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136 Cards in this Set
- Front
- Back
Explain the difference between concentric versus eccentric hypertrophy of the heart.
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Concentric is due to an increased afterload. Eccentric is due to volume-overload (preload problem).
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Holosystolic high pitched blowing murmur, loudest at the apex during systole. What heart murmur is this?
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Mitral regurgitation.
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Diamond shaped systolic ejection murmur following an ejection click. What heart murmur is this?
Where does it radiate? |
Aortic stenosis. Radiates to carotids.
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When does S3 and S4 heart sounds occur?
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S3 occurs in early diastole. S4 (decreased compliance) occurs in late diastole (atrial systole).
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Will there be left ventricular hypertrophy in mitral stenosis?
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No. No volume overload.
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What does mitral stenosis murmur sound like?
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Opening snap in early diastole followed by a rumbling murmur.
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What does an aortic regurgitation murmur sound like?
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High pitched blowing diastolic murmur. S3 and S4 would be present because LV overload. Increased intensity on expiration.
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What valve leaflet is hit by the dripping of blood from aortic regurgitation? Whats the murmur that is heard?
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Anterior leaflet of the mitral valve. Austin-Flint murmur.
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What is the most common cause of tricuspid stenosis? How do you differ tricuspid stenosis from mitral stenosis?
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Infective endocarditis. Tricuspid stenosis is louder with inspiration.
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What is the average weight of the heart? What is the average wall thickness of the left ventricle? Right ventricle?
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Average weight = 250-300g in females, 300-350g in males
Thickness: RV = 0.3-0.5, LV = 1.3-1.5 |
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What does azotemia indicate?
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If perfusion deficit of the kidney becomes sufficiently severe, impaired excretion of nitrogenous products may cause azotemia. LHF can cause this.
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What is anasarca?
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Generalized massive edema.
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What type of heart failure causes pulmonary edema?
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Left sided heart failure.
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What can be seen histiologically in the lungs of a person with chronic left heart failure?
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Heart failure cells: alveolar macrophages engulfing RBC's and breaking them down into hemosiderin.
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What is the main symptom of left heart failure?
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Dyspnea.
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Hydrostatic pressures increase where in right heart failure? Consequences?
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Backward failure: venous system. Neck vein distension, hepatomegaly (nutmeg liver), pitting edema. Possibly ascites.
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Paroxysmal nocturnal dyspnea. Right or left heart failure?
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Left heart failure. aka Pillow orthopnea, sleeping upright decreases VR and decreases pulmonary congestion.
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What type of heart failure does endotoxic shock cause?
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High-output failure by mass vasodilation. Increase stroke volume (hyperthyroidism), decrease blood viscosity (severe anemia), and arteriovenous fistulas (Paget's disease) can also cause high-output heart failure.
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How does estrogen protect against coronary artery disease?
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Increases HDL.
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How does cholestyramine protect against coronary artery disease?
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Decreases LDL by decreasing bile acid reuptake. Body must make new bile from cholesterol.
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What are the four types of ischemic heart disease?
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Angina pectoris, sudden cardiac death syndrome, myocardial infarction, chronic ischemic heart disease?
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What is sudden cardiac death syndrome? Cause of death?
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Patient dead within one hour of onset of symptoms. Autopsy reveals no thrombus, but severe coronary artery disease (atherosclerosis). Cause of death is VT.
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What is chronic ischemic heart disease?
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Progressive onset of CHF due to small infarcts. Ejection fraction falls too low.
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How do you determine if a patient with stable angina is a candidate for an angiogram?
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If they have ST depression of > 1.5 on exertion.
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What is the common cause/onset of Prinzmetal's variant angina? Male or female more common?
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Prinzmetal angina is secondary to coronary artery spasm. W > M.
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What does ST depression indicate?
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Subendocardial ischemia.
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What does the ST segment look like in Prinzmetal angina?
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ST elevation.Vasospams effects the full thickness of endocardium causing transmural (full thickness) ischemia.
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A patient who use to get pain on exertion now gets chest pain at rest. What do they have?
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Unstable angina.
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What is the most common manifestation of coronary artery disease?
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Angina pectoris
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What vessels can be used in coronary artery bypass graft?
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Internal mammary artery graft (10 years) or saphenous veins (10 years). Saphenous veins undergo arterialization of the vessels, fibrosis, and occlusion common after 10 years.
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What are the treatments for coronary artery diseases?
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Angina pectoris stable and Prinzmetal: nitroglycerin, Ca-channel blockers.
