Term
| T/F Renal disease is a risk factor for CVD. |
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Definition
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Term
| What type of dialysis is a CVD risk factor? |
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Definition
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Term
| What laboratory biomarkers are CVD/CHD risk factors? |
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Definition
| lipid studies, inflammatory markers (hsCRP), hypercoagulability markers (homocysteine) |
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Term
| Which lipid studies are CHD process prediction markers? |
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Definition
| lipid studies, homocysteine |
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Term
| Which lab studies are CHD/ACS event predictors? |
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Definition
| inflammatory markers, ischemia markers |
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Term
| Which laboratory markers are used for CHD/ACS diagnosis and risk prediction? |
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Definition
| ischemic markers, cardionecrosis markers, natriuretic |
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Term
| What is the most common cause of death in the US? |
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Definition
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Term
| What causes the greatest malpractice cost in the ER today? |
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Definition
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Term
| What is the sensitivity of ECG for ACS/AMI? |
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Definition
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Term
| What are ancillary studies besides EKG and cardiac enzymes to diagnose heart disease? |
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Definition
| coronary angiography, radioisotopic scans and diagnostic imaging, echocardiography, stress testing (+/- isotopic scan) |
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Term
| Why are females iwth ACS often misdiagnosed? |
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Definition
| they present with back/shoulder pain |
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Term
| Can an MI have no symptoms? |
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Definition
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Term
| In what layer of the artery do atherosclerotic plaques buildup? |
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Definition
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Term
| What happens when a plaque ruptures? |
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Definition
| leads to release of content including collagen and tissue thromboplastin. This in turn triggers a thrombotic cascade with platelet activation, fibrin formation--> thrombus development |
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Term
| What is the 2007 definition of MI |
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Definition
| rise or fall of cardiac biomarkers with at least one value above 99th percentile of the upper reference limit with evidence for myocardial ischemia including at least one of the following= symptoms of ischemia, ECG changes, development of pathologic Q waves, imaging evidance for new loss of viable myocardium and/or new regional wall motion abnormality |
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Term
| What do the cardiac enzymes need to be to diagnose an MI after PCI? |
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Definition
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Term
| What do the cardiac troponins need to be to diagnose MI after CABG? |
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Definition
| >5 x 99% in patients with normal baseline and at least one of the following new pathologic Q waves or LBBB, angiographically documented new graft or native coronary artery occlusion, imaging evidence of new loss of viable myocardium or new regional wall motion abnormality |
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Term
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Definition
| sponatneous MI related to ischemia due to a primary coronary occlusion event such as plaque rupture with thrombosis |
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Term
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Definition
| MI secondary to ischemia due to either increased oxygen demand or decreased supply (spasm, embolism, anemia, arrhythmia, hypo-or hypertension) |
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Term
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Definition
| sudden cardiac death, often with symptoms of myocardial ischemia, accompanied by new ST elevation or new LBBB, or verified coronary thrombus b y angiography and/or pathology, but death occuring before blood samples obtained |
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Term
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Definition
a= PCI related
b= RE: to stent thrombosis |
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Term
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Definition
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Term
| Name the biomarkers that are used in diagnosis of acute myocardial infarction? |
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Definition
| CKMB, troponins (Tn), myoglobin (Myo) |
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Term
| Which enzymes quickly leak through damaged cell membranes? |
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Definition
| soluble intracellular fluid and constitutents= CKMB, myoglobin, some (5%) troponin |
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Term
| Which cardiac markers require more severe cell damage nd longer time for release into systemic circulation? |
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Definition
| troponin because it is a structureal molecule of formed elements |
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Term
