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Abbey MSII Unit 3 > Pharm U3 L1. > Flashcards

Pharm U3 L1. Flashcards

1
Q

What is dopamine made from?

A

tyrosine

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2
Q

VMAT2

A

transports neurotransmitters (esp dopamine, NE, serotonin, histamine) from cellular cytosol into synaptic vesicles

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3
Q

DAT

A

dopamine transporter - recycles dopamine from synaptic cleft back into neuron

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4
Q

MAO A or B

A

inside of presynaptic membrane destroying dopamine

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5
Q

COMT

A

in synaptic cleft destroying dopamine

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6
Q

What is the main dopamine factory

A

substantia nigra

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7
Q

Nigrastriatal controls….

A

movement

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8
Q

Mesolimbic controls….

A

reward and perception

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9
Q

Mesocorticoal controls…..

A

executive function

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10
Q

Tuberoinfundibular controls….

A

pituitary prolactin function

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11
Q

Hyperfunctioning of mesolimbic = ?

A

addiction, hallucinations

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12
Q

Hyperfunctioning of mesocortical = ?

A

hypervigilance

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13
Q

Hyperfunctioning of nigrostriatal = ?

A

dyskinetic movement

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14
Q

Hypofunctioning of mesolimibic = ?

A

amotivation, apathy

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15
Q

Hypofunctioning of mesocortical = ?

A

inattention

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16
Q

Hypofunctioning of nigrostriatal = ?

A

diskinetic movement, parkinsonism

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17
Q

Hypofunctioning of tuberoinfundibulnar = ?

A

hyperprolactinemia

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18
Q

What are the dopamine enhancing drugs?

A

levodopa and carbidopa

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19
Q

Levodopa

A

precursor to DA that crosses BBB - promotes better movement by improving nigrostriatal functioning

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20
Q

Carbidopa

A

often combined with levodopa - prevents peripheral dopamine activity and lowers fatigue, dizziness, nausea (treats side effects)

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21
Q

Side effects of levodopa

A

too much DA - psychosis, mania, dyskinesia (involuntary movements) - usually hypotension, syncope, nausea, anxiety, fatigue

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22
Q

What is a treatment for depression?

A

increase folate in order to get more dopamine (some cycle where they are connected)

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23
Q

bupropion(XL) antidepressant

A

blocks dopamine transporter (DAT) - dopamine reuptake inhibition, leaving more DA in the synapse - increases DA activity in the mesocortical pathway

24
Q

Side effects of increased dopamine drugs (levodopa, bupropion)

A

think increase in norepinephrine = sympathetic stimulation = insomnia, anxiety, angitation, nausea, dry mouth, sweating, palpitations, mild increase BP

25
Q

Amphetamines MOA

A

block DAT like bupropion and also increases VMAT2 which ejects more DA from nerve terminals - more aggressive

26
Q

modafinil/armodafinil uses

A

stimulants, less addictive than amphetamines - used to treat narcolepsy, apnea, NOT ADHD

27
Q

modafinil/armodafinil side effect

A

may increase p450-3A4 enzymes - lowering birth control effectiveness; still addictive; psychosis at high doses; weight loss

28
Q

modafinil/armodafinil mechanism

A

increase histamine activity in tubermammilary nucleus - activating alertness in frontal cortex

29
Q

MAO-B inhibitors and treatment

A

selegiline and rasagiline - treat parkinson’s

30
Q

MAO A+B inhibition and treatment

A

isocarboxazid, phenelzine, tranylcypromine, selegiline - treat depression

31
Q

MAOi side effects

A

hypotension, dizziness, insomnia, weight gain - can also interfere with breakdown of serotonin and NE (drug-drug interactions that can be life threatening)

32
Q

MAOi mechanism

A

irreversibly inhibit MAO-A/B allowing build up of DA because it cannot be broken down

33
Q

What results in a hypertensive crisis?

