Brainscape's Knowledge GenomeTM

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


See full index

Cardiovascular: pharmacology > Drugs affecting the vasculature and blood pressure > Flashcards

Drugs affecting the vasculature and blood pressure Flashcards

1
Q

what is the role of endothelial cells?

A

provide a diffusion barrier but also inhibits platelet activation

more importantly - it can control the relaxation and contraction of smooth muscle cells

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

how do smooth muscle cells contract? the mechanisms is essentially the same as airway smooth muscle. Step 1-

A

calcium enters

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

how does calcium enter the SMC?

A

L-type channels or GPCR q11

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

what does calcium bind to once in the SMcell?

A

calmodulin

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

what does the Ca/calmodulin do?

A

converts MLCK into active MLCK

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

what does active MLCK do?

A

phosphorylates MLC causing contraction

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

which molecules is responsible for relaxation in SMC?

A

cGMP

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

what does cGMP do?

A

coverts MLC phosphatase into active form

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

what does active MLC phosphatase do?

A

dephosphorylaes MLC causing relaxation

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

which substances act on the endothelium to cause vasodilatation?

A

bradykinin
ADP
5HT

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

what do vasodilators on endotheliam dio?

A

allow GPCR to let in Ca into the cell ?

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

what does Ca in endothelial cells do?

A

binds to calmodulin

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

what does the Ca calmodulin complex do in endothlelial cells ?

A

activates nitric oxide synthase

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

what does nitric oxide synthase do?

A

converts L-arginine and oxygen to NO and citrulline

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

what does the NO producedby the endothelial cells then do?

A

diffuses into the SMC neighbouring it

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

what does NO in SMC do?

A

activates guanylate cyclase which converts GTP to cGMP

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

what does cGMP do?

A

causes relaxation through mechanism previously

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

what else can cGMP do?

A

activate protein kinase G activates Ca dependent K channels - causing K to leave and thus hyperpolarisation

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

what do organic nitrates do?

A

when metabolised they relesase NO into SMC and cause relaxation as above

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

in small doses what do organic nitrates do?

A

cause venorelaxation - decreases SV

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

what does small doses of organic nitrates do to the HR?

A

increase it so CO is maintained the same

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

what do organic nitrates do in larger doses?

A

cause arteriolar dilatation

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

what does arteriola dilatation cause?

A

decreases the arterial pressure so reduces afterload

- also decreases pulse wave reflection

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

why are organic nitrates useful in angina?

A

they cause decreased myocardial oxygen requirement via

1) decreased preload
2) decreased afterload
3) improved perfusion of the ischaemic zone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

how do Organic nitrates cause improved perfusion to ischaemic zones?

A

they cause dilatation of collateral vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what are organic nitrates used in?

A

angina and acute coronary syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is the danger in unstable angina?

A

danger that a cap of atheromatous plaque is going to form a thrombus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what are the two examples of ONs?

A

GTN and Isosorbide mononitrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is GTn most effective in?

A

prevention rather than relief

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is the acting time?

A

short acting 30 mins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is indicated if someone has a pain than goes away wtih GTN?

A

thye have angine and it is not an MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what is ISM acting time and what is it used for?

A

prophylaxis of angina and acting is 4 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what are the side effects and problems of GTN and ISM?

A
  • people can build up a tolerance
  • postural hypotension
  • headaches
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

how do the endothelium cause contraction in SMC?

A

they release endothelin which acts on ETa receptors in SMC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what kind of receptor is ETa?

A

GPCR- q11

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what does the activation of this receptor cause ?

A

increase in Ca levels and thus contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

how is the production of endothelin controlled?

A

either vasoconstrictor or dilators can influence the promotor region of the gene pre-proendothelin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what are some examples of vasoconstrictors?

A

adrenaline
angiotensin II
ADH (vasopressin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what are some examples of vasodilators?

A

nitric oxide
natriuretic peptide (ABC)
shear stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what does the RAAS system do?

A

increases bp and water retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

where is renin released from

A

granular cells in the kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what causes renin to be released?

A

there is a decrease in the renal blood supply

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

which cells sense this decrease in renal blood supply?

A

manca cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what could cause a decreased renal blood supply?

A

fall in renal BP or when there is a haemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what does renin do one in the circulation?

A

causes the conversion of angiotensinogen to angiotensin 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what happens to angiotensin 1?

A

it is converted to angiotensin 2 by ACE

47
Q

WHERE IS ACE LOCATED?

A

in the lungs

48
Q

what does AG2 do?

A

activates the AT1 receptor which is a GPCR leading to

1) contraction of smooth muscle in vasuclature
2) cell growth in the heart and arteries
3) aldosterone secretion from the adrenal cortex

49
Q

how is there contraction of vascular smooth muslce?

