Patho- Cardiovascular disorders Flashcards
(85 cards)
1
Q
what is hyperlipidemia ?
A
- elevated lipid content in blood
- elevated cholesterol, phospholipids, triglycerides in blood
- Apoproteins transport lipids
2
Q
lipid + apoprotein = ?
A
lipoprotein
3
Q
explain the density of lipoprotein
A
they can very in density
LDL, HDL, VLDL
4
Q
atheros?
A
soft paste
5
Q
sclerosis?
A
hardening
6
Q
what is an atherosclerosis ?
A
when an atheroma ( fibrofatty lesion) forms in intimate of larger arteries
7
Q
what does atherosclerosis cause?
A
affects perfusion–> ischemia ( restrictive blood flow because of some obstruction in the blood vessel at the local level)
—>schema can cause stroke, MI or PVD
8
Q
what is infarction?
A
tissue death due to ischemia
9
Q
what is hypercholesterolemia ?
A
excessive cholesterol in the blood
40 percent of Canadians experience this
10
Q
pathogenesis of atherosclerosis
A
insidious origin–> subtle endothelial injury from risk factors (inflam)
- -> monocytes and other inflam cells bind to endothelium
- -> monocytes enter intimate–> become macrophages—>
- –> 1. release free radicals by oxidizing lipids ( unstable damaged reactive cells)
2. engulf the lipids, are now foam called foam cells
3. release growth factors which cause proliferation of smooth muscle cells
All of this requires space so an atheroma forms which pushes into the lumen.
NOTE; centre is called necrotic core, blood goes inside and is a clot which can be dislodged to a thrombus
highest incidence of atherosclerosis are in the abdominal and iliac arteries
11
Q
what are the three lesion stages of atherosclerosis ?
A
fatty streak-
fibrinous atheromatous plaque– > clinical lesion, smooth muscle cells in intimate
complicated lesion—> changes inside the lumen
12
Q
is HDL good or bad?
A
HDL is good, 50 % carrier high density
13
Q
is LDL good or bad?
A
LDL is lousy because it contains 50 % cholesterol
14
Q
atherosclerosis facts
A
32 % of all deaths (1.3 of all Canadian deaths)
72000 deaths per year
15
Q
hypertension range?
A
when you can’t bring bp back to normal and its elevated all the time ( 140/90)
classified by type, cause and severity
16
Q
BP = ? x ?
A
BP = CO x PR
17
Q
systole?
diastole?
A
systole= pumping diastole= filling
18
Q
what are the four major control systems of hypertension ?
A
- arterial baroreceptors (aorta and wall of ventricles)
- renin- angiotensin system
- regulation of fluid volume ( by kidney with ADH and aldosterone)
- vascular auto regulation ( ability to dilate and constrict)
19
Q
how much blood in a person?
A
5-6 L
20
Q
what is normal bp?
A
21
Q
what is high normal BP ?
A
120- 139 over 80- 89
22
Q
Hypertension, what are the stages?
A
stage 1: mild
stage 2: moderate
stage 3: severe
23
Q
stage 1: mild hypertension?
A
140-159 over 90-99
24
Q
stage 2; moderate hypertension?
A
160-179 over 100-109
25
stage 3: severe hypertension?
>180 over >110
26
primary hypertension ?
```
idiopathic (unknown cause)
90 of cases
multifactorial aetiology (kidney involved but isn't due to kidney failure )
```
27
secondary hypertension ?
```
identifiable causes ( renal disease/ failure)
10 percent of cases
```
28
white coat hypertension?
hypertension in health care setting ( may develop to primary hyper tension
29
Systolic hypertension?
jut systolic pressure elevated > 140
mostly after age 50 due to; tissues changes, vessel compliance, dec elasticity
heart is pumping harder during systole but normal during diastole (filling)
30
Malignant hypertension?
```
same as persistent hypertension or resistant hypertension
sudden, quick, severe increase in bp
diastolic > 120
emergency
tiny vessels damaged causing shock
```
31
gestational hypertension ?
develops in pregnant women
most become normal after, some develop hypertension
problems with visual disturbances
32
Manifestations of hypertension?
- silent killer
- no early signs except bp
- later systemic manifestations, non specific; fatigue, palpitations, am headaches( bp highest in am due to circadian rhythms), blurred vision, dizziness
- progressive problems; organ damage to heart, kidneys, eyes and smaller blood vessels
33
treatment of hypertension
1. life style moderation (diet and exercise)
1st line- diuretic( excessive loss of fluid at the kidneys, loss of electrolytes)
2nd line- ACE inhibitor;blocks conversion of angiotensin1 to angiotensin2 --> will not form angiotensin2 and thus will stop potent vasoconstrictor, inc prod aldosterone, inc secretion of ADH
Angiotensin2 receptor blocker- blocks receptor of angiotensin2 , same results as ACE inhibitor
CA channel blocker; blocks channel where ca goes into cell calcium in heart and muscles --> decreased contraction of the heart causes decreased pressure
34
What is PVD
peripheral vascular disease
35
what does peripheral mean?
vessels away from heart (limbs, legs)
36
what does vascular mean?
