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Flashcards in SNS Agonists Deck (34)
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1

Most sympathetic post-ganglionic neurones release noradrenaline. State two exceptions.

Adrenal medulla – adrenaline (80%) and noradrenaline (20%)
Sweat glands – acetylcholine

2

State the difference between directly and indirectly acting sympathomimetics.

Directly acting – binds to the adrenoceptor and mimic the action of adrenaline and noradrenaline by stimulating the receptors
Indirectly acting – inhibits the uptake and breakdown systems leading to the accumulation of neurotransmitter in the synaptic cleft

3

Describe the mechanism of action of the four different types of adrenoceptor.

ALL adrenoceptors are G-protein coupled
Alpha 1 = PLC -> IP3 + DAG
Alpha 2 = decrease cAMP
Beta 1 + Beta 2 = increase cAMP

4

State the main actions of beta-1 receptors.

HEART – increase heart rate + increase contractility
KIDNEYS – increase renin release -> increase blood pressure
Lipolysis

5

State the main actions of beta-2 receptors.

Bronchodilation
Hepatic glucose output – glycogenolysis + gluconeogenesis
Vasodilation of vessels to skeletal muscle
Relaxation of the uterus (in women)

6

State some effects that are mediated by both alpha and beta-receptors.

Exocrine secretions (e.g. salivary gland secretions become thick)
GIT motility – decreased muscle motility and tone + contraction of sphincters

7

What receptors are responsible for the production of aqueoushumour by the ciliary body?

Beta receptors

8

State some effects of alpha-1 receptors.

Mydriasis (contraction of radial muscles of the iris)
Vasoconstriction
Constriction of trigone and sphincter in the bladder
Increased motility and tone of the ureters
Stimulates ejaculation (in males)
Lacrimation
Contraction of pilomotor muscle + increased localised secretion of sweat glands e.g. palm of hands
Hepatic glucose output (glycogenolysis and gluconeogenesis)
Lipolysis

9

What is the principle action of beta-blockers?

KIDNEYS – it inhibits the beta-1 mediated increase in renin secretion
It also decreases heart rate and contractility but its main action in reducing blood pressure is through the kidneys

10

Describe the relative selectivity of adrenaline and noradrenaline.

Noradrenaline is more selective for ALPHA-receptors
Adrenaline is more selective for BETA-receptors

11

Describe the action of pre-synaptic alpha-2 receptors.

Pre-synaptic alpha-2 receptors have a negative influence on noradrenaline synthesis and release

12

State five directly acting SNS agonists.

Phenylephrine – alpha-1
Clonidine – alpha-2
Dobutamine – beta-1
Salbutamol – beta-2
Isoprenaline – beta 1+ beta 2

13

Why is adrenaline more effective than noradrenaline in dealing with hypersensitivity?

During the hypersensitivity reaction, the most important problem to deal with is BREATHING.
Adrenaline is more selective for beta receptors than noradrenaline so is better at causing beta-2 mediated bronchodilation, thus opening up the airways.
Adrenaline also stimulates the heart via beta-1 to support blood pressure.
Adrenaline also acts on the alpha-1 receptors to cause vasoconstriction and an increase in TPR and blood pressure. Adrenaline can also slow down the release of histamine from mast cells via beta-2.

14

State two pulmonary obstructive conditions in which adrenaline is used therapeutically and explain why.

Asthma
Acute bronchospasm associated with chronic bronchitis or emphysema
It causes beta-2 mediated bronchodilation and it suppressors mediator release.

15

Which receptors are involved in the generation of aqueous humour in the eye?

Alpha-1 involved in vasoconstriction of the vessels in the ciliary body
Beta-receptors control the enzyme that makes the aqueous humour

16

Why is adrenaline used as a treatment for glaucoma?

Adrenaline can stimulate the alpha-1 receptors to cause vasoconstriction of the vessels in the ciliary body thus reducing the blood flow within the ciliary body -> reduced production of aqueous humour

17

State and explain three other clinical uses of adrenaline.

Cardiogenic Shock (the sudden inability of the heart to pump sufficientoxygenated blood)
 Beta-1 stimulation has a positive inotropic effect
 Cardiogenic shock can happen in MI or cardiac arrest
Spinal Anaesthesia
 Anaesthetising through the spine can take away the sympathetic output to the peripheral resistance vessels
 This leads to relaxation of the peripheral vasculature so the patient can’t maintain their blood pressure
 Giving a little adrenaline with the anaesthetic can constrict the blood vessels to maintain blood pressure
Local Anaesthesia
 Giving adrenaline with the LA can cause local vasoconstriction, which prevents clearance of the anaesthetic from that area
 This is due to alpha-1 mediated vasoconstriction

18

State some unwanted actions of adrenaline.

Secretions are reduced and thick
CVS – tachycardia, palpitations, arrhythmias, cold extremities, hypertension

19

Describe the resistance to degradation of phenylephrine.

Phenylephrine is MORE resistant to COMT degradation than adrenaline but it is NOT resistant to MAO degradation

20

State some clinical uses of phenylephrine.

Mydriatic
Nasal decongestant
It causes vasoconstriction

21

Describe and explain the effects of clonidine.

Clonidine stimulates alpha-2 receptors so has a negative effect on NA synthesis and release.
Decrease in NA release -> less vasoconstriction via alpha-1 action -> fall in TPR and blood pressure
Clonidine also has a central action on the brainstem – acts on baroreceptors and reduces the sympathetic drive coming out of the brain.
Reduction in sympathetic activity reduces TPR and reduces the amount of NA released at the nerve terminals thus reducing TPR further.
So there are two routes of clonidine action in reducing NA release and TPR.
Alpha-2 mediated reduction in NA release in the kidneys will also reduce renin release and hence reduce angiotensin II.

22

State some clinical uses of clonidine.

It is used to treat hypertension and migraine.

23

Describe the susceptibility to breakdown of isoprenaline compared to adrenaline.

Isoprenaline is less susceptible to uptake 1 and MAO breakdown

24

State three clinical uses of isoprenaline.

Cardiogenic Shock
Myocardial Infarction
Acute Heart Failure

25

What is a big problem with isoprenaline with regards to its action on beta 2 receptors?

Isoprenaline brings about positive effects via Beta-1 stimulation
However, stimulation of Beta-2 leads to vasodilation of blood vessels in the muscles -> pooling of blood within the muscles -> reduced venous return
Via the baroreceptors, you get a reflex tachycardia
So the beta-1 effects are good for patients with heart failure but the beta-2 effects are not

26

State a clinical use of dobutamine.

Cardiogenic shock
It lacks isoprenaline’s reflex tachycardia effect
Administration via IV infusion (half-life = 2 mins)

27

Describe the relative resistance of salbutamol to degradation.

Relative resistance to MAO and COMT

28

State and explain two clinical uses of salbutamol.

Asthma
 Beta-2 mediated relaxation of bronchial smooth muscle (bronchodilation)
 Inhibition of release of bronchoconstrictor molecules from mast cells
Threatened premature labour
 Beta-2 mediated relaxation of uterine smooth muscle
 This will prevent abortion

29

State some side effects of salbutamol.

Reflex tachycardia
Tremor
Blood glucose dysregulation

30

State two indirectly acting SNS agonists.

Cocaine
Tyramine