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Year 2 - Pharmacology and Therapeutics > Cholinoceptor Antagonists > Flashcards

Cholinoceptor Antagonists Flashcards

1
Q

Affinity?

A

Ability to bind to a receptor

BOTH agonists and antagonists

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2
Q

Efficacy?

A

Ability to induce a biological response

Agonist ONLY

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3
Q 
Which of the following drugs has efficacy for the muscarinic acetylcholine receptor?
x Acetylcholine
x Atropine
x Acetyl-cholinesterase
x Adrenaline
x Acetate
A

A!

A - has it is a agonist
B - its an antagonist so WILL NOT have efficacy
C - enzyme in synapse so NO
D - agonist BUT not for muscarinic BUT for adrenoceptor
E - breakdown product of Ach so NO

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4
Q

Another name for nicotinic receptor antagonists?

A

Ganglion-blocking drugs (GBDs)

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5
Q

How do GBDs act?

A

Either:
1. Block the nicotinic receptor

AND/OR

  1. Physically block the ion-channel itself i.e. CHANNEL BLOCKERS (technically not a receptor antagonist then)
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6
Q

Use-dependent blocks for GBDs?

A

Drug works best when channel is OPEN
i.e. the more the receptor is used, the more it is blocked

(weird because should be the opposite if have more agonist)

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7
Q

Incomplete blocking for GBDs?

A

Ion-channel blockade in only PARTIAL (some ions still pass through)

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8
Q

Do all GBDs have affinity?

A

NO!

x If blocking receptor = YES
x If blocking ion-channel = NO as just a physical block

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9
Q

2 examples of GBDs?

A

Hexamethonium

Trimetaphan

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10
Q

Difference between Hexamethonium and Trimetaphan in its MOA?

A

H:
ION-CHANNEL BLOCKER

(so not a lot of affinity)

T:
RECEPTOR ANTAGONIST

(so has affinity)

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11
Q

What effect would you see GBDs have on the body?

A

Depends upon body situation so if in:
x fight & flight
OR
x rest & digest

I.E. if PSN is dominant, will see its effect diminish

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12
Q 
Which of the following effects would 
be observed at rest after treatment 
with a ganglion blocking drug?
x Increased heart rate
x Pupil constriction
x Bronchodilation
x Detrusor contraction
x Increased gut motility
A

A & C!

  1. PSN slows the heart so YES
  2. Pupils are always partially constricted - driver by PSN so will see opposite
  3. Lungs are partially constricted via. PSN as will then allow further constriction or dilation so YES
  4. Detrusor under PSN control (allows bladder emptying) so would see relaxation if blocked
  5. PSN would drive gut motility so
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13
Q

When is Hexamethonium used?

A

One of the first anti-hypertensive drugs BUT had lots of side-effects as very general

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14
Q

When is Trimetaphan used?

A

When want hypotension

i.e. during surgery as short-acting

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15
Q

How/why does Hexamethonium cause hypotension when given at rest?

A

Heart:
NO BENEFICIAL EFFECTS as PSN keeps HR steady, so diminishing it acc speeds up HR

KIDNEY:
DECREASE RENIN production (so affects aldosterone and AGTII (no constriction))

BLOOD VESSELS:
DILATION of vessels so TPR decreases = BP decreases

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16
Q

GBDs affects on smooth muscle?

A

x Pupil DILATION
x DECREASED GI TONE
x Bladder DYSFUNCTION
x BronchoDILATION

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17
Q

GBDs affects on exocrine secretions?

A

DECREASE

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18
Q

Alpha-bungarotoxin?

A

Irreversible GBD (released as venom)

Need to replace whole receptor if want to restore function

19
Q

Difference between alpha-bungartoxin and Hexamethonium & Trimetaphan?

A

Alpha - bind mainly to SOMATIC nicotinic receptors (target skeletal muscles so cannot move or breathe)

H & T - bind mainly to AUTONOMIC nicotinic receptors

20
Q

Why can nicotinic receptors not be used therapeutically as much?

A

Has TOO many SIDE-EFFECTS (as found along the whole system)

21
Q

What are muscarinic receptor antagonists (MRAs) mostly?

A

Mainly PSN antagonist

only found in SN at sweat glands

22
Q

2 examples of MRAs?

A

Atropine

Hyoscine

23
Q

2 MRAs that affect CNS?

A

Atropine & Hyoscine

24
Q

Atropine affect on CNS?

A

Normal dose = little effect (M1 selective)

Toxic dose = mild restlessness –> agitation

25
Q

Hyoscine affects on CNS?

