Ch 8 Pathoma Cardiac Pathology Flashcards
Ischemic heart disease (IHD) are a group of syndromes related to ____. It is usually due to ___ of ___, which decreases ___ to the ___. Risk factors for IHD are similar to those of ____. Incidence increases with ___.
myocardial ischemia; atherosclerosis; coronary arteries; blood flow; myocardium; atherosclerosis (HTN, high cholesterol, smoking, diabetes, age, gender, genetics); age
Stable angina is ___ that arises with __ or ___. It is due to ___ of ___ arteries with greater than __% stenosis. The resultant decreased blood flow is not able to meet the ___ of the myocardium during ___.
chest pain; exertion; emotional stress; atherosclerosis; coronary; 70; metabolic demands; exertion
Stable angina represents reversible/irreversible injury to myocytes (yes/no necrosis). It presents as ___, lasting less than/more than 20 minutes, that radiates to the ___ or ___, and causes ___ and ___.
reversible; no; chest pain; less than; left arm; jaw; diaphoresis; SOB
Stable angina is relieved by these 2 things.
Rest or nitroglycerin (vasodilates veins - decreases preload - decreases work required by myocardium)
Name 3 types of angina and what they are due to
1) stable angina (due to atherosclerosis of coronary arteries); 2) unstable angina (due to rupture of an atherosclerotic plaque with thrombosis and incomplete occlusion); 3) prinzmetal angina (due to coronary artery vasospasm)
In stable angina the EKG shows ___ due to ____. In unstable angina, the EKG shows ___ due to ____. In prinzmetal angina the EKG shows ___ due to ____
ST segment depression; sub endocardial ischemia; ST segment depression; subendocardial ischemia; ST segment elevation; transmural ischemia
Nitroglycerin works by ___ arteries or veins. Describe more.
vasodilating; both; main function is to dilate veins, which decreases preload, which decreases work required by the myocardium
Unstable angina is ___ that occurs at ___. Usually due to ___ with ___ and complete/incomplete occlusion of a coronary artery.
chest pain; rest; rupture of an atherosclerotic plaque; thrombosis; incomplete
Unstable angina represents reversible/irreversible injury to myocytes (yes/no necrosis). It is relieved by ___. There is a high/low risk of progression to MI.
reversible; no; nitroglycerin; high
What is the hallmark of reversible injury to cells? What is the hallmark of irreversible injury to cells?
cellular swelling; membrane damage
Prinzmetal angina is ___ unrelated to ___. It is due to ____. It represents reversible/irreversible injury to myocytes (yes/no necrosis). It is relieved by __ or __.
episodic chest pain; exertion; coronary artery vasospasm (which transiently completely blocks the vessel!); reversible; no; nitroglycerin; calcium channel blockers (help to relieve calcium channel blockers
Of the 3 types of angina, which causes reversible injury? Which is due to exertion? Which causes ST segment depression? Elevation? Which is relieved by nitroglycerin? Calcium channel blockers? Rest?
all; stable angina; SA and unstable angina; prinzmetal angina; all; PA; SA
Myocardial infarction is ___ of ___. Usually due to ___ with __ and complete/incomplete occlusion of a coronary artery. Name 3 other potential causes.
necrosis; cardiac myocytes; rupture of an atherosclerotic plaque; thrombosis; complete; coronary after vasospasm (due to prinzmetal angina or cocaine use); emboli; vasculitis (e.g. kawasaki disease)
Name 4 clinical features of MI. Symptoms are/are not relieved by nitroglycerin.
1) severe, crushing chest pain (lasting more than 20 mins); 2) radiates to the left arm or jaw; 3) diaphoresis; 4) dyspnea; NOT
MI usually involves the ___ (part of the heart). The __ and __ are generally spared.
left ventricle; atria; right ventricle
What is the most common artery involved in MI? What is the second most common?
LAD (left anterior descending artery) - 45% of cases; RCA (right coronary artery)
Occlusion of the LAD leads to infarction of the __ and ___ of the ___. Occlusion of the RCA leads to infarction of the ___, ___, and ___ of the ___. Occlusion of the left circumflex artery leads to infarction of the ___ of the ___.
