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Year 2 CV > Exam2, Blood vessels gomez > Flashcards

Exam2, Blood vessels gomez Flashcards

1
Q

give examples of elastic arteries

A

large like aorta & large branches, pulmonary aa

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2
Q

give examples of muscular aa

A

medium sized branches from aorta

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3
Q

what are the vasa vasorum aa

A

feed medium and large arteries, found in the inter 1/2-2/3 media

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4
Q

what layer of arterioles change the lumen diamter

A

medial smooth muscle

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5
Q

what happens to resistance if you half the diameter in arteriole

A

resistance increases 16 fold

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6
Q

what aa have greets regulation affect on blood pressure

A

small muscular aa- arterioles

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7
Q

where dose leukocyte exudation and vascular leakage occur

A

in postcapillary venules

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8
Q

describe size and cell lining of a capillary

A

diameter of a RBC 7-8 um endothelial cell lining without media, has pericytes around it

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9
Q

describe the structure and function of lymphatics

A

endothelial, no media valves in larger lymph vessels return interstitial fluid and inflammarotyr cells to blood important pathway in disease dissemination

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10
Q

Where are weibel palade bodies found and what are they

A

found in endothelial cells they are membrae bound storage organelles with vWF

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11
Q

what are the 3 types of endothelial cells

A

fenestrated, discontinuous (sinusoidal) and continuous

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12
Q

what factors are expressed on endothelial cells

A

vWF, FVIII, CD34 and CD31(PECAM-1)

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13
Q

what are the anti-coagulant natural regulators

A

prostacyclin thrombomodulin heparin like molecules plasminogen activator

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14
Q

what are the natura prothrombotic regulators

A

vWF tisue factor plasminogen activator inhibitor

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15
Q

What are the ECM molecules that vasoconstrict and vasodilate

A

vasoconstrict: endothelin and ACE vasodilate: NO, prostacyclin

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16
Q

What are the natura regulators of inflammation and immunity in endothlium

A

IL1 IL6 chemokines adhesion: VCAM-1, ICAM, E-selectin, P-selectin histocompatability Ag

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17
Q

What molecules from endothelium stimulate growth? inhibit?

A

stimulators: PDGF, CSF, FGF inhibitors: heparin, TGF-beta

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18
Q

what are arteriovenous fistulas

A

rar abnormal communications between aa and vv most are congenital

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19
Q

What is fibromuscular dysplasia

A

focal irregular medial and intimal hyperplasia with thickening of walls of medium and large muscular aa most common in young women

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20
Q

What is HTN in adults >60

A

> 150/90

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21
Q

what are additional risks with HTN

A

coronary artery disease, cerebral vascular accidents, hypertensive heart disease aortic dissection, renal failure

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22
Q

What are the major factors that determine BP

A

age gender, BMI and diet genetic variation in genes of RAAS that increase Na retention

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23
Q

what is a hypertensive urgency

A

>220 / >120 with NO evidence of target organ damage

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24
Q

what is accelerated HTN

A

hypertensive emergency of significan increase in BP with organ damage

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25
Q

What is malignant HTN

A

target organ damage with papilledema

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26
Q

What are renal causes of secondary HTN

A

acute glomerulonephritis chronic renal disease polycystic disease renal artery stenosis renal vasculitis renin-producing tumors

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27
Q

What are the endocrine causes of secondary HTN

A

adrenocortical hyper function (cushing, primary aldosteronism, licorice ingestion) exogenous hormones pheochromocytoma acromegaly hypothyroidism hyperthyroidism pregnangyc induced

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28
Q

what are the cardiovascular causes of secondary HTN

A

coarctation of aorta polyarteritis nodosa increased intravascular volume increased CO rigidity of the aorta

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29
Q

what are the neurologic causes of secondary HTN

A

psychogenic increased intracranial pressure sleep apnea acute stress, including surgery

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30
Q

how does licorice ingestion cause HTN

A

molecule is similar structure to cortisol and aldosterone

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31
Q

what occurs in RAAS system with 11B-hydroxylase deficiency

A

increase mineralocorticoids

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32
Q

What is liddle syndrome

A

moderately severe salt sensitive HTN due to increased distal tubular reabsorption of Na with aldosterone stimulation

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33
Q

what are the 3 patterns of arteriosclerosis

A

monckeberg medial calcific sclerosis arterolosclerosis atherosclerosis

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34
Q

what is monckeberg medial calcific sclerosis

A

in muscular aa >50 y/o with no vessel umen narrowing

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35
Q

what is arterolosclerosis

A

in small arteries and arterioles

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36
Q

what is atherosclerosis

A

atheromas= atheromatous plaques develop in elastic aa and muscular aa

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37
Q

what systemid diseases is hyaline arterolosclerosis seen in

A

aging, DM, benign nephrosclerosis

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38
Q

what is hyperplastic arteriolosclerosis and what disease has this manifestation

A

cell death (onion skinning) sometimes necrotizing arteriolitis seen in malignant HTN

