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Pharmacology > Block 3 ANS neuro SG+slides > Flashcards

Block 3 ANS neuro SG+slides Flashcards

1
Q

ANS neurotransmission

A

sympathetic and parasympathetic

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2
Q

sympathetic

A

preganglionic fibers-short
acethylcholine-nicotinic receptor
posganglionic fibers- NE noropinephrine-Aplha & Beta
-involves with ‘fright/flight/fight’ response to stress or arousal

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3
Q

parasympathetic

A

long-acetycholine
nicotinic
posganglionic- Ach- muscarinic rec.

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4
Q

Cholinergic receptors

A

nicotinic and muscarinic

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5
Q

what are adrenergic/muscarinic receptors

A

they are on effector tissues (cardiac,smooth muscle,glands)

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6
Q

ANS drugs bind to adrenergic receptors on effectors and stimulate fight/flight response are?

A

adrenergic agonist & sympathomimetics

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7
Q

ANS drugs that bind to adrenergic receptors on effectors and block fight/flight response are?

A

adrenergic antagonist & sympatholytics

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8
Q

ANS drugs that bind to muscarinic receptors on

effectors and stimulate a rest/digest response:

A

cholinergic/muscarinic agonists & parasympathomimetics

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9
Q

ANS drugs that bind to muscarinic receptors on

effectors and block a rest/digest response:

A

Cholinergic/Muscarinic antagonists and

parasympatholytics

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10
Q

what are adrenergic receptors

A

All adrenoreceptors are similar in structure and belong to the family
of G-protein-coupled receptors

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11
Q

Alpha receptors:

A

a1- sympathetic effector tissue:brain

a2- presynaptic neuron

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12
Q

Beta receptors

A

b1- sympathetic effector tissue-heart,adipose tissue,GI tract,renal aterioles
b2- mast cells;brain
b3- adipose tissue

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13
Q

Non-selective Adrenergic Agonists MOA

A

Bind to α and β receptors
and stimulate a sympathetic nervous system
response

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14
Q

Clinical Uses

A

Treatment for cardiac arrest, hypotension, shock

• Management of acute anaphylaxis

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15
Q

Non-selective Adrenergic Agonists drugs

A

adrenaline
noradrenaline
ephedrine
dopamine

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16
Q

α1-Adrenergic Agonists MOA & drugs

A

Bind to α1 receptors and stimulate a sympathetic nervous system response
-phenylephrine

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17
Q

Clinical Uses

A

Treat hypotension, nasal congestion, red eyes (by
promoting vasoconstriction)
• Also used as a vasoconstrictor administered in combination with local anaesthetic

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18
Q

a1-Agonist : Common Adverse Effects

A
  • Hypertension
  • Blurred vision
  • Constipation
  • Urinary retention
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19
Q

α1-Adrenergic Antagonists MOA & drugs

A

Bind to α1 receptors and block a sympathetic nervous system response
- doxazosin

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20
Q

Clinical Uses?

A

Treat mild-moderate hypertension, decreases urinary retention in benign prostatic hyperplasia

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21
Q

Adverse Effects

A

Postural hypotension, urinary frequency, erectile

disorders, nasal congestion, fatigue

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22
Q

β1-Adrenergic Agonists MOA & drug

A

Bind to β1 receptors and stimulate a sympathetic nervous system response
• dobutamine

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23
Q

Clinical Uses?

A

Treat cardiac arrest, circulatory shock, hypoperfusion (by increasing heart rate and stroke volume)

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24
Q

Common adverse effects:

A

hypertension, tachycardia, constipation

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25
Q

β2-Adrenergic Agonists MOA & drugs

A

Bind to β2 receptors and stimulate a sympathetic nervous system response
• salbutamol, terbutaline, salmeterol, formoterol

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26
Q

• Clinical Uses?

