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Pharmacology > Pharm 9 - SNS Agonists > Flashcards

Pharm 9 - SNS Agonists Flashcards

1
Q

From which region of the spinal cord do sympathetic fibres originate?

A

Thoracolumbar

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2
Q

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

A

Sweat glands - acetylcholine

adrenal medulla - adrenaline

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3
Q

State two difference between directly and indirectly acting sympathomimetics.

A

Directly - binds to adrenoceptor and mimic the action of catecholamines by stimulating the receptor

indirectly acting - inhibits uptake and breakdown of the system leading to accumulation of the neurotransmitter in the synaptic cleft

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4
Q

Describe the mechanism of action of the 4 different types of adrenoceptors.

A

All are G protein coupled

Alpha 1 = PLC –> IP3 + DAG

Alpha 2 = decrease cAMP

beta 1+ 2= increase cAMP

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5
Q

State the main actions of beta-1 receptors

A

Heart - increase heart rate and contractility

kidneys - increase renin release which increases blood pressure

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6
Q

State the main actions of beta 2 receptors?

A
  • partial bronchodilation
  • hepatic glucose output - glycogenolysis + gluconeogenesis
  • vasodilation of vessels to skeletal muscle
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7
Q

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

A

Exocrine secretions

GIT motility

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8
Q

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

A

Beta receptors

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9
Q

State some of the effects of alpha 1 receptors.

A

vasoconstriction
increased motility and tone of ureters
mydriasis
hepatic glucose output

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10
Q

What is the principle action of beta blockers?

A

Inhibits beta 1 mediated increase in renin secretion

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11
Q

Describe the relative selectivity of adrenaline and noradrenaline

A

adrenaline = beta

noradrenaline = alpha

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12
Q

Describe the action of pre-synaptic alpha 2 receptors?

A

negative influence on noradrenaline synthesis and release

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13
Q

State 5 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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14
Q

Describe the development of hypersensitivity following the first exposure.

A

after the first exposure you generate antibodies to the antigen

these circulate and bind to mast cells

in subsequent exposure, the mast cells have the antibody on the surface

cross linking of the antibodies causes a huge release of stored mediators leading to the symptoms of hypersensitivity

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15
Q

State some of the symptoms of hypersensitivity.

A

Increase in capillary permeability leads to increased movement of fluid into the tissues.

depletes circulating fluid volume, causing decrease in blood pressure = anaphylactic shock

can also cause contraction of bronchial smooth muscle causing resp distress

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16
Q

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

A

adrenaline is more selective for beta receptors

so better as causing beta 2 mediated bronchodilation thus opening airways

airways is more important

adrenaline also stimulates heart via b1

acts on alpha 1 to cause vasoconstriction and increase TPR and blood pressure

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17
Q

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

A

asthma + acute bronchospasm

causes beta 2 mediated bronchodilation

18
Q

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

A

alpha1 - vasoconstriction of vessels in ciliary body

beta - control enzyme which makes humour

19
Q

Why is adrenaline used as a treatment for glaucoma?

A

adrenaline can stimulate the alpha 1 receptors to cause vasoconstriction of the vessels supplying the ciliary body and thus reducing the production of aqueous humour

20
Q

State 3 uses of adrenaline.

A

1) Cardiogenic shock
2) Spinal anaesthesia - constricts blood vessels to maintain BP
3) Local anaesthesia - constricts blood vessels so anaesthesia does not leave the site

21
Q

State some unwanted effects of adrenaline.

A

Secretion are thick

CVS - tachy, palpitations, arrhythmias, cold extremities, hypertension

22
Q

Describe the resistance to degradation of phenylephrine.

A

phenylephrine more resistant to COMT degradation than adrenaline

but not resistant to MAO degredation

23
Q

State some clinical uses of phenylephrine.

A

Mydriatic

Nasal decongestant

24
Q

Describe and explain the effects of clonidine.

A

Clonidine stimulates alpha-2 receptors so has a negative effect on NA synthesis and release. Decrease in NA release à less vasoconstriction via alpha-1 action à 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.

25
Q

State some clinical used of clonidine.

A

Hypertension and migraine

26
Q

Describe susceptibility to breakdown of isoprenaline compared to adrenaline.

A

isoprenaline is less susceptible to uptake 1 and MAO breakdown

27
Q

State 3 clinical uses of isoprenaline.

A

cardiogenic shock
myocardial infarction
acute heart failure

28
Q

What is the big problem with isoprenaline with regard to its actions on beta 2 receptors?

A

stimulates beta 2 receptors causing vasodilation of blood vessels — pooling of blood within muscles

+ reflex tachycardia

29
Q

State a clinical use of dobutamine

A

cardiogenic shock

30
Q

Describe the relative resistance of salbutamol to degradation.

A

relative resistance to MAO and COMT

31
Q

State two clinical uses of salbutamol.

A

asthma - beta 2 mediated relaxation of bronchial smooth muscle + inhibition of molecules from mast cells

Threatened premature labour - beta 2 mediated relaxation of uterine smooth muscle

32
Q

State some side effects of salbutamol.

A

Reflex tachycardia
Tremor
Blood glucose dysregulation

33
Q

State two indirectly acting SNS agonists.

A

cocaine

Tyramine

34
Q

Describe the mechanism of action of cocaine.

A

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

35
Q

Which nucleus within the hypothalamus uses dopamine as its neurotransmitter?

A

Nucleus accumbens

36
Q

Describe the effects of cocaine on the CNS?

A 
LOW = euphoria
HIGH = activation of chemotactic trigger zones, CNS depression, resp failure, death
37
Q

Describe the effects of cocaine on the CVS?

A

LOW - tachycardia, vasoconstriction

HIGH - ventricular fibrillation and cardiac failure

38
Q

What is tyramine and what food is it found in?

A

dietary amino acid

found in cheese, soy sauce and red wine

39
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

40
Q

In which subset of patients is tyramine a problem?

A

Patients taking MAO inhibitors

breakdown of NA is inhibited so accumulates

Pharmacology (10 decks)

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