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Medical Investigations PDF
Medical Investigations PDF
A- X-ray.
1. Introduction to chest X-ray…………………………… … 1
2. Chest X-ray …………………………………………..…… 9
3. Heart X-ray …………………………………………..…... 14
4. Bone X-ray ..…………………………………………..…... 20
5. GIT X-ray ...…………………………………………..…... 22
6. Urinary tract X-ray ...………………………...…..………. 26
B- ECG.
1. Introduction…………………………………….……...….. 29
2. Leads, Axis………………………………………...……….. 32
3. Chamber enlargement ………….…………………...….... 34
4. Conduction disturbance ………………………………..… 36
5. Coronary heart disease……………………………….…… 40
6. Drug Effects, Electrolyte Abnormalities, and
Metabolic Factors………………………………………….. 47
7. Pericardial, Myocardial, and Pulmonary Syndromes….…51
8. Wolff-Parkinson-White Preexcitation Patterns ................ 53
9. Arrhythmias ………………………………………………...53
10. Scheme……………………………………………………… 62
11. Comment……………………................................................ 64
12. Examples……………………………………………………..65
C - CLINCAL PATHOLOGY.
1. Blood report (Haematology)……………………………… 74
2. Serology report (immunology)…………………………… 96
3. Hepatitis markers profile (immunology)……...…………. 103
4. Urine analysis (microbiology)………….............................. 107
5. CSF report (microbiology)…...………………………….... 113
6. Stool analysis (microbiology)……........................................ 116
D - CHEMICAL PATHOLOGY.
1. Liver function tests …………............................................ 119
2. Kidney function tests …………......................................... 125
3. Blood sugar profile …………….......................................... 129
4. Thyroid profile………………………….………....………. 132
5. Cardiac enzymes and proteins ............................................ 133
1
2
Normal structures’ opacity Normal structures
Air = lung field is black Normal Posteroanterior view CXR is formed of
Water = heart and mediastinum are white Chest wall (ribs) Lung field
Bone is in between Mediastinum including the heart
Diaphragm
Bone
Chest wall
3
Position of the patient (centralization)
Both clavicles should be at same level and the midway between them should lie at the line of vertebral
spine.
Gender: female = breast shadow as the X-ray on the right.
Air Bronchogram
In a normal chest x-ray, the tracheobronchial tree is not visible
beyond 4th order. As the bronchial tree branches, the
cartilaginous rings become thinner and eventually disappears in
respiratory bronchioles. The lumen of bronchus contains air and
the surrounding alveoli contain air also. Thus there is no
contrast to visualize bronchi. The air column in bronchi beyond
4th order becomes recognizable if the surrounding alveoli is
filled, providing a contrast or if the bronchi get thickened.
4
The term air bronchogram is used for the former state and
signifies alveolar disease. Note in the adjacent CXR
branching radiolucent columns of air corresponding to
bronchi which occurs in RUL consolidation & this helps to
differentiate consolidation from effusion.
Cardiothoracic ratio
Normal ratio of the heart to thorax is 1:2
Chest x-ray consists of
Chest wall (ribs) the heart
Lung field (lobes) Diaphragm
Mediastinum
Mediastinum
It is formed of the tissues between the two lungs as heart, great vessels and LNs.
Deviation of the mediastinum is accessed by the position of the heart apex & trachea.
RIBS
First rib is the upper rib, highly curved than the
other ribs. It lies below the clavicle so it has a
common shadow with it. Ribs on the lt
hemithorax are counted from front the others on
the right hemithorax are counted from back
6th rib normally is the last rib crossing the
copula of the diaphragm. If the diaphragm
crosses at a lower ribs then there is
hyperinflation
5
The hilum costophrenic angles
Contains the pulmonary vessels and pulmonary LNs
Heart
Heart borders
1. RT border:
a- SVC. b- RT atrium.
c- Ascending Aorta.
2. Front of the heart: RT ventricle.
3. LT border :
a- Aortic knuckle (1st space).
b- Pulmonary a. (2nd space).
c- LT auricule (3rd space).
d- Waist = constriction bet. PA & LA. e- LT ventricle forming the apex.
The cardiac contour
PA view: straightening of the left heart order. A discrete bulge on the left 3rd intercostal space,
immediately below the pulmonary bay. A double shadow (opacity) seen through the right side of
the heart = border of the right and left atria. Lateral view: Pressure on the oesophagus
Ventricular enlargements
Right ventricle
Left ventricle
7
RVE LVE
Posteroanterior view
Increased cardiothoracic ratio
cardiac outline takes the triangular shape Elongation of the long axis of the left ventricle
Elevation of the apex Apex: rounding / displaced downward
Enlargement of the pulmonary artery Enlargement of the aorta
Lateral view
Obliteration of retrosternal space Obliteration of retrocardiac space
Ascending aorta Enlarged in volume overload (AR)
Pulmonary artery
LAE
RAE RVE LVE
3rd space
- RT border bulge -↑↑cardiothoracic -↑↑cardiothoracic
Double contour
- Elevated apex - Apex: rounding /
- ++ PA displaced downward
- shaped - ++ aorta
angle
Lung X-rays
OPACITY HYPERTRANSLUCENCY CAVITY
COPD
Lung abscess
Pneumothorax
Homogenous
Heterogeneous
Homogenous opacity
Massive pleural Effusion
Homogenous opacity right hemithorax.
Shift of mediastinum to the left.
Obliterated right costophrenic angle.
Absent bronchoalveolar markings in the lesion.
10
Atelectasis Left Upper Lobe
Homogenous opacity left lower zone of the lung
Central mediastinum.
Free both costophernic angles
RML Atelectasis
11
Right upper lobe consolidation
Homogenous opacity in the right upper lung
zone.
Central mediastinum
Clear angles.
Air bronchogram is clear in the lesion.
Difference between consolidation and collapse is air
bronchogram
Hydropneumothorax
The lesion occupies the Rt hemithorax with air /
fluid level and consists of 2 parts lower part
homogenous opacity & upper part Jet black
Compensatory emphysema Rt side
Shift of mediastinum to Rt side
Obliterated Lt costophrenic angle
12
B. Heterogeneous opacity
Milary shadow for DD
Bilateral diffuse nodules of uniform size of range
2-3 mm.
Central mediastinum
Clear costophrenic angles.
Causes
T.B. ▪ Alveolitis
Sarciodosis ▪ Haemosederosis
Pneumoconiosis
Bronchopneumonia
Diffuse bilateral opacities of fluffy cotton
appearance
Central mediastinum
Clear costophrenic angles.
Metastasis
Multiple bilateral rounded heterogeneous
opacities of different sizes largest is 3cm
diameter.
Central mediastinum
Clear costophrenic angles.
Localized bronchiectasis
Shows dilated bronchi at lower zones
Central mediastinum
Clear costophrenic angles.
Polycystic lungs
Diffuse soap bubble appearance
Central mediastinum
Clear costophrenic angles
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Honeycombing for DD
(Seen in end stage lung disease)
Bilateral multiple dilated tubular shadows + cystic
spaces with peribronchial fibrosis
Central mediastinum
Clear costophernic angles.
Causes: bronchiectasis, cystic fibrosis.
HYPERTRANSLUCENCY
Bronchial asthma
CXR of an asthmatic during an episode of
bronchospasm. Lungs are hyperinflated due
to air trapping. This normalizes once
bronchospasm is controlled.
COPD Pneumothorax
Lesion Hyperinflated > 6th rib is seen crossing Hyperinflated > 6th rib is seen crossing
the diaphragm the diaphragm
Bilateral hypertranslucency Unilateral Rt hypertranslucency
with presence of bronchoalveolar (jet black) with absence of
markings bronchoalveolar markings
Mediastinum Central Shifted to opposite side
+ shadow of the collapsed lung
Bony cage Wide intercostals space Wide + /- fracture of ribs
Heart Ribbon-shaped (compressed bilateral)
Diaphragm Depressed bilaterally Depressed on the same side
Emphysematous
bullae
Multiple bilateral basal
hypertranslucency sacs
Ribbon-shaped
Central mediastinum
Clear costophernic angles.
14
Cavity = lung abscess
Lesion : No. single
Shape rounded cavity
Size 5x6 cm
Site upper zone RT lung
Content upper part air----jet black lower part
fluid-opaque
Heart x-rays
Mitral stenosis (LAE)
LAE The cardiac contour is abnormal with bulging on
the right giving a double right heart border (1 )
prominence of the left atrial appendage = 3rd Lt space
(2) elevation of the left main bronchus (3), indicating
left atrial enlargement
Aortic regurgitation
Dilated ascending aorta
Normal sized aortic arch
LVE ++ cardiothoracic ratio, apex displaced
downwards.
Systemic Hypertension
LVE ++ cardiothoracic ratio, apex displaced
downwards
prominent aortic knuckle
permanent pacemaker is seen.
15
Pulmonary hypertension
RVE ++ cardiothoracic ratio, elevated apex, triangular
shape of the heart.
Prominent pulmonary artery (2nd left space).
Aortic aneurysm
The mediastinum is widened throughout
its length with increased lateral
convexity to the left.
Pericardial effusion
Flask (onion) shaped heart
Marked increased in cardiothoracic ratio
Both borders are well defined (no angulations)
with bugle of both cardiac borders
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Heart failure
17
1- LT atrial 2- LT ventricular 3- RT ventricular
enlargement enlargement enlargement
X-ray with contrast Plain X-ray Plain X-ray
(Ba swallow )
Lateral view
LAE with backward pressure on Obliteration of the retrocardiac Obliteration of the retrosternal
the oesophagus space space
Dextrocardia.
Heart is roated with LV and apex on Rt side, RA on LT
side.
Gastric air stomach on Lt side.
Situs inversus.
Heart is roated with LV and apex on Rt side, RA on LT
side.
Gastric air stomach on Rt side.
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Examples
1. Plain CXR (chest X-rays).
2. Postro-anterior view.
3. Gender : male.
4. Well centralized.
5. Central mediastinum.
6. Free bony cage.
7. Normal diaphragm.
8. Clear costo-phernic angles.
9. The heart shows
LAE (a). 3rd space bulge on the left heart border
(b) double shadow'on the right side of the heart.
Diagnosis: Mitralization (mitral stenosis)
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5. Central mediastinum. 6. Free bony cage.
6. Clear costo-phernic angles.
7. Normal diaphragm. .
9. The RT lung shows
Single rounded homogeneous opacity.
Lower zone.
Size 2x3 cm.
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Unilateral hypertranslucency (jet black) with
absence of bronchoalveolar markings.
Shadow of the collapsed RT lung.
Diagnosis : RT side pneumothorax
BONE X-rays
HANDS' X-rays
1. Acromegaly
Plain X-ray of RT hand & wrist.
● Enlarged bones size & shadows.
● Increased soft tissues shadow.
● Mushroom shaped appearance of terminal phalanx
(white arrows).
2. Rheumatoid arthritis
Plain X-ray of LT hand & wrist.
● Loss of bone density.
● Ulnar deviation at M-P
joints.
● Destruction of proximal I-P
joints.
● Z-shaped deformity of the
thumb.
● Amalgamated carpel bones.
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● Periarticular osteopenia.
3. Scleroderma
- Plain X-ray of LT hand & wrist.
● Tuft resorption.
● Soft tissue calcification.
4. Chronic haemolytic
anaemia.
Plain X-ray of LT hand & wrist.
● Decreased bone density.
● Metacarpal bones show…
Loss of waist (rectangular
shape).
Thin cortex.
expansion of medulla.
Skull X-rays
1. Acromegaly
Plain X-ray of skull.
Lateral view.
● Prognathism (prominent jaw).
● Enlargement of frontal air sinus.
● Prominent mastoids.
● Thick cortex.
● Saucerization صحن الفنجانof sella turcica
(black arrow).
Spinal X-rays
1. Extramedullary block. 2. Intramedullary block.
X-ray with contrast myeloid (myelography).
● RT unilateral block. ● Complete block.
● Short tails. ● Long tails.
● Saddle shaped. ● Fusiform-shaped.
● Site: lumber (big vertebrae), cervical (small ● Site: lumber(big vertebrae),cervical
vertebrae), thoracic (ribs). (small vertebrae), thoracic(ribs)
3. Lumber Spondylosis.
Plain X-ray of the spine.
● Variable intervertebral spaces.
● Loss of spinal lordosis.
● New bone formation (osteophytes, lipping).
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GIT X-rays
Oesophageal X-rays
1. Oesophageal varcies.
X-ray with contrast Ba swallow.
● Multiple irregular filling defects (grape shaped).
● Site: all over the whole oesophagus but mainly at
the lower end of the oesophagus.
2.Achalsia of cardia.
X-ray with contrast (Ba swallow).
● Body: dilated (sigmoid shaped).
● Lower end: narrow (pencil shaped).
● May shows air / fluid level.
3.Cancer oesophageus.
X-ray with contrast (Ba swallow).
Lesion.
● Shouldering + rate tail appearance = scirrhous tumour.
● Irregular filling defect = cauliflower قرنبيطmass.
(Mention site & size of the lesion).
Types of barium contrast radiology
Ba swallow shows oesophagus
Ba meal shows stomach and
duodenum
Ba follow through shows small
intestine
Currently all GIT radiology are
replaced by endoscope
Stomach X-rays
1. cancer stomach
X-ray with contrast (Ba meal).
