is not localized by ultrasonography I will do diagnostic laparoscopy
and orchidopexy.
124 STAGERS NOTES

Q/What are the benefits of orchidopexy?

-Psychological satisfaction of having both the testes in the scrotum.
-Maximize the prospect of normal spermatogenesis.
-Reduces the risk of torsion.
-Associated inguinal hernia is repaired.
-Minimize the risk of tumor development and diagnosis can be done early.

Q/What is the ideal time for orchidopexy?

-In majority of undescended testis, the testis descends into the scrotum by 3
months of age except in premature infants where it, descend by one year of age.
-Earlier it was said that the ideal time for operation is 5–6 years.
-But current consensus is that ideal time for orchidopexy is 6 months to 1 year.

Q/When will you consider orchidectomy in undescended testis?

- If there is complication, e.g. torsion or tumor, orchidectomy is necessary.
-If the testis is atrophic and is unlikely to function.
-If the testis cannot be mobilized to a sufficient length in spite of all maneuvers.

Q/Where from testis develops?

The testis develops from the genital ridge on the medial aspect of mesonephros
in the retroperitoneum during 4–6 weeks of gestation. The developing testis in
this site is attached to posterior abdominal wall by a fold of peritoneum called
meso-orchium through which testicular vessels and nerve enters the testis. The
primordial germ cells located at the caudal wall of the embryonic yolk sac
migrates to the genital ridge via the dorsal mesentery. Interstitial cells are
derived from the mesonephros. The gubernaculum develops in the 7th week of
intrauterine life extends from the developing gonad in the retroperitoneum to
the developing scrotum.

Q/What is processus vaginalis?

Before testis descends into the inguinal canal,
a fold of peritoneum descends into the
scrotum—this fold of peritoneum is called the
processus vaginalis. Later on the major part of
125 STAGERS NOTES

the processus vaginalis disappears except the most distal part which forms the
tunica vaginalis which encircles the testis.

Q/What is the effect on fertility in undescended testis?

Untreated bilateral undescended testis is usually associated with sterility. In
unilateral undescended testis infertility is usually not a problem but this may also
be associated with subfertility due to defective spermatogenesis in the normally
descended testis.

Q/What is ectopic testis?

It is one form of maldescent of testis where testis has deviated from the normal
route of descent and lies in a site other than the scrotum.

Q/Where an ectopic testis may lie?

An ectopic testis may lie at :
-Suprapubic region at root of penis
-Perineum
-Femoral triangle
-Opposite scrotal sac

-Superficial inguinal pouch which is

a space between the external
oblique aponeurosis and fascia of
Scarpa

Q/What is retractile testis?

The retractile testis is one which is withdrawn out of the scrotum by an active
cremesteric reflex but can be easily brought down into an orthotopic position
within the scrotum and remains there after the traction is withdrawn.
126 STAGERS NOTES

Q/How will you differentiate an ectopic testis and retractile testis in

superficial inguinal pouch?
- A retractile testis was in the scrotum at birth and then drawn up by reflex.
-The scrotum is well formed in retractile testis.
-The testis can be manipulated down to the scrotum in retractile testis.
-The retractile testis is normally developed.

Q/What are the complications of undescended testis?

1. Testicular atrophy.
2. Liable to repeated trauma.
3. Undescended testis is more liable to develop torsion due to long
mesorchium.
4. 10% of testicular tumors occur in undescended testis.
5. Subfertility or infertility.
6. Associated hernia—a patent processus vaginalis is found in 90% patient of
undescended testis.

Q/What is the risk of malignancy in undescended testis?

Undescended testis has 40 times greater risk of developing tumors than in
normally descended testis. The risk has been said to be 1 in 20 in abdominal
testis and 1 in 80 in inguinal testis.

Q/Which type of tumor is more common in undescended testis?

The most common tumor that develop in an undescended testis is seminoma.

Q/Does orchidopexy reduces the chance of malignancy?

This is controversial. There is emerging evidence that prepubescent orchidopexy
lessens the risk to some extent. Orchidopexy also allows thorough examination
and earlier detection if a tumor develops.
127 STAGERS NOTES

Penile conditions

Q/What is phimosis?
Phimosis is a condition when the preputial skin could
not be retracted beyond the corona glandis.

Q/How these patients usually presents?

-Difficulty in retracting the skin of prepuce beyond
the corona glandis
-In case with very small preputial orifice, the prepuce
may blow up during micturition
-Associated balanitis or balanoposthitis may cause
pain and purulent discharge.
Q/How will you treat this patient?
-I will do baseline investigations.
-I will do circumcision.

Q/What are the indications of circumcision?

1. On religious ground
2. Phimosis with recurrent attacks of
balanitis or balanoposthitis
3. Recurrent urinary tract infection
4. prevention of sexually acquired human
immunodeficiency virus (HIV) infection

Q/What are the complications of circumcision?

1. Bleeding
2. Wound infection
3. Removal of too much skin or too little skin
4. Injury to glans penis and urethra
5. Thermal or laser injury to the penis if these are used during circumcision.
128 STAGERS NOTES

Q/What is paraphimosis?
This is a condition where preputial skin is suddenly retracted beyond the corona
glandis and forms a constricting ring at this site and it cannot be pulled forward
leading to edema and swelling of glans penis. The preputial skin also becomes
edematous.
The constricting ring causes venous congestion and further aggravates the swelling
and can cause gangrene of glans penis.

Q/What are the complications of phimosis?

1. Recurrent balanitis and balanoposthitis
2. Paraphimosis
3. Preputial stenosis may cause ballooning of preputial skin and may cause
chronic retention of urine
4. Retained smegma may form calculi in the preputial sac
5. Chronic urinary retention may cause back pressure changes in bladder,
ureter and kidneys
6. Carcinomatous change. Phimosis with recurrent balanoposthitis is a
premalignant lesion. Retained smegma may also cause chronic irritation
129 STAGERS NOTES

leading to carcinomatous change.

Q/What is hypospadias?
Hypospadias is defined classically as association of three anatomic and
developmental anomalies of the penis:

1. An abnormal ventral opening of the urethral meatus, which may be located

anywhere from the ventral aspect of the glans penis to the perineum
2. An abnormal ventral curvature of the penis—chordee
3. An abnormal distribution of the foreskin with a hood present dorsally and
deficient foreskin ventrally.

Q/What are the different types of hypospadias?

131 STAGERS NOTES

Q/How will you manage this patient?

This is a distal penile type of hypospadias with a chordee and associated meatal
stenosis. So I will plan for an one stage operation for repair of this hypospadias.
131 STAGERS NOTES

stoma

Q/Define the stoma

A stoma is an opening in the skin, allowing
the connection of a hollow organ to the outside;
with a bag attached for the organ contents to
drain. Most commonly this is gastrointestinal
(colon, ileum), although urostomies are required
in some cases of invasive bladder or prostate
cancer. Stomas may be permanent or temporary,
with the intention of closing the latter at a later
date.

Q/ examination squences?
1. Introduction

• Introduce yourself and gain consent.

• Wash hands and apply gloves.
• Ensure that the patient is appropriately exposed (ideally this would be nipples to
knees—but to preserve dignity would normally just expose abdomen).

2. Inspection

• From the end of the bed: Look for abdominal scars, stoma position and
whether the patient appears unwell (unlikely in OSCE) and any other
indicators of systemic disease.
• Looking at the stoma: Note appearance (flush with skin or has a spout?),
health (colour should be pink/red and appear moist and glistening), stoma
contents (comment if absent) and colour, consistency and volume.
132 STAGERS NOTES

3. Palpation

• Check whether the patient is in any pain—both asking and reviewing

patient’s face for discomfort.

• Palpate abdomen for any surrounding tenderness, masses or the presence

of parastomal hernias.

• In addition you should percuss the abdomen and auscultate for bowel
sounds(indicating a functioning bowel).

4. Special tests

For completion you should offer to perform a digital stomal examination

using the index finger with gloves and lubricant (not expected in the OSCE).

1 Stoma Colostomy Ileostomy

2 Surface Mucosa sutured to and flush Spout appearance, proud from skin
with
skin
3 Location Usually in the left iliac fossa Usually in the right iliac fossa
4 Contents Brown solid formed stool, Green liquid stool, continuously
intermittently present present
5 Indications Colorectal carcinoma, Inflammatory bowel disease,
diverticular familial
disease adenomatous polyposis coli
6 more likely to develop fluid and
electrolyte problems

Temporary or defunctioning stomas are usually fashioned as loop stomas

A temporary colostomy may be transverse and sited in the right upper quadrant
133 STAGERS NOTES

Q/what is the sutible site of stoma?

away from bony prominences, skin folds and scars.
134 STAGERS NOTES

mass

Q/What is sebaceous cyst?

This is a retention cyst in relation to sebaceous gland due to blockage of sebaceous
duct and accumulation of secretion within the gland.

Q/Where sebaceous glands are absent?

Sebaceous glands are present throughout the body except in palms and soles.

Q/What are the complications of sebaceous cyst?

1. Infection
2. Ulceration
3. cock's peculiar tumor
4. Sebaceous horn formation
5. Rarely malignant change may occur. Usually a basal cell carcinoma.

Q/How will you differentiate dermoid cyst and sebaceous cyst?

Dermoid cyst occurs at the lines of embryonic fusion, whereas sebaceous cyst may
occur at any site.
Dermoid cyst lies in subcutaneous tissue and is free from the skin. The sebaceous
cyst lies deep to the epidermis and the skin is usually fixed to the cyst and there is
usually punctum over the skin.
135 STAGERS NOTES

Q/How will you differentiate a scalp dermoid from a sebaceous cyst?

1-The sebaceous cyst is tethered to the skin but dermoid cyst is subcutaneous and
skin is free in the dermoid cyst
2- Bony indentation is not found in sebaceous cyst but usually found in dermoid
cyst.

Q/What is lipoma?
Lipoma is a benign tumor arising from mature fat cells.

Q/Where do you find lipomas commonly?

The lipoma may be found anywhere in the body. It is commonly found in the
subcutaneous tissues of trunk, neck and limbs.

Q/How will you demonstrate slip sign?

Lipomas are freely mobile swellings. When the edge of the
swelling is pressed with the finger, the swelling along with
the edge gets displaced by the palpating finger. This is
called slip sign.
Q/What are the complications of lipoma?
The lipoma of long duration may undergo some secondary changes:

1. may attain huge size and cause cosmetic deformity

2. Saponification and calcification
3. Rarely malignant change—liposarcoma
4. myxomatous degeneration
5. Infection
6. Hemorrhage.
136 STAGERS NOTES

Surgical incision

Q/What are the different abdominal incisions?

The different abdominal incisions

2. Midline incision:
• Upper (above the umbilicus).
• Lower (below the umbilicus).
• Mid-midline (midline incision centreing the umbilicus).

Indicated in:

 emergency exploratory laparotomy

 gastric operations
 colonic resection
 abdominoperineal resection

2. Paramedian incision:

• Right paramedian incision— Vertical incision 2.5 cm to the right of midline.

Indicated in:
 gall bladder
 surgery, right hemicolectomy.

• Left paramedian incision—Same incision to the left of midline.

Indicated in:

 Gastric operations
137 STAGERS NOTES

 left hemicolectomy
 splenectomy.

3. Mayo Robson’s incision: Right upper paramedian incision extended like a

hockey stick to the midline.
Indicated in cholecystectomy.

4. Subcostal incision:

• Right subcostal incision (Kocher's subcostal incision)—Oblique incision 2 cm

below and parallel to the right costal margin, extending from midline to
138 STAGERS NOTES

beyond the tip of the costal cartilage.

Indicated in:

 Cholecystectomy
 CBD exploration
 biliary enteric bypass.

• Left subcostal incision—Same incision on the left subcostal region.

Indicated for
splenectomy.
• Roof top or chevron incision—Bilateral subcostal incision joined in the
midline. Indicated for :
 pancreatic surgery—Whipples’ operation
 pancreaticojejunostomy
 liver resection.

5. Transverse incision:
• Upper abdominal transverse incision. Indicated for:

 gallbladder surgery
 gastric operations.

• Infraumbilical transverse incision. Indicated for exploratory

laparotomy in children.
• Suprapubic transverse incision (Pfannensteil incision).
Indicated in :
 pelvic operations
 prostatectomy.

6. McBurneys’ gridiron incision: Indicated for appendicectomy.

7. Lanzs’ incision: Used for appendicectomy.
8. Inguinal incision: Incision at the inguinal canal running parallel to the
139 STAGERS NOTES

inguinal ligament. Used for hernia operations.

9. Loin incision or lumbar incision:

Incision from the lateral border of erector spinae downward and forward midway
between the 12th rib and the iliac crest upto the lateral border of rectus
abdominis. Used for operations in kidney.

10. Mercedez Benz incision: Bilateral subcostal incision with vertical incision
extending from
center of the ∧-shaped cut to the xiphoid process

Keloid and hypertophic sacr

Q/What is keloid scar?
Keloid is defined as a condition of proliferation of
fibroblast, collagen fibrils and immature blood vessel
usually on a preexisting scar

Q/Why it is not a hypertrophic scar?

Hypertrophic scar does not extend into normal tissue, has no claw like extension,
no itching, no sign of increased vascularity and gradually regresses after 6
months. Usually does not get worse after 1 year.

Q/Which factors are responsible for development of keloid?

1. Race: It is more common in negro population
2. Sex: Females are more affected than male
3. Familial: Familial predisposition in some cases
4. Site of scar: Incision across Langer's line increases chance of keloid formation
141 STAGERS NOTES

5. Tuberculosis: Increased incidence of keloid formation in patients suffering

from tuberculosis.

Q/How will you treat this patient?

1-Local steroid cream application (betamethasone or dexamethasone cream) may
help reduce the itching

2-If local application of steroid fails or the patient complains of severe itching,
intrakeloid injection of steroid, e.g. injection of triamcinolone into the keloid may
help. Injection is done at weekly interval for 4–6 weeks.

Q/What is the role of surgical treatment?

Surgery has a very limited role in management of keloid as there is high chance of
recurrence following surgery.
The surgery commonly practiced is intrakeloid excision and approximation of the
margin by suturing or split skin grafting.

Q/What are the complications of keloid?

1. Infection and suppuration
2. Ulceration due to itching or trauma. Rarely marjolin's ulcer may develop
3. Recurrence after excision.
141 STAGERS NOTES

Q/What are the characteristics of hypertrophic scar?

Hypertrophic scars are more cellular and vascular than the mature scars. There is
increased collagen production and breakdown. Hypertrophic scars appear as:
-Scar raised above the surface
-Does not extend to normal tissues
-Does not worsen after 6 months.

Q/what are the stages of wound healing ?

1. vascular constriction
Hemostasis 2. platelet aggregation, degranulation, and fibrin formation (thrombus)

1. neutrophil infiltration
2. monocyte infiltration and differentiation to macrophage
Inflammation
3. lymphocyte infiltration

1. re-epithelialization
2. angiogenesis
Proliferation 3. collagen synthesis
4. ECM formation (extracellular matrix.)

1. collagen remodeling
Remodeling 2. vascular maturation and regression
142 STAGERS NOTES

Pre operative preparation

we have to assess the general condition and fitness of the patient before elective
major surgery

1. detail history : ask about every system in detiaes

2. Detail physical examination:'

• General survey—mental state/nutrition/hydration status/any abnormalities of jaw

and neck/any skin infection

• Systemic examination:
− Cardiovascular system
− Respiratory system
− nervous system
− Gastrointestinal system
− Musculoskeletal system

3. Investigations:

• Baseline investigations
− Complete hemogram: Hb%, RBC count, PCV, tLC, DLC, platelet count
− Blood biochemistry: Blood sugar, urea and creatinine
− Urine for routine and microscopic examination
− CXR
− ECG, particularly in patients over 40 years and in patients with cardiac disease and
hypertension.
• Special investigations: Based on the suspected coexisting disease for example :
− In patients with cardiovascular disease:
» echocardiography.
143 STAGERS NOTES

» treadmill test.
» Coronary arteriography in patients with significant ischemic heart disease.

4. correction of the underlying coexisting medical disease

5. Informed consent

Pre-operative preparation in patient with colorectal surgery

Mechanical preparation of bowel:
• Diet:
− Low residue diet 48–72 hours before surgery
− On day before surgery only clear liquid is
allowed
− no feed on the day of surgery.
• Bowel wash: Balanced electrolyte solution
with polyethylene glycol—available as a powder
is to be dissolved in 2 litres of water and taken
on the day before surgery. This is
an effective way of bowel preparation. This brings about osmotic catharsis and may
render the whole gut empty.

Antibiotic preparation:
Mechanical wash of the colon does not sterilize the gut.
Bacterial count in the colon may be reduced by administration of luminal antibiotics
like neomycin 1 gram + erythromycin base 1 gram, on the day before operation at
1 PM, 3 PM and11 PM when surgery is planned at 9 AM next day.
A systemic antibiotic is also administered (e.g. ceftriaxone + metronidazole) before
induction of anesthesia and after 6 hours and 16 hours in postoperative period.
If there is contamination during surgery, the antibiotics may be continued for 2–3
days.
144 STAGERS NOTES

Pre- operative prepration of patient with gastric outlet obstructiion

1. Correction of dehydration: either by oral fluid or by intravenous normal saline

infusion.
Adequate urine output suggests proper hydration.
2. Correction of electrolyte imbalance: By intravenous infusion of normal saline.
Once adequate urine output is established potassium should be supplemented to correct
hypokalemia.
3. Correction of anemia: By blood transfusion.
4. Correction of hypoproteinemia: either by oral high protein diet or by amino acid,
fresh frozen
plasma or human albumin transfusion.
5. Gastriclavage: Gastric lavage is done before each feed 4–5 days prior to surgery.
Gastric lavage
removes the food residue, decreases the mucosal edema and also brings back the gastric
tonicity.
6. Correction of hypocalcemia: Intravenous calcium gluconate will correct associated
hypocalcemia.

Q/What are the electrolyte changes in patients with gastric outlet

obstruction ?
These patients are chronically dehydrated due to
vomiting and has electrolyte abnormalities.
Initially due to vomiting, the major loss is fluid rich in
hydrogen and chloride ion resulting in
hypochloremic metabolic alkalosis. At this stage
serum sodium and potassium is usually normal. to
compensate for this metabolic alkalosis the kidney
excretes low chloride and more bicarbonate. While
losing bicarbonate the kidney also loses sodium. The
reaction of urine is alkaline.
When the gastric losses continue the patient
becomes progressively more dehydrated and
145 STAGERS NOTES

hyponatremic. In an attempt to conserve the circulating volume and to conserve

sodium the kidney absorbs sodium preferentially and excretes hydrogen ion and
potassium ions. The

reaction of urine become acidic due to loss of hydrogen ion in urine.

At this stage in spite of metabolic alkalosis the kidney excretes an acidic urine. This
is called paradoxical aciduria. Hence, the alkalosis becomes more severe and the
hyponatremia and hypokalemia becomes more marked. Secondary to the
metabolic alkalosis plasma ionized calcium may fall and may result in tetany
and disturbances of conscious level.

Q/what are the pre-operative preparations for thyroid surgery and How
to know that the patient is ready for surgery?

1. 1-Carbimazole 30–40 mg day–1 is the drug of choice for preparation.

When euthyroid (after 8–12 weeks), the dose may be reduced to 5 mg 8-
hourly or a ‘block and replace’ regime used The last dose of carbimazole
may be given on the evening before surgery.
2. B-blockers: act on the target organs and
not on the gland itself.
Propranolol inhibits the peripheral
conversion of T4 to T3. This results in
very rapid control and operation may be
arranged within 1 week

The appropriate drugs are propranolol 40 mg t.d.s.,. The dose of -blocker is

increased to achieve the required, clinical response and quite often larger
doses (propranolol 80 mg t.d.s. or nadolol 320 mg once daily) are necessary
B-Blockers do not interfere with synthesis of thyroid hormones, and
hormone levels remain high during treatment and for
146 STAGERS NOTES

some days after thyroidectomy. It is therefore important to continue to give

the drug for 7 days postoperatively.

3. Iodine -blocker for the 10

days before operation. Iodide alone produces a transient remission and
may reduce vascularity, thereby marginally improving
safety.

Q/How to know that the patient is ready for surgery?

1. Symptomatic relief.
2. Gaining weight.
3. Sleeping pulse.(pulse alone is not an indicator of euthyroid as lnderal
will normalize pulse even before action of Neomercazol)
4. Serum T3 ,T4 level.
147 STAGERS NOTES

Diabetic foot
This patient is 65 years old male with 20 years history of diabetis ,
presented to you with leg ulcer , how can you mange him?

 Detailed history
 Physical examination:
A. General look to the patient : old age male sitting on the chair ,
confortable , not dysponeic looks pale , thers no cyanosis of
yellowish discoloration of the skin
B. Local examination:
Inspection:
1. Site: ex : on the hell of the right foot about 3 cm from
medical maelous
2. Size: ex about 4 cm in length , 3 cm in width and 1
cm in depth (use tape measure)
3. edge : usually puch out edge in neuropathic ulcer
4. color
 red : inflammation (cellulitis)
 black(gangareen)
 pale (anemic)
 normal as the surrounding
5. base: dry with dead necrotic tissue or wet with discharge
6. discharge
7. depth
8. amputation: local of major
9. state of local tissue : lymph nodes and surrounding skin
10.relation to the surrondings : joints , vessels , skin
11. skine thickness
12. dry kine
148 STAGERS NOTES

13. loss of tone

14. inspect between toes and left the foot and look for ulcer at dependent site
15. any dilated veins
16. foot deformity
17. muscle weasting
palpation
1. tenderness : usally painless
2. temperature : compare with other leg (use the dorsum of your hand )
 cold:ischemia
 hot : inflamtion
1. fell the base of the ulcer( wear gloves )
2. regional lymph node
3. pulses : dorsalis pedis, posterior tibial,popliteal and femoral artery (compare)
4. sensation
5. touch and pain by pinbrick and cotton
6. tuning fork for vibration
7. position sense : aske the patient to close his eye and look move his big toe up
and down
8. pitting edema
9. reflexes

general examination of the patient

 investigations :
general

1. RBS, blood urea and serum creatinine

2. CBC, ESR
3. GUE
4. WBC
5. CXR , ECG
6. Lipid profile

Spesefic :
149 STAGERS NOTES

1. Take swap for culture and sensitivity

2. X- ray for the foot :
 Amputation
 Bone deformity
 Gas ( due to gas forming anerbic organisms ex: clostridia prephrenges
 Callous formation
 Calcification (vessel or lymph nod )
 Forging body
 Soft tissue swelling
 Osteomyelitis

3. Bone isotops scan

4. Doppler US for blood flow in the leg and the foot
5. Bone biopsy : detecting osteomyelitis

 Treatment :

1. Control of the blood sugar

2. Debridement
3. Broad spectrum antibiotics according to the culture and sesntivity
4. Dressing
5. Keep it dry
6. Bed rest , avoid weight bearing
7. Avoid tight shoes
8. Trete anny diabetic complications: CVD , renal diseases
9. Regular exercise to the foot
10. Arerial surgery if possible
151 STAGERS NOTES

Q/ how can you classify the diabetic ulcer ?

According to Wagner's classification

Q/ how long swap culture takes ?

About 3 days

Q/ do you give the patient antibiotics before the result of the cultre
and sensitivity or you wait it ?
I will give broad spectrum antibiotics untile the result of the cultre and
sesnetivity

Q/ What are the facors that affect wound healing ?

Local Factors

Systemic Factors
151 STAGERS NOTES

uremia

-steroidal anti-inflammatory drugs,

chemotherapy

Q /What are the complications of DM?

Acute complications of DM
1- DKA
2- Non –ketotic hyperosmolar diabetic coma
3- Hypoglycaemia
4- lactic acidosis
Chronic complications
 Microvascular complications
a) retinopathy
b) peripheral nephropathy
c) neuropathy
d) diabetic foot
e) autonomic neuropathy
 Macrovascular complications
a) CVA
b) IHD ( MI & vascular disease )

Q/ what are the predisposing factors for diabetic foot ?

A. Vascular disease :caused by :

1. Atherosclerosis : leads to reduce the blood supply to the lower limb , so
thers delay in healing of minor wounds , coexist with increase the incidence of
152 STAGERS NOTES

trauma and injuries to that limb due to sensory dysfunction caused by DM (

neuropathy )

So low blood supply increses the chance for multi-organisms infections

especially anaerobic organisms

2. Calcifications of the arteries : due to prolonged diabetic metabolic

disturbance
3. Angiopathy :
 Decreases the blood pressure in large vessels
 Tunica media of muscular artries are calcified and incompressible
 Macro-angiopathy with thickening of the intima
4. Changes in blood elements :
 Increases the platelet adhesion
 Increases the platelet aggregation
 Increases the platelet turnover
 Increases the clotting factor leads to microthrombi and micro infarct

B. Neuropathy
Loss of pain perception: so small injres goes unnoticed

Paralysis of the small musceles of the foot leads to clowing of toes and reduces
the effective load bearing area under the fore foot

Autonomic neuropathy:

 Failure of the reflex dilatation in response to local injery

 Abnormal vasoconstriction in response to cold

C. Infection: increses the risk for infection due to:

 Abnormal immune response to inflammation
 Decreses the effecasy of process of repair
153 STAGERS NOTES

Q/what is the most common microorganism in that causes infection in

diabetic foot ?
This infection is caused by mutiorganisms that includes

 Enterococci
 Stphylococci
 Clostridia
 E coli

but bactroids are the most common organisms isolated

Q/ What is the cause of anemia in patient with diabetic foot ? how can
you you treat it ?
Due to blood haemolysis by clpstrdia prephrenges , it treated by eradicate the
infection by antibiotics

Q/ what are the indications of antibiotics therapy in patient with

diabetic foot ?
1.Treatment of cellulitis

 Its curative if thers no abscess

 It limte the sepreda of infection befor drainage if abscess present

2.Propylaxisis

 Prior to local or major amputation

154 STAGERS NOTES

Q/What are the types of amputation?

155 STAGERS NOTES

Fluid therapy

– Q/What are the types of fluid in general

1. Crystalloid (dextrose ,normal saline, glucose saline ,ringer lactate)

2. Colloids (whole blood, FFP ,albumin

3. Others such as manitol.

Q/What are the general indications of i.v. fluid therapy

1. Sever dehydration1
2. Moderate dehydration with:
3. Diarrhea more then 100cc/hr
4. Comatose pt.
5. 4-Repeated vomiting
6. 5-Pt. refuse taking the ORS
7. 6-Abdominal distention because of the paralytic ileus or gastric dilation

ISOTONIC SOLUTIONS
Normal saline 0.9%
Composition

0.9% Sodium chloride

Content:

 Na = 150 mmol/ l
156 STAGERS NOTES

 CL = 150 mmol/l
Osmolarity : 308 mosmol /l

Indications of NS 0.9%
1. Initiating treatment of sever dehydration
2. In initiating treatment of diabetic ketoacidosis
3. Drug administration
4. Gastric lavage , wound washing(not I.V.)
5. Mild hypernatremia’
6. Shock
7. metabolic alkalosis
8. use with blood transfusion

 NOTE: • Because this replaces extracellular fluid, don't use in patients with
heart failure, edema, or hypernatremia; can lead to overload.

Contraindications of NS 0.9%
1. Hypertensive patient
2. Infant < 2 month.

Side effect NS 0.9%

1. Circulatory over load

2. Hypernatremia
3. Acidosis
4. Hypokalemia
157 STAGERS NOTES

(5 %Dextrose in water) 5% D/W

Composition

Dextrose monohydrate 5gm

Osmolarity : 277 mOsm/l

Indications of 5% D/W

1. Dehydration .
2. Hypernatremia
3. Drug administration
4. To replace water loss not associated with
electrolyte disturbance
5. As nutrient to give calories when GIT feeding isn't accessible as in deep
coma ( but need higher concentration of glucose ex 10 % or 20 %)
6. in case of sever hypoglycemic coma(10%, 20%)

Contraindications of 5% D/W

—Diabetic patient

side effects

1. Hypokalemia .
2. Osmotic Diuresis – Dehydration .
3. Transient hyperinsulinism.
4. Water intoxication .

NOTES :

• Solution is isotonic initially; becomes hypotonic when dextrose is metabolized.

• Don't use for resuscitation; can cause hyperglycemia.
• Use cautiously in renal or cardiac disease; can cause fluid overload.
158 STAGERS NOTES

• Doesn't provide enough daily calories for prolonged use; may cause eventual
breakdown of protein.

Some important notes about NS and Dextrose

 Use dextrose for Hypertensive patient instead of NS
 Use NS of diabetic patient instade of dextrose
 Patient with liver disease : use dextrose instade of normal saline because
these patient has secondary hyperaldosteronism with salt and water
retension
 Patient with diarrohea and vomiting : use ringer or NS instated of dextrose
to replace fluid and electrolyts loss (dextrose has no electrolytes )
 In case of hyperkalemia , use dextrose (10%) instade of NS , since glucode
enhance the potassium to enter inside the cells
 In case of hypokalemia , use NS instde of dextrose when you give
potassium (slow IVI ), as above …
 If the patient has DM and HT at the same time : give dextrose with insulin
units or you can give ringer
 NS use for strilisation of the wounds , while dextrose not use …
 Some drugs are not mixed with dextrose (IVI)
 LASIX
 ferrous ampules

 Some drugs are not mixed with NS (IVI)

1- amiodarone >> used for heart rhythm disorders
2- amphotericin B >> for fungal infections
3- sodium nitroprusside >> a drug used to reduce very high
(blood pressure)
159 STAGERS NOTES

Ringer Lactate
Composition

 Na+ : 131mmol\L
 K+ : 5mmol\L
 Ca++ : 2mmol/L
 Cl- : 111mmol/L
 Hco3 : 29mmol/L

Osmolarity : 309 mOsm/l

The constituent of RL or ringer solution is

cloasly related to the normal electrolyts of the blood

# lactate metablised by the liver to bicarbonate and lactate

So we use it in case of metabolic acidosis but not used in case of lactic acidosis

#not used in liver disese because the liver unable to metablise it

#use with caution in case of renal failure because it conatins K

Indications of Ringer lactate

1. first line in resuscitation
2. in cases of blood loss
3. rehydration with good urine output

Contraindications of Ringer lactate

1. Hyperkalemia
2. No urine output

Side effect of Ringer lactate

1. If impaired urine out causehyper ururocemia

161 STAGERS NOTES

2. Electrolyte disturbances

Ringer solution

HYPOTONIC SOLUTIONS

0.45% sodium chloride (half-normal saline solution)

Indications

1) water replacement
2) DKA after initial normal saline solution and before dextrose infusion
3) Hypertonic dehydration
4) sodium and chloride depletion
5) gastric fluid loss from nasogastric suctioning or vomiting

NOTES :

• Use cautiously; may cause cardiovascular collapse or increased intracranial

pressure.

• Don't use in patients with liver disease, trauma, or burns.

HYPERTONICS SOLUTIONS
Dextrose 5% in half-normal saline solution
Indications :

• DKA after initial treatment with normal saline solution and half-normal saline
solution—prevents hypoglycemia and cerebral edema (occurs when serum
osmolality is reduced too rapidly)

• In patients with DKA, use only when glucose falls < 250 mg/dl.
161 STAGERS NOTES

Dextrose 5% in normal saline solution

Indications :

1) Hypotonic dehydration
2) Temporary treatment of circulatory insufficiency and shock if plasma
expanders aren't available
3) Syndrome of inappropriate antidiuretic hormone (or use 3% sodium chloride)
4) Addisonian crisis
5) 3% sodium chloride solution

Mannitol (osmotic diuresis)

Composition :

Mannitol

Osmolarity : 549 mOsm/l

Indications

1. Brain edema
2. Meningitis
3. Nephrotic syndrome
162 STAGERS NOTES

Fluid compartments
We have two majoir fluid compartements in the body :

1. intracellular fluid: the total amount of intracellular

fluid averages 40% of the person's body weight, or
about 28 L.
2. extracellular fluid :The total amount of extracellular
fluid averages 20% of the person's body weight, or
about 14 L.

