Brainscape's Knowledge GenomeTM

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


See full index

Cardiology > Vascular Biology > Flashcards

Vascular Biology Flashcards

1
Q

As arteries get smaller the velocity increases/decreases.

A

decreases –> cross sectional area –> promotes nutrient exchange

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

The amount of work that must be done to overcome friction between adjacent layers of fluid sliding over each other

A

shear force

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

Dilation of blood vessel after a period of ischemia is called:

A

hyperemia

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

Arteries that carry blood from the aorta to branch arteries

A

conduit arteries

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

Arterioles vasoconstrict/vasodilate in response to ischemia

A

vasodilate

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

Do large conduit arteries vasodilate to ischemia?

A

yes: 12-15%

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

4 molecules that promote vasodilation

A

NO/EDRF, prostacyclin (PGI2), bradykinin, acetylcholine

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

How does NO lead to vasodilation?

A

L-arginine is involved in production of eNOS (endothelial NO synthase) –> NO diffuses into smooth muscle cell –> activation of cGMP

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

How does Ach, substance P, bradykinin, B2 agonists lead to vasodilation?

A

G protein calmodulin pathway –> production of eNOS –> NO diffusion to smooth muscle cell –> cGMP

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

2 effects of ACh on blood vessels

A
  1. stimulates release of NO from endothelium leading to vasodilation
  2. vasoconstriction/contraction in circumstances with low NO (e.g. damaged endothelium) or with high doses of ACh (even low levels of ACh can cause constriction in diseased arteries)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

High ACh + low NO causes vasoconstriction/dilation

A

vasoconstriction

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

Which is more potent? NO or PGI2

A

NO

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

Angiotensin is a vasoconstrictor/dilator

A

constrictor –> breaks down bradykinin thereby preventing vasodilation by reducing production of NO and and PGI2

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

A high fat diet impairs endothelial mediated vasodilation/vasoconstriction for up to four hours after eating.

A

vasodilation

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

What is the difference between an angioblast and an endothelial progenitor cell?

A

angioblast is in utero and epc is what is modified during adulthood to create new vessels –> all under control of VEGF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What factors stabilize growing blood vessels?

A

angiopoetin 1 and ephrin b2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are 3 important growth factors for vessels?

A

pdgf, tgf beta, fgf

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

What growth factor can destabilize growing vessels leading to possible tumorigenesis?

A

angiopoetin 2

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

EPCs from patients with type II diabetes mellitus are characterized by:

A

decreased proliferation capacity and reduction of their adhesiveness and ability to form capillary tubes in vitro

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

What autosomal dominant condition can result from disruption of TGF beta signalling via abnormalities in one of two genes, endoglin (Eng) and activin-receptor-like kinase-1
(ALK1)?

A

HHT/Osler-Weber-Rendu

21
Q

4 consequences of HHT

A
  1. GI bleeding
  2. infection from septic emboli
  3. arteriovenous malformation in lungs causing shunting of blood and paradoxical emboli
  4. telangiectases
22
Q

3 classifications of anti-clot systems

A
  1. fibrinolytic - t-PA
  2. antithrombin - thrombomodulin, heparin
  3. antiplatelet - NO, prostacyclin, ADPases
23
Q

2 classifications of pro-clot systems

A
  1. anti-fibrinolytic - PAI1

2. angiotensin II stimulation of PAI1 (plasminogen activator inhibitor)

24
Q

_____ cleaves fibrin to produce progressively smaller degradation products

A

Plasmin

25
Q

Virchow’s triad

A

hypercoagulable state, endothelial injury, circulatory stasis –> clotting/DVT

26
Q

2 procoagulable properties of dysfunctional endothelium leading

A
  1. increase vwf production with increased platelet adhesion/aggregation
  2. increased synthesis of PAI1 resulting in impaired fibrinolysis
27
Q

All cell adhesion molecules are constitutively expressed on endothelium except:

A

ICAM II

28
Q

Migration of neutrophils, monocytes and
lymphocytes from the circulating blood to the inflammatory sites is directed by the expression of specific _____ on the
endothelium

A

cell adhesion molecules

29
Q

______ is a transcription factor involved in the expression of genes encoding many proinflammatory functions of
vascular wall cells and infiltrating leukocytes.

A

NFkB

30
Q

_________ acts as a proinflammatory factor by stimulating NFkB leading to expression of
_____, which mediates monocyte adhesion and of the chemokine _____, which attracts monocytes

A

Angiotensin-II, VCAM-1, MCP-1

31
Q

Angiotensin-II stimulates expression of

______, which provokes the acute-phase response leading to production of the systemic inflammatory marker _________..

A

interleukin (IL)-6, C-reactive protein

CRP

32
Q

Studies in hypercholesterolemic rabbits have

shown that ____ localizes in endothelium over foam cell–filled fatty streaks in the aorta.

A

VCAM

33
Q

T/F Endothelial leukocyte adhesion molecules play an important role in early plaque development

A

T

34
Q

____ stimulates production of endothelial

leukocyte adhesion molecules early in atherosclerotic lesion formation

A

OxLDL aka oxidative fat

35
Q

Spiral secondary flows and recirculation zones with lower shear stress result in round/elongated endothelial cells

A

round

36
Q

Do blood vessels have cholinergic innervation?

A

no –> only muscarinic receptors

37
Q

What stimulates NOS to produce NO from L-arginine?

A

shear stress, chemical mediateors like ACh

38
Q

Name a competitive inhibitor of L-arginine that indirectly inhibits NO production

A

ADMA

39
Q

What stimulates PGI2 release from endothelium?

A

shear stress, physiologic agonists, pathologic insult –> inhibits platelet activation, secretion, aggregation and maintains relaxation

40
Q

Vasoconstrictor or vasodilator? TxA2

A

constrictor

41
Q

Vasoconstrictor or vasodilator? PGI2

A

dilator

42
Q

Vasoconstrictor or vasodilator? NO

A

dilator

43
Q

Vasoconstrictor or vasodilator? endothelin

A

constrictor

44
Q

Vasoconstrictor or vasodilator? ACh

A

constrictor

45
Q

Vasoconstrictor or vasodilator? Angiotensin II

A

constrictor

46
Q

Vasoconstrictor or vasodilator? bradykinin

A

dilator

47
Q

Vasoconstrictor or vasodilator? substance P

A

dilator

48
Q

Vasoconstrictor or vasodilator? superoxide anion O2-

A

constrictor

49
Q

What happens to the number of EPCs in patients with risk factors for ischemic cardiovascular disease?

A

reduce number of endothelial preogenitors

Cardiology (41 decks)

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