PBL Meeting Notes u3 w1 Flashcards
(34 cards)
Stable and Unstable Angina
Stable -chest pain preceded by exertion, relieved by rest and nitroglycerin. Caused by underlying CAD, oxygen demand by heart cannot be met during exertion
Unstable - chest pain/discomfort caused by insufficient blood and oxygen. Caused most commonly by narrowing of coronary artery due to thrombus on disrupted atherosclerosis plaque. Consider this when chest pain increases or lasts 20-30 minutes
CAD - what is it?
atherosclerosis in the vessels supplying the heart
anatomy of a blood vessel
adventitia or tunica externa, then tunica media, tunica intima
which layer is the muscle in blood vessels?
tunica media, and in arteries it is bigger than in veins
damage to blood vessels is caused by
LDL, smoking, high blood pressure
dead macrophages called foam cell are where and are full of what?
under the endothelium of the blood vessel and are full of cholesterol
plaque in the artery is made of what?
fibrous cap and fatty streak
what percent of occlusion starts to cause down stream cellular injury and necrosis?
70% occlusion
Why does calcium deposit in the plaque?
the smooth muscle cells proliferate into the plaque and deposit calcium, causing the area to become more rigid. HDL is unable to help reduce this because of the LDL present
covid infection increase chance of myocarditis
x35, covid vaccination x3
Beta-1 specific blockers are specific to what tissues?
cardiac
don’t give sotalol to who?
patients with long QT syndrome because sotalol can worsen this
affect of aspirin on GI
epithelial injury, microvascular injury, chronic ulcer
cough associated with heart condition?
1) backflow to pulmonary veins causes fluid leak into lungs
2) ACE inhibitors increase cough reflex, possibly due to kinase II activity (accumulation of kinins, substance P, and prostaglandins)
Hypertensive Goals
under 130/80?
Dilated cardiomyopathy defined by how much left ventricular ejection fraction?
less than or equal to 40%
Dilated cardiomyopathy PE findings
rales, elevated JVP, S3 gallop, murmurs of functional mitral or tricuspid, regurgitation, cheyne-stokes breathing, pulsus alternans, pallor, cyanosis
Abnormal S2 splitting can be cause by:
1) paradoxical - delay in aortic valve closure, split occurs during expiration
2) persistent - prolonged left ventricular closure, split is more during inspiration but is present for both
3) fixed - wide s2 splitting present at baseline, wide splitting at both inspiration and expiration, atrial septal defect
NORMAL s2 splitting is caused on inspiration
eisenmenger syndrome
unoxygenated blood gets pushed through the left ventricle to the aorta, bypassing the lungs, caused sometimes by patent ductus arteriosus or other causes, flips the shunt
murmur assosicated with Patent Ductus Arteriosus
systolic, continuous “machinery” murmur
patent foramen ovale between the right and left atrium, occurs in what percent of the population?
occurs in 25% of people. 50% of cases self corrected by 6 months, 75% of cases closed by adulthood
Acyanotic Heart congenital heart defects
ventricular and atrial septal defects, patent ductus ateriosus, atrioventricular canal defect, pulmonary stenosis, aortic stenosis, aortic coarctation
cyanotic congenital heart murmurs
tetralogy of fallot, tricuspid atresia, ebstein’s anomaly, truncus arteriosis, total anomalous pulmonary venous return, transposition of the great arteries
how to test for recent strep infection?
ASO (antistreptolysin O), AntiDNase B (ADB). both negative means probably no strep infection