Send the link below via email or IMCopy
Present to your audienceStart remote presentation
- Invited audience members will follow you as you navigate and present
- People invited to a presentation do not need a Prezi account
- This link expires 10 minutes after you close the presentation
- A maximum of 30 users can follow your presentation
- Learn more about this feature in our knowledge base article
Copy of LiverDance
Transcript of Copy of LiverDance
The Steps in Diagnosis of Abnormal Liver Tests
Rx For Sanity, Norfolk VA
The Dance of the Liver Tests
Determine “Style” based on labs
Imaging studies or biopsy
First Step: Hepatitic or Cholestatic?
Primary Biliary Cirrhosis (PBC)
Primary Sclerosing Cholangitis (PSC)
Low platelet count in correct setting is suggestive of portal hypertension
Do Not Use the Term “Liver Function Tests” (LFTs!)
Alkaline Phosphatase (ALP)
History Appropriate to Lab Style
Hepatitic Lab Values
Transfusions, tattoos, IVDA, multiple sexual partners (>6/yr considered high risk), travel, work in day care or preschool, homosexuality Alcohol Induced: Precise ethanol intake
Amenorrhea, diabetes, thyroid disease, vitiligo, arthritis
FHx, diabetes, arthritis, impotence, FHx “early MI”
FHx, neonatal jaundice
FHx, personality changes, bone wasting, Fanconi’s syndrome, hemolytic anemia
Careful drug history
Cholestatic Lab Values
Itching, Worse at noc and on palms/soles, FHx connective tissue disease, Raynaud’s, sicca, GERD, xanthelasma
Itching, Sx of IBD (Ulcerative Colitis)
Hx biliary surgery, abdominal pain/fever, acholic stool
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
Step Four: Let’s order more labs
Hepatitis profile (incl HBsAb, HBsAg, HBcAb), HCV Ab, Fe, TIBC
Second round: ANA, ceruloplasmin, AIAT phenotype, AFP
AMA, ANA, early ultrasound to image liver
- Economical, Liver texture, bile duct diameter, stones, ascites, liver/spleen size, masses, Best for HCC screening
- masses, not too good for bile duct
- best image of biliary tree
- 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)
(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
Determine “Style” based on 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
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
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
Military personnel, Food handlers, Injection drug users, Travellers to endemic regions (essentially anywhere outside of North America, Western Europe and Japan)
Occupational risk including healthcare workers, employees of mental health facilities and sewage workers, consumers of high-risk foods (e.g. raw shellfish)
Patients with chronic liver disease - especially chronic hepatitis C - increased risk for fulminant hepatitis or death with HAV superinfection.
3. Hepatitis 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.
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.
In some individuals, HAV causes a biphasic illness with a second bout of jaundice and cholestasis six to 12 weeks after the primary infection.
Chronic HAV infection does not occur and liver enzymes are almost always normal within six months of infection.
= presence of the virus
= not detected in blood
= correlates with the viral replication and infectivity
= antibodies to the surface
= antibodies to the core can be either IgM (acute) or IgG (chronic)
= antibodies to e and indicates low infectivity and probable recovery
- usually involves medium and small arteries, appears early
- largely in children, liver disease is usually mild
- usually in older persons
Essential mixed cryoglobulinemia
- sometimes only a test tube finding
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.
may be seen either as presenting conditions or in association with hepatitis C.
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.
central obesity, type 2 diabetes mellitus, dyslipidemia, and metabolic syndrome
20 to 40 % of the general population
most asymptomatic, rare fatigue, malaise, and vague right upper abdominal discomfort
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)
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.
Invasive technique with significant complications
Let’s all rehearse the Liver Dance
2.HAV vaccination in :
: associated with hepatitis B antigen/antibody complexes.
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
Mooren corneal ulcers
Porphyria cutanea tarda
“I just drink one beer a day.”
The liver takes a beating
What are “Liver Function Tests” verses
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
Some specific diseases
What we won’t cover:
What we’ll cover today…