Brainscape's Knowledge GenomeTM

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


See full index

cardiovascular system > vascular endothelium 1 > Flashcards

vascular endothelium 1 Flashcards

1
Q

what are the anatomical and physiological aspects of the heart

A

muscular pump

generate flow

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

what are the anatomical and physiological aspects of the arteries

A

thick muscular walls

stabalise pulsatile flow

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

what are the anatomical and physiological aspects of the capillaries

A

very thin walls

fascilitate gas and solute exchange

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

what are the anatomical and physiological aspects of the veins

A

one way valves

maintain unidirectional flow

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

which way does the anatomy physiology relationship go

A

both directions
anatomy always determines function
in angiogenesis the function determines the anatomy

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

what is the vascular endothelium

A

single layer of cells that acts as a blood-vessel interphase

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

5 functions of the endothelium

A 
vascular tone 
thrombostasis and haemostasis 
absorbtion and secretion 
barrier 
growth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

describe vascular tone

A

secrete and metabolise vasoconstrictive substances - cause constriction and vasodilation

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

describe thrombostasis and haemostasis

A

mechanism to stop flow of blood - but ensure that clots don’t form unnecessarily

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

describe absorption and secretion

A

active or passive transport
diffusion or channels
nutrients, co2 and o2

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

describe action as a barrier

A

selective control of what enters and leaves

prevents atheromas and impedes pathogens

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

describe the growing action

A

mediate cell proliferation
if bv blocked so an area is not being perfused by blood
another bv grow in order to perfuse the other vessel with blood

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

what does regulation of hypertension depend on

A

downstream delivery and local forces

want ot be normotensive and adequately pressured

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

describe the normal relationship between vasodilation and vasoconstriction forces

A

they normally work in tandem

one way might pull slightly more than the other if needed

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

describe the hypertensive relationship between vasodilation and vasoconstriction forces

A

vasoconstriction more powerful than it should be

drugs can be used to balance both sides

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

describe laser doppler flowmetry

A

it measures the ACh response via endothelium to change the size of bv
the blue line is perfusion and is measured in arbituary units
in intact endothelium when ACh is supplied, after the 7th dose the perfusion plateaus
when no endothelium there is no response
when there is an exogenous NO donor (sodium nitropusside) a response is generated

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

describe flow mediated dilation

A

stimulate forearm ischemia - cuff at 300mmHg
want to increase sixe on bv - so that cells can get o2
dilate vessels and reduce resistance
the purple line on the ultrasound shows the blood vessel diameter

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

what is the colour of the hand caused by

A

Hb

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

describe the formation of prostacyclin and thromboxane

A

from phospholipids
phospholipase A2 makes Arachidonic acid
COX 1 and 2 make PGH2
[thromboxane synthase make thromboxane]
[prostacyclin synthase make prostacyclin]
also make PGD2, PGE2, PGF2 (prostaglandins for pain, fever and inflammation)

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

action of arachidonic acid

A

precursor for lots of things
lipoxygenase
leukotrienes
PGH2

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

PGD2, PGE2, PGF2 action

A

pain
fever
inflammation

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

prostacyclin action

A

vasodilator
anti-atherogenic
anti-platelet

these are useful characteristics

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

thromboxane A2 action

A

vasoconstrictor
proatherogenic
proplatelet

in time of haemostatic crisis - form plug for bleed

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

aspirin affect on COX 1 and 2

A

reduces the effect

25
Q

what is PGH2

A

prostaglandin precurser `

26
Q

explain how NO acts as a vasodilator

A

ACh binds to the GPCR on the endothelium membrane
this interacts with the membrane bound enzyme Phospholipase C
PLC converts PIP2 to IP3
IP3 triggers Ca influx from the ER
Ca upregulates eNOS - cytoplasmic enzyme
eNOS convert L-arg and O2 to NO and L cit
NO diffuse into vascular SM cell
activates GC (Guanylyl cyclase) which converts GTC to cGMP (cGMP can be broken down by to GMP by phosphodiesterase to reduce NO)
this upregulates PKG
activate K channels
membrane hyperpolarises
cell relaxes
vessel dilates

