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Pharmacology > CNS Pharmacology > Flashcards

CNS Pharmacology Flashcards

1
Q

Explain the 4 important CNS receptors.

A
  • voltage gated
  • ligand gated
  • GPCR (metabotropic) which directly acts on the channels
  • GPCR (metabotropic) which activates 2nd messenger, which activates the channel
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2
Q

Draw diagrams of inhibitory and excitatory synaptic transmission

A

-CNS pharm

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3
Q

What are the 4 criterions of a neurotransmitter?

A
  1. localized
  2. released by electrical or chemical stimulation via a Ca dependent mechanism
  3. produce a postsynaptic response similar to nerve stimulation
  4. mechanism for termination of transmitter action
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4
Q

What are the 5 types of CNS neurotransmitters?

A
  • amino acids
  • acetylcholine
  • monoamines
  • peptides
  • endocannabinoids
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5
Q

Glutamate

A
  • amino acid
  • excitatory
  • ionotropic Rs (NMDAR, AMPAR, KAR)
  • metabotropic (mGLUR1,2,3)
  • terminated by glia uptake
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6
Q

GABA

A
  • amino acids
  • inhibitory
  • ionotropic and metabotropic
  • GABAb can be presynaptic
  • Cl-
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7
Q

Glycine

A
  • inhibitory
  • ionotropic (Cl-)
  • limited expression (SC and brainstem)
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8
Q

Acetylcholine

A
  • ionotropic (nicotinic), metabotropic (muscarinic)
  • excitatory/inhibitory
  • cognitive functions (sleep, wakefulness)
  • target in treatment of Alzheimers disease
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9
Q

Monoamines

A
  • dopamine, NE, 5HT
  • derived from amino acids
  • synthesis enzyme/neuron dependent
  • small amount
  • complex functions (alertness, consciousness, mood)
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10
Q

Draw out the monoamine synthesis pathways

A

-CNS pharm

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11
Q

Neuropeptides

A
  • opioids, pain sensation, target of analgesics
  • metabotropic
  • can be release in conjunction with other NTs
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12
Q

What are 2 ways that neuropeptides differ from non peptide transmitters?

A
  1. synthesized in cell body and transported to nerve ending

2. no reuptake or enzyme degradation identified for termination of action

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13
Q

Endocannabinoids

A
  • lipid signalling molecules
  • produced on demand (not stored)
  • act at presynaptic Rs
  • memory, cognition, pain perception
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14
Q

Sedative vs Hypnotic Drugs

A

sedative (anxiolytic): reduces a person’s response to external stimuli
Hypnotic: drowsiness and sleep like state, a sedative drug at higher doses

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15
Q

Compare the dose response curves-benzos vs. barbs

A

-sedative hypnotic drugs lecture

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16
Q

Pharmacokinetics of Benzodiazepines

A
  • absorbed from the gut, rapidity of onset related to lipid solubility
  • the rate at which BZ crosses into the cerebrospinal fluid is dependent on protein binding, lipid solubility, ionization constant
  • easily cross the BBB and the placental barrier
  • duration of action determines use
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17
Q

BZs as a prodrug

A
  • half life represents the combined actions of the parent drug and its active metabolites
  • excreted as glucuronides or oxidized metabolites
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18
Q

T or F: the shorter the half life, the more aggressive the withdrawal symptoms

A

T

-also causes tolerance (triazolam gives early morning insomnia, day time anxiety, amnesia and confusion)

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19
Q

What are 3 drug interactions of sedative hypnotic drugs?

A
  1. BZ act in an additive manner with alcohol, barbs, anticonvulsants
  2. smoking induces P450 2C enzyme which metabolizes BZ
  3. SSRIs increase diazepam levels by altering clearance
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20
Q

Explain the effect of benzodiazepines on the GABA R

A

sedative hypnotic drugs lecture

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21
Q

Therapeutic uses of barbs

A
  • anesthesia-influenced by duration of action (thiopental, an ultra short acting barb used to induce surgical anesthesia_
  • anticonvulsant-phenobarbital used in long term management of tonic clonic seizures
  • anxiety-can be used as mild sedatives (anxiety and insomnia), mostly replaced by BZ
22
Q

