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MCM Test 4 > B2.069 Liver Case > Flashcards

B2.069 Liver Case Flashcards

1
Q

when does jaundice/icterus occur?

A

when the equilibrium between the production of bilirubin and the metabolism and excretion is disturbed
bilirubin > 2.5 mg/dL

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2
Q

how is bilirubin formed?

A

senescent erythrocytes release heme
heme oxygenase catalyzes production of biliverdin
biliverdin reductase catalyzes formation of bilirubin

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3
Q

what type of cell carries heme oxygenase and biliverdin reductase

A

macrophage (mononuclear phagocytic cell)

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4
Q

what protein carries bilirubin to the liver?

A

albumin

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5
Q

what are sources of unconjugated hyperbilirubinemia?

A

hemolytic anemia
resorption from internal hemorrhage
ineffective erythropoiesis

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6
Q

why does bilirubin complex with albumin?

A

it is insoluble and can’t be secreted otherwise

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7
Q

what can cause reduced uptake of bilirubin by the liver resulting in jaundice?

A

drug effects

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8
Q

what is the process of conjugation

A

hepatocytes take in bilirubin and form bilirubin glucuronides using UGT1A1

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9
Q

what are some sources of impaired conjugation?

A 
neonatal jaundice (decreased UGT1A1 Activity)
breast milk jaundice
Crigler-Najjar syndrome
Gilbert syndrome
viral hepatitis
drugs
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10
Q

Crigler Najjar syndrome

A

type 1: absent UT1A1

type 2: reduced UGT1A1

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11
Q

Gilbert syndrome

A

have about 30% of typical UGT1A1

presents jaundice under stress

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12
Q

what are some sources of impaired canalicular transport of bilirubin?

A

Rotor syndrome
Dubin-Johnson syndrome
Drugs

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13
Q

what structure transports bilirubin from the hepatocytes to the bile ducts?

A

bile canaliculus

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14
Q

what are some sources of obstructive jaundice?

A

bile duct obstruction
gallstones
carcinoma biliary
carcinoma pancreatic

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15
Q

what enzyme catalyzes the formation of urobilinogen?

A

bacterial b-glucuronidase

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16
Q

unconjugated bilirubin

A

indirect (can’t be directly measures)
insoluble
complexes tightly with serum albumin
cannot be excreted

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17
Q

conjugated bilirubin

A 
direct
water soluble
nontoxic
loosely bound to albumin
can be excreted in urine when in excess
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18
Q

reasons for increase in unconjugated bilirubin levels

A

excessive production
reduced hepatic uptake
impaired conjugation

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19
Q

reasons for increase in conjugated bilirubin

A

decreased hepatocellular excretion

impaired bile flow

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20
Q

conjugated: total bilirubin < 0.4

A

unconjugated hyperbilirubinemia

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21
Q

conjugated: total bilirubin > 0.4

A

conjugated hyperbilirubinemia

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22
Q

how do you evaluate hepatocyte integrity?

A

cytosolic hepatocellular enzyme levels
AST (aspartate aminotransferases)
ALT (alanine aminotransferases)

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23
Q

what is the typical presentation of apoptotic hepatocytes on IHC?

A

“dead red”

no nucleus

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24
Q

how do AST and ALT change with massive necrosis in hepatocytes?

A

rises and then falls once all hepatocytes are dead

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25
Q

how do you evaluate biliary excretory function?

A

serum bilirubin secreted in bile
plasma membrane proteins of bile ducts:
serum alkaline phosphatase
serum gamma-glutamyl transpeptidase (GGTP)

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26
Q

what makes up the portal triad?

A

hepatic artery
portal vein
bile duct

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27
Q

lab studies associated with acute liver disease

A

increased AST and ALT

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28
Q

lab studies associated with acute liver failure

A

increased AST, ALT, ammonia

prolonged PT

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29
Q

lab studies associated with obstructive/biliary liver disease pattern

A

increased alk phos, bilirubin, GGTP

30
Q

lab studies associated with cirrhosis pattern

A

decreased albumin and platelets

prolonged PT

31
Q

how is the prothrombin time related to liver function?

A

coagulation factors in extrinsic pathway are produced by the liver

32
Q

how do you evaluate hepatocyte function?

A

serum albumin
prothrombin time
serum ammonia

33
Q

why is serum ammonia relevant to liver function?

A

the liver converts nitrogen to usable products

ammonia is the biproduct

34
Q

what are clinical findings of hepatic encephalopathy?

A

alterations in mental status
disordered sleep
asterixis
coma and death

35
Q

characterize hepatic failure

A

80-90% of functional capacity gone

mortality = 70-95% without transplant

36
Q

what are two ways to get hepatic failure?

