Uworld

Friday, 20 March 2015 1:47 am

1. Fatty foods >> increase in CCK, contraction of gallbladder, hence increased pain in
Cholecystitis
a. Initiated by mechanical obstruction of the cystic duct
b. Stones disrupt the protective mucous layer; epithelium exposed to bile salts
i. Mucosal damage, lecithin hydrolysis
c. Release of lysolecithin and prostaglandins --> inflammation and edema
d. Distention of the gall bladder leads to compromise of blood supply
i. Secondary bacterial infection
ii. Gangrene and perforation
e. Pericholecystic abscess or generalised peretonitis
f. Dx:
i. USG - Suggestive, not diagnostic
1) Pericholecystic fluid
2) Wall thickening
3) Murphy's sign
ii. Nuclear medicine hepatobiliary scan (radionucleotide)
1) Tracer is injected IV and taken up by the liver
2) Excreted into biliary tract
3) Take images as it moves through the hepatobiliary system
4) In cholecystitis (acute/chronic)
a) Radiotracer will be excreted into the common bile duct and the
small intestine
b) Gall bladder wont be visualised

2. Somatostatin:
a. Inhibits GH and TSH
b. Also inhibits basically every other hormone in the GIT

3. Tumour markers:
a. Alpha fetoprotein - Hepatocellular carcinoma (HCC), Yolk sac tumours; not very
specific or sensitive but still useful
b. CEA - Colon cancer prognosis post surgery; not for screening.
c. CA-125: Marker for ovarian surface cancer
d. PSA: Screening for prostate cancer
e. HCG: Gestational trophoblastic disease, H. mole, embryonal carcinoma,
choriocarcinoma
f. CA 19-9: Carbohydrate antigen; Pancreatic carcinoma
g. DHEA: Elevated androgen synth; Adrenal neoplasia

4. Gastrojejunostomies:
a. Bypass the duodenum
b. Hence bypass the site for uptake of Fe; hence iron deficiency
c. Vit C (active), Pyridoxine = B6 (passive) in the distal bowel.
d. Vit B7 = Biotin, and B6 = Pantothenic acid; uptake by sodium dependent
multivitamin transporter

5. Alcoholic binge drinking:

a. Usually have poor nutrition and glucose intake is low
b. NADH is increased (Alcohol dehydrogenase and Aldehyde dehydrogenase enzymes
require reduction of NAD+ to NADH)
c. Increased NADH signals the hepatocytes to not produce glucose.
i. Depletion of the intermediates of gluconeogenesis
d. OAA converted to malate; Pyruvate converted to lactate --> acidosis

6. Cocaine causes hyperglycemia (adrenergic activation, by inhibiting reuptake of NE)

7. Localised superficial Candidiasis - T cell dysfunction

a. HIV
b. Mucocutaneous, cutaneous, vulvovaginal candidiasis

8. Disseminated candidiasis ie. Esophageal candidiasis - Low neutrophils

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 8. Disseminated candidiasis ie. Esophageal candidiasis - Low neutrophils
a. Neutrophils prevent hematogenous spread
b. Other organisms:
i. Aspergillus
ii. Mucor
iii. Rhizopus
c. Neutropenia:
i. Congenital
ii. Drugs
iii. Radiation / Chemotherapy for leukemia

9. Brunners glands:
a. Submucosal glands
b. Compound tubular ramified
c. Secretes alkaline mucous
d. Present only in the duodenum

10. Jejunum: More mucous glands, intense lymphocytic infilterate

11. Ileum: Peyer's patches

12. Ventral Pancreatic bud:

a. Inferior head
b. Uncinate process
c. Main duct (of Wirsung)

13. Pancreas divisum:

a. Usually clinically silent
b. May predispose to frequent bouts of pancreatitis
c. Failure of ventral and dorsal buds to fuse at 8th week

14. AST and ALT also require Pyridoxal phosphate (PLP) as an essential cofactor (B6)
15. ALA synthase - Cofactor required is Pyridoxal phosphate
a. Synthesis upregulated due to reduced heme
i. Ferrochetalase inactivation due to Pb toxiticiy
ii. Ala Dehydratase also reduced by Pb

b. Lipoic acid: oxoacid and glycine cleavage complexes; antioxidant and scavenges ROS
c. Retinoic acid: binds to retinoic acid receptors >> Gene transcription
d. Biotin: Carboxylation
e. Thiamine pyrophosphate: Dehydrogenases

16. CREST syndrome:

a. Typical:
i. Calcinosis
ii. Raynaud's
iii. Esophageal dysmotility (replacement of muscularis with fibrous tissue; Atonic
and dilated LES - unlike achalasia with increase LES tone) - No peristalsis?
iv. Sclerodactyly
v. Telangiectasias
b. Case presented:
i. Finger tip ulcerations (digital pitting)
ii. Telangiectasias
iii. Heartburn
iv. Risk of Barrets esophagus

17. Diffuse esophageal spasm:

a. Periodic non peristaltic esophageal muscle contractions
b. Corkscrew appearance on radiogram

18. Gallstone ileus:

a. Chronic cholelithiasis:
i. Large gallstone erodes into the intestinal lumen
ii. Cholecystenteric fistula between gallbladder and gut
1) Air enters gallbladder and biliary tree by this route
iii. Stone then lodges in the ileocecal valve; waxing and waning symptoms of:
1) Vomiting
2) Distention of abdomen
3) Cramping pain
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 3) Cramping pain
iv. Duodenum and Jejunum are large enough to allow stones to pass
v. Distended duodenum on an upper GI series; usually gallstones don’t have
enough calcium to be radio-opaque

19. Rhinoviruses are acid labile, hence don’t infect the GI tract unlike the other Picornaviruses
20. Question on lymphatic drainage
a. Lymphatic drainage of structures follows their embryological origin

21. Lipids:
a. Duodenum site for digestion of dietary lipids
b. Jejunum is the site for digestion of lipid absorption
c. Cholecystectomy increases rate of enterohepatic circulation
i. Such patients are less tolerant to heavy fatty meals

22. Fibrates + Bile acid binding resins:

a. Reduces LDL
b. Leads to increased incidence of cholesterol stones:
i. Increased excretion of Cholesterol through bile
ii. Hence increased uptake of LDL form circulation into Liver
iii. Hence corresponding increase in Bile shot out again (with more and more
amounts of cholesterol in it)
1) Increased cholesterol >> Increase in probability of gallstone formation

iv. Fibrates also suppresses cholesterol 7 alpha-hydroxylase; hence reduces

synthesis of bile acids. Bile acids have 2OH groups or 3OH groups (cholic acid)

v.

c. Fibrate used to reduce Hepatic secretion of bile: Ursodiol; reduces incidence of

gallstones
d. Ursodiol is also hepatotoxic

23. Gall bladder stones:

a. Estrogen upregulates HMG-CoA reductase >> more cholesterol secretion
b. Progesterone >> reduces bile acid secretion + slows gallbladder emptying

24. TCA toxicity:

a. Cardiac arrhythmias:
i. Can be fixed by NaHCO3

25. Annular pancreas:

a. Recurrent bilous vomiting soon after birth

26. Non caseating granulomas + stool bleeding = Hallmark of Crohns disease

a. Most commonly affects the ileum
i. Loss of bile acids, excess lipids bind to Ca+2
ii. Ca+2 cannot bind to oxalate to render It insoluble; hence oxalate is
reabsorbed and causes kidney stones.
b. Transmural ulcers
i. Chronic inflammation and fibrosis
ii. Leads to strictures
iii. FISTULAS
1) Perianal disease (fissures, abscesses, skin tags)
2) Enterocutaneous, enterovesical, enterovaginal, enteroenteric
c. Resemble sarcoidosis
d. Creeping mesenteric fat
e. Granulomas not seen in UC
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 e. Granulomas not seen in UC
f. Aphthous ulcers oral mucosa are common
g. Dull-gray, edematous and granular

27. Both ulcerative colitis and Crohns disease may lead to Toxic megacolon
28. If Crohns + enterovesical fistula + fever/pyuria is present; think struvite stone.

29. Protective mechanisms against trypsin activation within the pancreas

a. Serine peptidase inhibitor Kazal type 1 (SPINK-1) inhibits trypsin
i. Secreted by pancreatic acinar cells
b. Trypsin cleaves other trypsin molecules to inactivate them
c. SPINK-1 mutations or Trypsinogen mutations = Hereditary Pancreatitis

30. TB dissemination in kids:

a. Ineffective interferon signaling:
i. INF-gamma secreted by NK cells/Th1 cells in response to IL12 to kill infected
macrophages
ii. AR deficiencies = Infection by BCG strains usually given as vaccines:
1) INF gamma
2) IL12 receptor
3) STAT 1 molecular pathway
4) Intracellular killing enzymes

31. Leukocyte adhesion defect:

a. LAD
b. Delayed cord separation at birth
c. Defect in CD18 (component of Integrins)

32. Metronidazole & Nitazoxanide treats Giardia lamblia

a. Metronidazole also treats Trichomonas vaginitis

33. Inflammatory travelers diarrhoea (Blood + mucous) = Ciprofloxacin

a. Caused by ETEC (Enterotoxigenic E coli)
b. Fimbriae - attach to enterocytes (not invasive)
c. LT and ST
i. LT - Similar to Cholera toxin; increases cAMP activation
ii. ST - Increases cGMP
d. Toxin causes an increase in Cl- channels opening; large volume stool
e. Osmotic gap <50 [isotonic]

34. Erythromycin = Campylobacter since FQ resistant now

35. Hemochromatosis:
a. HFE gene on Chr - 6p
b. Mutation most commonly seen:
i. Missense mutation
ii. Cysteine to Tyr mutation at 282
c. Clinical features:
i. Fatigue, dry mouth
ii. Impotence (because of testicular damage)
iii. Skin hyperpigmentation (bronze discolouration)
1) Hemosiderin deposition within the dermis
iv. Liver disease
v. Insulin resistance (bronze diabetes; destruction of islet cells by hemosiderin
deposition)
vi. Cardiac dysfunction + hypertrophy
vii. Arthropathy

36. Cystic Fibrosis - mcc of death is pneumonia (respiratory complications)

37. Cystic Fibrosis and GIT:
a. Isotonic dehydration of secretions
b. Pancreatic ductal plugs >> Fibrosis of entire pancreas (not specifically the islets)
i. Leads to pancreatitis
ii. Decreased trypsinogen
iii. Think Pseudomonas aeruginosa infections too
c. Decreased intestinal secretions >> meconium ileus
i. Inspissated green mass
ii. Small bowel obstruction:
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 ii. Small bowel obstruction:
1) Bilious vomiting, air fluid levels, abdominal distention
2) Small bowel dilation
d. Pancreatic insufficiency can lead to fat malabsorption;
i. Vit A, E, D, K deficiencies
ii. Poor growth + Steatorrhea
iii. Not necessarily fatal though

