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Acute Care II - Summer 2017 > Weeks 3 & 4: Liver Function > Flashcards

Weeks 3 & 4: Liver Function Flashcards

1
Q

metabolic function of liver

A

detoxification/breakdown: toxins, hormones, drugs
synthesis: bile - for emulsification of fats in the lumen of the GI tract
protein: production - including amino acids, clotting factors, vitamins, albumin and various other hormones. Activation.
carbohydrate: including glyconeogenesis.
lipid: including cholesterol and triglyceride production
red blood cells: normal in the fetus but pathological in adults
storage: nutrients - glucose. vitamins & minerals: Vitamin A/D/B12, iron & copper
Immunological: kupffer cells lining sinusoids acts as antigen presenting cells

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2
Q

liver (hepatocyte) function and revelation after resection

A

removing metabolic waste production, hormones, drugs & toxins
producing bile to aid in digestion
processing nutrients absorbed from the digestive tract
storing glycogen, certain vitamins and minerals
Maintaining normal blood sugar
Synthesizing plasma proteins, albumin, and clotting factors
Producing immune factors & removing bacteria
Removing senescent red blood cells from the circulation
Excreting bilirubin

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3
Q

common lab liver tests

A 
Bilirubin
AST
ALT
GGTP
Alkaline phosphate
LDH
PT
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4
Q

what has recently happened to normal values

A

ALT

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5
Q

AST, normal range

A

<40

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6
Q

ALT normal range

A

19-35 for women, 29-33 for men

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7
Q

GGT normal range

A

< 60

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8
Q

alkaline phosphate normal range

A

< 112

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9
Q

what are the liver enzymes

A

ast, alt, ggt, alkaline phosphate

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10
Q

what are liver function tests?

A

bilirubin, albumin, prothrombin time

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11
Q

normal range for bilirubin

A

< 1.2

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12
Q

albumin normal range

A

3.5-4.5

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13
Q

prothrombin time normal range

A

< 14 seconds

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14
Q

WBC normal?

A

4000-11000

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15
Q

hematocrit normal?

A

> 40

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16
Q

platelet normal

A

> 150000

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17
Q

what should you say instead of liver function tests?

A

liver tests b/c more tests aren’t a function of liver function

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18
Q

what does ALT (alanine transaminase) do?

A

Produce in hepatocytes
Very specific marker of hepatocellular injury
Relatively low concentrations in other tissues so more specific than AST
Levels fluctuate during the day
Rise may occur with the use of certain drugs or during periods of strenuous exercise

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19
Q

what does AST aspartate transaminase do?

A

Occurs in two isoenzymes, indistinguishable on standard AST assays
The mitochondrial isoenzyme is produced in hepatocytes and reacts to membrane stresses in a similar way to ALT
The cytosolic isoenzyme is present in skeletal muscle, heart muscle and kidney tissue
Caution must be exercise in its use to evaluate hepatocellular damage
Usually rises in conjunction with ALT to indicate hepatocellular injury: a hepatitis picture

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20
Q

what does alkaline phosphatase (ALP) do

A

A group of isoenzymes that act to dephosphorylate a variety of molecules throughout the body
Produced in the membranes of cells lining bile ducts and canaliculi
Released in response to the accumulation of bile sales or cholestasis
Non-hepatic production in the kidney, intestine, leukocytes, placenta & bone
Physiological rise in pregnancy or in growing children
Pathologic rise in Paget’s disease, renal disease, and with bone metastases

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21
Q

what does GGT do (gamma glutamyl transferase)?

A

Present in liver, kidney, pancreas & intestine
It is found in the microsomes of hepatocytes and biliary epithelial cells
Elevation of GGT in association with a rise in ALP is highly suggestive of a biliary tract obstruction and is known as a cholestatic picture
Subject to rise with hepatic enzyme induction d/t chronic alcohol use or drugs such as rifampicin and phenytoin

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22
Q

what test is liver specific?