Lesion.
● Irregular filling defect → cauliflower tumour.
● Large ulcer w/o notch → ulcerative tumour.
● Linitis plastica → diffuse tumour.
(mention site & size of the lesion)
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Linitis plastica Filling defect Malignant ulcer
2. Chronic gastric peptic ulcer.
X-ray with contrast Ba meal.
Lesion…
● Lesser curve → ulcer niche (funnel protrusion).
● Greater curve → ulcer notch (filling defect = fibrosis).
N.B.:
There is also peptic ulcer occurring at the duodenum called duodenal
peptic ulcer.
Healing gastric peptic ulcer forms "Ba flake" in post-evacuation
film.
Healed one forms "hour glass stomach" due to fibrosis (also occurs
in gastric malignancy).
Differences between malignant ulcer & peptic one is the following
the malignant ulcer has 2 menisci (edges) but the peptic one has a
niche & a notch.
25
Biliary tract radiology
Plain x-rays X-ray with contrast
Intestinal X-rays
1. Crohn's disease.
Terminal ileum on barium follow-through
Lesion.
A long stricture is present (arrow A) and more
proximally there is ulceration with
characteristic 'rose thorn' ulcers (arrow B).
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2. Ulcerative colitis.
X-ray with contrast Ba enema (needle at anus).
Ba follow through (no needle).
Lesion…
● Colonic shorting.
● Loss of haustrations (pipe stem rigid appearance).
Urinary X-rays
1. KUB: plain x-ray of kidneys, ureters & urinary bladder.
Contrast…
2. IVU: x-ray with contrast (Urografin) of whole urinary tract.
3. IVP: as IVU but shows only renal pelvis upper ureters.
4. Descending cystograpy: as IVU but shows only urinary bladder & lower ureters.
5. Ascending cystograpy: x-ray with contrast (Urografin) of urinary bladder, dye is injected
inside the urethra with a needle is seen done in renal failure to see the bladder.
6. Urethrography: x-ray with contrast (Urografin) of the urethra.
1. Stone.
Plain X-ray = KUB.
Both kidneys show multiple staghorn stones at renal pelvis.
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4. Polycystic kidneys.
IVP (Urografin dye).
Lesion…
● Enlargement of the both kidneys.
● Smooth spider leg appearance.
● Elongation + attenuation & wide separation of
calyx (by the cysts in bet.).
29
Undergraduate syllabus
1. 1 degree heart block
st
2. LBBB, RBBB.
3. RVH, LVH, RAH, LAH.
4. Anterior, lateral, inferior MI (acute and old).
5. Anterior, lateral, inferior ischaemia.
6. AF, atrial flutter, extrasystoles, VT.
Usually one pathology is present.
Please study scheme P64
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INTRODUCTION
ECG PAPER : The ECG is usually recorded on a graph divided into millimeter squares, with darker lines
marking 5-mm squares. Time is measured on the horizontal axis. With a paper speed of 25 mm/sec, each
small (1-mm) box side equals 0.04 second and each larger (5-mm) box side equals 0.2 second. The
amplitude of any wave is measured in millimeters on the vertical axis
A, The resting heart muscle cell is polarized; that is, it carries an electrical charge, with the outside of the
cell positively charged and the inside negatively charged. B, When the cell is stimulated (S), it begins to
depolarize (stippled area).C, The fully depolarized cell is positively charged on the inside and negatively
charged on the outside. D, Repolarization occurs when the stimulated cell returns to the resting state. The
direction of depolarization and repolarization is represented by arrows. Depolarization (stimulation) of
the atria produces the P wave on the ECG, whereas depolarization of the ventricles produces the QRS
complex. Repolarization of the ventricles produces the ST-T complex.
A, A positive complex is seen in any lead if the wave of depolarization spreads toward the positive pole
of that lead. B, A negative complex is seen if the depolarization wave spreads toward the negative pole
(away from the positive pole) of the lead.C, A biphasic (partly positive, partly negative) complex is seen
if the mean direction of the wave is at right angles (perpendicular) to the lead
These three basic laws apply to both the P wave (atrial depolarization) and the QRS complex (ventricular
depolarization).
The P wave is positive (upward)
29
T wave is negative (downward).
The QRS complex is biphasic (partly positive,
partly negative)
The ST segment is isoelectric (neither positive
nor negative).
30
Notice that capital letters (QRS) are used to designate waves of relatively large amplitude and small
letters (qrs) label relatively small waves.
Ventricular depolarization (normal QRS complex)
The first phase of ventricular depolarization proceeds from the left wall of the septum to the right. A, An
arrow representing this phase points through the septum from the left to the right side. B, The second
phase involves depolarization of the main bulk of the ventricles. The arrow points through the left
ventricle because this ventricle is normally electrically predominant. The two phases produce an rS
complex in the right chest lead (V1) and a qR complex in the left chest lead (V6).
31
12 ECG Leads, AXIS
Standard bipolar limb leads: I, II, III
Bipolar limb leads aVR, aVL, aVF
Chest (percordial, ventricular) leads: V1 to V6
The LA electrode detects the electrical voltages of the heart that are transmitted to the left arm.
The RA electrode detects the electrical voltages transmitted to the right arm.
The LL electrode detects the electrical voltages transmitted to the lower limb.
: "unipolar” leads in that they measure the voltage in any one location relative to about zero
potential.
32
High
Strict
High Low
Strict Low
The depolarization stimulus spreads through the ventricles in different directions from instant to instant.
For example, it may be directed toward lead I at one moment and toward lead III the next. The mean
direction of the QRS complex, or mean QRS electrical axis, can also be described. If you could draw an
arrow to represent the overall, or mean, direction in which the QRS complex is pointed in the frontal
plane of the body, you would be drawing the electrical axis of the QRS complex. The term mean QRS
axis therefore describes the general direction in the frontal plane toward which the QRS complex
is predominantly pointed. Each lead has a positive and negative pole. As a wave of depolarization
spreads toward the positive pole, an upward (positive) deflection occurs. As a wave spreads toward the
negative pole, a downward (negative) deflection is inscribed. The cardiac axis is at right angles (90") to
the lead in which the R and S waves are of equal size. It may +ve if the difference bet QRS (lead I – lead
II) is +ve and vice versa.
33
CHAMBER ENLARGEMENT
Normal P wave < 2.5 small boxes. height & < 2.5 small boxes width. Ascending first part of P
wave is formed by RA since it contains the SAN so it is depolarized first followed by descending
part of late LA.LA is depolraized in opposite direction to lead V1 so it causes –ve deflection.
P mitrale wide, notched P waves in any lead and/or wide biphasic P waves wave > 2.5 small
boxes width in lead V1.
P pulmonale Tall narrow P waves (RAE/ RAH) wave > 2.5 small boxes height
34
The left ventricular hypertrophy exaggerates the normal pattern, causing deeper right precordial S
waves and taller left precordial R waves. By contrast, right ventricular hypertrophy shifts the QRS
vector to the right, causing increased right precordial R waves .
Big R inV1 R
≥S
Depressed ST
& inverted T
wave in :Vl →
V3 ( strain
pattern(
Right axis
deviation.
Strain pattern
May occur at the leads of hypertrophy due
relative ischaemia
35
CONDUCTION DISTURBANCES
36
37
38
Atrioventricular (AV) Heart Block
39
Abrupt nonconducted P waves without preceding changes in the PR
intervals sinus rhythm with 2:1 block alternating with 3:1 block (i.e., two consecutive nonconducted P
waves followed by a conducted one).
Type 2 heart block is simply seen as 2 succeeding Ps without QRS in between. Type I is preceded by
prolonged PR interval while it is not preceded by this change in type II.
independent atrial (P) and ventricular (QRS complex) activity. The
atrial rate is almost always faster than the ventricular rate. The PR intervals are completely variable.
Some sinus P waves fall on the T wave, distorting its shape. others may fall in the QRS and be “lost
Notice above that the QRS complexes are of normal width, indicating that the ventricles are being paced
from the atrioventricular junction.
Notice above that the QRS period may widen if it is paced by ventricular rhythm (idioventricular).
40
A With acute subendocardial ischaemia the electrical forces (arrows) responsible for the ST
segment are deviated toward the inner layer of the heart, causing ST depressions in lead V5,
which faces the outer surface of the heart.
B, With acute transmural (epicardial) ischaemia, electrical forces (arrows) responsible for the ST
segment are deviated toward the outer layer of the heart, causing ST elevations in the overlying
lead.
Characteristics of the normal ST segment and
T wave. The junction (J) is the beginning of the
ST segment. To comment as elevated ST
segment the J point should be above baseline by
1 s. sq. in limb leads or 2 s. sq. at chest leads.
Elevated ST segment (elevated J point) high take off of ST segment (isoelectric J point)
Angina pectoris
Type Site
Classic (Stable( Variant
Stable Angina
A, Baseline rhythm strip from the positive exercise
test of a patient with coronary artery disease.
B, Notice the marked ST depressions with increased
heart rate.
Prinzmetal's (variant) Angina
Prinzmetal's (variant) angina with transient ST elevations in a 30-year-old man with a history of
angina with exertion and at rest.
A, The baseline resting ECG shows nonspecific inferior lead ST-T changes.
B With chest pain, marked ST segment elevations occur in leads II, III, and aVF, and reciprocal
ST depressions are seen in leads I and aVL.
C The ST segments return to baseline after the patient is given nitroglycerin. Cardiac
catheterization showed severe right coronary obstruction with intermittent spasm producing total
occlusion and transient ST elevations.
41
Lateral Low (V 5,6) I (high) high) aVL)
InFerior II , III aVF
Septal V1, 2
Anterior (strict) V 3, 4
Antroseptal V 1,2,3,4
Extensive anterior V 1→ 5, 6
Anterolateral ANY 2 succeeding I aVL
chest lead
Posterior V 1,2,3 (reciprocal) V8 Usually ass. Inf. MI Tall R, Depressed ST
(inferoposterior)) V9 Upright T
Right ventricle V1r V3r Usually ass. Inf. MI
2 leads at least should present in the wall.
Antrolateral ischaemia.
42
Myocardial infarction
Type Site
Transmural Subendocardial
Q-wave infarction Non-Q-wave infarction
NSTEMI
Acute (recent) Chronic (Old)
Pathological Q wave is>1 small square in duration (width) & >1/4 preceding R wave (length) or single Q
wave in any lead rather than aVR . the mechanism of formation of Q wave is that Q wave is septal wave
escapes through infracted area.
Examples of pathological Q-wave
Evolving Resolving
Hyperacute Acute
0 – 6 h rs يتطور24 hr–3w Old > 3 weeks
6 - 24 hrs
43
A, Acute phase of an inferior wall myocardial infarction: ST elevations and new Q waves.
B, Evolving phase: deep T wave inversions+ pathological Q waves.
C, Resolving phase: partial or complete regression of ST-T changes (and sometimes of Q waves). In A
and B, notice the reciprocal ST-T changes in the anterior leads (I, aVL, and V2).
A, Acute phase of an inferior wall myocardial infarction: ST elevations and new Q waves. B, Evolving phase:
deep T wave inversions. C, Resolving phase: partial or complete regression of ST-T changes (and sometimes
of Q waves). In A and B, notice the reciprocal ST-T changes in the anterior leads (I, aVL, and V2).
Inferior MI
Lateral MI
44
Persistent ST elevation in a patient with a history of MI.
45
Tall R.
ST depression Ant. leads
Upright T.
Ass. inferior MI.
Non–Q wave infarction in a patient who complained of severe chest pain. Subsequently, the
patient's cardiac enzyme levels were elevated. Notice the marked, diffuse ST depressions in leads I, II, III,
aVL, aVF, and V2 to V6, in conjunction with the ST elevation in lead aVR. These findings are consistent
with severe subendocardial ischemia. Other abnormalities include a prolonged PR interval (0.28 sec) and
left atrial abnormality.
46
we expect it if there is inferior infarction. Here there is elevated ST
segment inferior and right leads.
Hyperkalaemia
47
T waves peaking (“tenting” )خيمة. Prolonged PR interval
P waves decrease in amplitude and may A sine-wave ) )جيب الزاويةpattern leads to
disappear asystole
QRS complexes widen and latter bizarre البوتاسيوم بتمط رسم القلب++
Hypokalaemia
50
PERICARDIAL, MYOCARDIAL, AND PULMONARY SYNDROMES
Acute pericarditis
Ventricular injury diffuse ST segment elevations in leads I, II, aVF, and V2 to V6, with reciprocal ST
depressions in lead aVR. A concomitant atrial injury PR segment elevations in lead aVR with reciprocal
PR depressions in the left chest leads and lead II.
Late pericarditis
Notice the diffuse T wave inversions in leads I, II, III, aVL, aVF, and V2 to V6.
Difference between pericarditis and myocardial infarction
No Q waves in percarditis.
Diffuse affection of all leads by ST changes.
PR change in acute pericarditis.
Pericardial effusion
Electrical alternans may develop in patients with pericardial effusion and cardiac tamponade. Notice the
beat-to-beat alternation in the P-QRS-T axis; this is caused by the periodic swinging motion of the heart
in a large pericardial effusion. Relatively low QRS voltage and sinus tachycardia are also present.
