Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

► Med Notes > GI Clin Med liver > Flashcards

GI Clin Med liver Flashcards

1
Q

Hepatitis

A

Inflammation of the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What can cause hepatitis

A

Hep A, B, C, D, E

Drugs and toxic agents

*clinical manifestations may be similar regardless of cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

True liver function tests

A

PT/INR
Albumin
Cholesterol

*alt/ast and alp and bilirubin ldh and get can come from other places “liver tests”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What causes mile elevations in ALT

A

Chronic hep b, c, d

Acute viral hep (A-E, EBV, CMV)

Steatosis/steatohepatitis

Hemochromatosis

Medications/toxins

Autoimmune hepatitis

Alpha-1 antitrypsin defiency

Wilson disease

Celiac disease

Glycogenic hepatopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Mild elevations AST

A

Alcohol related liver injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Nonhepattic mild elevations

A

Strenuous exercise

Hemolysis
Myopathy
Thyroid disease
Macro-ast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Severe elevations ast/alt

A 
Acute viral hepatitis a-e
Medications/toxins
Ischemic hepatitis
Wilson
Acute bile duct obstruction
Acute budd chairi syndrome
Hepatic artery ligation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Non hepatic sources bilirubin

A

Rbc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Non hepatic sources ast

A

Skeletal msucles, cardiac muscle, rbc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Non hepatic sources alt

A

Skeletal muscle, cardiac muscle, kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Nonhepatic source led

A

Heart, rbc,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Non hepatic source alkaline phosphatase

A

Bone, first trimester placenta, intestines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Hepatocellular disease-primary injury to hepatocytes

A

Ast, alt higher than alkaline phosphatase

Elevated direct bilirubin

Elevated or normal indirect bilirubin

Associated liver enzymes often elevated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Cholestatic liver disease-injury to bile ducts

A

Alkaline phosphatase higher than AsT, ALT

Elevation of alkaline phosphatase with near normal ast, alt levels

Normal direct bilirubin

Elevated indirect

No abnormal liver tests; no anemia, onset in late adolescence, fasting makes bilirubin rise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Hemolysis

A

Normal direct bilirubin

Elevation represents more than 90% of total bilirubin

Anemia usual; increased reticulocyte count, normal liver enzyme levels (LDH may be up)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Overall hepatocellular

A

ALT >AST

Both up

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cholestasis

A 
ALP up(if isolated consider bone involvement)
Check get
Elevated alp
Failure of bile to reach duodenum
Jaundice and pruritus
Pure cholstatsis 
Oral contraceptives, anabolic steroids sex hormones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Non inflammatory drug induced cholestasis

A

Anabolic steroids, azathripine, cyclosporine, estrogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Inflammatory drug induced cholestasis

A

Amoxicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Clinical presntation viral hepatitis

A

Malaise, nausea, vomiting, diarrhea, low grade fever followers by dark urging, jaundice and tender hepatomegaly; may be subclinical and detected on basis of elevated aspartate and alanine levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Hep a

A

Ss RNA hepatovirus (picornavirus family0

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Prodrome hep a

A

Anorexia, nausea, vomiting, malaise, aversion to smoking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Duration hep a

A

2-3 weeks

Complete clinical 9 weeks recovery 6-12 months no clinical sequelae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Risk factor hep a

A

1 international travel contaminated water or food, including inadequately cooked shellfish

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Symptoms hep a

A

Fever, malaise, myalgia, arthralgias, easy fatigability, upper respiratoy symptoms, anorexia, enlarged and tender liver, jaundice , nausea, vomiting, diarrhea or constipation

More severe in adults

Ab pain RUQ or epigastric

Alcoholic stools

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Transmission hep a

A

Fecal oral
Poor sanitation crowding
Excreted in feces for up to 2 weeks before clinical illness but rarely after the first week of illness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Labs hep a

A

Markedly elevated AST ALT

Elevated bilirubin and ALP-cholestasis

Anti hAC IgM early later IgG

Acute hep-IgM diagnose igG-protective and previous exposure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Vaccine HAV

A

Yup

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Hep with fulminant

A

ABD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Hep B

A

Hepadna virus partially dsDNA inner core and outer surface coat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Prodrome hep b

A

Anorexia, nausea, vomiting, malaise, aversion to smoking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Duration hep B

A

Acute illness usually subsides over 2-3 weeks->complete clinical laboratory recovery 16 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Risk factors hep b

A 
MSM
Inject drugs HIV
Hemodialysis
Physicians, dentists, nurses, personnel working in clinical and pathology laboratories and blood bands 
Incarcerated
STD
Blood transfusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Symptoms hep b

A

Fever low grade, enlarged and tender liver, jaundice

Asymptomatic w/o jaundice->a fulminating disease and death

Glomerulonephritis, serum sickness, and polyarthritis nodosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Transmission hep b

A

Blood or blood products
Sex
Perinatal Asia africa

HBsAg positive mothers 90% transmit to baby

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Labs hep b

A

Markedly elevated ALT AST easily higher than HAV

No cholestasis so ALP and bilirubin normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Vaccine HBV

A

Ok

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What percent of hep b is acute vs chronic

A

90% acute

10% chronic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Mortality hep b

A

Fulminant hepatitis less than 1% with mortality 60%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Prevent hep b

