Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

general path > Anteriosclerosis and Hypertension (CVI) > Flashcards

Anteriosclerosis and Hypertension (CVI) Flashcards

1
Q

what disease is responsible for more morbifiy and mortality than any other category of disease

A

Vacular disaese

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the principle mechanisms of vascular disase

A

Narrowing/obstruction of vascular lumina

weakening of vascular walls leading to dilation/rupture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is arteriosclerosis

A

Hardening of the artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what size of arteries does Atherosclerosis

A

Large and medium arties and arterioles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is monckeberg’s medial calcific sclerosis

A

Medial calcification without luminal narrowing or intimal disruption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are the types of arteriolosclerosis

A

Hyaline

Hyperplastic (proliferative)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is hyaline ateriolosclerosis

A

thickening of basement membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what causes hyaline arteriolosclerosis

A

Hypertension and diabetes mellitus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is hyperplastic (proliferative) arteriosclerosis

A

Firbocellular intimal thickening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what causes hyperplastic (proliferative) arteriosclerosis

A

Malignant hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

clinical signification of medial calcific sclerosis (monckeberg’s) Arteriosclerosis

A

no encroachment so clinically insignificant

- normal with aging

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what does hyaline arteriolosclerosis look like

A

lots of transudate PR so it apperas that there is a large basement membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what does hyperplastic arteriolosclerosis look like

A

s. muscle with collagen intermixed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is atherosclerosis associated with

A

With the formation of intimal lesions called atheromas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how do atheromas cause problems

A

Protrude into the lumen of a vessel

  • can enlarge and obstruct blood flow
  • weaken the underlying media of the artery
  • plaque can rupture resulting in catastrophic vessel thrombosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is a atheromas ook like

A
  • A fibrous cap (s. muscle, macrophage, foam cels, lymphcytes, collagen, elastin, proteoglycan, neovascularization)
  • necrotic center (cell debris, cholesterol crystals (LDL), foam cels, calcium)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

where is atherosclerosis common

A

US, western europe

and not common in africa and the far east

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is the peak death rate of myocardio infarcation

A

54% in the 60’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is the current death rate for all atherosclerosis related complications

A

50% (25% for myocardial infarcation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

non-modifiable risk factors for Atherosclerosis

A
  • Age(risk of acute myocardial infarction increases by 5x in men between 40 and 60)
  • Gender: men more than premenopausal women
  • genetics: family history of acute myocardial infarction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is the most important factors for atherosclerosis

A

Genetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what are the potentially modifiable risk factors for atherosclerosis

A

Cigarette smoking
diabetes mellitus
Hypertension (no specific level mentioned though)
hypercholesterolemia- specifically more LDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

how much does cig smoking increase risk for artherosclerosis

A

200% if a pack a day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are the added risk factors for artherosclerosis

A 
inflamtion (C-reactive protein, CRP-inflammatory marker)
hyperhomocysteinemia
Lipoprotein (a) levels
Metabolic syndrome (obesity)
Type A personality (stress)
Lack of exercise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what are the common sites of atheroma formation

A 
Major arterial branch points
Abdominal aorta
Coronary arteries
Popliteal arteries
Cerebral arteries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what are the progressive changes in plaques

A

Ulceration
fissure formation
Thrombosis
embolization (thrombus or debris from the central core)
calcification
hemorrhage into plaque from neovascualrization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what are the first steps in the response-to-injury hypothesis for atherosclerosis

A
  • Endothelial injury/dysfunction
  • accumulation of
  • lipoproteins in the vessel wall
    Monocyte adhesion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

how does Monocyte adhesion lead to atherosclerosis

A

Migration into intima with differentiation into macrophages and foam cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what are foam cells

A

MAcrophages that have ingested lipid

30
Q

how does foam cells cause problems

A

Tend to release lots of cytokines

31
Q

how doew release of cytokines from foam cells lead to atherosclerosis

A

Smooth muscle cell recruitment due to factors from activated platelets, macrophages, and vascular wall cells

32
Q

what does smooth muscle cell recruitment lead to

A

Cell proliferation and ECM(collagen) production to eventually create a fibrous cap and central lipid core

33
Q

when do fatty streaks appear

A

In most children independent of geograph, gender, race, and environment

34
Q

where do fatty streaks appear

A

Both sites prone and not prone to develop aterosclerosis

35
Q

can fatty straks develop in atheromas

A

Yes, some may

36
Q

do fatty streaks elevate themsleves

A

No, so no clinical remifications

37
Q

how can an atherosclerotic plaque change

A 
Calcification 
ulceration
fissure formation
thrombosis
Embolization
hemorrhage into plauqe
medial weakening
38
Q

where do lymphocytes tend to gether in an arthroma

A

Near the shoulder

39
Q

what can an advanced/vulnerable plaque develop into

A

Aneurysm and Rupture
Occlusion by Thrombus
Critical stenosis

40
Q

how can an advance/vulnerable plaque develop into an aneurysm and rupture

A

Mural thrombosis
embolization
wall weakening

41
Q

how can an advanced/vulnerable plaque develop into occlusion by thrombus

A 
Plaque ruptures
Plaue erosed
Plaue hemorrhages
Mural thrombosis
embolization
42
Q

how can an advanced/vulnerable plaque develop into critical stenosis

A

Progressive plaque growth

43
Q

complications of atherosclerosis

A 
Ischemic heart diseaes
Cerebral infarct (stroke)
gangrene
Renal artery stenosis
Aortic aneurysm
44
Q

how common is hypertension

A

very common, with 25% of US adults, soon to grow to 50%

45
Q

what are the guidelines for hypertension

A

Normal: less than 129/79
stage I: 130-139/80-89
stage II: greater than 140/90
crisis: greater than 180/120

46
Q

when do people show symptoms of hypertension

A

at stage II usually

47
Q

what are the guidlines for treatement for dentists with patients with hypertension

A

180/120: emergency room

160-> question

48
Q

how common is essential hypertension

A

90% of all hypertensios

49
Q

what is the contributing factors for essential hypertension

A 
Genetics
Stress
obesity
increased salt intake
Inactivity
cigs
50
Q

hat does untreated hypertension lead to

A

gets higher and shortens life

51
Q

when do symptoms of hypertension appear

A

once organ damage occurs

52
Q

what are some symptoms of hypertension that are not so bad

A

High BP leads to headaches, fatigue, dizziness, palpitations

53
Q

what is compensated hypertension

A

Concentric left ventricular hypertrophy

54
Q

what is decompensated hypertension

A

Left ventricular hypertrophy plus dilation and congestive heart failure

55
Q

what can artherosclerosis from essential hypertension lead to

A

Ischemic heart disease, stroke, and ischemic injury in other organs

56
Q

what does arterioloscerlosis from essential hypertension do to the eyes and kindey

A

retinal injury for visual disturbances

kidney damge or nephrosclerosis

57
Q

how can the kidney lead to essential hypertension

A

Reduced renal sodium excretion leads to increased plasma and increased cardiac output

58
Q

how can the vessels lead to essential hypertension

A

Increased peripheral vascular resistance (increased vascular reactivity

59
Q

what factors can lead to a change in blood volume

A

Sodium
mineralocorticoids
Atrial natriuretic peptide

60
Q

what humoral factors lead to constriction

A 
Angiotensin II
Catecholamines
Thromboxane
Leukotrienes
Endothelin
61
Q

what humoral factors lead to dilation

A

Postaglandins
Kinins
NO

62
Q

what neural factors lead to constriction and dilation

A

Constriction: Alpha adrenergic
Dialtion: beta adrenergic

63
Q

what local factors lead to peripheral resistance

A

Autoregulation
pH
hypozia

64
Q

what is compensated hypertensive heart disease

A

left ventricular concentric hypertrophy provides normal cardiac output

65
Q

what is decompensated hypertensive heart disease

A

hypertrophy no longer adequate to provide normal cardiac outpute deu to decreased myocardiacl contractility
- LV dilation and graduatl onset of congestive Heart failure

66
Q

what is concentric hypertrophy

A

Thickening of the left ventricle wall at the expense of the left ventricular chamber, with little to no increase in outside cardiac dimensions (lumen gets small)

67
Q

what is secondary hypertesion

A

kidney causes hypertesion due to lack of conrol

68
Q

what is dissection hypertension

A

blood blows into the media and pulls away the lining

69
Q

how long does ti take for accelerated (malignant) hypertension to start

A

Relatively rapid onset

- superimposed on previous hypertension

70
Q

what pressures are associated with accelerated malignant hypertesion

A

high systolic and diastolic pressure(200/120_)

71
Q

what complications are associated with Accelterated (malignant) hypertension

A 
Cerebral edema
Papiledema
encephalopathy
renal failure
cerebtral hemorrhage

general path (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions