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1
Q

complications of liver disease

A
  1. synthetic impairment
  2. cholestasis
  3. decreased clearance
  4. portal HTN
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2
Q

Tests of liver synthetic capacity

A

clotting factors
albumin
cholesterol: late complication of severe dysfunction

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3
Q

cholestasis

A

impairment of bile flow

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4
Q

Tests that measure liver clearance

A

bilirubin: imperfect

ammonia

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5
Q

portal HTN

A

portal blood is shunted around liver rather than processed by the liver

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6
Q

bilirubin

A

balance btwn input and removal by liver
increases with intrahepatic/extrhepatic obstruction
normal: 1

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7
Q

Tests that detect liver injury

A

aminotransferases: ALT, AST

ALP

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8
Q

AST (aspartate aminotransferase))

A

liver and muscle injury

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9
Q

ALT (alanine aminotransferase)

A

more specific for liver

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10
Q

ALP (alkaline phosphatase)

A

bile ducts: correlates with intrahepatic and extra hepatic injury or obstruction
level associated with increases synthesis
isoenzymes: Gut, Liver, Bone

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11
Q

Cholylglycine

A

serum bile salt

correlates with degree of cholestasis, intrahepatic of extra hepatic obstruction to bile flow

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12
Q

GGT (Gamma Glutamyl Transferase/Transpepidase)

A

many tissues
biliary
increased: cholestasis, biliary obstruction; Phenytoin and ethanol
limited clinical utility: many meds and chemicals increase it

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13
Q

isolated GGT elevation

A

due to medications or ETHANOL

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14
Q

ammonia

A

detoxified in liver by urea cycle and glutamine synthetase

correlation: hepatic encephalopathy

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15
Q

prolonged prothrombin time

A

clotting factor deficiency: I, II, V, VII, X
Vit. K deficiency
correlates with hepatic synthetic function

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16
Q

international standardized ratio (INR)

A

correlates with hepatic synthetic function

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17
Q

albumin

A

correlates with hepatic sun.
half life 20 days
rapidly changes with acute illness, malnutrition

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18
Q

Child Pugh score

score 1; 2; 3

A

prognosis after vatical bleeding
1. albumin: greater than 3.5; 2.8-3.5; less than 2.8
2. bilirubin: less than 2; 2-3; greater than 3
3. ascites: none; mild; mod.-sev.
4. encephalopathy: none; 1-2; 3-4
5. PT/INR: less than 1.71; 1.71-2.2; greater than 2.2
Grade A: 5-6
Grade B: 7-9
Grade C: 10-15
prognosis: grade A better survival (C nearly half die in 1-2 months)

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19
Q

Model of End-Stage Liver Disease (MELD)

A 
predictor of ALD survival
1. INR
2. bilirubin
3. creatinine: high is bad (should be low due to muscle wasting and malnutrition in liver disease)
High MELD: increase 90 day mortality
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20
Q

Where does the majority of liver blood flow come from?

A

Portal vein (splenic vein, splanchnic circulation)

rest: hepatic artery

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21
Q

How does chronic portal HTN lead to increased splanchnic blood flow and perfused capillary density?

A
  1. increased transvascular pressure gradient
  2. portosystemic shunting
  3. increase circulating levels of Glucagon and other vasodilators: decreases catecholamine sensitivity
  4. decreases splanchnic arteriolar resistance
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22
Q

How does chronic portal HTN lead to increased lymph flow?

A
  1. venous stasis
  2. capillary and postcapillary venule pressure (also due to decreased splanchnic arteriolar resistance)
  3. increase capillary filtration rate (also due to increased perfused capillary density)
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23
Q

What do venous collaterals in portal HTN cause (via what vein)?

