A.

food and water contamination

B. blood inoculation
1. HAV- A
2. HBV- B
3. HCV- B
4. HDV- B
5. HEV- A

6. spread by ingestion of contaminated water and food; shed in the stool for 2-3 weeks before and 1
week after the onset of jaundice- HAV
7. transmitted through blood inoculation, with IV drug use- HCV
8. acute coinfection after exposure to serum containing both HDV and HBV; superinfection of a
chronic carrier of HBV with a new inoculum of HDV- HDV
9. enterically transmitted, water borne infection; endemic in india- HEV
10. Transmitted vertically- HBV

11. nucleocapsid core protein- HBcAg

12. precore protein- HBeAg
13. envelope glycoprotein- HBsAg
14. transcriptional transactibator- HBV-X protein

15. HBeAg positive, high levels of HBV DNA (1billion IU/ml), normal serum aminotransferases,
low risk of liver damage- Immune tolerance
16. immune system attempts to clear virus resulting in liver damage, fluctuating ALT, variable levels
of HBV DNA- Immune active/ Immune clearance
17. immune system successfully controls virus, low HBV DNA, HB eAb positive, normal liver
function test= may completely eliminate HBsAg and develop HBsAb; resolution- Immune control
18. hepatitis B virus escapes immune control and begins to replicate again, despite the presence of
HBeAb, high HBV DNA, liver damage may again occur- Immune reactivation/ Immune escapes

19. acetaldehyde and acetic acid- Ethanol

20. glycol-aldehyde, glycolic acid, glyoxylic acid- Ethylene glycol
21. formaldehyde, formic acid- Methanol
22. acetone- Isopropyl alcohol

23. massive intake of solute free fluid- hyponatremia

24. dietary deficiency, gastric losses, leaky membranes, shifts from extracellular to intracellular-
hypokalemia
25. dietary deficiency, malabsorption, increased cellular uptake- hypophosphatemia
26. dietary deficiency, malabsorption, phosphorus deficiency- hypomagnesemia
27. extrahepatic biliary atresia; idiopathic neonatal sepsis- Neonatal cholestasis
28. prominent activated Kupffer cells and mild portal inflammation, hepatocyte necrosis is scant or
absent- Cholestasis of Sepsis
29. interlobular bile ducts actively destroyed by lymphocytic or plasmacytic inflammation with or
without granulomas (florid duct lesion)- Primary biliary cirrhosis
30. largest ducts- chronic inflammation with superimposed acute inflammation (similar to ulcerative
colitis), narrowing due to edema, subsequent scarring- Primary sclerosing cholangitis

Mechanism of injury excessive iron

31. lipid peroxidation by iron catalyzed free radical reactions
32. stimulation of collagen formation
33. direct irreversible oxidative damage of iron to DNA

Mechanism of injury excessive copper

34. promoting the formation of free radicals
35. binding to sulfhydryl groups of cellular proteins
36. displacing other metals in hepatic metalloenzymes

37. relatively small at the time of diagnosis- extrahepatic biliary tumors

38. jaundice, acholic stools, nausea and vomiting and weight loss from biliary obstruction-
extrahepatic biliary tumors
39. may cause symptoms only when much of the liver is replaced by tumor- intrahepatic biliary
tumor
40. nonspecific signs and symptoms such as weight loss, pain, anorexia, and ascites- intrahepatic
biliary tumor

hereditary hemochromatosis (decreasing order of severity)

41. liver- A
42. pancreas- B
43. heart- C
44. skin- D
45. joint synovial linings- E
46. testes- F

pathogenesis of hirschsprung disease

47. heterozygous loss of function mutations in receptor tyrosine kinase RET gene
48. normal migration of neural crest cells from cecum ro rectum disrupted
49. aganglionosis (lack of meissner submucosal plexus and auerbach myenteric plexus)
50. absent coordinated persitaltic contractions
51. bowel dilation proximal to the affected segment
52. Salient features of autoimmune hepatitis except
a. female predominance 70%
b. absence of serologic evidence of viral infection
c. presence of other forms of autoimmune dse
d. elevated serum IgM
53. Negative result for HBsAg may occur in the ff:
a. no infection
b. Immunization
c. core window period
d. A and C
e. ALL

Classify circulatory disorders of the liver according to:

54. Impaired blood flow into the liver- Hepatic Artery Inflow
55. Impaired blood flow through the liver- Cirrhosis and Passive Congestion
56. Hepatic Vein outflow obstruction- Budd-Chiari Syndrome

Impaired blood flow into the liver

57. Hepatic artery inflow
58. Portal vein obstruction and thrombosis
59. Peritoneal sepsis
60. Pancreatitis
61. Thrombogenic disease
62. Vascular invasion by primary or secondary cancer in the liver
63. Banti syndrome
64. Cirrhosis
65. intrahepatic thrombosis of portal vein radical
66. hepatoportal sclerosis

Impaired blood flow through the liver

67. Sickle cell disease
68. Disseminated intravascular coagulation

Hepatic vein outflow obstruction

69. Hepatic vein thrombosis (budd-chiari syndrome)
70. Sinusoidal obstruction syndrome

Drug/toxin induced liver diseases

71. Isoniazid- mimicking chronic viral hepatitis
72. Minocyclin- autoimmune-like hepatitis
73. Steatosis- total parenteral nutrition
74. Reye syndrome- aspirin
75. Type 1 DM
- massive autoimmune attack of the B cells of the pancreas from previous viral infection
- ketoacidosis is common
- childhood/ juvenile onset
- absolute deficiency of insulin
76. Type 2 DM
-dysfunctional B cells and insulin resistance
- responsive to oral hypoglycemic drugs
- inability of B cells to produce appropriate quantities of insulin

77. Which of the following is a characteristic of chronic hepatitis.

A.) T cell immunity
B.) Wrinkled baggy capsule
C.)Widespread scarring
D.) Muddy red mushy

78. Which of the ff. Is NOT the Characteristic of Pancreatic Carcinoma?

a.)60% part of the body
b.)highly invasive
c.)Trousseau syndrome
d.) Serum Carcinoembryonic and CA19-9 antigen.

79. Acute cholecystitis - gallbladder usually enlarged & tense; bright red or blotchy, violaceous color,
mucosal ulcerations, serosa frequently covered by fibrinous or fibrinopurulent exudate
80. Chronic cholecystitis - gallbladder may be contracted, normal size or enlarged, submucosa and
serosa thickened from fibrosis, mural lymphocytes
81. Gangrenous cholecystitis - gallbladder wall thickened, edematous and hyperemic into a green-
black necrotic organ
82. Empyema of gallbladder - contained exudate is mostly pus

Trace the probable pathogenesis of acute pancreatitis

83. obstruction and increase intraductal pressure
84. lipase secretion
85. local fat necrosis
86. injures periacinar myofibroblasts
87. leaky microbasculature
88. ischemic injury to acinar cells

Meconium Ileus
89. absence of epithelial cystic fibrosis transmembrane conductance regulator (CFTR gene)
90. defects in intestinal and pancreatic ductal chloride ion secretion
91. interference with bicarbonate, sodium, and water secretion
92. pancreatic intaductal concretions
93. autodigestion