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Copy of LiverDance

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Patricia Raymond

on 25 November 2013

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Transcript of Copy of LiverDance

Patricia L. Raymond MD FACG
The Steps in Diagnosis of Abnormal Liver Tests
LiverDance:
Rx For Sanity, Norfolk VA
The Dance of the Liver Tests
Determine “Style” based on labs
Imaging studies or biopsy
More Labs
Directed Physical
Directed History
First Step: Hepatitic or Cholestatic?
Hepatitic
Viral
Alcoholic
NASH
Autoimmune
Hemochromatosis
Alpha-1 Antitrypsin
Wilson’s Disease
Drug Induced
Cholestatic
Primary Biliary Cirrhosis (PBC)
Primary Sclerosing Cholangitis (PSC)
Structural Obstruction
Drug Induced
Low platelet count in correct setting is suggestive of portal hypertension
Do Not Use the Term “Liver Function Tests” (LFTs!)
Albumin
Cholesterol
Bilirubin
Prothrombin time
Hepatitic
SGOT/AST
SGPT/ALT
Cholestatic
Alkaline Phosphatase (ALP)
GGTP
5’ Nucleotidase
Second Step:
History Appropriate to Lab Style
Hepatitic Lab Values
Viral Hepatitis:
Transfusions, tattoos, IVDA, multiple sexual partners (>6/yr considered high risk), travel, work in day care or preschool, homosexuality Alcohol Induced: Precise ethanol intake
NASH:
Diabetes, hyperlipidemia
Autoimmune:
Amenorrhea, diabetes, thyroid disease, vitiligo, arthritis
Hemochromatosis:
FHx, diabetes, arthritis, impotence, FHx “early MI”
A1AT:
FHx, neonatal jaundice
Wilson’s:
FHx, personality changes, bone wasting, Fanconi’s syndrome, hemolytic anemia
Drug Induced:
Careful drug history
Cholestatic Lab Values
PBC:
Itching, Worse at noc and on palms/soles, FHx connective tissue disease, Raynaud’s, sicca, GERD, xanthelasma
PSC:
Itching, Sx of IBD (Ulcerative Colitis)
Structural:
Hx biliary surgery, abdominal pain/fever, acholic stool
Drug Induced:
Careful drug history
Step Three: Let’s Get Physical
Liver size and consistancy, palpable spleen or gallbladder
Spider nevi, palmar erythema, gynecomastia, caput medusae
Dupuytren's contractures, parotid gland enlargement, and testicular atrophy
An enlarged left supraclavicular node (Virchow's node) or periumbilical nodule (Sister Mary Joseph's nodule)
Assessment for ascites
Xanthelasmas
Kaiser-Fleisher Rings
Step Four: Let’s order more labs
Hepatitic:
Hepatitis profile (incl HBsAb, HBsAg, HBcAb), HCV Ab, Fe, TIBC
Second round: ANA, ceruloplasmin, AIAT phenotype, AFP
Cholestatic:
AMA, ANA, early ultrasound to image liver
Imaging Studies:
Ultrasound RUQ
- Economical, Liver texture, bile duct diameter, stones, ascites, liver/spleen size, masses, Best for HCC screening

CT
- masses, not too good for bile duct

ERCP/MRCP
- best image of biliary tree

Liver/Spleen scan
- Defines coloid shift, size- not too useful
Step Five (Last): The Liver Biopsy
Gold standard in liver diagnosis
Unclear etiology despite tests
Exclude other dx prior to rx with significant SE
Obtain tissue for diagnosis (Fe, Cu, neoplasm)
Obtain tissue for “staging” (HCV, NASH)
Side Step:
Discriminant
(Maddrey Score)
(4.6 X PT) + bili

If >32, 50% mortality in 1 month

Four-week course of Prednisolone (40 mg/day, typically stopped or followed by a taper over two to four weeks
Rehearsal!
Determine “Style” based on labs
Directed History
Directed Physical
More Labs
Imaging studies or biopsy
Case History #1
35 y/o male, malaise
SGOT 1200 SGPT 3000 T Bil 3.2 AP 120
Drinks “moderately” daily
Theraflu ingestion plus tylenol for flu
What do you do now?
Case History #2
70 y/o female, assymptomatic
SGOT 56 SGPT 74 AP 357 T Bil 2.1
Nocturnal pruritis
Case History #3
56 y/o male, executive, assymptomatic
SGOT 70 SGPT 85
Modest EToH (Social)
Extensive tattoos in past
Case History #4
80 y/o female, painless jaundice
SGOT 200 SGPT 350 AP 300 T Bil 12
Weight loss, acholic stools
Case History #5
48 y/o female, assymptomatic
SGOT 55 SGPT 47 AP nl T Bil nl
Mild obesity
Case History #6
35 y/o male, assymptomatic
SGOT 55 SGPT 45 AP nl T Bil nl
Moderate alcohol intake
Premature MI in relatives
Other stuff to learn:
Clinical presentation of autoimmune hepatitis and appropriate management

Indications for treatment and changes in treatment of chronic hepatitis C

Clinical presentation and management Gilbert’s syndrome

Some medications that may cause abnormal liver tests

Clinical presentation and diagnostic approach to Budd-Chiari syndrome
Alphabet Soup
Hepatitis A
1.Enteric
a.
Military personnel, Food handlers, Injection drug users, Travellers to endemic regions (essentially anywhere outside of North America, Western Europe and Japan)

b.
Occupational risk including healthcare workers, employees of mental health facilities and sewage workers, consumers of high-risk foods (e.g. raw shellfish)

c.
Patients with chronic liver disease - especially chronic hepatitis C - increased risk for fulminant hepatitis or death with HAV superinfection.
3. Hepatitis A
a.
Most HAV infections acquired in childhood are subclinical and anicteric, yet antibodies to the virus persist for life and provide immunity to further infection.