  1. anterior
  2. posterior
  3. superior
  4. inferior
A
  1. caput medusa (via umbilical vein)
  2. splenorenal shunt (via retroperitoneal veins)
  3. esophageal varcies (azygous)
  4. hemorrhoids/ anorectal varices
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24
Q

varices

  1. how many have them in newly Dx cirrhosis
  2. how many bleed within 2 year
  3. why do they bleed
  4. Tx
A

tortuous venous collaterals under high pressure
1. half (increases each year after Dx)
2. 1/3
3. high pressure, thrombocytopenia, impairment of clotting factors
4. volume resuscitation, correct coagulopathy, splanchnic vasoconstriction (decrease blood flow to intestine, stomach, collaterals); VASOPRESSIN, SOMATOSTATIN (blocks vasodilators like Glucagon)
MAJOR CAUSE of DEATH in liver disease

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25
Q

Tx of variceal hemorrhage

A
  1. endoscopic therapy to sclerose or band varices
  2. decrease portal pressure: Beta blockers, portosystemic shunt (surgical or transjugular intrahepatic), liver transplant
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26
Q

What causes ascites (3 pathways)?

A
  1. increased resistance to portal venous flow, increased flow to portal vein, increased lymphatic flow, leakage of lymphatic flow from the liver and intestines
  2. increased portosystemic shunting of vasodilators, systemic vasodilation
  3. decreased renal perfusion, increased renal vasoconstriction, increased Renin-Angiotensin, increased Na reabsorption
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27
Q

Hypotheses of Ascites

  1. traditional underfill concept
  2. overflow hypothesis
  3. revised underfill theory
A
  1. ascites formation, decreased effective volume, renal Na retention, ascites and edema
  2. primary renal tubular retention of Na, increase plasma volume, translocation of fluid out of splanchnic circulation as ascites
  3. primary peripheral vasodilation, imbalance of capacitance and volume (relative underfilling), renal Na retention
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28
Q

complications of ascites

A
  1. tense ascites: pressure on diaphragms and stomach, difficulty breathing and eating
  2. hepatic hydrothorax
  3. spontaneous bacterial peritonitis
  4. spontaneous bacterial peritonitis
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29
Q

spontaneous bacterial peritonitis

A

due to ascites (therefore liver disease)

  1. large amount of undrained fluid, low protein and complement
  2. bacterial translocation from intestines to blood, bacteremia infects ascites
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30
Q

Tx of ascites

A
  1. Na restriction
  2. diuretics
  3. Tx the underlying liver disease
  4. large volume paracentesis
    correct portal HTN
    other: transjugular/surgical portosystemic shunt, liver transplant
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31
Q

Two important effects of portal HTN

A
  1. ascites

2. varices

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32
Q

normal serum lab values

  1. ALT, AST, GGT
  2. ALP
A
  1. 10-60 U/L

2. 45-150 U/L

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33
Q

normal serum lab values

albumin

A

3.5-5.2 g/dL

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34
Q

normal serum lab values

alpha-1 antitrypsin

A

100-200 mg/dL

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35
Q

normal serum lab values

ammonia

A

7-27 micromol/L

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36
Q

normal serum lab values

amylase

A

30-110 U/L

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37
Q

normal serum lab values

bilirubin (total)

A

0.2-1.9 mg/dL

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38
Q

normal serum lab values

ceruloplasmin

A

25-63 mg/dL

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39
Q

normal serum lab values

copper

A

26-190 mcrgm/dL

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40
Q

normal serum lab values

creatinine

A

0.7-1.4 mg/dL

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41
Q

What population has a very high prevalence of alcoholic liver disease?

A

Native American

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42
Q

stages of alcoholic liver disease

A
  1. steatosis
  2. alcoholic hepatitis
  3. alcoholic cirrhosis
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43
Q

What can liver cirrhosis lead to?

A
  1. hepatocellular carcinoma

2. cholangiocarcinoma

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44
Q

How many drinks/day for alcoholic liver disease and how many years?

A

5 yrs

men: more than 6 drinks
women: 3 drinks

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45
Q

Why do women require less drinking than men to get alcoholic liver disease?

