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Pharmocology > SNS agonists > Flashcards

SNS agonists Flashcards

1
Q

What do SNS agonists do?

A
  • mimic the actions of adrenaline and noradrenaline by stimulating adrenoceptors
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2
Q

What is the molecular mechanism of alpha 1 adrenoceptors?

A

PLC is converted into IP3 and DAG

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3
Q

What is the molecular mechanism of alpha 2 adrenoceptors?

A

decrease cAMP

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4
Q

What is the molecular mechanism of beta 1 and 2?

A

increase cAMP

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5
Q

What effect will beta blockers have on the kidneys?

A

decrease renin release by blocking the B1 receptor - an increase in BP does not happen via the renin-angiotensin-aldosterone system

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6
Q

What effect will the beta blocker have on the heart?

A

the heart is controlled by beta 1 -to have positive inotropic and chronotropic effect
-this cannot happen with a beta blocker

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7
Q

What else will be effected besides the kidneys and heart with a beta blocker drug?

A
  • liver - blocked ability to break down glycogen to generate glucose
  • block the ability of the trachea and bronchioles to dilate
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8
Q

What adrenoceptors regulate blood vessels?

A

alpha 1

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9
Q

Which adrenoceptors can be activated by NA or adrenaline?

A
  • all
  • NA is more selective for alpha receptors
  • adrenaline is more selective for beta receptors
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10
Q

How is noradrenaline synthesized?

A
  • tyrosine from the diet is converted to DOPA by tyrosine hydroxylase
  • DOPA is then converted to dopamine, which is converted to noradrenaline
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11
Q

What receptor helps regulate noradrenaline synthesis?

A

Presynaptic alpha 2 receptors

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12
Q

How do alpha 2 receptors do this?

A

if NA concentration is high in the synapse it will stimulate presynaptic alpha 2 receptors to reduce production of NA and release

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13
Q

What adrenoceptor does phenylephrine favour?

A

alpha 1

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14
Q

what adrenoceptor does clonidine favour?

A

alpha 2

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15
Q

what receptor does dobutamine favour?

A

beta 1

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16
Q

what receptor does salbutamol favour?

A

beta 2

17
Q

what receptor does adrenaline favour ?

A

it is non-selective

bind to alpha and beta

18
Q

What does selectivity depend on?

A
  • CONCENTRATION
  • at low conc. these drugs will be relatively selective but as you increase conc. the chance of binding to other receptors increases
19
Q

How does hypersensitivity occur in the body?

A
  • after first exposure to the antigen your body generates antibodies that circulate around the body and bind to mast cells
  • in subsequent exposure the antigen cross-links with these antibodies and there is a massive release of mediators
20
Q

What are the symptoms of hypersensitivity?

A
  • lots of fluid moving into tissues as endothelial cells in blood vessel membranes move apart
  • fall in circulating fluid volume = fall in BP
  • anaphylactic shock that leads to a collapse in the circulatory system and hence unconsciousness
  • this can also lead to contraction of bronchial smooth muscle and constriction of the muscles around the throat
21
Q

Whys is adrenaline more effective than noradrenaline?

A

breathing- adrenaline acts more on beta receptors than NA which stimulates bronchodilation and relaxation of the throat muscles

  • slows down release of histamine from mast cells
  • tachycardia
  • acts on alpha receptors to get vasoconstriction
22
Q

List the other clinical uses of adrenaline?

A
  • asthma
  • acute bronchospasm associated with chronic bronchitis or emphysema
  • glaucoma
  • cardiogenic shock
  • spinal anaesthesia
  • local anaesthesia
23
Q

List the unwanted actions of adrenaline?

A
  • secretions become reduced and thickened mucus
  • tachycardias, palpitations, arrhythmias
    -cold extremities, hypertension
  • pulmonary oedema
    GIT- minimal
    -skeletal muscle tremor

Overdose can lead to cerebral haemorrhage

24
Q

How is phenylephrine different to adrenaline?

A
  • one hydroxyl group makes it more resistant to breakdown

- more resistant to COMT breakdown but NOT MAO degradation

25
Q

What are the clinical uses of phenylephrine?

A

vasoconstriction
nasal decongestant
mydriatic ( makes the pupil dilate)

26
Q

How does clonidine work?

A
  • stimulate presynaptic alpha 2 receptors
  • less noradrenaline release means there is LESS VASOCONSTRICTION, fall in TPR and BP
  • works on baroreceptors on the brainstem and reduces the sympathetic drive, reducing TPR
  • reduce release on NA in the kidney means reduced renin secretion and angiotensin II production
27
Q

What are the clinical uses of clonidine?

A
  • hypertension

- migraine

28
Q

Which adrenoceptors does isoprenaline favour?

A

beta 1 and beta 2

29
Q

How is isoprenaline different to adrenaline?

A

-less susceptible to uptake 1 and MAO breakdown

30
Q

Clinical uses of isoprenaline?

A
  • cardiogenic shock
  • acute heart failure
  • myocardial infarction
31
Q

What must you be cautious about when using isoprenaline?

A

stimulation of beta 2 receptors in vascular smooth muscle leads to dilation of vessels in the muscles and hence pooling of blood
-reflex tachycardia

32
Q

What are the clinical uses of dobutamine?

A
  • cardiogenic shock

- administration by IV

33
Q

How does salbutamol differ from adrenaline?

A

-relative resistance to COMT and MAO

34
Q

Clinical uses of salbutamol?

A
  • asthma ( beta 2 mediated relaxation of bronchial smooth muscle and inhibition of release of bronchoconstrictor substances from mast cells
  • threatened premature labour ( beta 2 mediated relaxation of uterine smooth muscle)
35
Q

what are the side effects of salbutamol?

A
  • reflex tachycardia
  • tremor
  • blood sugar dysregulation

Pharmocology (16 decks)

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