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Pharmacology MBBS > ANS-1 > Flashcards

ANS-1 Flashcards

1
Q

In a ganglion the receptors are of which subtype

A

Nn

Nicotinic receptor of neuronal subtype

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2
Q

The parts of the body when the neurotransmitter of post ganglionic sympathetic system is not norepinephrine

A
  1. Sweat glands (beta blockers cannot affect sweating)- Acetyl choline
  2. Adrenals- Acetyl choline
  3. Renal blood vessels- dopamine
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3
Q

Synthesis of Acetyl choline

A

Acetyl CoA from mitochondria + choline from systemic circulation
By choline-acetyl transferase

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4
Q

ACE Acetyl choline esterase

A 
Two sites: 
1. Esteratic site:
Breaks down the ester bond
2. Anionic site:
Choline’s + is attracted by this site
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5
Q

RDS of Acetyl choline synthesis

A

Reuptake of choline after action of ACE

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6
Q

Drugs which competes with choline for intake into the pre synaptic neuron

A

Hemicholinium

Used mostly in animal experiments

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7
Q

Drugs which inhibits the uptake of choline into the vesicle

A

Vesamicol

Used mostly in animal experiments

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8
Q

Drugs which block the pre synaptic Ca channel

A

Aminoglycosides

Produce neuromuscular toxicity by indirectly inhibiting Acetyl choline release

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9
Q

Drugs which directly inhibit Acetyl choline release into the synaptic cleft

A

Bungarotoxin
Botulinum toxin
Botulism: the patient dies by respiratory failure
Botox: migraine prophylaxis

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10
Q

Floppy infant

A

Muscle tone is lost
Infant with botulism
Acetyl choline is not released

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11
Q

Therapeutic uses of botulinum toxin

A 
As Botox injection:
1. Migraine prophylaxis
By decreasing CGRP (calcitonin gene related peptide) release
2. Achalasia 
3. Dystonia (abnormal movement)
4. Cosmetology
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12
Q

Receptors of the parasympathetic nervous system

A 
1. Muscarinic GPCR:
 A) Gq: Ca release
  M1, M3, M5
 B) Gi/o: relaxation by opening potassium channel
  M2, M4
2. Nicotinic:
 A) muscular (Nm): 
  myasthenia gravis
 B) neuronal (Nn):
  Adrenals, ganglions, CNS
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13
Q

Neurotransmitter of adrenals

A

Acetyl choline

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14
Q

M1 receptor

A 
Being Gq, it increases Ca release
CNS:
Increases action potential
Increases cognition 
Prevents Alzheimer’s syndrome
Agonist: Taclifensin

GIT:
Increases secretion

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15
Q

M3 receptors

A
  1. GIT: muscular contraction
  2. Glands: increased secretion
  3. Bronchoconstriction
  4. Detruser: contraction
  5. Iris: contraction or miosis
  6. Blood vessels:
    A) Endothelium (major effect)
    Stimulates Ca dependent ENOS producing NO ➡️ vasodilation
    B) Smooth muscle: minor vasocontraction
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16
Q

M5 and M4

A

Present in CNS

no clinical significance

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17
Q

M2 receptors

A

Heart
Block of SAN and AVN
i.e, bradycardia and block of AV conduction

A slight decrease in contraction of atrium greater than ventricle (clinically insignificant)

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18
Q

Classification of direct cholinergics

A
  1. Nicotinic
  2. Muscarinic:
    A) amides:
    All are lipid soluble except muscarine
    Can cross BBB
    Topical use
    B) choline esters:
    All are lipid insoluble
    No central side effects
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19
Q

Examples of direct cholinergics

A 
Nicotinic:
 Nicotine, Varenicline-smoking dependence
Muscarinic:
1. Amides
 Pilocarpine- c.a. glaucoma,...
 Cevimeline- xerostomia 
2. Choline esters
 Acetyl choline, esmolol, succinyl choline
 Bethanechol, carbachol, methacholine
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20
Q

Pilocarpine

A 
Treatment of:
1. xerostomia 
2. Miotic agent for closed angle glaucoma 
 Along with physostigmine, echothiophate
 Increases trabecular outflow

Adverse effects (miotic agents):

  1. Accommodation spasm (all M3 receptor) leads to
  2. Head ache
  3. Retinal detachment
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21
Q

Cevimeline

A

Drug of choice for xerostomia

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22
Q

Acetyl choline is metabolised in plasma by

A

Pseudocholinesterase
Very short acting like esmolol, succinyl choline
So no systemic use