A

GGTP - an isolate elevation of just one of the other test values should raise suspicion that a source other than the liver is the cause, when several liver test results are simultaneously out of normal range consideration of non-hepatic sources becomes irrelevant

GGTP level is too sensitive, frequently elevated when no liver disease is apparent. A GGTP is useful in only two instances

  1. it confers liver specificity to an elevated alkaline phosphate level
  2. in aminotransferase level elevations with AST/ALT ratio > 2, elevation of GGTP further supports alcoholic liver disease

in addition it can be used to monitor abstinence from alcohol

an isolated elevation of the GGTP level does not need to be further evaluated unless there are additional clinical risk factors for liver disease

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23
Q

differential diagnosis of increased AST

A 
primary liver disease
acute myocardial infarction
muscle trauma/diseases
pancreatitis
intestinal surgery
burns
renal infarction
pulmonary embolism
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24
Q

differential diagnosis of increased ALT

A 
primary liver disease
biliary obstruction
pancreatitits
ALT>AST viral hepatitis
AST>ALT alcoholic liver disease
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25
Q

differential diagnosis of increased ALP

A 
biliary obstruction
primary liver disease (changes parallel GGT)
infiltrative liver disease
bone diseases
hyperparathyroidism
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26
Q

differential diagnosis of increased GGT

A

biliary obstruction
primary liver disease (changes parallel ALP)
alcohol consumption
pancreatitis

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27
Q

differential diagnosis of increase bilirubin

A

biliary obstruction
primary liver disease
hemolytic anemias
hypothyroidism

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28
Q

medications & liver

A

may cause increases in one or more liver chemistry tests because of direct hepatotoxicity or cholestasis

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29
Q

ALT & AST?

A

are abundant liver enzymes

AST is also present in heart & muslce

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30
Q

where is ALP present?

A

in nearly all tissues, primarily bone & liver.

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31
Q

where is GGT?

A

abundant in liver, kidney, pancreas & intestine

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32
Q

do ALT & AST vary on lab?

A

yes, generally < 40

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33
Q

mild ALT & AST elevations?

A
  1. less than 5 times upper normal limit - they should be rechecked prior to extensive workup

possible causes: chronic hepatitis C or B, acute viral hepatitis, NAFLD, hemachromatosis, autoimmune hepatitis, medicaitons, alcohol-related liver injury, Wilson’s disease

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34
Q

moderately elevated ALT & AST?

A
  1. 5-15 times upper normal limit.

should be investigated w/o waiting to confirm the persistence of abnormal ALT,

possible causes - entire spectrum of liver diseases

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35
Q

severe ALT & AST elevations

A

> 15 times ULN

suggest severe acute liver cell injury

acute viral hepatits, ischemic hepatitis, or other vascular disorder, toxin mediated hepatitis, acute autoimmune hepatitis

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36
Q

what is bilirubin?

A

heme degradation product excreted in the bile, it requires conjugation in the liver before it is secreted

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37
Q

what should you do about hyperbilirubinemia?

A

investigate cause by direct (conjugated) or indirect (unconjugated) fraction of bilirubin

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38
Q

pre-hepatic causes (increased production, decreased liver uptake)

A

cause increase of indirect

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39
Q

intra-hepatic/post-hepatic causes

A

decreased hepatic excretion, increase of direct

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40
Q

increased production causes of hyperbiliirubinemia

A

hemolysis

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41
Q

decreased liver uptake causes of hyperbilirubinemia

A

Gilbert syndrome (5% of populatin - benign)

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42
Q

decreased hepatic excretion causes of hyperbilirubinemia

A

bile duct obstruction, primary biliar cirrhosis, primary sclerosing cholangitis, benign recurrent cholestasis, hepatitis, cirrhosis, medications, sepsis, total parenteral nutrition, Dublin-Johnson Syndrom,

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43
Q

what causes increased GGT?

A

alcohol consumption

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44
Q

what causes increased ALP & GGT

A

bile duct obstruction, primary biliary cirrhosis, primary sclerosing cholangitis, benign recurrent cholestasis, infiltrative disease of the liver (sarcoidosis, lymphoma, metastatasic disease)

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45
Q

causes of isolated elevated ALP (extra hepatic disease)

A

bone disease, pregnancy, chronic renal failure, lymphoma, congestive heart failure

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46
Q

causes of abnormal PT and albumin levels

A

indicate severe hepatic synthetic dysfunction & indicates progression to cirrhosis or impending hepatic failure

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47
Q

what is nonalcoholic fatty liver disease?

A

fatty infiltration (steatosis) of the liver, exceeding 5% of liver weight

requires exclusion of alcohol as potential cause. acceptable levels of alcohol consumption are controversial but in general < 20 grams/ day (2 drinks) in men & < 10 grams/day (1 drink) in women

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48
Q

what is primary NAFLD?