b.
In adults, 75 to 95% of infections are symptomatic, with jaundice in the majority of cases. Fulminant hepatic failure is rare but increases over the age of 40, and possibly in the context of underlying chronic liver disease.

c.
In some individuals, HAV causes a biphasic illness with a second bout of jaundice and cholestasis six to 12 weeks after the primary infection.

d.
Chronic HAV infection does not occur and liver enzymes are almost always normal within six months of infection.
Hepatitis B
HBsAg
= presence of the virus
HBcAg
= not detected in blood
HBeAg
= correlates with the viral replication and infectivity
anti-HBs
= antibodies to the surface
anti-HBc
= antibodies to the core can be either IgM (acute) or IgG (chronic)
anti-HBe
= antibodies to e and indicates low infectivity and probable recovery
Polyarteritis
- usually involves medium and small arteries, appears early

Glomerulonephritis
- largely in children, liver disease is usually mild

Polymyalgia rheumatica
- usually in older persons

Essential mixed cryoglobulinemia
- sometimes only a test tube finding

Guillain-Barre syndrome

Myocarditis
Very mild and often not clinically apparent.

Less than 15% of all cases of acute hepatitis in the USA.

Only about 15 - 25% of persons are jaundiced.

Antibodies to hepatitis C may take up to three months to detect .

Early diagnosis may be difficult.
About 20% of persons with acute hepatitis C fully recover and are felt to clear the virus

80% develop some form of chronicity.
Twenty-five percent of patients with chronic hepatitis will develop cirrhosis after 20 years

Of these, 5% will develop liver cell cancer and 5% decompensated cirrhosis.

Chronic hepatitis C infection causes chronic immune stimulation and autoimmune diseases are more frequent in hepatitis C.
Autoimmune diseases
may be seen either as presenting conditions or in association with hepatitis C.
Hepatitis D
Unique incomplete virus
Requires hepatitis B virus (HBV) for its replication

The RNA genome is covered by an outer coat of hepatitis B surface antigen.

Endemic in certain regions including the Mediterranean basin, the Balkan peninsula, the former Soviet Union, parts of Africa and the Middle East and the Amazon basin of South America.

Spread is intrafamilial and through sexual contact.
Depends on whether the virus was acquired as
a coinfection with hepatitis B

in acute self-limited hepatitis although fulminant hepatitis and death are well described.
a superinfection in an individual with a previously established chronic HBV infection.

typical course is one of a rapidly progressive chronic hepatitis.
Self-limited acute form of viral hepatitis that is typically spread by fecally contaminated water.

Endemic in developing countries

The most common cause of acute viral hepatitis worldwide, it is virtually unheard of in North America. Rare cases have been described in travelers returning from endemic regions.

The clinical hallmark of HEV infection is its extremely high mortality rate when infection occurs in pregnancy, particularly in the third trimester.

No HEV vaccine is yet available.

Comfry
Germander
Pennyroyal
Mistletoe
Kava
Chapparal
Ma-Huang
Ephedra
Senna
Cascara
Risk factors:
central obesity, type 2 diabetes mellitus, dyslipidemia, and metabolic syndrome

20 to 40 % of the general population

Symptoms:
most asymptomatic, rare fatigue, malaise, and vague right upper abdominal discomfort

Dx:
fat in liver (US), < 20 g alcohol daily, negative hepatitis B & C serology
AST and ALT elevated in 90 %
AST/ALT ratio is less than 1
Much lower than the ratio in alcoholic hepatitis (usually > 2)

Treatment:
Weight loss
Autosomal recessive defect of cellular copper export

Accumulation of copper, initially in the liver and then in other tissues, particularly the brain.

Hepatic, neurologic, hematologic, and renal impairment.
Kayser-Fleischer rings in 50 to 60 % with isolated hepatic involvement, > 90 % with neurologic involvement

Ceruloplasmin concentration < 20 mg/dL with Kayser-Fleischer rings is considered to be diagnostic.
Let’s Dance!
Invasive technique with significant complications
Let’s all rehearse the Liver Dance
2.HAV vaccination in :
Antigens
Antibodies
Hepatitis B
Extra-Hepatic Associations
: associated with hepatitis B antigen/antibody complexes.
Hepatitis C:
Acute
Hepatitis C:
Chronic
Hepatitis D:
Clinical Course
Hepatitis E
Medication
Almost any medication can cause an elevation of liver enzymes.

Common ones include nonsteroidal anti-inflammatory drugs, antibiotics, HMG-CoA reductase inhibitors, antiepileptic drugs, and antituberculous drugs.

In addition to prescription medications, herbal preparations and illicit drug use may also be the cause.
Herbs are safe
…not
NASH
Wilson’s Disease
Mooren corneal ulcers
Function
Diabetes
Mixed cryoglobulinemia
Thyroiditis
Erythema nodosum
Erythema multiforme
Glomerulonephritis
Hypothyroidism
Lichen planus
Polyarteritis
Urticaria
Porphyria cutanea tarda
Polymyalgia
B-cell lymphoma
LiverDance
“I just drink one beer a day.”
LiverDance
LiverDance
NASH
The liver takes a beating
Wilsons Disease
Wilsons Disease
Pretest
What are “Liver Function Tests” verses
“Liver Tests”?

What does SGOT/SGPT ratio tell you about the etiology of the liver damage?
What about AP out of proportion to TA elevation?
Do you know how to calculate discriminant
function? What do you do with it?
Interpreting liver tests

Alphabet soup
Some specific diseases

What we won’t cover:
Treatment
What we’ll cover today…
Full transcript