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Flashcards in Cardiovascular: Deck (53):
1

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

2

modifiable risk factors for coronary hert disease

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

3

hyperlipideia has what incidence

40% approx

4

hyperlipidemia=

high lipid content in blood
elevated cholesterol, phospholips nd triglycerides in blood

5

cholesterol

is a lipid biosynthesized by animals nec to form cell membrane

6

what transport lipids in blood

apoproteins

7

whats an apoprotein + a lipid

a lipoprotein
(fig 22-3)

8

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)

9

osis as a suffix=

deposition of

10

blood vessel layers

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

11

atheroma=
where do they form

fibrofatty lesion forms in intima of arger arteries

12

how do atheromas affect perfusion

they dec it>ischemia>stroke, MI or PVD

13

ischemia=

restricted blood flow at local level

14

death of tissue d/t ischemia=

infarction

15

what percentage of all deaths is caused by atherosclerosis

32%

16

3 types of lesions in atherosclerosis

initially fatty streak>fibrous atheromatous plaque>complicated lesion

17

initial lesion in atherosclerosis=
qualities
what does it contain

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

18

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

19

what is the third lesion in atherosclerosis
what does it do

complicated lesion
causes changes in lumen

20

when does atherosclerosis begin and manfest

mid to late 20s. mnfts in 50s60s

21

(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

22

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

23

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

24

incidence of HTN

22%

25

HTN=

Bp=cardiac output x total peipheral resistance

26

4 major control systems of BP

arterial baroreceptors
RAA
vascular autoregulation
regulation of lfuid volume

27

R coronary circuit from aorta

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

28

L coronary circuit

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

29

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

30

lookup in home notes the 4 major blood pressure control systems

l

31

normal ranges of BP

32

high normal BP

120-139 AND OR 80-89

33

Stage I mild

140-159 or 90-99

34

Stage 2: moderate

160-179 or 100-109

35

Stage 3: severe

>180 or >110

36

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

37

you can stage HTN by the numbers and also by _______

etiology

38

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)

39

2' (secondary) HTN
etiology
value

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

40

does secondary HTN follow primary?

no

41

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

42

what is white coat HTn

wc=d/t stress in health care settings

43

whats gestational HTn

during pregnancy
usually returns to normal after birth
eg eclampsia

44

malignant HTN

diastolic pressure is >120 and systolic is normal
unsure why

45

is edema a mnft of HTN

nope. complication

46

mnfts of HTN
late mnfts.

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

47

palpitation=

sensation of irreg, rapid, forceful heartbeat

48

when is Bp lowest

2-5am

49

why do some get blurred vision w HTN

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

50

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

51

if HTN is well managed what should manifest?

inc Bp only

52

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

53

systolic HTN

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