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Pharm Block 3 > 3 - Neuropsychoparmacology 1 > Flashcards

3 - Neuropsychoparmacology 1 Flashcards

1
Q

Where are norepi, serotonin, dopamine, and acetylcholine localized in the brain? Where do they send axons?

A

Norepi: locus coeruleus
Serotonin: Raphe nuclei
-Both NE and 5HT send axons down the spinal cord to modulate pain pathways

Dopamine: ventral tegmental area and substantia nigra
Ach: POMC, nucleus basalis, septal nuclei

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2
Q

What are dopaminergic pathways in the brain responsible for? What are the pathways?

A

Beneficial and adverse effects of many antipsychotic drugs.

  1. Midbrain mesocortical and mesolimbic pathways - schizophrenia
  2. Nigrostriatal pathway - degen in parkinsons
  3. Hypothalamus to anterior pituitary - regulates prolactin release
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3
Q

Where is GABA localized?

A

Substantia nigra, globus pallidus, hippocampus, limbic structures (amygdala), hypothalamus, and spinal cord.

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4
Q

What percentage of the population has a mood disorder? Of those people, what diagnosis is most common?

A

40% of the population.

Most of those (about 15%) are major depressive disorder.

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5
Q

What are the criteria for major depressive disorder?

A

Must have 5 or more for 2 weeks(one of these symptoms must be depressed mood or loss of pleasure:

Depressed mood, diminished interest or pleasure, weight change, insomnia/hypersomnia, fatigue, feeling worthless, inappropriate guilt, agitation, difficulty concentrating, suicidal ideation.

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6
Q

What occurs at the norepinephrine synapse?

A

Tyr brought in and made into DOPA, then dopamine (DA), then brought into vescicles where it’s turned into NE.

NE is released into the synapse and can bind to alpha and beta receptors.

NE left in synapse goes through reuptake and can be reused or metabolized by monoamine oxidase (MAO).

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7
Q

What is the effect of tricyclic antidepressants on noradrenergic transmission? What occurs after taking there for awhile?

A

Blocks reuptake of NE, causing more transmitter to be in the synapse.

After 2-3 weeks, you see more norepi in the synapse and less receptors (due to down-regulation).

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8
Q

What other drug types cause down regulation of receptors with chronic use?

A

TCAs
SSRIs
Mirtazapine
MAOIs

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9
Q

What is the restated monoamine hypothesis?

A

Depression is due to biogenic amine receptor or transmission imbalance.

The various drugs that we are discussing act to change the imbalance and restore a more normal affect.

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10
Q

What drugs are used to treat depressive disorders?

A 
SSRIs
SNRIs 
Atypical drugs 
TCAs 
MAOIs
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11
Q

What are examples of 5-HT uptake inhibitors (SSRIs)? How do their effects differ from TCAs? What are their side effects?

A

Fluoxetine and sertraline.

Similar in efficacy and time course to TCAs. Less acute toxicity than TCAs and MAOIs.

Side effects: nausea, insomnia, and sexual dysfunction. Serotonin reaction can occur if given with MAOIs.

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12
Q

FDA requires warnings about associated of SSRIs and SNRIs with _____ ______ ______. What did clinical studies show antidepressants can cause?

A

Neuroleptic malignant syndrome.

Increased risk of suicidal thinking and behavior in children and adolescents with depression and other psychiatric disorders.

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13
Q

What are symptoms of SSRI withdrawl? When do these symptoms begin?

A

Dizziness, light-headedness, vertigo, shock-like sensations, paresthesia, anxiety, diarrhea, fatigue, gait instability, headache, insomnia, irritability, nausea/vomitting, tremor, visual disturbances.

Symptoms begin within 1-7 days after stopping SSRI.

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14
Q

What are the approved uses of SSRIs?

A 
Major depression 
OCD
Panic disorder 
Social anxiety disorder
PTSD
Generalized anxiety disorder 
Premenstrual dysphoric disorder 
Hot flashes from menopause
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15
Q

What was the first SSRI on the market with a long half-life active metabolite that lasts 7 days or more and has effects on drug metabolism? What is it approved to treat and how is it given?

A

Fluoxetine.

Sustained release product for Premenstrual dysphoric disorder (PDD).

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16
Q

What SSRI has a similar action to fluoxetine with less effects on drug metabolism and a shorter half life? What is it used to treat?

A

Sertraline.

OCD, PTSD, and panic attacks.

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17
Q

What are the effects of SNRAs? What are their side effects?

A

Blcok both 5-HT and NE reuptake.

Side effect profile is more like SSRI-like than TCA-like.

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18
Q

What is a SNRI with a 12-18 hour half life? What is it used for and what considerations need to be made?

A

Duloxetine.

Also approved for neuropathic pain syndromes, fibromyalgia, back pain, and osteoarthritis.

Use with caution in pts with liver disease. Can cause withdrawl symptoms.

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19
Q

How are SNRIs and TCAs similar? How do they differ?

A

Both block serotonin and norepi reuptake, treat neuropathic pain and depressive disorders.

