Brainscape's Knowledge GenomeTM

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


See full index

YR2 LCRS Pharmacology > 8. SNS agonists > Flashcards

8. SNS agonists Flashcards

1
Q

where are sympathetic adrenoreceptors found?

A

all over the body at the ends of sympathetic nerves

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

in which 2 ways does activation occur in the sympathetic NS?

A

NERVOUS activation of receptors - nerves release NA

HORMONAL activation of receptors - adrenaline from the bloodstream can diffuse into tissues

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

what do directly acting SNS agonists do?

A
  • mimic actions of NA and A
  • bind to and stimulate adrenoreceptors
  • used principally for their actions on the CVS, eyes and lungs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what receptors are found in the heart and lungs?

A

heart - b1 = increased rate and contractility

lungs - b2 = dilation

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

how are blood vessels dilated and constricted?

A

dilation - activation of b2 receptors

constriction - activation of a1 receptors (dominant)

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

what is the order of selectivity of noradrenaline for receptors?

A

a1 = a2 > b1 = b2

NA is slightly more alpha selective

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

what is the order of selectivity of adrenaline for receptors?

A

b1 = b2 > a1 = a2

A is slightly more beta selective

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

what is NA derived from?

A

tyrosine from the diet

tyrosine -> DOPA -> Dopamine -> NA

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

where are all adrenoreceptors except a2 found?

A

post-junctional membrane

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

where is the a2 receptor found?

A

pre-junctional receptor found on the neurone itself (-ve feedback receptor that diminishes sympathetic effects by decreasing NA release)

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

give examples of directly acting SNS agonists

A
  • adrenaline (non-selective)
  • phenylephrine (a1)
  • clonidine (a2)
  • dobutamine (b1)
  • salbutamol (b2)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is anaphylaxis and what does a second exposure result in?

A

when someone becomes sensitive to a harmless agent

the next exposure results in recognition by mast cells coated with IgG antibodies -> mast cell degranulation -> histamine release -> bronchoconstriction + vasodilation

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

why do we give adrenaline to treat anaphylaxis?

A

A = Airways - acts on b2 to cause bronchodilation

B = Breathing - acts on b1 to cause tachycardia by increasing HR and CO

C = Circulation - acts on a1 to cause vasoconstriction to maintain normal BP

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

how does adrenaline stop degranulation?

A

it suppresses mediator release by acting on b-receptors on mast cells

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

what does mast-cell degranulation and release of inflammatory mediators cause in the heart and vascular system?

A
  • increased capillary permeability and entry of fluid into tissues
  • swelling of tissues e.g. tongue
  • loss of BP
  • reduced O2 to tissues
  • irregular heartbeat
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what does mast-cell degranulation and release of inflammatory mediators cause in the respiratory tract?

A
  • contraction of smooth muscle and constriction of throat and airways
  • difficulty swallowing
  • difficulty breathing
  • wheezing
17
Q

what does mast-cell degranulation and release of inflammatory mediators cause in the GI tract?

A
  • contraction of smooth muscle
  • stomach cramps
  • vomiting
  • diarrhoea
18
Q

what are other clinical uses of adrenaline?

A

b2 (airways):

  • asthma (emergencies)
  • acute bronchospasm (associated with chronic bronchitis or emphysema)

b1 (inotropic effects):
- cardiogenic shock (sudden inability of heart to pump sufficient O2-rich blood)

a1:
- spinal anaesthesia (maintain BP before surgery)
- local anaesthesia (vasoconstricts)

19
Q

what are the unwanted actions of adrenaline?

A
  • secretions: reduced and thickened mucous
  • CVS: tachycardia, palpitations, arrhythmias, cold extremities, hypertension
  • skeletal muscle: tremor
20
Q

describe the actions of phenylephrine as a SNS agonist

A
  • selective for a1
  • structurally similar to A and NA
  • more resistant to breakdown by COMT but not MAO (will last longer)
  • good nasal decongestant: a1-mediated vasoconstriction of vessels in nose
  • mydriatic (causes pupil dilation –> can use it for examination of the back of the eye)
21
Q

describe the actions of clonidine as a SNS agonist

A
  • selective for a2
  • negative feedback effect so decreases sympathetic function even though it is a SNS agonist
  • less NA release
22
Q

what is clonidine primarily used to treat?

A

glaucoma

23
Q

what is glaucoma?

A

an increase in intraocular pressure caused by poor drainage of aq. humour (formed from the ciliary body). the aq. humour is drained by the venous system. if untreated it permanently damages the optic nerve and can lead to blindness

24
Q

how does clonidine treat glaucoma?

A

there are a1 receptors on the blood vessels so stimulating this receptor causes vasoconstriction -> less blood supply to ciliary body -> less sq. humour produced

25
Q

what 2 receptors are found on the ciliary body?

A

a2 (inhibitory)

b1 (stimulatory - don’t want to activate)

26
Q

what are the other clinical uses of clonidine?

A
  • treats hypertension and migraines (reduces activation of heart, reduces vasoconstriction, reduces renin production)
  • reduces sympathetic tone (a2 adrenoreceptor mediated -> presynaptic inhibition of NA release)
27
Q

describe the actions of isoprenaline as a SNS agonist

A
  • beta selective

- more resistant to MAO and uptake 1 (longer lasting)

28
Q

what are the clinical uses of isoprenaline?

A
  • cardiogenic shock
  • acute heart failure
  • myocardial infarction
29
Q

why might b2 receptor stimulation by isoprenaline be a problem?

A

isoprenaline will drive the b1 receptors in the heart to support the heart in cardiogenic shock

HOWEVER

stimulation of b2 receptors in vascular smooth muscle -> dilation of blood vessels in muscles -> pooling of blood in muscles -> decreased venous return -> decreased venous BP -> stimulated baroreceptors -> reflex tachycardia -> exacerbate arrhythmias

30
Q

describe the actions of dobutamine as a SNS agonist

A
  • selective for b1
  • less risk of reflex tachycardia
  • HOWEVER rapidly metabolised by COMT (plasma half-life of 2mins)
31
Q

what are the clinical uses of dobutamine?

A

cardiogenic shock

32
Q

describe the actions of salbutamol as a SNS agonist

A
  • selective for b2

- similar to A and NA with similar resistance to MAO and COMT

33
Q

what are the effects of salbutamol?

A
  • bronchial smooth muscle relaxation
  • increased Na/Ca exchange
  • opens potassium channels
34
Q

what are the clinical uses of salbutamol?

A
  • treatment of asthma: b2 relaxation of bronchial smooth muscle, inhibition of release of bronchoconstrictor substances from mast cells
  • treatment of threatened premature labour: b2 relaxation of uterine smooth muscle, preventing the abortion of a foetus
35
Q

what are the side effects of salbutamol?

A
  • relex tachycardia
  • tremor
  • blood sugar dysregulation

YR2 LCRS Pharmacology (32 decks)

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