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AMC > Mental health > Flashcards

Mental health Flashcards

1
Q

Definition of delusions

A

Unshakeable, false beliefs that are not in keeping with an individual’s educational, cultural and social background.

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2
Q

Definition of hallucination

A

Perceptions in the absence of actual external stimuli

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3
Q

Schizophrenia diagnostic criteria

A

Includes psychotic phenomena, negative symptoms, cognitive symptoms and disorganisation. It is a chronic disorder, requiring at least 6 months of symptomatology and at least one month of psychotic symptoms. Disorders that meet the criteria for schizophrenia, but do not fulfil this timeframe, are classified as schizophreniform disorder

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4
Q

Psychotic disorders (schizophrenia, schizoaffective disorder, substance-induced psychosis, delusional disorder): aims of the treatment

A

facilitate recovery
prevent relapse, because repeated relapses are associated with poor short- and long-term outcomes
improve function, quality of life and physical health
prevent suicide

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5
Q

Psychotic disorder diagnosis

A

signs and symptoms of psychosis (including at least one positive sign or symptom) persist for at least 1 week and cause distress and functional impairment

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6
Q

Signs and symptoms in psychotic disorders

A

> Negative signs and symptoms

lack of motivation

poor self-care

blunted affect

reduced speech

social withdrawal

> Cognitive signs and symptoms

impaired planning

reduced mental flexibility

impaired memory and concentration

impaired social cognition [NB2]

> Excitement:

disorganised behaviour

aggression

hostility

catatonia

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7
Q

Signs and symptoms in Brief psychotic disorder

A

positive psychotic signs or symptoms that fully resolve within 1 month

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8
Q

Signs and symptoms in schizophreniform disorder

A

Both negative and positive signs or symptoms that fully resolve within 6 months

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9
Q

Signs and symptoms in substance-induced psychotic disorder

A

Positive psychotic signs or symptoms related to substance use that last longer than expected with intoxication or withdrawal, but less than 4 weeks

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10
Q

Signs and symptoms in schizophrenia

A

Negative and positive psychotic signs or symptoms and functional deterioration that persist for longer than 6 months

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11
Q

Signs and symptoms in schizoaffective disorder

A

Symptoms of schizophrenia with prominent mood symptoms consistent with those of major depression or bipolar disorder

Primarily experiences symptoms of psychosis, which may appear without a mood disorder. The DSM criteria require 2 weeks in which psychotic symptoms occur without mood symptoms

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12
Q

Signs and symptoms in Delusional disorder

A

Usually presents in middle to late life.

It is characterised by not bizarre delusions (grandiose, persecutory, erotomanic, somatic) lasting for at least 1 month and resulting in functional decline. Hallucinations, if present, are not prominent, and are related to the delusion

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13
Q

Assessment of psychotic disorders

A

> A comprehensive history, including:
details of the presenting symptoms
a developmental history, including details about relationships, employment, function and early life stress or trauma
family history, including mental and physical health
medical and psychiatric history, including treatment history
substance use, including alcohol, tobacco and other drugs
mental state examination
physical examination and neurological assessment; check blood pressure, heart rate, temperature and respiratory rate
investigations, including
full blood count
blood electrolytes (including calcium), creatinine and urea concentrations
liver biochemistry
blood glucose concentration
thyroid function tests
urine toxicology
inflammatory markers (eg erythrocyte sedimentation rate [ESR], C-reactive protein [CRP])
oxygen saturation (with or without blood gas measurement)
electrocardiogram (ECG)
brain imaging (eg computerised tomography [CT], magnetic resonance imaging [MRI]).
Additional assessments for people at risk of conditions associated with psychotic signs and symptoms, include:

hepatitis C serology for people at risk of hepatitis C
human immunodeficiency virus (HIV) antibody/antigen testing and syphilis serology for people at risk of a sexually transmitted infection
pain assessment in people at risk of delirium
electroencephalogram (EEG) when indicated (eg a history of head trauma, seizures)
antinuclear antibodies (ANA), N-methyl-D-aspartate (NMDA) receptor antibodies, and anti–glutamic acid decarboxylase (anti-GAD) antibodies for people at risk of autoimmune psychosis (eg NMDA receptor encephalitis); seek expert advice for further assessmen

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14
Q

Baseline parameters potentially affected by antipsychotic therapy

A

blood pressure and heart rate
weight, waist circumference and BMI
blood glucose and glycated haemoglobin (HbA1c) concentration
lipid concentrations, including triglycerides
level of physical activity
movement (involuntary or voluntary)
full blood count
blood prolactin concentration l
electrocardiogram (ECG)

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15
Q

Antipsychotic choice for a first episode of psychosis in adults - considerations

A

If antipsychotic therapy for a first episode of psychosis is considered necessary after observing the patient for 24 to 48 hours,

Amisulpride, aripiprazole, olanzapine, quetiapine, risperidone and ziprasidone have been shown in randomised controlled trials to have efficacy in treating a first episode of psychosis.

!!!!!!! Do not use olanzapine as first-line therapy for a first episode of psychosis because it has severe metabolic adverse effects.!!!!

1 amisulpride 100 mg orally, daily; increase to a target dosage of 400 to 600 mg daily in 2 divided doses [Note 5]. See Monitoring and titrating and Duration of therapy. Maximum daily dose is 1200 mg
OR

1 aripiprazole 10 mg orally, in the morning; increase to a target dosage of 15 mg daily. See Monitoring and titrating and Duration of therapy. Maximum daily dose is 30 mg
OR

1 quetiapine immediate-release 50 mg orally, twice daily on the first day; increase to 100 mg twice daily on the second day; increase to a target dosage of 200 mg twice daily on the third day [Note 6]. See Monitoring and titrating and Duration of therapy. Maximum daily dose is 800 mg
OR

1 quetiapine modified-release 150 mg orally, daily on the first day; increase to 300 mg daily on the second day; increase to a target dosage of 450 mg daily on the third day [Note 6]. See Monitoring and titrating and Duration of therapy. Maximum daily dose is 800 mg

OR

1 risperidone 1 mg orally, daily; increase to a target dosage of 2 to 4 mg daily (as a single dose or in 2 divided doses). See Monitoring and titrating and Duration of therapy. Maximum daily dose is 6 mg [Note 7]
OR

1 ziprasidone 40 mg orally, twice daily; target dosage is 40 to 60 mg twice daily. See Monitoring and titrating and Duration of therapy. Maximum daily dose is 160 mg [Note 8]
OR