A
  1. differences in volume of distribution
  2. decreased alcohol dehydrogenase activity
  3. differences in first pass metabolism
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46
Q

alcoholic hepatitis

A

40-60 yrs old
Sx: jaundice, muscle wasting, ascites, tender hepatomegaly, FEVER
AST over 2x ALT (both are rarely over 300)
also: elevated INR, leukocytosis

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47
Q

normal prothrombin time (PT)

A

10.7-15 s

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48
Q

normal INR

A

below 1.1

2-3 if on warfarin

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49
Q

ADH2*1 polymorphism

A

East Asian

increased susceptibility to alcoholic liver disease (flushing due to acetaldehyde build up)

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50
Q

TNF a-238 polymorphism

A

Caucasians

increased susceptibility to alcoholic liver disease

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51
Q

Mechanism of ALD pathogenesis

A
  1. ethanol, acetylaldehyde cause intestinal injury and increased permeability
  2. results in endotoxemia
  3. results in inflammatory response by Kupffer cells
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52
Q

Two hit theory of ALD

A

Hit 1: Fatty Liver: oxidative stress, increased NADH/NAD ratio, obesity/DM
fat sensitizes liver to 2nd hit
Hit 2: inflammation and necrosis; oxidative stress/hypoxia/immunological rxn

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53
Q

Maddrey score

A

modified discriminant function: predictor of survival in ALD
[4. 6 (PT- control)] + bilirubin
greater than 32: one month mortality is 1/3 to 1/2

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54
Q

Glasgow Alcoholic Hepatitis Score

score: 1, 2, 3

A

predictor of survival in ALD
greater than 9: bad
1. age: less than 50, greater than 50; no 3 score
2. WBC: less than 15,000, more than 15,000; no 3 score
3. BUN: less than 14, more than 14; no 3 score
4. INR: less than 1.5, 1.5-2, greater than 2
5. bilirubin: less than 7.4, 7.4-14.7, more than 14.7

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55
Q

C282Y mutation

A

location: HFE gene
missense: Cys to Tyr
hemochromatosis
decreased sensing of iron stores leads to excess iron absorption in intestine
decreases hepcidin

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56
Q

HFE gene

A

type I hemochromatosis

defect: can’t sense iron: absorb iron you don’t need

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57
Q

ALD patients with C282Y mutations had?

A

increased hepatic iron scores

higher rates of HCC

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58
Q

MZ or SZ

A

heterozygous

alpha-1 antitrypsin deficiency

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59
Q

ZZ

A

homozygous

alpha-1 antitrypsin deficiency

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60
Q

most important environmental factors in determining ALD risk

A

ethanol pattern

obesity and hyperglycemia

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61
Q

ALD Tx

A
  1. ABSTINENCE
  2. nutrition
  3. pentoxifylline
  4. immunosuppression with corticosteroids in some
    liver transplant
62
Q

How does heptaocellular steatosis occur in ALD?

A
  1. shunt substrates away from catabolism and toward lipid biosynthesis: increased generation of NADH by alcohol dehydrogenase and acetaldehyde dehydrogenase
  2. impaired assembly and secretion of lipoproteins
  3. increased peripheral fat catabolism of fat, releasing FFA into circulation
63
Q

nonalcoholic fatty liver disease (NAFLD)

A

obesity, T2DM, hyperlipidemia, metabolic syndrome

64
Q

Two conditions of NAFLD

A
  1. steatosis (limited progression)

2. NASH

65
Q

non-alcoholic steatohepatitis (NASH)

A

fatty liver, fibrosis, cirrhosis

increases risk of: HCC

66
Q

BMI of obesity

A

greater than 30

67
Q

Who has the highest rate of NAFLD? Lowest?

A

high: Mexican American
low: AA
gender equal

68
Q

Leading cause of pediatric liver disease?

