GIT MODULE:

ORAL CAVITY

DISEASES OF TEETH

1) Caries: tooth decay, demineralization of tooth by bacteria.

- Fluoro-apatite resists degradation by bacterial acids (flouride added in toothpastes)

2) Gingivitis: inflammation of gums (mucosa surrounding teeth) can lead to dental plaque (sticky,
colorless biofilm) calculus ( if plaque not removed it becomes calculus)

- Can lead to erythema, edema ,bleeding , most common in adolescence .

3) Periodontitis: inflammation that effect surrounding structures (periodontal ligament, alveolar bone,
cementum) , leads to loosening of tooth from the gums, preceding tooth loss.

- Mostly caused by anaerobic microaerophilic gram-ve flora.

- Adult periodontitis A/With aggregatibacter, actinomycetes, porphyromonas gingivalis, prevotella

intermedia.

- Systemic disease include: AIDS, leukemia,diabetes, crohn's, sarcoidosis, down syndrome, chedial-
higashi syndrome

- Mucocele; most common problem of salivary gland. (MCQ)

INFLAMMATORY LESIONS

1) Aphthous ulcers/ canker sores: Painful, superficial mucosal ulcers. Common in first 2 decades. Non-
contiguous.

- Unknown etiology.

- A/w celiac disease, IBD, behcet's disease .

- Appears as single or multiple hyperemic lesions, narrow zone of erythema.

- Resolve spontaneously in 7-10 days.

2) Fibrous proliferative lesions:

* Pyogenic granuloma: inflammatory peduncular lesion found on gingiva.

- Surface is red to purple, rapid growth may cause malignancy, have high vascular proliferation.

- occurs in children, young adults, and pregnant women. (MCQ)

* Peripheral ossifying fibroma: reactive growth of gingiva, not neoplastic, red, ulcerated, nodular lesions.

- unknown etiology but some arise as a result of long standing pyogenic granuloma.

* Peripheral Giant cell Granuloma:

Uncommon, reactive; not neoplastic ; covered by intact gingival mucosa or maybe ulcerated .

- histologically multinucleated giant cells separated by fibroangiomatous stroma , brown tumors.

INFECTIONS

1) Herpes simplex

- HSV-1 oral herpes- Primary occurs in children b/w 2-4 yrs (acute herpetic gingivostomatitis)

- Recurrent herpetic stomatitis (reactivation) can occur.

- Lesions resolve in 7-10 days, can persist in immunocompromised

2) Oral candidiasis

- Candida albicans is in normal flora, activated when immunity is low.

- 3 forms, pseudomembranous, erythematous, hyperplastic.

- Pseudomembranes most common, present as white grey layer that can be scraped off revealing an
erythematous base. (MCQ)

3) Deep fungal infections

- Fungi including histoplasmosis, blastomycosis, aspergillosis

- Usually in immunocompromised.

ORAL MANIFESTATIONS OF SYSTEMIC DISEASES:

1) Hairy leukoplakia:

- Due to EBV ,sometimes by HPV & HIV.

- White hair like patches usually on the lateral side of tongue that cannot be scraped off .

- Microscopically: hyperparakeratosis, acanthosis, balloon cells.

PRECANCEROUS AND CANCEROUS LESIONS:

1) Leukoplakia & Erythroplakia: Precancerous lesions (dysplastic & carcinoma in situ)

* Leukoplakia: white plaque that cannot be scraped off (MCQ )& cannot be characterized as any other
disease, Sharply demarcated borders.

- Tongue, palate, gingiva most common sites. Pre-cancerous stage.

- smooth and well-demarcated borders , diffuse irregular granular surface. More in males. Common RF:
TOBACCO.

* Erythroplakia: red velvety eroded area that cannot be scraped off. 17 times more malignant than
leukoplakia.

- sites: Vermillion border of lip (MC), buccal mucosa ,hard and soft palate, lower alveolar mucosa.

- cellular dysplasia, infiltration of lymphocytes and macrophages.

-R/F: tobacco (MC), alcohol, HPV, ill fitted dentures.

2) Squamous Cell Carcinoma of oral cavity: (ospie)

Multifactorial pathogenesis:

- Smoked tobacco (MC ) or Alcohol, Beetle nut and paan, Actinic radiations .

- Pathogenesis in patients of SCC with no known risk factors is unknown

- Mutation mostly involve p53, p63, NOTCH1

- HPV_associated SCC overexpress p16.

- Ventral surf of tongue (MC), floor of mouth, lower lip, soft palate, gingiva most favored sites.

- Morphology: Appear as raised pearly plaques, irregular roughened areas, can be mistaken with
leukoplakia.

- SCC begin as dysplastic or carcinoma in situ.

- Metastasis in lungs, liver, bones and mediastinal lymph nodes.

Pleomorphic adenomas (also known as mixed-type tumors) are the most common benign salivary gland
tumors. (MCQ) While most common malignant is mucoepidermoid.

SIALADENITIS and SIALOLITHIASIS

✨bacterial infl of major salivary gland , sec to calculus (MCQ)

✨caused by [Link] (MCQ )

✨sub mand 90% , parotid 10% (mostly by Mumps)

✨stone formation

BENIGN TUMOUR

- 65-80% involves parotid gland.

✨ pleomorphic adenoma most common (MCQ)

✨ Warthin tumor

✨ ductal papilloma

✨ oncocytoma.

PLEOMORPHIC ADENOMA

✨ most common salivary glands tumour 50%.

✨ female dominant most common parotid gl 60%.

✨ mixed tumour both show epithelial and mesenchymal (cartilaginous stroma) differentaition

✨ well demarcated mass less than 6cm.

✨ CLINICAL FEATURES: painless movable mass at angle of jaw , age 40 to 60 yrs

✨ TREATMENT: excision pariodectomy , ennucleation

✨ COMPLICATION : transform into adenocarcinoma aka carcinoma ex pleomorphic adenoma or

malignant mixed tumor.

WARTHIN TUMOUR (NOT MALIGNANT)

✨also known papillary cystadenoma lymphomatosum

✨male dominant, most common superficial lobe of parotid gland. (EXCLUSIVELY IN PAROTID)

✨8 times more common in smokers.

✨encapsulated .

✨cystic spaces filled with mucinous and serous. secretion (MCQ)

✨ Cystic spaces resting on lymphoid stroma.

MALIGNANT TUMOUR OF SALIVARY GLAND

✨mucoepidermoid carcinoma (most common)

✨adenoid carcinoma .

✨acinic cell carcinoma .

✨adenocarcinoma .

✨squamous cell carcinoma.

MUCOEPIDERMOID CARCINOMA

✨most common primary malignant tumour of salivary gland.

✨ located in parotid gland .

- 5 yrs survival rate; Low grade 90%, high grade 10%.

✨mix of neoplastic squamous cell, mucous secreting and INTERMEDIATE cells (MCQ)

- Lack well defined capsule.

ADENOID CYSTIC CARCINOMA

✨uncommon

- Commonly involve minor salivary gland .

- Slow growing has distinct features to invade perineural spaces (MCQ)

- Infiltrative and poorly encapsulated. Cribriform pattern.

CONGENITAL ABNORMALITIES:

1. ATRESIA: In esophageal atresia, a thin non-canalized cord replaces the segment of the esophagus,
causing a mechanical obstruction. Occurs at the bifurcation of trachea. A/w fistula (connection of upper
or lower esophagus to trachea). A fistula can be without atresia. See robins diagrams. A/w
polyhydromnios (MCQ)

2. Imperforate anus: failure of cloacal diaphragm to involute. Mc form of intestinal atresia

3. Stenosis: lumen is reduced , fibrous thickening. GERD, systemic sclerosis.

4. Diaphragmatic hernia: when incomplete formation of diaphragm allows the abdomen visceras to
herniate. Can cause pulmonary hypoplasia.

5. Omphalocele: when closure of physiological herniation does not complete, abdominal viscera
protrude with a ventral membranous sac.

6. Gastroschisis: similar to omphalocele but without membrane. Abdominal wall musculature fail to
close (MCQ)

7. Ectopia: ectopic gastric mucosa pt in upper gi referred as INLET PATCH. Similarly ectopic pancreatic
mucosa can also be ps in pylorus causing inflammation and scarring leading to obstruction.

8. Gastric heterotopia: small patches of ectopic gastric mucosa in colon with occult blood loss due to
peptic ulceration of adjacent mucosa.

9. Meckel diverticulum: true diverticulum ( a blind out pouching of all layers of alimentary canal) due to
failure of vitelline duct to regress. RULE OF 2's:

- 2% population

- Ps within 2ft of ileocecal junction

- 2 inches long (5cm)

- Symptoms appear at the age of 2.

- Diagnosis = technetium scan (gastric mucosa) (uworld MCQ)

- Ectopic pancreatic or gastric tissue may be ps.

- Lies in anti-mesenteric side of ileum (MCQ)

10. Pyloric Stenosis: hypertrophy of circular muscles of pylorus. More common in males. A/w trisomy 18
and Turner's syndrome.

- Projectile, non bilious vomiting 2-3 weeks after birth, regurgitation, demands for re-feed. (MCQ)

- Surgical splitting of muscularis is curative.

11. Zenker diverticulum: herniation of mucosal tissue at an area between thyropharyngeal and
cricopharyngeal parts of inf constrictor muscle (killiann triangle). It is false diverticulum ( only mucosa
and submucosal layer protrude out) . Mass in neck. (MCQ)

12. Hirschsprung disease: A/w down syndrome. Absence of myenteric and auerbach plexus.
Aganglionosis. (MCQ)

- Failure of NCC to form plexus. Abnormal peristalsis of colon. RET gene mutation. Megacolon formation
(in normal part of colon). Failure to pass meconium (MCQ), billious vomiting, Constipation.

13. Tracheoesophageal fistula: connection between esophagus n trachea.

- CF: frothing, bubbling, cyanosis, identified with first feed. A/w maternal polyhydromnios.

- Inability to pass NG tube.

- most common is type C pattern ie upper blind segment and fistula btw blind lower segment and
trachea.

14. Esophageal webs: protrusion of mucosa into lumen of upper esophagus. A/w plummer vinson
syndrome (dysphagia, iron deficiency anemia, middle aged woman, glossitis) inc risk of squamous cell
carcinoma of esophagus.

15. Esophageal rings: ring like protrusion. (A -ring Occur above gastro-esophageal junction. B -ring
Shatzki rings - occur at esophageal jx).