A

Vaccine

HBIG if exposure in unvaccinated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

HBc-AB IgG

A

Prior infx

Chronic infx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

HBsAg

A

Surface antigen, first evidence, positive during acute and carrier (chronic)

Before biochemical evidence of liver disease and persisting throughout the clinical illness

Persistence of HBsAg more than 6 months after the acute illness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

HBsAb

A

Surface antibody, immunity

Appears after clearance of HBsAg and after successfulvaccination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

HBcAg

A

Core antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

HBcAb IgM

A

Appears shortly after HBsAg is detected, ONLY THING DETECTABLE DURING GAP WINDOW PERIOF->CONSIDERED ACUTE HBV

Diagnose acute

Reappear during flares of previously inactive chronic hep b

IgG also persists but persists indefinitely

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

HBcAb IgG

A

Appears during late in acute phase and persists indefinitely, whether goes on to chronic infection or immunity (prior infx)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

HBeAg

A

Viral proliferation and infect iv its
+ acute and active chronic
Negative inactive chronic

Secretory form of HBcAg ->viral rep and infectivity

If persist beyond three months->chronic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

HBV DNA

A

Detectable during current infection, typically parallels the presence of HBeAg, more sensitive and precise marker of viral replication

More sensitive precise marker of viral replication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Hep D

A

Defective RNA virus needs HBV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Risk factor Hep D

A

HBV endemic Mediterranean basin ; spread predominantly by non percutaneous means

Nonendemic areas-spread percutaneous lh in HBsAg IV drug users or hemophiliac transfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Labs HDV

A

Ani HDV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Vaccine hepD

A

Vaccinate against hep b

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Mortality hep d

A

Enhances severity of HBV infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Hep E

A

RNA hepevirus hepevirdae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Risk factors hep e

A

Epidemic form in Asia, the Middle East, and North Africa, Central America , India

Pet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Tramsioson hep e

A

Enteric, cooked organ meat, spread by swine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Labs hep e

A

IgM anti HEV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Vaccine HEV

A

Approved in china

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Acute HEV chronic

A

Acute

But in transplant patients treated with tacrolimus instances of chronic with progression to cirrhosis have been reported

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Mortality hep e

A

Pregnant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Hep c

A

Flavivirus ss RNA Chronic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Risk factors hep c

A

HIV
Transfusion
Body piercing and tattooed, hemodialysis

Hospital and outpatient facility acquired transmission-re use syringes in caths

Unsafe medical practices

Bloody fisticuffs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Symptoms hep c

A

Mild and asymptomatic fluctuating elevations of serum ALT AST

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Labs hep c

A

HCV RNA

Enzyme immunoassay that detects antibodies to HCV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is someone has HCV ins drum, without HCV RNA in serum

A

Recovery from prior HCV infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Vaccine hep c

A

No but chronic carriers should be vaccinated against HAV HBV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Complications HCV

A

Cirrhosis, hepatocellular carcinoma, HIV coinfection, cryoglobulinemia and membranoproliferative glomerulonephritis, lichen Plano’s, autoimmune thyroiditis, lymphocytes sialadentis, idiopathic pulmonary fibrosis, sporadic porphyria cutaneous tarda, monoclonal gammatopathies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Prevent HCV

A

Test donated blood
Screen baby boomers
Safe sex
Don’t share razors of tooth brush

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Treat hep c

A

Curable with proper treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Chronic hepatitis

A

At least 6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Etiology chronic hepatitis

A

Hepatitis B virus, hep C, hep D, drugs (methyldopanitrofurantoin, isoniazid, dantrolene), autoimmune hepatitis, Wilson’s, hemochromatosis, a1-antitrypsin defiency)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Chronic hepatitis grade

A

Histologic assessment of necrosis and inflammatory activity based on exam of liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

State chronic hepatitis

A

Reflects the level of disease progression and is based not he degree of fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Presentation chronic hepatitis

A

Asymptomatic ALT AST Elevations
Acute fulminant
Fatigue, malaise, anorexia, low grade fever, jaundice , ascites, varices bleeping, encephalopathy, coagulopathy, hypersplenium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

When do people with chronic hepatitis get extrahepatic manifestations

A

HBV-urticaria, arthritis, polyarthritis nodosa, vasculitis, polyneuropathy, glomerulonephritis

HCV-mixed cryoglobulinemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

How ID presence or absence of fibrosis in chronic hep

A

Serum fibrosure and/or US elastography

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Toxic and drug induced hepatitis dose dependent

A

Onset in 48 hours, predictable , necrosis around terminal hepatic venue

Mushroom poisoning, acetaminophen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Toxic and drug induced hepatitis idiosyncratic

A

Variable dose and time of onset
Small number of exposed persons affected

May be associated with fever, rash, arthralgias, eosinophilia

Ioniazid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Treat toxic and drug induced hepatitis

A

Supportive -withdraw agent, gastric lovage and oral administration of charcoal
Liver transplant

Acetaminophen overdose, sulfhydryl compounds, use remark Matthew nomogram
-start therapy in 8 hours if ingestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Fulminant hepatitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Causes of fulminant hepatitis