38. Portal vein is anterior to IVC and immediately medial to Right lobe of liver (CT)

39. IVC - lies just anterior to the right renal artery, to the right of the aorta, enters into RA just
above the diaphragm above T8. IVC - common iliac veins join at L4 to form the IVC

40. Primary sclerosing cholangitis

a. Associated with ulcerative colitis (CREST, Celiac disease, RA)
b. Fatigue
c. ALP increased
d. Onion skinning and beading (Concentric bile duct fibrosis)

41. Primary biliary cirrhosis:

a. Lymphocytic infiltrates (autoimmune)
b. Granulomatous destruction of bile ducts
c. Pruritus (one of the first symptoms reported)
d. Xanthelasmas in eyes and tendons
e. Classical in middle aged women; rare in men
f. Raised ALP
g. Anti-mitochondrial antibodies [IgM]
h. Complications:
i. Steatorreha
ii. Portal hypertension
iii. Osteopenia (Vit D malabsorption); bone pain
i. Associated with:
i. CREST
ii. Scleroderma
iii. Hypothyroidism
iv. Celiac disease
v. Sjogrens
vi. Raynauds

42. Homeless people:

a. Acute cholangitis?
43. Alcoholism:
a. AST >> ALT
b. Increased GGT [important]
c. Pancreatitis
i. Ethanol induces high and low fluid pancreatic secretions
ii. Spasm of sphincter of Oddi
iii. Hypocalcemia because of all the Ca binding to saponified fat (non specific)
iv. May lead to deficiency in folic acid --> macrocytic anemia
d. Macrocytosis without anemia (>108 fl)
i. B12 and folate deficiency
ii. Direct marrow toxicity of alcohol

44. Clostridium difficile:

a. Causes Pseudomembranous colitis
i. Enterotoxin A - Watery diarrhoea
ii. Cytotoxin B - Colonic epithelial necrosis + fibrin deposition
b. Diagnosis - PCR test for stool Toxin A & B
c. Treatment:
i. Metronidazole (mild to moderate)
ii. Vancomycin (severe); not absorbed well through GIT
1) BACTERIOSTATIC against C diff.
2) Okay Katzung says Vancomycin is bactericidal, the argument is that
vancomycin is a slow killer of C diff. and doesn’t kill the spores.
iii. Fidaxomicin (narrow spectrum; less toxic)
1) BACTERIOCIDAL (kills faster and kills spores too)
2) In cases where recurrence is likely, give Fidaxomicin

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 d. Contact precautions - Hand washing important; kills spores that alcohol rubs don't
e. Clostridium difficile infections are inhibited in the normal state because of the
abundant bacterial flora present in the GIT. Hence only happen after they're killed
(antibiotic therapy)
i. FQ
ii. Clindamycin
iii. Broad spectrum Penicillins and cephalosporins

45. Histology (should have known this):

a. Surface - mucous glands
b. Upper glandular layer - Parietal cells
c. Deep glandular layer - Chief cells

46. Niacin side effects:

a. Facial flushing and warmth (release of prostaglandins; counter with aspirin)
b. Cutaneous pruritus
c. Worsens gout
d. Hyperglycemia (makes life worse for diabetics)
e. Biochemical effects:
i. Effectively raises HDL; doesn’t improve CVS outcomes though
ii. Suppresses FFA release from peripheral tissues, hence decreased hepatic VLDL
synthesis; and reduced conversion to LDL.

47. Drugs causing acute gout:

a. Hydrochlorothiazide
b. Niacin
c. Cyclosporine
d. Pyrazinamide

48. Fibrate + Statin = myopathy

49. Fibrate + Bile resins = Gall stones

50. Bile acid binding resins:

a. GI upset
b. Impaired absorption of nutrients and drugs
i. Fat soluble vitamins (A E D K)
ii. Drugs like warfarin and statins
c. Can worsen diverticulosis (because of constipation and bloating)

d. Hypertriglyceridemia
i. Interruption of enterohepatic cycling --> Upregulates bile acid production
ii. Increase in b100 LDL receptors allows for more of the blood LDL pool to be
utilised for synthesising bile acids.
iii. Does nothing to VLDL synthesis; contraindicated in hypertriglyceridemia since
it can worsen it [why?]
iv. Reduces uptake of statins; hence must space out at 4 hour intervals

51. Fibrates:
a. First line drugs for hypertriglyceridemia

52. Mallory Weiss syndrome:

a. Mucosal tear
b. Vomiting + hematemesis + Epigastric pain
53. Boerhaave syndrome:
a. Vomiting + Retching
b. Chest + Upper abdominal pain
c. Fever dyspnea septic shock
d. Air in mediastinum

54. Distal duodenum ulcer (beyond the bulb):

a. Non gastric neoplasm (Zollinger Ellison syndrome)
b. Abdominal pain + acid reflux
c. Diarrhoea - since the pancreatic enzymes are inactivated by gastric acid, hence
impaired digestion of nutrients. (vs VIPoma, persistent diarrhoea (with fasting),
achlorhydria, hypokalemia)
d. Zollinger Ellison syndrome Dx:
i. Serum gastrin (raised)
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 i. Serum gastrin (raised)
ii. BAO, MAO both raised (MAO - pentagastrin)
iii. BAO / MAO
iv. Check for Ca, Prolactin levels to exclude MEN1

55. Type A = Chronic gastritis + antral sparing: Autoimmune gastritis

a. Associated with B12 deficiency

56. Type B = Chronic gastritis antral predominant: H pylori

a. Gastrin secretion is increased:
i. Local alkalinsation by H pylori urease
ii. Inhibition of release of Somatostatin (chronic inflammation damages the delta
cells)
b. Increased risk for adenocarcinoma and MALT
c. Duodenal ulceration due to inability of [HCO3-] to neutralize the acid
d. Triple therapy:
i. Omeprazole (PPI)
ii. Clarithromycin (macrolide)
iii. Amoxicillin
iv. May add Bismuth (quadruple therapy)

57. H pylori gastric ulcers - local inflammatory response

a. Acid secretion may be low to normal in patients with gastric ulcers
b. Acid easily causes ulceration when the mucosal layer is degraded

58. Duodenal bulb - most exposed to increased gastric acid secretion

59. Diphenoxylate combined with atropine to reduce abuse laibility
a. Binds to mu opiod receptors and slows motility
b. Remember - miosis and constipation are side effects of opiods that don’t undergo
tolerance

60. Drugs to inhibit secretory diarrhoea:

a. Somatostatin analogs (Octreotide)
b. Bismuth salicylate
c. Probiotics

61. Polio oral vaccine (Sabin):

a. Leads to an increase in Secretory IgA in the duodenum
b. IgA dimers bind to plgR immunoglobulin receptors (synthesised in epithelial cells)
c. Undergoes transcytosis
d. Portion of plgR chain remains (Secretory component)
e. IgA
i. 10 proteins
1) Ig proteins x 8
2) J piece
3) Secretory component

62. Colon cancer:

a. Abdominal cramps, distention and nausea: symptoms of left sided colon cancer
i. Most common site for colon cancer is the rectosigmoid colon
ii. Are usually smaller, but infiltrate the wall of the colon; encircle it
iii. OBSTRUCTION - Altered bowel habits, constipation, abdominal distention
b. Weight loss and Progressive fatigue: Right sided colon cancer symptoms
i. Ascending colon second most common site
ii. Iron deficiency anemia due to slow blood loss

c. Tenesmus & thinning of stool = space occupying lesion of rectum; rectal

adenocarcinoma
d. Sporadic forms
i. APC mutation (5q - tumour suppressor - (responsible for intercellular
attachment)
ii. Most familial polyposis syndromes too

63. Grossly bloody stool = Ulcerative colitis

a. Neutrophils in the crypt lumina

64. Constipation alternating with pain = Irritable bowel syndrome

65. Hepatoblastoma - Part of the beckwith weidmann syndrome
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 65. Hepatoblastoma - Part of the beckwith weidmann syndrome
66. Intrahepatic cholangiocarcinoma:
a. Tree like pattern inside the fucking liver
b. Liver flukes
c. Fibropolycystic liver disease

67. Metastatic liver cancer:

a. 20x more common that HCC
i. HCC is also unifocal, infilterative (rarely multifocal)
b. Nodules end up replacing more than 80% of parenchyma
c. Severe parenchymal damage + bile duct obstruction: Leads to abnormal enzymes
d. Lots of round lesions
e. Rememeber - large white mass = barium stomach

68. Direct inguinal hernia

a. Breakdown of transversalis fascia medial to inferior epigastric vessles
b. Triangle of Hesselbach
c. Covered only by external spermatic fascia
d. Occurs in older men

69. Femoral hernias:

a. Mcc in women
b. Medial to femoral sheath (femoral vein) and lateral to lacunar ligament
i. Coopers ligament is behind the femoral canal, on the pubic bone
c. Features:
i. Femoral canal is small hence prone to incarceration
ii. Incarcerated bowel cant be reduced
1) Nausea
2) Vomiting
3) Abdominal pain + distention
iii. Impaired blood flow (few hours after incarceration) --> Strangulation
1) Ischemia and necrosis
2) Fever

70. Vibrio and Campylobacter:

a. Vibrio grows in alkaline media (TCBS agar); campylobacter cant
b. Vibrio cholerae:
i. Acid labile; risk factor for infection - achlorhydria
1) Drugs like omeprazole
2) Gastritis
ii. Stimulates IgA antibodies
iii. Non invasive (only Vibrio)
iv. Secretory diarrhoea (rice water stool)
v. Increase cAMP --> Decreased sodium reabsorption + increased Cl excretion +
vi. No
mucin
erythrocytes
ejection and no diarrhoea
c. Vibrio vulnificus - increased risk of infection in chronic liver failure

71. Charcot leyden crystals:

a. Intestinal parasitic infections
b. Strongyloidosis, Ancylostoma, Ascaris
c. Not with Entamoeba or Giardia

72. Leukocytosis + monocytic predominance - Salmonella typhi diarrhoea

73. Invasive diarrhoea - leukocytosis + neutrophilic predominance
a. Salmonella, Shigella, EIEC, Campylobacter, Entamoeba histolytica, Yersinia
b. Blood in diarrhea; low volume
c. Salmonella typhi and Yersinia can also cause systemic illness