2 asenapine 5 mg sublingually, twice daily [Note 9]. See Monitoring and titrating and Duration of therapy. Maximum daily dose is 20 mg [Note 10]
OR

2 brexpiprazole 1 mg orally, daily for 4 days, then increase to 2 mg daily; target dosage is 2 to 4 mg daily. See Monitoring and titrating and Duration of therapy. Maximum daily dose is 4 mg
OR

2 lurasidone 40 mg orally, daily; increase to a target dosage of 80 to 120 mg daily. See Monitoring and titrating and Duration of therapy. Maximum daily dose is 160 mg
OR

2 paliperidone modified-release 3 to 6 mg orally, daily; target dosage is 6 mg daily [Note 11]. See Monitoring and titrating and Duration of therapy. Maximum daily dose is 12 mg
OR

3 olanzapine 5 mg orally, daily; increase to a target dosage of 10 to 15 mg daily. See Monitoring and titrating and Duration of therapy. Maximum daily dose is 20 mg [Note 12].

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16
Q

Duration of antipsychotic therapy for a first episode of psychosis

A

The minimum duration of antipsychotic therapy for a first episode of psychosis depends on the duration of symptoms and how quickly the patient responds to treatment.

If symptoms last for longer than 6 months (ie the patient has schizophrenia or schizoaffective disorder) or the patient has delusional disorder, continue antipsychotic therapy for at least 2 years after symptom resolution—a longer duration is often required.
If symptoms resolve in less than 6 months and the patient does not have delusional disorder, continue antipsychotic therapy for at least 1 year after symptom resolution—a shorter duration may be adequate if the patient rapidly responds to treatment (eg symptoms resolve in a month). Consider the impact of the episode (eg risk of suicide or violence) and its context (eg comorbid substance use, family history of psychotic disorder).

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17
Q

Illusion: concept

A

e modifications of real objects or people that can be distorted in size
(micropsia or macropsia), shape (metamorphopsia), and color (dyschromatopsia).

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18
Q

Illusion categorization

A

illusions of completion,
illusions of affect,
pareidolia,
auditory illusions,
or tactile illusions.

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19
Q

Illusion risk factors

A

epilepsy and complex or focal seizures, but these misperceptions may also occur in individuals without a medical or psychiatric diagnosis

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20
Q

Dellusion categorization

A

bizarre (e.g., aliens living in one’s
body) or non-bizarre (e.g., boss thinking about firing them).

Delusions may be persecutory (being watched by CIA),

Grandiose (just drafted as an NFL quarterback),

Erotomanic (believing a famous movie star is married to you),

Somatic (believing eggs are hatching in one’s stomach),

Delusions of reference (believing the
President’s speeches are geared toward oneself),

Delusions of control (believing the Greek gods are controlling one’s movements and thoughts).

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21
Q

Explain the dopamine’s hypothesis of schizophrenia’s symptoms

A

The dopamine hypothesis attributes the symptoms of schizophrenia to
levels of dopaminergic activity in the mesocortical and mesolimbic tracts. Subnormal levels of dopamine in
the mesocortical tract are attributed to negative symptoms, while excessive dopaminergic activity in the
mesolimbic tract is attributed to positive symptoms.

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22
Q

Pathophysiology of negative symptoms

A

Subnormal levels of dopamine in
the mesocortical tract

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23
Q

Pathophysiology of positive symptoms

A

excessive dopaminergic activity in the
mesolimbic tract

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24
Q
A

excessive dopaminergic activity in the
mesolimbic tract

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25
Q

Follow up on clozapine use.

A

Weekly blood draws to ensure the white blood count is ≥ 3,500/mm3 and the absolute neutrophil count is ≥ 2,000/mm3. Patients who are on clozapine must be checked weekly during the first six months and then eventually once every four weeks.

A mild leukopenia (WBC = 3,000-3,500), with or without clinical symptoms such as lethargy, fever, sore throat, or weakness, should cause the psychiatrist to monitor the patient closely and institute a minimum of TWICE-weekly CBC tests with differentials included.

More serious leukopenia (WBC = 2,000 to 3,000) indicates DAYLY CBCs and stop the clozapine. It may be reinstituted after the WBCs normalize.

With an uncomplicated agranulocytosis (no signs of infection), the patient should be placed in protective isolation, the clozapine should be discontinued, and a bone marrow specimen may need to be gotten to see if progenitor cells are being suppressed. Clozapine must not be restarted in this latter case.

Additional side effects of clozapine include:
hyperglycemia
hypercholesterolemia.
Increased potential for seizures.

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26
Q

Follow up on chlorpromazine use

A

A slit-lamp examination of the eye is used to detect different stages of corneal or lenticular
pigmentation in patients

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27
Q

Esquizoaffective disorder’s criteria

A

In addition to the psychotic symptoms, patients with schizoaffective disorder must meet these criteria:

  • A major mood episode (either major depression or mania) that lasts for an uninterrupted period of time
  • Delusions or hallucinations for two or more consecutive weeks without mood symptoms
  • Mood symptoms are present for the majority of the illness
  • Symptoms are not related to substance use
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28
Q

Repetitive and involuntary series of oral-facial movements (primarily of the tongue and mouth

A

Tardive dyskinesia

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29
Q

Tardive dyskinesia - overview

A

Repetitive and involuntary series of oral-facial movements (primarily of the tongue and mouth

The onset of tardive dyskinesia generally occurs over the course of several months of use.

Tardive dyskinesia can be irreversible in many patients.

The first step in treating tardive dyskinesia is to discontinue the antipsychotic or switch to a different, second-generation antipsychotic.

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30
Q

Both mental and physical restlessness that can result in anxiety. Affected patients may be unable to sit still.

A

Akathisia

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31
Q

Akathisia - overview

A

Both mental and physical restlessness that can result in anxiety. Affected patients may be unable to sit still.

These types of extrapyramidal symptoms (EPS) generally occur over the course of several weeks on a first-generation antipsychotic and the symptoms are often reversible.

Propranolol as a short term measure for management of akathisia.

Diazepam if beta blockers are contraindicated (asthma, severe peripheral vascular disease).

It is recommended to reduce the dose OR discontinue the antipsychotic switch to a different one, like thioridazine

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32
Q

Prolonged and painful muscle contractions and/or spasm

A

Acute dystonia

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33
Q

Acute dystonia - overview

A

Prolonged and painful muscle contractions and/or spasm

Caused by excessive D2 dopaminergic receptor blockade.