A

• COPD, asthma (by promoting bronchodilation); stop premature labour (tocolytic)

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27
Q

Common adverse effects:

A

Fine muscle tremor, tachycardia, ↑ blood glucose

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28
Q

β–antagonists/ Beta-blockers MOA & drugs

A

Bind to β receptors and block a sympathetic nervous system response
-carvedilol, labetalol

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29
Q

• Clinical Uses?

A

• Cardiac disease, hypertension, migraine prophylaxis

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30
Q

β–antagonists/ Beta-blockers

Examples of b1 cardio-selective blockers

A

metoprolol, atenolol

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31
Q

Clinical Uses?

A

Ischemic Heart Disease -
Lowering of HR and force of contraction. Lessens work of heart
Hypertension - Effective only in hypertensive patients
Drop in BP is gradual
Reflex vasoconstriction is preserved. Less postural hypotension

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32
Q

Adverse Effects:

A
  • Dizziness
  • Lethargy
  • Insomnia
  • Diarrhoea
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33
Q

α2-Agonists-neg feedback mechanism

A

Majority of α2 receptors are located on the presynaptic neuron – binding of drugs to
these receptors stops release of more
catecholamines

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34
Q

Clinical Uses?
clonidine
apraclonidine

A

Clonidine and its derivative Apraclonidine are selective α2 receptor agonists. They block sympathetic nerve transmission associated with vasomotor tone

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35
Q

what is Clonidine used for?

A

hypertension

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36
Q

what is apraclonidine used for?

A

used as an adjunct in controlling glaucoma

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37
Q

Adverse effects

A

dizziness, drowsiness, dry nose/ mouth, nausea

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38
Q

Nicotinic receptors:

A

respond to stimulation by

nicotine

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39
Q

Muscarinic receptors:

A

respond to Muscarinic

extract obtained from toadstool mushroom. 5 subtypes M1-M5

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40
Q

where is nicotinic receptors found?

A

in the brain, autonomic ganglia , neuromuscular junction (skeletal muscle), adrenal medulla

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41
Q

where is muscarinic receptors found?

A

in all parasympathetic effectors

42
Q

what is anticholinesterases?

A
  • acetylcholine esterase inhibitors
43
Q

Muscarinic Agonist Drugs MOA & drugs

A

Bind to muscarinic receptors and stimulate
a parasympathetic nervous system response
-acetylcholine, pilocarpine

44
Q

Clinical Uses?

A

Miotics (by constricting pupils) for cataract surgery;

decrease intraocular pressure in glaucoma (by increasing drainage of aqueous humour)

45
Q

Common adverse effects:

A

Problems with eye accommodation; can get salivation or bronchospasm at high doses

46
Q

Nicotinic Agonists

A

Binding of nicotinic agonists to nicotinic receptors

47
Q

Nicotinic Agonists- Centrally in the brain

A

feeling of well-being and

relaxation

48
Q

Nicotinic Agonists- All autonomic ganglia

A

> Increase in autonomic tone
resulting in increased activity of both sympathetic
and parasympathetic nervous system

49
Q

Nicotinic Agonists-Adrenal Medulla

A

Release of adrenaline causing increased sympathetic activity

50
Q

Nicotinic Agonists-Skeletal Muscle

A

Depolarises skeletal muscle cells

51
Q

Nicotinic Agonists two main uses

A

-assist smoking cessation
(nicotine patch, gum, lozenge)
-short-acting muscle relaxant

52
Q

Nicotinic Agonist –

Depolarizing Muscle Relaxant MOA

A

Mimics ACh and binds to nicotinic receptors at the neuromuscular junction – causes a quick muscle contraction following by relaxation (AND short-lived blocking of the receptor to further stimulation)

53
Q

nicotinic agonist drug and clinical use

A

-suxamethonium

Short acting muscle relaxant for endoscopy, intubation or orthopaedic reductions

54
Q

Adverse effects

A

muscle spasms, hyperkalemia and malignant hyperthermia

55
Q

Anticholinesterase Drugs & MOA

A

Inhibits the enzyme acetylcholine esterase, effectively increasing the amount of ACh and hence cholinergic effects.

