Brainscape's Knowledge GenomeTM

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


See full index

Y2 LCRS Pharmacology and Therapeutics > sympathetic nervous system > Flashcards

sympathetic nervous system Flashcards

adrenoceptor antagonists 1: list the clinical uses, principal pharmacological features, mechanism of action and unwanted effects of selective and non-selective α and β adrenoceptor antagonists, and compare the pharmacology of selective and non-selective adrenoceptor antagonists

1
Q

what sections of spinal cord have sympathetic innervation

A

thoracic and lumbar

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

what sections of spinal cord have parasympathetic innervation

A

cervical and sacral

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

sympathetic innervation from thoracic section: effects

A

dilate pupil, inhibit salivation, relax bronchi, accelerate heart, inhibit digestive activity

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

sympathetic innervation from lumbar section: effects

A

stimulate glucose release by liver, secretion of adrenaline and noradrenaline from kidney, relaxes bladder, contracts rectum

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

effects of a1 adrenoceptor stimulation

A

vasoconstriction, relaxation of GIT

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

effects of a2 adrenoceptor stimulation

A

inhibition of transmitter release and contraction of vascular smooth muscle, CNS actions

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

effects of B1 adrenoceptor stimulation

A

increased cardiac rate and force, relaxation of GIT, renin release from kidney

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

effects of B2 adrenoceptor stimulation

A

bronchodilation, vasodilation (no PSNS innervation), relaxation of visceral smooth muscle, hepatic glycogenolysis

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

effect of B3 adrenoceptor stimulation

A

lipolysis

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

SNS synapse pathway (a1, B1, B2 and a2) in VSMCs

A

tyrosine to noradrenaline -> packaged in vesicles -> action potential down presynaptic sympathetic neurone -> release of noradrenaline by exocytosis and Ca2+ influx into synaptic cleft -> bind to and stimulation of a1, B1 or B2 receptor on postsynaptic VSMC -> effect e.g. vasoconstriction -> a2 receptor-mediated negative feedback by preventing further noradrenaline release from presynaptic neurone

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

non-selective (a1, B1 and B2) and selective a1 and a2 adrenoceptor antagonists

A

non-selective: carvedilol (B-blocker with a1 blockade, giving additional vasodilator properties), selective: phentolamine

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

selective a1 adrenoceptor antagonist

A

prazosin

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

selective B1 and B2 adrenoceptor antagonist

A

propranolol

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

selective B1 adrenoceptor antagonist (cardioblockers)

A

atenolol

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

4 clinical uses of adrenoceptor antagonist

A

treatment of: hypertension, arrhythmias, angina, glaucoma

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

what adrenoceptor antagonist can be used to treat hypertension

A

B-blockers and a-blockers, false transmitters

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

what adrenoceptor antagonist can be used to treat arrhythmias, angina and glaucoma

A

B-blockers

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

physiology: calculation of blood pressure

A

cardiac output x total peripheral resistance

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

pathophysiology of hypertension

A

consistently above 140/90 mmHg when sitting/lying for average male; risk factor for stroke, heart failure, myocardial infarction, chronic kidney disease

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

3 main contributers of blood pressure and targets for B-blockers

A

blood volume, cardiac output, vascular tone

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

tissue targets for anti-hypertensives and how they contribute to blood pressure

A

heart (cardiac output), sympathetic nerves that release noradrenaline (vasoconstrictor), kidney (blood volume and vasoconstriction), arterioles (determine peripheral resistance), CNS (determines blood pressure set point and regulation)

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

tissue targets for anti-hypertensives and relevant B adrenoceptors

A

heart (B1), sympathetic nerves that release noradrenaline (B1/B2), kidney (B1), CNS (B1/B2); arterioles have a adrenoceptors

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

effect of B-blockers when treating hypertension: heart

A

B-adrenoceptor coupled with adenyl cyclase so causes production of cAMP and drives cell activity, so antagonist will decrease heart rate and force of contraction, decreasing cardiac output

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

effect of B-blockers when treating hypertension: kidney

A

decrease sympathetic ability to produce renin, decreasing angiotenin II release, preventing vasoconstriction and aldosterone production (ultimately blood volume)

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

effect of B-blockers when treating hypertension: presynaptic B-adrenoceptors

A

block facilitatory effects of noradrenaline release, which may contribute to antihypertensive effect

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

2 other B-blockers which have other targets

A

nebivolol, sotalol

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

nebivolol therapeutic effect

A

B1 and potentiates NO (vasodilator)

28
Q

solatol therapeutic effect

A

B1, B2 and inhibits K+ channels (interferes cell hyperpolarisation)

29
Q

6 unwanted effects of selective and non-selective a and B adrenoceptor antagonists

A

bronchoconstriction, cardiac failure, hypoglycaemia, fatigue, cold extremities, bad dreams

30
Q

how might bronchoconstiction be a worse unwanted effect of selective and non-selective a and B adrenoceptor antagonists

A

wouldn’t give to patients with asthma/COPD

31
Q

why could selective and non-selective a and B adrenoceptor antagonists be problematic in patients with cardiac failure

A

need some sympathetic drive to heart

32
Q

why could selective and non-selective a and B adrenoceptor antagonists cause hypoglycaemia

A

mask symptom of hypoglycaemia/inhibit glycogen breakdown; wouldn’t give to diabetics

33
Q

why could selective and non-selective a and B adrenoceptor antagonists cause fatigue