69
Q

Other causes of NAFLD (besides obesity)

A
  1. nutrition abnormalities: total parenteral nutrition, starvation then re-feeding
  2. metabolic diseases: abetalipoproteinemia, hypobetalipoproteinemia
  3. occupational chemical exposure
  4. drugs
  5. surgery (with rapid, excessive wt. loss): jejunoileal bypass, gastric bypass
70
Q

drugs that cause NAFLD

A 
tamoxifen
corticosteroids
amiodarone
methotrexate
antiretrovirals
71
Q

pathogenesis of steatosis in NAFLD

A

normal: TG in chylomicrons travel via lymph to peripheral fat, hydrolyzed to FFA (stored in liver and oxidized by mitochondria)
disturbance of this
1. more lipogenesis
2. increased FFA from periphery to liver

72
Q

pathogenesis of insulin resistance in NAFLD

A
  1. insulin promotes uptake of glucose (stored as glycogen)
  2. inhibit lipolysis (increase in adipose tissue lipolysis?)
  3. increased insulin leads to increased lipogenesis: increased FFA
  4. increased mitochondrial FA oxidation: free radical formation and damage
73
Q

NAFLD: two hit hypothesis

A
  1. hepatic fat accumulation

2. oxidative stress via lipid peroxidation and free radicals

74
Q

Dx of NAFLD

A

Sx of most: NONE
nonspecific: fatigue
PE: obesity, hepatomegaly, SPIDER ANGIOMATA, PALMER ERYTHEMA
lab:
moderately elevated AST and ALT (up to 4x normal)
ALP up to 2x normal
can have normal LFTs but may have low platelets
Biopsy is the ONLY definitive way to Dx: controversial

75
Q

Histo definitions in fatty liver

  1. steatosis
  2. steatohepatisis
  3. fibrosis
  4. cirrhosis
A
  1. macro vesicular fat
  2. inflammation, hepatocyte degeneration, Ballooning and Mallory bodies
  3. pericellular then bridging
  4. 20% of patients within 10 yrs
76
Q

NAFLD/NASH Tx

A

WEIGHT REDUCTION

  1. optimize diabetic Tx
  2. must Tx hyperlipidemia to reduce cardiac risk
  3. BMI greater than 35: bariatric Sx: improves inflammation and fibrosis
  4. liver transplant
77
Q

most frequent genetic condition in Caucasians

A

hemochromatosis

78
Q

hepcidin

A

decreases iron absorption
normally: iron excess leads to up regulation; iron def. leads to down regulation

HEMOCHROMATOSIS: decreased hepcidin: leads to up increased intestinal iron absorption via upregulation of ferroportin

79
Q

HFE mutations

  1. C282Y homozygous
  2. C282Y/H63D or S65C
  3. homozygous for H6D3 or S65C
A
  1. most patients with hereditary hemochromatosis
  2. may have iron overload
  3. NOT associated with iron overload
80
Q

What organs is serum Fe in hemochromatosis loaded into and why?
What happens to these organs?

A

tissues with High Transferrin Receptors
liver, heart, pancreas, thyroid
increased oxidative stress and free radicals

81
Q

Hemochromatosis Sx

A

over 40 yrs in men; 50 yrs in women

general: fatigue, ARTHRITIS (most common)
liver: cirrhosis, HCC
heart: restrictive cardiomyopathy
skin: hyperpigmented
pancreas: bronze DM

82
Q

Type I hemochromatosis

A

HFE gene
adults
chromosome 6

83
Q

Type II hemochromatosis

A

Juvenile: 10-15yrs
defect in: HJV, HAMP gene
NO HEPCIDIN
more CARDIAC involvement

84
Q

HJV gene (hemojuvelin)

A

Type II hemochromatosis

85
Q

HAMP gene (hepacidin anti-microbial peptide)