Often presents during the initiation of first-generation antipsychotics (within hours).

Treatment with an anticholinergic (diphenhydramine or benztropine) can be used acutely, or even prophylactically. It is also recommended to discontinue the antipsychotic or to switch to a different one.

Benztropne: intravenous injection, most people respond within 5 minutes, if no response the dose can be repeated after 10 minutes.
Diphenhydramine: slow IV injection (not available in Australia as a parenteral preparation).
Promethazine: IV or IM is readily available in most ED. It may be useful alternative for the patient who has both dysctonia and significant anticholinergic symptoms from antipsychotic drugs.
Diazepam: IV or IM is used for the patients who don not respond to other treatment options.

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34
Q

Abnormal gait and/or cogwheel rigidity

A

Pseudoparkinsonism

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35
Q

Pseudoparkinsonism - overview

A

It is classified as a type of EPS and is similar in presentation to Parkinson disease.

Abnormal gait and/or cogwheel rigidity may be present.

This EPS occurs over several days of initiating first-generation antipsychotic therapy and can be treated with an anticholinergic (benztropine or diphenhydramine - both of which are also antihistamines), a dopamine agonist (amantadine), by decreasing the dose of the offending agent, or by switching to a different antipsychotic.

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36
Q

What first-generation antipsychotic have minimal appreciable effects on metabolic profiles, including blood
glucose, lipids, and weight gain?

A

Chlorpromazine

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37
Q

What’s the most common drug used by patients with schizophrenia.

A

Nicotine (90%),

cannabis (37%)

alcohol (34%)

cocaine (31%)

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38
Q

Main side effects: clozapine

A
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39
Q

Main side effects: chlorpromazine

A

is a medium-potency antipsychotic agent used for the treatment of schizophrenia in addition to bipolar disorder, attention deficit
hyperactivity disorder, and nausea. It can cause extrapyramidal and anticholinergic symptoms

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40
Q

Main side effects: haloperidol

A

is a high-potency antipsychotic agent that can cause extrapyramidal and anticholinergic adverse effects,

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41
Q

Main side effects: olanzapine

A

Is an atypical antipsychotic agent that commonly is used as a first-line treatment for schizophrenia. Adverse effects of olanzapine include
weight gain, hyperglycemia, and orthostatic hypotension, but it typically does not cause agranulocytosis

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42
Q

Main side effects: risperidone

A

An atypical antipsychotic agent that can cause hyperprolactinemia, which may lead to gynecomastia

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43
Q

Bipolar disorder with psychotic features - main feature

A

Primarily presents mood symptoms but can be associated with psychosis during manic or depressive episodes.

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44
Q

What personality disorder can be identified by the acronym ACID LIAR?

A

DSM-V criteria for Anti-social personality disroder:

The last 7 items are conduct disorders, of which ≥3 need to be evident before age 15:
* Age (can be diagnosed only if ≥ age 18, with conduct disorder diagnosed ≤ age 15, with at least 3 of 7 conduct disorders diagnosed)
* Criminality (DSM: “Disregards legal and social rules/norms”)
* Impulsivity (DSM: “Impulsive”)
* Disregard for safety (DSM: “Neglects safety [self/others”])
* Liar (DSM: Lies)
* Irresponsibility (DSM: “Irresponsible”)
* Aggression (DSM: “Irritable or Aggressive”)
* Remorselessness (DSM: “No remorse”)

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45
Q

What personality disorder shows splitting as a defense mechanism?

A

Borderline

The immature defense mechanism of splitting, in which people are grouped into extreme categories. It occurs when an individual perceives their surroundings as good or bad, focusing on the far sides of the spectrum in all things

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46
Q

Borderline personality disorder diagnostic criteria?

A

Borderline personality disorder is a pervasive pattern of instability in interpersonal relationships, self-image, and affects, along with marked impulsivity, as indicated, in the DSM-5 diagnostic criteria, by the presence of five (or more) of the following:

  1. Frantic efforts to avoid real or imagined abandonment
  2. A pattern of unstable and intense interpersonal relationships characterized by extremes
  3. Identity disturbance
  4. Impulsivity in at least 2 areas that are damaging (e.g., spending, sex, gambling, substance abuse)
  5. Recurrent suicidal behavior
  6. Instability in affect and/or mood
  7. Chronic feelings of emptiness
  8. Inappropriate or difficult-to-control anger
  9. Transient, stress-related paranoid ideation or severe dissociative symptom
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47
Q

Difference between OCD and OCDP?

A

Diagnosis requires both obsessions and compulsions to be present.

Obsessive-compulsive personality disorder (OCPD) is a condition where the patient is hyper-focused on order and control. However, in contrast to OCD, people with OCPD display ego-syntonic behavior. The recommended first-line treatment for OCD is cognitive-behavioral therapy combined with pharmacotherapy. Selective-serotonin reuptake inhibitors (SSRIs) are an effective choice for pharmacotherapy.

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48
Q

Avoidant personality disorder diagnostic criteria and treatment?

A

At least 4 out of the following 7 symptoms, all of which are all centered around the patient’s fear of not being accepted:

Avoidance of activities that involve significant interpersonal contact because of fears of criticism, disapproval, or rejection

Unwillingness to get involved with people unless certain of being liked

Showing restraint within intimate relationships because of the fear of being shamed or ridiculed

Preoccupied with being criticized or rejected in social situations

Inhibited in new interpersonal situations because of feelings of inadequacy

Self-perception as socially inept, personally unappealing, or inferior to others

Unusually reluctant to take personal risks or engage in any new activities because they may prove embarrassing

Treatment:

These patients can benefit from pharmacotherapy that suppresses the sympathetic nervous system, such as beta-blockers, and even selective serotonin reuptake inhibitors (SSRIs) if they have a comorbid major depressive disorder.
However, patients with avoidant PD derive the most benefit from psychotherapy particularly assertiveness training

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49
Q

Major depressive disorder: diagnosis?

