Cardiovascular: Flashcards by Willow Belanger

risk factors for coronary heart disease: non-modifiable

> male 45+

> family hx of CVD

- males under 55
 - females under 65

> postmenopausal female

45-55-65 males always first and menopause starts 40-51

How well did you know this?

Not at all

Perfectly

modifiable risk factors for coronary hert disease

>HTN
>Smoking
>dyslipedemia
   -low HDLs
   -elevated LDLs
>diabetes mellitus
>obesity
>L ventricular hypertrophy

How well did you know this?

Not at all

Perfectly

hyperlipideia has what incidence

40% approx

How well did you know this?

Not at all

Perfectly

hyperlipidemia=

high lipid content in blood

elevated cholesterol, phospholips nd triglycerides in blood

How well did you know this?

Not at all

Perfectly

cholesterol

is a lipid biosynthesized by animals nec to form cell membrane

How well did you know this?

Not at all

Perfectly

what transport lipids in blood

apoproteins

How well did you know this?

Not at all

Perfectly

whats an apoprotein + a lipid

a lipoprotein

fig 22-3

How well did you know this?

Not at all

Perfectly

lipoproteins what are the types in order of low density to high
what is more dense fat or protein

lipoproteins all contain some triglcerides, phospholipids and cholesterol
chylomicrons transport fat into the intestine (only 2% protein)
VLDL contains lots of triglcerides and 5-10% protein
LDL isnt as bad for you as VLDL contains 25% protein
HDL is 50% protein (they transport LDLs to liver for proc and return cholesterol to liver)

How well did you know this?

Not at all

Perfectly

osis as a suffix=

deposition of

How well did you know this?

Not at all

Perfectly

blood vessel layers

endothelial cells>CT>internal elastic membrane>Sm muscle cell>collagen and elastic fibres (typical artery)

How well did you know this?

Not at all

Perfectly

atheroma=

where do they form

fibrofatty lesion forms in intima of arger arteries

How well did you know this?

Not at all

Perfectly

how do atheromas affect perfusion

they dec it>ischemia>stroke, MI or PVD

How well did you know this?

Not at all

Perfectly

ischemia=

restricted blood flow at local level

How well did you know this?

Not at all

Perfectly

death of tissue d/t ischemia=

infarction

How well did you know this?

Not at all

Perfectly

what percentage of all deaths is caused by atherosclerosis

32%

How well did you know this?

Not at all

Perfectly

3 types of lesions in atherosclerosis

initially fatty streak>fibrous atheromatous plaque>complicated lesion

How well did you know this?

Not at all

Perfectly

initial lesion in atherosclerosis=
qualities
what does it contain

fatty streak
insidiious, subclinical
-yellowish discoloration inintima that contains defense cells and lipids

How well did you know this?

Not at all

Perfectly

what type of lesion comes after fatty streak in atherosclerosis
what does it contain

fibrous atheromatous plaque-basic clinical lesion in intima contains: defense cells, scar tissue, smooth muscle cells

How well did you know this?

Not at all

Perfectly

what is the third lesion in atherosclerosis

what does it do

complicated lesion

causes changes in lumen

How well did you know this?

Not at all

Perfectly

when does atherosclerosis begin and manfest

mid to late 20s. mnfts in 50s60s

How well did you know this?

Not at all

Perfectly

(my notes maybe use next slide?)process of atherosclerosis

endothelium gets damaged by risk factors eg smoking and lipids enter and deposit on intima

monocytes enter intima as well as platelets.
as lipids enter=fatty streak
macrophages enter and release free radicals such as hydroxyl that cause damage. they also engluf lipids and turn into foam cells
in Fibrous plaque the lipids form a core and smooth muscle begins to grow stim by foam cells releasign growth factors. at this point it would be 60% occluded
a complicated lesion will have changes in the lumen>hemmorhaging into the plaque>thrombus inside the vessel. its 90% occluded

How well did you know this?

