Patho- Cardiovascular disorders Flashcards
what is hyperlipidemia ?
- elevated lipid content in blood
- elevated cholesterol, phospholipids, triglycerides in blood
- Apoproteins transport lipids
lipid + apoprotein = ?
lipoprotein
explain the density of lipoprotein
they can very in density
LDL, HDL, VLDL
atheros?
soft paste
sclerosis?
hardening
what is an atherosclerosis ?
when an atheroma ( fibrofatty lesion) forms in intimate of larger arteries
what does atherosclerosis cause?
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
what is infarction?
tissue death due to ischemia
what is hypercholesterolemia ?
excessive cholesterol in the blood
40 percent of Canadians experience this
pathogenesis of atherosclerosis
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
what are the three lesion stages of atherosclerosis ?
fatty streak-
fibrinous atheromatous plaque– > clinical lesion, smooth muscle cells in intimate
complicated lesion—> changes inside the lumen
is HDL good or bad?
HDL is good, 50 % carrier high density
is LDL good or bad?
LDL is lousy because it contains 50 % cholesterol
atherosclerosis facts
32 % of all deaths (1.3 of all Canadian deaths)
72000 deaths per year
hypertension range?
when you can’t bring bp back to normal and its elevated all the time ( 140/90)
classified by type, cause and severity
BP = ? x ?
BP = CO x PR
systole?
diastole?
systole= pumping diastole= filling
what are the four major control systems of hypertension ?
- 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)
how much blood in a person?
5-6 L
what is normal bp?
what is high normal BP ?
120- 139 over 80- 89
Hypertension, what are the stages?
stage 1: mild
stage 2: moderate
stage 3: severe
stage 1: mild hypertension?
140-159 over 90-99
stage 2; moderate hypertension?
160-179 over 100-109
stage 3: severe hypertension?
> 180 over >110
primary hypertension ?
idiopathic (unknown cause) 90 of cases multifactorial aetiology (kidney involved but isn't due to kidney failure )
secondary hypertension ?
identifiable causes ( renal disease/ failure) 10 percent of cases
white coat hypertension?
hypertension in health care setting ( may develop to primary hyper tension
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)
Malignant hypertension?
same as persistent hypertension or resistant hypertension sudden, quick, severe increase in bp diastolic > 120 emergency tiny vessels damaged causing shock
gestational hypertension ?
develops in pregnant women
most become normal after, some develop hypertension
problems with visual disturbances
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
treatment of hypertension
- 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
What is PVD
peripheral vascular disease
what does peripheral mean?
vessels away from heart (limbs, legs)
what does vascular mean?
any vessel ( arteries, veins, lymphatic vessels) mostly refers to peripheral arteries similar to changes in coronary arteries
acute arterial occlusion?
acute interruption to perfusion; almost always due to thrombus or embolus
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
claudification
pain from ischemia
how does your body compensate for PVD?
vasodilation collateralization ( creation of new vessels that bypass block, takes time thus long term process )
anaerobic metabolism
complications from PVD
ulceration, gangrene–> amputation
what is an aneurysm?
localized dilation of artery d/t degeneration of vessel wall
is an aneurysm permanent?
yes
risks/ causes of aneurysms?
atherosclerosis, hypertension, trauma, infection, congenital defects
three types of aneurysms?
- fusiform
- saccular
- dissecting
shape of a fusiform aneurysm ?
both sides of vessel
shape of a saccular aneurysm ?
sac or pouch on one side
shape of dissecting aneurysm?
blood flows into and directs the layers of the wall, often at bends or divides
common sites for aneurysms?
thoracic and abdominal aorta, iliac, femoral, popliteal
complications from aneurysms?
rupture, blood slows, pools, blood clots develops—> thrombosis, distal embolization, applying pressure on surrounding areas
what is infarction?
necrosis d/t ischemia
stable angina?
fixed plaque
impedes perfusion
brief pain
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
variant angina
d/t spasm in arteries, can happen anytime
treatments of angina?
nitro glycerin (vaso dilator- reduces chest pain )
what is angina an manifestations of?
coronary artery disease
myocaridal infarction is caused by?
atherosclerosis, coronary artery spasm, hemorrhage
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
What is a transmural infarction?
involves all three layers of the heart
proximal occlusion
what is a subendochardial occlusion?
inner 1/3 to 1/2 of ventricular wall
distal occlusion
diagnostics used in MIs?
echocardiogram angiogram serum markers troponin 1 & T CKmb myoglobin
when is myoglobin present in the blood?
1 hr post MI
non specific marker
when is troponin 1 & T present in the blood?
elevated 3-10 hours after MI
when is CK mb present in the blood?
4-8 hours after MI
how do you treat an MI?
o2 pain control anticolagulants antiarrhythmics thrombolytics angioplasty (stient) bypass
what is cardiomyopathy?
idiopathic muscle disorder in the heart myocardium
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
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
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
what is the normal bpm ?
70 bpm
what is arrhythmias?
abnormal heart rhythms that affect cardiac cycle –> cardiac filling and perfusion
atrial flutter?
regular, fast rate atrial tachycardia ( 300 bpm)
regular inc ventricular rate ( 150 bpm)
atrial fibrillation
uncoordinated spontaneous muscle contractions ( 400- 600 bpm)
causes irregular ventricle rapid ventricular rate ( 80 -180 bpm)
Heart block?
block in the impulse from atria to ventricles
signal can’t pass from atria to ventricles
what is 1st degree heart block?
delayed av conduction, regular rhythms
what is 2nd degree heart block ?
only some signals go through
what is 3rd degree heart block ?
loss of av conduction
independent atria and ventricle contractions
what is ventricular fibrillation ?
ventricular quivering but no contractions
fatal within minutes–> needs defibrillation
treatment of arrhythmias ?
electrical ( defib, pacemakers)
ablation
drugs
what is valvular disease?
valves are damaged- allow for regurgitation or impeded slow ( stiff valve stenosis) due to damage
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
stenosis?
stiffening–> narrow opening–>obstructed flow
incompetent valve
floppy/ distorted –> closing problems—> improper shutting of valves—> regurgitation
hemodynamic
changes of pressure related to movement of blood from valves
treatment of valvular disease?
some drugs– force blood through valve
surgery ( repair of replace valve)