A

5 of the following being depressed mood everyday for 2 Weeks or sleep disturbances one of those

SIGECAPS

Sleep disturbances
Interest being low such as anhedonia.
Guilt
Energy changes
Concentration difficulties
Appetite changes
Psychomotor activity or retardation
Suicidal Thinking

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50
Q

Post-partum depression’s criteria and differentiation from baby blues

A

Mood symptoms during preganancy or within 4 weeks after childbirth

10-15% of women develop it

Baby blues is associated with period of crying and sadness, but without meeting at least 5 of SIGECAPS symptoms

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51
Q

Postpartum depression - prophylaxis

A

If high risk (mostly previous episode), initiate:

  • Antidepressants on the THIRD semester, if previously had good response in the later episode. Can also be initiated after delivery
  • If not: cognitive-behavioral therapy, interpersonal psychotherapy, or mindfulness based cognitive therapy
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52
Q

Most common symptoms of depression in children?

A

Angry and irritability

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53
Q

What’s the most important diagnosis to rule out in elderly patients with complaint of memory problem or a new onset cognitive problem?

A

Depression

It shall be considered in any elderly patient with poor concentration or focus or any changes in their cognition

(Pseudodementia)

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54
Q

Tricyclic antidepressants - overview (indication, side effects, toxicity)

A

They block reuptake of nora and sero

Use:
Major depression; OCD; Enuresis; fibromyalgia

SE:
Anticholinergic: tachycardia; urinary retention
Anti alpha adrenergic: sedation
Lower seizure threshold

Toxicity: 3 C
Convulsions.
COMA
Cardiotoxicity (arrythmia)

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55
Q

MAO I - Overview

A

Decrease MAO activity -> decrease amine degradation -> increased level of amine neutransmitters (importantly: tyramine)

Use:
Atypical depression
Resistant depression
Anxiety
Hypochondriasis

SE:
Hypertensive crisis - might be deadly (Due to tyramine rich diet like wine, cheese, fava beans, cured meats)
CNS stimulation - overexcitation
Orthostatic hypotension
Drowsiness
Weight gain
Dry mouth
Sexual and sleep dysfunction

Interaction with SNRI SSRI - Serotonin syndrome. Treated with cyproheptadine

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56
Q

SSRI - overview

A

Use: depression; OCD; PTSD; Panic; anxiety; bulimia; social phobia

SI:
Mild generally
weight gain
QTC prolongation
GI distress
Sexual dysfunction - bupropion or mirtazapine can treat
Insomnia
Serotonin syndrome

SSRI discontinuation syndrome:

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57
Q

SNRI - overview

A

Venlafaxine and Duloxetine

Use: depression; fibromyalgia; generalized anxiety; diabetic peripheral neuropathy

SI:
Mild generally
Hypertension
Sedation
Nausea
Anorexy, weight loss
Insomnia

SSRI discontinuation syndrome: flulike symptoms; electric-like shocks or zaps

Serotonin Syndrome

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58
Q

Serotonin Syndrome - symptoms

A

Fever
Agitation
Increased reflexes
Tremors
Sweating
Dilated Pupils
Diarrhea

MADAM’S TIPS:

Mental status change
Agitation
Diarrhea
Ataxia
Myoclonus
Shivering
Tachycardia
Increased reflexes
Pyrexia
Sweating

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59
Q

Serotonin Syndrome - treatment

A
  • Withdraw the offending agents.
  • Supportive therapy: ice packs and cold compresses.
  • Use Cyproheptadine ( antiserotonergic) orally if severe muscular excitation.
  • Chlorpromazine (5-HT receptor antagonist) IV infusion if oral intake impossible.
  • Consider benzodiazepines for sedation.
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60
Q

Bipolar disorder - risk factors

A

Family History
Onset of mood disorder before the age of 20
Past History of depression
Stressful lifestyle
Substance abuse

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61
Q

Bipolar disorder - Treatment

A

First line: Atypical antipsychotics (Olanzapine or Risperidone)

Second line: Haloperidol + Lithium carbonate, or Sodium valproate if renal failure, or Carbamazepine, Lamotrigine.

If there is failure to respond: combined therapy second degree antipsychotics plus Lithium.

If first episode of mania - continue treatment with mood stabilizer for 12 months after remission is achieved.

Consider ECT if not responding to drugs.

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62
Q

Bipolar disorder: types and diagnosis

A

BD I - at least one manic episode (for at least 7 days) and it’s often accompanied by depressed or hypomanic periods. CAUSES SOCIAL, WORK AND LIFE IMPAIRMENT

BDII - is marked by at least one hypomanic episode (for >=4 days) and at least one major depressive episode. DOESN’T CAUSE SOCIAL, WORK AND LIFE IMPAIRMENT

Mixed - is when depressed mood coexists with manic symptoms.

Rapid cycling - is the alternating periods of hypomanic periods with mild to moderate depressive symptoms intermixed over the course of two years. At least 4 mood episodes through a year

Cyclothymic disorder - numerous periods of both hypomania and depression within 2 years without meeting the criteria for BD.

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63
Q

Bipolar disorder difficult to treat - management during pregnancy.

A

Continue treatment with Lithium through the pregnancy.

  • Monitor for Ebstein’s anomaly (1: 1000) by high resolution US around 18-20 weeks.
  • The dose of Lithium is increased by 25% in third trimester.
  • Stop Lithium 24-48 hours before delivery. Restart after delivery.
  • Lithium is contraindicated in breastfeeding. If breastfeeding is desirable, consider atypical antipsychotic.
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64
Q

Acute depression in bipolar disorder - Management

A

Many mood stabilizers (olanzapine, risperidone) have bimodal effect. They can be used for treatment of both depression and mania. If a patient, who has successfully been stable on prophylactic dose of a particular mood­ stabilizer, develops acute depression two approaches can be considered with about the same efficacy:

Adding an antidepressant to the prophylactic mood stabilizer: the choices of the drug would be the same as for major depression. SSRls are first line options.
Increasing the dose of prophylactic mood stabilizer .

Cessation or dose reduction of a mood stabilizer can result in relapse of mania and is not appropriate.

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65
Q

Medication that can mimic Bipolar Disorder?

A

Steroids, sympathomimetics; bronchodilators, levodopa, antidepressants, anything that increases dopamine Maand any kind of alpha agonists

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66
Q

Mania symptoms?

A

DIGFAST

distractibility, insomnia, grandiosity, flight of ideas, activity or agitation, such as increased goal-directed activity, pressured speech and also thoughtless disregard of others.

If psychosis is present, shall be treated first, before mood symptoms.

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67
Q

Medicines that can enhance lithium levels? And diet?
What’s the therapeutic range?
Risk factors?

