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Gastrointestinal STEP 2 > Liver disease > Flashcards

Liver disease Flashcards

1
Q

all forms of chronic liver disease can produce

A
  1. ascites 2. coagulopathy 3. Asterixis (+ encephalopathy) 4. Hypoalbuminemia (+edema)
  2. spider angiomata + palmar erythema
  3. portal hypertension (–> varives)
  4. thrombocytopenia (from splenic sequestration)
  5. renal insufficiency (hepatorenal syndrome)
  6. hepatopulmonary syndrome
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2
Q

all cloating factor except … are made in liver

A

VIII

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3
Q

Ascites - paracentesis if

A
  1. new onset
  2. abdominal pain and tenderness
  3. fever
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4
Q

Serum ascites albumin gradient (SAAG is aka)

A

differencs or gradient between the serum and ascites

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5
Q

ascitis - causes regarding SAAG

A

if above 1.1 g/dL: infection, cancer

lower: Portal hypertension, CHF, hepatic vein thrombosis, constrictive pericarditis, Cirrhosis, nephrotic syndrome

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6
Q

ascitis - nephrotic syndrome - SAAG

A

according to MTB is above 1.1

according to medscape lower

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7
Q

spontaneous bacterial peritonitis (SBP)?

A

infection of the bowel without a perforation

we don’t actually know how bacteria gets there

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8
Q

spontaneous bacterial peritonitis (SBP) - organisms

A
  • E. coli is the MC
  • Anaerobes are rarely the cause
  • Pneumococcus also causes (for unknown reasons)
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9
Q

spontaneous bacterial peritonitis (SBP) - best initial test

A

cell count with more than 250 neutrophils is the basis upon which we start therapy (from abdominal cavity fluid)

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10
Q

spontaneous bacterial peritonitis (SBP) - gram stain

A

almost always negatie

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11
Q

spontaneous bacterial peritonitis (SBP) - most accurate test

A

fluid culture –> results are never available at the time we have to make a treatment decision

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12
Q

spontaneous bacterial peritonitis (SBP) - LDH

A

too nonspecific

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13
Q

spontaneous bacterial peritonitis (SBP) - treatment

A

cefotaxime or cefriaxone

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14
Q

spontaneous bacterial peritonitis (SBP) - recurrence

A

frequent

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15
Q

spontaneous bacterial peritonitis (SBP) - prophylaxis indcation

A
  1. ascitis when fluid albumin level is low
  2. all patients with SBP need lifelong prophylaxis
  3. all variceal bleeding
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16
Q

spontaneous bacterial peritonitis (SBP) - prophylaxis how

A

norfloxacin or TMP/SXM

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17
Q

spontaneous bacterial peritonitis (SBP) - treatment vs prophylaxis antibiotics

A

treatment: cefotaxime or cefriaxone
prophylaxis: norfloxacin or TMP/SXM

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18
Q

ascites + edema - treatment

A

spironolactone and other diuretics

serial paracenteses for large-volume ascites

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19
Q

coagulopathy and thrombocytopenia - treatment

A

FFP +/ platelets only if bleeding occurs

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20
Q

liver disease encephalopathy - treatment

A

lactulose + rifamixin

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21
Q

liver disease hypoalbuminemia - treatment

A

no specific therapy

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22
Q

spider angiomata + palmar erythema - treatment

A

no specific therapy

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23
Q

liver disease and varices - treatment

A

propranolol + banding via endoscopy

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24
Q

hepatorenal syndrome - treatment

A
  1. octreotide

2. midodrine (α1 agonist)

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25
Q

hepatopulmonary syndrome - treatment

A

no specific therapy

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26
Q

hepatopulmonary syndrome?

A

lung disease + hypoxia entirely on the basis of liver failure
Look for orthodeoxia

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27
Q

orthodeoxia?

A

hypoxia upon sitting upright

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28
Q

specific causes of cirrhosis

A
  1. Alcoholic liver disease
  2. primary biliary cirrhosis
  3. primary sclerosing cholangitis
  4. alpha 1-antitrypsin deficiency
  5. hemochromatosis
  6. chronic HBV + HCV
  7. wilson
  8. autoimmune hepatitis
  9. Nonalcoholic steatohepatitis or nonalcoholic fatty liver disease
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29
Q

Alcoholic liver disease - how to diagnose

A

it is a diagnosis of exclusion

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30
Q

Alcoholic liver disease - therapy

A

no specific therapy

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31
Q

Alcoholic liver disease - most accurate test

A

most of the causes of cirrhosis, except for sclerosing cholangitis, is liver biopsy

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32
Q

Alcoholic liver disease - specific lab characteristic

A

greater elevation in AST compared to ALT

BINGE drinking gives sudden rise in GGTP

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33
Q

binge drinking - lab test

A

sudden rise in GGTP

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34
Q

primary biliary cirrhosis - epidimiology

A

woman 40-50

associated with other autoimmune conditions (Sjogren, Hashimoto, CRREST, RA etc)

