PATH E3 - I don't HEART you

lunalovegood's version from 2015-11-09 04:51

Section 1

Question Answer
Right atrium ---> right ventricletricuspid valve
Left atrium ---> left venticlemitral valve
BIG tunica media. Artery or vein?artery

Section 2

Question Answer
"Hardening of arteries" - loss of elasticity in arterial wallsARTERIOsclerosis
Atheromatous plaques secondary to high cholesterolATHEROsclerosis (elevated fatty plaques)
Most common arteriosclerosisATHEROsclerosis (significant morbidity)
Hardening of arteriolesARTERIOLOsclerosis
Hyaline and hyperplastic variantsARTERIOLOsclerosis
Most often associated with HTN and DMARTERIOLOsclerosis
Thickening of vessel walls with lumenal narrowing that may cause downstream ischemic injuryARTERIOLOsclerosis
Calcific deposits in MEDIA of arteries in people >50Medial calcific sclerosis
Monckeberg arteriosclerosis aka...medial calcific sclerosis
MCS - do calcifications encroach on vessel lumen?NO!
Where are calcific deposits in MCS?media
MCS is for people > age ___.50


Question Answer
In atherosclerosis, where are the atheromatous plaques?vessel intima
Atheromatous plaques begin as...fibro-fatty streaks
Atheromatous plaques will protrude and obstruct vessel lumen. What does this cause?impairs blood folw, weakens tunica media, ulceration, calcification, thrombosis, hemorrhage, aneurysm formation, and embolization
High LDL, low HDL, HTN, cigarettes and cocaine, DM, bad genetics, increasing age, male, stress, obesity and couch potato predispose you for...atherosclerosis
Atherosclerosis - would 160 systolic or a 120 diastolic be more worrisome?high diastolic
Father or brother had complications before age ___. Mother or sister before age ___.50, 65
Being > age ____ for men. > ____ for women50, 55
1. Lipid infiltration (________) leads to _____ cell injury.insudation, endothelial cell
2. Encrustation (_________) leads to adhesion of _____.thrombogenic, platelets
2. Adhering platelets attract inflammatory cells like ____ which will infiltrate vessel walls.monocytes/macrophages
3. Response to injury - inflammatory factors cause migrations of ____ from ___ to _____ which become fibroblasts and deposit _____ leading to plaque formation.smooth muscles cells, from media to intima, collagen
1. _______ 2. _______ 3. Response to injury - formation of plaqueinsudation, thrombogenic
1. Coronary arteries --> CAD --> Angina --> ___MI
2. Cerebral arteries, Circle of Willis --> ___ ___brain stroke
3. Aorta --> ____aneurysm
4, 5, 6. T/F - Other common sites of atherosclerosis include peripheral artery disease, renal artery, and mesenteric artery.T
Name 5 complications of atherosclerosis. CUTAE.calcification, ulceration, thrombosis, aneurysmal dilatation and embolization
A dark red "glistening zone" coronary artery is about to...cause a heartattack
In aortic aneurysm, where does bulge appear?just above aortic bifurcation
Aortic aneurysm is prone to rupture at size _________-__cm.6-7cm
Pulsating mass in abdomen? What is it?probably an aortic aneurysm


Ischemic Heart Disease
Question Answer
Inadequate O2 to heart muscle secondary to CAD.ischemic heart disease
Atherosclerosis of coronary vessel, vasospasm of coronary vessel, aortic stenosis, rheumatic heart disease with mitral and aortic valve stenosis, degenerative calcific aortic stenosis, and aortic atresia.ischemic heart disease
IHD most common in men > ___ and women > ___.60, 70
At what age are IHD rates equal between men and women?80
IHD - greater than ___% lumen reduction is insufficient to meet moderate increases in demand of myocardium to oxygen.75%
Abrupt changes in plaque (stable angina --> acute MI)Acute Plaque Changes
Plaque ruptures, thrombogenic lipids and subendothelial collagen exposed, wave of platelet aggregation.Coronary Artery Thrombosis
There's a pre-existing plaque - perhaps releasing vasospastic mediators like thromboxane A2 from platelet aggregatesCoronary Artery Vasospasm
4 Clinical Manifestations.AP, MI, Chronic ischemic heart disease, sudden cardiac death
Paraoxysmal, intermittent chest pain cause by transient, but reverise myocaridal ischemia. Attacks of substernal chest pain too. Coronary vessel not completely blocked. Falls short of inducing necrosis that defines infarction.Angina pectoris
Episodic substernal chest pain with exertion - constricting, squeezing, knife-like stabbing lasting 15s to 15m, may radiate to left arm. Associated with fixed plaque occluding >75%. Pain is relieved with rest or NG.Stable Angina
Like stable angina, but increased frequency, more intense pain, and longer. Progressively less exertions. Harbinger of irreversible. Myocardial ischemia due to acute plaque changes --> Pre-infarction angina.Unstable angina