A

NSAID, Tetracycline, metronidazole, ACE inhibitors, diuretics, theophylline, osmotic diuretics like mannitol and acetazolamide,

Caffeine, high salt intake DECREASE lithium levels

Therapeutic range: 0.7 to 1.2 (0,4-1,0 (>0,6)mmol)

Toxic > 1,5 mmol/L
Lethal > 2,0 mmol/l

If above 3,0 -> dyalisis

Risk factors:
* Impaired kidney function
* Dehydration
* Age greater than 50 years
* Drug interactions (NSAID, ARBs, ACEI, Diuretics)
* Nephrogenic dial;,etes insipidus
* Hypothyroidism

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68
Q

Signs and symptoms of lithium toxicity? Therapeutic range? Management?

A

thirsty, weight gain, metallic taste, hair falling, tremor in their upper limbs (coarse tremor), weakness, dizzyness, nystagmus and it can eventually lead to stupor, coma, delirium, seizures, blurry vision and a heart arrhythmia.

  • CLASSIC:
    a fine tremor, sedation, ataxia, thirst or metallic taste in their mouth, polyuria, edema, and weight gain. GI problems, benign leukocytosis, thyroid enlargement. nephrogenic diabetes insipidus, coarse tremor and altered mental status.

mild toxicity can be managed by correcting the electrolyte disturbance through IV hydration.

Teratogenic effect: Ebstein’s anomaly (atrialization of the right ventricle, causing cyanosis and symptoms of heart failure)

Check kidney and thyroid panels

If >3 mmol/L - Do hemodialysis to protect the kidneys.

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69
Q

Other mood stabilizers?
Their most common indication and complication?

A

valproic acid, carbamazepine, and lamotrigine

Best option when there’s renal impairment - Valproic Acid

Lamotrigine - depressive phase (isn’t effective on mania)

Fetal anomaly caused by valproic acid and carbamazepine? Spina bifida,

70
Q

In Bipolar disorders, if the patient is pregnant in a severe mood disruption or any patient resistant to treatment, what’s the best option?

A

ECT

71
Q

Main difference between bullimia and anorexia?

A

In bullimia, the symptoms are ego-dystonic. Also, they tend to have an average BMI

Whereas in anorexia, patients find their symptoms ego-syntonic.

72
Q

Main difference between bullimia and binge eating?

A

In bullimia, there is compensatory behavior influenced by guilt and a perception of appearance.

73
Q

Bullimia’s criteria and overview

A

Recurrent episodes of binge eating, eating in a discrete period of time and a sense of lack of control.

At least 2 episodes per week for 3 months

Recurrent inappropriate compensatory behaviors to help prevent weight gain and the binge eating and inappropriate compensatory behaviors can both occur.

Their self-evaluation that’s unduly influenced by body, shape, and weight, and the disturbance does not occur exclusively during episodes of anorexia.

The severity is assessed by the frequency of inappropriate compensating or purging behaviours

74
Q

Binge eating: overview

A
  • Consuming an amount of food in a discrete period of time or so that is definitely larger than what most people would eat in a similar amount of time under similar circumstances is describing an episode of binge eating.
  • The episodes can occur, on average, at least once a week for about 3 months, and there’s no regular use of inappropriate compensatory behaviors.
  • That patient also feels a sense of lack
    of control from overeating
  • Co-comorbities frequently seen: specific phobias, social phobias, depression, PTSD, and alcohol abuse or substance dependence.
  • Binge eating treatment includesRumination Disorder
  • overvier individual psychotherapy and also behavioral therapy, a strict diet program and exercise routine.
75
Q

Rumination Disorder - overview

A

Rumination disorder is a behavioral disorder marked by repeated regurgitation of food, which may be re-chewed, re-swallowed, or spit out. This condition is not due to a medical disorder (GERD or pyloric stenosis) or other eating disorders (avoidant/restrictive food intake disorder, anorexia nervosa, binge eating disorder, or bulimia nervosa).

Seen in all ages but emerges sometime between 3 and 12 months of age

76
Q

Anorexia nervosa - overview and diagnostic criteria

A

Is an eating disorder characterized by self-imposed starvation and inappropriate dietary habits due to an intense fear of weight gain and disturbed perception of body shape and weight. Symptoms must be present for at least 3 months

Subtypes:

  • Restricting type: characterized by excessive starvation (weight loss is accomplished primarily through dieting, fasting, and/or excessive exercise)
  • Binge-eating/purging type: characterized by the use of drugs (laxatives, diuretics), induced vomiting, and excessive exercise as a means to reduce weight

Severity
Mild: BMI 17–18.49 kg/m2
Moderate: BMI 16–16.99 kg/m2
Severe: BMI 15–15.99 kg/m2
Extreme: BMI < 15 kg/m2

77
Q

Anorexia - what’s refeeding syndrome?

A

Constellation of metabolic disturbances that may occur due to refeeding of malnourished patients who are persistently starved.
Sudden increase in caloric intake causes an increase in insulin production.
Increase in insulin causes a sudden shifting of fluid and electrolytes into cells.
Marked electrolyte disturbances (hypophosphatemia), seizures, delirium, cardiac complications (cardiopulmonary failure), rhabdomyolysis
Aggressive nutrition without good monitoring can be fatal.

78
Q

Anorexia - complications?

A

Myocardial atrophy
Mitral valve prolapse
Pericardial effusion
Osteoporosis
Gastroparesis
Amenorrhea, infertility (functional hypothalamic amenorrhea due to low levels of LH and FSH)
Growth disturbances
Swelling of sallivary glands (purging subtype)
Lanugo
Cold intolerance (decreased thyroid hormones)
Russel sign (calloused knucles) in the purgin type
Hypercholesterolaemia
Hypophosphataemia

79
Q

Anorexia - involuntary hospitalization indication?

A

Temperature < 36.0℃ (96.8°F)

Pulse < 45/min

85% or less of expected weight

Lack of any weight gain or refractory symptoms as outpatient

Psychosis or suicidal ideations

Significant edema

Physiologic decompensation (e.g., serious cardiac arrhythmia,

significant electrolyte disturbances,

altered mental status, and orthostatic differential > 30 mm Hg)

The strongest indication for inpatient hospitalization in this patient is her significant lower extremity edema, which is most likely due to a loss of oncotic pressure secondary to low plasma protein levels, which is a sign of severe malnutrition.

80
Q

Factitious disorder - overview

A

Factitious disorder, formerly called Munchausen syndrome, is the intentional falsification of symptoms in order to assume the role of a sick person.

Purposeful misrepresentation of injury, impairment, or chronic sickness

Obvious acts of deception with no clear motive of secondary gain

More common in men than women

81
Q

Conversion disorder - Overview

A

The presence of symptoms or deficits that affect voluntary motor or sensory function in a way that suggests a neurological condition but is not explained by medical findings. Diagnosis is clinical, and management includes psychological and physical therapy. Unlike factitious disorder, there is no evidence of actual disease or deliberate falsification of symptoms.

82
Q

Malingering - overview

A

A disorder in which patients present with symptoms for secondary gain (e.g., avoiding the police, time off work, disability benefits). Determination of the external incentive distinguishes malingering from factitious disorder.

83
Q

What are the pos partum psychiatric disorders?

A
  • Postpartum (PP) blues: mild depressive symptoms that are transient and self-limiting in the perinatal period (first 2 weeks)
  • PP depression: depressive symptoms beginning within the 1st 12 months following childbirth and lasting for at least 2 weeks
  • PP psychosis: a psychiatric manifestation with abrupt onset after delivery that is characterized by psychotic symptoms
84
Q

Postpartum (PP) blues - Overview

A

Symptoms may include:
Feeling guilty and/or overwhelmed (especially about being a mother)
Crying, sadness
Rapid changes in mood and irritability
Anxiety
Poor concentration
Eating too much or too little
Insomnia or frequent awakenings at night
Symptoms are mild and do not interfere with activities of daily living.

Duration of symptoms:
Lasting up to and no more than 2 weeks

Management:
Resolves spontaneously
Provide reassurance.
Encourage self-care

85
Q

Postpartum Depression - overview

A

Symptoms may include:
Disinterest in self, in child, and in normal activities
Feeling isolated, unwanted, or worthless
Feeling a sense of shame or guilt about parenting skills
FEARFULL OF CRITICISM and anxiety about the wellbeing of the baby
↑ Anger outbursts
Suicidal ideation or frequent thoughts of death
Symptoms are more severe and patients have an inability to cope.

Duration of symptoms: > 2 weeks. Might initiate during pregnancy or up to 1 year after delivery.

Selective serotonin reuptake inhibitors (SSRIs) are the 1st-line treatment; best studied
Best options: paroxetine 10–50 mg/day, sertraline 50–200 mg/day (unlikely to have ↑ drug levels in breastfed infants)

Most women recover within 6–12 months.

Edinburgh Postnatal Depression Scale (EPDS) - to assess the suspected patient

86
Q

Postpartum Psychosis - Overview

A

Symptoms are similar to those of non-obstetric psychosis, which is a disturbance in an individual’s perception of reality.

Hallucination are usually BABY RELATED. Dellusions also presente

Onset: few days to 1 year after delivery (most commonly 2 WEEKS AFTER delivery). BEGINS ABRUPTLY

Severe physical anxiety (can’t stay still) + insomnia

Thoughts/plans of hurting themselvels or the baby

Frequently associated with Bipolar disorder

Admit to psychiatric mother-baby unit

Best options (expert opinion): older 2nd-generation antipsychotics (start with the following initial doses, with a higher dose given for severe symptoms):[21]
Quetiapine 50 mg once daily, up to 50 mg twice daily
Risperidone 0.5–1 mg/day
Olanzapine 2.5–5 mg/day

If previous episode, prophilaxy with: olanzapine OR risperidone + Lithium. If lithium, don’t breastfeed

87
Q

Postnatal adjustment disorder - Overview

A

Begins in the first 6 months

Symptoms of PP Blues + anxiety and fear of criticism

CBT; Psychodynamic therapy.

88
Q

Agoraphobia - overview

A

Fear or anxiety in a situation that would be difficult to leave or to obtain help in the event that one develops panic-like symptoms.

> > It’s needed at least 2 social situations (open spaces, enclosed spaces, etc).

Situations include being in public or open spaces, lines, crowds, or public transport.

If severe, the condition results in significant social and occupational disability in which patients actively avoid the situation, and in certain cases, refuse to leave their homes alone.

Diagnosis is clinical, based on the presenting symptoms. Agoraphobia occurs frequently with panic disorder.

Management is best approached with CBT and medications (selective serotonin reuptake inhibitors (SSRIs)).

89
Q

What antidepressants to avoid during pregnancy?

A

Paroxetine, fluoxetine, MAOI

90
Q

Panic disorder - overview

A

Characterized by spontaneous and recurrent panic attacks.
The number of attacks can vary from patient to patient. The episodes are short but leave lasting anticipatory
anxiety. For diagnosis of PD, patients must also have significant concerns and worries for at least 1 month about future panic attacks or their consequences.

  • Symptomatology:
    ‘PANICS’:
    Palpitations
    Abdominal distress
    Nausea
    Intense fear
    Chest pain, choking
    Sweating, short of breath

The single best treatment is CBT + selective serotonin reuptake inhibitors (SSRIs)

91
Q

Panick attack - overview

A

Is a transient period of sympathomimetic symptoms.

These symptoms can include chest pain,
shortness of breath, palpitations, diaphoresis, and sensations of choking.

They usually peak after 10 minutes and typically last approximately 30 minutes

92
Q

Social Anxiety disorder - overview

A

A persistent fear of one or more social or performance situations in which they are exposed to unfamiliar people or to possible scrutiny by others. These symptoms have to persist for at least 6 months.

They often suffer from panic attacks in these situations and fear they will act in a way that will be embarrassing and humiliating.

The SSRI class and beta-blockers (off-label use) have proven effective in treating performance anxiety, including public speaking. Other medications include monoamine oxidase inhibitors such as phenelzine. Psychotherapy is also a mainstay of treatment.

93
Q

Agoraphobia - definition

A

Fear of inescapable situations, such as open spaces or public spaces.

Diagnosis with ≥ 6 months of symptoms

Treatment: 1st-line: SSRI or CBT

94
Q

Delirium tremens - overview

A

DT is a severe form of alcohol withdrawal which usually presents 3–5 days following the last alcoholic drink.

Some important clinical features of DT include psychomotor agitation, severe global confusion, disorientation, hallucinations, tremors, fever, and excessive perspiration.

Signs of autonomic hyperactivity, such as tachycardia, hypertension, and tachypnea, are often present.

Positional nystagmus and mydriasis are important ocular signs of DT.

In addition, hallucinations frequently occur in DT and visual and tactile hallucinations are common.

95
Q

Wernicke - Korsakoff Syndrome - overview

A

Is classically characterized by the triad of confusion, nystagmus, and ataxia.

