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pharm - OBG > Parasympathetic NS > Flashcards

Parasympathetic NS Flashcards

1
Q

how do directly acting cholinomimmetic drugs produce their biological effect

A

exogenous agonists of specific ACh receptors

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2
Q

how do indirectly acting cholinomimmetic drugs produce their biological effect

A

inhibitions of Acetylcholinesterase- present in ALL cholinergic synapses,
this causes build up of Ash in synapse- therefore increasing its effect

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3
Q

why are directly acting cholinomimmetic drugs more selective in their actions than indirectly acting ones

A

because exogenous agonists only agonise specific receptors but anticholinesterases are found in all PNS synapses so bring about its effect in all of them

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4
Q

what is the structure of nicotinic receptors

A

Type 2- Ligand gated ion channels (fast)

Must have 2 alpha units and then a mix of 3 others (beta, delta, epsilon, gamma)

Ganglion (‘neuronal’) type: 2α 3β

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5
Q

what is the structure of muscarinic

+what are the 3 main subtypes

A 
3 main types of receptors (5total)
M1-salivary glands, CNS, stomach
M2- HEART
M3- Salivary/sweat glands+ bronchial/viceral SM+eye
M4/M5: in CNS

ODD: Gq (PIP2–>IP3+DAG)-excitatory
EVEN: Gi (cAMP)-inhibitory

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6
Q

where are muscarinic and nicotinic receptors found

A

muscarinic- effector organs on the postsynaptic side (PNS) and also act on SNS sweat glands

Nicotinic- are found on the all ANS ganglions (PNS and SNS)

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7
Q

how do cholinomimmetics produce most of their effect on the PNS when SNS also has nicotinic receptors

A

Lower concentrations of ACh required to stimulate muscarinic receptors than nicotinic, so cholinomimetics bring about PNS effects.

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8
Q

what are the muscarinic receptor agonists (aka direct acting cholinomimmetics) and what are their uses and pharmacokinetic properties

A

Choline esters - BETHANECHOL - M3 selective-limited brain access- half life: 3-4h
Uses: Assist bladder emptying and gastric motility after surgery

Alkaloids - PILOCARPINE-non selective- good lipid solubility- half life- 3-4h
Uses: GLAUCOMA

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9
Q

what are the anti-cholinesterase drugs (aka indirect acting cholinomimmetics

A

Reversible:
- PHYSOSTIGMINE-Competes with ACh - half life 30mins
donates carbamyl group to enzyme- slowly removed
Uses: Glaucoma, Atropine poisoning

  • Neostigmine:
    Uses:-Reverse non-depolarising NM Block
    -Treat Myaesthenia gravis

Irreversible:
- ECOTHIOPATE- eye drops
Organophosphate compounds Rapidly reacts with active site to leave a large phosphate blocking group-Stable and resistant to hydrolysis.–May require new enzymes (Days/weeks)
Uses: Glaucoma (Prolonged DofA)

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10
Q

how does pilocarpine (musc agonist) treat glaucoma

A

because the PNS mediates sphincter papillae contraction, giving a musc agonist causes Contraction of the sphincter pupillae –>opens a pathway for aqueous humour, allowing drainage via the Canals of Schlemm thus reducing IOP–in glaucoma this is impeded

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11
Q

whats the difference between closed and open angle glaucoma

A 
open= caused by obstruction in trabecular meshwork or canals of schlemm 
closed= fluid can't drain out of the eye in the first place because iris is too close to lens
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12
Q

what effect do anticholinesterases have on the CNS

A

Non-polar anticholinesterases can cross the blood brain barrier:

Low doses–excitation with possibility of convulsions.
High doses–unconsciousness, respiratory
depression, death

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13
Q

what are the side effects of cholinomimmetics

A 
Sweating
Impaired/blurred vision
Bradycardia
Hypotension
Respiratory difficulty/Arrest
GI disturbance/pain
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14
Q

what are the effects of CHOLINOMIMETICS on the CVS

A

causes a DROP IN BP:

heart via M2:decrease HR (effect on nodes) and CO (via less atrial contraction)
Reduction of cAMP causes:
1.Decreased Ca2+ entry–>Decreased CO.
2.Increased K+efflux–> Decreased HR

Vasculature via M3: decrease in TPR due to SM relaxation
ACh acts on vascular endothelial cells to stimulate NO release viaM3 AChR–> NO acts on SM–> relaxation and reduction of TPR
(note: most blood vessels do not have PNS innervation)

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15
Q

what are the effects of CHOLINOMIMETICS on non vascular smooth muscle

A

causes contraction of non vascular smooth muscle:

Lung: Bronchoconstriction

Gut: Increased peristalsis (motility)

Bladder: Increased bladder emptying

(the last two are how BETHANECHOL has its effect)

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16
Q

what are the effects of CHOLINOMIMETICS on Exocrine Glands

A

Digestion:
Salivation
Increased gastro-intestinal secretions (HCl)

