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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
Effects of beta 3 stimulation and mechanism
Postsynaptic GPCR Lipolysis, thermogenesis
26
Effects of adrenaline (receptors and clinical) Issues
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
27
Actions of dobutamine (receptor and clinical) Issues
Non selective beta agonist (no alpha) Chronotropy, ionotrophy Some vasodilation so may require concurrent alpha agonist
28
Actions of dopamine (receptor and clinical) Specific use
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
29
Actions of dopexamine (receptor and clinical) Issues
Beta 2 and peripheral D1 and 2 Inhibits NA reuptake Positive inotrope with peripheral vasodilation (splanchnic and renal) improving cardiac output
30
Actions of isoprenaline receptor and clinical) Use
Beta 1 and 2 agonist Treats Bronchospasm, bradycardia and heart block
31
Actions of noradrenaline (receptor and clinical) Issues
Primarily alpha agonist causing vasoconstriction Has some beta effects Can cause a reflex bradycardia if hypotension overcorrected
32
Actions of salbutamol (receptor and clinical) Uses Issues
Selective beta 2 agonist Relieves bronchospasm, causes uterine relaxation Some beta 1 effects including tachycardia at higher doses
33
Actions of clonidine ( preceptor and clinical) Uses
Alpha 2 agonist Inhibits neurotransmitter (NA) release causing decreased blood pressure Analgesia, sedative, prolongs epidurally administered local anaesthetics
34
Actions of metaraminol (receptor and clinical) Issues
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
35
Main uses of alpha 1 antagonists
Antihypertensives BPH
36
Cardiovascular effect effect of alpha blockade
Vasodilation with reflex increase in heart rate and cardiac output
37
Examples of alpha antagonists
Alfuzosin, doxazocin, tamsulosin, phenoxybenzamine
38
What receptors does phenoxybenzamine antagonise How does it bond and behave
Alpha 5HT Histamine Covalently bonds so detaches very slowly acting as competitive irreversible antagonist
39
Which beta blocker also blocks alpha receptors Clinical effect when given iV and oral
When IV predominant alpha blockade but reflex tachycardia reduced by the beta blockade function When given orally beta blockade predominates
40
What receptors do tamsulosin and alfuzosin effect
Alpha 1A receptors targeting prostate smooth muscle
41
Difference between selective and non selective beta blockers
Selective only target beta 1 Non selective target both
42
What is the effect of a beta receptor partial agonist
Stimulation at low levels then blockade at higher levels - may mitigate bradycardia effect and maintaining perfusion
43
Examples of full antagonist selective beta blockers
Atenolol Bisoprolol Betaxolol Exmolol Metoprolol Nadolol
44
Examples of non selective beta blockers full antagonists
Propranolol Sotalol Timolol
45
Examples of beta receptor partial agonists
Acebutalol Alprenolol Celiprolol Oxprenolol Pindolol
46
Uses of beta blockers
Htn Heart failure Angina Glaucoma Migraine Anxiety Thyrotoxicosis Phaeochormocytoma
47
Clinical effects of beta blockade
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
Which beta blockers are water soluble, Clinical effect
Atenolol, celiprolol, nadolol Sotolol Don’t penetrate bbb well Excreted in urine
49
Which beta blockers have minimal first pass metabolism
Bisoprolol Sotolol
50
Effect of beta blockers on myocardial demands
Reduces coronary blood flow but proportionally less than the reduction in myocardial oxygen demand
51
Side effects of beta blockers
Bradycardia Bronchoconstriction Hypoglycaemia esp on exercise Sleep disturbance Cold extremities
52
Bioavailability of atenolol Excretion?
