Cirrhosis & Portal HTN Flashcards
name two common examples of how the liver metabolizes toxins
1) converts ammonia to urea, 2) metabolizes alcohol
Phase 1 of drug metabolism occurs in zone ___ and uses _____ enzymes
zone 3; cytochrome P-450
Phase 2 of drug metabolism results in?
attachment of large molecules to improve water solubility (glucuronidate, methyl groups, acetic acid, sulfa groups)
what is the liver’s role in lipid metabolism?
cholesterol synthesis
what is the purpose of bile?
the emulsify fats (released from gallbladder after meals)
in liver injury, ____ cell activation leads to accum of scar matrix
stellate cell
____ cell activation accompanies liver injury and contributes to ____ activation of stellate cells
kupffer cell; paracrine
liver injury causes loss of hepatocyte ____ and sinusoidal endothelial _____
microvilli; fenestrae
name 4 genetic/hereditary etiologies of cirrhosis
hemachromatosis, wilson’s dz, a1-antitrypsin deficiency, inborn errors of metabolism
decompensated cirrhosis can have a mortality exceeding ___ at one year
50%
jaundice and scleral icterus are a result of?
liver’s inability to process bile
when bile pigments deposit in the skin, patient’s experience _____
pruritis
the liver’s inability to produce albumin results in?
acites and edema
___glycemia may occur in end-stage liver dz
hypoglycemia
clinical sx of portal HTN are seen when the portosystemic pressure gradient exceeds?
10-12mmHg (nl = 5)
portal pressure is directly related to ___ and ___
portal venous inflow & resistance to portal outflow
what influences portal venous inflow?
cardiac output (affects tone of mesenteric arterioles)
collateral blood flow secondary to portal HTN results in? (4 things)
hemorrhoids (rectal vein), caput medusae (umbilical vein), splenomegaly (splenic/left renal vein), varices (left gastric vein)
blood entering the portal venous circulation comes from the ____ arterioles
mesenteric
complications of cirrhosis that indicate decompensated dz (6 major)
variceal hemorrhage, ascites, spontaneous bacterial peritonitis, hepatorenal syndrome, hepatocellular carcinoma, hepatic encephalopathy (can also affect pulmonary system)
most devastating complication of cirrhosis and portal HTN
variceal hemorrhage
prevention of esophageal varices
1) screening EGD, 2) rx of portal HTN with non-selective beta-blockers, 3) endoscopic variceal ligation for primary prophylaxis
tx of acute bleeding varices
band ligation (by endoscope), sclerotherapy (BORTO), minnesota tube, transjugular intrahepatic portosystemic shunt
is ascites more frequently caused by liver or cardiac dz?
liver!
what is one way to distinguish between common and less common causes of ascites?
measure the serum-ascites albumin gradient (higher gradient means increased hydrostatic pressure - suggests heart or liver etiology)
management of ascites
1) low sodium diet, 2) diuretics (watch renal fnc and sodium closely because can cause renal failure)
interventions for refractory ascites
transjugular intrahepatic portosystemic shunt (TIPS), paracentesis, Denver shunt (peritoneovenous shunt)
spontaneous bacterial peritonitis is defined as?
peritoneal fluid with >250 PMN, infection typically from gut bacteria
tx SBP with?
3rd gen cephalosporin or quinolone
secondary prophylaxis for SBP includes?
norfloxaci, ciprofloxacin, or SMZ-TMP (mortality not tested)
hepatorenal syndrome is the end stage of a sequence of events that?
reduces perfusion to the kidneys, leading to acute renal failure
clinical presentation of hepatorenal syndrome (HRS)
oliguria (low urine output), low urine sodium, bland urine sediment, systemic hypotension, absence of another cause of renal failure
diagnostic criteria for HRS
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
which is the more severe type of HRS, type I or type II?
Type I (50% reduction of plasma creatinine clearance OR doubling of serum creatitine in less than 2 weeks)
treatment options for HRS
liver transplant (only tx for type I), midodrine & octreotide, norepi, vasopressin analogs, dialysis as bridge to transplant
how to midodrine and octreotide improve kidney perfusion?
midodrine –> systemic vasoconstriction, octreotide inhibits vasodilation of splanchnic vasculature (shunt blood)
prevention of HRS in setting of other liver dz
give albumin to px kidney failure in pts who have or are at risk for SBP; use of steroids or pentoxiphylline in alcoholic hepatitis
what is the most common cause of hepatocellular carcinoma worldwide? In the West (2)?
HBV worldwide (because of high rates in Asia); HCV and alcohol in West
how to dx HCC?
CT scan shows early enhancing and late portal “washout” on CT scan; elevated alpha-fetoprotein (AFP) is suspicious
why does HCC present with late phase portal washout?
because the tumor is only supplied by the hepatic artery, not the portal vein
what are the negative side effects of TIPS (portosystemic shunt)?
liver ischemia, hepatic encephalopathy from toxins bypassing liver
high levels of ____ derived from the gut can be measured by the ____ metabolite, but this is a poor test for dx of hepatic encephalopathy
nitrogenous substances; ammonia
high levels of nitrogen in helpatic encephalopathy cause derangements in the metabolism of?
glutamine, serotonin, GABA, catecholamines
what is the best dx tool for encephalopathy?
clinical exam (wide range of presentation, altered mental status) - can be sleep disturbance, personality changes, coma
what is the #1 important cause of hepatic encephalopathy that should be ruled out?
infection
six major causes of hepatic encephalopathy?
acidosis, infection, drugs, bleeding, hyponatremia, volume depletion
a normal ammonia level is useful to?
suggest an alternative diagnosis (such as alzheimer’s)
High grade HE includes patients that are unable to cooperate and present with?
confusion, lethargy, coma, etc.
low grade HE is more difficult to detect and most frequently results in?
decreased attention
name three treatment goals for HE
provide supportive care, identify precipitating factor(s), reduce nitrogen load from gut (poop, abx)
name an unexpected cause of HE
TIPS (can cause HE, other splanchnic shunts can tx HE)
factors that contribute to Child’s Pugh Scoring for severity of liver disease
bilirubin, albumin, INR, ascites, +/-encephalopathy
Pugh Classes go A-C; which has the best prognosis?
Class A
MELD, the model for end-stage liver dz, incorporates what three lab values?
serum bili, INR, serum creatinine
what is the only life-saving intervention for decompensated cirrhosis?
liver transplant (very effective) - list according to MELD score
