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Pharmacology CSA236 > Autonomic pharmacy > Flashcards

Autonomic pharmacy Flashcards

1
Q

What is the summary of sympathetic effects?

A

Heart –increase rate and force (b2)

Blood vessels— constriction (a1), dilation (B2)

Bronchi — dilation (b2)

GIT smooth muscle — relaxation (decrease motility) B2

Glands — no effect

Bladder smooth muscle — relaxation (b1)

Eye (pupil) – dilation (contraction of radial muscles) a1
Ciliary muscle — relaxation (far vision) (b2)

Sweat glands – Secretion (but muscarinic)

Lacrimal glands — no effect

Liver — increase in glycogenolysis and gluconeogenis (a1 and b2)

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2
Q

What is the summary of parasympathetic effects?

A

Heart — decrease in rate and force (m2)

Blood vessels — no effect

Bronchi — constriction (m3)

GIT smooth muscle — contraction (increase motility)

Glands — secretion

Bladder smooth muscle – contraction

Eye (pupil)— constriction (contraction of circular muscles)
ciliary muscle – contraction (near vision)

Sweat glands – no effect

Lacrimal glands – secretion

Liver – no effect

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3
Q

what does the autonomic nervous system do?

A

Maintains homeostasis
—-Blood pressure changes from sitting to a standing position

Coordinates responses to external stimuli

  • –Pupil changes in response to light
  • —Fight or flight response

Specific regulatory functions

  • —Contraction and relaxation of vascular and visceral smooth muscle
  • —Cardiovascular reflexes
  • —All exocrine and some endocrine secretions
  • —-Energy metabolism, particularly in the liver and skeletal muscle
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4
Q

What is the somatic efferent pathway?

A

a single motor neuron connects the CNS

to the skeletal muscle fibre

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5
Q

What is the autonomic efferent pathways?

A

consist of two neurons arranged in
series (with one exception – adrenal medulla)

The two neurons in the autonomic pathway are known as pre-
ganglionic and post-ganglionic.

Autonomic ganglia contain the nerve endings of preganglionic fibres
and the cell bodies of postganglionic neurons.

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6
Q

What does the parasympathetic nervous system do?

A

controls the rest and digest

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7
Q

How does the parasympathetic system direct ‘house keeping’ activities?

A

Directs ‘house keeping’ activities via the neurotransmitter acetylcholine

  • –Maintains resting heart rate
  • —Aids digestion (e.g. ↑ GI motility, gastric acid secretion)
  • –“SLUD” (salivation, lacrimation, urination, defecation)
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8
Q

What does the preganglionic and postganglionic neurons do in the parasympathetic nervous system?

A

Preganglionic neurons release acetylcholine (ACh)
—-ACh acts on nicotinic receptors in cell body of postganglionic neuron

Postganglionic neurons also release ACh
—ACh acts on muscarinic receptors on the effector tissue

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9
Q

What is a neurotransmitter?

A 
A neurotransmitter is 
chemical substance that is 
released at the end of a 
nerve fiber following an 
impulse to diffuse across 
the synapse or junction. 
Binding to a receptor 
causes the transfer of the 
impulse to another nerve, a 
muscle, or some other 
structure.
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10
Q

What is an example of a neurotransmitter involved in cholinergic transmission?

A 
Neurotransmitter: acetylcholine (Ach).
----widely distributed in the body:
---CNS
---ANS
---Somatic nervous system (voluntary control of 
skeletal muscles).
----Enteric nervous system

Cholinergic receptors are activated by
acetylcholine, and include:
—Nicotinic receptors, and
—-Muscarinic receptors.

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11
Q

What is the nicotinic Ach receptor?

A

Location

—Skeletal muscle (causing contraction)
—-Autonomic ganglia (allowing neurotransmission to continue between pre- and post-ganglion neurons)
—-Adrenal medulla (causing the release of
adrenaline)
—-Many regions of the CNS (excitatory)

Ligand-gated Na+ channel

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12
Q

What are the three locations of the Muscarinic receptor?

A

M1. receptors (‘neural’)
—–CNS, peripheral neurons and gastric parietal
cells

M2 receptors (‘cardiac’)
—-Heart, also presynaptic terminals of peripheral
and central nerves
—-Decreased heart rate and contractility and
causes neuronal inhibition (auto-inhibition)

M3 receptors (‘glandular/smooth muscle’)
—-Smooth muscle and glands
—Contraction of visceral smooth muscle,
relaxation of vascular smooth muscle and
glandular secretion

—G-protein coupled
receptor

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13
Q

What is the m1 receptor?