ESOPHAGUS:

1. Achalasia:

- triad of 3: inc tone of LES, no LES relaxation (due to loss of NO), aperistalsis. (MCQ)

- Results from degeneration of inhibitory neurons in myenteric /Auerbach plexus so No release of NO

and vasoactive intestinal peptide VIP in distal esophagus.

- Causes: idiopathic, chagas disease ([Link] inf, destruction of myenteric plexus), diabetic autonomic
neuropathy, sarcoidosis, amyloidosis.

- CF: dysphagia of solids and liquids, A/w esophageal cancer, weight loss, regurgitation, nocturnal cough.

- BIRD'S BEAK APPEARANCE on CXR. (Barium swallow) & Inc resting pressure in LES on manometry
(MCQ)

- Treatment: Ca channel blocker, nitrates, botulinum toxin inj.

2. Esophagitis: inflammation of esophagus. Ps with dysphagia. Types:

- Mallory wiese syndrome: partial thickness, longitudinal lacerations of GE jx, confined to mucosa and
submucosa, due to severe vomiting, hematemesis, alcohol use (MCQ), bulimia nervosa. Complications:
Boorehave synd (rupture of distal esophagus).

- Infectious esophagitis: candida (MC) white pseudomembranes, HSV (punched out ulcers MCQ), CMV
(linear ulcers), a/w immunosuppression.

- Medication induced esophagitis: 2° to bisphosphonates, tetracyclines, NSAIDs, ferrous sulphates, KCl.

- Reflux esophagitis: MC type 2° to Gerd. Morphology: basal zone hyperplasia, Eosinophils and
neutrophils, lamina propria elongate.

_Dx: if condition better with PPIs then it's GERD.

- Corrosive: 2° to caustic ingestion . E.g : lye , acid, detergents ingestion.

3. Hiatal hernia: herniation of stomach upwards into chest through esophageal hiatus. Types:
- sliding hernia: MC 95%, herniation of proximal stomach through widened diaphragmatic hiatus, GE jx is
displaced above the diaphragm.

- Rolling hernia (paraesophageal hernia): herniation of portion of stomach (greater curvature), GE jx

remain at the level of diaphragm.

- CF: heartburn and regurgitation. Paraesophageal can cause gastric volvulus.

4. Barrett's esophagus: metaplastic change in the lining mucosa of esophagus in response to chronic
GERD.

- From non keratinized Sq ep to non-ciliated columnar ep with GOBLET CELLS. A/w adenocarcinoma
(MCQ)

- Morphology: dysplasia:

- low grade : basal orientation of cell nuclei in ep cells.

- High grade: apical orientation of cell nuclei in ep cells.

- Red VELVET esophagus lining on endoscopy (MCQ)

- CF: heartburn, dysphagia, hematemesis, retrosternal pain.

- diagnosis : endoscopy, histology (intestinal metaplasia).

6. Esophageal Varices: dilated submucosal veins in lower third of esophagus 2° to portal HTN. MC cause
is cirrhosis. (MCQ)

-CF :hematemesis, fatal haemorrhage.

7. Esophageal tumours: ps with dysphagia first solids then liquids and wt loss.

- benign tumors include Leiomyomas (most common), fibromas, lipomas, hemangiomas.

- malignant include squamous cell CA (most common) and adenocarcinoma.

- Adenocarcinoma of lower esophagus most common.

- Squamous cell CA mutations: amplification of SOX2 gene, p53, E-cadherin, NOTCH1.

- Adenocarcinoma mutations: p53, EGFR, ERBB2, MET, CYCLIN D1, CYCLIN E genes.

STOMACH:

1. ACUTE GASTRITIS: inflammation of gastric mucosa.

- Causes: NSAIDs (most common -MCQ), alcohol, smoking, brain injury (cushing ulcers -MCQ), burn
injury (curling ulcers-MCQ), uremia, stress (MCQ), dec oxygen delivery at high altitude.

- MC site of Curling's ulcer is Duodenum (MCQ)

2. CHRONIC GASTRITIS: two types: Type A autoimmune gastritis & Type B [Link]:

A. Autoimmune Gastritis: autoantibodies against parietal cells so Decreased acid production-

achlorhydria with Hypergastrinemia

- body of stomach.

- Endocrine hyperplasia

- Vit 12 deficiency- megaloblastic anemia (Pernicious)

- Mucosal atrophy.

- CF: anemia, beefy red tongue, peripheral neuropathy (paresthesis and numbness). All B12 def
symptoms.

- A/w hashimoto's thyroiditis, DM-1, gastric adenocarcinoma.

- MCQ: Pt with DM1, Gastritis with T cells, destruction of Parietal cells.

Type B Helicobacter pylori: (MCQ)

- most common.

- Involves antrum and pylorus.

- Transmitted by feco-oral.

- Antral type gastritis: high acid production, dec interleukin 1B (MCQ), produces duodenal ulcer.

- Pangastritis: low acid production, high IL1B, causes adenocarcinoma.

- Non-invasive tests: Ag-Ab test , Stool antigen test/fecal antigen +ve in active inf (MCQ ), Urea breathe
test (+ve in active inf)

- Invasive: Endoscopic biopsy, Rapid urease test, PCR.

- Test to confirm [Link] has been eradicated after therapy: Urea breathe test (MCQ)

C. Eosinophilic Gastritis:

- antral/pyloric region

- Tissue damage A/w dense infiltrates of eosinophils.

- Inc in serum igE levels.

- Due to cows milk and soy protein.

- Atopic asthma, eczema .

D. Lymphocytic gastritis:

- a/with celiac disease.

- Affect entire stomach

- Referred as varioliform gastritis. (MCQ)

- Histologically inc no. Of intraepithelial lymphocytes.

E. Granulomatous Gastritis:

- a/with Crohn's disease, Sarcoidosis.

- Narrowing of gastric antrum.

Complications of Chronic Gastritis:

1. Peptic ulcer diseases: chronic mucosal ulceration affecting the duodenum or stomach.

* ulcers (VIVA): Localized defect of an organ or tissue caused by sloughing (shedding) of Necrotic
inflammatory tissue.

- Peptic, duodenal, oral, skin Ulcers.

- A/w [Link] (100% in duodenal ulcer, 70% in gastric ulcers), NSAIDS, cigarette smoking, Zollinger
ellison syndrome.

- Inc gastric secretions and dec bicarb secretions.

- MC in proximal duodenum, gastric ulcers located along lesser curvature near body and antrum.

- Morphology: sharply punched out defect (MCQ). Heaped margins are characteristic of cancer.

- CF: upper GI bleeding, burning pain, iron deficiency, hemorrhage (from lesser curvature-left gastric
artery, from post duodenal wall- gastroduodenal artery).

- PAIN DUE TO GASTRIC ULCER IS AGGRAVATED WITH FOOD, WHILE PAIN DUE TO DUODENAL ULCER IS
RELIEVED WITH FOOD (MCQ)

- Most common complication is Bleeding (MCQ)

- Gastric ulcers have 1-4% risk of cancer, while duodenal ulcers are NEVER malignant.

2. Mucosal Atrophy:
- long standing chronic gastritis lead to loss of parietal cell mass.

- A/w intestinal metaplasia, ps of goblets cells.

HYPERTROPHIC GASTROPATHIES:

1. MENTRIER DISEASE:

- excessive secretion of TGF-alpha.

- Diffuse hyperplasia of foveolar cells of body n fundus and hypoproteinemia.

- Gastric secretions contain excessive mucus, and lack HCl.

- A/w adenocarcinoma.

2. Zollinger Ellison Syndrome:

- gastric sec tumours.

- Doubling of Parietal/oxyntic mucosal thickness due to five fold inc of parietal cells.

- Fundus

- MEN-1 mutations

- No A/w adenocarcinoma.

GASTRIC POLYPS AND TUMOURS:

1. Inflammatory and hyperplastic polyps: 75% (MCQ)

- antrum, a/w [Link] and chronic gastritis.

- Elongated foveolar glands

2. Fundic glands polyp:

- sporadic. Germ line mutation in APC. so A/w FAP syndrome and Inc use of PPIs (MCQ)

- Body n fundus.

- No inflammatory infiltrates

- Risk factors: PPIs , FAP

3. Gastric cystica:
- body

- Trauma, prior surgery

4. Gastric Adenoma:

- low grade dysplasia.

- Antrum

- MC are of intestinal type .

5. Gastric adenocarcinoma:

- MC malignancy of stomach, 90% of all gastric cancers.

- MC site is lesser curvature of antrum-pyloric region.

- The depth of invasion and extent of nodal and distant metastasis remain most powerful prognostic
indicators of gastric adenocarcinoma (ospie)

- LAUREN CLASSIFICATION -Two types morphology:

A) intestinal type (bulky masses) 53%, Intestinal glands, expanding growth pattern.

B) diffuse type (signet ring cells- MCQ). Leather bottle appearance = linitis plastica (MCQ). IMP

-linitis plastica means that stomach wall becomes contracted and rigid! (MCQ)

- Wt loss anorexia, anemia.

- RF: [Link] most imp, smoked fish and meats, smoking, Chronic gastritis, gastric adenoma, Barrett
esophagus, FAP, HNPCC, male predominance.

- Metastasis: supraclavicular LN (Virchow's node), periumblical LN (Sister Mary Joseph nodules), left
axillary (Irish nodes), the ovary (Krukenberg tumour), pouch of douglass (blummer shelf).

- WNT signalling (APC)= intestinal type adenocarcinoma

- E-CADHERIN (CDH1)= diffuse gastric MCQ adenocarcinoma ....MCQ

6. Lymphoma: (5%)

- extranodal lymphomas arise virtually in GI tract esp in stomach.

- MC type is MALToma (Peyer patches) due to [Link] (MCQ )and chronic gastritis. It's only malignancy
which can be cured by antibiotics.

- Lymphoepithelial lesions.
- B-cell markers CD-19 and CD20 and CD43

- MC symptoms = dyspepsia and epigastric pain.

7. Carcinoid tumors:

- well differentiated neuroendocrine tumours (arise from EC cells)

- Most found in GI tract and 40% small intestine. (MCQ)

- Tumors that produce Gastrin may cause Zollinger ellison syndrome while ileal tumours cause carcinoid
tumours.

8. Gastrointestinal stromal tumour (GIST):

- MC mesenchymal tumor of abdomen.

- Arise from interstitial cells of cajal (Pacemaker cells)

- Carnay triad - non hereditary syndrome includes GIST, paraganglioma, pulmonary chondroma.

- Mutation of KIT.

- GIST contain spindle cells called epitheloid type.