A

Normal dose = sedation, amnesia (compare w. atropine!)

Toxic dose = CNS depression or paradoxical CNS excitation

26
Q

Why is there a difference seen between Atropine and Hyoscine on the CNS even though they are structurally very similar?

A

Hyoscine is very lipid-soluble so possibly due to a GREATER PERMEABILITY through the BBB into the brain (can access deeper brain structures more)

27
Q

Ophthalmic effects of MRAs?

A

Tropicamide - drug used

Used to prevent pupil constriction (PSN) as paralyses the muscles = pupil dilation = can EXAMINE RETINA more easily

28
Q

How are MRAs used as Anaesthetic pre-medication?

A

Lungs - BLOCKS constriction:
so causes vasodilation = if inhale anaesthesia, can take in more

Salivary glands - BLOCKS secretions:
prevents secretions going down airway as when anaesthetised cannot control this

Heart - BLOCKS reduce in HR & contractility:
Anaesthesia also reduces HR & C along with PSN so essentially protects HR from slowing down too much

ALSO has SEDATIVE effect

29
Q

MRAs use neurologically in motion sickness?

A

Hyoscine patch

Inhibits MRs in the VOMITING CENTRE:
x so sensory mismatch cannot induce vomiting when suffering from motion sickness

30
Q

How does motion sickness arise?

A

Sensory mismatch!

Visual coming from the eyes does NOT match information coming from the LABRYINTH in the ears (giving different info about balance & motion)

SO

this mismatch stimulates the vomiting centre

31
Q

Why does Parkinson’s Disease arise?

A

Loss of dopaminergic neurones in the substantia nigra

SO

less dopamine released into the striatum (D1R) = affects fine muscle tone & movement

32
Q

How can MRAs be used in Parkinson’s?

A

M4 receptors have an inhibitory effect on D1R

SO

Give MRAs = D1R MORE RESPONSIVE
x still producing less dopamine
BUT
x heightened D1R so can still respond to low levels of dopamine release

33
Q

Salbutamol?

A

Blue inhaler!

Acts as an AGONIST for the adrenoceptors = bronchodilation (beta-2)

34
Q

MRAs used in respiratory diseases such as asthma/OAD?

A

Ipratropium Bromide

not Atropine as much

35
Q

Why is one drug preferred more than the other in respiratory diseases such as asthma/OAD?

A

Ipratropium bromide has an additional nitrogen-polar group
SO
cannot cross mucosa (as easily as ATROPINE) so have a more LOCALISED EFFECT = reduces side-effects

36
Q

Difference between salbutamol and MRAs for respiratory diseases?

A

Salbutamol - AGONIST

MRAs - ANTAGONIST

37
Q

How are MRAs used in GIT?

A

Used for IBS (hyperactive gut)!

Decreases GI tone & secretions (M3 receptor antagonists)

38
Q

Unwanted effects of MRAs?

A

‘Hot as hell’
Decrease in sweating & thermoregulation defects

‘Dry as a bone’
Decreased secretions

‘Blind as a bat’
Cyclopegia (paralysis of ciliary muscles so no accommodation)

'Mad as a hatter'
CNS disturbance (i.e. tremors)
39
Q 
Which of the following drugs would you
administer to treat an atropine overdose?
x Bethanechol
x Ecothiopate
x Hyoscine
x Physostigmine
x Pralidoxime
A

A, B & D

A - stable version of Ach (longer-lasting)

B & D - cholinometrics (block acetyl-cholinesterase) so allows Ach to build up
• D is reversible, B is not so would choose D!

C - antagonist so NO as contributing to the block then

E - do not know what it is (rescues acetyl-cholinestease e.g. Is posionsed, would take this to recover some of the active enzymes)

I.E. would want to give a drug that either
x enhances Ach activity (anticholinesterase)
OR
x Inhibits atropine

40
Q

Bethanechol?

A

MRA

41
Q

Ecothiopate?

A

Irreversible anticholinesterase

42
Q

Physostigmine?

A

Anticholinesterase

Block this so prevent Ach from being metabolised = establish a COMPETITIVE AGONIST = so can restore MR function (which atropine diminished)

43
Q

Botulinum Toxin?

A

Prevents Ach exocytosis!

Binds to Ach vesicles ( blocking the SNARE complex) = cannot access skeletal muscles = paralysis

(this is BOTOX!!!)

Year 2 - Pharmacology and Therapeutics (9 decks)

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