A

any drug that raises NE + food source containing tyramine (fava beans, aged cheese, tofu) (causes immediate release of NE stores) - MAO-A used to breakdown tyramine

34
Q

Toxic levels of serotonin causes

A

tremor, muscle spasm, inc/dec vitals, hyperthermia, delirium, coma, death

35
Q

entacapone/tolcapone MOA

A

inhibition of COMTi - enzyme in the synapse that degrades monoamines as well - elevates DA or NE

36
Q

D2 receptor agonism - MOA and drugs

A

increases DA activity for treatment of parkinson’s and restless leg syndrome: bromocriptine, pramipexole, ropinerole, apomorphine injections

37
Q

Side effects of bromocriptine, pramipexole, ropinerole, apomorphine injections

A

nausea, fatigue, dizziness, mania

38
Q

What is the first line treatment for Parkinson’s

A

D2 receptor agonism (bromocriptine, pramipexole, ropinerole, apomorphine injections because dopa only works for a few years

39
Q

aripiprazole

A

partial agonist at D3 - promotes more alertness and energy, also partial agonist at D2 - antipsychotic for schizophrenia

40
Q

amantadine

A

treats parkinson’s and influenza - release DA from terminal vesicles, block DAT and stimulate D2 receptors - not really used anymore

41
Q

When would we want to decrease DA activity?

A

schizophrenia - decrease DA in mesolimbic to lower hallucinations and delusions

42
Q

Reserpine/tetrabenazine

A

dopamine synapse depleters - blocks VMAT

43
Q

What was reserpine originally intended to treat?

A

hypertension (less NE = less BP)

44
Q

D2 receptor antagonism

A

non selective - occurs in all DA pathways; high potency - blocking in mesolimbic alleviates psychosis, in nigrostriatal causes EPS

45
Q

EPS

A

extrapyramidal syndromes - when DA activity is forced too low. 1. akathisia (restlessness) 2. dystonia (muscle spasm) 3. parkinsonism (reversible) 4. neuroleptic malignant syndrome (hyperthermia, muscle rigidity, vital sign instability, rabdomyolysis)

46
Q

What are the FGAs and SGA

A

first generation antipsychotics and second generation

47
Q

Which drugs are very effective in parkinsonism EPS caused by FGA/SGA?

A

anticholinergic drugs (cholinergic muscarinic receptor antagonists) - inhibits cholinergic tone in basal ganglia, improving dopaminergic flow/tone in nigrostriatal pathway

48
Q

What are the anticholinergics? What are their side effects?

A

benztropine, trihexyphenadyl, diphenhydramine. SE = dry mouth, blurred vision, tachycardia, constipation, confusion, delirium, hallucinations

49
Q

Tardive Dyskinesia

A

chronic D2 receptor antagonism = abnormal movements

50
Q

What are the two types of FGAs?

A

low potency vs high potency - low potency manipulate other receptors associated with side effects

51
Q

What are the high potency FGA drugs?

A

haloperidol, fluphenzine, thiothixine

52
Q

What are the low potency FGA drugs?

A

chlorpromazine, thioridazine

53
Q

What is the SGA mechanism of action?

A

D2 receptor antagonism AND serotonin 2a(5HT2a) antagonism which lessens EPS risks - don’t need the anticholinergics and makes this the standard of care

54
Q

What are the SGA drugs?

A

dones (D2 blockade - more EPS); pines (more sedating and metabolic); ‘rips (aripiprazole) - partial agonist at D2 and D3

55
Q

What are the FDA precautions/boxed warnings for SGA?

A

suicide risk ages

56
Q

clozapine

A

used in refractory schizophrenia (SGA pine) - ALSO antagonizes D1 and D4, giving it multiple mechanisms to manipulate dopamine

57
Q

Which SGA has the most metabolic risk of any agent, but little to zero EPS/TD?

Abbey MSII Unit 3 (36 decks)

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