27
Q

how does shear stress affect vasodilation in brachial artery

A 
when there is low pressure in forearm - blood flows to forearm 
increase flow rate 
greater pressure
dilate 
also influences how much NO is produced
28
Q

effect of the endothelium:SM ratio on the effect of NO

A

when large there is a large effect

29
Q

effect of exogenous NO in the blood on SM

A

it diffuses across the endothelium and causes vasodilation

30
Q

effect of prostacyclin

A 
produced via COX 1 
diffuses into SM 
binds to IP receptor 
upregulation of andenylyl cyclase 
convert ATP to cAMP
inhibits MLCK (myosin light chain kinase) 
reduced cross bridge cycling 
cell relaxes 
vessel dilates 
[stops clots too]
31
Q

effect of Thromboxin A2 on SM

A 
thromboxane diffuses through apical and basement membrane 
binds to TPbeta on VSMC 
PLC migrate along the membrane 
PIP2 - IP3 
Ca release form SER and extracellular space 
upregulate MLCK
VSMC contracts 
vasoconstriction
32
Q

effect of TXA2 on platelets

A 
bind to TPalpha on platelets 
platelet becomes active 
makes more TXA2
positive feedback enhances the response 
platelets aggregate 
integration with the clotting cascade
33
Q

where is TXA2 more active SM, or plateleyt

A

platelet

34
Q

production of angiotensin 2

A

angiotensinogen - precursor
cleaved by renin - make angiotensin 1
ACE act on ang 1 to make ang 2

35
Q

where is ACE expressed

A

endothelial cells, lungs and kidneys

36
Q

effects of ANG2

A 
interact with the ADH secretion, aldosterone secretion, tubular sodium reabsorption - increase water retention 
arteriolar vasoconstriction (direct effect on bv - sm response), sympathoexcitation ( excite CNS - increase HR, pressure and constriction) - increased vascular resistance

both effects increase BP

37
Q

describe the mechanism of action for ANG2

A 
ang 2 diffuse across the endothelium 
bind to AT1 receptor on SM 
PLC 
PIP2 - IP3
Ca influx 
upregulate MLCK 
contraction
38
Q

alternative action of ACE

A

metabolise Bradykinin which casues vasodilation

39
Q

what is the balance between ANG 2 and bradykinin

A

if ACE high
net vasoconstriction by ANG2
little bradykinin effect

40
Q

endothelin - 1 mechanism of action on SM cell

A

endothelial cell nucleus produces Big endothelin 1
endothelin converting enzyme converts zymogen to ET- 1 on membrane
ET-1 bind to ET alpha and beta receptors on VSMC
PLC
PIP2-IP3
Ca influx
cell contracts
vessel constricts

41
Q

endothelin - 1 mechanism of action on endothelial cell

A 
ET-1 bind to ETb receptor 
upregulate eNOS 
increased NO production
diffuse into VSMC 
cell relaxes 
vessel dilates
42
Q

what is the main effect of ET-1

A

vasoconstriction

43
Q

what can change the affect of endothelin

A

molecule that intercommunicate and can interact and be sensed by the nucleus or membrane
Antagonists: PGI2, NO, ANP, heparin, HGF, EGF
Agonists: adrenaline, ADH, Ang II, IL-1

44
Q

what is the effect of ACE inhibitors and ANG blockers

A

block processes downstream

early phase treatment for hypotension

45
Q

describe the ratio between extracellular and intracellular Ca

A

extracellular 2mmol L-1
intracellular 100nmol L-1

up to 20000x difference

46
Q

effect of aspirin on COX 1

A

COX 1 is expressed all of the time

aspirin acetylation inactivates the enzyme

47
Q

effect of aspirin on COX 2

A

COOX 2 is upregulated at times of physiological insult

aspirin acetylation switches its function - to generating protective lipids

48
Q

general effect of aspirin on COX enzymes

A

causes irreversible inhibition
other non-specific NSAIDs cause reversible inhibition
COX- 2 specific inhibitors cause reversible inhibition of COX 2 only

49
Q

effect of aspirin on prostacyclin

A

no effect - nucleus makes more enzyme

50
Q

effect of aspirin on thromboxane

A

proportion of thromboxane decreases

greater effect in platelets - they cant make more COX enzymes (other way in prostacyclin)

51
Q

describe drug drug interactions

A

when keep adding drugs it makes biochemistry and lifestyle very complicated
the body can use the same chemicals for different processes
interaction between systems in the body
drugs not tissue specific
receptor expression and distribution varies between tissues
2 people taking same medication can have very different outcomes

52
Q

what is the BNF

A

catalogue of all dugs in the UK
biggest part of it is side effects
the number of people needed to show it is a side effect varies

53
Q

what system do the vasoconstrictors rely on

A

PLC

regulates Ca metabolism

54
Q

what do calcium blockers do

A

prevent Ca entering VSMCs

55
Q

mechanism of drug to treat hypertension

A

block flow of Ca into cells
impede cross bridge cycling which is ca dependant
this is endothelium dependant
the effect is on the vasculature, not the heart so it is a good drug

56
Q

issue with inhibiting cholinesterase enzymes

A

too complicated

ACh many other effects

57
Q

issue with inhibiting the phosphodiesterase enzyme - reduces breakdown on NO

A

undesired side effects

resold as Viagra

58
Q

issue with a medication that involves a NO functional group

A

too short acting to be useful - have to take it every 15minutes
it is used to treat angina though

cardiovascular system (22 decks)

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