A

common term for typical NAFLD associated w/ central obesity and/or DM2 or insulin resistance w/o another specific etiology

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49
Q

what is secondary NAFLD?

A

used to defined as NAFLD in the absence of insulin resistance and associated w/ other causes such as :

polycystic ovary syndrome
hypothyroidism
hypogonadism
hypopituitarism
medicaiton use (glucocorticoids, tamoxifen, amiodarone, HAART, diltiazem)
disorders of lipid metabolism (abetalipoproteinemia, lipodystrophy, Weber-CHristian syndrome, Andersen’s disease)
total parenteral nutrition and jejunoileal bypass surgery

many cases of secondary NAFLD likley represent an exacerbation of often unrecognized “primary” NAFLD

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50
Q

what is non alcoholic steatohepatitis (NASH)?

A

the more seer form of NAFLD characterized by inflammation, hepatocyte injury (ballooned hepatocytes) with or without fibrosis. it can progress to cirrhosis & possibly liver cancer

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51
Q

what is NASH cirrhosis

A

the presence of cirrhosis w/ current or previous evidence of steatosis or NASH

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52
Q

what is cryptogenic cirrhosis

A

a term used to define the presence of cirrhosis w/ no obvious etiology, frequently there is a history of DM & obesity.

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53
Q

do DM2 have > or < risk for cirrhosis

A

DM2 higher risk for cirrhosis compared to the general population, possibly d/t NAFLD

also at higher risk of hepatocellular carcinoma compared to the general population, possibly d/t NAFLD

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54
Q

race groups at higher risk for NAFLD?

A

non hispanic whites and hispanics at higher risk

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55
Q

what are predictors of more severe disease of NAFLD?

A 
age > 40-50 years
female
severe obesity
hypertension
DM
hypertriglyceridemia
elevated ALT, AST, GGT, AST/ALT ratio > 1
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56
Q

genetic predisposition for NAFLD?

A

single variant in an allele is strongly associated w/ liver fat & liver inflammation. allele is more common among Hispanics.

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57
Q

diagnosis of NAFLD requires?

A

presence of steatosis (by imaging or liver biopsy)

absence of significant alcohol consumption

competing cause of chronic liver disease

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58
Q

what are tests to rule out co-existing treatable conditions for NAFLD?

A

viral hepatitis C
autoantibodies
hemachromatosis

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59
Q

imaging methods to distinguish fatty liver and steatohepatitis?

A

no imaging methods to distinguish fatty liver & steatohepatitis

but imaging can help exclude biliary tract or focal liver disease

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60
Q

how to detect the presence of liver fat?

A

US is more sensitive than CT scan, less expensive & no radiation risk…

MRI primarily used in research settings to quantify the amount of fat in the liver

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61
Q

how to detect liver fibrosis

A

US based transient elastography measures tissue elasticity non invasively and correlates well w/ liver fibrosis in liver biopsy in patients with viral hepatitis. this method has been approved by FDA.

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62
Q

what is gold standard for NAFLD diagnosis

A

liver biopsy
staging (extent of injury)
& grading (degree of activity) of NAFLD

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63
Q

what is NAFLD activity score?

A

range from 0-8, composite score based on findings of steatosis, inflammation and hepatocyte injury

a higher NAS indicates greater damage

fibrosis is scored separately

64
Q

how is fibrosis scored?

A

0-4; 0-2 minimal, 3-4 bridging fibrosis & cirrhosis

65
Q

limitations of liver biopsy

A

patient inconvenience
potential for complications
sampling error

66
Q

what are non-invasive markers of fibrosis?

A

proprietary algorithm panel based fibrosis scores based on a combination of biochemical serum assays & routine lab tests and can reliably identify those with either minimal or advanced disease

however
substantial gray zone precluding accurate fibrosis diagnosis & staging

some are commercially available

limited dated are available of their utility in NAFLD

67
Q

what is the new word for liver function tests?

A

liver chemistries (ALT, AST, alkaline phosphate & bilirubin) are markers of liver injury (not liver function)

should be referred to as liver chemistries/liver tests

68
Q

what are markers of hepatocellular function that can be influenced by extrahepatic factors?

A

albumin, bilirubin, prothrombin time

69
Q

what tests require assessment & potential evaluation?

A

elevations of AST and/or ALT, alkaline phosphate & bilirbuin suggest hepatocelluar injury and are the abnormal liver chemistries that require assessment & potential evaluation

70
Q

which is more specific, ALT or AST

A

ALT more specific marker of hepatic injury

71
Q

how do you confirm an elevated alkaline phosphate level of hepatic origin?

