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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
What term do the following things describe? - Derangement of personaliy - Loss of contact with reality - Delusions - Hallucinations
**Psychosis**
26
Describe the **Dopamine Hypothesis** of Schizophrenia. What area of the brain does this refer to particularly?
Schizophrenia results from a _hyperactivity_ of _dopaminergic neurons_ or their receptors **particularly** in the _limbic areas._
27
What do _all effective antipsychotic_ drugs have in common?
They all interact with _dopamine systems._
28
What portion of Schizophrenia is dopamine hyperactivity of the **mesolimbic pathway** most responsible for?
It is most responsible for the _positive symptoms_ of schizophrenia.
29
What portion of Schizophrenia is diminished dopaminergic activity of the **mesocortical pathway** most responsible for?
It is most responsible for the _negative symptoms_ of schizophrenia.
30
How does the nigrostriatal pathway play a role in schizophrenia and its treatment?
Schizophrenia medications create increased extrapyramidal symptoms by blocking dopamine in this pathway.
31
What receptors are not utilized by anti-psychotic medications? Which receptor is utilized by Haloperidol? Which receptor is utilized by Clozapine?
D1 and D5 receptors are not utilized by anti-psychotic drugs. _D2_ is utilized by haloperidol. _D4_ is utilized by clozapine.
32
What primarily affects potency of anti-psychotic medications?
Their affinity for binding to the **D2 receptor**.
33
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?
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.
34
What is meant by the _extrapyramidal effects_ of anti-psychotic medications? (4 items)
1. Dystonia 2. Parkinsonism 3. Akathisia 4. Tardive dyskinesia
35
In order of early to late, when do EPS appear in anti-psychotic therapy generally?
Acute dystonia → Parkinsonism → Akathisia → Tardive dyskinesia
36
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?
1. Anticholinergic effects, Orthostatic hypotension, Hyperprolactinaemia, EPS 2. Cardiac effects of QT prolongation and possible Torsades de pointe 3. Olanzapine, Risperidone, Clozapine, Quetiapine
37
1. Describe **Neuroleptic Malignant Syndrome** presentation. 2. What does the treatment include?
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
1. What is the prototype **Phenothiazine** antipsychotic agent with an aiphatic side chain? 2. What is its relative _potency, sedative effect, major side effect_?
1. **Chlorpromazine** 2. Low to medium potency sedative in nature pronounce anticholinergic effects.
39
What class of drugs are the original antipsychotics that are less commonly used now?
**Phenothiazines**
40
1. What is the prototype **Phenothiazine** with a _piperidine_ side chain? 2. What is its relative potency, sedation, major side effects?
1. **Thioridazine** 2. **Low **potency * *Sedative** * *Decreased** EPS, **+ **Anticholinergic
41
1. What is the **Phenothiazine** with a _piperazine_ side chain? 2. What is its relative potency, sedation effects, side effects?
1. **Fluphenazine**, **Prochlorperazine** (Compazine) 2. **High **potency * *Less** sedative * *Increased **EPS, **Decreased** Anticholinergic
42
1. What butyrophenone derivative is a **Typical** antipsychotic that is pharmacologically similar to high-potency piperazine derivatives?
1.** Haloperidol**
43
What are some of the general benefits of atypical antipsychotics? (5 items)
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
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?
1. Blocks **D4 **and **5-HT2** receptors 2. **_Little_** effect on **D2** 3. Muscarinic _antagonist_
45
1. What are the benefits of **Clozapine** use? 2. What should the prescriber be cautious of? (2 items each)
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
1. What is the mechanism for **Olanzapine**?
1. _Potent_ **D1 and 2** and **5-HT2** _antagonist_ (Some D4)
47
1. What are the benefits of **Olanzapine**? 2. What are the drawbacks of **Olanzapine**?
1. **Few** EPS * *Less** seizure incidence than **Clozapine **(5HT \> D) * *NO** agranulocytosis 2. **Weight gain** * *_Diabetes_** related adverse events
48
What is the mechanism for **Risperidone**?
Combined **D2** and **5-HT2** _antagonism_
49
1. What are the benefits of **Risperidone**? 2. What is the active metabolite of **Risperidone**?
1. Greater **reduction** in _negative symptoms_ than traditional antipsychotics * *Less **_seizure activity_ than **Clozapine** 2. Paliperidone (Invega)
50
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?
1. In its _chemical structure_ 2. **Risperidone** and **Olanzapine** 3. **Shorter** half-life 4. **Depression**
51
1. What is the mechanism for **Aripiprazole**? 2. What is a secondary use for **Aripiprazole** (Abilify)?
1. *Partial* **D2** _agonist_ and **5-HT2** _antagonist_ 2. Adjunct in **depression** (augmentation)
52
Which anti-psychotics for this course are used for **manic episodes** and **bipolar disorder**?
Aripiprazole Olanzapine Quetiapine Risperidone
53
What antipsychotics are used for augmentation in depression?
Aripiprazole Olanzapine Quetiapine
54
What antipsychotic is also used for Tourette's syndrome?
Haloperidol
55
1. What is the general effect of **Lithium**? 2. What is unique about **Lithium** compared to other psychotherapeutic drugs?