Wernicke’s encephalopathy is an
acute, reversible condition caused by thiamine deficiency, which is characterized by ataxia, confusion, and ocular abnormalities.

Korsakoff’s syndrome is a chronic
amnestic syndrome characterized by anterograde amnesia and confabulation.

The earliest biochemical change seen in thiamine deficiency in the central nervous system is decreased α-ketoglutarate-dehydrogenase activity in the astrocytes, especially in those areas of the brain high in thiamine
content.

Acute thiamine deficiency is also associated with mitochondrial dysfunction in areas of the brain with the highest metabolic activity.

Other pathophysiologic changes associated with thiamine deficiency include increased astrocyte lactate levels, swelling of the astrocytes, increased extracellular concentration of glutamate, increased nitric oxide (from endothelial cell dysfunction), increased fragmentation of deoxyribonucleic acid (DNA) in the neurons, increased production of free radicals, increased cytokines, and breakdown of the blood-brain barrier.

96
Q

Wernicke’s encephalopathy - definition

A

Wernicke’s encephalopathy is an
acute, reversible condition caused by thiamine deficiency, which is characterized by ataxia, confusion, and ocular abnormalities.

97
Q

Korsakoff’s syndrome - definition

A

Korsakoff’s syndrome is a chronic
amnestic syndrome characterized by anterograde amnesia and confabulation.

98
Q

Akcoholic hallucinosis - Overview

A

It begins within 12 to 24 hours of abstinence, can even start while drinking heavily, and resolves within 48 hours.

Thee hallucinations are not associated with confusion—patients are aware that they are hallucinating. Vital signs are usually normal.

99
Q

Alcoholic hepatitis - overview

A

Classic clinical features include anorexia, fever, jaundice, and tender hepatomegaly.

Laboratory testing reveals moderately elevated transaminases (typically < 300
IU/mL), with an AST/ALT ratio of ≥ 2.

Patients may also present with right upper quadrant/epigastric pain, hepatic encephalopathy, and signs of malnutrition.

Decompensated cirrhosis can occur concurrently with acute alcoholic hepatitis.

Histologic findings in liver biopsies from patients with alcoholic hepatitis include steatosis, hepatocellular ballooning, infiltration by neutrophils and lymphocytes, Mallory-Denk bodies, fibrosis, cholestasis, and bile duct proliferation.

Mallory-Denk bodies are eosinophilic intracytoplasmic inclusions representing damaged intermediate filaments within the hepatocytes. They can also be seen in nonalcoholic steatohepatitis and are not specific for alcoholic hepatitis.

100
Q

Intermittent explosive disorder - Overview

A

Intermittent explosive disorder (IED) is an impulse control disorder characterized by recurrent episodes of violent aggressive outbursts, either verbal or physical, out of proportion to the provoking events and immediately followed by a sense of regret.

Psychotherapy:

CBT
Family therapy recommended for children/adolescents, and group therapy for older patients

Medication:

Antidepressants:
1st line: selective serotonin reuptake inhibitors (e.g., fluoxetine)
Mood stabilizers/anticonvulsants:
2nd-line treatment
Anticonvulsant medications (e.g., valproate, phenytoin, carbamazepine)

101
Q

Oppositional defiant disorder (ODD) - overview

A

Characterized by an angry or irritable mood, argumentative or defiant behavior, and/or vindictiveness over at least 6 months.

The behavior is typically directed to at least one individual who is not a sibling - a authority figure.

Does not involve aggressive behavior toward people/animals, destruction of property, or theft

102
Q

Disruptive mood dysregulation disorder - Overview

A

Patient is mainly angry all the time (most of the day and every day), with frequent outbursts, for at least > 12 months

Outbursts occur at least 3x per week in 2 different settings.

The child is always angry or irritable between outbursts.

Onset: 6–10 years of age

103
Q

Depersonalization/Derealization Disorder - Oveview

A

Depersonalization/derealization disorder (DDD) is a type of dissociative disorder characterized by a persistent experience of depersonalization (the feeling of being detached from oneself, like watching oneself from an external viewpoint) and derealization (the feeling of being detached from the real world, like the world is distant or hazy).

Crisis intervention therapy during the acute episodes, combined with psychotherapy during the asymptomatic period, is 1st-line treatment for this disorder.

104
Q

Difference between PTSD and Acute Stress Disorder?

A

In ASD, symptoms doesn’t last more than 1 month

105
Q

Alzheimer’s disesase - Overview

A

Onset of Symptoms - Insidious

Cognitive symptoms - Decline in memory and executive function

Motor symptoms - Usually rare

The main pathologic features are neuritic plaques, extracellular deposits of amyloid peptides, and neurofibrillary tangles.

Treatments for Alzheimer disease dementia:
- Acetylcholinesterase inhibitors (donepezil, galantamine, rivastigmine)
Increase the amount of available neurotransmitters and thus transmission of signals.
Long-term use modestly stabilizes cognitive decline for 6–12 months longer than no treatment.

106
Q

Vascular dementia - Overview

A

Onset of Symptoms - Stepwise progression

Cognitive symptoms - Decline in executive function

Motor symptoms - Depending on location of lesion

Reduction in cerebral perfusion → disruption of brain connectivity, cerebral atrophy

107
Q

Frontotemporal dementia - Overview

A

Onset of Symptoms - Pre-senile onset (the late 5os or early 60s)

Cognitive symptoms - Decline in executive function

Motor symptoms - Parkinsonian symptoms in certain cases

Changes in personality and social behavior or language, progressing over time to a more global dementia.

Other features include impaired initiation and planning, disinhibited behavior and social disgrace and mild abnormalities on cognitive testing. Apathy and memory deficits develop later in the course of the disease. A subset of patients may also exhibit symptoms of extrapyramidal or motor neuron involvement at some point in the disease process.

108
Q

Dementia with Lewy bodies - Overview

A

Onset of Symptoms - Insidious

Cognitive symptoms - Decline in executive and visuospatial function and Hallucinations (Recent onset forgetfulness and peculiar behavior and importantly visual hallucinations suggested by seeing people that do not exist)

Motor symptoms - Parkinsonian symptoms follow cognitive symptoms

Abnormal aggregation of protein (α-synuclein) within nerve cells is the chief component of Lewy bodies.

Presence of Lewy bodies alters the level of neurotransmitters and neuromodulators in the brain, principally dopamine.

