Unit 1: Liver Function Teest Flashcards by Wayne Glaiza Mappala

Yellow discoloration of the skin, eyes, and mucous
membranes

Jaundice

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3 Classifications of Jaundice

Pre hepatic
Hepatic
Post hepatic

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abnormality occurs before liver
metabolism

Pre hepatic jaundice

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abnormality occurs after liver
metabolism

Post hepatic

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Conjugation occurs but the problem is the
bilirubin in the form of B2 cannot be excreted
in the bile canaliculi causing jaundice and
causing its leaking in the bloodstream

Post hepatic jaundice

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serum or plasma sample with a yellow
discoloration due to an elevated bilirubin level

Icterus

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unconjugated hyperbilirubinemia

Pre hepatic jaundice

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Most commonly caused by an increased amount of bilirubin
being presented to the liver

Pre hepatic

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increased or continuous destruction of RBCs
so that, an increase in such causes now an
increased amount of bilirubin in the liver

Acute and chronic hemolytic anemias

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Pre hepatic lab results

Lab result: Elevated B1

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primary problem causing the jaundice resides in
the liver

Hepatic

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Caused by disorders of bilirubin metabolism (conjugation)
and transport defects (secretory functions of the liver)

Hepatic

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Syndrome of Chronic Nonhemolytic
Unconjugated Hyperbilirubinemia

Crigler-Najjar syndrome

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Associated with conjugation deficit

Crigler-Najjar syndrome

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complete absence of enzymatic bilirubin
conjugation

Crigler-Najjar syndrome type 1

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mutation causing a severe deficiency of
the enzyme (UDPGT) responsible for bilirubin
conjugation

Crigler-Najjar syndrome type 2

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Crigler-Najjar Syndrome lab result

Lab result: elevated B1

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Is caused by a genetic mutation in the gene
(UGT1A1) that produces UDPGT

Gilbert’s syndrome

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Gilbert’s syndrome Lab results

Lab result: Elevated B1

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Bilirubin excretion deficit

Dubin-Johnson syndrome and Rotor syndrome

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Dubin-Johnson syndrome and Rotor syndrome lab result

Lab result: Elevated B2

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A rare inherited disorder caused by a
deficiency of the canalicular multidrug
resistance/multispecific organic anionic
transporter protein (MDR2/cMOAT)

Dubin-Johnson syndrome

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Unique feature: appearance of dark-stained
granules on a liver biopsy sample

Dubin Johnson syndrome

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caused by mutations in SLCO181 and
SLCO1B3 genes (solute carrier organic
anion transporter fomily member 183/183
genes)

Rotor syndrome (Rotor hyperbilirubinemia)

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Neonatal hyperbilirubinemia a result of a deficiency in the enzyme UDPGT B1 is deposited in the nuclei of brain and nerve cells, causing kernicterus

Physiologic Jaundice of the Newborn

Treatment for Physiologic Jaundice of the Newborn

Phototherapy exchange transfusion pharmacological treatment

Baby is exposed to fluorescent lamp to convert B1 to water-soluble fragment ready for elimination

Conventional phototherapy

Applies a blanket (bili-blanket) ilagay sa likod ng baby to convert B1 into a double by-product for elimination.

Extensive phototherapy

Aliquot of blood from the baby and exchange with donors blood to solve hyperbilirubinemia.

Exchange transfusion

Will induce the activity of UDPGT

Phenobarbitone

Slow down the rate of hemolysis.

IV Immunoglobulins

Potent inhibitors of heme oxygenase. Competitive inhibitors.

Metalloporphyrins

Form of unconjugated hyperbilirubinemia caused by a circulating inhibitor of bilirubin conjugation

Lucey-Driscoll Syndrome

Lucey-Driscoll Syndrome lab result

Lab result: Elevated B1

o Occurs in breast-feed neonates (4-7th day of life). o Milk component inhibits enzyme UDPGT.

Breast Milk Jaundice Syndrome

Results from biliary obstructive disease (presence of gallstones or tumors) that prevent the flow of conjugated bilirubin into the bile canaliculi

Post hepatic

Stool becomes clay-colored

Post hepatic

Last stage of liver failure

Cirrhosis

adverse immune response directed against the liver itself

Autoimmune hepatitis

plasma protein; deficient in patients with hepatic cirrhosis

a1-antitrypsin deficiency

characterized by the accumulation of copper in the brain, liver, and in other organs

Wilson Disease

there is iron overload

Hemochromatosis

inborn error of carbohydrate metabolism

Galactosemia

there is liver inflammation and there will be presence of infiltrates in the liver not associated with alcohol

Nonalcoholic steatohepatitis (NASH)

Treatment of cirrhosis

o Abstaining from alcohol o Medications – hepatitis-related cirrhosis ▪ Interferon – viral hepatitis ▪ Corticosteroids – autoimmune hepatitis

Classification of tumors

Primary Metastatic Benign Malignant

Begins in the liver cells

Primary tumor

Tumors from other parts of the body spread to the liver

Metastatic tumor

hepatocellular adenoma, hemangiomas

Benign tumor

o is also known as Hepatic adenoma o Caused by massive oral contraceptive pill intake.

Hepatocellular adenoma

o Cavernous hemangiomas o Tangled blood vessels.

Hemangiomas

hepatocellular carcinoma (most common; 90% of primary liver cancers) and bile duct carcinoma

Malignant

Associated with elevated ammonia

Reye’s syndrome

Lab results of Reye’s syndrome

Lab results: mild hyperbilirubinemia; elevated levels of ammonia and aminotransferases (AST and ALT)

Most common caused of hepatic toxicity.