1. It blocks manic behavior 2. It is one of few psychotherapeutic drugs that has **no behavioral effects** in "normals."
56
What is the mechanism of **Lithium**?
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
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?
1. Complete absorption in **6 to 8 hours** 2. **18-36 hours** 3. It is **unbound** to plasma proteins
58
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?
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
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?
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
What are some side effects of **Lithium**?
Fatigue Muscular weakness Tremor (treated with beta-blockers) GI symptoms Slurred speech and ataxia
61
1. At what point does serious **Li** toxicity take place? 2. What does this look like?
1. At **2 to 3 times** therapeutic levels 2. Impaired consciousness Rigidity and hyperactive DTRs Coma
62
What are the clinical uses for **Lithium**?
Mania and Bipolar Disorder Unipolar depression Aggressive/Violent/Antisocial behavior Cluster Headaches
63
1. What is **Carpamazepine** in terms of Psychiatry? 2. How does it work? 3. What are its side effects?
1. An alternative to Lithium 2. **Na channel** inhibition 3. Sedation, Confusion, Ataxia
64
1. What is **Valproic acid** used for in Psychiatry? 2. What is its major side effect?
1. **Valproic acid** is a first line drug in bipolar disease 2. It is sedating
65
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?
1. **Haloperidol** 2. **Olanzapine **and **Fluoxetine**
66
How can **Carbamazepine **affect the metabolism of other drugs?
It **induces **hepatic enzymes.
67
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?
1. Partial Seizures 2. Absence seizures 3. Diplopia and Ataxia GI upset Drowsiness Rare blood dyscrasias
68
1. What is the mechanism of action for **Valproic Acid**? 2. What is the protein binding, distribution and effect on metabolism of other drugs?
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
What are the therapeutic uses for **Valproic Acid**?
1. **Absence** seizures 2. **Absence** seizures with concomitant **Tonic-clonic** seizures 3. Generalized **tonic-clonic **seizures 4. **Myoclonic** seizures
70
What are two non-dose related effects of **Valproic Acid**?
1. Idiosyncratic hepatotoxicity 2. Teratogenicity - Spinal bifida
71
1. What is the amino acid that GABA is derived from? 2. What type of cell is the GABA receptor?
1. Glutamate 2. Cl- ion channel
72
1. How are Benzodiazepines related to GABA? 2. What drug has opposing action to benzos?
1. They are **agonists** of the GABA Cl- channel. 2. **Flumazenil **is a GABA/Benzo receptor antagonist.
73
What benzodiazepines, for this course, are used to treat anxiety disorders? (4 items)
Diazepam Chlordiazepoxide Alprazolam Lorazepam
74
What is the non-benzo anxiolytic for this course? What is its MOA?
**Buspirone**: Partial agonist for 5HT1A which inhibits adenylate cyclase and opens K+ channels
75
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?
1. **Alprazolam** depresses primarily _Forebrain_ and **Diazepam** causes _broad CNS depression_. 2. **Alprazolam **has a _short duration_. **Diazepam** has a _long duration_.
76
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?
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
1. Which benzos have active metabolites? 2. Which benzos do not have active metabolites? 3. How are all benzos eliminated?
1. Chlordiazepoxide, Diazepam, Alprazolam 2. Lorazepam, Flurazepam 3. Conjugation and Urinary Excretion
78
What are the CNS effects of benzodiazepines and their accompanying clinical use?
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
1. What is a common anti-convulsant benzo? 2. What is a commong ETOH withdrawal benzo?
1. Diazepam 2. Chlordiazepoxide
80
What is an important consideration when discontinuing a benzo?
Gradual dose reduction is necessary to prevent a withdrawal syndrome
81
What are three benzos used as hypnotics for sleep disturbance?
Flurazepam, Lorazepam, Zolpidem
82
What three major effects do benzos have on the normal sleep cycle?
1. Decreased latency to sleep 2. Increases in Stage 1 and Stage 2 sleep 3. Decreased Stage 3,4 and REM sleep
83
What non-benzodiazepine binds to the BDZ receptor on the GABA receptor complex to produce hypnosis, weak anxiolysis, and muscle relaxation?
**Zolpidem** (Ambien)
84
1. What are the benefits of Zolpidem over other benzos for sleep aid? 2. How is a Zolpidem overdose treated?
1. Preserves Stage 3 and 4 sleep with only minor effects on REM sleep. 2. Flumazenil reverses it as well.
85
1. What is the mechanism of action of barbiturates? 2. What are the two major clinical uses for barbiturates?
1. Bind to GABAa Cl- ion channel. Enhances GABA and increases inhibition. 2. Hypnotic - rarely used today Anticonvulsant - **Phenobarbital**
86
What is **chloral hydrate?** What is an advantage to its use?
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
1. What is the general concept behind skeletal muscle relaxants? 2. What are two primary GABAergic Agents for muscle relaxation?
1. Reduce spastic tone by inhibiting the stretch reflex arc and higher centers in the brain. 2. **Diazepam **and **Baclofen**
88
1. What is the mechanism of action for Baclofen? 2. What is the benefit of using it?
1. GABAB bindingresulting in hyperpolarizaiton and presynaptic inhibition 2. It is atleast as effective in reducing spasm as Diazepam and much less sedating
89
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?
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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