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CV II Exam 2 > Blood Vessels II > Flashcards

Blood Vessels II Flashcards

1
Q

benign HTN

A

essential

-controlled with no short term problems

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2
Q

HTN urgency

A

systolic > 220
diastolic > 120

no evidence target organ damage

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3
Q

accelerated HTN

A

increase in BP with target organ damage

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4
Q

malignant HTN

A

increased in BP with target organ damage

ALSO papilledema

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5
Q

secondary causes of HTN

A

renal
endocrine
caardiovascular
neurological

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6
Q

licorice

A

glycrrhizin
-similar to cortisol and aldosterone

can go to aldosterone receptors

result is secondary HTN

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7
Q

high cortisol

A

binds aldosterone receptors

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8
Q

vasoconstriction

A 
ANG II
catecholamines
thromboxane
endothelin
alpha-adrenergic
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9
Q

vasodilation

A 
NO
prostacyclin
kinins
ANP
beta-adrenergic
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10
Q

renovascular HTN

A

stenosis - decreased glomeruli pressure

> renin release
RAAS activation
vasoconstriction
increased blood volume

leads to HTN

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11
Q

RAAS control

A

only 2% of sodium reabsorption

98% reabsorbed rest of kidney

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12
Q

hydroxylase deficiency

A

results in HTN

congenital adrenal hyperplasia

associated with androgen and mineralocorticoid excess
-masculinization and HTN

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13
Q

liddle syndrome

A

mutations in ENaC

  • overresponseive to aldosterone
  • large Na reabsorption
  • more blood volume

> HTN

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14
Q

arteriosclerosis

A

hardening of artery

3 patterns:

  • monckeberg
  • arteriolosclerosis
  • atherosclerosis
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15
Q

monckeberg

A

medial calcific sclerosis
-muscular arteries of patients > 50yo with no vessel lumen narrowing**

**not clinically significant

may be seen in mammogram as calcified vessels

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16
Q

arteriolosclerosis

A

small arteries and arterioles

two subtypes

  • hyperplastic
  • hyaline

result in small lumen - clinically significant

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17
Q

hyaline arteriolosclerosis

A

plasma proteins leak across endo cells - cell matrix synthesis

hyaline thickening with luminal narrowing

more severe in those with HTN

in aging, diabetic microangiography and nephrosclerosis

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18
Q

hyperplastic arteriolosclerosis

A

with severe malignant HTN
-onion-skinning lesion**

concentric laminated thickening of walls with luminal narrowing

in malignant HTN - accompanied by fibrinoid deposits and vessel wall necrosis - necrotizing arteriolitis (kidney)

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19
Q

atherosclerosis

A

intimal lesions - atheromas (atheromatous plaques)

raised soft, yellow, grumous core of lipid

can rupture and weaken underlying media

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20
Q

50% of deaths and serious morbidity in US

A

atherosclerosis

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21
Q

primary intervention

A

prevent onset of disease

22
Q

secondary intervention

A

patient already has problem - lets help them out

asymptomatic patient

23
Q

tertiary prevention

A

prevent recurrences with disease

-symptomatic patient

24
Q

atherosclerotic plaque

A

atheromas or atheromatous plaques

  • obstruction
  • thrombi
  • weaken media
25
Q

prone to atherosclerosis

A

turbulent flow and low shear stress

26
Q

laminar flow

A

endothelial genes for agents against atherosclerosis - superoxide dismutase

27
Q

turbulent flow

A

increased blood hitting vessel wall
> endo cell takes beating
> endo dysfunction
> increased risk of plaque formation

-also inflammation causes endo dysfunction

28
Q

type I atherosclerotic lesion

A

fatty dot

29
Q

superoxide dismutase

A

expressed by endo cells with laminar flow

-protects against atherosclerosis

30
Q

problems with atherosclerosis

A

obstruction

plaque rupture

weaken vessel wall - aneurysm

31
Q

constitutional risk factors for ischemic heart disease

A

non-modifiable
age
gender
genetics

32
Q

modifiable risk factors for ischemic heart disease

A

hypercholesterol
HTN
smoking
DM

33
Q

additional risk factors for ischemic heart disease

A 
inflammation
hyperhomocystinemia
metabolic syndrome
lipoprotein a
hemostatic factors
34
Q

endo injury response

A

intimal thickening

-presence of lipids - atheroma forms

35
Q

atheromas more common

A

branch points - high turbulence

36
Q

oxidized LDL

A

taken up by macrophages - form foam cells
-scavenger receptors

pro-inflammatory response

37
Q

fatty dot

A

stage I

-to fatty streak

38
Q

stage 6 plaque

A

complicated - when endo denuded

-sets off thrombi**

39
Q

dark spots on atherosclerotic lesion?

A

thrombi

-means it is complicated -stage 6

40
Q

trichrome stain

A

for collagen

-collagen in atheroma - means its been there long time

41
Q

atheroma structure

A

fibrous cap

  • necrotic center
  • media destroyed
42
Q

plaque stenosis

A

at 70% occlusion

43
Q

new plaque

A

thinner fibrous cap
-more likely to break apart

aka vulnerable plaque

44
Q

stable plaque

A

thicker fibrous cap

  • older
  • more stable
45
Q

MI risk at 60

A

5x risk at 40

46
Q

genetics of atherosclerosis

A

familial hypercholesterolemia

47
Q

male

A

more likely to get atherosclerosis

48
Q

2 risk factors together

A

4x risk

49
Q

3 risk factors together

A

7x risk

50
Q

BP > 169/95

A

60% increased risk of IHD

51
Q

cigarette smoking

A

death rate from HID increased > 200%

52
Q

inflammation measure

A

C-reactive protein

-increased risk of atherosclerosis

CV II Exam 2 (18 decks)

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