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DMD 5247 > Blood Vessel Pathology > Flashcards

Blood Vessel Pathology Flashcards

1
Q

vessels most affected by atherosclerosis

A
  • abdominal aorta
  • coronary arteries
  • popliteal arteries
  • carotid arteries
  • vessels of the circle of Willis
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2
Q

contents of a plaque

A

fibrous cap
necrotic center
media

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3
Q

step 1

A

chronic endothelial injury

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4
Q

high blood pressure damages the endothelium and activates:

A

inflammation

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5
Q

high blood pressure promotes:

A

turbulent flow in a blood vessel

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6
Q

this turbulent flow is particularly evident in areas of:

A

branching or constriction of the blood vessel

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7
Q

what effect does endothelial damage have on cholesterol invasion and clot formation

A

increases the likelihood

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8
Q

step 2

A

endothelial dysfunction

monocyte adhesion and emigration

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9
Q

step 3

A

macrophage activation

smooth muscle recruitment

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10
Q

step 4

A

leukocytes and smooth muscle cells engulf lipid

hyperlipidemia is a primary player in the etiology

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11
Q

step 5

A

smooth muscle proliferation
collagen and extracellular lipid deposition
(complicated plaque)

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12
Q

major non-modifiable risk factors

A

age
gender
genetics

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13
Q

major modifiable risk factors

A

lifestyle
cigarette smoking
diabetes
inflammation

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14
Q

complications of atherosclerosis

A

stenosis
thrombosis/embolus
aneurysm
calcification

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15
Q

what must occur for cholesterol to be a problem

A

oxidation

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16
Q

major steps of atherosclerosis

A
  1. LDL enters the intima through the inner endothelium
  2. Intimal LDL is oxidized into pro-inflammatory lipids
  3. Oxidized LDL causes adhesion and entry of monocytes and T lymphocytes across the endothelium
  4. monocytes differentiate into macrophages which then consume large amounts of LDL: forming foam cells
  5. foam cells release cytokines: that encourage atherosclerosis
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17
Q

How many patterns or types of LDL cholesterol are there

A

2

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18
Q

Type A cholesterol

A

Large, less dense

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19
Q

Type B cholesterol

A

small, more dense

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20
Q

Which one more easily penetrates the endothelium

A

Type B

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21
Q

Risk factors for pattern B

A

genetics
oral contraceptives
diet

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22
Q

what effect does increased glutathione activity have on atherosclerotic development?HMG

A

slows the atherosclerotic development

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23
Q

Statins

A

HMG-CoA Reductase inhibitors

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24
Q

most circulating cholesterol is synthesized de novo

A

80% in the liver
10% in the intestine
5% in the skin

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25
Q

HMG-CoA reductase inhibitors

A

May prolong life in those with previous cardiovascular event history
provide very little primary protection
increases risk of diabetes
other side effect

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26
Q

side effects of statins

A 
increases the risk of diabetes
kidney failure
liver failure
muscle pain
rhabdomyolysis: muscle break down
--perhaps a function of reduced ubiquinone(Coenzyme Q10)
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27
Q

What does reduced ubiquinone (Coenzyme Q10) cause

A 
Myopathy: muscle weakness and pain
reduced mitochondrial function
oxidative stress
intima media thickness increase
cataracts
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28
Q

What does cholesterol do that is so important

A 
cell membranes
steroid synthesis
bile salts
vitamin D
ubiquinone
29
Q

hypertension

A

affects 25% of the population

asymptomatic until later

30
Q

what are the different types of hypertension

A

benign and malignant

31
Q

benign hypertension

A

essential: 95% of cases

secondary

32
Q

essential benign hypertension

A
  • primary hypertension
  • idiopathic
  • appears to be a mix of genetic and environmental factors
  • erroneously assumed to result from weight gain
33
Q

secondary benign hypertension

A

-resulting from structural, renal, or endocrine defects

34
Q

structural defect causing secondary benign hypertension

A

aortic coarctation

35
Q

renal defect causing secondary benign hypertension

A

renal artery stenosis

36
Q

endocrine defect causing secondary benign hypertension

A

adrenocortical hyperfunction

37
Q

benign hypertension increases risk of:

