Cardiac Pathology Flashcards
What are the three types of angina? How is each related to exertion? What is the cause of each types? Does it respond to nitroglycerin? What will the EKG show?
Stable - chest pain that arises with exertion; caused by >70% stenosis of coronary arteries from atherosclerosis that cannot meet the oxygen demands of the myocardium during exertion; relieved by nitroglycerin and rest; EKG shows ST segment depression
unstable - chest pain that occurs at rest; caused by rupture of an atherosclerotic plaque and thrombosis that leads to incomplete occlusion of the coronary arteries; relieved by nitroglycerin; EKG shows ST segment depression
Prinzmetal - episodic chest pain that are unrelated to exertion; caused by coronary artery vasospasm; not relieved by nitroglycerin and calcium channel blockers relieve vasospasm; EKG shows ST segment elevation
Why is nitroglycerin used to treat chest pain/angina?
Nitroglycerin (like all nitrates) is converted to nitric oxide which is a potent vasodilator. It’s main mechanism of action is to increase the dilation of veins, decreasing the preload of the heart and decreasing the amount of blood the ventricles have to pump, decreasing the amount of oxygen the ventricles need.
Ischemia leads to what type of cellular changes? Infarction leads to what type of cellular changes?
Ischemia leads to reversible cell damage
Ischemia >20 minutes leads to necrosis
Infarction leads to necrosis
What are the causes of myocardial infarction?
1) rupture of atherosclerotic plaque with thrombosis and complete occlusion of the coronary artery
2) coronary artery vasospasm for longer than 20 min
3) emboli that causes complete occlusion of the coronary artery
4) vasculitis of coronary artery (Kawasaki disease) that damages the endothelium and generates a thrombus that completely occludes the coronary artery
Occlusion of the left anterior descending artery causes damage to what structure of the heart? Occlusion of the right coronary artery? Occlusion of the left circumflex artery?
LAD - anterior wall of left ventricle, anterior wall of interventricular septum.
RCA - posterior wall of left ventricle, posterior portion of inter ventricular septum, papillary muscle of the LV
circumflex - lateral wall of left ventricle
What are the cardiac enzymes used to diagnose myocardial infarctions? When do these rise, peak and fall?
Troponin I - Most sensitive and specific for initial infarction. Rises 2-4 hours after infarction, peaks at 24 hrs, returns to normal in 7 days
CK-MB - useful for detecting another infarction days after initial infarction. Rises 4-6 hours after infarction, peaks at 24 hours, returns to normal in 72 hours
What are the microscopic changes after 4-24 hours after infarction? 1-3 days? 4-7 days? 1-3 weeks? months?
4-24 hours - coagulative necrosis 1-3 days - neutrophil infiltration 4-7 days - macrophage infiltration 1-3 weeks - granulation tissue months - fibrosis/scar
What are the major complications in the 4-24 hours after infarction? 1-3 days? 4-7 days? 1-3 weeks? months?
Cardiogenic shock, (the heart can’t pump blood so blood pressure plummets and blood supply to vital organs cannot be maintained), congestive heart failure, arrhythmia
4-24 hours - arrhythmia (if the conduction system was damaged)
1-3 days - fibrinous pericarditis
4-7 days - rupture (ventricular wall - cardiac tamponade; inter ventricular septum - shunt; papillary muscle - mitral valve insufficiency)
1-3 weeks - nothing
months - aneurysm, mural thrombus, Dressler syndrome (pericarditis due to formation of autoantibodies against the pericardium)
What coronary artery feeds the papillary muscle? If the papillary muscle ruptures, what disease will that lead to?
Right Coronary Artery. Mitral insufficiency
How does hypertension lead to left sided heart failure?
HTN causes left ventricular hyperplasia. Since the oxygen demand is greater but the diffusion capacity is lower in the hyperplastic heart, the cardiac tissue eventually becomes ischemic. The ischemic wall becomes weak and can no longer pump all the blood out of the ventricle, causing the blood to back up in the lungs
What are the clinical findings of left-sided heart failure?
1) Blood backs up in the lungs (pulmonary congestion) leading to:
pulmonary edema with dyspnea
paroxysmal nocturnal dyspnea (dyspnea after laying flat for a few hours)
orthopnea (dyspnea after laying flat for a few minutes)
crackles
heart failure cells (alveolar macrophages that eat up the RBCs and iron from exploded capillaries making them hemosiderin-laden macrophages)
2) decreased forward perfusion leading to
activation of renin-angiotensin system
What are the causes of right sided heart failure (cor pulmonale)?
left heart failure (most common)
left-to-right shunt
chronic lung disease (hypoxia induces blood vessels in the lung to constrict, backing up blood in the right ventricle)
What are the clinical findings of right-sided heart failure?
