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Diagnostic medicine > “LFTS” & Hepatitis Serology > Flashcards

“LFTS” & Hepatitis Serology Flashcards

1
Q

typical values given in LFTs

A 
Albumin
Bilirubin
Bilirubin Direct (conjugated)*
Bilirubin Indirect (unconjugated)*
Alkaline Phosphatase
Total Protein
ALT (Alanine aminotransferase)
AST (Aspartate transaminase)
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2
Q

we mat may see _____ on a typical LFTs

A

GGT

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3
Q

which values must be ordered separately from a LFTS

A

PT, which is usually ordered with INR

and Labs indicative of liver infection (e.g. hepatitis labs)

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4
Q

which two typical LFTs values are not included in the CMP and what must you order to obtain these values?

A 
Bilirubin Direct (conjugated)*
Bilirubin Indirect (unconjugated)*
you must order a Hepatic function panel to get these values
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5
Q

which value patterns would you expect to see in typical inflammation or hepatocellular damage

A

above normal ALT and AST

above normal Possible GGT

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6
Q

In the case of inflammation/damage, which labs values would only rise if inflammation is severe
such as in acute hepatitis

A

above normal Bilirubin
above normal Bilirubin Direct
above normal Bilirubin Indirect

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7
Q

which value patterns would you expect to see in typical case of cholestatis
such as in obstruction

A

above normal Bilirubin
above normal Bilirubin Direct (conjugated)
above normal Alkaline Phosphatase
possible above normal GGT

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8
Q

clinical significance of GGT or Gamma-Glutamyl Transpeptidase

A

Used to determine source of Alkaline Phosphatase (ALP) elevation, whether is it bone or liver sourced
If GGT also elevated, source likely liver

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9
Q

what lab value can be used as a marker of alcohol consumption

A

GGT, however it can be too sensitive and results can be elevated by small amounts of alcohol or various other drugs

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10
Q

which value patterns would you use as an indication of reduced liver function

A

Albumin is low
Total protein is low
and PT, if ordered is, is prolonged (high)

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11
Q

urine Urobilinogen in chloestasis is ______

A

decreased

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12
Q

common cause of chloestasis related to the gallbladder

A

gallstones in the common bile duct

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13
Q

medical term for gallstones in the common bile duct

A

choledocholithiasis

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14
Q

patients with choledocholithiasis typically present with

A

pain specifically biliary colic
jaundice
clay colored stools
and cola colored urine

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15
Q

other causes of choledocholithiasis

A

tumors such as in pancreatic cancer

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16
Q

choledocholithiasis causes

A

an the extra-hepatic obstruction, resulting in inhibited hepatic bile flow into the duodenum

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17
Q

results of an extra-hepatic obstruction

A

the conjugated bilirubin formed within the hepatocytes is unable to be excepted in the bile and is passed to the blood stream

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18
Q

why does choledocholithiasis or extra-hepatic obstruction cause dark urine

A

Because conjugated bilirubin is water soluble (unlike unconjugated bilirubin), it can then be excreted by the kidneys into the urine. Urine looks dark and cola colored as a result

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19
Q

typically the bilirubin is excerpted as bile and

A

is able to reach the intestine

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20
Q

no urobilinogen & no stercobilin in the intestine causes

A

acholic white stools

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21
Q

how should you test for a bile duct obstruction such as choledocholithiasis

A

test for bilirubin in the blood for more accurate results

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22
Q

what type of obstruction is choledocholithiasis classified as

A

a post-hepatic obstruction

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23
Q

when would you expect to see a isolated elevation of Indirect (Unconjugated) Bilirubin

A

often is it due to Gilbert Syndrome

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24
Q

Gilbert syndrome

A

Benign condition
Results from defect in the promotor of the gene that encodes the enzyme uridine diphosphoglucuronate-glucuronosyltransferase 1A1 (UGT1A1),
Usually only see Indirect Bilirubin in homozygotes so many pts present as isolated cases
During times of stress (e.g. dehydration, fasting, disease, menstruation, overexertion), can see episodes of jaundice

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25
Q

what does the UGT1A1 enzyme cause if working properly

A

which is responsible for the conjugation of bilirubin with glucuronic acid

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26
Q

how to diagnosis Gilbert syndrome

A

ruling out other causes of ↑Indirect Bilirubin

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27
Q

Alkaline phosphatase is derived from

A

liver and bone

also a very small contribution is made from the intestines

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28
Q

which expensive test would indicate the source of an elevated Alk phos value

A

Alk phos isoenzymes

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29
Q

common cause of reduced liver function

A

cirrhosis or serve acute injury such as severe hepatitis or toxic insult like acetaminophen overdose

