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FUN F > F5 Autonomic pharmacology > Flashcards

F5 Autonomic pharmacology Flashcards

1
Q

describe how an action potential block occurs

A
  • blockage of voltage-gated sodium ion channels (main channel that triggers depolarisation)
  • prevents excitation of both pre and postsynaptic cells
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2
Q

what 2 drugs can block action potentials?

A
  • lidocaine (local anaesthetic)
  • lamotrigine (anti epileptic)
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3
Q

describe lamotrigine effects

A
  • acts in the CNS
  • voltage-gated sodium ion channel blocker
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4
Q

describe how lidocaine can block sodium ion channel pore

A
  • blocks the pore of the channel after it has opened by docking into it
  • prevents the passage of ions so no triggering of an action potential
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5
Q

what does the inhibition of synthetic enzymes lead to?

A

depletion of transmitter

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6
Q

what is methyl-DOPA and what happens when it is supplied?

A
  • a false substrate for DOPA decarboxylase
  • gets converted by DOPA decarboxylase and produces methyl-dopamine (can’t be converted into noradrenaline)
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7
Q

what does the production of methyl-dopamine by DOPA decarboxylase lead to?

A
  • saturation of cell by making false products that aren’t useful or making noradrenaline
  • depletion of vesicles
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8
Q

what can not be converted into noradrenaline?

A

methyl-dopamine

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9
Q

what is the precursor for noradrenaline?

A

dopamine

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10
Q

how can L-DOPA be used?

A
  • therapy in Parkinson’s disease
  • gets converted into dopamine in the CNS and alleviates some symptoms
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11
Q

what can prevent vesicle loading?

A
  • inhibition of vesicle transporter
  • reserpine blocks NA uptake (and other monoamines)
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12
Q

what does reserpine do?

A

blocks neurotransmitter loading

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13
Q

what happens if neurotransmitter fails to load?

A
  • vesicles fail to load / package
  • stores are depleted by ongoing activity
  • there won’t be anymore neurotransmitter released because they’re not packaged into vesicles
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14
Q

what does calcium trigger in synapses?

A
  • vesicle fusion and transmitter release
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15
Q

what does conotoxin do?

A
  • blocks calcium channels
  • used in experiments for further studies on how to block calcium channels, not used therapeutically
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16
Q

what does botulinum toxin (botox) do?

A
  • degrades vesicle release machinery
  • very potent, a small amount can shut down synaptic transmission
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17
Q

what does antagonism of ionotropic receptors cause?

A

prevents depolarisation of the postsynaptic cell

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18
Q

what are the several mechanisms of antagonism of ionotropic receptors?

A
  • occupy NT binding site
  • prevent channel opening
  • block the open pore
19
Q

explain the mechanism of the antagonists of ionotropic receptors: occupy NT binding site

A

competitive antagonist and blocks ion channel

20
Q

explain the mechanism of the antagonists of ionotropic receptors: prevent channel opening

A

make a molecule that binds to an allosteric site which will cause a conformational change in the binding site

21
Q

explain the mechanism of the antagonists of ionotropic receptors: block the open pore

A
  • similar to Lidocaine
  • binds to the pore of the open channel which prevents any influx
22
Q

what does antagonism of metabotropic receptors cause?

A
  • prevents target cells from responding to released NT
23
Q

what do antagonists that bind to metabotropic receptors do?

A

occupy binding site or allosteric site or inhibit G protein activation

24
Q

what does inhibition of transporters / degradation enzymes lead to?

A

prolonged activation of postsynaptic cell

25
Q

what does amitriptyline do?

A
  • inhibits NA uptake
  • antidepressant that inhibits noradrenaline reuptake
  • leads to more NA at the synapse to bring about more signalling
26
Q

how are drugs used on the ANS? 2 methods

A
  • aimed at correcting defects in the ANS itself
  • (more commonly) exploit the ANS to correct other problems
27
Q

give examples of defects in the ANS that drugs can be used to target

A
  • primary or secondary autonomic dysfunction
  • diabetic neuropathy (neurons in the CNS are dying off so drugs are used to correct this issue)
28
Q

give some examples of issues that can be corrected by drugs targeting the ANS that are not ANS specific

A
  • hypertension
  • asthma
  • incontinence
29
Q

give 3 examples of antagonist drugs (1 mAChR blocker, 1 beta AR blocker and 1 alpha AR blocker)

A
  • Tropicamide (mAChR blocker)
  • Atenolol (beta AR blcoker)
  • Tamsulosin (alpha AR blocker)
30
Q

give 3 examples of agonist drugs (1 beta AR agonist, 1 mAChR agonist and 1 nAChR agonist)

A
  • Salbutamol (beta AR agonist)
  • Pilocarpine (mAChR agonist)
  • Nicotine (nAChR agonist)
31
Q

what are the indications for beta blockers?

A
  • hypertension
  • angina
  • arrhythmias
32
Q

what are the contraindications for beta blockers?

A
  • asthma
  • COPD
  • bradycardia (slow heart rate)
  • severe peripheral arterial disease
33
Q

what is bradycardia a contraindication for beta blockers?

A
  • beta blockers reduce heart rate
  • don’t want to reduce a heart rate that is already slow
34
Q

side effects of beta blockers

A
  • bronchospasm
  • GI disturbances
  • hypotension
  • bradycardia
  • visual disturbances
  • headache
  • dizziness
35
Q

general effects of beta blockers

A
  • counteracts sympathetic input
  • reduce cardiac output
  • risk of pulmonary side effects
36
Q

what are antimuscarinics?

A
  • antagonists for muscarinic acetylcholine receptors
  • eg. Hyoscine, Atropine, Oxybutynin
37
Q

what are the indications for antimuscarinics?

A
  • bradycardia
  • GI disorders
  • urinary incontinence
  • ophthalmology
  • premedicants to dry bronchial and salivary secretions (especially during surgery
38
Q

contra-indications for antimuscarinics

A
  • glaucoma
  • myasthenia graves (muscle weakness)
  • urinary retention
39
Q

side effects of antimuscarinics

A
  • dry mouth
  • blurred vision
  • constipation
  • tachycardia
  • palpitation
  • arrhythmias
40
Q

general effects of antimuscarinics

A
  • enhances sympathetic activities, counteracts parasympathetic input
  • inhibits glandular secretion
  • blocks smooth muscle contraction
41
Q

what can cause over dilation of pupils?

A
  • too much activation of sympathetic nervous system
  • too much suppression of the parasympathetic system
42
Q

what are on and off target side effects?

A
  • on target: hitting the right target in the wrong place
  • off target: hitting the wrong target
43
Q

what are pharmacodynamics?

A

what target does the drug bind to?

44
Q

what are pharmacokinetics?

A

where does the drug go in the body?

FUN F (9 decks)

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