```
any vessel ( arteries, veins, lymphatic vessels)
mostly refers to peripheral arteries
similar to changes in coronary arteries
```
37
acute arterial occlusion?
acute interruption to perfusion; almost always due to thrombus or embolus
38
Atherosclerotic occlusive disease
causes pain, pooling of blood (venous statius)
hydrostatic pressure increases causing edema
venous or lymphatic stasis
severe inc waster and fluid accumulation causing ischemia causing tissue damage
39
claudification
pain from ischemia
40
how does your body compensate for PVD?
```
vasodilation
collateralization ( creation of new vessels that bypass block, takes time thus long term process )
```
anaerobic metabolism
41
complications from PVD
ulceration, gangrene--> amputation
42
what is an aneurysm?
localized dilation of artery d/t degeneration of vessel wall
43
is an aneurysm permanent?
yes
44
risks/ causes of aneurysms?
atherosclerosis, hypertension, trauma, infection, congenital defects
45
three types of aneurysms?
1. fusiform
2. saccular
3. dissecting
46
shape of a fusiform aneurysm ?
both sides of vessel
47
shape of a saccular aneurysm ?
sac or pouch on one side
48
shape of dissecting aneurysm?
blood flows into and directs the layers of the wall, often at bends or divides
49
common sites for aneurysms?
thoracic and abdominal aorta, iliac, femoral, popliteal
50
complications from aneurysms?
rupture, blood slows, pools, blood clots develops---> thrombosis, distal embolization, applying pressure on surrounding areas
51
what is infarction?
necrosis d/t ischemia
52
stable angina?
fixed plaque
impedes perfusion
brief pain
53
unstable angina?
unfixed plaque--> may break off
can become embolisms
if disrupted platelet aggregation, thrombosis, de granulate and release prostaglandin --. constriction of vessels
plaque collects fibrin, platlets and cellular debris
pain; severe longer
54
variant angina
d/t spasm in arteries, can happen anytime
55
treatments of angina?
nitro glycerin (vaso dilator- reduces chest pain )
56
what is angina an manifestations of?
coronary artery disease
57
myocaridal infarction is caused by?
atherosclerosis, coronary artery spasm, hemorrhage
58
extent of infarction based on ?
proximal or diastal occlusion( close or far away), duration of ischemia,
if other blood vessels were supplying the same area
59
What is a transmural infarction?
involves all three layers of the heart
| proximal occlusion
60
what is a subendochardial occlusion?
inner 1/3 to 1/2 of ventricular wall
| distal occlusion
61
diagnostics used in MIs?
```
echocardiogram
angiogram
serum markers
troponin 1 & T
CKmb
myoglobin
```
62
when is myoglobin present in the blood?
1 hr post MI
| non specific marker
63
when is troponin 1 & T present in the blood?
elevated 3-10 hours after MI
64
when is CK mb present in the blood?
4-8 hours after MI
65
how do you treat an MI?
```
o2
pain control
anticolagulants
antiarrhythmics
thrombolytics
angioplasty (stient)
bypass
```
66
what is cardiomyopathy?
idiopathic muscle disorder in the heart myocardium
67
what is hypertrophic cardiomyopathy?
when cell are excessively larger
ventricles hypertrophy
as ventricles get larger they grow inwards and the intra ventricular septum thickens
genetic
68
what is dilated congestive cardiomyopathy ?
cardiomyopathy d/t decreased elasticity in heart wall --> congested, pooling of blood because heart can't dilate
decreased ejection fraction
69
what is restrictive cardiomyopathy?
walls or heart become rigid
loose elasticity --> don't fill enough---> don't empty enough
incomplete ventricular filling --> dec CO
leads to CHF
70
what is the normal bpm ?
70 bpm
71
what is arrhythmias?
abnormal heart rhythms that affect cardiac cycle --> cardiac filling and perfusion
72
atrial flutter?
regular, fast rate atrial tachycardia ( 300 bpm)
| regular inc ventricular rate ( 150 bpm)
73
atrial fibrillation
uncoordinated spontaneous muscle contractions ( 400- 600 bpm)
causes irregular ventricle rapid ventricular rate ( 80 -180 bpm)
74
Heart block?
block in the impulse from atria to ventricles
| signal can't pass from atria to ventricles
75
what is 1st degree heart block?
delayed av conduction, regular rhythms
76
what is 2nd degree heart block ?
only some signals go through
77
what is 3rd degree heart block ?
loss of av conduction
| independent atria and ventricle contractions
78
what is ventricular fibrillation ?
ventricular quivering but no contractions
fatal within minutes--> needs defibrillation
79
treatment of arrhythmias ?
electrical ( defib, pacemakers)
ablation
drugs
80
what is valvular disease?
valves are damaged- allow for regurgitation or impeded slow ( stiff valve stenosis) due to damage
81
etiology of valvular disease?
```
congenital defects
trauma
infarction/ ischemic damage
tissue deterioration with age
inflammation causing valves falling back or scar tissue causing hardening of valves
```
82
stenosis?
stiffening--> narrow opening-->obstructed flow
83
incompetent valve
floppy/ distorted --> closing problems---> improper shutting of valves---> regurgitation
84
hemodynamic
changes of pressure related to movement of blood from valves
85
treatment of valvular disease?
some drugs-- force blood through valve
| surgery ( repair of replace valve)