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35
Q

primary biliary cirrhosis - presentation

A
  • fatique and itching
  • xanthalesma/xanthoma
  • osteoporosis
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36
Q

primary biliary cirrhosis - labs

A
  • normal bilirubin –> elevated in in very far advanced
  • ## elevated ALP
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37
Q

primary biliary cirrhosis - tests

A
  • most accurate test: liver biopsy
  • most accurate blood test: antimitochondrial antibody
  • normal bilirubin and IgM –> elevated in in very far advanced
  • elevated ALP
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38
Q

primary biliary cirrhosis - treat with

A

ursodeoxycholic acid

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39
Q

primary biliary cirrhosis - antibodies

A

antimitochondrial antibody

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40
Q

primary sclerosing cholangitis - epidimiology

A

over 80% of primary sclerosing cholangitis occurs in association with IBD
middle aged men

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41
Q

primary sclerosing cholangitis - presentation

A
  1. pruritus

2. elevated ALP and GGTP as well as bilirubin levels

42
Q

primary sclerosing cholangitis - most accurate test (results?)

A

MRCP or ERCP –> beading, narrowing or strictures in the biliary system

43
Q

primary sclerosing cholangitis - MRCP vs ERCP

A

MRCP is generally done because there is no therapeutic need for ERCP

44
Q

primary sclerosing cholangitis - biopsy

A

you can iagnose it from biopsy if it was done for other reasons –> but is not essential foe establishing the diagnosis
primary sclerosing cholangitis is the only cause of cirrhosis for which a biopsy is not the most accurate

45
Q

primary sclerosing cholangitis - treatment

A

cholestyramine or ursodeoxycholic acid (same as primary biliary cirrhosis

46
Q

primary sclerosing cholangitis - association with IBD treatment

A

does not improve or reslove with IBD resolution

even after colectomy in UC, the patient may still progress to needing a liver transplantation

47
Q

primary sclerosing cholangitis vs primary biliary cirrhosis - biopsy image

A

primary sclerosing cholangitis –> concentric onion skin bile duct fibrosis –> alternating dilation of intra + extrahepatic
primary biliary cirrhosis –> granulomas of intralobular bile duct

48
Q

alpha 1-antitrypsin deficiency - look for

A

combination of liver disease and empysema ina young patient (under 40)

49
Q

alpha 1-antitrypsin deficiency - family

A

COPD in early age

50
Q

alpha 1-antitrypsin deficiency - treamtent

A

replace enzyme

51
Q

hemochromatosis - mechanism

A

genetic disroder leading to OVERABSORPTION of iron in the duodenum
(mutation in the C282y gene)

52
Q

hemochromatosis - men vs women

A

men present earlier than women because estruation delays the onset of liver fibrosis + cirrhosis

53
Q

hemochromatosis - presentation

A
  • fatique + joint pain (pseudogout)
  • erectile dysfunction in men, amenorrhea in women (from pituitary involvement)
  • skin darkening
  • diabetes
  • cardiomyopathy
54
Q

hemochromatosis - best initial test

A

iron studies that show:

  • increased serum iron + ferritin
  • decreased iron binding capacity
55
Q

hemochromatosis - most accurate test

A

liver biopsy for increased iron

56
Q

hemochromatosis - EKF

A

conduction defects

57
Q

hemochromatosis - Echo

A

dilated or restrictive cardiomyopathy

58
Q

hemochromatosis - routine testing

A

it may be found on routine testing with mildly abnormal liver function or iron levels

59
Q

hemochromatosis - infections

A
  1. vibrio vulnificus
  2. Yersinia
  3. Listeria
    because organisms feed on iron
60
Q

blood test are associated with hemochromatosis - next step

A

MRI (increased iron deposition o in the liver) + gene testing –> can spare the need for a liver biopy

61
Q

hemochromatosis - treatment

A

phlebotomy

2nd line: chelation: defeferoxamine, deferasirox, or deferiprone

62
Q

hemochromatosis - medications for chelation

A
  1. if cannot be managed with phlbotomy
  2. are anemic + hemochromatosis from overtransfusion such as thalassemia
    - -> deferasirox + deferiprone are huge breakthrough medications because they are effective orally
    - -> defeferoxamine has to be given lifelong by injection
63
Q

hemochromatosis - liver fibrosis - treatment

A

liver fibrosis can resolve if phlebotomy is begun before cirrhosis develops

64
Q

beside cirrhosis + cancer, both chronic HBV + HCV are also associated with

A

polyarteritis nodosa

65
Q

chronic hepatitis B - definition

A

surface antigen + for longer than 6 months

66
Q

chronic hepatitis B - e antigen - epidemiology

A

most patients are (+)

