Exam (elaborations)
ACNP Diagnosis & Management Exam 1: Q’s And A’s
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ACNP Diagnosis & Management Exam 1: Q’s And A’s
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ACNP Diagnosis & Management Exam 1: Q’s And A’sLectures Covered:
1. Ischemic Heart Disease
2. Hypertension
3. Pericarditis
4. Heart Failure+APE
Ischemic Heart Disease Right Ans - Myocardial O2 demand > Myocardial
O2 supply --> spectrum of clinical syndromes
Results in myocardial hypoxia and accumulation of waste metabolites
Most common cause: atherosclerotic disease of coronary arteries
-reduction in coronary blood flow
-inadequate perfusion of region of myocardium supplied by affected artery
Risk Factors for CAD Right Ans - Obesity
Sedentary lifestyle
DM/insulin resistance
High LDL
Low HDL
smoking
Each of these cause a disturbance of normal functions of vascular endothelium
(maintenance of antithrombotic surface, control of vascular tone - blood
supply, control of inflammatory cell adhesion)
Angina Pectoris Right Ans - chest discomfort produced by myocardial
ischemia - 2 types
Stable Angina Right Ans - Chronic pattern of transient angina pectoris,
precipitated by physical activity or emotional upset
Relieved by rest within a few minutes; pain follows a predictable pattern
Episodes often associated with temporary ST depression, but no permanent
myocardial damage *EKG changes return to normal!*
,Unstable Angina Right Ans - Pattern of increased frequency and duration of
angina episodes, sometimes at rest; risk of progression to MI if untreated
Pain is NOT relieved by rest or nitroglycerin!
Cardiac biomarkers (troponin, CK) are normal!
Myocardial Infarction Right Ans - Prolonged cessation of blood supply
leads to region of myocardial necrosis
Most often results from acute thrombus at site of coronary atherosclerotic
stenosis
Atherosclerotic Plaques Right Ans - Develop at sites of fatty streaks, where
there are accumulations of foam cells
Soft vs. hard plaques --> ratio of foam cells to fibrous tissue
Softer plaques may be more likely to rupture (because of the higher number
of foam cells!!!)
Acute Coronary Syndrome Right Ans - A spectrum of disease including:
-unstable angina
-NSTEMI
-STEMI
NSTEMI Right Ans - Clinical feature of unstable angina PLUS:
-evidence of myocardial necrosis, as indicated by cardiac biomarkers
-may have some EKG changes --> ST segment depression, T wave inversions
-but, NO ST SEGMENT ELEVATION
Creatinine Kinase (CK) Right Ans - Non-specific for cardiac injury, rises 4-8
hours after insult and returns to normal in 48-72h
(Elevates with cardiac and other muscle damage)
Rises faster than Troponin!
, Troponin I Right Ans - *Very specific for cardiac injury*, but can also be
elevated in PE, SIRS, HF, ESRD,
Takes longer than CK to rise --> do 2-3 sets over 6-12h if first test is negative
May stay elevated for 1-2 wks following MI.
NSTEMI Treatment Right Ans - Continuous EKG monitoring--> watch for
progression to STEMI
Nitrates --> paste or SL, IV gtt if pain persists after 3 doses (be sure to ask
about phosphodiesterase inhibitor use, warn about HA associated w/ nitrates,
monitor BP for drop)
Beta-blockers --> target HR of 50-60 bpm (ask about cocain use
ASA 325 mg --> chewed, non-enteric coated
Heparin --> unfractionated
Early invasive strategy vs. conservative --> cardiac cath/stent vs. lifestyle
modifications
ACE Inhibitor when stable for pt with HTN, HF, DM --> this is not for the tx of
HTN is for the prevention of L ventricular modeling!
STEMI Right Ans - Chest pain is the most common presenting complaint
(pressure, squeezing, crushing)
Associated diaphoresis strongly suggestive
Total occlusion of an epicardial coronary artery produces ST-segment
elevation on EKG (>1 mm in 3 contiguous leads!)
Cardiac biomarkers elevated --> may not be elevated immediately following
injury!!
-1/4 of pt have signs of sympathetic hyperactivity (tachycardia, high BP)
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