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30
Q

Cirrhosis results from

A

chronic liver disease

due to chronic inflammation / hepatocellular damage causing scarring that can not be repaired

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31
Q

scarred or fibrotic livers

A

the liver does not function like healthy liver

may be unable to detoxify harmful substances, “clean” blood, make vital proteins

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32
Q

cirrhosis patient signs & symptoms

A

Fatigue
Portal hypertension
Ascites
Jaundice (will see ↑Bili) – obstruction of flow, failure of hepatocyte conjugation, failure of excretion of bile [since unconjugated bilirubin is fat soluble – and cannot be excreted – it accumulates in fatty tissues (most notably the skin)]
Easy bruising / bleeding due to low platelets (thrombocytopenia) – that result from throbopoeitin, splenic sequestration, and increased destruction
Others

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33
Q

why do we see portal hypertension is cirrhosis

A

due to scarring obstructing flow

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34
Q

ascites and cirrhosis

A

causes an accumulation of fluid in the abdomen – partially due to portal hypertension

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35
Q

why do we see jaundice in cirrhosis patients

A

obstruction of flow causes failure of hepatocyte conjugation and failure of excretion of bile
since unconjugated bilirubin is fat soluble and cannot be excreted, it accumulates in fatty tissues, most notably the skin)]

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36
Q

why do we see easy bruising and bleeding in cirrhosis patients

A

due to low platelets (thrombocytopenia) that result from throbopoeitin, splenic sequestration, and increased destruction

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37
Q

how to diagnosis cirrhosis

A

a definitive diagnosis & staging requires liver biopsy

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38
Q

normal LFTs do not mean

A

the liver is normal

Patients with normal ALT & AST levels can have significant liver disease

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39
Q

is ALT or AST more specific

A

ALT

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40
Q

risk factors for liver damage and disease

A 
Family history
ETOH consumption
Obesity
Diabetes
Hyperlipidemia
Medications / Supplements
Autoimmune disease
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41
Q

hepatitis risk factors

A 
IVDU / cocaine use
High-risk sexual behavior
Foreign travel
History of transfusion(s)
Tattoos
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42
Q

Medications and vitamins/herbals that can cause elevations in transaminases (ALT & AST)

A 
Herbals/Vitamins
Ephedra
Kava
Vitamin A
ANY
Medications
Acetaminophen (often combined with opiates!)
Statins
Antifungals / Azoles
Antibiotics
Anti-TB drugs
NSAIDs
Tegretol
OTHERS
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43
Q

The easiest way to determine if a medication is responsible is to

A

stop it and see if the lab value returns to normal

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44
Q

Differential diagnosis for elevated transaminases (↑ALT & AST)

A 
Hepatitis
HAV, HBV, HCV, autoimmune, others
Alcoholic liver disease
Fatty liver/ Nonalcoholic steatohepatitis
Medications
Hemochromatosis
Rare conditions
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45
Q

Differential diagnosis for elevated transaminases that are uncommon to have elevated transaminases

A

Celiac disease

Hypothyroidism

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46
Q

rare conditions causing elevated transaminases

A

Alpha-1 antitrypsin deficiency

Wilson’s disease

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47
Q

Modest elevations in ALT (& AST) are ____ and often ____

A

are common and often asymptomatic

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48
Q

when to worry about Elevated Transaminases

A

Other liver tests are abnormal

Clinical signs & symptoms of disease
greater than 3-5 fold elevation of any enzyme level

Persistently abnormal levels for > 6 months

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49
Q

Mildly elevated AST & ALT

A

less than 3 times normal level likely due to fatty liver or ETOH consumption

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50
Q

fatty liver is associated with

A

Obesity
Type 2 DM
Hyperlipidemia

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51
Q

Elevated AST

A

Alcoholic hepatitis
Common bile duct obstruction (choledocholithiasis) – will also see ↑Alk Phos & Direct Bili
Cholangitis (infection that can result from choledocholithiasis) – will also see ↑Alk Phos & Direct Bili

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52
Q

AST:ALT ratio of > 1 suggest

A

ETOH liver disease, especially if GGT > 2X normal

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53
Q

AST:ALT ratio of < 1 (ALT higher) suggest

A

Acute or chronic viral hepatitis

NASH (Nonalcoholic steatohepatitis)

