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Diagnostic Studies, Unit IV > LFTs and Gamma-Glutamyl Transferase (GGT) > Flashcards

LFTs and Gamma-Glutamyl Transferase (GGT) Flashcards

1
Q

Normal Ranges, GGT

(just view, don’t memorize)

A

Peds + Adults > 45 yo: 8-38 units/L

Adults > 45 yo: 5-27 units/L

Elderly: slightly higher values

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2
Q

Indications, GGT

(1 general, 4 specifics)

A

General: Sensitive indicator for hepatocellular disease

Specifics: most sensitive liver enzyme for detecting

  1. Billiary obstruction
  2. Cholangitis
  3. Cholecycstitis
  4. Alcohol abuse
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3
Q

GGT Clinical Function and Location

A

Function: involved in transmembrane amino acid and peptide movement

Location: highest concentrations in

  1. Liver
  2. Biliary tract
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4
Q

Differentials, Inc GGT

(4)

A
  1. Liver disease
    • Hepatitis
    • Cirrhosis
  2. Hepatic tumor/mets
  3. EtOH ingestion (acute)
  4. EBV (due to hepatosplenomegaly)
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5
Q

Liver Function Test (LFT) Pannel

(9 tests)

A
  1. Total protein
  2. Albumin
  3. Alkaline phosphatase
  4. AST (SGOT)
  5. ALT (SGPT)
  6. LDH
  7. Total bilirubin
  8. Direct bilirubin
  9. Indirect bilirubin
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6
Q

Indication, Total Protein

(5)

A

Used to diagnose, evaluate, and monitor malabsorption-related disaeses:

  1. Liver disease
  2. Intestinal/renal protein wasting states
  3. Immune disorders
    • ​All antibodies are made of protein
  4. Impaired nutrition
  5. Chronic edamatous states
    • ​Leaked fluid is pulled back by albumin. Low albumin = high edema
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7
Q

Clinical Significance of Protein

(5 functions)

A
  1. Muscle structure
  2. Enzyme structure
  3. Transport substances
  4. Cell membrane structure (specifically, channels)
  5. Osmotic pressure
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8
Q

Total Protein Components

(3 c defining characteristics/functions)

A
  1. Prealbumin
    • function - transport thyroxine, a thyroid hormone
  2. Albumin​
    • ​formed w/i liver
    • ~60% of total serum PRO
    • 1/2 life = 12-18 days, so change in albumin prdctn may not be realized for months
    • function - transport drugs, hormones, enzymes
  3. Globulins
    • ​key components of the following
      • antibodies
      • glycopro
      • lipid pro
      • clotting factors
      • complement pro
    • three types
      • alpha
      • beta
      • gamma
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9
Q

Globulin Subtypes

(3, major roles of each)

A
  1. Alpha - all in GI and pulmonary tissues
    • **Alpha 1 antitrypsin **- prevent lung elastic tissue breakdown, deficiency will cause emphasema
    • Haptoglobin
    • Prothrombin
    • Cholinesterase
  2. Beta
    • ​Lipopro
    • Plasminogen
    • Fibrinogen
  3. Gamma
    • ​Immune globulins
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10
Q

Differential, Increased Gamma Globulin Levels

(5)

A

Antibody responses

  1. Multiple myeloma - pro leak from neoplastic plasma cells
  2. Chronic inflmmatory disease - RA, SLE, etc have asst autoantibodies
  3. Malignancy - leukemias and lymphomas (esp CLL - plasma cell leukemia)
  4. Cirrhosis - pathophys unknown
  5. Infection - acute or chronic, resulting in antibody response

*Note - first you will see an increase in total protein then order a protein electrophoresis to reveal gamma globulin specifically *

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11
Q

Differential, Decreased Gamma Globulin Levels

(2 categories, 1/3 specifics)

A
  1. Genetic immune disorders
  2. Secondary immune deficiency
    • ​Steroid use - anti-inflammatory effect depresses gamma
    • Nephrotic syndrome - losing protein thru kidney
    • Leukemia - * abnormal WBC aren’t producing appropriate antibody levels *
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12
Q