74. Leptin:
a. Produced by adipocytes (adipokine)
b. Causes Satiety
i. Decreases production of neuropeptide Y in arcuate nucleus of hypothalamus
ii. Leptin stimulates POMC in the arcuate nucleus
iii. Alpha-MSH produced by cleavage of POMC
c. Knockout mice:
i. Increased production since receptor interaction is blocked
ii. Would be zero production if leptin gene was mutated
d. Humans:
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 d. Humans:
i. Sustained elevation of leptin due to increased fat stores = desensitization

75. Superior mesenteric artery:

a. Originates at L1 lower border
b. Courses down near the 3rd part of duodenum
i. Tumour can damage superior mesenteric artery, vein; uncinate process of
pancreas

76. Portal vein is retroperitoneal

77. O157:H7 characteristics: (EHEC)
a. Shiga like toxin, inactivate 60S ribosomal subunit [ADP ribosylation]
b. Don’t ferment sorbitol on MaConkeys agar
c. Doesn't produce glucuronidase
d. Toxin production enhanced by iron deficiency
e. Undercooked beef
f. Causes

78. Bacterial toxins:

a. cAMP activation - Bordatella pertussis, Bacillus anthracis, ETEC (LT), Campylobacter
jejuni, Bacillus cereus, Cholera
b. cGMP activation - ETEC (ST), Y. enterocolitica
c. EF-2 inactivation (ADP ribosylation of EF2) - Corynebacterium diphtheriae,
Pseudomonas aeruginosa (Exotoxin A)
d. Cytoskeletal disruption (actin polymerisation) - C. difficile.
i. Toxin A (enterotoxin); Toxin B (Cytotoxin; more virulent)
ii. Act on signal transduction proteins; Acts on actin cytoskeletal structure
iii. Recruit neutrophils, induce apoptosis

79. Metabolism:
a. 1g protein - 4 cal
b. 1g carbohydrate - 4 cal
c. 1g fat - 9 cal
d. 1g Ethanol - 7 cal

80. Shigella infectivity

a. Doesn’t form H2S on TSI
b. Non-lactose fermenter (shigella sonnei is late lactose fermenter, and most common
subtype )
c. Only small doses of shigella are required to infect (200)
d. Lots of neutrophils
e. Invades into the intestinal M cells (overlying payers patches)
i. Lyses containment vacuole
ii. Enters cytosol
iii. Apoptosis of host cell + spread laterally to other cells via protrusions (actin
polymerisation)
f. Shiga toxin production isn't necessary for infectivity; non-toxigenic strains also
produce dysentery
i. Toxin (ST / SLT)
1) Removal of a specific adenine residue on 60S ribosome
2) Inhibits tRNA binding; hence inhibits protein synthesis
ii. Mucosal cell death + toxic to renal tubular cells [not why HUS happens]
g. Diarrhoea >> Dysentery
h. Tenesmus
i. Transmitted by feco-oral route; dirty hands, fomites, unhygienic food handlers
j. Other high infectivity organisms:
i. Giardia (1)
ii. Entamoeba histolytica (1)
iii. Campylobacter (500)
iv. Clostridium perfringens (500)

81. Serum albumin and PT = Liver biosythnetic activity measurement

a. Increased PT + Decreased albumin = poor prognosis
82. MHC I - never processed in lysosomes
83. MHC II - lysosomal processing involved

84. Bile acids: Reabsorbed in the terminal ileum (Enterohepatic cycling)

85. Cricopharyngeal dysfunction:
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 85. Cricopharyngeal dysfunction:
a. Zenker diverticulum
b. More force required to push food down the esophagus
i. Herniation of pharynx through the posterior hypopharynx
ii. False diverticulum (pulsion)
c. Dysphagia, choking, recurrent aspiration

86. False diverticulum:

a. Pulsion diverticula
b. Herniation of mucosa and partly submucosa through the weak spots in the colonic
muscular layer
i. Weak spots - where the mesenteric arteries perforate into the gut

87. Traction diverticula - true diverticula

a. Secondary to scarring and inflammation
i. Mucosa, submucosa, muscularis
b. Midesophageal diverticula: mediastinal lymphadenitis, TB

88. True diverticulum:

a. Seen in the mid esophagus
b. TB, fungal infections
c. Also Meckel's diverticulum

89. Whipple disease treatment:

a. Antibiotics - Tropheryma whippelii
i. PAS +
ii. Diastase resistant
b. Remember no bleeding in stool in Whipple

CMV Linear ulcerations Intranuclear and cytoplasmic inclusions (Owl

eye) Blood supply of rectum:
90. HSV - 1 Small vesicles, typical punched Cowdry type A inclusions in multinuclear i. Superior rectal artery (inferior mesenteric)
out ulcers squamous cells ii. Middle and inferior rectal artery (internal iliac)
Candida Grey white pseudomembranes Yeast cells + psudohyphae

91. CT - calcifications in chronic pancreatitis; pancreatitis may also lead to left sided pleural
effusion
a. Increased stool fat

92. Head neck and body of pancreas - retroperitoneal; tail - intraperitoneal

a. Overlies the L1 and L2 vertebrae
b. Head overlies the L2 vertebrae; sits next to the curve of the duodenum

93. Celiac disease - best diagnosed with small intestine biopsy

a. Flattening of villi in the background of diffuse enteritis
b. Intense lymphocytic infiltrate (some plasma cells, eosinophils etc in the lamina
propria)
c. Strong genetic basis
d. Deep gland pits
e. Antibodies:
i. Anti gliadin (IgA and IgG)
1) Cross reacts with reticulin; protein found in anchoring fibrils of
epidermal basement membrane --> Dermatitis herpetiformis
ii. Anti endomysial (IgA)
iii. Anti tissue transglutaminase (IgA + IgG)
iv. Anti reticulin
f. Dermatitis herpetiformis (kinda looks like the clustered lesions in herpes)
i. Eruptions on the extensor surfaces
ii. Bilateral and symmetrical
iii. Microabscesses - fibrin and neutrophils present at dermal papillae tips; maybe
even eosinophils; coalesce to form subepidermal blisters
iv. Buttocks, elbows, back

94. Gastric erosion:

a. Mucosa (into but not through muscularis mucosae)
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 a. Mucosa (into but not through muscularis mucosae)
b. NSAIDS, surgical stress, smoking, head trauma (Cushings' ulcers), burns (Curlings
ulcers), alcohol consumption
i. Curling ulcers - burns/trauma --> proximal duodenum
ii. Cushing ulcers - head injury (increased ICP) --> duodenum / esophagus /
stomach
c. Later heals with full repithelisai
d. Histology:
i. Small defects (erosions / ulcers)
ii. Unremarkable adjacent mucosa
e. Pathogenesis
i. Compression of the Vagus nerve by increased ICP
ii. Increased stimulation of parietal cells --> HCl

95. Atresias of the intestine:

a. Duodenal - failure of recanalisation; associated with Downs syndrome
b. Distal intestinal - vascular accidents:
i. Ischemia of vessel in utero
ii. Fibrosis or complete loss of bowel segment
iii. Distal ileum assumes a spiral configuration around the ileocolic vessel (Apple
peel defect)

96. Lysosomal enzymes released as a result of acinar damage activate trypsinogen in

pancreatitis
a. Lack of anti-zymogen enzymes further perpetuates damage
b. Leads to pancreatic necrosis
c. High propensity for bacterial infection

97. Superior mesenteric artery syndrome:

a. Transverse duodenum is entrapped between the SMA and Aorta
b. Partial intestinal obstruction
i. Low body weight
ii. Recent weight loss
iii. Surgical correction of scoliosis
iv. Pronounced lordosis
98. Mesenteric adenitis:
a. Yersinia enterocolitica
b. Children 5-14
c. No fistulas
d. Presents with symptoms that can be confused with appendicitis

99. GGT is done to clarify importance of increased ALP

100. Aflatoxin mediated mutations:
a. G:C to T:A transversion in codon 249 of p53 gene
b. Aflatoxins released by Aspergillus parasticius and Aspergillus flavus
c. "Mouldy grains" = Aspergillus or some fungi
d. HCC risk increases

101. Fulminant hepatic failure:

a. Shrunken liver on autopsy
b. Can be caused by crazy alcohol intake
c. Halothane anaesthetic
i. Presents 2 weeks - 4 days post operation; (general anaesthesia)
ii. Hepatocellular injury - centrilobular [why?]
1) Halothane metabolites
2) Autoantibodies against liver proteins
iii. Massive hepatic necrosis; 80% mortality rate
1) LFT raised
2) Hepatomegaly
3) Liver tenderness
d. HBV + HDV superinfection, and viral hepatitis

102. HDV:
a. ssRNA; circular
b. Needs HBsAg to coat it to be effective
i. Hence only coinfection or superinfection of chronic HBV carrier

103. Reye's syndrome:

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 103. Reye's syndrome:
a. Microvescicular steatosis (vs Macrovescicular - nucleus may be displaced
eccentrically - in ethanol consumption)
b. Similar morphology to acute fatty liver of pregnancy
i. Rx for acute fatty liver of pregnancy = must deliver the baby

104. Fatty liver due to alcohol intake:

a. Hepatic steatosis
b. Increased TG accumulation in the hepatocytes
i. Decreased beta oxidation
ii. Acyl CoA dehydrogenase is inhibited by increased availability of NADH
produced from alcohol metabolism.
c. Also inhibition of gluconeogenesis due to the same reason
d. Stain fat with Sudan black or Oil Red O
e. Impaired lipoprotein assembly

105. Pyloric gastric glands:

a. Secrete mucous and lysozyme
106. Osmotic laxatives:
a. Polyethylene glycol
b. Magnesium citrate

107. Congenital Lactase deficiency:

a. Congenital lactase deficiency
b. AR disorder
c. Prevents the breakdown of Lactose --> Galactose + Glucose
d. Bacterial fermentation of lactose >> fatty acids + hydrogen
i. Increased breath H2 test
ii. Decreased stool PH
iii. Low increase in blood glucose (<20 mg/dl)
108. Lactase deficiency can be acquired too:
a. Celiac sprue
b. Viral gastroenteritis
c. Damaged cells slough off, and dissacharidase enzyme is destroyed since it is present
on the brush border epithelium

109. Bacteriodes fragilis

a. Seen in intraabdominal abscesses post trauma / surgery
b. Also causes Endometritis
c. Gram negative
d. Surface polysaccharides favour abscess formation
e. Others:
i. E coli
ii. Enteroccoci
iii. Streptococci

110. Imperforate anus:

a. Cloacal derivative
b. Associated with genitourinary defects
c. Less common:
i. VACTERL:
1) Vertebral defects
2) Anal atresia
3) Cardiac abnormalities
4) Tracheoesophageal fistulal
5) Renal abnormalities
6) Limb abnormalities
d. Associated with genitourinary defects like:
i. Bladder extrophy
ii. Hypospadias
iii. Epispadias