A

by elevation of the GGT or fractionation of alkaline phosphate

72
Q

Signs/symptoms of NAFLD

A

most common: asymptomatic, fatigue, right upper quadrant pain

palmar erythema, spider angiomas in cirrhosis

clinical findings associated w/ metabolic syndrome commonly seen

hepatomegaly, acanthosis nigricans in children

lipoatrophy/lipodystrophy

73
Q

is mildly elevated serum ferritin common in patients w/ NAFLD?

A

mildly elevated serum ferritin is common in patients with NAFLD

if serum ferritin & transferrin saturation are both elevated then this is suggestive of hemochromatosis & genetic testing is justified

74
Q

non-pharmacologic treatment of NAFLD

A

diet & exervise are cornerstones of therapy. weight lostt 5-6% effetively improves steatosis & other histological features of NAFLD and reduces risk of progression

75
Q

notes for weight loss on NAFLD treatment

A

avoid rapid weight loss, can cause histological exacerbation

76
Q

what about exercise w/o weight loss for NAFLD treatment?

A

evidence suggests it may help, encourage increased physical activity level even in the absence of weight loss

77
Q

diet composition for NAFLD treatment?

A

effects of specific diets on NAFLD are not known

recommended balanced diet such as that endorsed by ADA or AHA

78
Q

pharmacologic treatment for NAFLD

A

obeticholic acid, improved histological features of NAFLD. adverse effects: increase in LDL & pruritits

79
Q

thizolidinediones for treatment of NAFLD

A

pioglitazone significantly improves histological outcomes & b/c of other benefits in treatment in DM2, can be considered drug of choice for NAFLD in those w/ DM2

80
Q

biguanides for NAFLD?

A

metformin usually only used in research data.

81
Q

antioxidants in NAFLD?

A

pilot data suggest improvement w/ vitamin E

82
Q

cytoprotective agents:

A

large RCT showed use of ursodeoxycholic acid shows no histologic benefits

83
Q

gold standard for NAFLD?

A

biopsy, used to diagnose, stage and grade NAFLD, not routinely performed

84
Q

common initial approach to NAFLD?

A

lab tests to rule out other potential causes of liver disease are most common initial approach

85
Q

what is a cornerstone to initial management

A

lifestyle changes

86
Q

is there FDA approved medication therapy?

A

no FDA-approved medication therapy
although thiazolidinediones may be preferred in patients with both NAFLD
and T2DM

87
Q

non hepatic source of abnormal bilirubin?

A

red blood cells (hemolysis, intra-abdominal bleed, hematoma)

88
Q

non hepatic source of abnormal AST

A

skeletal muscle, cardiac muscle, red blood cells

89
Q

non hepatic source of abnormal alt

A

skeletal muscle, cardiac muscle, kidneys

90
Q

non hepatic source of abnormal ldh

A

heart, red blood cells (hemolysis)

91
Q

non hepatic source of abnormal alkaline phosphate

A

bone, first trimester placenta, kidneys, intestines

92
Q

aminotransferases (AST & ALT) abnormal in?

A

hepatocellular injury: ethanol, hepatitis, ischemic injury, NAFLD, acute biliary obustruction

Rare: hyperthyroidism, celiac disease, skeletal muscle disease

93
Q

alkaline phosphate abnormal in

A

cholestasis, canalicular injury, children during bone growth, bone disease, pregnancy (placenta origin)

94
Q

GGT abnormal in ….

A

cholestasis, medications, ethanol, rarely anorexia nervosa, hyperthyroidism, myotonic dystrophy

95
Q

bilirubin abnormal in…

A

any acute or chronic liver disease, congenital disorders of bilirubin metabolism

96
Q

what is hepatitis?

A

inflammation of the liver
many causes:
toxic agents (drugs, ETOH, mushrooms, organic solvents, dietary supplements)
infectious A-E, CMV, HSV, EBV
mechanical - injury, obstruction, thrombus, Budd-Chiarai
autoimmune

97
Q

common drugs that induce hepatitis

A

acetaminophen & methotrexate

98
Q

what is fibrosis?

A

scarring, possibly reversible

99
Q

what is cirrhosis?

A

scarred non-functional tissue - will not regenerate

can compensate with cirrhosis

100
Q

what is liver failure?

