Brainscape's Knowledge GenomeTM

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


See full index

LSS Cadiovascular System > circulation > Flashcards

circulation Flashcards

vascular endothelium: recall the structure and function of the vascular endothelium, and recall its role in inflammation

1
Q

define vascular endothelium

A

single cell layer of cells (tunica intima) that acts as the blood-vessel interface on top of a basement membrane

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

5 key physiological functions of vascular endothelium

A

vascular tone, thrombostasis, absorption and secretion, barrier, growth (and angiogenesis)

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

key physiological functions of vascular endothelium: vascular tone

A

secretes and metabolises vasoactive substances

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

key physiological functions of vascular endothelium: thrombostasis

A

prevents clots forming or molecules adhering to vessel wall

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

key physiological functions of vascular endothelium: absorption and secretion

A

allows active/passive transport via diffusion/channels (regulates flux of fluids and molecules from blood to tissues)

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

key physiological functions of vascular endothelium: barrier

A

prevents atheroma development and impedes pathogens

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

key physiological functions of vascular endothelium: growth

A

mediates cell proliferation

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

what are prostaglandins

A

group of compounds that affect vascular tone

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

what is the first stage of prostahlandin synthesis

A

phospholipase A2 catalyses conversion of membrane phospholipids to arachidonic acid

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

what is the second stage of prostaglandin synthesis

A

COX-1 and COX-2 convert arachidonic acid to PGH2 precursor

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

what three compounds can be synthesised from PGH2

A

thromboxane A2 (pro-platelet vasoconstrictor); prostacyclin (anti-platelet vasodilator); prostaglandins associated with inflammation, pain and fever

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

2 vasodilator molecules

A

nitric oxide, prostacyclin

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

key features of vasodilator molecules

A

use -yl second messenger in vascular smooth muscle cells and xTP/cXMP to cause vascular smooth muscle cell relaxation and platelet inhibition

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

exogenous source of nitric oxide

A

diffuse from blood to vascular smooth muscle cells

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

endogenous source of nitric oxide

A

produced in response to Ach/bradykinin binding and shear stress (upregulates eNOS)

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

nitric oxide: production after ACh stimulation

A

ACh binds to GPCR → PLC migrates along membrane → converts PIP2 to IP3 → IP3 triggers Ca2+ influx from ER → upregulate eNOS → nitric oxide produced

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

nitrix oxide: pathway and effect on vascular smooth muscle cells

A

diffuses into vascular smooth muscle cell → activates guanylate cyclase → upregulates protein kinase G → activates K+ channels, causing hyperpolarisaton, relaxation of cells and vessel dilation

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

2 sources of prostacyclin

A

phospholipids (converted to arachidonic acid), PIP2 (phospholipase C converted to IP3 and diacyl glycerol, which is converted by DAG to arachidonic acid)

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

prostacyclin synthesis

A

COX-1 or COX-2 convert arachidonic acid to PGH2, which is converted to PGI2 (prostacyclin)

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

prostacyclin: pathway and effect on vascular smooth muscle cells

A

PGI2 diffuses into vascular smooth muscle cell → binds to membrane IP receptors → upregulates adenyl cyclase→ cAMP inhibits MLCK → reduced cross bridge cycling, causing relaxation of cells and vessel dilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

3 vasoconstrictor molecules

A

thromboxane A2, angiotensin II, endothelin I

22
Q

what does thromboxane A2 do

A

vasoconstrictor that activates platelets

23
Q

2 sources of thromboxane A2

A

phospholipids (converted to arachidonic acid), PIP2 (phospholipase C converted to IP3 and diacyl glycerol, which is converted by DAG to arachidonic acid)

24
Q

thromboxane A2 synthesis

A

COX-1 or COX-2 convert arachidonic acid to PGH2, which is converted to TXA2

25
Q

thromboxane A2: pathway and effect on vascular smooth muscle cells

A

TXA2 binds to TPB receptor on vascular smooth muscle cell → phospholipase C migrates along membrane → converts PIP2 to IP3 and DAG → IP3 causes Ca2+ to diffuse in → upregulates MLCK → VSMC contracts and the vessel constricts

26
Q

thromboxane A2: pathway and effect on platelets

A

TXA2 binds to TPa receptor on platelets → activates and releases more TXA2 (positive feedback) → increased ability to aggregate and stick to endothelium

