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Pharmacology > Dawn Livingstone > Flashcards

Dawn Livingstone Flashcards

1
Q

What causes the establishment of membrane potential?

A

The uneven distribution of ions inside and outside the cell

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2
Q

What is the name of the equation which determines the equilibrium potential? And from the equation what determines equilibrium potential?

A

Nerst equation

  1. Relative concentrations of ion inside and outside the cell
  2. Valency: charge that the ion carries
  3. Temperature
  4. Energy
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3
Q

Entry of positive ions during the action potential causes depolarisation of the membrane just ahead and threshold to be reached.
This initiates the action potential conduction along the axon …(1) only, as the Na+ channels enter the …(2)

Na+ channels are present at high density in the …(3)

AP ‘leap’ from one NoR to the next: …(4)

A

(1) in one direction
(2) refractory period
(3) Nodes of Ranvier
(4) saltatory conduction

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4
Q

How many efferent nerve(s) are there in the somatic and autonomic nervous system?

A

Somatic: one somatic efferent

ANS: two efferent nerves between the CNS and effector tissue

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5
Q

Where is the cell body of the autonomic neurones located?

A

Spinal cord which projects to the ganglion then effector tissues

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6
Q

Describe the synthesis of Ach

A

Acetyl-CoA (release from the mitochondrion) + choline -> acetylcholine

Enzyme: choline acetyltransferase

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7
Q

Describe the storage of Ach

A

Ach is transported into the vehicle by a specialised transporter. Once transported the vesicles are stored at the nerve endings ready to be released.
Each synaptic vesicles contains thousands of molecules of Ach

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8
Q

Describe the release of Ach

A
  • Neurotransmitter is released from the pre-synaptic nerve terminals following entry of calcium ions via Ca voltage gated channels
  • Since the synaptic cleft has a very small volume, high conc. of Ach is achieved
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9
Q

Describe the activation and termination of Ach

A

Ach binds to its receptor (either nicotinic or Muscarinic receptor) in the post-synaptic nerve terminals. Eliciting a response in the post-synaptic nerve.

It is degraded rapidly by the enzyme acetylcholine esterase into choline and acetate. The product of the degradation is transported back to the pre-synaptic terminals.

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10
Q

What is the antagonists for nicotinic Ach receptor and Muscarinic Ach receptor?

A

Nicotinic: curare

Muscarinic: atropine

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11
Q

Explain why nAchR is denoted as a cation channel and which region of the channel twist and causing the channel to open when Ach is bound to it?

A

The subunits are arranged so that the pore is lines with TM2. This formed a negatively charged ring in the pore, hence it attracts cations.

The TM2 regions of the channel twist to open the channel.

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11
Q

State what mAchR can activate and inhibit.

A

Activate:

  • phospholipase C to cause the production of IP3 and diacyl glycerol
  • K+ channels

Inhibit:

  • adenylate cyclase causing a decrease in the levels of cAMP
  • Ca2+ channels
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11
Q

Name the different types of mAchR and state where they are found.

A

M1 - neural
M2 - cardiac (decrease HR and force of contraction - parasympathetic)
M3 - secretion, contraction of smooth muscle in the gut, vascular relaxation
M4 and M5 - found in CNS

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12
Q

name a drug which:

  1. block the transport of choline into terminal (synthesis)
  2. inhibits transport of Ash into vesicles (storage)
  3. blocks NaVGC (release)
A
  1. hemicholinium
  2. vesamicol
  3. TTX
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13
Q

describe the mechanism of botulinum toxin

A

it prevents the fusion synaptic vesicles with membrane of the presynaptic terminal

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14
Q

which Ace receptor is present in the neuromuscular junction?

A

nicotinic Ach receptor

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15
Q

define EPP

A

binding of Ach in postsynaptic membrane which causes sodium ions to flow into the postsynaptic cell causing depolarisation

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16
Q

which receptor does bungratoxin target

A

potent nAChR antagonist

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17
Q

name a drug that inhibits the transport of choline into nerve terminal

A

hemicholinium

18
Q

name a drug that blocks the transport of acetylcholine into vesicles

A

vesamicol

19
Q

which process does botulinum toxin prevents?

A

prevent fusion of synaptic vesicles with membrane of the presynaptic terminal

20
Q

name the treatments of botulinum toxin

A
  • eyelid spasm
  • bladder overactivity
  • excessive muscle tone
21
Q

explain what is meant by EPP

A

the activation of Ace receptor channels causes sodium ions to flow into post-synaptic cells causing depolarisation

22
Q

define non-depolarising blockers which class of drug can overcome the blocking action of non-depolarising drug?

name an example of such drug

A

compete with acetylcholine for the agonist binding site on the nAchR. therefore they are competitive receptor antagonists.

anti-cholinesterase drug which increases [agonist]

atracurium which is short acting non-depolarising blockers

23
Q

define depolarising blockers. name a drug in this class, describe its structure its mechanism of action.

