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Pharmacology Module 1-11 > Module 14 > Flashcards

Module 14 Flashcards

1
Q

What is neuropharmacology

A

study of how drugs affect the function of the central nervous system

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2
Q

How do drugs affect neuropharmacology?

A

treat the symptoms not the cause

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3
Q

What is the brain composed of?

A

millions of neurons

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4
Q

what are neurons

A

cells in the brain that act to process and transmit signals and information

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5
Q

How do neurons function

A

excitable cells that transmit information by electrical and chemical signalling

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6
Q

where does start of information transfer begin?

A

the dendrite

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7
Q

what are action potentials

A

electrical signalling that propagate along the axon of the neuron

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8
Q

how does action potential transmit from presynaptic nerve terminal?

A

release of neurotransmitters (chemical signalling) to pass across the synapse

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9
Q

Action potentials role

A

cell-to-cell communication

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10
Q

what is the resting membrane potential of cells

A

-70mV

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11
Q

What is depolarization

A

positively charged Na+ ions enter the cell through voltage gated Na+ channels

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12
Q

What is repolarization

A

Na+ channels close and potassium channels open allowing potassium to leave the cell during repolarization (current overshoots)

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13
Q

Synapse

A

junction between a presynaptic and postsynaptic neuron

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14
Q

What happens once an action potential reaches a synapse? (4)

A

1) influx of calcium
2) calcium causes vesicles containing neurotransmitters to fuse with the pre-synaptic membrane
3) vesicles release neurotransmitters into the synaptic cleft (the space between the neurons)
4) neurotransmitters bind to receptors on the post-synaptic nerve membrane and the signal continues

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15
Q

Classes of neurotransmitters (3)

A
  • monoamines
  • amino acids
  • other
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16
Q

4 monoamines

A
  • norepinephrine
  • epinephrine
  • dopamine
  • serotonin
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17
Q

Norepinephrine (associated disease, type)

A
  • depression and anxiety

- monoamine

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18
Q

Epinephrine (associated disease, type)

A
  • anxiety

- monoamine

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19
Q

Dopamine (associated disease, type)

A
  • parkinson’s and schizophrenia

- monoamine

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20
Q

Serotonin (associated disease, type)

A
  • depression and anxiety
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21
Q

4 Aminoacids

A
  • Glutamate
  • Asparate
  • GABA
  • Glycine
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22
Q

Excitatory amino acids

A
  • glutamate

- aspartate

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23
Q

Inhibitory amino acids

A
  • GABA

- Glycine

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24
Q

Glutamate (associated disease, type)

A
  • alzheimer’s

- excitatory amino acid

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25
Q

Aspartate (associated disease, type)

A
  • Alzheimer’s

- excitatory amino acid

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26
Q

GABA (associated disease, type)

A
  • anxiety

- inhibitory amino acid

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27
Q

Glycine (associated disease, type)

A
  • anxiety

- inhibitory amino acid

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28
Q

Acetylcholine (associated diseases)

A

alzheimer’s and Parkinson’s

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29
Q

Basic mechanisms of CNS drug action (5)

A

1) replacement
2) agonists/antagonist
3) inhibiting neurotransmitter breakdown
4) blocking reuptake
5) nerve stimulation

30
Q

Replacement (CNS drug action)

A

the drug acts to replace neurotransmitters that are low in diseases

31
Q

Agonists/Antagonist (CNS drug action)

A

a drug that directly binds to receptors on the post-synaptic membrane

32
Q

Inhibiting neurotransmitter breakdown (CNS drug action)

A

neurotransmitter metabolism is inhibited

33
Q

Blocking reuptake (CNS drug action)

A

neurotransmitter reuptake into the pre-synaptic neuron is blocked

34
Q

Nerve stimulation (CNS drug action)

A

the drug directly stimulates the nerve causing it to release more neurotransmitter

35
Q

Parkinson’s disease

A
  • progressive loss of dopaminergic neurons in the substantia nigra of the brain
  • normal to lose some, but patients with PD lose 70-80% of dopaminergic neurons
36
Q

Parkinson’s disease - prognosis

A
  • without treatment = progresses in 5-10 years to a state where patients are unable to care for themselves
37
Q

Symptoms of Parkinson’s disease (6)

A

1) Tremor - mostly in the extremities including hands, arms, legs, jaw, face
2) Rigidity (joint stiffness and increased muscle tone)
3) bradykinesia (slowness of movement/slow to initiate movemnts)
4) masklike face (cant show face expression and have difficulty blining and swallowing)
5) postural instability (balance impaired)
6) dementia (later in disease)

38
Q

Pathophysiology of Parkinson’s disease

A

1) dopamine release is decreased, so there is not enough dopamine present to inhibit GABA release
2) there is a relative excess of acetylcholine compared to dopamine, which results in increased GABA release
3) excess GABA release causes the movement disorders

39
Q

Etiology of Parkinsons (6)

A
  • largely idopathic (aka unknown) but there are 5 factors
    1) drugs - a by product of ilicit street durgs synthesis produces MPTP, which causes irreversible death of dopaminergic neurons
    2) genetics (mutations in 4 gens = alpha synuclein, parkin, UCHL1 and DJ-1)
    3) Environmental Toxins (certain pesticides)
    4) brain trauma
    5) oxidative stress (ex diabetes induced oxidative damage and PD)
40
Q

4 mutations to lead to parkinsons

A
  • alpha synuclein, parkin, UCHL1, DJ-1
41
Q

Drug treatment for Parkinson’s disease (2)

A
  • ideal = reverse degeneration of dopaminergic
  • either….
    1) increase dopamine
    2) decrease acetylcholine
42
Q

