Path 3 - Ischemia

Front 1

to what point is ischemia reversible?

Back 1

disruption of cellular membranes

Front 2

how long after the loss of coronary blood flow does the myocardium cease to contract?

Back 2

60 sec

Front 3

coronary artery disease

Back 3

ischemia is late manifestation
present in 90% pts
begins in childhood
fatty streak progresses to occulusive plaque

Front 4

risk factors for CAD

Back 4

smoking
diabetes
hypercholesterolemia
HTN
men
age

Front 5

Metabolic syndrome

Back 5

obesity, HTN, DMII, dyslipidemia, mincroalbuminuria
2-3 fold inc in heart disease

Front 6

Hormone replacement therapy's interaction on CAD

Back 6

improved lipids
improves endothelial fxn
antioxidants
dec adhesion molc
dec C-rxtv P

Front 7

The health risks of hormone replacement therapy

Back 7

stroke
CAD
PE
breast cancer

Front 8

statin therapy

Back 8

inc HDL
dec triglycerides
dec LDL
no gender specificity

Front 9

C reactive protien

Back 9

marker of inflam expanded core in atheromatous plaques

Front 10

C reactive protien is increased in

Back 10

smokers
obese
diabetics
metabolic syndrome

Front 11

homocystine

Back 11

may cause endothelial dysfunction
interferes w NO fxn

Front 12

Fatty streak propagation

Back 12

activated SM in the presence of hypercholesterolemia
collagen, elastin & matrix P elaborated

Front 13

smooth muscle is stimulated by?

Back 13

PDGF
FGF
TGF a

Front 14

stable plaques

Back 14

raised intimal lesions
fibrous cap
protected subendothelial center
necrotic center
induces collateral circulation
70% occulusion

Front 15

unstable plaques

Back 15

eccentric
loss of fibrous caps
large inflam center
shoulder stress
50-70% occulusion

Front 16

acute plaque changes

Back 16

mechanical stress, adrenergic stim w peak in am,
inc BP, platelet activity & MI

Front 17

acute injury to plaque

Back 17

loss of fibrous cap
exposure of collagen
fragmented
capillary damage

Front 18

inflammatory mediators activity

Back 18

attract leukocytes & propagate cytokines promoting unstable plaque core

Front 19

examples of inflammatory mediators

Back 19

ICAM, VCAM, E/P selectins
TNF a, IL6, INFy
metalloproteinase

Front 20

what does ICAM, VCAM, E/P Selectins do?

Back 20

leukocyte adherence & migration

Front 21

what does TNF, IL6, INFy do?

Back 21

stimulate endothelium & mp

Front 22

what does metalloproteinase do?

Back 22

degrades the collagen cap

Front 23

thrombis causing total occlusion causes?

Back 23

transmural infarct

Front 24

thrombis causing partial occulsion causes?

Back 24

subendothelial infarct
unstable angina
sudden death

Front 25

Symptoms in angina are

Back 25

transient...
squeezing chest pain
L arm, neck, jaw pain
relieved w rest
ST segment changes

Front 26

Stable angina

Back 26

inc myocardial demand
critical flow reduction
stable plaque
improves w rest

Front 27

unstable angina

Back 27

unstable plaque
inc freq & duration
MAY OCCUR @ REST

Front 28

Women and ischemia

Back 28

less symptomatic
lower risk below 60 same after

Front 29

Race and ischemia

Back 29

more common in whites
less common in AA

Front 30

Prinzmetals angina

Back 30

sx @ rest
vasospasm related
may or may not have CAD
ST segment elevation

Front 31

what EKG change do you see with prinzmetal angina?

Back 31

ST segment elevation

Front 32

Chronic ischemia causes?

Back 32

fibrosis of the myocardium
loss of myocardial compliance & contractility

Front 33

left ventricular hypertrophy due to HTN is

Back 33

concentric

Front 34

By controlling BP in the elderly, there was a decrease in the risk for?

Back 34

stroke
CAD
CHF
crebrovascular disease
*** ind of cholesterol

Front 35

What is the ventricular hyertrophy load theory

Back 35

afterload is the primary determinant of ventricular hypertrophy

Front 36

early heart disease - diastolic dysfunction

Back 36

thick myocardium dec filling
normal systolic fxn
greater diastolic filling in LV

Front 37

altered gene expression in early heart disease

Back 37

fetal protien forms
inc fibrosis
c-myc, c-fos, c-jun

Front 38

what is the histology in early hypertrophy?

Back 38

inc myocyte size
pleomorphism
fibrosis

Front 39

inc O2 demand of hypertrophy causes

Back 39

inc HR
inc ionotropy

Front 40

Myocardial apoptosis is inhibited by

Back 40

NO

Front 41

myocardial apoptosis is increased by

Back 41

Ang II that inc p53

Front 42

EKG changes with hypertrophy

Back 42

prolonged P wave
high voltage QRS

Front 43

what is the strongest predictor of subsequent cardiac events?

Back 43

EKG changes

Front 44

Defects in NO cause

Back 44

impaired relaxation
endothelial dysfunction
inc arteriolar resistance

Front 45

Angiotensin II causes

Back 45

reduced LV mass
improved coronary blood flow

Front 46

what does the humoral theory state?

Back 46

locals vasoactive mediators initiate hypertrophic changes

Front 47

the salt theory says that if you increase dietary salt intake you get..

Back 47

inc LV mass
independent of atrial pressure
ind of tot peripheral resitance

Front 48

clincial heart failure in late hypertrophic heart disease

Back 48

loss of 40-50% myocytes
<50% LV EF
SOB (pulmonary edema)
renal dysfunction
dec exercise tolerance
jugulovenous distention

Front 49

Gender & HTN heart disease

Back 49

systolic BP inc w age M>F
heart failure 2X M & X3 F
EKG evidence in men

Front 50

race & HTN heart disease

Back 50

AA more common

Front 51

Acute cor pulmonale

Back 51

dialated RV
pulmonary embolis

Front 52

Chronic cor pulmonale

Back 52

prolonged inc R heart pres
1 pulmonary HTN
recurrent emboli
radiation induced injury
vasculitis
COPD
restrictive lung disease