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GI / Hepatology > 4 - Jaundice & LFTs > Flashcards

4 - Jaundice & LFTs Flashcards

1
Q

Elevated ALT - Cause

A

I don’t fucking know. That shit just happens sometimes

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2
Q

15% of patients with Chronic Liver disease (HCV or NAFLD)

A

Have NORMAL liver tests despite having histologic damage

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3
Q

New Recommendations for the cut off for aminotransferases

A

Men - 31

Women - 30

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4
Q

Dangerzone - Hepatocytes

A 
Well-differentiated
80% of cytoplasmic mass
Have the ability to replicate in injury
Secrete bile acids
Take up digested material
Synthesize albumin
Metabolize and detoxify exogenous compounds
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5
Q

Dangerzone - Biliary Tree

A

Bile is secreted by hepatocytes
Cholestasis is caused by alterations in microfilaments surrounding bile canaliculus
Alterations can be induced by toxins, infection or obstruction
Obstruction may be intrahepatic or extrahepatic

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6
Q

Liver Functions

A

Measure of SYNTHETIC activity, not inflammation!!!!!!

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7
Q

“True” liver function tests measure

A

Protein synthesis (albumin, coag factors)
Nutrient Metabolism (Gluconeogenesis - the last thing to go)
Biotransformation (bilirubin glucoronidation)
Immune Defense
Bile Acid Synthesis

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8
Q

Synthetic Function Tests

A

PT - Production of coag factors
Most have half-lives between 6 - 96 hours and prolonged within a day with hepatic synthetic dysfunction

Albumin - Produced in hepatocytes half life is 20 days but not specific can be abnormal because of the other factors that can lower, including poor nutrition,

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9
Q

Bilirubin Test

A

Can be a marker of impaired synthetic function

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10
Q

Labs - Bilirubin

A

Breakdown product of heme cells released from senescent red blood cells and from hemoprotein in the liver
Natural compound circulates with albumin and is taken up by liver and secreted in the bile

If bile secretion is impaired, conjugated bilirubin may leak into plasma and cause jaundice

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11
Q

Alkaline Phosphatase

A

A family of isoenzymes that catalyze the hydrolysis of phosphatase esters

Found in liver, bone, intestine, placenta, kidney, leukocytes

In liver associated with sinusoidal and canalicular membranes

Obstruction to bile flow causes an increase in AP secondary to the induction of AP synthesis

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12
Q

Aminotransferases (AST, ALT)

A

Naturally found in the serum at low levels

AST is also found in cardiac muscle, skeletal muscle, kidney, pancrease, lungs, leukocytes

Both enzymes are released in the blood in increasing amounts when the hepatocyte membraen is damaged

Correlated in injury byt not to chance of recovery

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13
Q

INR of 2

A

Bad

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14
Q

γGlutamyl Transpeptidase (GGT)

A

Catalyzes transfer of glutamyl groups of peptides suc has glutathione to other amino acids

Found in liver, kidney, seminal vesciles, liver, spleen, heart, brain, not bone

VERY SENSITIVE, limited specificity

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15
Q

AST - Location

A

Mitochondria and cytosol of hepatocytes, heart and muscle

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16
Q

ALT - Location

A

Cytosol of hepatocytes

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17
Q

Alk Phos

A

Microvilli of the bile canaliculi, bone, placenta

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18
Q

Hepatocellular Pattern

A 
AST +++
ALT +++
Alk Phos +
TB +
GGT +
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19
Q

Cholestatic Pattern

A 
AST +
ALT +
Alk Phos +++
TB +++
GGT +
20
Q

Infiltrative Pattern

A 
AST +
ALT +
Alk Phos +++
TB +
GGT +
21
Q

Ultrasound - Use

A

Biliary Obstruction, Masses, Vasculature
$

Biliary Tree:
Rule out obstruction
Evaluate for presence of stones

Vasculature:
Evaluate flow, rule out obstruction
Screen for thrombus
Screen for stricture

22
Q

CT or MRI/MRCP - Use

A

HCC, Mets
$$

3D imaging
Demonstrates morphology of the liver
Evaluate for size, position
Evaluate for bleeding
Evaluate for tumors, both benign of malignant

Will not evaluate for liver function and is not sensitive enough to detect fibrosis of the liver
Rarely reveals exact etiology of disease

23
Q

ERCP - Use

A

Evaluate and Treat Biliary Obstruction
$$$$

Endoscopic cannulation of the ampulla with injection of contrast into the biliary tree
Diagnosis and therapy

24
Q

EUS

A

Endoscopy using ultrasound technology to locate masses, lymph nodes, evaluate bile ducts