Antihistamines

A
  • some histamine antagonists cross BBB (e.g. diphenhydramine, hydroxyzine, doxepin)
  • produce sedation via H1 mediated red in Ach release in reticular nuclei
  • used to treat mild insomnia and anxiety
23
Q

Buspirone

A
  • MOA mediated by 5-HT1A Rs
  • treatment of generalized anxiety disorders
  • little sedation, anti convulsant or muscle relaxant properties
24
Q

Zolpidem

A
  • imidazopyridine derivative
  • binds directly to BZ R, increases GABA mediated inhibition
  • short term treatment of insomnia
25
Q

Ramelteon

A
  • activates melatonin Rs in suprachiasmatic nuclei
  • decreases latency of sleep onset
  • min rebound insomnia and abuse potential
26
Q

Orexin antagonists

A
  • suvorexant
  • hypnotic
  • orexin is a peptide found in the hypothalamus and is involved in wakefulness
27
Q

A short acting BZ

A

triazolam

28
Q

An intermediate action BZ

A

-alprazolam

29
Q

A long acting BZ

A

flurazepam

30
Q

An ultra short acting barb

A

thiopental

31
Q

A short acting barb

A

-secobarbital

32
Q

A long acting barb

A

-phenobarbital

33
Q

Monoamine Oxidase

A
  • a mitochondrial enzyme found in neural and other tissues that inactivates excess monoamines in nerve endings
  • causes their degradation
34
Q

What is the mechanism of action of MAO inhibitors

A
  • inhibit the enzyme
  • more NE/5HT is taken up
  • more is released in response to stimulus
35
Q

What are the adverse effects of MAO inhibitors?

A
  • hypertensive crisis can result due to increased NE stores
  • tyramine levels can increase
  • risk of serotonin syndrome
36
Q

Tricyclic and heterocyclic antidepressants

A

-inhibit reuptake of NE and 5HT in synapse

37
Q

What are 4 adverse effects of TCAs?

A
  1. excessive sedation
  2. antimuscarinic effects (effects GI motility)
  3. sympathomometic effects
  4. orthostatic hypotension (block in peripheral adrenergic Rs), EEG abnormalities
38
Q

SSRIs

A
  • selectively inhibit serotonin uptake

- used to treat depression, eating disorders, anxiety disorders, OCD

39
Q

What are 5 adverse effects of SSRIs?

A
  1. nausea
  2. headache
  3. anxiety, agitation
  4. insomnia
  5. sexual dysfunction
    - fewer anticholinergic side effects than TCAs
40
Q

Mirtazapine

A

-blocks presynaptic alpha2 Rs, increases NE and 5HT release-blocks feedback inhibition

41
Q

Buproprion

A
  • weak inhibitor of DA, 5HT, NE uptake
  • few side effects
  • used for quitting smoking
42
Q

The Neurotrophic Hypothesis of Depression

A
  • GFs such as BDNF critical to regulation of neural plasticity
  • stress, pain, depression assoc with decreased BDNF levels and structural atrophy in hippocampus, frontal cortex
  • antidepressant drugs assoc with increased BDNF levels, synaptogenesis with chronic administration
43
Q

Draw out the serotonin hypothesis which explains why it takes time for antidepressant drugs that increase monoamines to have therapeutic effects

A

-antidepressants lecture

44
Q

Draw out dopamine pathways in the striatum that lead to Parkinson’s.

A

-anti parkinsons lecture

45
Q

Drugs that increase dopamine levels in the treatment of Parkinson’s.

A
  • levodopa
  • carbidopa
  • COMT inhibitors
  • selegiline
46
Q

Bromocriptine and Peroglide

A
  • dopamine R agonists

- act on post synaptic Rs

47
Q

Benztropine

A

-block striatal muscarinic Rs

48
Q

Amantadine

A
  • inhibits DA reuptake
  • facilitate presynaptic DA release
  • used in patients that don’t respond well to L-dopa
49
Q

Draw the dopaminergic pathways associated with psychoses

A

-antipsychotics

50
Q

Typical/first generation anti psychotic drugs

A
  • phenothiazines (chlorpromazine)
  • butyrophenones (haloperidol)
  • thioxanthenes (fluphenazine)
  • ability to relieve positive symptoms of schizophrenia
  • antagonism of D2 R of mesolimbic pathways

Pharmacology (9 decks)

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