Hepatology Flashcards
(182 cards)
1
Q
Development of liver starts at ——— weeks of gestation from ————- from —— wall of foregut
A
3-4 weeks
proliferating endodermal bud
ventral
2
Q
FGF for liver formation is produced by
A
cardiogenic mesoderm
3
Q
BMP-7 is produced by
A
septum transversum
4
Q
common marker for all hepatoblasts
A
AFP
5
Q
marker for hepato blast forming cholangiocyte
A
SOX-9
6
Q
marker for hepato blast forming hepatocyte
A
HNF-4 alpha
7
Q
connective tissue framework of liver is formed from
A
septum transversum
8
Q
Marker of mature hepatocyte
A
cytokeratin 8 and 18
9
Q
cytokeratin 8 and 18 are expressed in which type of cancer
A
SCC
10
Q
ytokeratin 8 and 18 are normally expressed in which cells
A
mature hepatocytes
glandular epithelium
transitional epithelium
11
Q
defect in Jagged 1/NOTCH2 pathway causes
A
Alagille syndrome
12
Q
Features of Alagille syndrome
A
1.paucity of intrahepatic bile ducts ——->cholestasis
2. pulmonary stenosis
3. ophthal - posterior embryotoxon
4. butterfly vertebrae
5. Renal obstruction
13
Q
structures of mesodermal origin in the liver (3)
A
connective tissue framework
glisson capsule
stellate cells
14
Q
—-% of blood supply and —-% of O2 supply from portal vein
A
70,40
15
Q
—-% of blood supply and —-% of O2 supply from hepatic artery
A
30,60
16
Q
embryonic structures forming portal vein
A
inferior segments of left and right vitelline veins
17
Q
zone of hepatocytes most prone to ischemiq
A
zone 3 - centrilobular
18
Q
Hepatic artery is —— to the portal vein and —- of the bile duct
A
anterior , left
19
Q
Glissons capsule covers all structures except ————
A
hepatic vein
20
Q
function of stellate cells
A
vitamin A storage
21
Q
HOX-1 and HOX-2 are respectively present in (cell organelle)
A
smooth ER and mitochondria
22
Q
ATP requiring step in bilirubin metabolism
A
Excretion of bilirubin diglucuronide into bile
23
Q
Membrane protein requires for bilirubin re entry in bilirubin hopping
A
OATP B1/B3
24
Q
Deficiency of MRP2 causes
A
Dubin Johnson syndrome
25
Deficient of OATP B1/B3
rotor syndrome
26
daily production of bilirubin
300 mg / day
or
4mg /kg
27
indirect hyperbilirubinemia : ——% of total br is indirect
Direct hyperbilirubinemia : ——% of total br is direct
>85%
>50%
28
indirect hyperbilirubinemia : ——% of total br is indirect
Direct hyperbilirubinemia : ——% of total br is direct
>85%
>50%
29
Drugs causing indirect hyperbilirubinemia (2)
rifampicin
probenecid
30
condition where AST high and ALT normal (2)
MI
rhabdomyolysis
31
liver condition where AST> ALT
alcoholic hepatitis
32
AST/ALT ratio for definitive diagnosis of alcohol hepatitis
3:1
33
Causes for chronic mild elevations of ALT>AST (5)
1. chronic viral hepatitis
2. Wilson’s
3. NASH
4. AI hepatitis
5. Hemochromatosis
after ruling out coeliac and hyperthyroidism ^
34
Chronic hepatitis with mild elevations AST> ALT is characteristic of
cirrhosis (decreased sinusoidal uptake of AST)
35
ALP is produced from ——— of hepatocytes
canalicular membrane
36
Conditions causing intrahepatic cholestasis (5)
1. drugs
2. Primary sclerosing chloangitis
3. Primary biliary cirrhosis
4. sarcoidosis
5. sepsis
37
reduced ALP is only seen in —— (condition)
Wilson’s disease
38
Drug causing vanishing bile duct syndrome
Amoxiclav
Macrolides
39
Name type of hepatitis caused by each
1.Anabolic steroids
2. Azathioprine
3. NSAIDs
4. Allopurinol
5. Procainamide
6. Amoxiclav
7. Macrolides
1. bland cholestasis
2,3 : Cholestatic hepatitis
4,5 : granulomatous hepatitis
6,7: Vanishing bile duct syndrome
40
Negative acute phase reactant proteins produced by liver are : (4)
albumin
AFP
transferrin
transthyretin
41
———- is seen in autoimmune hepatitis (wrt albumin globulin)