Angina pectoris unstable: percutaneous transluminal coronary agnioplasty (PTCA), stenting, coronary bypass graft MI: same as unstable angina plus thrombolysis |
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What is the difference between a myocardial infarction and angina pectoris?
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Angina is myocardial ischemia without cellular necrosis (no infarction).
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What is reperfusion injury?
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Restored blood flow reintroduces oxygen and superoxide free radicals that damages cells.
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What are the most common coronary artery occlusions in MI?
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LAD > RCA > circumflex
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What does the left anterior descending artery supply?
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The anterior portion of the heart and the anterior 2/3rds of the IV septum.
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What does the right coronary artery supply?
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The posterior side of the heart. The posterior 1/3rd of the IV septum. The entire right ventricle. Also supplies posterior-medial papillary muscle of the mitral valve. AV node.
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Obstruction of which can cause bradycardia: RCA or LAD?
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RCA. It supplies the AV node.
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How many hours/days after an MI is the heart the softest and at risk of rupture?
What type of necrosis do you see? After how many hours/days? |
Between 3-7 days.
Coagulation necrosis (low oxygen) after ~12-24 hrs. |
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At point does tachycardia compromise filling of the coronary arteries?
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180 bpm
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What is this showing?
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Day 7 of acute MI in the posterior wall of LV. Yellow area is surrounded by dark, red granulation tissue.
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What is the appearance of an MI 1-3 days after event? 4-7?
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1-3: myocyte nuclei disappear, neutrophils lyse dead myocardial cells.
4-7: red granulation tissue, macrophages removing necrotic debris. |
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Patient presents with severe retrosternal pain radiating down the left arm. The patient presents with sweating, anxiety, and hypotension. His symptoms are not relieved by nitroglycerin. What does he have?
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MI
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What does this show?
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Fibrinous pericarditis
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What does this show? Look at thin wall on the inferior portion of the ventricle.
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Left ventricle aneurysm. Thin wall of scar tissue. Rupture is uncommon.
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What is a mural thrombosis? How do you treat?
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Thrombosis on the wall of the ventricle (most often LAD). Mixed characteristics of venous (stasis) clot and platelet-like clot. Asprin (platelet-like) and heparin/warfarin (venous-like).
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MI complications:
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Arrhythmia
Congestive heart failure Rupture (anterior wall, posterior papillary muscle, IV septum) Aneurysm (mural thrombus) Fibrinous pericarditis (early, late autoimmune) |
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What is the most common arrhythmia caused by MI? Most common cause of death?
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Ventricular premature beat. V-fib.
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What is the consequence of an anterior wall rupture due to an MI? Where does the occlusion commonly occur?
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Causes cardiac tamponade (fluid in pericardial cavity). This rupture is associated with thrombosis of the LAD coronary artery.
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What is the consequence of an IV septal rupture as a result of an MI?
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This rupture is associated with LAD coronary artery thrombosis. It produces a L to R shunt causing RHF.
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What is the most common cause of death after a ventricular aneurysm?
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A ventricular aneurysm as a result of an MI is clinically recognized within 4-8 weeks. CHF due to lack of contractile tissue is the cause of death.
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What is Dressler's syndrome?
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Autoimmune phenomenon resulting in fibrinous pericarditis several weeks post-MI.
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Three weeks out of MI patient notices his chest bulging. What does he have? Whats the most common complication?
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Ventricular aneurysm. Heart failure (<<EF)! (Not rupture).
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CK-MB appears within ___to___ hours; peaks at ___ hours; disappears within ___to___ days.
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4 to 8
24 hours 1.5 to 3 |
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cTnI and cTnT appear within __to__ hours; peak at ___ hours; disappear within __to__ days.
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3 to 6
24 7 to 10 |
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How do you diagnose reinfarction?
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CK-MB, because it shows up again 3 days later.
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What is the LDH (1-2) flip?
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Normally, LDH2 is higher than LDH1. In acute MI, LDH1 in cardiac muscle is released causing the "flip."
Appears within 10 hours; peaks at 2 to 3 days; disappears within 7 days |
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What murmur would you here with this pathology?
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Click (midsystolic) followed by late systolic murmur (not snap, murmur). Most common valvular lesion.
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Whats the pathophysiology of mitral valve prolapse?
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Redundancy of valve tissue:
Myxomatous degeneration of the mitral valve leaflets due to excess production of dermatan sulfate |
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What valvular diseases most commonly causes hemolytic anemia with schistocytes?
