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45 Cards in this Set
- Front
- Back
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list the valvular heard diseases
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degenerative calcific aortic valve stenosis
mitral valve prolapse mitral annular calcification |
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pathogenesis of degenerative calcific aortic valve stenosis
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subendothelial rigid calcific masses within valsalva sinuses
lead to thickening and immobility of valve cusps with narrowing of orifice Usually LVH 2degree to pressure overload |
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what are bicuspid aortic valves prone to develop
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calcification - asymptomatic until stenosis reaches critical point when congestive heart failure rapidly ensues
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epidemiology of mitral annular calcification
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genreally in older people
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what is mitral annular calcification
is it affected by IE? |
degenerative non inflammatory calcific deposits within mitral annulus
rarely a focus for infective endocarditis |
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how does mitral annular calcification present?
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patients present with regurgitation arrhythmias 2ndary to impinging on conduction pathways
valve stenosis 2ndary to bulky depostis on leaflets, calcification of valve ring. these leaflets may damage surrounding tissue |
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how does mitral valve prolapse present?
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usually asymptomatic and found only as a ********midsystolic****** click on auscultation. but may also be associated with atypical chest pain, dyspnea, fatigue or psych symptomes.
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what does mitral valve prolapse increase the risk of?
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IE
slow, progressive valvular insufficiency --> CHFF arrhythmias - atrial & ventricular sudden death!! |
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what is mitral valve prolapse?
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interchordal ballooning of valve leaflets, elongated, occasionally ruptured chordae tendinea, no commisural fusion.
fibrous thickening of valve leaflets, thickened left ventricle endocardium at sites of friction ATRIAL THROMBOSES behind ballooing cusps. CALCIFICATION OF MITRAL ANNULUS annulus=the outer ring |
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what increases risk of infectiv endocarditis
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1/ mitral valve prolapse
2. degenerative calcific stenosis 3. bicuspid aortic valve 4. prosthetic valve |
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what is infective endocarditis
who mostly affected? |
infection of the native of prosthetic valve or endocardium
occurs most often in ppl with recognized heart disease when you have damage to the endocardium and bacteria manages to lodge itself in the damaged tissue. it can stay there and grow, meanwhile eating away at body's tissue. |
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how is diagnosis confirmed?
where does IE directly affect and what can IE lead to? |
by blood culture
direct injury to valves, myocardium, or aorta can have thrombotic events to heart, brain , spleen, kidneys ***antigen antibody complex-mediated glomerulonephritis --> nephrotic syndrome or renal failure |
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gross look at IE
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friable microbe-laden vegetations present on one or more valves
acute --> vegetations cause erosion or perforations of leaflets. They may be adjacent to myocardium or aortic wall to produce abscess cavities subacute --? smaller vegetaions that rarely erode or penetrate leaflets |
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how is IV drug use related to IE
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can cause IE. usually right sided, but can be left
organism is usually s. aureus |
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acute vs subacute IE.
what kind of infection organisms? |
these are bacterial infective endocarditis infections
acute - S aureus subacute - usually strepococcus viridans |
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what is non bacterial thrombotic endocarditis?
what patient group seen in? |
inflammation of the endocardium, not due to bacterial infection, and commonly seen on undammaged valves
often seen in cancer patients, px's with debilitating illness (renal failure, chronic sepis), thought to be 2ndary to DIC or other hypercoag condidtion. May embolize to brain IV DRUG USERS |
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large important difference of non bacterial endocarditis compared to bacterial?
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smaller vegetations, but they are very prone to embolize
does not induce inflammatory response from body |
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what is liebman sacks endocarditis
clinical presentation? |
endocarditis associated with Systemic lupus erythematous
valvular (mitral and tricuspid) disease seen in SLE and antiphospholipid syndrome, according to robbins - does not have a preferred location to affect - can affect the undersurface or valve or even move to endocardium |
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gross presentation of liebman sacks endocarditis
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mitral and tricuspid fibrinoid necrosis, mucoid degerneration.
small, fibrinous Sterile vegetations on either side of valve |
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what are the congenital heart defect classes?
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Left to right shunt, right to left shunt, obstructive congenital anomolies
Obstructive - coarctation of aorta |
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left to right shunt defects
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ASD, VSD, PDA
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right to left shunts
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Tetrology of fallot, truncus arteriosus, tricuspid atresia, transposition of the great arteries
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obstructive congenital anomolies
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coarctation of aorta, pulmonary valve stenosis
aortic valve stenosis and atresia |
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tetrology of fallot
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1. VSD
2. aorta overriding the VSD 3. pulmonary stenosis, w/ right ventricle outflow obstruction 4. RVH |
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why are left to right shunts called late cyanotic
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left to right shunts cause either right sided heart failure or right sided hypertrophy and pulmonary artery pressure. and after this, they become right to left shunts. when this occurs person become cyanotic
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what CHD is more common in children of diabetics?
