Liver disease Flashcards
(102 cards)
1
Q
all forms of chronic liver disease can produce
A
- ascites 2. coagulopathy 3. Asterixis (+ encephalopathy) 4. Hypoalbuminemia (+edema)
- spider angiomata + palmar erythema
- portal hypertension (–> varives)
- thrombocytopenia (from splenic sequestration)
- renal insufficiency (hepatorenal syndrome)
- hepatopulmonary syndrome
2
Q
all cloating factor except … are made in liver
A
VIII
3
Q
Ascites - paracentesis if
A
- new onset
- abdominal pain and tenderness
- fever
4
Q
Serum ascites albumin gradient (SAAG is aka)
A
differencs or gradient between the serum and ascites
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
6
Q
ascitis - nephrotic syndrome - SAAG
A
according to MTB is above 1.1
according to medscape lower
7
Q
spontaneous bacterial peritonitis (SBP)?
A
infection of the bowel without a perforation
we don’t actually know how bacteria gets there
8
Q
spontaneous bacterial peritonitis (SBP) - organisms
A
- E. coli is the MC
- Anaerobes are rarely the cause
- Pneumococcus also causes (for unknown reasons)
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)
10
Q
spontaneous bacterial peritonitis (SBP) - gram stain
A
almost always negatie
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
12
Q
spontaneous bacterial peritonitis (SBP) - LDH
A
too nonspecific
13
Q
spontaneous bacterial peritonitis (SBP) - treatment
A
cefotaxime or cefriaxone
14
Q
spontaneous bacterial peritonitis (SBP) - recurrence
A
frequent
15
Q
spontaneous bacterial peritonitis (SBP) - prophylaxis indcation
A
- ascitis when fluid albumin level is low
- all patients with SBP need lifelong prophylaxis
- all variceal bleeding
16
Q
spontaneous bacterial peritonitis (SBP) - prophylaxis how
A
norfloxacin or TMP/SXM
17
Q
spontaneous bacterial peritonitis (SBP) - treatment vs prophylaxis antibiotics
A
treatment: cefotaxime or cefriaxone
prophylaxis: norfloxacin or TMP/SXM
18
Q
ascites + edema - treatment
A
spironolactone and other diuretics
serial paracenteses for large-volume ascites
19
Q
coagulopathy and thrombocytopenia - treatment
A
FFP +/ platelets only if bleeding occurs
20
Q
liver disease encephalopathy - treatment
A
lactulose + rifamixin
21
Q
liver disease hypoalbuminemia - treatment
A
no specific therapy
22
Q
spider angiomata + palmar erythema - treatment
A
no specific therapy
23
Q
liver disease and varices - treatment
A
propranolol + banding via endoscopy
24
Q
hepatorenal syndrome - treatment
A
- octreotide
2. midodrine (α1 agonist)
25
hepatopulmonary syndrome - treatment
no specific therapy
26
hepatopulmonary syndrome?
lung disease + hypoxia entirely on the basis of liver failure
Look for orthodeoxia
27
orthodeoxia?
hypoxia upon sitting upright
28
specific causes of cirrhosis
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
29
Alcoholic liver disease - how to diagnose
it is a diagnosis of exclusion
30
Alcoholic liver disease - therapy
no specific therapy
31
Alcoholic liver disease - most accurate test
most of the causes of cirrhosis, except for sclerosing cholangitis, is liver biopsy
32
Alcoholic liver disease - specific lab characteristic
greater elevation in AST compared to ALT
| BINGE drinking gives sudden rise in GGTP
33
binge drinking - lab test
sudden rise in GGTP
34
primary biliary cirrhosis - epidimiology
woman 40-50
| associated with other autoimmune conditions (Sjogren, Hashimoto, CRREST, RA etc)
35
primary biliary cirrhosis - presentation
- fatique and itching
- xanthalesma/xanthoma
- osteoporosis
36
primary biliary cirrhosis - labs
- normal bilirubin --> elevated in in very far advanced
- elevated ALP
-
37
primary biliary cirrhosis - tests
- most accurate test: liver biopsy
- most accurate blood test: antimitochondrial antibody
- normal bilirubin and IgM --> elevated in in very far advanced
- elevated ALP
38
primary biliary cirrhosis - treat with
ursodeoxycholic acid
39
primary biliary cirrhosis - antibodies
antimitochondrial antibody
40
primary sclerosing cholangitis - epidimiology
over 80% of primary sclerosing cholangitis occurs in association with IBD
middle aged men
41
primary sclerosing cholangitis - presentation
1. pruritus
| 2. elevated ALP and GGTP as well as bilirubin levels
42
primary sclerosing cholangitis - most accurate test (results?)
MRCP or ERCP --> beading, narrowing or strictures in the biliary system
43
primary sclerosing cholangitis - MRCP vs ERCP
MRCP is generally done because there is no therapeutic need for ERCP
44
primary sclerosing cholangitis - biopsy
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
primary sclerosing cholangitis - treatment
cholestyramine or ursodeoxycholic acid (same as primary biliary cirrhosis
46
primary sclerosing cholangitis - association with IBD treatment
does not improve or reslove with IBD resolution
| even after colectomy in UC, the patient may still progress to needing a liver transplantation
47
primary sclerosing cholangitis vs primary biliary cirrhosis - biopsy image
primary sclerosing cholangitis --> concentric onion skin bile duct fibrosis --> alternating dilation of intra + extrahepatic
primary biliary cirrhosis --> granulomas of intralobular bile duct
48
alpha 1-antitrypsin deficiency - look for
combination of liver disease and empysema ina young patient (under 40)
49
alpha 1-antitrypsin deficiency - family
COPD in early age
50
alpha 1-antitrypsin deficiency - treamtent
replace enzyme
51
hemochromatosis - mechanism
genetic disroder leading to OVERABSORPTION of iron in the duodenum
(mutation in the C282y gene)
52
hemochromatosis - men vs women
men present earlier than women because estruation delays the onset of liver fibrosis + cirrhosis
53
hemochromatosis - presentation
- fatique + joint pain (pseudogout)
- erectile dysfunction in men, amenorrhea in women (from pituitary involvement)
- skin darkening
- diabetes
- cardiomyopathy
54
hemochromatosis - best initial test
iron studies that show:
- increased serum iron + ferritin
- decreased iron binding capacity
55
hemochromatosis - most accurate test
liver biopsy for increased iron
56
hemochromatosis - EKF
conduction defects
57
hemochromatosis - Echo
dilated or restrictive cardiomyopathy
58
hemochromatosis - routine testing
it may be found on routine testing with mildly abnormal liver function or iron levels
59
hemochromatosis - infections
1. vibrio vulnificus
2. Yersinia
3. Listeria
because organisms feed on iron
60
blood test are associated with hemochromatosis - next step
MRI (increased iron deposition o in the liver) + gene testing --> can spare the need for a liver biopy
61
hemochromatosis - treatment
phlebotomy
| 2nd line: chelation: defeferoxamine, deferasirox, or deferiprone
62
hemochromatosis - medications for chelation
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
hemochromatosis - liver fibrosis - treatment
liver fibrosis can resolve if phlebotomy is begun before cirrhosis develops
64
beside cirrhosis + cancer, both chronic HBV + HCV are also associated with
polyarteritis nodosa
65
chronic hepatitis B - definition
surface antigen + for longer than 6 months
66
chronic hepatitis B - e antigen - epidemiology
most patients are (+)
67
HBV - best way to determine viral replication activity
PCR
68
HBV - biopsy
biopsy to detect bridging necrosis no longer has any significant meaning
69
HCV - becomes chronic
80%
70
how to determine the time of HCV infection
no way
71
the most accurate way to determining disease activity in HCV
PCR RNA viral load
72
acute HCV is treated with
interferon, ribavirin, and either telaprevir or boceprevir
73
hepatitis virus - biopsy
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
treatment of chronic HBV
one of the following
1. adenofovir 2. lamivudine 3. Telbivudine
4. Entecavir 5. Tenofovir 6. INF
75
treatment of chronic HCV
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
treatment of chronic HCV vs HBV regarding the number of drugs
HBV --> 1
| HCV never with 1
77
Best way to follow chronic HCV + HBV
both with PCR
78
goal for therapy for chronic HCV + HBV
sustained viral response or a permanently undetectable PCR viral load
79
interferon SE
arthralgias, thrombocytopenia, depression, leukopenia
80
Ribavirin SE
anema
| teratogenic
81
Adefovir - SE
renal dysfunction
82
Lamivudine - SE
none
83
Wilson disease - mechanism
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
Wilson - copper builds up in
LIVER, KIDNEY, RBCs, and NERVOUS SYSTEM
85
wilson disease - presentation (beside the common features of cirrhosis)
1. neurological symptoms
2. Coombs (-) hemolytic anemia
3. renal tubular acidosis or nephrolithiasis
86
wilson disease - neurological symptoms
psychosis, tremor, dysarthria, ataxia or seizures
87
wilson disease - best initial test
slit-lamp examination for Kayser-Fleischer rings
88
Kayser-Fleischer rings?
a brownish ring around the eye from copper deposition
89
wilson disease which is the more sensitive and which is the most specific test to to detect abnormally increased heaptic copper
biopsy
90
wilson disease - labs
ceruloplasmin is usually low
91
wilson disease - the most accurate diagnostic test
looking at an abnormally increased amount of copper excretion into the urine after giving penicillamine
92
wilson disease - decreased ceruloplasmin is not the most accurate test - WHY
all plasma proteins can be decreased in those with dysfunction + cirrhosis
93
wilson disease - treatment (and explain)
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
autoimmune hepatitis - epidemiology
look for women with signs of liver inflammation with a positive ANA
95
autoimmune hepatitis - antibodies
ANA
96
autoimmune hepatitis - treatment
prednisone and/or azathioprine
97
autoimmune hepatitis - most specific test
1. liver-kindey microsomal antibodies
2. high gamma globulin (IgG)
3. anti-smooth muscle antibodies
4. anti-liver/kidney microsomal antivodies
98
autoimmune hepatitis - most accurate test
liver biopsy
99
Nonalcoholic steatohepatitis or Nonalcoholic fatty liver disease - very common cause of
mildly abnormal function tests
100
Nonalcoholic steatohepatitis or Nonalcoholic fatty liver disease - most accurate test
biopsy: microvesicular fatty deposits you would find in alcoholic liver disease (but without history of alcohol)
101
Nonalcoholic steatohepatitis or Nonalcoholic fatty liver disease - it is associated with
1. obesity
2. diabetes
3. hyperlipidemia
4. corticosteroids
102
Nonalcoholic steatohepatitis or Nonalcoholic fatty liver disease - management
1. exclude more serious liver disease
2. correct the underling cause
3. no specific drug therapy