LAD: anterior wall; anterior septum; left ventricle;
RCA: posterior wall; posterior septum; papillary muscles; left ventricle
LcircumflexA: lateral wall; left ventricle
Initial phase of infarction leads to ___ necrosis involving less than __% of myocardial thickness. EKG shows ___. Continued or severe ischemia leads to ___ necrosis involving most of the wall. EKG shows ___.
subendocardial; 50; ST-segment depression; transmural (full wall); ST-segment elevation
During MI, lab tests detect elevated ___. Name 2.
cardiac enzymes; troponin I; CK-MB
Which is the most sensitive and specific cardiac enzyme marker for MI (gold standard)? Which is useful for detecting reinfarction?
troponin I; CK-MB
Troponin I levels rise __ hours after infarction, peak at __ hours, and return to normal by ___. CK-MB levels rise __ hours after infarction, peak at __ hours, and return to normal by ___.
Troponin: 2-4 hrs; 24hrs; 7-10 days
CK-MB: 4-6 hrs; 24hrs; 72 hrs (makes it more useful for detecting reinfarction)
Name the 6 treatments used for MI
1) aspirin and/or heparin (limits thrombosis); 2) supplemental O2 (minimized ischemia); 3) nitrates (vasodilates veins and coronary arteries); 4) B-blocker (slows HR, decreasing O2 demand, and risk for arrhythmia); 5) ACE inhibitor (decreases LV dilation); 6) fibrinolysis or angioplasty (opens blocked vessel)
In MI, what do we give to limit thrombosis? What do we give to minimize ischemia? What do we give to vasodilate veins and coronary arteries?
aspirin and/or heparin; supplemental O2; nitrates;
In MI, what do we give to slow HR (decreased O2 demand and risk for arrhythmia)? What do we give to decrease LV dilation (decrease after load by preventing arteriole constriction and decrease blood volume by preventing release of aldosterone)?
Beta-blocker; ACE inhibitor
In MI, we do fibrinolysis or angioplasty to ___. Name to complications of them.
Open blocked vessel; 1) contraction band necrosis (reperfusion of irreversibly damaged cells leads to calcium influx causing hyper contraction of myofibrils); 2) reperfusion injury (return of oxygen and inflammatory cells may lead to free radical generation further damaging myocytes)
During the first 4 hours of MI, what are the gross and microscopic changes, and what are complications?
No gross or microscopic changes; cardiogenic shock (massive infarction), CHF (reduced EF), and arrhythmia
During the 4-24 hours after MI, what are the gross and microscopic changes, and what are complications?
gross: dark discoloration; micro: coagulative necrosis; complication: arrhythmia
During the 1-3 days after MI, what are the gross and microscopic changes, and what are complications?
gross: yellow pallor; micro: neutrophils; complication: fibrinous pericarditis (if there was transmural infarction) - it presents as chest pain with friction rub
During the 4-7 days after MI, what are the gross and microscopic changes, and what are complications?
gross: yellow pallor; micro: macrophages (eat up necrotic debris so wall is at its weakest); complications: rupture! (of ventricular free wall leads to cardiac tamponade; of inter ventricular septum leads to shunt; of papillary muscle leads to mitral insufficiency)
During the 1-3 weeks after MI, what are the gross and microscopic changes, and what are complications?
gross: red border emerges as granulation tissue enters from edge of infarct; micro: granulation tissue (scar) with plump fibroblasts, collagen (primarily type 1), and bv’s; no complications
During the month after MI, what are the gross and microscopic changes, and what are complications?
gross: white scar (not as strong as wall); micro: fibrosis; complications: aneurysm, mural thrombus (since scarred wall does not move well) or Dressler syndrome
Dressler syndrome is a complication seen ___ after an MI. It is a ___ reaction, in which the body creates ___ against ___, causing ___.