A 
ABCDE
Drugs
Ischemia
Budd chiari syndrome
Idiopathic chronic active hep
Acute Wilson’s disease
Reye’s syndrome acute fatty liver of pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Clinical fulminant hepatitis

A

Encephalopathy
Rapidly shrinking liver side, raising bilirubin, prolongation PT, clinical signs of confusion, disorientation, somnolence, ascites and edema-hepatic failure with encephalopathy, ALT AST fall
Cerebral edema,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Mortality fulminant hepatitis

A

Common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Treat fulminant hepatitis

A

Maintain fluid balance, support of circulation and respiration, control bleeding, correction of hypoglycemia, and tratment of other complications of the comatose state in anticipation of liver regeneration and repair

Restrict protein intake
Oral lactulose or neomycin
Prophylactic antibiotics -improves survival
Liver transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Alcoholic liver disease

A

80 mg a day men 30-40 mg a day women

Often denied in exam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Men or women more susceptible to get advanced liver disease with less alcohol intake

A

Women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Cofactors in alcoholic liver disease

A

Hep B and B malnutrition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Fatty liver alcohol

A

Asymptomatic and goes away with stopping alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Alcoholic hepatitis

A

Asymptomatic->severe liver failure with jaundice, ascites, GI bleeding and encephalopathy
Anorexia, nausea, vomiting, fever, jaundice, tender hepatomegaly, RUQ pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Alcoholic hepatitis AST ALT

A

AST ALT 2:1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Diagnosis alcoholic hepatitis

A

Biopsy hepatocyte swelling, mallory denk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Adverse prognosis alcoholic hepatitis

A

Critically ill
A maddreys discriminates function (PT and serum bilirubin involved)-over 32 associated with poor prognosis

MELD score of end stage liver disease->21 is also significant mortality

Glasgow alcoholic hepatitis scare-predicts mortliaity based on age, serum bilirubin, BUN, prothrombin time, and WBC
Over 9 who receive glucocorticoids had higher survival rates compared to those that didn’t

Ascites, varices hemorrhage, encephalopathy, hepatorenal syndrome poor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Lab of alcoholic hepatitis

A 
Mild liver enzymes
Anemia
Leukocytosis
Leukopenia
Thrombocytopenia
ALP GGT up
PT up
Depressed albumin and gamma globulin up
Increased transferrin saturation, hepatic iron stores, and sideroblastic anemia
Folic acid defiency by
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Imaging hepatic alcoholic

A

UD exclude biliary obstruction and identifies subclinical ascites
CT IV MRI
Serum fibrosure and or US elastography can identify presence or absence of fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Liver biopsy of alcoholic hepatitis is identical to what

A

Non alcoholic steatohepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Treat alcoholic hepatitis

A

Abstinence is essential
Multivitamin
G;ucose administation increases thiamine requirement and can precipitate wernicke korsakoff syndrome if thiamine is not co administered

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Wernicke encephalopathy

A

Confusion, ataxia, involuntary abnormal eye movements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Korsakoff syndrome

A

Severe memory issues

Confabulation/make up stories to fill in the gaps

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Treat korsakoff

A

Correct K Mg and phosphate deficiencies

Transfusions of packed rbc, plasma as necessary
Monitor glucose

Severe alcholic hepatitis(discrimination function>32 MELD >20) steroids

Pentoxifylline increase survival

Liver transplantation-but must obstinate from alcohol for 6 months to be considered

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Non alcoholic fatty liver disease

A

Asymptomatic elevated ALT AST hepatomegaly
Steatosis without fibrosis

Common 20-45% of Americans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Causes oris factors non alcoholic fatty liver disease

A

Obesity, DM, hyper TG, insulin resistance

Hispanic

Vinyl chloride

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Histology non alcoholic fatty liver

A

Focal infiltration by polymorphonuclear neutrophils and mallory hyaline similar to non alcoholic steatohepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Symptoms NAFLD

A

Asymptomatic mild URQ discomfort

Hepatomegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Lab NALFLD

A

Milf elevation ALT AST

Maybe normal though

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Imaging NAFLD

A

CT< US< MRU see macrovascular steatosis

MRU-quantify fat content

US elastography-assess liver stiffness can be used to estimate hepatic fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Primary biliary cirrhosis

A

Progressive non supportive destructive intrahepatic cholangitis
Chronic
Autoimmune destruction
FEMALE over 50

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Symptoms primary biliary cirrhosis

A

Asymptomatic isolated elevation in ALP or impaired bile excretion->liver failure and cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Risk of primary biliary cirrhosis

A

UTI
Smoking
Hormone replacement therapy
Hair dye

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Clinical manifestations PBC

A

Pruritus, fatigue, jaundice, xanthelasma, osteoporosis, steatorrhea, skin hyperpig, portal hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Associated disease PBC

A

Sjirgen autoimmune

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Diagnose PBC

A

AMA 90%

ALP GGT bilirubin, cholesterol IgM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Treat PBC

A

Ursodeoxycholic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Autoimmune hepatitis 1

A

More common
Anti smooth msucle antinuclear
Antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Type II autoimmune hepatitis

A

Women

Antiliver.kidney microsomal antibodies anti LKM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Clinical manifestation autoimmune hepatitis type I