  • pyridostigmine
  • neostigmine
56
Q

Clinical Uses?

A

– Treat Myasthenia gravis

– Post-op reversal of neuromuscular blockade and treatment of urinary retention

57
Q

Adverse Effects

A

salivation, diarrhoea, bradycardia, hypotension, bronchospasm, urinary urgency

58
Q

Muscarinic Antagonists

A

antimuscarinics or anticholinergics

59
Q

Muscarinic Antagonists MOA & drugs

A

binds to muscarinic receptors and blocks
ACh from binding; inhibits a parasympathetic response
-atropine
-glycopyrronium

60
Q

Clinical Uses: atropine

A

“Pre-med” pre-surgery to counter-balance the effect of
vagal nerve stimulation associated with general
anaesthesia; decreases respiratory secretions
• Dilation of the pupil prior to eye surgery
• Antidote for organophosphate poisoning

61
Q

Clinical uses: glycopyrronium

A

treatment of gastric ulcers or pre-med (by decreasing gastric secretions)
• treatment of asthma/COPD - long-acting muscarinic antagonist
asthma inhaler/LAMA (by promoting bronchodilation)

62
Q

Clinical uses: ipratropium

A

treatment of asthma/COPD – short-acting muscarinic antagonist inhaler/SAMA (by promoting bronchodilation)

63
Q

clinical uses: benzatropine

A

anticholinergic drug use to Treatment of Parkinson’s disease (crosses blood-brain
barrier to reduce tremor and rigidity by fixing balance
of dopamine/acetylcholine activity)

64
Q

clinical uses: hyoscine

A

Treatment of GI spasm or nausea/vomiting

65
Q

Typical anticholinergic adverse effects

A
  • Dry Mouth
  • Blurred vision
  • Urinary retention
  • Constipation
  • Tachycardia
66
Q

Nicotinic Antagonists -

Non Depolarizing Muscle Relaxant MOA & drug

A

binds to nicotine receptors at neuromuscular junction and blocks ACh from binding and leads to complete paralysis of the muscle
-rocuronium

67
Q

Clinical Uses?

A

Pre-med for neuromuscular blockade (muscle relaxant) -
slower onset of action and longer half life than
suxamethonium so can be used for longer procedures

68
Q

Adverse Effects:

A

Decreased BP (then reflex tachycardia – Marey’s Law!

69
Q

what are organophosphates?

A

anticholinesterases

acetylcholinesterase inhibitors

70
Q

What would happen to a person who is poisoned with

organophosphates?

A

mnemonic SLUDGEM (Salivation, Lacrimation, Urination, Defecation, Gastrointestinal motility, Emesis, Miosis)

71
Q

What would the antidote be?

A

atropine

72
Q

stimulation of the sympathetic nervous system results in

A

an increase in heart rate and blood pressure and dilation of the bronchioles to the lungs promoting an increased supply of oxygen to the tissue.

73
Q

stimulation of Parasympathetic nervous system

A

opposite stimulation. ‘rest and repose’. Blood pressure and heart rate drop, less
oxygen is needed so the bronchioles constrict while increased blood flow
is supplied to the digestive system with concurrent stimulation of peristalsis and increased release of digestive secretions such as saliva.

74
Q

drugs that stimulate sympathetic NS are

A

sympathomimetics- mimic

the neurotransmitter involved in the sympathetic nervous system and produce a sympathetic nervous system response.

75
Q

Drugs that stimulate the parasympathetic nervous system

A

parasympatholytics- they block the parasympathetic

nervous system response.

76
Q

MOA of ANS drugs

A

(neuron) receives impulses/input signals at specialized projections termed dendrites. If the stimulus reaches a threshold, a nerve
impulse (action potential) will be conducted down the axon to the terminal branches, stimulating the release of specialised chemical messenger molecules called neurotransmitters

77
Q

noradrenaline binds only to

A

adrenergic receptors.