SMALL INTESTINE

INTESTINAL OBSTRUCTION

cm: pain, distension, vomiting & constipation

1) HERNIAS:

Most frequent cause of obstruction

protrusion of serosa lined pouch of peritoneum , obstruction occurs due to external herniation ( visceral
protrusion)

Pressure at neck of pouch can cause incarceration, strangulation & infarction

2) ADHESIONS: Most common!

Fibrous bridges

Can result in internal herniation

3) VOLVULUS:

Twisting of a loop about its mesenteric point

Causes both obstruction and infarction

Most common in sigmoid colon

4) INTUSSUSCEPTION:

-Constricted wave of peristalsis telescopes into distal segment , pulls the mesentery along

-Most common in children under 2 yrs of age

-Mostly idiopathic, can be associated with rotavirus vaccine (reactive hyperplasia of peyers patches)

- Sausage like protrusion, complete constipation (MCQ)

- Contrast enemas used for treatment

ISCHEMIC BOWEL DISEASE

Mucosal infarction

Mural infarction

Transmural ( by acute vascular obstruction)

Pathogenesis: first phase; hypoxic injury

2nd phase; reperfusion

Severity also depends on vascular anatomy

Watershed zones (splenic flexure, sigmoid colon &rectum) more susceptible

Surface epithelium of intestinal capillaries vulnerable to ischemia

Morphology: often segmental and patchy lesions

Congested dusky to purple red bowel

Blood tinged mucus or flank blood

Coagulative necrosis of musculris propria(1-4days)

Hyperpoliferative crypts

In chronic ischemi fibrous scarring of LP

Bacterial superinfection induce pseudomembrane formation ( resembles clostridium)

CF: left abd pain, sudden cramps, desire to defecate

MALABSORPTION : Defective absorption

Hallmark: steatorrhea
4 phases:

1) intraluminal digestion: breakdown of food into simplest forms

2) Terminal digestion: hydrolysis of carbs n peptides in brush border

3) Transepithelial transport: transport of nutrients

4) lymphatic transport of fats

DIARRHEA

Inc in stool mass, frequency, fluidity greater than 200gm per day/ 3 or more loose stools per day (mcq)

Bloody diarrhea; dysentery

4 types:

1) Secretory: isotonic stool, no electrolyte loss

2) Osmotic: due to unabsorbed luminal solute ( lactase deficiency)

3) Malabsorptive: failure of nutrient absorption (steatorrhea)

4) Exudative: due to inflammatory disease

CYSTIC FIBROSIS

due to absence of CFTR (chloride channels gene)- thick secretions mainly in lungs, pancreas...

Failure of intraluminal phase

Treated with oral enzymes.

CELIAC DISEASE /Gluten sensitivity ( immune mediated)

-Pathogenesis: gliadin (alcohol soluble fraction of gluten) is the disease causing component , induce IL5->
activation of CD8+ -> expression of NKG2D ( receptor for mic-A) -> attacked by lymphocytes

*variant HLA-DQ2 or HLA-DQ8 allele present in patients

- Associations include DM 1, Sjogren's syndrome, IgA nephropathy, thyroiditis, neurological disorders

(down, turner syndrome, epilepsy)

- Morphology: duodenum or proximal jejunum are diagnostic parts.

- Inc CD8+, Crypt hyperplasia and villus atrophy (MCQ)

- IgA antibodies against tissue tranglutaminase, Most sensitive test is Anti- endomysial IgA antibodies,
Anti- gliadin IgA antibodies , endoscopy is Gold standard. (MCQ)
- CF: often asymptomatic, diarrhea bloating chronic fatigue.

- Paediatric CD diagnosed at 6-24 months

- Characteristic dermatitis herpitiformis (10% patients)

- Complications: anemia, female infertility, osteoporosis, cancer ( higher than normal rate of malignancy
in CD)

- Tx: life-long gluten free diet.

ENVIRONMENTAL ENTEROPATHY

- tropical sprue, disease of developing countries, with poor hygiene conditions

- Underlying cause unknown but maybe defective intestinal barrier or exposure to fecal pathogens

- No accepted criteria for diagnosis available

AUTOIMMUNE ENTEROPATHY

- X linked

- Germline mutation in FOXP3 gene

- Txt: immunosuppresants in rare cases hematopoietic stem cell transplant

LACTASE DEFICIENCY /LACTOSE INTOLERANCE:

lactase-> brush border enzyme

-CF: chronic diarrhea with inc osmotic gap, bloating ,abd distention, NO STEATORRHEA.

1) congenital

- Autosomal recessive ie mutation in code encoding lactase

- Rare, presents with explosive diarrhea symptoms, abate by terminating milk products.

2) Acquired

- Due to down regulation of lactase gene expression following viral/bacterial inf.

- Dx: Hydrogen breathe test

- lactose free diet.

ABETALIPOPROTINEMIA
- autosomal recessive ,mutation in MTP

- Intracellular lipid accumulation ,vacuolization of small intestine epithelial cells (by oil red-O stain)

- Presents in infancy, failure to thrive, diarrhea, steatorrhea, def of fat sol vitamins, lipid membrane
defects recognized by acanthocutic red cells (burr cells)

WHIPPLE DISEASE:

- Described as intestinal lipodystrophy caused by tropheryma whippelii (gram +ve actinomycete)

- Triad of Wt loss, diarrhea (impaired lymphatic transport),arthralgia. Also lymphadenopathy (MCQ)

- Foamy macrophages present in laminated propria of small intestine, mesenteric LN, synovial
membranes of joints, cardiac valves and brain.

- Hallmark; foamy macrophages in Lamina Propria (PAS positive) MCQ

- Acid fast stain used to differ b/w intestinal TB and Whipple.

POLYPS:

- More common in colo-rectal region

- Most common: adenoma

•NON NEOPLASTIC POLYPS (ospie)

1) Hyperplastic: Most Common! ( In stomach, most common is Inflammatory polyps)

- Benign epithelial proliferation

- Pathogenesis: dec cell turnover & Shedding (piling up of goblet & absorptive cells)

- Morphology: Most common in left colon/recto-sigmoid junction (<5mm) histologically mature goblet
&absorptive cells

- Hallmark; Serrated surface architecture.

- NO MALIGNANT POTENTIAL.

2) Inflammatory

- Triad of rectal bleeding, mucus discharge & inflammation of ant rectal wall .

- Cause; impaired relaxation of anorectal sphincter.

- Can also form from chronic cycle of injury and healing.

- Histologically inflammatory infiltrates, erosion, epithelial hyperplasia.

3) Hamartomatous (Abnormal mixture of cells and tissues)

_ Sporadic or due to genetic or aquired syndromes

A) Juvenile polyps

- most common polyps in children (MCQ)

- SMAD4 mutated gene

- Focal malformation of epithelium &LP

- Most common in rectum (rectum bleeding) intussusception, obstruction, polyp prolapse may occur

Sporadic jp usually solitary (MCQ)

B) Juvenile Polyposis syndrome:

- Autosomal dominant synd. have from 3 to 100 polyps ( require colectomy)

- Extraintestinal. Manifestation: pulmonary arteriovenous malformation, clubbing.

- Morphology: pedunculated, reddish lesions with cystic spaces cysts filled with mucin and inflammatory
debris

- Juvenile polyposis syndrome A/w dysplasia not sporadic JP.

- MALIGNANT POTENTIAL (MCQ)

C) Peutz Jeghers syndrome:

- Autosomal dominant presents at 11 yrs multiple hamartomatous polyps (MCQ )& mucocutaneous
hyperpigmentation ( pigmented/melanotic macules- dark blue to brown),similar as freckels but
differentiated by presence in buccal mucosa

- Inc risk of MALIGNANCY (also cancers of other locations)

- STK11 mutated gene.

- Morphology: most common in small intestine (MCQ), large & pedunculated, smooth muscles mixed
with LP (difference b/w PJ syndrome & JP)

NEOPLASTIC POLYPS

- most common; Adenomas aka Adenomatous polyps.

- Ranges from small pedunculated to large sessile polyp.

- Size correlates with malignancy (>4cm has foci of cancer)

- Male dominant.

- Clinically asymptomatic except large polyps that produce bleeding cause anemia and billohs adenomas
that cause hypoproteinemic hypokalemia

- Morphology: velvet texture,

- Hallmark; hyperchromasia, elongation and stratification (epithelial dysplasia)

- Dec goblet cells.

- INC RISK OF ADENOCARCINOMA.

3 class:

i) tubular: small sessile, rounded tubular glands. Most common type. Malignant potential. Most
common site is colon (90%)-MCQ

ii) villous: large and sessile ,covered by villi. GREATEST RISK OF MALIGNANCY (MCQ)

iii) tubulovillous; mix of both

- Sessile serrated adenomas; common in right colon, resembles hyperplastic polyps (serrated
architecture)

- No dysplasia present.

- Intramucosal carcinoma; dysplasia breach the basement membrane and invade LP or muscularis.

FAMILIAL ADENOMATOUS POLYPOSIS (FAP):

_ Most common!

- Autosomal dominant

- Mutation in APC (WNT signalling pathway)

- APC holds ß-catenin in a resting cell. Under WNT signalling, APC detaches with ß-catenin which cause
cell proliferation. So loss of function mutation in APC causes overprolif of cells by ß-catenin.

- Numerous colorectal adenomas in teenage.

- Atleast 100 polyps required for diagnosis (MCQ)

- Dysplastic crypts present

- Colorectal adenocarcinoma develop in untreated patients.

- Txt: prophylatic colectomy

- Particularly occur in stomach and adj to ampulla of vater

- Extra-intestinal Manifestations: hypertrophy of retinal pigment epithelium (detected at birth) IMP

- ASSOCIATIONS: Gardner syndrome, Turcot syndrome.

- Gardner syndrome : FOReSt (MCQ)

1. F= FAP

2. O= osteomas
3. Re= retinal epithelium hypertrophy

4. St= supernumerary teeth

If all above + brain involvement = turcot syndrome.

HEREDITARY NON-POLYPOSIS COLORECTAL CANCER (HNPCC )/Lynch syndrome:

- most common. Young age.

- Autosomal dominant.

- Mutation in genes that encode proteins responsible for detection, excision and repair error of DNA
replication.

- Majority have mutation in MSH2 or MLH1.

- cancers at many sites in body.

- Inc risk of endometrial and ovarian cancer in females.

COLON ADENOCARCINOMA:

- most common malignancy of GIT.

- MC site is Rectosigmoid colon. (MCQ)

- Pathogenesis: in genetic abnormality 2 pathways involved APC/ ẞ- catenin and microsatellite

instability.