polyclonal hypergammaglobulinemia
42
———- is an excellent marker of hepatic synthetic function in patients with chronic liver disease with cirrhosis
albumin
43
IV fluid of choice for acute hep A infection and dose
3 pints of 10% dextrose / day
(150 g dextrose per day to replenish glucose)
44
Most common cause of acute fulminant hepatic failure in India
HEV
45
Drugs inducing liver injury independent of dose
RIFAMPICIN (even 1 dose)
INH
valproate
PTU
phenytoin
carbamazepine
nitrofurantoin
46
what is used to predict risk of hepatotoxicity in PCT poisoning
Rumack Matthews nomogram
47
Rumack Matthews nomogram is used to
predict risk of hepatotoxicity in PCT poisoning
48
Kings college hospital indicators of poor prognosis in ALF PCT:
arterial pH <7.25 more than 24 hours after drug ingestion
PT > 100 sec or INR>6.5
S Cr >3.4 mg/dL or anuria
Grade 3 to 4 encephalopathy
49
Functional cause of cirrhosis
decrease in sinusoidal nitric oxide—-> vasoconstriction and defenestration of sinusoids —-> activation of stellate cells
50
First evident clinical finding in Portal Hypertension
Splenomegaly
51
First evident biochemical finding in PoHTN
Thrombocytopenia (spleen trapping platelets)
52
Signs of decompensation in liver(4)
Jaundice
Ascites
Encephalopathy
Bleeding varices
53
PoHTN is defined as increase in sinusoidal pressure >______
6 mm Hg
54
At the hilum, —- drains in to left portal vein and —— drains to right portal vein
umbilical vein ; cystic vein
55
EHPVO is characterised by
UGI bleeding and massive splenomegaly
no cirrhosis
56
Budd Chiari syndrome is characterised by
Ascites and hepatomegaly
57
Drug used to treat portal hypertension that decreases portal flow (best drug)
non selective beta# - Carvedilol
58
Indications for endoscopic variceal ligation (2)
1. unable to tolerate beta#
2. target HVPG not achieved w beta#
59
Drug of choice in acute variceal bleed with dosage
Terlipressin
2 mg iv every 4th hourly for 48 h
+ 3 more days
60
High SAAG low protein ascites is seen in
portal hypertension or cirrhosis
61
Low SAAG low protein ascites is seen in
nephrotic syndrome
62
Low protein high SAAG ascites is seen in
peritoneal carcinomatosis
63
High SAAG high protein ascites seen in
Budd chiari syndrome
64
First sign of decompensation of liver is ——— except in ———-
ascites, fulminant hepatic failure
65
min ascitic fluid detectable in USG
100 ml
66
min ascitic fluid for shifting dullness
500 ml
67
min ascitic fluid for fluid thrill
1500 ml
68
Grade of ascites where treatment is started
grade 2
69
most common organism causing SBP
E.coli
70
Criteria for SBP (3)
1. ascitic fluid culture +
2. WBC >= 500/mcL or PMN >=250 cells /mcL
3. No evident intra abdominal, surgically treatable source of infection
71
Most common cause of Low SAAG ascites
peritoneal carcinomatosis
72
Treatment for SBP
Inj Cefotaxime 2g IV TDS x 5days
73
drug of choice for prophylaxis of SBP
Norfloxacin
74
Starting and maximum dose of spironolactone in ascites
100 mg , 400 mg
75
Starting and maximum dose of furosemide in ascites
40 mg, 160 mg
76
drugs used in treatment of ascites
spironolactone
furosemide
77
Type B HE is assoc with
TIPSS
78
cell involved in HE
Alzheimer type 2 astrocyte
79
Toxins playing a role in HE (top 4)
1. NH3
2. Mercaptans
3. Aromatic aa
4. Manganese
80
High grade edema is seen in Type —— HE
A (due to fulminant hepatic failure )
81
Precipitating factors for HE
1. inc NH3 - UGI bleed, sepsis
2. Alkalosis
3. uremia
4. dehydration
5. BZDs
82
Criteria used for assessing HE
West Haven criteria
83
rigidity hypertonia and clonus is seen in grade ——— WHC in HE
grade III
84
triphasic wave on EEG is seen in grade —— of WHC
grade IV
85
Which drug is preferred in treatment of HE and why?