Extracellular fluid can be broken down further

into:
 interstitial fluid, which surrounds the cells,
 intravascular fluid, or plasma, which is the liquid portion of blood.
 In an adult, interstitial fluid accounts for about 75% of the extracellular
fluid. Plasma accounts for the remaining 25%.
163 STAGERS NOTES

Renin-angiotensin-aldosterone system

Atrial natriuretic peptide

The renin-angiotensin-aldosterone system isn't the only factor at work balancing
fluids in the body. A cardiac hormone called atrial natriuretic peptide (ANP) also
helps keep that balance. Stored in the cells of the atria, ANP is released when atrial
pressure increases. The hormone counteracts the effects of the renin-angiotensin-
aldosterone system by decreasing blood pressure and This powerful hormone:

• suppresses serum renin levels

• decreases aldosterone release from the adrenal glands
• increases glomerular filtration, which increases urine excretion of sodium and
water
• decreases ADH release from the posterior pituitary gland
• reduces vascular resistance by causing vasodilation.
164 STAGERS NOTES

Classification of the fluid

A. Crystalloids

1. Isotonic solutions
 Contain about the same concentration of osmotically active particles as
extracellular fluid, so fluid doesn't shift between extracellular and
intracellular spaces
 Osmolality: 240 to 340 mOsm/kg
 Example: D5W, normal saline solution, and dextrose 5% in normal saline
solution
2. Hypotonic solutions
 Are less concentrated than extracellular fluid, which allows movement
from the bloodstream into the cells, causing cells to expand
 Osmolality: less than 240 mOsm/kg
 Example: half-normal saline solution
 Can cause cardiovascular collapse from vascular fluid depletion or
increased ICP from fluid shifting into brain cells
 Avoid using in patients at risk for increased ICP, such as those who have
had a stroke, head trauma, or neurosurgery
 Also avoid using in patients who suffer from abnormal fluid shifts into the
interstitial space or body cavities, such as in liver disease, burns, or trauma
3. Hypertonic solutions
 Are more concentrated than extracellular fluid, which allows movement
of fluid from cells into the bloodstream, causing cells to shrink
 Osmolality greater than 340 mOsm/kg
 Examples include dextrose 5% in half-normal saline solution, 3%
sodium chloride solution, and dextrose 10% in normal saline solution
 May not be tolerated by those with cardiac or renal disease
 May cause fluid overload and pulmonary edema
 Should not be used in patients at risk for cellular dehydration, such as
those with DKA

B. Colloids
 Act as plasma expanders
 Are always hypertonic, pulling fluid from cells into the bloodstream
 Examples: albumin, plasma protein fraction, dextran, and hetastarch
165 STAGERS NOTES

 Require close monitoring for signs and symptoms of hypervolemia, such as

increased blood pressure, dyspnea, and bounding pulse

Delivery methods
• Methods include peripheral and central I.V. therapy
• Choice based on purpose and duration of therapy; patient's diagnosis, age,
and health history; condition of the veins
• Catheters and tubings are selected according to type of therapy and site used
• Complications of I.V. therapy
• Infiltration: leakage of fluid from vein into surrounding tissue when access
device dislodges from the vein

Complications of I.V. therapy

1) Infection: may occur at the insertion site; requires monitoring for purulent
drainage, tenderness, erythema, warmth, or hardness at the site
2) Phlebitis: inflammation of the vein
3) Thrombophlebitis: irritation of the vein with clot formation
4) Extravasation: leakage of fluid into surrounding tissues; results when
medications seep through veins, producing blistering and eventually necrosis
5) Severed catheter: dislodgment of a piece of catheter into the vein (rare)
6) Allergic reaction: may result from I.V. fluid, medication, catheter, or latex
port in the I.V. tubing
7) Air embolism: entry of air into a vein; results in decreased blood pressure,
increased pulse, respiratory distress, increased ICP, and loss of consciousness
8) Speed shock: too-rapid infusion of I.V. solutions or medications; results in
facial flushing, irregular pulse, decreased blood pressure, and possibly loss of
consciousness and cardiac arrest
9) Fluid overload: gradual or sudden occurrence; produces neck-vein
distention, increased blood pressure, puffy eyelids, edema, weight gain, and
respiratory symptoms
166 STAGERS NOTES

Some important notes about acid base balance

• Acids—molecules that can give hydrogen molecules to other molecules;

include solutions with a pH below 7
• Bases—molecules that can accept hydrogen molecules; include solutions with
a pH above 7
• Must maintain a delicate balance for the body to work properly
• Metabolism and body functions affected by slight imbalances
• Imbalance caused by infection, trauma, and medications

Understanding pH
• pH—calculation based on the percentage of hydrogen ions and the amount of
acids and bases in a solution
• Normal blood pH—7.35 to 7.45, which represents the balance between
hydrogen ions and bicarbonate ions

Deviation from normal pH

• Acidosis—blood pH is below 7.35 and either the hydrogen ion concentration
has increased or the bicarbonate level has decreased.
• Alkalosis—blood pH is above 7.45 and either the hydrogen ion concentration
has decreased or the bicarbonate level has increased.
• A pH below 6.8 or above 7.8 is generally fatal.
• Deviation compromises well-being, electrolyte balance, activity of critical
enzymes, muscle contraction, and basic cellular function.

Maintaining acid-base balance

Chemical buffer systems

• Bicarbonate buffer system—buffers blood and interstitial fluid
• Phosphate buffer system—reacts with acids and bases to form compounds
that alter pH; especially effective in the renal tubules
167 STAGERS NOTES

• Protein buffer system—acts inside and outside the cell; binds with acids and
bases to neutralize them

Respiratory system
• Functions as the second line of defense
• Responds to pH changes in minutes
• Makes temporary adjustments to pH
• Regulates carbon dioxide levels in the blood by varying the rate and depth of
breathing
• Compensates with quick and deep breathing so more carbon dioxide is lost
when bicarbonate levels are low
• Compensates with slow, shallow breathing so more carbon dioxide is retained
when bicarbonate levels are high
• Regulates carbonic acid production
Kidneys
• Make long-term adjustments to pH
• Reabsorb acids and bases or excrete them into urine

• Produce bicarbonate to replenish lost supply

• Regulate bicarbonate production
• Compensate with bicarbonate retention and increased acid excretion when
Paco2 level is high
• Respond with bicarbonate excretion and increased acid retention when Paco2
level is low

Anion gap
• Represents the level of unmeasured anions in extracellular fluid
• Normally ranges from 8 to 14 mEq/L
• Helps differentiate acidotic conditions
168 STAGERS NOTES
169 STAGERS NOTES

Important anatomical and physiological

notes

Q/What are the boundaries of inguinal canal ?

inguinal canal is an oblique canal with a length of about 3.8 cm, situated at the
lower part of anterior abdominal wall and extends from the deep inguinal ring to
the superficial inguinal ring.
This canal is bounded:

 Anteriorly: By the external aponeurosis along its whole length and reinforced
laterally by the muscular fibers of the internal oblique.
 Posteriorly: By the fascia transversalis throughout and reinforced medially by
the conjoint tendon.
 Medially: By the lateral border of the rectus sheath.
 Roof: Formed by the conjoined tendon and arched fibers of internal oblique
and transverses abdominis.
 Floor: Formed by the lacunar ligament medially and the inguinal ligament
laterally.
171 STAGERS NOTES

Q/What is Hesselbach’s triangle?

The medial part of the inguinal canal is Hesselbach’s triangle being bounded:

 Laterally by the inferior epigastric vessels.

 Medially by the lateral border of the rectus sheath.
 Base is formed by the upper concave surface of the medial part of the
inguinal ligament and the lacunar ligament.

Q/What are the contents of inguinal canal?

The inguinal canal contains:

 Spermatic cord in male and round ligament of uterus in female.

 in addition, the ilioinguinal nerve traverses through the inguinal canal.
 The nerve does not come through the deep ring enters the inguinal canal by
piercing the internal oblique muscle and emerges out through the superficial
inguinal ring.
171 STAGERS NOTES

Q/ What are the coverings of spermatic cord?

The coverings of spermatic cord are outside inwards:

 External spermatic fascia: Derived from the external oblique aponeurosis and
covers the cord beyond the superficial inguinal ring.
 Cremesteric muscle and fascia: Derived from the internal oblique aponeurosis.
 Internal spermatic fascia: Derived from the fascia
transversalis.

Q/ What is the anatomy of deep inguinal ring?

The deep inguinal ring lies 1.25 cm above the inguinal ligament at the midinguinal
point (A point midway between the symphysis pubis and anterior superior
iliac spine). This is actually not an opening but the mouth of a prolongation of
fascia transversalis dragged down by the gubernaculum. The inferior epigastric
vessels lies medial to the deep inguinal ring.
The spermatic cord in male and round ligament in female emerges through the
deep inguinal ring.
172 STAGERS NOTES

Q/What is the anatomy of superficial inguinal ring ?

The superficial inguinal ring is formed by splitting of external oblique aponeurosis
at its insertion medially. Base is 1.25 cm and the height is 2.5 cm.
The boundary of superficial inguinal ring are
Base: Formed by the pubic crest.

 Medially: Superomedial crus of external oblique aponeurosis.

 Laterally: inferolateral crus of external oblique aponeurosis
• The two crura are joined by intercrural fibers.
173 STAGERS NOTES

Q/What is the boundary of femoral ring ?’

 Anteriorly: inguinal ligament.

 Posteriorly: Fascia covering pectineus and cooper’s ligament.

 Medially: concave margin of lacunar ligament.
 Laterally: Septum separating the femoral vein.

Q/What are the arterial supply of stomach ?

 Vessels along the lesser curvature:

• Left gastric artery—branch of celiac trunk.
• Right gastric artery—branch of hepatic
artery.

These two arteries anastomose along the

lesser curvature and divides into anterior and
posterior branches and supplies the body
and pyloric part of the stomach.
174 STAGERS NOTES

 Vessels along the greater curvature:

• Right gastroepiploic artery—a branch of gastroduodenal artery.
• Left gastroepiploic artery—a branch of splenic artery.

These two arteries anastomose along the greater curvature and gives off
branches which
supplies the body and pyloric part of the stomach.

 Short gastric arteries,

which are branches of splenic artery runs along the gastrosplenic

ligament and supplies the fundus of the stomach.
Some branches from gastroduodenal artery supplies the pyloric part of the
stomach.

Q/What is the venous drainage of stomach?

„ Veins along the lesser curvature:
• Right gastric vein drains into the portal vein.
• Left gastric vein drains into the portal vein.
„ Veins along the greater curvature:
• Right gastroepilploic vein drains into the superior mesenteric vein.
• Left gastroepiploic vein drains into the splenic vein.
• Short gastric vein drains into the splenic vein.
Prepyloric vein of Mayo runs anterior to the pylorus of the stomach and connects
the right gastric vein with the right gastroepiploic vein.

Q/What is the arterial supply of colon ?

 Cecum: Supplied by anterior and posterior cecal artery which are branches of
inferior division of ileocolic artery.
 Ascending colon: Supplied by right colic artery which is a branch of superior
mesenteric artery. The right colic artery divides into ascending and
descending branches. The ascending branch joins with the right branch of
175 STAGERS NOTES

middle colic artery and the descending branch joins with the superior branch
of ileocolic aretry.
 Right colic flexure: This is supplied by the ascending branch of right colic
artery and the right branch of middle colic artery.

 Transverse colon:
 Right 2/3rd of transverse colon develops from the midgut, hence is
supplied by the middle colic branch of superior mesenteric artery and
 the left 1/3rd develops from the hind gut and is supplied by the inferior
mesenteric artery.
 The middle colic artery divides into right and left branch.The right branch
joins with the ascending branch of right colic artery and the left branch
joins with ascending branch of left colic artery.
 The end arteries vasa recti arises from the marginal artery running along
the mesenteric border of the colon.
 Descending colon: Supplied by the left colic branch of the inferior mesenteric
artery.
 Sigmoid colon: Supplied by the sigmoid branches of the inferior mesenteric
artery.
176 STAGERS NOTES

Q/What is the average weight of liver

 The liver is the largest organ of the body.
 in adult male—1.4 kg. to 1.8 kg.
 in adult female—1.2 kg to 1.4 kg.

Q/What are anatomical lobes of liver?

the liver is demarcated into right and left lobes anatomically by the attachment of
falciform ligament in front and above and below and behind by the fissure for
ligamentum teres and ligamentum venosum. the right lobe constitutes 5/6th and
the left constitues1/6th of the liver.
177 STAGERS NOTES

Q/What are ligaments in relation to the liver

 Falciform ligament: A sickle shaped peritoneal fold connects the liver to the
undersurface of diaphragm and anterior abdominal wall up to the umbilicus.
it consists of two layers of peritoneum and at the free margin contains
ligamentum teres.
 Coronary ligament: it consists of upper layer reflected from the liver to the
diaphragm and lower layer reflected from the liver to the kidney (Hepatorenal
ligament).
 Right triangular ligament connects right lateral surface of the liver to the
diaphragm.
 Left tr iangular lig ament: it connects the upper surface of the left lobe to
the diaphragm.
 Lesser omentum: it consists of two layers of peritoneum and connects the
lesser curvature of the stomach and proximal 2.5 cm of duodenum to the
liver.
178 STAGERS NOTES

Q /What is porta hepatis?

This is a nonperitoneal transverse fissure on the under surface of the liver through
which the heaptic artery (right and left branches) and the portal vein (right and left
branches) enters into the liver and the hepatic ducts (right and left branches) and
lymphatics exit from the liver.
The relation of structures at the porta hepatis from before backwards are:

 Hepatic ducts in the front

 Branches of hepatic artery
 Branches of portal vein.
179 STAGERS NOTES

Q/What is ligamentum teres?

Ligamentum teres is the remnant of left umbilical vein and runs from the umbilicus
to the fissure for ligamentum teres and ends in left branch of portal vein in the
inferior surface of liver. This runs in the free margin of the falciform ligament.

Q/What is the blood supply of gallbladder and biliary tree ?

The gallbladder is supplied by the cystic artery
which is usually a branch of right hepatic
artery. The cystic artery arises behind the
common hepatic duct, crosses behind and
enters the gallbladder .
An accessory cystic artery arising from the
gastroduodenal artery may also supply the
gallbladder .
The bile duct is supplied by two vertical
arteries arising from the hepatic artery
running along the bile duct at 3 and 9 o’clock
position and giving off circumferential arteries anteriorly and posteriorly.
181 STAGERS NOTES

Q/How venous drainage of gallbladder occurs?

the cystic veins draining the gallbladder does not accompany the cystic artery.
These veins pierces the fossa for the gallbladder and drains into the intrahepatic
part of portal vein. Rarely cystic vein drains into the right
branch of portal vein.

Q/What is the lymphatic drainage of biliary tree ?

The lymphatics of gallbladder drain into the cystic lymph node of Lund. The cystic
lymph node lies at the junction of cystic duct and common hepatic duct.The
efferent from the cystic lymph nodes drains into the pericholedochal lymph nodes
and lymph nodes at the porta hepatis and supeorior and posterior pancreatico
dudenal lymph nodos. These lymphatic then passes into the celiac lymph nodes.

Q/What is the boundary of Calot’s triangle ?

The calot’s triangle is bounded:

 Above by the inferior surface of liver

 Below by the cystic duct and
 Medially by the common hepatic duct.

What are the functions of gallbladder?

Gallbladder performs a number of functions:

 Storage of bile: Gallbladder stores the bile during fasting. in fasting state the
bile secreted by the liver is diverted into the gallbladder via the cystic duct as
the sphincter of oddi remains in spasm.
 Concentration of bile: Gallbladder concentrates the bile by active absorption
of water, sodium bicarbonate and sodium chloride.The gallbladder is 5-10
times concentrated than the liver bile.
 Emptying of bile: in response to feeding, the gallbladder contract and the
sphincter of oddi relaxes, resulting in emptying of bile into the duodenum.
This is mediated by the hormone cholecystokinin.
181 STAGERS NOTES

 Secretion mucus-Gallbladder has the capacity of secretion of mucus. About

20 mL of mucus is secreted by the gallbladder mucosa per day. if the cystic
duct is obstructed due to any reason the bile cannot enter into the
gallbladder and the mucus secreted by the gallbladder remains pentup in the
gallbladder resulting in mucocele of gallbladder.

Q/What is the location and parts of pancreas?

Pancreas (Greek Word- “Pan” means all and “kreas” mean flesh) weigh approximately 80–90
gm and is located in the retroperitoneum behind the stomach and from the
concavity of the duodenum to the hilum of the spleen.
The pancreas consists of following parts:

 Head: Lies within the concavity of the duodenum. constitute about 30% of
the mass of pancreas.
 Neck: The junctional area between the head and body of the pancreas. The
neck of the pancreas overlies the superior mesenteric vein and the formation
of portal vein. extends from the left margin of the portal groove to the tail of
the pancreas.
 Tail: The extreme left portion of pancreas lying between two layers of
lienorenal ligament extending upto the hilum of the spleen.
 Uncinnate process- This is a triangular projection from the lower and left
portion of the head of pancreas which passes upwards and medially behind
the superior mesenteric vessels.

 Body
182 STAGERS NOTES

Q/What is pancreas divisum ?

Pancreas divisum is a congenital anomaly where there is failure of fusion of dorsal
and the ventral pancreatic duct.
In this condition the dorsal pancreatic duct draining the body and tail of the
pancreas opens into the minor duodenal papilla.
The ventral pancreatic duct draining the head and neck of the pancreas opens into
the major duodenal papilla.
This may result in functional obstruction of the minor duodenal papilla draining the
major part of the pancreas resulting in recurrent pancreatitis.

Q/What are the islet of Langerhans?

These are endocrine cells in the pancreas and constitutes about 10–20% of
pancreatic mass. This consists of:

 Beta cells (70%): Secretes insulin.

 Alpha cells (20%): Secretes glucagon.
 Delta cells: Secretes somatostatin.
 Pancreatic polypeptide cells: Scretes pancreatic polypeptide.
183 STAGERS NOTES

 VIP cells: Secretes vasoactive intestinal polypeptide.

Q/What is the arterial supply of pancreas

 Head and neck: Supplied by superior and inferior pancreaticoduodenal

arteries.
 Superior pancreaticoduodenal artery is the branch of gastroduodenal
artery, and inferior pancreaticoduodenal artery is the branch of superior
mesenteric artery. Each of these arteries gives off dorsal and ventral branches
and an anastomotic network is formed on the ventral and dorsal aspect of the
head of pancreas.
 Body and tail: Supplied by the pancreatic branches of splenic artery. One of
these branches is large and accompanies the main pancreatic duct and is
known as arteria pancreatica magna.
 Occasionally a dorsal pancreatic branch arising from splenic artery or coeliac
trunk may supply the dorsal surface of the pancreas.
 A capillary plexus supplies the islet cells and the acini.
 Venous drainage: The veins follows the arteries and drains into the superior
mesenteric vein, splenic vein and the portal vein.
184 STAGERS NOTES

Q/Where the base of appendix is

located
The base of the appendix is attached to
the posteromedial wall of the cecum 2
cm below the ileocecal junction.
if the taenia coli in the cecum are traced
downwards all the three taenia coli
converges to the base of the appendix
and continue as the longitudinal muscle
coat of the appendix.
on the surface the base of the apendix
lies at MacBurney’s point which is located
at the right spinoumbilical line (Line joining between the anterior superior iliac
spine and the umbilicus) at the junction of medial two-thirds and lateral one-third.

Q/What is mesoappendix?
This is the mesentery of the appendix
attached to the mesenteric border of the
appendix. The mesoappendix contains the
appendicular vessels. The mesoappendix does
not extends up to the tip of the appendix and
the appendicular vessels stops just before the
tip of the appendix.
The tip of the appendix is the least vascular
area, and in obstructive type of appendicitis
the commonest site of gangrene is the tip of
the appendix

Q/Which vessels supply the appendix?

The appendix is supplied by appendicular artery which is a branch of inferior
division of ileocolic artery. The appendicular artery is an end artery.
185 STAGERS NOTES

Sometimes an accessory appendicular artery may arise from the posterior cecal
artery and may supply the appendix in addition to appendicular artery.

Q/What are the branches of celiac trunk

This is the 1st ventral branch of abdominal aorta. This subdivides into:

 Left gastric: Runs along the lesser curvature and anastomose with the right
gastric artery. Gives off branches to esophagus, fundus of stomach, body and
cardiac end of stomach.
 Hepatic artery: The hepatic artery runs in the gastrohepatic omentum. Part
of the hepatic artery from its origin to the origin of gastroduodenal artery is
called the common hepatic artery. Part of the hepatic artery from the origin of
gastroduodenal artery to its bifurcation is called the hepatic artery proper.
The branches of hepatic artery includes:

• Gastroduodenal which divides into superior pancreaticoduodenal and

right gastroepiploic artery.
• Right gastric.
• Branches to bile duct: Arteries to the bile duct runs at 3 o’clock and 9
o’clock position.
• cystic artery arises from the right branch of the hepatic artery.
• two terminal branches: Right and left hepatic branches supplying the
corresponding lobes of the liver.
• An accessory hepatic artery may arise from the superior mesenteric
artery or left gastric artery.

 Splenic artery: Runs along the upper border of pancreas and reaches the
splenic hilum. The branches of splenic artery are:

• Short gastric branches

• Left gastroepiploic artery.
186 STAGERS NOTES

Q/What are the branches of superior mesenteric artery

The superior mesenteric artery is a ventral branch of abdominal aorta and arises at
the level of L1 vertebra. The branches includes:

 inferior pancreaticoduodenal: Runs in the pancreaticoduodenal groove and

anastomose with the superior pancreaticoduodenal artery.
 Middle colic
 Right colic
 Ileocolic
 Jejunal and ileal branches.
187 STAGERS NOTES

Q/What are the branches of inferior mesenteric artery ?

inferior mesenteric artery is a ventral branch of the aorta at the level of L3
vertebra.The branches includes:

 Left colic artery.

 Sigmoid artery: May be more than one in number.
 Superior rectal artery: inferior mesenteric artery continues as the superior
rectal artery.
188 STAGERS NOTES

Q/Describe anatomy of portal vein ?

The portal system of veins carries blood from the abdominal part of the
gastrointestinal system, spleen, pancreas and gallbladder to the liver.
The blood in the portal system traverses through two sets of capillaries:
„ 1st set of capillary in the wall of the gut
„ 2nd set of capillary at the liver where the blood drains into the sinusoids and from
there the blood is returned via the hepatic veins and the inferior vena cava.
„ Origin of portal vein: This is formed by the union of superior mesenteric vein and
the splenic vein behind the neck of the pancreas.
„ Course of portal vein:
The portal vein ascends behind the neck of the pancreas and the pyloric part of the
stomach and runs in the free margin of the lesser omentum running inbetween and
behind the bile duct and the hepatic artery. The bile duct lies in the right free
margin and the hepatic artery lies to the left of the duct. As the vein reaches to the
porta hepatis it divides into the right and
189 STAGERS NOTES

left branches and enters into the liver.

Tributaries of portal vein:
 Superior mesenteric vein.
 Splenic vein (inferior mesenteric vein drains into the splenic vein).
 Right gastric vein.
 Left gastric vein (coronary vein).
 cystic vein.
 Sometimes prepyloric vein.
 Superior pancreaticoduodenal vein.
 Paraumbilical vein drains into left branch of portal vein.

Q/What are the sites of portacaval anastomosis ?

-At the abdominal part of the esophagus:
• Portal: esophgeal tributaries of left gastric vein.
• Systemic: esophageal tributaries of azygos and accessory hemiazygos vein.
-At the dentate line of anal canal:
191 STAGERS NOTES

• Portal: Superior rectal vein.

• Systemic: Middle and inferior rectal veins.
-Around the umbilicus:
• Portal: Paraumbilical vein.
• Systemic: Thoracoepigastric and superficial epigastric.
in portal hypertension these veins forms a bunch of dilated veins around the
umbilicus
(caput medusae).
-In the bare area of liver:
• Portal: Veins from the liver.
• Systemic: Diaphragmatic veins.
-In the retroperitoneum:
• Portal: Veins of colon and duodenum.
• Systemic: Retroperitoneal veins and veins from kidney.
-If due to developmental error the ductus venosus remains patent, then there is
direct communication between the left branch of portal vein and the inferior vena
cava providing a portacaval anastomosis.
191 STAGERS NOTES

Q/What are ligament of Cooper?

These are fibrous strands extending from the breast
parenchyma to the skin of the breast. When cancers cells
spreads along these fibrous strands there appears
dimpling of the skin due to attachments of the ligaments
to the skin.

Q/What are the layers of scalp ?

The scalp is the soft tissue covering of the skull and consists of:
S: Skin
c: Subcutaneous tissue
A: Galea aponeurotica and occipitofrontalis
L: Loose connective tissue
P: Pericranium.

Q/What is the blood supply of the scalp ?

The scalp has a rich blood supply and a small cut may cause profuse bleeding. The
following arteries supply the scalp:
i. Supratrochlear and supraorbital arteries, branches of ophthalmic artery run along
the corresponding nerves
ii. Superficial temporal artery, the smaller terminal branch of the external carotid
artery runs up infront of the tragus along with auriculotemporal nerve.
iii. Posterior auricular artery, a branch of external carotid artery ascends pehind the
pinna.
iv. occipital artery, a branch of external carotid artery runs up in occipteal region
along with greater occipital nerve.
The venous drainage occurs through:
i. Supratrochlear and supraorbital veins, which joins at the medial angle of the orbit
to form the facial vein
ii. Superficial temporal vein, which joins with the maxillary veins in the substance of
the parotid gland to form the retromandibular vein.
192 STAGERS NOTES

ii. Posterior auricular vein, which joins with the posterior division of the
retromandibular vein to form the external jugular vein.
iv. occipital vein, which drains into the occipitial venous plexus. The occipitial
venous drains into both the vertebral vein or internal jugular vein.
The veins of the scalp freely anastomose with each other and are connected to the
diploic veins of the skull bone. These veins also communicates with the intracranial
venous sinuses through the valveless emissary veins.

Q/Where is the thyroid gland located?

The thyroid gland is located in the thyroid region.
each of the lateral lobes extends above up to the oblique line of the thyroid
cartilage and
193 STAGERS NOTES

below upto the 4th or 5th tracheal ring.

The isthmus of the thyroid gland lies over the 2nd, 3rd and 4th tracheal rings.

Q/What is the disposition of the isthmus of the thyroid gland?

The isthmus of the thyroid gland joins the two lobes and lies over the 2nd, 3rd and
4th tracheal rings.
The isthmus has superior and inferior borders and anterior and posterior surfaces.
The posterior surface lies over the 2nd, 3rd and 4th tracheal rings.

Q/What are the different triangles in the neck ?

There are different triangles in the neck. Broadly these are :
„ Anterior triangle: Boundary
• Anteriorly: Midline of the neck from chin to the suprasternal notch.
• Posteriorly: Lateral border of the sternocleidomastoid.

• Base: Lower border of the mandible and a line joining between the angle of
mandible
and mastoid process.
• Apex: Lies at the suprasternal notch.
„ Posterior triangle: Boundary:
• Anteriroly lateral border of sternocleidomastoid.
• Posteriorly medial border of trapezius.
• Base is formed by the clavicle.
• Apex at the mastoid process where trapezius and the sternocleidomastoid meet.
194 STAGERS NOTES

Q/What is ansa cervicalis ?

This is a loop of nerve lying in front of the carotid sheath and the larynx and
supplies the infrahyoid muscles.
*Formation:
• Superior root: From the descending branch of hypoglossal nerve. its fibers are
derived from the ventral rami of 1st cervical nerve.
• inferior root is formed by the branches from ventral rami of 2nd and 3rd cervical
nerve.
− Supply: Branch from the superior root supplies the superior belly of omohyoid.
− Branch from the ansa supplies the sternohyoid, sternothyroid and inferior belly of
omohyoid.

Q/What are the coverings of testis?

The coverings of the testis are the layers of the scrotum and the intrinsic coverings
195 STAGERS NOTES

of the testis.
These are from outside inwards:
- Skin
-Dartos muscle
-external spermatic fascia
- cremesteric fascia
- internal spermatic fascia
- Parietal layer of tunica vaginalis
- intrinsic coverings of the testis. The intrinsic coverings of the testis includes the
visceral layer
of tunica vaginalis, tunica albuginea and tunica vasculosa.

Q/What is the internal structure of testis ?

Q/What is the blood supply of testis ?

Arterial supply:
The testis is principally supplied by the testicular artery which is a lateral branch of
abdominal aorta at the level of L1 vertebra.
The testis may also be supplied by the artery to the vas which is a branch of
superior vesical artery.
A minor supply may come from cremasteric artery which is a branch of inferior
epigastric artery.
196 STAGERS NOTES

Venous drainage:
The testis is drained by pampiniform plexus formed by 15–20 veins emerging from
the upper pole of the testis. At the level of the superficial inguinal ring these veins
join to form 4–5 veins and at the level of deep inguinal ring these veins join further
to form 2 veins and at the retroperitoneum these two veins join to form a single
testicular vein. The right testicular veins drain at the inferior vena cava and the left
testicular vein drains into the left renal vein.

Q/How does the lymphatic of testis drains ?

The lymphatics of testis follows the vessels and drains into the para aortic lymph
nodes at the level of L1 vertebra.
197 STAGERS NOTES

Q/What are the common sites of perforating veins?

in great saphenous system:
„ Saphenofemoral junction at saphenous opening—largest perforator
„ Adductor canal perforator at mid thigh
„ Perforator above the knee
„ Perforator below the knee

„ Medial ankle perforator at 5 cm, 10 cm

and 15 cm above the medial side of the
leg

„ Perforators at the level of ankle

„ Apart from these constant perforators

there are some other inconstant
perforators at different level joining the
superficial and deep system of veins.
in short saphenous system:
„ Saphenopopliteal junction situated at 2
cm below to 15 cm above the knee joint
line.
198 STAGERS NOTES

STAGERS NOTES
CLINICAL MEDICINE
DVT 199
RF 207
Asthma 222
COPD 235
DM 246
HF 272
IHD 282
AF 292
CVA 294
Auscultation from back 306
BP measurment 312
Pleural effusion 316
CXR 321
Examination Of Precordium 328
JVP 332
Basic & Advanced life support 332
examination of the speech 337
7th cranial nerve 339
fever 346
Pleural effusion 352
ECG notes 362
Drugs in medicine 370
Radiology 383
Blood transfusion 400
199 STAGERS NOTES

Case NO. 1 DVT

Q/ what are the findings on examination in DVT?

on examination we have to look for

a) On inspection:
1. Swelling ( by using tap measure , 10 cm
bellow tibial tuberosity takes the diameter
of both legs and compare)
2. Color( blue of dark red in venous
obstruction, pale in A. obstruction)
3. Hair distribution
4. Scar or ulcer
5. Site for trauma
6. Discoloration
7. The texture of the skin ( thin skin , shiny,
scaling)
8. Any amputation
9. Bleeding sites
10. Bruses
b) On palpation looks for first you have to aske the patient about
any pain
1. Temperature(cobararism using the back of your hand)
2. Tenderness
3. Edema : pitting or not pitting( using your thump..press about 15 sec. then
palpate the site of pressure …

If you found pitting edema on the dorsal apect of the foot then ascend upward
untell it disappear)

4. Pulses
211 STAGERS NOTES

 Posterior tibial( 2 cm below and behind the medial malleolus)

 Anterior tibial ( midway between boath maleoi anteriory
 Doralis pedis ( lateral to the extensor holloses longus tendon, you
have to flex the big toe the tendon becomes clear then palpate lateral
to it)
 Popliteal A. (by flextionthe leg , it defecult to palpate , if the vessel
easly palpable …think of popliteal A. aneurism)

5. Homan’s sign (pain in the calf or behind the knee on dorsiflexion of the ankle)
not used nowadays

Q/ What are the causes of recurrent DVT and DVT in young age ?
SLE , anti-phospholipid antibody syndrome and congenital anticoagulant
deficiency

Q/ what is the benefit of know that this case of DVT due to APA?
In this case we have to increses the INR to reduces the recuurence

Q/ what is INR?
Q/ what are the congenital causes of DVT?
Defecieny of

 Antithrombin
 Protein C , Protein S
 Prothrombin G20210A
 Factor V Leiden

Q/ what are the DDx of leg swelling ?

Unilateral
 Deep vein thrombosis
 Soft tissue infection
 Trauma
211 STAGERS NOTES

 Immobility, e.g. hemiplegia

Bilateral
 Heart failure
 Chronic venous insufficiency
 Hypoproteinaemia, e.g. nephrotic syndrome, kwashiorkor, cirrhosis
 Lymphatic obstruction, e.g. pelvic tumour, filariasis
 Drugs, e.g. non-steroidal anti-inflammatory drugs, nifedipine, amlodipine,
fludrocortisone
 Inferior vena caval obstruction
 Thiamine deficiency (wet beri-beri)
 Milroy's disease (more common in females, unexplained lymphoedema which
appears at puberty)
 Immobility

Q/ what are the risk factors for DVT?