Blood backs up into the organs (congestion)
jugular venous distension
painful hepatosplenomegaly
dependent pitting edema
What direction is the shunt in a ventricular septal defect? How does the size effect the direction of the shunt? What disease is this associated with?
If the ventricular septal defect is small, the shunt will be from left to right and is often asymptomatic. If the VSD is large, initially the blood will be shunted left to right. As blood is shunted to the right, the blood pressure increases in the pulmonary system resulting in pulmonary HTN and right ventricular hypertrophy. Eventually, the pulmonary BP gets higher than the systemic BP so the shunt reverses and goes right to left and causing cyanosis, hypoxia and a reactive polycythemia. VSD is associated with fetal alcohol syndrome.
What is Eisenmenger syndrome?
When a congenital heart defect (VSD, ASD, PDA) initially causes a left-to-right shunt but later switches to a right-to-left shunt because pulmonary BP rose higher than systemic BP.
What direction is the shunt in an atrial septal defect? What can be heard on auscultation?
Left-to-right shunt. An S2 split can be heard on auscultation because there is an increased amount of blood in the right side of the heart, delaying the closure of the pulmonic valve.
What are the valvular disorders?
Acute rheumatic fever, Chronic rheumatic heart disease, aortic stenosis, aortic regurgitation, mitral valve prolapse, mitral regurgitation, mitral stenosis
How do you diagnose acute rheumatic fever? What are the signs and symptoms?
JONES criteria
1) evidence of prior group A strep infection from elevated ASO titers or anti-DNase B titers
2) minor criteria - fever, elevated ESR
3) major criteria
Joints - migratory polyarthritis usually in large joints
O (heart) - endocarditis (mitral valve), myocarditis (Aschoft bodies filled with fibrinoid material, giant cells and Anitschkow cells - histiocytes with slender, wavy, caterpillar nuclei), pericarditis
Nodules (subcutaneous)
Erythema marginatum
Syndenham chorea
What causes acute rheumatic fever? What is the progression of this disease?
pharyngitis due to group A beta-hemolytic streptococci (other infections with same bacteria do not cause ARF). The bacterial M protein resembles proteins in human tissue so once the patient makes antibodies to the M protein, the antibodies can attack the patient’s tissue.
The acute attack usually resolves, but it can progress to chronic rheumatic heart disease
What causes chronic rheumatic heart disease? What valves does it affect and what does it do to the valves?
CRHD is caused by progression of acute rheumatic fever.
It attacks
mitral valve - (usually) causes thickening of chordae tendinae and cusps
aortic valve - (occasionally) causes scarring and fusion of the commissures
What causes aortic stenosis? What are the risk factors for AS? What type of murmur is heard in AS? What are the complications?
Aortic stenosis is due to fibrosis and calcification from “wear and tear” of the valve. Risk factors are increasing age and a bicuspid aortic valve. A systolic ejection click followed by a crescendo-decrescendo murmur is heard. Complications are left ventricular hypertrophy, angina and syncope with exercise, microangiopathic hemolytic anemia
What are the causes of aortic regurgitation? What type of murmur can be heart in aortic regurgitation? What are the clinical signs and symptoms?
Valve damage (e.g. from infectious endocarditis) or an aortic root dilation (e.g. from syphilitic aneurysm)
Characterized by an early, blowing diastolic murmur.
Patients will have an increased pulse pressure (i.e. an increase in the difference between the systolic BP and the diastolic BP) leading to bounding pulses and head bobbing. Left ventricle dilation and hypertrophy.
What is mitral valve prolapse? What is the pathogenesis? What type of murmur can be heard?
MVP is a ballooning of the mitral valve into the left atrium during systole. It’s etiology is unknown but it is characterized by myxoid degeneration (accumulation of ground substance) of the valve, making it floppy.
The murmur is a mid-systolic click. Can be followed by a regurgitation murmur if regurgitation is present as well.
What are the causes of mitral regurgitation? What type of murmur can be heard?
mitral valve prolapse, left ventricular dilation, infective endocarditis, acute rheumatic fever, papillary muscle rupture after MI
Holosystolic “blowing” murmur that gets louder with squatting or expiration
What are the causes of mitral stenosis? What type of murmur can be heard? What are the complications of mitral stenosis?
