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23 Cards in this Set
- Front
- Back
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requirements for cardiac biomarkers
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-measurability
-incremental value -patient management -patient impact |
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myoglobin
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-O2-bearing heme protein found in skel muscles and the heart
-early maker of AMI -rapidly cleared by renal filtration -non-specific AMi marker |
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rise of myoglobin
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-rises 1 hr after MI
-peaks 2-12 hours after -return to normal in 24 hours |
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what other conditions cause inc myoglobin?
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-skeletal muscle injury
-chronic renal failure (retention) |
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creatine kinase
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-3 cystolic isoenzymes
-CKMM, CKMB, CKBB -CKMB is high in heart -CKMB/totalCK>3% suggests cardiac damage |
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rise of CKMB
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-rises within 2-4 hours
-peaks at 12-24 hours -returns to normal 48-72 hours |
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causes of increased CK
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-myocardial disease
-skeletal muscle disease/injury -miscellaneous (hypotyroid, prolonged hypothermia, cerebral injury) |
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cardiac troponin
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-important regulatory component of myocardial contractile apparatus (thin filament)
-its release from cardiomyocyte denotes serious and probably irreversible injury -highly specific |
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what causes cTN release into blood
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-ANY type of myocardial injury (not just ischemic injury)
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ESC/ACC definition of AMI
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-detection of rise/fall of cardiac biomarkers and at least one of the following:
-symptoms of ischemia, pathological Q waves in ECG, ST elevation or depression, imaging evidence |
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what is the preferred biomarker for the dx and risk stratification of pts with AMI
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-cTn
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what does an elevated cTn signal
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-higher acute risk
-adverse longterm prognosis |
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relationship with troponin I and T
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-not linear
-hemolysis cause dec cTnT and inc cTnI in some assays |
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analytical factors of cTn assays
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-serum vs plasma
-heparin can bind cTn masking epitopes -hemolysis cause dec cTnT and inc cTnI in some assays -lack of consistency btw assays |
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coronary artery disease as a precursor to AMI
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-begins with atherosclerosis, thickening of coronary arteries by lipid-filled plaques
-stable angina --> unstable -AMI occurs when thrombus fully occludes the coronary artery |
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c reactive protein
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-vascular inflamm to plaque rupture to ischemia to cell death to myocardial dysfunction
-measures vascular inflammation |
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hsCRP used for..
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-seen as strongest univariate predictor of AMI risk
-golden marker for inflamm and coronary artery disease |
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what are BNP and NTproBNP used for
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-dx of CHF
-differentiate CHF and COPD |
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brain natriuretic peptide (BNP)
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-32 AA hormone produced by ventricles of the heart
-in response: myocardial stretching, vol overload, inc ventricular filling pressures -counteracts effects of renin-angio-aldo system |
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NY heart Assoc categories of CHF (correlation with BNP)
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-I: without limitation on physical activity
-II: slight limit (may result in fatigue, palpitations, dyspnea, angina) -III: marked limit -IV: inability to carry on any physical activity without discomfort |
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BNP/NTproBNP
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-perform as part of diagnosis, but not really diagnostic
-low BNP means you can probably rule out CHF -level correlates to severity of HF |
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BNP vs NTproBNP
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-proBNP secreted by cardiomyocytes
-proBNP cleaved in circulation to BNP and NTproBNP -are proportional |
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BNP consideration
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-normal levels of BNP and NTproBNP increase with age
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