- Epigenetic ;methylation induced gene silencing

- Typically include mutation of APC additional mutation of KRAS

- In patients with DNA mismatch mutation in microsatellite repeats called microsatellite instability (MSI)

- So MUTATIONS: APC, K-RAS, SMAD4, p53.

- R/f: Dietary factors (low fibres, high red meat, high fats, dec calcium), Age, cigarette, FAP, HNPCC, IBD
(UC>>CD).

- Morphology: distributed equally mostly but tumor in proximal colon are mostly polypoid exophytic
mases

- In distal colon annular lesions ;napkin ring configuration/ Apple-core sign (MCQ)

- Most tumors have tall columnar cells (resembling dysplastic epi)

- Desmoplastic response

- May have signet ring cells

- CF: right sided colon present with fatigue( b12 deficiency)

- Left sided with occult bleeding,cramping,left lower quad discomfort

- Dx: fecal occult blood test, Colonoscopy with biopsy (Gold standard), Barium enema, DNA test,SERUM
CARCINOEMBRYONIC ANTIGEN (CEA) is used to detect recurrence.

- Metastasize to Liver (MC), lungs, bones, peritoneal cavity.

- Imp prognosis: depth of invasion & lymph node metastasis. (Imp)

HEMORRHOIDS:

- These are not varicose veins.

- Elevated venous pressure in hemorrhoidal plexus

- Common cause; constipation , pregnancy can also develop with portal HTN.

- Morphology: thin walled dilated submucosal vessels protrude the anal or rectal mucosa.

- Internal hemorrhoids: dilated superior hemorrhoidal complex, above dentate line/ anorectal line,
Painless

- External hemorrhoids: Dilated inf hemorrhoidal complex, below dentate /anorectal line, Painful.

APPENDICITIS:

MOST COMMON medical emergency. Common in youngs, acute or chronic. More In males.

- Inspected at McBurney's point. (At lateral 1/3 of ASIS and Umbilicus)

- Causes: Obstruction by Lymphoid hyperplasia (children), Fecalith (adults), ball of worms, tumors,
Gallstone.

Histological criteria: neutrophilic infiltration of muscularis propria, Not MUCOSAL INFILTRATION.

- CF: Pain at first periumbilical area, then at Rt lower quadrant (MCQ), Nausea, vomiting, Rebound
tenderness, inc WBC 15k-20k /micro litre.

- Complications: perforation, appendix mass, abscess, gangrenous necrosis, rupture, suppurative

perotinitis, bacteremia.

TUMORS OF APPENDIX: Most common is BENIGN CARCINOID (NEUROENDOCRINE)- TIP OF APPENDIX.

- others include adenoma, adenocarcinoma, mucocele, mucus cystadenoma, mucus

cystadenocarcinoma.
PEROTINITIS: Infl of peritoneum, usually due to fungal or bacterial inf.

- causes: burst stomach ulcer, burst appendix, diverticulitis, pancreatitis, surgery, trauma, cirrhosis.

- S/S: Abd pain, abd distention, fever, nausea vomiting, diarrhea, reduced urine output, fatigue.

C/F: Rebound tenderness.

- Most likely Associated organism with perotinitis: [Link] (MCQ)

- Leakage of bile into abd cavity: Sterile perotinitis (MCQ)

TUMORS OF PERITONEUM:

- Primary: Mesothelioma (A/w ASBESTOSIS)& Soft tissue tumors. Round cell tumor.

- Secondary/ metastatic.

LIVER

- Ballooning degeneration is a type of injury occurring when the hepatocyte loses its normal polygonal
shape and becomes swollen and rounded. Leads to lytic necrosis (swell and burst). It is seen in Ischemic
and hypoxic injury.

- Feathery degeneration: swollen hepatocytes with diffuse, yellow, foamy appearance seen in
Cholestatic liver disease.

-Steatosis/ fatty liver: accumulation of TAG fat droplets within hepatocytes. 2 types

1) Microvesicular steatosis: multiple tiny fat droplets which don't displace nucleus. Seen in acute fatty
liver of pregnancy, valproic acid toxicity.

2) Macrovesicular steatosis: single large fat droplet which displace the nucleus. Seen in DM, obesity,
alcoholic liver dis/ALD ,Hep C

- Centrilobular hemorrhagic necrosis refers to necrosis of hepatocytes immediately around the terminal
hepatic vein. Caused by ischemic injury and drug toxicity.

Results from LHF (hypoperfusion)& RHF (retrograde congestion). Liver has mottled appearance due to
hemorrhage and necrosis in Centrilobular regions referred as "Nutmeg liver"

* Cirrhosis: end-stage liver dis characterized by irreversible "diffuse" fibrosis with formation of
REGENERATIVE NODULES In chronic injury. (MCQ)
* Causes: ALD (most common 60 70%), Hep B,C, PBC, PSC, Hemochromatosis, Wilson's dis, alpha 1
antitrypsin def, non-alcoholic liver dis.

- Hepatic stellate cells (MCQ)ps in perisinusoidal space converts to myofibroblasts in acute and chronic
hepatic injury - form collagen, which compress nearby sinusoids and central vein- Inc pressure inside
sinusoids (MCQ)- Portal HTN -fluid pushed into tissues & large open spaces like peritoneal cavity/
ASCITES -leads to congestive splenomegaly due to fluid regurgitation thru portal vein back in splenic vein
to spleen - followed by Portal systemic shunts.

- CF: initially asymptomatic, anorexia, wt loss, jaundice, coagulopathy (less coagulation factors),
encephalopathy (less detoxification leads to more toxins like ammonia, gamma butyric acid which are
neurotoxins), Portal HTN .

-signs: jaundice, spider angioma & palmar Erythema & gynecomastia due to inc esterogen bcz not
metabolized by liver, Asterixis/ flapping tremors in hepatic encephalopathy, splenomegaly, ascites,
Caput medusae.

- Labs: elevated bilirubin, PT INR, aminotransferases, Dec albumin & sodium, CBC shows anemia,
leukopenia, thrombocytopenia.

- Dx: Liver biopsy (MCQ). Collagen fibers visible as blue on TRICHOME STAIN.

- Complications: progressive heart and liver failure, hepatorenal syndrome, hepato pulmonary
syndrome, Hepatocellular carcinoma.

* Portal HTN: portal venous pressure above 12 mmhg.

Prehepatic causes: Portal vein thrombosis, splenic vein thrombosis.

Hepatic causes: Cirrhosis (MC), metastatic malignancy, Sarcoidosis.

Post hepatic causes: Budd Chiari syndrome, RHF, constrictive pericarditis (leads to RHF eventually
pooling/ regurg of blood back to liver & systemic circulation).

- CF: Splenomegaly is cardinal finding, Ascites, Caput medusae, hepatic encephalopathy, CRUVEILHIER-
BAUMGARTEN SYNDROME : venous hum on auscultation from distention of para-umbilical veins.

* Budd Chiari syndrome: thrombosis of larger hepatic veins and sometimes IVC.

- causes: idiopathic, Primary PV oral contraceptives & pregnancy (hypercoaguable states), inherited
disorders of coagulation.

- CF: painful hepatomegaly, sudden onset of abd pain, marked Ascites, occasionally liver failure.

- inc Lfts, ascites, MRI or venography.

- Tx: thrombolysis with streptokinase

* Ascites refers to fluid more than 500 ml in peritoneal cavity.

- Signs: fluid thrill and shifting dullness.

- Managed by diuretics, sodium restriction, large volume paracentesis, trans jugular intrahepatic
portosystemic shunt.

- Exudative ascites is a protein rich and cell-rich fluid hence the diff btw serum and ascitic fluid albumin
is much less

- Transudative ascites is a protein poor and cell-poor fluid, hence the diff btw serum and ascitic fluid
albumin is much high.

* Portosystemic shunts: formed when portal systemic pressure increased, flow is reversed from portal
to systemic circulation - dilation of collateral vessels.

1) Esophagus: Esophageal varices- formed btw esophageal br of left gastric vein (portal) & esophageal
veins draining middle 3rd of esophagus into Azygous vein (systemic)

- Presents as HEMATEMESIS. Managed by beta blockers like propanolol, endoscopy with band ligation
in acute bleeding.

2) Umbilicus: Caput medusae - formed by para-umbilical veins connecting left br of portal vein with
superficial veins of Ant abd wall (systemic)

3) Rectum: Hemorrhoids- formed btw Sup rectal veins (portal) and middle & inf rectal veins (systemic)

* Hepatic encephalopathy: neuro-psychotic syndrome caused by cirrhosis, which progresses from

confusion to coma.

- less detoxification leads to more toxins like ammonia, gamma butyric acid which are neurotoxins.

- CF: progressive mental deterioration (confusion, drowsiness, aggressiveness, coma), Flapping tremors/
Asterixis, constructional apraxia (inability to draw objects), Hyper reflexia; bilateral extensor plantar
responses.

- Tx: Lactulose (laxative), Neomycin to dec bacterial content of bowel.

BILIRUBIN METABOLISM

* RBC broken down into Hb and membranes. Hb consists of Heme (which comprises 4 protoporphyrin
rings & Fe) & globin chains.

* Heme degraded to Biliverdin and Fe by HEME OXYGENASE which reduced to Bilirubin by BILIVERDIN
REDUCTASE.
* Unconjugated/ Indirect bilirubin is lipid soluble, end product of heme degradation. Binds to albumin
and transported to liver hepatocytes.

* Conjugated /Direct bilirubin is water soluble. Formed by conjugation of UCB by UDP

glucoronyltransferase (UGT1A1). Stored in GB , transported to duodenum via CBD where converted to
urobilinogen by intestinal bacteria.

* 80% Urobilinogen is converted to urobilin and excreted in feces gives characteristic brown color.

* 20% urobilinogen recycled to liver (90%) and kidneys ie in urine (10%).

- In Criggler najjar and Gilbert syndrome UGT1A1 deficiency ( Unconjugated high), while in Dubin
Johnson and Rotor syndrome defect in canalicular transport In bile (Conjugated bilirubin high)- MCQ

* AUTOIMMUNE HEPATITIS: Chronic , progressive hepatitis with all the features of autoimmune diseases
also associated with them. More in females. Inc Plasma cells (MCQ), Hepatocellular "rossettes" in areas
of marked activity.

- by CD4, CD8 (MCQ)

1) Type 1: More common. In elders. Characterized by ANA, SMA, anti-SLA/LP, AMA antibodies.