A

Women
Abrupt onset 1.3 insidious 2/3

Progressive jaundice, anorexia, hepatomegaly, abdominal pain, epistaxis, ever, fatigue

Healthy woman-spider telangiectasia, cutaneous striae, acne, hirstisum, hepatomegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Autoimmune hepatitis and cirrhosis

A

Leads to itwhich causes death if untreated risk of hepatocellular cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Extrahepatic manifestations autoimmune hepatitis

A

Rash, arthralgias, keratoconus TI is sicca, thyroiditis, hemolytic anemia, nephritis, UC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Treat autoimmune hepatitis

A

Glucocorticoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Hemochromatosis

A

Elevated iron saturation or serum ferritin or a FH
Most asymptomatic
Recognized after 5th decade

120
Q

What does hemochromatosis cause

A

Hepatic abnormalities, cirrhosis, heart failure, hypogonadism and arthritis

121
Q

Genetics hemochromatosis

A

HFE gene mutation AR

122
Q

Iron in hemochromatosis

A

Liver, pancreas, heart, adrenals, testes, pituitary, kidneys

123
Q

Symptomsand signs of hemochromatosis

A

Earlier in men
Early-fatigue
Later-arthropathy, hepatomegaly, hepatic dysfunction, KSIN pigmentation, cardiac enlargement, DM

124
Q

Hemochromatosis increased risk for infection with what

125
Q

Lab hemochromatosis

A

Milf ALT AST
Elevated iron and transferrin saturation
Elevated ferritin

126
Q

Imaging hemochromatosis

A

MRI CCT overload iron

MRI quantitiate

127
Q

Liver biopsy hemochromatosis

A

Homozygous C282Y

Serum ferritin less than 1000, serum AST normal, hepatomegaly absent

128
Q

Risk factors hemochromatosis

A

Male sex, excess alcohol consumption and DM

129
Q

Screen HFE

A

All first degree family members

130
Q

Treat hemochromatosis

A

Avoid foods rich in iron such as red meat, alcohol, vitamin C, raw shellfish, and supplemental iron

PHLEBOTOMIES every week

Monitor hematocrit and serum iron

Chelating agents deferoxamine for patients with hemochromatosis and anemia or secondary iron overload tue to thalassemia who cant tolerate phlebotomies

131
Q

Complications hemochromatosis

A

Anthropathy, DM, heart disease, portal hypertension, fibrosis, cardiac conduction defects and insulin requirements

132
Q

Wilson disease

A

AR under 40

Excessive deposition of Copper in liver and brain

133
Q

Serum ceruloplasmin urine copper wilson

A

Serum ceruloplasmin low

Urinary excretion high

134
Q

Genetic wilson

A

ATP7B

Heterozygous ok

135
Q

Where is copper in wilson

A

Copper deposition, espicially in the liver, brain, cornea, and kidney

136
Q

Who do we consider Wilson’s in

A

Liver disease in adolescents and neuropsychiatric disease in young adults

Any young kid with hepatitis, splenomegaly with hypersplenism, Coombs negative hemolytic anemia, portal hypertensiona nd neurologic psychiatric abnormalities

137
Q

Neuro wilson basal ganglia

A

Akinetic rigid Parkinsonism , tremor, ataxia , dystonia syndrome , dysarthria, dysphagia, migraines, seizures

Behavior and personality changes

138
Q

Diagnose wilson

A

Low ceruloplasmin, high urine copppper up
Jayden flies her
MRI brain increased basal ganglia and brainstem and cerebellar copper
ATB 7B

139
Q

Budd chiari

A

Tender, painful hepatic enlargement RUQ pain jaundice, splenomegaly, ascites, frequently complicated by hepatocellular carcinoma

140
Q

Imaging budd chiari

A

Occlusion/absence of flow in hepatic vein or inferior vena cave

141
Q

What predisposes a patient to budd chiari

A

Hereditary and acquired hypercoagulable states
(Polycythemia very, specific mutation V617F) in gene of JAK2

Thrombosis-activated protein C resistance (factor V Leiden mutation, protein C or S or antithrombin defiency,

142
Q

Liver and budd chiari

A

Canal webs->right sided heart failure->NUTMEG LIVER

143
Q

In India china and South Africa, what is budd chiari syndrome associated with

A

Poor standard of living

144
Q

Presentation budd chiari

A

Fulminant, acute, subacute or chronic

Mainly subacute

145
Q

With chronic disease what complications from budd c

A

Bleeding varices, hepatic encephalopathy, hepatopulmonary syndrome

146
Q

Imaging budd chiari

A

Prominent caudate lobe
Contrast enhanced CEUD

Pulsed Doppler US
MRI-see obstructed vein

Direct venography-delineate canal webs and occluded hepatic veins (spider web pattern ) most precisely

147
Q

Liver biopsy budd c

A

Percutaneous or transjugular

Nutmeg-ventricular congestion and fibrosis

148
Q

Alpha 1 anti trypsin

A

AR

Accumulated in hepatocytes causing liver damage and decreased levels of protease inhibitors