TCAs are “dirty” drugs and binds lots of receptors to cause other effects such as H1 receptors (sedation), muscarinic receptors (burred vision, retention, constipation, glaucoma), and alpha adrenergic receptors (hypotension, dizziness, and reflex tachy).

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20
Q

What are Atypical antidepressants?

A

Drugs without typical tricyclic structure or SSRI or SNRI action. May or may not block catecholamine uptake.

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21
Q

What atypical antidepressant is also approved for nicotine withdrawl and seasonal affective disorder? What is its action? What are benefits?

A

Bupropion: weakly blocks NE and dopamine uptake.

No weight gain or sexual dysfunction.

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22
Q

What atypical antidepressant increases apetite and is often used for AIDs patients? How does this drug work?

A

Mirtazapine.

Blocks presynaptic alpha2 receptors in the brain.

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23
Q

What is the function of tricyclic antidepressents?

A

Block NE and 5-HT reuptake.

Now used secondarily to SSRIs and other new compounds,

Long plasma half-life: 8-100 hrs.

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24
Q

What are some pharmacological properties and effects of TCAs?

A

Elevation in mood after 2-3 wks.

Decreases REM and increases stage 4 sleep.

Prominent anticholinergic effects: can cause cardiac abnormalities like palpitations, tachy, and arrythmias.

Sedation.

Overdose/acute toxicity: hyper or hypotension, seizures, coma, and cardiac conduction effects.

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25
Q

What drugs do TCAs interact with?

A

Sympathomimetic drugs, particularly indirect acting agents (because these increase the release of NE).

Effects absorption and metabolism of other drugs.

26
Q

What are the therapeutic uses of TCAs?

A

MDD
Enuresis in childhood
Chronic pain: amitriptyline

27
Q

What is the function of MAO inhibitors?

A

Block the oxidative deamination of biogenic amines such as NE, DA, and 5-HT.

Two forms: MAO-A and MAO-B. Antidepressant action is probably due to inhibition of MAO-A.

28
Q

What drug is an irreversible inhibitor of MAO?

A

Phenelzine.

29
Q

What effects do MAO inhibitors have? What are symptoms of acute toxicity?

A

Antidepressant action takes 2 wk or more. Mood elevation in depressed pts that may progress to hypomania in bipolar disease.

Corrects sleep disorders in depressed pts. May causes stimulation in normal individuals.

Acute toxicity: agitation, hallucinations, hyperpyrexia, convulsions, and changes in BP.

30
Q

What must a patient be willing to do if they are prescribed an MAOI?

A

Adhere to food restritcions because tyramine that gets into blood stream can cause sympathetic nerves to release norepi and cause huge increases in BP and organ damage.

MAO normally metabolize tyramine, but people taking MAOIs have no other way to metabolize it making it dangerous.

31
Q

What are the therapeutic uses of MAOIs?

A

Major depression (not drug of first choice)

Narcolepsy

32
Q

What are characteristics of psychosis?

A

Derangement of personality, loss of contact with reality, delusions, and hallucinations.

33
Q

What is the prevalence of schizophrenia?

A

About 1% of the US adult population.

34
Q

What are the central criteria for a schizophrenia diagnosis? What are the core positive symptoms?

A

Two or more symptoms during a one month period, at least one must be a core positive symptom.

Core positive symptoms: delusions, hallucinations, disorganized speech. (typical antipsychotics better at treating these)

35
Q

Other than the core positive symptoms, what symptoms are associated with scizophrenia? are

A

Grossly disorganized or catatonic behavior.

Negative symptoms: blunted affect, lack of spontaneity, poor abstract thinking, poverty of thought, an social withdrawl (atypical antipsychotics are better at treating these).

36
Q

What are the subtypes of schizophrenia?

A

There are NO subtypes, only specifiers.

37
Q

What is the dopamine hypothesis?

A

Schizophrenia results from hyperactivity of dopaminergic neurons or their receptors, particularly in the limbic areas of the brain.

Abnormal dopamine neurotransmission in the frontal cortical areas responsible for negative symptoms.

(all effective antipsychotics interact with dopamine synthesis)

38
Q

______ pathways in the brain are responsible for the beneficial and adverse effects of many antipsychotic drugs.

A

Dopaminergic (DA) pathways.

39
Q

What is the mesolimbic tract and what is it associated with? Where does it originate? What does dopamine hyperactivity result in here?

A

Originates in A10.

Arousal, memory, stimulus processing, locomotor activity, and motivational behavior.

Dopamine hyperactivity causes positive symptoms.

40
Q

Where does the the mesocorticol tract orginate? What function is it associted with? What occurs with altered dopaminergic activity?

A

Originates in the A10.

Functions in cognition, communication, and social activity.

Altered dopaminergic activity causes negative symptoms.

41
Q

Where does the nigrostriatal pathway originate? What is a result of dopamine blockade? What about 5-HT blockade?

A

Originates in A9.

Dopamine blockade increases extrapyramidal symptoms.

Blockade of 5HT causes decreased extrapyramidal symptoms and can cause parkinsonism.

