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2.2Elizi ex 2 GI 2 Exam 2 COPY > Jaundice DSA - McGowan > Flashcards

Jaundice DSA - McGowan Flashcards

1
Q

transfusion reactions, sickle cell anemia, thalassemia (inadequate Hg), autoimmune disease

A

prehaptic

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2
Q

hepatitis, cancer, cirrhosis, congenital disorders, drugs

A

intrahepatic

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3
Q

gallstones, inflammation, scar tissue or tumors that block the flow of bile into the intestines

A

posthepatic

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4
Q

primary injury is to the hepatocytes

  • primarily AST/ALT elevation
  • ALT more specific for liver injury than AST
A

hepatocellular injury

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5
Q

primary injury is to the bile ducts

  • primarily Alk Phos and bilirubin elevated
  • failure of bile to reach duodenum
  • jaundice and pruritis
  • pure cholestasis (no signs of hepatocellular necrosis)
A

cholestatic injury

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6
Q

what are the TRUE liver function tests that McGowan wants us to know?

NOTE: AST/ALT, Alk Phos and bilirubin (LDH, GGT) can come from other sources and are not accurate to determine liver’s function

A
  • PT/INR
  • albumin
  • cholesterol
  • ammonia
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7
Q

what are the 4 main DDx for unconjugated (indirect) jaundice?

A
  1. hemolytic syndrome (anemia/reaction)
  2. Gilbert syndrome
  3. Criggler-Najjar syndrome
  4. viral hepatitis
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8
Q

what are the 5 main DDx for conjucated (direct) jaundice?

A
  1. hepatitis (acute/chronic, infectious/non-infectious)
  2. cirrhosis
  3. obstruction
  4. Dubin-Johnson syndrome
  5. Rotor syndrome
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9
Q

what are the first steps in evaluating pt with jaundice?

A
  1. determine conjugated vs unconjugated

2. other biochemical liver tests are normal

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10
Q

how to diagnose jaundice

A
  • order CBC to look for anemia and thrombocytopenia
  • order chemistry labs: AST/ALT, total bilirubin, Alk phos (will need to request fractionated bilirubin to tell you indirect vs. direct)
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11
Q

when ALP is elevated, what is your next step?

A

fractionate by ordering gamma glutamyl transferase (GGT)

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12
Q

what if ALP and GGT are elevated?

A

most commonly coming from liver source

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13
Q

what if ALP elevated, but GGT is normal?

A

consider bone or other source (placenta) for elevated ALP

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14
Q

what would you order to look for anemia and thrombocytopenia?

A

CBC

- can check for hemolysis: haptoglobin (low), reticulocyte count (elevated) and LDH (elevated)

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15
Q

reduced activity of uridine diphosphate glucuronyl transferase

  • unconjugated (indirect) bilirubin
  • benign, asymptomatic hereditary jaundice, hyperbilirubinemia increased by 24-36 hour fast
A

Gilbert syndrome

  • no tx required
  • assoc with reduced mortality from cardiovascular disease
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16
Q

AR, absent UGT1A1 activity

  • no liver pathology
  • fatal in neonatal period
A

Crigler-Najjar Type 1

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17
Q

AD with variable penetrance, decreased UGT1A1 activity

  • no liver pathology
  • generally mild, occasional kernicterus
A

Crigler-Najjar Type 2

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18
Q

AR, decreased UGT1A1 activity

  • no liver pathology
  • innocuous (not harmful) clinical course
A

Crigler-Najjar Type 3

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19
Q

AR, impaired biliary excretion of bilirubin glucuronides due to mutation in canalicular multidrug resistance protein (MRP2)

  • pigmented cytoplasmic globules
  • innocent clinical course
A

Gilbert Syndrome

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20
Q

what is the main serum antibody present in acute viral hepatitis?

A

IgM

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21
Q

what is the main serum antibody present in chronic?

A

IgG

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22
Q

viral, drugs, ischemia, Budd-Chiari

  • pt has aversion to smoking
  • stools my be acholic (no bile = pale yellow)
  • dx: CVC, CMP, PT/INR, acetaminophen level (use rumack-matthew nomogram)
A

acute hepatitis

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23
Q
  • ssRNA virus
  • aversion to smoking
  • 2-3 week incubation
  • enlarged tender liver, jaundice, acholic stools
  • fecal-oral transmission
  • elevated bilirubin and alk phos = cholestasis
  • both IgM and IgG are detectable in serum soon after onset
A

Hep A
- vaccine!