51
Pulmonary embolism
PE showers form Sinus tachycardia, Massive PE causes S waves in lead I with Q waves and T wave
inversions in lead III (SI, QIII, TIII pattern), Submassive PE makes slow R wave progression with T
wave inversions in chest leads especially V1 & V2 resulting from acute right ventricular overload
COPD
52
Notice the characteristic combination of relatively low voltages in the limb leads, right axis deviation, right atrial
overload pattern (“P pulmonale”), and slow R wave progression. The P wave axis is also more rightward than usual
(almost +90°). RVH may be also present.
Notice the characteristic triad of the WPW pattern: wide QRS complexes, short PR
intervals, and delta waves (arrows) that are negative in some leads (e.g., II, III, and
aVR) and positive in others (aVL and V2 to V6). The Q waves in leads II, III, and aVF
are the result of abnormal ventricular conduction (negative delta waves) rather than an
inferior myocardial infarction. This pattern is consistent with a bypass tract inserting
into the posterior wall of the left ventricle
ARRHYTHMIAS
Arrhythmias
Arrhythmia is change in heart rate, rhythm or both. They are divided according the source of the pace
maker i.e. sinus, nodal (junctional), atrial and ventricular.
53
Sinus tachycardia: Pacemaker: SAN, regular & rapid rate >100.
Pacemaker is AVN, P wave: Absent or inverted (retrograde), regular & slow rate.
Paroxysmal supra-ventricular tachycardia (PSVT) AV nodal reentrant tachycardia (AVRT)
Pacemaker: atrial ectopic foci (small P or superimposed on the preceding T waves).usually regular, any rate.
Atrial fibrillation
54
Pacemaker: multiple atrial foci. P wave is replaced by fibrillatory (f) waves which appears as rapid
oscillation of the baseline, irregular rapid (usually) heart rate. (if slow rate it is then called slow AF).
Atrial flutter
Usually regular. Rate: any. Pacemaker: reentrant atrial focus. P wave is replaced by flutter “F” waves it
appears as classic “saw tooth” waves. They (F) are multiple per QRS here it is 4:1. If atrial flutter with
irregular heart rate then it it is atrial flutter with variable block.
Wandering atrial pacemaker (WAP)
Pacemaker: Multiple atrial foci (one of them is SAN). More than three different P waves are present.
Regularity: irregular. Rate: usually slow.
Multifocal atrial tachycardia (MAT)
It is a type of WAP but rapid rate. (look like AF but with Ps).
Ventricular tachycardia
(VT)
Monomorphic…………
Polymorphic…………..
Torsades de pointes
(twisting of points)…….
Regularity: marked irregular. Rate: any. Pacemaker: multiple ventricular ectopic foci. Fibrillatory
waves are of variable shape, size and direction. QRS complex are lost
Ventricular Flutter
Pacemaker: Macro reentrant focus. Flutter waves. Regularity: regular. Rate: very rapid >300.
55
Escape idioventricular rhythm
Pacemaker: ventricular. Regularity: regular. Rate: slow < 40.Wide QRS duration.
Accelerated idioventricular rhythm
Escape beats: Sinus rhythm is interrupted by sinus pause followed by an ectopic beat
Escape atrial beat
Escape junctional beat
Escape ventricular beat
Premature beats (premature contraction PC, extrasystole): Sinus rhythm is interrupted by
premature beat followed by a pause.
Premature atrial beat Premature junctional beat
Premature ventricular beat
ESCAPE ATRIAL BEAT
56
JUNCTIONAL PREMATURE BEAT
Pause
Premature beat + compensatory pause periods = periods of 2 beats i.e. full compensation.
PREMATURE BEAT WITH NON-CONDUCTED P
Premature beat occurring during ventricular contraction (QRS and/or T wave) only pause is left.
MONOFOCAL PREMATURE BEAT
57
VENTRICULAR TRIGEMINY
Premature beat (X) falls between two normal beats, in which case it is interpolated. No pause.
Notice the
transition in lead
V3.
Somewhat
delayed R wave
progression, with
the transition in
lead V5.
Early transition
in lead V2.
R waves in the chest leads normally become relatively taller from lead V1 to the left
chest leads.
58
Early transition “poor” or preferably “slow” R wave progression
Anterior myocardial infarction (death of ventricle = R wave)
RVH LVH
RBBB LBBB
chronic lung disease
Before taking an ECG, the operator must check to see that the machine is properly calibrated, so
that the 1-mV standardization mark is 10 mm tall.2 large boxes.
A, Electrocardiograph set at normal standardization.
B, One half standardization.
C, Two times normal standardization.
59
DIFFERNTIAL DIAGNOSIS
lead II (= arrhythmias)
Sinus bradycardia: normal regular heart but slow.
1st degree HB: like normal but slow rate + FIXED prolonged PR interval.
2nd degree HB: 2 succeeding P waves with no QRS
3rd degree HB: P waves everywhere.
Nodal rhythm: absent P, inverted P:.
Idioventricular rhythm: wide QRS, characteristic shape.
Hypokalaemia: T wave flattening + u wave.
Slow AF.
Tachycardia.
Supraventicular (sinus, atrial, nodal) …. Normal QRS
Normal P waves… sinus
Absent or inverted ….nodal
Replaced: AF, atrial flutter.
Ventricular (abnormal QRS).
VF, VT, ventricular flutter
Axis
Normal
LAD
LVH: SV1+ RV5 or 6 ≥ 7 b. sq.
LBBB: RsR' complex (M -shaped, notched R ) in V6, Deep QS complex lead V1(notched
S)
LAHB: deep S in inferior leads esp. aVF.
Bifasicular: LAHB + RBBB.
Normal
RAD
LPHB: deep S in lateral leads
Normal
PE, COPD, Lateral infarction
V1 Big R wave
RVH: deep S in V6 + strain pattern in V1-V2
RBBB: rSR' complex
Posterior MI: associated inferior MI
VI deep S wave
LVH: SV1+ RV5 or 6 ≥ 7 b. sq.
T wave inversion
Subendocardial ischaemia: NO elevated cardiac enzymes
Evolving transmural infarction: elevated cardiac enzymes
Left or right ventricular hypertrophy (formerly called “strain” pattern)
Secondary T wave alterations: bundle branch blocks, Wolff-Parkinson-White patterns
Digitalis effect: Scooping of the ST-T complex ST segment and T wave are fused together
T wave hyperacute
AMI
Hyperkalaemia: long PR, lost P, wide QRS.
ST segment elevation
Hyperacute MI: NO pathological q wave
60
Acute MI: pathological q wave
Both acute and hyperacute MI are associated with chest pain + enzyme elevation.
Old MI + aneurysm: pathological q wave + ST elevation without chest pain or enzyme elevation
Prinzimetal angina (vasospastic): NO pathological q wave no enzyme elevation anginal chest pain.
Pericarditis: diffuse ST elevation.
Hyperkalemia (usually localized to V1 and V2)
ST segment depression
Subendocardial ischaemia: NO elevated cardiac enzymes
Subendocaridal infarction: elevated cardiac enzymes
Reciprocal change with acute transmural ischemia
Left or right ventricular hypertrophy (formerly called “strain” pattern)
Pathological Q
Myocardial infarction
Myocarditis
QRS duration
Intrinsic intraventricular delay (IVCD):Left bundle branch block and variants,
right bundle branch block and variants.
Extrinsic (“toxic”) intraventricular delay: Hyperkalemia, drugs: class I antiarrhythmic drugs and
other sodium-channel blocking agents
Ventricular beats: premature, escape, or paced
Ventricular preexcitation: Wolff-Parkinson-White pattern and variants
Ectopic beats
Escape beats (pause precedes the beat) or premature (beat precedes the pause).
Atrial (upright P wave), junctional (inverted or absent P wave), ventricular (long, bizarre, wide
QRS).
If regular…. bigeminy, trigeminy, qaudriqeminy.
Same shape (monofocal), different shape (multifocal).
Scheme postgraduate
1. Lead II arrhythmias
2. LI / LIII axis
3. Limb leads
Q wave … MI
Deep S waves in inferior leads LAHB in lateral leads LPHB
SIQIIITIII massive PE
P wave atrial enlargement
4. V1: Big R wave: RVH, RBBB and Posterior MI.
5. V6: LBBB, LVH
6. All leads ST segment, T wave, pathological Qs
Arrhythmias
Upright normal P waves: sinus arrhythmia
Inverted , absent superimposed P waves: supraventricular arrhythmia
Inverted , absent P waves: nodal arrhythmia
superimposed P waves over T waves or replaced by F or f waves: atrial arrhythmia
Wide + bizarre: ventricular arrhythmia.
61
SCHEME UNDERGRADUATE
comment diagnosis
Lead II
1. Rhythm Sinus (+ve P wave) Bradycardia: 1st degree HB,
N: regular Not sinus (–ve or absent) Nodal rhythm, Slow AF.
constant R-R Irregular (variable R-R) Tachycardia:
2. Rate If regular = 300/no of big sq bet Supraventicular (sinus,
N: HR 60-100 2R atrial, nodal) Normal QRS
> 100 = Tachy If irregular = no QRS in (see P wave). Ventricular
< 60 = brady 6sec(15cm) x10 (abnormal QRS): VF, VT,
ventricular flutter
3. P-wave Tall peaked (P-pulmonale > 2.5 ↑) right atrial enlargement
Normal +ve in Broad ± Bifid (P-mitrale > 2.5 left atrial enlargement
L II size 2.5 x small boxes ↔ )
2.5 small boxes. Absent P AF ,SVT ,VT ,nodal rhythm
Inverted P nodal rhythm
Flutter wave (absent P) Atrial flutter
Fibrillatory waves Atrial fibrillation
4. P-R interval Normal < 1 big box
AV conduction Prolonged > 1 big box 1st degree heart block
Axis L I / L III or L I / L aVF
5. Axis Extreme RAD ( both –ve )
Normal axis RAD ( L I –ve , L III +ve ) RVH, Lat. infarction
both +ve LAD ( L I +ve , L III –ve ) LVH, LBBB,
Chest leads … start with V1 & V6
6. QRS Big R wave RVH, RBBB
voltage SV1+ (RV5or6)≥35 s.sq (7 b. sq.) LVH
7. QRS Normal (<2.5 small boxes)
duration Wide + rSR' (M-shaped V1) RBBB
Wide + RsR' (M-shaped V6) LBBB
8. Path. Q V 1,2 Septal infarction
is>1 s sq width or V 3,4 Strict anterior infarction
>1/4 R wave or V 1,2,3,4 Antroseptal infarction
single Q V1→6 Extensive anterior infarction
II , III , aVF InFerior infarction
I, aVL(low) V 5,6 (high) Lateral infarction
9. ST Seg. Raised Recent MI
Normal (iso- Depressed VH , BBB(strain) ,
electric) ischaemia
10. T wave Inverted (normal in lead aVR) Same causes of depressed
ST
62
Arrhythmia
Check QRS complex
Ventricular arrhythmia
Accelerated idioventricular rhythm
Escape idioventricular rhythm
Ventricular ptachycardia (VT): wide
regular QRS complex.
Ventricular Fibrillation (VF):
irregular wide QRS complex.
Ventricular Flutter: as VTac.but HR>
300
Premature atrial beat: early atrial beat
followed by pause
Escape atrial beat: pause followed by
atrial beat
Premature ventricular beat: early
ventricular beat followed by pause
Escape ventricular beat: pause
followed by ventricular beat
63
COMMENT
regular or irregular.
: … beats per minute.
: normal (2.5 x 2.5 small squares), tall, wide. Upright, inverted, absent, replaced by flutter
or fibrillatory waves.
normal (1 big square), prolonged, short.
normal, elevated (1 small square limb leads or 2 small squares chest leads),
depressed (1 small square limb leads or 2 small squares chest leads).
upright, inverted, flat.
In hypokalaemia.
EXAMPLES
64
ST elevations are localized to leads V1, V2, V3, I, and aVL reciprocal ST
depressions in leads II, III, and aVF..
inverted II, III & aVF, hyperacute V2,V3.
.
regular. normal.
: 100 beats per minute. normal.
: normal.
wide in premature beats, normal.
leads II, III, aVR, aVL. aVF, V3. normal.
: high in premature normal, inverted leads II, III,
beats, leads II, III, aVF. aVF, V2.
absent.
65
irregular. : normal
: 75 beats per minute. absent.
: absent replaced by fibrillatory normal.
waves. downsloped leads I, II,
absent. V2- V6.
normal. normal.
normal.
regular. : normal
: 200 beats per minute. absent.
: absent (buried in QRS). normal.
absent. normal.
normal. normal.
normal.
66
regular. : normal
: 150 beats per minute. absent.
: normal. normal.
normal. depressed leads I, II, aVL,
left axis. V3-6.
normal. normal.
normal.
regular. absent.
: 75 beats per minute. normal.
: peaked especially lead II. : big R wave lead V1 &V2
normal. normal.
right. inverted leads II, II, aVF, V1-3
normal. (strain pattern).
: normal
67
irregular. : normal
: 80 beats per minute. absent.
: normal. normal.
normal. normal.
normal. normal.
normal.
regular. : high V4
: 150 beats per minute. absent.
: absent replaced by flutter waves. normal.
absent. normal.
normal. normal
normal.
68
regular. absent.
: 75 beats per minute. normal.
: normal. elevated II, II, aVF,
normal. depressed aVL, V2,3.
normal. normal.
normal.