A

the organ is non-functional or severely impaired, also called decompensated.

101
Q

acute liver failure?

A

also called fulminant - liver failure that develops in days to weeks

hyperacute 2-7 days,

sub acute up to 6 months

102
Q

chronic liver failure?

A

progressive fibrosis over time with continued exposure to provocatory agent

often can live for a while without transplant (just using medication)

103
Q

causes of acute liver failure

A

usually drugs

drugs: tyelnol, herbal supplements, NSAIDs,
hepatitis a, b, e
cancer
Budd-Chiari (venous malformation)
toxins
auto-immune
metabolic
104
Q

causes of chronic liver failure

A 
alcohol
hepatitis C
NASH/NAFLD
primary biliary cirhhosis
primary sclerosing cholangitis
medications/toxins: methotrexate, tylenol, supplements
metabolic

day to day exposure over long periods of time

105
Q

signs & symptoms of liver failure

A

jaundice, ascites, edema, dark urine, pale stools, palmar erythema, odor - fector hepatic, caput medusae, encephalopathy, day/night reversal, hepatomegaly, splenomegaly, umbilical hernia, pruritus, nausea/malaise

106
Q

labs for liver failure

A

hyperbilirubinemia, hypoalbunemia, hyponatremia, hypoglycemia, transaminitis, thrombocytopenia, increased creatinine, azotemia, coagulopathy, increased serum ammonia.

107
Q

should I measure serum ammonia?

A

no, doesn’t really do anything to trend ammonia

give lactulose if high

you would send an ammonia if they are somnolent

108
Q

CV sequellae liver failure

A

hypotension, pulmonary hypertension, arrhythmias

109
Q

respiratory sequellae of liver failure

A

dyspnea, hepatic hydrothorax, aspiration from encephalopathy

110
Q

infection sequellae of liver failure

A

SBP, cholangitis, sepsis

111
Q

GI sequellae of liver failure

A

anorexia, constipation, GI bleeds, varies

112
Q

renal sequellae of liver failure

A

hepato-renal syndrome, hyponatremia

if someone has 2 weeks of kidney issues list them for a kidney/liver transplant

113
Q

heme sequellae of liver failure

A

anemia, coagulopathy

114
Q

ONC sequellae of liver failure

A

hepatocellular carcinoma

115
Q

endocrine sequellae of liver failure

A

hypoglycemia

116
Q

neuro sequellae of liver failure

A

encephalopathy, RUQ pain

117
Q

derm sequellae of liver failure

A

pruritus

118
Q

initial lab results for liver failure

A

WBC normal to low
UA - proteinura common, bilirubinemia before jaundice
significantly elevated ALT & AST > 500 (marker of inflammation & insult of parnchymea)
elevated bilirubin & alkaline phosphate (obstruction of biliary tree) elevated after ALT/AST normalize

119
Q

where is alkaline phosephate also?

A

in bones, so you want to send fractioned alk phose to tell if bone or liver.

GGT or GTT to tell if actively drinking

120
Q

prognosis with acute hepatitis

A

remove offending agent and you recover

acute hepatitis turns into acute liver failure and you need liver tx

you get better but go on to chronic liver failure which may necessitate a liver transplant

121
Q

what is MELD?

A

model for end stage liver disease

122
Q

supportive care for liver failure

A

monitor INR, CBC, bilirubin, and LFTs
Encephalopathy - limit po protein & give lactulose
Hypoglycemia – 10 % glucose infusion
Coagulopathy – Vitamin K, FFP

Hyponatremia – free water restrict
• Ascites – low Na diet, diuretics prn,
– careful paracentesis (significant loss albumin, 6-8 gm of albumin per kilo of fluid removed)

123
Q

what are the ‘real lfts’

A

hypoglycemia, hypoalbminemia, elevated INR

124
Q

why low salt diet?

A

Na would leak into the tissues and water will follow the Na

125
Q

why low protein diet?

A

breakdown protein - get ammonia - liver can’t handle the ammonia

126
Q

what kind of diet for liver failure

A

high carb diet, low Na, & fluid restriction. page 14

127
Q

why do paracentesis for liver failure?

A

remove fluid

128
Q

why do thoracentesis for liver failure

A

remove fluid - hepatic hydrothorax

129
Q

what other interventions are there for liver failure?

