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Primary Pharmacology > ANS Pharmacology > Flashcards

ANS Pharmacology Flashcards

1
Q

What is the structure of ach

A

Quaternary amine in the choline moiety
Ester with a negative charge

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2
Q

What type of muscurinic receptors are antagonised by atropine
Where are they found

A

M1-3
M1 CNS, autonomic ganglia and gastric parietal cells
M2 heart and presynaptic sites
M3 smooth muscle, vascular endothelium, exocrine glands

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3
Q

Examples of muscarinic agonists

A

Carbachol, pilocarpine

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4
Q

Structure of pilocarpine and consequences of this

A

Like ach except
Quaternary amine to a tertiary amine
Removed the ester
Increased length of the aliphatic component

Effects are decreased potency but also decreased hydrolysis so increased half life.

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5
Q

Uses of muscarinic agonist

A

Pupillary constriction to reduce IOP in glaucoma
Improve micturation by increasing detrusor muscle contraction

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6
Q

Systemic effects of muscarinic agonists

A

Bradycardia
Hypotension
Low SVR
Increased rs mucus production
Bronchoconstriction
Increased gi propulsion
Increased gi secretions
Urinary sphincter tone decreased
detrusor tone increased
Miosis
Lacrimation increased muscle

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7
Q

Examples of mucarinic antagonists
Which are naturally occurring
Structure and consequence

A

Atropine, glycopyrrolate, hyoscine

Nat occurring are atrop and hyoscine - these are tertiary amines and can cross the bbb
Glycopyrrolate is synthetic quaternary amine and can’t cross bbb

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8
Q

Effects of muscarinic antagonists

A

Increase Herat rate
Increase Bp
Inhibit secretions and sweating
Decreased ruination
Dilated pupils, blocked accommodation and blurred vision
Bronchodilation

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9
Q

What is atropines structure

A

Similar to ach but with an aromatic group instead of the acetyl group and a tertiary amino group in place of the quaternary one
Synthesised from plants as S but spontaneously becomes racemic

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10
Q

What local anaesthetic is atropine related to
Consequence

A

Cocaine!
Weak local anaesthetic effect

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11
Q

Effect of atropine on CNS

A

Crosses bbb
Causes initial excitement then depression

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12
Q

What drug dose glycopyrronium have a similar duration of action too?

A

Neostigmine

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13
Q

Which form of atropine and hyoscine have most clinical effect

A

L form

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14
Q

What are the different preparations of hyoscine and what is it used for
What is the iV dose difference

A

Hydrobromide (scopolamine) - CNS depression (sedative and antiemetic)
Butylbromide - smooth muscle relaxant (GI and GU spasm reduction
100fold dose difference! Hydrobromide approx 400mcg sc, butylbromide 20mgSC

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15
Q

Example of nicotinic ACh agonist
Effect?

A

Nicotine!
Mainly autonomic ganglia - vasoconstriction, hypertension, sweating, salivation

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16
Q

Examples of nicotinic ACh antagonists

A

Muscle relaxants
D-turobocurane blocks ganglia - drops Bp, causes postural hypotension

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17
Q

What substances prevent neurotransmitter release
How

A

Magnesium and Aminoglycosides - inhibit presynaptic calcium entry into cells
Botulinum and beta bungarotoxin - bind to nicotinic nerve terminals preventing neurotransmitter release

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18
Q

Effect of anticholinesterases and organophosphates
Clincial effects

A

Block acetylcholinesterase
Initially cause parasympathetic response, in high enough dose cause a depolarising neuromuscular block

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19
Q

Order of effect of adrenaline, noradrenaline and isoprenaline on alpha adrenoreceptors

A

Noradrenaline > adrenaline > isoprenaline

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20
Q

Order of effect of adrenaline, noradrenaline and isoprenaline on beta adrenoreceptors

A

Isoprenaline > adrenaline > noradrenaline

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21
Q

Effects of alpha 1 stimulation and mechanism

A

Postsynaptic excitatory GPCR Gq
Vasoconstriction, gut smooth muscle relaxation, salivation, hepatic glycogenolysis