42
Q

What occurs with dopamine blockade of the tuberoinfundibular tract?

A

Increase in prolactin release.

43
Q

What are the types of dopamine receptors?

A

All GPCRs.

D1-like family: subtypes D1 and D5. Activation coupled to Gas activates adenylyl cyclase leading to increase in cAMP.

D2-like family: subtypes D2, D3, and D4. Activation coupled to Gai, inhibits adenylyl cylase and leads to a decrease in cAMP. Also autoreceptors that decrease dopamine synthesis when stimulated by dopamine.

44
Q

What is potency of antipsychotics determined by?

A

The ability to block D2 receptors.

45
Q

What are some atypical antipsychotics? What is their function?

A

Newer drugs such as clozapine and risperidone. Have additional neurochemical effects in addition to DA receptor blockade.

Block 5-HT2 receptors in the forebrain. Often with greater potency than for DA receptors.

46
Q

What are the actions of antipsychotic drugs?

A

Decrease in psychotic behavior: typical drugs differ in potency only. Negative symptoms not well treated by older typical agents. Atypicals can treat positive and negative.

Sedation: from blocking H1 receptors.

Extrapyramidal effectsL dystonias, parkinsonism, akathisia (restlessness), tardive dyskinesia.

47
Q

What are side effects of antipsychotic mediations in the order by which they occur temporally?

A

Acute dystonia(1-5 days): spasm of muscles of face, neck, and back.

Parkinsonism(5-30 days): bradykinesia, tremor, rigidity, shuffling gait.

Akathisia (5-60 days): compulsive, restless movement, symptoms of anxiety.

Tardive dyskinesia(months to years): dyskinesis, choreoathetoid movements.

48
Q

What are other actions (side effects) of antipsychotic drugs besides the main four?

A

Orthostatic hypotension.

Anticholinergic: dry mouth, blurred vision, urinary retention.
Decreased seizure threshhold (clozapine)

Weight gain- diabetes more common with atypicals.

49
Q

What is neuroleptic malignant syndrome? How is it treated?

A

Potentially lethal hypodopaminergic side effect of antipsychotic drugs.

Hyperthermia, parkinson-like symptoms (rigidity and tremor), and possible death.

Treatment includes cooling and hydration.

50
Q

What are the three types of typical antipsychotic drugs and examples?

A
  1. Phenothiazines - Chlorpromazine
  2. Thioxanthine derivatives
  3. Butyrophenone - Haloperidol (haldol)
51
Q

Name five atypical antipsychotics?

A
  1. Clozapine
  2. Olanzapine
  3. Risperidone
  4. Quetiapine
  5. Aripiprazole
52
Q

What are the advantages of atypical antipsychotics?

A

Lower incidence of extrapyramidal symptoms (better compliance)

Possible lower incidence of tardive dyskinesia.

Improve negative symptoms better than typicals.

Less impact on cognitive function.

53
Q

What atypical antipsychotic blocks D4 and 5HT receptors, has little effect on D2, and is a muscarinic antagonist? What is the advantage and disadvantage of this drug?

A

Clozapine.

Improves + symptoms and - symptoms. Lower seizure threshhold more than other antipsychotics (5-10%).

Can cause fatal agranulocytosis

54
Q

What atypical antipsychotic is a potent 5HT antagonist, is a D1 and 2 antagonist, and has some effects on D4. What are the benefits and side effects?

A

Olanzapine

Few extrapyramidal symptoms (5HT>D), less seizure incidence than clozapine. No agranulocytosis.

Weight gain and diabetes. Can be abused.

55
Q

What atypical antipsychotic is a combined D2 and 5HT antagnoist and has greater reduction in negative symptoms and less extrapyramidal symptoms than traditional antipsychotics? What are benefits and what does it treat?

A

Resperidone (prodrug).

Less seizure activity and less antimuscarinic effects than clozapine. Available intramuscular.

56
Q

How does quetiapine differ from other atypical antipsychotics? How is it similar?

A

Similar to risperidone and olanzapine in effects on schizophrenia symptoms and side effects.

Shorter half life. Approved for augmentation in depression. Some reports of abuse.

57
Q

What drug is a partial D2 agonist and 5HT antagnoist that’s also approved as an adjunct in depression and for bipolar 1? What form of the drug is available?

A

Aripiprazole

Long acting forms available (one month or more)

Increases impulsive behavior in young men.

58
Q

Which antipsychotic drugs can be used to treat manic episodes and bipolar disorder?

A

Aripiprazole
Olanzapine
Quetiapine
Risperidone

59
Q

Which antipsychotic drug can be used for augmentation in depression?

A

Aripiprazole
Olanzapine
Quetiapine

60
Q

Which antipsychotic drugs can be used to treat Tourette’s syndrome?

A

Haloperidol

Aripiprazole

61
Q

What are the uses of antipsychotic drugs besdies manic episodes, schizoeffective disorder, augmentation in depression, and tourette’s syndrome?

A

Acute psychotic episodes - regardless of the cause

Chronic schizophrenia

Antiemesis

Pharm Block 3 (15 decks)

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