1.

Cleft lip and palate:

Introduction: Oro-facial clefts (OFCs) are common congenital malformations of the lip, palate, or both
caused by complex genetic and environmental factors. OFC may involve the lip, hard palate, or the soft
palate.

Etio/Risk factors: - More common in Asians

- Maternal folic acid and other nutritional deficiencies

- Maternal smoking, alcohol, drugs like PHENYTOIN
- Chromosomal abnormalities- trisomy 13, Treacher Collins

Pathogenesis:

- Development of face/lips- 5 processes/lobes

1 from the top of the head-> down towards the future upper lip (frontonasal prominence);

2 from the cheeks, which meet the first lobe to form the upper lip (maxillary prominence);

2 two additional lobes grow from each side below, which form the chin and lower lip (mandibular
prominence).

- Development of palate- 2 palatal shelves (left and right) which fuse together as well as anteriorly
with the upper lip.

Any abnormality during development will lead to their abnormal fusion causing cleft lip, cleft palate or
both.

Gross/types:

Cleft lip- Unilateral/ bilateral; complete/incomplete

Cleft palate- Incomplete/ complete(soft and hard palate)

Combined cleft lip and palate

Sequelae:

- Difficulty in feeding

- Difficulty in speech
- Recurrent ear infections (Eustachian tube defects)
 - Psychosocial issues

Clinical features: Defect seen in upper lip/ palate/both

Investigations: - Antenatal diagnosis on ultrasound, otherwise clinical diagnosis

-For fitness for surgery, Millards rule of 10: 10 weeks of age, 10 pounds weight, 10g% hemoglobin

Treatment:

Cleft lip- REPAIR AT 3 MONTHs

- Millards repair freshen the edges of the cleft and suture

Cleft palate- Staged repair depending on severity between 6-12 months of age, or later

- Repair of soft palate, hard palate, alveolar grafting, hearing aids and speech therapy

2. DENTIGEROUS CYST

Introduction: An odontogenic cyst formed in relation with the crown of an unerupted/partially erupted
tooth.

E/Rf: Early life-> Teenagers

Pathogenesis: -The pressure exerted by an erupting tooth on the follicle may obstruct venous flow
inducing accumulation of exudate between the reduced enamel epithelium and the tooth crown.

In addition to the developmental origin, some authors have suggested that peri-apical inflammation of
teeth in proximity to the follicles of the unerupted permanent tooth may be a factor for triggering this
type of cyst formation.

Gross: Cyst in relation with unerupted tooth filled with straw coloured fluid

Micro: Cyst lined by stratified squamous non-keratinized epithelium

Sequelae: -Rapid growth of cyst may lead to pathological fracture of jaw

-muco-epidermoid carcinoma
Clinical features: Cystic swelling usually at the site of upper or lower unerupted 3 rd molars

Investigations: Radiographically (Orthopantomogram) appears unilocular with well defined margins and
often sclerotic borders, sometimes it may be multilocular/SOAP BUBBLE in appearance and may have a
continuous cystic membrane .

Treatment: Excision of cyst alongwith unerupted tooth/ marsupialisation of cyst.

3. Dental cyst/Periodontal cyst/Radicular cyst

Introduction: Odontogenic cyst that develops at apex/crown of chronically infected tooth

E/RF: Dental caries

- Middle aged

- Dental trauma

Pathogenesis: Untreated dental caries -> bacteria to reach the level of the pulp -> access to the
periapical region of the tooth through deeper infection of the pulp, traveling through the roots-> pulpal
necrosis-> release toxins at the apex of the tooth -> periapical inflammation -> cyst formation

Gross: Cyst related to erupted caries tooth

Sequelae: Erosion of maxilla

C/F: Discoloration of affected tooth, cystic swelling in jaw.

Inv: Orthopantomogram: Unilocular cystic lesion in maxilla at root of caries tooth.

Treatment: Resection/marsupialization of cyst + treatment of caries tooth.

