12 terms

Patho Test 4

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Perfusion
The body's ability to deliver oxygen and nutrients (via the heart pumping blood) to all cells and to remove waste products of cellular metabolism.
Atherosclerosis of coronary arteries
Disease of the intima (inner lining). Chronic, progressive, inflammation starts the process
Coronary Artery Disease (CAD)
Patho:
1. Inflammation - endothelium damaged - lipids deposited; lipids are oxidized and attract monocytes; monocytes enter the intima, become macrophages which ingest LDLs, then are transformed into foam cells; foam cells release cytokines which cause inflammation and injury.
2. Fatty streak (yellow, lipid-filled smooth muscle cells - an organized collection of foam cells); starts causing some narrowing.
3. Fibrous plaque (fatty streak, collagen, elastic fibers); causing further narrowing.
4. Complicated (advanced) lesion - fibrous plaque (lesion) hemorrhages, causes clot formation and obstruction.
Development of CAD
Fatty streak starts to develop in early 20s in males
-Chronic and progressive
-No signs or symptoms of CAD until artery 60% or more occluded.
Number 1 killer in US and other developed countries
Risk Factors of CAD
1. Cigarette smoking (direct + passive)
A. Nicotine - epinephrine released, increase HR and vasoconstriction
B. increase platelet adhesiveness (stickiness) - increase clot formation
C. CO (carbon monoxide) - attaches to Hgb molecule; less O2 carried to tissues
2. Hypertension - increase P.V.R. (peripheral vascular resistance); increase workload of heart accelerates process of atherosclerosis.
3. Hyperlipidemia
A. advanced age
B. male gender (under 60) then male/female risk equal
C. genetic predisposition - especially family history before age 55.
D. hyperlipidemia (increase serum lipoproteins) caused by: increase dietary fat intake, diabetes, and genetics. Lipoproteins = lipids, phospholipids, cholesterol and triglycerides bound to carrier proteins.
4. Diabetes mellitus (type 1 - insulin dependent) occurrence of CAD X 2 greater in men; X 4 more in women, CAD occurs earlier and more severely with diabetes; increase blood glucose accelerates CAD.
5. Women and CAD - higher mortality rate after acute myocardial infarction; number 1 killer of american women (more deaths than all cancers combined); detection more difficult; less favorable outcomes after surgery and procedures than men.
6. Cocaine/Methamphetamine use: increase BP and HR; cause vasoconstriction of coronary arteries.
7. Hyperhomocysteinemia
A. homocysteine is amino acid (from animal protein); normally, broken down in the liver with help of vitamins B6, B12, and folic acid
B. causes injury to arterial wall
C. treat/prevent with folic acid (folate)
8. Role of inflammation in development of CAD - C-reactive protein (CRP) high sensitivity ("cardiac" CRP) increase and measures inflammation
Myocardial Ischemia
local and temporary deficiency of blood supply due to obstruction of coronary circulation.
Imbalance between supply decrease in blood flow to myocardium and demand myocardium's need for O2 and nutrients
leads to
myocardial cells becoming ischemic within 10 seconds (myocardial O2 deficit)
leads to
anaerobic (without O2) metabolism
leads to
lactic acid accumulation
leads to
chest pain (angina)
Clinical manifestations of myocardial ischemia
Classical (typical): transient 3-20 min.
sub-sternal pain, discomfort, heaviness, pressure, tightening, squeezing or aching
may radiate to neck, left arm, jaw, teeth, back
Non-classical (atypical): indigestion, upper back pain, jaw pain only, increasing fatigue
Types (stable angina progresses to acute coronary syndrome)
1. Stable
predictable; similar events initiate attack (stress, activity); similar type of sensation with each attack; relief with rest and nitrates
2. Acute coronary syndrome - sudden coronary artery obstruction due to: thrombus formation over atherosclerotic plaque
-unstable angina - indicates advanced CAD; unpredictable - sensation often occurs with rest
-myocardial infarction may be associated with sudden death
Myocardial infarction - "heart attack"
CAD leads to myocardial ischemia leads to irreversible hypoxia leads to cellular death
Cause: narrowed coronary artery (CAD) + clot formation (coronary artery 100% occluded)
A. cellular injury - reversible; first 30-60 seconds of hypoxia - EKG changes; myocardial cells deprived of O2 and nutrients lose contractility
B. Cellular death - irreversible hypoxia; (after 20 mins) cellular death and necrosis (infarction); remodeling - thin, poorly contracting ventricular walls; cell membranes rupture - intracellular enzymes spill out into the blood stream
Zone of:
1. ischemia - collateral circulation causes healing
2. injury - same as ischemia
3. infarction - does not heal: becomes scar tissue
C. Repair (healing) - scar formation (zone of infarction); weak, mushy (10-14 days post MI); strong scar (6 weeks), but does not contract/pump
Clinical manifestations of MI
Classical:
-sub-sternal pain, discomfort, heaviness, pressure, tightness, squeezing or aching
-may radiate to neck, left arm, jaw, teeth, back
-indigestion, nausea, vomiting
-diaphoresis (sweating)
-cool, clammy skin
-change in BP and/or HR and rhythm
-nitroglycerin usually does not relieve pain
Non-classical (atypical):
-weakness, fatigue, SOB, upper back pain (between scapula), no symptoms
High risk for non-classical:
-women (back pain); diabetics (no symptoms); elderly (>75 years old)
MI diagnosed
1. Hx/PE (history/physical exam) - history of CAD and clinical manifestations
2. lab data
A. Enzyme - increase CK - MB (creatinine phosphokinase)
B. troponin - increase cardiac muscle cells
C. WBC - increase reflects inflammatory response
D. Glucose (blood sugar) - increase elevates with stress
3. 12 - lead EKG - identifies if MI occured and where
Post - MI complications
Depends on site and size of infarction
1. heart failure/cardiogenic shock - decreased ejection fraction (EF) - % of blood (L) ventricle ejects; normal = 50-60% and above
2. arrhythmias/dysrhythmias
-disturbance of cardiac rhythm
-occurs with 80-90% of MI's most common complication