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Cardio > pathophysiology of vascular disease > Flashcards

pathophysiology of vascular disease Flashcards

1
Q

blood flow to donwstream tissue is inadequate if (2)

A
  1. perfusion pressure too low

2. resistance too high

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2
Q

vasculature fails to meet demands for increased blood flow if

A

resistance to flow can not be sufficiently lowered in order to increase flow

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3
Q

most important adaptive mechanism for PVD

A

collateral pathways

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4
Q

how does the body compensate for reduced blood flow caused by a blocked artery?

A
  1. dilation of arterioles distal to stenosis
  2. collateral artery formation
  3. reduced tissue metabolism
  4. increased oxygen extraction
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5
Q

progressive disease involving the development of arterial wall lesions. As they grow, these lesions may narrow or occlude the arterial lumen. Complex lesions may also become unstable and rupture, leading to acute coronary events, such as unstable angina, myocardial infarction, and stroke.

A

atherosclerosis

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6
Q

Turbulent flow and low shear stress leads to

A

endothelial injury and build-up of atherogenic material on the vessel wall.

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7
Q

High shear stress (I.e. post-stenotic dilatation) causes

A

vessel dilation

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8
Q

PVD becomes clinically apparent when diseased vessels become over _____ stenotic. Tandem lesions will cause greater symptoms.

A

50-70%

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9
Q

tight enough to have an impact on flow at rest or during increased demand

A

significant PVD

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10
Q

effort induced pain caused by accumulation of

A
  1. anaerobic metabolites

2. lactic acid and adenosine monophosphate

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11
Q

calf claudication, ischemic foot ulceration/gangrene

A

tibial atherosclerosis

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12
Q

calf claudication

A

supertifical femoral atherosclerosis

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13
Q

muscle ache, buttock/leg claudication, impotence

A

aortoiliac atherosclerosis

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14
Q

loss of neurological function, transient ischemic event, amaurosis fugax, stroke

A

carotid atherosclerosis

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15
Q

chest pain/discomfort, myocardial infarction, acute coronary syndrome, chronic stable angina

A

coronary atherosclerosis

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16
Q

do not alter resistance to blood flow and have no impact on flow

A

non-obstructive blockages

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17
Q

Blockages that do not restrict blood flow at rest but prevent flow increases needed meet increased demands (e.g. exertional angina)
Very tight blockages restrict flow at rest and at stress (e.g. rest pain)

A

obstructive blockages

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18
Q

Claudicants can have a wide range of ABI. Less than ______ is considered severe PVD.

A

0.4

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19
Q

Doppler systolic occlusion pressure at ankle versus arm measures pressure gradient between the two vascular beds at rest and with exercise (exercise increases flow (F))

A

ankle brachial index

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20
Q

increasing myocardial oxygen demand leads to (2)

A
  1. coronary vasodilation- decrease in resistance

2. increases coronary blood flow- increase in flow

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21
Q

cardiac stress test is done to

A

stress the coronary vascular bed

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22
Q

If the resistance cannot be sufficiently lowered to meet the requirements for coronary flow the heart becomes _____

A

ischemic

23
Q

ection of radio-opaque contrast dye to create an image of the arterial lumen
Allows more direct measurement of blockage
Give limited information about how sufficient are the collaterals

A

contrast angiography

GOLD STANDARD

24
Q

is useful for post operative follow up of bypass grafts and carotid endarterectom

-used to measure lumen area and the velocity of blood traveling across a stenosis which is proportional to the severity of the obstruction and the driving pressure.

A

Ultrasound

25
Q

Wall tension (T) is proportional to

A

radius (R) and pressure (P or blood pressure).

26
Q

Aneurysms form with ____________ particularly when the vascular radius is large (e.g. aorta) and the wall thickness is low.

A

increasing pressure (e.g. hypertension)

27
Q

Wall tension is reduced by ______

A

increased blood vessel wall thickness.