1. Patient factors
 Age > 40 years
 Obesity
 Varicose veins
 Previous DVT
 Oral contraceptive
 Pregnancy/puerperium
 Dehydration
 Immobility
2. Surgical conditions
 Surgery, especially if > 30 minutes' duration ,Abdominal or pelvic
,Orthopaedic to lower limb

3. Medical conditions
 Myocardial infarction/heart failure
 Inflammatory bowel disease
212 STAGERS NOTES

 Malignancy
 Nephrotic syndrome
 Homocystinaemia
4. Haematological disorders
 myloproliferative disorders as
o Primary polycythaemia ,
o Essential thrombocythaemia,
o Myelofibrosis
 Paroxysmal nocturnal haemoglobinuria
5. Deficiency of anticoagulants
 Antithrombin
 Protein C , Protein S
 Prothrombin G20210A
 Factor V Leiden
6. Antiphospholipid antibody
 Lupus anticoagulant ,
 Anticardiolipin antibody
213 STAGERS NOTES

Q/why DVT occurs more frequently in pregnancy than non-pregnant

women?
1. increases the pressure on the left iliac vein
2. Progesterone effect
3. Inhibition for fibrinolysis?

4. Protein s deficiency

Q/ what are the most common malignancy that cause DVT ?

A/ pancreatic malignancy

Q/ this patient presented to you with DVT , how can you diagnose him ?
Clinical suspicion of DVT classified into low , intermediate & high probability

according to Well’s criteria. According to these criteria each of the

following represents one point:

1. Active cancer
2. Paralysis, paresis, or recent cast
3. Bedridden for >3 days; major surgery <12 weeks
4. Tenderness along distribution of deep veins
5. Entire leg swelling
6. Unilateral calf swelling >3 cm
7. Pitting edema
8. Collateral superficial nonvaricose veins. While if alternative diagnosis is at
least as likely as DVT 2 points should be ditracted (-2)

A high probability for DVT exists in patients with a score of greater than 3; a
moderate probability with score of 1 to 2; and low pretest probability with score of
0 or less.
214 STAGERS NOTES

Investigations:
1. D-dimers are degradation products of cross-linked fibrin by plasmin
that are detected by diagnostic assays, its negative predictor , means it
use ot exclude not to confirm DVT
2. Doppler ultrasonography
3. CT or MRI
4. The classic “gold standard” is contrast venography.

Q/ What are the causes of elevation of D-dimer other than DVT?

1. Trauma
2. recent surgery
3. hemorrhage
4. cancer Deffrences in leg cercumfrence between
5. sepsis two leg is significant if > 3 cm

6. DIC
7. MI
8. Pneumonia
215 STAGERS NOTES

9. Pregnancy
10. cardiac & renal failure

Q/ what is the appropriate treatment in this case?

1. Low molecular weight heparin SC
2. Warfarin is initiated simultaneously with heparin, and both therapies are
overlapped for a minimum of 4 to 5 days and until the INR has reached the
therapeutic range (2-3) for two measurements taken 24 hours apart.
3. In selected cases of severe iliofemoral thrombosis, catheter-directed
thrombolysis
4. Inferior Vena Caval (IVC) Filters indicated in two conditions:
 active bleeding that precludes anticoagulation and
 recurrent venous thrombosis despite intensive anticoagulation

Q/ What are the duration of the treatment in patient with DVT?

1. patients with an underlying prothrombotic risk or a history of previous emboli
should be anticoagulated for life.
2. If the cause is identified and reversible …. 3 ms treatment
3. DVT that is idiopathic or associated with certain congenital thrombophilic
conditions has high rate of recurrence after 6 to 12 months of therapy;
therefore, longer-term therapy is recommended. To reduce the risk for
bleeding and the need for INR testing lower-intensity anticoagulation
regimen (INR, 1.5–2.0) after the initial 3 to 6 months of therapy in patients
with a high risk for DVT recurrence is reasonable.

Q/ Why we give heparine simtenously with warfarine

1. Warfarine inhibits protein S and proein C (vit. K dependent )so increases the
risk for thrombosis
2. Slow onset action of heparien (about 72 h)
216 STAGERS NOTES

Q/ Patient with DVT develops sudden attack of SOB what do you think
he have .?
A/ PE

Q/When DID the patient presented with bilateral DVT ?

IF thers IVC obstruction

Q/ What are the ECG finding of PE?

Q/ what are the CXR finding in PE
Q/ what are the investigation of choice in patient with PE
Q/ What are the types of heparine
Q/ what are the complications of hepatrine therapy
Q/ what are the complications of warfarinen therapy
What are the indications of use thrombolytic in patient with DVT ?
What are ophlegmasia cerula dolens
Leg cellulitis :erethema
Shiness
Tender
Well demarckate

d-dimer has negative predictive value (means if negative exclude DVT)

217 STAGERS NOTES

CASE NO.2 Renal failure

Q/ define CRF?
A/ irreversible deterioration in renal function which classically develops over a
period of years

Q/ What are the stages of CRF?

STAGE DESECREPTION GFR

(ml/min/1.73m2)
1 Kidney damage with normal or high GFR ≥91
2 Kidney damage with slightly low GFR 60-89
3 Moderately low GFR 30-59
4 Severe low GFR 15-29
5 Kidney failure < 15 or dialysis
218 STAGERS NOTES

Q/ what is the most common cause of CRF?

A/ DM (20-40 %)
Q/what are the features of CRF that differentiate it form ARF ?

1. eydoetoydoetso renal
 Osteomalacia
 Osteoporosis
 Osteosclerosis
Uremic pericardidtis
 Hyperparathyroidism
-Concave st segment elevation in all
2. segn hs nioy leads except V1 & Avr
 Bruises
-Depress PR interval
 Earthy color
-Low voltage and electrical alternance-
 Scratching
3. noieoet dso oooghn -ST elevation while T inversion

 Parasthesia T- ‫ ترجع طبيعية يال تصير‬ST ‫ ال‬MI ‫نفرقهة عن ال‬

inversion
 Foot drops
4. gdosfor A-V fistula
5. syoneygya
6. Hypocalcemia : fits and muscle twitching
7. Endocrine chanes
 Hyperparathyroidism
 Hypoglycemic attacks in patient with DM
8. US :
 Small size kidney( normal size kidney 3,6,12)
 Cortical thikness ( normally about 2 cm)….< 1 cm (poor cortical
thickness in CRF)
219 STAGERS NOTES

Q/ What are the effect of CRF on CVS?

1. atherosclerosis + IHD Patient with CRF
2. HT with Na and water retention asymptomatic until GFR >
3. Uremic pericarditis 30 ml/min/1,73
4. LVH
5. Diastolic dysfunction

Q/ What are the causes of anemia in RF?

1. Decrease erythropoiesis due to toxic effect of ureic acid on bone marrow
2. Decrease erythropoietin
3. Decrease RBCs lifespan
4. Decrease iron absorption: due to nausea , vomiting and anorexia
5. Increases the bleeding : due to increase capillaries fragility

Important note
In CKD, the patient can tolerate mild to moderate anemia, because there is more
release of oxygen from hemoglobin. The mechanisms are—in CKD patient, there is
acidosis and high 2, 3 DPG level in RBC, which shifts the oxygen dissociation curve to
the right and more oxygen is released from
hemoglobin. So, the patient doesn’t require blood transfusion in mild to moderate
anemia.
Target hemoglobin is 11 to 12.5 g/dL.

Q/ What is the cause of bleeding tendency in RF?

Thromboesthenia (platelet function defect)

Coagulation casced defect

Q/ what is the cause of osteoporosis in CRF ?

A/ due to decreases the activation of vitamin D by the kidney
211 STAGERS NOTES

Q/ What are the causes of dyspnea in patient

with RF?
Peripheral neuropathy in CRF due to:
1. Anemia
2. Uremic pericarditis 1. Uremia
3. HT 2. DM
4. IHD

Q/Why theirs increases the risk of thrombosis in patient nephrotic

syndrome ?
Because thers loss of antithrombin C so increases the risk of the thrombosis
So we have to give all patient heparin in large dose
Why we give heparin in large dose ?
Because heparin potentiate antithrombine , in patient with nephrotic thers loss of
antithrombine , so we need large dose of heparin to act effectively
Note / warfarin is highly protein bound , in patient with nephrotic syndrome theirs
loss of protein , so these patien are highly sensitive to warfarin

Q/ What are the causes of myopathy in patient with RF?

1. Increase PTH
All electrolytes affect the
2. Poor neutretion
3. Vit D defecency consciousness level except K

Q/ What are the causes of non oliguric ARF? ( causes of ARF in

hemodynamically stable patient)
1. Urinary tract obstraction
2. Drugs and toxiens : NSAIDs , ACEI, cisplatin, amphotracine B. snake bite, crush
syndrome
3. Vascular event

malignant hypertension and haemolytic uraemic syndrome

4. Rapidly progressive glomerulonephritis (RPGN) SLE and vasculitis

5. Acute interstitial nephritis
211 STAGERS NOTES

Q/ What are the electrolyte changes in patient with CRF?

1. Hyperkalemia
2. Hypermagnsemia Polycytic kidney diseas
3. Hyperphosphatemia
1. Congenital (young age patient about 20 years
4. Hypernatremia (or hypo Na) presented with hypertension
5. Hydrogen retention 2. Acquired: in chronic dialysis
6. hypocalcemia

Q/ what are the causes of encephalopathy in patient with CRF?

1. Uremic encephalopathy
2. Hypernatremia
3. Fluied overload

Q/ what is the target of hemoglobin in patient with CRF ? AND WHY?

 10-12 mg/dl
 If higher it will increase the viscosity which result in reduce the kidney
perfusion

Q/ Why patient with CRF tolerate low Hb (10-12 mg/dl) better than
normal person?
 Hb- O2 dissociation curve shift to right due to
acidosis results in increases of 2,3
diphosphgluconate ( enzyme found in RBC) which
increses the delivery of O2 to the tissue

Q/ what are the causes of low Hb in patient with

CRF?
1. GIT bleeding ( pletlet dysfunction)
2. Anorexia and malabsorbtion
3. Folate deficiency due to dialysis

Q/ what are the ECG findings in hyperkalemia?

1. Tented T wave Patient with CRF received ACEI ..then
he develops sudden deterioration in
renal fuction think of RAS as the
cause of RF
212 STAGERS NOTES

2. Wide QRS
3. Prolonged QRS
4. Absence P wave
5. signet wave sign
6. Then stand still

Q/ What are the treatment of hyperkalemia?

1. Stabilise cell membrane potential:
 Intravenous calcium gluconate (10 ml of 10%
solution)
2. Shift K into cells
 Inhaled β2 agonist, e.g. s albutamol
 Intravenous glucose (50 ml of 50% solution) and
insulin (5 U Actrapid)
 Intravenous sodium bicarbonate2 (100 ml of 8.4% solution)
3. Remove K from body

Intravenous furosemide and normal saline

Ion-exchange resin (e.g. Resonium) orally or rectally
Dialysis
213 STAGERS NOTES

Q/ what are the causes of atherosclerosis in RF?

1. HT
2. Increases Ca and phosphate ( accelerate atherosclerosis)

Q/ what are the most common cause of death in CRF?

 IHD

Q/ What are the sites of action of diuretics drugs?

Q/ causes of CRF with normal size kidney ?

1. DM
2. Polycytic kidney diseas
3. Amyloidosis
4. Multiple myloma
214 STAGERS NOTES

Thiazide diuretic not

5. Obstruction uoropaathy act in low GFR , so we
use loop diuretic
Q/ how clould DM cause RF ?
1. nephropathy (glomerular dises)
2. Autonomic neuropathy (neurogenic bladder )
3. Reccurent UTI (cause interstitial disese )

Q/What are the defrences between uremia and uremia ?

 Azotemia :high concentration of urea and creatinin in the blood without
symptoms
 Uremia :high concentration of urea and creatinin in the blood with symptoms

Q/define ESRF (end stage RF )

 Means death is likely without renal replacement therapy

Q/ What are the indications of renal replacement therapy in ARF?

1. Increased plasma urea and creatinine. Plasma urea > 30 mmol/l (180 mg/dl)
and creatinine > 600 μmol/l (6.8 mg/dl) are undesirable.
2. Hyperkalaemia. A plasma potassium > 6 mmol/l with failure of medical
therapy
3. Metabolic acidosis. This will often occur together with hyperkalaemia and
raise the plasma potassium further
4. Fluid overload and pulmonary oedema. In patients with continued urine
output, this may be controlled by careful fluid balance and use of diuretics,
but in oligo/anuric patients may be an indication for RRT
5. Uraemic pericarditis/uraemic encephalopathy..

All diuretics are dose related except thiazide

215 STAGERS NOTES

Impo note: vit. D pass in two steps in the activation

25-hydroxycholycalceferol in the liver

1-25 hydroxycholycalceferol in the kidney (so that we give 1-alph

to patient with CRF)

Q/ Causes of edema in CRF? Acute renal failure

1. Protein loss needs 8 week to

convert to CRF
2. Water retention

Q. What is CKD and what is ESRD?

 CKD is the irreversible deterioration of renal function, classically developing
over a period of years
 End stage renal disease or failure (ESRD) is a stage when renal replacement
therapy is compulsory either dialysis or renal transplantation, without which
death is likely.

Q. What is acute renal failure? What are the causes?

Sudden deterioration in renal function, occurring within weeks or
months (<3 months), biochemically detected by high urea and
creatinine level. This is usually reversible.
Causes of ARF:

1. Prerenal:
 Fluid loss due to diarrhea, vomiting, dehydration, etc
 Blood loss due to hemorrhage.
 Plasma loss in burn
216 STAGERS NOTES

 Hypotension due to myocardial infarction, shock, vasodilator drugs, heart

failure
 Rhabdomyolysis
 Hemolytic uremic syndrome
 Hepatorenal syndrome
 Renal artery occlusion or stenosis
 Disease affecting arterioles.

2. Renal (intrinsic renal disease

 Acute tubular necrosis or toxic or septic renal failure (85%)
 RPGN, due to:
o Primary GN, e.g. MCGN, IgA nephropathy
o Systemic disease such as SLE, rheumatoid arthritis,
systemic sclerosis, multiple myeloma, vasculitis

 Tubulo-interstitial disease (10%) due to drugs (NSAIDs,

ciprofloxacin, allopurinol, sulfonamide, cyclosporine).

3. Post renal:
 Urethral—phimosis, paraphimosis, stricture, stone, blood
clot, slaughed papilla.
 Bladder neck—prostatic hypertrophy, malignancy, stone.
 Bilateral ureteric—calculus, following surgery, pelvic tumor,
uterine prolapse, retroperitoneal fibrosis (due to radiation,
methysergide, idiopathic).

Q/ What are the causes of CKD?

 Glomerular diseases (30 to 40%), e.g. IgA nephropathy, MCGN
 Diabetes mellitus (20 to 40%)
 Hypertension (5 to 20%)
217 STAGERS NOTES

 Obstructive uropathy
 Chronic pyelonephritis
 Tubulointerstitial diseases (5 to 10%)
 Systemic inflammatory diseases (5 to 10%), e.g. SLE, vasculitis
 Renal artery stenosis (5%)
 Congenital and inherited (5%), e.g. polycystic kidney disease, Alport’s
syndrome
 Unknown (5 to 20%).

Q/what are the metabolic abnormalities in CRF?

4. Hyponatremia, hyperkalemia or sometimes hypokalemia
5. Metabolic acidosis (due to increased tissue catabolism and retention of
organic acids)
6. Hyperuricemia and gout
7. Hypocalcemia, hyperphosphatemia
8. Lipid abnormalities (hypercholesterolemia, hypertriglyceridemia).

Q/What are Endocrine abnormalities in CRF?

1. Secondary hyperparathyroidism, may be tertiary
2. Prolonged half-life of insulin, due to reduced tubular metabolism of insulin.
Also, insulin requirement in a diabetic patient decreases. But in advanced
CKD, there may be end organ resistance to insulin, leading to impaired
glucose tolerance
3. Hyperprolactinemia (presents with galactorrhea in men as well as women, loss
of libido and sexual dysfunction in both sexes).

4. Others—increased LH, decreased serum testosterone (erectile dysfunction,

decreased spermatogenesis), oligomenorrhea or amenorrhea (in female),
impaired growth in children, abnormal thyroid hormone levels (hypothyroid
feature), partly because of altered protein binding.
218 STAGERS NOTES

Q/Bone diseases in CRF (renal osteodystrophy)?

1. Osteomalacia (or ricket called renal ricket)
2. Osteoporosis
3. Osteosclerosis (in vertebral body, giving rise to Rugger Jersey spine)
4. Osteitis fibrosa cystica.

Q/What is renal osteodystrophy?

This is a group of metabolic bone disease secondary to chronic renal failure and
comprises the following:

1. Osteomalacia (or ricket, called renal ricket)

2. Osteoporosis
3. Osteosclerosis (in vertebral body, giving rise to Rugger jersey spine)
4. Osteitis fibrosa cystica.

what are the causes of enlarge kideny

Q/ How to treat CKD? In acute kidney injery

Tubules has the ablitly to regenerate

As follows:
CRF has no ablity to regeneralte
A. General measures:
1. Fluid restriction
2. Salt restriction
3. Protein restriction (0.5 g/kg body weight/day). However, this is
controversial. Severe protein restriction is avoided. Excess consumption of
protein should be avoided
4. Smoking should be stopped
5. Social and psychological support.
B. Symptomatic and supportive:
1. Hypertension: Good control of blood pressure delays renal deterioration.
Target control of BP is 130/80 mm Hg (if UTP < 1g/day) and 125/75 mm Hg
(if UTP > 1g/day)
 ACE inhibitor, increased to maximum dose
 ARB is added, if goal is not achieved (in case of type 2 DM, treatment
should be started with ARB)
219 STAGERS NOTES

 Diuretic to prevent hyperkalemia and to help control BP. High and single
dose is preferable
 Calcium channel blocker (verapamil or diltiazem), added if goal is not
achieved.
2. Statins for dyslipidemia
3. Hyperkalemia:

1. Stabilize cell membrane potential : Intravenous calcium gluconate (10 ml of

10% solution)
2. Shift K into cells : Inhaled β2 agonist, e.g. salbutamol, Intravenous glucose (50
ml of 50% solution) and insulin (5 U Actrapid) and Intravenous sodium
bicarbonate2 (100 ml of 8.4% solution)
3. Remove K from body: Intravenous furosemide and normal saline, Ion-
exchange resin (e.g. Resonium) orally or rectally and Dialysis

4. Acidosis:
• Sodium bicarbonate (1.26%, IV) or calcium carbonate (upto 3 g/day).
Bicarbonate should be maintained above 22 mmol/L.
5. Calcium and phosphate control and suppression of PTH:
 Hypocalcemia should be treated with calcitriol or alpha-calcidol and
calcium supplementation. Serum calcium should be monitored
frequently to avoid hypercalcemia.
6. For hyperphosphatemia—dietary restriction of phosphate containing food
(milk, cheese, eggs) and phosphate binding drugs like calcium carbonate,
aluminium hydroxide and lanthanum carbonate may be used with food to
prevent phosphate absorption. Polymer based phosphate binders may be
used.
221 STAGERS NOTES

7. Anemia:

1. Synthetic (recombinant) human erythropoietin (EPO). Side effects are

hypertension and thrombosis (may occur in arteriovenous fistula, used for
hemodialysis)
2. If there is no response after 300 IU/kg weekly, or a fall in hemoglobin after a
satisfactory response, then erythropoietin is likely to be ineffective, which may
be due to iron deficiency, bleeding, infection, malignancy, formation of anti-
EPO antibody or aluminum overload that occur in dialysis. These should be
searched and treated. If iron is needed, it should be given intravenously.
3. Blood transfusion may be given in severe anemia. Risk of blood transfusion in
CKD patient—fluid overload, potassium overload, increased chance of graft
rejection after kidney transplant, so blood transfusion is better to be avoided.
In severe anemia, BT should be given during hemodyalisis.

C. Definitive treatment of CKD – renal replacement therapy may be

given, such as:
1. Hemodialysis
2. Hemofiltraiton
3. Peritoneal dialysis
4. Renal transplantation.

D. Treatment of primary cause, if any:

1. Diabetis melitus—insulin
2. Hypertension—antihypertensive
3. APKD—sirolimus decreases the cyst size
4. Removal of obstruction in obstructive uropathy.

Q/ What are the indications of renal replacement therapy?

1. Serum creatinine > 600 to 800 µmol/L (7 to 9 mg/dL), or e.GFR< 8 to 10
2. Hyperkalemia (plasma potassium > 6 mmol/L despite medical treatment)
3. Metabolic acidosis (H+ > 56 nmol/L, pH < 7.25), HCO3< 10 mmol/L
4. Fluid overload and pulmonary edema
221 STAGERS NOTES

5. Uremic pericarditis or encephalopathy

6. Sepsis (tentative evidence for mediator removal), CRRT (continuous renal
replacement therapy).

Q/ What are the hemodialysis Complications?

1. Hypotension during dialysis due to fluid removal and hypovolemia. There
may be chest pain and leg cramps
2. Cardiac arrhythmia due to potassium and acid base shift
3. Hemorrhage due to anticoagulation. Also,
venous needle disconnection may lead to
hemorrhage
4. Anaphylactic reaction
5. Sepsis, usually involving vascular access devices
6. Pulmonary edema due to fluid overload
7. Hemolytic reactions
8. Air embolism
9. Hard water syndrome
10. Dialysis disequilibrium due to rapid correction
of uremia.

Q/what are the examinations findings in patient with CRF?

222 STAGERS NOTES

Asthma
Short history

Difficulty in breathing
Cough
Wheeze and tightness in the chest

Mainly at late night and early morning

Q /why we give hydrocortisone in patient with asthma?

1. Anti-inflammatory
2. Protect the adrenal gland because it maximally stimulated

Q /Why we give hydrocortisone in acute asthmatic attack not

dexamethason
Hydrocotison is acive form

Q/general examination findings in patient with asthma?

 The patient is dyspneic
 Decubitus is propped up
 No anemia, jaundice, cyanosis, edema, clubbing,
koilonychia or leukonychia
 No lymphadenopathy or thyromegaly
 Neck vein: Not engorged
 Purse lip: Absent
 Nasal polyp: Present on both sides
 Pulse: 120/min
 BP: 120/70 mm Hg
 Respiratory rate: 24/min.
223 STAGERS NOTES

Q/What are the DDx in this case ?

1. COPD
2. HF
3. Bronchitis
4. Pneumonia

Q/What are the respiratory system examination in patient with bronchial

asthma?
Inspection:
-Shape of the chest—Normal
-There is indrawing of intercostal spaces, suprasternal and supraclavicular
excavation and prominent accessory muscles of respiration.

Palpation:
-Trachea: Central. Tracheal tug absent
-Apex beat: In the left 5th intercostal space in midclavicular
line, 8 cm from midsternal line, normal in character
-Chest expansion: Reduced
-Vocal fremitus: Normal.
Percussion:
- Percussion note: hyperresonance in both sides
-Area of liver dullness: In 5th ICS in the right midclavicular
line
-Area of cardiac dullness: Normal.
Auscultation:
-Breath sound: Vesicular with prolonged expiration
-Vocal resonance: Normal
-Added sounds: High pitched rhonchi are present in both sides of the chest, more
marked on expiration.
FET (forced expiratory time): > 6 seconds (normally <6 seconds).
Examination of other systems reveals no abnormalities.
224 STAGERS NOTES

Q/Why not chronic bronchitis?

In chronic bronchitis, there is presence of cough
Asthmatic patient
with sputum production not attributable to other
develops cataract ,,, due
causes, on most of the days for at least 3 consecutive to steroid side effect

months in a year for at least 2 successive years.

Q/What are the causes of resistant ashma ?

1. Poor complint
2. Poor technique of nebulizer
3. Thyrotoxicosis Asthmatic patient recently

4. Chronic infection with mycoplasma develops polyuria ,,think of DM

due to steroid side effect
5. Steroid resistant asthma
6. GERD
7. Unrecognized allergene

Q/What is cardiac asthma?

Cardiac asthma means left ventricular failure in which the patient usually presents
with sudden severe dyspnea and cough with profuse mucoid expectoration. On
examination, there are bilateral basal crepitations and no rhonchi or wheeze.

Q/What is bronchial asthma?

A. It is a chronic airway inflammatory disorder characterized by hyper-
responsiveness of the airways to various stimuli, presenting as breathlessness,
cough, chest tightness and wheeze. It is reversible.

Q/How can you diagnose bronchial asthma?

A. Typical history (cardinal features like paroxysmal breathlessness, cough, wheeze
and chest tightness) plus any of the following:
- FEV1 ≥ 15 % (and 200 mL) increase following the inhalation of bronchodilator.
225 STAGERS NOTES

(Global Initiative for Asthma accepts an increase of 12%).

- FEV1 ≥ 15 % decrease after 6 minutes of exercise.
- PEFR shows > 20% of diurnal variation on ≥ 3 days in a week for 2 weeks.

Q/what is cough variant asthma?

A. It is a type of asthma in which there is chronic dry cough with or without sputum
eosinophilia, but no abnormalities in airway function. It is also called eosinophilic
bronchitis, common in young children. Cough is the only symptom, mostly at night.
Examination during day may not reveal any abnormality. Cough may be increased
with exercise, exposure to dust, strong fragrances or cold
air. Methacholine challenge test is positive.

Q/what is excersise induce asthma?

A. When exercise produces asthma, it is known as
exercise-induced asthma. 10% or more reduction of FEV1
after exercise is diagnostic.
Cold dry air that enters into the lungs during exercise is
the main trigger factor. Increased ventilation results in
water loss from the pericellular lining fluid of the
respiratory mucosa trigger mediator release. Heat loss from the respiratory mucosa
is also involved.

Q/what is occupation induce asthma?

A. It may be defined as “asthma induced at work by exposure to
occupation related agents, which are mainly inhaled at the
workplace”. The most characteristic feature is symptoms that
worsen on work days and improves on Atopic individual and
smoker are at increased risk. Commonly found in chemical
holidays. grain handlers, cigarette workers, farmers,
manufacturers, fabric, dye, press and printing workers,
laboratory workers, poultry breeders, wood and bakery workers.
Measurement of 2 hourly peak at and away from work is helpful for diagnosis.
226 STAGERS NOTES

Treatment:
-Avoidance of further exposure
-Using mask at work
-If no response, step care asthma management plan.

Q/What is drug induce asthma?

A. Symptoms of asthma that occurs after use of certain drugs such as aspirin, beta
blocker, some nonsteroidal anti-inframmatory drugs (NSAIDs), etc. These drugs can
cause bronchospasm.
Treatment: Avoidance of triggering drugs. Safe NSAIDs are paracetamol, tramadol,
also etoricoxib.

Q/What is extrinsic and intrinsic asthma?

A. As follows:
-Intrinsic asthma (non atopic or late onset asthma): When no causative agent can
be identified. It is not allergic, usually begins after the age of 30 years, tends to be
more continuous and more severe.

-Extrinsic asthma (atopic or early onset asthma): When a definite external cause is
present. There is history of allergy to dust, mite, animal danders, pollens, fungi, etc.
It occurs commonly in childhood and usually shows seasonal variations.

Q/what is acute sever asthma ?

A. It is defined as “severe acute persistent attack of asthma without any remission
in between and not controlled by conventional bronchodilator”. Previously it was
called status asthmaticus.
Q/how to asses the severity of of acute bronchial asthma?
A. Acute severe asthma is assessed by the following points:

1. Inability to complete a sentence in one breath

2. Respiratory rate > 25/min
3. Pulse rate > 110/min
4. PEFR 33 to 50% of predicted (< 200 L/min).
227 STAGERS NOTES

Q/ what are the causes of acute dyspnea without chest pain?

 Pulmonary embolism
 Pneumothorax
 Metabolic acidosis
 Hypovolaemia/shock
 Acute left ventricular failure/pulmonary oedema

Q/ what are the causes of acute dyspnea with Pleuritic chest pain?

 Pneumonia
 Pneumothorax
 Pulmonary embolism
 Rib fracture

Q/ what are the causes acute dyspnea with central chest pain?

 Myocardial infarction with left ventricular failure

 Massive pulmonary embolism/infarction

Q/ what are the causes acute dyspnea with Wheeze and cough?

 Asthma
 COPD

Q/ what are the causes of dyspnea that starts within minutes ?

1. Pulmonary
2. Thromboembolism
3. Pneumothorax
4. Asthma
5. Inhaled foreign body
6. Acute left ventricular failure

Q/ what are the drugs that cause Bronchoconstriction?(take care in

asthma )
1. Beta-blockers
2. Opioids
228 STAGERS NOTES

3. Non-steroidal anti-inflammatory drugs

Q/What are the features of life threatening asthma?

A. As follows:

1. Exhaustion, confusion or coma

2. Cyanosis
3. Silent chest
4. Feeble respiratory effort
5. Bradycardia or hypotension or arrhythmia
6. PEFR < 33% of predicted (< 100 L/min)
7. Blood gas analysis – SpO2 < 92% or
PaO2 <8 kPa (60 mm Hg) even with O2
8. Normal or raised PaCO2 (> 6 kPa) and low or falling blood pH.

Q/This patient presented to you to the ER department with acute severe

asthma how can you treate him ?
A. As follows:

1. High flow O2—40 to 60% (to maintain O2 saturation above 92%).

2. Nebulized sulbutamol 5 mg or terbutaline 10 mg. May be repeated 2 to 4
hourly.
3. Nebulized ipratropium bromide 0.5 mg may be added with nebulized
sulbutamol.
4. Injection hydrocortison 200 mg IV 4 hourly. After 24 hour, oral prednisolone
60 mg daily should be given for two weeks, then taper.
5. If no response, IV infusion sulbutamol 3 to 20 mg/min or terbutaline 1.5 to 5
mg/min or magnesium sulphate IV 1.2 to 2 gm over 20 minutes may be
given.
6. In some cases, injection aminophyllin 5 mg/kg loading dose over 20 minutes,
then continuous infusion at 1 mg/kg/h.
7. Correction of fluid and electrolytes (repeated use of salbutamol may cause
hypokalemia).
229 STAGERS NOTES

8. If no response with this regime, the patient may be shifted ICU for assisted
ventilation.

Q/What is the management of chronic asthma ?

231 STAGERS NOTES

Q/What is the indications for assited ventilation ?

1. Coma, severe exhaustion, confusion, drowsiness, respiratory arrest.
2. Deterioration of arterial blood gas despite optimal therapy:

 PaO2 < 8 kPa (< 60 mm Hg) and falling

 PaCO2 > 6 kPa (> 45 mm Hg) and rising
 PH low and falling (H+ high and rising)
 Failure to maintain above 92% (or O2 saturation <90%).

Q. What are the criteria for discharge?

1. Stable on discharge medication
2. Without nebulisation for at least 24 hours
3. PEFR 75% of predicted or personal best.

Q. What are the steroid sparing drugs?

1. Methotrexate
2. Cyclosporine
3. Intravenous immunoglobulin
4. Etanercept
5. Anti-IgE monoclonal antibody (omalizumab).

Amonophlline : loading 250mg in 100 ml G/W over 30 min

Maintenance 1mg /kg infusion

231 STAGERS NOTES

Q/ What are the differences between bronchial asthma and COPD?

COPD Bronchial asthma
Age of onset Middle age, usually >40 Any age
years
Smoking history Common, >20 pack years May or not be present
Allergy Uncommon Common—rhinitis,
eczema, skin
prick positive,
eosinophilia
Family history Not common Common
Cardinal features Cough, expectoration Dyspnea, cough,
and dyspnea wheeze, and
chest tightness
Sputum Often copious Infrequent
Symptom free It is chronic and There is recurrent attack
period progressive but the
without any symptom patient is usually
free period symptom free in
between attacks.
However, in
chronic bronchial
asthma, the
features may be
persistent
Dyspnea Progressive, persistent Intermittent and
(with variable, vary from
exacerbation) day to day and peak at
night and in
early morning
Spirometry Airway obstruction is Airway obstruction is
irreversible reversible
Bronchodilator May not be satisfactory Usually satisfactory
response
232 STAGERS NOTES

Q/ What are the differences between wheeze and stridor?

Wheeze
Wheeze occurs in both inspiration and expiration but is always louder in the
latter. It implies airway narrowing and is common in asthma and chronic
obstructive bronchitis. In asthma, the wheeze is episodic and clearly associated
with shortness of breath, fulfilling the definition of ‘variable wheezy
breathlessness’.

Caused by small airway obstruction

Stridor
Stridor is a harsh inspiratory and expiratory noise which can be
imitated by adducting the vocal cords and breathing in and out.

Caused by large airway obstruction

Asthma with hypertension

Management of asthma is same. Regarding antihypertensive drugs, remember the
following points:

1. Avoid b blocker. However, cardioselective b blocker can be used.

2. Drug of choice—calcium channel blocker or ARB (losartan, valsartan). ACE
inhibitor is avoided as it may induce cough.

Asthma with Arrhythmia

1. Digoxin and amiodarone may be used

2. Aminophylline or theophylline should be avoided.

Asthma with Pain

1. Paracetamol and tramadol are preferred for pain management. COX 2
inhibitor can be used.
2. NSAIDs like aspirin, diclofenac, etc. should be avoided
3. Steroid may be given, if needed
233 STAGERS NOTES

Q/What are the side effect of aminophylline ?

