Ischemic diseases and MI pathology 12/02 Flashcards
In what states there are no cells necrosis?
Stable angina, unstable angina, prinzmetal angina.
Which states ar primary to chest pain, which secondary? What mechanisms?
Primary - ischemic myocardium, e.i. unstable angina.
Secondary - due to coronary narrowing or spasm, e.i. stable angina (secondary to atherosclerosis) and prinzmetal/vasospastic angina.
Which state is in 70proc. occlusion?
Stable angina.
Which state is in incomplete occlusion?
Unstable angina.
Which state is in complete occlusion?
MI.
Which state is caused by exertion?
Stable angina.
Which state is caused by emotional stress?
Stable angina.
Which state is caused at rest?
Unstable angina.
Which state is episodic and not related to exertion?
Prinzmetal angina.
Subendocardial ischemia causes ST…………….
Depression.
Transmural ischemia causes ST …………….
Elevation.
Which angina has ST depression and which elevation?
Depression - stable and unstable.
Elevation - prinzmetal.
Which angina has subendocardial ischemia?
Stable and unstable angina.
Which angina has transmural ischemia?
Prinzmetal.
Which angina has high risk of progression to MI?
Unstable.
Which angina is relieved by nitroglyrecin?
Stable, unstable and prinzmetal.
Which angina is relieved by CCB?
Prinzmetal angina. (because of smooth muscle relaxation).
Which angina is relieved by rest?
Stable angina.
Smoking is a risk factor, hypertension and hypercholesterolemia are not. What type of angina?
Prinzmetal.
What are 4 risk factors for prinzmetal angina?
Smoking, cocaine, alcohol, triptans.
Treatment of stable angina?
Rest, Nitroglycerine.
Treatment of unstable angina?
Nitroglycerine.
Treatment of prinzmetal angina?
Nitroglycerine, CCB, smoking cessation.
What type ischemia and ECG changes are at stable angina?
Subendocardial. ST depression.
What type ischemia and ECG changes are at unstable angina?
Subendocardial. ST depression and/or T wave inversion.
What type ischemia and ECG changes are at vasospastic angina?
Intramural. ST elevation.
How long last ST elevation and prinzmetal angina?
Transient.
Is there increase of biomarkers in angina?
No.
What other part of ECG is affected in unstable angina?
T wave. It can be conversed with ST depression or only its conversion.
Clinical symptoms of stable angina.
Pain <20 min, radiates to left jaw, arm, diaphoresis, shortness of breath.
What is principle of Coronary steal syndrome?
Shunted artery –> bellow it decreases pressure, artery dilates –> from good perfused arteries via collaterales blood goes down to pressure gradient –> dilated artery with decreased perfusion gets blood.
What drugs dilate normal vessels in coronary steal syndrome? How affect vessels?
Dipyridamole, regadenoson.
Vasodilation.
How act drugs used in coronary steal syndrome?
Dilate normal (not shunted) vessels –> blood goes to good perfused areas, not below shunted artery –> Ischemia in myocardium perfused by stenosed/shunted artery.
How is diagnosed coronary steal syndrome?
Pharmacologic STRESS TEST with coronary vasodilator, e.i. dipyridamole, regadenoson.
What changes in ECG are seen in coronary steal syndrome stress test?
ST segment depression.
What is the main reason of sudden cardiac death?
Ventricular artthythmia (VF).
What disease cause 70-90proc. of sudden cardiac death?
CAD/atheroslerosis.
What are 5 causes of sudden cardiac death?
CAD, cardiomyopathy (dilated, hypertrophic), cocaine abuse, MV prolapse, hereditary ion channelopathies (long QT syndrome, Brugada syndrome).
What prevents sudden cardiac death?
ICD - implantable cardioverter defibrillator.
What is chronic ischemic heart disease? What is the outcome?
Poor myocardial function due to chronic ischemic damage. Progress to CHF.
NSTEMI. How many wall is affected, what is ECG change?
Subedocardial (inner 1/3 wall). ST depression.
STEMI. How many wall is affected, what is ECG change?
Transmural (full thickness). ST elevation, Q waves.
When are indicated cardial biomarkers?
in MI. Not in Angina.
Common occluded coronary arteries.»_space;>
LAD>RCA>circumflex.
Symptoms of MI.
Severe, crushing retrosternal pain. Pain in left arm, jaw, shoulder, back. Pain longer than 20 min. Nausea, vomiting, fatigue. Diaphoresis, shortness of breath. Nitroglycerin doesn’t relieve symptoms.
In what disease there is cell necrosis?
MI.
What is the main cause/mechanism of MI?
Rupture of atherosclerotic plaque –> COMPLETE obstruction of a coronary artery.
What 4 causes of MI?
Rupture of atherosclerotic plaque, vasospasm (Prinzmetal, cocaine abuse), emboli, vasculitis (Kawasaki disease).
What part of the heart is usually involved in MI?
Left ventricle.
What parts are affected by LAD occlusion?
Anterior wall and anterior septum of LV.
What parts are affected by RCA occlusion?
Posterior wall and posterior septum. PAPILLARY MUSCLES of LV.
What artery occlusion cause rupture of LV papillary muscles?
RCA.
What parts are affected by LCX occlusion?
Lateral wall of LV.
What changes of myocardium are in initial phase of MI?
Subendocardial necrosis. ST depression.
What changes of myocardium are in continued or severe phase of MI?
Transmural necrosis. ST elevation.
What necrosis (myocardial wall) is in severe MI?
Transmural.
What is gold standart cardiac enzyme for MI?
Troponin I.
What are 2 main cardiac enzymes in MI?
Troponin I and CK-MB.
When is Troponin I rise?
Rise after 2-4h after MI, peak after 24. Return to normal after 7-10 days.
When is CK-MB rise?
After 4-6h (6-12h FA). Peak after 24h, returns to normal by 72h (48 FA).
Why is CK-MB important?
Useful in diagnosing reinfarction following acute MI, because levels return normal after 48 h FA (by 72h in Pathoma).
What are changes <4h from MI?
No gross or micro.
What are complications 0-24 hours from MI?
Cardiogenic shock (massive MI), CHF, ventricular arrhythmia.
What are changes 4-24h from MI?
Gross - dark discoloration/mottling. Micro - coagulative necrosis. Necrotic cell contents in blood. Edema, hemorrhage, wavy fibers. Appear neutrophils.
What are complications 4-24h from MI? ISTRTINTI, Palikti 0-24, kur kardiogeninis sokas etc
Arrhythmia.
What are changes 1-3 days from MI?
Gross - yellow pallor; hyperemia. Micro - Extensive coagulative necrosis. Acute infl. with Neutrophils.
What are complications 1-3 days from MI?
Fibrinous pericarditis (chest pain with friction rub).
What are changes 3-7 days from MI? ISTRINTI SITA
Gross - yellow pallor. Micro - Macrophages.
What are complications 3-14 days from MI?
Ventricular wall rupture –> tamponade.
Papillary muscule rupture –> mitral regurgitation/mitral insufficienty.
Intraventricular septum rupture –> shunt.
LV pseudoaneurysm –> risk of rupture.
What causes interventriculat septum rupture in MI?
It’s macophage mediated structural degradation.
What are complications 3-14 days from MI?
Ventricular wall rupture –> tamponade.
Papillary muscule rupture –> mitral regurgitation/mitral insufficienty.
Intraventricular septum rupture –> shunt.
LV pseudoaneurysm –> risk of rupture.
What are changes 3-14 days from MI?
Gross - hyperemic border; central yellow-brown softening. Micro - granulation tissue at margins with: fibroblasts, collagen and blood vessels.
What are changes 2 weeks to several months from MI?
Gross - white scar. (+recanalized arteries).
Micro - fibrosis (completed scar).
What are complications 2 weeks to several months from MI?
Dressler syndromes, HF, arrhythmis, true ventricular aneurysm (risk of mural thrombus).
What leads change in Anteroseptal STEMI?
V1-V2
What leads change in Anteroapical STEMI?
V3-V4
What leads change in Anterolateral STEMI?
V5-V6
What leads change in Lateral STEMI?
I, aVL.V5-V6
What leads change in Inferior STEMI?
II, III, aVF.
What leads change in Posterior STEMI?
V7-V9, ST depression in V1-V3 with tall R waves.
Treatment of acute coronary syndromes.
Unstable angina/NSTEMI - anticoagulants (heparin), antipltelets (aspirin), ADP inhibitoriai (clopidogrelis), Beta blockers, ACE inhibitors, Statins. Symptoms controled with nitroglycerine and morphine.
STEMI - same as above, but reperfusion therapy is most important.