50% Urinary excretion
53
Vaughn Williams classification
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
Half life of esmolol How
9 minutes Red cell esterases
55
Bioavailability of propranolol Lipid solubility and proteins binding
10-30%: Highly lipid soluble and protein bound
56
Action of carbidopa
Inhibits dopa decarboxilase preventing formation of dopamine Doesn’t cross bbb thus formation still occurs in CNS
57
Actions of methyldopa
False substrate for dopa decarboxilase forming methylnoradrenaline which is inactive. Causes displacement of true neurotransmitter thus reduces blood pressure
58
Mechanism of reserpine
Blocks uptake and reuptake of na, dopamine and 5HT
59
Effect of guanethidine
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
Which calcium channel blocker is used to treat vascular spasm in SAH
Nimodipine
61
How does sodium nitroprusside work
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
Effect of nitrates and sodium nitroprusside
Vasodilation (mainly venous) Decreases preload thus lower myocardial work and oxygen demand Higher doses dilate arterioles reducing afterload and dilating coronary arteries
63
Metabolism of GTN
Rapidly hydrolysed by liver Small amounts of GDN which is mildly active with t1/2 w hrs
64
Pharmacokinetics of isosobide dinitrate
Slow release preparation gradually absorbed Converted to IMN in liver T1/2 4 hrs
65
Use of inhaled nitric oxide
Treats pulmonary hypertension
66
Why doesn’t inhaled nitric oxide have a systemic effect
Enters vascular system and combines with hb forming methaemoglobin
67
How is sodium nitroprusside administered Side effects
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
How is sodium nitroprusside monitored
Thiocyanate levels
69
Example of potassium: channel activator Mechanism
Nicorandil Opens k channels, hyperpolarisation so reduced electrical activity, relaxes smooth muscle reducing SVR Also dilates coronary arterioles
70
Mechanism of ivabradine
If current inhibitor Reduces slow depolarisation stage thus reducing heart rate
71
Examples of endothelin receptor antagonists Mechanism Uses
Bosentan, sitaxsentan Endothelin causes increased free calcium thus vasoconstriction Agonists thus cause vasodilatation and can be used in pulmonary hypertension
72
Examples of prostacyclins Uses
Epoprostenol, iloprost Vasodilation and inhibition of platelet aggregation Pulmonary hypertension
73
Class and effect of sildenfil
Pde5 inhibitor Inhibits nitric oxide stimulation of guanylyl cyclase thus causes smooth muscle relaxation and vasodilation
74
What is diazoxide Mechanism
A thiazide that causes sodium and water retention!
75
What is hydralazine
Causes vascular smooth muscle relaxation and some alpha blocking actions
76
Mechanism of action of phenylephrine
Alpha 1 agonist
77
Effect of adrenaline in gi tone and splanchnic blood flow
Decreases
78
Effect of adrenaline on renal blood flow
Increases
79
Metabolim of adrenaline
Comt in liver Mao in neurones To inactive metabolites
80
General strength of atropine preparation
600mcg in 1ml
81
Oral bioavailability of atropine
10-25%
82
Intra operative dose of atropine Organophosphate poisoning dose of atropine
300-600mcg 2mg
83
Contraindications to atropine
Glaucoma, hyperpyrexia
84
Non cardiovascular effects of atropine
Bronchodilator Reduced rs secretions Reduced gi motility Antispasmodic Pupillary dilatation and increased IOP
85
Metabolism of atropine
Hydrolysed to Tropine and tropic acid in liver Excreted by urine
86
Structure of atropine
Tertiary amine
87
Onset, peak and Duration of action of clonidine
10mins, 30-60mins, 3-7hrs
88
Effects of clonidine
Transient increase in SVR and Bp from alpha 1 Then decreased SVR and Bp from alpha 2 Analgesia
89
Metabolism of clonidine
65% unchanged in urine , 20% in faeces, 15% inactivated in liver
90
Effects of increasing dopamine infusions
1-5mcg/min increases renal blood flow 5-15 inotropic 15-20 vasoconstrict
91
Side effects of dopamine
Nausea, tachycardia, arrhythmias, prolactin inhibition
92
Elimination of ephedrine
99% unchanged in urine
93
Bioavailability of gycopyrrolate
5%
94
Excretion of glycopyrrolate
85% unchanged in urine and 15% in faeces
95
Issue with glycopyrrolate
High doses can be nicotinic antagonist effecting myasthenia gravis patients
96
Metabolism of hyoscine dervivitives
Hepatic to scopine
97
Dosing of labetaolol
Slow bonuses of 50mg at 50 minute intervals IV infusion at 15-160mg/hr
98
Half life of labetolol Metabolism
60 mins Hepatic
99
Effect of NA on gravis uterus
Reduces perfusion so can cause fetal hypoxia

Primary Pharmacology (18 decks)

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