2) Type 2: Usually in children and teenagers. Characterized by anti-LKM1, ACL-1 antibodies.

* VIRAL HEPATITIS: infl of hepatocytes by virus- viral proteins displayed on cells by MHC I- CD8+ T cells
recognize -cytotoxic killing - Cell apoptosis (Councilman bodies)- liver damage. (MCQ)

CF:

1) Asymptomatic stage: minimal elevation of serum aminotransferases, Ps of antiviral antibodies,

asymptomatic inf most common in HCV.

2) Prodromal stage: fever, painful hepatomegaly, elevated serum aminotransferases (ALT>>>AST),

atypical lymphocytosis (CD8)

3) Icteric stage: Jaundice (UCB+ CB), Dark urine, light colored stool, Pruritis.

* Morphology: Hepatocyte injury in form of Ballooning degeneration, cholestasis, kupffer cells

hypertrophy and hyperplasia, COUNCILMANN BODIES ie hepatocytes undergoing lobules. (MCQ )

- ONLY HEP B&C HAVE CARRIER STATES & RISK OF HEPATOCELLULAR CARCINOMA, BOTH RESPONSIBLE
FOR CHRONIC HEPATITIS + CIRRHOSIS. (MCQ)

- ONLY HEP B HAS DOUBLE STRANDED DNA, WHILE REST HAS SINGLE STRANDED RNA. (MCQ)

-BOTH HAV & HEV lack an envelope and are not destroyed by the gut.
* Hep A: single stranded RNA, incubation period 2-6 weeks (MCQ), transmitted by Feco-oral route
(MCQ) contaminated food (MCQ), more in Travellers, day care centers, prisons.

- Active inf: Anti -HAV IgM

Recovery : Anti -HAV IgG (protective antibody)

*HEP B: DOUBLE STRANDED DNA (MCQ), Incubation period 4-26 weeks, mode of transmission via blood
(MCQ )ie IV, sexual, pregnancy, Breast feeding.

- Uses RNA dependant DNA polymerase/ Reverse transcriptase to convert mRNA to DNA to be packaged
in capsid. (For TB: DNA dependant RNA polymerase)

- Serology:

Hep B Surface antigen HBsAg is first marker due to which there is GROUND GLASS HEPATOCYTES
(MCQ ),also sanded nuclei.

- Dane particles are the complete, infectious virions of the Hepatitis B virus (HBV).

- HBeAg and HBV- DNA= infective particles (MCQ)

Anti-HBc (core)- IgM= window phase

Anti-HBs =protective antibody /vaccination (MCQ)

- prevented by recombinant vaccination

- Tx: interferon alpha, lamivudine (MCQ), liver, transplantation.

* HEP C: single stranded RNA, incubation period 2-26 week, mode Of transmission via blood ie IV, sexual
contact, child birth.

- Bile duct epithelial cell proliferation, lymphoid aggregate formation.

- Serology:

episodic elevation in serum aminotransferases

HCV RNA -IgG is not protective antibody.

-Recombinant immunoblot assay RIBA is confirmatory.

* HEP D: single stranded RNA, transmit by blood. Almost always ps along with HBV.
- COINFECTION with HBV results in fulminant hepatits, recovery, or chronic hepatitis (less likely)

- SUPERINFECTION with HBV results in fulminant Hepatitis, acute severe Hepatitis, or chronic hepatitis
(more likely)

- HDV IgG not protective, IgM active inf.

*HEP E: single stranded RNA, incubation period 2-8 weeks, transmission is WATER BORNE (MCQ)

- only causes Acute hep, FULMINANT HEPATITIS IN PREGNANT WOMEN (MCQ)

- No vaccine.

* Chronic Hepatitis: if more than 6 months.

- portal tract infl, interface hepatitis, and bridging necrosis

- Hallmark of chronic hepatitis is deposition of fibrotic tissue and regenerative nodules ie Cirrhosis.

- only by HBV (10%) and HCV (60%)

* Fulminant Hepatitis: hepatic encephalopathy occurring within 2-3 weeks of hepatitis (acute liver
failure)

- causes: Drug and chemical toxicity=52% (paracetamol, isoniazid, antidepressants, methyl dopa), HAV or
HAB 12%, HEV IN PREGNANT WOMEN, Idiopathic 18%, Reye syndrome.

* ALCOHOLIC LIVER DISEASE: refers to hepatic changes in pts with chronic alcohol consumption.

- AST>>>>ALT (2:1 ratio). Also Inc ALP.

- Presents in 3 forms:

1) Hepatic steatosis /Fatty liver:

- bcz of more fat production due to its low oxidation and more synthesis.

- Larger, yellow, greasy liver. Micro and Macrovesicular steatosis.

- It is completely REVERSIBLE if alcohol intake is stopped.

2) Alcoholic Hepatitis:

Liver is mottled red with bile stained areas, cell swelling and necrosis, MALLORY BODIES -MCQ
(damaged intermediate filaments visible as cytoplasmic inclusions), neutrophilic infiltration, fibrosis
3) Alcoholic Cirrhosis:

- Pericellular or CHICKENWIRE LIKE FIBROSIS around HEPATOCYTES (MCQ)

- Micronodular cirrhosis and Macro nodular cirrhosis giving "HOBNAIL APPEARANCE" on surf of liver.

- "LAENNEC CIRRHOSIS" ie formation of broad and tough scar tissue from ischemic necrosis.

- IRREVERSIBLE

- portal HTN and it's complications.

* NON-ALCOHOLIC FATTY LIVER DISEASE (NAFL)

- it is a condition that resembles alcohol induced liver dis, but occurs in non-alcoholics.

- accounts for 70% cases of chronic hepatitis of unknown cause, cirrhosis in 10-30% cases, most common
cause of " cryptogenic cirrhosis"

- Inc risk of hepatocellular carcinoma.

- R/F: Metabolic syndrome (HTN, insulin resistance, DM type 2, hyper-insulinemia, Obesity,

Dyslipidemia) MCQ.

- Pathogenesis : due to less response of insulin receptors - more fat storage, less fat oxidation- less
secretion of FA into bloodstream (lipoproteins)- inc syn of FFA & uptake unto Hepatocytes

* CF: asymptomatic, abnormal LFTs, ALT>>>AST, INC GGT

* Non-alcoholic Steatohepatitis (NASH): intermediate form of liver damage.

- steatosis, multifocal parenchymal infl, Mallory hyaline, necrosis, and sinusoidal fibrosis.

* HEMOCHROMATOSIS: excessive accumulation of body iron, leading to tissue injury.

- Types:

1) Hereditary Hemochromatosis: Autosomal recessive, mutation of HFE gene on Chr 6, mostly C282Y
gene resulting in inc uptake of iron in intestines. Male dominant, above 40 yrs.

2) Secondary Hemochromatosis: Blood transfusions, ineffective erythropoiesis (thalassemia etc), inc

intake, CLD, porphyria cutanae tarda.

* CF: Liver (Micronodular cirrhosis and HEPATOCELLULAR CARCINOMA), Pancreas ( DM ie bronze

diabetes), Skin (hyperpigmentation), Heart (Restrictive cardiomyopathy, CHF), Gonads (hypogonadism),
Bones and joints (arthropathy of metacarpophalangeal joints)

* Diagnosis: Inc Iron, ferritin, dec TIBC, Transferrin saturation> 45%. Ecg, HFE screening,

* Liver biopsy shows inc iron content, which can be quantified by PRUSSIAN BLUE/ PERL'S STAIN.
* Tx: weekly phlebotomy of 500 ml blood (250mg iron), Deferoxamine to excrete iron.

* WILSON'S DISEASE: aka Hepatolenticular degeneration which is a genetic disorder of copper

metabolism resulting in accumulation of toxic levels of Cu.

- Autosomal recessive, characterized by dec synthesis of CERULOPLASMIN due to mutation of WD gene/

ATP7B gene on chr 13. Which normally forms ceruloplasmin and excrete excess Cu in bile.

- so Cu from intestines is absorbed and taken to Liver, where it can't be incorporated into ceruloplasmin
also can't be excreted in bile so accumulates in liver.

- CF: Liver (acute or chronic hepatitis), Eyes (KAYSER- FLEISCHER RINGS ie greenish brown discoloration
of cornea due to it's deposition in Descemet's membrane- 60% cases), CNS ( movement disorders if
deposit in putamen, hemi-ballismus if deposit in Subthalamus, Dementia if deposit in cerebral cortex)

- Dx: Dec serum Ceruloplasmin (BEST), inc hepatic Cu, inc Cu in urine.

- best seen by RHODININE stain! (MCQ)

- Avoid high Cu diet, Penicillamine which inc it's excretion, Zinc Dec it's absorption.

* α1 - antitrypsin AAT def: Autosomal recessive disorder marked by low levels of AAT, which is a
protease inhibitor ie inhibits elastase which are normally released from neutrophils during acute infl.

- means no inhibition of elastase - elastase breaks - Liver (neonatal hep, Micronodular cirrhosis, risk for
HEPATOCELLULAR CARCINOMA) & Lungs (Pan-acinar emphysema) -MCQ.

- most commonly diagnosed genetic liver dis in infants and children.

- AAT is produced by Pi (Protease inhibitor)gene on chr 14. Normal genotype is PiMM.

- most common abnormal allele is Z : PiZ (MCQ)

- PiZZ variant: homozygotes with extremely low levels of AAT, high risk pts

PiMZ variant: heterozygotes with moderately low levels of AAT, medium risk pts.

- Characteristic feature is RED cytoplasmic granules which are PAS STAIN POSITIVE and diastase
resistant.

- Pooled AAT given IV.

* PRIMARY BILIARY CIRRHOSIS (PBC):

- Chronic progressive cholestatic liver dis of unknown cause, possibly Autoimmune ie T cell mediated.
Characterized by destruction of intra-hepatic bile ducts -bile leakage.
- CF: middle ages women, Pruritis is initial complaint, jaundice, osteomalacia (due to def of Fat soluble
vitamins), osteoporosis, Skin xanthomas, hepatosplenomegaly, leads to liver failure.

- A/w other autoimmune dis like Sjogren's syndrome, Raynaud's phenomenon, Celiac dis, systemic
sclerosis, autoimmune hep.

- Dx: elevated serum cholesterol, CHOLESTATIC JAUNDICE ie Inc CB, ALP, GGT. Confirmed by liver biopsy,
inc serum IgM, ANTI-MITOCHONDRIAL ANTIBODY (AMA)- 95%.

- Morphology: Lymphocytic infiltrate in portal tracts, granulomatous destruction of bile ducts.