149
Q

PiM

150
Q

PiS

A

Mildly recused

151
Q

PIX

A

Homozygous severe reduction in enzyme

152
Q

How does alpha 1 antitrypsin cause increased risk of HCC

A

Micronodular cirrhosis

153
Q

Presentation a1 antitrypsin

A

Baby-liver fail-liver transplan
Older-pulmonary emphysema at young age
Don’t smoke and liver transplant

154
Q

Ischemic hepatitis

A

Ischemic hepatopathy, hypoxichepatitis, shock. Liver, acute cardiogenic liver injury

Acute fall in cardiac output due to MI, arrhythmia, septic or hemorrhagic shock, hypotension

155
Q

Treat ischemic hepatitis

156
Q

Hallmark ischemic hepatitis

A

ALT AST increased
Greater than 5000
Early rapid rise in the serum lactate dehydrogenase

Alp bilirubin mild
Jaundice worse outcomes

PPT prolonged, encephalopathy, or hepatopulmonary syndrome

157
Q

Mortality ischemis hepatitis

158
Q

Right heart failrue

A

Passive congestion liver nutmeg

Serum bilirubin up alp normal
ALT AST mild up
HEPATOJUGULAR REFLUX PRESENT WITH TRICUSPID REGURGIATION THE LIVER MAY BE PULSATILE
ASCITES(high SAAG serum ascites albumin gradient over 1)

Increased N terminal proBNP

159
Q

Causes of non cirrhosis portal hypertension

A

Portal vein thrombosis
Splenic vein obstruction
Schistomiasis

160
Q

Risk factors non cirrhosis portal hypertension

A

OC, preg, treatment f thrombocytopenia with eltrombopag

161
Q

Signs of non cirrhosis portal hypertension

A

Acute portal vein thrombosis causes abdominal pain
Splenomegaly
GI bleed

162
Q

Lab noncirrhotic portal hypertension

A

Normal
But hypercoagulable stage is found in many patients with portal vein thrombosis

JAK stat factor V Leiden mutation, protein C and S defiency

163
Q

Imaging non cirrhosis portal hypertension

A

Color Doppler US and contrast enhanced CT, MRA of portal system is generally confirmatory, EUS

164
Q

Treatnon cirrhotic, portal hypertension

A

Splenectomy
Anticoagulation particularly with low molecular weight heparin
Anti helmets

165
Q

Pyogenic hepatic abscess signs

A

Fever, RUQ pain, jaundice (charcots triad..)

Often ins eating of biliary disease

166
Q

How can the liver be invaded by bacteria:pyogenic hepatic abscess

A

Bile duct, portal vein, hepatic artery, direct extension, traumatic implantation

167
Q

Risk factors pyogenic hepatic abscess

168
Q

Pyogenic liver abscess

A

Increased risk of GI malignancy

169
Q

Ascending cholangitis

A

Resulting from biliary obstruction due to a stone , stricture, or neoplasm is most common identifiable cause of hepatic abscess in US

170
Q

Appendicitis diverticulitis

A

10% of liver abscess

171
Q

40% of liver abscesses

A

Dental source

172
Q

Most common organisms of pyogenic hepatic abscess

A

E. coli, klebsiella, proteus vulgarisms, enterobacter aerogenes, microaerophilic and anaerobic species

173
Q

Pyogenic hepatic abscess hepatocellular carcinoma

A

Rare can present as a pyogenic abscess because of tumor necrosis, biliary obstruction, and superimposed bacterial infection

174
Q

What must always be considered with pyogenic liver abscess

175
Q

Pyogenic hepatic abscess symptoms and signs

A

Insidious
Fever
Pain
Jaundice, tenderness RUQ,

176
Q

Labs pyogenic hepatic abscess

A

Leukocytosis with shift left
Normal liver test
Blood culture positice

177
Q

Imaging pyogenic hepatic abscess

A

Chest x ray-elevation diaphragm if abscess in right love
US, CT< MRI intrahepatic lesions
MRI-high signal intensity T2

178
Q

Cavernous hemangioma

A

Incidental finding US CT MRI
Enlarge in women on hormonal therapy
Surgical resection of cavernous hemangiomas is rarely necessary

179
Q

Focal nodular hyperplasia

A

All ages
Not oc
Asymptomatic
Hypercascular mass central stellate scar on CT MRI

Stain positive for glutamine synthetase with central stellate scare

Not a neoplasm

180
Q

Hepatocellular adenoma

A

Women 30-40
OC
Acute ab pain if tumor undergoes necrosis or hemorrhage
Occurs with glycogen storage disease and FAP

Hypovascular

181
Q

Hepatocellular Adelina microscopically

A

Consists of sheets of hepatocytes w/o portal tracts or central veins

182
Q

Clinical benign liver neoplasms-cavernous hemangioma adenoma

A

Palpable mass
Liver function normal
Arterial phase helical CT and multiphase dynamic MRI with contrast can distinguish an adenoma from focal nodular hyperplasia in 80-90% of cases

183
Q

Treat focal nodular hyperplasia

A

OC not discontinue
Should do US every teat for 2-3 years to ensure the lesion is not enlarging
Excellent prognosis

184
Q

Treat hepatocellular adenoma

A

Bleeding, necrosis, rupture——hormone therapy, third trimester, men

Resection is advised in all who is 5 cm

Discontinue OC get regression

Transarterial embolization is the initial treatment for adenomas complicated by hemorrhage