: normal
regular. : normal
: 100 beats per minute. absent.
: normal. normal.
prolonged. normal.
normal. normal.
normal.
69
regular. absent.
: 100 beats per minute. : RsR' complex (M -shaped,
: normal. notched R ) in leads I, aVL, V5 & V6.
normal. Deep rS complex lead V1-3.
left. normal.
broad complex. inverted leads I, aVL, V6.
: insignificant
regular. : normal
: 60 beats per minute. absent.
: normal. : rSR' in lead V1-6.
normal. normal.
normal. inverted V1.
broad complex
70
regular. absent.
: 75 beats per minute. tall R leads V3-6.
: normal. deep s leads V, 2.
normal. depressed leads v3-v6 (strain
left. pattern).
normal. inverted leads I, II, aVL & V3-6.
: high in chest leads.
regular. : normal
: 50 beats per minute. leads II, II, aVF.
: normal. : peaked (hyperacute) leadsV2-3.
normal. normal.
left. inverted II, aVF & V6, hyperacute
normal. V2 &V3.
71
regular. : normal
: 90 beats per minute. absent.
: normal. normal.
normal. depressed I, II, V2-6.
normal. normal.
normal.
irregular.
: 90 beats per minute.
normal.
: normal
absent.
72
VVV. imp. Clinical pathology exam is about lab. investigations ONLY
73
Blood report
Blood
Plasma Cells
Nongranulocytes Granulocytes
74
Leucoerythroblastic anaemia: Immature cells (myelocytes, promyelocytes, metamyelocytes,
normoblasts) seen in film. Due to marrow infiltration (eg malignancy) when these cells are
displaced; also seen in anorexia, sepsis, severe haemolysis.
Blasts: Nucleated precursor cells. They are not normally in peripheral blood, but are seen in
myelofibrosis, leukaemia or malignant infiltration by carcinoma.
Burr cells: Irregularly shaped cells occurring in uraemia.
Howell-Jolly bodies: DNA nuclear remnants in RBCs, which are normally removed by the
spleen (fig 8). Seen post-splenectomy and in hyposplenism (eg sickle cell disease, coeliac
disease, congenital, UC/Crohn's, myeloproliferative disease, amyloid). Also in
dyserythropoietic states: myelodysplasia, megaloblastic anaemia.
Leukaemoid reaction: A marked Leucocytosis (WCC>50,000/cmm). Seen in severe illness eg
with infection or burns, and also in leukaemia.
Reticulocytes: 0.5-2% Young, larger RBCs (contain RNA) signifying active erythropoiesis.
Increased in haemolysis, haemorrhage, and if B12, iron or folate is given to marrow that lack these
• Reticulocytosis: indicates hyper-active BM as in
- Haemolytic anaemia. - Acute haemorrhage.
- Anaemia under specific treatment, especially megaloblastic, Fe def. anemia .
- Recovery from BM suppression.
• Absent reticulocytes: occurs in
- Aplastic anaemia ( B.M. failure ) - Dyshaemopoietic anaemia ( def. of Fe , B12 )
Nucleated red blood cells (normoblasts)
Marrow infiltration
Severe haemolysis
Myelofibrosis
75
Stem cells and growth factors in haematopoietic cell development. (BFU-E = blast-forming unit-
erythroid; CFU-Meg = colony-forming unit-megakaryocyte; CFU-GM = colony-forming unit-
granulocyte, monocyte; CFU-E = colony-forming unit-erythroid; IL = interleukin; SCF = stem cell factor;
GM-CSF = granulocyte macrophage-colony stimulating factor; Epo = erythropoietin; Tpo =
thrombopoietin; G-CSF = granulocyte-colony stimulating factor; M-CSF = macrophage-colony
stimulating factor)
• RBC's • WBC's
HB 12- 16 o TLC 4000 – 11000/ cmm
PCV 46 o Differential count Relative Absolute
RBC's count 4.5-5.5m Basophils 0-1% 10-100
MCV 76-96 Eosinophils 1-6% 40-400
MCHC Neutrophils 40-75% 2500-7500
MCH 34
Lymphocytes 20-40% 1500-2500
27-32
Reticulocytes Monocytes
2-10% 200-800
0.5-2.5
• Platelets 150-450 • ESR ♂ ♀
thousand 1st hour 5 10
2nd hour 8 16
Causes of anaemia
RBC’s count
Increased Decreased
Corpuscular
membrane HB Enzyme
PNH SCA
Spherocytosis Thalassemia G6PD def.
Extracorpuscular
NB: haemolytic anaemia is also divided clinically into acquired, inherited and miscellaneous.
1- Hereditary.
a- Membrane defect (hereditary spherocytosis).
b- HGB defect (Thalassemia, SCA).
c- Metabolic (G6PD)
2- Acquired.
a-Immune: (autoimmune haemolytic an., incompatible blood transfusion, drug induced,
paroxysmal cold HGBuria).
b- Non immune: PNH, microangipathy, valve prosthesis, malaria).
3- Miscellaneous.
An approach to haemolytic anaemia
Haemolysis is the premature breakdown of RBCs, before their normal life span of ~120 d. It occurs in the
circulation (intravascular) or in the reticuloendothelial system i.e. macrophages of liver, spleen and bone
marrow (extravascular). In sickle-cell anaemia, lifespan may be as short as 5d. Haemolysis may be
asymptomatic, but if the bone marrow does not compensate sufficiently, a haemolytic anaemia results.
An approach is to first confirm haemolysis and then find the cause try to answer these 4 questions:
Is there increased red cell breakdown?
o Anaemia with normal or ↑‘MCV.
o ↑‘Bilirubin: unconjugated, from haem breakdown (prehepatic jaundice).
o ↑‘Urinary urobilinogen (no urinary conjugated bilirubin).
o ↑‘Serum lactic dehydrogenase (LDH), as released from the RBC.
Is there increased red cell production?
o ↑‘Reticulocytes, causing ↑‘MCV (reticulocytes are large immature RBCs) and
polychromasia.
Is the haemolysis mainly extra- or intravascular?
Extravascular haemolysis may lead to splenic hypertrophy and splenomegaly. Features of
intravascular haemolysis are:
o ↑‘Free plasma haemoglobin: released from RBCs.
78
o Methaemalbuminaemia: some free Hb is broken down in the circulation to produce haem
and globin; haem combines with albumin to make methaemalbumin.
o ↑“Plasma haptoglobin: mops up free plasma Hb, then removed by the liver.
o Haemoglobinuria: causes red-brown urine, in absence of red blood cells.
o Haemosiderinuria: occurs when haptoglobin binding capacity is exceeded, causing free
Hb to be filtered by the renal glomeruli, absorption of free Hb via the renal tubules and
storage in the tubular cells as haemosiderin.
Investigations of spherocytosis? See below
Investigations of sickle cell anemia? See below.
Investigations of G6PD? See below.
Investigations of thalassemia?. See below.
U Investigations of haemolytic anemia
I. For diagnosis of hemolytic anemia:
1. CBC:
Normocyte normochromic anemia with normal MCV & normal MCHC.
Macrocytic anemia may occur in megaloblastic crisis or in severe reticulocytosis.
Microcytic hypochromic anemia may occur in case of thalassemia.
Reticulocyte count: High ......... this is the rule.
Reticulocyte count: Low ......... in aplastic crisis.
Blood film may reveal characteristic red cells, e.g. sickle cells, spherocytes.
WBC's & platelets usually normal, BUT may t due to hyperactive BM.
2. Bone marrow examination:
Hyperplastic BM: this is the rule. 3. Measure of life span of RBCs:
Hypoplastic BM: in aplastic crisis. "using Cr - labeled red cells "
Megaloblastic BM: in megaloblastic crisis. Shortened life span of RBCs.
4. Bile pigments: 5. Increased serum LDH.
Serum bilirubin: increased mainly the indirect
Stools: increased stercobilinogen
Urine: increased urobilinogen, absent bilirubin.
II. For diff. bet. Intravascular & Extravascular haemolysis:
Investigations
80
decreased red cell indices ( MCV , MCHC ) = Micro..Hypchromico
- WBC : usually normal
Eosinphilia if ancylostoma infection
- Platelets : usually normal
2- Bone marrow examination
Erythroid hyperplasia
Decreased iron stores in the bm 's macrophages
3- Evidence of iron deficiency
decreased ………...serum iron , stored iron (ferrtin) .
iron carrier ptn (transferring saturation )
increased………....TIBC (total iron binding capacity)
FEP ( free erythrocyte protoporphyrin)
4- 5-
Test Result
Decreased 4- Achlorohydria - Stomach function test - ↓↓ HCl
absorption 5- Malabsorption - Stool -↑↑ fats (steatorrhoea)
syndrome - Urine (D-Xylose - Urine collecres after 5 hrs
test) show < 5gm D-xylose
- Malabsorption pattern
- Ba follow through - diagnostic
- Jeujenal biopsy
6-7-8
Test Result
Increased 6- Hge bl. disease Purpura Haemophilia
loss Platelet count -- N
Bleeding time ++ N
Hiss test +ve -ve
Clotting time N ++
APTT N ++
7- GIT bleeding - Stool - occult blood / ancylostoma
- Endoscopy - oesophagoscopy ,
gasroduodnoscopy , colonscopy
- Ba follow Ba enema , Ba meal
through - arteriography , radioisotope scan
- Bleeding
8- Ancylostoma - Blood - eosinophilia , hypoalbuminaemia
- stool - ova
Most 2 important inv. in Fe def. an.
- decreased reticulocytes
- Iron profile
Investigations of acute leukaemia?
Leukaemias are malignant disorders of the haematopoietic stem cell compartment, characteristically
associated with increased numbers of white cells in the bone marrow and/or peripheral blood. The
course of leukaemia may vary from a few days or weeks to many years, depending on the type.
NB: pluripotent stem cells Myeloid stem cells platelets, RBCs, granulocyts, monocyts.
Lymphoid stem cells T and B cells.
Investigations for acute leukaemia
1- CBC: -- HGB, -- platelets, ++ TLC with ++ blast cells (blast cells may be few in AML).
TLC usually 100,000 up to 500,000, AML's TLC count may be lower because it is mainly in
Bone marrow. Myeloblast should be differentiated from Lymphoblast by a) Auer bodies
81
present in myeloblast b) Ag myeloid are CD13, CD33 while lymphoid are CD10 (B cells)
c)karyotyping (chromosomal analysis)
2- BM aspirate or better biopsy (most vulnerable diagnosis): hypercellular BM + leukaemic
blast cells.
Investigations of CLL?
This is a monoclonal proliferation of non-functional mature B lymphocytes (T cell CLL occurs
rarely). CLL constitutes 25% of all leukaemias♂:♀ 2:1. It is a disease of the elderly, median age at
diagnosis is ~65 years.
Investigations for CLL
1- CBC: Hb normal or low; WBC raised, and may be very high; platelets normal or low
Lymphocytes increased above 5000/cmm.
2- Bone marrow. Reflects peripheral blood, often very heavily infiltrated with lymphocytes.
3- Immunoglobulins. Low or normal.
4- Immunophenotyping shows mainly CD19/20 + CD5+ B cells. They may weakly express
surface immunoglobulin. Blood count. Hb normal or low; WBC raised, and may be very
high; platelets normal or low. Blood film. Lymphocytes increased above 5 × 109/L.
5- Later: autoimmune haemolysis (+ve Commb's test),
Investigations of CML?
Chronic myeloid leukaemia is a myeloproliferative stem cell disorder resulting in proliferation of all
haematopoietic lineages but manifesting predominantly in the granulocytic series.
Investigations for CML
1- CBC: WBC ++ (often >100,000/ cmm) with whole spectrum of myeloid cells ie
neutrophils, myelocytes, basophils, eosinophils. Hb ++ or normal, platelets variable. Uric
acid ++, B12++. LDH ++.
2- BM aspirate or better biopsy: bone marrow is hypercellular. Ph found on cytogenetic
analysis of blood or bone marrow.
Causes of polycythaemia?
Primary Polycythaemia Vera
Secondary
Due to an appropriate increase in erythropoietin
o High altitude
o Lung disease
o Cardiovascular disease (right-to-left shunt)
o Heavy smoking
o Mutant high oxygen affinity haemoglobin, e.g. congenital polycythaemia
Relative ('Apparent' polycythaemia) Dehydration, Burns
Due to an inappropriate increase in erythropoietin
o Congenital: Chuvasch polycythaemia
o Renal disease: tumours, cysts
o Liver disease: hepatocellular carcinoma, cirrhosis
o Endocrine: adrenal tumours
o Tumours: cerebellar haemangioblastoma, massive uterine fibroma, bronchial carcinoma
Causes of aplastic anaemia?
Most cases are autoimmune, triggered by drugs, (viruses eg Parvovirus, hepatitis) or
irradiation. May also be inherited eg Fanconi anaemia
Pancytopenia is reduction in all the major cell lines: red cells, white cells and platelets.
Causes are due to
++ marrow production: aplastic anaemia, infiltration (eg acute leukaemia, myelodysplasia,
myeloma, lymphoma, solid tumours, TB), megaloblastic anaemia, paroxysmal nocturnal
haemoglobinuria , myelofibrosis, SLE.
++ peripheral destruction: hypersplenism.
Causes of haemophilia?
