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Owenpharm Block 3 > Neuropsychopharm > Flashcards

Neuropsychopharm Flashcards

1
Q
  1. Where are the neurons that contain NE in the brain and where do they project?
  2. Where does serotonin originate in the brain?
  3. Where are dopamine containing neurons and where do they project?
A
  1. Neurons are located in locus coeruleus and innervate nearly every part of CNS
  2. Raphe nuclei
  3. Substantia nigra projects to the striatum. Ventral tregmentum projects to prefrontal cotex and limbic system.
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2
Q

Where are the 6 sites of GABA localization?

A
  1. Sustantia Nigra
  2. Globus Pallidus
  3. Hippocampus
  4. Limbic structures - Amygdala
  5. Hypothalamus
  6. Spinal cord
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3
Q

What is the difference between DSM-IV depression categorization and DSM-5 categorization?

A

DSM-IV denotes Major Depressive Disorder under which include unipolar and bipolar. DSM-5 separates Bipolar disorder from Major Depressive Disorder

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4
Q

What is the difference between the classic theory of depression vs. current theory of depression?

A

The classic (Monoamine Theory) was insufficient transmission of NE and 5-HT in CNS. The current theory is that there is an imbalance of amine receptor or transmission imbalance in CNS.

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5
Q
  1. How does efficacy and time course of SSRIs compare with TCAs?
  2. How does acute toxicity of SSRIs compare to TCAs and MAOIs?
  3. How soon do withdrawal symptoms begin after cessation of SSRIs?
  4. What are 4 unique symptoms of withdrawal?
A
  1. Efficacy and time course are about the same.
  2. Acute toxicity is less.
  3. 1-7 days
  4. Shock-like sensations and paresthesia, dizziness, gait instability, visual disturbances.
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6
Q

What are the approved uses for SSRIs? (8 items)

A
  1. Major Depression
  2. OCD
  3. Panic disorder
  4. Social Anxiety Disorder
  5. PTSD
  6. Generalized Anxiety Disorder
  7. Premenstrual Dysphoric Disorder
  8. Hot flashes associated with menopause
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7
Q
  1. What are two examples of SSRIs?
  2. Which has the longer half-life? Why?
  3. Which has less effects on drug metabolism?
A
  1. Fluoxetine and Sertraline
  2. Fluoxetine. It has an active metabolite
  3. Sertraline
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8
Q
  1. What drug is an SNRI that blocks 5-HT and NE reuptake?
  2. What is its half-life?
  3. What non-psychiatric conditions is this drug approved for?
  4. What patients should this drug be used with caution?
A
  1. Duloxetine
  2. 12-18 hours
  3. Chronic pain syndromes: fibromyalgia, back pain, neuropathic pain.
  4. Patients with liver disease.
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9
Q
  1. What are two atypical antidepressants?
A
  1. Bupropion and Mirtazapine
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10
Q
  1. What is the mechanism for Bupropion?
  2. What are non-depression uses for Bupropion?
  3. What is the benefit in terms of side effects of Bupropion?
A
  1. Bupropion weakly blocks NE and dopamine uptake.
  2. Nicotine withdrawal, Seasonal Affective Disorder
  3. No weight gain or sexual dysfunction as with SSRIs
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11
Q
  1. What is the mechanism for Mirtazapine?
  2. What is a side effect of Mirtazapine?
A
  1. Blocks pre-synaptic alpha2 receptors in brain
  2. It increases appetite
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12
Q
  1. What are two examples of TCAs?
  2. What is the mechanism of TCAs?
  3. What is the relative absorption and distribution of TCAs?
  4. Which TCA has an active metabolite that is also used as a drug?
  5. What is the plasma half-life of TCAs?
A
  1. Amitriptyline and Clomipramine
  2. Blocks NE and 5-HT reuptake
  3. Rapid absorption and high concentrations in brain and heart.
  4. Amitriptyline
  5. Long: 8-100 hours.
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13
Q
  1. How long does it take for TCAs (Amitriptyline and Clomipramine) to improve depressive symptoms?
  2. What effect do TCAs have on sleep?
  3. What are some prominent side effects of TCAs?
  4. What type of patient are TCAs contraindicated?
A
  1. 2-3 weeks
  2. Decreased REM and increased stage 4 sleep
  3. Anti-cholinergic effects, Sedation, Cardiac abnormalities
  4. Patients with recent M.I.
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14
Q

What are the major therapeutic uses for TCAs? (4 items)

A
  1. Major depressive disorder
  2. Enuresis in childhood
  3. Chronic pain - Amitiptyline
  4. OCD - Clomipramine
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15
Q

What is the hallmark MAOI for this course?