185
Q

Cirrhosis

A

Development of liver fibrosis , regenerative nodules, decreased liver function

Portal hypertension

186
Q

Cirrhosis reversible

A

If remove cause

187
Q

4 types of cirrhosis

A

Compensated, compensated with varices, decompensated

188
Q

Symptoms cirrhosis

A

Anorexia, nausea, vomiting, diarrhea, vague RUQ pain, fatigue, weak, ab pain glisson capsule , ascites,

189
Q

Signs cirrhosis

A 
Spider telangiectasia, palmar erythema, dupuytren contractures
Glossitis cheilosis (vitamin deficiencies)
Weigh loss
Jaundice
Capture Medusa
Ascites
Encephalopathy 
Fecer
190
Q

Labs cirrhosis

A 
Anemia
Pancytopenia
PT up
Hyponatremia, alkalosis
Glucose disturbances, hypoalbuminemia
191
Q

What decreases cirrhosis

A

Coffee tea

192
Q

Most common causes of cirrhosis

A

Alcohol
Chronic hepatitis C infection
NAFLD
Hepatitis B infection

193
Q

Most common genetic disorder that causes cirrhosis

A

Hemochromatosis

Also wilson, a1 antitrypsin, PBD, heart failure, autoimmune (SMA antiLKM)

194
Q

Diagnostic cirrhosis

A 
Viral hepatitis
Hemochromatosis
AMA primary biliary cirrhosis
SMA anti LKM autoimmune
Ceruloplasmin wilson
A1 anti

US-liver size

NEED BIOPSY

195
Q

Complications cirrhosis

A

CMP or hepatic function panel

PE for ascites and encephalopathy

196
Q

Problems with cirrhosis

A

DM and vitamin D defiency

197
Q

Portal hypertension

A

Increased hydrostatic pressure
Caused by increased intrahepatic resistance to the passage of blood flow through the liver together with increased splanchnic blood flow due to vasodilation within the splanchnic vascular bed

198
Q

Consequences of portal hypertension

A 
Varices with hemorrhage
Ascites
Hypersplanism
Hepatic encephalopathy
Spontaneous bacterial peritonitis
Hepatorenal syndrome 
Hepatocellular carcinoma
199
Q

EGD or capsule endoscopy

A

To determine whether varices are present

200
Q

Treat portal hypertension

A

Beta adrenergic blockers to reduce risk of hemorrhage in patients with small varices who have varices red wale marks or advanced cirrhosis (B or C)

201
Q

Symptoms esophageal varices

A

Bleeding,
Retching or dyspepsia
Varices DP not cause symptoms
UGIB0life threatening, most common cause of GIB due to portal HTN

202
Q

Risk of bleeding with esophageal varices

A

Size over 5 mm
Presence at endoscopy or red wale markings
Child score B or C
Active alcohol cause

203
Q

Diagnose esophageal varices

A

Upper endoscopy

204
Q

Treat esophageal varices

A

60% recur

Acute resuscitation in ICU
Rapid rectus situation with fluids and blood products

-give fresh frozen plasma or platelets be patients have coagulopathy duct to cirrhosis
VK intravenous! For abnormal prothrombin time

205
Q

Antibiotic prophylaxis esophageal varices

A

Don’t want gram negative infection-50% get
Fluoroquinolone or IV third generation cephalosporins

Reduce risk of serious infection in 10-20% as well as hospital mortality, espicially in patients with child Pugh C

206
Q

Esophageal varices and somatostatin and octreotide

A

Infusions reduce portal pressures vasoactive drugs

207
Q

Lactulose esophageal varices

A

Encephalopathy may complicate GIB in patients with severe liver disease

208
Q

Prevent re bleed

A

Nonselective beta adrenergic blockers (propranolol, nadolol) reduce risk or rebleeding

Long term treatment with band ligation reduces

209
Q

Emergent endoscopy esophageal varices

A

Hemodynamically stable with active bleeding->endotracheal intubibation to protect against aspiration during endoscopy

Preformed to exclude other or associated causes of UGIB -immediate banding

210
Q

Complications emergent endoscopy

A

20-30% chest pain, fever, bacteremia, esophageal ulceration, stricture, perforation

211
Q

Balloon tube tamponade esophageal varices

A

Mechanical tamponade with specially designed nasogastric tubes containing large gastric and esophageal balloons -Minnesota or sengstaken blkemore tubes

212
Q

Balloon tube tamponade effectiveness

A

Initial control of active hemorrhage in 60-90% rebleeding in 50%

213
Q

Complications balloon tube tamponade

A

Prolonged inflation

Esophageal and oral ulceration , perforation, aspiration, airway obstruction

214
Q

Why is balloon tube tamponade a temporary measure in patients not controlled with pharm or endoscopic technique

A

High rate of complications

215
Q

What must be done before balloon tube tamponade

A

Endotracheal intubation

216
Q

Transvenous intrahepatic portoystemic shunt

A

Over a wire that is passed through a catheter inserted in the jugular vein, an expandable wire mesh stent is passed through the liver parenchyma, creating a portosystemic shunt from the portal vein to the hepatic vein