54
Q

alk phos elevation usually more prominent than transaminase elevations in

A

cholestatic disease

55
Q

fatty liver medical term

A

Hepatic steatosis

56
Q

Fatty infiltration + associated inflammation creates

A

NASH a liver disease that is clinically and histologically indistinguishable from alcoholic steatohepatitis

57
Q

NAFLD can lead to

A

cirrhosis, which can lead to liver failure and/or hepatocellular carcinoma

58
Q

what causes the progression from steatosis to steatohepatitis

A

the etiology is unknown

59
Q

prevalence of NAFLD (2008)

A

11% in population, accounting for 75% of chronic liver disease

60
Q

NAFLD & NASH

Risk Factors

A 
Obesity
Hypertriglyceridemia / Dyslipidemia
Insulin resistance &amp; DM
Medications
E.g. corticosteroids, estrogen, tamoxifen, amiodarone, anti-HIV medications
61
Q

clinical symptoms of

A

NAFLD & NASH
most patients asymptomatic or have fatigue
elevated ALT or ALT & AST are simply noted on routine labs
hepatomegaly may also be appreciated during physical exam
labs may be normal

62
Q

↓Albumin & ↑PT (protime) may occur with

A

advanced disease of NAFLD & NASH such as the progression to cirrhosis

63
Q

Definitive diagnosis of NAFLD and NASH

A

Demonstration of hepatic steatosis by imaging or biopsy
Exclusion of significant alcohol consumption
Exclusion of other causes of hepatic steatosis`

64
Q

initial test in NAFLD and NASH imaging

A

an ultrasound
echogenicity, ability to bounce sound, is increase
however this can only detect steatosis, not cirrhosis

65
Q

other imaging and results for NAFLD and NASH

A

CT – decreased attenuation (reduced intensity of X-ray beams)
MRI – ↑fat signal

66
Q

liver biopsy NAFLD and NASH

A

Need for liver biopsy determined by specialist may be needed if diagnosis is unclear or if you need to assess progression of disease (stage)

67
Q

NASH (steatohepatitis) assoc. with _____ risk than NAFLD (Fatty Liver)

A

higher

68
Q

General approach to management of NAFLD and NASH

A

Weight loss for patients who are obese
Hep A & B vaccinations
Avoid alcohol consumption
Treatment of risk factors for cardiovascular disease

69
Q

Hereditary Hemochromatosis (HH)

A

Hereditary disorder of iron metabolism

Autosomal recessive

70
Q

Hereditary Hemochromatosis (HH) genetic mutation

A

Mutation of HFE gene is most common cause
Can be caused by other mutations that result in disordered iron regulation

Genetic mutation results in increased iron absorption from the gut→ leads to accumulation of iron in the: liver, kidney, pancreas, heart, adrenals, testes, pituitary

71
Q

HFE gene encodes

A

HFE protein thought to be responsible for regulating the uptake of circulating iron

72
Q

Hereditary Hemochromatosis (HH) prevalence

A

homozygotes in Caucasians in U.S. ≈ 0.5%; heterozygotes ≈ 10%
A different disorder of iron overload has been identified in African Americans – but HH is uncommon in African & Asian Americans

73
Q

Hereditary Hemochromatosis Diagnosis

A

Clinical symptoms generally absent until the 5th decade

Symptoms appear earlier in men

Often diagnosed earlier due to family history or incidental ↑LFTs (ALT & AST) noted on routine lab

74
Q

Hereditary Hemochromatosis symptoms

A

Symptoms initially non-specific – fatigue, malaise
Later manifestations (classic triad is cirrhosis, DM, bronze skin pigmentation)
Cirrhosis
Cardiac enlargement / cardiomyopathy
DM
Skin hyperpigmentation

75
Q

steps to diagnosing HH

A

If patient has: ↑ALT & AST (& possibly Alk phos), symptoms, or 1st degree relative
Check serum transferrin saturation (transferrin is the main iron-binding protein) & ferritin (marker of iron storage)
If transferrin saturation (TS) < 45 (normal) & ferritin normal – no further evaluation
If TS ≥ 45 (high) and/or ferritin elevated – check for HFE genotype

76
Q

Hereditary Hemochromatosis Prognosis

A

f not identified and managed – can result in cirrhosis leading to an hepatocellular carcinoma
As noted before, can also lead to DM, cardiomyopathy, hypopituitarism, hypogonadism, hypothyroidism, extra-hepatic cancer
Major cause of death is decompensated (severe) cirrhosis, HCC, DM, & cardiomyopathy