4. Salivary gland tumours/Pleomorphic adenoma

Salivary glands- Parotid, submandibular, Sublingual- Major

- Minor- throughout the oral cavity

Classification of salivary tumours (WHO-2004)

1. Benign epithelial- Pleomorphic adenoma (MC), Warthin’s tumour, oncocytoma,

myoepithelialoma, cystadenoma
2. Malignant epithelial- Mucoepidermoid CA (most common malignant salivary tumour), acinic cell
CA, cystadenoCa, Oncocystic CA
3. Soft tissue- Hemangioma, angiosarcoma
4. Lymphoid- Hodgkins, Diffuse B cell
5. Secondaries- Oral CA, Melanoma

Pleomorphic adenoma:

Introduction: It is a common benign salivary gland neoplasm characterised by neoplastic proliferation of

glandular cells along with myoepithelial components, having a malignant potentiality. It is the most
common type of salivary gland tumor and the most common tumor of the parotid gland. It derives its
name from the architectural Pleomorphism (variable appearance) seen by light microscopy. It is also
known as "Mixed tumor, salivary gland type", which refers to its dual origin from epithelial and
myoepithelial elements as opposed to its pleomorphic appearance.
Etiology/Risk factors: M>F, usually 40-60 years

Pathology:

Gross- Usually located in the superficial lobe of parotid. Borders show finger like extensions
(pseudopodia) which need to be removed along with tumour- thus simple enucleation can’t be done-
high rate of recurrence

Microscopy-Classically it is biphasic and is characterized by an admixture of polygonal epithelial and

spindle-shaped myoepithelial elements in a variable background stroma that may be mucoid, myxoid,
cartilaginous or hyaline. Epithelial elements may be arranged in duct-like structures, sheets, clumps
and/or interlacing strands and consist of polygonal, spindle or stellate-shaped cells (hence
pleiomorphism).

Sequelae: Malignant transformation- carcinoma ex pleomorphic adenoma.

Clinical features: Slow growing, painless tumour below ear lobe, nodular to feel. Features of facial nerve
palsy indicate malignant transformation.

Diagnosis: USG of swelling- nodular tumour in superficial lobe of parotid

-FNAC- to differentiate benign vs malignant

-Trucut biopsy- Contraindicated for fear of seeding the tract-high recurrence

Treatment: Surgery is the only treatment modality.

-Superficial parotidectomy (removal of superficial lobe with preservation of facial nerve) is treatment of
choice. Incision- lazy S/Blairs incision OR

- Extra-capsular excision of pleomorphic adenoma (new procedure with lower complications)

-Complications of surgery- Facial nerve palsy

Freys syndrome (gustatory sweating)- due to injury to auricotemporal nerve fibres which regenerate
and fuse with sympathetic nerves on face. Patients presents with sweating on same side of face while
eating, or even at sight/smell of food. Diagnosed by starch iodine test. Managed by antiperspirants,
Botox injection, or tympanic neurectomy (med/MiSx/Sx)

5. SPINAL ANESTHESIA :

Method of blocking the spinal nerves (thoracolumbar) by giving local anesthetic injection in the
subarachnoid space.
INDICATIONS :

Surgical procedures to the lower body - lower limb amputation, peri-anal surgeries (piles, fissure,
fistula), inguinal hernia, LSCS.

Drugs used :

Heavy bupivacaine with adjuvants – opioids, dexmeditomedine, clonidine etc.

Mechanism of action:

Results in a rapid onset of block, usually within 3 minutes. Maximal effects may take up to 30
minutes. Acts mainly at spinal nerve roots, although some effect is possible at the cord itself.
Smaller sympathetic fibres are more easily blocked than larger sensory and motor fibres. Hence, the
‘sympathetic’ level is higher than the sensory level.