| Which components of cardiac muscle cells are released into the blood directly upon necrosis? lymph? |
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Definition
blood= smaller proteins like myoglobin
lymph= larger proteins such as CKMB and troponin |
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Term
| What are the current recomendations for cardiac enzymes upon arrival? |
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Definition
| one definitive marker (troponin) and optional early marker (myoglobin) |
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Term
| How often do you remeasure cardiac enzymes after first measurement on admit? |
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Definition
| 3-6 hrs= definitive marker and optional if measured on admit; 6-9 hours= definitive; 12 hrs= definitive marker (+24 hr opt) |
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Term
| How quickly should cardiac enzyme enzymes be read? |
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Definition
| 60 minutes or less from vein to brain on first 2 collections if acute interventions available |
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Term
| What is the function of CK? |
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Definition
| creatine kinase= enzyme catalyzes reversible conversion of muscle pohsphocreatine to creatine + ATP |
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|
Term
| What is the structure of creatine kinase? |
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Definition
| exists as a dimer composed of 2 subunits, M and B; and thus 3 isoenzymes (MM, MB, BB) |
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Term
|
Definition
| skeletal muscle (95+) and cardiac muscle (60-80) |
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|
Term
|
Definition
| cardiac muscle (20-40%) and skeletal muscle (3-5%, but largest MB source) |
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|
Term
| What is the largest source of CKMB? |
|
Definition
|
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Term
|
Definition
| brain (CNS) and smooth muscle |
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Term
| What is the main use of CK total activity? |
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Definition
| biochemical assay= calculate CKMB % relative index |
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Term
| What is the old method for measuring CK isoenzymes? |
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Definition
|
|
Term
| CK isoenzymes measured by electrophoresis= |
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Definition
| almost entirely MM, usually no detectable BB; small amount of MB |
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Term
| How is CKMB currently measured? |
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Definition
|
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Term
| What are potentially confounding variables that can be corrected for when measruing someones cardiac enzymes? |
|
Definition
| URL method and gender of patient |
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|
Term
| How do you calculate CKMB % relative index? |
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Definition
|
|
Term
| What information does the CKMB percent relative index give you? |
|
Definition
if <3%= skeletal muscle source
if >5%= strong evidence for cardionecrosis
trace elevation= 3-5% (gray zone) |
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|
Term
| What are the CKMB isoforms? |
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Definition
|
|
Term
| What is the course of a CK-MB level following an acute cardiac episode? |
|
Definition
| beings to rise in 3-4 hours; peaks in 12 to 24 hours, returns to baseline in 24 to 36 hours; reinfarction (secondary rise)and extension (remain elevated) |
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Term
| What does a high CK index do to your specificity and sensitivity? |
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Definition
| adds specificity to high CK-MB as a gauge of cardiac injury and AMI, but decreases sensitivity |
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Term
| T/F Every MI has a positive CKMB index. |
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Definition
|
|
Term
| T/F it is uncommon to find nondiagnostic "trace" elevations of CK-MB index. |
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Definition
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|
Term
| Besides AMI and unstable angina, what other cardiac issues can cause trace CKMB? |
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Definition
| cardiac catheterization, tachyarrhythmias, myocardiits, some cardiomyopathies, etc. |
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Term
| What non cardiac causes can cause CK MB? |
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Definition
| rhabdomyolysis, hypothyroidism, degenerative skeletal myopathies (duchene's, renal failure with associated dialysis) |
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Term
| CKMB is _____but not truly cardiospecific. |
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Definition
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Term
| What percent of troponins are structurally bound within the cell and requires time for release? |
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Definition
|
|
Term
| LIst the three types of troponins? |
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Definition
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|
Term
|
Definition
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|
Term
|
Definition
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|
Term
|
Definition
| binds tropomyosin; localizes troponin complex along actin filaments |
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Term
|
Definition
| binds tropomyosin; localizes troponin complex along actin filaments |
|
|
Term
| Why are troponins so specific for cardiac muscle? |
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Definition