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22
Q

Effects of alpha 2 stimulation and mechanism

A

Inhibitory GPCRs on presynaptic membrane Gi
Inhibit of autonomic (NA and ACh) neurotransmitter releases, stimulation of platelet aggregation

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23
Q

Effects of beta 1 stimulation and mechanism

A

Postsynaptic excitatory gpcr Gs
Increases heart rate, contractility. Causes gut smooth muscle relaxation and lipolysis

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24
Q

Effects of beta 2 stimulation and mechanism

A

Postsynaptic inhibitory GPCRs
Vasodilation, bronchodilation, viceral smooth muscle relaxation, glycogenolysis, muscle tremor

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25
Q

Effects of beta 3 stimulation and mechanism

A

Postsynaptic GPCR
Lipolysis, thermogenesis

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26
Q

Effects of adrenaline (receptors and clinical)
Issues

A

Mainly beta with moderate alpha
Both inotropy and chronotropy
Vasoconstriction generally but dilation of skeletal muscle arterioles
Sensitises myocardium to arrhythmia and makes it hyper excitable

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27
Q

Actions of dobutamine (receptor and clinical)
Issues

A

Non selective beta agonist (no alpha)
Chronotropy, ionotrophy
Some vasodilation so may require concurrent alpha agonist

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28
Q

Actions of dopamine (receptor and clinical)
Specific use

A

Dopamine receptors, Non selective beta but also mild alpha 1 agonist
Dose dependent - just dopamine receptors at lower doses then starts effecting beta then alpha with increasing dose
Dopamine receptors peripherally are located renally and cause vasodilation thus maintains renal perfusion

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29
Q

Actions of dopexamine (receptor and clinical)
Issues

A

Beta 2 and peripheral D1 and 2
Inhibits NA reuptake
Positive inotrope with peripheral vasodilation (splanchnic and renal) improving cardiac output

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30
Q

Actions of isoprenaline receptor and clinical)
Use

A

Beta 1 and 2 agonist
Treats Bronchospasm, bradycardia and heart block

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31
Q

Actions of noradrenaline (receptor and clinical)
Issues

A

Primarily alpha agonist causing vasoconstriction
Has some beta effects
Can cause a reflex bradycardia if hypotension overcorrected

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32
Q

Actions of salbutamol (receptor and clinical)
Uses
Issues

A

Selective beta 2 agonist
Relieves bronchospasm, causes uterine relaxation
Some beta 1 effects including tachycardia at higher doses

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33
Q

Actions of clonidine ( preceptor and clinical)
Uses

A

Alpha 2 agonist
Inhibits neurotransmitter (NA) release causing decreased blood pressure
Analgesia, sedative, prolongs epidurally administered local anaesthetics

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34
Q

Actions of metaraminol (receptor and clinical)
Issues

A

Mixed alpha and beta agonism (mainly alpha)
Increases SVR and PVR
Bradycardia, reduces cerebral and renal blood flow, increases uterine tone, increases BM in diabetics

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35
Q

Main uses of alpha 1 antagonists

A

Antihypertensives
BPH

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36
Q

Cardiovascular effect effect of alpha blockade

A

Vasodilation with reflex increase in heart rate and cardiac output

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37
Q

Examples of alpha antagonists

A

Alfuzosin, doxazocin, tamsulosin, phenoxybenzamine

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38
Q

What receptors does phenoxybenzamine antagonise
How does it bond and behave

A

Alpha
5HT
Histamine
Covalently bonds so detaches very slowly acting as competitive irreversible antagonist

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39
Q

Which beta blocker also blocks alpha receptors
Clinical effect when given iV and oral

A

When IV predominant alpha blockade but reflex tachycardia reduced by the beta blockade function
When given orally beta blockade predominates

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40
Q

What receptors do tamsulosin and alfuzosin effect

A

Alpha 1A receptors targeting prostate smooth muscle

41
Q

Difference between selective and non selective beta blockers

A

Selective only target beta 1
Non selective target both

42
Q

What is the effect of a beta receptor partial agonist

A

Stimulation at low levels then blockade at higher levels - may mitigate bradycardia effect and maintaining perfusion

