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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
Amphetamines MOA
block DAT like bupropion and also increases VMAT2 which ejects more DA from nerve terminals - more aggressive
26
modafinil/armodafinil uses
stimulants, less addictive than amphetamines - used to treat narcolepsy, apnea, NOT ADHD
27
modafinil/armodafinil side effect
may increase p450-3A4 enzymes - lowering birth control effectiveness; still addictive; psychosis at high doses; weight loss
28
modafinil/armodafinil mechanism
increase histamine activity in tubermammilary nucleus - activating alertness in frontal cortex
29
MAO-B inhibitors and treatment
selegiline and rasagiline - treat parkinson’s
30
MAO A+B inhibition and treatment
isocarboxazid, phenelzine, tranylcypromine, selegiline - treat depression
31
MAOi side effects
hypotension, dizziness, insomnia, weight gain - can also interfere with breakdown of serotonin and NE (drug-drug interactions that can be life threatening)
32
MAOi mechanism
irreversibly inhibit MAO-A/B allowing build up of DA because it cannot be broken down
33
What results in a hypertensive crisis?
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
Toxic levels of serotonin causes
tremor, muscle spasm, inc/dec vitals, hyperthermia, delirium, coma, death
35
entacapone/tolcapone MOA
inhibition of COMTi - enzyme in the synapse that degrades monoamines as well - elevates DA or NE
36
D2 receptor agonism - MOA and drugs
increases DA activity for treatment of parkinson’s and restless leg syndrome: bromocriptine, pramipexole, ropinerole, apomorphine injections
37
Side effects of bromocriptine, pramipexole, ropinerole, apomorphine injections
nausea, fatigue, dizziness, mania
38
What is the first line treatment for Parkinson’s
D2 receptor agonism (bromocriptine, pramipexole, ropinerole, apomorphine injections because dopa only works for a few years
39
aripiprazole
partial agonist at D3 - promotes more alertness and energy, also partial agonist at D2 - antipsychotic for schizophrenia
40
amantadine
treats parkinson’s and influenza - release DA from terminal vesicles, block DAT and stimulate D2 receptors - not really used anymore
41
When would we want to decrease DA activity?
schizophrenia - decrease DA in mesolimbic to lower hallucinations and delusions
42
Reserpine/tetrabenazine
dopamine synapse depleters - blocks VMAT
43
What was reserpine originally intended to treat?
hypertension (less NE = less BP)
44
D2 receptor antagonism
non selective - occurs in all DA pathways; high potency - blocking in mesolimbic alleviates psychosis, in nigrostriatal causes EPS
45
EPS
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
What are the FGAs and SGA
first generation antipsychotics and second generation
47
Which drugs are very effective in parkinsonism EPS caused by FGA/SGA?
anticholinergic drugs (cholinergic muscarinic receptor antagonists) - inhibits cholinergic tone in basal ganglia, improving dopaminergic flow/tone in nigrostriatal pathway
48
What are the anticholinergics? What are their side effects?
benztropine, trihexyphenadyl, diphenhydramine. SE = dry mouth, blurred vision, tachycardia, constipation, confusion, delirium, hallucinations
49
Tardive Dyskinesia
chronic D2 receptor antagonism = abnormal movements
50
What are the two types of FGAs?
low potency vs high potency - low potency manipulate other receptors associated with side effects
51
What are the high potency FGA drugs?
haloperidol, fluphenzine, thiothixine
52
What are the low potency FGA drugs?
chlorpromazine, thioridazine
53
What is the SGA mechanism of action?
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
What are the SGA drugs?
dones (D2 blockade - more EPS); pines (more sedating and metabolic); ‘rips (aripiprazole) - partial agonist at D2 and D3
55
What are the FDA precautions/boxed warnings for SGA?
suicide risk ages
56
clozapine
used in refractory schizophrenia (SGA pine) - ALSO antagonizes D1 and D4, giving it multiple mechanisms to manipulate dopamine
57
Which SGA has the most metabolic risk of any agent, but little to zero EPS/TD?
clozapine

Abbey MSII Unit 3 (36 decks)

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