217
Q

TIPS effectiveness

A

Control acute hemorrhage in over 90% of patients
Increased risk of encephalopathy
Lowers risk of rebleeding but not mortality

218
Q

Who gets TIPS

A

Recurrent episodes of varices bleeding that have failed endoscopic or pharm therapies

219
Q

Liver transplant varices

A

Treat with band ligation or TIPS to control bleeding pre transplant

220
Q

Hepatic encephalopathy

A

Altered mental status and cognitive function occurring in presence of liver failure

Acute reversible, chronic and progressice

221
Q

States of encephalopathy

A

Mild confusion, drowsiness, stupor, coma

222
Q

Diagnose hepatic encephalopathy with clinical features

A

Confusion, slurred speech, change in personality, violent and hard to manage, sleepy and difficult to arouse, asterixis——coma

Encephalapp-stoop test ask name color of written word

223
Q

Pathophysiology hepatic encephalopathy

A

Gut derived neurotoxins ammonia elevated not removed by liver

But severity not due to height of ammonia levels

224
Q

Precipitates hepatic encephalopathy

A

GI bleeding, azotemai, constipation, high protein diet

225
Q

Treat hepatic encephalopathy

A

Remove precipitates and orrect electrolyte imbalances

Lactulose -colonic acidification and diarrhea-WANT THIS want to increase stools

Liver transplant

226
Q

Ascites cirrhosis cause

A

Portal hypertension; hypoalbuminemia

Urinary Na concentration low

Free water excretion impaired->hyponatremia

227
Q

Two categories of ascites

A 
Normal peritoneum
Diseased peritoneum(More common with portal HTN and cirrhosis)
228
Q

Signs and symptoms ascites

A

Increasing abdominal girth
Elevated jugular venous pressure, right sided heart fail, large tender liver (budd, acute alcoholic hep), asterisks, anasarca, shifting dullness

229
Q

Risk factors ascites

A

Alcohol transfusion tattoos, injection drug use, history or viral hep, jaundice, birth in endemic area of hepatitis

230
Q

Diagnose ascites

231
Q

Labs ascites

A

Abdominal paracentesis -new onset and has cirrhosis and ascites

When patients deteriorate to exclude bacterial peritonitis

232
Q

White cell in ascites

A

Spontaneous bacterial peritonitis

Over 500 leukocytes
Over 250 PMC

TB or peritoneal carcinomatosis

233
Q

Albumin and total protein in ascite

A

SAAG portal HTN 1.1
Non portal hypertension lesss than 1.1

Subtract ascites fluid albumin from serum albumin

234
Q

Culture and gram stain ascites

A

Aerobic and anaerobic culture

235
Q

imaging ascites

A

US distinguish ascites with portal and nonportal
Doppler-budd c
LAD-

CT-see causes of portal and nonportal , see budd c, LAD

236
Q

SAAG greater than or equal to 1.1

A

Portal hypertension
-hepatic congestion (heart failure, constrictive pericarditis, tricuspid insuffiency, budd C, Venmo occlusive)

or liver disease (cirrhosis, alcoholic hep, fulminant hepatic failure, fibrosis

237
Q

SAAG less than 1.1

A 
Diseased peritoneum (bacterial, TB, fungal, HIV)
Infections, malignant (carcinomatosis, mesothelioma, pseudomyxoma, cancer)
238
Q

SAAG less than 1.1 hypoalbuminemia

A

Nephrotic syndrome
Protein losing enteropathy
Severe malnutrition

239
Q

Miscellaneous conditions SAAG less than 1.1

A

Myxedema greater than 1.1!!

Rest pancreatic, bile, nephrotoxicity, ovarian disease

240
Q

Spontaneous (primarY0 bacterial peritonitis is common with what history

A

Chronic liver disease and ascites

Absence of an apparent intra abdominal source of infection

241
Q

Peritoneal signs and spontaneous bacterial peritonitis

242
Q

Neutrophil in spontaneous bacterial peritonitis

A

Higher than 250

243
Q

How get spontaneous bacterial peritonitis

A

Translocation of enteric bacteria across the gut wall or mesenteric lymphatics leads to seeding of the ascetic fluid

Monomicrobial

  • e coli klebsiella (enteric gram -)
  • strep p, viridans, enterococcus(gram +)

NO ANAROBIC

244
Q

Signs and symptoms spontaneous bacterial peritonitis

A

Subtle
Fever ab pain
Change in mental status
Worsening or renal function

Chronic liver disease with ascites

245
Q

Lab findings primary bacterial peritonitis

A

Abdominal paracentesis -PMN over 250

246
Q

Secondary bacterial peritonitis

A

Secondary to intra abdominal infection

Appendicitis, diverticulitis, perforated peptic ulcer, gallbladder, multiple organisms,

247
Q

Prevent SBP

A

Oral once a day antibiotics

248
Q

Treat peritoneal infection

A

Third gen cephalosporin
Beta lactam/beta lactamase agent
-not aminoglycosides bc of nephrotoxicity