1. Nausea and vomiting Asthma causes respirator failure
2. Arrhythmia late in the coars tof the disease

3. convulsions While fibrosing alveolitisis

causing asthma early in the coarse

Q/What is the deffrence between obstructive and restrictive lunge

disease ?
234 STAGERS NOTES

Q/How to use a metered-dose inhaler?

• Remove the cap and shake the inhaler
• Breathe out gently and place the mouthpiece into the mouth
• Incline the head backwards to minimise oropharyngeal deposition
• Simultaneously, begin a slow deep inspiration, depress the
cannister and continue to inhale
• Hold the breath for 10 seconds
235 STAGERS NOTES

COPD

Q/ What is COPD?
A. COPD is characterized by airflow limitation, which is not fully reversible. It is
usually progressive, and associated with an abnormal inflammatory response of the
lung to noxious particles or gases.

FEV1< 80% predicted and FEV1: FVC < 70% predicted. Bronchodilator reversibility
test shows<15% increase in FEV1 after giving bronchodilator.

Q/What are the examination findings in patient with COPD

Inspection:

1. Shape of the chest: Barrel shaped.

2. Movement of the chest: Bilaterally restricted.
3. Intercostal space: Full.

Palpation:

1. Trachea: Central
2. Apex beat: Difficult to localize
3. Chest expansion: Reduced
4. Vocal fremitus: Normal.

Percussion:

1. Percussion note: Hyperresonant

2. Area of liver dullness: In the right 7th ICS in midclavicular line
3. Area of cardiac dullness: Impaired.
236 STAGERS NOTES

Auscultation:

1. Breath sounds: Vesicular with prolonged expiration

2. Added sounds: Plenty of rhonchi, in both lung fields, present in both
inspiration and expiration
3. Vocal resonance: Normal.

Q/What are the features of COPD?

The patient is a heavy smoker, taking ... cigarettes a day for ... years, there is chronic
cough with breathlessness, which is progressively increasing day by day.

Q/what is the deffrential diagnosis of COPD?

1. Chronic severe or persistent bronchial asthma
2. Bronchiectasis
3. Chronic bronchitis
4. Congestive cardiac failure.
237 STAGERS NOTES

Q/ What is the basic difference between bronchial asthma and COPD?

A. Bronchial asthma is reversible, but COPD is not fully reversible and it is
progressive.

Q/ What are the findings in spirometry?

A. As follows:

1. FEV1< 80% predicted

2. FEV1: FVC < 70% predicted
3. Bronchodilator reversibility test shows <15% increase in FEV1 after giving
bronchodilator.

Q/ What investigations should be done in COPD?

A. As follows:
1. Complete blood count (there may be polycythemia and increased PCV due to
persistent hypoxemia).

2. Chest X-ray PA view (there may be features of hyperinflation – increased

translucency, low flat diaphragm, tubular heart, widening of intercostal space,
emphysematous bullae).

3. ECG (usually normal. In cor pulmonale, there may be features of RVH).

4. Echocardiogram (may show features of cor pulmonale).
5. Lung function tests:

 FEV1and FVC are reduced. Ratio of FEV1: FVC is also reduced (indicates
obstructive airway disease)
 Post bronchodilator FEV1 < 80% of the predicted value and FEV1/FVC is <
70%
 Other tests: Lung volumes may be normal or increased. Gas transfer
coefficient of carbon monoxide is low, when significant emphysema is present
238 STAGERS NOTES

6. PEFR (reduced).
7. Blood gas analysis:

 Often normal at rest

 PO2 (reduced)
 PCO2 (normal or increased)
 PH (acidosis).

8. High resolution CT—assessment of COPD, characters of emphysema, particularly

bullae.
9. Sputum examination (if superadded infection).
10. b1 antitrypsin deficiency—may be done in young, nonsmoker patient with basal
emphysema.

Q/ What are the presentations of COPD?

Usually the patient is above 40 years, male and smoker. There is:

1. Chronic cough and sputum production, which is progressively increasing

2. Progressive breathlessness
3. There may be hemoptysis, edema and morning headache (due to
hypercapnia).

Q/What are the causes of edema in patient with COPD ?

1. Steroid side effect
2. Cor-pulmonale
3. Hypoxia and hypercapnea induce salt and water retension
239 STAGERS NOTES

Q/What are the deffrence between chronic bronchitis and emphysema ?

241 STAGERS NOTES

Q/ What are the systemic features in COPD?

Muscular weakness, peripheral edema due to impaired salt and water excretion,
weight loss due to altered fat metabolism, increased osteoporosis, increased
circulating inflammatory markers.

Q/ What are the risk factors or causes of COPD?

A. Multiple factors may be responsible for COPD, such as:
1. Exposure to:

1. Smoking (the most common)—active or passive

2. Indoor and outdoor air pollution
3. Occupation—exposure to dust, fumes, smokes, chemicals, etc. (e.g. coal
miners and those who work with cadmium)
4. Urban dweller
5. Low socioeconomic status
6. Low birth weight
7. Poor lung growth which may be due to childhood infections or maternal
smoking
8. Infections—recurrent lung infection, persistent adenovirus in lung tissue, HIV
infection is associated with emphysema
9. Cannabis smoking (controversial).

2. Host factors:

1. Genetic factors—a1 antitrypsin deficiency

2. Airway hyper-reactivity
3. More in male and Caucasians
4. Biofuel mass.

Q/ What organisms are associated with acute exacerbation of COPD?

A. Common organisms: Haemophilus influenzae and Streptococcus pneumoniae.
Other less common organisms are Moraxella catarrhalis, Chlamydia pneumoniae
and Pseudomonas aeruginosa.
241 STAGERS NOTES

Q/ What are the complications of COPD?

1. Pulmonary hypertension
2. Cor pulmonale
3. Respiratory failure
4. Secondary infection
5. Polycythemia.

Q/ How to manage acute exacerbation of COPD (type II respiratory

failure)?
1. Oxygen: Continuous low concentration oxygen via Venturi mask to raise PaO2
> 8 kPa (60 mm Hg). Initially 24% or 28% oxygen is given and increased
gradually provided PaCO2 does not rise unacceptably. If PaCO2 rises and pH
falls below 7.25, artificial ventilation or a respiratory stimulant should be
given.
2. Bronchodilator nebulized short acting b2 agonist (e.g. salbutamol) with an
anticholinergic agent(e.g. ipratropium).
3. Oral prednisolone 30 mg daily for 10 days.
4. Antibiotic: Given if infection is suspected.
5. Diuretic: If peripheral edema.
6. Chest physiotherapy. Secretions should be removed by suction.
7. Respiratory support: If above treatment fails or there is tachypnea and
acidosis (pH < 7.35).
Noninvasive ventilatory technique like BiPAP is used first. CPAP is occasionally
needed.
8. Respiratory stimulant: Less used. Doxapram 1.5 to 4.0 mg/min by slow IV
infusion may be helpful.

Q/What are the indications of hospitalization in patient

with COPD?
1. severe symptoms or acute worsening that fail to respond
to outpatient management
2. Presence of cyanosis
242 STAGERS NOTES

3. Peripheral edema
4. Alteration of consciousness
5. Co-morbidity and poor social circumstances.

Q/ Why low concentration O2 given in COPD? Or what happens when

high flow O2 given?
A. In COPD, the patient is dependent on hypoxic drive for respiration. High flow
oxygen blunts the chemoresponsiveness of the respiratory center in the medulla
(part of the brainstem) and thus aggravates respiratory failure (Type 2 respiratory
failure). To avoid this, low flow oxygen is given.

Q. What is pink puffer and blue bloater?

Pink puffer:

1. The patient is not cyanosed (pink), but dyspneic with lip pursing (puffer). No
edema
2. Usually lean and thin
3. It is found in emphysema, commonly panacinar, age 50 to 75 years
4. Usually there is no cor pulmonale
5. Exertional dyspnea is the main feature, and cough less common
6. Arterial PO2 and PCO2 are relatively normal.

Blue bloater:
1. The patient is cyanosed (blue) and edematous (bloater). But not dyspneic (or
mild dyspnea)
2. It is found in chronic bronchitis, age 40 to 45 years. Edema is due to cor
pulmonale
3. Cough with sputum is the main feature, dyspnoea is less common
4. Pulmonary hypertension, right ventricular hypertrophy, cor pulmonale and
secondary polycythemia may develop (patient may appear plethoric)
243 STAGERS NOTES

5. There is marked arterial hypoxemia and hypercapnia (low PO2 and increased
PCO2).

Q/ What are the discharge criteria of COPD patient?

1. The patient should be clinically stable and no parenteral therapy for 24 hours
2. Inhaled bronchodilators are required less than 4 hourly
3. Oxygen delivery has ceased for 24 hours
4. The patient is able to eat and sleep without significant episodes of dyspnea
5. The patient or caretaker understands and is able to administer medications

Follow up and home care arrangements (As for example home oxygen, home care,
Meals on Wheels, community nurse, allied health, GP, specialist) have been
completed The patient is ambulating safely and independently, and performing
activities of daily living.

Q/ What are the causes of dyspnea on exertion?

1. COPD
2. Bronchial asthma
3. DPLD (Interstitial lung disease)
4. LVF
5. Valvular diseases of the heart
244 STAGERS NOTES

6. Anemia.

Q/ What is cor pulmonale?

A. Cor pulmonale may be defined as “right ventricular hypertrophy or dilatation
with or without right sided heart failure due to causes of lung parenchyma,
pulmonary vasculature or chest wall”.

Q. What are the causes of chronic cor pulmonale?

A. As follows:
1. Respiratory disorders:

 Obstructive: COPD or chronic bronchitis with emphysema, chronic persistent

asthma
 Restrictive: DPLD (interstitial lung disease).

2. Pulmonary vascular disorders:

 Primary pulmonary hypertension

 Vasculitis of the small pulmonary arteries.

3. Chest wall or bony abnormality: kyphoscoliosis, ankylosing spondylitis, obesity

(Pickwickian syndrome).

Q/ What are the signs of pulmonary hypertension (PH)?

Signs of pulmonary hypertension are:

1. Low volume pulse

2. JVP is raised
3. Prominent ‘a’ wave in JVP
4. Left parasternal heave (indicates RVH)
5. Palpable P2
6. Loud P2 on auscultation
7. Epigastric pulsation (indicates RVH)
245 STAGERS NOTES

8. Early diastolic murmur (Graham Steel murmur due to pulmonary

regurgitation).

Q/ What are the causes of right heart failure?

A. As follows:

1. Secondary to left sided failure (the most common cause)

2. Secondary to mitral stenosis
3. Cor pulmonale
4. Myocardial infarction
5. Pulmonary valvular disease (PS, PR)
6. Tricuspid regurgitation
7. Eisenmenger’s syndrome (pulmonary hypertension with reversal of shunt in
ASD, VSD, PDA)
8. Cardiomyopathy
9. Chronic constrictive pericarditis.

Q/ What is Pack-year?
It is a way to measure the amount a person has smoked over a long period of time.
It is calculated by multiplying the number of packs of
cigarettes smoked per day by the number of years the
person has smoked.
For example, 1 pack year is equal to smoking 20 cigarettes
(1 pack) per day for 1 year, or 40 cigarettes per day for half
a year, and so on.
One pack year equals 365 packs of cigarettes.

Q/ what are the clinical features that suggest obstructive sleep apnea?
• Excessive daytime somnolence
• Intellectual deterioration and irritability
• Early-morning headaches
• Snoring
• Restless nights
• Social deteroriation (e.g. job, marriage, driving difficulties)
246 STAGERS NOTES

Diabetes mellitus

Q/ how to examine patient with DM ?

 Look for evidence of weight loss and dehydration .
 Smell the patient’s breath for the sweet smell of ketones
(diabetic ketoacidosis).
 Examine the skin: look for signs of infection and rashes. Look
for xanthelasma and xanthomata . Examine insulin injection sites for evidence
of lipohypertrophy (which may cause unpredictable insulin release),
lipoatrophy (rare) or signs of infection (very rare).
 Measure pulse and BP and examine the cardiovascular and
peripheral vascular systems.
 Examine the respiratory and gastrointestinal systems.
 Examine the central nervous system.
 Test visual acuity and examine the eyes and optic fundi
 Perform urinalysis

Q/What is DM ?
It is a clinical syndrome characterized by hyperglycemia caused by absolute or
relative deficiency of insulin secretion ,action or both and due to dysregulated
hepatic glucose production.
247 STAGERS NOTES

Q / What are laboratory tests of blood sugar ?

1) normal level ( fasting & postprandial)
2) impaired blood glucose level( abnormal either fasting level and / or
postprandial)
3) diabetic blood level ( fasting & postprandial)

Q/ How we diagnose DM ?
1) clinical features of DM(polyuria, polydipsia)with one value of diabetic blood
sugar range ,
or :
2) two reading of diabetic range of blood sugar on two different occasions

Q/ What is the criteria for diagnosis of DM ?

Symptoms of DM (polyuria,polydepsia and unexpalied weight loss) plus one of the

follwing :

 RBS >200 mg
 FBS > 126 mg
 Hb A1c>6.5 %
 2 hours PG >200 mg/dl during OGTT

Q/ What are types of DM ?

 Type 1 DM either immune mediated or idiopathic

 Type 2 DM
 Other specific types : include the following :
1- Genetic defect of B- cell function
2- Genetic defect of insulin action
3- Pancreatic disease ( eg . pancreatitis , pancreatectomy, cystic fibrosis ,
haempochromocytosis.
4- Excess endogenous production of hormonal antagonist to insulin ( Growth
hormone = Acromegally , Glucocorticoied = Cushing syndrome , Glucagon =
Glucogonoma , Catech olamines = Phaeochromocytoma , Thyroid hormone =
Thyrotoxicosis )
5- Drug induced : ( corticosteroid , thiazid diuretics , phenytoin )
6- Viral infection : ( congenital rubella , mumps
248 STAGERS NOTES

7- Associated with genetic disorder s (Down syndrome , Klienfillter , Turner

syndrome , DIDMOAD = Diabetus Inspidus . Diabetus Mellitus , Optirc
Atrophy , Deafness )

 Gestational DM

Q/ what are the symptom of DM ?

1) Thirst, dry mouth

2) Polyuria
3) Nocturia
4) Tiredness, fatigue, lethargy
5) Noticeable change in weight (usually weight loss)
6) Blurring of vision
7) Pruritus vulvae, balanitis (genital candidiasis)
8) Nausea; headache
9) Hyperphagia; predilection for sweet foods
10) Mood change, irritability, difficulty in concentrating, apathy

Q/ What Is syndrome X ?
Syndrom X or Reaven syndrome : It describe the
co-segregation in population of group of risk factor
factors for atherosclerosis , manifested by
disease ( coronary , peripheral , macrovascular
cerebral ) and excess of mortality ,It is not discrete
clinical disorder and associated with polycystic
ovarian syndrome , non alcoholic fatty liver )

FEATURES OFX- SYNDROM :

1. Hyperinsulinaemia
2. Type 2 diabetes or impaired
3. glucose tolerance
4. Hypertension
5. Low HDL cholesterol;
249 STAGERS NOTES

6. elevated triglycerides
7. Central (visceral) obesity
8. Microalbuminuria
9. Increased fibrinogen
10. Increased plasminogen
11. activator inhibitor-1
12. Increased C-reactive
13. protein (CRP)
14. Elevated plasma uric acid

.Q/What are important investigation to diagnose DM ?

A. 1-Urine testing for

 glucose ( by dip stick ) very cheap ,used as screening test , urine sample
must be passed in 1-2 h after meal for better sensitivity . This test if +ve
need blood sample to confirm. It`s disadvantage is the low renal threshold
which is the commonest cause of +ve glucosuria , as well as in pregnancy
251 STAGERS NOTES

 ketones ( by nitroprusside reaction , using tablets or dipstick to measure

acetoacetic acid)
 ketonuria found in : normal person after fasting or severe exercise, after
repeated vomiting, or after heavy fatty meal with low CHO . If ketonuria is
associated with glucosuria the diagnosis of DM is high
 protein ( dipstick for albumin) : this detect urine protein > 300mg/L
.Thus microalbuminuria only measured by specific test ,( if +ve in absence
of UTI may be an early indicator of DM nephropathy)
B. 2-blood sample

 blood glucose: using either glucose oxidase reaction or colorimetric

method to diagnose DM , an accurate method rather then portable
method must be used to check blood sugar . venous plasma glucose value
is the most reliable for diagnosis of DM.
glucose concentration in venous are lower than that in arterial or capillary
(finger prick) whole blood glucose concentration is lower than that of
plasma

Q / What is HbA1c ? What is benefit of it ? What is the normal range ?

Mention condition at which HbA1c is low ?
HbA1c

slow non- enzymatic covalent attachment of glucose to

hemoglobin ( glycation ) in DM the ratio of glycated adult
HbA ( HbA1c ) to the non glycated adult (HbA1) is used to
check glycaemia .The rate of formation of HbA1C is
directly related to the degree of hyperglycemia , a rise of
1% of HbA1C corresponds to increase of 36 mg/dl in
blood glucose.

Benefit

HbA1C can be used for diagnosis of DM, and for checking glycaemic control in the
previous weeks to months
Normal range :

Normal range 4.0% - 6.0%

251 STAGERS NOTES

HbA1c low in :

anemia and pregnancy

Q/ What is OGTT ? What are indication ?How is be done ? What are

result of OGTT?
OGTT :

Oral Glucose Tolerance Test

Indication :

1) fasting plasma glucose = 110 – 125 mg/dl ( 6.1 – 7.0 mmol/L )

2) random plasma glucose =140 – 199 mg/dl (7.8 – 11.0 mmol/L)
3) in pregnant women is very useful to diagnose Gestational DM

OGTT DONE :

 unrestricted CHO diet for 3 days

 fasting overnight for at least 8 hours
 rest for 30 minutes
 stay at rest during the test without smoking
 plasma glucose measured before and 2 hours after 75g of unhydrated
glucose orally

Result:
252 STAGERS NOTES

NOTE: Women with gestational diabetes should have glucose tolerance re-assessed
after pregnancy (generally at 6 weeks post-partum or later). If post-partum glucose
tolerance has returned to normal (fasting glucose < 6.1 mmol/L (110 mg/dL) and 2
hour glucose < 7.8 mmol/L (140 mg/dL)) advice on lifestyle changes should be
given to minimize the long-term risk of developing type 2 diabetes.

Q/ During follow up patient with DM , Why some people may gain

weight while other get weight loss ?

Weight gain means that they are not adherent to diet .

Weight loss means that there worsening of Beta-cell function.

Q/ What are level of control in DM ?

1) Tight control (intensive care) ( meticulous) ,in which we try to keep 24

h blood sugar level near normal, this is by using insulin multiple injections or
insulin pump , this is very difficult and carries the risk of hypoglycaemia so it
is unsuitable for eldery , those autonomic neuropathy . It is used for
pregnancy to avoid DM complications of DM

2) b- Conventional standard care: this should be considered for all patients of

type 2 DM whenever possible . This need to make the patients free of
symptoms by good control using diet , OHD , or insulin

3) c-Minimal care : this is for selected patients ( terminal disease,advanced CA,

those with advanced DM complication such as severe retinopathy, very young
or very old patients)

Q/ In type 1 DM at diagnosis ,tight blood sugar control prevent

microangiopathy OR macroangiopathy ?
In type 1 DM at diagnosis ,tight blood sugar control can prevent and even slow
microangiopathy , retinopathy Nephropathy and increased survival and when
combined with blood pressure and lipid control Can be very cost-effective
There is less clear benefits from tight control of blood sugar in TYPE 1 DM in
regard to Macrovascular complication of DM
253 STAGERS NOTES

Q/What are the frequency of blood glucose (BG) testing in diabetes?

Patient treated with insulin:

• Regular BG monitoring should be performed by all patients
to adjust the insulin dose and detect hypoglycaemia
• Daily pre-prandial and bedtime measurements are usually
recommended
• Target BG levels are typically 5–8 mmol/L (∼90–140
mg/dL),
although target ranges may be lower (e.g. in gestational
diabetes) or higher (e.g. in impaired awareness of
hypoglycaemia)

Patient treated with anti-diabetic drugs

• BG monitoring is optional in many patients with stable type 2 diabetes
• BG monitoring is most useful in patients taking sulphonylureas (risk of
hypoglycaemia), during intercurrent illness and prescription of corticosteroids, and
during changes in therapy
• BG is usually measured before breakfast (typical target 4–7 mmol/L (∼72–126
mg/dL)) and 2 hrs after food (typical target 4–10 mmol/L (∼72–180 mg/dL))

Q/What is gestational DM ?
Diabetes with first onset or recognition during pregnancy.
this definition will include a small number of women with pre-
existing (and previously clinically undetected) type 1 or type 2
diabetes, the majority of women can expect to return to normal
glucose tolerance immediately after pregnancy .

Q/ What are risk factors for DM ?

1) obesity.
2) ethnicity (South Asian, black, Hispanic, Native
American).
3) family history of type 2 diabetes.
254 STAGERS NOTES

4- previous glucose abnormalities during pregnancy .

5- previous macrosomia .

Q/ How gestational DM is diagnose ?

 Perform a 75-g OGTT, with plasma glucose measurement fasting and at 1 and
2 h,at 24–28 weeks of gestation in women not previously diagnosed with
overt diabetes.
 The diagnosis of GDM is made when any of the following plasma glucose
values are exceeded:
 Fasting: ≥92 mg/dL (5.1 mmol/L)
 1 h: ≥180 mg/dL (10.0 mmol/L)
 2 h: ≥153 mg/dL (8.5 mmol/L)

Q/ What are effects of DM on pregnancy ?

A. Early :first 6 weeks of development:
Hyperglycemia has teratogenic effect such :
cardiac, renal and skeletal malformations, of which the caudal regression
syndrome is the most characteristic.
B. Later hyperglycaemia in pregnancy: macrosomia and neonatal hypoglycaemia

Q/what are the precusion measures that the pregnant patient with DM
needs to take to avoid the risks of DM on the pregnancy ?
1) Pregnancy in women with established diabetes : insulin doses must be
increased substantially to overcome physiological insulin resistance.
2) Pre-conception preparation: strict glycaemic control very early in pregnancy
prevents fetal malformations.
3) Pregnancy should be planned: folic acid supplementation is introduced
before conception and patients with type 2 diabetes should usually be
converted to insulin therapy. If possible, use basal-bolus insulin regimens.
4) Monitoring:
255 STAGERS NOTES

5) Frequent self-monitoring of blood glucose, including post-prandial

measurements, plus HbA1c.
6) Maintain strict glycemic control, i.e. HbA1c close to the non-diabetic range. Do
not strive for normoglycaemia at the expense of hypoglycaemia.
7) Check blood glucose periodically during the night.
8) Check overnight sample of urine for ketones regularly; increase intake of
carbohydrate and dose of insulin to eliminate ketonuria.
9) Microalbuminuria and retinal screening should be performed on three
occasions during the pregnancy.
10) Regular monitoring of fetal size, and screening for fetal abnormalities*.

Q// What are the anti diabetic drugs that can use during pregnancy ?
1-insulin
2-metformin
3- glibenclamide

NOTE : GLIBENCLMIDE is only sulphonylurea can use during pregnancy

Q/ Enumerate anti-diabetics drugs ?

1) Sulphonylureas group& Meglitinides

2) Biguanides
3) Acarbose
4) Thiazolidenidiones ( TZD) or glitazones
5) Incretine mimetic
6) gliptins
7) 7-SGT2 inhibitors
8) insulin
256 STAGERS NOTES

Q/ What is effect of metformin ? What are indications of metformin ?

What are contraindication ?
EFFECT :

1) it increases insulin sensitivity and increases

peripheral uptake of glucose by stimulating
cAMP-regulated Kinases in the muscles
2) it decreases the absorption of glucose from GIT
3) inhibits glucose production in the liver
4) at molecular level it inhibits mitochondrial
respiration leading to intracellular AMP and this
lead to decrease gluconeogenesis

INDICATIONS :
1) first line drug choice in type 2 DM ( especially obese type 2 DM)
2) added to sulphonylureas when fail to achieve optimum control
3) combined with other antidiabetic drugs including Insulin

CONTRAINDICATION :
1) renal impairment
2) hepatic insufficiency
3) those who use alcohol heavily ( risk of lactic acidosis )
4) it should be stopped during severe illness , shock , hypoxaemia state and
septicaemia
5) vit B12 level is lowered during therapy
6) should be discontinued during radiographic contrast material

Q/ What is effect of sulphonylurea ? Indication ? Enumerate drugs

involve in this group ?

EFFECT :
stimulate insulin secretion
257 STAGERS NOTES

INDICATION:
They are used add-on therapy for non-obese type 2 DM not responding to diet
and metformin especially of recent onset(<5 years).

EXAMPLE :

1) the first generation and most mild one is Tolbutamide used mainly for elderly
because it is less likely to cause hypoglycaemia, needs to be given 2-3 times/d
2) the second generation include : gliclazide and glibizide
3) glibenclamide causes hypoglycaemia and should be avoided in elderly
4) glimeprideandmodified gliclazide cause less hypoglycaemia , long acting can
be used once/day .

#All sulphonylureas are most effective in their lower doses and no

additional benefits by increasing the doses .

Q/ Enumerate types of insulin ?

According to duration of action :

1- rapid acting insulin ( insulin –analogue such as ( Lispro and aspart )

start action in less than half hour
2- short acting ( soluble ) insulin start action about half hour
3- intermediate insulin ( isophane ) start action after 1-2 hours and last 14 hours
4- long acting ( protamin-zinc insulin )act after 2-4 hours and last 30 hours
5- long acting insulin with analogue (glargine)start in 1 – 2 hours and last
24hour

Q/ What is insulin regime ?

This depend on : the desired degree of glycaemic control , patient`s life style , the
ability of the patient to adjust the dose
1- short acting ( soluble )insulin + intermediate insulin /2 / day before meals ,
the morning dose is 2/3 of total dose 1/3 the evening dose . The soluble
ratio to intermediate is ½
258 STAGERS NOTES

2- short acting ( soluble ) 3 / d / before meals + intermediate acting insulin at

bed time
3- fast acting (insulin analogue ) before meals /3 times / d + morning
intermediate acting insulin

Q/ During insulin therapy despite day blood sugar control , some

patients develop fasting hyperglycemia, Why ?
 CAUSES ARE :
 Dawn phenomenon
the fasting hyperglycaemia is caused by the release of counter-
regulatory hormones circardian rhythm
 Somogy`s phenomenon
this is a rebound hyperglycaemia in the early morning due to insulin
induced hypoglycaemia in the late night usually due to higher evening
dose of long acting and intermediate insulin ,( here the patient get
weight gain)

Q/ Enumerate side effect of insulin ?

1- Hypoglycaemia
2- Weight gain
3- Peripheral oedema (insulin treatment causes
salt and water
retention in the short term)
4- Insulin antibodies (animal insulins)
5- Local allergy (rare)
6- Lipodystrophy at injection sites

Q/ Enumerate complication of DM ?
A. Acute complications of DM
1- DKA
2- Non –ketotic hyperosmolar diabetic coma
3- 3-Hypoglycaemia
4- lactic acidosis
B. Chronic complications
259 STAGERS NOTES

1- microvascular complications
 a-retinopathy
 b-diabetic nephropathy
 c-peripheral neuropathy
 d-diabetic foot
 e =autonomic neuropathy
2- macrovascular complications
 a-CVA
 b-IHD ( MI & vascular disease )

Q/ What are criteria for diagnosis of DKA ?

Its criteria :
 hyperglycemia ( blood glucose ≥ 250 mg /dl )
 ketosis ( ketone bodies in the blood and urine )
 acidosis ( pH ≤ 7.3 or HCO3 ≤ 15 meq/l )

Q / What are precipitating factors for DKA ?

Precipitating factors for DKA
1- infection ( 30 % ) even mild respiratory or urinary tract infection
2- new onset DM ( 25 % )
3- problem in insulin therapy ( 20 %)
4- stress

Q/ Enumerate keton bodies ?

1- hydroxybuterate
2- acetoacetate
3- aceton

Q/ How you manage patient with DKA ?

A. History of : ( infection , new onset DM , proplem in insulin therapy , stress)
B. Physical examination
C. Investigation :
 checking plasma : glucose , urea ,acetone , electrolytes , lipids , amylase
261 STAGERS NOTES

 ECG
 complete blood cell count and differentia
 arterial blood gases
 urine examination and ketone bodies in urine
 blood culture
 abdomenal US or CT scan , CXR as dictated
 calculate anion gap and serum osmolality

D. Treatment :
1) use short acting ( soluble ) insulin
2) fluid replacement
3) potassium replacement
4) antibiotic if there is infection
5) chart follow up during management for monitoring : vital signs, fluid input &
output , blood glucose , BUN, creatinine , electrolyte , blood gases and
HCO3

Insulin treatment for DKA

This is best given by infusion pump . Using 50 units of soluble insulin in 50 ml of 0.9
% NaCL, initially given in a rate of 6 U / hour ( checking blood glucose hourly if
there is no reduction in blood glucose the infusion rate should be increased )
when blood glucose reach about 270 mg/dl ( 15 mmol/ ) , the rate of insulin should
be reduced to 3U/hour . And when blood glucose about 180 mg/dl ( 10 mmol /L)
the insulin should be reduced to 2 U / h The target of lowering blood glucose
should be in the range of 55 – 110 mg/dl per hour
DKA treatment (continue)

Fluid replacement
r%9.0saline (NaCl) I.V
1L over 30 mins
1L over 1 hr
1L over 2 hrs
1L over next 2-4 hrs
When blood glucose < 15 mmol/L (270 mg/Dl) Switch to 5%
dextrose, 1 L 8-hourly
261 STAGERS NOTES

If still dehydrated, continue 0.9% saline and add 5% dextrose, 1 L per 12 hrs
Typical requirement is 6 L in first 24 hrs but avoid fluid overload in elderly
patients
Subsequent fluid requirement should be based on clinical response including
urine output

Potassium replacement
 non in the first liter of fluid unless plasma K < 3mmol/L
 when plasma K is < 3.5 mmol/L give only 20 mmol of potassium per hour
 when plasma K is > 3.5 mmol/L give 10 mmol of potassium per hour
Additional procedures

NOTES :DKA occure mainly in type 1 DM , but can occur in type 2 DM during
infection or stress state .
Every patient with DKA is K + DEPLETED

Q/ Why would K concentration drops after insulin treatement?

BECAUSE :

1) Dilution of extracellular k by IV fluid

2) Insulin cause shifting of K from extracellular to intracellular
3) Contineous renal loss of K

# Abdominal pain is a feature of DKA IN CHILDREN

Serum amylase may be raised in a patient with DKA but rarely indicate
# associated Pancreatitis
262 STAGERS NOTES

Q/ How hypoglycemia been diagnosed ?

To diagnose hypoglycaemia we must fulfill the criteria of Whiple`s triad

which are :
 patients symptoms of hypoglycemia
 low blood glucose measurement at the time of
the symptoms
 symptoms resolved on correction of
hypoglycemia

Q/ Mention the reading from which we consider that the patient is

hypoglycemic in both diabetic and normal people ?
1) In normal non diabetic symptoms of hypoglycaemia develop when blood
sugar ( 45 – 54 mg/dl) after injection of rapid acting insulin.
2) but in diabetic patients symptom may develop higher at (blood glucose < 3.5
mmol/l (63 mg/dl) .

Q/ What are the differential diagnosis of hypoglycemia ?

263 STAGERS NOTES

Q// What are the main symptoms of hypoglycemia ?

1-Autonomic
• Sweating • Hunger
• Trembling • Anxiety
• Pounding heart
2-Neuroglycopenic
• Confusion • Inability to concentrate
• Drowsiness • Incoordination
• Speech difficulty • Irritability, anger
3-Non-specific
• Nausea • Headache
• Tiredness

N.B. Symptoms differ with age; children exhibit behavioral changes (such as
naughtiness or irritability), while elderly people experience more prominent
neurological symptoms such as visual disturbance and ataxia.

Q/ What are risk Factors for sever hypoglycemia ?

1) Strict glycaemic control

2) Impaired awareness of hypoglycaemia
3) Age (very young and elderly)
4) Increasing duration of diabetes
5) Sleep
6) C-peptide negativity (indicating complete insulin deficiency)
7) History of previous severe hypoglycaemia
8) Renal impairment
9) Genetic, e.g. angiotensin-converting enzyme (ACE) genotype

Q/ What are causes of hypoglycemia ?

1) Missed, delayed or inadequate meal

2) Unexpected or unusual exercise
3) Alcohol
4) Errors in oral anti-diabetic agent(s) or insulin dose/
schedule/administration
264 STAGERS NOTES

5) Poorly designed insulin regimen, particularly if predisposing

to nocturnal hyperinsulinaemia
6) Lipohypertrophy at injection sites causing variable insulin
absorption
7) Gastroparesis due to autonomic neuropathy
8) Malabsorption, e.g. coeliac disease
9) Unrecognised other endocrine disorder, e.g. Addison’s
disease
10) Factitious (deliberately induced)
11) Breastfeeding by diabetic mother

Q/ How you treat patient with hypoglycemia at emergency department ?

Mild (self-treated)
• Oral fast-acting carbohydrate (10–15 g) is taken
as glucose
drink or tablets or confectionery
• This should be followed with a snack containing
complex
carbohydrate

Severe (external help required)

• If patient is semiconscious or unconscious, parenteral
treatment is required:
I.v. 75 mL 20% dextrose (=15 g; give 0.2 g/kg in children)*
or
I.m. glucagon (1 mg; 0.5 mg in children)
• If patient is conscious and able to swallow:
Give oral refined glucose as drink or sweets (=25 g)
or
Apply glucose gel or jam or honey to buccal mucosa

Q/ What are risk factors for diabetic nephropathy ?

1) poor control of DM
2) long duration of DM
265 STAGERS NOTES

3) presence of other microvascular complications

4) pre-existing hypertension
5) family history of diabetic nephropathy or hypertension

Q/ When did the patient with DM should be screen for

microalbumenemia ?

• Patients with type 1 diabetes annually from 5 yrs after diagnosis

• Patients with type 2 diabetes annually from time of diagnosis

Q/When you say that the patient enter to nephropathy and have
microalbumenemia ?

Microalbuminuria present if:

Males : ACR 2.5–30 mg/mmol creatinine in urine
Females : ACR 3.5–30 mg/mmol creatinine in urine

#Established microalbuminuria if 2 out of 3 tests positive

Q/How you manage patient with diabetic nephropathy ?

1-improve glycaemic control : metformin should be abandoned (if serum

creatinine is more than 1.7 mg/dl) , long acting sulphonylurias should be replaced
by short acting ones
2 -aggressive reduction of high blood pressure by:

• using ACE-inhibitors ( if there are contraindication for their use such as ,renal
artery stenosis or hyperkalaemia , calcium channel blockers such as
Deltiazem or Verapamil can be used
• aggressive CVD risk factor control( such as hyperlipidaemia )
3-renal replacement therapy may benefit diabetic patients if carried out early
before ESRD
4-renal transplant improve life expectancy ,but macrovascular and microvascular
diabetic diseases continue in its progress. The progression of recurrent diabetic
nephropathy in the allograft is too slow
5-pancreatic transplant can delay or reverse microvascular diseases
266 STAGERS NOTES

Q/What are risk factors of diabetic retinopathy ?

1) Lone duration of DM
2) Poor glycemic control
3) Hypertension
4) Hyperlipidemia
5) Pregnancy
6) Nephropathy/renal disease
7) Others:obesity and smocking

#Classification of diabetic retinopathy according to the prognosis

of vision:
1=Background retinopathy (non – prolifrative )
2=Maculopathy
3=pre-prolifrative
4=prolifrartive
267 STAGERS NOTES

Q/How you manage patient with diabetic retinopathy ?

1- Good glycaemic control(HbA1c around 53 mmol/mol (7%)
2- appropriate blood pressure (< 130/80 mmHg) should be maintained to
prevent onset and delay progression of diabetic eye disease
3- Retinal photocoagulation (laser treatment) is indicated in:
• severe proliferative or
• very severe nonproliferative retinopathy;
• new vessels elsewhere with vitreous haemorrhage;
• new vessels without vitreous haemorrhage in type 2 diabetes;
Q/ Enumerate types of diabetic neuropathy ?
Somatic
1) Polyneuropathy
2) Symmetrical, mainly sensory and distal
3) Asymmetrical, mainly motor and proximal (including amyotrophy
4) Mononeuropathy (including mononeuritis multiplex)
Visceral (autonomic(
1) Cardiovascular
2) Gastrointestinal
3) Genitourinary
4) Sudomotor
5) Vasomotor
6) Pupillary

Q/ What are clinical feature of autonomic neuropathy ?

1) Cardiovascular
• Postural hypotension
• Resting tachycardia
• Fixed heart rate
2) Gastrointestinal
• Dysphagia, due to oesophageal atony
• Abdominal fullness, nausea and vomiting, unstable
glycaemia, due to delayed gastric emptying (‘gastroparesis’)
268 STAGERS NOTES

• Nocturnal diarrhoea ± faecal incontinence

• Constipation, due to colonic atony
3) Genitourinary
• Difficulty in micturition, urinary incontinence, recurrent
infection, due to atonic bladder
• Erectile dysfunction and retrograde ejaculation
4) Sudomotor
• Gustatory sweating
• Nocturnal sweats without hypoglycaemia
• Anhidrosis; fissures in the feet
5) Vasomotor
• Feet feel cold, due to loss of skin vasomotor responses
• Dependent oedema, due to loss of vasomotor tone and
increased vascular permeability
• Bullous formation
6) Pupillary
• Decreased pupil size
• Resistance to mydriatics
• Delayed or absent reflexes to light

CLINICAL SENARIO
Q/ A25 yrs old diabetic female on metformin , she get pregnancy
during pregnancy her blood glucose became uncontroll, What your
management ?

She remain on metformin and add insulin

Q/A 30 yrs old diabetic female on glibizide , What do you do about

her drug ?

Change Gligizide to Glibenclmide ( only sulphonylurea drug used during pregnancy

) and add insulin if blood sugar uncontrolled
269 STAGERS NOTES

Q/A 60 yrs old diabetic male on glibenclimide drug admitted to the

emergency unit his blood glucose is 40 mg/dl , what is you
management ?

- the pt should recirve 5 % DEXTROSE and remain in the hospital for 2 days
because hypoglycemia result from glibenclmide which have long half life 36 hour.

Q/ Diabetic patient develop ischemic heart disease , How you are

manage him ?

Primary prevention of myocardial infarction

• Strict glycaemic control
• Aggressive control of hypertension
• Cholesterol reduction with a statin
Immediate measures in acute myocardial infarction
• Primary angioplasty or thrombolysis/fibrinolysis
• Aspirin and clopidogrel
• ACE inhibitor
• β-blocker
• ? Intravenous insulin
Secondary prevention of myocardial infarction
• Aspirin
• β-blocker
• ACE inhibitor
• Cholesterol reduction with high-dose statin
• Intensive subcutaneous insulin or anti-diabetic medication
271 STAGERS NOTES

Q/ A 20 yrs old diabetic female , she get pregnancy , during pregnancy she
complained of sever epigastric pain ,nausea and vomiting , her bloog glucose
level 400 mg/dl , urine test show proteinurea and keton positive , What are
likely diagnosis ? and how you are manage her ?

- Diagnosis is DKA

-Management : mentioned above

Q // When measure insulin level & C- Peptide , We find the following :

1= Both Insulin & C –peptide are low

2= Both Insulin & C-peptide are high

3= Insulin is high & C-peptide in low

How you interpret ate this result ?

Answer :

1= BOTH ARE LOW :Alcohol , drugs

2= BOTH ARE HIGH : Sulphonylurea , insulinoma

3= Insulin high , C-peptide low : Exogenous insulin

Q// A50 yrs old diabetic male obes his BMI is 30 kg/ m2 ,He had history of
hypertention , on urine test done for him he had microalbuminurea , he is on
metformin and not take any drug for hypertention , his blood sugar is 300 mg
/dl , BP= 20/10 mmHg :

1= What is drug of choice for diabetes in this case ?

2= What is drug of choice for hypertention in this case ?

3= What is target BP AND blood glucose ?

271 STAGERS NOTES

4=What is diagnosis ?

1= Insulin

2= ACE –inhibitor for both hypertension and proteinurea

3= target BP is less than 140/ 80 mmHg

Target blood glucose : fasting below 108 mg/dl

Preprandial 72- 126 mg /dl

Postprandial 72-137 mg/dl

4=Diagnosis is diabetic nephropathy.

Q// Diabetic patient develop renal failure , what is best drug for him ? WHY ?

1) Metformin should be avoided when creatnin level above 1.7 mg/ dl decause
risk of lactic acidosis
2) Sulphonylurea is avoided because secretion of it mainly by kidney so in
patient with renal failure the secretion of sulphonylurea is impaired result in
increase in half life and more risk of hypoglycemia so should be abonded
3) INSULIN is drug of choice
272 STAGERS NOTES

HF
Q1/ define HF?
describe the state that develops when the heart cannot
maintain an adequate cardiac output or can do so only at
the expense of an elevated filling pressure.

Q2/ What are the Causes of HF?

1- Ischemic Heart disease (IHD) which is the commonest.
2- HTN or Hypertensive Heart disease with end Organ damage.
3- Valvular Heart disease, the commonest cause is Rheumatic heart disease.
4- Cardiomyopathy.
5- Congenital heart disease.
6- Cor-pulmonale.
7- Constrictive pericarditis.
8- Heart failure with high cardiac output like thyrotoxicosis, severe anemia

Q3/ Wht are the factors the preceptate HF in patient with preexisting
heart diseas? Also the causes of decompensation of CHF?
Also causes of acute on chronic HF ?
1) Myocardial ischaemia or infarction
2) Intercurrent illness, e.g. infection
3) Arrhythmia, e.g. atrial fibrillation
4) Inappropriate reduction of therapy
5) Administration of a drug with negative inotropic properties (e.g. β-blocker)
or fluid-retaining properties (e.g. NSAIDs, corticosteroids)
6) Pulmonary embolism
7) Conditions associated with increased metabolic demand, e.g. pregnancy,
thyrotoxicosis, anaemia
8) Intravenous fluid overload, e.g. post-operative i.v. infusion
273 STAGERS NOTES

Q4/ how can you deferrentiate between right and left side heart failure
in clinical signs?
1. Left heart failure develops pulmonary oedema may present with:
 breathlessness
 Orthopnoea
 paroxysmal nocturnal dyspnoea
 inspiratory crepitations over the lung bases.
2. Right heart failure produces a
 high JVP
 hepatic congestion
 peripheral oedema.
 Ascites pleural effusion
 cardiac cachexia

Q5/ What are the findings on examinations in patient with HF ?

274 STAGERS NOTES

Q6/where is the first site that the patient develops edema first?
 In ambulant patients the oedema affects the ankles
 whereas in bed-ridden patients it collects around the thighs and sacrum.

Q7/Define cardiac cachexia

marked weight loss sometimes associated with
Chronic HF caused by a combination of :

1. anorexia and impaired absorption due to

gastrointestinal congestion
2. poor tissue perfusion due to a low cardiac
output
3. skeletal muscle atrophy due to immobility.

Q8/define cardiac asthma?what is the importance to defrentiate it from

true asthma?

Cardiac asthma is a medical diagnosis of wheezing, coughing or shortness of breath

due to congestive heart failure. It is known as cardiac asthma because the
symptoms mimic ordinary asthma

The distinction between true asthma and cardiac asthma is especially important
because some treatments for true asthma, including inhalers, may actually worsen
cardiac asthma and cause severe heart arrhythmias.

Q/New York Heart Association classification of heart failure?

Grade
I No symptoms at rest, dyspnoea only on vigorous exertion
II No symptoms at rest, dyspnoea on moderate exertion
III May be mild symptoms at rest, dyspnoea on mild exertion, severe dyspnoea on
moderate exertion
IV Significant dyspnoea at rest, severe dyspnoea even on very mild exertion. Patient often
bed-bound
275 STAGERS NOTES

Q/ clinical features of chronic HF?

Classical pleural
• Fatigue on minimal exertion effusion in HF is
• Exertional dyspnoea bilateral or unilateral

• Peripheral oedema (right side)

• Abdominal discomfort (from hepatic distension)

• Nocturia (reversal of diurnal rhythm)
• Weight loss and cachexia

Q9/ what are CXR findings in left heart failure?

1. abnormal distension of the upper lobe pulmonary veins (with the patient in
the erect position)
2. The vascularity of the lung fields becomes more prominent
3. the right and left pulmonary arteries dilate
4. septal or 'Kerley B' lines :horizontal lines in the costophrenic angles
(thickened interlobular septa and dilated lymphatics due to interstitial oedema.)
5. More advanced changes due to alveolar oedema cause :
 A hazy opacification spreading from the hilar regions
 pleural effusions.
276 STAGERS NOTES

Q10/ what are the causes of RF in HF?

1. poor renal perfusion due to a low cardiac output
2. diuretic therapy
3. ACE inhibitors and angiotensin receptor blockers.

Q11/ What are the drugs that cause peripheraledema?

Sodium retention: fludrocortisone, non-steroidal anti-inflammatory agents

Increasing capillary permeability: nifedipine, amlodipine

Q12/ what are the causes of hypokalemia in HF?

1. treatment with diuretics
2. hyperaldosteronism caused by activation of the RAS.

When we give ACEI , we have to do B,urea , S,creatinin and S.K after one week

It should be stopped if thers deterioration in renal fuction or K level above 5.5 mmol /dl
277 STAGERS NOTES

Q13/ what are the causes of hyperkalemia in HF?

1. the effects of drug treatment, particularly the combination of angiotensin-
converting enzyme (ACE) inhibitors and spironolactone
2. renal dysfunction.

Q14/ what are the causes of hyponatrenia in HF?

1. diuretic therapy
2. inappropriate water retention due to high ADH secretion
3. failure of the cell membrane ion pump.

Q15/ what are the causes of jaundice in HF?

This due to liver dysfunction caused by:
'Adding oral β-blockers
1. hepatic venous congestion gradually in small incremental
2. poor arterial perfusion doses to standard therapy
including ACE inhibitors in
Q16/ what are the causes of DVT in HF? people with heart failure
reduces the rate of death or
1. the effects of a low cardiac output
hospital admission
2. immobility

Q17/what are the causes of CVA in HF?

1) atrial fibrillation
2) intracardiac thrombus complicating conditions such as mitral stenosis or LV
aneurysm.

Q18/ what are the causes of arrythemia in HF?

1) electrolyte changes (e.g. hypokalaemia, hypomagnesaemia)
2) the underlying structural heart disease
3) the pro-arrhythmic effects of increased circulating catecholamines
4) drugs (e.g. digoxin)

When we give Na nitroprosside or angesed IV infusion we have to cover the fluied and giving set
because it react with the sunlight and convert to cyanide which is toxic
278 STAGERS NOTES

Q19/ what are the complications in HF ?

1) Renal failure
2) Hypokalaemia
3) Hyperkalaemia
4) Hyponatraemia
5) Impaired liver function
6) Thromboembolism
7) Atrial and ventricular arrhythmias

In patient with HF , blood transfusion if the blood Hb below than 8 mg/dl because he or she cannot
tolerate , he is already hypoxic and anemia will increses the load on the heart

Q/ how can you mange patient with acute heart failure (acute pulmonary
edema)?
1. Short history and vital signs
2. Sitting upright
3. Cannula and moniter ECG (treate any arrytmia)
4. Send for investigation while continue treatment
5. O2 therapy : the aim is for SPO2 >95 (OR >90 with COPD)
6. IV morphine 2.5-10 mg IV slowly (caution in liver failure and COPD)
7. Furosemide 40-120 mg IV
8. IV nitrate infusion( GTN useful in significant HF (contraindicated if systolic BP
less than 90 mmHg)
9. Withdraw any drug contribute to HF (CCB and NSAIDs)
10. If the patient is worsening then further dose of furosemiode (40-80 mg),
CAPAP, or increases nitate infusion but keep systolic BP above 100 mmHg.
11. Aortic ballone
12. Ultrafiltration of the fluid
279 STAGERS NOTES

The major benefit of ACE inhibitor therapy in heart failure is a reduction in afterload; however,
there may also be an advantageous reduction in preload and a modest increase in the plasma
potassium concentration.

Q/ management of patient with chronic HF?

A. NON- pharmacological measures

1. Salt and water restruction (< 2 L / day)
2. Avoid heavy exersize
3. Avoid psychological distress
B. Pgamacological measures

For volume overload :diuretics ex : loop diuretics or thiazide

1. ACEI or ARAB:

Angiotensine 2 cause
281 STAGERS NOTES

• Cardiac musle death

• Potent vasoconstrictor
• Na and fluied retention
• Atherogenic

So we use ACEI and ARAB in treatment of HF

 ACEI useful in any type and in any stage of HF

 Contraindications of ACEI are?
• Bilateral RAS
• Pregnancy
• Hyperkalemia
 So we uses angeside and hydralazine instade of it
 ACEI prolonged survival in patient with heart failure
2. B- blockers: starts with low dose then bulid up the dose gradually
3. Spironolactone:gives as early as possible because it
• Reduce atherogenesis
• Improve left ventricular systolic dysfuction

Side effect: painful gynecomastea and hyperkalemia

4. Digoxine:not prolonge survival but reduce the rate of hospital admission and
symptomatic relief

Can cause arrhythmia

Frequency of plureal effusion
5. Anticoagulation: warfarine in case of :
1-right side
Af and mural thombi on ECHO
2-bilateral
6. Statine
7. Avoid drugs the preceptate HF :
• Steroids
• NSAIDs
• All antiarrytmtic drugs are cardiosupressor except amiodarone and flecanide(class
1C)
281 STAGERS NOTES

Q/Causes of non-cardiogenic pulmonary edema?

Q/ Defrential diagnosis of HF?
Any causes of SOB

B-blockers are contraindicated in acute HF

SINCE the heart deoends up on sympathetic activity

Q/ define phantom tumor?

An accumulation of fluid in the interlobar spaces of
the lung occurring as a result of congestive heart
failure and appearing radiologically as a neoplasm.
Disappear on diretic therapy
282 STAGERS NOTES

IHD
Q/ What aare the risk factors for CHD?

Modifiable risk factors:

 Hypertension (high blood pressure)

 Tobacco use
 Raised blood glucose (diabetes)
 Physical inactivity
 Unhealthy diet
 Cholesterol/lipids
 Overweight and obesity
 stress

Non modifiable risk factors :

 Age
 Gender
 Family hx
 Heredity and race
 menopause

Q/What are The physical signs that you found on examination in patient
with MI?

 Prolonged cardiac pain

o Chest, throat, arms, epigastrium or back
 Anxiety and fear of impending death
 Nausea and vomiting
 Breathlessness
 Collapse/syncope
283 STAGERS NOTES

Physical signs
 Signs of sympathetic activation
o Pallor, sweating, tachycardia
 Signs of vagal activation
o Vomiting, bradycardia
 Signs of impaired myocardial function
o Hypotension, oliguria, cold peripheries
o Narrow pulse pressure
o Raised jugular venous pressure
o Third heart sound
o Quiet first heart sound
o Diffuse apical impulse
o Lung crepitations
 Signs of tissue damage
o Fever
 Signs of complications, e.g. mitral regurgitation, pericarditis
(see text)

ECG canges in patient with MI

anteroseptal infarction, ST- elevation found in one or more leads from V1 to V4

anterolateral infarction produces changes from V4 to V6, in aVL and in lead I

Inferior infarction is best shown in leads II, III and aVF, while at the same time
leads I, aVL and the anterior chest leads may show 'reciprocal' changes of ST
depression

(Infarction of the posterior wall of the left ventricle does not cause ST elevation or
Q waves in the standard leads, but can be diagnosed by the presence of reciprocal
changes (ST depression and a tall R wave in leads V1-V4). inferior infarction may
associated with right ventricle MI; this may be identified by recording from
additional leads placed over the right precordium. V3R &V4R
284 STAGERS NOTES

Q/What are the etiology of I.H.D

• Atherosclerosis of the coronary artery is the cause of I.H.D in almost all cases

• other rare causes include:

1) coronary artery spasm

2) severe Aortic stenosis or HOCM[hypertrophic obstructive CM]
3) coronary arteritis such as PAN or other collagen disease
4) Coronary embolism e.g. SBE or Paradoxical embolism
5) Syphilitic aortitis involving coronary ostium

The progression of IHD

Silent ischemia staple angina UA non STEMI STEMI Sudden death

Q/ what are the causes of silent MI?

1. DM
2. Old age
3. Cardiac transplantation

Q/ What are the Echocardiographic findings in acute MI?

1. regional wall abnormaly [hypokinesia, dyskinesia]
2. assessing left and right ventricular function
3. detecting important complications such as
 mural thrombus
 cardiac rupture Diagnosis of MI

 ventricular septal defect
 mitral regurgitation
 pericardial effusion.
Increases cardiac enzymes plus one of the following
 Classical chest pain
 ECG changes(ST segment elevation, Q wave)
 New LBBB
285 STAGERS NOTES

Q/ how can you manage this case ?

1) Short history and vital signs

2) High-flow oxygen
3) I.v. access and send for important
investigations
4) ECG monitoring
5) 12-lead ECG
6) I.v. analgesia (morphine 5-10 mg) and antiemetic(metchlopromide 10 mg IV)
7) Aspirin 300 mg (Chewing and hold in mouth)
8) Clopedogrel 300-600 mg loading dose
9) IV B-blockers like metoprolol 5mg IV (before giving B-blockers you have to
search for contindications :
 asthma
 systolick BP below 90 mmHg
 acute HF
10) GTN sublingual (500 microgram) or IV infusion
Contraindications for GTN are"
 systolick BP below 90 mmHg
 prior sildenafil (Viagra) in previous 24 hours or tadalafil (Cialis) in
previous 5 days
11) Reperfusion therapy
Q/indications for reperfusion therapy are:
 ST segment elevation > 2mv in at least two adjacent chest leads
 ST segment elevation > 1mv in at least two adjacent limp leads

 New LBBB
 True posterior MI
We have to send the patient to hospital in which PCI facilties are available , if not
available then we have to start with chmecal thrombolysis using Alteplase within 6
hours from onset of MI
286 STAGERS NOTES

Q/How to give alteplase?

If body weight > 65 then :

 15 mg IV bolus followed by:

 50 mg over 30 min
 35 mg over 60 min( total 100 mg over 90 min)

If body weight < 65 then weight adjusted

Q/What are the contraindications to thrombolysis?

Absolute
Inferior MI management is the
1. Any prior intracranial haemorrhage same excpt drugs that cause
2. Ischemic strock within 3 months reduction in BP:
3. Ischemic strock within 3 months
Diuretics ,ACEI & B-blockers
4. Intracranial A-V malformation
5. Intracranial malignant neoplasm
6. active bleeding or bleeding diathesis

Relative
1. Sever HT (systolic>180mmHg, diastolic >110 mmHg)
2. Pregnency
3. Prolonged CPR
4. Non compressible vascular puncture
5. Major surgery within 3 weeks
6. Internal bleeding within 2-4 weeks
7. Active peptic ulcer
8. Current anticoagulant use
9. For streptokinase : prior exposure to streptokinase
287 STAGERS NOTES

Q/What we have to do if the patient have contraindication to

thrombolysis?
A/Considered PCI

Q/ what are the complications of acute MI?

A. Immediate
1. VT,VF
2. Complete heart block
3. Hypotension
4. Cardiogenic shock
5. Pulmonary edema
B. Early( within days)
1. New murmer
2. Mitral regerge
3. Ventricular septal repture
4. Repture of myocardial wall
5. Mural thrombi and systemic empolization
6. Pericarditis
C. Late complications(within weeks)
1. Dresslers syndrome
2. VT,VF
3. Left ventrecullar aneurism

12)Late management of myocardial infarction

Lifestyle modification

 Stop smoking
 Regular exercise
 Diet (weight control, lipid-lowering)

Secondary prevention drug therapy

 Antiplatelet therapy (aspirin and/or clopidogrel)

 β-blocker
 ACE inhibitor
288 STAGERS NOTES

 Statin
 Additional therapy for control of diabetes and hypertension

Q/ what is the deference between stable angina , unstable angina and

MI?
Stable angina Ischaemia due to fixed atheromatous stenosis of one or more
coronary arteries
Unstable Ischaemia caused by dynamic obstruction of a coronary artery due
angina to plaque rupture with superimposed thrombosis and spasm
Myocardial Myocardial necrosis caused by acute occlusion of a coronary
infarction artery due to plaque rupture and thrombosis

Q/ what are the classification of UA?

1. Any recent severe angina within first week
2. Stable angina which change its character (frequent attacks , poor effort
tolerance not relief to previous dose of antianginal drugs
3. Variant angina
4. Post MI angina

Q/ what are the features of angina pain ?

• Brought on by physical or emotional exertion
• Relieved by rest
• Usually crushing, squeezing or constricting in nature
• Usually retrosternal
• Often worse after food or in cold winds
• Often relieved by nitrates

Q/ what are the deferential diagnosis of chest pain at

rest ?
• Myocardial infarction
• Unstable angina
• Dissecting aortic aneurysm
• Oesophageal pain
289 STAGERS NOTES

• Pericarditis
• Pleuritic pain
• Musculoskeletal pain
• Herpes zoster (shingles)

Q/ what are the benefits of B-blocker in acute MI?

1. Prolonged survival
2. Protect form arrhythmia
3. Pain killer
4. Reduce blood pressure

Q/How to defrrentiate STEMI from Non-STEMI & UA?

UA: ST segment depression or T wave inversion with normal enzymes

Non-STEMI: ST segment depression or T wave inversion with elevated enzymes

STEMI: ST segment elevation with elevated enzymes

Q/What are the bad prognostic sign for MI?

Ddx of tall R wave in lead V1:
1. big size of infarctionm
2. unstable vital sign -RVH
3. Q type of ECG\
-WPWs
4. anterior MI
5. Acute ST elevation ‫مثل الشراع‬ -RBBB

6. Hx of arrhythmia -Dextrocardia
7. LV dysfunction
8. Old age DM
9. Extensive ECG changeshifg titer of troponin
10. Prior IHD
11. 3 vessle disease

Q/ What are the indications for PCI in acute MI

(HIGHT RISK PATIENTS)

1. Hight troponin level
291 STAGERS NOTES

2. Reccurent chest pain

3. Extensive ECG changes
4. LV dysfunction
5. Old age DM
6. High rik exsersise test
7. 3 vessle disease

Q/What are the defrences between X-syndrome and syndrome –X

Metabolic syndrome X vs cardiac X-syndrome
Cardiac syndrome X is angina (chest pain) with signs associated with decreased
blood flow to heart tissue but with normal coronary arteries. Cardiac syndrome X is
sometimes referred to as microvascular angina when there are findings of
microvascular dysfunction.

 +ev ECG
 +ev enzymes
 Chest pain
 Mainly in young female

Metabolic syndrome is a disorder of energy utilization and storage, diagnosed by

a co-occurrence of three out of five of the following medical conditions: abdominal
(central) obesity, elevated blood pressure, elevated fasting plasma glucose, high
serum triglycerides, and low high-density lipoprotein (HDL) levels. Metabolic
syndrome increases the risk of developing cardiovascular disease and diabetes
291 STAGERS NOTES

Q/Define prinzmetal angina

Prinzmetal angina (variant angina) is a syndrome typically

consisting of angina at rest that occurs in cycles. It is
caused by vasospasm, a narrowing of the coronary arteries
caused by contraction of the smooth muscle tissue in the
vessel walls rather than directly by atherosclerosis

Q/ What are the drugs that improve survival in MI?

Asprine

ACEI

B blocker

Q/ contraindications of ACEI ?
1. Pregnancy
2. Hyperkalemia
3. Systolic BP less than 100 mmHg

What is the cause of bradycardia in patient with right sided MI ?

LAD : widow macker , supply about 90 % from the left ventricle

292 STAGERS NOTES

AF
Q/ what are the causes of AF?

 Coronary artery disease (including acute myocardial infarction)

 Valvular heart disease, especially rheumatic mitral valve disease
 Hypertension
 Sinoatrial disease
 Hyperthyroidism
 Alcohol
 Cardiomyopathy
 Congenital heart disease
 Chest infection
 Pulmonary embolism
 Pericardial disease
 Idiopathic (lone AF)
293 STAGERS NOTES
294 STAGERS NOTES

CVA
Q/Define CVA ?
Stroke may be defined as sudden development of focal
neurological deficit due to nontraumatic vascular cause, lasting
more than 24 hours.

Q/Define TIA
Transient ischaemic attack (TIA). Describes a stroke in which symptoms resolve
within 24 hours
Q. What is stroke? What are the types of stroke?
Stroke may be defined as sudden development of focal neurological deficit due to
nontraumatic vascular cause, lasting more than 24 hours. It is of following types:

1. Transient ischemic attack (TIA)—sudden neurological dysfunction due

to cerebral ischemia lasting less than 24 hours and the patient recovers
completely within 24 hours
2. Stroke in evolution—the symptoms worsen gradually or in a step wise
pattern over hours or days and the neurological deficit persists for more than
24 hours
3. Completed stroke—clinical signs of neurological deficit are persistent
Reversible ischemic neurological deficit (RIND)—neurodeficit persists for more
than 24 hours, but recovers totally within 3 weeks
4. Partial non-progressive stroke (PNS)—neurodeficit persists for more
than 3 weeks, but is either partial or ends up with minimal residual deficit.

Q/what are the features of cerebral thrombosis?

onset is slow. There is no history of vomiting, unconsciousness or convulsion.
Q/ what are the features of cerebral embolism?
In cerebral embolism, onset is sudden (seconds to minutes), called stormy onset.
295 STAGERS NOTES

Q/ what are the defrrential diagnosis of strock and TIA?

1. Primary cerebral tumours
2. Metastatic cerebral tumours
3. Subdural haematoma
4. Peripheral nerve lesions(vascular or compressive)
5. Cerebral abscess
6. Todd’s paresis (after epileptic seizure)
7. Demyelination
8. Hypoglycaemia
9. Encephalitis
10. Conversion disorder
11. Migrainous aura (with or without headache)
12. Ménière’s disease or other vestibular disorder
13. Focal seizures
Q/Patient presented to you with sudden attack of weakness what is the
first investigation you have to do ? and why
First I have to do ergent CT scan to the brain , to defrentiate ischemic strock from
haemorrhagic one , because thers deferent lines of managements

Brain damage resulting from an ischemic stroke may take more than
24 hours to manifest on CT, so CT is expected to be normal initially.

Q/what are the risk factors stroke ?

1. modifiable
 High blood pressure
• Heart disease (atrial fibrillation, heart failure, endocarditis)
• Diabetes mellitus
• Hyperlipidaemia
• Smoking
• Excess alcohol consumption
• Polycythaemia
• Oral contraceptives
• Social deprivation
296 STAGERS NOTES

2. Non modifiable
• Age
• Gender (male > female, except in the very young and very old)
• Race (Afro-Caribbean > Asian > European)
• Heredity
• Previous vascular event, e.g. myocardial infarction, stroke or
peripheral embolism
• High fibrinogen

Q/Indications for emergency CT in acute stroke

• Patient on anticoagulants or with abnormal coagulation
• Consideration of thrombolysis or immediate anticoagulation
• Deteriorating conscious level or rapidly progressing deficits
• Suspected cerebellar haematoma, to exclude hydrocephalus

Q/ why we do CT scan instade of MRI in ER Head trauma and

strock patient?
Short time for scan (few min)
Better results than MRI for haemorrhage and bone fracture
Q/ What are the features of cerebral hemorrhage?
A. In cerebral hemorrhage, onset is sudden (seconds to minutes) and usually
associated with loss of consciousness, vomiting or convulsion.

Q/ What are the features of subarachnoid hemorrhage?

A. In subarachnoid hemorrhage, the patient is usually young. There is history
of sudden severe headache mostly in the occipital
region followed by vomiting and loss of
consciousness. Features of meningeal irritation, like
neck rigidity and Kernig’s sign, are usually present.
Fundoscopy shows subhyaloid hemorrhage (boot
shaped concave).
297 STAGERS NOTES

Q/ What you have examined in the heart?

A. Any arrhythmia like atrial fibrillation. Also any valvular lesion, e.g. MS.
Q/ Have you examined the neck? Why?
A. Yes. I have seen carotid bruit (thrombus from carotid may be dislodged
and cause cerebral thrombosis).

Q/ What investigations do you suggest?