Contraindications
Localised sepsis
Patient refusal
Bleeding disorders or anticoagulated patients

Anatomy
The spinal cord terminates at L1/2 in adults and L3 in infants. The line joining the iliac crests is at
L3/4 and is called Tuffier’s line. The subarachnoid space ends at S2 in adults and lies lowers in
children. The subarachnoid space extends laterally along the nerve roots to the dorsal root ganglia.
Technique
Preoperative assessment of the patient, as for a general anaesthetic. Facilities for resuscitation and
progression to general anaesthesia must be available. Establish full monitoring. Obtain IV access
before commencing the block.
Figure 6: Anatomy of the spinal cord, epidural space and the subarachnoid space.
 The patient should be sitting or lying on their side. Back flexion opens the intervertebral spaces. The
back is cleaned using standard antiseptic solution. The anaesthetist should adopt an aseptic
technique. Aim to identify the L3/4, L4/5 or L5/S1 interspace (use Tuffier’s line). The chosen
interspace is infiltrated with local anaesthetic. The spinal needle (most commonly used is Quincke’s
needle) is inserted in the midline, aiming slightly cranially. Resistance increases as the ligamentum
flavum is entered and when the dura is encountered, with a sudden "give" as the dura is pierced.
Correct placement of the needle is confirmed by cerebrospinal fluid at the hub.
1. The paramedian approach requires less back flexion (may be limited in certain patients). Infiltrate
with local anaesthetic 1.5 cm lateral to the cranial border of the spinous process at the interspace.
Aim the needle medially and cranially until the resistance of the ligamentum flavum is felt. If the
lamina is engaged, walk the needle off its cranial edge.
Complications :
1. Total spinal anesthesia leading to respiratory and cardiac arrest
2. PDPH- post dural puncture headache
3. Localized abscess at puncture point , Meningitis or sepsis
4. Hypotension/Neurogenic shock

6. EPIDURAL ANESTHESIA :

Method of blocking spinal nerves by delivering local anesthetic injection into epidural space.

Indications :
Orthopedic surgery - Major hip and knee surgery, pelvic fractures
Obstetric surgery - Cesarean delivery, labor analgesia
Gynecologic surgery - Hysterectomy, pelvic floor procedures
 Pediatric surgery - Inguinal hernia repair, orthopedic surgery
Ambulatory surgery - Foot, knee, hip, anorectal surgery
Urologic surgery - Prostatectomy, cystectomy, lithotripsy,
Amputation of lower extremity, revascularization procedures
Medical conditions - Autonomic hyperreflexia, myasthenia gravis,
pheochromocytoma, known or suspected malignant hyperthermia

Drugs used :

Bupivacaine/ Lignocaine/ Ropivacaine / Levobupivacaine with adjuvants –

opiods, dexmeditomedine, clonidine etc.

Mechanism of action:

Results in a slow onset of block, usually takes minimum 10 minutes. Maximal effects may take up
to 30 minutes. Requires larger volume of the drug as compared to spinal anesthesia.

Contraindications
Localised sepsis
Patient refusal
Bleeding disorders or anticoagulated patients
Severe refractory hypotension

: Anatomy of the spinal cord, epidural space and the subarachnoid space.
 Patient position – Sittiing or Lateral decubitus

Approach – Midline or paramedian

Structures through which epidural needle passes before reaching epidural space-
Skin, subcutaneous tissue, supraspinous ligament, interspinous ligament, Ligamentum
flavum (piercing this structure gives the classical feeling of loss of resistance )

Complications :
1. Epidural abscess
2. Epidural hematoma
3. Accidental dural puncture

7. Local anesthesia :
It is loss of sensation in a circumscribed area of the body caused by depression of
excitation in nerve endings or an inhibition of the conduction process in peripheral
nerves.

Indications:
1. Superficial surgeries: Lipoma/fibroadenoma excision
2. LN biopsy (cervical)
3. EVLA for varicose veins (tumescent anesthesia)
4. Pain relief
5. Diagnostic endoscopies

Advantages :
Widely used method of pain control
Painless and comfortable treatment to patient
Less time of onset
Low systemic toxicity
No permanent alteration of nerve structure

Mechanism of action :
Decreased permeability of sodium ions through nerve membrane leading to inhibition of
sodium conduction and neural excitation.

Commonly used local anesthetics :

Lignocaine- 4 to 5 mg/kg. If combined with adrenaline, then 7 mg/kg.
Bupivacaine (longer acting)
Prilocaine
 Ropivacaine

Technique: Area to be anesthesized is cleaned an draped. Permitted dose of local

anesthetic is taken in syringe with hypodermic needle. Needle pierced in subcutaneous
plane, aspirated (to rule out entry into vessel) and anesthetic injected in the region
desired.