111. Crigler Najjar type-1:

a. AR
b. Absence of UGT1A1
c. Neurological symptoms due to increased UCB
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 c. Neurological symptoms due to increased UCB
d. Fatal jaundice and kernicterus

112. Dubin Jhonson:

a. AR
b. Impaired bile transport (MRP2)
c. Increased CB
d. Brown discoloured liver

113. High concentrations of anaerobes and Staph aureus:

a. Deconjugation of bile acids
i. Also occurs in - bowel stasis, blind loops, extensive diverticulosis
b. Less soluble and cant form micelles
c. Lipid malabsorption

114. CEA isn't useful for diagnosis (not specific), but useful for monitoring tumour recurrence
after surgery
a. Grading: Histological features
i. Differentiation
ii. Degree of aneuploidy
iii. Number of mitotic figures
b. Staging: Extent of spread (important for determining prognosis)
i. Staging > than clinical symptoms (many are asymptomatic)
c. Type of resection + Extent of spread: Depends on tumour stage

115. Colon carcinoma staging:

Stage A Confined to the mucosa
Stage B Involves the muscularis
a.
Stage C Lymph node spread
Stage D Distant metastasis
116. Caput medusae:
a. Superficial umblical veins >> Superficial and inferior epigastric veins
117. Esophageal varices:
a. Left gastric >> Esophageal veins (tributary of azygos vein)

118. Paneth cells = Secrete lysozyme; present at the base of crypts of lieberkhun
119. Colon with endometriosis:
a. Benign disease
b. May be symptomatic, responds to estrogen and grow

120. Abetalipoproteinemia:
a. AR
b. RBC findings: Acanthocytes
c. Inability to secrete TG rich lipoproteins (anything containing Apo B)
i. B100 - VLDL
ii. B48 - Chylomicrons
d. MTP (microsomal triglyceride transfer protein) mutation; no assembly of
chylomicrons
i. MTP is responsible for proper folding of Apo B
ii. Involved in transfer of lipids to CM and VLDL
e. Epithelial cells:
i. Fat vacuoles present
ii. Foamy appearance
f. Absence of Apo B containing plasma lipoproteins; Apo B gene is normal
g. Clinical picture:
i. Failure to thrive
ii. Steatorrhea
iii. Diarrhoea
iv. Fat soluble vitamin deficiencies
1) Vitamin E: Acanthocytes, ataxia, retinitis pigmentosa

121. Bacillus cereus:

a. Emetic type diarrhoea
b. Fried rice infected
122. Undercooked shellfish:
a. Vibrio cholerae
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 a. Vibrio cholerae
b. Norwalk virus
c. HAV
123. Vibrio parahemolyticus:
a. Rice water stool similar to cholera
b. Caused by consumption of contaminated shellfish

124. Raw egg + chicken = Salmonella

125. Canned food:

a. Clostridium botulinum spores
b. Preformed toxin; adult botulism
i. Descending flaccid paralysis

126. Phenytoin:
a. Enzyme inducer - Increases the metabolism of Warfarin
127. Amiodarone + Cimetidine:
a. Cimetidine also has potent anti androgenic effects
b. Enzyme inhibitor - Decreases metabolism of Warfarin
c. Amiodarone + Warfarin = Rx of Atrial Fibrillation; hence important to keep this
d. Other
toxicityenzyme
in mindinhibitors: metronidazole and TMP-SMX

128. Meckel diveritculum:

a. 2% population
b. 2 ft from ileocecal valve
c. 2 inches long
d. Males x2 times more likely
e. 2% asymptomatic

129. Meckel diverticulum ectopic tissue:

a. Gastric tissue
i. Detected by 99mmTc-pertechnetate scan
ii. Ulceration of adjacent tissue because of acid
iii. Painless malena (lower GI bleed)

iv. Inflammation --> presents as acute appendicitis

v. Predisposes to intussusception - current jelly stool

b. Pancreatic acini
c. Intestinal glands (not ectopic then is it lol)
d. Endometrial tissue

130. Muscles of mastication:

a. Supplied by V3 --> Foramen ovale
b. Temporalis / Masseter / Lateral and medial pterygoids

131. Stacked brick pattern of intestinal adhesion - EAEC; developing countries infants

132. GIT lymphomas:

a. Atypical lymphocyte infiltration in the lamina propria

133. Gastric tissue supplied by short gastric arteries at risk of ischemia (poor anastomoses)
a. Region of the proximal greater curvature above the splenic artery

134. HAV anicteric infection sometime in infancy:

a. Anti HAV IgM --> Negative (vs Positive IgM in acute HAV)
b. Anti HAV IgG --> Positive
135. HAV in children - anicteric; in adults it's acute self limiting jaundice, RUQ pain, malaise
fatigue etc etc
a. Fever + dark urine
b. Also strange aversion to smoking
c. Raw/steamed shellfish
d. Contaminated food/water
136. HAV is an acute & self limiting hepatitis
a. Ballooning degeneration
b. Hepatomegaly and Jaundice
c. AST and ALT spike early in disease; bilirubin and ALP increase later
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 c. AST and ALT spike early in disease; bilirubin and ALP increase later

137. HBV is an enveloped virus, has partially circular dsDNA; and also has reverse transcriptase
a. Nucleocapsid core + Outer lipoprotein envelope
b. DNA (repaired in the nucleus) --> (+)RNA --> DNA
c. Has no direct cytopathic effect
d. Proliferative phase
i. HBsAg and HBcAg expressed with MHC-I on hepatocyte surface
ii. Increases CD8+ T cell response
e. Integrative phase
i. HBV DNA incorporated into host genome of surviving hepatocytes; risk of HCC
stays the same.
ii. HBV can't however cause HCC without integrating with hepatocyte DNA
1) HBx protein - activates synthesis of IGF -II and IGF-I receptors; hence
stimulating cell proliferation.
2) Suppression of p53 (but this effect isn't by HBeAg!!)
3) Basically - you need integration of viral genome into host cells!

138. Serological markers for HBV:

a. HBsAg - active infection; anti-HBs - post vaccination or infection
i. Appearance of HBsAg is just before the onset of symptoms
ii. Time lag btw appearance of anti-HBsAg after HBsAg clears = window period
b. HBcAg - sequestered within HBs coat; anti-HBc (IgM - acute HBV infection)
i. HBcAg cannot be detected
ii. Anti-HBc is useful in the window period when anti-HBs hasn’t risen
1) Most specific marker for acute HBV infection
c. HBeAg and HBV DNA - markers for active viral replication [you fucking knew this]
i. Pre-core mutant doesn’t have HBeAg
d. Carrier for HBV:
i. Persistence of HBsAg
ii. Chronic non infective = No HBeAg; detectable Anti HBeAg
iii. Chronic infective HBV = Carrier + HBV DNA + HBeAg
e. Notes:
i. Anti HBs Ab functions by binding to the HBsAg as it attaches to a hepatocyte,
preventing it from interacting with hepatocyte receptors.
ii. Can spread by sexual contact (common) and blood
iii. Vertical transmission possible too
iv. Incubation period = 1 to 6 months
v. Rise in AST/ALT (ALT>AST) is preceded by the onset of symptoms
1) Malaise
2) Fever and joint pain
3) Pruritus
4) Anorexia, RUQ pain, Jaundice
vi. HBV vaccination:
1) Prevents HBV and HDV

139. Transplacental transmission of hepatitis - 3rd trimester

a. HBeAg [+] - transmission risk is 95%
b. If infected, the infant has a high risk of progressing to chronic hepatitis:
i. Mild elevation of liver enzymes and persistent serum antigens in neonate
1) Mild elevation because neonatal immune system isn't fully developed
yet (hence minimal necrosis) + no HBV direct cytopathic effect
ii. Progresses to cirrhosis or HCC
c. Hence passively immunize all newborns of HBV active mothers with HBV IgG,
followed by active HBV vaccine.

140. Honey - carries spores of Clostridium botulinum; causes disease in infants

a. Spores germinate in GIT
i. Intracellular toxin production
ii. Bacteriolysis --> toxin release
iii. Mild systemic absorption
iv. Produces a subterminal spore
b. Toxin itself is heat labile
c. Constipation, poor feeding, weakness and lethargy
d. Neuromuscular paralysis after GI symptoms
i. SNARE proteins are cleaved by botulinum toxin; causes impaired release of
neurotransmitter vesicles.
ii. Reduced Ach release --> Dry mouth, ptosis, difficulty swallowing,
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 ii. Reduced Ach release --> Dry mouth, ptosis, difficulty swallowing,

e. Stool tests for bacterial toxins:

i. ELISA and PCR

141. Acute viral hepatitis - AST/ALT 1000s

142. Chronic viral hepatitis - AST/ALT 100s

143. Hepatocytes and ammonia:

a. Two enzyme systems keep blood levels of NH3 low
i. Periportal: glutaminase + urea cycle
ii. Perivenous: glutamine synthase

144. Hepatic abscess:

a. Developing countries: Usually parasitic; Echinoccocus, Entamoeba
i. Ascending infection from portal vein
b. Developed countries: Usually bacterial (80%)
i. Dx: USG / CT
ii. Hematogenous seeding - Staph aureus
iii. Ascending biliary tract infection (ascending cholangitis), direct invasion from
adjacent area
1) Klebsiella
2) E coli
3) Enterococcus
iv. Portal vein pyemia (appendicitis, diverticulitis)

145. Squamous cell carcinoma of esophagus

a. Upper 2/3 of the esophagus
b. Alcohol, Smoking, N-nitroso foods (betel nuts and shit)
c. Esophageal webs, Zenker diverticulum, Achalasia
d. Morphology:
i. Keratin pearls (dysplasia; well differentiated)
ii. Intercellular bridging
iii. Eosinophilic cytoplasm
iv. Plaque like mucosal thickening
e. Symptoms:
i. Progressive dysphagia - first solids then liquids
ii. Weight loss
f. Poor prognosis

146. HCV infection:

a. Rare from blood since it's screened for that shit now
b. Progresses to stable chronic hepatitis (most common outcome)
c. Extra hepatic disease manifestations:
i. MPGN type I
ii. Mixed cryoglobulinemia
d. Less than 50% progress to cirrhosis
e. Multiple quasi species:
i. Imperfect RNApolymerase activity
ii. No 3' → 5' exonuclease activity of the RNA polymerase (NS5A/B)
iii. Leads to hypervariable surface E2 (envelope) antigens
1) (E1 and E2 code for two envelope glycoproteins)

147. Achalasia caused by an infection:

a. Trypanosoma cruzi - Chagas disease
i. Arthropod vector - reduviid bug
b. Causes damage to myenteric plexus
i. LES is incapacitated (increased tone)
ii. Proximal dilation of esophagus
iii. No peristalsis
c. May also lead to megacolon and megaureter
d. Rx: Nifurtimox (trypanothione reductase inhibitor) for trypanosomes