25
Q

Liver biopsy

A

Provides diagnostic and prognostic information
Performed if expected benefit exceeds risk of procedure
Complications requiring hospitalization (1.4 - 4%)
Severe hemorrhage, pneumo, peritonitis (.1 - .3%)
Mortality rate of 9/100,000

26
Q

Disease Identification - Hepatocellular Disease

A

History, Serology, Virology, Biopsy

```
Viral Hepatitis
A, B, C, D, E, EBV, CMV
Drug Induced Liver Disease
(Acetaminophen, INH)
Autoimmune Hepatitis
~~~

27
Q

Disease Identification - Cholestatic Disease

A

Imaging

Obstruction of Biliary Tree
Gallstones, Pancreatic Mass, Ampullary Mass
Drug Induced Liver Injury
(Augmentin)

28
Q

Disease Identification - Infiltrative DIsease

A

Imaging, Biopsy

Sacroid, Tuberculosis, Fungal Infections, Lymphoma

29
Q

Painless Jaundice

Double Duct Sign

A

Know what that means I was scanning my shit

30
Q

Elevated Unconjugated Bilirubin

A

Kids with something

Conditions overwhelming the system:
Sickle Cell Patients
ABO Mismatch blood transfusions –> Massive hemolysis

31
Q

Approach to Jaundice

A

Indirect/Unconjugated OR Direct/Conjuaged

32
Q

Jaundice - Indirect/Unconjugated

A

Hemolysis

Defect in Conjugation

33
Q

Jaundice - Direct/Conjugated

A

Hepatocellular

Cholestatic

34
Q

Jaundice - Direct/Conjugated - Cholestatic

A

Intrahepatic

Extrahepatic

35
Q

Drug Induced Liver Injury (DILI)

A

Liver is the most common target organ for toxicity
Hepatotoxicity has been linked to over 1000 drugs
Accounts for >50% of cases of acute liver failure
Most common cause of death from acute liver failure
Most frequent reason for withdrawal of drugs from the market

36
Q

Natural History of DILI

A

Wide spectrum of presentation from asymptomatic to fulminant hepatic failure
Mortality 8 - 10%
Mortality rate is higher in patients with jaundice at presentation

37
Q

Factors associated with injury - DILI

A 
Female Gender
Age
Diabetes
Obesity
Chronic Viral Disease
Alcohol**
Possible Nutritional Deprivation
Renal Function
38
Q

Causative Agents - DILI

A

73% of cases are from a single prescription agent:

Antimicrobials - 45%
CNS agents - 15%
Immunomodulatory Agents - 5.5%
Analgesics
Antihypertensives
Antineoplastic
Lipid Lowering Agents - 3.4%

9% dietary supplements

39
Q

Mechanisms of Liver Injury

A

Binding of Drug to intracellular proteins:
Ionic gradients
Decline in ATP
Actin disruption, cell swelling & cell rupture

Drugs that affect transport proteins at the canalicular membrane

Drugs bound to enzymes (adducts):
Antibody Formation
Direct cytolytic T-Cell Responses with cytokine formation

Activation of TNF receptor or FAS

Inhibition of mitochondrial function

40
Q

Types of hepatotoxicity - Intrinsic

A 
More predictable
Affects all individuals
Cause toxicity in dose-dependent manner
liver as target-injury to the tissue occurs at doses below those that are lethal
Predictable pathology
41
Q

Sensitivity to Intrinsic Hepatotoxins

A

Inflammatory Stress - LPS

Environmental Cofactors - Alcohol (Induction of CYP2E1 - increased reactive metabolite)

42
Q

Acetaminophen Toxicity

A

Cluguronide and sulfate metabolites (85 - 95%)

Toxite Metabolite NAPQI
Mercapturic Acid Cysteine Conjugates (5 - 10%)

NAPQI leads to depletion of intracellular glutathione which inactivates the potent electrophile. This electrophile then binds to cell macromolecules and disrupts mitochondrial function

43
Q

Types of hepatotoxicity -Idiosyncratic

A 
Infrequent
Attacks susceptible individuals
Not clearly dose related
Variable Onset (average 5 - 90 days)
Variable Pathology
Not predictable with animal testing
44
Q

Idosyncratic Liver Injury - Allergic Reactions

A

Fever, rash, eosinophilia
Latency 1 month or less
Rapid recurrence after re-exposure (example, sulfa drugs)

45
Q

Idiosyncratic Liver Injury - Non-Allergic

A 
No features of hypersensitivity
Long latency (often many months)
Re-challenge does not consistently reproduce the injury (example amiodarone)
46
Q

Stevens Johnson Syndrome

A

Sulfa Drugs

Phenytoin

GI / Hepatology (28 decks)

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