Haemophilia A: Factor VIII deficiency
82
Haemophilia B (Christmas disease): Factor IX deficiency
Causes of DIC?
Disseminated intravascular coagulation (DIC): This is pathological widespread activation of
coagulation, due to release of procoagulant agents into the circulation. Clotting factors and
platelets are consumed, with ++ risk of bleeding. Fibrin strands fill small vessels, haemolysing
passing RBCs, and fibrinolysis is also activated.
Causes: Malignancy, sepsis, trauma, obstetric: OHCS p88.
laboratory investigations of DIC? –Platelets ++ PTT ++ APTT –fibrinogen (correlates
best with severity); ++ fibrin degradation products (D-dimers). Film: broken RBCs (schistocytes).
Causes of thrombophilia? Thrombophilia is an inherited or acquired coagulopathy
predisposing to thrombosis, usually venous: DVT or PE (venous thromboembolism: VTE).
Inherited
Activated Protein c (APC) resistance/Factor V Leiden: Commonest cause of inherited
thrombophilia. Present in ~5% population, although most will not develop thrombosis. Usually
associated with a single point mutation in factor V (Factor V Leiden), so that this clotting factor is
not broken down by APC. Risk of venous thromboembolism (DVT or PE) is increased 5-fold in
patients who are heterozygous for the mutation, and 50-fold in homozygotes. Thrombotic risk is
increased in pregnancy and those on oestrogens.
Prothrombin gene mutation: Leads to high prothrombin levels and increased thrombosis due to
down-regulation of fibrinolysis, by thrombin-activated fibrinolysis inhibitor.
Protein C and Protein S deficiency: These vitamin K-dependent factors act together to cleave and
thus neutralize Factors V and VIII. Heterozygotes deficient for either protein risk thrombosis.
Skin necrosis also occurs, especially if on warfarin. Homozygous deficiency for either protein
causes neonatal purpura fulminans fatal, if untreated.
Antithrombin deficiency: Antithrombin is a co-factor of heparin, and inhibits thrombin. Less
common, affects 1 : 500. Heterozygotes' thrombotic risk is greater than Protein C or S deficiency
by ~4-fold. Homozygosity is incompatible with life.
Acquired
Causes: newer 3rd generation progesterones in the oral contraceptive pill and the antiphospholipid
syndrome (APL) when serum antiphospholipid antibodies are found (lupus anticoagulant آ±
anticardiolipin antibody) predisposing to venous and arterial thrombosis, thrombocytopenia, and
recurrent fetal loss in pregnant women. In most it is a primary disease, but it is also seen with
SLE.
Causes of thrombocytosis Platelets >450,000/L may be a reactive phenomenon, seen with
many conditions including:
Bleeding
Infection
Chronic inflammation, e.g. collagen disorders
Malignancy
Trauma
Post-surgery
Iron deficiency
Causes of purpura? See latter.
Causes of coagulopathy? See latter.
Myelofibrosis
There is hyperplasia of megakaryocytes which produce platelet derived growth factor, leading to
intense marrow fibrosis and myeloid metaplasia (haemopoiesis in the spleen and liver)→massive
hepatosplenomegaly.
The myeloproliferative disorders
These form a group of disorders caused by proliferation of a clone o
f haematopoietic myeloid stem cells in the marrow. While the cells proliferate, they also retain the
ability to differentiate into RBCs, WBCs or platelets.
83
Classification
is by the cell type which is proliferating
RBC ++ Polycythaemia rubra vera (PRV).
WBC ++ Chronic myeloid leukaemia (CML).
Platelets ++ Essential thrombocythaemia.
Fibroblasts ++ Myelofibrosis.
Philadelphia chromosome
(Ph) Present in >80% of those with CML. It is a hybrid chromosome comprising reciprocal
translocation between the long arm of chromosome 9 and the long arm of chromosome 22 (9;22)
forming a fusion gene BCR/ABL on chromosome 22, which has tyrosine kinase activity. Those
without Ph have a worse prognosis. Some patients have a masked translocation cytogenetics do
not show the Ph, but the rearrangement is detectable by molecular techniques.
Gold
penicillamine
Carbimazole
Captopril, enalapril,
nifedipine
Phenytoin, sodium
valproate,
carbamazepine
Sulphonamides,
penicillins,
cephalosporins
Ranitidine
84
Haemostatic
disorders
Purpura Coagulopathy
1. Bone marrow failure 1. Autoimmune: 1. Antiplatelet: e.g. aspirin e.g. glanzmann's disease
2. Bone marrow infilteration o 1ry → ITP 2. Autoimmune: SBE
3. Megaloblastic anemia o 2ry → SLE 3. Multipule myeloma
4. Myelodysplastic 2. Acute infection 4. uraemia
syndromes 3. Hypersplenism 5. Thrombocytosis
85
check RBCs
> 5.5 millions/mm3 4.5 - 5.5 millions / mm3 < 4.5 millions / mm3
++ WBC's >20,000 --platelets --platelets & --WBC's all normal ++coagulation time
Leukaemia Thrombocytopenia Pancytopenia Haemophilia
Check MCV, MCH
check blast cells
low high normal
++blast no blast
Microcytic Macrocytic Normocytic
Acute Chronic
hypochromic (megaloblastic) normochromic
Leukaemia Leukaemia
anemia anemia anemia
if eosinophilia If reticylocytosis
++lymphocytes ++monocytes think of → haemolytic an.
CLL CML ancylostoma
86
U
I. Tests for purpura:
1. Bleeding time: Normally: 2-4 minutes.
• Measures platelet plug formation in vivo. Cuff of sphygmomanometer for 10 minutes is
inflated at pressure 40mmHg + small incision by a pin is made then count the time needed
for bleeding to stop.
• Depends on platelets & capillaries.
• It is prolonged in purpura.
2. Platelet count: Normally: 150,000-400,000/cmm
• Reduced in thrombocytopenic purpura if <40,000/cmm bleeding may occur.
87
Basophils 0 %
Eosinophils 1 %
Staff 2 %
Segmented 15 %
Lymphocytes 80 %
Monocytes 2 %
Platelet count 250,000 /cmm
1.- Ineffective erythropoiesis is evident in all types of hemolytic anemia.
a. True b- false
2- In which of the following is the Philadelphia chromosome most likely to be found?
a. chronic lymphocytic leukemia c. acute lymphocytic leukemia
b. chronic myelogenous leukemia d. acute myelogenous leukemia
3- In which of the following situations would the platelet count be decreased:
a. in idiopathic thrombocytopenic purpura c. post splenectomy
b. in Essential Thrombocythemia d. in polycythemia rubra vera
4. Which of the following test results would most likely be seen in Hemophilia A:
a. an abnormal PT c. abnormal von Willebrand factor level
b. an abnormal Bleeding Time d. an abnormal APTT
5- What is the deficient coagulation factor in Hemophilia A:
a. F VII b. F VIII c. F I X d. F XII
Report 2
Haemoglobin 8.5 g/dl
PCV (haematocrit) 26 %
Red cell count 2,830,000 /cmn
Reticulocytic count 0.2 % -
MCV 92 fl
MCH 30 Pg
MCHC 33 g/dl
TLC 150,000 /cmn
Basophils 0 %
Eosinophils 0 %
Staff 2 %
Segmented 7 %
Lymphocytes 2 %
Monocytes 14 %
Myeloblasts 50 %
Promyelocytes 25 %
Platelet count 30,000 /cmm
88
a. increased total bilirubin c. decreased haptoglobin
b. direct bilirubin levels will remain normal d. the reticulocyte count will decrease
5-All of the following occur in intravascular hemolysis except:
a. haptoglobin levels decrease c. hemopexin levels decrease
b. methemalburnin levels increase d. serum iron levels decrease
89
TLC 96,000 /cmm
Basophils 0 %
Eosinophils 0 %
Staff 1 %
Segmented 5 %
Lymphocytes 0 %
Monocytes 1 %
Blasts 93 %
Peroxidase stain of blasts positive
Platelet count 28.000 /cmm
1.- Intrinsic factor is necessary for the absorption of:
a. folic acid b. iron c. vitamin B6 d. vitamin B12
2- Which of the following patients is most likely to have peroxidase positive blasts:
a. a child with Burkitt's leukemia/lymphoma
b. a child with acute myelogenous leukemia
c. a child with B acute lymphoblastic leukemia
d. a child with T acute lymphoblastic leukemia
3- hyperbilirubinemia is present in acute post-hemorrhagic anemia
a. true b. false
4. The red cell count is decreased in hemolytic anemia
a. true b. false
5- What is the deficient coagulation factor in Hemophilia B:
a. F VII b. F VIII c. F I X d. F X
Haemoglobin 14 g/dl
PCV (haematocrit) 44 %
Report Red cell count 4,500,000 /cm
5 Reticulocytic count 0.2 %
MCV 92 fl
MCH 30 Pg
MCHC 33 g/dl
TLC 24,000 /cmm
Basophils 0 %
Eosinophils 0 %
Neutrophils
-Band 20 %
-segmented 75 %
Lymphocytes 5 %
Monocytes 0 %
Platelet count 300,000 / cmm
1.- the reticulocyte count is increased in both acute post-hemorrhagic anemia & hemolytic anemia
a. true b. false
2- the red cell survival time is decreased in acute post-hemorrhagic anemia
a. true b. false
3-normal adult male reference range of HGB
a. 10 g/dl b. 12 g/dl c. 16 g/dl d. 20 g/dl
4-.Normocytic normochromic anemia is characterisd by
a. increase MCV b. decrease MCV c. normal MCV
5- Thalassemia causes:
90
a. Normocytic normochromic anemia c. Macrocytic hyperchromic anemia
b. Microcytic hypochromic anemia d. Aplastic anaemia
91
Lymphocytes 20 %
Monocytes 4 %
Platelet count 250,000 /cmm
Bleeding time 3 minutes
Coagulation time 15 minutes
92
5- Philadelphia chromosome is
a. present in 60% of patients with CML c. presence denotes bad prognosis
b. found in the BM d. All of the above
Report 9
Haemoglobin 7.5 g/dl
PCV (haematocrit) 25 %
Red cell count 2,400,000 /cmm
Reticulocytic count 20 %
MCV 92 fl
MCH 30 Pg
MCHC 33 g/dl
TLC 18,000 /cmm
Basophils 1 %
Eosinophils 2 %
Staff 20 %
Segmented 60 %
Lymphocytes 13 %
Monocytes 4 %
Platelet count 150 000 /cmm
Report 10
Haemoglobin 19.0 g/dl
PCV (haematocrite) 60 %
Red cell count 7,800,000 /cmm
Reticulocytic count 2 %
MCV 92 fl
MCH 30 Pg
93
MCHC 33 g/dl
TLC 20,000 /cmm
Basophils 0 %
Eosinophils 2 %
Staff 10 %
Segmented 60 %
Lymphocytes 25 %
Monocytes 3 %
Platelet count 700,000 /cmm
ESR 1st Hour 1 mm
nd
2 Hour 3 mm
1.- normal adult male reference range of PCV
a. 25 % b. 35 % c. 45% d. 55%
2-Malaria causes …. haemolysis
a. Intracorpuscular b. Extracorpuscular
3-All of the following are causes of haemolytic anemia except
a. Thalassemia b. Sickle cell anemia c. PNH d. spherocytosis
4. In polycythaemia rubra vera there is increased
a. RBC c. platelets e. All of the above
b. WBC d. a+b
5- Philadelphia chromosome is
a. present in 60% of patients with CML c. presence denotes bad prognosis
b. found in the BM d. None of the above
Report 11
Haemoglobin 11.5 g/dl
PCV (haematocrit) 35 %
Red cell count 3,800,000 /cmm
Reticulocytic count 2 %
MCV 92 fl
MCH 30 Pg
MCHC 33 g/dl
TLC 35,000 /cmm
Basophils 0 %
Eosinophils 1 %
Staff 2 %
Segmented 15 %
Lymphocytes 80 %
Monocytes 2 %
Platelet count 250,000 /cmm
1.- In thalassemia the following occur except
a. Reticulocytic count is decreased c. Microcytic hypochromic anemia
b. HB electrophoresis is important d. BM aspirate is important
2- The red cell survival time is decreased in acute post-hemorrhagic anemia
a. true b. false
3- Normal adult male reference range of HGB
a. 10 g/dl b. 12 g/dl c. 16 g/dl d. 20 g/dl
94
4- Spherocytosis is caused by
a. Congenital b. Acquired c. Both
5- ESR > 100 is caused by
a. Malignancy b. TB c. SLE d. All of the above
Answers
1. 1- b 2- b 3- a 4- d 5- b 7. 1- d 2- a 3- d 4- e 5- a
2. 1- b 2- d 3- a 4- d 5- d 8. 1- b 2- a 3- a 4- e 5- b
3. 1- c 2- a 3- d 4- d 5- e 9. 1- a 2- a 3- b 4- a 5- d
4. 1- d 2- b 3- b 4- a 5- c 10. 1- c 2- b 3- c 4- b 5- b
5. 1- a 2- b 3- c 4- c 5- b 11. 1- a 2- b 3- c 4- c 5- d
6. 1- e 2- a 3- d 4- b 5- d
95
a) True b) false
17. Blast cells that are myeloperoxidase positive and contain Auer rods most likely belong to
which cell
a) lymphoid b) AML c) ALL d) myeloma
18. Which FAB type of myelodysplastic syndrome shows less than 1% blasts in the peripheral
blood, less than 5% blasts in the bone marrow, and ringed sideroblasts in at least 15% of the
nucleated RIBC in the bone marrow
a) refractory anaemia
b) refractory anaemia with ring sideroblasts
c) refractory anaemia with excess blasts
d) refractory anaemia with excess blasts in transformation
19. All of the following are characteristic of M3 leukaemia EXCEPT:
a) the myeloperoxidase and sudan black stain are positive
b) patients may develop DIC
c) a translocation between chromosomes 15 and 17 is common
d) the predominate cell on the peripheral smear is monocyte
20. In which of the following situations the platelet count could be decreased
a) ITP c) postsplenectomy
b) essential thrombocythaemia d) polycythaemia rubra vera
21. Hyperbilirubinaemia is present in acute post-haemorrhagic anaemia
a) True b) false
22. Oral anticoagulant is monitored by
a) PT b) PC c) APTT d) INR
23. Bleeding time is prolonged in
a) Purpura c) Patient on oral anticoagulants
b) Haemophilia d) anaemias
24. ESR> 100 mm in the first hour occurs in … EXCEPT
a) breast abscess c) pulmonary TB
b) breast cancer d) lupus nephritis
25. Unfractionated heparin is monitored by
a) PT b) PC c) APTT d) INR
26. Low molecular weight heparin is monitored by
a) PTT b) INR c) both d) none
27. Evidence of intravascular haemolysis are all… EXCEPT
a) ++ free HB c) ++ metHB
b) ++ haptoglobin d) haemosiderinuria.