148. Achalasia:
a. Bird beak appearance
b. Dysphagia
c. Regurgitation, chest pain, weight loss
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 c. Regurgitation, chest pain, weight loss
d. Heart burn
149. Normal Esophageal manometry:
i. Cricopharyngeus contracts --> Peristalsis in the esophagus --> LES relaxes
a. Achalasia:
i. Normal cricopharyngeal tone (vs cricopharyngeal dysfunction --> Choking
sensation, pain during swallowing, Dx: video fluroscopy)
ii. Decreased amplitude of peristalsis
iii. No LES relaxation
b. Diffuse esophageal spasm:
i. Multiple irregular contractions from middle to lower esophagus
c. GERD:
i. Decreased LES pressure; it fails to contract after transfer of food to stomach

150. Profuse watery diarrhoea in immunocompromised - Isospora belli

151. Oral leukoplakia - Tobacco use
152. Oral hairy leukoplakia - EBV (non cancerous)

153. Liver cirrhosis

a. Increased lactate (decreased hepatic clearance)
b. Hyperestrinism -
i. Decreased metabolism of estrogen
ii. In alcoholic liver disease - upregulation of SHBG
1) Decreased free testosterone
iii. Leads to gynaecomastia, spider angiomas, testicular atrophy, decreased body
hair

154. Ulcerative colitis:

a. Crypt abscesses + multiple pseudopolyps
i. Inflammation extends to the mucosa and submucosa
b. Continuous mucosal involvement (vs skip lesions in Crohns)
c. Bloody diarrhoea (with or without abdominal pain)
i. Abdominal pain is always present in Crohns
d. Rectum is always involved
e. Complications:
i. Sclerosing cholangitis
ii. Colorectal adenocarcinoma
iii. Toxic megacolon
1) Pain and distention
2) Fever, diarrhea, and signs of shock
3) Risk of perforation:
a) Hence no barium or colonoscopy studies
4) Plain X-Ray - distended colon (transverse) with or without fluid levels
5) Rx:
a) Conservative therapy - fluids, steroids, immunosuppressants
b) Surgery (total colectomy / ileostomy)

155. Hepatic granulomatosis (what is this?)

a. Hydralazine
b. Methyldopa
c. Quinidine

156. Drug induced Cholestasis:

a. OCP
b. Niacin
c. Anabolic steroids
d. Chlorpromazine
e. 6MP

157. Alkylating agents - Black tarry stools; since rapidly dividing cells are damaged (hair, skin,
mucosa of GIT)
158. Autoimmune hepatitis - Antigenic mimicry with self antigen recognizing CD4+ T cells

159. Anal fissures:

a. Bright red blood while shitting
b. Most commonly on the posterior midline
i. Because posterior midline is poorly perfused
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 i. Because posterior midline is poorly perfused
ii. Mucosa is sensitive to tears by hard fecal matter
c. Distal to dentate line (somatic sensations)
i. Hence sharp pain while taking a shit
d. Associated with constipation and low fiber diets

160. Chronic NSAID use - increased risk for GI blood loss (+ fecal occult blood test)

161. Gilbert syndrome

a. LFT stays mostly normal
b. Unconjugated hyperbilirubinemia (indirect)
i. Normal LFT
ii. Normal CBC, Reticulocyte count, Blood smear normal
c. 5' mutation (insertion of 2 extra bases) in the UGT1A1 promoter region
d. Reduced transcription; hence impaired glucuronidation
e. Precipitated by triggers such as febrile illness, hemolysis, exertion etc

162. Dubin Jhonsons syndrome:

a. AR
b. Conjugated hyperbilirubinemia
i. Direct bilirubin increases
c. MDR2 channel defect; cant export bile from hepatocytes once conjugated
d. Pigmented hepatocytes (epinephrine metabolites)
e. Liver is grossly black
f. Intermittent self resolving jaundice; mild symptoms
i. Icterus evident only with onset of contraceptive usage, infections, pregnancy
whatever
g. Urine test: High urinary coproporphyrin I

163. HNPCC
a. Lynch I and Lynch II (Lynch II - colon + extraintestinal)
b. Defect in DNA mismatch repair
i. MLH 1, MSH 2, MSH 6, PMS 2
ii. Mechanism of action:
1) MutS detects a mismatch by checking the methylation status.
a) Methylated = paternal
b) Non-methylated = daughter
2) Mut S recruits MutL; Endonuclease makes occasional nicks in the
daughter strand;
3) Exonuclease 1 removes the mismatched region (and a bit more either
side). ssDNA binding proteins stabilise the single strand.
4) DNA polymerase delta (5' --> 3') makes a new strand, ligase seals the
remaining nick.
c. Causes colon and endometrial carcinoma
d. Features:
i. Right sided colon cancers
ii. Multiple cancers
iii. Arise from macroscopically normal areas
1) Mucosa here is however dysplastic

164. Hirschprung disease

a. Arrest of migration of neural crest cells
i. Migration takes place along the vagus nerve
ii. 8th week enters the proximal colon
iii. 12th week it enters into the rectum
1) Most common site affected
b. Colon is narrow and cannot relax; aganglionic
c. No passage of intestinal contents
d. Failure to pass meconium within 48 hours

165. Colorectal carcinoma associated with intake of charred / fried foods; Gastric carcinoma
with Alcohol, tobacco, dietary nitrates and H pylori infection.

166. Fibrates - Reduce serum triglycerides and help prevent pancreatitis

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 166. Fibrates - Reduce serum triglycerides and help prevent pancreatitis
a. Act via PPAR alpha receptors

167. Parietal cells are stimulated by Gastrin:

a. Eosinophilic cells
b. Lots of mitochondria and tubulovesicular system
c. Secretion of HCl and proliferroation/hyperplasia of parietal cells
d. Zollinger ellison syndrome - visibly enlarges the fundic mucosal folds

168. Proximal duodenal ulcer:

a. 90% due to H. pylori; 10% due to NSAID use
b. Treat with triple therapy (14 days):
i. Clarithromycin + amoxicillin + PPI
ii. Bismuth may be used

169. Metoclopramide: D2 antagonist, used as an antiemetic and to treat diabetic / post

operative gastroparesis & prevent nausea and vomiting.

170. Barrett's esophagus (Dysplastic + metaplastic condition):

a. Lower 1/3 of esophagus
b. Severe long standing gastroesophageal reflux
c. Mucosal damage, causing inflammation + necrosis
d. Replacement of normal stratified squamous epithelium with intestinal columnar
cells + Goblet cells
i. Goblet cells no stain with H&E
ii. What are those purple things then?
e. May progress to esophageal adenocarcinoma (need to be monitored for dysplastic
cells)
i. Silent till it obstructs the lumen

171. Gastric banding surgery:

a. Restrictive bariatric surgery; slows the passage of food, increases satiety and limits
the amount of food consumed.
b. Band has to pass through the lesser omentum
c. Lesser omentum:
i. Gastroduodenal ligament
ii. Hepatogastric ligament
d. Careful about the arteries and structures enclosed by each ligament

172. Congenital pyloric stenosis:

a. Non bilious vomiting; projectile
b. Visible epigastric peristalsis
c. Olive sized mass in distal stomach (upper right abdomen)
d. Hypertrophy pyloric muscularis mucosae (hypertrophy of smooth muscle)
e. Rx: Surgical splitting of muscle

173. Acquired pyloric stenosis:

a. Neoplasm (carcinoma, lymphoma)
b. Gastritis
c. Peptic ulcer disease

174. Gallstone formation:

a. Female sex hormones, OCP usage, increased aromatase activity
b. Fibrates, Octreotide (somatostatin analog), Ceftriaxones
c. Malabsorption of bile acids (ilieal disease, resection)
d. Total parenteral nutrition, advanced age, fasting
e. Dx: USG

175. Pigment stones - increased activity of beta glucuronidase; enzyme deconjugates bilirubin.
Free bilirubin complexes with calcium, and precipitates in the bile.
a. Enzyme is released by bacteria and damaged hepatocytes

176. Vitamin A required to maintain mucous secreting columnar epithelium and other
specialised epithelia; deficiency leads to squamous metaplasia to keratinizing epithelium

177. Alpha amantin

a. Mushroom toxin (very potent)
b. Concentrated in hepatocytes by organic acid transporting polypeptide (OATP) and
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 b. Concentrated in hepatocytes by organic acid transporting polypeptide (OATP) and
sodium taurocholate co-transporter (NCTP)
c. Other areas damaged - GIT and renal tubules
d. Inhibits RNA polymerase II (no mRNA synthesis)
i. Cells die by apoptosis
e. Symptoms:
i. Abdominal pain
ii. Watery diarrhea
iii. Vomiting
f. Urine test for alpha amantin is confirmatory

178. Ricin (Ricinus communis) cleaves rRNA component of eukaryotic 60S

179. Iron poisoning:
a. Stage 1 - Nausea, diarrhoea, abdominal pain; haemorrhage and hypovolemia
(malena too)
b. Stage 2 - GI symptoms resolve
c. Stage 3 - Metabolic acidosis, hepatic dysfunction, hypoglycemia
d. Stage 4 - Scarring of GIT

180. Colon cancer - increased risk with low fibre diet

a. Inactivating mutation in DCC

181. Pancreatic cancer [this question was testing your knowledge of neoplasia]
a. Palpable gallbladder, non tender
b. Adenocarcinoma of the head of pancreas, probably compressing common bile duct
i. Obstructive jaundice symptoms
c. Adenocarcinoma of tail --> Late onset symptoms, only when splanchnic plexus
invasion takes place.
d. Risk factors:
i. Age (6th and 7th decade)
ii. Smoking
iii. Diabetes
iv. Chronic pancreatitis (heavy alcohol consumption; not moderate)
v. Genetic: MEN, Hereditary, HNPCC and FAP sometimes

182. Ezetimibe - reduces intestinal cholesterol and phytosterol absorption

183. Adenomatous polyposis

a. Premalignant
b. Mutations in APC gene [inactivating mutations]
c. Step wise mutations (AK53):
i. Methylation abnormalities
ii. COX 2 overexpression
1) COX inhibitors (Aspirin) reduces incidence of colon cancer
iii. K-RAS activation
iv. DCC inactivation
v. P53 inactivation
d. Screening + Timely excision --> Prevents colon carcinoma