NOTE: detection of IgN anti-HAV is excellent test for dx acute Hep A

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24
Q
  • partially dsDNA
  • acute illnes usually subsides over 2-3 weeks, 5-10% chronic
  • low-grade fever, enlarged and tender liver, jaundice
  • assoc with polyarteritis nodosa
  • parenteral, sexual, perinatal transmission
  • endemic in sub-saharan Africa and SE Asia
  • HBsAg-positive mothers may transmit HBV at delivery, risk of chronic infection in infant is 90%
  • elevated aminotransferases early in course (higher than HAV infection)
  • substantial risk for cirrhosis -> HCC
A

Hep B

- vaccine!

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25
Q

what is the window period of HBV infection?

A

between HBsAg disappearing and HBaAb appearing, which may take several weeks

  • pt is still considered to have acute HBV
  • infection is only detectable with HBcAb IgM

NOTE: VERY important when screening blood donations

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26
Q

persistence of HBsAg more than 6 months after acute illness signifies what?

A

chronic Hep B

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27
Q

what appears in most individuals after clearance of HBsAg and after successful vaccination against Hep B?

A

anti-HBsAb

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28
Q

what does IgM anti-HBc indicate?

A

acute Hep B

- may also reappear during flares of previously inactive chronic Hep B

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29
Q

what appears during acute Hep B but persists indefinitely?

A

IgG anti-HBc

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30
Q

what is HBeAg?

A

Hep B envelope Ag = secretory form of HBcAg

  • in serum shortly after detection of HBsAg
  • indicated viral replication and infectivity
  • persistence of HBeAg beyond 3 months = increased likelihood of chronic Hep B
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31
Q

defective RNA virus that required HBV for replication

  • endemic among HBV carriers in Mediterranean Basin
  • spread by non-percutaneous (not skin) means
  • non-endemic areas (US, Europe) spread percutaneously (skin)
A

Hep D

- vaccinate against HBV!

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32
Q

ssRNA flavi-like virus (7 genotypes)

  • coinfection with HCV found in 30% of HIV patients
  • accounts for 90% of transfusion-assoc hepatitis
  • IV drug use accounts for >50% of cases
  • boxers! bloody fisticuffs can transmit
  • most sentitive serum indicator is RNA
  • cirrhosis, HCC, mixed cryoglobulinemia, MPGN, increased risk non-Hodgkin lymphoma
A

Hep C
- pt with chronic liver dz should be vaccinated against HAV and HBV

NOTE: occasional persons found to have anti-HCV in serum, without HCV RNA in serum -> recovery from prior HCV infection (spontaneous clearance)

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33
Q

what are the CDC and USPSTF screening recommendations for HCV?

A

all persons born between 1945-1965 should be screened

  • vaccinate against HAV and HBV
  • check for co-infection with HIV
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34
Q

ssRNA hepevirus

  • risk factor for immunocompromised hosts
  • endemic in Asia, middle east, North Africa, Central America, India
  • fecal-oral transmission, waterborne epidemics, spread by swine
  • chronic infection with progression to cirrhosis reported in transplant patients treated with tacrolimus (immunosupressant)
  • high mortality in pregnant women
A

HEV

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35
Q

what is the main cause of drug-induced hepatitis?

A

acetaminophen

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36
Q

what is the tx of drug-induced hepatitis (DILI)?

A

supportive

  • withdraw suspected agent
  • include use of gastric lavage and oral administration of charcoal or cholestyramine
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37
Q

what is the #1 cause of acute liver failure?

A

acetaminophen

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38
Q

nausea, vomiting, icterus and jaundice, itching, elevated liver enzymes

  • life threatening coagulation abnormalities
  • hepatic encephalophathy
  • asterixis
A

acute liver failure

NOTE: in acetaminophen toxicity, AST/ALT > 500 u/L

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39
Q

what is the tx of acetaminophen overdose?