Answers
1) d 8) d 15) a 22) d
2) a 9) c 16) a 23) a
3) d 10) b 17) b 24) a
4) d 11) a 18) b 25) c
5) d 12) a 19) d 26) d
6) a 13) b 20) a 27) b
7) a 14) a 21) b
SEROLOGY report
I-Widal test:
Value :
Salmonella agglutination test in enteric (typhoid) fever
96
Measures body's Abs causing agglutination of Salmonella Abs .
Ag are H (flagellar) , O (somatic) , Vi ( capsular) .
Interpretation :
Positive from the second week (to detect salmonella before that do blood culture)
Positive when the titer > 180 or rising titer
Recent infection = rising Anti O or Anti Vi Ab.
Type of infection = AntiH Ab
False positive test = previous vaccination or infection
Amanasetic reaction = nonspecific reaction in fever causing rise of all types
of Anti H abs
The salmonella are detected in blood from the first week by blood culture , second week
antibodies in blood by Widal test, third week by stool and urine culture.
Drawbacks of Widal test :
Needs 2 weeks to be positive
Needs a rising titre ( not only positive)
Affected by antibiotics
Widal test
check Anti O
97
Direct : detect fixed RBCs Ab
Indirect : detect free RBCs Ab in serum (severe cases)
VII- Antibodies:
IgM (Produced first in immune response)
The antibody is confined mainly to the intravascular pool. It is a large pentameric molecule, bound
together by the joining 'J' chain. It does not cross the placenta, and is not normally produced in the child
until after birth. Therefore, if present in the newborn infant, antigen-specific IgM is a good marker for
intrauterine infection. It is usually a sign of acute infections.
IgG (Dominant class of antibody)
This is the most abundant immunoglobulin in serum, present as a monomer. IgG is the antibody of
secondary response, and has high antigen affinity. It is the only antibody to cross the placenta in
significant quantities. IgG antibody is involved in resistance to infection, as patients who are lacking in
IgG suffer with recurrent, even life-threatening bacterial infections. Those with isolated IgA or IgM
deficiency have much less severe problems.
IgA (Found in mucous membrane secretions)
This is mainly the antibody of secretions, being present in the respiratory, gastrointestinal and urinary
tracts. IgA is mainly monomeric in the serum, but dimeric in secretions, the two molecules being
complexed by a joining (J) chain. For IgA responses, localized antigen exposure gives rise to generalized
mucosal immunity, which is of importance in vaccination. This is because after encountering antigen, IgA
precursor B cells in the mucosal lymphoid follicles journey to regional lymph nodes. After clonal
expansion the cells return to the systemic circulation via the thoracic duct and circulate to settle widely in
the mucosa-associated lymphoid tissue (MALT, not just the area where antigen exposure occurred.
IgD (Found almost solely on lymphocyte membrane)
Serum levels are very low and its function at this site is uncertain.
IgE (Responsible for symptoms of allergy; used in defence against nematode)
IgE is a monomer that is normally present in very low levels in serum, as most is membrane-bound to the
high-affinity receptors on mast cells and basophils. Its main physiological role is its antinematode
(parasites) activity, but its most common clinical relevance is in the pathogenesis of type 1
hypersensitivity (atopic or allergic) disease.
VIII- autoimmune profile:
Plasma autoantibodies (Abs): disease associations. Always interpret in the context of clinical findings:
Rheumatological
ANA antinucleic antibody in most of autoimmune disease.
Rheumatoid Factor (RhF): +ve in (%)
Sjogren's syndrome 100% Mixed connective tissue disease 50%
Felty's syndrome 100% SLE 40%
RA 70% Systemic sclerosis 30%
Infection (endocarditis, Hepatitis)50% Normal 2-10%
Rheumatoid factor measured by Rose-Waaler , Bentonite ,Latex test. It is an antibody against
immunoglobulin
Anti-histone Ab: Drug-induced SLE (~100%).
Anti-double stranded DNA (dsDNA): SLE (60%, more specific than ANA).
Anti-phospholipid Ab (eg anti-cardiolipin Ab): antiphospholipid syndrome, SLE.
Anti-centromere Ab: limited systemic sclerosis.
Anti-extractable nuclear antigen (ENA) antibodies (usually with +ve ANA)
Anti-Ro (SSA): SLE, Sjogren's syndrome, systemic sclerosis. Associated with congenital heart
block. Associated with congenital heart block
Anti-La (SSB): Sjogren's syndrome, SLE (15%).
Anti-Sm: SLE (20-30%)
Anti-RNP: SLE, mixed connective tissue disease.
Anti Jo-1; Anti-Mi-2: Polymyositis, dermatomyositis.
98
Anti-Scl70: Diffuse systemic sclerosis.
GastroIntestinal
Anti-mitochondrial Ab (AMA): Primary biliary cirrhosis (PBC: >95%). Also: autoimmune
hepatitis (30%), idiopathic cirrhosis (25-30%).
Anti-smooth muscle Ab (SMA): Autoimmune hepatitis (70%), PBC (50%), idiopathic cirrhosis
(25-30%).
Gastric parietal cell Ab: Pernicious anaemia (>90%), atrophic gastritis (40%). Also: autoimmune
thyroid disease (40%), normal controls (10-15%).
Intrinsic factor Ab: Pernicious anaemia (50%).
gliadin Ab, anti-tissue transglutaminase, anti-endomysial Ab: Coeliac disease.
Endocrine
Thyroid peroxidase Ab (TPO): Hashimoto's thyroiditis (80-95%), Graves' (50-80%).
Islet cell Ab (ICA), glutamic acid decarboxylase (GAD) Ab: Type 1 DM (75%).
Renal
Glomerular basement membrane Ab (GBM): Goodpasture's syndrome.
Anti-neutrophil cytoplasmic Ab (ANCA): vasculitis
Neuromuscular
Acetylcholine receptor (ACR) Ab: Myasthenia gravis (90%).
Consumed C3 and C4 and ESR > 100 also indicate autoimmune activity.
Typhus are tested by Weil-Felix test.
Report 1
Anti-O : 1/80. Anti-H para-A : 1/80.
Anti-H typhoid: 1/80. Anti-H para-B : 1/80
1-Normal Anti O titre is 1/80 d. Non of the above
a. true 4-Increased Anti O Ab titre means
b. False. a. Recent infection
2.- Widal test is positive from the b. Amenestic reaction
a. Frist week c. both
b. Second week d. none of the above
c. Third week 5-The diagnosis is
d. Fourth week a. Recent typhoid infection.
3- The H antigen is b. Recent para-typhi A infection.
a. flagellar antigen c. Old para-typhi B infection
b. Somatic antigen d. Vaccinated person
c. Capsular antigen
Report 2
Anti-O : 1/240. Anti-H para-A : 1 / 80.
Anti-H typhoid: 1/240. Anti-H para-B : 1 / 80
1- Normal Anti H typhoid titre is d. droplet
1/80 4- Blood culture for salmonella is positive
a. True . during the
b. False. a. Frist 2 week
2.- False positive Widal test occurs in b. Second 2 week
a. Previous infection c. Third 2 week
b. Past vaccination d. Fourth 2week
c. Both 5-The diagnosis is
d. none of the above a. Recent typhoid infection.
3- Typhoid is transmitted by b. Recent para-typhi A infection.
a. injection c. Old para-typhi B infection
b. sexual
c. feco-oral
d. Vaccinated person
Report 3
99
Anti-O : 1/240. Anti-H para-A : 1/240.
Anti-H para-B : 1 / 80
Anti-H typhoid: 1 / 40.
1- Normal Anti H paratyphoid A titre is 4- Which type of theses Abs rise frist during
1/80 an immune reaction
a. True . a. Ig A
b. False. b. Ig G
2.- positive Widal if c. Ig M
a. Rising titre
b. Titre>1/80
d. Ig D
c. Titre>1>160 e. Ig E
d. All of the above 5-The diagnosis is
3.- Stool culture is positive during a. Recent typhoid infection.
a. Frist - Second week b. Recent para-typhi A infection.
b. Second - Fourth week c. Old para-typhi B infection
c. Fourth -Fifth week d. Vaccinated person
Report 4
Anti-O : 1 / 80. Anti-H para-A : 1/160.
Anti-H typhoid: 1/160. Anti-H para-B : 1/160
1- Normal Anti H paratyphoid B titre is d. Hydate disease
1/80 4- Increased Anti O Ab titre means
a. True . a. Recent infection
b. False. b. Amenestic reaction
2.- Widal test is positive from the c. a or b
a. Frist week
b. Second week
d. none of the above
5- The diagnosis is
c. Third week
d. Fourth week a. Recent typhoid infection.
3. Casoni test is done for b. Recent para-typhi A infection.
a. Salmonella c. Old para-typhi B infection
b. TB d. Vaccinated person
c. Taenia saginata
Questions
1- Recent vaccination elevates c) 1 samples 10 days apart from first week
a) Anti-O d) 1 samples 10 days apart from second
b) Anti-H week
c) both 4- Widal antibodies
d) none a) Anti-H rises early and disappears late
2- Recent infection increases b) Anti-O rises early and disappears late
a) Anti-O c) Anti-O rises early and disappears late
b) Anti-H d) None of the above
c) Both 5- Detection of salmonella in the first week
d) none a) Blood culture
3- Ideal method of Widal sampling b) Stool culture
a) 2 samples 10 days apart from first week c) Widal test
b) 2 samples 10 days apart from second d) None of the above
week
ANSWERS
1 2 3 4 5
Report 1
Report 2
Report 3
Report 4
100
1- To which of the following classes of immunoglobulins do the allergy-mediated antibodies
belong
a) IgA c) IgM e) IgE
b) Ig G d) IgD
2- Which of the following antibody classes is the frist to be produce in an immune response to a
given antigen?
a) IgA c) IgM e) IgE
b) Ig G d) IgD
3- In the most of normal persons; what is the percentage of IgG in the whole
immunoglobulins?
a) 10% c) 50% e) Over 70%
b) 25% d) 60%
4- Which one of the following immunoglobulins is the principle immunoglobulin exocrine
secretion?
a) IgA c) IgM e) IgE
b) Ig G d) IgD
5- Which of the following statements about IgM is true?
a) it is reaginic antibody
b) it is important in the first few days of the primary immune response
c) it increases in serum concentration after IgG has reached its peak serum concentration
d) it is the smallest of the immunoglobulin molecules
e) it is involved in allergic reactions
6- Actively acquired immunity can be caused by all of the following EXCEPT?
a) The specific disease.
b) Exposure to subclinical doses of the disease causing organism
c) Vaccination with appropriate antigen.
d) Injection with immune serum containing appropriate antibodies.
7- Which of the following substances may be passively transferred from the mother to the fetus
during the third trimester
a) IgG c) Anti-Rh antibody
b) IgM d) Natural isohaemagglutinis
Answers
1) e 3) e 5) b 7) a
2) c 4) a 6) d
Report 1
Widal test
Anti-H para-A: negative. Anti-O: negative.
Anti-H para-B: negative Anti-H typhoid: 1/40.
Monospot test: negative Brucella (latex):positive
1- Titer of brucella agg. > 1/160 indicates a. acute brucellosis
chronic brucellosis b. chronic brucellosis
a. True . c. both
b. False. d. None of the above
2.- Brucella is characterized by 4- Dick test is done for
a. Aplastic anemia a. Salmonella
b. polycythaemia b. Scarlet fever
c. leucocytosis c. Taenia saginata
d. leucopenia d. Hydate disease
3- Elisa test is done for
101
5- Which of the following is passively b. IgM
transmitted from a mother to her foetus during c. Anti-Rh antibodies
pregnancy d. Natural isohaemoagglutinins
a. IgG
Report 2
ESR:
1sthour 54 mm
nd
2 hour 82 mm
Rheumatoid Factor:
Latex Positive
Rose Waaler 64 DAT (up to 16) up to 16)
ASO: 125 Todd Units (up to 250) up to 166)
CRP: Positive
ESR Increased
ASO 100 Todd,s units
ANA Positive
103
■ Its presence indicates high infectivity.
