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Neuroscience > Pharmacology > Flashcards

Pharmacology Flashcards

0
Q

What is the sequence of dopamine synthesis?

A
  • Tyrosine enters cell
  • Converted into L-DOPA
  • L-DOPA converted into dopamine
  • Dopamine transported into vesicles
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1
Q

What drugs interfere with neuronal uptake of NA in the CNS?

A

Cocaine inhibits high affinity neuronal uptake

Amphetamine/ephedrine displaces NA from vesicles and causes non-exocytotic release of NA

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4
Q

What is the sequence for catecholamine biosynthesis?

A
  • Tyrosine enters cell
  • Converted to L-DOPA
  • L-DOPA converted to dopamine
  • Dopamine is transported into vesicle
  • Dopamine converted into NA
  • NA converted into Adr
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5
Q

How does cocaine act?

A
  • Blocks uptake of NA, dopamine and serotonin
  • Dopaminergic action linked to dependence
  • NAergic and serotonergic actions related to euphoria and reward
  • Blocks Na+ channels (anaesthetic drugs)
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6
Q

What type of ligand-gated ion channels are in the CNS?

A

Excitatory (nicotinic) - Na+ influx causes depolarisation

Inhibitory (GABA A) - Cl- influx causes hyperpolarisation

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7
Q

What is the effect of receptor location on neurons?

A

Receptors on post-synaptic cleft can generate APs

Receptors in pre-synaptic cleft can modulate neurotransmitter release

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8
Q

What neurotransmitters are implicated in movement disorders?

A

-Dopamine: degeneration of dopaminergic neurons in Parkinson’s disease (RX L-DOPA and Dopa decarboxylase inhibitor)
-GABA: GABA deficiency in Huntington’s disease (RX GABA agonist and dopamine antagonist)
(Concept: Multiple neurotransmitters can be involved in disease)

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9
Q

What pathways is dopamine involved in?

A

-Movement: basal ganglia
-Behaviour: schizophrenia
-Dependence and reward: nucleus accumbens and ventral tegmental area
-Pituitary function: prolactin secretion
(Concept: a single NT can be involved in multiple diseases)

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10
Q

What regulates nerve excitability?

A

Ion channels and receptors

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11
Q

What is the MOA of local anaesthetics?

A
  • reversibly block conduction of nerve impulses at the axonal membrane
  • Bind to transmembrane domain IV of Na+ channels
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12
Q

What are 3 classes of local anaesthetics?

A
  • Aminoesters (e.g. procaine) - short acting (enzymatic hydrolysis)
  • Aminoamides (e.g. lignocaine) - longer acting (hepatic metabolism)
  • Benzocaine
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13
Q

What are the mechanisms of local anaesthetic binding to Na+ channels?

A
  • Hydrophobic binding does not depend on activity of Na+ channels (e.g. MOA of benzocaine)
  • Hydrophilic binding depends on the activity of Na+ channels (e.g. aminoester and aminoamides): hydrophilic drugs are charged and require Na+ channel to be open in order to bind to active site
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14
Q

What are the adverse effects of local anaesthetics?

A

Side effects that are proportional to blood concentration:

  • hypotension (excl cocaine)
  • myocardial depression
  • inhibits inhibitory fibres: excitation, tremor, convulsion, resp arrest

Allergic reactions (independent of blood concentration):

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15
Q

What are the stages of general anaesthesia?

A

Stage 1: amnesia and euphoria
Stage 2: Excitement and delirium
Stage 3: Unconscious, regular resp, decreased eye movements
Stage 4: resp arrest, cardiac depression and arrest

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16
Q

What are some adverse effects of general anaesthetics?

A
  • depression of resp centre
  • obstruction of airways
  • peripheral vasodilation
  • cardiac arrythmias
  • depress cardiac contractility
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17
Q

What are the MOA of general anaesthetics?

A
  • Lipid theory: potency related to lipid solubility - accumulates in lipid space
  • Receptor interaction: inhibit excitatory receptors and enhance the effects of inhibitory receptors
18
Q

What are ways to modulate nerve excitability?