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39
Q

what type of flow dynamics are prone to atherosclerosis

A

turbulent flow and low shear stress

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40
Q

how does laminar flow protect you from atherosclerosis

A

induces endothelial genes for products that protect against atherosclerosis (superoxide dismutase)

41
Q

what are the nonmodifiable risks for atherosclerosis

A

genetic abnormalities, family history, increasing age, male gender

42
Q

what are the modifiable risks for atherosclerosis

A

hyperlipidemia hypertension cigarette smoking diabetes inflammation

43
Q

If you have 3 of the risk factors for atherosclerosis what is your risk

A

ischemic heart disease

44
Q

obesity increases risk for what syndromes

A

diabetes, HTN, hypertriglyceridemia

45
Q

what metabolic syndromes are at increased risk from obesity

A

obesity, dyslipidemia, HTN, insulin resistance

46
Q

What are the 2 major pathways for cholesterol metabolism

A

2/3 LDL receptor pathway 1/3 Scavenger R pathway

47
Q

what apolipoproteins does LDL bind to

A

B-100 and E

48
Q

cholesterol released from LDL suppresses cholesterol synthesis how

A

inhibits 2HMG coenzyme A reductase

activates cholesterol acyltransferase (storage of excess cholesterol)

down regulates synthesis of cell surface LDL R

49
Q

oversupply of cholesterol inhibits what processes in the metabolism pathway

A

HMG CoA reductase

synthesis of LDL receptors

50
Q

what decreases risk of hyperlipidemia

A

exercise and alcohol

increased HDL

51
Q

what type of fats are okay

A

omega 3 beneficial

52
Q

what are the effects of estrogen on HDL and LDL

A

increase HDL and LDL

however replacement therapy does not decrease risk of MI in post menopausal women

53
Q

What causes familial hypercholesterolemia

A

mutations in LDL R gene

impair the intracell transport and catabolism of LDL

impair transport of IDL

cause elevated LDL cholesterol in the plasma

54
Q

What is the scavenger R pathway for LDL

A

oxidized LDL R

found on macrophages, monocytes, smooth m and endothelial cells

55
Q

amount catabolized by scavenger R pathway is directly related to what plasma level

A

cholesterol

56
Q

how does oxidized cholesterol affect cells in body

A

in macrophages it contributes to atherosclerosis and xanthoma formation

endothelial and smooth muscle cells

57
Q

What is the most common mutation in cholesterol metabolism

A

class II R protein transport from ER to golgi apparatus is impaired from abnormal protein folding

58
Q

What are the genetics behind familial hypercholesterolemia

A

Autosomal dominant

heterozygotes 2-3x elevation of plasma cholesterol levels

homozygotes 5x elevation of plasma cholesterol levels

59
Q

what are symptoms and signs of homozygous familial hypercholesterolemia

A

develop severe atherosclerosis, mitral valve stenosis, corneal arcus, xanthomas

60
Q

elevated plasminogen activator inhibitor 1 is a strong predictor of what

A

major atherosclerotic events

sedentary life style

stress

61
Q

what is the role of C reactive protein

A

roles in opsonizing bacteria and activating complement

62
Q

how does CRP contribute to atherosclerosis

A

involved in endothelial adhesion of WBCs and thrombosis

63
Q

what is elevated CRP a strong independent predictor for

A

risk of MI, stroke, PAD, and sudden cardiac death

64
Q

will lowering of CRP reduce cardiovascular risk

A

no

65
Q

what is the pathogensis of arterial wall changes in response to injury hypothesis

A

chronic endothelial injury

accumulation lipoproteins with subsequent oxidation

adhesion of monocytes with migration into intima

adhesion and activation of platelets

migration os smooth muscle cells becoming neointimal smooth muscle cells

accumulation of lipids in macrophages (foam cells) smooth muscle cells and extracellular spaces

66
Q

what infections can lead to atherosclerosis

A

chlaymydia pneumonia, herpesvirus and cytomegalovirus

67
Q

what cellular process leads to aneurysms and rupture

A

macrophage matix metalloproteinases and inflammation induced smooth muscle apoptosis

68
Q

What is celebrex or celexoib and what does in inhibit

A

Cox inhibitor, preferentially Cox 2 so prostacyclin, leads to prothormbotic state because COX2 not inhibited

69
Q

What are the most important causes of abdominal aortas

A

atherosclerosis (aortic)

HTN via medial cystic degeneration (thoracic)

70
Q

What are some syndromes that are associated with AAA

A

marfan syndrome

loeys dietz syndrome

ehlers danlos syndrome

scurvy

trauma

congenital defects

syphilis and vasculitides

71
Q

what are mycotic aneurysms caused by

A

septic embolus (infective endocarditis)

extension of an adjacent suppurative process

circulating organisms infecting the arterial wall

72
Q

what are the types of true aneurysms

A

saccular aneurysm-apears rounded

fusiform aneurysm- involves long segment of artery and is not rounded

73
Q

what is a pseudoaneurysm

A

false aneurysm

hematoma secondary to transmural rupture

74
Q

what is the demographic distribution of AAA

A

M>F

smokers and age>50

75
Q

What are inflammatory AAA

A

rich in lymphocytes, plasma cells and macrophages

often giant cells

cause uncertain

occur at younger age

76
Q

What infects mycotic AAA

A

salmonella gastroenteritis

77
Q

at what size are AAA surgically repaired

A

5 cm

78
Q

what are they types of syphilitic (Luetic) aneurysms

A

obliterative endarteritis– tertiarty stage syphilis with the arterioles of thoracic aorta

syphilitic aortitis– obliterative endarteritis of vasa causing ischemic injury of media causing loss of the medial elastic fibers and muscle cells

79
Q

how does syphilitic aortitis lead to aortic valve incompetence

A

can lead to aneurysmal dilation that can include aortic annulus

can involve coronary ostia

80
Q

What is an aortic dissection

A

dissection of blood between planes of the media

81
Q

What population are aortic dissections most common in

A

>90% in men 40-60 with HTN

82
Q

what procedure can cause iatrogenic aortic dissection

A

arterial cannulation

83
Q

How do you Tx an aortic dissection

A

antiHTN therapy and aortic plication

84
Q

what is characteristic symptoms onset of aortic dissection

A

sudden onset of excrutiatin pain, usually involves anterior chest, radiating to the back, and moving downard as the dissection progressesl

85
Q

where do aortic dissections usually occur

A

within 10 cm aortic valve

86
Q

what is the genetic basis of marfan syndrome

A

loss of function mutation of fibrillin

>500 mutations of FBN1 gene for fibrillin 1

prevents normal assemly of microfibrils

87
Q

what is the genetic inheritance of marfan syndrome usually

A

autosomal dominant. familial

88
Q

why does loeys dietz syndrome have similar signs to marfan

A

because fibrillin decrease leads to increase TGF beta

Loeys Dietz syndrome involves mutations in TGF beta R

89
Q

What are the skeletal manifestations of marfan syndrome

A

slender with abnormally long legs, arms and fingers. high arched palate, hyperextensibility of joints, spinal deformities

pectus excavatum or pigeon breast

90
Q

what are they eye manifestations of marfan syndrome

A

bilateral dislocation of lens from wekaness suspensory ligaments

91
Q

what are the CV manifestations of marfan syndrome

A

aneurysmal dilation and aortic dissection, dilation of the aortic valve ring (aortic incompetence)

mitral and tricuspid valve floppy calce syndrome giving rise to congestive cardiac failure

92
Q

What does marfan look like on cross section of aortic media

A

areas devoid of elastin that resemble cystic spaces that are filled with proteoglycans

93
Q

What are types of ANCA mediated vasculitis

A

wegener granulomatosis (PR3-ANCA/c-ANCA)

Microscopic polyangiitis/polyarteritis (MPO-ANCA/p-ANCA)

Churg-Strauss syndrome (MPO-ANCA/p-ANCA)

94
Q

What are the direct Ab mediated vasculitis

A

Goodpastures syndrome (anti-glomerular basement membrane Ab)

Kawasaki disease (anti-endothelial Ab and also anti smooth muscle cell Ab)

95
Q

What are the immune complex mediated causes of vasculitis

A

infection induced (Hep B or C)

Henoch-Schonlein purpura

SLE and RA

polyarteritis nodosa

Drug induced HS reactions

cryoglobulinemia

serum sickness

96
Q

what are the nonspcific Sx with vasculitis

A

fever

weight loss

myalgia

arthralgia

malaise

fatigue

97
Q

what are the types of large vessel vasculitis

A

giant cell (temporal ) arteritis: polymyalgia, usually patients older than 50

takayasus arteritis: grnaulomatous inflammation in patients younger than age 50

98
Q

What are types of medium vessel vasculitis

A

polyarteritis nodosa: necrotizing inflammation typically involving renal aa but sparing pulmonary vessels

kawasaki disease: arteritis with mucocutaneous lymph nodes. occurs in children

99
Q

what are types of small vessel vasculitis

A

wegener granulomatosis- PR3 ANCA

churg strauss syndrome- MPO ANCA, eos rich granulomatous inflammation

microscopic polyangiitis- MPO ANCA, necrotizing

Year 2 CV (31 decks)

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