Chronic rheumatic heart disease.
On auscultation, you can hear an opening snap followed by diastolic rumble.
Mitral stenosis leads to volume overload in the left atrium -> dilation of the left atrium -> pulmonary congestion with pulmonary edema and alveolar hemorrhage -> pulmonary HTN and right-sided heart failure. Dilation of LA also leads to stretch of the atrial wall, messing up the conduction system -> atrial fibrillation -> increased risk for mural thrombi.
What two organs are connected by the ductus arteriosus? What direction is the shunt in a PDA? What are the signs/symptoms of PDA? What disease is PDA associated with? How can you treat a PDA?
Connects the pulmonary artery and aorta after the first three major branches of the aortic arch (brachiocephalic trunk, left common carotid, left subclavian). Initially a left to right shunt. Over time, can progress to a right to left shunt, resulting in lower extremity cyanosis. The head and upper extremities are unaffected because the DA connects after the first three major arteries off the aorta. Congenital rubella. Treat with indomethacin which blocks prostaglandin E and closes the PDA. (PGE keeps the PDA open)
What is the embryological failure that results in the Tetralogy of Fallot? What are the four anatomical findings in tetralogy of Fallot?
The aorticopulmonary septum doesn’t equally divide the truncus arteriosus, giving the aorta an abnormally large lumen and the pulmonary artery an abnormally narrow lumen. The anatomical findings are 1) VSD 2) an aorta that overrides the VSD 3) pulmonary artery/right ventricular outflow tract stenosis 4) right ventricular hypertrophy
What defect is present in transposition of the great vessels? What is the treatment? What disease is this defect associated with?
The aorta arises from the right ventricle and the pulmonary artery arises from the left ventricle, creating two independent circuits. Treatment involves administering prostaglandin E to maintain a patent ductus arteriosus until surgical repair is performed. Associated with maternal diabetes.
What defect is present in truncus arteriosus? How does it present?
Truncus arteriosus occurs when the truncus fails to divide, creating a single large vessel that arises from both ventricles. Oxygenated blood from the left ventricle mixes with deoxygenated blood from the right ventricle so patient present early on in life with cyanosis.
What defect is present in coarctation of the aorta? What are its two forms? How are the forms different?
In coarctation of the aorta there is a narrowing of the aorta. The two forms are
Infantile – narrowing lies distal to the aortic arch but proximal to the PDA so the infant presents with lower extremity cyanosis at birth but no hypertension. Associated with Turner syndrome.
Adult - narrowing lies distal to the aortic arch but there is no PDA. The patient presents much later in life with upper extremity hypertension and hypotension and weak pulses in the lower extremities. Collateral circulation develops across the intercostal arteries. These engorged arteries cause ‘notching’ of the ribs on x-ray. Associated with bicuspid aortic valve.
What is the most common cause of endocarditis? What is the pathogenesis of this type of endocarditis? Do the valves get destroyed?
Strep viridans. Requires prior damage to the heart valves. Damaged valves develop thrombotic that trap the bacteria if they get into the blood. Once emeshed in the thrombi, the bacteria grow small vegetations that do not destroy the valve (subacute endocarditis).
What are other bacterial causes of endocarditis? What are they associated with?
Staph aureus – associated with IV drug abusers. Destroys the heart valve causing acute endocarditis
Staph epidermidis – associated with prosthetic valves
Strep bovis – associated with colorectal carcinoma
HACEK organisms – associated with endocarditis with negative blood cultures because these organisms are so difficult to grow. Haemophilus, actinobacillus, cardiobacterium, Eikenello, Kingella.
What are the clinical findings in endocarditis?
Fever
Heart murmur
Janeway lesions – erythematous, nontender lesions on palms and soles
Osler nodes – painful lesions on fingers and toes
Splinter hemorrhages in nail bed – embolization of vegetations
Anemia of chronic disease – chronic bacteremia causes continuous inflammatory response
What are the types of non-bacterial endocarditis?
Thrombotic endocarditis is due to sterile vegetations (thrombi) that form due to a hypercoagulable state or underlying adenocarcinoma.
Libman-Sacks endocarditis is due to sterile vegetations that form due to SLE. Sterile vegetations on BOTH sides of the valve is a finding unique to Libman-Sacks endocarditis.