Paracetamol (acetaminophen)

Lab results: slight elevations in AST, ALT, and GGT; biopsy shows fatty infiltrates in the vacuoles of the liver

Alcoholic fatty liver

Lab results: moderately elevated AST, ALT, GGT, and ALP; total bilirubin (> 30 mg/dL); AST/ALT ratio > 2; decreased serum albumin; prolonged PT

Alcoholic hepatitis

Lab results: increased liver function tests (AST, ALT, GGT, ALP, total bilirubin); decreased serum albumin; prolonged PT

Alcoholic cirrhosis

Implies injury to the liver characterized by the presence of inflammation in the liver tissue

Hepatitis

prolonged elevation of serum transaminase (ALP, AST, etc.) level (longer than 6 months – chronic hepatitis)

HBV and HCV

Routes of transmission Fecal-oral

HAV HEV

Route of transmission Parenteral sexual

HBV, HCV, HDV

Basis of commonly used methods today

CLASSIC DIAZO REACTION

Bilirubin + diazotized sulfanilic acid -> colored product (urine sample)

CLASSIC DIAZO REACTION

found that the diazo reaction may be applied to serum samples only in the presence of an accelerator (solubilizer)

VAN DEN BURGH

first clinically useful methodology for the quantitation of bilirubin in serum samples

EVELYN AND MALLOY

Evelyn and malloy o Accelerator: o Diazo A: o Diazo B: o Diazo Blank:

o Accelerator: 50% methanol (solubilizer) o Diazo A: 0.1% Sulfanilic Acid + HCl o Diazo B: 0.5% Sodium Nitrite o Diazo Blank: 1.5% HCl

pink to purple azobilirubin (red-purple) ▪ pH 1.2 ; 560 nm

Final reaction Evelyn and Malloy

candidate reference method for total bilirubin Requires the addition of buffer

JENDRASSIK AND GROF

Jendrassik and Grof Accelerator

caffeine sodium benzoate

Buffer of Jendrassik and Grof

Sodium Acetate

Jendrassik and Grof Final reaction:

pink to blue azobilirubin

Jendrassik and Grof required wavelength

600 nm

Involves the measurement of reflected light from the skin using two wavelengths that provide a numerical index

BILIRUBINOMETRY

Bilirubin found in Dubin-Jonnson

Delta bilirubin (measured as B2)

Total bilirubin 3 fractions:

Unconjugated, Conjugated, and Delta bilirubin

serum is preferred in this method

Evelyn and Malloy

Bilirubin conversion factor

17.1

Absence of urobilinogen from the urine and stool

Complete biliary obstruction

Urobilinogen reacts with p- dimethylaminobenzaldehyde (Ehrlich’s reagent) to form a ____ color, which is then measured spectrophotometrically.

Red

Spx for urine urobilinogen

fresh 2-hour urine specimen

most liver specific enzyme

Alanine amino transferase

Method AST

Karmen Method

Karmen method indicator

Malate dehydrogenase

Karmen Method Optimal pH

7.3 to 7.8

Karmen method wavelength

340 nm

METHOD: ALT

Coupled enzymatic reaction

Indicator method ALT

Lactate dehydrogenase Ph 7.3 to 7.8 340 nm

Found in very high concentrations in cases of extrahepatic obstruction

Alkaline phospatase

Is considered the most useful single technique for ALP isoenzyme analysis

ELECTROPHORESIS

ALP activity is measured before and after heating the serum at 56°C for 10 minutes.

HEAT FRACTIONATION / STABILITY TEST / HEAT DENATURATION

A continuous-monitoring technique which allows calculation of ALP activity based on the molar absorptivity of p- nitrophenol

BOWERS AND MCCOMB

Serum levels become significantly elevated in hepatobiliary disease

5’ - NUCLEOTIDASE

Highest levels of GGT are seen in biliary obstruction

Y-GLUTAMYLTRANSFERASE (GGT)

GGT substrate

: y-glutamyl-p-nitroaninide

High serum levels may be found in metastatic carcinoma of the liver.

Lactate dehydrogenase

L → P reaction (Lactate to pyruvate

WACKER METHOD (FORWARD/ DIRECT)

P → L reaction (Pyruvate to lactate)

WROBLEUSKI LA DUE (REVERSE/INDIRECT)

May be useful in following the progression of disease and the assessment of the risk of bleeding

Prothrombin time (Vit. K response test)

Prolonged PT

Severe Diffuse Liver Disease

Useful in quantitating the severity of hepatic dysfunction

SERUM PROTEINS

low due to decreased protein synthesis o Low/reduced in case of alcoholic cirrhosis, alcoholic hepatitis

Albumin

decreased in chronic liver disease o Low or absent α-globulin – α1-antitrypsin deficiency ▪ Deficient in patients with hepatic cirrhosis

a- Globulin

transiently increased in acute liver disease and remain elevated in chronic liver disease

Y-globulin

elevated in chronic active hepatitis

IgG and IgM

primary biliary cirrhosis

IgM

alcoholic cirrhosis

IgA

Fasting sample Lipemic

Bilirubin conc. Falsely ⬆️

Hemolysed sample

Bilirubin conc. falsely ⬇️

Fecal urobilonogen Spx

Aqueous extract of fresh feces

Any urobilin present is reduced to urobilinogen by treatment with ——- before Ehrlich’s reagent is added

alkaline ferrous hydroxide

Unit 1: Liver Function Teest Flashcards

(111 cards)