77
Q

Hereditary Hemochromatosis Management

A

Therapeutic phlebotomy
No optimal regimen – usually removal of 1 unit of blood every 1-2 weeks
Avoid iron rich foods (e.g. red meat, vit. C)
Avoid insult to liver (no alcohol)

78
Q

Autoimmune hepatitis

A

A chronic hepatitis characterized by autoimmune features, generally including presence of circulating autoantibodies

possible genetic susceptibility with environmental trigger

Affects all ethnic groups and can occur at any age

most commonly diagnosed in pts in their 40s or 50s

3.6 to 1 female predominance

79
Q

Autoimmune hepatitis pervalence

A

Prevalence 11-25 per 100,000

80
Q

Autoimmune hepatitis Diagnosis

A

Clinical manifestations & severity variable

Symptoms range from asymptomatic (no symptoms) to acute liver failure

Diagnosis based on characteristic serologic (blood) and histologic (biopsy) findings & by excluding other diseases

Liver biopsy may be needed if diagnosis uncertain

81
Q

Autoimmune hepatitis labs

A

in addition to ↑ALT & AST (and other possible abnormal LFTs):
Increased total IgG (gamma-globulin) levels
+ ANA (antinuclear antibodies)
+ ASMA (anti-smooth muscle antibodies
+ others

82
Q

autoimmune hepatitis managment

A

Refer to hepatologist

Corticosteroid (prednisone) often prescribed

83
Q

Wilson disease Background

A

Very rare hereditary disorder of cellular copper transport

Autosomal recessive

84
Q

Wilson disease genetic abnormality

A

leads to impaired biliary copper excretion → leads to accumulation of copper in several organs, most notably: liver, brain, cornea

85
Q

Wilson disease prevalence

A

1 case in 30,000

86
Q

Wilson disease Diagnosis

A

Variable age of onset (may be due to differences in mutation penetrance)

majority are diagnosed between ages 5 & 35

Children usu. present with liver disease / hepatitis 1st

Adults usu. present with neurologic symptoms 1st (dysarthria, gait abnormalities, dystonia, tremor, Parkinsonism, drooling), may have less liver involvement

Signs of liver disease variable – from asymptomatic to signs of steatosis to cirrhosis

Kayser-Fleischer rings in about ½ of pts with liver disease

87
Q

Wilson disease Kayser-Fleisher ring

A

Fine pigmented granular deposits in the cornea

Color is brownish or gray-green

Detected by naked eye or slit lamp exam

Disappears with treatment

88
Q

Wilson disease labs

A

↑ALT & AST
May have labs consistent with cirrhosis: ↓Albumin, ↑PT, thrombocytopenia (low platelets)

LOW ceruloplasmin

89
Q

Wilsons disease refer to specialist for

A

definitive diagnosis

90
Q

Wilson disease Prognosis

A

Untreated Wilson disease universally fatal – due to cirrhosis (or HCC) or neurologic disease

Prognosis for those who receive treatment is excellent

91
Q

Wilson disease Management

A

By specialist
Lifetime therapy aimed at treating copper overload

D-penicillamine, a copper chelator (binds to copper for removal from body)

92
Q

Approach to an asymptomatic patient with mildly elevated transaminases step one

A

Check for risk factors for hepatitis, liver damage, & conditions associated with NAFLD or NASH

Screen for Hepatitis C & B

ask about Alcohol, medications/supplements (if present, stop & recheck)

Obesity, dyslipidemia, DM → if present, screen for NAFLD/NASH with ultrasound

Can also check labs for hereditary hemochromatosis (especially if family history of liver disease) → if ↑transferrin saturation & ↑ferritin, refer to specialist for genetic testing

93
Q

Approach to an asymptomatic patient with mildly elevated transaminases (ALT & AST) step 2

A

Consider other causes of elevated ALT & AST

Celiac disease
Hypothyroidism
Adrenal insufficiency

94
Q

Approach to an asymptomatic patient with mildly elevated transaminases (ALT & AST) step 3

A

Consider screening for rare liver conditions
Autoimmune hepatitis → IgG, ANA, ASMA
Wilson disease → ceruplasmin (looking to see if it’s low)

may often be done by specialist

95
Q

Approach to an asymptomatic patient with mildly elevated transaminases (ALT & AST) step 4