A

Phenelzine

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16
Q
  1. How long do MAOIs take to achieve their effect?
  2. Used with caution in bipolar depression. Why?
A
  1. About 2 weeks.
  2. Can progress to hypomania
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17
Q
  1. Do MAOIs worsen or improve sleep disorders in depressed patients?
  2. What effect would MAOIs have in a normal patient?
A
  1. They correct sleep disorders.
  2. They may produce stimulation
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18
Q

What are some symptoms of MAOI toxicity?

A
  1. Agitation
  2. Hallucinations
  3. Hyperpyrexia
  4. Convulsions
  5. Changes in blood pressure
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19
Q

What is the primary dietary concern with MAOIs? Why?

A

Tyramine containing foods (cheese, wine, chocolate, processed meats) can cause hypertensive crisis by increasing release of NE because Tyramine is broken down my MAO.

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20
Q

What are the two major therapeutic uses for MAOIs?

A
  1. Major depression – no longer drug of first choice
  2. Narcolepsy
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21
Q

What is a non-specific blocker of NE and 5-HT used to treat depression?

A

Amitriptyline

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22
Q

What are the selective serotonin reuptake inhibitors for this course?

A

Fluoxetine and Sertraline

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23
Q

What is the mechanism of action for Duloxetine? What is it used for?

A

Inhibits the reuptake of Serotonin and Norepinephrine. It is used for depression.

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24
Q

What is the mechanism of action for Phenelzine? What is it used for?

A

It inhibits the action of Monoamine Oxidase and therefore inhibits the breakdown of monoamines like serotonin and norepinephrine. It is used for depression.

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25
Q

What term do the following things describe?

  • Derangement of personaliy
  • Loss of contact with reality
  • Delusions
  • Hallucinations
A

Psychosis

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26
Q

Describe the Dopamine Hypothesis of Schizophrenia.

What area of the brain does this refer to particularly?

A

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

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27
Q

What do all effective antipsychotic drugs have in common?

A

They all interact with dopamine systems.

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28
Q

What portion of Schizophrenia is dopamine hyperactivity of the mesolimbic pathway most responsible for?

A

It is most responsible for the positive symptoms of schizophrenia.

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29
Q

What portion of Schizophrenia is diminished dopaminergic activity of the mesocortical pathway most responsible for?

A

It is most responsible for the negative symptoms of schizophrenia.

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30
Q

How does the nigrostriatal pathway play a role in schizophrenia and its treatment?

A

Schizophrenia medications create increased extrapyramidal symptoms by blocking dopamine in this pathway.

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31
Q

What receptors are not utilized by anti-psychotic medications?
Which receptor is utilized by Haloperidol?
Which receptor is utilized by Clozapine?

A

D1 and D5 receptors are not utilized by anti-psychotic drugs.
D2 is utilized by haloperidol.
D4 is utilized by clozapine.

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32
Q

What primarily affects potency of anti-psychotic medications?

A

Their affinity for binding to the D2 receptor.

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33
Q
  1. What is the only difference between typical anti-psychotics?
  2. What is not well treated by older typical agents?
  3. Why are atypical drugs generally more desirable?
A
  1. Potency is the only difference.
  2. Negative symptoms are not well treated.
  3. They are more effective in treating the negative symptoms. In addition to treating the positive symptoms.
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34
Q

What is meant by the extrapyramidal effects of anti-psychotic medications? (4 items)

A
  1. Dystonia
  2. Parkinsonism
  3. Akathisia
  4. Tardive dyskinesia
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35
Q

In order of early to late, when do EPS appear in anti-psychotic therapy generally?

