Clinical Enzymology Cardiac markers Flashcards
Type of cardiovascular disease affecting the heart
Coronary heart disease
Manifestation of coronary heart disease
Angina/angina pectoris (chest pain), acute myocardial infarction
Type of cardiovascular disease affecting the brain
Cerebrovascular diseases
Conditions under cerebrovascular diseases
Stroke, transient ischemic attacks (lack of blood supply)
Type of cardiovascular disease associated with ischemic conditions
Peripheral arterial disease
Symptoms of peripheral arterial disease
Acute localized pain in arms and legs
Type of cardiovascular disease associated with increased blood pressure
Aortic Atherosclerotic Disease
Cause of aortic atherosclerotic disease
Build-up of fatty streaks or plaques
Complication of aortic atherosclerotic disease
Formation of blood clots
Consequence of abnormal weakening of the artery
Aneurysm
Condition related to tears in the thoracic or abdominal aorta
Aortic dissection
Types of cardiac markers
Myoglobin, CK-MB, Troponin I, Troponin T, CK, LDH
Angina also known as
Chest pain
Type of angina after strenuous activity without underlying injury
Stable angina
Characteristics of stable angina
Activity-related, no increase in cardiac markers
Type of angina associated with acute myocardial infarction
Unstable angina
Effect of unstable angina on cardiac markers
Increases cardiac markers
Classic manifestation of angina
Chest pain (squeezing pain), burning feeling, difficulty in breathing
CK isoenzymes
CK-BB (CK-1), CK-MB (CK-2), CK-MM (CK-3)
CK-BB (CK-1) characteristics
Widely distributed, not detected normally, fastest in electrophoresis
CK-MB (CK-2) characteristics
Found in the heart
CK-MM (CK-3) characteristics
Present in skeletal muscle and the heart
Tissue sources of CK
Brain, Heart, Skeletal muscle
Pronounced elevation of CK (>5x UL)
Duchenne’s muscular dystrophy, polymyositis, dermatomyositis, myocardial infarction
Mild to moderate elevation of CK (2-4x UL)
Acute agitated psychosis, alcoholic myopathy, severe exercise, delirium tremens, severe ischemic injury, pulmonary infarction, intramuscular injections, hypothyroidism, muscular trauma
Reference range for CK in males
15–160 U/L
Reference range for CK in females
15–130 U/L
CK-MB normal percentage of total CK
<6% of total CK
Main form of CK in serum
94%-100% is CK-MM
Cofactor and activator of CK
Magnesium Ion
CK isoenzyme with fastest migration to the anode
CK-BB (CK-1)
CK isoenzyme found in the heart
CK-MB (CK-2)
CK isoenzyme present in skeletal muscle and heart
CK-MM (CK-3)
Non-clinically significant CK isoenzyme
Macro-CK
CK isoenzyme associated with immunoglobulin and seen between CK-MM and CK-MB
Macro-CK
CK isoenzyme detected in extensive tissue damage and poor prognosis
Mitochondrial-CK
CK isoenzyme detected in malignant tumors and cardiac abnormalities
Mitochondrial-CK
Specimen consideration for CK determination
Avoid prolonged storage (CK1 most labile), avoid chelators and gross hemolysis (adenylate kinase)
Total CK analysis method with decreasing pattern
Tanzer-Gilvarg (Forward method)
pH for Tanzer-Gilvarg method
Alkaline at 9.0
Reaction in Tanzer-Gilvarg method
Creatine to creatine phosphate conversion, Diphosphate reacts with phosphoenolpyruvate (uses pyruvate kinase)
Product in Tanzer-Gilvarg method
Lactate + NAD
Preferred method for CK determination
Oliver-Rosalki (Reverse method)
pH for Oliver-Rosalki method
37050
Reaction in Oliver-Rosalki method
Creatine phosphate to creatine
Product in Oliver-Rosalki method
6-Phosphogluconate + NADPH
Regulator of calcium dependent interactions of actin and myosin filament; attached to actin via tropomyosin
Cardiac troponin