-Tx: Urodeoxycholic acid- it slows progression of dis (main) , Cholestyramine -anion binding resin used
for Pruritis.

* SECONDARY BILIARY CIRRHOSIS: due to prolonged extrahepatic biliary obstruction, which results in
intra-hepatic injury.

- prolonged extrahepatic biliary obstruction results from Gall stones (MC), biliary atresia, bile duct
strictures, pancreatic head CA.

-similar CF.

- Diff from PBC by negative serum IgM, and AMA.

*PRIMARY SCLEROSING CHOLANGITIS (PSC): Chronic progressive cholestatic liver dis of unknown cause
possibly Autoimmune. Characterized by progressive infl and fibrosis accompanied by extrahepatic and
intrahepatic bile strictures.

-CF: same as of Obstructive jaundice. Inc risk of CHOLANGIOCARCINOMA.

- A/w Ulcerative colitis (MC), Crohn's dis (both IBDs), chronic pancreatitis.

- Dx: Cholestatic jaundice- inc CB, inc ALP, GGT. Inc IgM, p-ANCA.

"BEADING APPEARANCE" ie multiple areas of bile duct strictures and dilatations seen on MRCP/ERCP.

- PERI-DUCTAL PORTAL TRACT "ONION SKIN" FIBROSIS and infl.

-Tx: Urodeoxycholic acid- it shows progression of dis, Cholestyramine -anion binding resin used for
Pruritis.

* BENIGN LIVER TUMORS:

1) Cavernous hemangioma: Most common benign tumor.

- discrete ,red blue soft nodules <2cm located beneath capsule.

- tumor consists of vascular channels in bed of CT.

- chief significance: not to be mistaken for metastatic tumors.

- rare cause of intraperitoneal hemorrhage.

2) Liver cell Adenoma: more common in women and A/w oral contraceptives (estrogen), regresses with
termination of use.

- Clinical significance: if ps as intrahepatic mass- mistaken as Hepatocellular CA. Subcapsular adenomas

have tendency to rupture, esp during pregnancy (under estrogen stimulation)- life threatning. Rarely can
transform into Hepatocellular CA esp in pts with glycogen storage dis

- ps in form of cords and sheets, Portal tracts are absent, instead arterial vessels and veins are
distributed thruout, therefore it's a highly vascular tumor.

- Mutations : HNF-@, ẞ CATENIN, GP130.

3) Nodular Hyperplasia: solitary or multiple hepatocellular nodules may develop in non-cirrhotic liver.

- two conditions:

A: Nodular focal hyperplasia: well- demarcated but poorly capsulated ,lesion is lighter (yellow) than liver.

B: Nodular Regenerative hyperplasia: liver entirely transformed into nodules.

* MALIGNANT TUMORS:

1) HEPATOCELLULAR CARCINOMA (HCC): Most common primary malignant tumor of liver. 3rd leading
cause of cancer deaths.

- More in males, 4 to 6 decade.

- causes: Chronic HBV, HCV, Cirrhosis, Aflatoxin released by aspergillus molds which induce mutation of
p53 gene (MCQ), Hereditary Hemochromatosis, Wilson's dis, AAT def, Exposure to PVC, arsenic or
thorotrast (MCQ), Oral contraceptives, NOT A/W SMOKING.

- Morphology: Focal, multi focal or diffusely infiltrative. Neoplastic cells characteristically contain BILE.

- CF: Mostly asymptomatic, discovered on screening. Portal HTN symptoms.

- Metastatize to LUNGS first, then to other sites via hepatic vein system.

- Production of ectopic hormones : Erythropoietin (2° polycythemia), insulin like factor (hypoglycemia)

- Dx: inc ALPHA FETO-PROTEIN (AFP)-50 to 75% cases. Sudden inc in ALP GGT. Liver biopsy.

2) CHOLANGIOCARCINOMA:
Most common malignancy of biliary tree. Arises from bile ducts within and outside the liver.

- R/F: PSC, Choledochal cyst, Liver fluke, Thorotrast exposure, HBV HCV

- site: Ampulla of Vater & CBD (most common)20 30%, Junc of rt and left hepatic duct (Klatskin
tumor)60%, intrahepatic ducts 10%.

- extremely firm and gritty. Tubular glandular structures lined by cuboidal epithelium, non-bile stained
neoplastic cells.

-CF: Obstructive jaundice, COURVOISIER'S SIGN ie palpable non-tender GB. Poor prognosis.

3) HEPATOBLASTOMA:

- Rare tumor, most common liver tumor of young childhood (MCQ). Fatal if not treated. More in males.

- epithelial and mixed type & mesenchymal type.

- Characteristic feature is frequent activation of WNT signalling pathway- inc FOXG1 expression which is
regulator of TGF B pathway.

* METASTATIC TUMORS: Most common liver cancer.

- Lungs most common, Breast, Colon, leukemia, lymphoma.

*CHOLELITHIASIS: 2 types

1) Cholesterol stones: more common. Contains 50-100% cholesterol.

- 80-90% are radiolucent (not visible on x-ray) while 10-20% are radio-opaque due to ps of Calcium
carbonate.

- Supersaturation of bile with cholesterol (mcq) due to hypersecretion of cholesterol by Hepatocytes &
Gall bladder stasis.

R/F: More in West, aging , obesity, rapid wt reduction, female gender (oral contraceptives, pregnancy)

2)Pigment stones/ Bilirubin stones: less common

A) Black stones: composed of oxidized inorganic Ca salts + CB which are 50-75% radio-opaque. STERILE
GB.

B) Brown stones: composed of pure inorganic Ca salts + UCB which are radiolucent due to calcium
soaps.

- soft Nd greasy

- Sign of infected GB eg [Link], Ascaris, liver fluke.

R/F: More in Asians, rurals, chronic hemolytic syndromes, biliary infection, Git dis like Crohn's dis, ileal
bypass, cystic fibrosis.

*CF: asymptomatic 70 80% cases, take years, Biliary colic ie sudden dull post prandial pain (several hrs)
in Rt upper quadrant. Pain is "colicky" in nature .may radiate to RT SHOULDER or BACK.

- nausea, vomiting, dyspepsia, flatulence, NO FEVER!!

-complications: Cholecystitis (most common), CBD obstruction, GB cancer, GB ileus, Acute pancreatitis,
perforation.

*ACUTE CHOLECYSTITIS: acute infl of GB. Almost always A/w Gallstones.2 types

1) Acute calculous cholecystitis: obstruction of neck and cystic duct by gallstones.

2) Acute acalculous cholecystitis: results from causes not A/w stones eg severe trauma/burns,
multisystem organ failure, post partum state, post op.

-CF: FEVER, nausea, vomiting after 15-30 mins after eating.

- Pain is epigastric initially then radiates to RUQ, referred to RT SCAPULA!!

- MURPHY'S SIGN: RUQ tenderness during inspiration by the examiner's Rt subcostal palpation.

- COURVOISIER'S SIGN: palpable non-tender GB.

-Labs: leukocytosis, ALT AST normal, elevated ALP ,inc CB, U/S is gold standard. (MCQ)

- morphology: GB is large and tense. Lumen contains turbid bile, with large amount of fibrin, frank pus,
& hemorrhage. Stones maybe ps.

- Empyema of GB: occurs when exudate is virtually pure pus (MCQ)

- Gangrenous cholecystitis occurs in severe cases characterized by green-black necrotic organ with
perforations. Due to ischemia by compression of vessels.

* CHRONIC CHOLECYSTITIS: Chronic infl of GB. Most common symptomatic disorder of GB.

- causes: recurrent cholecystitis, cholelithiasis (90%), Chronic infl, [Link] & enterococci (1/3)

-Morphology: ROKITANSKY-ASCHOFF SINUSES ( outpouchings of mucosal epithelium thru the wall)

- Complications:

1) HYDROPS of GB: atrophic, obstructed GB containing clear secretions.

2) XANTHOGRANULOMATOUS CHOLECYSTITIS: shrunken, nodular, & chronically infl GB.

3) PROCELAIN GB: rare form, dystrophic calcification within GB, A/w inc cancer risk.

* CHOLESTEROLOSIS: aka Strawberry GB

- characterized by excess cholesterol in bile -yellow speckled mucosal surf.

- microscopically collections of lipid-laden macrophages within lamina propria.

- not directly A/w GB formation.

* CA of GB: most common malignancy of extrahepatic biliary tract. Most common R/F is Gallstones
(95%). Female domination. 70 yrs

- Most common type is adenocarcinoma. Most common site is fundus and neck.

- Liver invasion occurs early and centrifugally

- growth pattern: infiltration (common) and exophytic

- Metastatize: Peritoneum, Git, lungs.

PANCREAS

PANCREATIC DIVISUM:

- most common congenital anomaly of pancreas. Results from dorsal and ventral pancreatic bud to fuse

- Dorsal panc duct( santorini) drains the bulk of pancreas thru minor papilla.

- the ventral panc duct (wirsung) which is normally the main panc duct remains short and drains only a
part of head of panc thru major papilla (of Vater)

- imc risk of chronic pancreatitis.

Annular pancreas: refers to band like ring of pancreas encircling the 2nd portion of duodenum.

- due to failure of complete rotation of ventral panc bud in the 5th week embryogenesis.

- may cause duodenal obstruction and present with gastric distention and vomiting.

ECTOPIC PANCREAS: ps of panc tissue in the submucosa of other parts of GIT.

- common sites: stomach most, duodenum, jejunum, Meckel's diverticulum.

ACUTE PANCREATITIS: acute infl of pancreas.

- Causes: GET SMASHED (gall stones most common MCQ, Ethanol, Trauma, Steroid, Mumps,
Autoimmune, Scorpion venom, Hyperlipidemia, Endoscopy, Drugs thiazides diuretics, azathioprine)

- Results from autodigestion of pancreas by inappropriate activation of panc enzymes.

- can be mutation of trypsin: hereditary pancreatitis (MCQ)

- Morphology: Fat necrosis and deposition of Ca soaps, Destruction of blood vessels and hemorrhage
(MCQ), edema, acute infl, proteolytic destruction of panc parenchyma.

- Acute interstitial pancreatitis: mild form, characterized by interstitial edema and focal areas of fat
necrosis.

- Acute necrotizing Pancreatitis: Moderate form, necrosis of acinar and ductal tissues and islets.

- Acute hemorrhagic pancreatitis: Most severe form, parenchymal necrosis with diffuse hemorrhage.

- CF: Epigastric pain (cardinal), sitting forward relieve pain (MCQ), pain radiates to back, nausea
vomiting.