A

1) through activation of smooth muscle AT1 receptors

2) through increased release of noradrenaline from sympathetic nerves

50
Q

what does the aldosterone secretion causE>

A

tubular reabsorption of Na and salt retention

51
Q

overall what does the RAAS system do?

A

increases MABP and BLood volume

52
Q

what is the role of ACE? it has 2 roles

A

1- Converts inactive angiotensin I to angiotensin II (vasoconstrictor)
2- Inactivates bradykinin (vasodilator)

53
Q

give an example of an ace inhibitor?

A

lisinopril

54
Q

what do ARBs do?

A

they are receptor antagonists of AT1 - so block the action of angiotensin 2

55
Q

give an example of an ARB

A

losartan

56
Q

what are the effects of ACE inhibitors ?

A

they cause venous dilatation (decreased preload) and arteriolar dilatation (decreased afterload and TPR)

57
Q

what increases the effect of ACE inhibitors?

A

if the person is hypertensive or ont

also if the person is having diuretic therapy as there will be increased renin secretion

58
Q

where do ACE inhibitors have the greatest effect?

A

in angiotensin sensitive vascular beds - like the brain, heart, kidney – important because this may help maintain perfusion of critical organs

59
Q

what are some adverse effects of ACE inhibs

A

May initially cause hypotension – especially in patients treated with diuretics
Dry cough - this is because bradykinin is present in the airways and where it stimulates irritant receptors

60
Q

why would an ARb be used instead of an ACE?

A

if the perosn has a cough

61
Q

when are both ARBs and ACE inhibitors contraindicated>

A

in pregnancy (foetal toxicity) and should be not be used in bilateral renal artery stenosis (although ACEIs are used in diabetic nephropathy)

62
Q

what are the clinical uses of ARB and ACE inhibitors? there are three

A

1- hypertension
2- cardiac failure
3 - following MI

63
Q

what is the benefit of ARB and ACE in hypertension?

A

they

1) reduced TPR and MABP and
2) possible suppression of proliferation of smooth muscle cells in the media of resistance vessels

64
Q

what is the benefit of ARB and ACE in HF and post MI ?

A

HF is associated with inappropriate activation of the RAAS. ACEIs 1) decrease vascular resistance improving perfusion; 2) increase excretion of Na+ and H20; 3) cause regression of left ventricular hypertrophy

65
Q

what are adrenoceptors?

A

g-protein coupled receptors that are activated by the sympathetic transmitter noradrenaline and the hormone adrenaline

66
Q

what are the different types of adrenoceptor?

A

a1,2

b1,2,3

67
Q

what is the clinical use of beta adrenoceptor antagonists ?

A
  • treatment of angina pectoris
  • treatment of hypertension
  • treatment of HF
68
Q

what do B blockers do in angina? 3 things

A

1) decrease myocardial O2 requirement (decrease HR, SV, Work, O2)
2) counter elevated sympathetic activity associated with ischaemic pain
3) increase the amount of time spent in diastole (decrease HR) improving perfusion to the left ventricle

69
Q

what do B blockers do in HT treatment ?

A

reduce CO

reduce renin release from the kidneys

a CNS action that reduces sympathetic activity

70
Q

what do B blockers do in HF?

A

In combination with other drugs they suppress adverse effects associated with elevated activity of the sympathetic nervous system and RAAS

71
Q

what do Ca antagonists do?

A

they prevent the opening of L-type channels in exciteable tissues in response to depolarisation and hence limit Ca entry

72
Q

where are Ca channels found ?

A

in the heart and in smooth muscle

73
Q

what do Ca antagonists do in AP of SA and AV nodes?

A

they modify upstroke and reduce the rate and conduction through the AV node

74
Q

what do Ca antagonists do in AP of ventricular myocytes?

A

they act on phase 2 - reducing the force of contraction

75
Q

what is the first step in calcium entry in vascular smooth muscle?

A

noradrenaline is released from sympathetic neurones to act on A1 adrenoceptors

76
Q

what does the noradrenaline acting on a1 receptors cause? 2 things

A

leads to the release of Ca from intracellular stores (sarcoplasmic reticulum)

ALSO alpha 1 can activate Na receptors

77
Q

what does the activation of Na receptors cause?

A

depolarisation via plasma membrane cation channels

78
Q

what does depolarisation by Na channels cause?

A

the opening of ROCcs (calcium channels leading to an influx in Ca in plasma membrane l- type channels

79
Q

what o Ca antagonists do?

A

they prevent the ROCC opening

80
Q

give three examples of Ca antagonists

A

1) verapamil
2) amlopidine
3) diltiazam

81
Q

what is verapamil relatively selective for?