28
Q

Laplace’s law on risk of anuerysm

A

Risk of aneurysm rupture increases with size due to Laplace’s law

29
Q

Defined as 50% or greater increase in diameter of vessel

A

arterial aneurysm

30
Q

Ascending thoracic aortic aneurysm risk factors (4)

A

Hypertension
Marfan
Ehlors-Danlos
Bicuspid aortic valve associated aneurysm

31
Q

Descending thoracic aortic aneurysm risk factors

2

A

Atherosclerosis

Hypertension

32
Q

Abdominal aortic aneurysm

3

A

Infrarenal: 95%
Atherosclerosis
Hypertension

33
Q

best imaging test for pre-operative planning. The thrombus seen adherent to the vessel wall in the aneurysmal aorta is common, and has no clinical significance.

A

CT

34
Q

Spontaneous disruption of intima
“False channel” created within wall of aorta
Propagation of tear distally
May occlude branch vessels (viscera, extremities)
May lead to vascular rupture
Aorta, carotid arteries and coronary arteries are often sites

A

arterial dissection

35
Q 
Lipid infiltration and into vascular wall
Macrophage activation
Lipid oxidation
Cellular proliferation
Calcification, atheroma formation
Responsive to LDL-C lowering
A

atherosclerosis

36
Q 
Plaque rupture
Mural thrombus
Arterial disease often platelet-dependent thrombus formation
Responsive to anti-platelet therapy
Aspirin
P2Y12 blockers
A

thrombosis

37
Q

ASCVD Pathogenesis: 1-2 Punch

A
  1. abnormal lipid metabolism

2. systemic inflammation

38
Q 
Atherogenic lipoproteins
LDL
VLDL/IDL
Cholesterol
Triglycerides
A

abn. lipid metabolism

39
Q 
Diabetes
Obesity
Tobacco
Hypertension
Age
A

systemic inflammation

40
Q

Abnormal lipids (Dyslipidemia)
Elevated low density lipoprotein cholesterol (LDL-C)
Decreased high density lipoprotein cholesterol (HDL-C)
Elevated triglycerides, particularly with low HDL-C
Diabetes mellitus
Hypertension
Smoking tobacco products

Family history of premature coronary artery disease (CAD)
First degree male relatives < 55 years or females < 65 years.
Obesity and lack of exercise particularly in relation to Diabetes
Male sex
Advanced age
Others: Lipoprotein a (Lp(a))

A

risk factors for atherosclerotic CAD

41
Q

Women develop ASCVD approximately 10 years after men following ______

A

menopause

42
Q

Aspirin may be less effective at preventing ASCVD in women

A

true

43
Q

The onset of ASCVD following menopause may be caused by the ______

A

loss of estrogen

  • no benefits in replacement trials
44
Q

monogenetic lipid disorders

A
  1. familial hyercholesterolemia

2. familial combined hyperlipidemia- Elevated triglycerides and LDL-C

45
Q

_____ are remnant particles that started as VLDL and IDL and transport cholesterol and some triglycerides to tissues (forward cholesterol transport

A

Low Density Lipoproteins (LDL)

46
Q

_______ transport cholesterol back to liver for disposal in bile (reverse cholesterol transport)

A

High Density Lipoproteins (HDL)

47
Q

Derived from VLDL->IDL
Rich in esterified and non-esterified cholesterol
Protein: Apo B-100
Hydrophobic Core
Bind LDL-Receptor as well as scavenger receptors
Toxin to endothelium that incite blood vessel wall inflammation
“Bad Cholesterol”

A

LDL

48
Q

Synthesized empty
Protein: Apo-A-I and –A-II
HDL particles pick-up cholesterol from tissues
Reverse cholesterol transport
CETP exchanges cholesterol between different lipoproteins
“Good cholesterol”

A

HDL

49
Q

Genetic studies support a strong causal relationship between LDL-C levels ASCVD

A

yep

50
Q

HMG-CoA Reductase Inhibitors

A

Statins:

51
Q

High Intensity Statin used for

A

Secondary Prevention of ASCVD

52
Q

Moderate Intensity Statin used for

A

Primary Prevention of ASCVD

53
Q

aspirin

A

platelet inhibition

Cardio (26 decks)

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