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Pharm Unit 3 > CNS I and II (Dopamine and pals) > Flashcards

CNS I and II (Dopamine and pals) Flashcards

1
Q
  1. You need ____ to make dopamine and from there it is packaged into and stored in ____ by what?
A

TYROSINE; vesicles; VMAT2 (vesicular monamine transporter)

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2
Q
  1. To terminate dopamine’s actions, what things can be used?
A
  1. MAO A or B (in mito inside the presyn neuron) after using the dopamine transporter (DAT) to bring dopamine back in
  2. COMT can break down dopamine
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3
Q
  1. For the five dopamine pathways, list what they are and origin and destination:
A
  1. Nigrastriatal: controls MOVEMENT (substantia nigra to basal ganglia or striatum)
  2. Mesolimbic: controls REWARD and PERCEPTION (midbrain ventral tegmental area to nucleus accumbens)
  3. Mesocortical: controls EXECUTIVE FUNCTION (midbrain ventral tegmental area and sends axons to areas of prefrontal cortex)
  4. Tuberoinfundibular pathway: controls pituitary PROLACTIN function (hypothalamus to anterior pituitary gland)
  5. Thalamic
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4
Q
  1. Consequences of hyperfunctioning in four dopamine pathways :
A
  1. Mesolimbic: addiction, hallucinations (HAM)
  2. Mesocortical: hyperVIGILANCE
  3. Nigrostriatal: dyskinetic movement
  4. Tuberoinfundibular: HYPOprolactinemia
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5
Q
  1. Hypofunctioning in four dopamine pathways consequences :
A
  1. Mesolimbic: amotivation, apathy
  2. Mesocortical: inattention
  3. Nigrostriatal: dyskinetic movement, PARKINSONISM
  4. Tuberoinfundibular: HYPERprolactinemia
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6
Q
  1. Basic concept of what the X- and Y-axes are in the inverted U shaped curve:
A

X axis: want to be in the MIDDLE of the U (too low is distractible/inattentive and PARKINSONISM, vs. too high being hyperVIGILANT, addicted, hallucinating, dyskinetic)
Y axis: Want to be higher in terms of OPTIMAL FUNCTIONING

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7
Q
  1. For COMT, what can lead to too much DA breakdown?
A

Abnormal gene (valine substitution) that leads to agggressive COMT and too much DA broken down (now perhaps DEPRESSION)

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8
Q
  1. Facts about levodopa:
A
  1. Precursor to DA and crosses BBB
  2. In CNS, converted to DA proper and can promote better MOVEMENT by improving nigrostriatal functioning
  3. SE: dosed too HIGH, can lead to dyskinetic movements and hallucinations;
    Do NOT start patients on this because you could have those dyskinetic movements over a span of 15-30 years
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9
Q
  1. When do we use carbidopa?
A

COMBINED WITH LEVODOPA: prevents PERIPHERAL dopamine activity and lowers FATIGUE, DIZZINESS, NAUSEA (potentially associated with levodopa)

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10
Q
  1. SE’s of levodopa:
A
  1. Psychosis
  2. Mania
  3. Dyskinesia
  4. Hypervigilant;
    also hypotension, nausea, anxiety/agitation, fatigue (Hyper FAN)
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11
Q
  1. Depression could come from a low _____ state; what two molecules can help with production of dopamine?
A

DA (amotivation and no reward/enjoyment in life);
L-methylfolate allows DA neurons to make more DA with tyrosine conversion, and SAMe can help do the same, both INCREASING THE 1-CARBON CYCLE

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12
Q
  1. SE’s of drugs like L-methylfolate or s-adenosyl methionine:
A

None, maybe GI upset

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13
Q
  1. What does an NDRI do and give an example? Side effects
A

NE-DA reuptake inhibitor;
Bupropion antidepressant:
1. Blocks DAT (aka dopamine reuptake inhibition, DRI)
2. DA in the synapse increased and INCREASED DA activity in mesocortical pathway –> lower depression syndromes;

SE’s: less aggressive in CNS and not a 100% agonist of DA system; if too much, think insomnia, jitteriness/hypervigilance, seizures (HIS);
Increased NE: anxiety, agitation, dry mouth, nausea, sweating, palpitations, slight increase in BP (think fleeing from an animal)

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14
Q
  1. For ADHD, what drugs can be used and what are their mechanisms?
A

Stimulants like amphetamines and methylphenidate products;
1. Amphetamines (dextroamphetamine, mixed amphetamine salts, lisdexamfetamine): block DAT, maybe REVERSE it, increase VMAT2 to eject more DA
2. Methylphenidate products: blocks DA transporter;
DONE THROUGHOUT THE BRAIN so greater DA and NE side effects, whereas bupropion is limited more to the cortex

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15
Q
  1. Random fact about lisdexamfetamine:
A

PRODRUG!!

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16
Q
  1. Classification of modafinil/armodafinil:
A
  1. Stimulant class of medications (pseudostimulants?)
  2. Class IV addictive (less addicting)
  3. Good for fatigue due to narcolepsy, apnea, shifwork (NAS)
  4. Less severe but similar SE’s to other stimulants and might increase p450-3A4
17
Q
  1. Modafinil/armodafinil mech:
A
  1. Increase histamine activity in tuberomammillary nucleus (TMN), activating alertness in frontal cortex
  2. Could increase OREXIN activity
  3. Requires operating DAT system and might block this pump, akin to DRI
  4. Could actually manipulate NE receptors post-synaptically
18
Q
  1. With stimulants, what SE’s are we looking at?
A
  1. Addiction now an issue
  2. Super high doses: psychosis
  3. Moderate doses: appetite and weight loss
  4. Any dose: NE and DA side effects
19
Q
  1. What do MAOi’s do? Give examples; SE’s of these guys?
A

