GI MEGAQUIZ LIVER Flashcards

1
Q

extrahepatic complications of chronic HBV

A

-due to circulating hep B antigen-antibody immune complexes
-polyarteritis nodosa- inflammation of medium sized vessels -> cancer sx
-glomerular disease

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2
Q

chronic HBV treatment

A

-based on circulating virus, HBeAg, LFTs, cirrhosis +/-
-nucleoside or nucleotide analog
-OR pegylated interferon
-fu and monitor for nontreated pts and cirrhosis pts

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3
Q

most important factor that increases progression of liver disease to chronic

A

-longer the duration of infection
-coinfection with hep D does not increase chance of becoming chronic

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4
Q

extrahepatic complications for HCV

A

-fatigue
-jaundice rare
-Hematologic diseases- essential mixed cryoglobulinemia and lymphoma
-Renal disease- membranoproliferative glomerulonephritis
-Autoimmune disorders- thyroiditis
-Dermatologic conditions- porphyria cutanea tarda and lichen planus
-Diabetes mellitus

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5
Q

chronic HVC treatment

A

-f/u monthly
-quantitivative HCV RNA test at 4 weeks of therapy
-virologic response to tx- viral load at 12 weeks after therapy
-fu- HCC screenings, LFTs, US, AFP, EGD

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6
Q

autoimmune hepatitis

A

-high autoantibodies and serum globulin concentration
-can affect anyone -> middle age women MC
-can follow viral illness- insidious
-asymptomatic - debilitation sx
-ANA and ASMA elevated*
-high bili, AST, ALT
-liver bx required
-tx- prednisone +/- azathioprine
-vaccinate
-monitor if cirrhosis

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7
Q

primary biliary cholangitis

A

-rare autoimmune- environmental trigger
-intrahepatic bile duct - small
-female > male
-high LFTs
-asymptomatic usually -> if any, pruritis, fatigue
-cholesterol deposits
-high alk phos, high AMA
-MRCP
-liver bx
-tx- ursodeoxycholic acid, fat soluble vitamins if deficient
-monitor bone density
-monitor if cirrhosis
-associated with sjrogens

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8
Q

primary sclerosing cholangitis

A

-intra and extrahepatic bile ducts affected
-large -> stent
-males > females
-associated with IBD (ulcerative collitis)

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9
Q

hemochromatosis

A

-increased accumulation of iron as hemosiderin in organs
-autosomal recessive - HFE +
-asymptomatic until > 40 in males and postmenopause in females
-heart failure, arrhythmias, type 2 diabetes, hypogonadism, cognitive changes, arthropathy, bronze colored skin
-high ferritin/iron/transferrin labs
-tx- phlebotomy

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10
Q

alcoholic liver disease

A

-steatosis
-steatohepatitis
-asymptomatic hepatomegaly - end stage cirrhosis
-rule out other causes of liver disease
-AST>ALT**, high alk phos, GGT, bili
-anemia, thrombocytopenia, prolonged PT, low albumin
-imaging to view fat, and r/o other liver disease
-bx not often necessary
-tx- lifestyle -> if severe, methyprednisone, pentoxifyline

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11
Q

nonalcoholic fatty liver disease (NAFLD)

A

-steatosis with or without inflammation
-nonalcoholic fatty liver- NAFL (steatosis) -> labs wnl
-nonalcoholic steatohepatitis- NASH -> mildly elevated aminotransferases and alk phos
-MC liver disorder
-obesity, diabetes, high triglycerides, meds
-RUQ pain, asymptomatic
-ALT > AST- NORMAL THOUGH
-REQUIRMENT FOR DX:
-r/o other causes of liver disease
-imaging or bx for steatosis
-no excessive EtOH
-normal LFTs**

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12
Q

nonalcoholic fatty liver disease tx and referral

A

-Weight loss-5-7% body wt
-Diabetes tx
-Hyperlipidemia tx
-Vaccinate
-Vitamin E if NASH
-Referral:
-LFTS remain elevated despite loss of ≥5 percent of body weight
-Clinical features of advanced liver disease (eg, ascites, splenomegaly, jaundice)
-Advanced Inflammation/fibrosis on liver biopsy
-Advanced fibrosis on a noninvasive liver assessment
-MELD> 10-refer for transplant

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13
Q

cirrhosis MC causes, classification, labs

A

-MC causes- chronic hep c, alcohol, NASH -> chronic inflammation or cholestasis
-fibrosis and nodular regeneration
-histologic classification- micronodular, macronodular, mixed forms
-elevated LFTs, bili
-thrombocytopenia, prolonged prothrombin time
-anemia
-high or low WBC