- signs: PERIUMBILICAL DISCOLORATION (CULLEN'S SIGN,), FLANK DISCOLORATION (GREY TURNER'S

SIGN)

- Labs: Inc serum amylase and lipase (MCQ),x-ray shows Sentinal loop sign and colon cut-off sign.

- Complication: organ failure, DIC, abscess, pseudocyst, chronic pancreatitis, edema, shock, ARDS (MCQ)

- management: NPO, IV fluids, analgesia.

CHRONIC PANCREATITIS:

Causes: Alcohol (MC), panc duct obstruction, hereditary pancreatitis, neoplasms.

- Morphology: Progressive parenchymal FIBROSIS. reduced no and size of acini with relative sparing of
islets.

- CF: Abd pain (severe, recurrent, epigastric, radiates to back), Endocrine insufficiency (DM), exocrine
insufficiency (anorexia wt loss steatorrhea)

- ERCP shows Dilated chains of Lakes ie sacculations with intervening short strictures.

PANCREATIC CYSTS AND TUMORS:

PANC PSEUDOCYST:

- MOST COMMON Panc cyst (75%)

- refers to localized collections of necrotic -hemorrhagic material rich in panc enzymes.

- called "pseudo" bcz it lacks epithelial lining and wall is formed by granulation tissue.

Causes: acute and chronic panc, trauma.

INSULINOMA: /BETA CELL TUMOR

- most common islet cell tumor. Produces insulin.

- WHIPPLE TRIAD: Episodic hypoglycemia, CNS dysfucn (confusion, anxiety, coma), Dramatic reversal of
symp by glucose intake.

- Labs: elevated Insulin, Dec glucose, no ketoacids, C-peptide elevated in insulinoma but not in
exogenous insulin intake.

GASTRINOMA: /G -CELL TUMOR

- often a malignant tumor, produces gastrin.

- A/w ZOLLINGER ELLISON SYNDROME (MEN-1): elevated gastrin, hyperacidity, recurrent peptic ulcer
dis.

- most common benign tumor of pancreas: Serous cystic. (MCQ)

PANCREATIC CARCINOMA:

- most common is Adenocarcinoma (MCQ) 95% are exocrine.

- RF: Smoking, high fat diet, chronic pancreatitis, DM, liver cirrhosis, alcohol.

-Mutations: K-RAS (early),p16 (intermed stage), p53 SMAD4 & BRCA2 (LATE STAGE) MCQ

- location: Head (60%),body 15%, tail 5%, entire gland 20%.

- Morphology: Most common type: Ductal adenocarcinoma (MCQ) highly invasive, elicits "Desmoplastic
response" ie non-neoplastic host rxn composed of fibroblasts, lymphocytes, ECM.

- Carcinoma of Head of PANC: produces symp early, mostly jaundice bcz obstructs CBD and cause
distention of biliary tree.

- Carcinoma of body and tail: prod no symptoms, remains silent bcz not impinge on CBD.

- CF: Painless Obstructive jaundice (CA of head) MCQ, epigastric pain, anorexia, Wt loss, Palpable non-
tender GB (COURVOISIER'S SIGN)

- Serum levels of CARCINOEMBRYONIC ANTIGEN (CEA) & CA19-9 ANTIGEN are often elevated but not
diagnostic. (MCQ)

MICROBIOLOGY
* Spore forming Gram +ve rods: Bacillus and Clostridium.( MCQ)

* Bacillus cereus: Food Poisoning/reheated rice syndrome. (MCQ)

* 2 enterotoxins: one same as cholera toxin (inc cAMP by ADP ribosylation of G protein -MCQ) AND
other as staph enterotoxin (act as Supra antigen ie by inc IL1&2)

*2 syndromes: Emetic type (4 hrs incubation time, cause emesis), Diarrhoeal type (8 hrs incubation
period cause bloody diarrhea)

* Only symptomatic Tx given.

2)C. Botulinum: Botulism aka FLOPPY BABY SYNDROME in children. Transmit by preformed toxins in
CANNED foods, contaminated vegetables & meat (MCQ)

* Blocks release of Ach ie inhibit motor neurons. (MCQ)

* 5 Ds: Descending paralysis (flaccid), Diplopia, Dysphagia, Dysarthria, Dyspnea.

*2 forms: wound and infant botulinum.

3) C. Perfringens: causes Gas Gangrene and Food Poisoning.

* Gas Gangrene: Spores from soil, it produces alpha toxin LECITHINASE (MCQ) in traumatized muscles
which cause hemolysis, degraded enzyme produce gas in tissues.

- Pain, swelling and gangrene in wound site like stab (MCQ)

- identified by sugar fermentation rxn and organic acid production.

- Penicillin G is DOC.

* FOOD POISONING: exotoxin from ingested meal. Member of normal flora of colon but not in small
bowels where it causes diarrhea, acts as supra antigen. No essay for toxin. Symptomatic Tx given.

Both salmonella and shigella are gram -ve , non lactose fermenting so not Grow on MacConkey's agar,
instead by Hektoin agar or TSI agar (ospie ),oxidase -ve , and invade through M cell of peyer's patches.

SALMONELLA:

- most common food poisoning (MCQ)

- black on Hektoin agar (Shigella Green on Hektoin agar) .All motile.

- Indole -ve , H2S production (MCQ)

- Acid labile.
- Invades through macrophages to get into colon.

- SALMONELLA ENTERICA: causes inflammatory diarrhea, by eating undercooked meat like chicken.

- SALMONELLA PARATYPHI: causes Paratyphoid fever, most common cause of osteomyelitis in sickle cell
patients. (MCQ)

- SALMONELLA TYPHI: always from a human source, cause: typhoid fever, gall bladder (carrier), red
spots, typhoid marry, step ladder Fever (MCQ), cause pea soup diarrhea, live attenuated vaccine.

- 3 antigen (OHK)

- humans are reservoir (MCQ)

- Three phases: 1. Constipation followed by diarrhea , headache, fever. 2. Rose spots in 2nd week (MCQ)
3. Bacteremia.

- High temperature but slow pulse. Characteristic STEPLADDER TYPE FEVER (MCQ)

- High ID50 atleast 100,000 organisms.

- 4 tests: blood culture 1st week (MCQ)

- Stool isolation (2nd week)

- Felix Widal test Confirmatory: detects IgG & IgM against outer membrane protein (O and H)

- Typhidot test: serological test to detect IgM and IgG antibody. Quick and early diagnosis compared to
traditional blood cultures.

- complications: Gallbladder cancer, intestinal perforation (MCQ), arthritis, hemorrhage.

- DOC is Ciprofloxacin (MCQ)

SHIGELLA:

- Humans

- Spread via cell to cell, no hematogenous

- No H2S production , no flagella (immotile), no lactose ferment.

- Endotoxin ie shiga [Link] binds to 60s subunit of ribosomes and inhibit translation.

- Low ID50 (MCQ) like 100 organisms.

- Acid stable

- Effect of antimicrobial on fecal excretion = shortens duration ( SHigella= SHortens )

- Abdominal pain --> tenesmus, bloody mucus stools (bacillary dysentery= enterocolitis)

- most common cause of dysentery (MCQ) similar to EIEC (MCQ)

- No vaccine

- 4 F's= finger, flies, food, feces.

- Invasion of M cell in Peyer's patches is key pathogenicity

- Stool culture.

- Methylene blue test for neutrophils. If + , can be salmonella and shigella and campylobacter

- Shigella = green colonies on Hektoin agar (indole +), different from Salmonella which grow black.

- Renal failure , low platelets, HUS (e-coli also causes this)

- tx by FQ or Macrolide.

Lactose fermenting enteric bacteria: MacConkey's agar= pink colonies.

CEEKS milk.

1. C= citrobacter

2. E= [Link]

3. E= Enterobacter

4. K= klebsiella

5. S= serratia

YERSINIA ENTEROCOLITICA:

- gram - , pleomorphic with bipolar staining.

- Pets feces, contaminated milk or pork

- Acute bloody diarrhoea

- Pseudo-appendicitis

- Reactive arthritis in adults

- ALL CURVED RODS ARE OXIDASE +ve:

1. Campylobacter. 2. [Link]. 3. Vibrio cholera

CAMPYLOBACTER JEJUNI:

- camp = camp fire , grows at 42°C

- Gram -ve , comma shaped polar flagella, oxidase +ve

- Major cause of bloody diarrhea in children

- Feco oral or via ingestion of undercooked contaminated poultry or meat (MCQ)

- Gullian barre syndrome and reactive arthritis.

- Foul smelling diarrhea

ESCHERICHIA COLI:

- gram -ve , indole +ve rod.

- Normal flora of colon.

- Virulence factor= fimbriae i.e pilli (MCQ )~ cystitis and pyelonephritis, capsular -K antigen ~ pneumonia
and neonatal meningitis, Flagellar- H antigens, LPS toxin~ septic shock. MC cause of gram -ve sepsis.

- MC cause of UTI in pregnant women (MCQ)

- form pink colonies on MacConkey's agar/ lactose fermenting (MCQ)

- 4 Species:

1) Enteroinvasive (EIEC): invades mucosa causing bloody diarrhea like Shigella (MCQ)

2) Enterotoxigenic (ETEC) cause traveller's diarrhea by producing two toxins:

SG = stable , cGMP

LA= labile , cAMP.

3) Enteropathogenic (EPEC) no toxin, no infl, but produce diarrhea usually in children.

4) Enterohemorrhagic (EHEC) classic serotype [Link] 0157: H7. Doesn't invade but produce shiga-like
toxin that cause bloody diarrhea (MCQ ). Usually from undercooked beef. Causes HUS in 10% people
(triad of hemolytic anemia, thrombocytopenia And acute RF)

* ONLY [Link] WHICH DOES NOT FERMENT SORBITOL!

VIBRIO CHOLERA:

- gram -ve , flagellated, comma shaped, oxidase +ve, no H2S. COLOURLESS COLONIES on MacConkey's
agar, while form Yellow colony on TCBS AGAR.

- Acid labile.

- not invasive.
- Major pathogenic strain in world is 01. (MCQ) Other is 0139 (Chennai) in developing world.

- Produce rice water diarrhea via enterotoxin that activates Gs, inc cAMP.

- High ID50, ingestion of contaminated water or by raw/ contaminated seafood like shellfish (MCQ)

- Cholera O antigen differentiates it between pathogenic and non-pathogenic strain (MCQ)

- [Link] causes cellulitis~ high serum iron patients.