A

TIPS: transjugular intrahepatic protosystemic shunt, improves ascites but decreases LOC, makes encephalopathy worse b/c it doesn’t clear ammonia
ERCP/EGD
biopsy - gold standard for disease process figuring out
transplant

130
Q

medications used to manage liver failure

A

lactulose: encephalopathy - give lactulose until brain is OK
rifaximin: abx changes gut flora & helps to keep those that will keep ammonia
spironolactone/furosemide: diuretic
midodrine: increase NP
cipro or daily abx: bactrim to prevent spontanesou bacterial pertinotis
propranolol: assist w/ portal HTN, keep pressure low in portal varices
octreotide
pantoprazole

131
Q

how do you determine the mode of transmission of Hep A-E?

A

if it’s a vowel - fecal / oral route

if its a consonant: blood/mucosal transmission

132
Q

prodromal phase

A

malaise, myalgia, arthralgia & fatigue
anorexia, nausea & vomiting common
diarrhea or constipation
rash, arthritis or serum sickness in early HBV
fevers <104F
mild constant RUQ or epigastric abdominal pain, increased w/ exertion

133
Q

icteric phase

A

dark urine & clay colored stool
jaundice at onset or within 10 days
intensified prodromal symptoms BUT some patients are asymptomatic
tender helaptomegaly
splenomegaly
posterior cervical lyphadenopathy rare but some patients have normal exam

134
Q

chronic liver failure

A

reduce metabolic function
impaired bile formation and flow
produces multisystem organ failure, encephalopathy, increased incidence of infection: spontaneous bacterial peritonitis (E. coli, klebsiella, strep)

135
Q

hepatitis A

A

caused by HAV
fecal / oral transmission
incubation period 15-50 days, average 28 days
diagnosis by blood test - positive HAV IgM
not a common cause of liver failure

136
Q

new infections for hep A 2015

A

2800

137
Q

new infections hep B 2015

A

21900

138
Q

living with Hep C

A

3.5 million

139
Q

what helped decline of hep a virus?

A

hep a vaccine, declined 95% since 1995

140
Q

hep a sign/symptoms

A

young children often asymptomatic
abrupt onset: fever, fatigue, anorexia, N/V, abd pain, dark urine, clay colored stools, joint pain, jaundice
-symptoms last < 2 months
-HAV can live outside the body for months
-chlorinated water kills it
-can’t get reinfected

141
Q

what can offer short term protection for HAV?

A

IG, must be given within 2 weeks after exposure

142
Q

is hep E more or less common if have another hepatitis?

A

more common if have another hepatitis

143
Q

HEV

A
  • fecal oral route
  • symptoms: fever, fatigue, anorexia, N/V, abd pain, jaundice, dark urine, clay stools, joint pain
  • treatment: supportive, avoid ETOH
  • clinical course: self limited - acute illness.
  • no FDA approved test for HEV
144
Q

hep b transmission

A
  • blood mucous
  • must have mucosal/percutaneous contact with infectious blood/body fluid
  • not spread through food, water, casual contact, sharing utensils, breastfeeding
145
Q

hep B symptoms

A

same as all other hep: fever, fatigue, anorexia, N/V, and pain, jaundice, dark urine, clay colored stools, joint pain

tend to be sicker at beginning and into icteric phase faster

146
Q

who’s at risk for hep b

A

-infants born to infected mothers
-sex partners of infected persons
-MSM
IVDA
-household contact of those infected
occupational
HD patients
travelers to countries w/ intermediate/high prevalence of HBV infection
unprotected sex, > 1 sex partner in previous 6 months, non-monogamous relationship

147
Q

incubation period for HBV

A

60-160 days, average 90 days

148
Q

clinical illness (jaundice for HBV)?

A

> 5 years, 30-50%

149
Q

acute case fatality rate for HBV

A

0.5-1%

150
Q

chronic infection rate for hbv

A

infants >90%, >5y/o 25-50%

premature mortality from chronic liver disease 15-25%

151
Q

hep b surface antigen

A

person is infected

152
Q

hep b surface antibody

A

indicates recovery or immunity from infection/indicates seroconversion from vaccination

153
Q

hep b core antibody

A

appears at the onset of symptoms in acute Hep b, persists for life

154
Q

IgM antibody to anti-Hbc

A

recent infection (<6 months), acute infection

IgM - smoking gun = you’re infected

155
Q

Hep B e antigen

A

active viral replication

156
Q

Hep B DNA

A

quantitative, viral load

Acute Care II - Summer 2017 (10 decks)

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