■ Its persistence more than 3 months indicates chronicity
6 .HBeAb (Anti - HBe antibodies):
■ Its presence indicates low infectivity
7. PCR for HBV DNA:
■ It is the most sensitive index for viral replication.
Summary
Incubational period: HBsAg, HBcAb IgM.
Acute hepatitis: as incubational period + HBcAb IgG.
Post-infection immunization: HBsAb + HBcAb IgG
Postvaccination immunization: HBsAb only.
Chronic infection: HBsAg + HBcAb IgG.
Follow up viral ttt therapy: HBV DNA PCR + HBVeAg + liver enzymes.
Window phase HBcAb are positive and the rest are negative
104
Acute hepatitis
Hepatitis A Hepatitis C
Early recovery
105
Report 1
Urine analysis
NORMAL VALUES
1-Volume 500 - 1500 cc /day
2-Colour - aspect: amber yellow , clear
3-Specific gravity: 1015 - 1025
4-Reaction "pH" : acidic - 5.5 - 6.5
5-Chemical contents :
a-Nitrogenous: urea, creatinine, uric ammonium.
b-Non nitrogenous : ketone & glucose are absent
c-Enzymes & small MW proteins
6-Microscopic examination :
a-Cells : RBCs : N: 0 - 4 / HPF -Pus cells : N: 0 - 4 / HPF
b-Bacteria - parasites - ova : absent
c-Casts
d-Crystals : - Acidic urine : ca oxalate, uric acid.
- Alkaline urine : phosphate
a) Volume of urine:
Polyuria: ++ urine volume more than 1500 CC / 24h: ++ fluid intake, DM, DI.
Oliguria: -- urine volume less than 400 CC / 24h.
Causes:
Prerenal causes as shock, dehydration
Renal causes as ARF, CRF, Acute GN.
Postrenal cause: obstructive uropathy
b) Aspect: Turbid in infection or phosphate or urate deposits.
c) Colour:
pale yellow if diluted
Red in bleeding, Rifampicin.
pigments as vitamin B complex … dark yellow
Green yellow in infection.
107
Black in metastatic melanoma or phenol derivatives.
Milky urine due to rupture of lymphatics, sever infection, phosphate.
d) Specific gravity:
It depends on amount of solute and volume of urine.
e) Urinary casts: coagulated protein cast formed in tubular lumen
Red casts in nephritic syndrome.
Fatty casts in nephrotic syndrome.
f) Sterile pyuria: no culture on ordinary culture media despite the presence of pus cells in urine >
10/HPF (high power field).
Causes:
Renal TB Recent antimicrobial therapy
Female genital tract infection Prostatitis
Non-gonnocal urtheritis Renal neoplasms, calculi.
Infection by anaerobic bacteria
.
108
Check urine volume ( N: 800 - 1500 ml / day )
Nephrotic
Turbid (aspect) Reddish (colour) Brown or dark red (colour) syndrome
Acute
Haematuria Jaundice Obstructive Bilirubin Urobilinogen
pyelonephritis
Examples
+ pus cells Haemolytic Bilirubin Urobilinogen
Jaundice
Hepatocellular
Jaundice Bilirubin Urobilinogen
109
Jaundice
Jaundice
# Answers of urine analysis reports
Report 1: Urinary infection in diabetic patient.
Report 2: Urinary infection.
Volume 100 ml 200 ml 4000 2500 3500 500 ml/24h
101 (Random 201 (Random ml/24h ml/24h ml/241
Colour Amber yellowsam Amber yellowamp Pale yellow Pale yellow Pale Smoky
Reaction Alkaline ple) Acidic le) Alkaline Acidic Acidic Acidic
Specific Gravity 1030 1025 1002 1040 1010 1035
Aspect Turbid Turbid Clear Clear Clear Clear
Protein + ++ Nil + + +
Sugar + Nil Nil ++++ Nil Nil
Acetone Nil Nil Nil Nil Nil Nil
Bile Pigment Nil Nil Nil Nil Nil Nil
Urobilinogen Normal trace Normal trace Normal trace Normal trace Normal trace Normal trace
Epithelial Cells + ++ Nil + Nil +
Pus Cells 15-20 > 100 0-1 1-3 0-1 1-5
RBC's 8-10
/HPF 2-3
/HPF 0-1
/HPF 0-1
/HPF 0-1
/HPF 10-20
Crystals Amorphous Nil /HPF
Nil Nil Nil Nil
phosphate
Triple phosphate
Casts Nil Nil Nil Hyaline Hyaline & Red Casts
Ova Nil Nil Nil Nil granular
Nil Nil
Report 3: Diabetes insipidus or functional polyurea.
Report 4: Diabetic proteinuria.
Report 5: Chronic renal failure or, Diuretic stage of acute renal failure.
Report 6: Nephritic syndrome.
110
Examples
Volume 1000 1400 2500 500 ml/24 600 3500
ml/24h ml/24 hours ml/24 hours hours ml/24 hours ml/24 hours
Colour Amber yellow Brown Pale yellow Amber yellow Smoky Watery
Reaction Alkaline Alkaline Alkaline Acidic Alkaline Alkaline
Specific Gravity 1025 1018 1040 1035 1010 1010
Aspect Turbid Clear Clear Clear Clear Clear
Protein + + +++ Nil + +
Sugar Nil Nil ++++ Nil Nil Nil
Acetone Nil Nil Nil Nil Nil Nil
Bile Pigment Nil ++ Nil Nil Nil Nil
Urobilinogen Normal trace Normal trace Normal trace Normal trace Normal trace Normal trace
Epithelial Cells + + Nil NIL + Nil
Pus Cells 15-20 /HPF 0-1 /HPF 1-3 1-3 3-5 35-40
RBC's 3-5
/HPF /HPF 0-1 /HPF 1-3
/HPF 1-3
/HPF 25-30
/HPF 5-7
/HPF
Crystals Nil Nil Nil /HPF
Nil Nil /HPF
Nil
Casts Hyaline & White Hyaline Hyaline & Fatty Nil Hyaline, Red cell Hyaline, White
Ova cell
Nil Nil Casts
Nil Nil & Granular Casts Nil
Nil cell & granular
Casts
Bile salts
# Answers of urine analysis reports
Report 1:Pyelonephritis.
Report 2:Cholestasis..
Report 3:Diabetic nephrosis (KW
syndrome)..
Report 4:Pre-renal uraemia or functional
oliguria.
Report 5: Acute renal failure (Acute tubular necrosis).
Report 6:Chronic pyelonephritis & chronic renal failure.
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Report 1
Volume 1000 ml/24h
Colour Amber yellow
Reaction Alkaline
Specific Gravity 1025
Aspect Turbid
Protein +
Sugar Nil
Acetone Nil
Bile Pigment Nil
Urobilinogen Normal trace
Epithelial Cells +
Pus Cells 15-20 /HPF /HPF
RBCs 3-5 /HPF
Crystals Nil
Casts Hyaline & White cell
Ova Nil
1-What is your diagnosis:
a) Acute nephritic syndrome. c) nephrotic syndrome
b) Chronic renal failure d) pyelonephritis
2- increased urine volume occurs in all …. except:
a) D.M. c) Chronic renal failure.
b) D. insipidus d) acute Renal failure
3- haematuria occurs in …except
a- Acute nephritic syndrome. c- bilharsiasis
b- Crystals d- Nephrotic syndrome
4- Turbid urine indicates
a- Acute nephritic syndrome. c- nephrotic syndrome
b- pyelonephritis d- All of the above.
5- proteinuria occurs in
a- Nephrotic syndrome c- Acute pyelonephritis
b- Chronic G.N. d- All of the above
Report 2 Volume 4000 ml/24h
Colour Pale yellow
Reaction Alkaline
Specific Gravity 1002
Aspect Clear
Protein Nil
Sugar Nil
Acetone Nil
Bile Pigment Nil
Urobilinogen Normal trace
Epithelial Cells Nil
Pus Cells 0-1 /HPF
RBCs 0-1 /HPF
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Crystals Nil
Casts Nil
Ova Nil
1-What is your diagnosis:
a-- Acute nephritic syndrome. c- Diabetes iinsipidus
b- Chronic renal failure d- pyelonephritis
2- The cause is in :
a-- Pituitary gland. b- Kidney c- both d- none
3- investigation needed is
a- serum ADH. c- both
b- serum insulin level d- none
4- Very low specific gravity occurs in
a-- D.M. c- ch. Renal failure
b- D. insipidus d- acute Renal failure
5- Anuria characterized by all except
a- means complete absence of urine output for more than 12-24 hours
b- occurs in bilateral ureteric obstruction
c- occurs in renal failure d- occurs in nephotic syndrome
1- d 2- d 3- d 4- b 5- d 1- c 2- c 3- c 4- b 5- d
CSF profile
The pressure: (N: 80-120 mm CSF)
1. Causes of high pressure:
- Meningitis. - Brain tumour & abscess.
- Haemorrhage. - Idiopathic increased ICT
2. Causes of low pressure:
- Subarachnoid block. - Excessive CSF aspiration.
The colour & aspect (N: clear & colourless):
1. Red: in haemorrhage.
2. Yellow:
- After subarachnoid haemorrhage. - Subarachnoid block.
3. Turbid: in meningitis.
The proteins (N:20-40 mg/dl):
1. High with excessive WBCs: in meningitis.
2. High with excessive RBCs: in haemorrhage.
3. High with normal cells: in "cyto-albuminous dissociation":
- Subarachnoid block. - Multiple sclerosis.
- Infective polyneuritis. - Some brain tumours as acoustic neuroma.
The cells (N: no cells):
1. Neutrophils: in septic meningitis. meningitis.
2. Lymphocytes: in tuberculous & viral 3. RBCs in haemorrhage.
The sugar (N: 40-80 mg/dl):
1. It is low in meningitis especially septic type.
2. It is high in diabetes and haemorrhage.
The chlorides (N: 115-130 mmol/L).
1. It is low in meningitis especially tuberculous.
2. It may be high in uraemia.
Froin tirade (Occurs in extramedullary block in paraplegia)
1) Spontaneous coagulation
2) Xanthochromia
3) Cytoalbuminous diss. ( ++ ptn , N. cell count )
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T.B Septic Viral Extrmed. Intramed.
- pressure Increased Normal decreased increased
- Colour Turbid Clear Yellow Clear red
/ aspect (xanthoch.)
- ptn ++ ++++ ++ ++
- chloride -- N N N
- sugar -- N N N
- cells Lymph. PMN Lymph. N RBC
- Culture +ve +ve -ve No organism
Septic = pyogenic meningitis is caused by meningococcal.
Check colour/aspect
Check sugar/cells
Normal sugar
-- Sugar -- Sugar ++ Lymphocytes
++ Lymphocytes ++ PMN
Intramedullary Viral
T.B. Septic block meningitis
meningitis meningitis
Examples
Septic (pyogenic) meningitis
Aspect Turbid
Colour Colourless
Protein 150 mg/dl (15-45mg/dl)
Sugar 5 mg/dl (45-80 mg/dl)
Chloride 115 mmol/1 (115-130 mmol/1)
Cells 300 Cell/ul (Polymorph nuclear)
Viral meningitis
Aspect Clear
Colour Colourless
Protein 40 mg/dl (15-45 mg/dl)
Sugar 60 mg/dl (45-80 mg/dl)
Chloride 125 mmol/1 (115-130 mmol/I)
Cells 90 Cell/ul (Lymphocytes)
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Extramedullary block
Aspect Clear
Colour Xanthochromic
Protein 200 mg/dl (15-45 mg/dl)
Sugar 65 mg/dl (45-80 mg/dl)
Chloride 120 mmol/1 (115-130 mmol/I)
Cells 5 Cell/ul (mononuclear)
1- In septic meningitis the CSF shows:
a- Decreased chloride. b- Increased sugar. c- Increased lymphocyte.
d- Increased PMN (polymorph nuclear leucocytes).
2- The following precutions must be done during CSF aspirate procedure except:
a- The procedure is done under complete aseptic conditions.
b- The sample must be put in sterile tube and taken immediately to the lab and not leave it in the
fridge.
c- The sample must be put in the three sterile tubes.
3- Increased lymphocytes in
a- Septic meningitis meningitis d- A+B.
b- Tuberculous c- Viral meningitis. e- B+C.
4- In viral meningitis the CSF shows:
a- Decreased chloride. b- Increased sugar. c- Increased lymphocyte.
d- Increased PMN (polymorph nuclear leucocytes).
5- Decreased pressure occurs in
a- Septic meningitis c- Viral meningitis.
b- Tuberculous meningitis d- Paraplegia.
6- Pyogenic meningitis differ from TB meningitis in
a- pressure c- colour of CSF e- amount of sugar
b- cellular type d- amount of ptn
7- Viral meningitis shows increased ptn and decreased chloride
a- True b- False
8- Negative culture of CSF occurs in
a- Septic meningitis b- Tuberculous meningitis c- Viral meningitis.
9- Clear CSF occurs in
a- Septic meningitis b- Tuberculous meningitis c- Viral meningitis.