6-8 weeks; autoimmune; antibodies; pericardium; pericarditis
The papillary muscle of the heart is fed by the ___. Infarction in that artery can cause rupture of the ___, leading to ___, usually arising ___ after an MI.
RCA; papillary muscle; mitral insufficiency; 4-7 days
Fibrinous pericarditis is a post-MI complication seen ___ after an MI, and only occurs with a ___ infarction. It presents with these 2 symptoms.
1-3 days; transmural; chest pain; friction rub
Sudden cardiac death is unexpected death due to ___. It occurs with/without symptoms or less than __ after symptoms arise. Usually due to ___. Most common etiology is ___. __% of pts have pre-existing severe atherosclerosis. Name three less common causes
cardiac disease; without; 1 hour; fatal ventricular arrhythmia; acute ischemia; 90; mitral valve prolapse; cardiomyopathy; cocaine abuse (vasospasm related to cocaine)
Chronic ischemic heart disease is poor ___ due to ___ (with/without infarction). It progresses to ___.
myocardial function; chronic ischemic damage; with or without; CHF
Congestive heart failure is ___. Divided into __ and __ failure
pump failures; left and right sided
Name 5 causes of left sided heart failure
1) ischemia; 2) hypertension (causes LV hypertrophy, which is harder to oxygenate); 3) dilated cardiomyopathy (dilation of all chambers, leads to stretched muscle, can’t contract as well); 4) MI; 5) restrictive cardiomyopathy (can’t fill heart so it can’t pump properly)
Clinical features of left-sided heart failure are due to ___ and ___.
decreased forward perfusion; pulmonary congestion
Pulmonary congestion (due to left sided heart failure) leads to ___. It results in these 4 symptoms.
pulmonary edema; dyspnea; paroxysmal noctural dyspnea (due to increased venous return when lying flat); orthopnea; crackles (fluid in interstitia)
In pulmonary congestion, small congested capillaries may __, leading to ___, which is marked by ____ (aka ‘__’ cells)
burst; intraalveolar hemorrhage; hemosiderin-laden macrophages; heart-failure
(pulmonary congestion due to left sided heart failure
Left sided heart failure can also cause decreased flow to the ___, leading to activation of the ____ system. Which leads to increased ___ and ___, further exacerbating CHF. Mainstay of treatment for left sided heart failure is __.
kidneys; renin-angiotensin; TPR (angiotensin II); blood volume (angiotensin II - aldosterone); ACE inhibitor
Right sided heart failure is most commonly due to ___. Name 2 other important causes.
left-sided heart failure; left-to-right shunt; chronic lung disease (cor pulmonale) - failure of R side of heart due to pulmonary stenosis (pulmonary vessels constrict with hypoxia from disease)
Right sided heart failure clinical features are due to ___. Name 3 features.
congestion; 1) JVD; 2) painful hepatosplenomegaly with characteristic ‘nutmeg’ liver, may lead to cardiac cirrhosis; 3) dependent pitting edema (due to increased hydrostatic pressure)
In coagulative necrosis, seen ___ after an MI, myocardium loses ___, but there are still no ___.
4-24hrs; nuclei; neutrophils (they come 1-3 days later)
Congenital heart defect arise during ___ (usually ___ through __) seen in __% of live births. Most are genetic/sporadic. Often result in ___ between left (systemic) and right (pulmonary) circulations
embryogenesis; wks 3-8; 1; sporadic; shunting
Defects with left-to-right shunting may be __ at birth, but the shunt can reverse. Increased flow through the pulmonary circulation results in __ of pulmonary vessels and ___. Increased pulmonary resistance eventually leads to ___, leading to ___ (___ syndrome). Can end up with these 3 symptoms
asymptomatic; hypertrophy; pulmonary hypertension; reversal of shunt; cyanosis; Eisenmenger syndrome; right ventricular hypertrophy (b/c pumping against pHTN), polycythemia (deoxygenated blood - hypoxemia - inc EPO), clubbing (due to cyanosis)
Defects with right to left shunting usually presents as __ shortly after __.
cyanosis; birth
What is the most common congenital heart defect?
ventricular septal defect