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23 Cards in this Set
- Front
- Back
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Whats the most common malformation overall?
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Ventricular septal defect. 40% of cases.
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Whats the most common malformation in adults?
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Atrial Septal defect. This is because most of the people with VSD will die.
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The biggest cause of CHD is
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unknown. 90%
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What happens in a right to left shunt?
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leads to cyanosis. permit emboli from venous sources directly into systemic circulation.
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What happens in left to right shunt?
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right-sided heart overload with 2ndary pulm HTN and right ventricle hypertrophy. with the increase in right sided pressure shut becomes right to left, with cyanosis presenting later. Left to right shunt is more common.
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What are the left to right shunts?
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This causes late cyanosis.
ASD-asympt. until adulthood VSD- most common PDA- want to close early *early surgical correction to prevent embolism. |
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What are the Right to left shunts?
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Early cyanosis:
Tetralogy of Fallot Transposition of Great Vessels Truncus Arteriosus Tricuspid atresia |
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features of tetralogy of fallot
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1. Right vetricular hypertrophy
2. Pulmonary stenosis 3. Overriding aorta 4. Ventricular septal defect *cyanosis is present at birth |
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What is the one factor that often allows a child with CHD to survive?
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Getting enough o2 in the system. A PATENT DUCTUS. It typically closes off in one to two days. In signifanct HD, it’s the one thing that keeps the kid alive.
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What causes valve diseases?
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aging process, calcification around valve ring, leaflet calcification
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Syphilis and aortic valve disease...
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hardly ever see syphilitic aortic/valve disease anymore, but since it’s the poster child for aortic valve disease, it’s good to know syphilitic aortititis disease and the ascending aorta that may be damaged by untreated syphilis. If someone came from faraway and has untreated syphilis, they may carry aortic disease.
carcinomas that cause fibrin and plately grunge that causes the stuff to hang on the leaflets. Potential for embolization. Doesn’t destroy, but can embolize |
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Mitral Valve prolapse. how can it be detected?
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by hearing a midsystolic click. occurs in people 20-40, common with Marfans. balloon of valve leaflets, ofttime ruptured chordae tendinae
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What is infective endocarditis?
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blood-borne bacteria secondary to infection elsewhere in body. increased risk with congential heart anomalies. may come from staph aureus for acute, and strep for subacute.
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#1 thing for everything bad is
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age.
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What is the response to injury hypothesis of atherosclerosis?
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-chronic endothelial injury
-accumulation of LDL -oxidation of lipoproteins -adhesion of monocytes -release of platelet factors-> smooth muscle cell migration into intima -proliferation of SMC -increase lipid accumulation |
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Medial Calcific Sclerosis
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seen on xrays of extremities. seen as focal calcifications in media of small muscular arteries. no inflammation. if it's less than 5cm there's a chance for tx. more than 5cm less chance.
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What does hyperplastic arteriolosclerosis look like?
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onion skin arteriolar thickening. this is a malignant hypertension. will see fibrin desposition and wall necrosis- necrotizing arteriolitis.
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Transmural vs Subendocardial MIs
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transmural- full thickness of the ventricular wall usually 2ndary to severe coronary atherosclerosis w plaque disruption.
Subendocardial- limited to the inner third to half of ventricular wall all affect left ventricle. |
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Pathogenesis of MI
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most vulnerable plaques have a relatively soft core of lipids separated from the lumen by a thin fibrous cap. Thrombosis follows the acute plaque change.
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Timing of MI
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time b/w onset and irreversible injury is 20-40 minutes.
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cause of subendocardial
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diffuse coronary atherosclerosis and global border line perfusion made transiently critical by increase demand. no thrombus usually. just a slow insidious MI.
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ventricular rupture can happen when?
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within first 10 days. have have a rupture of a free wall. pericardial hemorrhage and tamponade and rupture of the septum. left to right shunt with right heart volume overload. sudden death.
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gross changes and timing
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6-12 hr inapparent, but may see lesion
18-24 hrs pale to cyanotic 1st wk yellow and soft 7-10 days hyperemic granular tissue 6 wks white fibrous scar established. |