Three-protein complex in cardiac troponins
TnT, TnI, TnC
Preferred sample for cardiac troponins
Heparinized plasma
High sensitivity troponins
Can detect acute myocardial infarction (MI)
Reference value for troponins
0-10 ng/mL
Troponins during heart injury
Elevates during/after injury to the heart
Marker for cardiac injury
Troponin T and I
General marker for muscle injury; nonspecific to heart
Myoglobin
First for muscle injury (rise time)
1 to 4 hours
Rise time of lactate dehydrogenase
8-12 hours or 12-24 hours
Rise time of AST
6-8 hours
Rise time of CK-MB
4-6 hours
Rise time of troponin I and T
3-4 hours or 3-12 hours
Rise time of myoglobin
1-3 hours
Peak time of myoglobin
5-12 hours
Peak time of troponin I
14-20 hours
Peak time of CK-MB
12-24 hours
Peak time of AST
18-24 hours
Peak time of LD
48-72 hours
Normalizing time of myoglobin
18-30 hours
Normalizing time of troponin I
5-10 days
Normalizing time of CK-MB
2-3 days
Normalizing time of AST
4-5 days
Normalizing time of LD for monitoring
10 days
Cardiac marker similar to myoglobin but more specific to the heart; higher sensitivity but lower specificity
Heart type fatty acid binding protein (H-FABP)
H-FABP appears _____ after angina
3-6 hours
Predictor of acute myocardial infarction (AMI)
Ischemia-Modified Albumin (IMA)
Binding of ischemia-modified albumin
Binds copper, not always present
Markers of plaque instability
Myeloperoxidase (MPO), C-reactive protein (CRP), Myeloid related protein 18/4 (MRP-18/4), Pregnancy associated plasma protein A (PAPP-A)
Similar to Troponin in early detection of AMI
Markers of plaque instability
Used to rule out congestive heart failure
B-Type Natriuretic Peptide and C-reactive protein
Linked to atherosclerosis and thrombosis
Homocysteine
Least tissue specific enzyme
Lactate dehydrogenase (LDH)
Tissue source for LD1 (fastest)
Heart, RBCs, Renal cortex
Tissue source for LD2
Lungs, lymphocytes, spleen, pancreas
Tissue source for LD3
Liver, skeletal muscles
Tissue source for LD4 and LD5 (slowest)
Liver, skeletal muscles
Normal serum LD ratio
LD2 > LD1
Flipped ratio LD1 > LD2 indicates
MI, hemolytic disease, megaloblastic anemia, renal function issues
Significance of LD-6 elevation
Arteriosclerotic cardiovascular failure, grave prognosis (impending death)
Intracellular ratio of LD
LD1 > LD2
Pronounced elevation of LD (greater than 5x normal)
Megaloblastic/pernicious anemia, renal infarction, systemic shock, hypoxia, hepatic metastases, hepatitis
Moderate elevation of LD (3-5x normal)
Myocardial infarction, hemolytic conditions, pulmonary infarction, muscular dystrophy, delirium tremens, leukemias, IM
Slight elevation of LD (up to 3x normal)
Most liver diseases, nephrotic syndrome, hypothyroidism, cholangitis
Specimen considerations for LD determination
Avoid hemolysis, avoid cold storage (LD5 most cold labile), avoid chelators
LDH-5 elevation significance
Occurs concurrently with LD6 in severe circulatory insufficiency
Role of LD6 in alcohol metabolism
Metabolizes alcohol; not normally found in the blood
Macromolecular complex of LDH
LDH complexed with IgA and IgG; migrates between LDH-3 and LDH-4
Condition with highest total LD
Pernicious anemia
LD elevation in liver disorders, AMI, pulmonary infarction
2-3x increase
LDH isoenzyme elevated in skeletal muscle disorders
LD5
Method for LD testing (forward reaction)
Wacker method
Reaction in Wacker method
Lactate + NAD+ → Pyruvate + NADH + H+
Product of Wacker method
NADH + H+
Method for LD testing (reverse reaction)
Wroblewski-Ladue method
Reaction in Wroblewski-Ladue method
Pyruvate + NADH + H+ → Lactate + NAD+
Product of Wroblewski-Ladue method
Lactate + NAD+
Reference range for LD
100–225 U/L (37°C)