168. Diffuse esophageal spasm

a. May mimic the pain of angina pectoris
b. Crampy pain vs the burning pain of GERD

c. Normal:
i. Food bolus distends the esophagus
ii. This stimulates contractions to start just above the bolus
iii. Propels the food down
d. DES:
i. Several segments of the esophagus contract simultaneously
ii. No propogation of food forward
iii. Manometry:
1) Disorganised non peristaltic contractions
2) Large amplitude and duration
iv. Corkscrew esophagus on barium
v. Typically not associated with exertion and isn't relieved by rest / food
1) Do a cardiac work up to exclude that shit though

169. Herpetic gingivostomatitis

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 169. Herpetic gingivostomatitis
a. Most common clinical manifestation of primary HSV-1
b. Tzanck smear (Wright Giemsa stain) to epithelial scrapings from ulcer base
i. Multinucleated giant cells
ii. Intranuclear inclusions (HSV or VZV)
c. Symptoms:
i. Fever
ii. Swollen gums
iii. Cervical lymphadenopathy

170. Giardia lamblia

a. Trophozoite (pathogenic); pear shaped and contains 2 nuclei
b. Cyst (infective); oval with 4 nuclei
c. Transmission:
i. Drinking contaminated water (campers / travelers to endemic areas)
d. Pathogenesis:
i. Adheres to mucosal cells and releases molecules --> inflammation
ii. Villous atrophy and crypt hyperplasia
e. Diagnosis:
i. Watery diarrhoea + abdominal cramps
ii. Foul smelling stool
iii. Ova and paraistes microscopy / Fecal immunoassays (Giardia antigens)
f. Risk factors:
i. IgA deficiency
ii. X-Linked agammaglobulinemia
iii. Common variable immune deficiency

171. Healthy patient + GI bleed --> ↑ BUN; (vs decreased BUN in hepatic failure GI bleeds. This
happens because NH3 cant be converted to Urea in hepatic failure)
172. Hepatic encephalopathy
a. Sequalae of Hepatic failure
b. BUN is low; NH3 is high
c. ↑NH3 alters amino acid transport across the blood brain barrier. Decreased
glutamate and catecholamine release, increase in GABA
d. Flapping tremor (Asterixis)
e. Precipitating factor:
i. Drugs (Sedatives, narcotics)
ii. Hypovolemia (diarrhea and vomiting)
iii. Excessive nitrogen load
1) GI bleeding, Constipation, Too much protein
2) Bacteria convert proteins into NH3
3) Portal shunting (capillarisation of sinusoids) leads to reduced conversion
of NH3 to urea
iv. Infections
1) Pneumonia, UTI, Spontaneous bacterial peritonitis
v. Metabolic
1) Hypokalemia (stimulates renal NH3 production), Metabolic alkalosis
(NH3>NH4+), Hypoglycema [why?]
vi. TIPS (shunting) will make things worse!
f. Rx:
i. Stop offending agent / drug
ii. Lactulose - bacterial action leads to acidification
1) Breakdown to lactic acid + acetic acid
2) NH3 trapped as NH4+ --> Luminal distention & osmotic defect (out via
potty)
iii. Rifamixin - Kills bacteria

173. Omphalomesenteric duct

a. Connects midgut lumen with yolk sac cavity in early embryonic life
b. Normally obliterates in the 7th week
i. Persistent vitelline duct
1) Meconium discharge from the umbilicus after birth
ii. Meckel diverticulum (most common)
1) May present with a fibrous band attached from umbilicus to the ilium
2) Bowel loop may get stuck over this
iii. Vitelline sinus
1) Open to the umblicus
2) Closed on the side of the gut
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 2) Closed on the side of the gut
iv. Vitelline duct cyst
1) Enterocyst; central part remains as a cyst, the proximal and distal bits
degenerate

174. Odynophagia in HIV

a. Caused by Candida
b. Painful linear esophageal ulcers (mucosal disruption)
i. Diagnosis - Endoscopy with biopsy
ii. White plaques on an erythematous mucosa
c. Leads to painful swallowing
d. Other causes - HSV

175. Octreotide - causes B12 deficiency (by decreasing gastric secretion of intrinsic factor)
176. Wilsons disease - Basal ganglia atrophy (Hepatolenticular degeneration)
a. <30 years of age + chronic hepatitis
b. No predisposition to pancreatitis though
c. Neurological symptoms:
i. Parkinsonism like tremor
ii. Ataxia & slurred speech
iii. Personality changes (depression / paranoia)
iv. Rigidity and catatonia
d. Liver disease (increased AST / ALT)
e. ATP7B gene mutation; Chr 13
f. Excess circulating free copper; causes damage to cells via ROS generation
i. May cause Fanconi syndrome
g. Dx:
i. Liver biopsy; quantitative demonstration of copper > 250 mcg/g dry weight
ii. Low Ceruloplasmin
iii. Increased Cu excretion
iv. Kayser Fleischer rings (cornea) identified on slit lamp examination
h. Rx:
i. Penicillamine (Cu chelator) + Triethylenetetramine (trientine)

177. Echinococcus granulosus

a. Endemic regions
b. Sheep / Dog handlers
c. Initial infection: asymptomatic
d. Subsequent signs and symptoms:
i. Size of cyst
ii. Location of cyst
e. Cyst formation occurs in capillaries when some larvae survive despite monocytic and
eosinophilic infiltration
f. Wall of cysts:
i. Layers of delicate gelatinous sheets
ii. Thick fibrous capsule
g. Treatment:
i. Surgery
ii. Albendazole etc
iii. Don’t aspirate because you will spill shit --> Anaphylactic shock

178. Echinococcus mulilocularis --> Multiple cysts

179. Retroperitoneal hematoma due to trauma:

a. Associated with abdominal / pelvic crush injuries
b. Pancreatic injury
i. Direct abdominal blows by malpositioned seat belts during crash
ii. Mild symptoms / asymptomatic
iii. May be ignored due to other injuries
iv. Dx: Abdominal CT, conservative management
c. Abdominal aorta hemorrhage would be huge and the patient would be in fucking
shock. He wouldn’t be alive to be complaining about mild pain.
d. Spleen is intraperitoneal

180. Spleen is the most common intra-abdominal organ injured

a. It is intraperitoneal (dorsal mesentery)
b. Mesodermal derivative [should have caught this; since the liver is endodermal]

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 181. Xylose is a monosaccharide [stupid…]
a. Used to measure brush border absorptive function independent of pancreatic
function. (Intestinal vs pancreatic malabsorption)
182. Serum trypsinogen is decreased in:
a. Chronic pancreatitis
b. Subtotal pancreatectomy
c. Cystic fibrosis

183. Alpha 1AT deficiency:

a. Panacinar emphysema (flat diaphragm, hyperlucent lung)
b. Hepatitis:
i. Neonatal hepatitis with cholestatic jaundice is common
ii. Adult disease is asymptomatic till very severe
iii. Cirrhosis, HCC
c. Test patients who have premature COPD, aswell as non smokers with COPD for
A1AT. Neonatal hepatitis - makes A1AT more probable

184. ETEC, Yersinia enterocolitica (cGMP), Vibiro, Campylobacter:

a. AB toxins, A and 5Bs
b. Stimulate G-proteins

185. Pancreatic pseudocyst:

a. Complication of acute pancreatitis
i. Disruption of pancreatic ducts --> leakage into peripancreatic space (3rd
spacing)
ii. Pancreatic enzymes cause inflammation; fibrosis and granulation tissue
develops
b. Walls of pseudocyst - granulation tissue; no epithelial lining
i. Walls of true cyst - lined by epithelial cells
c. Most common location:
i. Lesser peritoneal sac (posterior to stomach)
ii. Adherent to surrounding hollow organs

d. 'maturation' of pseudocyst takes 4-6 weeks after acute pancreatitis

186. Pancreatic neoplasm histology:

a. Glycogen rich cuboidal epithelium - Serous pancreatic neoplasms
b. Columnar mucinous epithelium - mucinous cystic neoplasm
c. Atypical cells + papillae - Papillary adenocarcinoma

187. Pringle maneuver - pinching the hepatoduodenal ligament to identify source of bleed
a. If bleeding doesn’t stop:
i. IVC bleed
ii. Hepatic vein bleed
b. Venous bleeds are non-pulsatile; arterial bleeds are pulsatile

188. Hepatitis viruses:

a. Hepatitis A and E [+] ss RNA (non enveloped)
b. Hepatitis C [+] ss RNA (enveloped)
c. Hepatitis B - dsDNA
d. Hepatitis D[-] ss circular RNA(enveloped)

189. Hepatitis E virus

a. Shed in stool in the early stages of infection
b. Incubates for 6 weeks
c. HEV antigen / HEV RNA --> Detected in stool before onset of clinical disease
d. High mortality in pregnant females
e. No chronic phase / no carcinoma

190. Selective COX2 inhibitors - anti-inflammatory effects and spares the GI mucosa (helps
reduce GI ulceration)
a. Does not inhibit platelet aggregation (Platelet function is COX1), useful in some
cases but can predispose to CVS events.
b. Worsens renal impairment, hypertension and angina.

191. Hepatocellular carcinoma:

a. Major etiologies
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 a. Major etiologies
i. Viral infection
1) 85% of the HCC cases in the world are endemic to countries with high
rates of HBV infection
2) HCC presents at a younger age in these countries
3) Vaccination would therefore help reduce that
ii. Alcoholism
iii. Food toxins (Aflatoxins)
b. Serum AFP increases
c. Suspect HCC in patients with otherwise stable cirrhosis who suddenly decompensate

192. Hepatic adenoma

a. Middle aged and young women with history of OCP use
b. Anabolic steroids (young atheletes)
c. Right hepatic lobe (usually)

193. Total parenteral nutrition:

a. Increased risk of gallstone formation:
i. Decreased enteric stimulation --> Decreased CCK
ii. Decreased enterohepatic circulation in patients with ileal resection
1) This isn't a concern with jejunal resection
b. Decreases gastrin
c. Rx: Exogenous CCK

194. Damaged hepatocytes - impaired ability to extract bile acids from portal blood;
195. Pancreatic secretin stimulation:
a. Increased flow rate of secretions
i. Increased HCO3-, decreased Cl-
1) Counter transporter at apical membrane of pancreatic ductal cells
2) Stimulated by secretin
ii. Same conc of Na and K as plasma (isotonic) [vs intestinal secretions, where at
high HCO3- excretion, there is an increased K+ excretion]

196. Acute pancreatitis

a. Common causes:
i. Gall stones
ii. Alcoholism
b. Rare causes:
i. ERCP procedure
ii. Drugs (Didanosine, azathioprine, sulfonamides (sulfasalazine, furosemide),
valproate)
iii. Infections (mumps,coxsackie virus, mycoplasma pneumoniae)
iv. Hypertriglyceridemia (>1000 mg/dl)
1) Increase FFA production by pancreatic lipase in the capillaries, normally
bound to albumin
2) At >1000 however, FFA concentration too high for albumin; therefore
causes direct injury
v. Pancreatic ductal abnormalities, ampulla abnormalities
vi. Surgery (gastric, biliary)
vii. Hypercalcemia

