Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

cardiovascular system > vascular endothelium 1 > Flashcards

vascular endothelium 1 Flashcards

(58 cards)

Start Studying
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

Study These Flashcards
A

reduces the effect

25
what is PGH2
prostaglandin precurser `
26
explain how NO acts as a vasodilator
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
how does shear stress affect vasodilation in brachial artery
``` 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
effect of the endothelium:SM ratio on the effect of NO
when large there is a large effect
29
effect of exogenous NO in the blood on SM
it diffuses across the endothelium and causes vasodilation
30
effect of prostacyclin
``` 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
effect of Thromboxin A2 on SM
``` 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
effect of TXA2 on platelets
``` bind to TPalpha on platelets platelet becomes active makes more TXA2 positive feedback enhances the response platelets aggregate integration with the clotting cascade ```
33
where is TXA2 more active SM, or plateleyt
platelet
34
production of angiotensin 2
angiotensinogen - precursor cleaved by renin - make angiotensin 1 ACE act on ang 1 to make ang 2
35
where is ACE expressed
endothelial cells, lungs and kidneys
36
effects of ANG2
``` 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
describe the mechanism of action for ANG2
``` ang 2 diffuse across the endothelium bind to AT1 receptor on SM PLC PIP2 - IP3 Ca influx upregulate MLCK contraction ```
38
alternative action of ACE
metabolise Bradykinin which casues vasodilation
39
what is the balance between ANG 2 and bradykinin
if ACE high net vasoconstriction by ANG2 little bradykinin effect
40
endothelin - 1 mechanism of action on SM cell
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
endothelin - 1 mechanism of action on endothelial cell
``` ET-1 bind to ETb receptor upregulate eNOS increased NO production diffuse into VSMC cell relaxes vessel dilates ```
42
what is the main effect of ET-1
vasoconstriction
43
what can change the affect of endothelin
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
what is the effect of ACE inhibitors and ANG blockers
block processes downstream | early phase treatment for hypotension
45
describe the ratio between extracellular and intracellular Ca
extracellular 2mmol L-1 intracellular 100nmol L-1 up to 20000x difference
46
effect of aspirin on COX 1
COX 1 is expressed all of the time | aspirin acetylation inactivates the enzyme
47
effect of aspirin on COX 2
COOX 2 is upregulated at times of physiological insult | aspirin acetylation switches its function - to generating protective lipids
48
general effect of aspirin on COX enzymes
causes irreversible inhibition other non-specific NSAIDs cause reversible inhibition COX- 2 specific inhibitors cause reversible inhibition of COX 2 only
49
effect of aspirin on prostacyclin
no effect - nucleus makes more enzyme
50
effect of aspirin on thromboxane
proportion of thromboxane decreases | greater effect in platelets - they cant make more COX enzymes (other way in prostacyclin)
51
describe drug drug interactions
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
what is the BNF
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
what system do the vasoconstrictors rely on
PLC | regulates Ca metabolism
54
what do calcium blockers do
prevent Ca entering VSMCs
55
mechanism of drug to treat hypertension
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
issue with inhibiting cholinesterase enzymes
too complicated | ACh many other effects
57
issue with inhibiting the phosphodiesterase enzyme - reduces breakdown on NO
undesired side effects | resold as Viagra
58
issue with a medication that involves a NO functional group
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.
© 2025 Bold Learning Solutions. Terms and Conditions