A

N-acetylcysteine (NAC)

  • provides a reservoir of sulfydryl groups to bind to the toxic metabolites or by stimulating synthesis of hepatic glutathione
  • should be given within 8 hours of ingestion
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40
Q

development of hepatic encephalopathy within 8 weeks after the onset of acute liver disease
- coagulopathy (INR 1.5 or higher)

A

fulminant hepatic failure

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41
Q

development of hepatic encephalopathy between 8 weeks - 6 months

A

subfulminant hepatic failure

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42
Q

acute deterioration in liver function in pt with preexisting chronic liver disease

A

acute-on-chronic liver failure

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43
Q

massive hepatic necrosis with impaired consciousness occurring within 8 weeks of onset of illness

  • rapidly shrinking liver size + rapidly rising bilirubin level
  • marked prolongation of PT
  • disorientation, somnolence, ascites, edema
A

fulminant hepatitis

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44
Q

what is the tx/management of fulminant hepatitis?

A

supportive, maintenance of fluid balance, support of circulation, respiration

  • oral lactulose and neomycin administered
  • meticulous intensive care + prophylactic abx coverage can improve survival
  • consider liver transplant
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45
Q

what is the dx of chronic hepatitis?

A

biopsy -> histologic classification
classified based on:
- grade (necrosis and inflammatory activity)
- stage (disease progression/degree of fibrosis)

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46
Q

classic, ANA (most common) and/or ASA (anti-smooth muscle antibodies)

A

Type 1 autoimmune hepatitis

47
Q

associated with anti-liver/kidney microsomal (anti-LKM antibodies)

A

Type 2 autoimmune hepatitis

48
Q

what is the dx of AIH?

A
  • *serologic abnormalities**
  • type 1: hypergammaglobulinemia, smooth muscle Ab, ANA
  • type 2: anti-LKM Ab

**serum aminotransferase levels may be greater than 1000 units/L, and total bilirubin is usually increased

49
Q

what is the tx of AIH?

A

glucocorticoids

complications: leads to cirrhosis -> increased risk HCC

50
Q

excessive alcohol use can cause fatty liver

  • exceeds 80g/day in men and 30-40g/day in women
  • Hep B and C may be cofactors in dvlpment of liver disease
A

alcohol liver disease

51
Q

asymptomatic -> severe liver failure with jaundice, ascites, GI bleeding, encephalopathy

  • typical anorexia, nausea vomiting, fever, jaundice, tender hepatomegaly and RUQ pain
  • 2:1 AST:ALT ratio
  • Mallory-Denk bodies
A

alcohol liver disease

52
Q

what is the main risk of alcoholic cirrhosis?

A

> 50 grams of alcohol (5 drinks) daily for over 10 years

53
Q

what is the tx/management of alcohol liver disease?

A

abstinence from alcohol!

  • glucose administration increase the thiamine requirement and can precipitate Wernicke-Korsakoff syndrome if thiamine is not coadministered
  • if severe, can consider Pentoxifylline or liver transplantation (pt’s must abstain from alcohol for 6 months to be considered)
54
Q

what are the complications of alcoholic liver disease?

A
  • Wernicke encephalopathy (confusion/ataxia)
  • Korsakoff syndrome (severe memory issues)
  • adverse prognostic factor: critically ill pts with alcoholic hepatitis have 30-day mortality rates >50%
55
Q

what does the Glasgow Alcoholic hepatitis score predict?

A

mortality based on:

  • age
  • serum bilirubin
  • BUN
  • prothrombin time
  • peripheral WBC count
56
Q

what is a Model for End-Stage Liver Disease (MELD) score > 21 associated with?

A

significant mortality in alcoholic hepatitis

57
Q

triad: (only 10% have all 3)
- confusion
- ataxia (staggering/stumbling/lack coordination)
- treat with thiamine

A

Wernicke encephalopathy

58
Q
  • permanent
  • progressive from Wernicke
  • severe memory issues
  • confabulate/make up stories to fill in gaps
A

Korsakoff syndrome

59
Q

a way to estimate disease severity and mortality risk in patients with alcoholic hepatitis

  • patients with a DF value > 32: have high short-term mortality and may benefit from treatment with glucocorticoids
  • those with lower scores have low short term-mortality and do not appear to benefit from glucocorticoids
A

Maddrey discriminant function

60
Q

what does a GAH score > 9 mean?

A

survival benefit for those who received glucocorticoids compared with those who did not

61
Q

what does a GAH score < 9 mean?