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Aortic stenosis
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You hear an early diastolic murmur and notice a bunding pulses (water hammer pulse), head nodding, and a pulsating uvula. What is the diagnosis?
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Aortic regurgitation.
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What is shown?
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Acute rheumatic fever. Uniform, verrucoid-appearing sterile vegetations appear along the line of closure of the mitral valve.
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What is the pathogenesis of Rheumatic fever?
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Pathology: Immune-mediated disease that follows group A streptococcal infection. Antibodies develop against group A streptococcal M proteins. Antibodies cross-react with similar proteins in human tissue. Type II hypersensitivity reaction
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What causes Rheumatic fever?
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Group A streptococcal pharyngitis.
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How is acute rheumatic fever diagnosed?
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Increased antistreptolysin (ASO) titers, positive throat culture, leukocytosis, increased PR interval, increased C-reactive protein.
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What valvular disease are commonest in rheumatic fever?
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Mitral regurgitation > aortic regurgitation. In chronic infection: mitral stenosis.
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What are Aschoff bodies?
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They are present in myocarditis caused by rheumatic fever. They are a central area of fibrinoid necrosis surrounded by reactive histiocytes.
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What is Sydenham's chorea?
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Reversible rapid, involuntary movements affecting all muscles. It results from childhood infection with Group A beta-hemolytic Streptococci (rheumatic fever).
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Mitral senosis is most often caused by chronic rheumatic fever. Give four clinical findings in mitral stenosis.
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Dyspnea (pulmonary capillary congestion).
Atrial fibrillation (atrial dilation/hypertrophy). Pulmonary venous hypertension (leads to RVH). Dysphagia for solids (compression of the esophagus). |
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Give the most common causes of mitral regurgitation.
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Mitral valve prolapse, LHF, infective endocarditis, and dysfunction of the papillary muscle.
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What causes aortic stenosis?
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Dystrophic calcification of a normal or bicuspid aortic valve. Chronic rheumatic fever.
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What causes aortic regurgitation?
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Isolated aortic valve root dilation.
Infective endocarditis. HTN. Rheumatic fever. Aortic dissection. Coarctation |
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Name the microbial pathogens responsible for infective endocarditis.
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Streptococcus viridians – most common cause of IE.
Staphylococcus aureus – most common cause of IE in IV drug abuse. Staphylococcus epidermidis – most common cause of IE due to prosthetic device. Streptococcus bovis – most common cause of IE in ulcerative colitis or colorectal cancer. |
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Patient presents with fever, splenomegaly, splinter hemorrhages, and a pansystolic murmur which is heard louder on expiration. What does this patient have?
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Infective endocarditis causing mitral valve regurgitation.
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What produces sterile vegetations on the mitral valve surface?
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SLE associated Libman-Sacks endocarditis.
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Patient presents with fever, chest pain, CHF. Labs show increased CK-MB, troponins. What virus could cause these symptoms? What protozoa?
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Coxsackievirus. Trypanosoma cruzi. A lymphocytic infiltrate is highly predictive of coxsackievirus.
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What are the clinical features of pericardial effusion?
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Muffled heart sounds, hypotension associated with pulsus paradoxus, Kussmaul's sign (jugular vein distention).
Water bottle configuration on CXR. |
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Patient presents with hypotension and the heart on ausculation has a distinctive knock. What does this patient have?
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Constrictive pericarditis. TB is the most common cause worldwide. the pericardial knock is due to the ventricles hitting the thickened parietal pericardium.
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Define cardiomyopathy. What three types are there?
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Group of diseases that primarily involve the myocardium and produce myocardial dysfunction.
Dilated, hypertrophic, restictive. |
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Name the causes of cardiomyopathy.
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Idiopathic > genetic causes > drugs (doxorubicin, cocaine), postpartum > thiamine deficiency (EtOH).
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Patient presents with an EF < 40%, CXR shows a global enlargement of the heart, and echo shows poor contractility. What type of cardiomyopathy is this?
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Dilated.
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What is the most common cause of sudden death in young individuals?
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Hypertrophic cardiomyopathy. Familial form in young individuals: mutation in heavy chain of beta-myosin and in the troponins.
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What is the pathophysiology of hypertrophic cardiomyopathy?
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Hypertrophy IV septum + anterior MV leaflet drawn against septum = decreased CO.
Conduction system in the IV septum is damaged = sudden death. |
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How is the ejection murmur created by hypertrophic cardiomyopathy affected by preload?
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Increased preload decreases the murmur (reclining, negative inotropic drugs).
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What is Pompe's disease? Why type of cardiomyopathy can it cause?
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Autosomal recessive glycogen storage disease. Lysosomal storage disease with a deficiency in alpha-glycosidase. The muscular weakness can lead to restrictive cardiomyopathy.
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Name the infiltrative causes of restrictive cardiomyopathy.
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Pompe's glycogenosis, amyloidosis, hemochromatosis. Sarcoidosis.
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Loeffler endocarditis?
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Cardiac damage caused by the damaging effects of eosinophil granule proteins (ex. major basic protein) is known as Loeffler endocarditis
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The afferent pain fibers from the heart run centrally in the thoracic cardiac branches of the sympathetic trunk and enter spinal cord segments at the same dermatome level as __to__.
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T1 - T5
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The innervation of the pericardium is supplied by the phrenic nerve. Pain sensation is referred to __to__ dermatomes.
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C3 -C5
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The epicardium is also known as what layer of the heart?
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The visceral layer of serous pericardium.
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What percent of cases is the cause of myocardial ischemia due to atherosclerotic coronary arterial obstruction?
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90%. This IHD is often termed coronary artery disease.
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During which weeks of embryogenesis do congenital heart defects occur?
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Gestational weeks 3-8 when major cardiovascular structures develop.
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What is the primary site for gas exchange in the fetus?
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Chorionic villus.
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What fetal vessel has the highest amount of oxygen? Lowest?
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Highest: umbilical vein
Lowest: umbilical arteries (2) |
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Why do newborns have polycythemia?
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HbF has a higher affinity for oxygen. To supply sufficient oxygen to tissue the baby increases the number RBC.
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What vasodilator keeps the ductus arteriosus open?
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Prostaglandin E2 made by the placenta.
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What shunts lead to a step up in oxygen content? What shunt leads to a step down?
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Step up = left-to-right (75 to 80)
Step down = right-to-left (95 to 80) |
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What are the clinical findings in left-to-right shunts?
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Pulmonary hypertension which will cause right ventricular hypertrophy. Reversal of the shunt occurs when pressure in RV overrides LV pressure, which leads to cyanosis (Eisenmenger syndrome).
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Name the left-to-right cardiovascular defect shunts.
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ASD, VSD, AVSD, patent ductus arteriosus.
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Name the types of atrial septal defects.
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Secundum ASD (90%), primum ASD and sinus venosus (5% each). Patent foramen ovale is present in up to 1/3rd of individuals and may/may not be considered an ASD.
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Atrial septal defects are associated with ______ and ______.
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Fetal alcohol syndrome and Down syndrome. Down syndrome is actually an AVSD.
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Which left-to-right cardiovascular shunt commonly spontaneously closes?
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VSD. Types: membranous and infundibular VSDs.
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Ventricular septal defects are associated with _____,_____, and _____.
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Cri du chat syndrome, trisomy 13, and trisomy 18.
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A continuous machine-like murmur is heard during systole and diastole. Additionally the patient has a pink upper body and a cyanotic lower body. Diagnosis?
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Patent ductus arteriosus which as reversed to a right-to-left shunt.
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Patent ductus arteriosus is associated with _____.
PDA can be closed with _____. |
Congential rubella.
Indomethacin. Inhibits PGE2. |
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What are the clinical features of right-to-left shunt
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Cyanosis. With chronic cyanosis patients can develop hypertrophic osteoarthropathy (clubbing), polycythemia, and infective endocarditis
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Name the right-to-left cardiovascular shunts.
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Tetralogy of Fallot, complete transposition of the great vessels, truncus arteriosus, tricuspid atresia, total anomalous pulmonary venous connection.
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What are the four features of tetralogy of Fallot? Which feature determines the severity?
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VSD, pulmonary stenosis, overriding aorta, and right ventricular hypertrophy. The degree of pulmonary stenosis determines the severity of the disease.
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Name two cardioprotective shunts that would aid the survival of someone with tetraology of Fallot.
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PDA and ASD.
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What is the congenital defect in total anomalous pulmonary venous return?
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Pulmonary vein empties oxygenated blood into the right atrium.
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Name the obstructive congenital anomalies.
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Coarctation of the aorta, pulmonary stenosis/atresia, and aortic stenosis/atresia.
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Hows does adult and infantile aortic coarctation differ?
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Infantile is preductal while adult is distal to the ligamentum arteriosum.
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Patient presents with a systolic murmur, decreased blood pressure in the lower extremities (>10 mmHg less than upper), leg claudication and hypertension. What is your diagnosis?
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Adult coarctation.
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Infantile coarctation is associated with _____.
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Turner's syndrome.
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What is paradoxical embolization?
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In right to left shunts, emboli from peripheral veins can bypass the normal filtration action of the lungs and enter the systemic circulation.
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A 9 year old girl is diagnosed with acute rheumatic fever. Instead of recovering she dies. What is the cause of death?
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The most common cause of death that occurs during acute rheumatic fever is cardiac failure secondary to myocarditis.
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What is Sydenham chorea?
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A central nervous system manifestation of acute rheumatic fever. It is characterized by involuntary, purposeless muscular movements, and bizarre grimaces, as well as emotional lability.
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In what disease is the bundle of Kent present? What does the characteristic ECG look like?
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Wolf-Parkinson White syndrome. ECG has prolonged QRS with a delta wave.
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Describe the ECG tracing of atrial fibrillation. How do you treat?
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Irregularly irregular and no discrete P waves. Coumadin to prevent clot formation.
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Describe the ECG tracing of atrial flutter. How do you treat?
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Sawtooth appearance. Class IA, IC or III antiarrhythmics.
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Describe the ECG's of AV heart blocks.
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First degree: prolonged PR (>.2)
Second degree: Mobitz I: progressively longer PR intervals till P wave is dropped. Mobits II: consistent PR's from beat to beat until one drops. Third degree: independent atria and ventricular beats. |
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How would a LBBB appear on an ECG tracing?
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Wide QRS which are mostly negative in V1-2. M morphology in V5-6.
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How would a RBBB appear on an ECG tracing?
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QRS is mostly positive with M morphology in V1-2. Large S wave in V5-6.
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Tosades de pointes can be caused by:
a. prolonged PR b. absent T c. prolonged QT d. tachycardia |
c. Prolonged QT interval can predispose to torsades de pointes. It shows up on ECG as a sinusoidal waveform around the isoelectrical point.
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Does hyperkalemia or hypokalemia increase the risk of ventricular fibrillation?
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Hyperkalemia. Nerst equation includes -(K in/K out). Increasing K out makes the membrane potential less negative and closer to the threshold potential, therefore it is easier to elicit an AP.
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What are the pacemaker rates at the SA, AV, and His-Purkinje system?
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SA = 60-80, AV = 40-60, Purkinje = 20-40
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What antiarrhythmic drug class is used to treat acute ventricular arrhythmias?
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Class IB - lidocaine. Lidocaine is best used in post-MI conditions, because it acts on damaged tissue, not normal myocytes.
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What is the best antiarrhythmic drug to use for paroxysmal supraventricular tachycardia?
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Adenosine.
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Hyperthyroidism can cause _____ in the heart.
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Arrhythmia. Most often tachycardia.
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What are the three types of atria fibrillation?
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Paroxysmal - recurrent episodes that are self-limiting within 7 days
Persistent - recurrent episodes that are not self-limiting Permanent - last than more than a year |
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What is the atrial rate (of impulses) in atrial fibrillation? In this condition what is the rate in the ventricles?
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400-600 bpm, but most are blocked in the AV node and the ventricles are normally 80-180 bpm.
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What antiarrhythmias would you use in atrial fibrillation to control the rate in the ventricles?
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Beta blockers which suppress abnormal pacemakers by decreasing the slope of phase 4. Ca channels also work at the AV nodal cells (verapamil).
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How many premature ventricular contractions qualifies as ventricular tachycardia?
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3 or more.
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What is sick sinus syndrome? What are some causes?
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Both fast and slow arrhythmia due to a malfunctional SA node.
Can be caused by sarcoidosis, amyloidosis, Chagas, cardiomyopathies |
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In what situation is the antiarrhythmic Mg (2+) used?
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Torsades de pointes and digoxin toxicity.
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What antiarrythmic drug class can cause bradycardia?
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Beta blockers.
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What is the Jones criteria used for?
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Diagnoses of Rheumatic Fever. Major criteria: erythema marginatum, migratory polyarthritis, subcutaneous nodules, chorea, carditis. Minor: fever, arthralgia, leukocytosis, increased ESR, ECG heart block, ASO, etc. Diagnosis: 2 major and + culture or 1 major, 2 minor, + culture.
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