A
  • atherogenesis
  • aortic dissection
  • stroke
38
Q

hypertension causes what types of small blood vessel disease

A

hyperplastic arteriosclerosis

hyaline arteriosclerosis

39
Q

malignant hypertension

A

lethal in 1-2 years if left untreated

40
Q

malignant hypertension usually accompanies:

A
  • renal failure
  • retinal hemorrhages
  • papilledema (blurred disk margins)
41
Q

RAAS Dysfunction

A
  • insulin increases kidney sodium reabsorption
  • insulin increases aldosterone secretion
  • a very slight increase in plasma insulin is capable of eliciting an antidiuretic effect
42
Q

Enhanced growth factor activity

A

receptors in capillary endothelial cells

  • vascular cells are esponsive to insulin
  • hypertrophy of the vascular wall leads to narrowing of vascular lumen
43
Q

SNS

A

insulin causes a dose-related increas in norepinephrine release
subsequent increase in pulse and blood pressure

44
Q

dyslipidemia

A 
reduced HDL
increased VLDL
increased LDL
-pattern B
Increased triglycerides
45
Q

nitric oxide

A

NO reduces blood pressure: made from L-arginine
insulin increases NO production
NO is a potent vasodilator

46
Q

aneurysm

A

localized abnormal vessel dilation

47
Q

true aneurysm

A

involves all three layers

48
Q

false aneurysm

A

hole covered with a hematomq (extravascular connective tissue)

49
Q

causes of an aneurysm

A
  • caused by atherosclerosis
  • wall degeneration
  • trauma
  • congenital defects (Marfan Syndrome)
  • infection
50
Q

aortic dissection

A

aortic wall tears and blood pours into wall

51
Q

Type A1 of aortic dissection

A

originates in ascending aorta, propagates to the ascending aorta and often beyond it distally

52
Q

Type A2 of aortic dissection

A

Originates in ascending aorta and is confined to the ascending aorta

53
Q

Type B3 of aortic dissection

A

originates in the descending aorta, rarely extends proximally but will extend distally

54
Q

aortic dissection can be caused by

A

hypertension

trauma

55
Q

Vasculitis

A

inflammation of blood vessels

56
Q

Giant-cell artheritis

A

most common vasculitis
chronic granulomatous inflammation of the large to small arteries
accompanied by fever, headache, vision loss
treatment: corticosteroids

57
Q

takayasu arteritis

A

granulomatous vasculitis of the aortic arch
severe narrowing in upper extremities
ocular disturbances

58
Q

polyarteritis nodosa

A

different stages coexist in the same artery
varied symptoms
fatal if untreated, but steroids are curative

59
Q

wegener granulomatosis

A

lung granulomas, renal disease, vasculitis
T-cell mediated hypersensitivity
fatal if untreated within a year
c-ANCA positive

60
Q

churg-strauss syndrome

A

similar to wegener but more related to alergies and asthma, without the renal disease

61
Q

microscopic poly angitis

A

widespread necrotizing vasculitis of smaller vessels
antibody response to the drug or bug
neutrophils heavily present in vessels
possibly type 3 hypersensitivity
removing offending agent usually resolves the problem

62
Q

tumors

A

hemangioma
glomus tumor
kaposi sarcoma
angiosarcoma

63
Q

capillary hemangioma

A

skin, oral mucosa, sometimes organs

strawberry type present at birth, regresses

64
Q

cavernous hemangioma

A 
organs, sometimes skin
cosmetic problem (unless brain)
65
Q

pyogenic granuloma

A

rapidly growing red nodule on skin, in mouth

microscopically resembles granulation tissue

66
Q

glomus tumor

A

benign but painful
arise from glomus body cells
distal digits, especially under fingernails
excise

67
Q

kaposi sarcoma

A 
low-grade malignancy of endothelial cells 
4 forms
-chronic
-african
-transplant-associated
-AIDS associated

clinical course varies: chronic is the best prognosis
excise

68
Q

angiosarcoma

A

high-grade malignancy of endothelial cells
often in skin, soft tissue, breast, liver
arsenic and PVC increase risk
covers a spectrum from well-differentiated to anaplastic
metastasize rapidly

DMD 5247 (13 decks)

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