A

decrease cardiac output and muscle perfusion (B2 adrenoceptors cause dilation of skeletal muscle)

34
Q

why could selective and non-selective a and B adrenoceptor antagonists cause cold extremities

A

loss of B-receptor mediated vasodilation in cutaneous vessels

35
Q

advantage of atenolol over propranolol

A

atenolol is more selective for B1 receptors, so doesn’t have disadvantages of bronchoconstriction and hypoglycaemia (can give to asthmatics and diabetics), as these have B2 adrenoceptors

36
Q

advantage of carvedilol over atenolol

A

more powerful hypotensive effect: carvedilol is a dual acting B1 and a1 antagonist, with a1 blockade preventing arteriole vasoconstriction, thus reducing peripheral resistance; also induces decrease in heart rate, cardiac output and blood volume (B effect in heart and kidneys; wanes with chronic use)

37
Q

features of a1 adrenoceptors

A

Gq-linked (stimulatory), with effect on postsynaptic VSMCs

38
Q

featurs of a2 adrenoceptors

A

Gi-linked (inhibitory), with effect of presynaptic autoreceptors inhibiting noradrenaline release

39
Q

example of a non-selective a-blocker

A

phentolamine

40
Q

what was phentolamine used to treat

A

pheochromocytoma-induced hypertension (block a1 to dilate vasculature)

41
Q

side effects of non-selective a-blocker e.g. phentolamine

A

fall in arterial pressure causing postural hypotension, causing reflex response of increasing cardiac output and heart rate (B receptors); also increased GIT motility, causing diarrhoea

42
Q

example of an a1 specific blocker

A

prazosin

43
Q

effect of prazosin and clinical use

A

inhibits noradrenaline vasoconstrictor activity, but only has modest blood pressure lowering effects so used as adjunctive treatment

44
Q

why do a2 receptors and baroreceptors reduce phentolamine effectiveness

A

a2 is inhibitory, so phentolamine reduces inhibition of release of noradrenaline (prevents negative feedback), so competition between noradrenaline and phentolamine in synapse; baroreceptors detect drop in arterial pressure so decrease firing, increasing SNS activity further

45
Q

phentolamine vs prazosin

A

both cause vasodilation and fall in arterial pressure; prazosin induces less reflex tachycardia as no a2 action so don’t increase noradrenaline release from nerve terminals, and fall in venous pressure due to dilation causes decreased cardiac output; doesn’t affect cardiac function much, but postural hypotension is troublesome; also causes increased HDL and lower LDL; both cause baroreceptor firing rate to drop and compensatory increase in SNS activity though

46
Q

define arrhythmia

A

abnormal or irregular heart beats

47
Q

main cause of death due to arrhythmias

A

myocardial infarction

48
Q

what can precipitate or aggravate arrhythmias

A

increase in sympathetic drive to heart via B1

49
Q

treatment of arrhythmias using B1 adrenoceptor antagonists: 2 features

A

decrease sympathetic drive to heart, and increased refractory period of AVN, interfering with AV conduction in atrial tachycardias and slowing ventricular rate (better blood flow from atria to ventricle)

50
Q

drug used to treat arrhythmias

A

propranolol

51
Q

features of propranolol which make it effective in treating arrhythmias

A

non-selective B-antagonist but mainly B1, reduces mortality of patients with myocardial infarction, with particular success in arrythmias occuring during exercise or mental stress

52
Q

3 types of angina (in order of normal progression)

A

stable, unstable, variable

53
Q

define angina

A

pain that occurs when O2 supply to myocardium is insufficient for its needs

54
Q

pain distribution of angina

A

chest, arm, neck

55
Q

when is angina typically brought on

A

exertion or excitement

56
Q

features of stable angina

A

pain on exertion; increased demand on heart; due to fixed narrowing of coronary vessels e.g. atheroma

57
Q

features of unstable angina

A

pain with less and less exertion, culminating with pain at rest; platelet-fibrin thrombus assoicated with ruptured atheromatous plaque, but without complete occlusion of vessel; risk of infarction

58
Q

features of variable angina

A

occurs at rest; caused by coronary artery spasm; associated with atheromatous disease

59
Q

drug used to treat angina

A

low dose metoprolol

60
Q

how does metoprolol treat angina

A

B1-selective, so reduces heart rate and myocardial contractile activity, blood flow better matched to tissue demand; doesn’t affect bronchial smooth muscle, so reduces O2 demand whilst maintaning same degree of effort

61
Q

negative effects of metoprolol and other B-blockers

A

impair ability to do exercise

62
Q

what causes glaucomas, what are they characterised by and what is untreated outcome

A

caused by poor drainage (or excess production) of aqueous humour, with increase in intraocular pressure resulting; if untreated, permanant damage to optic nerve, causing blindness

63
Q

route of aqueous humour in normal eye

A

produced by blood vessels in ciliary body (by carbonic anhydrase) -> flows into posterior chamber, through pupil, to anterior chamber -> drains into trabecular network and into veins and canal of Schlemm

64
Q

what is aqueous humour production indirectly related to

A

blood pressure and blood flow in ciliary body

65
Q

what is used to treat glaucoma, and how does it work

A

B1-selective adrenoceptor by decreasing aqueous humour production on ciliary body (B1 receptor on carbonic anhydrase, so no production of HCO3- for aqueous humour)

Y2 LCRS Pharmacology and Therapeutics (68 decks)

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