249
Q

Major cause of death PB

A

Kidney injury give IV albumin

250
Q

Treat SBP

A

Broad spectrum metronidazole or third gen cephalosporin

251
Q

Most effective treatment for recurrent spontaneous bacterial peritonitis

A

Liver transplant

252
Q

Prognosis spontaneous bacterial peritonitis

A

Over 30% mortliatiy

But if treated and seen early less than 10

253
Q

Malignant ascites

A

Peritoneal carcinomas

254
Q

What are the most common tumors causing carcinomatosis

A

Ovary, uterus, pancreas, stomach, colon, lung, breast

255
Q

How do tumors metasticize to peritoneal

A

Lymphatic obstruction, hepatocellular carcinoma

256
Q

Cytology malignant ascits

257
Q

Malignant ascites SAAG

A

Less than 1.1

258
Q

Malignant ascites respond to diuretics

259
Q

Familial Mediterranean fever SAAG <1.1

A

Rare AR in Mediterranean ancestry where they lack a protease in serosa fluids that inactivate interleukin 8 and the chemotactiv complement factor 5A

260
Q

Symptoms familial Mediterranean fever

A

Before 20
Episodic bouts of acute peritonitis that may be associated with serositis involving the joints and pleura

Sudden fever, ab pain, ab tender, guarding or rebound

261
Q

Familial Mediterranean fever untreated

A

Resolve in 34-48 Horus

262
Q

Why may someone with familial Mediterranean fever undergo laparotomy unnecessarily

A

Mimic surgical peritonitis

263
Q

Colchicine

A

Decreased frequency of familial Mediterranean fever

264
Q

Main cause of death familial Mediterranean fever

A

Secondary amyloidosis

265
Q

Mesothelioma SAAG

A

Primary abdominal malignant mesothelioma

Asbestos

266
Q

Signs of mesothelioma

A

Ab pain, bowel obstruction, increased abdominal girth, and small to moderate ascites

267
Q

Chest radiograph mesothelioma

A

Pulmonary asbestosis

268
Q

Ascites in mesothelioma

A

Hemorrhagic

269
Q

Cytology mesothelioma

270
Q

CT PET-CT mesothelioma

A

Sheet like masses involving the. Mesentery and omentum

271
Q

Diagnosis mesothelioma

A

Laparotomy or laparoscopy

272
Q

Chylothorax ascites SAAG<1.1

A

Lipid rich lymph in peritoneal cavity milky appearances TG greater 1000

273
Q

Why get chylothorax ascites

A

Lymphatic obstruction or leakage caused by malignancy, espicially lymphoma

Post op trauma, cirrhosis, TB, pancreatitis, filariasis

274
Q

Pancreatic ascites

A

Accumulation of pancreatic secretions due to disruption of pancreatic duct or to a pancreatic pseudocyst in patients with chronic pancreatitis and complicates acute pancreatitis

275
Q

Pain with pancreatic ascites

A

No be enxymes not active

276
Q

Describe fluid of pancreatic ascites

A

High protein amylase high excess 1000

277
Q

Bile ascites SAAG<1.1

A

From complications of biliary tract surgery, percutaneous lvier biopsy or abdominal trauma

278
Q

Pain bile ascites

A

Unless infected no pain , fever, or leukocytosis

279
Q

Paracentesis bile ascites

A

Yellow fluid

280
Q

Ration of ascites bilirubin to serum bilirubin in bile ascites

A

Greater than 1

281
Q

Most important treatment of cirrhosis

A

Abstinence from alcohol

F

282
Q

Other cirrhosis treatment

A

If HAV HBV get pneumococcal vaccines and a yearly flu vaccine

Liver transplant

Nonsteroidal anti inflammatory drugs contraindicated
Don’t use angiotensin converting enzyme inhibitors and angiotensin II antagonists

283
Q

Complication paracentesis

A

Bleeding, infection, bowel perforation

284
Q

How treat ascites and edema

A

Dosing intake restricted
Bed rest
Fluid intake restricted

Diuretics

285
Q

What diuretic for ascites and edema

A

Spironolactone with furosemide

286
Q

TIPS and ascites

A

Lower ascites recurrence and hepatorenal syndrome

287
Q

What is associated with increased mortality with TIPS

A

Chronic kidney disease, diastolic cardiac dysfunction, refractory encephalopathy, hyperbilirubinemia

288
Q

Complication fo TIPS

A

Hepatic encephalopathy, infection, shunt stenosis, shunt occlusion

289
Q

Hepatorenal syndrome

A

Histology kidneys morale get acute decreased in cardiac output precipating event

290
Q

Treat hepatorenal syndrome

A 
Discontinue diuretics 
IV albumin 
Vasoconstrictor 
TIPS
Liver ranspaotn
291
Q

Acute liver failurefulmient or sub most common cause

A

Acetaminophen

Suicide or unintentional

292
Q

Second most common cause of acute liver failure

A

Anti TB drugs, antiiepileptics, antibiotics

293
Q

Characterization fulminant hepatic failure

A

Development of hepatic encephalopathy within 8 weeks and 6 months

Acute onchronic liver failure too

294
Q

Liver transplant

A

If irreversible
Abstinent for 6 months
Prioritzaion based on MELD and CHILD

295
Q

What is given after liver transplant

A

Immunosuppressant

296
Q

What order to calculate MELD

A

CMP (serum bilirubin, creatinine) and PT/INR

297
Q

What MELD score is required for liver transplant

A

14 or over

► Med Notes (62 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions