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Cardiology 3

Patient has chest pain that gets better when they lean forward Fibrinous pericarditis
Person with transmural infarct. 6 wks later – fever, muscle aches & pains, 3 component friction rub in chest. Autoimmune pericarditis: i. When had infarct, damaged pericardial surface --> develop Abs against your own pericardial tissue (6 wks to get high enough titer), systemic sx’s related to that immunologic reaction, treat with NSAIDs
If pt had mitral regurg, related to postero-medial papillary dysfxn or rupture, what coronary vessel was occluded? right coronary artery because the RCA supplies the papillary muscles of the mitral valve
If patient develops mitral regurg during an MI, what vessel caused the MI? right coronary artery because the RCA supplies the papillary muscles of the mitral valve
3 days after an MI, patient comes back in heart failure and you hear a new murmur you hadn't heard before: pansystolic murmur heard at the apex, increases on expiration, S3 S4 right coronary artery occlusion --> caused rupture of the papillary muscles of the mitral valve. The murmur is a mitral regurg murmur. Failed left heart --> everything backs up into the lungs.
3 weeks after an MI, patient comes back with pain, and his chest bulges out. What is the most common complication of this condition? Ventr aneurysm, which is a complication of MI. This aneurysm doesn't rupture because it's all scar tissue. What you fear is that the patient goes into cardiac failure due to the decreased contractility of all that scar tissue in his heart (very low EF).
For a patient with MI, what is the best prognostic indicator of how well this patient will do in recovery? Ejection fraction. High ejection fraction is good prognosis.
For a patient who had an MI, when would you expect to see elevated levels of CK-MB? starting 4-8 hours after MI, peaks at 24 hrs, and is gone by 3 days
For a patient for whom you know had an MI 4 days ago, what does it mean if you measure CK-MB and find it elevated? Reinfarction because CK-MB disappears after 3 days.
For a patient who had an MI, when would you expect to see elevated levels of troponin? appears 3-6 hours after MI, peaks at 24 hrs, lasts 7 to 10 days
What is the normal LDH profile of someone with no MI? LDH1 < LDH2
In a person who just had an MI, what would the LDH levels be? LDH1 > LDH2 (LDH flip)
For a patient who had an MI, when would you expect to see elevated levels of LDH1? LDH "flip" happens 10 hours after MI, peaks at 3 days hrs, lasts 7 days
What pathologic changes would you see in the heart of a patient who died of sudden cardiac death syndrome? They died so fast (within one hour of the MI) there were no time for changes like pallor or coagulation necrosis
Indications for heart transplant - adult 1. dilated/congestive cardiomyopathy (all chambers of heart are dilated --> dec contractility --> dec ejection fraction) 2. chronic ischemic heart disease
Indications for heart transplant - child 1. endocardial fibroelastosis
Formula for stroke volume SV = EDV x EF = EDV – ESV
Formula for ejection fraction EF = SV/EDV = (EDV - ESV)/EDV
Irregularly irregular pulse atrial fibrillation
Patient has rheumatic fever. What is the valvular dysfunction? Mitral regurg because all parts of the heart are inflamed. Pericardium --> friction rubs. Myocardium --> myocarditis. Endocardium --> valves with the vegetation
Patient has hx of multiple attacks of rheumatic fever. What is the valve that is most likely involved? Mitral --> stenosis.
In post-pharyngitis rheumatic fever, what is the organism you want to look for and where would you look for it? Group A strep. Will get a pos throat cx, but won't find it in bld because pathogenesis of RheumFev is Type II hypersen: body made Abs to GAS, but those Abs x-react w antigens on mitral valve n joints. Therefore, no infectious agents in the blood stream.
Young person with swollen, painful joints, something that looks like a zit on the skin, holosystolic heart murmur, and positive antistreptolysin A titers post-infectious (group A strep) acute rheumatic fever.
