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Bloc E - GI & Metabolism > Feb22 M1,2-Hepatic Function Liver Disease > Flashcards

Feb22 M1,2-Hepatic Function Liver Disease Flashcards

1
Q

true liver function tests

A
  • total serum protein and albumin
  • total bilirubin
  • prothrombin time (PT, INR)
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2
Q

fake LFTs

A
  • ALT
  • AST
  • AP
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3
Q

ALT charact

A

released when liver cells damaged

normal 5-40

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4
Q

AST charact

A

can come from liver but also heart muscle intestine pancreas

normal 8-20

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5
Q

AST:ALT ratio in alcoholics

A

2:1 AST:ALT

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6
Q

AP charact

A

normal 20-70. found in liver (can frac or do isoenzymes to check if not from bone)
marker of OBSTRUCTION or infiltrative disease (cholestatic disease)

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7
Q

how to check if AP shows cholestatic liver injury (bile not emptying properly)

A

GGT (gamma GT) must be elevated too

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8
Q

(EXAM) bilirubin source and 2 types

A

indirect (unconjugated): from old RBCs.

conjugated (direct): after liver adds glucuronic acid to make it water soluble for excretion

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9
Q

(EXAM) bilirubin excretion

A

stool (makes it brown)

urine (high bilirubin = black urine)

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10
Q

(EXAM) normal total bilirubin

A

0.3-1.0 mg per dL

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11
Q

(EXAM) direct bilirubin tells what

A

amount of bilirubin liver was able to manage

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12
Q

(EXAM) how bilirubin made from heme

A

IN MACROPHAGES:

  1. heme oxygenase transforms open alpha group on heme: makes biliverdin
  2. biliverdin reduced by biliverdin reductase to make bilirubin
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13
Q

(EXAM) what happens to bilirubin in hepatocytes

A

conjugated to form bilirubin diglucuronide (DIRECT) by UDP-glucuronyl transferase

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14
Q

(EXAM) what happens to bilirubin diglucuronide in bacteria of the gut

A

transformed in urobilinogen (which is what goes to urine) and stercobilinogen (in the stool)

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15
Q

3 types of jaundice (also called icterus)

A

(jaundice = serum bilirubin over 3 mg per dL)

prehaptic, intrahepatic, posthepatic

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16
Q

prehepatic jaundice

A

hemolytic anemia, increased load of bilirubin

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17
Q

intrahepatic jaundice

A

problem inside liver in making direct bilirubin (infection, chemical, drug, genetics, autoimmune, neonatal)

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18
Q

posthepatic jaundice

A

intrahepatic bile ducts (drug, PBC, cholangitis)

extrahepatic bile ducts (gallstones, pancreatic tumor, cholangiocarcinoma)

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19
Q

2 types of drug injuries to the liver

A
  • predictable (tylenol): we know the quantity

- by chance

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20
Q

elevated bilirubin and jaundice: which is up direct or indirect?

A

both. DIRECT is the most of it. (bc still transforming to direct, it’s a clearance problem)

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21
Q

LFTs in liver problem

A

direct bilirubin up
indirect bilirubin up
albumin down
INR up

22
Q

steps in determining what kind of jaundice is present

A
  1. check the conjugated bilirubin (is normal in pre, but is high in intra and post)
  2. ask for color of stools (are light colored if extrahepatic)
23
Q

other way to distinguish posthepatic jaundice

A

high ALP (AP) and NO urine urobilinogen

24
Q

(IMPORTANT)extrahepatic causes of biliary obstruction + most common of these

A
  • choledocholithiasis
  • malignancy (cholangio, PANCREATIC IS MOST COMMON, GB, ampullary)
  • PSC
  • AIDS cholangiopathy
25
Q

(IMPORTANT) causes of intrahepatic biliary obstruction

A
  • TPN (total parenteral nutrition)
  • sepsis
  • PSC
  • PBC
  • intrahepatic mass
26
Q

main things that kill the liver

A
  1. fat
  2. alcohol
  3. autoimmune (PSC and PBC)
  4. viruses
  5. drugs
    …
27
Q

how to dx the etiology of liver disease using the fake LFTs (liver enzyme tests)

A
  • enzymes less 300 = alcohol, cirrhosis, obstruction (AST:ALT 2:1 for alcohol
  • enzymes 500-1000 = ACUTE biliary obstruction
  • enzymes over 1000 = ischemia, toxin, virus/
28
Q