27
Q

what is angiotensin II produced by

A

renin-angiotensin-aldosterone system

28
Q

basic angiotensin II synthesis

A

angiotensinogen (liver) → angiotensin I (bloodstream by renin) → angiotensin II (lungs by ACE)

29
Q

what else does ACE do

A

metabolises bradykinin to reduce nitric oxide synthesis

30
Q

5 angiotensin II mechansisms

A

increase ADH secretion (more vasoconstriction and water retention), increase aldosterone secretion (more Na+ absorbed so more water retention), increase kidney Na+ reabsorption, upregulates sympathetic system excitation to cause vasoconstriction and increase heart rate, arteriolar vasoconstriction

31
Q

angiotensin II: endothelial pathway and effect on vascular smooth muscle cells

A

binds to AT1 receptor → PLC migrates along membrane → converts PIP2 to IP3 → IP3 triggers Ca2+ influx from ER → Ca2+ upregulates MLCK → vascular smooth muscle cells contract

32
Q

what does endothelin I stimulate

A

majorl stimulation of vasoconstriction, minor stimulation of vasodilation

33
Q

agonist sources of endothelin I

A

adrenaline, angiotensin II, ADH

34
Q

antagonist sources of endothelin I

A

nitric oxide, heparin, prostacyclin

35
Q

endothelin-1: production after ACh stimulation

A

big endothelin 1 produced in endothelial cell nucleus → converted to ET-1 in presence of endothelin converting enzyme

36
Q

endothelin-1: pathway and effect on vascular smooth muscle cells in presence of agonists

A

ET-1 binds to ETA and ETB receptors on vascular smooth muscle cells → activates PLC → PIP2 converted to IP3 → Ca2+ influx → cell contracts and vessel constricts

37
Q

endothelin-1: pathway and effect on endothelial cells and subsequently vascular smooth muscle cells in presence of antagonists

A

ET-1 binds to ETB receptor on endothelial cells → upregulates eNOS → increased nitric oxide production → nitric oxide diffuses into vascular smooth muscle cells → cell relaxes and vessel dilates

38
Q

blood vessel structure from lumen to exterior

A

lumen → tunica intima (endothelium) → internal elastic tissue → tunica media (smooth muscle) → external elastic tissue → tunica adventitia (fibrous connective tissue)

39
Q

role of lumen

A

hollow area through which blood flows

40
Q

roles of tunica intima (endothelium)

A

one cell thick, allows for exchange and homeostasis, production of: adhesion molecules, matrix molecules, anti-thrombotic or procoagulant factors, vasodilating or vasoconstricting factors, growth factors

41
Q

features of resting endothelium

A

inactivated and anti-inflammatory, anti-thrombotic and anti-proliferative

42
Q

features of activated endothelium

A

pro-inflammatory, pro-thrombotic and pro-proliferative

43
Q

activating factors of endothelium

A

viruses, smoking, thrombosis, mechanical stress, hypertension, hyperglycaemia, inflammation (chronic activation leads to pro-inflammatory and pro-thrombotic effects)

44
Q

activated endothelium processes

A

thrombosis, senescence, increased permeability, increased leukocyte recruitment

45
Q

describe senescence

A

damaged or aging cells undergo growth arrest to halt proliferation in response to stress or damage

46
Q

advantage of senescence

A

stops damaged cells replicating

47
Q

disadvantages of senescence

A

pro-inflammatory, contributes to cardiovascular disease

48
Q

effect of increased permeability

A

allows plasma protein leakage, and for lipoproteins to pass over and bind to proteoglycans

49
Q

fate of lipoproteins bound to proteoglycans

A

oxidised before macrophages engulf them to form foam cells

50
Q

how is there increased leukocyte recruitment

A

bind strongly using integrin, not selectin, and transmigrate to tissues in post-capillary venules

51
Q

increased leukocyte recruitment in large arteries

A

leukocytes adhere strongly using integrin to endothelium, transmigrate, and become stuck in the subendothelial space

52
Q

formation of endothelial tight junctions

A

monolayer that stop proliferating when they touch (contact inhibition), forming tight junctions

LSS Cadiovascular System (40 decks)

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