Side effects :
Local : Hematoma
Pain
Failure of anesthesia
Local necrosis
Systemic : Overdose of local anesthesia
Allergic reaction to local anesthesia
Clinical manifestation of local anesthesia overdose : confusion ,
apprehensiveness,slurred speech, muscular twitching , elevated HR,RR and BP,
auditory and visual disturbances, hallucinations, loss of consciousness.

8. General anesthesia (including management of airway)

DEFINITION : General anesthesia is defined as “an induced state of unconsciousness accompanied

by partial or complete loss of protective reflexes, including the ability to independently maintain an
airway and respond purposefully to physical stimulation or verbal command.”

SURGERIES PERFORMED UNDER GENERAL ANESTHESIA:

Head and neck surgery
Modified radical MASTECTOMY
Exploratory LAPAROTOMY, Laparoscopic surgeries
PEDIATRIC SURGERY

DRUGS USED IN GENERAL ANESTHESIA ;

1. IV INDUCTION AGENTS : propofol, thiopnetone
2. INHALATIONAL AGENTS : sevoflurane,desflurane
3.MUSCLE RELAXANTS: atracurium, succinylcholine
4. OPIOIDS: fentanyl,morphine

STEPS OF GENERAL ANESTHESIA :

1. induction of anesthesia with IV or INhalational agent
2. Muscle relaxation with neuromuscular blocking agent
3. securing airway - by - bag and mask ventilation, endotracheal intubation (inserted with the
help of direct laryngoscope) or supraglottic airway device/Laryngeal mask airway
4. maintenance of anesthesia with opiods and inhalational agents
5. reversal of neuromuscular blockade
6. removal of ETT( extubation)
POST OPERATIVE SIDE EFFECTS OF GA:
sore throat, due to ETT(endotracheal tube)
temporary confusion and memory loss,
dizziness
difficulty passing urine
posst op nausea and vomiting
post op shivering

Management of difficult airway (add only if specifically asked)

DEFINITION: A Difficult Airway is defined in the American Society of Anesthesiologists (ASA)
guidelines as the clinical situation in which a conventionally trained anesthesiologist experiences
difficulty with face mask ventilation of the upper airway, difficulty with endotracheal intubation, or
both.

Examples of anticipated difficult airway:

1.Obesity, obstructive sleep apnea, history of snoring
2.Ankylosis, degenerative osteoarthritis,
3.subglottic stenosis, lingual thyroid or tonsillar hypertrophy,
4.Treacher-Collins, Pierre Robin or Down syndrome

COMPLICATIONS OF DIFFICULT AIRWAY

1. Hypoxia
2. Brain damage
3.Pneumothorax
4. Death

TESTS FOR EVALUATION OF A DIFFICULT AIRWAY:

Mallampatti classification
Cormack Lehane grading'Sternomental distance
Thyrmental distance
LEMON criteria

DIFFICULT AIRWAY GUIDELINES FOR UNANTICIPATED DIFFICULT AIRWAY:

1. Intubation - Maximum 4 attempts - with bougie,stylette,change of attemptors
2. Insertion of Supraglottic airway device/LMA
3. Bag and mask ventilation
4. Front of neck access - cricothyroidotomy, tracheostomy
 9. TOTAL INTRAVENOUS ANESTHESIA (TIVA)

Total intravenous anesthesia (TIVA) is a technique of general anesthesia which uses a

combination of agents given exclusively by the intravenous route without the use of
inhalation agents (Gas Anesthesia)

Indications of TIVA :
• Malignant hyperthermia risk • Long QT Syndrome (QTc≥500 ms) • History of
severe PONV • ‘Tubeless’ ENT and thoracic surgery • Patients with anticipated
difficult intubation/extubation • Neurosurgery—to limit intracranial volume •
Surgery requiring neurophysiological monitoring • Myasthenia
gravis/neuromuscular disorders to avoid NMBs • Anaesthesia in non-theatre
environments • Transfer of anaesthetised patient between environments • Day-
case surgery • Trainee teaching • Patient choice

Advantages of TIVA :
1.Reduced incidence of post-operative nausea and vomiting
2.Reduced atmospheric pollution,
3. more predictable and rapid recovery,
4. greater hemodynamic stability,
5.reduction in intracerebral pressure and reduced risk of organ toxicity.

