NBME CBSE LATEST 2026 EVALUATION EXAMS QUESTIONS
AND SOLUTIONS GUARANTEE A+
✔✔McArdle - ✔✔Glycogen phosphorylase
(glycogen --> G1P)
exercise intolerance (arrhythmia, m cramps)
✔✔Cori - ✔✔*Debranching *(glycogen-->G1P)
hypoglycemia; Hepatomegaly; Ketoacidosis
increased *limit dextrin*
✔✔Reye - ✔✔VZV/flu + ASPIRIN
microvesicular steatosis
encephalopathy
NH4 *damage mt*
✔✔Hemochromatosis - ✔✔*AR - HFE *
inactive *transferrin-R*
--> GI absorbes FE
--> *HEMOSIDERIN *
Black liver, Blue on stain
✔✔Hemochromatosis complications - ✔✔*HCC,* DM,
Pigment, Hypogonad,
Arrhythmia, *Dilated cardiomyopathy,*
MCP arthropathy
✔✔Hepatic encephalopathy - ✔✔CAUSE: H*C*V + GI bleed (N absorption)
high NH3 = high *GLUTAMINE*
ATAXIA
✔✔Tx of hepatic encephalopathy - ✔✔*Lactulose*
- decrease GI pH, increase NH4
*Rifaximin*
- decrease synth/abs of NH3
- Metabolized by *CYP3A4*
✔✔HAV - ✔✔Self limiting
Ballooning degeneration
Monocellular infiltrates
Eosinophilic apoptosis
,✔✔Portal vein thrombosis causes - ✔✔portal hypertension
esophageal varices
large spleen
✔✔Portosystemic anastomoses - ✔✔PORTAL // IVC
-*Left gastric* // esophageal
-Paraumbilical // superficial, inferior epigastric
...........................................-->internal iliac
-superior rectal // middle, inferior rectal
-->IMV-->Splenic..........-->internal iliac
✔✔CD31 - ✔✔PECAM-1
✔✔CD31/PECAM1 - ✔✔*vascular endothelial tumor *
LIVER ANGIOSARCOMA
✔✔liver angiosarcoma caused by what toxins - ✔✔arsenic and polyvinyl Cl
✔✔Aspergillus aflatoxin induces what mutation that causes what in the liver - ✔✔p53
mutation --> HCC
✔✔bile rate limiting step - ✔✔cholesterol 7a-hydroxylase
requires NADPH
(inhibited by *fibrates*)
✔✔what "cofactor" does bile require - ✔✔NADPH
✔✔What starts the process of bilirubin syntehsis - ✔✔heme
✔✔Bilirubin synthesis - ✔✔heme --> biliverdin --> unconj --> conj --> unconj -->
urobilinogen
✔✔Unconj bili to Conj bili - ✔✔*UGT*
(UDP glycoronsyl transferase)
✔✔UGT low in - ✔✔*Gilbert*: jaundice w fasting/exercise
*Crigler Najjar* (none): kernicterus
✔✔Crigler Najjar - ✔✔no UGT = death from *kernicterus* (super high unconj)
✔✔Gilbert - ✔✔low UGT = high *unconj*
jaundice w fasting/exercise
✔✔Conj bili to Unconj bili - ✔✔B-glucuronidase
,✔✔high conj - ✔✔Dubin Johnson + Rotor
Cholestasis / Obstruction
✔✔high unconj - ✔✔Hemolysis
Gilbert
Crigler Najjar
✔✔Dubin Johnson + Rotor - ✔✔obstruction (PBS, PBC)
= *high conj *
BLACK liver
✔✔PBC - ✔✔FEMALE
lymphocytes destroy *intralobar* ducts
(*granulomas*)
ITCHING
✔✔PBC dx - ✔✔high AlkPhos
+anti-mt
IgM
✔✔tx PBC - ✔✔UDC acid to replace BA
✔✔PSC - ✔✔MALE
onion skin beading of *intra+extra*lobar ducts