A

Type II hemochromatosis

86
Q

Type III hemochromatosis

A

transferrin receptor mutation

87
Q

Type IV hemochromatosis

A

ferroportin mutation

88
Q

Dx of hemochromatosis

A
  1. transferrin saturation (serum Fe/TIBC) greater than 45%: suspect iron overload
  2. serum Ferritin more than 1000 mcg/l predicts advanced fibrosis/cirrhosis
    TIBC: transferrin
  3. gene test for homo C282Y
  4. biopsy: confirm HIC/age greater than 1.9; assess liver injury; Dx those without HFE mutation (type II, III)
89
Q

Screening for HFE

  1. who
  2. how
  3. for children of hemochromatosis parent

if have

  1. hetero or homo C282Y and elevated ferritin
  2. hetero or homo C282Y and normal ferritin
A
  1. all 1st degree relatives
  2. check ferritin/TS and HFE mutation
  3. check other parent: don’t have it, then children are heterozygotes and don’t need further testing
  4. start Tx: phlebotomies
  5. monitor Fe normally
90
Q

Other causes of iron overload (other than hemochromatosis)

A
  1. ineffective erythropoiesis (Thalassemia, sideroblastic anemia)
  2. parenteral iron overload from transfusions
  3. chronic liver disease
  4. aceruloplasminemia
  5. congenital atransferrinemia
91
Q

Hemochromatosis Tx

A
  1. phlebotomy (until ferritin is less than 50g/ml)
  2. Fe chelation: desferoxamine, deferasirox
  3. avoid Vit. C (increases Fe absorption), undercooked seafood (risk of infection with Vibrio; also at risk of Listeria, Yersinia)
  4. decrease: alcohol and iron intake (no longer recommended)
92
Q

Results of hemochromatosis Tx do?

A
  1. improve survival if initiated before cirrhosis/DM
  2. reversal of fibrosis (but not cirrhosis)
  3. improved glycemic control and cardiac function
  4. reduction in portal HTN
  5. elimination of HCC risk (if before cirrhosis)
  6. reduction in skin pigmentation
93
Q
  1. What can hemochromatosis NOT reverse?

2. What should cirrhotic hemochromatosis pts. be screened for?

A
  1. hypogonadism, arthropathy, cirrhosis

2. HCC

94
Q

Wilson’s Sx

  1. liver
  2. brain
  3. kidney
  4. blood
A

AR
presents EARLY in life
excess Cu
ATP7b defect
1. chronic hepatits, cirrhosis, acute liver failure
2. psych Sx, basal ganglia (parkinson like: tremor, dystonia, lack of coordination, dysphasia, spasticity, etc)
3. proximal tubular disease
4. hemolytic anemia
other: cardiomyopathy, pancreatitis, osteoporosis, arthritis, nephrolithiasis
KAYSER-FLEISCHER RING

95
Q

Cu metabolism

A

intestinal Cu transported to hepatocyte

  1. into circulation bound to ceruloplasmin
  2. biliary Cu excretion into feces
96
Q

ATP7b gene

A

encodes ATPase that transports Cu in hepatocytes
reduced/absent: WILSON’S: reduced Cu excretion in bile and inability to incorporate Cu into ceruloplasmin
chromosome 13

97
Q

Where does Cu go in Wilson’s?

A

increase in serum free Cu

some goes to: urine and extra-hepatic sites

98
Q

Labs in Wilson’s

A
  1. low ceruloplasmin
  2. high free Cu in plasma
  3. high Cu in liver
99
Q

Kayser-Fleischer Ring

A

Cu in Descemet’s membrane of cornea
WILSON’S
can be absent in isolated hepatic Wilson’s
also seen in: PBC, PSC

100
Q

Wilson’s: fulminant liver failure

A
  1. liver failure
  2. encephalopathy
  3. coagulopathy: hemolytic anemia (Coomb’s neg)
  4. low serum ALP
  5. ALP/Bil less that 2
  6. AST/ALT less than 2000
    Tx: LIVER TRANSPLANT only
101
Q

