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USMLE > Psychiatry > Flashcards

Psychiatry Flashcards

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USMLE® Step 1 flashcards
1
Q

What is schizophrenia?

What are the biochemical and histological features?

A

Schizophrenia is a chronic mental disorder with periods of psychosis, disturbed behaviour and thought, and decline in functioning lasting >6 months.

Associated with increased dopaminergic activity and reduced dendritic branching. Ventriculomegaly on brain imaging.

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2
Q

Diagnosis of Schizophrenia requires?

A

At least two of the following (at least positive symptom):

  1. Delusions
  2. Hallucinations
  3. Disorganised speech
  4. Disorganised or catatonic behaviour
  5. Negative symptoms.
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3
Q

How are the following different to Schizophrenia?

Brief psychotic disorder

Schizophreniform disorder

Schizoaffective disorder

A

Brief psychotic disorders last less than one month. Schizophreniform disorder last between one and six months. Schizoaffective disorder meets criteria for Schizophrenia in addition to major mood disorder. Psychotic features must be for longer than two weeks without a major mood episode.

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4
Q

What are the preferred medications for BPAD?

A

Lithium

Sodium valproate

Carbamazepine

Lamotrigine

Atypical antipsychotics

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5
Q

What are the preferred medications for OCD?

A

SSRIs

Venlafaxine

Clomipramine

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6
Q

What are the preferred medications for Panic Disorder?

A

SSRIs

Venlafaxine

Benzodiazepines

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7
Q

How do the Typical and Atypical Antipsychotics work?

A

Block Dopamine D2 receptors. Atypicals also have varied effects on 5-HT, Dopamine, and Histamine receptors.

Reduce activity of the mesocortical (negative) and mesolimbic (positive) pathways. Also block the nigrostriatal and tuberoinfundibular pathways, hence the EPS and pituitary side effects.

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8
Q

What are the high and low potency Typical Antipsychotics? What are the common side effects of each class?

A

(TRI to FLy High) (CHeating THIeves are low)

High potency = Trifluoperazine, Fluphenazine, Haloperidol

Side effects = EPS

Low potency = Chlorpromazine, Thioridizine

Side effects = anticholinergic and antihistamine, alpha blockade.

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9
Q

Clozapine is helpful for?

What is a feared side effect?

A

Clozapine can be used in treatment resistant Schizophrenia or Schizoaffective disorder. Also used for suicidality in Schizophrenia.

Must watch bone marrow CLOZely for agranulocytosis.

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10
Q

Olanzipine causes?

A

Obesity and metabolic syndrome.

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11
Q

Risperidone causes?

A

Hyperprolactinaemia.

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12
Q

Advantages and disadvantages of Atypical compared to Typical Antipsychotics?

A

Fewer EPS and amticholinergic side effects.

More QT prolongation.

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13
Q

Mechanism of action

Clinical use

Adverse effects of:

Lithium

A

Inhibition of the phosphoinositol cascade.

Mood stabiliser for BPAD; blocks relapse and acute manic attacks

(LiTHIUM): Low Thyroid, Heart (Ebstein abnormality), Insipidus, unwanted Movements.

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14
Q

Mechanism of action

Clinical use and advantages of:

Buspirone

A

Stimulates 5-HT1a receptors.

Generalised anxiety disorder.

Does not cause sedation, addiction or tolerance.

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15
Q

Mechanism of action

Clinical use

Adverse effects of:

SSRIs

A

(Fluoxetine, Paroxetine, Citalopram, Setraline)

Inhibit 5-HT reuptake.

Used for depression, GAD, PD, OCD, bulimia, social anxiety disorder, PTSD, premature ejaculation, premenstrual dysphoric disorder.

Sexual dysfunction, GI distress, can precipitate mania in BPAD.

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16
Q

Mechanism of action

Clinical use

Adverse effects of:

SNRIs

A

(Venlafaxine, Duloxetine, Milnacipran)

Inhibit both 5-HT and NE uptake.

Depression, GAD, diabetic neuropathy, social anxiety disorder, PD, PTSD, OCD. Duloxetine is also indicated for fibromyalgia.

Hypertension most common. Sedation, nausea.

17
Q

What is Serotonin syndrome?

Which medications can cause it?

What is the treatment?

