Blood Vessels II

Question 1

benign HTN

Answer 1

essential

-controlled with no short term problems

Question 2

HTN urgency

Answer 2

systolic > 220
diastolic > 120

no evidence target organ damage

Question 3

accelerated HTN

Answer 3

increase in BP with target organ damage

Question 4

malignant HTN

Answer 4

increased in BP with target organ damage

ALSO papilledema

Question 5

secondary causes of HTN

Answer 5

renal
endocrine
caardiovascular
neurological

Question 6

licorice

Answer 6

glycrrhizin
-similar to cortisol and aldosterone

can go to aldosterone receptors

result is secondary HTN

Question 7

high cortisol

Answer 7

binds aldosterone receptors

Question 8

vasoconstriction

Answer 8

ANG II
catecholamines
thromboxane
endothelin
alpha-adrenergic

Question 9

vasodilation

Answer 9

NO
prostacyclin
kinins
ANP
beta-adrenergic

Question 10

renovascular HTN

Answer 10

stenosis - decreased glomeruli pressure

> renin release
RAAS activation
vasoconstriction
increased blood volume

leads to HTN

Question 11

RAAS control

Answer 11

only 2% of sodium reabsorption

98% reabsorbed rest of kidney

Question 12

hydroxylase deficiency

Answer 12

results in HTN

congenital adrenal hyperplasia

associated with androgen and mineralocorticoid excess
-masculinization and HTN

Question 13

liddle syndrome

Answer 13

mutations in ENaC

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

> HTN

Question 14

arteriosclerosis

Answer 14

hardening of artery

3 patterns:

• monckeberg
• arteriolosclerosis
• atherosclerosis

Question 15

monckeberg

Answer 15

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

**not clinically significant

may be seen in mammogram as calcified vessels

Question 16

arteriolosclerosis

Answer 16

small arteries and arterioles

two subtypes

• hyperplastic
• hyaline

result in small lumen - clinically significant

Question 17

hyaline arteriolosclerosis

Answer 17

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

Question 18

hyperplastic arteriolosclerosis

Answer 18

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)

Question 19

atherosclerosis

Answer 19

intimal lesions - atheromas (atheromatous plaques)

raised soft, yellow, grumous core of lipid

can rupture and weaken underlying media

Question 20

50% of deaths and serious morbidity in US

Answer 20

atherosclerosis

Question 21

primary intervention

Answer 21

prevent onset of disease

Question 22

secondary intervention

Answer 22

patient already has problem - lets help them out

asymptomatic patient

Question 23

tertiary prevention

Answer 23

prevent recurrences with disease

-symptomatic patient

Question 24

atherosclerotic plaque

Answer 24

atheromas or atheromatous plaques

• obstruction
• thrombi
• weaken media

Question 25

prone to atherosclerosis

Answer 25

turbulent flow and low shear stress

Question 26

laminar flow

Answer 26

endothelial genes for agents against atherosclerosis - superoxide dismutase

Question 27

turbulent flow

Answer 27

increased blood hitting vessel wall > endo cell takes beating > endo dysfunction > increased risk of plaque formation -also inflammation causes endo dysfunction

Question 28

type I atherosclerotic lesion

Answer 28

fatty dot

Question 29

superoxide dismutase

Answer 29

expressed by endo cells with laminar flow | -protects against atherosclerosis

Question 30

problems with atherosclerosis

Answer 30

obstruction plaque rupture weaken vessel wall - aneurysm

Question 31

constitutional risk factors for ischemic heart disease

Answer 31

non-modifiable age gender genetics

Question 32

modifiable risk factors for ischemic heart disease

Answer 32

hypercholesterol HTN smoking DM

Question 33

additional risk factors for ischemic heart disease

Answer 33

``` inflammation hyperhomocystinemia metabolic syndrome lipoprotein a hemostatic factors ```

Question 34

endo injury response

Answer 34

intimal thickening | -presence of lipids - atheroma forms

Question 35

atheromas more common

Answer 35

branch points - high turbulence

Question 36

oxidized LDL

Answer 36

taken up by macrophages - form foam cells -scavenger receptors pro-inflammatory response

Question 37

fatty dot

Answer 37

stage I | -to fatty streak

Question 38

stage 6 plaque

Answer 38

complicated - when endo denuded | -sets off thrombi**

Question 39

dark spots on atherosclerotic lesion?

Answer 39

thrombi | -means it is complicated -stage 6

Question 40

trichrome stain

Answer 40

for collagen | -collagen in atheroma - means its been there long time

Question 41

atheroma structure

Answer 41

fibrous cap - necrotic center - media destroyed

Question 42

plaque stenosis

Answer 42

at 70% occlusion

Question 43

new plaque

Answer 43

thinner fibrous cap -more likely to break apart aka vulnerable plaque

Question 44

stable plaque

Answer 44

thicker fibrous cap - older - more stable

Question 45

MI risk at 60

Answer 45

5x risk at 40

Question 46

genetics of atherosclerosis

Answer 46

familial hypercholesterolemia

Question 47

male

Answer 47

more likely to get atherosclerosis

Question 48

2 risk factors together

Answer 48

4x risk

Question 49

3 risk factors together

Answer 49

7x risk

Question 50

BP > 169/95

Answer 50

60% increased risk of IHD

Question 51

cigarette smoking

Answer 51

death rate from HID increased > 200%

Question 52

inflammation measure

Answer 52

C-reactive protein | -increased risk of atherosclerosis