When to suspect Wilson’s

A
  1. less than 40 with elevated AST/ALT
  2. Neuropsychiatric disease with liver disease
  3. young patient with liver failure
102
Q

Dx of Wilson’s

A
  1. ceroloplasmin less than 5 mg/dl
  2. free Cu greater than 25 ugm/dl
  3. 24 hour Cu urine greater than 100 mg
  4. liver Cu concentration greater than 250 ugm/gram (can get false neg if have severe fibrosis)
    too many mutations for genetic mutation (unless family member already Dx)
103
Q

Tx of Wilson’s

A
  1. chelating agent: penicillamine, trientene, tetrathiomolybdate
  2. Zinc
  3. Liver transplant
104
Q

Rx of choice for Wilson’s

A

trientene and zinc

105
Q

Alpha-1 anti-trypsin

A

neutralized neutrophil elastase

106
Q

SERPINA1 gene

A

chromosome 14
alpha1 antitrypsin deficiency
alleles: M, S, Z
only Z

107
Q

alpha-1 anti-trypsin

  1. M
  2. S
  3. Z
A
  1. normal
  2. mutated: slow moving
  3. mutated: slowest: disease; cannot be secreted by liver (excess in liver, low in lung and serum)
108
Q

alpha-1 antitrypsin deficiency
Sx
Dx
Tx

A
  1. lung: EARLY EMPHYSEMA (uncontrolled elastase activity)
  2. liver: accumulation: liver injury, neonatal jaundice
    can have either one or both
    Dx: ZZ phenotype, liver biopsy
    Tx: if smoke STOP, replace aAT (useful for emphysema only)
    liver transplant for cirrhosis
109
Q

Risk of HCC in

  1. hemochromatosis
  2. Wilson’s
  3. Alpha-1 AT def.
A
  1. HIGH
  2. low
  3. middle
110
Q

impact of liver transplant in

  1. hemochromatosis
  2. Wilson’s
  3. Alpha-1 AT def.
A
  1. can theoretically recur (rare); no impact on extra hepatic sites
  2. cures disease, may improve neurological disease
  3. cures hepatic disease, emphysema irreversible
111
Q

causes of hepatic encephalopathy

A
  1. acute liver failure
  2. portosystemic shunt without liver failure
  3. chronic liver failure
112
Q

proposed mechanisms of hepatic encephalopathy

A
  1. ammonia, nitrogenous waste
  2. increased intracellular glutamine
  3. astrocyte swelling, cerebral edema
  4. inflammatory cytokines alter BBB
  5. increased benzodiazepine receptors
  6. increase neurosteroids, increased GABA receptor activity
  7. manganese: neurotoxin that deposits in basal ganglia
113
Q

acute hepatic encephalopathy

A
  1. coagulopathy and altered mental status within 2 weeks of jaundice
  2. alteration of BBB
  3. associated with acute cerebral edema resulting in cerebral herniation
    MAJOR cause of death in acute liver injury
114
Q

chronic hepatic encephalopathy

A

slow and subtle
milder Sx
missed by coworkers or physicians (often noticed by family)
REVERSIBLE (possibly mild decrease in mentation)

115
Q

stages of hepatic encephalopathy

  1. Grade I
  2. Grade II
  3. Grade III
  4. Grade IV
A
  1. irritable, insomnia, agitation
  2. indefferent, personality change, short term memory impairment, mildly disoriented about time or place
  3. drowsy but arousable, significantly confused and disoriented to time and place
  4. coma
116
Q

Sx of hepatic encephalopathy

A

asterixis, myoclonus (jerking) with hyperextension of ankles
confusion
NO tachycardia, HTN, other sensory/motor/cerebellar deficient to suggest other causes

117
Q

asterixis

A

hyperextend wrist and observe flap motion

inability to sustain grip

118
Q

conditions that need to be treated in hepatic encephalopathy

A
  1. hypovolemia
  2. hypokalemia
  3. GI bleed
  4. remove some medications (sedatives), substance abuse
  5. infection: MENINGITIS
  6. exclude INTRACRANIAL HEMORRHAGE (falls with thrombocytopenia, coagulopathy)
119
Q