67
Q

HBV - best way to determine viral replication activity

A

PCR

68
Q

HBV - biopsy

A

biopsy to detect bridging necrosis no longer has any significant meaning

69
Q

HCV - becomes chronic

A

80%

70
Q

how to determine the time of HCV infection

A

no way

71
Q

the most accurate way to determining disease activity in HCV

A

PCR RNA viral load

72
Q

acute HCV is treated with

A

interferon, ribavirin, and either telaprevir or boceprevir

73
Q

hepatitis virus - biopsy

A

determines the degree of inflammation and fibrosis. It can help you understand the urgency for treatment is fibrosis is present or worsening
biopsy to detect bridging necrosis no longer has any significant meaning in HBV

74
Q

treatment of chronic HBV

A

one of the following

  1. adenofovir 2. lamivudine 3. Telbivudine
  2. Entecavir 5. Tenofovir 6. INF
75
Q

treatment of chronic HCV

A

use combination of ledipasvir and sofosbuvir
INF, ribavirin and boceprevir are added when treatment fails
Ribavirin and sofosbuvir can be used orally without INF in some cases

76
Q

treatment of chronic HCV vs HBV regarding the number of drugs

A

HBV –> 1

HCV never with 1

77
Q

Best way to follow chronic HCV + HBV

A

both with PCR

78
Q

goal for therapy for chronic HCV + HBV

A

sustained viral response or a permanently undetectable PCR viral load

79
Q

interferon SE

A

arthralgias, thrombocytopenia, depression, leukopenia

80
Q

Ribavirin SE

A

anema

teratogenic

81
Q

Adefovir - SE

A

renal dysfunction

82
Q

Lamivudine - SE

A

none

83
Q

Wilson disease - mechanism

A

disorder abnormality of decreased copper excretion from the body.
Because of decrease in ceruloplasmin, copper in not excreted and it builds up in the body in the LIVER, KIDNEY, RBCs, and NERVOUS SYSTEM

84
Q

Wilson - copper builds up in

A

LIVER, KIDNEY, RBCs, and NERVOUS SYSTEM

85
Q

wilson disease - presentation (beside the common features of cirrhosis)

A
  1. neurological symptoms
  2. Coombs (-) hemolytic anemia
  3. renal tubular acidosis or nephrolithiasis
86
Q

wilson disease - neurological symptoms

A

psychosis, tremor, dysarthria, ataxia or seizures

87
Q

wilson disease - best initial test

A

slit-lamp examination for Kayser-Fleischer rings

88
Q

Kayser-Fleischer rings?

A

a brownish ring around the eye from copper deposition

89
Q

wilson disease which is the more sensitive and which is the most specific test to to detect abnormally increased heaptic copper

A

biopsy

90
Q

wilson disease - labs

A

ceruloplasmin is usually low

91
Q

wilson disease - the most accurate diagnostic test

A

looking at an abnormally increased amount of copper excretion into the urine after giving penicillamine

92
Q

wilson disease - decreased ceruloplasmin is not the most accurate test - WHY

A

all plasma proteins can be decreased in those with dysfunction + cirrhosis

93
Q

wilson disease - treatment (and explain)

A

penicillamine will chelate copper + remove it from the body. Additional therapies are:

  1. ZINC: interferes with intestinal copper absorption
  2. trientine: an alternate copper-chelating compound
94
Q

autoimmune hepatitis - epidemiology

A

look for women with signs of liver inflammation with a positive ANA

95
Q

autoimmune hepatitis - antibodies

A

ANA

96
Q

autoimmune hepatitis - treatment

A

prednisone and/or azathioprine

97
Q

autoimmune hepatitis - most specific test

A
  1. liver-kindey microsomal antibodies
  2. high gamma globulin (IgG)
  3. anti-smooth muscle antibodies
  4. anti-liver/kidney microsomal antivodies
98
Q

autoimmune hepatitis - most accurate test

A

liver biopsy

99
Q

Nonalcoholic steatohepatitis or Nonalcoholic fatty liver disease - very common cause of

A

mildly abnormal function tests

100
Q

Nonalcoholic steatohepatitis or Nonalcoholic fatty liver disease - most accurate test

A

biopsy: microvesicular fatty deposits you would find in alcoholic liver disease (but without history of alcohol)

101
Q

Nonalcoholic steatohepatitis or Nonalcoholic fatty liver disease - it is associated with

A
  1. obesity
  2. diabetes
  3. hyperlipidemia
  4. corticosteroids
102
Q

Nonalcoholic steatohepatitis or Nonalcoholic fatty liver disease - management

A
  1. exclude more serious liver disease
  2. correct the underling cause
  3. no specific drug therapy

Gastrointestinal STEP 2 (8 decks)

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