Patient access :
As TIVA is conducted exclusively via an intravenous infusion, the choice must be
made from either a peripheral or a central venous access device.

Choice of agents :
Drugs with fast onset and offset times are most useful for balancing adequate
hypnosis/analgesia with rapid recovery. Most commonly used agents for TIVA
are Propofol and Remifentanil.

10. Squamous cell carcinoma

Introduction: Ca arising from skin or mucous membrane

Etiology/Risk factors: -UV radiation

- Fair skinned individuals

- Chimney sweepers/Kangri cancer(Kashmir)
- Oral cavity sq. cell CA- smoking, spirits, spices, sepsis, sharp tooth
- Premalignant lesions: Erythoplakia/leukoplakia, Solar keratosis, Xeroderma
pigmentosum (DNA mismatch repair mutation), Papillomas
- Chronic ulcers, burns, long standing scars (Marjolins)
Pathology:

-Gross: Exophytic/ Ulcerative with heaped up/everted edges /indurated

-Micro: Keratin pearls, cells arranged in whorls

-Spread: LN mets common, hematogenous is rare

Clinical features: Usually at sun exposed skin. Rapidly growing ulcer, everted edges, bleeds
on touching. Regional nodes may be palpable.

Staging: Like CA breast/Penis

Investigations: 4 quadrant wedge biopsy for confirmation. CT/FNAC of nodes for mets.

Treatment: 1. Surgery: Wide local excision with 2 cm margin and regional LN excision. If
involving bone, then limb amputation

2. Radiotherapy: Curative for early stage.

IF SAQ is Marjolin’s ulcer:

Introduction: Sq. cell Ca occurring in a long standing scar

Etio/RF: Mentioned in SCC

Patho: -Gross: Same is SCC

-Micro: Same as SCC

- Spread: Its locally invasive but no LN/hematogenous spread is noted as tumour is formed
in previous scars with destroyed lymphatics

C/f: Same as SCC

Investigations and treatment: Same as SCC (no radiotherapy, no LN excision)

11. Basal Cell Carcinoma/ Rodent ulcer

 Introduction: The most common type of skin cancer, more than 85% of all skin cancers

Etio/RF: Same as SCC

Gross: Ulcerative type with beaded edges/ Cauliflower like/ Noduloulcerative/nodulocystic

Micro: Palisading appearance of stratum basale

Sequelae: Locally invasive like a rodent. LN/Hematogenous mets are rare (as cells as large and clustered)

C/F: Common site- above the line joining the ear lobe to angle of mouth on face

-Ulcer with beaded margins

Investigations: 4 quadrant wedge biopsy

Treatment: Wide local excision with facial reconstruction with full thickness skin graft/local flaps

Moh’s micrographic excision

12. Melanoma:

Introduction: Malignant tumour of melanocytes. (Naevus is choristoma/benign tumour of

melanocytes)

Etio/RF:

-Congenital Giant Nevus/Dyplastic Nevus

Pathology:

-Gross/Types:

1. Superficial spreading: Most common type, horizontal spread, less invasion, radiating borders

2. Nodular: 2nd MC type, seen at mucocutaneous junction, vertically spreading and invasive

3. Lentigo maligna: Seen in elderly, can occur from pre-existing nevus, horizontal spread
 4. Acral lentigerous: Seen at palms and soles

5. Amelanotic: Less pigmented, aggressive, poorly differentiated

Microscopy: Clarkes classification of melanomas based on depth

1- Epidermis
2- Upper papillary dermis
3- Lower papillary dermis
4- Entire Dermis
5- Subcutaneous

Spread: MC site of melanoma- head and neck, also trunk. Rare sites: Iris, meninges

LN- Regional

Hematogenous: Lungs (cannon ball)

C/F: Danger signs (in a pre-existing nevus):

A- asymmetry
B- Borders are irregular
C- Colour(variegated)
D- Diameter > 6mm
E- Everted edge

Other features: Rapidly growing, bleeding on touch, satellite lesions

Staging: Pathological based on depth of invasion/Breslow’s staging

T1- <1 mm depth

T2- 1 to 2 mm

T3- 2 to 3 mm

T4- >3 mm

Investigation:

To confirm: Excision biopsy with 2 cm margin

For mets: FNAC of LN, CT scan

Treatment:

Surgical: Wide local excision + LN clearance

If pre-op no LN evident, then intra-op SLNB

Adjuvant Chemo (vincristin) + Radio + Immunotherapy

Limb warming chemotherapy: type of intra-arterial chemotherapy

** Moh’s micrographic surgery: Excision of skin tumours(SCC/BCC) in the vicinity of cosmetic structures
where 2 cm margin is not possible. In that case, excise tumour with minimal margin (1-2mm) under
microscopic vision and send for histopathology (micrography) after marking the quadrants of the
tumour if any quadrant shows tumour then excise only that quadrant. Repeat micrography if margin
remains involved.

*Include Moh’s technique if SAQ on SCC/BCC/Marjolin is asked.

13. Pilonidal sinus/Jeep bottom

Introduction: Sinus usually occurring at natal cleft containing dead hair (without roots).

Etiology/Risk factors: - 2nd-3rd decade

- Hairy males
- Obesity
- Hairdressers

Pathogenesis/Theories:

1. Congenital theory- Hodges-> Occur due to congenital sinus tracts not accepted
anymore
2. Acquired theory: Constant friction at natal cleft region breach in epitheliumtips of
broken hair irritate the damaged epitheliumsinus tract formation

Gross: MC site is upper part of natal cleft (overlying coccyx).

Superficial sinus tract (extending into subcutaneous tissue) consisting of dead hair.

Sequelae: Abscess, malignancy

C/F: Usually presents as an abscess at natal cleft- pain, fever and pus discharge

Investigations: Sinogram/MRI of lower spine to rule out prolapsed intervertebral disc

Treatment: Treat the abscess with antibiotics and incision and drainage.

For sinus:

1. Wide excision with marsupialization (do not close the tract primarily)
2. Wide excision with flap cover(Limberg rotation flap)
3. Bascoms procedure

14. Hirschsprung’s disease/ Congenital megacolon/Colonic Aganglionosis

Introduction: Congenital abnormality characterized by failure of normal neuronal development of

terminal part of colon and rectum

Etio/RF: - Males>Females

-Downs syndrome

- Maternal infections
Pathogenesis: Normal development-> Neural crest cells migrate to the hindgut->Neural
innervation of colon begin from proximal to distal-> Intrauterine accidentFailure of migration of
neural crest cells-> absence of myenteric plexus in distal colon/rectum->Hirschsprung

Gross: Extent of aganglionosis is distal to proximal, with rectum being most common (similar to
Ulcerative colitis). This segment fails to relax and proximal segment dilates

Micro: Aganglionosis in affected segment, proximal colon is NORMAL (contrast to achalasia

where proximal segment shows reduced ganglions)

Sequelae: Intestinal obstruction

C/F: Usually 1st decade of life depending on severity-> Constipation in an infant, Intestinal
obstruction.

Investigation: CT with rectal contrast/Barium enema is the first investigation.

Rectal biopsy is investigation of choice-> Will show aganglionosis of rectum

Treatment: Surgery is the only treatment, depending on age and severity of presentation.

If diagnosed with intestinal obstruction, then temporary diversion colostomy

After stabilization-> Resection of affected segment with colo-anal anastomosis (Swenson’s pull
through procedure/Duhamel procedure).

15. Bariatric surgery:

Introduction: Surgery done for patients with morbid obesity with the intent of weight loss and
reduction in obesity associated co-morbidities (diabetes/hypertension etc.)