A

Ultimately may need specialty consult for definitive diagnosis

Gastroenterologist (GI) or hepatologist determine need for biopsy

96
Q

Hepatitis A facts

A

causes “infectious / endemic hepatitis”

does not lead to chronic disease or to cirrhosis or (HCC)

Spread is fecal-oral route

Incubation period 10-50 days

Excreted in feces up to 2 week before clinical illness – rarely after first week of illness

In U.S. in 2015 acute symptomatic cases of HAV have gone down

97
Q

HAV transmission

A 
Household contacts
Daycare centers, nursing homes
Sexual contacts
Persons living in high risk areas
Persons traveling to high risk areas 
Injection &amp; non-injection drug users
98
Q

HAV – clinical presentation

A

Fever, jaundice are main symptoms

> 90% childhood infections asymptomatic
Just 25-50% adult infections asymptomatic

99
Q

HAV prognosis

A

99% of cases recover completely
Very few pts experience permanent liver damage
Fatal for ~0.1% of individuals

100
Q

HAV Post-exposure prophylaxis

A 
Healthy individuals (12 months to 40 years old) 
Vaccinate as soon as possible within 2 wks of exposure

For those < 12 months, > 40 y/o, or if there is a contraindication to vaccine, give immunoglobulin (IG)

101
Q

HAV – prevention

A

Hygiene (hand washing)
Vaccinate children between 12-23 months of age
Consider for people 2 & older, anyone who wants protection

Vaccinate those who are at risk or at risk of complications from HAV

102
Q

HAV high risk population

A

Persons living in/traveling to areas with intermediate/high rates of infection
Men who have sex with Men (MSM)
Injection & non-injection drug users
Those with chronic liver disease (e.g. NAFLD or NASH, hemochromatosis)
Those with clotting factor disorders
Contacts of people with HAV

103
Q

HAV labs

A

ALT & AST can be in the hundreds or low thousands
also causes elevated bilirubin

Hep A Antibodies

104
Q

If patient is IgM anti-HAV neg & IgG anti-HAV pos, this indicates

A

past infection and/or immunity

105
Q

Hepatitis B (HBV)

A

Transmitted by blood, sexual contact, parenteral (injection) contact
HBV is a leading cause of cirrhosis & hepatocellular carcinoma worldwide

106
Q

HBV prevalence

A

Affects ≈ 240 million persons
Worldwide 780,000/year die from chronic active HBV, related cirrhosis or HCC

In U.S. 850,000 – 2.2 million with chronic HBV

107
Q

HBV risk factors

A 
multiple sex partners 24% 
other 23%
Injecting drug users 20%
Men who have sex with men 17% 
sex contact 13%
household 3%
108
Q

Acute HBV

A

Presence of signs/symptoms varies
Most children < 5 y/o & newly infected immunosuppressed adults are asymptomatic
30-50% of those ≥ 5 y/o have initial signs & symptoms – looks like hepatitis – fever, jaundice (N/V, dark urine)
Acute phase of hepatitis B rarely fulminant or fatal (only ≈ 0.5%)

109
Q

chronic HBV clinical presentation and who gets affected

A

usu. asymptomatic until late disease
90% infected as infants
25-50% infected from ages 1-5
5% infected as adults

110
Q

chronic HBV prognosis

A

Premature death due to cirrhosis or HCC
25% infected as children
15% infected after childhood
In U.S. ≈ 1800 / year die due to chronic HBV

111
Q

acute HBV management

A

supportive

112
Q

chronic HBV management

A

with antiviral medications – treatment usually is directed by a specialist

113
Q

HBV prevention vaccination “more important”

A 
Avoid high risk behaviors
important: 
Vaccination
--All infants, beginning at birth 
--All children aged <19 years who have not been vaccinated previously 
--Persons with HIV infection 
Persons seeking evaluation or treatment for a sexually transmitted disease 
---Men who have sex with men 
--Injection drug users
114
Q

HBV prevention vaccination “less important”

A

Avoid high risk behaviors
important:
Vaccination
—Susceptible sex partners of hepatitis B surface antigen (HBsAg)-positive persons
—Sexually active persons who are not in a long-term, mutually monogamous relationship
–Susceptible household contacts of HBsAg-positive persons
–Health care and public safety workers at risk for exposure to blood or blood-contaminated body fluids
–Persons with end-stage renal disease, including predialysis, hemodialysis, peritoneal dialysis, and home dialysis patients
–Residents and staff of facilities for developmentally disabled persons
–Travelers to regions with intermediate of high rates of endemic HBV Persons with chronic liver disease
–Unvaccinated adults with diabetes mellitus who are aged 19 through 59 years (discretion of clinicians for unvaccinated)