A

‘neutral’

Mainly found in the CNS, peripheral neurons and gastric parietal cells

receptor activation causes neuronal excitation and gastric secretion

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14
Q

What is the m2 receptor?

A

‘cardiac’

found mainly in the heart, also the presynaptic terminals of peripheral and central nerves

receptor activation causes decreased HR and contractility and causes neuronal inhibition (auto-inhibition)

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15
Q

What is the m3 receptor?

A

‘glandular/smooth muscle’

—found on smooth muscle and glands

—receptor activation causes contraction of visceral smooth muscle, relaxation of vascular smooth muscle and glandular secretion

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16
Q

Parasympathetic effects (muscarinic)

A

M2 —- heart: reduced HR and reduced contractility

M3 —- smooth muscle: contraction, lung, bladder, GI, eye

M3—— Exocrine glands: secretion, salivation, lacrimation

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17
Q

Parasympathetic nervous system effects. M3 smooth muscle

A

M3 - smooth muscle

blood vessels – no parasythathic control but drugs can cause dilation

Bronchial — bronchoconstriction

GI smooth muscle – defacetaion

Bladder smooth muscle — urination

Eye (pupil) — constriction
Eye (ciliary muscle) – near vision

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18
Q

Parasympathetic nervous system effects M3 exocrine glands?

A

M3 exocrine glands

Sweat glands —- no parasympathetic control ut muscarinic receptors response to sympathetic control

Lacrimal glands — increased tears

Salivary glands — increased salivation

Bronchial glands — mucous secretion

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19
Q

What is the sympathetic nervous system?

A

The sympathetic nervous system controls the ‘fight or flight’
response:

↑HR and BP, increased blood supply skeletal muscle, bronchodilation,
pupil dilation, ↑sweating, ↑ energy metabolism

—Preganglionic neurons release acetylcholine (ACh)

—-ACh acts on nicotinic receptors in cell body of postganglionic neuron

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20
Q

What do most postganglionic neurons release in the sympathetic nervous system?

A

Most postganglionic neurons release noradrenaline (NA)

—NA acts on α- or β-receptors on the effector tissue

Exceptions:

  • innervation of sweat glands: ACh acts on muscarinic receptors
  • innervation of adrenal medulla: ACh acting on nicotinic receptors
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21
Q

What is involved in the noradrenergic transmission?

A

In noradrenergic transmission, noradrenaline is the neurotransmitter.

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22
Q

What is the function of Noradrenaline in the CNS and PNS?

A

Noradrenaline (NA) is present in the central peripheral nervous systems:

—-In the central nervous system, its functions are related to arousal, mood and regulation of blood pressure.

—-In the peripheral nervous system, its functions are associated with the sympathetic nervous system

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23
Q

What completes the activity of noradrenaline?

A

The activity of noradrenaline is complemented by adrenaline, a hormone
secreted by the adrenal medulla.

Noradrenergic receptors (or adrenoceptors) are activated by noradrenaline and
adrenaline, and include:
——α receptors, and
—–β receptors

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24
Q

What are alpha noradrenergic receptors and what do they do?

A

Alpha

a1 receptor— mainly found on smooth muscle (increase contraction)
Activation causes release of intracellular ca2+ stores —- excitatory effects.

a2 receptor— located presynaptically ( presynaptic inhibition of noradrenaline release)

—activation causes inhibitory effects

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25
Q

What are the Beta noradrenergic receptors and what do they do?

A

Beta

b1 receptor —- mainly located on cardiac muscle — increased HR and contractility
—Activation causes increased ca2+ conductance

b2-receptor —- mainly on smooth muscle (relaxation)

— activation causes phosphorylation of intracellular proteins

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26
Q

sympathetic nervous system effects of a1?

A

a1

Blood vessels, skin — contraction — internal organs in the main cavities of the body

Pupil — contraction — dilation (mydriasis)

Liver —– increase glycogenolysis and glucogenogensis

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27
Q

sympathetic nervous system effects of a2?

A

a2

GI smooth muscle — relaxation, decrease motility

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28
Q

sympathetic nervous system effects of b1

A

b1

heart — increase rate and force of contraction

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29
Q

sympathetic nervous system effects of b2

A

B2

Smooth muscle relaxation

  1. Bronchi – bronchidilation
  2. GI – decrease motility
  3. Bladder - decrease urination
  4. eye: ciliary muscle - far vision

B2
Liver - increase in glycogenolysis and gluconeogenesis

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30
Q

Parasympathetic nervous system. What do the pre and post-ganglionic neurons release?