Types of procedures:

1. Restrictive : Where stomach is reduced in size reduction in meal size lower calorie
intake Weight loss
Examples: Sleeve gastrectomy, adjustable gastric band

2. Mal-absorptive: Where segment of intestine is bypassed less absorptive area

Lesser absorption of food weight loss
Examples: Biliopancreatic diversion/Duodenal switch, Mini-gastric bypass
 3. Combined: Where both of above effects are applicable
Example: Roux-en-Y gastric bypass

4. Endoscopic bariatric procedures: Non-surgical, purely by endoscopic approach

Example: Gastric balloon, Endoscopic gastroplasty (principally same as restrictive
procedures)

WHO classification of obesity based on BMI:

Category BMI
Normal 18.5 to 24.9
Overweight 25 to 29.9
Obese- Class I 30 to 34.9
Obese- Class II 35 to 39.9
Obese- Class III >40

*Morbid obesity: BMI > 40 or BMI >35 with obesity associated diseases (Diabetes, HTN,
Sleep apnoea etc.)

Indication for bariatric surgery (worldwide): 1. BMI > 40 with/without co-morbidites OR

2.BMI >35 with co-morbidities

*In Asians, BMI points are reduced by 2.5 for above indications

Complications of bariatric surgery:

1. Related to surgery: Post operative bleed, post operative staple line leak, internal
hernia, band erosion
2. Related to obesity: Deep vein thrombosis, pulmonary embolism, respiratory failure
3. Related to reduced food intake/malabsorption: Hyop-proteinemia, anemia, vitamin
deficiencies (Vit B12/Vit D etc.)

16. Benign breast disease

Intro: Congenital or acquired diseases of the breast of benign nature

E/Rf/Types:

A) Congenital- Amazia/Polymazia, Diffuse hypertrophy

B) Trauma- Fat necrosis.Hematoma
C) Inflammatory- Mastitis, Abscess, Periductal mastitis (duct ectasia)
D) Tumours (Benign)- ANDI, Fibroadenoma
 E) Misc-Breast cysts, Mondor’s diseas

Pathogenesis of ANDI: Normal menstrual cycle hormonal influence growth of

parenchyma Involution any aberration abnormality of growth or involution Nodularity
and cysts formation ANDU

Pathogenesis of abscess: Lactation Trauma to areola and nipple  Entry of staph aureus into
lactiferous ducts inflammation  Mastitis  occlusion of ducts Collection of secretions
Formation of pus due to staph Breast abscess

Gross: ANDI- Nodules, cysts, papillomas. Solitary/multiple

Fibroadenoma- Hard/Soft, capsulated

Micro: ANDI- fibroadenosis

Fibroadenoma- Staghorn arrangement

Sequelae: Abscess- Septicemia

C/F: FA- Mouse in breast

ANDI- Cyclical mastalgia, bilateral nodularity

Abscess- Redness, severe pain, tenderness, fever with chills

Investi- Triple assessment (describe from practicals notes)

Rx- Abscess- Antibiotics + Aspiration or Incision and drainage

ANDI- Table 53.1 from bailey

FA- Enucleaiton if large > 5 cm or symptomatic or cosmesis or suspicious

17. Hashimoto’s thyroiditis/Chronic Lymphocytic thyroiditis

Introduction: Autoimmune inflammation and destruction of thyroid gland

Etio/Rf: Associated with other autoimmune diseases like T1 Diabetes, RA, Pernicious anemia
etc.
Pathogenesis: Any r/f Environmental trigger Antibodies mediated destruction Initial
hyperthyroidism (transient) Euthyroidism Hypothyroidism

Gross: Bossellated, enlarged thyroid

Micro: Lymphoid follicles infiltrate

Sequelae: Permanent hypothy. Risk of papillary CA

C/F: Middle aged Female

Hypothyroidism features

Bosselated/nodular goiter

Investi: Same as practicals

1. TFT- Hypothyroidism (Inc TSH, dec T3/T4)

2. USG neck with FNAC
3. Antibodies- Anti TPO/Anti TG

Rx: Medical Correct hypothyroidism

No role of steroids

Surgery (Total Thyroidectomy) if compression/cosmesis/complications

18. Buerger’s disease/Thromboangitis obliterans/Smoker’s Arteritis

Intro: Inflammatory small and medium vessel arteritis of LL leading to PVD.

