Cirrhosis & Portal HTN

Question 1

name two common examples of how the liver metabolizes toxins

Answer 1

1) converts ammonia to urea, 2) metabolizes alcohol

Question 2

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

Answer 2

zone 3; cytochrome P-450

Question 3

Phase 2 of drug metabolism results in?

Answer 3

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

Question 4

what is the liver’s role in lipid metabolism?

Answer 4

cholesterol synthesis

Question 5

what is the purpose of bile?

Answer 5

the emulsify fats (released from gallbladder after meals)

Question 6

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

Answer 6

stellate cell

Question 7

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

Answer 7

kupffer cell; paracrine

Question 8

liver injury causes loss of hepatocyte ____ and sinusoidal endothelial _____

Answer 8

microvilli; fenestrae

Question 9

name 4 genetic/hereditary etiologies of cirrhosis

Answer 9

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

Question 10

decompensated cirrhosis can have a mortality exceeding ___ at one year

Answer 10

50%

Question 11

jaundice and scleral icterus are a result of?

Answer 11

liver’s inability to process bile

Question 12

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

Answer 12

pruritis

Question 13

the liver’s inability to produce albumin results in?

Answer 13

acites and edema

Question 14

___glycemia may occur in end-stage liver dz

Answer 14

hypoglycemia

Question 15

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

Answer 15

10-12mmHg (nl = 5)

Question 16

portal pressure is directly related to ___ and ___

Answer 16

portal venous inflow & resistance to portal outflow

Question 17

what influences portal venous inflow?

Answer 17

cardiac output (affects tone of mesenteric arterioles)

Question 18

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

Answer 18

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

Question 19

blood entering the portal venous circulation comes from the ____ arterioles

Answer 19

mesenteric

Question 20

complications of cirrhosis that indicate decompensated dz (6 major)

Answer 20

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

Question 21

most devastating complication of cirrhosis and portal HTN

Answer 21

variceal hemorrhage

Question 22

prevention of esophageal varices

Answer 22

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

Question 23

tx of acute bleeding varices

Answer 23

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

Question 24

is ascites more frequently caused by liver or cardiac dz?

Answer 24

liver!

Question 25

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

Answer 25

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

Question 26

management of ascites

Answer 26

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

Question 27

interventions for refractory ascites

Answer 27

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

Question 28

spontaneous bacterial peritonitis is defined as?

Answer 28

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

Question 29

tx SBP with?

Answer 29

3rd gen cephalosporin or quinolone

Question 30

secondary prophylaxis for SBP includes?

Answer 30

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

Question 31

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

Answer 31

reduces perfusion to the kidneys, leading to acute renal failure

Question 32

clinical presentation of hepatorenal syndrome (HRS)

Answer 32

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

Question 33

diagnostic criteria for HRS

Answer 33

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

Question 34

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

Answer 34

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

Question 35

treatment options for HRS

Answer 35

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

Question 36

how to midodrine and octreotide improve kidney perfusion?

Answer 36

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

Question 37

prevention of HRS in setting of other liver dz

Answer 37

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

Question 38

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

Answer 38

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

Question 39

how to dx HCC?

Answer 39

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

Question 40

why does HCC present with late phase portal washout?

Answer 40

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

Question 41

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

Answer 41

liver ischemia, hepatic encephalopathy from toxins bypassing liver

Question 42

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

Answer 42

nitrogenous substances; ammonia

Question 43

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

Answer 43

glutamine, serotonin, GABA, catecholamines

Question 44

what is the best dx tool for encephalopathy?

Answer 44

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

Question 45

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

Answer 45

infection

Question 46

six major causes of hepatic encephalopathy?

Answer 46

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

Question 47

a normal ammonia level is useful to?

Answer 47

suggest an alternative diagnosis (such as alzheimer's)

Question 48

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

Answer 48

confusion, lethargy, coma, etc.

Question 49

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

Answer 49

decreased attention

Question 50

name three treatment goals for HE

Answer 50

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

Question 51

name an unexpected cause of HE

Answer 51

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

Question 52

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

Answer 52

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

Question 53

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

Answer 53

Class A

Question 54

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

Answer 54

serum bili, INR, serum creatinine

Question 55

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

Answer 55

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