Give the differential diagnosis for polyarthritis in children: a. acute rheumFev, b. Juvenile RA, c. Henoch Schoenlein (Small vessel vasculitis. Type III Hypersensitivity. IgA immune complexes form and deposit within the skin and affected organs. Purpuric rash on legs.), d. Rubella (fever, rash, arthritis)
What is an Aschoff nodule? Aschoff's bodies or nodules are reactive histiocytes, characteristic lesion of acute rheumatic fever
What is the most common overall cause of infective endocarditis? Strep viridans, infects damaged valves only
What is the most common cause of infective endocarditis for an IV drug user? Staph aureus, infects both normal and damaged valves
What is the most common cause of infective endocarditis due to prosthetic devices? Staph epi
What is the most common cause of infective endocarditis associated with ulcerative colitis and colorectal cancer? Strep bovis
What is the most common valve involved in infective endocarditis? Mitral
What are the most common valves involved in infective endocarditis in IV drug users? Tricuspid (they’re injecting things into their veins, which goes into the right side of the heart) and aortic
When you brush your teeth, what is the most common organism that can get into your blood stream? Strep viridans, infects damaged heart valves only
What is carcinoid heart disease? carcinoid tumor of small int. Mets to liver n heart. Serotonin in tumor nodules-> hepatic vein tributaries-> venous bld --> bathes R side of heart --> serotonin produces fibrous tissue response on valve --> TIPS (tricuspid insuff & pulmonic stenosis)
What type of immune response is seen in infective endocarditis? Type III Hypersensitivity
Splinter hemorrhage associated with what disease? Infective endocarditis. Small areas of bleeding under fingernails or toenails. Ass w infxn of heart valves (endocarditis) n may be caused by vessel damage from swelling of vessels (vasculitis) or tiny clots that damage small capillaries (microemboli).
What is the difference between Osler's nodes and Janeway lesions? What are they associated with? Osler's- painful lesions on finger pulps/soles of feet - subac Infective endocard (10-20%), immune complex dep. Janeway are non-tend, macules/nodules in palms/soles, pathognomonic of infective endocarditis. Type III hypersen rxn.
Fundoscopy exam shows red spot with white center Roth's spots are retinal hemorrhages with white or pale centers composed of coagulated fibrin. They are usually caused by immune complex mediated vasculitis often resulting from bacterial endocarditis.
What is infective endocarditis? bacteria sits on valves, damaging the valves, seeding other areas in the body
Young woman positive for anti-nuclear antibody has vegetations on her heart valves Libman Sacks endocarditis
Most common cause of myocarditis and pericarditis Coxsackie virus, biopsy of endocardium will show lymphocytic infiltrate (what you would expect for a viral infection)
Most common cause of viral meningitis Coxsackie virus
Most common cause of hand foot mouth disease Coxsackie virus
Most common cause of herpangina Coxsackie virus
Most common cause of sudden death in an athlete hypertrophic cardiomyopathy. Muscles are not orderly – conduction bundles screwed up, conduction defects --> vtach at any time
Young 16 yo boy dies while playing basketball at school hypertrophic cardiomyopathy. Muscles are not orderly – conduction bundles screwed up, conduction defects --> vtach at any time
What is endocardial fibroelastosis? Restrictive cardiomyopathy – preventing ventricle from filling up. Most common reason for child to get a heart transplant. Most common disease producing restrictive myocardiomyopathy in children
What is the most common heart tumor in adults? cardiac myxoma. Benign. Causes problems because the tumor blocks the mitral valve --> simulates mitral stenosis --> causes syncope.
What is the most common heart tumor in children? rhabdomyoma.
What disease are rhabdomyomas associated with? tuberous sclerosis in children.
What is pulsus paradoxus? Exaggeration of the normal: during the inspiratory phase of respiration, the pulse becomes weaker as one inhales and stronger as one exhales. In this case the pulse of the radial artery becomes much weaker on inspiration (>10mmHg drop in BP).
What is Kussmaul sign? observation of a jugular venous pressure (JVP, the filling of the jugular vein) that rises with inspiration. Breathe in –> blood sucked into the R heart, but it can’t distend so it backs up into the neck veins.
Pt has: muffled heart sounds (don’t hear anything), inspiration – neck veins distend (neck veins should collapse on inspiration), radial artery – pulse decreases with inspiration, 10 mmHg drop in BP on inspiration. CXR has water bottle configuration. Pericardial effusion
young woman with unexplained pericardial effusion or pleural effusion She has SLE -- Inflammation of membranes is a feature of SLE. Leaks fluid --> effusions
How can you distinguish between constrictive pericarditis and a pericardial effusion? Constrictive pericarditis will have a pericardial knock (sound from the sudden cessation of ventricular filling early in diastole)
Created by: christinapham



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