A

Preganglionic neurons release acetylcholine (ACh)
—-ACh acts on nicotinic receptors in cell body of postganglionic neuron

Postganglionic neurons also release ACh
—-ACh acts on muscarinic receptors on the effector tissue

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31
Q

What does the neuromuscular junction consist of?

A
  • —–The presynaptic terminal of a motor neuron
  • —The synaptic cleft
  • —-The postsynaptic membrane of a skeletal muscle cell

The efferent neuron releases acetylcholine, which binds to
nicotinic receptors on skeletal muscle

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32
Q

What are non-polarising blocking drugs at the NMJ?

A

Non-depolarising blocking drugs e.g. atracurium, pancuronium etc.

—-Block nicotinic receptors and depolarisation cannot occur

Non-depolarising and depolarising NMJ-blocking drugs are used clinically as adjuncts to general anaesthesia

Blockade of NMJ can be an adverse effect of drugs, poisons and venoms e.g. curare

Botulinum toxin
—Blocks release of Ach and prevents contractions: used in muscle spasticity

33
Q

What are depolarising blocking drugs?

A

suxamethonium

—Activate nicotinic receptors and depolarisation block
—Nicotinic receptors are activated result in initial twitching
—Continued receptor activation activated and muscle cells stay in their refractory
period and are no longer excitable

34
Q

What is pilocarpine?

A

Muscarinic agonist

—–Treats glaucoma (ocular administration) –contraction of ciliary body and miosis;
Aqueous humor can drain more easily via
Canal of Schlemm

—-Adequate lipid solubility to cross conjunctival membrane

—-Ocular adverse effects: ↓ night vision,
reduced distant vision

—–Systemic adverse effects rare with correct
administration

35
Q

What does the muscarinic agonist bethanechol do?

A

—Treats bladder and GI hypotonia

—Administered orally

—Systemic adverse effects possible with large doses

36
Q

What is an example of a muscarinic receptor antagonist?

A

Competitive antagonists
—block muscarinic receptor

Naturally occurring

  • –Deadly nightshade (Atropa
    belladonna) → atropine

—Thorn apple (Datura
stramonium) → hyoscine
(scopolamine)

—Lipid soluble – posing produces CNS effects as well as peripheral effects

37
Q

What effects do antimuscarinic have on CNS?

A

Low doses: mild sedation, confusion. high doses: agitation, disorientation, fever

38
Q

What effects do antimuscarinic have on cardiovascular?

A

Increased HR at rest (e.g. to 80-90bpm – loss of existing parasympathetic tone)

39
Q

What effects do antimuscarinic have on visceral smooth muscle?

A

GI - Decreased GI motility (constipation)

Bladder - relaxation (urinary retention)

Lungs - Relaxation of bronchial smooth muscle (bronchodilation)

40
Q

What effects do antimuscarinic have on eye?

A

Relaxation of ciliary muscle → cycloplegia (paralysis of accommodation) – distant
vision facilitated, near vision impaired

Relaxation of constrictor pupillae muscle → mydriasis, increased IOP (only important in glaucoma patients)

41
Q

What effects do antimuscarinic have on exocrine glands?

A

Inhibition of secretions (dry mouth, eyes and skin)

42
Q

what is one example of an antimuscarinic?

A

Atropine (carried by paramedics)

—Non-selective, lipid soluble muscarinic receptor antagonist.

—Indications: e.g. bradycardia, organophosphate poisoning (neuromuscular blockade) (iv injection).

—Adverse effects: tachycardia, arrhythmias, constipation, urinary retention, dry mouth,
dry eyes, blurred vision, confusion.

—-Precautions: atrial fibrillation, glaucoma

43
Q

An example of antimuscarinic other than Atropine?

A

Ipratropium (Atrovent) (carried by paramedics)

—-Non-selective, water soluble muscarinic receptor antagonist.

Indications: bronchospasm associated with asthma or COPD (inhaled).

Adverse effects: similar to atropine, but only in high doses.

Precautions: glaucoma (avoid contact with eyes).

NB: Does not work immediately – must be used with an immediate-acting
bronchodilator (salbutamol).

Tiotropium (Spiriva) used chronically in COPD

43
Q

An example of antimuscarinic other than Atropine?