A. As follows:
1. CT scan of the head (first investigation to be done)
2. Complete blood count with ESR
3. Blood sugar
4. Blood urea and serum creatinine
5. Serum lipid profile
6. Serum electrolyte
7. Chest X-ray P/A view
8. ECG
9. Source of the event:
 Doppler study of extracranial/intracranial vessels
 Echocardiography—transthoracic or transesophageal
 MRA or CTA of the cerebral vessels

10. Other tests according to suspicion of cause:

 For collagen vascular disease—ANA, anti-dsDNA, anti-cardiolipin and anti-

phospholipid antibody
 pANCA, cANCA
 Coagulation screening, serum antithrombin III, protein C and protein S level
 Others—red cell mass (PRV), chromatographic test in serum and urinary
level of homocysteine or methionine (homocystinuria), TPHA and VDRL
(syphilis).
298 STAGERS NOTES

Q/ How to treat CVD?

A. As follows:
1. General measures:
1. Oropharyngeal suction
2. IV channel
3. Nasogastric tube feeding
4. Maintenance of nutritional status
5. Regular change of posture (2 hourly)
6. Care of bowel
7. Care of bladder (catheterization)
8. Care of mouth (to prevent fungal infection)
9. Care of eyes (tear naturale or taping of the affected eye shut).

2. Control of risk factors or cause, if any. For example:

1. Control of hypertension
2. Control of diabetes mellitus
3. Control of hyperlipidemia
4. Other treatment according to the cause.

3. If cerebral edema: Dexamethasone or mannitol.

4. Specific treatment according to the type of stroke (after CT scan):

*Cerebral infarction—antiplatelet drugs (e.g. aspirin, clopidogrel). Cerebral
vasodilator like vinpocetine should be given. If atrial fibrillation, heparin followed by
warfarin should be considered

*Cerebral hemorrhage—for massive hemorrhage, neurosurgical intervention may be

required. Other treatment is symptomatic and supportive

*Subarachnoid hemorrhage—nimodipine can be given, neurosurgical intervention is

essential.
299 STAGERS NOTES

5. To reduce morbidity and improve quality of life:

*Physiotherapy
*Speech therapy
*Occupational therapy.
Treatment of hypertension in stroke:
1. If the patient is known hypertensive—continue the antihypertensive if the BP is
normal or high.
2. If the patient is not known to be hypertensive and BP is mildly or moderately
high, then observe the patient and monitor BP for 7 to 10 days. If after this period
BP is still high, then antihypertensive agents should be considered.

3. If the patient is not known to be hypertensive, antihypertensive drug should be

started if:
*There is evidence of target organ damage—such as hypertensive retinopathy or
evidence of enlargement of heart.
* BP is severe—>220/110 mm Hg
*Co-morbidity—myocardial infarction, cardiac failure.
4. In CVD, following antihypertensive may be given:
* ACEI or ARB
*Calcium channel blocker
* Beta blocker
*Diuretics.

Q. What are the complications of acute

stroke?

1. Raised intracranial pressure

2. Hydrocephalus
3. Aspiration pneumonia
4. Convulsion
5. Pressure sores
6. DVT
311 STAGERS NOTES

7. Pulmonary embolism
8. Electrolyte imbalance
9. Painful shoulder
10. Urinary infection
11. Constipation
12. Depression and anxiety
13. Alteration of sleep wake cycle.

Q/ What are the causes of CVD in a young patient?

1. Mitral stenosis with atrial fibrillation (cerebral embolism from cardiac source)
2. Other cardiac cause—PFO, VSD, TOF
3. Antiphospholipid syndrome
4. SLE
5. Hematological disease—sickle cell anemia, polycythemia rubra vera, inherited
deficiency of naturally occurring anti-coagulant (protein C, protein S,
antithrombin III, factor V Leiden). In all these conditions, there is increased
tendency of thrombosis.
6. Vasculitis. Behcet’s disease
7. Vascular malformation—AVM, berry aneurysm causing SAH
8. Arterial dissection
9. In female—oral contraceptive pill, eclampsia
10. Homocystinuria
11. Syphilis
12. Premature atherosclerosis may occur in familial hyperlipidemia
13. Rarely, migraine may cause cerebral infarction
14. Drugs like amphetamine, cocaine.

Q/What are the risk factors for hemorrhagic stroke?

1. Hypertension
2. AVM
3. Aneurysm
311 STAGERS NOTES

4. Amyloid angiopathy
5. Cavernous angioma
6. Anticogulant therapy
7. Hypercoagulable disorder
8. Drugs—cocaine, amphetamine
9. Vasculitis—SLE, PAN, isolated CNS vasculitis
10. Septicemia
11. Hemorrhage into brain tumor.

Cerebral thrombosis:
The most common site is internal capsule and commonest vessel involvement is
middle cerebral artery

Risk factor—atherosclerosis, systemic hypertension, diabetes mellitus,

polycythemia rubra vera, collagen vascular disease, dyslipidemia, smoking, obesity,
oral contraceptive pill, alcohol, obesity, carotid artery occlusion

Cerebral embolism:

Onset—very acute or stormy (develops quickly in seconds), during exertion or

activity, no warning sign of TIA

Site—left sided vascular lesion is common as left common carotid artery arises
directly from the aorta. Left middle cerebral artery is commonly involved

There is usually a source of embolus or vulvular heart disease with atrial fibrillation

Cause—atherosclerosis, mitral stenosis with atrial fibrillation, infective endocarditis,

paradoxical embolism, myocardial infarction.

Cerebral hemorrhage:
312 STAGERS NOTES

Site—near internal capsule in basal ganglia. Other site—pons, thalamus, cerebellum

and cerebral white matter

Common vessel involved is the lenticulostriate branch of the middle cerebral

artery
Onset—usually sudden. There may be mental stress or strain
Q/ What are the causes of coma or unconsciousness?
IT'S COMA
I nfection -> meningitis, encephalitis, sepsis
T rauma
S eizures

C VA, e.g. stroke

O verdose -> Opioids, poisoning, e.g. CO
M etabolic, e.g. hypoglycemia, hyponatremia
A lcohol

Q/What are the features of LMNL?

1. Paralysis
2. Hypotonia
3. Hyporeflaxia
4. Wasting
5. fasciculation

Q/what are the features of UMNL?

1. Paralysis
2. Hypertonia
3. Hyperreflaxia
4. No wasting( except in long standing cases )
5. No trophic changes
313 STAGERS NOTES

Q/What is papniski sign? Where will be positive?

Definition : dorse flextion of the bog toe with or without
faning of other toes
Causes : pyramidal and extra pyramidal tract lesion
Deep sleep, deep coma, deep ansthesia

Q/What are lacunae?

Small vessel strokes that result from lipohyalinosis of a
small-caliber artery or
arteriole, often secondary to HTN

Q/What is amaurosis fugax?

Transient, painless monocular visual loss associated with central retinal artery
occlusion; often a result of artery-artery embolus from a carotid artery atheroma

Q/The anterior circulation comprises what vessels?

The internal carotids, their branches (the MCA and ACA), and smaller branches
from those vessels

Q/The posterior circulation comprises what vessels?

The vertebral arteries, the basilar artery, the PCAs, and smaller branches from
those vessels. The posterior circulation is also called the “vertebrobasilar system.”
Q/What basic neurologic deficits result from occlusion
of the MCA?
MCA stroke results in contralateral face, arm, and some leg weakness associated
with aphasia (if on the dominant side of the brain, which is usually the left side)
314 STAGERS NOTES

or neglect (if on the nondominant side of the brain)

Q/What neurologic deficits result from occlusion of the

ACA?
ACA stroke results in contralateral leg weakness.

Q/What neurologic deficits result from occlusion of the PCA?

PCA stroke results in contralateral hemianopsia.

Q/What are the features of Horner syndrome?

Unilateral miosis, ptosis, enophthalmos(inward or posterior displacement of the
eye), and anhydrosis

Q/What can be done for secondary stroke prevention?

Aspirin and other antiplatelet agents have been shown to decrease the annual risk
of repeat stroke by approximately25%–30%. Statins have also been shown
to reduce stroke risk. Control vascular risk factors

Q/What risk factors are associated with a first stroke?

HTN (the most important risk factor), dyslipidemia, DM, smoking, and
advancing age

Q/How is stroke prevented in the patient with atrial fibrillation or

another cardioembolic source of stroke?
Anticoagulation with warfarin is the most effective treatment and may lessen the
risk of cardioembolic stroke in such patients by 60%–80%.
315 STAGERS NOTES

Q/What is the classic presentation of the patient with

SAH?
The acute onset of the “worst headache of my life,” with or without focal
neurologic deficits

Q/How is the diagnosis of SAH made?

CT of the head reveals a pattern of subarachnoid blood in approximately 90% of
cases if performed early.

Q/If the CT is negative and the clinical suspicion for SAH is high, what is
the next test?
An LP should be performed to look for blood in the CSF. The absence of
xanthochromia (yellow appearance due to prolonged hemolysis of RBCs) or a
decreasing number of RBCs over serial tubes helps distinguish a traumatic tap
from SAH.
316 STAGERS NOTES

Auscultation from back

Q/auscultate this patient from back?

1. Greeting the patient and introduce
yourself
2. Stand on the right side of the patient
3. Excuse
4. Explain
5. Expose
6. Ask the patient to bend his arms in
front of his chest
7. Don't touch the patient unless you ask him about any pain
8. By using the diaphragm of the stetoscop , ascultate 8 areas (4 areas on each
side)
9. Avoid ascultaton directly on the spines
10. Interpretation of the results
We have to describe the following :
 Type of breathing :vascular or bronchial
 Air entry : good ,poor, no
 Added sounds: rhonchi , friction rub ,crepitation
 Compare

Interpretation of the results:

First you have to generally describe the patient

Ex: middle age male sitting upright , seems to be comfortable

On auscultation there's good/poor air entry bilaterally , with normal vascular

breathing/bronchial breathing, no added sounds/ with late fine /coarse
inspiratory crepitation's
317 STAGERS NOTES

Q/Causes of bronchial breath sounds

Common
 Lung consolidation (pneumonia)

Uncommon
 Localized pulmonary fibrosis
 At the top of a pleural effusion
 Collapsed lung (where the underlying major bronchus is
patent)

Q/Causes of diminished vesicular breathing?

Reduced conduction
 Obesity/thick chest wall
 Pleural effusion or thickening
 Pneumothorax

Reduced air flow

 Generalized, e.g. COPD
 Localized, e.g. collapsed lung due to occluding
lung cancer

Q/Causes of crackles?
Phase of
inspiration Cause
Early Small airways disease as in bronchiolitis
Middle Pulmonary oedema
Late Pulmonary fibrosis (fine)
Pulmonary oedema (medium)
Bronchial secretions in COPD, pneumonia, etc.
(coarse) lung abscess, tubercular lung cavities
(coarse)
Biphasic Bronchiectasis (coarse)
318 STAGERS NOTES

Q/ what are the red flag symptoms in patient with respiratory disease?
Haemoptysis. May be a symptom of cancer, although most are due to
infection. Chest x-ray required.
• Persistent symptoms of chest infection. May be underlying cancer.
Chest x-ray required.
• Right lower lobe collapse. Enquire about choking fit. May be
foreign body.
• Absent breath sounds and wheeze in a breathless patient. Not necessarily a
good sign. May imply severe asthma with little air movement.
• Equal inspiratory and expiratory wheeze may in fact be stridor from a central
obstruction. If there is also a hoarse voice consider laryngeal carcinoma.
• In a patient with apparently mild COPD (chronic obstructive pulmonary
disease) who develops oedema or excessive sleepiness consider type 2 respiratory
failure.
• In a patient with a ‘fat face’ and full neck consider SVC (superior vena cava)
obstruction and look for dilated veins over the chest wall.
• If clubbing develops in a patient with COPD this is likely to be due to a
carcinoma.

Q/how to examine the respiratory rate ?

1. Observe whether the patient is breathless at rest
2. Observe chest movements (surreptitiously) while feeling the pulse
3. count the number of respirations per minute.

normal respiratory rate is 14-18 breath / min

Q/ what are the causes of tachpnoea and brady pnoea ?

319 STAGERS NOTES

Q/What are the breathing pattern?

Cheyne-Stokes breathing: is characterized by a period of increasing rate and
depth of breathing followed by diminishing respiratory effort and rate, usually
ending in a period of apnoea or hypopnoea.
Causes are :
1. stroke involving the brain stem
2. severe cardiac failure.
3. normal during sleep in the elderly.

Hyperventilation is a common response to acute anxiety or emotional distress

and is often associated with respiratory alkalosis with low arterial carbon dioxide
tension.
Küssmaul respiration ('air hunger'): occurs is a response to the reduced arterial
pH in metabolic acidosis.
Causes are :
1. acute renal failure
2. lactic acidosis
3. diabetic ketoacidosis
4. salicylate and methanol poisoning.

Q/What are the causes of clubbing ?

Thoracic
1. Tumours: benign or malignant

 Lung
CA
 Mesothelioma
 Pleural fibroma
 Oesophageal cancer
 Oesophageal leiomyoma
 Thymoma
 Atrial myxoma
2. Sepsis
 Bronchiectasis
 Lung abscess
311 STAGERS NOTES

 Cystic fibrosis
 Bacterial endocarditis
3. Interstitial lung disease

 Fibrosing alveolitis
 Asbestosis
4. Arteriovenous shunting

AV malformations in the lung

Cyanotic congenital heart disease

Non-thoracic
 Hepatic cirrhosis
 Coeliac disease
 Ulcerative colitis
 Crohn's disease

Familial
Q/What are the causes of central and prephral cyanosis ? where are the
best site to detect them?
Central Cyanosis
The best place to look is the mucous membranes of the lips
and tongue.

The most common causes are :

1. Decrease Oxygen transfer due to lung disease: fibrosing alveolitis,

severe pneumonia, COPD, massive pulmonary embolism
2. right to left shunt :(cyanotic congenital heart disease)
3. Methaemoglobinaemia, sulfhaemoglobinaemia
4. Acute comditions : asthma, pneumothorax, inhaled foreign body, left
ventricular failure
311 STAGERS NOTES

peripheral Cyanosis
The peripheries, the fingers and the toes, are blue with normal
mucous membranes.

1. All causes of central cyanosis

2. Cold exposure
3. Raynaud’s phenomenon
4. Arterial occlusion
5. decrease Cardiac output e.g. shock, left ventricular
failure
312 STAGERS NOTES

BP measurement

1. The patent should be at rest about

five min
2. Confortable position
3. Aske the patient if he smock, drink
tea or coffe in previous 30 min
4. Greeting the patient and introduce
yourself
5. Stand on the right side of the
patient
6. Excuse
7. Explain
8. Expose
9. Chose the arm that don't contains canulla
10. The arm should be at the level of the heart (support it with table)
11. Ask about any pain
12. Support the patient's arm comfortably at about heart level.
13. Measure the BP first using palpation :
 Palpate the brachial pulse.
 Inflate the cuff until the pulse is impalpable. Note the pressure on the
manometer. This is a rough estimate of systolic pressure.
 Now use the stethoscope for measuring Bp , and inflate the cuff another
10 mmHg above previous reading on palpation
 Compare both arms
 Postural hypotension: by measuring Bp on boath standing and sitting
postion
313 STAGERS NOTES

Q/ what is the cause of BP differences between two

arms?
BP is different in each arm: a difference >10 mmHg
suggests the presence of subclavian artery disease.
Unequal brachial BP is a marker of increased cardiovascular
morbidity and mortality

Q/ if one reading higher than the other wich reading does we take ?
The higher one

Q/Why we measure BP by palpation before auscultation?

Auscultatory gap: up to 20% of elderly hypertensivepatients have Korotkoff sounds
which appear atsystolic pressure and disappear for an interval
between systolic and diastolic pressure. If the first appearance of the sound is
missed, the systolic pressure will be recorded at a falsely low level.
Avoid this by palpating the systolic pressure first
314 STAGERS NOTES

Q/Why we measure BP on standing and sitting?

To detect Orthostatic hypotension: it is defined as a fall in systolic blood pressure
of at least 20 mm Hg or diastolic blood pressure of at least 10 mm Hg when a
person assumes a standing position.

Causes are :

1. Hypovolemia
2. Addison's disease
3. Diabetes
4. pheochromocytoma

5. Medication: tricyclic antidepressants, monoamine oxidase inhibitors & Alpha-

1 blockers

Q/What do you know about Korotkoff

sounds?
These sounds are produced between systole
and diastole because the artery collapses
completely and reopens with each heart beat,
producing a snapping or knocking sound
These sounds are produced between systole
and diastole because the artery collapses
completely and reopens with each heart beat,
producing a snapping or knocking sound

Q/Causes of hypertension?
• Primary/idiopathic (95% of cases)
• Obesity
• Obstructive sleep apnoea
• Alcoholism
• Renal artery stenosis
• Parenchymal renal disease
315 STAGERS NOTES

• Renal tumours
• Gestational
• Pre-eclampsia
• Congenital adrenal hyperplasia
• Hypothyroidism
• Hyperthyroidism
• Acromegaly
• Conn’s syndrome (primary hyperaldosteronism)
• Cushing’s syndrome
• Phaeochromocytoma
• Polycythaemia vera
• Acute intermittent porphyria
• Raised intracranial pressure
• Medication-induced (oral contraceptives, corticosteroids, cyclosporin)

Q/Deffrential diagnosis of hypotension?

Impaired cardiac output
• Myocardial infarction
• Pericardial tamponade
• Massive pulmonary embolism
• Acute valve incompetence
Hypovolaemia
• Haemorrhage
• Diabetic precoma
• Dehydration from diarrhoea or vomiting
Excessive vasodilatation
• Anaphylaxis
• Gram-negative septicaemia
• Drugs
• Autonomic failure
316 STAGERS NOTES

JVP
Q/define JVP?
is the indirectly observed pressure over the venous system
via visualization of the internal jugular vein. (normally<7
mmHg/9 cmH2O)
The sternal angle is approximately 5 cm above the right
atrium, so the JVP in health should be ≤4 cm above this
angle
If right atrial pressure is low, the patient may
have to lie flat for the JVP to be seen

squences of examination
1. Greeting the patient and introduce yourself
2. Stand on the right side of the patient
3. Excuse JVP behind not infront
4. Explain sternocledomastoied
5. Expose
6. Good light source
7. Position the patient supine, reclined at 45°, with the head on
a pillow to relax the sternocleidomastoid muscles.
8. Look across the patient’s neck from the right side
9. Identify the jugular vein pulsation in the suprasternal notch
or behind the sternocleidomastoid muscle.
10. If you are uncertain , Use the abdomino-jugular test or occlusion to confirm it
is the JVP.: you have to aske the patient about any abdominal pain , then
press on right hypochondrium about 10 seconds
Occlusion: the JVP waveform is obliterated by gently occluding the vein at the
base of the neck with your finger
317 STAGERS NOTES

Q/ what are the differences between carotid artery and

jugular venous pulsation
Carotid Jugular
Rapid outward movement Rapid inward movement
One peak per heartbeat Two peaks per heartbeat (in sinus
rhythm)
Palpable Impalpable
Pulsation unaffected by pressure at Pulsation diminished by pressure at
the root of the neck the root of the neck
Independent of respiration Height of pulsation varies with
respiration
Independent of position Varies with position of patient
Independent of abdominal pressure Rises with abdominal pressure

The normal JVP waveform

• ‘a’ wave corresponds to right atrial contraction and occurs just before the first
heart sound. In atrial fibrillation the ‘a’ wave is absent.
• ‘v’ wave is caused by atrial filling during ventricular systole when the tricuspid valve
is closed.
• Rarely, a third peak (‘c’ wave) may be seen due to closure of the tricuspid valve.

Q/Causes of large 'a' wave

 tricuspid stenosis
 Right heart failure
 Pulmonary hypertension

Q/causes of cannon 'a' wave (atria contracting against closed tricuspid

valve)
 Atrial flutter
 Premature atrial rhythm (or tachycardia)
 third degree heart block
 Ventricular ectopics
318 STAGERS NOTES

 Ventricular tachycardia

Q/Causes of absent 'a' wave

 atrial fibrillation

Q/Causes of large 'v' wave (c-v wave)

 Tricuspid regurgitation

Q/ causes of parodoxical JVP (Kussmaul's sign: JVP rises with

inspiration, drops with expiration)

 Pericardial effusion
 Constrictive pericarditis
 Pericardial tamponade

Q/ causes of absent 'x' descent

 Tricuspid regurgitation (sometimes 'x' wave is replaced by a positive wave)

Q/ causes of prominent 'x' descent

 Constrictive pericarditis

Q/ causes of prominent & Deep 'y' descent

 Constrictive pericarditis

Q/ what are the findings on examination of the hands that you look for
in patient with CVD?
1. Clubbing
2. Sweating
3. Splinter haemorrhages
4. Palmar erythema
5. Nicotine staining
6. Osler’s nodes
7. Janeway’s lesions
319 STAGERS NOTES

8. Q/ what are the findings on examination of the abdomin that you

look for in patient with CVD?
1. Hepatomegaly
2. Ascites
3. Aortic aneurysm

Q/ what are the deffrential diagnosis of rised JVP?

• Congestive or right-sided heart failure
• Tricuspid regurgitation
• Pericardial tamponade
• Pulmonary embolism
• Iatrogenic fluid overload
• Superior vena cava obstruction

Q/ what is the vein that you examine and why ?

I examine the IJV because thers no valves between it and the right atrium , so it
reflect the right atrial pressure , and the venous waveform provides information
about cardiac function

Q/Where you find the IJV?

Behind the sternocleidomastoid muscle

Q/Why we donot use the external jugular vein for examination?

as the external jugular vein is more superficial and prominent. We do not examine
this routinely because it is prone to kinking and partial obstruction as it traverses
the deep fascia of the neck.

Q/What is the normal JVP?

Mean right atrial pressure is normally < 7 mmHg (9 cmH2O). Since the sternal angle
is approximately 5 cm above the right atrium the normal jugular venous pulse
should extend not more than 4 cm above the sternal angle
321 STAGERS NOTES

Q/ if we cannot detect the JVP what will you do?

press firmly over the centre of the abdomen for a few seconds after explaining to
the patient what you are about to do. This increases venous return to the heart,
transiently increasing right atrial pressure and the height of the jugular venous
pulse by 2-3 cm (abdominojugular reflux).

Q/What are the feature of elevation JVP in patient

with SVC obstruction ?
 Rise non pulsatile JVP
 Not decreases with inspiration
 Negative hepatogegular reflux
321 STAGERS NOTES

CXR interpretations
322 STAGERS NOTES

1. Name,age,sex, date
2. Exposure : good exposure when the intervertebral disk nearly visible
under-exposed image will be too white and an over-exposed image will be
too black

3. Rotation : The sternal ends of the clavicles should symmetrically overlie the
transverse processes of the 4th or 5th thoracic vertebrae. A rotated film can
alter the position of structures, eg rotation to the right projects the aortic arch
vessels over the right upper zone, appearing as though there is a mass.
4. Any lines, leads or tubes
5. Start with the soft tissue in the chest and neck: possible abnormalities are
surgical emphysema ,masses and forging bodies
6. Look for the bone : ribs , clavicles, sternum and the spine for any lytic lesions ,
fractures and abnormal position
 The spaces between the ribs are wide in hyperinflation or pneumothorax
and crowded in collapse
7. Look for the trachea: any tracheal deviation , normally it slightly deveated to
the right
Deviated by collapse (towards the lesion), tension (away from the lesion), or
patient rotation. Check heart position
8. Look for mediastinum
Causes of wide mediastinum are :
1. mediastinal fat
2. retrosternal thyroid
3. unfolded aorta, or aortic aneurysm
4. lymph node enlargement (sarcoidosis,
lymphoma, metastases, TB);
5. tumour (thymoma, teratoma)
6. cysts (bronchogenic, pericardial)
7. paravertebral mass(TB).
323 STAGERS NOTES

9.look for the Hila

The left hilum is higher than the right or at the same level (not lower); they
should be the same size and density. May be pulled up or down by fibrosis or
collapse.
deffrential diagnosis of enlarged hila:
1. Lymph nodes
2. pulmonary arterial hypertension
3. bronchogenic ca.

deffrential diagnosis of hillar Calcification:

1. Sarcoid
2. past TB
3. silicosis
4. histoplasmosis
Sarcoidosis
5. Inflation: There should be 5 to 7 ribs visible anteriorly (or
10 posteriorly). Hyperinflation can be abnormal, eg
COPD.

10.look at the lung field: masses,collapse,consolidation opacifaction

11.look at cardiac shadow

Normally less than half of the width of the thorax (cardiothoracic ratio <0.5).
⅓ should lie to the right of the vertebral column, ⅔ to the left. It may appear
elongated if the chest is hyperinflated (COPD); or enlarged if the image is AP
or if there is LV failure , or a pericardial effusion. Are there calcified valves?

 slouting sign: if the mass obliterate cardiac shadow, its position infront
of the heart
 if the mass behind the heart , the cardiac shadow clearly visible
 cardiomegaly
 arotic neckle

12.the diaphragm : falt in case of hyperinflated chest

324 STAGERS NOTES

 elevation of one hemidaiphragm :paralysis of hemidiaphragm

13.subdiaphragmatic area:

 gass shadow in the stomach

 air under diaphragm
 dilated bowel loop
 donot forget the apex of the lung

Deferential diagnosis of Bilateral hilar lymphadenopathy

1. TB
2. Sarcoidosis
3. Lymphoma
4. Others: bronchial carcinoma, metastatic tumours,
recurrent chest infections,
5. AIDS, berylliosis, silicosis

Deferential diagnosis of Cavitating lung lesions

1. Abscess (Staphylococcus aureus, Klebsiella,
Pseudomonas aeruginosa, TB, histoplasmosis)
2. Tumour (particularly squamous cell carcinoma),
lymphoma
3. Infarct
4. Inflammatory: Rheumatoid nodule, Wegener’s
granulomatosis

Deferential diagnosis of Coin lesions

1. Tumours: bronchial carcinoma, metastatic deposit
(e.g. breast cancer, renal cell carcinoma,
hamartoma, adenoma, fibroma)
2. Infection: pneumonia, TB, abscess, hydatid cyst
3. Infarction
4. Encysted pleural effusion
325 STAGERS NOTES

5. Rheumatoid nodule
6. Vasculitides (e.g. Wegener’s granulomatosis)
7. AV malformation

Deferential diagnosis of Airspace/alveolar shadows

1. Pus (consolidation)
2. Fluid (pulmonary oedema)
3. Blood (pulmonary haemorrhage)
4. Cells (lymphangitis carcinomatosis, alveolar cell carcinoma)

Deferential diagnosis of Reticulonodular shadows

1. Pulmonary fibrosis: Cryptogenic fibrosing

alveolitis
2. Connective tissue diseases: scleroderma,
SLE, sarcoidosis, rheumatoid arthritis,
ankylosing spondylitis
3. Drugs (amiodarone, busulphan, bleomycin,
nitrofurantoin),
4. Radiation
5. Extrinsic allergic alveolitis (e.g. farmers’
lung, bird fancier’s lung, malt worker’s lung)
6. Pneumoconioses (coal workers’ pneumoconiosis, asbestosis, silicosis,
berylliosis)

Other DDX of reteculonodular shadow according to the lung zones

1. Upper zone: TB, allergic bronchopulmonary aspergillosis, radiation,
extrinsic allergic alveolitis,
ankylosing spondylitis, sarcoidosis.
2. Middle zone: sarcoidosis
326 STAGERS NOTES

3. Lower zone: cryptogenic fibrosing alveolitis, drugs, asbestosis, rheumatoid

arthritis,
scleroderma

Deferential diagnosis of White hemithorax

1. Large pleural effusion
2. Pneumo nectomy
3. Congenital absence of lung/extensive
hypoplasia
4. Collapse

Deferential diagnosis of multiple nodelos?

1. miliary tuberculosis (TB)
2. dust inhalation
3. metastatic malignancy
4. healed varicella pneumonia
5. rheumatoid disease

Deferential diagnosis of Ring shadows, tramlines and tubular shadows

Bronchiectasis

Deferential diagnosis of Increased translucency in CXR?

1. Bullae
2. Pneumothorax
3. Oligaemia
327 STAGERS NOTES

Deferential diagnosis of Unilateral and bilateral hilar enlargement:

• Unilateral hilar enlargement: TB, bronchial carcinoma, lymphoma
• Bilateral hilar enlargement: sarcoid, lymphoma, TB, silicosis

What are the causes of hillar congestion in CXR ?

1. Asthma
2. Hypertension
3. bronchitis
328 STAGERS NOTES

Examination Of Precordium

Inspection:

 Deformity of the chest wall (kyphosis, scoliosis, lordosis, pectus

excavatum or carinatum)
 Visible cardiac impulse (visible apex beat)
Other impulses: epigastric, suprasternal, supraclavicular
 Any scar mark: in the midline (valve replacement or coronary artery
bypass), thoracotomy scar
(valvotomy in mitral stenosis)
 Pacemaker or cardioverter defibrillator box may be seen (mention, if
any).

Palpation:
1. Apex beat:

 Site (localize the intercostal space. Beware of dextrocardia)

 Distance from the midline (in cm)
 Nature (normal, taping, heaving, thrusting, diffuse or double apex
beat).

Thrusting : LVH

Double apex beat :HOCM and ventricular aneurism

Heaving :in left parasternal area for RVH

2. Thrill:

 Site (apical, basal or any other space)

 Nature (systolic or diastolic, by feeling the carotid pulse at the same
time. If coincides with carotid pulse, it is systolic and if it does not
coincide, it is diastolic).
329 STAGERS NOTES

3. Left parasternal heave: Place the flat of right palm in left parasternal area
and feel by giving gentle
sustain pressure (presence of left parasternal heave indicates RVH)
4. Palpable P2 (in left second intercostal space): It indicates pulmonary
hypertension
5. epigastric pulsation.

Auscultation:
1. First and second heart sounds in all four areas
(mitral, aortic, pulmonary and tricuspid areas). At the
same time, palpate the right carotid pulse with thumb
simultaneously. 1st heart sound coincides with carotid
pulse, but 2nd sound does not (comes before or after).
See also other heart sounds, if present (3rd and 4th).

2. Murmur:

 Site (apical, parasternal, aortic or pulmonary area)

 Nature—systolic (pansystolic or ejection systolic), diastolic (mid diastolic
or early diastolic)— by feeling carotid pulse at the same time (systolic
coincides with carotid pulse and diastolic does not coincide
 Radiation (pansystolic murmur to left axilla, ejection systolic murmur to
neck)
 Relation with respiration (right sided murmur increases on inspiration
and left sided murmur increases on expiration)

 Grading of murmur (e.g. 2/6, 4/6).

3. Added sounds (pericardial rub, opening snap, ejection click, metallic plop.

4. Others: Auscultate the back of the chest for crepitations (found in

pulmonary edema).
331 STAGERS NOTES
331 STAGERS NOTES

Grades of intensity of murmur?

Grade 1 Heard by an expert in optimum conditions

Grade 2 Heard by a non-expert in optimum conditions
Grade 3 Easily heard; no thrill
Grade 4 A loud murmur, with a thrill
Grade 5 Very loud, often heard over wide area, with

Sites and radiation of murmer

Cause
Tricuspid regurgitation
Pulmonary stenosis
Mitral regurgitation
Aortic regurgitation
Aortic stenosis
Ventricular septal defect
Primary site
Lower left sternal edge
Upper left sternal ege
Apex
Left sternal edge
Apex
Left sternal edge
Radiation
Lower right sternal edge,
liver
Towards left clavicle,
beneath left scapula
Left axilla, beneath left
scapula
Down left sternal edge
towards apex
Towards upper right sternal
edge, over carotids
All over pericardium

Mitral stenosis Apex Does not radiate

Q/What are the causes of normal apex beat position with tracheal
deviation?
1. Apical fibrosis
2. Lymph node or tumor
3. Thyroid mass (retrosternal goiter)

Q/What are the causes of normal tracheal position with abnormal apex
beat ?
 Cardiomegaly
332 STAGERS NOTES

Basic & Advanced life support

(Management of cardiac arrest)

333 STAGERS NOTES

Q/ this patient has been arrive to the hospital , how can you mange him?
334 STAGERS NOTES

Q/Wht is this device ?

This is direct current cardio version

Q/What are the position of the pads ?

The right one on the sternum , the left one on

the apex
Q/How to use DC ?
1. Expose the chest of the patient
2. Turn O2 off
3. Get all the staff and the relative away from the bed
4. Remove the moniter
5. Put gel on the paddles
6. If the patient conscious and we need to shock him/her ,we have to give
analgesia ex: morphine
7. Use the DC as monitor for heart rhythm (by turning the key onto monitor
option )
8. Asynchronized (VF) or synchronized (VT)

Asynchronized (VF) (Asynchronized‫) الجهاز اصال على‬

synochronize(VT): for VT, AF, SVT as needed , here you have to press on the key
on the machine to turn it on the synochronised

9. by turning the key into the needed number of joule

10. If not response , CPR for two min then increases the voltage then DC again

Q/If thepatient has VT what you have to do?