A

Acute dystonia → Parkinsonism → Akathisia → Tardive dyskinesia

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36
Q
  1. What are some common side effects of anti-psychotic drugs?
  2. What is a unique side effect of Thioridazine?
  3. Which drugs should one be more cautious about diabetes when prescribing?
A
  1. Anticholinergic effects, Orthostatic hypotension, Hyperprolactinaemia, EPS
  2. Cardiac effects of QT prolongation and possible Torsades de pointe
  3. Olanzapine, Risperidone, Clozapine, Quetiapine
37
Q
  1. Describe Neuroleptic Malignant Syndrome presentation.
  2. What does the treatment include?
A
  1. Hyperthermia, Parkinson-like symptoms (muscular rigidity and tremor), mutism
  2. Cooling the patient, hydration, and administration of bromocriptine and dantrolene are all very important to patient survival.
38
Q
  1. What is the prototype Phenothiazine antipsychotic agent with an aiphatic side chain?
  2. What is its relative potency, sedative effect, major side effect?
A
  1. Chlorpromazine
  2. Low to medium potency
    sedative in nature
    pronounce anticholinergic effects.
39
Q

What class of drugs are the original antipsychotics that are less commonly used now?

A

Phenothiazines

40
Q
  1. What is the prototype Phenothiazine with a piperidine side chain?
  2. What is its relative potency, sedation, major side effects?
A
  1. Thioridazine
  2. Low potency
    * *Sedative
    * *Decreased     EPS, **+ **Anticholinergic
41
Q
  1. What is the Phenothiazine with a piperazine side chain?
  2. What is its relative potency, sedation effects, side effects?
A
  1. Fluphenazine, Prochlorperazine (Compazine)
  2. **High potency
    * *Less     sedative
    * *Increased **EPS, Decreased Anticholinergic
42
Q
  1. What butyrophenone derivative is a Typical antipsychotic that is pharmacologically similar to high-potency piperazine derivatives?
A

1.** Haloperidol**

43
Q

What are some of the general benefits of atypical antipsychotics? (5 items)

A
  1. Lower incidence of EPS
  2. Lower incidence of tardive dyskinesia
  3. Possible improvement in negative symptoms
  4. May help in refractory patients
  5. Possible decreased impact on cognitive function
44
Q
  1. What is the mechanism of the Atypical antipsychotic Clozapine?
  2. To what extent does it affect D2 receptors?
  3. What effect does it have on muscarinic receptors?
A
  1. Blocks **D4 **and 5-HT2 receptors
  2. Little effect on D2
  3. Muscarinic antagonist
45
Q
  1. What are the benefits of Clozapine use?
  2. What should the prescriber be cautious of?

(2 items each)

A
  1. Improves positive symptoms in refractory psychosis
    * *Improves** negative symptoms
  2. Lowers seizure threshold more than other drugs (5-10%)
    * *Agranulocytosis **(possibly fatal) - requires monitoring
46
Q
  1. What is the mechanism for Olanzapine?
A
  1. Potent D1 and 2 and 5-HT2 antagonist (Some D4)
47
Q
  1. What are the benefits of Olanzapine?
  2. What are the drawbacks of Olanzapine?
A
  1. Few EPS
    * *Less** seizure incidence than **Clozapine (5HT > D)
    * *NO     agranulocytosis
  2. Weight gain
    * *Diabetes** related adverse events
48
Q

What is the mechanism for Risperidone?

A

Combined D2 and 5-HT2 antagonism

49
Q
  1. What are the benefits of Risperidone?
  2. What is the active metabolite of Risperidone?
A
  1. Greater reduction in negative symptoms than traditional antipsychotics
    * *Less **seizure activity than Clozapine
  2. Paliperidone (Invega)
50
Q
  1. How is Quetiapine similar to Clozapine?
  2. What drugs are its effects on Schizophrenia similar to?
  3. What is the relative half-life compared to other atypicals?
  4. What other psychiatric condition is Quetiapine approved for?
A
  1. In its chemical structure
  2. Risperidone and Olanzapine
  3. Shorter half-life
  4. Depression
51
Q
  1. What is the mechanism for Aripiprazole?
  2. What is a secondary use for Aripiprazole (Abilify)?
A
  1. Partial D2 agonist and 5-HT2 antagonist
  2. Adjunct in depression (augmentation)
52
Q

Which anti-psychotics for this course are used for manic episodes and bipolar disorder?

A

Aripiprazole
Olanzapine
Quetiapine
Risperidone

53
Q

What antipsychotics are used for augmentation in depression?

A

Aripiprazole
Olanzapine
Quetiapine

54
Q

What antipsychotic is also used for Tourette’s syndrome?

