Cirrhosis & Portal HTN Flashcards

1
Q

name two common examples of how the liver metabolizes toxins

A

1) converts ammonia to urea, 2) metabolizes alcohol

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2
Q

Phase 1 of drug metabolism occurs in zone ___ and uses _____ enzymes

A

zone 3; cytochrome P-450

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3
Q

Phase 2 of drug metabolism results in?

A

attachment of large molecules to improve water solubility (glucuronidate, methyl groups, acetic acid, sulfa groups)

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4
Q

what is the liver’s role in lipid metabolism?

A

cholesterol synthesis

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5
Q

what is the purpose of bile?

A

the emulsify fats (released from gallbladder after meals)

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6
Q

in liver injury, ____ cell activation leads to accum of scar matrix

A

stellate cell

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7
Q

____ cell activation accompanies liver injury and contributes to ____ activation of stellate cells

A

kupffer cell; paracrine

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8
Q

liver injury causes loss of hepatocyte ____ and sinusoidal endothelial _____

A

microvilli; fenestrae

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9
Q

name 4 genetic/hereditary etiologies of cirrhosis

A

hemachromatosis, wilson’s dz, a1-antitrypsin deficiency, inborn errors of metabolism

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10
Q

decompensated cirrhosis can have a mortality exceeding ___ at one year

A

50%

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11
Q

jaundice and scleral icterus are a result of?

A

liver’s inability to process bile

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12
Q

when bile pigments deposit in the skin, patient’s experience _____

A

pruritis

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13
Q

the liver’s inability to produce albumin results in?

A

acites and edema

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14
Q

___glycemia may occur in end-stage liver dz

A

hypoglycemia

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15
Q

clinical sx of portal HTN are seen when the portosystemic pressure gradient exceeds?

A

10-12mmHg (nl = 5)

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16
Q

portal pressure is directly related to ___ and ___

A

portal venous inflow & resistance to portal outflow

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17
Q

what influences portal venous inflow?

A

cardiac output (affects tone of mesenteric arterioles)

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18
Q

collateral blood flow secondary to portal HTN results in? (4 things)

A

hemorrhoids (rectal vein), caput medusae (umbilical vein), splenomegaly (splenic/left renal vein), varices (left gastric vein)

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19
Q

blood entering the portal venous circulation comes from the ____ arterioles

A

mesenteric

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20
Q

complications of cirrhosis that indicate decompensated dz (6 major)

A

variceal hemorrhage, ascites, spontaneous bacterial peritonitis, hepatorenal syndrome, hepatocellular carcinoma, hepatic encephalopathy (can also affect pulmonary system)

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21
Q

most devastating complication of cirrhosis and portal HTN

A

variceal hemorrhage

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22
Q

prevention of esophageal varices

A

1) screening EGD, 2) rx of portal HTN with non-selective beta-blockers, 3) endoscopic variceal ligation for primary prophylaxis

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23
Q

tx of acute bleeding varices

A

band ligation (by endoscope), sclerotherapy (BORTO), minnesota tube, transjugular intrahepatic portosystemic shunt

24
Q

is ascites more frequently caused by liver or cardiac dz?

A

liver!

25
Q

what is one way to distinguish between common and less common causes of ascites?

A

measure the serum-ascites albumin gradient (higher gradient means increased hydrostatic pressure - suggests heart or liver etiology)

26
Q

management of ascites

A

1) low sodium diet, 2) diuretics (watch renal fnc and sodium closely because can cause renal failure)

27
Q

interventions for refractory ascites

A

transjugular intrahepatic portosystemic shunt (TIPS), paracentesis, Denver shunt (peritoneovenous shunt)

28
Q

spontaneous bacterial peritonitis is defined as?

A

peritoneal fluid with >250 PMN, infection typically from gut bacteria

29
Q

tx SBP with?

A

3rd gen cephalosporin or quinolone

30
Q

secondary prophylaxis for SBP includes?

A

norfloxaci, ciprofloxacin, or SMZ-TMP (mortality not tested)

31
Q

hepatorenal syndrome is the end stage of a sequence of events that?

A

reduces perfusion to the kidneys, leading to acute renal failure

32
Q

clinical presentation of hepatorenal syndrome (HRS)

A

oliguria (low urine output), low urine sodium, bland urine sediment, systemic hypotension, absence of another cause of renal failure

33
Q

diagnostic criteria for HRS

A

cirrhosis with ascites; serum creatinine >1.5mg/dl; no response to diuretic withdrawal and IV albumin; absence of shock, nephrotoxic drugs, and parenchymal kidney dz

34
Q

which is the more severe type of HRS, type I or type II?

A

Type I (50% reduction of plasma creatinine clearance OR doubling of serum creatitine in less than 2 weeks)

35
Q

treatment options for HRS

A

liver transplant (only tx for type I), midodrine & octreotide, norepi, vasopressin analogs, dialysis as bridge to transplant

36
Q

how to midodrine and octreotide improve kidney perfusion?

A

midodrine –> systemic vasoconstriction, octreotide inhibits vasodilation of splanchnic vasculature (shunt blood)

37
Q

prevention of HRS in setting of other liver dz

A

give albumin to px kidney failure in pts who have or are at risk for SBP; use of steroids or pentoxiphylline in alcoholic hepatitis

38
Q

what is the most common cause of hepatocellular carcinoma worldwide? In the West (2)?

A

HBV worldwide (because of high rates in Asia); HCV and alcohol in West

39
Q

how to dx HCC?

A

CT scan shows early enhancing and late portal “washout” on CT scan; elevated alpha-fetoprotein (AFP) is suspicious

40
Q

why does HCC present with late phase portal washout?

A

because the tumor is only supplied by the hepatic artery, not the portal vein

41
Q

what are the negative side effects of TIPS (portosystemic shunt)?

A

liver ischemia, hepatic encephalopathy from toxins bypassing liver

42
Q

high levels of ____ derived from the gut can be measured by the ____ metabolite, but this is a poor test for dx of hepatic encephalopathy

A

nitrogenous substances; ammonia

43
Q

high levels of nitrogen in helpatic encephalopathy cause derangements in the metabolism of?

A

glutamine, serotonin, GABA, catecholamines

44
Q

what is the best dx tool for encephalopathy?

A

clinical exam (wide range of presentation, altered mental status) - can be sleep disturbance, personality changes, coma

45
Q

what is the #1 important cause of hepatic encephalopathy that should be ruled out?

A

infection

46
Q

six major causes of hepatic encephalopathy?

A

acidosis, infection, drugs, bleeding, hyponatremia, volume depletion

47
Q

a normal ammonia level is useful to?

A

suggest an alternative diagnosis (such as alzheimer’s)

48
Q

High grade HE includes patients that are unable to cooperate and present with?

A

confusion, lethargy, coma, etc.

49
Q

low grade HE is more difficult to detect and most frequently results in?

A

decreased attention

50
Q

name three treatment goals for HE

A

provide supportive care, identify precipitating factor(s), reduce nitrogen load from gut (poop, abx)

51
Q

name an unexpected cause of HE

A

TIPS (can cause HE, other splanchnic shunts can tx HE)

52
Q

factors that contribute to Child’s Pugh Scoring for severity of liver disease

A

bilirubin, albumin, INR, ascites, +/-encephalopathy

53
Q

Pugh Classes go A-C; which has the best prognosis?

A

Class A

54
Q

MELD, the model for end-stage liver dz, incorporates what three lab values?

A

serum bili, INR, serum creatinine

55
Q

what is the only life-saving intervention for decompensated cirrhosis?

A

liver transplant (very effective) - list according to MELD score