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Unit 3 Pharm > CNS Drugs: Dopaminergic Agents > Flashcards

CNS Drugs: Dopaminergic Agents Flashcards

1
Q

The pathway that projects from the SN to the BG/striatum, is part of the extrapyramidal nervous system and controls motor function and mvmt is called what?

A

Nigrostriatal dopamine ptwy

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2
Q

The mesolimbic dopamine ptwy projects from where to where, areas involved in what?

A

Midbrain ventral tegmental area to the nucleus accumbens, a part of the limbic system thought to be involved in behaviors such as pleasurable sensations, the powerful euphoria of drugs of abuse, as well as delusions and hallucinations of psychosis.

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3
Q

Ptwy projecting from midbrain tegmental area to PFC, where the role is in mediating cognitive symptoms (DLPFC) and affective symptoms (VMPFC) of schizophrenia

A

Mesocortical dopamine ptwy

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4
Q

The tuberoinfundibular dopamine ptwy projects from the hypothalamus to the ant pit gland and controls what?

A

Prolactin secretion

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5
Q

What area of the brain known as the vigilance center fails to activate in ADHD, thus preventing the storage of memory in hippocampus and causing wrong parts of brain to compensate?

A

Anterior cingulate.

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6
Q 
Hyperfunctioning in the following dopamine pathways leads to what:
Mesolimbic- 
Mesocortical-
Nigrostriatal-
Tuberoinfundibular-
A

Addiction, hallucinations.
Hypervigilance.
Dyskinetic mvmt.
Hypoprolactinemia.

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7
Q 
Hypofunctioning in the following dopamine pathways leads to what:
Mesolimbic- 
Mesocortical-
Nigrostriatal-
Tuberoinfundibular-
A

Amotivation, apathy.
Inattention.
Dyskinetic mvmt, parkinsonism.
Hyperprolactinemia.

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8
Q

One of the first biogenetic markers of depression is the activity of COMT, in which a valine substitution has what effect on COMT?

A

Makes COMT aggressive and COMT breaks down too much DA in the synapse and you may develop symptoms

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9
Q

What two PD drugs are used to treat the low DA states?

A

Levodopa and carbidopa

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10
Q

L-dopa promotes better mvmt by improving [ ] ptwy functioning. If dosed too high, it can create what?

A

Nigrostriatal. Dyskinetic mvmt with choreic, quirky tic like mvmts, hallucinations.

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11
Q

What agent is often combined with Levodopa, as it promotes peripheral DA activity and lowers fatigue, dizziness, nausea.

A

Carbidopa.

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12
Q

Worst side effects of levodopa? Avg side effects?

A

Psychosis, mania; dyskinetic abn involuntary mvmts. More common S.E.s are hypotension, nausea, anxiety/agitation, fatigue, and hypervigilance and insomnia. L-dopa is “messy”.

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13
Q

How can we increase the 1C cycle to allow DA neurons to make more DA to improve a depressed patient’s apathy?

A

Give L-methylfolate and SAMe.

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14
Q

How can we increase DA in the synapse? What does this type of drug do to tx depression?

A

Give a NDRI like bupropion. Blocks DAT, leaving more DA in the synapse to increase DA activity in the mesocortical ptwy, lowering depression symptoms.

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15
Q

Why are S.E.s of buproprion in the CNS less/more than levodopa? What are the S.E.s?

A

Not a 100% agonist of the DA system. The S.E.s are sympathetic stim, like insomnia, anxiety, agitation, nausea, dry mouth, sweating, palps, mild increases in blood pressure. ‘Sweaty, shaky, jittery’

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16
Q

Stimulants for ADHD are even stronger than bupropion and have stronger S.E.s why?

A

Block the DAT more aggressively and more throughout the brain than bupropion, therefore you can have greater DA and NE S.E.s

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17
Q

Amphetamines (dextro-, mixed amph salts, lisdexamfetamine (prodrug)) are stimulants that act how?

A

Block DAT, may even reverse it, inc VMAT2 transport ejecting more DA from nerve terminals.

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18
Q

Methylphenidate is a stimulant that does what?

A

Blocks DAT

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19
Q

Modafanil/Armodafanil are ‘pseudostimulants’ with what mech of action?

A

Theoretically inc histamine activity in the TMN, thus activating alertness in the frontal cortex. Also may inc orexin activity. May block DAT. May also manipulate NE receptors postsynaptically.

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20
Q

Modafanil/Armodafanil are approved for what and used off-label for what? By virtue of their induction of p450-3A4 enzymes, they lower the effectiveness of what other drug type?

A

Fatigue due to narcolepsy, apnea, shiftwork, but not ADHD. ADHD. BCPs.

21
Q

Because stimulants block DAT and NET and thus inc DA and NE activity in the cortex AND mesolimbic pathways (reward center), what can thus be a problem? At super high doses, this can occur? At mod doses, what happens?

A

Addiction. Psychosis. Wt loss and appetite loss.

22
Q

We can diminish DA degradation by giving what drugs? What do they do?

A

MAOIs. Irrev inhibit MAO-A/B in the neuron.

23
Q

Selegiline and Rasagiline inhibit MAO-B or A? For what disease?

A

MAO-B for PD.

24
Q

By cranking up the dose, these drugs are more aggressive and thus can block MAO-B and A and tx what disease? List the drugs.

A

Depression. Isocarboxazid, phenelzine, tranylcypromine, selegiline (high dose).

25
Q

MAOi side effects. For depression, there are greater effects for MAO-A also interfering with the ability to break down what, allowing for what dangerous things to happen?