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23
Q

Uses of Acetyl choline

A

Miotic agent in ocular surgeries

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24
Q

Bethanechol and carbochol

A

Resistant to both ACE and pseudocholinesterase
M1,3 more than M2
1. Bethanechol has 0 nicotinic effect, hence preferred for bladder atony and gastroparesis (M3)
2. Carbochol has maximum nicotinic effect so no systemic and topical use
Miotic agent in ocular surgery (like Acetyl choline)

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25
Q

Methacholine

A

Resistant to pseudocholinesterase only
M2 more than M1,3
Moderate nicotinic effect
Used in bronchial challenge test in diagnosis of bronchial asthma

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26
Q

Examples of indirect cholinergics

A 
1. Organophosphates
•Warfare agents •Echothiophate, Fluostigmine
•Insecticides 
2. Carbamate
 •Physostigmine
 •Donepezil, Rivastigmine, Galantamine
 •Pyridostigmine, Neostigmine-Myasthenia gravis
 •Edrophonium
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27
Q

Organophosphates

Original uses

A 
Binds to the esteratic site of ACE
Irreversible binding(after ageing)
Warfare agents (nerve gas) like Sarin, cyclosarin, tabun, Soman, Vx
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28
Q

Ageing of ACE

A

After the binding and breakage of the bond between esteratic site and organophosphates ,
the esteratic site forms stronger irreversible bonds

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29
Q

ACE reactivators

A

Oximes

They have positive charge and bind to the anionic site thus removing organophosphate from the esteratic site

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30
Q

Organophosphates clinical uses

A 
Echothiophate
Fluostigmine
Miotic agent in closed angle glaucoma (no more preferred)
Side effects:
1. Common miotic agent side effects
2. Iris cysts (echothiophate)
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31
Q

Organophosphates as insecticides and pesticides

A

Induce spastic paralysis (increased stimulation)
For suicide cases of cholinergic poisoning:
1. Agitation
2. Increased secretions: patient drowns in his own secretions
3. Pin point pupil:
due to severe miosis
opioid toxicity or pontine myelinosis

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32
Q

Organophosphate poisoning treatment

A

Atropine is the drug of choice (saves the life)
Then to treat nicotinic symptoms oximes are used like:
1. pralidoxime (most commonly used oxime in India)
2. obidoxime
3. diacetyl monoxime

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33
Q

Most specific drug in organophosphate poisoning is

A

Oximes
Because it reverses the effect of organophosphates (reactivation of ACE)
Though it is not the life saving drug (atropine)

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34
Q

Carbamates

Mechanism

A

Binds to both esteratic site and anionic site
(So in case of carbamate poisoning oximes are useless
Drug of choice is atropine)
This binding is reversible after a long time or pseudoirreversible
Exception:
Edrephonium-
binds only to anionic site via ionic bonds
So it is short acting

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35
Q

Carbamates

Examples of drugs

A 
1. Tertiary amines:
Lipid soluble
Like physostigmine, donepezil, rivastigmine, galantamine
2. Quaternary amines:
Lipid insoluble
3. Herbicides, fungicides, pesticides
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36
Q

Physostigmine

A 
Example of tertiary amine of carbamate 
Use:
1. Closed angle glaucoma (miotic agent)
2. Atropine toxicity (both crosses BBB)
Belladonna poisoning/ datura poisoning
Sources: physostigma venenosum (calabar beans)
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37
Q

Donepezil, rivastigmine, galantamine are used in

A

Alzheimer’s disease

They are tertiary amine (carbamates) that can cross BBB

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38
Q

Myasthenia gravis

A

Anti Nm antibodies which competitively inhibit Ach
Drug of choice is Edrephonium for Tensilon test, diagnosis
Neostigmine for both diagnosis and treatment
Pyridostigmine DoC for treatment (usually)
Premedication of atropine required for removing muscarinic side effects

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39
Q

Edrephonium

A

Edrephonium ,unlike other carbamates ,binds only to anionic site via ionic bonds
So it is short acting
Hence used for
1. Tensilon test, diagnosis of myasthenia gravis
2. Differential diagnosis of myasthenia gravis and cholinergic crisis
3. Treatment of PVST (paraoxysmal supraventricular tachycardia)

40
Q

Neostigmine

A

Quaternary amine (carbamate)