A

cardiac L-type channels

82
Q

what is amlopidine relatively selective for?

A

dihydropyridine compound - relitively selective for smooth muscle L-type channels

83
Q

what are Ca antagonists used for clinically ?

A

1) hypertension - amlopidine
2) angina
3) arrhythmias

84
Q

how do Ca antagonists work in Hypertension?

A

they reduce Ca entry into vascular smooth muscle cells causing generalized arteriolar dilatation, reducing TPR and MABP.

85
Q

where the the major effect of Ca antagonists on smooth muscle?

A

on the arteries and arterioles with little effect on the veins

86
Q

what are the adverse effects of Ca antagonists acting on smooth muscle?

A

hypotension, dizziness, flushing and ankle oedema

87
Q

what are calcium blockers used for in angina?

A

as prophylactic treatment

88
Q

what are ca antagonists often used in combination with if B blockers are contraindicated in the treatment of angina?

A

GTN

89
Q

why are calcium blockers of use in angina? 2 things

A

1) they cause peripheral arteriolar dilatation decreasing afterload and myocardial oxygen requirement - preload is not significantly changed
2) they produce coronary vasodilatation

90
Q

diltiazam and verapamil produce negative inotropic effects, what offsets this?

A

the activation of the baroreceptor reflex in response to vasodilatation and increased sympathetic activity

91
Q

what do Ca antagonists treat in arrhythmias?

A

atrial fibrilation

92
Q

how do Ca antagonists treat AF?

A

they reduced ventricular rate by suppression of conduction through the AV node

93
Q

what should verapamil not be used in combination with?

A

B blockers

94
Q

how do potassium channel openers cause relaxation?

A

they open ATP modulated K channels creating a hyperpolarisation effect as K leaves the cell. This switches off Ca L-type channels.

95
Q

where are these ATP modulated K channels located?

A

in vascular smooth muscle - K openers act potently and primarily upon arterial smooth muscle

96
Q

name a K opener that is used as a drug of last resort in severe hypertension ?

A

minoxidil

97
Q

what are the adverse effects of minoxidil?

A

causes reflex tachycardia (prevented by a β-blocker) and salt and water retention (alleviated by a diuretic)

98
Q

name a K opener that is used in Angina?

A

nicorandil

99
Q

what do A1 receptor antagonists do?

A

Cause vasodilatation by blocking vascular α1-adrenoceptors. Reduced sympathetic transmission results in decreased MABP

100
Q

give examples of a1 receptor antagonists ?

A

prazosin and doxazosin - both are competative antagonists

101
Q

what are a1 blockers also used for?

A

also provide symptomatic relief in benign prostatic hyperplasia (an abnormally enlarged prostate that compresses the urethra) and are particularly indicated for hypertensive patients with this condition

102
Q

give an adverse effect of A1 blockers

A

hypotension

103
Q

what do diuretics do?

A

they act on the kidney to increase the excretion of Na, Cl and H20 and exert additional indirect , relaxant effects upon the vasculature

104
Q

what are the two major classes of diuretics?

A

loop and thiazide

105
Q

what do thiazide diuretics do?

A

inhibit NaCl reabsorption by the distal tubule by blocking te Na/Cl co-transporter

106
Q

what percentage of filtered Na do they cause to be excreted alongside water?

A

up to 5% producing a moderate diuresis

107
Q

what do loop diuretics do?

A 
Inhibit NaCl reabsorption in
the thick ascending limb of 
the loop of Henle by 
blocking the Na+/K+/2Cl- 
co-transporter
108
Q

what percentage of filtered Na do they cause to be excreted alongside water?

A

Cause up to 15-25% of
filtered Na+ to be excreted
with accompanying H20
producing a strong diuresis

109
Q

what is undesirable about diuretics?

A

Thiazides and loop agents both produce an undesirable loss of K+
(that occurs through Na+/K+ exchange in the late distal tubule).

110
Q

how is the loss of K corrected?

A

Corrected by co-administration of a ‘potassium sparring diuretic’
or K+ supplements

111
Q

what are thiazides used in treatment for?

A

mild heart failure

hypertension

and also in severe resistant oedema (with a loop agent)

112
Q

give an example of a thiazide diuretic?

A

bendroflumethiazide

113
Q

what are loop diuretics used for?

A

Are used to reduce salt and water overload associated with:

  • acute pulmonary oedema
  • chronic heart failure

Benefit in these conditions occurs as a result of an absorption of extracellular fluid
contributing to oedema into capillaries as a consequence of diuretic-induced
reduction of blood volume

114
Q

give an example of a loop diuretic

A

furosemide

Cardiovascular: pharmacology (6 decks)

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