A

depolarising blockers activate the nicotinic receptor.

suxamethonium is two acetylcholine molecules linked together by their acetyl group

Suxamethonium produces a sustained depolarisation at the endplate that ultimately lead to receptor inactivation (pore does not open in response to agonist binding)

24
Q

why does depolarising blocker have short duration of action? what is the implication and name their side effects

A

because they are broken down cholinesterase therefore only used in brief procedures.

side effect:
- bradycardia (direct muscarinic action, low heart rate)

25
Q

what is myasthenia graves (MG) and which receptor does it affect?

A

MG is an autoimmune disease characterised by muscle weakness. due to antibody attacking the nAchR (post synaptic) at the NMJ.

26
Q

name a drug use to treat MG and what does this drug do?

A

neostigmine

It is a reversible AchE inhibitor, it increases the conc. of Ach in the synaptic cleft increasing the chance of interaction with functional receptor

27
Q

what is observed in the electrical and mechanical response in MG patients?

A

they decrease overtime whereas control, the response is sustained.

28
Q

remember that muscarinic receptors mediate the action of PSNS, therefore what can it activate and inhibit?

A

activate:
- phospholipase C -> production of IP3 and DAG (diacyl glycerol)
- K+ channels

inhibit:

  • Ca2+ channels
  • adenylate cyclase -> decrease in cAMP
29
Q

M1, M2 and M3 name where these receptors are present

A

M1: neural (slow EPSP in ganglia)

M2: cardiac (mediate decrease of rate and force of contraction)

M3: smooth muscle in the gut, vascular relaxation

30
Q

referring to the structure of Ach, which group addition accounts for the selectivity for muscarinic AchR? name an example of the drug

A

addition of methyl group in Ach molecule makes compound more selective for muscarinic

metacholine and bethanecol

31
Q

which group substitution makes a compound resistance to AchE break down?

A

substitution of methyl for amine group

32
Q

describe the action of carbachol

A

have both effects in the muscarinic and nicotinic receptors but resistant to AchE because have amine group at the end

33
Q

name the therapeutic uses of atropine

A
  • myocardial infarction: blockade of Sino-atrial node muscarinic receptors -> allow sympathetic dominance
  • pre-anaesthetic
  • ophthalmological: muscarinic receptor blockade causes pupil dilation
  • PD’s: muscarinic blockade in the basal ganglia, restore balance in cholinergic and dopaminergic systems
  • poisoning of cholinomimetics: counteract the effect of over activation of muscarinic receptor
34
Q

name two cholinesterases

A
  1. acetylcholinesterase: found in ALL cholinergic synapse

2. butyrylcholinesterase: hydrolyses other esters such as suxamethonium

35
Q

name two reversible cholinesterase inhibitors and explain of it inhibits AchE

A
  • physostigmine
  • neostigmine

binds to catalytic site and catalysed the transfer of caramel to serine. Carbamyl-serine can be hydrolysed re-storing the enzyme function

36
Q

explain how irreversible AchE inhibits AchE and name a drug that could restore the enzyme

A

phosphorylation of the enzyme which can be re-phosphorylate by pralidoxime, re-storing the enzyme function

37
Q

side effect of activation and blockade of muscarinic receptors

A

activation: bradychardia
blocking: tachycardia

38
Q

name the effects mediated by M3 receptors

A
  • exocrine gland secretion
  • increase gut motility
  • increase miosis in spinchter
  • increase accommodation via cilliary
  • bronchoconstriction
  • bronchodilation
39
Q

name four cholinergics and state what they treat

A
  1. metacholine: bronchospasm in asthma challenge test
  2. bethanechol: post op and urinary retention
  3. carbachol: glaucoma
  4. pilocarpine: cystic fibrosis sweat test and glaucoma

these are also considered as mAchR agonist

40
Q

name six anti-acetylcholinesterase and what they treat

A
  1. edrophonium: diagnostic of MG to differentiate it with cholinergic crisis
  2. neostigmine: to treat MG, urinary bladder atony, reversal of non-depolarising blockNO BBB
  3. physostigmine: atropine overdose (intoxication by antimuscarinic drug) can cross BBB
  4. echotiophate: glaucoma
  5. donepezil: Alzheimer’s
    (balance between cholinergic and dopaminergic system, in Alzheimer’s patient, Ach level is low)
  6. tacrine: Alzheimer’s (balance between cholinergic and dopaminergic system, in Alzheimer’s patient, Ach level is low)
41
Q

name 5 mAchR antagonists and state what they treat

A
  1. atropine
  2. ipratopium: treat asthma, bronchodilator of smooth muscle in the airways
  3. benztropine: atropine derivatives, treats PD’s
  4. oxybutynin: urinary incontinence, reduce bladder spasm
  5. pirenzepine: peptic ulcers
42
Q

name the drugs use to treat anti-AchE poisoning

A

atropine to counteract bradycardia and excessive secretion (remember stimulation of M3 associated with exocrine gland secretion)

pralidoxime to reactivate the enzyme due to irreversible inhibition of AchE

43
Q

what happened to the rats that were given atropine in the learning of the location of the platform?

A

they take longer to learn, this concludes that the mAchR are associated with spatial learning

44
Q

in the hippocampus, what prolonged the synaptic potential and which drug blocks it?

A

prolonged by physostigmine (AchE) and blocked by antagonist atropine

Pharmacology (8 decks)

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