197. Cervicofacial actinomycosis

a. Oral trauma
b. Draining yellow pus form a firm growing mass
c. Actinomyces israelii
d. Treatment:
i. Chronic penicillin therapy
ii. Surgical debridement

198. Colonic polyps

a. Non Neoplastic
i. Hyperplastic - well differentiated; glands and crypts
ii. Hamartomatous - Peutz Jegher / Juvenile polyposis
1) AD
2) Pigmented mucocutaneous macules, hamartomatous polyps in GIT
iii. Inflammatory - Crohns / UC (regenerating intestinal mucosa)
1) Ulcerative colitis - pseudopolyps
iv. Lymphoid - in children, lymphocytic infiltration
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 iv. Lymphoid - in children, lymphocytic infiltration

b. Neoplastic adenomatous polyps (can transform into adenocarcinoma)

i. Degree of dysplasia
ii. Histological pattern
1) Villous > Tubulovillous > Tubular (Descending malignant potential)
iii. Size:
1) >4cm - 40% risk of malignancy
2) <1cm - probably benign

iv. Adenoma to carcinoma sequence [takes about 10 years]

1) APC - small polyp
2) K-RAS (proto-oncogene)- uncontrolled cell proliferation; increase in size
3) P53 / DCC - malignant transformation

199. Midgut malrotation

a. Normal - 270° anticlockwise rotation
b. Abnormal rotation:
i. Cecum may be fixed in the RUQ
ii. Fibrous bands (Ladd's bands) may be present attached to the second portion
of the duodenum
1) Bilious vomiting
2) Intestinal obstruction
c. Twisting of intestine around the SMA - midgut volvulus / intestinal gangrene +
perforation

200. Acute acalculous cholecystitis

a. Acute inflammation of the gallbladder
b. Predisposing conditions:
i. TPN
ii. Trauma
iii. Coronary heart disease
iv. Major burns
v. Surgery
vi. Opiate usage
c. Pathophysiology:
i. Secondary to gallbladder stasis & ischemia
ii. Causes inflammation and injury
iii. Gangrene, perforation & emphysematous cholecystitis
d. Treatment:
i. Antibiotics
ii. Cholecystectomy + abscess drainage

201. Corticosteroid therapy and liver enzymes

a. Upregulation of gluconeogenesis (Increased PEPCK, Glucose 6 phosphatase)
b. Increased glycogen synthesis (Glycogen synthetase)
c. Peripheral insulin antagonism
i. Catabolic state
ii. Hyperglycemia (diabetogenic)
d. In peripheral tissues, there is increased catabolism:
i. Skeletal muscle
1) Caused by cortisol proteolysis + Hypokalemia (mineralocorticoid action
of cortisol)
2) Proximal muscle weakness + BUN increase
ii. Skin thinning + purple stirae (impaired fibroblast proliferation)
iii. Potent immunosuppressive agents
1) Impaired T cell function
2) Decreased leukocyte count; except neutrophils (demargination hence
increase)
iv. Decreased bone mass
1) Decreased GIT Ca+2 absorption, increased renal calcium excretion, and
decreased osteoblast bone forming activity

202. Travel vaccination (Africa, Asia, South America)

a. HAV
b. Salmonella (typhoid fever)

203. Typhoid fever:

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 203. Typhoid fever:
a. Salmonella typhi penetrates the intestinal mucosa, travels into mesenteric lymph
nodes, multiplies and phagocytosed by macrophages (doesn’t get degraded)
b. Rose spots on abdomen
c. Fever
204. Travellers diarrhoea - E coli (ETEC), Campylobacter, Shigella, Salmonella, Giardia,
Entamoeba

205. VIPoma , Pancreatic cholera, WDHA

a. Hyper secretion of VIP from the pancreas (non alpha, non beta)
i. Otherwise released from preganglionic parasympathetics of GIT
b. Inhibits Gastrin secretion, Relaxes GI smooth muscle
c. Increases HCO3- and Cl- secretion from pancreas
d. Secretory Diarrhoea
i. Low stool osmotic gap <50mOsm/kg
ii. No blood or pus
iii. Doesn’t improve with dietary modification (not osmotic)
iv. Increased intestinal water and electrolyte secretion
1) Hypokalemia, Hyponatremia
e. Somatostatin - Treats VIPoma

206. Xanthelasmas
a. Contains lipid laden macrophages (foam cells)
b. Papules, yellow (due to its location in the superficial dermis)
c. Associated with
i. Primary / Secondary hyperlipidemia
ii. Chronic cholestatic processes
1) Obstructive biliary lesions
2) Primary biliary cirrhosis

207. Liver failure --> Hypersplenism --> mild thrombocytopenia

208. Enterobius vermicularis (pin worm)

a. Perianal pruritus
b. School age children
c. Simple life cycle, hence high prevalence
d. Adult worm:
i. Cecum and Appendix
ii. Female worm migrates into the perianal region to deposit eggs (at night)
e. Eggs:
i. Larvae inside mature in about 6 hours
ii. Asymmetrically flattened on one side
iii. Scotch tape test
f. Rx: Albendazole + Pyrantel Palmoate (Nm depolarisation; spastic paralysis of
worms. Doesn’t work on Trematodes or cestodes)

209. Peptic ulcers:

a. Duodenal uclers are always benign; caused by H. pylori
i. Non invasive; present in the mucous layer, or attached to the epithelium
b. Gastric ulcers may be malignant; hence biopsy
i. Gastric MALToma (H pylori is a risk factor for this)
ii. Gastric adenocarcinoma
iii. Penetration into:
1) Proximal lesser curvature --> Left gastric artery
2) Distal lesser curvature --> Right gastric
3) (similar logic for greater curvature)

210. Carcinoma of distal colon - annular lesions (grow within the walls)
a. Leads to bowel constricton
b. Heaped up edges
c. Ulcerated central region
d. Risk factors:
i. Age
ii. FAP
iii. Sporadic?
iv. Inflammatory bowel disease

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 211. Pill induced esophagitis:
a. Tetracylines (Doxycycline)
i. Can also cause tooth enamel hypoplasia, permanent tooth discoloration in
kids
b. Bisphosphonates
c. KCl

212. GERD:
a. Nocturnal cough, dysphagia, sore throat = GERD
b. Heartburn may or may not always be present
c. Pathophysiology:
i. Decreased LES tone
ii. Acid refluxes into the esophagus - epithelial repair initiated
iii. High risk of metaplasia
d. Characteristic histological findings:
i. Erosions / ulcerations if severe
ii. Basal zone hyperplasia
iii. Elongation of the lamina propria papillae
iv. Inflammatory cells
1) Neutrophils
2) Eosinophils
3) Lymphocytes
e. Diagnosis by upper GI endoscopy, and pH testing

213. All acute viral hepatitis have the same histopathological findings
a. Ballooning degeneration
b. Panlobular lymphocytic (mononuclear) infiltrates (look at that image in notes)
c. Hepatocyte apoptosis; councilman bodies (pink staining)
d. Regenerative attempts [chronic hepatitis; not HAV]
i. Pseudoacini of dividing hepatocytes
ii. Numerous mitotic figures

214. Acute pancreatitis:

a. Pathogenesis:
i. Ductal obstruction - stasis of pancreatic secretions
1) Digestion of adipose cells by lipase
2) Fatty acids - bind calcium and precipitates as insoluble calcium salts
b. Acute interstitial pancreatitis
i. Edema --> Compression of acinar blood supply
ii. Activation of trypsin by ischemic damage; autolysis of pancreatic tissue
iii. Focal fat necrosis
c. Acute necrotic pancreatitis (progression of acute interstitial)
i. Destruction of blood vessel walls --> hemorrhage into necrotic areas
ii. Areas of white chalky necrosis visible
iii. Spreads to mesentery and abdominal cavity
iv. Gross: Black areas of hemorrhage
d. Diagnosis:
i. Pancreatic Amylase
ii. Pancreatic lipase

215. High amylase in pleural effusion fluid

a. Pancreatitis
b. Pancreatic pseudocyst
c. Esophageal rupture
d. Lung adenocarcinoma

216. Mesenteric ischemia - bowel is dusky red in colour; ecchymosis (subserosal) + edema may
be present

217. Peritonitis
a. Intestinal perforation
b. Bacterial peritonitis:
i. Peritoneal surfaces with white-yellow suppurative exudate

218. Classical Galactosemia

a. Impaired liver function
b. Hyperchloremic metabolic acidosis (normal anion gap)
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 b. Hyperchloremic metabolic acidosis (normal anion gap)
c. Aminoaciduria
d. Clinical features:
i. Failure to thrive as soon as breastfeeding is started
ii. Vomting + lethargy

219. Urease breath test

a. Test for H. pylori infection
b. Consumption of radiolabeled Urea (C13 - Urea)
i. Rad-CO2 + NH3 produced
1) Increases pH (alkaline); turns Phenol Red pink.
ii. Rad-CO2 exhaled by the lungs after being absorbed into the bloodstream

220. Porcelain gallbladder:

a. Increased risk of carcinoma (11-33%); recommend surgical removal
b. Bluish, brittle, calcium laden gallbladder - chronic cholecystitis
i. Diagnosed on radiograph
ii. Firm, painless mass in the RUQ
c. Intramural deposition of calcium salts; secondary to chronic irritation from
gallstones or natural progression of chronic inflammation.

221. Infection of biliary tree - brown pigment stones

a. Organisms:
i. Opisthorchis sinensis (Clonorchis sinensis)
ii. Ascaris lumbircoides
iii. E coli
b. Release of enzyme beta glucuronidase from injured hepatocytes & microorganisms
leads to an increase in deconjugation of CB, forming UCB. This increases the risk of
forming brown pigment stones.
c. Beta glucuronidase deficiency - Sly syndrome; mucopolysaccharidoses VII

222. Black stones = sign of hemolysis; excess CB --> converted to UCB (I'm assuming by beta
glucuronidase) which combines with Ca --> Calcium bilirubinate stones.