Tx of hepatic encephalopathy

A
  1. lactulose: decreases glutamine absorption, reduced syn. and absorption of NH3
  2. zinc sulfate: cofactor in NH3 metabolism (def. is common in liver disease)
  3. antibiotics: alter intestinal flora; decrease NH3, intestinal glutaminase, coliform bacteria that produce NH3
  4. NUTRITION
    do NOT restrict protein
120
Q

chronic neuropsychiatric complications of cirrhosis

A
  1. decreased functional capacity despite medical therapy
  2. dementia
  3. Parkinson’s like syndrome
  4. cerebral edema
121
Q

hepatic Parkinsonism

A

symmetrical

rigidity, lack tremor

122
Q

hepatic dementia

A

flutuating Sx

attention deficit, dysarthia, apraxia (inability to carry out learned movements)

123
Q

hepatic cerebral edema

A

ACUTE liver failure or decompensated cirrhosis

worsened with hyponatremia, rapid fluid shifts

124
Q

hepatic myelopathy

A

demyelination of pyramidal tract
progressive spastic paraparesis
hyper-reflexia
dementia

125
Q

hepatocerebral degeneration

A 
risk with recurrent hepatic encephalopathy
neuropsych disorders
movement disorders, myoclonus
cerebellar Sx
myelopathy
126
Q

hepatocerebral degeneration MRI

A

increased intensity in globus pallidus with T1
associated with severity and worsened NH3 levels
IMPROVED within 3 mo. of LIVER TRANSPLANT, IMPROVEMENT in BASAL GANGLIA ABNORMALITIES (his publication)

127
Q

renal complication associated with liver disease

A
  1. hepatorenal syndrome
  2. IgA nephropathy
  3. membranoproliferative glomerulonephritis
  4. membranous glomerulomephritis
128
Q

hepatorenal syndrome

A

liver failure causes renal arterial vasoconstriction and renal failure
Sx: cirrhosis and ascites; serum Cr greater than 1.5 mg/dL
Dx: exclusion; lack of return of renal function with intravascular volume depletion
reversed with Tx of liver failure

129
Q

hepatorenal syndrome

  1. Type 1
  2. Type 2
A
  1. rapid worsening Cr greater than 2.5 mg/dL or decrease in CrCl less than 20 ml/min within 2 wks
  2. slow progression, often with worsening liver disease
130
Q

Mechanism of hepatorenal syndrome

A
  1. peripheral artery vasodilation
  2. stimulation of renal sympathetic nervous system, renin-angiotensin-aldosterone
  3. cardiac dysfunction
  4. cytokinees, vasoactive mediators
131
Q

hepatorenal syndrome Tx

A
  1. intravascular volume repletion
  2. Tx underlying infection
  3. AVOID NSAIDs and CONSTRAST
  4. optimize renal perfusion with midodrine and octreotide
  5. hemodialysis until liver transplant
132
Q

IgA nephropathy

A

most common secondary cause: liver disease
IgA, C3 deposition (decreased clearance)
IFN worsens dysfunction
association: HEP C and B

133
Q

membranoproliferative glomerulonephritis

A

associated with: CHRONIC HEPATITIS C

CRYOGLOBULINEMIA

134
Q

cryoglobulinemia

A

proteins precipitate in chilled tube of blood

see bruises in distal extremeties

135
Q

drug-induced liver disease

Sx

A

RASH, EOSINOPHILIA, FEVER

other: asymptomatic, fatigue, abnormal liver enzymes, jaundice, liver failure

136
Q

intrinsic vs. idiosyncratic hepatotoxin

  1. predictability
  2. dose dependency
  3. reproducibility in animals
  4. what drugs
A 
intrinsic
1. predictable 
2. dose dependent
3. easily reproduced in animals
4. carbon tetrachloride, acetaminophen
idiosyncratic
1. unpredictable
2. not reproduced in animals
3. not dose dependent
4. MOST medications
137
Q

