ACNP
ACNP Diagnosis and Management Exam
1 2025
Ischemic Heart Disease - Correct 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 - Correct 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 - Correct Ans-chest discomfort produced by myocardial ischemia - 2
types
Stable Angina - Correct 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 - Correct 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!
ACNP
,ACNP
Myocardial Infarction - Correct 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 - Correct 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 - Correct Ans-A spectrum of disease including:
-unstable angina
-NSTEMI
-STEMI
NSTEMI - Correct 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) - Correct 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 - Correct 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 - Correct Ans-Continuous EKG monitoring--> watch for progression
to STEMI
ACNP
, ACNP
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 - Correct 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)
-1/2 of those with inferior infarct have parasympathetic signs (bradycardia, low BP)
STEMI Treatment - Correct Ans-ASA 325 mg (chewed, non-enteric coated --> want
buccal absorption)
Supplemental O2
Morphine --> reduces pain and sympathetic stimulation (decreases preload!)
Nitrates --> NOT for use in inferior/posterior MI!
Beta-blockers --> reduces magnitude and rate of re-infarction (do not use in pt with
CHF, will exacerbate!)
P2Y12 Inhibitor --> reduce platelet aggregations! e.g., Plavix (clopidogrel), Brilinta
(ticagrelor)
ACNP
ACNP Diagnosis and Management Exam
1 2025
Ischemic Heart Disease - Correct 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 - Correct 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 - Correct Ans-chest discomfort produced by myocardial ischemia - 2
types
Stable Angina - Correct 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 - Correct 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!
ACNP
,ACNP
Myocardial Infarction - Correct 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 - Correct 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 - Correct Ans-A spectrum of disease including:
-unstable angina
-NSTEMI
-STEMI
NSTEMI - Correct 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) - Correct 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 - Correct 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 - Correct Ans-Continuous EKG monitoring--> watch for progression
to STEMI
ACNP
, ACNP
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 - Correct 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)
-1/2 of those with inferior infarct have parasympathetic signs (bradycardia, low BP)
STEMI Treatment - Correct Ans-ASA 325 mg (chewed, non-enteric coated --> want
buccal absorption)
Supplemental O2
Morphine --> reduces pain and sympathetic stimulation (decreases preload!)
Nitrates --> NOT for use in inferior/posterior MI!
Beta-blockers --> reduces magnitude and rate of re-infarction (do not use in pt with
CHF, will exacerbate!)
P2Y12 Inhibitor --> reduce platelet aggregations! e.g., Plavix (clopidogrel), Brilinta
(ticagrelor)
ACNP