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14
Q

what features cause cirrhosis symptoms

A

-hepatic cell dysfunction
-portal hypertension
-portosystemic shunting

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15
Q

cirrhosis complications

A

-UGI bleeding - Varices, portal hypertensive gastropathy, or gastroduodenal ulcer
Ascites
-Spontaneous bacterial peritonitis
-Hepatorenal syndrome
-Hepatic encephalopathy
-Carcinoma of the liver
-prevention:
-low Na, restrict fluid, diuretics, TIPS
-avoid ACE inhibitor, NSAIDs, drugs heavy on liver
-tx infection

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16
Q

cirrhosis dx and tx

A

-US
-Liver Bx (gold std but not always necessary)
-Elastography vs fibrosure
-monitor and treat underlying
-end stage liver disease MELD > 10- transplant eval

17
Q

hepatic encephalopathy

A

-CNS dysfunction
-ammonia high
-asterixis
-tx- control protein intake, lactulose

18
Q

hepatocellular carcinoma

A

-Arise from parenchymal cells
-85% associated with cirrhosis
-Chronic hepatitis B and C infections, ETOH, NASH** hemochromatosis
-Men > women
-mass + on US
-bx
-PET scan for staging
-high AFP

19
Q

Child-Pugh score

A

-grades liver disease severity
-bilirubin
-albumin
-prothrombin time
-ascites
-encephalopathy

20
Q

causes of jaundice

A

-hemolysis
-obstruction
-genetic mishandling
-hepatocellular disease

21
Q

unconjugated vs conjugated bilirubinemia

A

-unconjugated- hemolysis, genetic disease, drug rx
-stool and urine are normal
-conjugated- hepatocellular disease, obstruction, hereditary cholestatic syndrome
-urine dark, stool light

22
Q

acute hepatitis phases

A

-prodromal- abrupt, nausea, vomiting, diarrhea, constipation, RUQ/epigastric pain, fatigue
-icteric phase- 5-10 days after, alcoholic stools
-convalescent phase- resolution of sx
-general signs: hepato and splenomegaly, lymphadenopathy, liver tenderness

23
Q

acute hepatitis labs

A

-WBC normal to low
-proteinuria (kidney)
-bilirubinuria- precedes jaundice
-AST/ALT elevated
-PT/INR- prolonged

24
Q

length of different acute hepatitis

A

-2-3 weeks usually
-6-9 hep A
-12 hep B
-B, D, C, G can become chronic
-incubation:
-Hep A- 28 days (2 weeks prior infectious stool)
-Hep B- 1-5 months

25
Q

hepatitis A

A

-RNA
-no chronic carrier state
-HAV and Anti HAV IgM - acute infection
-Anti HAV IgG- prior infection or vaccine

26
Q

hepatitis B

A

-8 genotypes
-sexually transmitted, vertical transmission
-higher chance of chronic in young children
-HBcAg does not appear in serum -> test for Anti-HBc
-HBeAg > 3 months increases chronic likelihood

27
Q

hepatitis C

A

-6 genotypes
-blood
-asymptomatic usually, fatigue, no jaundice usually
-Anti HVC does not mean recovery -> means you have been exposed *****
-HCV RNA PCR- infectious
-tx- treat ASAP or try to let them clear and treat at 12 weeks

28
Q

hepatitis E

A

-waterborne
-no carrier state**
-higher mortality rate in pregnant women

29
Q

fulminant vs subfulminant

A

-fulminant- encephalopathy within 8 weeks
-subfulminant- encephalopathy within 8 weeks and 9 months
-acute hepatic failure

30
Q

causes of acute hepatic failure and tx

A

-acetaminophen toxicity #1 -> NAC
-viral hepatitis- 12% -> antiviral
-parvovirus B 19
-liver transplant

31
Q

acute hepatic failure symptoms and complications

A

-acute liver atrophy
-systemic inflammatory response
-GI symptoms
-hemorrhagic phenomena
- +/- jaundice early
-complications:
-Coagulation defects
-Electrolyte imbalance
-Acid base disturbances
-Renal failure
-Hypoglycemia
-Encephalopathy

32
Q

cirrhosis symptoms

A

-jaundice
-splenomegaly
-ascites*
-peripheral edema
-encephalopathy
-anemia
-spider nervi
-palmar erythema
-liver flap- hands flap
-monitor for US, AFP q 6 mos, EGD
-complications:
-UGI bleeding -Varices, portal hypertensive gastropathy, or gastroduodenal ulcer
Ascites
-Spontaneous bacterial peritonitis
-Hepatorenal syndrome
-Hepatic encephalopathy
-Carcinoma of the liver

33
Q

albumin and total protein

A

-low may indicate liver damage

34
Q

alkaline phosphatase (ALP)

A

-alk phos can be high with bone diseases and liver disease
-order GGT to differentiate -> elevated only with liver damage
-AMA should be ordered when alk phos is high as well -> autoantibodies against mitochondria

35
Q

alpha 1 antitrypsin deficiency

A

-can cause chronic hepatitis
-associated with emphysema
-AAT allows for neutrophil elastase to uncontrollably produce -> attacks lung tissue -> decrease recoil
-jaundice, ascites, weight loss