Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

how is bilirubin formed?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what type of cell carries heme oxygenase and biliverdin reductase

A

macrophage (mononuclear phagocytic cell)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what protein carries bilirubin to the liver?

A

albumin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are sources of unconjugated hyperbilirubinemia?

A

hemolytic anemia
resorption from internal hemorrhage
ineffective erythropoiesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

why does bilirubin complex with albumin?

A

it is insoluble and can’t be secreted otherwise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

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

A

drug effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the process of conjugation

A

hepatocytes take in bilirubin and form bilirubin glucuronides using UGT1A1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Crigler Najjar syndrome

A

type 1: absent UT1A1

type 2: reduced UGT1A1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Gilbert syndrome

A

have about 30% of typical UGT1A1

presents jaundice under stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are some sources of impaired canalicular transport of bilirubin?

A

Rotor syndrome
Dubin-Johnson syndrome
Drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

bile canaliculus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are some sources of obstructive jaundice?

A

bile duct obstruction
gallstones
carcinoma biliary
carcinoma pancreatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what enzyme catalyzes the formation of urobilinogen?

A

bacterial b-glucuronidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

unconjugated bilirubin

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

conjugated bilirubin

A 
direct
water soluble
nontoxic
loosely bound to albumin
can be excreted in urine when in excess
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

reasons for increase in unconjugated bilirubin levels

A

excessive production
reduced hepatic uptake
impaired conjugation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

reasons for increase in conjugated bilirubin

A

decreased hepatocellular excretion

impaired bile flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

conjugated: total bilirubin < 0.4

A

unconjugated hyperbilirubinemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

conjugated: total bilirubin > 0.4

A

conjugated hyperbilirubinemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

how do you evaluate hepatocyte integrity?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is the typical presentation of apoptotic hepatocytes on IHC?

A

“dead red”

no nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

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

A

rises and then falls once all hepatocytes are dead

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
how do you evaluate biliary excretory function?
serum bilirubin secreted in bile plasma membrane proteins of bile ducts: serum alkaline phosphatase serum gamma-glutamyl transpeptidase (GGTP)
26
what makes up the portal triad?
hepatic artery portal vein bile duct
27
lab studies associated with acute liver disease
increased AST and ALT
28
lab studies associated with acute liver failure
increased AST, ALT, ammonia | prolonged PT
29
lab studies associated with obstructive/biliary liver disease pattern
increased alk phos, bilirubin, GGTP
30
lab studies associated with cirrhosis pattern
decreased albumin and platelets | prolonged PT
31
how is the prothrombin time related to liver function?
coagulation factors in extrinsic pathway are produced by the liver
32
how do you evaluate hepatocyte function?
serum albumin prothrombin time serum ammonia
33
why is serum ammonia relevant to liver function?
the liver converts nitrogen to usable products | ammonia is the biproduct
34
what are clinical findings of hepatic encephalopathy?
alterations in mental status disordered sleep asterixis coma and death
35
characterize hepatic failure
80-90% of functional capacity gone | mortality = 70-95% without transplant
36
what are two ways to get hepatic failure?
sudden massive destruction | end point of progressive damage to liver as part of chronic liver disease
37
what accounts for 50% of acute liver failure cases in the US?
acetaminophen overdose
38
what are some general causes of acute liver failure?
``` viral infection drug induced autoimmune ischemia mushroom poisoning ```
39
what is ascites?
a decrease in albumin causes a decrease in oncotic pressure | water pools in the belly
40
what are the 3 main results of cirrhosis?
decrease in detox portal hypertension decrease in protein synthesis
41
results of decrease in protein synthesis in liver
less coag proteins PT time lengthened bleeding tendency
42
results of portal hypertension
ascites esophageal varices: hypovolemia hepatorenal syndrome
43
results of decrease in detoxification in liver
hyperestrinemia: due to less breakdown of estrogen -gynecomastia, testicular atrophy ammonia toxicity -encephelopathy
44
causes of cirrhosis
``` viral hepatitis alcoholic liver disease NAFLD biliary disease primary hemochromatosis wilson disease A1AT deficiency cryptogenic cirrhosis ```
45
pathogenesis of cirrhosis
progressive fibrosis and reorganization of vascular microarchitecture of the liver types 1 & 3 collagen
46
what do activated Kupffer cells do?
release cytokines | activate stellate cells
47
how are Kupffer cells activated?
apoptosis of hepatocytes
48
what is the function of activated stellate cells?
myofibroblasts | secrete type 1 collagen and form irreversible fibrous bands
49
what parts of your body can be affected by cirrhosis induced shunting of blood flow?
``` esophageal varices spider angiomata splenomegaly hemorrhoids periumbilical caput medusa ```
50
why does spenomegaly occur?
blood pools in the spleen | platelets are sequestered
51
which zone of the liver acinus has the most oxygen?
zone 1 (outside)
52
which zone of the liver acinus has the most cytochrome p450
zone 3 (inside)
53
what pattern of necrosis in the liver lobule is associated with APAP?
centrilobular
54
how do centrilobular necrosis zones appear on IHC?
pale
55
what is the toxic metabolite of APAP?
NAPQI
56
what compound neutralizes NAPQI?
gluthathione
57
what happens when glutathione stores are depleted in the liver?
NAPQI covalently binds to cell proteins triggers mitochondrial permeability transition leads to necrosis
58
what are the 3 possible metabolites of APAP?
``` sulfate moiety (nontoxic) glucuronide moiety (nontoxic) NAPQI (toxic) ```
59
what is the antidote to APAP overdose?
NAC replenishes glutathione stores most effective in 1st 12 hours
60
characterize cytolytic acute liver injury
spotty necrosis submassive necrosis massive necrosis APAP, psychotropic drugs, herbal medicines, cocaine, carbon tetrachloride
61
characterize cholestatic acute liver injury
intrahepatic cholestasis- mostly in centrilobular hepatocytes, formation of canalicular plugs anabolic or contraceptive steroid use
62
steatosis
fat deposition in liver
63
what causes steatosis in alcoholic induced liver disease
excess reducing equivalents (NADH and H+) shunting of normal substrates away from catabolism and toward lipid biosynthesis dysfunction of membranes hypoxia oxidative stress
64
what is the progression of alcohol induced liver disease?
steatosis steatohepatitis cirrhosis
65
what are some features of steatohepatitis?
liver cell necrosis inflammation Mallory bodies fatty change
66
can you reverse alcohol induced liver disease?
steatosis -yes steatohepatitis- yes cirrhosis - no
67
how do fat droplets appear on IHC?
cytoplasm replaces with white instead of pink
68
what is Mallory hyaline?
ubiquinated cytokeratin intermediate filaments | appears dark purple in ballooned hepatocytes
69
what contributes to non alcoholic fatty liver disease?
obesity dyslipidemia hyperinsulinemia insulin resistance
70
what is the most likely cause of increased AST and ALT?
non alcoholic fatty liver disease
71
what is metabolic syndrome
``` one of: DM impaired glucose stuff insulin resistance AND two of: high BP dyslipidemia central obesity microalbuminuria ```

MCM Test 4 (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions