Arteriosclerosis and Hyptertension Flashcards

1
Q

What is an atheroma

A

accumulation of degenerative material in the inner layer of artery walls

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2
Q

Define arteriosclerosis

A

hardening of the arteries

they become thick and stiff

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3
Q

How is atherosclerosis characterized?

A

by atheroma in large or medium arteries

-it’s a specific type of arteriosclerosis

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4
Q

Monckeberg’s medial calcific sclerosis

A

medial calcification WITHOUT luminal narrowing or intimal disruption –> occurs when you get calcium deposits in muscle walls

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5
Q

Hyaline arteriosclerosis

examples

A

thickening of the basement membrane

ie hypertension and diabetes mellitus

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6
Q

Hyperplastic/proliferative arteriosclerosis

A

fibrocellular intimal thickening

i.e. - malignant hypertension and scleroderma (chronic hardening of skin and CT)

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7
Q

Non-modifiable risk factors for atherosclerosis

A

age - risk of MI increases 5X in men 40-60 yrs old

gender - men > premenopausal women

genetics - MOST IMPORTANT FACTOR

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8
Q

Potentially modifiable risk factors for atherosclerosis

A

smoking - 1 pack per day increases death rate by 200%
-once one stops, gradually decreases
diabetes mellitus
hypertension - no specific level identifies increased risk
hypercholesterolemia - higher LDL and cholesterol, the greater the risk. higher the HDL, the lower the risk

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9
Q

Additional risk factors for atherosclerosis

A
inflammation (C-reactive protein)
hyperhomocysteinemia - inc in levels of homocysteine
lipoprotein (a) levels
metabolic syndrome (obesity)
type A personality (stress)
lack of exercise
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10
Q

Common sites of atheroma formation

A
branches of main arteries
papliteal artery - knee
coronary arteries - heart
abdominal aorta
carotid arteries - head and neck
cerebral arteries - brain
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11
Q

What does plaque contain?

A
collagen
lipid
macrophage
myofibroblasts
neovascularization (proliferation of bv in tissues not normally containing them)
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12
Q

What makes up a fibrous cap?

A

myofibroblasts (smooth muscle cells) and collagen.

these cover a central core of lipid/cellular debris with CHOLESTEROL

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13
Q

Plaque can progress into…

A

ulcerations
fissure formation
thrombosis
embolization of thrombus or debris from central core
calcification
hemorrhage into plaque from neovascularization

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14
Q

What is a fatty streak?

A

the first grossly visible lesion in the development of atherosclerosis
-characterized by lipid-laden cells in the intimia

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15
Q

Where do fatty streaks occur?

A

in infants and children in atherosclerotic or nonatherosclerotic areas

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16
Q

What can result from a fatty streak?

A

they can regress
or
they can progress to atheromas

17
Q

complications of atherosclerosis

A

ischemic heart disease - reduced BF to <3

aneurysm formation due to pressure atrophy of the media with altered balance of collagen synthesis/degradation

18
Q

hypertension prevalence in adults from USA?

A

about 25%, prevalence increases with age

19
Q

guidelines for hypertension

A

BP < 140/90 –> normal
BP > 160/106 –> moderate to severe
BP = 140/90 to 159/104 –> mild

20
Q

What does essential hypertension mean?

It accounts for what % of hypertension?

A

hypertension without a known cause

90%

21
Q

Contributing factors to essential hypertension include:

A
genetics
obesity
stress
increased salt
inactivity
cigarette smoking
22
Q

Symptoms of essential hypertension

A

most patients have no symptoms until organ damage has occurred

23
Q

High BP causes:

A

headache
dizziness
fatigue
palpitations

24
Q

Concentric left ventricular hypertrophy (compensated)

A

LV thickens to adapt to inc in stress to wall. Provides normal CO

25
Q

LV hypertrophy (decompensated) occurs when?

A

when the LV is no longer able to adequately provide normal CO

26
Q

what does LV hypertrophy (decompensated) lead to?

A

dilation and CHF

27
Q

Atherosclerosis leads to…

A

ischemic heart disease
stroke
ischemic injury to other organs (nephrosclerosis)
gangrene - dead tissue

28
Q

Arteriosclerosis leads to…

A
retinal injury (visual disturbances) 
kidney damage or nephrosclerosis (renal failure)
29
Q

How does a dissecting hemotoma of the aorta occur?

A

a longitudinal tear in the media because of a complication from hypertension

30
Q

Pathogenesis of hypertension

A

BP = CO x peripheral resistance

  1. peripheral vascular resistance (vasoconstriction)
  2. reduced sodium excretion –> salt and water retention –> increased plasma volume and CO
31
Q

How is secondary hypertension controlled

A

it’s controlled when the underlying disease is controlled

32
Q

Relatively rapid onset of very high BP is….

A

malignant hypertension

33
Q

Complications stemming from malignant hypertension…

A
cerebral edema with papilledema ->blindness
cerebral hemorrhage
retinal hemorrhage
severe headache
vomiting
convulsions
encephalopathy - brain disease
renal failure
heart failure
34
Q

How does one treat malignant hypertension?

A

promptly, but being cautious of not decreasing BP too quickly