  1. Treatment and diagnosis of myasthenia gravis with atropine as premedication
  2. NDMR (non depolarising muscle relaxants) reversal which also competitively inhibit Nm receptor
  3. Cobra bite treatment: damaged post synaptic membrane
  4. Bladder stone
  5. Gastroparesis
41
Q

Pyridostigmine

A

Oral long acting drug in quaternary amine of carbamate
Uses:
1. DoC for treatment of myasthenia gravis
2. Postural hypotension

42
Q

Myasthenia gravis treatment

A 
1. Generalised MG:
DoC pyridostigmine
If not steroids if not immunomodulators 
2. Ocular MG:
DoC pyridostigmine if not immunomodulators 
3. Myasthenic crisis:
DoC IV Ig
(IV Ig is also used in Guillain barre syndrome, Kawasaki disease)
If not plasmapheresis
43
Q

Anti cholinergic drug classification

A
  1. Muscarinic inhibitors
  2. Nicotinic inhibitors
    A. Nn inhibitors:
    ganglionic blockers
    2nd line drugs in hypertension
    (side effects: postural hypertension)
    B. Nm inhibitors- muscle relaxants
44
Q

Examples of Nn blockers /ganglioside blockers (anti cholinergic)

A
  1. Tetra ethyl ammonium-research
  2. Mecamylamine-Taurette syndrome
  3. Trimethaphan-HTN emergency
  4. Hexamethonium
    These drugs are used as second line anti hypertensive drugs
45
Q

Examples of muscarinic receptor blockers

A
  1. Tropicamide (shortest acting)
  2. Atropine (most potent)
  3. Homatropine
  4. Cyclopentolate
46
Q

Tetraethyl ammonium

A

Nn blockers
So anti hypertensive
Used only as a research drug as it causes potassium channel blockage

47
Q

Trimethaphan

A 
Nn inhibitors (anti cholinergic)
Used by intravenous route for treatment of hypertensive emergency
48
Q

Mecamylamine

A

Nn inhibitor (anti cholinergic)
Treatment of Tourette syndrome
Adjunct to nicotine patch in smoking dependence

49
Q

Effects of anti muscarinic drugs (anti cholinergics)

A
  1. CNS: (M1) decreased cognition
  2. Pupils: (M3) mydriasis and cycloplegia
  3. Oropharyngeal secretions: decrease
  4. Lungs: bronchodilatation
  5. Heart:
    increase HR and AVN conduction
  6. GIT: decrease HCl secretions, decrease contraction
  7. Bladder: decrease detruser concentration
50
Q

Why is scopolamine called truth serum

A

Anti muscarinic drugs decrease cognition (M1 receptor inhibition)
So it is used for narcoanalysis
Though the drug of choice for narcoanalysis is thiopentone

51
Q

The drug of choice for narcoanalysis is

A

Thiopentone

52
Q

Uses of mydriatics

And their examples

A

Examples: muscarinic receptor blockers like:

  1. Tropicamide: shortest acting so preferred for adults
  2. Atropine: most potent so preferred in children
  3. Fundus examination
  4. To prevent synechae formation for patients with uveitis, corneal ulcer
53
Q

The anti muscarinic drugs used as pre anaesthetic medication

Why

A

Glycopyrrolate is used as a pre anaesthetic medication to decrease oropharyngeal secretion (preventing aspiration pneumonia as the cough reflex is suppressed)
It is a quaternary amine so it does not cross the BBB

54
Q

Uses of muscarinic acid blockers wrt cycloplegia

A
  1. Decreases pain in iridocyclitis

2. Refractive error test

55
Q

Uses of anti muscarinic drugs wrt lungs

A
  1. DoC for COPD

2. Bronchial asthma treatment

56
Q

Drug of choice for COPD is

A

Anti muscarinic drugs cause bronchoconstriction
Other effects like fibrosis and sclerosis are not reversible
1. Ipratropium: short acting, QID
2. Oxitropium and Aclidineum:
intermediate action, BD
3. ‘Tiotropium’, Umeclidineum, Revefenacin:
Long acting (so DoC), OD

57
Q

Atropine and heart

A
  1. Treatment of bradyarrythmia
  2. AVN block reversal
    Atropine is an anti arrhythmic drug
58
Q

Side effects of the DoC for COPD

A 
Anti muscarinic drugs 
Side effects:
1. Dry mouth
2. Glaucoma
3. Urine retention
59
Q