78
Q

Adrenergic receptors are found on

A

effectors in the sympathetic nervous system

79
Q

adrenergic antagonists are drugs that will bind to

A

adrenergic receptor and stop the neurotransmitter,

noradrenaline from binding.

80
Q

Removal of Neurotransmitters from the Synaptic Cleft

A

To avoid continual stimulation by neurotransmitters remaining in the synaptic cleft forever removal mechanisms must exist.

81
Q

There are two main mechanisms used for this: Re-uptake

A

of the released neurotransmitter by the neuron that released
it.eg. one way in which noradrenaline is removed is by the amine re-uptake pump located on the presynaptic neuron (the neuron in which noradrenaline was released from).

82
Q

There are two main mechanisms used for this: Enzymatic breakdown

A

by the action of enzymes that degrade or breakdown the neurotransmitter. eg.enzyme
acetylcholinesterase breaks down the neurotransmitter acetylcholine.

83
Q

how is noradrenaline removed?

A

y removed by both mechanisms. It is removed from the synapse by the amine re-uptake pump and then degraded by an enzyme called monoamine oxidase.

84
Q

If a drug inhibits or blocks the enzymes involved in neurotransmitter breakdown the neurotransmitter is going to be around for longer.

A

result of this will be prolonged stimulation of the receptors and hence further
stimulation of either the parasympathetic or sympathetic nervous system

85
Q

Each neurotransmitter has a process for its removal after release.

A

Drugs may selectively modify this process.

86
Q

Neurotransmitters transmit impulses between what?

A

neurons or from a

neuron to an effector tissue.

87
Q

drugs may do what to neurotransmitter

A
  • mimic
  • block neurotransmitter’s receptor
  • affect concentrations
88
Q

Neurotransmitters vary between different nerve tracts.

A

key ones are acetylcholine (binds to cholinergic receptors) and noradrenaline (binds to adrenergic receptors). Depending on their molecular shape, drugs may also bind to these receptors. This enables drug action to be more
specific.

89
Q

what is dopamine and where can it be found?

A

a neurotransmitter found in the CNS

90
Q

what is the clinical use of dopamine?

A

restoring circulation and tissue perfusion in circulatory shock

91
Q

Adrenergic Adverse Effects occur how?

A

occur as a result of
drug action on adrenergic receptors at sites other than where the desired
effect is wanted.

92
Q

What is the role of the 2-receptors?

A

Binding of noradrenaline to the 2-receptor results in inhibition of further release of neurotransmitter from the same axon terminal

93
Q

what is a Apraclonidine?

A

It is a selective 2-

agonist used to treat glaucoma

94
Q

how is Acetylcholine released?

A

released in a cholinergic synapse, diffuses across and

combines with a postsynaptic cholinergic receptor.

95
Q

what is Autonomic ganglion ?

A

continuation of impulse to postganglionic fibres in BOTH the sympathetic and parasympathetic fibres

96
Q

nicotinic receptors-Somatic NS effect

A

increase in skeletal muscle tone, muscle contraction

97
Q

nicotinic receptors- what happen when there is a release of adrenaline and
noradrenaline from adrenal
medulla ?

A

increased heart rate.

98
Q

Muscarinic receptors- ANS parasympathetic NS results in?

A

m1- GI tract – increased gastric acid & saliva secretion
m2- Heart -decreased rate and force of contractions
m3- Increased GI tract secretions –saliva, pancreatic juice, bile and motility
-Increased insulin secretion
-Pupils contract (miosis) as eyes accommodate for close vision
-Bronchoconstriction, increased mucus secretion
-Promotion of micturition &
defecation

99
Q

Muscarinic receptors- Sympathetic NS- cholinergic synapses results in?

A

m3- vasodilation in skeletal

muscles; sweating

100
Q

Muscarinic receptors- CNS

A

effect improves memory enhanced cognition

Pharmacology (7 decks)

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