MAOi’s irreversibly inhibit MAO-A/B within the neuron and allow DA buildup;
1. Selegiline (MAO-B inhibitor at low dose) for PARKINSON’S or depression (full MAO A+B inhibition)
2. Rasagiline (MAO-B inhibitor) for PARKINSON’S!!
Notice these guys can both SELECTIVELY INHIBIT MAOB;
SE’s: hypotension, dizziness, insomnia, WEIGHT GAIN!! HDWI-fi
MAOi of MAO-A can interfere with breakdown of serotonin and NE which could have fatal drug-drug interactions

20
Q
  1. In which case can you have a hypertensive crisis?
A

Food source with TYRAMINE (heart attack or stroke) when on a MAOi that knocks out MAO-A;
think spoiled meat/fish, fava beans, aged cheese, tofu, smoked meats!!

21
Q
  1. MAOi leads to less breakdown of ___, leading to ____ syndrome; what drugs shouldn’t be given in this case and what are SE’s?
A

serotonin; serotonin;
think antidepressants, narcotic pain meds, antihistamines;
SE’s: tremor, muscle spasm, inc/dec vitals, hyperthermia, delirium, coma, death (

22
Q
  1. Entacapone, tolcapone: what do they try to do, SE’s
A

Inhibit COMT, which could help degrade dopamine or NE otherwise; use for PARKINSON patients;
Enta: nausea, fatigue, diarrhea, dyskinesias
Tol: Also has liver failure

23
Q
  1. D2 receptor agonism: what does phasic mean and what can this treat? Examples of drugs? SE’s
A 
Phasic = rapidly fluctuating;
increase DA activity in Parkinson's or RLS;
1. bromocriptine
2. pramipexole
3. ropinerole
4. apomorphine injections;
SE's: nausea, fatigue, dizziness, mania
24
Q
  1. D3 receptor agonism: what does tonic mean? example of drug,
A

Tonic = gradual fluctuation and undulate rather than peak and trough;
Aripiprazole (antipsychotic for schizo but also approved to treat depression)
Receptors: partial agonist at D3 (alertness, energy) and D2; at D3, 30% receptor activity so net increase in DA activity

25
Q
  1. Amantadine: therapeutic, mech, SE’s
A

Thera: treat Parkinson’s and influenza
Mech: release DA from terminal vesicles, block DAT, stim D2 receptors
SE’s: nausea, dizziness, psychosis, insomnia, seizures!! Nausea DIPS

26
Q
  1. What can deplete the synapse of dopamine?
A
  1. Reserpine: blocks VMAT and used for hypertension, but less NE and DA means more depression, and less BP and maybe less psychosis, respectively
  2. Tetrabenazine: used to treat Huntington’s chorea (VMATi to help lessen movements)
27
Q
  1. FGA Mech of Action and where do the high potency agents work?
A

Mech: D2 receptor antagonism and occurs in all DA pathways
High potency: HIGH AFFINITY for D2 receptor antagonism; in mesolimbic alleviates psychosis and in nigrostriatal can cause low DA and extrapyramidal side effect (PARKINSON’S)

28
Q
  1. FGA High potency SE’s:
A

If DA activity is too low

  1. Akathisia (restlessness)
  2. Dystonia (muscle spasm)
  3. Parkinsonism (potentially reversible)
  4. Neuroleptic Malignant Syndrome (hyperthermia, muscle rigidity, vital sign instability, rhabdo)
29
Q
  1. How do anti-Ch drugs relate to Parkinson’s? Examples? SE’s
A

Inhibit Ch tone in basal ganglia = improving dopaminergic flow/tone in nigrostriatal pathway (very effective in EPS caused by first and second generation antipsychotics);
Benztropine, triheyphenadyl, diphenhydramine
SE’s: Hallucinations, delirium, confusion, AND dry mouth, blurred vision, tachy, constipation

30
Q
  1. Chronic D2 receptor antagonism could cause
A

permanent movement disorder called tardive dyskinesia

31
Q
  1. For the low potency FGA’s,
A

there is low affinity for D2 antagonism and they also deal with other receptors:

  1. H1 receptor antagonism: fatigue and increased appetite/weight
  2. Anti-Ch: dry mouth, blurry vision, constipation
  3. Alpha 1 receptor antagonism (orthostasis
  4. D2 receptor antagonism chronically: EPS
32
Q
  1. Examples of high potency FGA drugs are; low potency FGA drugs are
A

High potency: Haloperidol, fluphenazine, thiothixine;

Low potency: chlorpromazine, thioridazine

33
Q
  1. SGA mech of action; how is it improved over FGA’s?:
A
  1. D2 receptor antagonism (improve psychosis, mania, aggression: PAM)
  2. Serotonin 2a antagonism (lessen EPS risk);
    IMPROVED SELECTIVITY since the blocking is going on primarily in the mesolimbic system (where psychosis reigns)
34
Q
  1. Dones main SE; Pines main SE’s
A

Dones: Possible more EPS/TD (like the FGA’s)
Pines: More sedating with its anti-H1 activity; more METABOLIC SYNDROME induced, so weight gain and eating more (think DIABETIC patient)

35
Q
  1. SGA SE’s besides those listed for the dones and pines?
A

Think suicide risk <25 and stroke in dementia patients!!

36
Q
  1. Clozipine: thera, mech, SE’s, misc
A

Thera: used for refractory schizo
Mech: antagonize D2 and 5HT2a; also D1 and D4; block NMDA glutamate receptors
SE’s: risk of agranulocytosis (monitor WBC and ANC); most metabolic risk of any agent
Misc: Little to zero EPS/TD

Pharm Unit 3 (12 decks)

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