- can CAUSE SEVERE LIFE THREATENING DIARRHEA (MCQ)

- 3 stages:

A) Stage of evacuation: watery diarrhea in 24 hrs, vomiting

B) Stage of Collapse: Dehydration, sunken eyes, SCAPHOID/CONCAVE ABDOMEN, washerman hands

feet, cramps, RF.

C) Stage of Recovery

- Culture used is TSI (MCQ)

- Erythromycin is DOC (MCQ)

HELICOBACTER PYLORI:

- gram -ve , curved, urease +ve , catalase +ve , oxidase +ve.

- Virulence factors include urease (major virulence factor), Catalase, Adhesins, Cytotoxin Associated
gene A (CagA) toxin

- Urease produce acidic environment for h pylori to survive (MCQ)

- feco-oral route.

- Antrum of stomach

-gastric ulcer, Gastritis, Gi adenocarcinoma, MALToma.

- Stool antigen test, urea breathe test. Biopsy is confirmatory but is invasive.

- Triple and quadruple therapy.

CESTODES/ TAPEWORMS

- head (scolex), have suckers ,hooks.

1. taenia solium:

- pork tapeworm -MCQ (intermediate host),in pig’s skeletal muscles.

- Defintive host of both taenia is human.

- proglottid head seen on O&P, hookers present around 4 suckers. (MCQ)

- larvae->taeniasis, ingested egg->cysticercosis (through faeces of infected human)

- neurocysticerosis, presents with seizure, looks like swiss cheese on MRI.

- Pumpkin - seeds like appearance on stool examination (MCQ)

- txt: albendazole, dead cystecerci causes inflammation in organs (specially in brain) MCQ

- txt: praziquantel for taeniasis.

2. taenia saginata:

- 4 suckers on scolex, no hooks (MCQ)

- larvae causes taeniasis (undercooked meat)

- malaise,mild cramps occur

- motile proglottids present

- txt: praziquantel

3. diphylobothium latum* (longest tapeworm)

- fish tapeworm

- fresh water fish and crustaceans are intermediate bost (MCQ)

- 2 sucking grooves on scolex

- wide proglottids segments on o&P

- causes diarrhea ,b12 def causing megaloblastic anemia

- diagnosis by egg with OPERCULUM in stool.

- txt:praziquental or niclosamide

4. echinococcus granulosus

- dog tapeworm (via dog faeces)/ definite host (MCQ)

- intermediate hosts: sheep

- scolex has 3 proglottids

- causes unilocular hydatid cyst disease (MCQ)

- egg shell calcification in liver(migrates primarily to liver)

- bloody sputum in lungs

- headache, focal neurologic signs in cerebral cyst

- anaphylactic shock when cyst rupture

- brood capsule containing multiple protoscoleses present microscopically

- serologic test; hemagglutination test

- eosinophillia present

- while removing cyst,inject ethanol or hypertonic saline (protoscolicidal agent)

- txt: albendazole

TREMATODES

1. Schistosoma species

- blood fluke

- intermediate host; snails

- Enter thru skin (MCQ), migrate against portal flow.

~Schistosoma mansoni ~; large lateral spine on egg in urine sample (MCQ ), main affected site: veins of
colon (damages walls of large intestine)

Schistosoma japonicum; spine is small or absent, round egg , affected site: veins of small intestine and
liver(damages walls of both large & small intestine)

- Both of these cause jaundice , liver cirrhosis, portal htn leading to abd distention , itching where the
larvae penetrates the skin

- complications; splenomegaly & hepatomegaly , most common cause of death; ruptured esophageal
varices (severe loss of blood)

Schistosoma haematobium; large terminal spine, affected site: veins of bladder

cause hematuria (diagnostic) of bladder, risk of bladder cancer(carcinoma) MCQ

- TXT: praziquental (MCQ)

- diagnostic tests; stool & urine culture

2. Clonorchis sinesis

- chinese liver fluke

- intermediate host: snails then transferred to fish

- causes chlonorchiasis due to consuming raw fish

- biliary tract obstruction and inflammation (obs jaundice and pancreatitis), can cause b.t fibrosis

- complications; pigmented gallstones, cholangiocarcinoma

- small, brownish operculated eggs on o&p

- txt: praziquental

3. paragonimus westermani

- lung fluke

- intermediate hosts: snails

- causes paragonimiasis ,chronic cough with bloody sputum (resembles TB),recurrent pneumonia

- due to eating raw crabs (has larvae)

- operculated eggs in stool

- txt: Praziquantel (MCQ)

NEMATODES

1. enterobius vermicularis

- pinworm infection

- female worms lay eggs in anus (scotch tape test- MCQ), anal itching occurs, eggs are not found in stool

- perianal pruritis occur.

- ELONGATED OVAL, IRREGULAR EGGS.

- txt: pyrantel pamoate (kills worm not egg; reinfection is common), albendazole

2. Trichuris

- whipworm infection (MCQ)

- causes diarrhea , causes rectal prolapse in children

- BARREL shaped eggs (MCQ)

- txt: mebendazole
3. ascaris lumbricoides

- largest intestinal nematodes (giant worms)

- causes ascariasis

- lives in intestinal wall but doesnot attach to gut wall

- from feces, egg hatches in intestine travels to lungs(major damage)

- respiratory symptoms ,eosinophilic pneumonitis (loefflers syndrome), Intestinal obstruction at ileocecal

junction (abd pain)

- txt: albendazole & PAM (MCQ)

4. ancylostomata* (old) & nector(new)

- hookworms

- penetration through skin (feet and legs),travels to lungs

- loss of blood at attachment site, causes microcytic anemia (iron def -MCQ), malnourished, ground itch
occurs at site.

- pneumonia & eosinophilia

- txt: PAM, albendazole

5. strondyloides stercoralis*

- causes strongyloidiasis.

- Lives in Soil (EXCEPTION cz rest all lives in body)

- penetrates in skin of feet travels to lungs

- autoinfection by eggs in intestine

- larvae found in stool , eosinophilia

- txt: ivermectin is DOC -MCQ, albendazole

6. trichinella spirals*

- causes trichinosis.

- occurs due to eating undercooked meat.

- develops cysts in striated muscle cells (nurse cells)

- diarrhea with fever , myalgia, periorbital edema, eosinophilia, vomiting.

- txt: albendazole.

INTESTINAL PROTOZOA:

1. Giardia lamblia:

- watery, foul smelling, non -bloody fatty diarrhea, FLATULENCE.

- Seen in campers/ hikers

- Cysts in water

- Men sex with man

- Trophozoites - pear shaped having 2 nuclei and 4 pairs of flagella.

- Cysts= 4 nuclei, internal fibres.

- Does not invade mucosa instead attach to it's wall & cause Duodenal inflammation (MCQ) leading to
malabsorption.

- PCR , stool antigen detection (ELISA)

- Dx by String test (MCQ)

- Metronidazole.

2. E .histolytica:

- Amoebiasis- bloody diarrhea ، liver abscess (anchovy paste appearance), RUQ pain.

- 4 nuclei in cysts (MCQ) & 1 in trophozoite.

- Flask shaped ulcers in colon esp prox colon like cecum (MCQ)

- Dx by trophozoite or cyst in stools and,

- characteristic feature, it's trophozoites shows endocytosed RBCs (MCQ)

- Metronidazole is DOC, Paromomycin & Iodoquinol for asymptomatic cyst passers.

3. Cryptosporidium :

- immunocompromised pts (AIDS)

- Watery diarrhea bcz no invasion, JEJUNUM.

- Oocysts in water, feco-oral route.

- Partially acid fast stain.

- oocytes can be removed via filtration bcz highly resistant to chlorination.

- Tx by Nitazoxanide.

*Viruses:*

11. Poliovirus:

- non-enveloped, icosahedral, ssRNA, no polymerase.

- Humans are only reservoir. 3 serological types (MCQ)

- Feco-oral route, replicates in oropharynx and intestinal tract.- retrograde thru nerves to CNS, replicates
in ANTERIOR HORN of spinal cord (MCQ)

- Bulbar poliomyelitis (with resp paralysis), rarely damages cerebral cortex.

- headache, sore throat, nausea, vomiting, aseptic meningitis, FLACCID paralysis.

- PCR for poliovirus RNA.

-2 vaccines:

_ inactivated poliovirus vaccine (IPV, Salk): cannot cause vaccine- associated polio. Only forms IgG,not
IgA.

_ Live attenuated oral polio vaccine (OP , Sabin) triggers local immunity in GI mucosa ie IgA. Rarely
reversion of attenuated virus to virulent state.

* No polio vaccine is to be administered within 3 weeks of TONSILLECTOMY. also in Diarrhea.

* It is the most sensitive vaccine to HEAT!

12. *Rotavirus* {REOVIRUS}

- SEGMENTED, dsRNA (UNIQUE), icosahedral capsid, has RNA dependant RNA polymerase.

- *Infective Stage:* Ingestion of fecally contaminated material.

- Major cause of severe gastroenteritis in infants (MCQ) watery diarrhea.

- Vaccination has reduced prevalence.

- Detection in stool by ELISA (MCQ)

- 2 vaccines: both contain live virus and are given orally. A/E: Intussusception!
CANDIDA ALBICANS

✨ normal flora of mouth, intestines skin and vagina.

- most common opportunistic fungal inf.

- Dimorphic: unicellular budding yeast at 20° and True hyphae at 42°.

✨CLINICAL FINDINGS : oral thrush (esp in steroid inhlaed pts) , esophagitis in HIV (white
pseudomembranes), valvovaginitis (cottage cheese appearance) , diaper rash (beefy red plaques)

- women taking antibiotics are at risk.

✨ lab diagnosis: gram positive culture grows yeast colonies, forms germ tubes at 37°, PCR to detect DNA.

✨treatment: tropical azole ( vaginal disease, diaper rash) , nystatin ( oral thrush ) , fluconazole
( esophagitis , candidemia),Caspofungin for resistant strains.

IMPORTANT

Bloody diarrhea:-

Salmonella, Shigella, Enterohemorrhagic E. Coli, EnteroInvasive [Link], Campylobacter, Yersinia,

Schistosoma, CMV. Also entamoeba histolytica.

-bloodEY SCENES: Mnemonic for bloody diarrhea causing organisms.

Here N Means Nothing :)

Watery diarrhea:-

[Link] (ETEC), Rota virus, Cryptosporidiosis.

Rice water:-

V. Cholera

Foul smelling diarrhea:-

C difficile, Rota Virus, Giardia lamblia

---Bloody diarrhea most are inflammatory

Watery are mostly non-inflammatory.