A

Haloperidol

55
Q
  1. What is the general effect of Lithium?
  2. What is unique about Lithium compared to other psychotherapeutic drugs?
A
  1. It blocks manic behavior
  2. It is one of few psychotherapeutic drugs that has no behavioral effects in “normals.”
56
Q

What is the mechanism of Lithium?

A

It inhibits the recycling of inositol substrates may cause depletion of second-messenger source PIP2 and therefore reduce IP3 and DAG.

It also has effects on GSK.

57
Q
  1. How long does complete absorption take for Lithium?
  2. What is the half-life for Lithium?
  3. What degree of plasma binding does it have?
A
  1. Complete absorption in 6 to 8 hours
  2. 18-36 hours
  3. It is unbound to plasma proteins
58
Q
  1. How is its volume of distribution of Lithium determined?
  2. What level of CNS penetrance does it have?
  3. How is the majority of Lithium eliminated?
A
  1. Lithium’s volume of distribution is equal to total body water.
  2. Its CSF concentration is 40 to 50% of plasma concentration.
  3. 95% of a single dose is eliminated in urine.
59
Q
  1. What is the relationship between serum Na and Li levels?
  2. What medications or physiologic activity can create the same effect?
  3. Why is frequent monitoring necessary?
A
  1. Decreased serum Na increases Li levels.
  2. Thiazide diuretics, ACE-I, ARBs or losses of fluids/electrolytes
  3. It has a narrow therapeutic window
60
Q

What are some side effects of Lithium?

A

Fatigue
Muscular weakness
Tremor (treated with beta-blockers)
GI symptoms
Slurred speech and ataxia

61
Q
  1. At what point does serious Li toxicity take place?
  2. What does this look like?
A
  1. At 2 to 3 times therapeutic levels
  2. Impaired consciousness
    Rigidity and hyperactive DTRs
    Coma
62
Q

What are the clinical uses for Lithium?

A

Mania and Bipolar Disorder
Unipolar depression
Aggressive/Violent/Antisocial behavior
Cluster Headaches

63
Q
  1. What is Carpamazepine in terms of Psychiatry?
  2. How does it work?
  3. What are its side effects?
A
  1. An alternative to Lithium
  2. Na channel inhibition
  3. Sedation, Confusion, Ataxia
64
Q
  1. What is Valproic acid used for in Psychiatry?
  2. What is its major side effect?
A
  1. Valproic acid is a first line drug in bipolar disease
  2. It is sedating
65
Q
  1. What typical antipsychotic can be used for initial control of manic symptoms?
  2. What combination of drugs is used for depressive episodes associated with bipolar disease?
A
  1. Haloperidol
  2. **Olanzapine **and Fluoxetine
66
Q

How can **Carbamazepine **affect the metabolism of other drugs?

A

It **induces **hepatic enzymes.

67
Q
  1. What is **Carbamazepine **a drug of choice for in Neurology?
  2. What type of condition is it contraindicated for?
  3. What does Carbamazepine toxicity look like?
A
  1. Partial Seizures
  2. Absence seizures
  3. Diplopia and Ataxia
    GI upset
    Drowsiness
    Rare blood dyscrasias
68
Q
  1. What is the mechanism of action for Valproic Acid?
  2. What is the protein binding, distribution and effect on metabolism of other drugs?
A
  1. Blocks repetitive neuronal firing by reducing T-type Ca++ currents and increasing GABA concentrations.
  2. Bound to plasma protein (competes with phenytoin)
    Distributes in extracellular fluid
    Inhibits metabolism of phenobarb., phenytoin, and carbamazepine
69
Q

What are the therapeutic uses for Valproic Acid?

A
  1. Absence seizures
  2. Absence seizures with concomitant Tonic-clonic seizures
  3. Generalized **tonic-clonic **seizures
  4. Myoclonic seizures
70
Q

What are two non-dose related effects of Valproic Acid?

A
  1. Idiosyncratic hepatotoxicity
  2. Teratogenicity - Spinal bifida
71
Q
  1. What is the amino acid that GABA is derived from?
  2. What type of cell is the GABA receptor?
A
  1. Glutamate
  2. Cl- ion channel
72
Q
  1. How are Benzodiazepines related to GABA?
  2. What drug has opposing action to benzos?
A
  1. They are agonists of the GABA Cl- channel.
  2. **Flumazenil **is a GABA/Benzo receptor antagonist.
73
Q

What benzodiazepines, for this course, are used to treat anxiety disorders? (4 items)

A

Diazepam
Chlordiazepoxide
Alprazolam
Lorazepam

74
Q

What is the non-benzo anxiolytic for this course? What is its MOA?