Indications, Albumin Testing

(3)

A

Measure the following parameters

  1. Nutritional status
  2. Hepatic fctn
  3. Renal fctn
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13
Q

Clinical Significance, Albumin

(4)

A
  1. Hepatic synthesis
  2. Approximately 60% of plasma PRO
  3. Major contributor to plasma osmotic pressure
    • ​​*Push albumin c IV fluids to prevent edema *
  4. Significant in transport of
    • ​Fatty acids
    • Thyroid hormones
    • Steroid hormones
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14
Q

Differential, Increased Albumin

(1)

A

Dehydration

*As intravasular volume decreases, [albumin] increases *

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15
Q

Differential, Decreased Albumin

(7)

A
  1. Malnutrition (causes lack of aa and liver dysfunction)
  2. Pregnancy (increased demands)
  3. Hepatic disease (site of albumin synthesis)
    • Hepatitis
    • Cirrhosis
    • Metastatis liver tumor
  4. Malabsorption syndrome
    • Crohn’s disease
  5. Nephrotic syndrome
  6. Third space losses
    • Ascites
    • Third degree burns
  7. Overhydration
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16
Q

Indications, Alkaline Phosphatase

(2)

A

Detect and monitor changes in the sites of alkaline phosphatase prdctn:

  1. Liver
  2. Bone
17
Q

Location/Function, Endogenous Alkaline Phosphatase

(3)

A
  • Liver*
  • Location - liver and biliary tract epithelial Kepffer cells
  • Bone*
  • Most frequent extrahepatic ALP source
  • New bone growth = inc. ALP
    • consider this when reviewing labs of peds
18
Q

Alkaline Phosphatase Isoenzymes

(list 2 and their functions)

A

Function: distinguish between bone and liver disease

  1. ALP1 = liver
  2. ALP2= bone
19
Q

Differential, Inc Alkaline Phosphatase Levels

(6)

A
  1. Primary cirrhosis
  2. Biliary obstruction
    • ​Intrahepatic
    • Extrahepatic
  3. Liver tumor
    • ​Primary
    • Metastatic
  4. Normal bones of growing children
  5. Healing fx
  6. Paget’s Disease (bone growth/destruction disease)
20
Q

Aspartate Aminotransferase (AST) Alternate Name

A

Serum Glutamic Oxaloaceitic Transaminase (SGOT)

Only really referred to as AST

21
Q

Indications, AST testing

(2)

A
  1. Suspected occlusive CAD
    • ​Old method for MI determination
  2. Suspected hepatocellular disase
22
Q

Endogenous AST

(6 locations, life process)

A

Process: released from lysed cells

  • Directly related to # of cells injured
  • Correlates to time of injury
    • elevates 8 hrs post injury
    • peaks 24-36 hrs post injury
    • normalizes 3-6 days post inury

Location:

  1. Heart
  2. Liver
  3. Skeletal muscle
  4. Pancreas
  5. RBC
  6. Kidney

*Note: not a helpful test by itself *

23
Q

Differential, Increased AST

(5 categories, 4/4/4/1/1 specifics)

A
  • Cardiac
    1. MI
    2. Cardiac surgery
    3. Cardiac catheterization
    4. Angioplasty
  • Liver
    1. Hepatitis - inc up to 20x normal (~700)
    2. Cirrhosis
    3. Hepatic mets
    4. Infectious mono c hepatitis
  • Skeletal muscle
    1. ​Trauma
    2. Noncardiac surgery
    3. Severe deep burns
    4. Seizure
  • Pancreas
    1. Acute pancreatitis
  • Acute extrahepatic obstruction
    1. ​​Gallstone - inc 10x normal
24
Q

Differential, Decreased AST

(2)