Question Answer
Prolonged ischemia, >20 minutes leads to...MI
US - per year - how many acute MI? how many die?1 million, 1/2 million (and 1/2 of those die before they receive assistance)
Men age 45-55 are _________ times more likely to develop MI than women.5 times
Chest pain >20m, sweating, nausea vomiting, shortness of breath, anxiety, fatigueMI
Chest pain radiates to ___ arm, neck/lower jaw and or back.left
___-___ % of MI cases are painless. Usually seen in ___, ___, or ____ patients.20-30%, diabetics, HTN, elderly
ECG - ST segment is abnormal and T-wave is ___.inverted
Electric abnormalities of ischemic myocardium cause..arrhythmias
Sudden cardiac death may occur due to lethal arrhythmia in _________% of cases.25% (many deaths of MI before hospital)
MI pt who reach hospital. ____% are gooood. No further complications.20%
MI pt who reach hospital. ___% develop complications - cardiac arrhythmias, left ventricular failure with pulmonary edema, rupture of septum and thromboembolism.80%
When O2 is cutoff, what shuts down?ATP
When ATP shuts down, what is not pumped out of cells?Na + (the cell will swell now)
O2 cutoff, ATP shut down, Na+ in cell, ___ enters cellCa2+ (most important chemical in irreversible cell damage)
What does Ca2+ entering the cell do?activates phospholipase (tears down cell membrane - cell rupture)
4 treatments for MIThrombolytic, angioplasty, change of life style, bypass surgery


Transmural vs. Subendocardial MI
Question Answer
Full thickness of heart ventricular wall (endo, myo and pericardium)Transmural
Localized area of tissue death limited to inner 1/3 to 1/2 of heart wallSubendocardial (may extend laterally)
Usually associated with coronary atherosclerosis with superimposed thrombosis of a single coronary arteryTransmural
May be caused by a spasm in a small coronary arterySubendocardial


Histopathology of Infarct
Question Answer
Contraction bands, coagulation necrosis1-2 days
Striation lost, acute inflammation2-3 days
Reduced inflammation5-7 days
Evidence of collegen1-2 weeks
Fibrosis3-4 weeks
bright eosinophilic bands of condense contractil proteins that run at right angles to the long axis of the cardiac myocytecontraction bands


MI enzymes/proteins
Question Answer
Rise in 2-4 hrs, peaks in 24, sensitive but non-specific, returns to normal in 72 hrscreatine kinase
Rise in 2-4 hrs, peaks in 18-24 hrs, return to normal in 48hrs, more specific "cardiac" CK isoenzymeCK-MB
Detectable in 2-6 hrs, elevated for 10 daysTroponins
Peaks in 4-6 hrs, may imply very recent injury to the heart or other muscle tissuemyoglobin
Remains elevated the longestTroponins (10 days)
Rises in like 2 hours CK, CK-MB, Troponin (2-4, 2-4, 2-6)
May actually be a result of injury to another muscle tissuemyoglobin
Sensitive, but non-specificCreatine kinase
Returns to normal in 48 hoursCK-MB
Returns to normal in 72 hoursCK
Peaks at 24 hoursCK (but also CK-MB peaks at 18-24 hours)
Other enzymesLDH, AST, SGOT
Returns to normal the fastestmyoglobin (according to graph)
Rises the fastestmyoglobin (according to graph)


Question Answer
___% of people 65 of older76%
Affects ___ million in US5.7 million (300k new cases every year, 1 mil hospital cases each year)