115
Q

HBV acute labs

A

↑ALT & AST (in the hundreds or thousands)

When ALT & AST that high – will see high Bilirubin too

116
Q

HBV chronic labs

A

↑ALT & AST (mildly elevated)
Diagnosis may be made by incidental ↑ALT and/or AST on routine lab
Do not see other abnormal labs until later disease (e.g. progression to cirrhosis)

117
Q

antigen labs HBV

A

review from foundations

Hep B surface antigen (HBsAg): protein on surface of the virus (part of the virus).
Hep B surface antibody (anti-HBs): anti-HBs appears during recovery, usu. indicates recent infection or immunity; anti-HBs also develops in a person who has been successfully vaccinated.
Total Hep B core antibody (anti-HBc): appears at onset of symptoms in acute hepatitis B & persists for life; indicates previous or ongoing infection with HBV in undefined time frame.
IgM antibody to Hep B core antigen (IgM anti-HBc): indicates acute or recent infection with HBV (≤6 months).
Hep B e antigen (HBeAg): a secreted product of the nucleocapsid gene of HBV (part of virus) found in serum during acute and chronic hepatitis B; indicates that the virus is replicating and infected person has high levels of HBV.
Hep B e antibody (HBeAb or anti-HBe): produced by immune system temporarily during acute HBV infection or consistently during or after a burst in viral replication; spontaneous conversion from e antigen to e antibody (a change known as seroconversion) is a predictor of long-term clearance of HBV in patients undergoing antiviral therapy → indicates lower levels of HBV.

118
Q

Hepatitis C

A

Transmitted primarily through large or repeated percutaneous exposures to infectious blood

Incidence in 2014 was ≈ 30,500 acute cases
Prevalence of chronic HCV in U.S. is ≈ 2.7-3.9 million
(more than HBV)

119
Q

leading cause for liver transplants

A

chronic HCV

120
Q

how is HCV transmitted frequently

A

Injection drug use (currently the most common means of HCV transmission in U.S.)

Receipt of donated blood, blood products, and organs (once a common means of transmission but now rare in the US since blood screening became available in 1992)

Needlestick injuries in health care settings

Birth to an HCV-infected mother (not spread through breast-feeding)

121
Q

how is HCV transmitted infrequently

A

Sex with HCV-infected person
Sharing personal items contaminated with infectious blood, such as razors or toothbrushes
Invasive procedures, such as injections

122
Q

acute HCV clinical presentation

A

20-30% who acquire HCV may become symptomatic, usu. mild
Can see fever, jaundice (N/V, dark urine)
Ave. time from exposure to symptom onset = 4-12 wks

123
Q

acute HCV prognosis

A

25% will clear the infection
75% will develop chronic infection

of those chronically infected & not treated
65% will develop chronic ds
5-20% will develop cirrhosis over 20-30 yr period
1 in 5 will die from consequences of chronic infection (cirrhosis or HCC)

124
Q

chronic HCV

A

usually asymptomatic until late disease
Symptoms of late liver disease
Fatigue/Malaise
Signs of liver not functioning such as ascites, jaundice

125
Q

HCV management

A

Acute & Chronic HCV managed similarly
Depends on genotype (1-6) & subtype (there are > 50)
Genotype 1 is most common in U.S

126
Q

HCV therapy

A

in 2011 a highly effective (curative) HCV protease inhibitor was released however it is very expensive

127
Q

prevention of HCV

A

Avoid high risk behaviors & exposures

128
Q

Prevention og HCV complications

A 
Screen (with HCV Ab):
Everyone born 1945 to 1965
Injection drug users
Recipients of blood products before 1992
Persons with HIV
Persons with known exposure

Test* anyone with signs or symptoms, like an ↑ALT or AST

129
Q

HCV labs

A

Start with HCV antibody
If +, check for HCV RNA
If HCV RNA virus is +, pt has HCV
if HCV RNA not present – may have cleared infection (most likely) or HCV antibody was a false positive.
If pt has HCV – refer to specialist who will do viral genotyping & may assess degree of liver damage prior to initiating treatment

130
Q

does having Hep C in the past provide immunity for re infection

A

no, unlike other infections, having had Hep C does not provide immunity to re-infection

Diagnostic medicine (9 decks)

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