5 drugs that increase dopamine neurotransmission

A

1) dopamine replacement
2) dopamine agonist
3) dopamine releaser
4) catecholamine-O-Methyltransferase Inhibitor
5) monoamine oxidase-B (MAO-B) inhibitor

43
Q

Levodopa

A

dopamine replacement drug to treat parkinson;s

44
Q

What is the most effective drug for treating parkinson;s disease

A
  • levodopa (dopamine replacement)

- however beneficial effects of L-DOPA decrease over time as the disease progresses

45
Q

L-DOPA mechanism of action (3)

A
  • L-DOPA is inactive on its own but is converted to dopamine in dopaminergic nerve terminals
  • conversion of L-DOPA to dopamine is mediated by decarboxylase enzymes in the brain
  • the cofactor pyridoxine (vitamin B6) speeds up this reaction
46
Q

L-DOPA and getting into cells

A

crosses the blood brain barrier via an active transport protein

47
Q

Why give levodopa instead of dopamine (2)

A

1) Dopamine does not cross the BBB

2) dopamine has a very short half life in blood

48
Q

L-DOPA adverse effects

A
  • nausea and vomiting (dopamine activation of chemoreceptors)
  • dyskinesias (abnormal involuntary movements)
  • cardiac dysrhythmias (L-DOPA to dopamine in periphery can intervere with cardiac beta 1 receptors)
  • orthostatic hypotension
  • psychosis (20% of patients will have hallucinations, vivid dreams, paranoid thoughts)
49
Q

L-DOPA - peripheral metabolism

A
  • only 1% of total DOPA dose reaches the brain, as the remaining dose is metabolized in the peripheral tissue (Esp. intestine)
50
Q

L-DOPA - peripheral metabolism - solution

A
  • solution = give L-DOPA with a carbidopa (decarboxylase inhibitors that inhibits peripheral metabolism)
  • 10% of L-DOPA reaches the brain
  • RESULT = lower dose of L-DOPA administered, decreased risk
51
Q

2 types of loss of effect from L-DOPA

A

1) wearing off (gradual loss of effect)

2 on-off - abrupt effect

52
Q

Wearing off (loss of effect from L-DOPA)

A
  • usually occurs at the end of the dosing interval and indicates that drug levels might be low
53
Q

how to minimize Wearing off (loss of effect from L-DOPA) (3)

A

1) shortening the dosing interval
2) give a drug that inhibits L-DOPA metabolism (ex a COMT inhibitor)
3) add a dopamine agonist to the therapy

54
Q

On-Off (loss of effect from L-DOPA)

A
  • can occur even when drug levels are high
55
Q

how to minimzie On-Off (loss of effect from L-DOPA) (3)

A

1) dividing the medication into 3-6 doses per day
2) using a controlled release formulation
3) moving protein-containing meals to the evening

56
Q

Dopamine agonist - Parkinson’s disease

A
  • produce their effects by directly activating dopamine receptors on post-synaptic cell membrane
57
Q

Dopamine agonist - use

A
  • not as effective as L-DOPA

- often used as first line treatment for patients with milder symptoms

58
Q

Adverse effects of dopamine agonist (3)

A
  • hallucinations
  • daytime drowsiness
  • orthostatic hypotension
59
Q

Dopamine Releaser - action

A
  • acts to stimulate release of dopamine from dopaminergic neurons and in addition, it also blocks dopamine reuptake into pre-synaptic nerve terminals, and blocks NMDA receptors
60
Q

Dopamine Releaser - response time

A
  • rapid, 2-3 days
61
Q

Dopamine releaser - efficacy

A

not as effective as L-DOPA

62
Q

Dopamine releaser - effect of blocking NMDA

A

decrease dyskinesia side effect of L-DOPA

63
Q

Dopamine releaser - adverse effects

A
  • dizziness
  • nausea
  • vomiting
  • lethargy
  • anticholinergic side effects
64
Q

Catecholamine-O-Methyltransferase (COMT)

A
  • COMT - an enzyme that adds methyl group to dopamine and L-DOPA
  • methylated dopamine and L-DOPA = inactive
65
Q

Catecholamine-O-Methyltransferase (COMT) inhibitor

A
  • inhibiting COMT results in a greater fraction of L-DOPA and L-DOPA available to be converted to dopamine
  • moderately effective (combine with L-DOPA)
66
Q

Catecholamine-O-Methyltransferase (COMT) inhibitor - adverse effects

A
  • similar to adverse effects of L-DOPA =
  • nausea
  • orthostatic hypotension
  • vivid dreams
  • hallucinations
67
Q

Monoamine oxidase-B (MAO-B)

A
  • enzyme that metabolizes dopamine and L-DOPA through oxidation (thus inactivating them)
  • present in the periphery and in the brain
68
Q

Monoamine oxidase-B (MAO-B) inhibitor

A
  • inhibiting oxidative metabolism of L-DOPA allows more conversion to dopamine, and allows more dopamine to remain in nerve terminals and be released
69
Q

Monoamine oxidase-B (MAO-B) inhibitor efficacy

A

moderately effective, often combined with L-DOPA

70
Q

Monoamine oxidase-B (MAO-B) inhibitor adverse effects

A
  • insomnia
  • orthostatic hypotension
  • dizziness
  • *at therapeutic doses, MAO-B inhibitors do not inhibit MAO-B in liver –> dont cause hypertensive crisis when patients eat tyramine-containing foods
71
Q

Acetylcholine excess

A
  • diaphoresis (excess sweating)
  • salivation
  • urinary incontinence

Pharmacology Module 1-11 (2 decks)

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