Not at all

Perfectly

pathogenesis of atherosclerosis

insidious origin w subtle endothelial injury>inflm (CRP)
monocytes and other inflm cells bind to endothelium
monocytes enter intima>become macrophages>release free radicals (from oxidizing the lipids) causing injury and engulf lipids to bcome foam cells
sm muscle cells proliferate
atheroma forms

sites of severe atherosclerosis in order of frequency

1=abdominal aorta and iliac arteries
2=proximal coronary arteries
3=thoracic aorta, femoral and popliteal arteries
4=internal carotid arteries
5=vertebral, basilar, and middle cerebral arteries

incidence of HTN

22%

HTN=

Bp=cardiac output x total peipheral resistance

4 major control systems of BP

arterial baroreceptors RAA vascular autoregulation regulation of lfuid volume

R coronary circuit from aorta

``` aorta R coronary artery R marginal artery arterioles capillaries in myocardium venules small cardiac vein coronary sinus R atrium ```

L coronary circuit

``` L coronary artery circumflex or atrioventricular artery arterioles capillaries in myocardium venules middle or great cardiac vein ```

passage of blood through heart and large vessels eg aorta

deoxy blood enters R atrium via superior vena cava passes tricuspid R atrioventricular valve into R ventricle through pulmonary semilunar valves nto pulmonary trunk then to lungs through pulmonary arteries after lungs the pulmonary veins carry oxygenated blood to the left atrium past the mitral valve (L atrioventriular valve) into L ventricle from L ventricle to body passing the aortic semilunar vve

lookup in home notes the 4 major blood pressure control systems

normal ranges of BP

high normal BP

120-139 AND OR 80-89

Stage I mild

140-159 or 90-99

Stage 2: moderate

160-179 or 100-109

Stage 3: severe

>180 or >110

if you have a pt w 150/105 how would you stage their HTN? why?

use the higher value to err on the side of caution. THey would be stage 2. diastolic and systolic are of equal importance. use the higher number

you can stage HTN by the numbers and also by _______

etiology

1' (primary) HTN value etiology

``` >140/90 essential or idiopathic etiology is multifactorial kidneys are implicated this is more common (90% of pts have this form of HTN) ```

2' (secondary) HTN etiology value

identifiable etiology such as renal disease | 10% of those w HTN have secondary HTN

does secondary HTN follow primary?

why does systolic HTN mostly occur after age 50

wear and tear At rest TPR is stable but TPR fluctuates. With aging their is change in compliance of the vessels. When heart pumps the vessels dont have the elasticity to comply. Because peripheral resistance is dec cardiac output must inc

what is white coat HTn

wc=d/t stress in health care settings

whats gestational HTn

during pregnancy usually returns to normal after birth eg eclampsia

malignant HTN

diastolic pressure is >120 and systolic is normal | unsure why

is edema a mnft of HTN

nope. complication

mnfts of HTN | late mnfts.

inc BP only | late: fatigue, palpitations, morning headaches, blurred vision, dizziness

palpitation=

sensation of irreg, rapid, forceful heartbeat

when is Bp lowest

2-5am

why do some get blurred vision w HTN

retina is made up of tiny blood vessels which are easily affected

if HTn isnt well managed what could happen

Progressive organ damage - the heart because it is the pump - the kidneys receive a large amount of blood - vessel walls

if HTN is well managed what should manifest?

inc Bp only

Tx of HTn

``` lifestyle modification (diet, exercise, weight) (theyll initially take Bp, have you try the above then remeasure if still HTN then move onto drugs) ``` -1st line diuretic! (must maintain normal blood volum) diuretics inc fluid loss from kidneys >dec blood volume>dec HTN. you also lose electrolytes then, if nec add one or more of these in any order calcium channel blocker-dec contraction of heart and on smooth muscle in blood vessels angiotensisn II receptor blocker ACE inhibitor

systolic HTN

systolic P >140, diastolic pressure of dec elasticity>inc systolic pressure but not diastolic pressure