A

Buspirone: Partial agonist for 5HT1A which inhibits adenylate cyclase and opens K+ channels

75
Q
  1. What is the difference between Alprazolam and Diazepam in terms of location of depression in CNS?
  2. What is the difference in their duration of action?
A
  1. Alprazolam depresses primarily Forebrain and Diazepam causes broad CNS depression.
  2. **Alprazolam **has a short duration. Diazepam has a long duration.
76
Q
  1. What is the reason for Diazepam’s fast onset compared to Lorazepam’s slower onset and longer duration?
  2. What is the difference in the metabolites of these two drugs?
A
  1. Diazepam is more lipophilic than Lorazepam. It enters the brain faster but is rapidly redistributed after single dose.
  2. **Diazepam **has active metabolites and Lorazepam has NO active metabolites.
77
Q
  1. Which benzos have active metabolites?
  2. Which benzos do not have active metabolites?
  3. How are all benzos eliminated?
A
  1. Chlordiazepoxide, Diazepam, Alprazolam
  2. Lorazepam, Flurazepam
  3. Conjugation and Urinary Excretion
78
Q

What are the CNS effects of benzodiazepines and their accompanying clinical use?

A
  1. Decreased anxiety – General anxiety disorders
  2. Sedation and Hypnosis – Sleep disorders
  3. Muscle relaxation – muscle relaxant
  4. Anterograde amnesia – procedural sedation
  5. Anticonvulsant action – Seizures, ETOH withdrawal
79
Q
  1. What is a common anti-convulsant benzo?
  2. What is a commong ETOH withdrawal benzo?
A
  1. Diazepam
  2. Chlordiazepoxide
80
Q

What is an important consideration when discontinuing a benzo?

A

Gradual dose reduction is necessary to prevent a withdrawal syndrome

81
Q

What are three benzos used as hypnotics for sleep disturbance?

A

Flurazepam, Lorazepam, Zolpidem

82
Q

What three major effects do benzos have on the normal sleep cycle?

A
  1. Decreased latency to sleep
  2. Increases in Stage 1 and Stage 2 sleep
  3. Decreased Stage 3,4 and REM sleep
83
Q

What non-benzodiazepine binds to the BDZ receptor on the GABA receptor complex to produce hypnosis, weak anxiolysis, and muscle relaxation?

A

Zolpidem (Ambien)

84
Q
  1. What are the benefits of Zolpidem over other benzos for sleep aid?
  2. How is a Zolpidem overdose treated?
A
  1. Preserves Stage 3 and 4 sleep with only minor effects on REM sleep.
  2. Flumazenil reverses it as well.
85
Q
  1. What is the mechanism of action of barbiturates?
  2. What are the two major clinical uses for barbiturates?
A
  1. Bind to GABAa Cl- ion channel. Enhances GABA and increases inhibition.
  2. Hypnotic - rarely used today
    Anticonvulsant - Phenobarbital
86
Q

What is chloral hydrate?

What is an advantage to its use?

A

A prodrug metabolized to trichloroethanol, the active form, and is pharicologically similar to barbiturates.

It has less effects on stages of sleep than benzos or barbiturates.

87
Q
  1. What is the general concept behind skeletal muscle relaxants?
  2. What are two primary GABAergic Agents for muscle relaxation?
A
  1. Reduce spastic tone by inhibiting the stretch reflex arc and higher centers in the brain.
  2. **Diazepam **and Baclofen
88
Q
  1. What is the mechanism of action for Baclofen?
  2. What is the benefit of using it?
A
  1. GABAB bindingresulting in hyperpolarizaiton and presynaptic inhibition
  2. It is atleast as effective in reducing spasm as Diazepam and much less sedating
89
Q
  1. What is the mechanism for Tizanidine?
  2. What is it used for? How effective is it?
  3. What are the side effects?
  4. What important drug interacts does it have?
A
  1. Alpha2 adrenergic agonist that enhances pre- and post- synaptic inhibition
  2. Used for muscle relaxation and similar efficacy to Baclofen and Diazepam.
  3. Drowsiness, dry mouth, weakness
  4. Cipro and fluvoxamine (CYP1A2 inhibitors)

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