A

Ipratropium (Atrovent) (carried by paramedics)

—-Non-selective, water soluble muscarinic receptor antagonist.

Indications: bronchospasm associated with asthma or COPD (inhaled).

Adverse effects: similar to atropine, but only in high doses.

Precautions: glaucoma (avoid contact with eyes).

NB: Does not work immediately – must be used with an immediate-acting
bronchodilator (salbutamol).

Tiotropium (Spiriva) used chronically in COPD

43
Q

An example of antimuscarinic other than Atropine?

A

Ipratropium (Atrovent) (carried by paramedics)

—-Non-selective, water soluble muscarinic receptor antagonist.

Indications: bronchospasm associated with asthma or COPD (inhaled).

Adverse effects: similar to atropine, but only in high doses.

Precautions: glaucoma (avoid contact with eyes).

NB: Does not work immediately – must be used with an immediate-acting
bronchodilator (salbutamol).

Tiotropium (Spiriva) used chronically in COPD

44
Q

How do anticholinesterase drugs work?

A

Muscarinic effects can be achieved by either binding to the M
receptor (agonists), or by increasing the ACh lifetime (decreasing
degradation)

Inhibit the enzyme acetylcholinesterase which normally deactivates
ACh

Increased ACh at cholinergic synapses → enhanced ACh transmission

Increased ACh at NMJ → increased muscle contraction….. But with high
doses: depolarisation block and paralysis

45
Q

Examples of anticholinesterases?

A

Neostigmine and pyridostigmine

  • —Water-soluble compounds that cannot cross the BBB.
  • —Tend to affect the neuromuscular junction more than the autonomic nervous system.
  • —Used to treat myasthenia gravis (an autoimmune disease where antibodies destroy nicotinic receptors at the NMJ) or reversal of neuromuscular blockers following surgery
46
Q

What is physostigmine and what does it do?

A

Anticholinesterase
Physostigmine

  • –Lipid soluble (crosses the BBB).
  • —Tends to affect the autonomic nervous system more than the neuromuscular junction.
  • —Used to treat antimuscarinic poisonin
47
Q

What are Donepezil, galantamine, rivastigmine and what do they do?

A

Lipid soluble (crosses the BBB), used to treat Alzheimer’s disease (degeneration of cholinergic neurons in the the hippocampus and frontal cortex)

48
Q

What are organophosphates and what do they do?

A

Highly lipid soluble (absorbed through the skin and crosses the BBB).

  • —Irreversibly inhibits AChE.
  • —Used as pesticides, chemical warfare
49
Q

When to use AChE inhibitors - antimuscarinic poisoning?

A

Ingestion of deadly nightshade or thorn apple, or overdose of medical
antimuscarinics:

Excitement, irritability, hyperactivity, agitation, disorientation, considerable rise in body temperature (accentuated by loss of sweating)

Peripheral antimuscarinic effects

50
Q

What is the antidote for antimuscarinic poising?

A

Antidote: physostigmine (hospital treatment)

Inhibit AChE

  • -increase ­amount of ACh in synapse
  • —Competitively overcomes block
  • –Physostigmine is a lipid soluble anticholinesterase: crosses BBB

Remember: Distribution of antidote in the body must match the distribution of
poison in the body

51
Q

What is AChE inhibitor poisoning?

A

Organophosphate poisoning

Causes

Accidental: farm workers (organophosphate insecticides)

Warfare/terrorism: e.g. sarin gas, Novichok, VX

52
Q

Symptoms of organophosphate poisoning?

A

Autonomic cholinergic effects:
—–Severe bradycardia, hypotension, bronchoconstriction, diarrhoea, pupil constriction,
sweating, salivation etc.

Depolarising neuromuscular junction blockade:
—-Motor and respiratory paralysis.

Excess ACh transmission in the CNS:

  • –Initial excitation → convulsions.
  • –CNS depression → unconsciousness.

Neurotoxicity:
—-Peripheral nerve demyelination → progressive weakness and sensory loss (unrelated
mechanism)

53
Q

What is Obidoxime?

A

Used to treat organophosphate poisoning by “luring” the poison away from
AChE (chemically binds the organophosphate)

Needs to be used promptly

After a few hours, the organophosphate-enzyme bond strengthens and obidoxime can no longer win the competition

54
Q

Why is obidoxime not the ideal antidote?

A

Not the ideal antidote: does not cross BBB.

—-Needs to be used with atropine to treat CNS effects and augment treatment of peripheral effects (obidoxime and atropine in ComboPen auto-injector).