1- d 2- c 3- e 4- d 5- d 6- b 7- b 8- c 9- c
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stool analysis
1- Volume :
- < 200 gm / day ( unless excess dietary fibers are ingested )
-Diarrhea = loose stool, frequent motion > 4 times / d. or both
-Constipation = infrequent bowel evacuation (> 48 hr.) + passage of hard small stools
2- Consistency : soft, well formed
3- Colour : light to dark down
4- Odour : fecal (not offensive)
5- Reaction : alkaline
6- Contents : - mucus , pus , RBC : absent
- fat < 6 gm / day
Normal Increased
> 6 gm / day or > 25 % of total weight
Check mucus & pus cells
Malabsorption
syndrome
check split/unsplit fats
Intestinal Maldigestion
Malabsorption (pancreatic -
syndrome hepatobiliary
)
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Stool Report
Diagnosis Normal Amebic Bacillary
dysentery dysentery Malabsorption Maldigestion
(intestinal) (pancreatic - hepatobiliary)
Contents
-Mucus - excess slight + slight + slight +
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LIVER FUNCTION TESTS
1- Bile pigments & salts tests
Bile pigments & salts
120
SUMMARY of LIVER FUNCTION TESTS
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Total Bilirubin 0.85 mg/dl (N: 0.1-1.0)
Direct Bilirubin 0.35 mg/dl (N: 0.0-0.25)
AST 95 U/L (N: 0-37)
ALT 5 U/L (N:0-40)
ALP 140 U/L (N: 40-117)
Total Protein 7.4 g/dl (N: 7-9)
Albumin 2.9 g/dl (N: 3.5-5.5)
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Total Bilirubin 0.88 mg/dl (N: 0.1-1.0)
Direct Bilirubin 0.35 mg/dl (N: 0.0-0.25)
AST 95 U/L (N: 0-37)
ALT 57 U/L (N:0-40)
ALP 140 U/L (N: 40-117)
Total Protein 7.4 g/dl (N: 7-9)
Albumin 2.9 g/dl (N: 3.5-5.5)
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Normal Nephrotic syndrome CRF
Blood urea 10-50 mg/dl Normal 250
Serum creatinine 0.5-1.5 mg/dl Normal 10
Serum uric acid 3.5-7 mg/dl Normal
Serum phosphorus 2.5-5.0 mg/dl Normal
Serum calcium 8.5-10.5 mg/dl Normal
Serum Na 135-145 mmol/L Normal
Serum K 3.5-5.2 mmol/L Normal
Serum Glucose 70-110 mg/d1 Normal
Serum total protein 6.6-8.6 mg/d1 Normal normal
Serum albumin 3.5-5.6 mg/d1 2.3 normal
Serum cholesterol 100-250 mg/dl 350
Kidney profile
Nephrotic Chronic
syndrome renal failure
- Serum albumin < 2.3 - Blood urea > 250
- Serum cholesterol > 350 - Serum creatinine > 10
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Nephritic syndrome Nephrotic syndrome Acute renal failure Chronic renal failure
1-Urine analysis
- Gross
1) Volume Oliguria Normal Oliguria<400ml/day, upto Polyuria3-4L/day,then
2) Aspect, colour Smoky/dark/haematuria Frothy, amber yellow anuria oliguria
3) Sp. Gravity Increased Increased Dark بول غامق مركز Pale بول فاتح مخفف
4) pH Acidic Low+fixed 1010 in ATN Low+fixed 1010 in ATN
5) ptn ptnuria < 3.5 gm/day Heavy ptnuria >3.5
- Microscopic gm/day Mild ptnuria Mild ptnuria
6) cells RBC most imp.
7) casts Red cell most imp. Epith. + RBC
Lipid v. specific to it. Granular v. specific to it Broad casts specific to it
2-Kidney funct. IMPAIRED
- urea, creatinine , urea , creatinine normal unless renal
uric acid may . failure occurs
- creat. clearance ( -- GFR ) ,, ,, ,, ,,
3-Biopsy. If prolonged case To see the pathology If persistent ARF > 4 weeks Reveals pathology
4-Radiology Normal Normal PUT , U/S in postrenal obst.
5-C&S if pus Normal Normal Normal Normal
cells
6-Bl. Electrolyte
- K
+
, H+ N -- K+ ++ K+ & ++ H+ As ARF but
+
- Na , HCO
-
O -- Na+ -- Na+ & - - HCO- Variable Na+
2+
- Ca , P
3+
R -- Ca2+ -- Ca2+ & ++ P3+ & hyperlipidaemia
- ptn M -- mainly albumin
- lipids AL ++Chlolest. / TGA
7-CBC Anemia(--ptn) ,++ESR Anemia(--ptn) Anemia Anemia(--erythropoetin)
Nephritic syndrome = 1) oliguria 2) nephritic oedema 3) HTN 4) haematuria
Nephrotic syndrome = 1) heavy ptnuria 2) hypoalbuminaemia 3) generalized oedema 4) hyperlipidaemia
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Report 1
Blood urea 250 mg/dl N 10-50mg/dl
Serum creatinine 10.5 mg/dl N 0.4-1.4 mg/dl
Serum uric acid 9.0 mg/dl N 3.2-7mg/dl
Serum phosphorus 7.0 mg/dl N 2.5-5.0 mg/dl
Serum calcium 7.1 mg/dl N 8.5-10.5 mg/dl
Serum Na 139 mmol/1 N 135-145 mmol/1
Serum K 5.8 mmol/1 N 3.5-5.2 mmol/1
Serum Glucose 96 mmol/1 N 70-110 mmol/1
Serum total protein 7 mmol/1 N 6.6-8.6 mmol/1
Serum albumin 4.6 mmol/1 N 3.5-5.6 mmol/1
Serum cholesterol 150 mg/dl N 100-250 mg/dl
1-Serum creatinine
a- Is affected by liver disease c- Always elevated in nephrotic syndrome
b- Mainly endogenous in origin d- Not related to muscle mass
2- What is your diagnosis:
a-- Acute nephritic syndrome. b- Chronic renal failure
c- Nephrotic syndrome d- Chronic active hepatitis
3-In chronic renal failure:
a- Serum creatinine and uric acid are increases hypophosphataemia
b-There is metabolic alkalosis d-Serum AST and ALT are always elevated.
c-There is hypocalcemia and
4- Serum urea:
a- Is mainly excreted through GIT d-Its rate of synthesis does not depend on
b- Increases in chronic renal failure exogenous intake of nitrogen
c- Is higher in females than males
5- In nephrotic syndrome:
a- There is hypoalbuminaemia and proteinuria Less than 3 g/day
b- There is hypoalbuminaemia and hypocholesterolaemia
c- There is heavy proteinuria and hypoalbuminaemia
d- Increased urea and creatinine is a constant feature
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1- In nephrotic syndrome:
a- Cholesterol is usually increased c- urea and creatinine are affected early
b- Heavy proteinuria is a cardinal symptom d- All of the above
2- What is your diagnosis:
a- Acute nephritic syndrome. c- Nephrotic syndrome
b- Chronic renal failure d- Chronic active hepatitis
3-In acute nephritic syndrome:
a- Serum creatinine and uric acid are increased glomerulonephritis
b- ASO titre may be elevated d- All of the above.
c- RBC casts are highly suggestive of
4- Serum urea:
a- Is mainly excreted through GIT d-Its rate of synthesis does not depend on
b- Increases in chronic renal failure exogenous intake of nitrogen
c- Is higher in females than males
5- In nephrotic syndrome:
a- There is hypoalbuminaemia and proteinuria Less than 3 g/day
b- There is hypoalbuminaemia and hypocholesterolaemia
c- There is heavy proteinuria and hypoalbuminaemia
d- Increased urea and creatinine is a constant feature
1. 1- b 2- b 3- a 4- b 5- c 2. 1- d 2- b 3- d 4- b 5- c
Check FPG
check FPG
70-110 >126
>126 >200
check 1 hrs PPG check 2 hrs PPG
(peak) D.M.
70- 140 140-200
<160 160 >160
IFG IGT
Flat Lag
curve curve
check urine
glucose absent
Renal Normal
glycosuria
130
Examples
Blood sugar Urine Sugar Acetone
IGT Fasting: 130 mg/dl Nil Nil
30 min: 180 mg/dl Nil Nil
60 min: 170 mg/dl Nil Nil
90 min: 170 mg/dl Nil Nil
120 min: 150 mg/dl Nil Nil
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thyroid profile
Check FT3
Increased Decreased
+ low TSH
Check TSH
Primary
hyperthyroidism Increased Decreased
Primary Secondary
hypothyroidism hypothyroidism
Examples
1. Primary hypothyroidism. 3. Hyperthyroidism (primary).
FT3 0.4pg/dl (N: 1.3-5.0) . FT3 6.7 pg/dl (N: 1.3-5.0).
FT4 0.2 pg/dl (N: 0.8-2.0).
FT4 4.9 pg/dl (N: 0.8-2.0).
TSH 85 IU/ml (N: 0.3-5.0).
TSH 0.01 IU/ml (N: 0.3-5.0).
2. Pituitary hypothyroidism.
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2- Increased serum T3 & T4 with increased serum TSH is a charecteristic of
a- Primary hypothyroidism c- Primary Hyperthyroidism.
b- Secondary hypothyroidism d- Secondary hyperthyroidism
3- To differntiate Primary from Secondary hypothyroidism the following test is
done
a- Fee T3 b- Free T4 c- TSH d- PTH
4- FT4 is better than total T4 beacause it is affected by
a- Fasting c- Blood glucose level
b- Plasma ptn d- Muscle mass
5- In thyrotxicosis oral glucose tolerance test is
a- Flat curve c- Lag curve
b- Diabetic curve d- Normal curve
ANSWERS 1- c 2- a 3- c 4- b 5- c
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check CK-MB
> 40 N : 20
Check AST
AMI
Within 3 days <23 Decreased
AMI OMI
Within 2 weeks Within 2 weeks
U diagnosis of ami
1- TYPICAL chest pain of infarction U importance of enzymes
2- ECG 1- Confirm diagnosis
3- Cardiac enzymes 2- Timing of infarction
3- Detect the efficacy of the ttt
Changes in plasma enzyme
concentrations after myocardial
infarction. Creatine kinase (CK) and
troponin T (TnT) are the first to rise,
followed by aspartate
aminotransferase (AST) and then
lactate (hydroxybutyrate)
dehydrogenase (LDH). In patients
treated with a thrombolytic agent,
reperfusion is usually accompanied
by a rapid rise in plasma creatine
kinase (curve CK (R)) due to a
washout effect; if there is no
reperfusion, the rise is less rapid but
the area under the curve is often
greater (curve CK (N)).
134
2- One of the following plasma enzymes is frequently abnormal in acute myocardial
infarction:
a- Alkaline phosphatase c- LDH
b- Amylase d- Glucose-6-phosphate dehydrogenase.
3- In patients with acute myocardial infarction:
a- AST is the first enzyme to return to normal
b- After one week LDH is still elevated.
c- CK-MB reaches its peak after one week.
d- CK starts to rise 3 days after the pain.
4- This cardiac profile probably belongs to a case of :
a- Angina pectoris c- Recent myocardial infarction
b- Unstable angina d- Acute myocardial infarction > two WEEKS
5- CK:
a- Its estimation is only useful in cases of muscle dystrophy.
b- It is of great value in diagnosis old myocardial infarction
c- Returns to normal in about 3 days following onset of pain.
d- Is not a useful marker of myocardial infarction .
o CK-MB 5 U/I N: 0-24 U/L
o CK 80 U/I N: 0 -170 U/L
o AST 30 U/I N: 0-32 U/L
o LDH 500 U/I N: 240-480 U/L
1- CK-MB:
a- Peaks 30 min after the onset of pain
b- Is the last of the cardiac enzymes lo return in normal.
c- ls cardiac isoenzyme of CK
d- Its determination is useful in the second week , following the infarction
2- LDH
a- Reaches its peak 6 hours after the onset of pain.
b- Is the last of the cardiac enzymes lo return to normal.
c- Is specific to the myocardium.
d- Returns to normal levels 2 days after the onset of pain
3- AST:
a- Is the first of the cardiac enzymes to rise and to return to normal.
b- Is elevated only in cases of acute myocardial infarction.
c- elevated in patients suffering from acute viral hepatilis.
d- Returns to normal 48 hours following the onset of pain.
4- The diagnosis of this case may be:
a- Acute pancreatitis.
b- Recent myocardial infarction.
c- Angina pectoris.
d- Myocardial infarction occurring more than 5 days ago.
5- One of the following plasma enzymes is frequently normal in acute myocardial infarction:
a- Alkaline phosphatase
b- Amylase
c- LDH
d- Glucose-6-phosphale dehydrogenase.
1- a 2- c 3- b 4- c 5- c 1- c 2- b 3- c 4- d 5- c
135
Oral questions in clinical pathology
U Laboratory investigations of …….
Blood: Anaemias , Leukaemia , Purpura.
GIT: Jaundice, Liver functions, hepatitis markers.
Infection: Widal test, Brucella, IBV.
Cardiology: Cardiac enzymes.
Nephrology: Laboratory investigations ARF, CRF.
Neurology: Differentiation bet. CSF.
Rheumatology: SLE, Rheumatoid arthritis.
Endocrine : DM
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