ANS Flashcards

1
Q

What are the locations of M1, M2, M3

A

M1- ALPHA 1
M2- BETA 1
M3-BETA 2

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2
Q

Where does M1, M2, M3, APLHA 1, BETA 1 AND BETA 2 ACT

A

M1- STOMACH
M2- HEART
M3 - EXOCRINE GLANDS

ALPHA 1- VESSELS
BETA 1- HEART, JGC, KIDNEYS
BETA 2- BRONCHI, UTERUS

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3
Q

Describe direct acting cholinergic agonists

A

Examples: ACH, Betanachol, carbachol, pilocarpine

MOA: Mimic ACH by binding directly to cholinoreceptor
PSNS stimulation; miosis, redness, decreases blood pressure

Indications: Urinary retention, Megacolon, Atonic bladder –> Bethanechol
Treatment glaucoma, optic nerve neuropathy d/t increase of intraocular pressure- > pilocarpine
Sjogren syndrome-> Pilocarpine

S/E:
DIARRHEA
URINATION
MIOSIS/MUSCLE WEAKNESS
BRONCHORREA
EMESIS
LACRIMATION
SWEATING
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4
Q

INDIRECT ACTING CHOLINERGIC AGONIST: Reversible

A

Examples: Edrophonium, neostigmine, physostigmine

MOA: ache inhibitors block ash esterase to stop to from cleaving ACH. act then accumulates in the synaptic cleft.

Indications: Dx of myasthenia graves

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4
Q

INDIRECT ACTING CHOLINERGIC AGONIST: Reversible

A

Examples: Edrophonium, neostigmine, physostigmine

MOA: ache inhibitors block ash esterase to stop to from cleaving ACH. act then accumulates in the synaptic cleft.

Indications: Dx of myasthenia gravis (when antibodies attack the NMJ receptors causing muscle weakness) –> Edrophonium
tx of myasthenia gravis—> Physostigmine
Alzheimers—-> Tacrine, Donezipil, Rivastigmine, Glutamine
Glaucoma—-> Pilocarpine

S/Es: Nausea, Abdominal pain, decrease blood pressure, Redness/ Flushing, Bronchospam) cholinergic stimuLATION
Diarrhea, GI distress

C/I: Peritonitis, IBD

*Atropine is given in a cholinergic crisis

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5
Q

Indirect acting cholinergic agonist: Irreversible

A

Example: Ecothiophate (Short Acting)
MOA: Covalently binds to ACHe–> Longer half life–> choline
Indications: Glaucome (Not 1st line)
Long DOA–> 3 weeks

Side Effects: Nausea, abdominal pain, decrease in BP, Redness/ flushing, diarrhoea, GI DISTRESS*

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6
Q

AntiMuscarinic / Cholinergic Antagonist

A

MOA: Blocks cholinorecptors—> Antimuscarinic effect

Indications: Cholinergic Reactions
Parkinsons
organophosphate poisoning  (Atropine)
COPD (Ipatropium)
Scopolamine is used for amnesia in OBGYN along with morphine

Atropine and tropicamide–> PSNS Antagonist

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7
Q

Characterise a atropine overdose

A

Dilation—> Blurred vision
Tachyarrythmia
Red b/c pix won’t sweat
Temp increase making them red

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8
Q

What medication is taken in the case of a atropine overdose?

A

Take reversible acting cholinergic agonist

Such as Edrophonium, Neostigmine, Physostigmine

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9
Q

Can acetylcholine be used as a drug?

A

No it cleaved by ACHe too fast

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10
Q

Symptoms of cholinergic drug overdose

A

Nausea, Vomiting, Flushing, Pupil constriction/ miosis, Diarrhea

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11
Q

Antidote for cholinergic overdose

A

atropine

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12
Q

symptoms of atropine poisoning

A

constipation, dry mouth, urinary retention, pupil dilation, myodriasis, Dry/ sandy eyes

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13
Q

Antidote for atropine poisoning

A

Physostigmine

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14
Q

Alpha 1 agonist

MOA
USE
SIDE EFFECTS

A

MOA: Stimulates vasoconstriction and may increase BP

Use: Cardiogenic shock( hypotensive state), septic shock, CHF
Side Effect: Orthostatic hypotension, tacharrythmias

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15
Q

Alpha 2 agonist

MOA
USE

A

Presynaptic they are auto regulatory Because a portion of NE will circle back and react with this receptor

A2 Stimulation—> Feedback inhibition of ongoing release of NE.
This inhibitory action decreases further action from the output from the adrenergic neutron

So this acts as a modulating mechanism for when there is high sympathetic activity.

USE= HYPERTENSION

16
Q

B1 AGONIST

MOA
USE

A

Produces cardioslective stimulation increasing cardiac output.
Due to positive isotropy (leading to increased HR) and positive chronotropy (leading to increased heart contractility)

USE: Cardiogenic Shock and Heart Block
To speed up HR
CHF

17
Q

B2 AGONIST

A

In bronchi and uterus stimulation occurs leading to bronchodilator and uterine relaxation

it is used in preterm labour and asthma

18
Q

What is the first line treatment for cariogenic shock in ED

A

Adrenaline/ Epinephrine

It works by acting on all adrenergic receptors

Alpha 1 —> Increase total peripheral resistance at vasoconstriction
Beta 1——> Increases cardiac output plus a positive inotropic and chronotrophic effect

19
Q

Drugs used in treatment for hypertension

A

Clonidine (A2 Agonist)
Nebivolol. (B1 Blocker)
Propranolol (Non-selective beta blocker)
Labetolol (A1, B1, B2)

20
Q

Nasal decongestants
Class
MOA

A

Example: Phenylephrine, Oxymetazolone
MOA: They are alpha 1 and alpha 2 agonist that cause vasoconstriction and decrease congestion in nasal vessels

21
Q

MOA of direct acting agonists

A

Thye bind to the adrenergic receptor without interacting with presynaptic neurone

22
Q

Indirect acting agonist

A

They enhance norepinephrine release from the presynaptic terminals or inhibit norepinephrine uptake

23
Q

Mixed Action Adrenergic agonist

A

They active postsynaptic adrenergic receptors and induce the release of NE from the presynaptic terminals

24
Q

What drugs are contraindicated in Asthma and COPD

A

Non selective beta blockers such as propranolol, timolol and nadolol are contraindication in asthma & COPD as they also block b2 leading to bronchoconstriction

25
Q

Side effect of alpha 1 antagonists

A

Tachyarrythmias

Orthostatic hypotension

26
Q

SIDE EFFECTS OF BETA BLOCKERS

A

Reflex tachycardia

Vasodilative properties—> Decrease in heart beat so the heart tries to compensate by beating fast

27
Q

Main form of treatment in glaucoma

A

Pilocarpine

it decreases intraocular pressure

28
Q

Long Acting beta adrenergic agonist

A

Formoterol

Salmeterol

29
Q

Short acting beta adrenergic agonist

A

fenoterol

salbutamol