43
Q

Examples of full antagonist selective beta blockers

A

Atenolol
Bisoprolol
Betaxolol
Exmolol
Metoprolol
Nadolol

44
Q

Examples of non selective beta blockers full antagonists

A

Propranolol
Sotalol
Timolol

45
Q

Examples of beta receptor partial agonists

A

Acebutalol
Alprenolol
Celiprolol
Oxprenolol
Pindolol

46
Q

Uses of beta blockers

A

Htn
Heart failure
Angina
Glaucoma
Migraine
Anxiety
Thyrotoxicosis
Phaeochormocytoma

47
Q

Clinical effects of beta blockade

A

CVS - negative chronotrophy and inotropy, decreased BP and myocardial work, decreased coronary blood flow
RS - bronchoconstriction
Renal - decreseased renin secretion
Metabolic - less free fatty acid realises, reduced glycogenolysis, and insulin release, lipolysis, thermogenesis
Eye - reduced production of aqueous humour
Central - reduced sympathetic tone, reduced anxiety, tiredness, nightmares, sleep disturbance

48
Q

Which beta blockers are water soluble,
Clinical effect

A

Atenolol, celiprolol, nadolol Sotolol
Don’t penetrate bbb well
Excreted in urine

49
Q

Which beta blockers have minimal first pass metabolism

A

Bisoprolol
Sotolol

50
Q

Effect of beta blockers on myocardial demands

A

Reduces coronary blood flow but proportionally less than the reduction in myocardial oxygen demand

51
Q

Side effects of beta blockers

A

Bradycardia
Bronchoconstriction
Hypoglycaemia esp on exercise
Sleep disturbance
Cold extremities

52
Q

Bioavailability of atenolol
Excretion?

A

50%
Urinary excretion

53
Q

Vaughn Williams classification

A

1 - Na blockade
1a - moderate reduction phase 0 slope, increases AP duration and refractory period
1b - mild reduction phase 0 slope, reduces AP duration and refractory period
1c - significant reduction phase 0 slope, no effect on AP duration and refractory period
2 beta blockers
3 k blockers
4 ca blockers

54
Q

Half life of esmolol
How

A

9 minutes
Red cell esterases

55
Q

Bioavailability of propranolol
Lipid solubility and proteins binding

A

10-30%:
Highly lipid soluble and protein bound

56
Q

Action of carbidopa

A

Inhibits dopa decarboxilase preventing formation of dopamine
Doesn’t cross bbb thus formation still occurs in CNS

57
Q

Actions of methyldopa

A

False substrate for dopa decarboxilase forming methylnoradrenaline which is inactive. Causes displacement of true neurotransmitter thus reduces blood pressure

58
Q

Mechanism of reserpine

A

Blocks uptake and reuptake of na, dopamine and 5HT

59
Q

Effect of guanethidine

A

Causes release of NA then inhibits release of diminishing levels of NA
Used in chronic pain medicine regionally (like a biers block) to stop reflex sympathetic dystrophy

60
Q

Which calcium channel blocker is used to treat vascular spasm in SAH

A

Nimodipine

61
Q

How does sodium nitroprusside work

A

Same as organic nitrates (NO3-)
Converted in vascular smooth muscle to nitrates NO2- then react with hydrogen ions to form nitric oxide NO
Stimulates guanylyl cyclase thus GTP to cGMP
cGMP relaxes smooth muscle

62
Q

Effect of nitrates and sodium nitroprusside

A

Vasodilation (mainly venous)
Decreases preload thus lower myocardial work and oxygen demand
Higher doses dilate arterioles reducing afterload and dilating coronary arteries

63
Q

Metabolism of GTN

A

Rapidly hydrolysed by liver
Small amounts of GDN which is mildly active with t1/2 w hrs

