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Farmer > SNS Agonists > Flashcards

SNS Agonists Flashcards

1
Q

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

A

Adrenal medulla – adrenaline (80%) and noradrenaline (20%)

Sweat glands – acetylcholine

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2
Q

State the difference between directly and indirectly acting sympathomimetics.

A

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

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3
Q

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

A

ALL adrenoceptors are G-protein coupled
Alpha 1 = Gq
Alpha 2 = Gi (inhibitory)
Beta 1 + Beta 2 = Gs

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4
Q

State the main actions of beta-1 receptors.

A

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

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5
Q

State the main actions of beta-2 receptors.

A

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

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6
Q

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

A 
Exocrine secretions (e.g. salivary gland secretions become thick) 
GIT motility – decreased muscle motility and tone + contraction of sphincters
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7
Q

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

A

Beta receptors

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8
Q

State some effects of alpha-1 receptors.

A

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

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9
Q

What is the principle action of beta-blockers?

A

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

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10
Q

Describe the relative selectivity of adrenaline and noradrenaline.

A

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

(Nora = Mora -A)

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11
Q

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

A

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

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12
Q

State five directly acting SNS agonists.

A 
Phenylephrine – alpha-1 
Clonidine – alpha-2 
Dobutamine – beta-1 
Salbutamol – beta-2 
Isoprenaline – beta 1 + beta 2
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13
Q

Describe the development of hypersensitivity following first exposure.

A

After the first exposure you generate antibodies to the antigen and these circulate around the body and bind to mast cells. In the subsequent exposure, the mast cells are primed with the antibody on its surface. Cross-linking of these antibodies on the surface of mast cells causes massive release of the stored mediators leading to the symptoms of hypersensitivity.

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14
Q

State some symptoms of hypersensitivity.

A

Increase in capillary permeability leads to increased movement of fluid into the tissues. This depletes the circulating fluid volume leading to a drop in blood pressure -> ANAPHYLACTIC SHOCK (and collapse the circulatory system leading to unconsciousness) This can also lead to contraction of bronchial smooth muscle and constriction of muscles around the throat causing respiratory distress. It can also constrict GI smooth muscle causing vomiting and diarrhoea.

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15
Q

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

A

During hypersensitivity reaction, priority BREATHING. Adrenaline is more selective for beta receptors than noradrenaline, meaning more beta-2 mediated bronchodilation, opening up the airways/

Adrenaline also stimulates the heart via beta-1, supports BP. It also acts on alpha-1 receptors to cause vasoconstriction and increase TPR and BP. Adrenaline also slows down histamine release from mast cells via beta-2.

(HYDROCORTISONE GIVEN ALONGSIDE AS SUPPORTIVE TREATMENT SOMETIMES)

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16
Q

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

A

Asthma
Acute bronchospasm associated with chronic bronchitis or emphysema
It causes beta-2 mediated bronchodilation and suppressors mediator release from mast cells. Selective beta-2 agonists are preferable, though adrenaline is useful in a hypotensive crisis.

17
Q

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

A

Alpha-1 involved in vasoconstriction of the vessels in the ciliary body

Alpha-2 involved in humour formation

Beta-receptors control the enzyme that makes the aqueous humour

18
Q

Why is adrenaline used as a treatment for glaucoma?

A

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

19
Q

State and explain three other clinical uses of adrenaline.

A

Cardiogenic Shock (sudden inability of heart to pump sufficient oxygenated blood) Beta-1 stimulation has a positive inotropic effect. Cardiogenic shock can happen in MI or cardiac arrest.

Spinal Anaesthesia - Anaesthetising through spine takes away sympathetic output to peripheral resistance vessels, leads to relaxation of the peripheral vasculature. Patient can’t maintain BP. Giving a little adrenaline with anaesthetic constricts the blood vessels to maintain BP.

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

20
Q

State some unwanted actions of adrenaline.

A

Secretions are reduced and thick CVS – tachycardia, palpitations, arrhythmias, cold extremities, hypertension
Overdose of adrenaline can lead to: cerebral haemorrhage, pulmonary embolism

21
Q

Describe the resistance to degradation of phenylephrine.

A

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

22
Q

State some clinical uses of phenylephrine.

A

Mydriatic

Nasal decongestant It causes vasoconstriction

23
Q

Describe and explain the effects of clonidine.

A

Clonidine stimulates alpha-2 receptors (negative effect on NA synthesis and release.) Decrease in NA -> less vasoconstriction via alpha-1 action -> fall in TPR and BP.

Clonidine also has central action on brainstem – acts on baroreceptors and reduces the sympathetic drive from brain. Reduced sympathetic activity reduces TPR and the amount of NA released at the nerve terminals further reducing TPR.

Alpha-2 mediated reduction in NA release in the kidneys will also reduce renin release and hence reduce angiotensin II.

24
Q

State some clinical uses of clonidine.

A

It is used to treat hypertension and migraine.

25
Q

Describe the susceptibility to breakdown of isoprenaline compared to adrenaline.

A

Isoprenaline is less susceptible to uptake 1 and MAO breakdown

26
Q

State three clinical uses of isoprenaline.

A

Cardiogenic Shock
Myocardial Infarction
Acute Heart Failure

27
Q

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

A

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

28
Q

State a clinical use of dobutamine.

A

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

29
Q

Describe the relative resistance of salbutamol to degradation.

A

Relative resistance to MAO and COMT

30
Q

State and explain two clinical uses of salbutamol.

A

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

31
Q

State some side effects of salbutamol.

A

Reflex tachycardia
Tremor
Blood glucose dysregulation

32
Q

State two indirectly acting SNS agonists.

A

Cocaine

Tyramine

33
Q

Describe the mechanism of action of cocaine.

A

Cocaine inhibits uptake 1 for both noradrenaline and dopamine leading to an accumulation of dopamine or noradrenaline within the synapse

34
Q

Which nucleus within the hypothalamus uses dopamine as its neurotransmitter?

A

Nucleus accumbens

35
Q

Describe the effects of cocaine on the CNS and CVS.

A

CNS
Low dose = euphoria
High dose = activation of chemotactic trigger zones (causing vomiting), CNS depression, respiratory failure, convulsions, death

CVS
Low dose = tachycardia, vasoconstriction, raised blood pressure
High dose = ventricular fibrillation and cardiac arrest

36
Q

What is tyramine and what foodstuffs is it found in?

A

It is a dietary amino acid Found in cheese, soy sauce and red wine

37
Q

Describe the mechanism of action of tyramine.

A

Tyramine acts as a false transmitter It acts as a weak agonist at the effector organ at which NA will be stimulating receptors It piggy backs on the uptake systems and competes with NA for the uptake 1 site Tyramine starts being taken up into vesicles and it displaces NA from the vesicles Normally MAO breaks down the displaced NA

38
Q

In which subset of patients is tyramine a problem?

A

Patients taking MAO inhibitors This means that the breakdown of NA is inhibited so it accumulates in the synapse leading to a hypertensive crisis

Farmer (33 decks)

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