Atropine is a muscarinic antagonist, and will block the effects of excess ACh at
muscarinic receptors.
ìIt will have no effect at the NMJ (nicotinic receptors).

NOTE: Atropine carried by Tas paramedics, obidoxime and atropine carried by NSW paramedics

55
Q

What is the first step in noradrenergic transmission?

A

Preparation

Uptake of precursor (tyrosine), synthesis of NA

Uptake of NA into synaptic vesicles via vesicular monoamine transport (VMAT)

56
Q

What is the second step in noradrenergic transmission?

A

Depolarisation

— influx of ca2+

57
Q

What is the third step in noradrenergic transmission?

A

Release of transmitter by exocytosis

  • –diffusion to postsynaptic membrane
  • —binding to postsynaptic receptors
  • – Binding with presynaptic receptors (a2 auto-inhibitory receptors)
58
Q

What is the fourth step in noradrenergic transmission?

A

Clean-up

— Reuptake of transmitter by nerve terminal via uptake 1 (recycles 75% of NA)

—Uptake of transmitter by non-neuronal cells via uptake 2

59
Q

What are the cardiovascular effects of a and b agnonist?

A

A - contraction vascualr smooth muscle

B
B1 - increased HR and contractility
B2- relaxation of smooth muscle

60
Q

What agnostics are involved with adrenaline?

A

a and b agonist

combination of both actions

61
Q

Wat are agonists are involved in Noradrenaline?

A

Predominantly α-agonist (no β2 effect)

  • —Vasoconstriction
  • —Increased systolic and diastolic pressure
  • –Reflex bradycardia
62
Q

What are the agonists involved in Isoprenaline?

A

Predominantly β-agonist
• Vasodilation β2
• Increased cardiac force and rate
• Fall in mean arterial pressure

63
Q

What are some drugs affecting noradrenergic transmission?

A

Sympathomimetics –mimic the effects of the SNS

—-a1 , β1, β2 agonists

Indirect-acting sympathomimetics

  • –Uptake 1 inhibitors
  • –MAO inhibitors (old antidepressants)

Sympatholytics –block the effects of the SNS
—a1 antagonist, a2 agonists, β1/ β2 antagonists

64
Q

What is an example of a sympathomimetic?

A

Adrenaline(carried by paramedics)

—Non-selective α and β receptor agonist.

Indications: asystole, inadequate perfusion, bradycardia, anaphylaxis, severe asthma, severe croup (iv injection / iminjection / inhaled, depending on indication and severity).

Adverse effects: tachycardia, arrhythmias, hypertension, pupil dilation, hyperglycaemia, anxiety, nervousness, tremor.

Precautions: any medical condition that may be worsened by the adverse effects

65
Q

What is another example of a sympathomimetic?

A

Salbutamol(carried by paramedics)

Selective β2 receptor agonist.

Indications: respiratory distress with suspected bronchospasm –asthma, COPD, severe allergic reactions, smoke inhalation (inhaled or iv injection depending on severity / access).

Adverse effects: tachycardia, arrhythmias, nervousness, tremor (usually only with iv or high-dose inhaled).

Precautions: any medical condition that may be worsened by the adverse effects

66
Q

Information about sympathomimetics?

A

Topical administration as nasal and ocular decongestants (e.g.
phenylephrine, naphazoline)

a1 agonist—vasoconstriction

—-shrinkage of swollen mucous membranes

—-decongestion of nose and eyes in colds and allergies

Caution: prolonged topical use result in rebound congestion

Combination of local ischaemia and receptor down regulation (fewer
receptors, diminished responsiveness)
—-Rapid tachyphylaxis(tolerance) to drug
—-Use only for 3-5 days at a time

67
Q

What is an example of a oral decongestant sympathomimetic?

A

Phenylephrine: selective a1 agonist

Pseudoephedrine: a1 agonist and indirect acting
sympathomimetic: increases amount of noradrenaline in synapse
(see next slide)

—non-selective sympathomimetic effects
—-CNS and cardiac stimulation, increased blood pressure,
hyperglycaemia(topical safe).
13

68
Q

What are indirect-acting sympathomimetics?

A

Amphetamine, pseudoephedrine, tyramine

Transported into nerve terminals by uptake 1
—-Taken up into vesicles by vesicular monoamine
transporter (VMAT)
—- increase NA available to act on adrenoceptors

Non-specific sympathomimetic effects:
bronchodilation, increase BP, increase HR, increase force of myocardial
contraction, decrease GI motility, CNS stimulation
(potential for abuse)

69
Q

What are other sympathomimetics?