223. Acetaminophen liver damage occurs after a latent period; prevented by N-acetyl cysteine
(Glutathione donor)

224. Hepatic angiosarcoma - Exposure to Polyvinylchloride, thorotrast or arsenic

a. CD31 - PECAM1 (endothelial marker; responsible for leukocyte transmigration)
i. Aresenic - pesticides
ii. Thorotrast - old radiocontrast agent
iii. PVC - plastic industry

225. Henoch Schonlein purpura (HSP)

a. Kids (3 - 10 years old)
b. Symptoms:
i. Abdominal pain (GI bleeding due to vasculitis)
ii. Proteinuria (Renal involvement read below)
iii. Arthralgias
c. Small vessel vasculitis - palpable purpura
d. [IgA - Anti IgA] immune complex in circulation (Type III hs):
i. Deposition in renal walls
ii. Deposition in renal mesangium
iii. May cause crescent formation (NOT RPGN)
e. Deposition leads to activation of complement --> Inflammation

226. Crohns disease and gallstones

a. Decreased enterohepatic cycling of bile acids due to terminal ileal disease
b. Loss of bile acids --> Increased CH:Bile salt ratio
i. Gallstones

227. Chronic mesenteric ischemia

a. Main findings:
i. Postprandial epigastric pain + food aversion (end up losing weight because of
pain avoidance)
ii. History of generalized atherosclerosis
1) Carotid artery disease
2) Coronary artery disease
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 2) Coronary artery disease
b. Pathogenesis:
i. Atherosclerosis of the mesenteric arteries
ii. Intestinal angina: hypoperfusion of the bowel when more blood is needed for
digestion/absorption of nutrients
c. Dx:
i. Duplex USG
ii. Angiography

228. Acute mesenteric ischemia - aortic dissection, arterial embolism

229. Biliary colic also causes post prandial epigastric pain (no atherosclerosis, food aversion
absent)

230. Intussusception
a. Impaired venous return from invaginated segment of bowel --> Ischemia and
necrosis of the intestinal wall
b. Clinical presentation
i. Intermittent abdominal pain
ii. Nausea and vomiting
iii. RLQ palpable mass maybe?
iv. Bright red stools + mucous (currant jelly)
c. Sites and causes:
i. Most commonly at the ileocolic junction (size difference btw bowels)
ii. Most common in children < 2 years old
iii. Age >2 years:
1) Meckels
2) Foreign body
3) Intestinal tumour
d. Barium enema (both diagnostic and therapeutic); else surgery

231. Secretin released from S-cells in the crypts of Lieberkuhn once stimulated by the delivery
of acidic chyme (pH < 4.5)
a. Pancreas stimulated to release HCO3- and Water
b. Does not have any role to play in release of exocrine pancreatic enzymes (that's the
job of CCK)
c. Also promotes insulin release

232. Salivary gland secretions

a. Isotonic at the acini
b. In the ducts:
i. Na and Cl are reabsorbed (aldosterone does do something here)
ii. K+ and HCO3- are secreted
c. Saliva is hypotonic because more Na and Cl is reabsorbed and the ducts are
impermeable to water.
d. At high flow rates; Na and Cl is high, and K+ low in saliva because the ducts don’t
have enough time to take up stuff.

233. Squamous cell carcinoma of Head and Neck - usually associated with tobacco and alcohol
abuse.
a. Site of development
i. Ventral tongue
ii. Floor of mouth
iii. Lower lip
iv. Soft palate + gingiva

234. Ischemic colitis

a. Common cause of lower GI hemorrhage in the elderly
b. Causes:
i. Hypoperfusion (Cardiac disease / shock)
ii. Occlusion of vasculature
1) Atherosclerosis - accompanied by diminished peripheral pulses
2) Embolism
3) Thrombosis
c. Presenting features:
i. Crampy abdominal pain
ii. Tenderness
iii. Diminished bowel sounds
iv. Diminished cardiac output (cardiac disease, prolonged shock)
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 iv. Diminished cardiac output (cardiac disease, prolonged shock)
d. Histological findings
i. Moderate ischemia - patchy necrosis, mucosal hemorrhages, ecchymoses
ii. Severe ischemia - muscularis involvement; bowel thickens and becomes
edematous; frank blood
iii. Finally --> transmural infarct, leading to perforation

235. Bile salts are emulsifying agents; hence can disrupt the surface membrane of bacteria
(gram negative enterics)
a. Look out for increased bacterial proliferation in those with obstructed CBD

236. Leiomyoma of the esophagus is detected on barium swallow If intramural.

237. Multiple, rapidly appearing acanthosis nigricans (brown, black thickened plaques) is a sign
of malignant gastric cancer.
a. Or liver / lung cancer too (but classically gastric cancer)

238. FAP - Familial adenomatous polyposis (AD)

a. Extraintestinal manifestations - soft tissue tumours of skin, hepatoblastoma

239. Virchow's node (left supraclavicular)

a. Abdominal viscera
i. Hence is enlarged in occult abdominal malignancies
b. Left hemithorax viscera
i. Lung cancer
ii. Breast cancer

240. Trypsinogen activated to trypsin by Enterokinase

a. Trypsin further activates other enzymes
b. Enterokinase (Enteropeptidase) deficiency - typical protein malabsorption signs
i. Diarrhoea
ii. Growth retardation
iii. Hypoproteinemia

241. Watershed area - splenic flexure

a. Systemic hypotension leads to ischemic colitis
i. Necrosis and ischemia of the intestinal wall
ii. Abdominal pain + bloody diarrhoea

242. Morphine (mu receptor analgesic)

a. Causes constriction of smooth muscles in the sphincter of oddi
i. Increased CBD pressures
ii. Cause biliary colic
b. Rare side effect, but severe RUQ pain is seen in this disease
c. Doesn’t happen with meperidine
i. Opioid of choice In biliary / pancreatic pain
ii. NSAIDS (diclofenac / ketorlac) may be better though

243. Staph aureus: preformed heat stable toxin

a. Direct inoculation from food handlers
b. Food at room temperature:
i. S aureus multiplies and produces toxin (enterotoxin)
1) Mayonnaise
2) Meat, egg, fish products
3) Cream, milk, dairy products
ii. Causes nausea, vomiting, abdominal cramps (not much diarrhoea)
iii. Symptoms occur within 6 hours (preformed hence rapid)

244. Measuring achlorhydria:

a. pH of a gastric aspirate before and after stimulation with a gastric analog

Cholecystokinin I cells
GIP K cells
245.
Somatostatin D cells (pancreatic islets + intestine)
GLP-1 L cells
246. Tongue innervation:
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 246. Tongue innervation:
a. Anterior and posterior parts are delineated by the terminal sulcus (with the foramen
cecum in the midline)
b. Motor:
i. Hypoglossal nerve (XII)
ii. Palatoglossus - Vagus(X)
c. General sensory:
i. Anterior 2/3 of the tongue - Mandibular branch of trigeminal (V)
ii. Posterior 1/3 - XI
iii. Root of the tongue - X
d. Taste:
i. Anterior 2/3 - Chorda tympani (VII)
ii. Posterior 1/3 - CN IX
iii. Posterior area of root of tongue (CN X)

247. Granulomatous gastritis - benign, granulomatous, secondary to transmural inflammation

248. Gastric adenocarcinomas - features of subtypes are important:

a. Diffuse
i. Signet ring cells
ii. Loss of E-cadherin
iii. Leather bottle appearance, infiltrate the stomach wall
iv. Risk factors:
1) Chronic gastritis
2) Barret esophagus
3) H pylori, nitrate consumption, no fruits and vegetables, cigarette smoke
b. Intestinal
i. Similar to colonic carcinoma
ii. Arises from precursor lesions
iii. Intraluminal expansion

249. GI irritation induced nausea and vomiting (mediated by increased activation of 5HT3
(serotonin) receptors on vagal and spinal afferent nerves:
a. Relay to the medullary vomiting center --> Emesis
b. 5HT3 receptor antagonists (Ondansetron) useful in these conditions
i. Travelers diarrhoea / Chemo / General anaesthesia
c. Side note:
i. Dopamine receptor antagonists also act as antiemetics (more useful in central
neural causes of nausea)
1) Metoclopramide, promethazine
2) Very toxic:
a) Sedation
b) Extrapyramidal side effects
ii. First generation H1 antagonists are useful in treating nausea due to vestibular
sickness (Diphenhydramine, meclizine) and ach antagonists (scopolamine)
1) Significant sedation

250. Campylobacter:
a. Transmitted from domestic animals to humans
i. Puppies, cattle, sheep, chickens
ii. Contaminated food (undercooked poultry, unpasteurized milk)
b. Curved rod; corkscrew motility
c. Tenesmus and abdominal cramping
d. Invasive + inflammatory diarrhoea; blood may be present

251. Budd Chiari syndrome

a. Thrombotic occlusion of the hepatic veins, or intra/suprahepatic IVC
i. Portal hypertension
ii. Ascites
iii. Hepatomegaly
iv. Splenomegaly
b. Hepatic centrilobular necrosis or congestion will be seen (vs portal vein thrombosis)

252. Carcinoid tumours of GIT:

a. Metastatic - carcinoid syndrome will manifest
b. Localized (to GIT) - carcinoid syndrome wont happen because all the serotonin is
metabolized by the liver
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 metabolized by the liver
i. Remember a localized bronchial carcinoid will show serotonin syndrome
ii. Also produces other kinins apart from serotonin
c. Clinical findings:
i. Flushing of skin, telangiectasias, cyanosis
ii. Watery diarrhoea
iii. Bronchospasm, dyspnea, wheezing
iv. Cardiac valvular plaques (right sided; Tricuspid regurg and Pulm stenosis)
v. Elevated 24hr 5-HIAA excretion
vi. Hypotension [vs the hypertension of Pheo]
d. Rx: Octreotide and surgery

253. Octreotide uses:

a. Carcinoids
b. Acromegaly
c. Varices
d. VIPoma

254. Vitamin A - stored in the perisinusoidal stellate cells (ito cells); lasts 6 months

255. Portal vein thrombosis:

a. Portal hypertension + normal liver biopsy
b. Esophageal varices, splenomegaly will be present, but sinusoidal hypertension will
be absent.
c. No ascites (since liver is normal)

256. Extrahepatic biliary atresia:

a. Congenital obstruction of extrahepatic bile ducts
b. Persistent jaundice beginning around the 3rd or 4th week of life
c. Clinical features:
i. Dark urine
ii. Light stools
iii. Firm enlarged liver
iv. Will progress to cirrhosis within 6 months of life if nor surgically corrected
d. Lab findings:
i. Increased ALP, Direct bilirubin
ii. Gamma-glutamyl transferase
e. Biopsy findings:
i. Marked intrahepatic bile duct proliferation
ii. Portal tract edema + fibrosis
iii. Parenchymal cholestasis (bile lakes?)

257. Short bowel syndrome:

a. Extensive delivery of intestinal fluid + osmotically active solutes to the colon -->
Diarrhoea

258. Choledochal cyst - congenital dilation of the common bile duct

259. Increased mucous in stool - Crohn's disease, giardiasis, inflammation

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Hepatnotice.
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