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15 Cards in this Set

  • Front
  • Back

What are the primary functions of the liver

>bile secretion, excretion

>glucose homeostasis (glycogenisis/olysis, gluconeogenesis)

>coagulation (clotting factors, fibrinogen)

>detox (conjugation, NH3 to urea)

>infectious (complement)

>oncotic pressure (albumin)

>lipid metabolism (digestion, absorption)

What are the clinical manifestations of cirrhosis/end stage liver disease

external: jaundice, testicular atrophy, muscle wasting, ascites (fluid buildup in belly), bruising, edema
internal: encephalopathy (brain injury), cirrhosis (hepatocytes replaced by fibrin and nodules from scarring), tea colored urine
in end stage liver disease: malnutrition, portal hypertension with dilation, hyponatremia (low blood sodium, fat malabsorption

Why do liver disease patients suffer from malnutrition

-one of the most important prognosis in liver cirrhosis. in 80% of patients.
-primarily due to decreased intake. anorexia (common), early satiety, impaired gastric emptying, functional dyspepsia (heart burn), abdominal pain.
-secondary are malabsorption and maldigestion. GI tract and hepatocyte dysfunction. decreased muscle and visceral proteins, increased metabolic/catabolic state.
-vitamin deficit from poor absorption, can't store fat soluble vitamins, can't convert them to active forms
-AA. aromatics and met, glu, his increased. BCAA decreased.

nutritional recommendation for patients with liver disease?

-adequate calories, protein (except in encephalopathy), nutrients to support hepatocyte regeneration, vitamins

-frequent feeding to maintain glucose and decrease catabolism

-physical activity to prevent muscle loss

-fluid restriction, diuretics

-sodium restriction

-consistent CHO intake (due to inhibited insulin secretion and insulin resistance)

-enteral (via GI) for ill patients. give BCAA

-parenteral (via vein or artery) not advised due to complications.

hepatic encephalopathy

buildup of toxins in blood, leading to neuro problems like confusion, altered state. reversible by consuming BCAA, antibiotics, laxatives.


bile can't flow from liver to duodnum, due to mechanical (gall stone) or inhibited bile formation

Whatis the definition of nonalcoholic fatty liver disease (NAFLD)? how is it diagnosed?

most common cause of chronic liver disease. macrovesicular fat in >5% hepatocytes, and absence of other causes of fatty liver.
-clinical: most pt are asymptomatic. RUQ pain, hepatomegaly, abnormal aminotransferase. most children are obese, association with metabolic syndrome (hyperinsulin, truncal obesity, dyslipidemia, hypertension).
-diagnosis: usually use ultrasound. MRI is most sensitive but expensiveliver biopsy is best.

how is NAFLD diagnosed?

-diagnosis: usually use ultrasound. MRI is most sensitive but expensive. liver biopsy is gold standard. aminotransferase (ALT) lvl not useful for early stages of disease. non invasive biomarkers are european liver fibrosis score (ELF) and serum cytokeratin (CK18) which is a filament cleaved by caspase-3.

what's the progression of NALFD?

steatosis- intracellular fat deposition (fatty hepatocytes)

non alcoholic steatohepatitis (NASH)- fat depo, inflammation, fibrosis with necrosis

cirrhosis- nodules surrounded by fibrosis

finally, hepatocellular carcinoma.


what are the complications of NAFLD?

cardiovascular and all-cause mortality

children: dyslipidemia, hypertension, insulin resistance, metabolic syndrome,

hepatic steatosis may have more adverse health impact on CVD than liver disease itself.

describe the multi-hit hypothesis for development of NAFL

first hit: steatosis

second hit: progression to inflammation and fibrosis form oxidative stress, mito dysfunction, overproduction of cytokines, genetic predisposision.

treatment options for NAFLD?

-diet and exercise is primary therapy. gradual weight loss correlated with NAFLD improvement in kids and adults.

-weight loss camp for kids

-bariatric surgery best for adults, clears steatosis and fibrosis. however, rapid weight loss can inflame liver. no data for kids.

-LCPUFA: encouraging data, but still weak

-metformin: insulin sensitizer. yes, helps.

-vitamin E helps, but still weak.

neither vitaE or metformin significantly reduced ALT or fibrosis

who gets liver transplants?

cholestatic cirrhosis, autoimmune hepatits, liver cancer, drug induced liver injuty, metabolic errors like wilson's disease, cystic fibrosis.

-loss of fulction (coagulopathy, encephalopathy, cholestasis)

-structural complications (ascites or fluid in belly, portal bleed)


what are benefits of living donor liver transplant? disadvantages?

advantages: timing of procedure, no graft ischemia, potential long term immunological advantage, bonding experience

disadvantage: small risk to donor, reduced size graft (bililary, vascular problems)

Whatare the common complications affecting people with liver transplants

allograft problems, infection, medication interactions and side effects, metabolic complications, malignant complications, health care maintenance, vaccination and other prophylaxis.

lots of detail to be filled in for each category