A

no survival benefit with glucocorticoids

62
Q

what is the threshold used to allow diagnosis of NAFLD?

A

<20 g of alcohol per day in women and <30g in men

63
Q

what is steatosis?

what is steatohepatitis?

A 
steatosis = fatty liver
steatohepatitis = fatty liver than causes liver inflammation
64
Q

what is the most common cause of chronic liver disease in the US?

A

NAFLD

65
Q

obesity, DM, hypertriglyceridemia in association with insulin resistance as part of the metabolic syndrome -> increased risk for cardiovascular disease, chronic kidney disease and colorectal cancer

A

principal causes of NAFLD

66
Q

asymptomatic, or may have mild RUQ discomfort

  • hepatomegaly is up to 75% of cases
  • labs may show mildly elevated aminotransferase and alk phos
  • macrovascular steatosis may be seen on US or CT
  • biopsy: focal infiltration by polymorphonuclear neutrophils and Mallory hyaline indistinguishable from alcoholic hepatitis and referred to as nonalcoholic steatohepatitis (NASH)
A

NAFLD

67
Q

what is the tx of NAFLD?

A

lifestyle modification

  • weight loss, dietary fat restriction, exercise, vitamin E
  • statins are NOT contraindicated
68
Q

HFE gene mutation on chromosome 6

  • men>women
  • elevated iron saturdation or serum ferratin
  • increased accumulation of iron as hemosiderin in liver, pancreas, heart, adrenals, testes, pituitary, and kidneys
  • hepatic and pancreatic insufficiency, heart failure, and hypogonadism may develop
A

hemochromatosis

- increased iron absorption in the duodenum

69
Q

what is the classic tetrad of hemochromatosis?

A
  • cirrhosis with hepatomegaly
  • abnormal skin pigmentation
  • DM
  • cardiac dysfunction
70
Q

what are the later clinical manifestations of hemochromatosis?

A
  • arthropathy (and ultimate need of joint replacement)
  • hepatomegaly
  • skin pigmentation
  • DM
  • ED in men
71
Q
  • elevated plasma iron with greater than 45% transferrin saturation
  • elevated serum ferretin
  • liver biopsy: homozygous for C282Y
  • HFE mutation
A

hemochromatosis

72
Q

what is the tx/management of hemochromatosis?

A
  • avoid foods right in iron
  • weekly phlembotomies of blood
  • PPI -> reduces intestinal iron absorption
  • chelating agent deferoxamine (for pt with hemochromatosis and anemia)
73
Q

what is the main association/complication that McGowan wants us to know with hemochromatosis?

A

Yersinia infection

74
Q

AR, mutation in ATP7B

  • people under age 40
  • results in impaired copper excretion into bile and a failure to incorporate copper into ceruloplasmin
  • leads to hemolytic anemia (copper is toxic to RBC)
  • liver disease in adolescents and neuropsychiatric disease in young adults
A

Wilson disease

75
Q

what is the pathognomic sign of Wilson disease?

A

Kayser-Fleischer rings (brown-green rings around the iris)

- represents fine pigmented granular deposits in Descemet membrane in the cornea

76
Q

elevated liver enzymes:

  • AST/ALT
  • alk phos
  • bilirubin
  • low serum ceruloplasmin

molecular analysis of ATP7B mutations can be diagnostic

A

Wilson disease

- tx: oral penicillamine increases urinary extretion of chelated copper

77
Q

AR, defective a1AT

  • most commonly diagnosed inherited hepatic disorder in infants and children
  • Pi gene chromosome 14
  • development of pulmonary (panacinar) emphysema
  • causes liver disease as a consequence of hepatocellular accumulation of the misfolded protein
A

alpha-1 antitrypsin deficiency

- tx: smoking abstinence/cessation and liver transplant

78
Q 
HBsAg: +
HBcAb IgM: +
HBcAb IgG: +
HBeAg: +
HBV DNA: +

HBs Ab: -

A

chronic Hep B infection

79
Q
  • African Americans have higher rate of chronic disease, but lower fibrosis
  • coffee slows progression
  • pts have normal AST/ALT
  • high risk of cirrhosis and HCC (higher risk in genotype 1b)
A