Drug induced liver disease: what do you see on histo (not sure if correlate)

  1. amiodarone
  2. CCl4
  3. androgens
  4. chlorpromazine
  5. floxuridine
  6. azathioprine
  7. sulfonamides
  8. chlorpromazine
  9. halothane
A
  1. ALD
  2. fatty liver
  3. cholestasis
  4. bile duct injury
  5. sclerosing cholangitis
  6. veno-occlusive Dis
  7. granulomas
  8. cholestasis
  9. fatal immune-mediated hepatitis
138
Q

hepatocellular injury in drug induced liver disease

A

acute and chronic hepatitis
fulminant hepatitis
steatohepatitis
cirrhosis

139
Q

cholestatic injury in drug induced liver disease

A

cholestasis
acute and chronic cholangitis
sclerosing cholangitis
vanishing bile duct syndrome

140
Q

oral contraceptive drug induced liver disease

A

idiosyncratic
bland cholestasis
estrogen decreases membrane fluidity
decrease Na/K ATPase activty and bile salt transport

vascular complications, Budd-Chiari, peliosis hepatitis, focal nodular hyperplasia, hepatic adenomas, HHC (rare)

141
Q

acetaminophen and ethanol

A
  1. decreased glutathione
  2. increase CYP induction
  3. increase toxic metabolites
    Tx: N-acetylcysteine; discontinue alcohol and tylenol
    LOW dose acetaminophen in alcoholic is all it takes
142
Q

fulminant hepatic failure

A

massive necrosis of liver cells without preceding liver disesae
HIGH MORTALITY
LESS THAN 2 WEEKS

143
Q

Causes of fulminant hepatic failure

  1. viral
  2. drug/toxin
  3. ischemic
  4. metabolic
  5. misc.
A
  1. Hep. A, B, D, E; herpes, CMV, EBV, varicella, adeno
  2. acetaminophen, halothane, NSAIDs, herbals
  3. hypoxia, shock, budd-chiari
  4. wilson, fatty liver of pregnancy, Reye’s
  5. CA, bactierial infection
    MOST are viral or toxic
144
Q

viral fulminant hepatic failure

  1. pregnancy
  2. immunocompromised
  3. rare, usually greater than 40 yrs
  4. other
A

MOST COMMON cause

  1. HEV
  2. HSV, CMV, EBV, varicella, adeno
  3. HAV
  4. HBV (most common of virus; half infected with HDV)
145
Q

second most common cause of fulminant hepatic failure

A

drugs

halothane, NSAID, ISONIAZID, acetaminophen, mushroom, herbals, alcohol

146
Q

acetaminophen liver toxicity

A

oxidation causes the problem, sulfonation, glucoronidation help fix
metabolized by CYP to NAPQI (toxic)
glutathione detoxifies NAPQI

147
Q

HBsAg

A

Hep. B surface antigen

ongoing infection

148
Q

anti-HBc

A 
Ab to Hep B core antigen
prior infection (IgM indicates recent)
149
Q

anti-HBs

A

Ab to Hep B surface protein

immunity and/or recovery

150
Q

Hep. B

  1. type 1
  2. type 2
  3. type 3
A
  1. clear
  2. chronic (greater than 6 mo)
  3. fulminant hepatic failure
151
Q

Wilson’s Tx in acute liver failure

A

transplant

don’t bother with chelating

152
Q

Sx of acute hepatic failure

  1. general
  2. bad/late
  3. if was from chronic
A
  1. Jaundice, large liver (or small with collapse), vomit
  2. increased HR and BP, fever
    if do to chronic: no liver Hx, small 3. hard liver, splenomegaly, vascular collaterals

GI (12 decks)

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