64
Q

Pharmacokinetics of isosobide dinitrate

A

Slow release preparation gradually absorbed
Converted to IMN in liver
T1/2 4 hrs

65
Q

Use of inhaled nitric oxide

A

Treats pulmonary hypertension

66
Q

Why doesn’t inhaled nitric oxide have a systemic effect

A

Enters vascular system and combines with hb forming methaemoglobin

67
Q

How is sodium nitroprusside administered
Side effects

A

Protected from light - brown syringe, yellow infusion lines
Metabolism produces cyanide ions which cause methaemoglobin
Also forms thiocyanate which combines with b12 forming cyanocobalamin
In high doses cyanide will interupt electron transfer chain

68
Q

How is sodium nitroprusside monitored

A

Thiocyanate levels

69
Q

Example of potassium: channel activator
Mechanism

A

Nicorandil
Opens k channels, hyperpolarisation so reduced electrical activity, relaxes smooth muscle reducing SVR
Also dilates coronary arterioles

70
Q

Mechanism of ivabradine

A

If current inhibitor
Reduces slow depolarisation stage thus reducing heart rate

71
Q

Examples of endothelin receptor antagonists
Mechanism
Uses

A

Bosentan, sitaxsentan
Endothelin causes increased free calcium thus vasoconstriction
Agonists thus cause vasodilatation and can be used in pulmonary hypertension

72
Q

Examples of prostacyclins
Uses

A

Epoprostenol, iloprost
Vasodilation and inhibition of platelet aggregation
Pulmonary hypertension

73
Q

Class and effect of sildenfil

A

Pde5 inhibitor
Inhibits nitric oxide stimulation of guanylyl cyclase thus causes smooth muscle relaxation and vasodilation

74
Q

What is diazoxide
Mechanism

A

A thiazide that causes sodium and water retention!

75
Q

What is hydralazine

A

Causes vascular smooth muscle relaxation and some alpha blocking actions

76
Q

Mechanism of action of phenylephrine

A

Alpha 1 agonist

77
Q

Effect of adrenaline in gi tone and splanchnic blood flow

A

Decreases

78
Q

Effect of adrenaline on renal blood flow

A

Increases

79
Q

Metabolim of adrenaline

A

Comt in liver
Mao in neurones
To inactive metabolites

80
Q

General strength of atropine preparation

A

600mcg in 1ml

81
Q

Oral bioavailability of atropine

A

10-25%

82
Q

Intra operative dose of atropine
Organophosphate poisoning dose of atropine

A

300-600mcg
2mg

83
Q

Contraindications to atropine

A

Glaucoma, hyperpyrexia

84
Q

Non cardiovascular effects of atropine

A

Bronchodilator
Reduced rs secretions
Reduced gi motility
Antispasmodic
Pupillary dilatation and increased IOP

85
Q

Metabolism of atropine

A

Hydrolysed to Tropine and tropic acid in liver
Excreted by urine

86
Q

Structure of atropine

A

Tertiary amine

87
Q

Onset, peak and Duration of action of clonidine

A

10mins, 30-60mins, 3-7hrs

88
Q

Effects of clonidine

A

Transient increase in SVR and Bp from alpha 1
Then decreased SVR and Bp from alpha 2
Analgesia

89
Q

Metabolism of clonidine

A

65% unchanged in urine , 20% in faeces, 15% inactivated in liver

90
Q

Effects of increasing dopamine infusions

A

1-5mcg/min increases renal blood flow
5-15 inotropic
15-20 vasoconstrict

91
Q

Side effects of dopamine

A

Nausea, tachycardia, arrhythmias, prolactin inhibition

92
Q

Elimination of ephedrine

A

99% unchanged in urine

93
Q

Bioavailability of gycopyrrolate

A

5%

94
Q

Excretion of glycopyrrolate

A

85% unchanged in urine and 15% in faeces

95
Q

Issue with glycopyrrolate

A

High doses can be nicotinic antagonist effecting myasthenia gravis patients

96
Q

Metabolism of hyoscine dervivitives

A

Hepatic to scopine

97
Q

Dosing of labetaolol

A

Slow bonuses of 50mg at 50 minute intervals
IV infusion at 15-160mg/hr

98
Q

Half life of labetolol
Metabolism

A

60 mins
Hepatic

99
Q

Effect of NA on gravis uterus

A

Reduces perfusion so can cause fetal hypoxia

Primary Pharmacology (18 decks)

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