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transposition of great arteries
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most common CHD
most common presenting as adults |
VSD
ASD |
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types of atrial septal defects
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primum 5% associated w/ mitral valve deformities
secundum 90% sinus venosus 5% |
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what is acute rheumatic fever
supporative vs. nonsupporative? what infection? |
it is a delayed non supporative disease.... meaning it is non puss forming. not many WBCs
Strep group A infection proliferative inflammatory lesion in connective tissue of joints, heart, skin, and central nervous tissue |
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how does rheumatic fever begin?
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starts with upper resp tract infection
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what age group do we see highest infection rate of acute rheumatic fever?
what climate? |
5-15yrs
cooler months |
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what pathogen involved in acute rheumatic fever?
properties of pathogen? |
group A streptococcus pyogenes
gram positive cocci in chains catalase negative lactic acid fermenter (ferment sugars into lactic acid) |
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pathogenesis of acute rheumatic fever?
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evidence supports autoimmune phenomenon
immunoglobulin and complemen deposits Heart reactive Abs in serum Px demonstrate hyperimmune response to strep antigens rheumatic heart valves show T-cell infiltration |
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clinical diagnosis - evidence of what ?
what are criteria |
lab evidence of recent strep infection and presence of 2 or 1maj and 2 minor jones criteria
Major - carditis, polyarthritis, erythema marginatum subQ nodules, sydenham's chorea Minor - arthalgia, fever, previous rhem fever *****prolonged PR interval** elevated ESR, c-reactive protein or leukocytes |
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what are jones criteria?
name them, atleast name the most common |
Major
****** polyarthritis (MOST COMMON 80 %)******* carditis (40-50%) , erythema marginatum subQ nodules, sydenham's chorea Minor - arthalgia, fever, previous rhem fever *****prolonged PR interval** elevated ESR, c-reactive protein or leukocytes |
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what is laboratory diagnosis for acute rheumatic fever
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screen with streptozyme test
if positive do ASO (>500 units) can also do acute phase reactants - will be elevated in any inflam response ESR, CRP, PMNs etc |
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Treatment for actue rheumatic fever
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salicylates 4-8 weeks
prednizone reserved for px's with severe carditits |
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prevention of acute rheumatic fever
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primary reaction - prompt recognition and treatment of strep throat
secondary attack - continuous long term prophylaxis with penecillin 5-10 yrs |
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classifications of infective endocarditis - 4
give their most likely organism |
acute infective endocarditis - Staph Aureus
subacute infective endocarditis - strep viridans group A IV drug use infective endocarditis - staph Aureus Prosthetic valve endocarditis - Early - staph Epi... late - strep viridans |
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In infective endocarditis...
where is damage to heart commonly from? where is bacteria commonly from? specifically what gets affected with some of these |
damage - heart disease, drugs, toxins
bacteria - dental, IV introduction (Tricuspid), pulmonary(mitral) |
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pathogenesis of infective endocarditis
3 steps |
usually starts with traumatized valves - leading to non bacterial thrombotic vegetations -
endothelial damage, collagen removed, plateltes aggragate, fibrin deposits, bacteria colonize - form vegetations, stimulate thromi OR via Venturi effect cardiac abnormalities --> high and low pressure areas through narrowings - platelet-fibrin aggregate on low pressure side highvelociy jets damage endocardium - platelet fibrin thrombi--> focus of bacterial infection bacteria survive host defenses and adere to vegetations |
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clnical diagnosis of AIE
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abrupt onset of fever, riors, prostration and leukocytosis
skin may show ecidence of embolic pustules or DIC janeway lesions - on palms or soles heart murmur********** |
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clinical diagnosis of SIE
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presents as an ill define wasting disease
patient not feeling well, often anorexia and weight loss **heart murmur, splenomegaly, and petechiae ***splinter hemorrhage common Osler nodes and Roths spots |
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lab diagnosis for infective endocarditis
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blood cultures - for AIE 3 during 1-2 hr period
SIE - 3 cultures per day for 2 days DO ECHOCARDIOGRAM |
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treatment of IE
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antibiotics
monitor with cultures and serum bactericidal levels shoudl be 1:8 surgery |