A

Tricyclic antidepressants, cocaine: block uptake 1
—- Increase amount of noradrenaline in synapse
—-Lipophillic: cross blood-brain-barrier
Noradrenaline accumulates –treatment of depression

MAO-inhibitors: phenelzine and tranylcypromine
—-Inhibit the enzyme monoamine oxidase (responsible for breaking
down noradrenaline)
—-Noradrenaline accumulates –treatment of depression (rarely used
now)

70
Q

What are selective a1-receptor antagonists?

A

Prazosin(short half-life), terazosin, tamsulosin: longer half-
lives allow once-daily dosing

Highly selective for a1-receptors

  • –cause vasodilation and fall in arterial blood pressure
  • —relaxation of the smooth muscle of bladder neck and prostate

Clinical use

  • – Hypertension (other agents preferred)
  • –Benign prostatic hypertrophy (BPH)
  • – Incidence increases in males > 50 years
71
Q

What are cardiovascular use of B - antagonists?

A

E.g. metoprolol and atenolol (relatively cardioselective) and propranolol

Ischaemic heart disease
—Decreased HR reduction of myocardial O2 demand

— Arrhythmias
 Reduction in myocardial contractility

—Hypertension
 Decreased HR and myocardial contractility  decreased afterload

Congestive heart failure

  • –Cardiac output insufficient to meet body’s circulatory needs
  • –SNS activity increases in attempt to increase cardiac output
  • –Maintained SNS activity -down-regulation of receptors and deleterious positive feedback cycle
  • –b-blockers antagonise the adverse effects of excessive activation of SNS

Caution: bradycardia (start low, go slow)
18

72
Q

What are some other uses of b-antagonists?

A

Anxiety (propranolol)
—-Control of somatic symptoms, eg. tremor (b2), tachycardia (b1), palpitations (b1).

Hyperthyroidism

  • –Thyroid hormones up-regulation of b-receptors.
  • – b-blockers control symptoms of hyperthyroidism (tremor, tachycardia, palpitations, agitation).

Glaucoma

  • –Timolol eye drops reduce formation of aqueous humor
  • –Non-selective -blocker
  • – Contraindicated in asthma, COPD as systemic side effects are possible.
Migraine prophylaxis (propranolol)
---The precise mechanism of action of b-blockers in prevention of migraine is unknown.
19
73
Q

What are some adverse effects of b-receptor antagonists?

A

Bronchoconstriction
—-Of little significance in the absence of airways disease, but can be life-
threatening in asthmatic and COPD patients (b2)

Bradycardia and cardiac depression
—-Can lead to signs of heart failure or life-threatening heart block, particularly
in the elderly (b1)

Fatigue
—Reduced cardiac output (b1) and skeletal muscle perfusion (b2) in exercise

Cold extremities
—Loss of b2-receptor-mediated vasodilation in cutaneous vessels

Nightmares
—CNS action (less likely with atenolol: lower lipid solubility)
20

74
Q

How does b-receptor antagonist cause hypoglycemia?

A

Low blood glucose —-SNS stimulation

Activation of β1-receptors Increased HR

Activation of β2-receptors –tremor

Activation of β2-receptors also —increased gluconeogenesis and
glycogenolysis in the liver

75
Q

What are precautions to the use of B-blockers?

A 
Asthma and COPD
Bradycardia
Uncontrolled heart failure
Peripheral vascular disease
Diabetes
76
Q

What are some centrally acting a2-agonist?

A

Clonidine, methyldopa: Selective a2-agonists: activate a2-
receptors in the medulla and inhibit NAD release (decrease SNS outflow)

Lowers blood pressure
—-Methyldopa used for hypertension in pregnancy (safer than other
drugs)

Sedation, analgesia, anxiolytic
—-Clonidine used in ADHD, adjunct to anaesthesia, drug withdrawal
(alcohol/opiates), menopause (hot flushes)

77
Q

What are some important things to know concerning centrally acting a2-agonists?

A

Prevent sudden drug cessation

Normal activation of SNS —sudden and dangerous increase in BP
(rebound hypertension)

Withdrawal syndrome: rapid rise in BP, headache, flushing, sweating,
insomnia, agitation and tremor

Adverse effects are common: drowsiness, fatigue, bradycardia,
dizziness (all due to decreased SNS activity)

Pharmacology CSA236 (3 decks)

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