Lactulose bowel wash:
1. reduces pH
2. fermented by colonic bacteria to produce volatile fatty acids and hydrogen (no NH3)
3. laxative
86
Charcots triad and condition
RUQ pain, fever, jaundice
Cholangitis
87
Gene involved in Wilson’s disease
ATP 7B , chromosome 13q
88
Wilson’s disease only manifests after —— years of age because —-
3, body has enough metallothioneins until 3 years of age
89
Cu is excreted in
bile
90
most important marker to screen Wilson
serum ceruloplasmin < 10 mg
91
Wilson presenting with fulminant hepatic failure will always also have ——
Coombs negative haemolytic anemia + low ALP
92
EM changes in Wilson
tennis racquet appearance due to mitochondrial involvement
93
Where is Cu deposited in Wilson’s?
Kupffer cells
not hepatocytes
93
anyone <20 years with neuropsychiatric or Parkinsonism manifestations, always suspect —-
Wilson’s
94
Type of tremor seen in WD
Wing beating tremor
95
most common neurological manifestation in WD
dysarthria
96
Eye signs in WD (2)
KF ring
Sunflower cataract
97
MC endocrine presentation in WD
hypoparathyroidism
98
Gold standard test to diagnose WD
biopsy + quantitative Cu concentration in liver
99
False high Ceruloplasmin is seen in (2)
Acute inflammation (it’s a positive APR)
hyper estrogenic states like pregnancy
100
Nazer prognostic index is used in
WD
101
DOC Wilson’s disease
D- penicillamine 250 mg OD
102
adverse effects of D - pencillamine (4)
1.Drug induced lupus
2.secondary membranous nephropathy
3.aplastic anemia
4.myasthenic crisis
103
Radiological signs in WD(4)
1. Face of giant panda sign
2. Mercedes- benz sign
3. Brighton Claustrum sign
4. Bisected pontine hyperintensity
104
Defective gene in hereditary hemochromatosis
HFE gene on 6p
105
Non HFE related genes in hemochromatosis
HJV
Hepcidin
TFR-2
106
Only individuals homozygous for ——— develop hereditary hemochromatosis
C282Y
107
Non HFE related genes in hemochromatosis
HJV
Hepcidin
TFR-2
108
C282Y heterozygous individuals are at an increased risk of developing —-(2)
Porphyria cutanea tarda
NASH
109
Best screening test for hereditary hemochromatosis
Transferrin saturation (>=45%)
110
Joint finding in hereditary hemochromatosis
PSUEDO- OA
deposition of calcium pyrophosphate dihydrate crystals in MCP/wrist joint
111
Heart finding in hereditary hemochromatosis
dilated > restrictive cardiomyopathy
112
Organs involved in hereditary hemochromatosis
1. liver
2. heart
3. joint
4. pancreas
5. gonad
6. skin
113
Gold standard test for hereditary hemochromatosis
C282Y genetic analysis
114
Treatment of hereditary hemochromatosis
Weekly phlebotomy of 1 unit of whole blood
if not, then S/C Desferrioxamine
115
——- and —— do not reverse after phlebotomy in hereditary hemochromatosis
joint and gonad manifestations
116
Antibody specifically seen in PBC and what is it directed against
Anti mitochondrial antibody against PDH-E2 enzyme
117
which bile ducts are involved in PBC?
intralobular / small intrahepatic bile ducts
118
Autoimmune associations of PBC (2 most imp)
Sjögren
distal RTA (type 1)
119
Diarrhea, steatorrhea, weight loss, metabolic bone disease seen in :
PBC (no bile —-> fat malabsorption —->Vit D malabsorption )
120
earliest HPE finding in PBC
loss of canals of Hering
121
Most imp diagnostic clue in HPE for PBC
ductopenia
122
most characteristic HPE finding in PBC
florid duct lesion + non caseating epithelioid granulomas
123
ducts involved in PSC
fibrosis of intra and extra hepatic bile ducts
124
ioc for PSC
MRCP
125
Bx finding of PSC
onion skin like concentric periductal fibrosis
126
Antibodies seen in PSC
Atypical P-ANCA
127
PSC is strongly associated with
Ulcerative colitis
128
HLA association of PSC
HLA-B8 and DR3
129
Interface hepatitis is classically seen in
Type 1 autoimmune hepatitis
130
Histology features in type 1 AI hepatitis (4)
1. interface hepatitis
2. lymphoplasmacytic inflammation
3. Emperipolesis (one cell engulfing another without killing)