A
  • enhance inhibitory inputs (e.g. enhance GABA receptor activity)
  • limit excitatory nerve activation (e.g. inhibit Na+ channels)
  • inhibit T-type Ca++ channels
  • inhibit NMDA receptor
19
Q

What is the scientific basis of benzodiazepines?

A

-enhance GABA A receptors (ligand gated ion channels) leading to decreased neuronal excitability and depressed CNS function which can reduce muscle contractions
therefore used in practice as a sedative, hypnotic and muscle relaxant

20
Q

What is the MOA of benzodiazepines?

A
  • Bind to specific binding site on GABA A receptor
  • Increases receptor affinity for GABA (increased sensitivity)
  • Increases the frequency of Cl- channel openings
  • Allosteric modulator
21
Q

What is potency?

A

Relative position of dose-effect curve along the dose axis
High potency not related to therapeutic effect
The higher the potency, the lower the dose administered

22
Q

What is efficacy?

A

The ability of a drug to have a particular action
Pharmacological efficacy = strength of receptor activation
(full agonist has high efficacy and partial agonist has low efficacy)
Clinical efficacy = strength of the beneficial effect

23
Q

How do benzodiazepines and barbituates compare?

A

Both potentiate the effect of GABA through GABA A receptor but
BDZs increase frequency of Cl- channel openings but does not change maximum response of the channel
BDZs increase the potency of GABA
Barb prolong Cl- channel openings and increase the maximum response of the channel
Barbs increase the efficacy of GABA
BDZs have wider therapeutic index than barb

24
Q

What are actions of dopaminergic drugs?

A
  • increase DA synthesis (L-DOPA and DCC inhibitor)
  • increase DA release
  • DA receptor agonists
  • reduce DA metabolism (inhibit COMT to reduce metabolism of L-DOPA and inhibit MAO B to reduce metabolism of DA)
25
Q

What are key transmitter systems in the brain reward pathway?

A

Dependence related to increased DA in nucleus accumbens
Transmitters which modulate DA transmission:
-ACh, serotonin, NA, GABA, glutamate, opioids

26
Q

What issues are associated with amphetamine use?

What are the adverse effects?

A

Dependence related to DAnergic actions in the nucleus accumbens

Ecstasy: releases DA and serotonin
psychological dependence, sympathomemetic, disrupted thermoregulation, potential degeneration of neurons caused by toxic metabolites (possible effects on mood, memory, sleep and appetite), psychosis

27
Q

What is MOA of TCA?

A
  • inhibits neuronal uptake of NA and 5-HT
  • poorly selective
  • takes weeks for clinical effects to develop
  • narrow therapeutic window (limited efficacy)
28
Q

What is MOA of MAOIs?

A
  • inhibit metabolism of 5-HT, NA, and DA
  • serotonin syndrome (tyramine-containing foods can precipitate hypertensive crisis)
  • weight gain
  • liver toxicity
29
Q

MOA of SSRIs?

A
  • inhibit uptake of 5-HT selectively
  • high therapeutic index
  • increased anxiety and suicidal tendencies in adolescents
  • sexual dysfunction
30
Q

What are the components of noradrenergic transmission?

A
  • Influx of Ca++ causes release of NA in vesicles
  • NA can activate alpha and beta receptors on postjunctional folds
  • NA can also activate alpha receptors on prejunctional folds
  • NA can be inactivated via neuronal uptake (high affinity) and degradation by MAO as well as via extraneuronal uptake (low affinity) and degradation by MAO and COMT
33
Q

What are the components of chemical neurotransmission that can be used as targets for drug action?

A
  • Synthsis/storage of neurotransmitter
  • Release of vesicles containing neurotransmitter (Ca++ influx)
  • Inactivation of neurotransmitter (uptake or metabolism)
  • Receptors (pre and postjunctional folds)

Neuroscience (9 decks)

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