If haemodynmically stable …. IV lidocain or amiodaron

If haemodynmically unstable….synochronized DC
335 STAGERS NOTES

Q/You are sitting in the ER department , 60 years patient presented to

you with cardiac arrest , how would you mange him ?
1. Put the patient on the bed
2. Call for help (ask the staph to bring DC machine , put cannula , sucker… )
3. If there’s abnormal breathing (gasping ) start CPR (30:2)
4. expose the chest of the patient
5. press on the chest effectively and rapidly
6. if there’s secretion from the mouth of the patient , use the sucker to clean it
7. while you doing this , take short history from the relatives (how did this
condition occur ?)
8. when the staph bring DC machine , put gel on the pads , put the pads on the
chest of the patient , one on the sternum and the other on the apex
9. first use it as monitor :
 if thers asystole :then IV adrenaline and CPR (30:2) for two minutes then
look to the moniter again :
 still asystole : CPR (30:2) with IV adrenaline every 3-5 minutes
 VT or VF : then immediately DC shock (start at 150-200 j) then CPR for 2
min..then check with moniter again m still VT or VF , shock again(increase
the joules ) …CPR for 2 min … moniter …still … shock again

10. After the 3rd shock give adrenaline and 300 mg amiodaron (2 ampoule )
11. Then CPR again with monitoring flowed by monitoring … between each CPR
section give adrenaline (1 ampule)
12. We have two outcomes here :
 the CPR success and he start to do vital activates (coughing ,
breathing,sinus rhythem) moniter the brething pattern of the patine , if
he cannot breath , her we have to intubate and ventilate the patient …
then send for investigations to know the cause of his condition
 or the patient turn into asystole … as above , do CPR ..
13. after 15-20 minutes if thers no signs of life and still asystole, the start to
confirm death :
 check the heart sounds by stethoscope
 check the breathing sounds
336 STAGERS NOTES

 Pupillary Light Reflex

 Corneal Reflex
 Gag Reflex
 With no electrical activites on the moniter
337 STAGERS NOTES

examination of the speech

You have to examine 6 things :

1. Comprehension:
2. fluency
3. repetition : function of arcuate fasculus
4. writing: ex: agrafia
5. reading
6. naming: function of angular gyrus

we have two ares responsible about the speech :

the sensory speech area(wernickes area) :paraital lobe, responsible about reception
and understanding of the speech

the motor speech area (brocas area): in the infeirior portion of the frontal lobe

we have 3 disorder of the speech

1. dysphasia:
 Receptive dysphasia: the patient doent understand you and talk a lot
Caused by strock , trauma or tumor affecting the posterior superior
temporal lobe(dominant)
 Expressive dysphasia: the patient understand you but cant talk
 Caused by strock , trauma or tumor affecting the inferiolateral frontal
lobe(dominant)

2. Dysarthria : disorder in articulation

Cerebellar disease: slurred, scanning speech
Bulbar palsy: nasal speech
338 STAGERS NOTES

Pseudobulbar palsy: slow, indistinct, effortful (spastic speech)

Extrapyramidal disease: soft, monotonous
3. Dysphonia : disorder in production of the voice
339 STAGERS NOTES

Examine facial nerve

We examin 4 things:
1. Inspection for asymmetry (the face deviate to normal part)
2. Tets 1 :Rise the eye brow…to see the wrinkling (muscle responsible is
occeptofrontal)
3. Tets 2 :Close the eye against resistance (muscle responsible orbicularis
occuli)
4. Tets 3 :the teeth (muscle responsible orbicularis oris)
5. Tets 4 : Blow out the checks
6. Taste for sensation

In UMNL :
the patient able to do test 1 and 2

Preserve of wrinklings

Loss of nasolabial folds

Inability to do test 3 and 4

In LMNL :
the patient unable to do all tests
341 STAGERS NOTES

Q/ define bells phenomina?

a sign of peripheral facial paralysis,
manifested by the upward and outward
rolling of the eyeball when the affected
individual tries to close the eyelid. It
occurs on the affected side in
peripheral facial paralysis.

Q/ why not all fucnctions of fascial nerve are affected in UMNL?

Because fascial nerve is bilaterally represented

causes o facial pulsy
a) Unilateral
1. Bell’s palsy (idiopathic) or pathologies along the course of the nerve VII:
2. Brainstem: infarction, demyelination, tumours
3. Cerebellopontine angle: acoustic neuroma
4. Basal meningeal inflammation/infiltration: TB, sarcoidosis, lymphoma
5. Middle ear: middle ear infection or herpes zoster
6. Face/parotid: surgery, trauma

b) Bilateral
1. Congenital facial diplegia
2. Guillain–Barr e syndrome
3. Sarcoidosis
4. Motor nurone disease
5. Myasthaenia gravis
6. Muscular dystrophy
7. Infections: Lyme disease, HIV
341 STAGERS NOTES

Neurological examination

of the lower limb

a) Inspection:
 Posture of the ptient
 Decorticated postion : flextion of the the elbow and the wrist , adduction of
the hand, and hyperextension of the lower limb , this posture occurs in
CVA
 Decereprated position :this patient has internal rotation of the sholder ,
extension of the elbow , flextion of the wrist with hyperexternsion of the
lower limb, this posture occurs in brain stem lesion
 Muscle bulk :
 Muscle atophy : in LMNL and cachexia
 Muscle hypertrophy : athletic people and duchen hypertrophy
 Movements :
 Fasculation: in LMNL
 Hyokunesia
 Hyperkinesia
 Tremer
o resting : in parkinsons disease
o intension tremor : occurs on voluntary activity tword target and
disappears at rest occurs in crec=bullar disease
o postural tremer :tremer when the limb maintain against gravity
and dsiiapears at rest , occurs in hyperthyroidism and drugs
ex(salbutamol)
o flapping tremer :mjor organ failure
 other movements:
 tics
342 STAGERS NOTES

 chorea
 athetosis

b) Tone
 normal tone
 hypotonea in LMNL
 hypertonia in UMNL

Examination sequence
1. Ask the patient to lie supine on the
examination couch, and to relax and ‘go
floppy’. Enquire about any painful joints
or limitations of movement before
proceeding
2. Passively move each joint tested through
as full a range as possible, both slowly
and quickly in all anatomically possible
directions. Be unpredictable with these
movements, both in direction and speed,
to prevent the patient actively moving
with you; you want to assess passive
tone.
c) Roll the leg from side to side, then
briskly lift the knee into a flexed position,
observing the movement of the foot
.Typically the heel moves up the bed, but
increased tone may cause it to lift off the
bed due to failure of relaxation.
343 STAGERS NOTES

power :
 you have to grade it :

Medical Research Council scale for muscle power

0 No muscle contraction visible

1 Flicker of contraction but no movement
2 Joint movement when effect of gravity eliminated
3 Movement against gravity but not against examiner’s
resistance
4 Movement against resistance but weaker than normal
5 Normal power

examination sequence
1. Ask about pain which may interfere with testing.
2. Test lower limb power with the patient reclining.
3. Ask the patient to undertake a movement. First assess whether he can overcome
gravity, e.g. instruct the patient ‘Lift your right leg off the bed’ to test hip flexion.
Then apply resistance to this movement testing across a single joint, e.g. apply
resistance to the thigh in hip flexion, not the lower leg.

4. Observe the patient getting up from a chair and walking.

Assess individual muscles depending on the history.
344 STAGERS NOTES

d) reflexes:
 knee jerk L3,L4
 Ankle jerk S1 , S2
 Babinisky sign : in UMNL
there will be hallux up with
faninig of the other toes

IF the reflex is weak or

absence aske the patient to clench the teeth and interlock the flexed fingers

Examination sequence

1. Ask the patient to lie supine on

the examination couch with the
limbs exposed. He should be as
relaxed and comfortable as
possible, as anxiety and pain can
cause an increased
response.
2. Flex your wrist and allow the
weight of the tendon hammer
head to determine the strength
of the blow. Strike the tendon,
not the muscle or bone.
3. Record the response as:
increased
normal
diminished
present only with reinforcement
absent.
345 STAGERS NOTES

Principal reflexes
1. Ensure that both limbs are positioned identically with the same
amount of stretch.
2. Compare each reflex with the other side; check for symmetry
of response
3. Use reinforcement whenever a reflex appears absent. For knee
and ankle reflexes, ask the patient to interlock the fingers and
pull one hand against the other on your command, immediately
before you strike the tendon (Jendrassik’s manœuvre;
4. To reinforce upper limb reflexes, ask the patient to clench the
teeth or to make a fist with the contralateral hand. The patient
should relax between repeated attempts. Strike the tendon
immediately after your command to the patient.

If you have exagurated reflexes what is the next step in the

examination ?
We Do clonus

e) Examine: the cerebellar function: hell-shin test

346 STAGERS NOTES

fever
Q/Take short history from patient with fever ?
 How long have you been suffering from fever?
 When does it start (morning, evening, night, etc.)? How long
does it persist (few hours or throughout the day or night)?
Is there any evening rise of temperature associated with
night sweats?
 What was the highest recorded temperature?
 Is it associated with chills and rigors? Does it subside with sweating?

 Does it subside spontaneously or with antipyretic? If there is spontaneous

remission, ask about the length of each episode of fever and the duration of
the intervening afebrile period. However, if there is no spontaneous
remission, ask if the temperature fluctuate more than 2ºC or not more than
1ºC? (to find whether the fever is continuous, remittent or intermittent).
 Is the fever punctuated by apyrexial period? (Undulant or Pel-Ebstein).
 Is the fever associated with skin rash or purpura?
 Is there any other associated symptom? (urinary complain, cough, chest pain,
pain abdomen, headache, impaired or loss of consciousness, weight loss,
polyarthritis).
 Is there any history of sexual exposure, homosexuality, travel abroad?
 Are you taking any drugs? (to exclude any drug fever).
347 STAGERS NOTES

Q/Your case is male patient ,55 years old , his chief complaint if
increses the body temperature for one week , what are going to look
for on the examionation ?
If a febrile patient looks unwell, rapidly assess the mental state, pulse rate,
respiratory rate, blood pressure and pulse oximetry(SpO2). If the history and
general examination suggest severe sepsis or septic shock, begin resuscitation
immediately
Most patients with bacterial infection have localising symptoms or signs, e.g.
tender swelling of an abscess or murmurs of bacterial endocarditis, but it is
essential to examine the patient from head to toe because clues may be in any
system.

1) Examine the head and neck:

 Look at the tympanic membranes with an otoscope for
middle-ear infection.
 Percuss the frontal and maxillary sinuses for tenderness
(sinusitis).
 Palpate the temporal arteries for tenderness (giant cell
arteritis).
 Examine the nose for congestion and discharge (clear or
purulent).
 Look in the mouth at the oropharynx and gums for
inflammation , oral candidiasis
immunodeficiency, e.g. HIV, or recent broad-spectrum
antibiotic use.
 Examine the sclerae for conjunctivitis or jaundice.
 Use an ophthalmoscope to examine the retinae for Roth’s spots
(endocarditis)
 Gently flex the neck to detect discomfort, stiffness, or both,
indicating meningism.
 Palpate for neck lymphadenopathy
348 STAGERS NOTES

2) Percuss and auscultate the lungs for crackles, signs of

consolidation (pneumonia) or effusion (empyema).
3) Listen to the heart for murmurs (endocarditis).
4) Examine the abdomen for enlargement and tenderness of
the liver and spleen.
5) Percuss the flanks for renal tenderness (pyelonephritis).
6) In women, pelvic examination may reveal cervical
motion or adnexal tenderness; in men, look for urethral
discharge or local genital tenderness .
7) Perform a rectal examination looking for tenderness
and swelling, suggesting perirectal abscess (which may be
occult in immunocompromised patients) and prostatic
8) enlargement or tenderness (urinary or prostate infection).
Examine the major joints for swelling, erythema and tenderness
(joint infection or rheumatologic disorder).

Q/What is the normal body temp?

Normal body temperature is 36.8ºC (mouth), 36.4ºC (axilla), 37.3ºC (rectum).
Temperature > 37.3ºC in mouth or 37.7ºC in rectum is considered as fever.
Q/What do you means by hyperthermia?
Temperature above 41.1ºC is called hyperthermia or hyperpyrexia. This may
occur in severe infection, pontine hemorrhage, heat stroke, malignant
hyperthermia, neuroleptic malignant syndrome, thyroid crisis, lobar
pneumonia, datura poisoning. Hypothermia means temperature less than
35ºC.

Q/What are the types of fever?

Pel-Ebstein fever : one week fever and one week no fever ex: lymphoma
Intermittent fever.: Fever that persists for several hours and always touches the
baseline between attacks is called
349 STAGERS NOTES

Remittent fever: If the fever fluctuates > 2ºC (3ºF) but does not touch the
baseline, it is called remittent.
This is found in any

 pyogenic infection (pyogenic liver abscess, acute bronchopneumonia, acute

tonsillitis, septicemia, acute pyelonephritis)
 miliary tuberculosis
 lymphoma.

Continued fever: If the fluctuation of fever is not > 1ºC (1.5ºF) and the fever
does not touch the baseline, it is called continued. This is found in typhoid,
typhus, miliary tuberculosis, meningococcal meningitis, rheumatic fever, drug
fever.

Factitious fever: Sometimes patient purposefully show false rise of temperature.

Usually found in young woman.
Hectic temperature: It means sudden rise of very high temperature usually
associated with chill and rigor, persist for few hours and then fall with profuse
sweating. This may be found if pus is anywhere in the body, e.g. lung abscess,
pyogenic liver abscess, empyema thoracis, subphrenic abscess, empyema of
gallbladder, perinephric abscess, etc. Sometimes in septicemia or pyemia.

Q/What are the cause of fever without infection?

Aseptic (non-infectious) fever: Fever without infection. May be found in SLE,
lymphoma, leukemia, pontine hemorrhage, drug fever, early stage of acute
myocardial infarction, heat stroke, thyrotoxic crisis, acute gout, excessive use of
atropine injection rheumatic fever, drug fever.

Q/What are the drugs that cause fever?

Drug causing fever: A wide variety of drugs can cause drug fever. Common are—
MAO inhibitor, tricyclic antidepressant, alpha-methyldopa, beta-lactam antibiotics,
salicylate poisoning, LSD, ecstasy, procainamide, anticonvulsant, sulfonamide.
351 STAGERS NOTES

Neuroleptic malignant syndrome may be caused by phenothiazine, butyrophenone

Q/what are the causes of Fever with chill and rigor

acute pyelonephritis, acute cholangitis, subacute bacterial endocarditis,
subphrenic abscess, pyogenic lung abscess, septicemia, lobar pneumonia,
pyrogenic reaction after infusion or transfusion.

Q/What are the causes of Fever with unconsciousness

—cerebral malaria, meningitis, encephalitis, pontine hemorrhage.

Q/What are the causes of Fever with neck rigidity

meningitis, encephalitis.

Q/What are the causes of Fever with drenching

night sweat
lymphoma, tuberculosis.

Q/What are the causes of Low grade fever with evening rise
tuberculosis.

Q/What are the causes of Fever with myalgia

viral infection (e.g. influenza, dengue).

Q/What are the causes of Fever with skin rash (according to the day of
appearance of rash)—Remember:
“Very sick person must take double eggs.”

• 1st day—Varicella (chicken pox)

• 2nd day—Scarlet fever
• 3rd day—Pox (small pox)
• 4th day—Measles, german measles (rubella)
• 5th day—Typhus
351 STAGERS NOTES

• 6th day—Dengue
• 7th day—Enteric fever (rose spot)
• Drug rash may appear anytime.

Q/What are the causes of Fever with relative bradycardia

Normally, for 1ºF rise in temperature, pulse increases by 10 beats per
minute. If the rise of pulse rate is less than that, it is called relative bradycardia. It
occurs in viral fever, 1st week of enteric fever, brucellosis, psittacosis, Weil’s disease,
etc.
352 STAGERS NOTES

pleural effusion

Q/what are the examinations findings in plueral effusion?

Inspection:

1. Movement is restricted on lower part of right side of

the chest with fullness of intercostal spaces
2. (Mention, if any puncture mark, gauze and tape
indicating aspiration of pleural fluid).

Palpation:

1. Trachea is shifted to the left side

2. Apex is shifted to the left (in 6th intercostal space in the anterior axillary line),
normal in character
3. Vocal fremitus is reduced in right lower chest up to … ICS (tell where)
4. Chest expansion is restricted over the right lower chest.

Percussion:
There is stony dullness in the right lower chest up to … ICS (tell where).
Auscultation:

1. Breath sound—diminished (or absent) in the right lower chest

2. Vocal resonance—diminished (or absent) in the right lower part of chest
3. No added sound.

Q/What is pleural effusion?

Accumulation of excessive amount of fluid in pleural cavity is called pleural effusion.

Q/ Why not consolidation?

There is stony dullness and reduced breath sound and vocal resonance in the
affected area along with mediastinal shifting. These are against consolidation (In
consolidation, there is woody dullness, bronchial breath sound, increased vocal
resonance and no shifting of the mediastinum).
353 STAGERS NOTES

Q/ Why not collapse?

In case of collapse, the apex beat and trachea will be shifted to the same side. In
addition, if there is collapse with patent bronchus, there will be bronchial breath
sound and increased vocal resonance.
Q/ Why not pneumothorax?
In pneumothorax, there is hyper-resonance on percussion.

Q. What investigations do you suggest?

1. X-ray chest P/A view

2. Hb%, TC, DC, ESR (high ESR in TB, leukocytosis
in pneumonia)
3. Mantoux test (MT)
4. Aspiration of pleural fluid for analysis

1. Physical appearance (straw colored, serous,

hemorrhagic, chylous)
2. Gram-staining, cytology (routine) and
exfoliative cytology (malignant cells)
3. Biochemistry (protein and sugar), also a simultaneous blood sugar, protein
and lactate dehydrogenase (LDH) may be done
4. ADA (high in tuberculosis)
5. Culture and sensitivity (C/S)
6. AFB and mycobacterial C/S

5. Pleural biopsy by Abram’s or Cope’s needle

6. Other investigation of pleural fluid (according to suspicion of cause):

1. Cholesterol, LDH and rheumatoid factor (in rheumatoid arthritis)

2. Amylase (high in acute pancreatitis, esophageal rupture, malignancy)
3. Trigycerides (in chylothorax)
354 STAGERS NOTES

7. Sputum (if present) for Gram staining, C/S, AFB, mycobacterial C/S and
malignant cells
(exfoliative cytology)
8. If palpable lymph node: FNAC or biopsy (for lymphoma, metastasis)
9. Other investigations according to suspicion of causes include:
1. ANF, anti-ds DNA (SLE)
2. Liver function tests
3. Urine for protein and serum total protein (nephrotic syndrome)
4. CT scan in some cases (it helps to clarify pleural abnormalities more readily
than chest X-ray and ultrasonogram, and also helps to distinguish between
benign and malignant diseases).

Q/ What are the definitive signs of pleural effusion?

Stony dullness on percussion and reduced or absent breath sound (confirmed by
aspiration).

Q/ How to confirm if there is small effusion? (if not detected by chest X-

ray PA view.)
1. X-ray in lateral decubitus position
2. Ultrasonogram (USG) of lower part of the chest
3. Occasionally, CT scan of chest may be needed.

Q/ What are the characteristics of pleuritic chest pain?

A. Pleuritic chest pain is localized, sharp or lancinating in nature, worse on
coughing, deep inspiration or movement.
Q/ What are the causes of dullness on percussion over lower chest?
1. Pleural effusion (stony dullness)
2. Thickened pleura
3. Consolidation (woody dullness)
4. Collapse of the lung
5. Raised right hemidiaphragm (due to hepatomegaly or liver pushed up)
6. Mass lesion.
355 STAGERS NOTES

Q/ Supposing, clinically it is pleural effusion but no fluid is coming after

aspiration. What are the possibilities?

1. Fluid may be thick (empyema)

2. Thickened pleura
3. Mass lesion.

Q/What are the common causes of pleural effusion?

1. Pulmonary tuberculosis
2. Parapneumonic (also called postpneumonic)
3. Bronchial carcinoma
4. Pulmonary infarction.

if the patient is young, common causes are

1. Pulmonary tuberculosis
2. Parapneumonic
3. Others—Lymphoma and SLE in female (also pulmonary infarction).

if the patient is middle age or elderly, common causes are:

1. Pulmonary tuberculosis
2. Parapneumonic
3. Bronchial carcinoma.

Q/ What are the causes of predominantly right or left sided pleural

effusion?
Causes of right-sided pleural effusion

1. Liver abscess
2. Meig’s syndrome
3. Dengue hemorrhagic fever.
356 STAGERS NOTES

Causes of left-sided pleural effusion

1. Acute pancreatitis
2. Rheumatoid arthritis
3. Dressler’s syndrome
4. Esophageal rupture (Boerhaave’s syndrome)
5. Dissecting aneurysm.

Q/ What are the causes of bilateral effusion?

1. All causes of transudative effusion (CCF, nephrotic syndrome, cirrhosis of liver,

malabsorption or malnutrition or hypoproteinemia).
2. Collagen diseases (rheumatoid arthritis and SLE).
3. Lymphoma.
4. Bilateral extensive pulmonary TB.
5. Pulmonary infarction.
6. Malignancy (usually multiple metastases involving both lungs).

Q. What are the causes of exudative and transudative pleural effusion?

A. As follows:
1. Exudative (protein >3 g%):

1. Pulmonary tuberculosis
2. Pneumonia
3. Bronchial carcinoma
4. Pulmonary infarction
5. Collagen disease (SLE, rheumatoid arthritis)
6. Lymphoma.
7. Dressler’s syndrome (post-myocardial infarction syndrome characterised by
pain, pyrexia, pericarditis, pleurisy and pneumonitis).
8. Others—acute pancreatitis, subphrenic abscess, liver abscess, pleural
mesothelioma, secondaries in the pleura, yellow nail syndrome, etc.
357 STAGERS NOTES

2. Transudative (protein <3 g%):

1. Congestive cardiac failure (CCF)

2. Nephrotic syndrome
3. Cirrhosis of liver
4. Malnutrition
5. Hypothyroidism
6. Meig’s syndrome (ovarian fibroma, ascites and right sided pleural effusion)
7. Chronic constrictive pericarditis
8. Acute rheumatic fever.

Q/ How to differentiate between exudative and transudative pleural

effusion?
According to Light’s criteria

Pleural fluid is an exudate if one or more of the following criteria

are met:
• Pleural fluid protein:serum protein ratio > 0.5
• Pleural fluid LDH:serum LDH ratio > 0.6
• Pleural fluid LDH > two-thirds of the upper limit of normal serum LDH

Q/ What are the types of pleural effusion according to the color?

1. Serous (hydrothorax)
2. Straw
3. Purulent (empyema or pyothorax)
4. Hemorrhagic (hemothorax)
5. Milky or chylous (chylothorax)

Q/What are the causes of hemothorax (blood stained fluid)?

1. Chest injury or trauma
2. Bronchial carcinoma
358 STAGERS NOTES

3. Pleural mesothelioma
4. Pulmonary infarction
5. Others – SLE, lymphoma, acute pancreatitis.

Q/What are causes of empyema?

1. Bacterial pneumonia
2. Lung abscess (bursting in pleural cavity)
3. Bronchiectasis
4. Tuberculosis
5. Secondary infection after aspiration
6. Rupture of subphrenic abscess or liver abscess
7. Infected hemothorax.

Q/ How to treat empyema thoracis?

A. According to cause:
1. Non-tuberculus:
1. Drainage of pus with wide bore intercostal tube using water seal drainage.
2. Antibiotic for 2 to 6 weeks. IV Co-amoxiclav or cefuroxime plus
metronidazole. May be given according to C/S.
3. Surgical intervention if pus is thick or loculated. Surgical decortication of the
lung may be needed, if visceral pleura is grossly thickened.

2. Tuberculous empyema:
1. Antitubercular drug
2. Wide bore needle aspiration or intercostal tube drainage
3. Sometimes surgical ablation of pleura.

Q/ What are the causes of recurrent pleural effusion? How to treat

recurrent pleural effusion?

1. Bronchial carcinoma
2. Pleural mesothelioma
359 STAGERS NOTES

3. Lymphoma
4. Collagen disease (SLE)
5. All causes of transudate (CCF, nephrotic syndrome, cirrhosis of liver).

Treatment of recurrent pleural effusion is done by pleurodesis in the following

way:

1. A plain rubber tube is introduced in the intercostal space, and fluid is

removed as far as possible. Introduce the drug, tetracycline (500 mg) or kaolin
or talc through the tube, clamp it and keep for4 to 8 hours (may be
overnight). In malignant pleural effusion, bleomycin 30 to 60 mg is
introduced.
2. Patients’ posture should be changed 2 hourly to allow the drug to spread in
pleural space.
3. After 4 to 8 hours, remove any remaining fluid and take out the drainage tube
at the height of inspiration.
4. The patient usually complains of severe chest pain after pleurodesis. In such
case, analgesic should be given.

Q/ How can you suspect malignant effusion?

A. As follows:
Clincally—elderly emaciated or cachexic patient having clubbing with nicotine
stain, palpable
lymph node, radiation mark on the chest, etc.
Pleural fluid is hemorrhagic and there is rapid accumulation after aspiration.
Q/ What is pseudotumor (phantom tumor)?
A. It is the accumulation of fluid in interlobular fissure, usually found
along the lateral chest wall.
Chest X-ray shows rounded homogeneous opacity, misdiagnosed as
a tumor. It is confirmed by USG(localized or encysted effusion) or CT
scan. It disappears with resolution of effusion. It is commonly found
in CCF.
361 STAGERS NOTES

Q/ What are the characteristics of tuberculous pleural effusion?

A. As follows:

1. Straw or amber color

2. Exudative
3. High lymphocyte in pleural fluid
4. AFB is found in 20% cases
5. Culture for AFB is found in one-third cases
6. Pleural biopsy is positive in 80% cases.

Q. What are the causes of low pH and low glucose in pleural fluid?

1. Infection (empyema)
2. Tuberculosis
3. Advanced malignancy
4. SLE
5. Rheumatoid arthritis
6. Esophageal rupture.

Q/ What is the treatment of pleural effusion?

A. Treatment should be according to cause. For example:
If tuberculosis: Full course antitubercular therapy. Prednisolone 20 to 30 mg
daily may be given for 4 to 6 weeks, especially in large effusion.

If parapneumonic: Aspiration of fluid, may be repeated if necessary. Antibiotic

should be given.
If complicated case, especially empyema, thoracostomy may be done.
Sometimes, if all fails, thoracotomy with decortication may be necessary.

Q/ How much fluid may be drawn at a time?

A. Usually up to 1500 mL. If more is drawn, there may be risk of re-expansion
pulmonary edema.
The mechanism is because of effusion, lung is compressed and there is ischemia to
361 STAGERS NOTES

lung parenchyma and necrosis of pulmonary vessels. If more fluid is drawn, there is
rapid expansion of the lung, as no regeneration of necrotic vessels. As a result,
more leakage of fluid causing pulmonary edema.
362 STAGERS NOTES

ECG NOTES

How many ECG leads do we have ?

We have 12 ECG leads as folwos :

 6 chest leads are: V1,V2,V3,V4,V5,V6

 6 chest leads :
 Unipolar : aVR,aVL,aVF
 Bipolar:1,2,3

 V1–V2 : Septal wall

 V3–V4 : Anterior wall
 I, aVL ,V5-V6 : Lateral wall
 II, III, aVF : Inferior wall

 P wave-atrial depolarization
 QRS complex-ventricular depolarization
 ST segment, T wave-ventricular repolarization

Q/ what are the correct positions of the chest

leads?
 V1: Right side of sternum, fourth intercostal space
 V2: Left side of sternum, fourth intercostal space
 V3: Midway between V2 and V4
 V4: Left midclavicular line, fifth intercostal space
 V5 : Left anterior axillary line; same level as V4
 V6: Left midaxillary line; same level as V
363 STAGERS NOTES

How to intrepretate an ECG paper ?

1. ID and date
2. Look for standarisation and Avr lead (to know the conection)
3. Rate
4. Rhythem
5. Axis
6. P – wave
7. P-R intervals
8. QRS complex
9. ST segment and T wave abnormalities
10.Hypertrophy
11.Bundle branch block

1. ID and date
Ex: this ECG for Mr. Ahmed Ali Mohamed , taken at 20 of july /2015
2. Look for Avr lead (to know the conection)
All waves should be negatives in Avr unless the limb leads are wrongle
connected or dexrtocardia

3. Rate
How to calculate the rate of an ECG?
Normal heart rate between 60-100 bpm(3-5 larg squares between R-R)
 Regular rhythms can be quickly determined by counting the number
of large graph boxes between two R waves. That number is divided into
300 to calculate bpm. Ex: 3 large squares (300/3=100 bpm)
364 STAGERS NOTES

 If the distance between R-R waves just one large square or 1.5
large square , here we count the number of small squares then:
 1500/number of the large squares
 The best method for measuring irregular rates with varying R-R
intervals is to count the number of R waves in a 6-sec strip and multiply
by 10. (calculate the number of QRS in 30 large squares strep and
multiply by 10)This gives the average number of bpm.
 The following example : 7 x 10 = 70 bpm

4. Rhythem

Look to the strep : (you can use ruler)

 Regular : regular intervals beteen two R waves

 Irregular : iregular intervals between two R waves
5. Axis
Look to QRS complex in leads 1 and AVF
365 STAGERS NOTES

Q/ what are the causes of riht and left axis deviation?

Left axis deviation (LAD)

1. Left anterior hemiblock
2. MI (inferior wall)
3. Wolff–Parkinson–White syndrome (some types)
4. Ventricular tachycardia (left ventricular focus)
5. Obesity, pregnancy, congenital heart defects (e.g. endocardial cushion
defects)

Right axis deviation (RAD)

1. Right ventricular hypertrophy (e.g. secondary to COPD), pulmonary embolism
2. MI (antero-lateral)
3. Wolff–Parkinson–White (left-sided accessory pathway)
4. Dextrocardia
5. Left posterior hemiblock (rare)

6. P – wave indicating atrial depolarization (and contraction)

 P Mitrale ( Left Atrial Enlargement)
 Wide (>0.12 second) and notch P waive
 P Pulmonale ( Right Atrial Enlargement)
 Peaked P wave (>2.5 mm in lead 2)

DDx of absence P wave

1. Atrial fibrillation
2. Hyperkalaemia
3. Sinoatrial block, junctional (AV nodal) rhythm

DDx of tall P wave

1. Pulmonary hypertension (primary, secondary to pulmonary emboli, COPD)
2. Pulmonary stenosis
3. Tricuspid stenosis
366 STAGERS NOTES

4. P-R intervals : normally 3-5 mm

 First degree heart block : > 5 mm and remains constant from beat
to beat

 2nd degree heart block

 Mobtiz type 1 block(wenckebach phenomenon ):

Progressive lengthinig of P-R interval flwedd by drop beat

 Mobtiz type 2

 3rd degree heart block :

 Thers no relation between p and QRS complex , and has P wave
more than QRS

5. QRS complex
6. ST segment and T wave abnormalities
DDx of ST segment depression
1. Myocardial ischaemia
2. Myocardial infarction (posterior)
3. Drugs (digoxin, quinidine)
4. Ventricular hypertrophy

DDx of ST segment elevation

1. Myocardial infarction (acute)
2. Pericarditis
3. Prinzmetal angina
4. Left ventricular aneurysm
5. Brugada syndrome (downsloping ST elevation; may be caused by mutations
in the cardiac sodium channel gene SCN5A, associated with sudden cardiac
death)
6. High take-off
367 STAGERS NOTES

7. Hypertrophy
 Left ventricular hypertrophy :
 Sum of the hight of R wave in leads V5 or V6 and the depth of S
wave in lead V1 = > 7 large squares

 Right Ventricular Hypertrophy

 R wave in lead V1 divided by S wave in lead V1 =>1
368 STAGERS NOTES

8. Bundle branch block

Right Bundle Branch Block

 Wide QRS complex
 RSR pattern or rabbit ears pattern in V1
 Broad and slurred S wave in lead 1 and V6(the major criteria)
 Riht axisi deveation my be oresent

What are the causes of RBBB?

1. Right bundle branch block (RBBB)
2. Ischaemic heart disease
3. Cardiomyopathy
4. Massive pulmonary embolism
5. Atrial septal defect, Ebstein’s anomaly
369 STAGERS NOTES

Left bundle branch block

 Wide QRS duration (>3mm)
 Deep and broad S wave in V1 with no R wave
 Broad and slurred R wave (RR pattern) without Q wave in lead 1 and V6

 Always associated with LAD

What are the causes of LBBB?