A

sudden massive destruction

end point of progressive damage to liver as part of chronic liver disease

37
Q

what accounts for 50% of acute liver failure cases in the US?

A

acetaminophen overdose

38
Q

what are some general causes of acute liver failure?

A 
viral infection
drug induced
autoimmune
ischemia
mushroom poisoning
39
Q

what is ascites?

A

a decrease in albumin causes a decrease in oncotic pressure

water pools in the belly

40
Q

what are the 3 main results of cirrhosis?

A

decrease in detox
portal hypertension
decrease in protein synthesis

41
Q

results of decrease in protein synthesis in liver

A

less coag proteins
PT time lengthened
bleeding tendency

42
Q

results of portal hypertension

A

ascites
esophageal varices:
hypovolemia
hepatorenal syndrome

43
Q

results of decrease in detoxification in liver

A

hyperestrinemia: due to less breakdown of estrogen
-gynecomastia, testicular atrophy
ammonia toxicity
-encephelopathy

44
Q

causes of cirrhosis

A 
viral hepatitis
alcoholic liver disease
NAFLD
biliary disease
primary hemochromatosis
wilson disease
A1AT deficiency
cryptogenic cirrhosis
45
Q

pathogenesis of cirrhosis

A

progressive fibrosis and reorganization of vascular microarchitecture of the liver
types 1 & 3 collagen

46
Q

what do activated Kupffer cells do?

A

release cytokines

activate stellate cells

47
Q

how are Kupffer cells activated?

A

apoptosis of hepatocytes

48
Q

what is the function of activated stellate cells?

A

myofibroblasts

secrete type 1 collagen and form irreversible fibrous bands

49
Q

what parts of your body can be affected by cirrhosis induced shunting of blood flow?

A 
esophageal varices
spider angiomata
splenomegaly
hemorrhoids
periumbilical caput medusa
50
Q

why does spenomegaly occur?

A

blood pools in the spleen

platelets are sequestered

51
Q

which zone of the liver acinus has the most oxygen?

A

zone 1 (outside)

52
Q

which zone of the liver acinus has the most cytochrome p450

A

zone 3 (inside)

53
Q

what pattern of necrosis in the liver lobule is associated with APAP?

A

centrilobular

54
Q

how do centrilobular necrosis zones appear on IHC?

A

pale

55
Q

what is the toxic metabolite of APAP?

A

NAPQI

56
Q

what compound neutralizes NAPQI?

A

gluthathione

57
Q

what happens when glutathione stores are depleted in the liver?

A

NAPQI covalently binds to cell proteins
triggers mitochondrial permeability transition
leads to necrosis

58
Q

what are the 3 possible metabolites of APAP?

A 
sulfate moiety (nontoxic)
glucuronide moiety (nontoxic)
NAPQI (toxic)
59
Q

what is the antidote to APAP overdose?

A

NAC
replenishes glutathione stores
most effective in 1st 12 hours

60
Q

characterize cytolytic acute liver injury

A

spotty necrosis
submassive necrosis
massive necrosis
APAP, psychotropic drugs, herbal medicines, cocaine, carbon tetrachloride

61
Q

characterize cholestatic acute liver injury

A

intrahepatic cholestasis- mostly in centrilobular hepatocytes, formation of canalicular plugs
anabolic or contraceptive steroid use

62
Q

steatosis

A

fat deposition in liver

63
Q

what causes steatosis in alcoholic induced liver disease

A

excess reducing equivalents (NADH and H+)
shunting of normal substrates away from catabolism and toward lipid biosynthesis
dysfunction of membranes
hypoxia
oxidative stress

64
Q

what is the progression of alcohol induced liver disease?

A

steatosis
steatohepatitis
cirrhosis

65
Q

what are some features of steatohepatitis?

A

liver cell necrosis
inflammation
Mallory bodies
fatty change

66
Q

can you reverse alcohol induced liver disease?

A

steatosis -yes
steatohepatitis- yes
cirrhosis - no

67
Q

how do fat droplets appear on IHC?

A

cytoplasm replaces with white instead of pink

68
Q

what is Mallory hyaline?

A

ubiquinated cytokeratin intermediate filaments

appears dark purple in ballooned hepatocytes

69
Q

what contributes to non alcoholic fatty liver disease?

A

obesity
dyslipidemia
hyperinsulinemia
insulin resistance

70
Q

what is the most likely cause of increased AST and ALT?

A

non alcoholic fatty liver disease

71
Q

what is metabolic syndrome

A 
one of:
DM
impaired glucose stuff
insulin resistance
AND
two of:
high BP
dyslipidemia
central obesity
microalbuminuria

MCM Test 4 (19 decks)

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