Anti muscarinic drugs and stomach

A

Decrease HCl secretions so used in treatment of peptic ulcer disease
Pirenzepine
Tesenzepine
It also decreases contractility

60
Q

Anti muscarinic drugs used as anti spasmodics

A

They decrease contraction
Glycopyrrolate
Dicyclomine
Scopolamine (hyoscine)

61
Q

DoC for motion sickness

A

Scopolamine (hyoscine)
It is given as transdermal patch
Applied atleast 4-5 hours before journey (acts for 2-3 days)
Also used as an anti-spasmodic

62
Q

Anti muscarinic drugs and bladder

Effect

A

Decrease detruser concentration

Used against overactive bladder/ detruser instability ➡️ spontaneous contraction ➡️ urge incontinence

63
Q

The various examples of drugs used in treating urge incontinence of bladder

A 
Anti muscarinic drugs
1. Non selective anti muscarinic: FFOTT
 Flavoxate
Fesoterodine
Oxybutinin (very toxic so used as transdermal patch)
Tolterodine
Trospium-only quaternary amine (so does not cross BBB)
2. Selective M3 blockers: DS
 ‘Darifenacin’-most selective so DoC
 Solifenacin
64
Q

Classification of sympathomimetics

A 
1. Catecholamines
 A. Endogenous
 B. Exogenous
2. Non catecholamines
3. Norepinephrine depletors
65
Q

Epinephrine

A

Agonist of α and β1 and β2 (vasodilation) receptors
So more potent cardiac stimulator
1. DoC for cardiac arrest
2. DoC for anaphylactic shock (IM route with multiple dose, if no effect then IV)
3. DoC for brittle asthma
4. Local vasoconstrictor to reduce bleeding
5. Used along with local anaesthetics to increase the duration of action
6. Glaucoma

66
Q

Norepinephrine

A 
Agonist of α and only β1 receptors
More potent vasoconstrictor, so:
1. DoC for vasodilatory shock (sepsis)
2. Cardiogenic shock 
Side effects:
If given via IM route causes muscle necrosis
67
Q

1:1000 dilution for epinephrine

A 
Used for systemic effect
Used via:
1. IM
2. Subcutaneous
3. Endotracheal
68
Q

1:10,000 dilution for epinephrine

A

For systemic effect

  1. IV
  2. Intracardiac route
  3. Intraosseous route
69
Q

1:100,000 dilution for epinephrine

A

When used as a local vasoconstrictor

70
Q

1:200,000 dilution for epinephrine is used

A

Used along with local anaesthetics

71
Q

Dale’s phenomenon

A

When epinephrine is given to a living system:
Initially epinephrine acts on α1, so bp increases
Then epinephrine gets metabolised, so bp falls to normal
Then epinephrine acts on β2 receptors, so the bp decreases
The body then produces catecholamines to bring the level back to normal

72
Q

VMAT2

Inhibitors of it

A 
Vesicular mono amine transporter of the vesicle
It transports dopamine of the axon endings into the vesicle
Inhibitors are:
1. Reserpine
2. Tetrabenazine
3. Derivatives of tetrabenazine like:
     Deutetrabenazine
     Valbenazine
73
Q

Exogenous catecholamines

A
  1. Dobutamine- acute CHF, stress ECG
  2. Fenoldopam and Dopexamine- hypertensive emergency
  3. Isoprenaline (isoproterenol)-bradycardia, AV Nodal block, bronchial asthma
  4. Droxidopa-postural hypotension
74
Q

RDS of norepinephrine or dopamine formation

Inhibitor of this step is

A

The first step of hydroxylation of tyrosine to DOPA by tyrosine hydroxylase
Metyrosine is an analog of tyrosine which inhibits this step

75
Q

Formation of norepinephrine occurs in

How

A

Vesicle

The dopamine is converted into norepinephrine in the vesicle by Dopamine β hydroxylase

76
Q

Fate of norepinephrine after it stimulates the receptors

A
  1. Reuptake back into the pre synaptic neuron (most common 95%)
  2. Can be metabolised MAO, COMT
  3. Diffusion from the synaptic cleft
77
Q

Metyrosine is used in

A 
Analogue of tyrosine
Inhibits the RDE
Used in:
1. Hypertension
2. Pheochromocytoma as an add on drug
78
Q

Reserpine is used in

A

Treatment of tardive dyskinesia

Treatment of hypertension

79
Q

Tetrabenazine

A

Inhibitor of VMAT2 of norepinephrine synthesis pathway (like Reserpine, Deutetrabenazin, Valbenazine)