E/Rf: Smoking, Young < 40 years, Male gender

Pathogenesis/Theories: Nicotine exposure Inflammatory response in vessels Vasospasm

Persistent smoking Recurrent vasospasm Thrombosis Also affects adjacent veins and
nerves thrombophlebitis and peripheral neuritis

Gross: Multiple segmental small/medium vessel occlusions

Sequelae: same as PVD (Ulcer/gangrene)

C/F: Triad of : Intermittent claudication in distal limb (lower calf/foot) + Thrombophlebitis +

Raynauds phenomenon- cyclical color changes on cold exposure (practical notes)

Examination- Absent dorsalis pedis, ATA, PTA. Popliteal and larger arteries are spared

Investi (Same as prax): Doppler (arterial) of LL

May require angiography (CT/MR/DSA)

Rx: Medical (prax notes)

MiSx- (Prax notes)

Sx- Revascularization by Arterial Bypass or amputation if gangrene

19. Hypospadiasis

Introduction: Congenital abnormality characterized by abnormal opening of urethra on under

surface(ventral) of penis instead of terminal opening.

Etiology/Risk factors: Genetic mutations

-Intra utero accidents-> maternal infection

-Associated with other genitor-urinary abnormalities-WAGR syndrome (seen in WILMS’)

Pathogenesis: Normal genitalia (tubercles) differentiates to penis under the influence of

androgens in 8th-12th weekurethra develops from urogenital sinus grows into penis any
intrauterine accident arrest in development of urethra opening is formed proximally 
hypospadiasis

Gross/Types: Normal urethral meatus is terminal. In hypospadiasis, MC type of opening is seen

on glans.
Glandular hypospadiasis is associated with prepuce covering the opening giving it a “hooded
prepuce” appearance. The missing distal part of urethra is replaced by fibrous tissue, leading to
ventral bending of penis->chordee of penis

Sequelae: Difficulty in micturition and scrotal excoriation. In severe forms (scrotal/perineal),

difficulty in intercourse

C/F: Glandular form is asymptomatic. Severe forms are diagnosed at birth by neonatologist.
Evaluate for other associated syndromic abnormalities

Investigations: Clinical diagnosis. USG abdomen for WILMS’.

Treatment: Glandular form usually requires conservative management. For severe forms->
Reconstruction (urethroplasty) with release of chordee done between 6 to 12 months (Nesbitt
repair). In neonates with diagnosed hypospadiasis-> CIRCUMCISION IS CONTRA-
INDICATED, as prepuce is used to neo-urethra reconstruction.

**EXTRA POINTS:

1. Complications of Splenectomy:
- Related to surgery: Left lobe basal atelectasis (MC), acute gastric dilatation (due to
devascularation of short gastric vessels during splenectomy), injury to tail of pancreas
- Related to asplenia: Risk of infections from capsulated organisms->
OPSI(overwhelming post splenectomy sepsis) --> occurs few months to years after
splenectomy Prevented by vaccination against PNEUMOCOCCI,MENINGOCOCCI
AND H.INFLUENZA atleast 2 weeks prior to elective splenectomy. If emergency
 splenectomy (trauma), then vaccinate at the earliest after surgery. Repeat booster
vaccines as per protocol.

2. Classification of pancreatic cancers:

-Glandular elements (Exocrine): Adenoma, Adenocarcinoma
- Cystic elements: Serous cystadenoma, mucinous cystadenoma, IPMN(intra-ductal
pancreatic mucinous neoplasm)
- Endocrine tumours: Insulinoma, gastrinoma (Zollinger Ellison), glucagonoma

3. Weigart Meyer law:

In duplicated/double ureter, the upper ureter gets inserted lower down in bladder
(neck/prostatic urethra), while the lower ureter opens normally in trigone. In males, its
asymptomatic, while in females it presents with urinary incontinence