6 causes of fulminant hepatic failure (mnemonic ABCDEF)

A 
A: acetaminophen
B: hepB
C: hepC, cryptogenic
D: hepD, drugs
E: esoteric (Wilson's Budd-Chiari)
F: fatty infiltration (acute fatty liver of pregnancy, Reye's)
29
Q

ddx of ascites + main one

A

-PORTAL HTN (85%)
-malignancy
-infection
-renal
-endocrine
…

30
Q

(EXAM) what to do to investigate ascites

A

measure serum-ascites albumin gradient (SAAG): more than 11 is high

31
Q

(EXAM) meaning of SAAG

A
  • high SAAG = transudative process = LIVER CAUSE
  • low SAAG = exudative process = PERITONEUM CAUSE (peritoneal carcinomatosis, peritonitis, pancreatic ascites, bile leak, nephrotic syndrome,.._
32
Q

(imp?) when ascites associated with portal htn

A

when SAAG over 1.1

33
Q

(EXAM) main pathophgy of ascites (2)

A
  1. Na retention secondary to splanchnic and systemic vasodilation (dereased arterial volume led to Na retaining mechanisms)
  2. extrahepatic: CHF, constrictive pericarditis, Budd Chiari syndrome)
34
Q

(EXAM) portal htn def and value

A

portal system branches into sinusoids (and then these will drain in hepatic venous system).
**portal htn = portal vein P over 11

35
Q

(EXAM) prehepatic causes of portal htn

A
  • congenital atresia or stenosis (portal vein)
  • thrombosis of portal vein
  • splenic vein thrombosis
  • extrinsic compression (tumor)
36
Q

(EXAM) intrahepatic causes of portal htn

A
  • cirrhosis (sinusoidal obstruction)
  • bilharzial periportal fibrosis
  • sinusoidal obstruction syndrome (chemo)
37
Q

(EXAM) posthepatic causes of portal htn

A
  • Budd Chiari (hepatic vein thrombosis)
  • cardiac disease (valvular disease or constrictive pericarditis)
  • right heart failure
38
Q

(EXAM) cirrhosis pathophgy of ascites and other pathophgies

A
  • increased intrahepatic resist due to fibrosis, regenerative nodules, hepatic venular vasoconstriction = sinusoidal htn
  • lymph leakage in sinusoids
  • TB
  • peritoneal lymph leakage
  • bile ascites
  • pancreatic ascites
39
Q

most important risk factor for liver disease + 2nd most important

A

alcohol

2nd is obesity (fat)

40
Q

ALT of 70 (normal below 35) approach

A

means nothing. repeat the test

41
Q

AST 55 (normal <30), ALT 70 (normal <35), ALP 70 (normal <90) conclusion

A
  • NOT alcohol bc AST:ALT not 2:1

- statistically, more likely cause is fat (NASH)

42
Q

(IMPORTANT) when liver enzymes and bilirubin go up

A
  • ALT and AST up acutely bc hepatocytes destroyed

- AP and bilirubin up after days bc have to be manufactured and excreted

43
Q

liver zones and fct

A

1 = near portal triad (duct, arteriole, venule): FA oxydation, glucose synthesis
zone 2 = in between
zone 3 = near central vein (glycogen synthesis and glycolysis + coag factors synth)

44
Q

injuries where in liver and meaning

A
  • usually zone 1

- zone 3 = toxic (get high INR, low glucose)

45
Q

UC patient with high enzymes and bilirubin

A

PSC

46
Q

high INR patient high bilirubin

A

zone 3 injured: toxic = fulminant (acute) liver failure

47
Q

acute vs chronic hepatitis

A 
acute = 10 fold elevation of ALT
chronic = 1.5-10 fold elevation of ALT
48
Q

high AP and GGT, normal INR, jaundice, palmar erythema, spider angiomata, splenomegaly (signs of portal htn) dx

A

PBC

49
Q

all normal except bilirubin of 56 dx

A

Gilbert’s syndrome

50
Q

how to check liver problem cause with bilirubin

A

bilirubin < 250 = obstruction

bilirubin > 250 not obstruction

51
Q

end stage of any chronic liver disease

A

cirrhosis: regenerative nodules, fibrous septation

2 stages: compensated and decompensated

52
Q

(EXAM) pathophgy of portal htn in cirrhosis

A

distorted sinusoidal architecture leads to increased resistance. backup in porto-caval anastomoses

Bloc E - GI & Metabolism (58 decks)

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