chronic HCV

80
Q

passive congestion of the liver nutmeg liver

  • ischemic hepatitis = ischemic hepatopathy, hypoxic hepatitis, shock liver, acute cardiogeneic liver injury
  • statin therapy prior to admission may protect against ischemic hepatitis
  • hepatojugular reflex is present -> tricuspic regurg may be pulsatile
  • jaundice associated with worse outcomes
A

right heart failure

81
Q
  • markedly elevated serum N-terminal-proBNP or BNP
  • rapid and striking elevation of serum aminotransferase (often greater than 5000 units/L)
  • early rapid rise in the serum lactate dehydrogenase
A

right heart failure

82
Q

development of liver fibrosis to the point that there is architectural distortion with formation of regenerative nodules -> decreased liver function

A

cirrhosis

mexican and blacks > whites

83
Q

what are the 3 types of cirrhosis?

A
  1. compensated
  2. compensated with varices
  3. decompensated
84
Q

what has been reported to reduce the risk of cirrhosis?

A

higher coffee and tea consumption

85
Q
  • spider telangiectasias
  • palmar erythema
  • dupuytren contractures
  • glossitis and cheilosis
  • jaundice
  • caput medusae
  • asterixis
A

signs of cirrhosis

86
Q

what are the diagnostic studies of cirrhosis?

A
  • CBC: pancytopenia, anemia
  • prolonger PT/INR
  • glucose disturbances
  • hypoalbuminemia
87
Q

definitive diagnosis of cirrhosis depends on what?

A

liver biopsy

- histologic classification (grade and stage)

88
Q

what is the tx/management of cirrhosis?

A
  • *abstinence from alcohol!**
  • pts should receive HAV, HBV, pneumococcal, and yearly flu vaccines
  • transjugular intrahepatic portosystemic shunt (TIPS/TIPSS)
  • *NSAIDS ARE CONTRAINDICATED**
  • Ang-converting enzyme inhibitors and Ang II antagosnists should be avoided
89
Q

SAAG > 1.1 g/dL

A
  • portal HTN

- myxedema

90
Q

SAAG < 1.1 g/dL

A
  • hypoalbuminemia

- diseased peritoneum (peritonitis, peritoneal cancer)

91
Q

increasing abdominal girth

  • alcohol consumption, transfusions, tattoos, IV drug use, hx of viral hepatitis or jaundice
  • fevers -> infected peritoneal fluid
  • PE: elevated JVP, asterixis, shifting dullness
A

ascites

92
Q

what diagnostic tool reliably establishes the presence of fluid?

A

abd US + Doppler
- abdominal paracentesis: development of fever, adb pain, rapidly declining renal function, or worsened hepatic encephalopathy -> exclude SPONTANEOUS BACTERIAL PERITONITIS

93
Q

what are the routine studies on ascitic fluid?

A

CBC:

  • WBC with diff = most important test -> increase in ascitic white blood cell count highly suggestive of SBP
  • albumin: serum-ascites albumin gradient (SAAG) is best single test for ascites classification
94
Q

how is SAAG calculated?

A

subtract ascitic fluid albumin from serum albumin

- the gradient correlates directly with portal pressure

95
Q

alteration in mental status and cognitive function occuring in the presence of liver failure

  • elevated ammonia levels
  • confusion, slurred speech, change in personality, asterixis (flapping tremor)
  • precipitated by GI bleeding, azotemia, constipation
A

hepatic encephalopathy

- tx: lactulose, or rifaximin if lactulose not tolerated

96
Q

spontaneous bacterial infection

  • occurs in the absence of apparent intra-abdominal source of infection
  • caused by monomicrobial infection
  • NOT assoc with anaerobic bacteria
  • hx of chronic liver disease and ascites
A

SBP
- IMPERATIVE THAT ANY PATIENT PRESENTING WITH ASCITES, ESPECIALLY WITH INFECTION SX GET A PARACENTESIS TO RULE OUT SBP

97
Q

what is the dx of SBP?

A
  • WBC count with diff is MOST important test (NL = less than 500 leukocytes, less than 250 PMNs)
  • ascitic fluid PMN count GREATER THAN 250
98
Q

what is the most effective tx of SBP?

A

liver transplant
- empiric abx: third-generation cephalosporin IV (ceftriaxome)

NOTE: kidney injury develops in 40% of patients and is a major cause of death

99
Q

what must spontaneous bacterial peritonitis be distinguished from?

A

SECONDARY bacterial peritonitis
- secondary: ascitic fluid has become secondarily infected by an intra-abdominal infection

  • tx: broad-spectrum abx
100
Q

male: female ratio 4:1
- tumor usually develops in cirrhotic liver
- high incidence in Asia and Africa
- Aflatoxin exposure contributes to etiology and leaves molecular signature -> mutation in codon 249 of p53 gene

A

HCC

101
Q
  • pt with known liver disease develops an abnormality on
  • US
  • rising AFP
  • abnormal liver function tests/liver enzymes
A

HCC

102
Q

what is the tx/management of HCC?

A
  • surgical resection or liver transplantation
  • radiofrequency ablation
  • transcatheter arterial embolization (TACE)
103
Q

stones in common bile duct

A

choledocolithiasis

- tx: ERCP with sphincterotomy and stone extraction

104
Q

charcot triad: RUQ pain, fever, jaundice
Raynold pentad: triad + altered mental status, hypotension

labs show positive blood culture for E.coli, klebsiella, or enterococcus

A

ascending cholangitis

105
Q

chronic liver diease

  • autoimmune destruction of small intrahepatic bile ducts and cholestasis
  • asymptomatic isolated elevation in alk phos
  • PE: pruritis, jaundice, xanthelasma
  • dx: positive AMA in 90-95%, elevated serum alk phos, bilirubin, cholesterol, and IgM
  • biopsy: florid duct lesion
A

primary biliary cirrhosis/cholangitis (PBC)

- tx: ursodeoxycholic acid, calcium and vit D given for osteoporosis

106
Q
  • associated with IBD (primarily UC)
  • men (20-50 years old)
  • beads on a string on MRCP or ERCP
  • onion skinning on liver biopsy
  • smoking and coffee consumption decrease risk of UC and PSC
  • associated with increased risk of cholangiocarcinoma
A

primary sclerosing cholangitis (PSC)

  • no proven therapy exists
  • symptomatic treatment with steroids, bile salt chelators for pruritis
  • liver transplant
107
Q

female

  • 95% AMA positive
  • florid duct lesions and loss of small ducts only
A

primary biliary cirrhosis

108
Q

male

  • 70% associated with IBD
  • 65% ANCA positive
  • strictures and beading of large bile ducts, pruning of smaller ducts
A

primary sclerosing cholangitis

109
Q

occlusion of hepatic veins or IVC

  • caval webs (on venography), right sided heart failure
  • hypercoaguable state (75% of patients)
  • in India, China, South Africa is associated with poor standard of living
  • tender, painful hepatic enlargement (RUQ pain), jaundice, splenomegaly, ascites, nutmeg liver
  • imaging: prominent caudate liver lobe
  • screening test of choice is contrast-enhanced CEUS
  • color or pulsed-Doppler US
A

Budd-Chiari syndrome

- tx: symptomatic, sometimes anticoag or thrombolytic therapy

110
Q

painless jaundice, weight loss, steatorrhea

  • if there is pain, is worse at night laying down
  • trousseau sign of malignancy
  • courvoisier sign
  • CA19-9 elevated
A

pancreatic cancer

111
Q

conjugated hyperbilirubinemia

  • reduced excretory function of hepatocytes
  • benign, asymptomatic hereditary jaundice
  • gallbladder does not visualize on oral cholecystography
  • liver DARKLY PIGMENTED on gross exam
A

Dubin-Johnson syndrome

112
Q

conjugated hyperbilirubinemia

  • reduced hepatic reuptake of bilirubin conjugates
  • similar to Dubin-Johnson, but liver is NOT pigmented, and the gallbladder IS visualized on oral cholecystography
A

Rotor syndrome

113
Q

predominantly conjugated hyperbilirubinemia

  • cholestasis
  • benign cholestatic jaundice, usually occuring in third trimester of pregnancy
  • itching, GI symptoms, abnormal liver excretory function tests
  • cholestasis noted on liver biopsy
  • excellent prognosis, but recurrence with subsequent pregnancies or use of oral contraceptives
A

intrahepatic cholestasis of pregnancy

2.2Elizi ex 2 GI 2 Exam 2 COPY (6 decks)

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