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old patho 154 > Cardiovascular: > Flashcards

Cardiovascular: Flashcards

1
Q

risk factors for coronary heart disease: non-modifiable

A

> 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

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2
Q

modifiable risk factors for coronary hert disease

A 
>HTN
>Smoking
>dyslipedemia
   -low HDLs
   -elevated LDLs
>diabetes mellitus
>obesity
>L ventricular hypertrophy
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3
Q

hyperlipideia has what incidence

A

40% approx

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4
Q

hyperlipidemia=

A

high lipid content in blood

elevated cholesterol, phospholips nd triglycerides in blood

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5
Q

cholesterol

A

is a lipid biosynthesized by animals nec to form cell membrane

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6
Q

what transport lipids in blood

A

apoproteins

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7
Q

whats an apoprotein + a lipid

A

a lipoprotein

fig 22-3

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8
Q

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

A

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)

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9
Q

osis as a suffix=

A

deposition of

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10
Q

blood vessel layers

A

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

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11
Q

atheroma=

where do they form

A

fibrofatty lesion forms in intima of arger arteries

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12
Q

how do atheromas affect perfusion

A

they dec it>ischemia>stroke, MI or PVD

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13
Q

ischemia=

A

restricted blood flow at local level

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14
Q

death of tissue d/t ischemia=

A

infarction

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15
Q

what percentage of all deaths is caused by atherosclerosis

A

32%

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16
Q

3 types of lesions in atherosclerosis

A

initially fatty streak>fibrous atheromatous plaque>complicated lesion

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17
Q

initial lesion in atherosclerosis=
qualities
what does it contain

A

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

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18
Q

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

A

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

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19
Q

what is the third lesion in atherosclerosis

what does it do

A

complicated lesion

causes changes in lumen

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20
Q

when does atherosclerosis begin and manfest

A

mid to late 20s. mnfts in 50s60s

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21
Q

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

A

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
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22
Q

pathogenesis of atherosclerosis

A
  • 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
Q

sites of severe atherosclerosis in order of frequency

A

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
Q

incidence of HTN

A

22%

25
Q

HTN=

A

Bp=cardiac output x total peipheral resistance

26
Q

4 major control systems of BP

A

arterial baroreceptors
RAA
vascular autoregulation
regulation of lfuid volume

27
Q

R coronary circuit from aorta

A 
aorta
R coronary artery
R marginal artery
arterioles
capillaries in myocardium
venules
small cardiac vein
coronary sinus
R atrium
28
Q

L coronary circuit

A 
L coronary artery
circumflex or atrioventricular artery
arterioles
capillaries in myocardium
venules
middle or great cardiac vein
29
Q

passage of blood through heart and large vessels eg aorta

A

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
Q

lookup in home notes the 4 major blood pressure control systems

A

l

31
Q

normal ranges of BP

A
32
Q

high normal BP

A

120-139 AND OR 80-89

33
Q

Stage I mild

A

140-159 or 90-99

34
Q

Stage 2: moderate

A

160-179 or 100-109

35
Q

Stage 3: severe

A

> 180 or >110

36
Q

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

A

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
Q

you can stage HTN by the numbers and also by _______

A

etiology

38
Q

1’ (primary) HTN
value
etiology

A 
>140/90
essential or idiopathic
etiology is multifactorial
kidneys are implicated
this is more common (90% of pts have this form of HTN)
39
Q

2’ (secondary) HTN
etiology
value

A

identifiable etiology such as renal disease

10% of those w HTN have secondary HTN

40
Q

does secondary HTN follow primary?

A

no

41
Q

why does systolic HTN mostly occur after age 50

A

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
Q

what is white coat HTn

A

wc=d/t stress in health care settings

43
Q

whats gestational HTn

A

during pregnancy
usually returns to normal after birth
eg eclampsia

44
Q

malignant HTN

A

diastolic pressure is >120 and systolic is normal

unsure why

45
Q

is edema a mnft of HTN

A

nope. complication

46
Q

mnfts of HTN

late mnfts.

A

inc BP only

late: fatigue, palpitations, morning headaches, blurred vision, dizziness

47
Q

palpitation=

A

sensation of irreg, rapid, forceful heartbeat

48
Q

when is Bp lowest

A

2-5am

49
Q

why do some get blurred vision w HTN

A

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

50
Q

if HTn isnt well managed what could happen

A

Progressive organ damage

  • the heart because it is the pump
  • the kidneys receive a large amount of blood
  • vessel walls
51
Q

if HTN is well managed what should manifest?

A

inc Bp only

52
Q

Tx of HTn

A 
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
Q

systolic HTN

A

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

old patho 154 (18 decks)

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