CANCER assoc
✔✔PSC dx - ✔✔pANCA
IgM
✔✔Biliary atresia - ✔✔<2 yo
high *GGT *
*obstruct* extrahepatic = high DIRECT
dark urine, pale stool, jaundice
✔✔Gallbladder hypomobility causes - ✔✔biliary sludge
✔✔Cholelithiasis - ✔✔LUCENT = high Chol
OPAQUE = high bilirubin
low BA
low phosphatidylcholine
✔✔cholelithiasis dissolves with - ✔✔Bile Acid (ursoeoxycholic acid)
, ✔✔pigment cholelithiasis
(what increases risk?) - ✔✔*UNCONJ *- not visualized on scan
Forty, Fat, Female, Fertile
Female: *E* = chol synth
Fertile: *P *inhibit gb empty
✔✔low B-glucoronidase - ✔✔brown pigment stones
assoc w E coli + Helminths
✔✔Cholecystitis located - ✔✔cystic duct
✔✔Colic cholelithiasis located - ✔✔at neck
✔✔Acalculous cholecystitis - ✔✔inflammation, *no stone*
in *SICK pt *(sepsis)
✔✔Gallstone ileus - ✔✔SI obstruction w
air in gb and biliary tree
✔✔prolonged obstruction of gb causes - ✔✔fat sol *vit* deficiency (ex: vit A)
✔✔porcelain gb has a risk for - ✔✔adenocarcinoma
✔✔avoid WHAT in GB disease - ✔✔*fibrates *
(inhibit chol-7a-hydroxylase)
causes stones
✔✔Cholestyramine - ✔✔BA binding
low LDL
high TAG
✔✔Fibrates - ✔✔inhibit *chol-7a-hydroxylase*
do not take w statin
OR if GB disease
✔✔Ezetimibe - ✔✔inhibit cholesterol absorption
(via inhibiting *NPC1L1*)
increase *LDL-R*
✔✔Statin - ✔✔HMG-CoA reductase inhibitor
increase LDL-R density
AND SOLUTIONS GUARANTEE A+
✔✔McArdle - ✔✔Glycogen phosphorylase
(glycogen --> G1P)
exercise intolerance (arrhythmia, m cramps)
✔✔Cori - ✔✔*Debranching *(glycogen-->G1P)
hypoglycemia; Hepatomegaly; Ketoacidosis
increased *limit dextrin*
✔✔Reye - ✔✔VZV/flu + ASPIRIN
microvesicular steatosis
encephalopathy
NH4 *damage mt*
✔✔Hemochromatosis - ✔✔*AR - HFE *
inactive *transferrin-R*
--> GI absorbes FE
--> *HEMOSIDERIN *
Black liver, Blue on stain
✔✔Hemochromatosis complications - ✔✔*HCC,* DM,
Pigment, Hypogonad,
Arrhythmia, *Dilated cardiomyopathy,*
MCP arthropathy
✔✔Hepatic encephalopathy - ✔✔CAUSE: H*C*V + GI bleed (N absorption)
high NH3 = high *GLUTAMINE*
ATAXIA
✔✔Tx of hepatic encephalopathy - ✔✔*Lactulose*
- decrease GI pH, increase NH4
*Rifaximin*
- decrease synth/abs of NH3
- Metabolized by *CYP3A4*
✔✔HAV - ✔✔Self limiting
Ballooning degeneration
Monocellular infiltrates
Eosinophilic apoptosis
,✔✔Portal vein thrombosis causes - ✔✔portal hypertension
esophageal varices
large spleen
✔✔Portosystemic anastomoses - ✔✔PORTAL // IVC
-*Left gastric* // esophageal
-Paraumbilical // superficial, inferior epigastric
...........................................-->internal iliac
-superior rectal // middle, inferior rectal
-->IMV-->Splenic..........-->internal iliac
✔✔CD31 - ✔✔PECAM-1