1. Ischaemic heart disease
2. Cardiomyopathy
3. Left ventricular hypertrophy (aortic stenosis, hypertension)
4. Conduction system fibrosis
371 STAGERS NOTES

Drugs in medicine

Atropine
Atropine ampoule 0.6 mg/ ml or 600microgram/ml

Route :IM IV

Dose : 0.6mg – 3mg

Indication :

1. asystole
2. bradycardia
3. hypotention
4. organophosphorous poisning
5. anasthetic premedication

Side effect :

1. cholinergic side effect ( dry mouth , mydriasis , visual disturbance

,constipation )
2. Hallucination and fit in high dose
3. Nausea and vomiting

Contraindication :

1. allergic reaction
2. closure angle glaucoma
3. urine retention
4. prostatic enlargement
371 STAGERS NOTES

Adrenaline ampoule 1mg/ml

Route : IV IM

Dose: 1mg iv every 3-5v min

Indication :

1. cardiac arrest
2. anaphylaxis shock

Side effect :

1. hypertention
2. dyspnea
3. palpitation

Contraindication :

1- hypertension
2- pulmonary edema

Hydrocortisone vial 100mg/ 2ml

Route : IV, IM & IVI

Indication :

1- Acute asthmatic attack

2- acute exacerbation of COPD
3- anaphylactic shock

Side effect :

1- hyperglycemia
2- osteoporosis
3- cataract
4- cushing syndrome
372 STAGERS NOTES

5- peptic ulcer

Contraindication :

1- 1-hypersensivity
2- pregnancy
3- 3- infection
4- 4- peptic ulcer
5- 5- hypertention
6- 6- D M

4-Angeside : ( Glyceryl trinitrate tab 0.5 mg )

Route :

 sublingual
 buccal

Indication : Ischemic heart disease

Side effect :

 Headache
 hypotention

Contraindication :

1- Inferior MI
2- hypotention
3- withen 24 hours of sildenafil drug

Amiodarone ampoule 150 mg /3ml Class III antiarrythmic drug

Route : IV Oral

Dose : 5mg /kg over 12o min then 15 mg /kg over 24 hours
373 STAGERS NOTES

Indication :

 serious or resistance atrial and ventricular arrhythmias ( i.e cardiac arrest due
to VF resistance to DC )

Side effect :

1- photosensivity
2- hypotension
3- thyroid dysfunction
4- skin discoloration
5- corneal deposit
6- nausea and vomiting
7- hepatotoxicity
8- peripheral neuropathy
9- Torsade pointes
10- potentiate digoxin and warfarin

Contraindication :

1- hyperthyroidism
2- hypotention
3- second trimester of pregnancy
4- breast feeding

Amiodarone shouid be avoided to take with this medication :

1- antiarrythmic drug class III sotalol

2- class Ia disopyramide
3- antineoplastic drug ciclosporin
4- antiparasitic Pentamidin
5- neuroleptic chloropromazine
6- Ca channel blocker verapamil
374 STAGERS NOTES

Frusemide ( Lasix) ampoule 20mg /2ml

Route : IV, IM & PO

Dose : in acute pulmonary edema ( 50-100 mg )

Indication :

1- acute heart failure ( acute pulmonary edema )

2- nephrotic syndrome
3- hypertention

Side effect :

1- hypokalemia
2- hyperurecemia

Contraindication :

1- anurea
2- hypotention

Aminophylline ampoule 250mg /10ml

Route : IVI & PO

Dose :

 loading dose 5mg /kg over 20 min

 follow by 1mg /kg /hr infused slowly at 200cc of 5% Dextrose

Indication : Acute asthmatic attack

Side effect :

1- nausea and vomiting

2- arrhythmia
3- tachycardia
4- C N S( irritability, headache ,seizure )
375 STAGERS NOTES

Adenosine ampoule 6mg /2ml

Route : IV only

Dose : 3mg over 2 second injected rapidly IV follow by 6mg then 12 mg at interval
1-2 minutes

Indication : SVT

Side effect :

1- flushing
2- dyspnea
3- chest pain

Contraindication : ASTHMA

Aspirin tab 100mg

Route : PO

Dose : in MI (3 TAB of aspirin (300mg ) chewing within 12 hrs of MI follow by 75

mg tab single dose daily for life )

Indication :

1- Ischemic heart disease

2- APAS
3- strok

Side effect :

1- Bronchospasm
2- peptic ulcer

Contraindication : 1- asthma 2- peptic ulcer

376 STAGERS NOTES

Heparin
Route : SC

Dose : in ACS ( 6000 IU sc )

Types of heparin :

1- Low molecular weight heparin ( enoxaparin

dose 1mg /kg every 12 hrs )
2- Unfractionated heparin
3- Pentasaccchride ( fondaparinux dose 2.5 mg
single dose daily )

Indication :

1- Acute coronary syndrome

2- DIC

Side effect :

1- heparin induce TCP

2- hemorrhage
3- long term ( osteoporosis )

Contraindication :

1- TCP
2- Active bleeding

Calcium gluconate ampoule 10 ml of 10 %

Route : IVI

Dose : 10% in 10 ml in 5% dextrose over 10 min (

Role of 10 )

Indication :

1- hyperkalemia ( membrane stabilizing )

377 STAGERS NOTES

2- hypocalcemia

Side effect : hypercalcemia

KCL ampoule contain 20 mmol of K

Route : IVI (slowly over 2 hours )

Indication :1- DKA ( DOSE 20 mmol/l NOT in

the first pind ) 2- Hypokalemia ( dose 20- 40
mmol/l )

Digoxin
Route : IV &PO

Dose : IV ( 0.5 mg over 30 min Then 0.25 – 0.5 mg 4-8 hourly to maximum dose of
1mg )

PO ( 0.5 mg 6hourly for 2 doses then 0,125- o,25 mg daily )

Indication :

1- treatment and prevention of SVT

2- Rate control in AF
3- 3- Heart failure due to AF )

Side effect : ( Digoxin toxicity )

 Cardiac : bradycardia ,VT ,VF ,atrial

tachycardia
 Extra cardiac : nausea , vomiting , diarrhea ,altered color vision ( Xanthopsia
)
378 STAGERS NOTES

Dopamine ampoule 200 mg /5ml

Route : IVI

Indication : cardiac arrest

Side effect : nausea , vomiting , dyspnea

Warfarin tab 5mg

Route : PO

Dose : adjusted according To INR

Indication : DVT , pulmonary embolism , AF ,

APAS , stroke

Side effect : bleeding

Clopidogrel ( plavix tab )

Route : PO

dose : in MI ( 600 M g within 12 hrs follow by

150 mg over 1 week Then 75 mg for 12 month

Indication :

1- Acute coronary syndrome

2- strok

Side effect : haemorrge

379 STAGERS NOTES

Actilyse : Alteplase (human tissue plasminogen activator )

2 ampoule 50mg
Route : IVI

Dose : take 15 mg from first ampoule and give it in bolus dose ( 15 mg ) then take
the second ampoule ( 50mg ) and give it during 30 min Then the remaining from
first ampoule ( 35 mg ) give it through one hour

Indication:

1- in M.I within 12 hrs ( STEMI )

2- new onset LBBB

contrindications :

 absolute :
1. previous intracranial haemmorage at
any time
2. ischemic heart disease
3. brain tumor
4. AV malformation
5. suspected aortic dissection
5- active internal bleeding
 relative :
1-sever uncontrolled hypertention 180/110 mmhg
2-Hx of ischemic strok more than 3 months
3- bleeding tendency
4- current use of anticoagulant
5- trauma ( include traumatic CPR )
6-pregnancy
7- active peptic ulcer
381 STAGERS NOTES

Verapamil ( Isopten ) (Non dihydroperdin Rate limiting CA channel blocker)

Route: IV & PO

Dose :

 IV 5-10 mg over 30 min

 PO 40-120 mg 1x3 ( 8 hourly )

Indication :

1. Rate limiting in AF
2. Prevention of SVT
3. ACS

Side effect :

1. Constipation
2. bradycardia
3. hypotension

Metoprolol ( selective B- blocker )

Route : IV PO

Dose :

 IV 5mg over 20 min with maximum 15 mg

 PO 50- 100 mg ( 1x3 ) 8hourly

Indication :

1. treatment and prevention of SVT

2. Acute Coronary Syndrome ( effect are decrease pain , decrease risk of
arrhythmia , improve mortality )
3. In chronic heart failure at low dose
4. prevention of ectopic beat
381 STAGERS NOTES

Side effect :

1. bradycardia
2. bronchospasm
3. cold periphery

Atenolol
Route : IV PO

Dose : IV 2-5 mg with 1mg /min at 5 min

interval with maximum dose 10 mg

Indication and Side effect : as metoprolol

Bisoprolol
Route : only oral no IV route

Dose : 2.5 – 10 mg single dose daily

Indication and side effect : as metoprolol

Lidocain
Route : only IV

Dose : 50-100 mg ( 4mg /min for 30 min Then 2mg/min

for 2hr Then 1mh/min for 24 hrs)

Indication : In short term treatment and prevention of

VT & VF

Side effect : myocardial suppression , confusion , convulsion

382 STAGERS NOTES

Magnesium sulfate : ampoule 5ml of MgSO4 ( 50mg /ml )

Indication :

1. Asthma persist after salbutamol and hydrocortisone

2. Torsade point
3. pre eclampsia

Side effect :

1. C NS side effect like convulsion

2. Respiratory suppression
3. Hyperreflexia

Dose in asthmatic attack :

1.2 g- 2 g Iv over 2 minutes

383 STAGERS NOTES

Radiology

CXR interpretations
384 STAGERS NOTES

9. Name,age,sex, date
10. Exposure : good exposure when the intervertebral disk nearly visible
under-exposed image will be too white and an over-exposed image will be
too black

11. Rotation : The sternal ends of the clavicles should symmetrically overlie
the transverse processes of the 4th or 5th thoracic vertebrae. A rotated film
can alter the position of structures, eg rotation to the right projects the aortic
arch vessels over the right upper zone, appearing as though there is a mass.
12. Any lines, leads or tubes
13. Start with the soft tissue in the chest and neck: possible abnormalities
are surgical emphysema ,masses and forging bodies
14. Look for the bone : ribs , clavicles, sternum and the spine for any lytic
lesions , fractures and abnormal position
 The spaces between the ribs are wide in hyperinflation or pneumothorax
and crowded in collapse
 Look to the vertebral colomin , normally thers no calcification of
intervertebral disc , no osteoophyts or paravertebral lesions (TB ,
osteosarcoma )
15. Look for the trachea: any tracheal deviation , normally it slightly
deveated to the right
Deviated by collapse (towards the lesion), tension (away from the lesion), or
patient rotation. Check heart position
Also looks for main bronci :
Right main bronchus is more vertical , while left one is more horezental
Looks for carena : normally its angle < 60 degres , wider occurs in MS and
subcarenal LAP
16. Look for mediastinum
Causes of wide mediastinum are :
8. mediastinal fat
9. retrosternal thyroid
10. unfolded aorta, or aortic aneurysm
385 STAGERS NOTES

11. lymph node enlargement (sarcoidosis, lymphoma, metastases, TB);

12. tumour (thymoma, teratoma)
13. cysts (bronchogenic, pericardial)
14. paravertebral mass(TB).

9.look for the Hila

The left hilum is higher than the right or at the same level
(not lower); they
should be the same size and density. May be pulled up or
down by fibrosis or collapse.
deffrential diagnosis of enlarged hila:
4. Lymph nodes
5. pulmonary arterial hypertension
6. bronchogenic ca.
deffrential diagnosis of hillar Calcification:
6. Sarcoid
7. past TB
8. silicosis
9. histoplasmosis
Sarcoidosis
10. Inflation: There should be 5 to 7 ribs visible anteriorly
(or 10 posteriorly). Hyperinflation can be abnormal,
eg COPD.

10.look at the lung field: masses , collapse ,consolidation pacification

NOTE: when thers mass or lesion in the lung you have to describe it according to
lunge zone , we hhave 3 lunge zones , upper ,middle and
lower :

Upper zone : its lower border at anterior 2nd rib

Middle zone: from the lower border of anterior 2nd rib to
the lower border of anterior 4nd rib
386 STAGERS NOTES

Lower zone: from the lower border of anterior 4nd rib below
11.look at cardiac shadow

Normally less than half of the width of the thorax (cardiothoracic ratio <0.5).
⅓ should lie to the right of the vertebral column, ⅔ to the left. It may appear
elongated if the chest is hyperinflated (COPD); or enlarged if the image is AP
or if there is LV failure , or a pericardial effusion. Are there calcified valves?

 slouting sign: if the mass obliterate cardiac shadow, its position infront
of the heart
 if the mass behind the heart , the cardiac shadow clearly visible
 cardiomegaly
 arotic neckle

12.the diaphragm : falt in case of hyper inflated chest

 elevation of one hemidaiphragm :paralysis of hemidiaphragm

 look at costo-phrenic angle
 right himidiaphragm is higher than left one

13.subdiaphragmatic area:

 gass shadow in the stomach

 air under diaphragm
 dilated bowel loop
 donot forget the apex of the lung

14.don’t forget to llok to the hidden areas :

 Below the clavicles (apex of the lung)

 Hilar and retrohilar areas
 Cardiac shadow
 Retrophrenic area
 Subdiaphragmatic
387 STAGERS NOTES

Deferential diagnosis of Bilateral hilar lymphadenopathy

6. TB
7. Sarcoidosis
8. Lymphoma
9. Others: bronchial carcinoma, metastatic tumours,
recurrent chest infections,
10. AIDS, berylliosis, silicosis

Deferential diagnosis of Cavitating lung lesions

5. Abscess (Staphylococcus aureus, Klebsiella,
Pseudomonas aeruginosa, TB, histoplasmosis)
6. Tumour (particularly squamous cell carcinoma),
lymphoma
7. Infarct
8. Inflammatory: Rheumatoid nodule, Wegener’s
granulomatosis

Deferential diagnosis of Coin lesions

8. Tumours: bronchial carcinoma, metastatic
deposit (e.g. breast cancer, renal cell carcinoma,
hamartoma, adenoma, fibroma)
9. Infection: pneumonia, TB, abscess, hydatid cyst
10. Infarction
11. Encysted pleural effusion
12. Rheumatoid nodule
13. Vasculitides (e.g. Wegener’s granulomatosis)
14. AV malformation

Deferential diagnosis of Airspace/alveolar shadows

5. Pus (consolidation)
6. Fluid (pulmonary oedema)
7. Blood (pulmonary haemorrhage)
8. Cells (lymphangitis carcinomatosis, alveolar cell carcinoma)
388 STAGERS NOTES

Deferential diagnosis of Reticulonodular shadows

7. Pulmonary fibrosis: Cryptogenic fibrosing

alveolitis
8. Connective tissue diseases: scleroderma,
SLE, sarcoidosis, rheumatoid arthritis,
ankylosing spondylitis
9. Drugs (amiodarone, busulphan, bleomycin,
nitrofurantoin),
10. Radiation
11. Extrinsic allergic alveolitis (e.g. farmers’
lung, bird fancier’s lung, malt worker’s lung)
12. Pneumoconioses (coal workers’ pneumoconiosis, asbestosis, silicosis,
berylliosis)

Other DDX of reteculonodular shadow according to the lung zones

4. Upper zone: TB, allergic bronchopulmonary aspergillosis, radiation,
extrinsic allergic alveolitis,
ankylosing spondylitis, sarcoidosis.
5. Middle zone: sarcoidosis
6. Lower zone: cryptogenic fibrosing alveolitis, drugs, asbestosis, rheumatoid
arthritis,
scleroderma

Deferential diagnosis of White hemithorax

5. Large pleural effusion
6. Pneumo nectomy
7. Congenital absence of lung/extensive
hypoplasia
8. Collapse
389 STAGERS NOTES

Deferential diagnosis of multiple nodelos?

6. miliary tuberculosis (TB)
7. dust inhalation
8. metastatic malignancy
9. healed varicella pneumonia
10. rheumatoid disease

Deferential diagnosis of Ring shadows, tramlines and tubular shadows

Bronchiectasis

Deferential diagnosis of Increased translucency in CXR?

4. Bullae
5. Pneumothorax
6. Oligaemia

Deferential diagnosis of Unilateral and bilateral hilar enlargement:

• Unilateral hilar enlargement: TB, bronchial carcinoma, lymphoma
• Bilateral hilar enlargement: sarcoid, lymphoma, TB, silicosis

What are the causes of hillar congestion in CXR ?

4. Asthma
5. Hypertension
6. bronchitis

how to deffrentiate CT from MRI ?

look to the bone :

in CT scan the bone is white

in MRI : bone is black

391 STAGERS NOTES

how to know the right from the left in CT or MRI ?

suppose yopurself standing at the end of the bed while he lying in supine position when
he being scan

Q/how to deffrentiate epidural from subdural haematoma in CT scan ?

Dura maters enters the sutures of the skulls , so the blood above it (epidural ) become
compressed between the skull and the dura ….appears as lens shape

Subdural space is not limted by the sutures ,nstade it limed by falx cerbri …so the bllod
will deefusly destrbuted ,,,,appears as crescent shape

Subarchnoid haemorrhage : obliteration of the sulci

391 STAGERS NOTES

Cardiotoracic ratio :
 50 % in adults
 > 60 % in pediatrics

Cardiac diameter about 15-16 CM in adults

What are Kerley’s lines in Chest X-ray?

There are two type of Kerley’s line seen in chest X-rays:
Kerley’s A lines: These are 1–2 mm nonbranching lines radiating from the hilum, 2–6
cm long. This is due to thickened interlobular septa.
Kerley’s B lines: These are transverse 1–2 mm nonbranching lines at lung bases
perpendicular to the pleura,1–3 cm long. This is also due to thickened interlobular
septa.
392 STAGERS NOTES

Air under diaphragm

What are the causes of such X-ray appearance?
1. Perforation of hollow viscera containing gas :
• Peptic ulcer perforation—gastric or duodenal
• Perforation of malignant gastric ulcer
• Small gut perforation due to typhoid ulcer,
tubercular ulcer, crohn's disease.
• Large gut perforation due to tubular ulcer, crohn’s
or ulcerative colitis.
− Blunt trauma abdomen causing perforation or
transaction of small or large gut.
2. Penetrating injury abdomen causing peritoneal penetration, with or without
underlying visceral injury.
3. Bullet injury abdomen—with peritoneal penetration and with or without
underlying hollow viscus injury.
4. Following laparoscopic procedure or following abdominal operation—due to
entrapment of carbon dioxide gas or air.
5. Following tubal insufflation test for tubal patency.

Plain abdominal X rays shows multiple air-fluid level

Why do you say these gas filled loops are jejunal loops?
These gas filled intestinal loops are likely to be jejunal loops
because of following characteristics:
-These gas filled loops are centrally located in the abdomen.
- They are arranged in a stepladder pattern.
- There are closely packed valvulae connivantes indicated by
white lines in the gas filled gut.
What are the characteristics of gas filled ileal loops?
- These are also central in location and may have step ladder
pattern of arrangement.
393 STAGERS NOTES

-But the valvulae conniventes if present are very sparse and incomplete.
- The gas filled ileal loops are typically described as characterless.
Q/What are the characteristics of colonic gas shadows?
The characteristics of colonic gas shadows are:
- The colonic gas shadows are situated more
peripherally.
- There are haustrations in the walls. These are
incomplete mucosa folds in the walls placed at
different levels.

Q/Which X-ray is important for evaluation of patient with acute intestinal

obstruction?
A supine abdominal film gives better delineation of the gas filled gut loop and an
erect film is not required routinely.

Q/How many fluid levels in abdomen X-ray may be regarded as normal?

In adults two inconstant fluid levels—one at duodenal cap another at terminal ileum
may be regarded as normal.
In infants few fluid levels (2–4) in small gut may be regarded as normal.
394 STAGERS NOTES

Plain X ray shows cecal and sigmoid volvulus

Q/What are the causes of intra abdominal calcifecations ?

Concretions

These are discrete precipitates in a vessel or organ. They are sharp in outline but
the density and shape vary but in some cases they may be virtually
pathognomonic:

 stones
o renal stones
o ureteric stones
o bladder stones
o gallstones
 pancreatic ductal calcification
 nodal calcification - most commonly
from tuberculosis or histoplasmosis 1
 phlebolith
 appendicolith
 calcified granuloma

Conduit calcification

Calcification within the walls of any fluid-filled

hollow tube:

 abdominal aorta
 pancreatic ducts
 vas deferens
 large veins

Cystic calcification

Calcification in the wall of a mass such as a cyst, pseudocyst or aneurysm. Hallmark

is a smooth curvilinear rim of calcification.

 simple serous cysts

 aneurysms
395 STAGERS NOTES

 echinococcal cysts
 haematoma
 'porcelain' gallbladder
 calcified appendiceal mucocoele

Solid mass calcification

Diverse features which generally show extensive but variable calcification.

 mesenteric nodes
 uterine fibroids
 primary tumours, e.g. ovarian dermoid
 metastases
 adenoma
 spleen (sickle cell disease)

Radioopraq shadow in the right hypochondrium

Q/What percentage of gallstone and kidney stones are radiopaque?

About 10% gallstones are radioopaque and about 90% kidney stones are
radiopaque.

Q/What are the D/D of a radiopaque shadow in Rt. Hypochndrium ?

1-Kidney stone
2-Gallstones
3-Pancreatic calculi
4- Foreign body
5- Fecolith
5-Phleboliths
6- calcified lymph node
7- calcified renal tuberculosis
8- calcified adrenal gland
9-chip fracture of a transverse process of vertebra or calcification of costal cartilage
396 STAGERS NOTES

Q/How will you confirm your diagnosis?

*I will take a lateral view
• Gall stone lies anterior to the vertebral body
• Kidney stone lies posterior to the vertebral body or overlaps the vertebral body
*confirmation will be by an ultrasonography.

Ultrasonography will show the gallbladder outline. The gallbladder wall thickness
may be assessed and stone in the gall bladder will be confirmed by the presence
echogenic mass inside the gallbladder, which casts acoustic shadows. The size of
the common bile duct and presence of any stone in the bile duct may also be seen.
Kidney can be seen and its size may be measured. cortex and medulla can be
delineated.
The pelvicalyceal system can be seen and presence of renal calculi may also be
demonstrated by demonstrating the echogenic mass in the pelvicalyceal system
showing acoustic shadows.

Q/Which type of renal stones are radiopaque?

-oxalate stones
-Phosphate stones
-cystine stones
-Xanthine stones.

Q/What are the complications of renal stones?

-Renal infection—Acute pyelonephritis or pyonephrosis.
-Obstruction—Hydronephrosis, hydroureter.
-Ureteral stricture—Passage of stone may result in desquammation leading to
fibrosis and stricture formation in ureter, calyces or renal pelvis.
-Chronic renal failure—In bilateral calculi with associated infection or obstruction.
-Calculous anuria.
-Epidermoid carcinoma—presence of stones in the renal pelvis may cause squamous
metaplasia and squamous cell carcinoma of the renal pelvis.
397 STAGERS NOTES

Canon ball metastasis

Q/What are the important causes of cannon ball shadows in chest X-ray?
This may be due to
„ Metastasis
„ Benign lesion
• Fungal infection—Histoplasmosis, coccidioodomycosis,
aspergillosis.
• Parasitic infection—Filarial infection, hydatid disease.
• Sarcoidosis.
• Wegener’s granulomatosis.
• Rheumatoid nodules.

Q/What are the important primary sites, which can cause metastasis to
the lungs?
The important primary sites are: (PUBLIK-TS)
-Prostate
-Uterus and ovary
-Breast
-Lungs
-Stomach/Intestine
-Kidney
-Testis
-Thyroid
-Soft tissue sarcomas
-osteosarcomas.

Q/What are the important causes of miliary shadows in chest X-ray?

Miliary shadows in chest X-ray may be due to:
-Miliary tuberculosis
-Tropical eosinophilia
- Metastatic—Particularly from thyroid carcinomas
- Fungal infections—Especially coccidiodomycosis and aspergillosis
-occupational lung diseases—Asbestosis, byssinosis, silicosis.
398 STAGERS NOTES

ERCP
Q/What are the complications of ERCP?
ERcP may be associated with a number of complications:
-cholangitis
-Acute pancreatitis
-Bleeding
- Duodenal injury.

Q/What is the normal dimension of pancreatic duct?

In the head region—5 mm
In the body—3 mm
In the tail—2 mm.

IVU
Q/How will you prepare patient for intravenous
urography study?
-no fluid restriction is required.
-Patient should avoid solid food 6 hours before the procedure.
- oral purgative and antiflatulent tablet—the night before the
procedure.

Q/How intravenous urography is done?

„ At first a control X-ray of the KUB region is done to exclude any radiopaque calculi
or any calcification in the KUB region.
„ About 50 mL of contrast agent 76% urograffin (sodium diatrizoate) is injected
slowly intravenously and then serial radiographs are taken:
• one minute film will give a nephrogram phase.
• Five minute film will show early filling of the pelvicalyceal system and the ureter
may be visualized and any filling in the lower ureter may be seen well. In the
delayed film, the lower ureter will be overlapped by the full bladder.
If there is no obstruction an abdominal compression is applied with a belt and
exposure of renal area is taken at 10 minutes—the pelvicalyceal system is well
visualized.
399 STAGERS NOTES

• once the bladder gets filled in 10–15 miutes time the oblique views are taken to
look for any irregularity in the blader wall.
• If an urethrogram is required, patient is asked to pass urine and a micturating
cystourethrogram may be obtained in an oblique view.

Tension pneumothorax
Q/How will you diagnose tension pnemothorax?
-Severe respiratory distress.
-cyanosis.
-Mediastinal shift (trachea and apex beat shifted to opposite
side).
-Hyperresonant percussion note.
-Absent breath sound

Q/How will you relieve tension pneumothorax?

If tension pneumothorax is present, it should be relieved immediately by inserting a
wide bore needle in 2nd intercostal space at the midclavicular line.
411 STAGERS NOTES

BLOOD TRANSFUSION

Q/ Whar are blood product ?

1. Whole blood
2. Packed red cell
3. Platlate
4. 4-Fres Frozen Plasma
5. 5-Cryopreciptdte

Q/ What are content of whole blood ? what is indications ? What is

degree of storage ?
Content :
Fibrinogen , coagulation factors , plasma

Indication :
In acute blood loss

Store at :
4 Centigrade for ( 34 days )

Whole blood avoided in patient with

1-Renal failure
2- Heart failure
411 STAGERS NOTES

Q/ What are content of Packed red cell ? What is indications ? What is

degree of storage ?

Content : Only red cell

Indications:
1-Anaemia
2-Renl failure
3-Heart failure

Degree of storage :
4centigrade for( 34 days )

Q/ What is content of platlate ? What is indication of platlate ?

transfusion ? What is degree of storage ?
Content :
Only Platlate

Indication :
Thrombocytopnia ( platlate below 10 x10 9 )

Storage :
At 22Centigrade ( at room temperature ) for 5days

#Each unit of platlate is transfused increase platlate by 5000- 10,000 .

# Platelets more effective if compatible with patient's ABO type
#Plasma in group O platelets can haemolyse red cells of group A patient.
412 STAGERS NOTES

Q/ What are content of FFP ? What are indications ? What is degree

of storage ?

CONTENT :
Fibrinogen , antithrombin , albumin , protein S,C .

INDICATIONS :
1. Warfarin effect
2. coagulopathies
3. TTP ( Thrombotic thrombocytopenic purpura )
4. Liver disease
5. DIC

STORAGE :
At -30 Centigrade for 12 months

Q / What are content of Cryopreciptate ? What are indication :?

-CONTENT :
1. Fibrinogen
2. factor VIII
3. von Willebrand factor
INDICATION :
1. von Willebrand disease
2. haemophilia

Q/ Enumerate types of cryopreciptate ? Indication ?

1-Coagulation factors VIII , IX : Used in treatment of VWD, Haemophilia .
2-Intravenous immunoglobulin IVIG : Used in treatment of Immune
thrompocytopenic purpura , Gillian Barre syndrome
3-Human albumin : two types
@ 5% solution in plasma exchange
413 STAGERS NOTES

@20% solution in ( Hypoalbuminemia ,eg: nephrotic syndrome and chronic liver

disease

Q/ What are the main tests that should be done before transfusion ( pre
transfusion tests ) ?
1-Blood group ABO
2-Rh
3-Red cell antibodies
4- HIV
5- Hepatitis B , C
6-Syphilis

Q/ What arte safe transfusion procedure ?

 Taking blood for pre-transfusion testing. Positively identify the patient at the
bedside ( NAME OF PATIENT ) . Label the sample tube and complete the
request form clearly and accurately after identifying the patient. Do not write
forms and labels in advance.
 Administering blood. Positively identify the patient at the bedside. Ensure that
the identification of each blood pack matches the patient's identification.
Check that the ABO and RhD groups of each pack are compatible with the
patient's. Check each pack for evidence of damage. If in doubt, do not use
and return to the blood bank. Complete the forms that document the
transfusion of each pack.
 Record-keeping and observations. The reason for transfusion, the product
given, any adverse effects and the clinical response should be recorded in the
notes. Transfusions should only be given in a situation where the patient can
be observed. Blood pressure, pulse and temperature should be monitored
before and 15 minutes after starting each pack. If the patient is conscious,
further observations are only needed if the patient has symptoms or signs of
a reaction. An unconscious patient should have pulse and temperature
checked at intervals during the transfusion. Signs of abnormal bleeding
during the transfusion could be due to DIC resulting from an acute
haemolytic reaction
414 STAGERS NOTES

#During blood transfusion ,OBSERVE the following :

1-The reason for transfusion, 2- the product given, 3- adverse effects and the
clinical response should be recorded in the notes 4- Expire 5- Blood group and
Rh

TRANSFUSION REACTION :
# If the patient develop signs of acute transfusion reaction like fever , tachycardia
,ARDS, bronchospasm , abdominal pain Do the following :

1-stop transfusion

2-check vital signs B.P ,pulse , temperature , oxygen saturation

3- check compatibility

A) @ If the patient is compatible and develop fever less than 1.5 Centigrade

– stop transfusion for half hour

-Give paracetamol

-Restart transfusion slowly and observe frequently

If the patient is compatible and develop mild urticaria @

Stop blood transfusion for half hour-

- Anti histamine : Chlorphenamin 10 mg IV

-Restart transfusion slowly and observe frequently

415 STAGERS NOTES

B)If the patient is INCOMPATIBLE , Do the following :

-Stop blood transfusion

-Return blood to the blood bank

-Monitor urine output

-Saline infusion

-Give Lasix if UO less than 100 ml / hr

-Treat DIC with FFP

-Inform the hospital transfusion department immediately

C) If the patient is compatible and develop seves allergic reaction ( Bronchospasm,

abdominal pain , hypotention , angioedema ) :

-Stop transfusion

- Give antihistamin allermin 10mg slowly IV

-Oxygen

-Salbutamol nebulizer

-if the patient is severly hypotensive give Adrenalin 0.5 mg IM

-Send blood sample to the lad

- Return blood to blood bank

D)If the patient is compatible and develop bacterial contamination ( Blood pack
discolor , rapid onset hypo or hypertension ,rigor or collapse ) ,Do the following :

- return the blood to blood bank

-Take blood sample and send for culture,cross matching , urinanalysis, biochemistry
, coagulation screen

-Monitor urine output

416 STAGERS NOTES

-Broad spectrum antibiotics

-Oxygen and fluid support

Q/What is primary hemorrhage?

Bleeding during operation or at the time of injury.
Q/What is reactionary hemorrhage?
Reactionary hemorrhage occurs within 24 hours following operation or injury after
the primary hemorrhage is controlled.
This may be due to slippage of a ligature or dislodgment of a clot. Resuscitation
from shock may increase the blood pressure and may cause reactionary
hemorrhage.

Q/What is secondary hemorrhage?

Secondary hemorrhage usually occurs 7–14 days following the operation or injury.
This is usually due to infection and sloughing of vessels.
The secondary hemorrhage is often proceeded by ‘warning hemorrhage’ which are
brighi red stains of hemorrhage from the wound followed by sudden and severe
hemorrhage.

Q/What are the characteristics of arterial, venous and capillary

bleeding?
Arterial bleeding: Bright red bleeding in spurts which rise and fall with the pulse
wave.
Venous bleeding: Dark red bleeding occurring steadily and if large veins are injured
flow may
be copious.
Capillary bleeding: Bright red, continuous, often rapid ooze.
Q/What are the approximate blood volume in an adult and an infant?
In adult normal blood volume is approximately 7% of body weight. So a 70 kg adult
has a blood volume of 5 liters.
The blood volume in a child is approximately 8–9% of body weight (80–90 mU/kg
417 STAGERS NOTES

of body
weight).
418 STAGERS NOTES

STAGERS NOTES
CLINICAL PDEIATRICS

COMING SOON..