Increased bronchial secretions
Increased sweating (SNS-mediated)- due to sweat glands having musc receptors
17
Q

what are the signs and symptoms of anti cholinesterase poisoning

A

Low dose
– Enhanced muscarinic activity (see above)

Moderate dose
– Further enhancement of muscarinic activity
– Increased transmission at ALL autonomic ganglia (nAChRs)
– This is because the anticholinesterase increases the acetylcholine concentration at ALL cholinergic synapses, muscarinic and nicotinic

High dose (toxic)
– Depolarising block at autonomic ganglia & NMJ
– Nicotinic receptors get over stimulated -->SHUT DOWN
18
Q

what are the treatments for anti cholinesterase poisoning

A

Treatment = IV-atropine, artificial respiration, IV-pralidoxime- this unblocks the acetylcholinesterase enzymes

19
Q

explain how nicotinic receptor antagonists(ganglion blocking drugs, GBD’s) work

A

they affect ALL ANS ganglions (mostly PNS at rest and SNS during exercise)

MOA: Blocks receptor and/or channel pore
Channel pore bloackage:
   Use-dependent block (↑ agonist present = more accessible channel)
   Incomplete block (ion leakage)
20
Q

what effect do GBD have on body

A

depending on the situation they reduce activity of SNS or PNS

ie:
-At rest the reduce the PNS- , you would expect
to see an increased HR and bronchodilation after giving GBD
-During fight or flight they reduce the SNS

  • CVS effects: ^HR but hypotension–blood vessel vasoconstriction inhibited (as weirdly SNS tone dominates at rest) kidney renin secretion inhibited (so no AngII)-also SNS .
  • Smooth muscle effects: pupil dilation, decreased GI-tone, bladder dysfunction, bronchodilation.
  • Exocrine secretions: decreased secretions
21
Q

what are the main nicotinic receptor antagonists(ganglion blocking drugs, GBD’s) + toxins

A
  • Hexamethonium= 1st Anti-hypertensive (Blocks receptor and channel)
  • Trimetaphan = Hypotension during surgery, short acting (Blocks receptor only)

Toxin made by snake: alpha-bungarotoxin: irreversible, covalent block-Affects ANS + Skeletal muscles+Paralyses diaphragm and respiratory muscles

22
Q

what are the main musc receptor antagonists

A

Mainly PNS antagonist except sweat glands (SNS)

Atropine:
Normal dose – Little effect
Toxic dose - Mild restlessness  Agitation
(Less M1 selective)

Hyoscine:
Normal dose – Sedation, amnesia
Toxic dose – CNS depression or paradoxical CNS excitation (associated with pain)
(Greater permeation into CNS – more lipid soluble; more M1 selective)

Tropicamide: used for ophthalmic exam

23
Q

what are the clinical uses of MR antagonists:

A

o Opthalmology: Retina examination
-Tropicamide blocks PNS constriction of pupils  pupil dilation

o Pre-surgery:
-Blocks PNS bronchoconstriction – so anaesthetic has better access (as dilation takes place)
-Reduce saliva and GI secretions – prevent aspiration
Counteract HR decrease (many anaesthetics lower HR - dangerous)
-Sedation: Hyoscine

0 Motion sickness:
-Hyoscine patch: muscarinic receptors in the vomiting centre so the sensory mis-match cannot induce vomiting when suffering from motion sickness

o Parkinson’s Disease:
Muscarinic neurones inhibit dopamine release into striatum from alternative source (not SNc), therefore inhibiting the musc, prevents inhibition of dopamine release–>^dopamine in striatum

o Asthma/Obstructive airway disease
Blocks PNS bronchoconstriction–>bronchodilation(Atropine or Ipratropium Bromide)

o Irritable bowel syndrome (hyperactive gut)
Blocks (M3r-mediated) gut motility + tone, secretions

24
Q

what are the side effects of musc receptor antagonists

A

Hot as hell - less sweating, thermoregulation
Dry as a bone - less secretions
Blind as a bat - cyclopegia- Paralysis of the ciliary
muscle of the eye, resulting in a loss of
accommodation.

Mad as a hatter - CNS disturbance

25
Q

what are the signs and symptoms of atropine poisoning

A

Hot as hell - less sweating, thermoregulation
Dry as a bone - less secretions
Blind as a bat - cyclopegia- Paralysis of the ciliary
muscle of the eye, resulting in a loss of
accommodation.

Mad as a hatter - CNS disturbance

basically the side effects but worse

26
Q

how can you treat atropine poisoning

A

Treat with Physostigmine- (Anticholinesterase)-Increases [Ach], which outcompetes antagonist

27
Q

how does botulinum toxin work

A

Botulinum binds to the ACh vesicles and stops them
docking with the inner membrane.
Forms SNARE complexes—> no ACh released at NMJ—> paralysis

pharm - OBG (25 decks)

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