✔✔CD31/PECAM1 - ✔✔*vascular endothelial tumor *
LIVER ANGIOSARCOMA
✔✔liver angiosarcoma caused by what toxins - ✔✔arsenic and polyvinyl Cl
✔✔Aspergillus aflatoxin induces what mutation that causes what in the liver - ✔✔p53
mutation --> HCC
✔✔bile rate limiting step - ✔✔cholesterol 7a-hydroxylase
requires NADPH
(inhibited by *fibrates*)
✔✔what "cofactor" does bile require - ✔✔NADPH
✔✔What starts the process of bilirubin syntehsis - ✔✔heme
✔✔Bilirubin synthesis - ✔✔heme --> biliverdin --> unconj --> conj --> unconj -->
urobilinogen
✔✔Unconj bili to Conj bili - ✔✔*UGT*
(UDP glycoronsyl transferase)
✔✔UGT low in - ✔✔*Gilbert*: jaundice w fasting/exercise
*Crigler Najjar* (none): kernicterus
✔✔Crigler Najjar - ✔✔no UGT = death from *kernicterus* (super high unconj)
✔✔Gilbert - ✔✔low UGT = high *unconj*
jaundice w fasting/exercise
✔✔Conj bili to Unconj bili - ✔✔B-glucuronidase
,✔✔high conj - ✔✔Dubin Johnson + Rotor
Cholestasis / Obstruction
✔✔high unconj - ✔✔Hemolysis
Gilbert
Crigler Najjar
✔✔Dubin Johnson + Rotor - ✔✔obstruction (PBS, PBC)
= *high conj *
BLACK liver
✔✔PBC - ✔✔FEMALE
lymphocytes destroy *intralobar* ducts
(*granulomas*)
ITCHING
✔✔PBC dx - ✔✔high AlkPhos
+anti-mt
IgM
✔✔tx PBC - ✔✔UDC acid to replace BA
✔✔PSC - ✔✔MALE
onion skin beading of *intra+extra*lobar ducts
CANCER assoc
✔✔PSC dx - ✔✔pANCA
IgM
✔✔Biliary atresia - ✔✔<2 yo
high *GGT *
*obstruct* extrahepatic = high DIRECT
dark urine, pale stool, jaundice
✔✔Gallbladder hypomobility causes - ✔✔biliary sludge
✔✔Cholelithiasis - ✔✔LUCENT = high Chol
OPAQUE = high bilirubin
low BA
low phosphatidylcholine
✔✔cholelithiasis dissolves with - ✔✔Bile Acid (ursoeoxycholic acid)
, ✔✔pigment cholelithiasis
(what increases risk?) - ✔✔*UNCONJ *- not visualized on scan
Forty, Fat, Female, Fertile
Female: *E* = chol synth
Fertile: *P *inhibit gb empty
✔✔low B-glucoronidase - ✔✔brown pigment stones
assoc w E coli + Helminths
✔✔Cholecystitis located - ✔✔cystic duct
✔✔Colic cholelithiasis located - ✔✔at neck
✔✔Acalculous cholecystitis - ✔✔inflammation, *no stone*
in *SICK pt *(sepsis)
✔✔Gallstone ileus - ✔✔SI obstruction w
air in gb and biliary tree
✔✔prolonged obstruction of gb causes - ✔✔fat sol *vit* deficiency (ex: vit A)
✔✔porcelain gb has a risk for - ✔✔adenocarcinoma
✔✔avoid WHAT in GB disease - ✔✔*fibrates *
(inhibit chol-7a-hydroxylase)
causes stones
✔✔Cholestyramine - ✔✔BA binding
low LDL
high TAG
✔✔Fibrates - ✔✔inhibit *chol-7a-hydroxylase*
do not take w statin
OR if GB disease
✔✔Ezetimibe - ✔✔inhibit cholesterol absorption
(via inhibiting *NPC1L1*)
increase *LDL-R*
✔✔Statin - ✔✔HMG-CoA reductase inhibitor
increase LDL-R density