4. rosette formation
131
Type 1 AI is associated with which AI disorder
SLE
132
Antibodies in type 1 AI hepatitis
1. anti ANA
2. anti SMA
3.AAA
4. SLA
5. atypical p ANCA
133
Autoantibodies in type 2 AI hepatitis (2)
anti LKM-1
anti liver cytosol type 1
134
LKM-1 seen in
AI hepatitis type 2, chronic HCV
135
LKM-2 seen in
drug induced hepatitis
136
LKM-3 seen in
chronic HDV
137
Polyclonal hypergammaglobulinemia is a sign of
autoimmune conditions
138
Type 2 AI hepatitis is associated with HLA——
HLA DR7
139
Effects of alcohol on the cell (5)
HESST
1. hypoxia (mitochondrial damage)
2. Endoplasmic reticulum —> Mallory hyaline body
3. Super oxides (cytP2e1)
4. SAM less and SAH more
5. Toxic effects of acetaldehydes
140
best serum marker for ALD
carbohydrate deficient transferrin
141
3 classical features of alcoholic hepatitis on HPE
1. Mallory bodies
2. ballooning degeneration
3. neutrophilic infiltration
142
Prognostic scores in alcoholic liver disease (3)
1. discrimination fraction >= 32
2. MELD >= 18
3. Glasgow >=9
143
Conditions with micronodular cirrhosis (6)
1. alcohol
2. Biliary cirrhosis
3, indian childhood cirrhosis
4 cystic fibrosis
5 BCS
6 Hemochromatosis
144
Microvesicular steatosis is seen in (7)
PRETTY Visits JAMAICA with ALCOHOL and ACID
Pregnancy
Reye’s
Tetracycline
Valproate
Jamaican sleeping sickness
Alcohol
Acid lipase deficiency
145
Swollen mitochondria reduced in number seen in
Reye’s syndrome
146
Conditions which lead to HCC without cirrhosis (2)
NASH
hep B
147
important drugs causing fatty liver (6)
1. L asparaginase
2. Bleomycin
3. tetracycline
4. Griseofulvin
5. valproate
6. amiodarone
148
Drug of choice in NASH
Vitamin E (800-1000 IU/d)
149
most common acquired cause of BCS
polycythaemia rubra vera
150
M/C inherited cause of BCS
factor V leiden mutation
151
BCS is typically seen in
females 30-40y post partum
152
ioc BCS
CECT
153
screening test for BCS
hepatic venous doppler
154
classical presentation of EHPVO
3-8 year child with ugi bleed and spleenomegaly
155
Best marker for high infectivity and high replication for HBV
HBV DNA load
156
best marker for acute hepatitis B
anti HBc IgM
157
HBV is ——- times as infective as HIV and ——- times as infective as HCV
100,10
158
All body fluids contain HBV except ———
stools
159
M/C genotype of HBV is
A
160
Genotype — of HBV is associated with HCC
C
161
90/10 rule in pregnancy for HBV
HBsAg + HBeAg + —>90%
HBsAg + HBeAg- —> 10% risk of transmission
162
M/C cause of Post transfusion hepatitis
CMV > EBV > HCV
never HBV
163
Maximum risk of transmission of hep B in pregnancy is in —-trimester
3rd
164
HBIg dose
0.06 ml/kg
165
Anti Hbs titre for which only one booster dose is needed
10-100 IU
166
Anti Hbs titre which is considered unvaccinated
<10 IU
167
which patients require 4 doses of HBV vaccine
CKD
0,1,2,6
168
Adult dosage of HBV vaccine and course
20 mcg = 1mL over deltoid 0,1,2 or 6
169
170
to diagnose acute on chronic hepatitis B : (4)
1. no h/o
2. quantitative HBsAg> 1000IU/L
3. HBV DNA levels high
4. severely symptomatic
171
extrahepatic manifestations of chronic hepatitis (3)
arthritis - dermatitis
membranous nephropathy
polyarteritis nodosa
172
Scenarios where treatment is required for chronic hepatitis without fibrosis
ALT > 2x normal
AND
HBeAg+ and HBV DNA >20,000IU/mL
or
HBeAg- and HBV DNA >2000IU/mL
173
174
DOC for HBV and dose
Tenofovir alafenamide 25 mg OD
175
anti LKM-3 antibody is seen in
chronic HDV infection
176
chronic HDV infection shows which antibody (not related to virus)
anti LKM-3
177
Hep C virions bind to
VLDL/LDL particles
178
which hep virus is associated with fatty liver
C
179
most variable region of HCV
E2
180
Extra hepatic manifestations in HCV (7)
1.Sjogren
2.essential mixed cryoglobulinemia
3.lichen planus
4.porphyria cutanea tarda
5.MPGN type 1
6.thyroid illness
7.DM
181
Treatment for HCV without cirrhosis and with cirrhosis
Velpatasvir + Sofosbuvir x 12weeks
cirrhosis : + Ribavirin