A

Hypotension, dizziness, insomnia, wt gain. To bkdn Ser and NE which may allow for many drug-drug interactions.

26
Q

Adding NE raising drugs can elevate bp when on an MAOi. Adding any food source with what in can cause this type of crisis? Name it.

A

Tyramine hypertensive crisis (MAO-A breaks down tryamine)

27
Q

MAOi decrease the bkdn of serotonin, thus if you add an aggressive serotonin drug (like some antidepressants, antihistamines like chlorpheniramine, narcotics) you may create toxic levels of CNS serotonin causing what symptoms?

A

Tremor, muscle spasm, inc/dec vitals, hyperthermia, delirium, coma, death, rhabdo, kidney failure.

28
Q

COMTi can help in PD. Name the two and their peculiar S.E.s.

A

Entacapone - nausea, fatigue, dizziness

Tolcapone - liver failure, nausea, fatigue, dizziness

29
Q

We can agonize DA receptors to give a better background of dopaminergic activity without adding extra dopamine. Which DA receptors control phasic DA pathways involved in reward? Which DA receptors are more gradual and allow gradual undulations of wakefulness and tiredness?

A

D2. D3.

30
Q

Name the 4 D2 agonists (phasic DA) that increase DA activity in treating PD or RLS. What’s the point in using these?

A

Bromocriptine, Pramipexole, Ropinerole, Apomorphine injections (n/f/diz/mania S.E.’s for all). They prolong the time to when L-dopa will be needed.

31
Q

Aripiprazole: type, uses, agonism

A

Antipsychotic for schizo but approved for depression. Partial D3 agonist promoting alertness and energy perhaps. Also partial D2 agonist (30%).

32
Q

Amantadine: uses, agonism, mech, S.E.s. What is this drug NOT compared to stimulants?

A

PD and influenza. Theorized to release DA from terminal vesicles, block DAT, and stim D2 receptors. N/diz/psychosis/insomnia/seizures. Not addicting, it’s weak.

33
Q

Name the 2 synapse DA depleters and their uses

A

Reserpine blocks VMAT and is used for htn. Tetrabenazine is a VMATi used for Huntington’s Chorea.

34
Q

FGA (typicals) D2 receptor antagonists: list the high potency and low potency drugs

A

Haloperidol, fluphenazine, thiothixine. Chlorpromazine, thioridazine.

35
Q

FGA mech of action. Selective or not in regard to ptwy?

A

D2 receptor antagonism. Not selective, occurs in all DA pathways.

36
Q

High potency FGAs unique feature and why? What ptwy is the action helpful in returning high DA activity back to normal in?

A

High affinity for D2 blockage thus few side effects outside those from lowering D2 activity. Mesolimbic.

37
Q

FGA side effects

A

EPS (low DA in nigrostriatal ptwy), akisthisia (restlessness), dystonia (spasm), parkinsonism, NMS (hyperthermia, rigidity, vital sign instab, rhabdo).

38
Q

Name 3 anticholinergics and say why they’re used when taking dopamine receptor blockers

A

Benztropine, trihexyphenadyl, diphenhydramine. Lower parkinsonism EPS caused by FGA/SGA.

39
Q

Chronic D2 receptor antagonism may cause this permanent mvmt disorder.

A

Tardive Dyskinesia.

40
Q

Low potency FGA S.E.s due to their “messiness”

A

D2 receptor antag can cause EPS; H1 antag can cause fatigue and inc’d appetite and wt; anticholinergic musc antag can cause dry mouth, blurry vision, constipation; a1 antag can cause orthostasis.

41
Q

SGA (atypicals) mech of action

A

D2 receptor antagonism improves psychosis, mania, aggression. 5HT2a antagonism lessens EPS risks and helps in depression too I think. Improved ptwy selectivity compared to FGA. (Can block DA in mesolimbic where psychosis originates, but thru feedback more DA is allowed to stay in nigrostriatal ptwy.)

42
Q

Some SGA agonize this to help anxiety? Antagonize this to help depression? These properties to treat depression? What type of blockade lowers aggression in autism? And lowers mania in bipolar?

A

5HT1a. 5HT2c, 3, 7. SRI and NRI. D2 blockade. D2 blockade.

43
Q

SGA drugs: list

A

‘Dones, ‘Pines, ‘Rips.

44
Q

General side effects of the dones?

A

Possibly more EPS

45
Q

General side effects of the pines?

A

More sedating due to more histamine activity (anti H1). More metabolic syndrome inducing, less EPS.

46
Q

SGA side effect of slowing metabolism is by virtue of desensitizing the leptin system allowing wt gain, inc chol, inc blood glucose. What’s the antagonism responsible here?

A

5HT2c antagonism

47
Q

The headaches, GI problems, insomnia, and anxiety seen in SGA is due to what agonism and antagonism?

A

5HT1a partial agonism, 5HT3,7 antagonism. Also, the SRI/NRI properties do this.

48
Q

SGA FDA boxed warnings

A

Suicide risk under 25 yrs old, metabolic syndrome, TD/EPS, stroke in dementia patients.

49
Q

The original antipsychotic used for refractory schizophrenia is called what? Actions. Risks. What risk does it not carry?

A

Clozapine. Antagonizes D2 and 5HT2a (lessening EPS risk), also antags D1 and D4. May block NMDA Glu receptors. Risk of agranulocytosis and the MOST risky agent for metabolic syndrome. Little to no EPS/TD.

Unit 3 Pharm (8 decks)

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