A

A syndrome characterised by neuromuscular hyperActivity, Autonomic stimulation, and Agitation.

Any drug that increases 5-HT: MAOIs, SSRIs, SNRIs, TCAs, Tramadol, Ondansetron, Linezolid, Triptans, MDMA, Dextromethorphan.

Cryoheptadine is the treatment (5-HT antagonist)

18
Q

Mechanism of action

Clinical use

Adverse effects of:

TCAs

A

(Amitriptyline, Imipramine, Clomipramine, Doxepin)

Inhibit NE and 5-HT reuptake

Major depression, OCD, peripheral neuropathy, chronic pain, migraine prophylaxis, nocturnal enuresis.

Tri C’s: Coma, Convulsions, Cardiotoxicity. Sedation, postural hypotension, anticholinergic effects, can prolong QT interval.

19
Q

Mechanism of action

Clinical use

Adverse effects of:

MAOIs

A

(Tranylpromine, Phenelzine, Isocarboxid, Selegiline)

Non-selective MAO inhibition which increases levels of amine NTs.

Used for depression and PD (Selegiline)

CNS stimulation with hypertensive crisis, especially with Tyramine (found in cheese and wine). Contraindicated with SSRIs, TCAs, and St John’s wort.

20
Q

Mechanism of action

Clinical use

Adverse effects of:

Bupropion

A

Inhibits reuptake of both NE and Dopamine.

Depression and smoking cessation.

May help alleviate sexual dysfunction. Stimulant effects.

21
Q

Mechanism of action

Clinical use

Special uses and adverse effects of:

Mirtazapine

A

Alpha-2 agonist, stimulates NE and 5-HT.

Depression and stimulates appetite and weight gain.

Useful for anorexia and elderly. Sedation and dry mouth.

22
Q

Mechanism of action

Clinical use

Adverse effects of:

Trazodone

A

(traZZZZoBONE)

Primarily blocks 5-HT, alpha adrenergic, and H-1 receptors Used for insomnia. High doses need for depression.

Sedation and priapism.

23
Q

Mechanism of action

Clinical use

Adverse effects of:

Vortioxetine

A

Inhibits 5-HT reuptake Atypical antidepressant for major depressive disorder.

Causes nausea, sexual dysfunction, and abnormal dreams.

24
Q

What are the medications used for treating alcoholism?

How do they differ in their mechanism of action?

A

Naltrexone blocks the mu-opioid receptor and reduces the craving for alcohol, it blocks the rewarding and reinforcing effects of alcohol. It can still be used while patients are drinking.

Disulfiram inhibits aldehyde dehydrogenase and has an aversive mechanism of action. It should only be used in patients who are motivated to abstain.

Acamprosate modulates glutamate neurotransmission and can only be used after a period of sustained abstinence.

25
Q

Describe the pathophysiology of alcohol withdrawal:

A

Alcohol is a CNS depressant that binds to GABA-A receptors, enhancing the inhibitory effects of GABA. Chronic use alcohol of alcohol leads to down regulation of GABA receptors. Withdrawal therefore leads to reduced inhibitory GABA and therefore CNS stimulation.

26
Q

Which of the opioid receptors is responsible for effecting:

Respiratory and cardiac depression?

Miosis?

Antidepressant effects?

Sedation?

Reduced GI motility?

Analgesia?

Where does Naloxone bind with most affinity?

A

Respiratory and cardiac depression? Mu

Miosis? Kappa

Antidepressant effects? Delta

Sedation? Mu and Kappa

Reduced GI motility? Mu

Analgesia? Mu and Kappa

Naloxone binds Mu with greatest affinity.

27
Q

Describe the pharmacology of TCAs:

What 5 receptors do they inhibit?

A

TCAs assert their antidepressant effects through inhibiton of serotonin and NE reuptake.

However, they also inhibit:

Muscurinic Ach receptors (cholinergic effects)

Peripheral alpha 1 receptors (orthostatic hypotension)

Cardiac fast sodium channels (arrhythmias)

Histamine receptors (flushing, sedation)

28
Q

In what situation would you use MAOIs for depression?

A

In treatment resistant depression or in atypical depression.

Atypical depression is characterised by mood reactivity, leaden paralysis, rejection sensitivity, and the reversed vegetative signs of increased sleep and appetite.

USMLE (14 decks)

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