  1. DoC in Huntington’s chorea
  2. Treatment of tics associated with Taurette syndrome
80
Q

Deutetrabenazine and valbenazine

A

Longer-acting Tetrabenazine derivatives
Inhibitor of VMAT2 of norepinephrine synthesis pathway (like Reserpine, tetrabenazine)

DoC in Tardive dyskinesia

81
Q

Dopamine β hydroxylase is inhibited by

A

Disulfiram

No clinical significance

82
Q

Drugs which inhibit reuptake of norepinephrine

A
  1. TCA (Tricyclic antidepressants)
  2. SNRI (Serotonin norepinephrine reuptake inhibitors)
  3. Cocaine

Increased norepinephrine ➡️

  1. Increased blood pressure
  2. Arrhythmia
83
Q

DoC for deaddiction of cocaine

A

Bromocriptine stimulates D2 receptors and gives similar effect
The kick of cocaine is due to increased dopamine ➡️ D2 receptor stimulation (brain)
Cocaine also inhibitors reuptake of norepinephrine

84
Q

Common side effects of drugs like metyrosine, reserpine, tetrabenazine, deutetrabenazine, valbenazine

A

These drugs inhibit norepinephrine (depression, hypotension) and dopamine synthesis (Parkinsonism).

85
Q

Receptors of sympathetic system are which type of receptors

A

GPCR
Both α and β

α1, α2 and β2 have hyperglycaemic effects via different mechanisms

86
Q

α1 receptors

A

Gq subtype of receptors of post-synaptic membrane
Increases Ca
1. Vasoconstriction
2. Contraction of prostatic urethra and bladder sphincter
3. Contraction of radial muscles of iris ➡️ mydriasis
4. Relaxation of GIT smooth muscle due to Ca-dependent K-channels opening
5. Increased glycogenolysis and gluconeogenesis in liver and muscle

87
Q

α2 receptors

explain

A

Gi subtype of receptors on the pre synaptic
Exception:
1. Post synaptic and Gq subtype in blood vessels ➡️ vasoconstriction
2. β islet cells is post synaptic Gi subtype ➡️ decreases insulin release ➡️ hyperglycaemia

Stimulated at high concentration
Blocks the release of norepinephrine (autoreceptor)

Clonidine is an agonist

88
Q

Auto receptors

examples

A

They reduce the secretion of their own neurotransmitter

  1. α2 receptors of sympathetic
  2. M2 of parasympathetic system
  3. H3 of histaminergic system
  4. 5HT1 of serotonergic system
89
Q

Clonidine

A

α2 receptor agonist given for hypertension patients via IV route
Slow infusion of oral:
presynaptic receptor ➡️ decreases norepinephrine ➡️ vasodilation
Fast infusion (contraindicated):
Post synaptic receptor ➡️ vasoconstriction

90
Q

β receptors

A

All are Gs subtype of GPCR

β1,2,3

91
Q

β1 receptor

A

Gs subtype
1. Heart:
cAMP increases ➡️ Ca channel phosphorylation ➡️ Increased Ca ➡️ increased CO, HR and conduction
2. JG cells (kidney)
Increased renin ➡️ increased blood pressure

92
Q

β2 receptors

explain

A

Gs subtype of receptors on the pre synaptic neuron
Stimulated at low concentrations
Stimulates norepinephrine release

93
Q

β2 receptor functions and locations

A 
1. Smooth muscle:
cAMP➡️ activates MLCP, inhibits MLCK, opens K+ channels ➡️ relaxation:
 Vasodilation
 Bronchodilation
 Relaxation of uterus
2. Cardiac and skeletal muscles:
increased cAMP ➡️ phosphorylation of Ca channels ➡️ increased contractility (palpitations, tremors)
3.  Hyperglycaemia
94
Q

β2 receptor and blood glucose level

A

Gs subtype of GPCR ➡️ increases cAMP:

  1. Induces glycogenolysis and gluconeogenesis (liver and muscle) ➡️ hypoglycaemic
  2. Increases insulin release

Predominantly hyperglycaemic

95
Q

β3 receptors

A
  1. Detruser muscle:
    Increased cAMP ➡️ relaxation
  2. Adipocytes:
    Increased cAMP ➡️ activates hormone sensitive lipase HSL➡️ lipolysis

Treatment of obesity

Pharmacology MBBS (19 decks)

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