A
  1. Acute renal disease
  2. Chronic renal dialysis
25
Alanine Aminotransferase (ALT) Alternate Name
Serum Glutamic Pyruvic Transaminase (SGPT)
26
Indications, ALT Testing | (2)
*Hepatocellular disease management, **more liver-specific** than other LFTs:* 1. Disease identification 2. Treatment monitoring
27
Endogenous ALT
Injury or disease to liver cells will release this enzyme
28
Indications, ALT Testing
**Most commonly used c AST in dtermining the type of liver disease** Both sensitive and specific
29
Differential, Increased ALT | (6)
1. Hepatitis 2. Hepatic necrosis 3. Cirrhosis 4. Cholestasis - stagnant bile, usually secondary to obstruction 5. Hepatotoxic drugs 6. Obstructive jaundice
30
Indications, Lactic Dehydrogenase (LDH) Testing (7)
Release of the intracellular enzyme in one of the following tissues 1. Heart 2. Liver 3. RBC 4. Kidney 5. Skeletal muscle 6. Brain 7. Lung
31
Endogenous LDH
* Intracellular enzyme found in many tissues * not a specific test for dx * Diseased or injured cells lyse and release LDH into bloodstream * **5 total isoenzymes comprise total LDH** * **​**LDH1 - heart * LDH2 - reticuloendothelial system (majority) * LDH3 - lungs * LDH4 - kidney, placenta, pancreas * LDH5 - liver, striated muscle
32
LDH Progression c MI
* Initial rise = 24-48 hours post MI * Peak = 2-3 days post MI * Normalize = 5-10 days post MI *Usefulness (not highly utilized)* * Determine MI severity * Track healing
33
Differential, Increased LDH | (7)
1. RBC disease *(hemolytic or megaloblastic anemia)* 2. MI 3. Pulmonary disease *(embolism, infarction, pneumonia, CHF)* 4. Hepatic disease 5. Muscular dystrophy 6. Renal parenchymal disease 7. Neoplastic states
34
Categories of Bilirubin Testing | (3)
1. Total bilirubin 2. Direct/conjugated bilirubin: 70-85% total 3. Indirect/conjugated bilirubin: 15-30% total
35
Indications, Bilirubin Testing | (3)
1. Evaluate liver fctn 2. Hemolytic anemias 3. Newborn jaundice, often result of ABO incompatibility b/w mother and baby
36
Bilirubin Prdcn Process
1. RBC breakdown by spleen 2. Hgb release 3. Hgb → heme + globin 4. Heme → biliverdin (intestines) 5. Biliverdin → **indirect bilirubin** (travels to liver) 6. **Indirect bilirubin → direct bilirubin (in liver)** 7. Direct bilirubin excreted in bile 8. Bile breakdown by gut bacteria into urobilinogen and stercobilinogen 9. Excretion * ​Stercobilinogen - feces (gives feces brown color) * Urobilinogen - kidneys + reabsorbed
37
Jaundice | (corresponding lab result, 3 causes)
_Causes_: 1. Bilirubin metabolism defect 2. Bilirubin excretion defect 3. Physiologic newborn jaundice * ​Insufficient amt of conugating enzymes due to ABO compatibility from mother * High unconjugated bili * Left untreated (via phototherapy), may cross BBB to cause encephalopathy (kernicterus) _Lab_: TBili \> 2.5 mg/dl
38
Adult Jaundice | (2 pathophys, 2/4 causes)
***Post-Conjugated*** _Pathophy_: increase in **direct bilirubin** due to defect after conjugation _Causes_: extrahepatic dysfunction at common bile duct 1. Gallstone obstruction 2. Tumor ***Pre-Conjugated*** _Pathophys_: defect before conjugation, increasing **indirect bilirubin** _Causes_: intrahepatic or extrahepatic 1. Hepatocellular dysfunction - hepatitis, cirrhosis 2. Hemolysis 3. Drugs 4. Gilbert syndrome - congenital enzyme deficiency that interrupts bilirubin conjugation

Diagnostic Studies, Unit IV (7 decks)

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