| because ther are specific forms of TnI and TnT that exist in both skeletal and cardiac muscle |
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|
Term
| Which type of troponin is used? |
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Definition
| either TnI or TnT b/c they are equally useful; 1st generation CTnT assays showed cross-rx with skeletal muscles but newer assays are OK. CTnI more common in US, CTnT more common in Europe |
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|
Term
| What is the course of troponin I after MI? |
|
Definition
| rise detectable in 3-6 hrs; peaks in 12 to 24 hours; remains elevated 4-7 days or more |
|
|
Term
| What is the significance of a normal TnI at 12+ hours after event? |
|
Definition
| nearly 1000% predictive value for no MI |
|
|
Term
| What is the course of troponin T levels after MI? |
|
Definition
| rise detectable in 3-6 hours; peaks in 12 to 24 hours; remains elevated as long as 10-14 days |
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|
Term
| Can troponins I and T be used outside of the acute setting? |
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Definition
| yes; can be used to assess risk of future cardiac complications and later development of MI |
|
|
Term
| What can cause false positives in troponin use? |
|
Definition
| cross reactions (less common with monoclona lantibodies), heterophile antibodies, non-specific binding (switch to plasma versus serum) |
|
|
Term
| What are the standardization issues with troponins? |
|
Definition
| CTnI in "many flavors" in blood: can be free (10-15%), binary complex with CTnC (80-90%), ternary complex with T and C, oxidized, reduced phosphorylated etc.This means that different assay antibodies don't see the same TnI so cuttoff points are highly method dependent |
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|
Term
|
Definition
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|
Term
| Why is the sustained elevation of troponin after initial acute cardiac event a disadvantage in some ways? |
|
Definition
| difficulty in detecting reinfarction or MI extension; look for secondary rise in CTn and/or use CKMB |
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|
Term
| What is the "false" false positive perception that might become a problem with troponins? |
|
Definition
| because troponins cannot identify the etiology of cardiac damage, MDs may come to not trust abnormal CTn values |
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|
Term
| T/F Both acute and chronic CHF can cause elevated troponins. |
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Definition
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|
Term
| T/F Asymptomatic patients after noncardiac surgery can have elevated troponins. |
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Definition
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|
Term
| T/F Renal failure can cause elevated troponins. |
|
Definition
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|
Term
| T/F Critically ill patients, esp with diabetes, can have elevated troponins. |
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Definition
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|
Term
| T/F Hypothyroidism can elevate troponins. |
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Definition
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|
Term
| T/F pumonary embolism can elevate troponins. |
|
Definition
|
|
Term
| T/F Amyloidosis can cause troponin elevation. |
|
Definition
|
|
Term
| What is the earliest practical MI marker? |
|
Definition
| myoglobin; rises 1.5 to 3 hrs after cardiac or skeletal muscle damage |
|
|
Term
| What is the course of myoglobin levels after MI? |
|
Definition
| rise in 1.5 to 3 hours; peak at 6-9 hours; return to baseline in 12 to 24 hours |
|
|
Term
| What are the problems with using myoglobin to assess cardiac necrosis? |
|
Definition
| high myoglobin not specific for cardiac injury, renal failure patietns have elevated baselines |
|
|
Term
| What is the main use of myoglobin levels when assessing patients for ACS? |
|
Definition
| to rule out an MI b/c it has a high negative predictive value |
|
|
Term
| T/F CTn is highly specific for both myocardial injury and acute myocardial infarct. |
|
Definition
| false; specific for myocardial injury but that can be due to many things besides AMI |
|
|
Term
| What are the three types of natriuretic peptides? |
|
Definition
|
|
Term
|
Definition
| atria in response to stretch |
|
|
Term
|
Definition
| ventricles in response to stretch |
|
|
Term
|
Definition
| formed in brain and vascular endothelium |
|
|
Term
| What's another name for the natriuretic peptides? |
|
Definition
|
|
Term
| What is the action of natriuretic peptides? |
|
Definition
| all three cause vasodilation and decrease in circulatory volume via natriuresis; antagonists of renin/angiotensin/aldosterone |
|
|
Term
| Which natriuretic peptide is measured and why? |
|
Definition
| BNP is most useful as cardiac biomarker; CNP exists at very low levels; ANP has much shorter half life than BNP |
|
|
Term
| What forms of BNP are measured? |
|
Definition
| both active hormone (BNP or B-type natriuretic peptide) and inactive fragment (NT-proBNP or N-terminal prohormone BNP) |
|
|
Term
| What are teh steps of formation and release of BNP? |
|
Definition
| pre-proBNP is cleaved into signal peptide and proBNP; proBNP is cleaved and both BNP and NT-proBNP are released into the blood |
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|
Term
| T/F BNP and NT-proBNP are both independent risk predictors in ACS. |
|
Definition
|
|
Term
| What's the difference between measuring NT-proBNP versus BNP? |
|
Definition
| NT-proBNP has greater half life in vivo and stability in vitro. It is also more dependent on renal clearance |
|
|
Term
| T/F Both BNP and NT-proBNP can be used interchangeably. |
|
Definition
|
|
Term
| What can interfere with natriuretic peptide levels? |
|
Definition
| obesity lowers both BNP and NT-proBNP, CKD increases both (NT-proBNP>BNP), CKD requires new C/Os, BNP assay not useful to monitor Natrecor Rx |
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