109
Q

Attention Deficit Hyperactivity Disorder - Overview

A

Attention deficit hyperactivity disorder is a neurodevelopmental disorder characterized by a pattern of inattention and/or hyperactivity-impulsivity that occurs in at least 2 different settings for more than 6 months.

Although the patient has normal intelligence, the disease causes functional decline.

The onset usually occurs before 12 years of age and often persists into adulthood.

The 1st line of treatment is stimulant medications but may include non-stimulant medications and behavioral therapy.

Atomoxetine (Non-stimulant medications): Usually 2nd-line therapy
Mechanism of action via norepinephrine reuptake inhibitor Indicated with comorbid anxiety, tic disorder, or insomnia
Side effects: increased suicidal ideation in children

110
Q

Schizofrenic patient with hyponatremia - most likely diagnosis?

A

Psychogenic polydipsia

Self-induced water intoxication should always be considered in the differential diagnosis of confusional states and seizures in schizophrenic patients.

As many as 20% of patients with a diagnosis of schizophrenia drink excessive amounts of water. At least 4% of these patients suffer from chronic hyponatremia and recurrent acute water intoxication.

In psychogenic polydipsia, urine osmolality is < 100 mOsm/kg (100 mmol/kg). Decreasing water intake gradually will lead to decreasing urine output, increasing plasma and urine osmolality and serum sodium concentration.

Medications that cause excessive water retention, such as lithium and carbamazepine, can aggravate the symptomatology.

111
Q

Ddx between griev and complicated grief reaction

A

In complicated grief reaction, we find:

Intense feeling of guilt and blame
Functional impairment
Might occur psychotic thoughts or suicidal
SYMPTOMS LAST MORE THAN A YEAR
Ttx: antidepressants, antipsychotics, ECT

112
Q

Treatment with antidepressants: avaluating initial response

A

Assess the patient in 2 WEEKS:

  • If responding well, continue treatment
  • If partial response, increase the dose further
  • If no initial response, switch to different drug
  • If not possible, switch to different drug
  • If inadequate responde AFTER 6 WEEKS, change to different drug (can be of the same class).
113
Q

Changing antidepressants - management

A
  • Taper the drug by halving the dose each week to avoid discontinuation syndrome.
  • Washout period: 2 - 4 days; 1 week (Fluoxetine ); 2 weeks (MAOI).
  • The new drug should be started at a low dose.
  • Monitor closely for serotonin toxicity.
114
Q

Antidepressants and Hypertension

A

SNRIs

SSIRs like: paroxetine, reboxetine

TCA

MAOI

Bupropion

115
Q

Antidepressants and sexual dysfunction

A

Less implicated:

Desvenlafaxine, mirtazapine, escitalopram

Methylphenidate can be added to SSRI to boost the antidepressant action and it can reduce SSRI-induced sexual effect.

116
Q

Discontinuation Syndrome - overview

A

FINISH:
* Flu-lÍke symptoms (headache, myalgia, arthralgia)
* Insomnia (vivid dreams, nightmares)
* Nausea
* Instability of gait ( ataxia ), tremor
* Sensory disturbances ( electric shock-lik:e sensation)
* Hyperarousal (anxiety, irritability, anger, panic, low mood)

Management: restart the drug in the original dose before beginning to taper slowly: reduce the dose by 25 - 50%, wait 2 - 4 weeks, repeat. Liquid medication may be required.

117
Q

Antidepressants in Pregnancy

A

Drugs to avoid in pregnancy: Paroxetine, Fluoxetine, MAOI.

  • Paroxetine can increase the risk of withdrawal syndrome in newbom baby due to rapid absorption.
  • First trimester: cardiovascular malformation.
  • Third trimester: pulmonary hypertension in fetus.
118
Q

Paroxetine overdose - Management

A

It can cause nausea, vomiting, cold and clammy extremities, bradycardia and a fall in the BP, disorientation, restlessness and incoherence of speech.

Most patients recover with conservative management and require little intervention.

Deaths involving paroxetine toxicity have generally been a result of ingestion of multiple drugs, and not from paroxetine alone ——»> Evaluate for coingestants is the MOST important thing to be done

119
Q

TCA Toxicity - overview

A
  • Cardiotoxicity with cardiovascular collapse:
  • Reduced cardiac contractility.
  • Hypotension.
  • Broad complex dysrhythmias (abnormal conduction).
  • ECG: sinus tachycardia, wide QRS
    tall R wave in a VR prolonged QTc. prominent S wave in lead I
    CNS depression: drowsiness, sedation, coma, convulsions, ataxia.
120
Q

Truancy - overview

A

Escaping the school and going to games and parlours on the one hand and being tearful and withdrawn on the other hand does not fit into the diagnosis of depression.
Truancy is any intentional unauthorised or illegal absence from compulsory schooling.Children who run away from school to do other things (truancy) rather than stay home usually have different problems from those who do not want to go to school.
They may be wanting to get attention, trying to impress their friends or they may be angry because of school or home problems.Truancy may happen when there are learning problems.Children who truant a lot sometimes go on to break the law as they get older.
Children who truant usually try not to let their parents find out.Truancy sometimes happens when parents are not very interested in the child getting a good education, and perhaps don’t get on very well with the school themselves.

Children with depressive disorders feel sad, lack interest in activities they previously enjoyed, criticise themselves, and are pessimistic or hopeless about the future.Thinking that life is not worth living, they may contemplate suicide.
They may also be irritable and aggressive. They may be indecisive and have problems concentrating. They tend to lack energy and to have problems sleeping

121
Q

Reactive attachment disorder - overview

A

Clinical features (some evidenced <5 years)

Insufficient care (eg, neglect, abuse, inconsistent caregiving, prolonged institutionalization)
Does not seek or respond to comfort
Poor social responsiveness, limited positive affect
Unexplained irritability/fear/sadness even during safe encounters

Associated features

Toileting & sleep difficulties
Anxiety, aggression, hyperactivity/impulsivity

Differential diagnosis

Adjustment disorder, posttraumatic stress disorder
Global developmental delay, intellectual disability
Autism spectrum disorder
Anxiety disorders (eg, social anxiety disorder, selective mutism)
Depressive disorders

Management

Early intervention promoting:
safe, stable & enriching environment
consistent, responsive caregiving
Psychological services (eg, parenting skills, individual/family counseling)

122
Q

Whats paraphrenia?

A

Late onset eschizophrenia

123
Q

Paraphrenia - CF, age of onset, most common symptoms

A

symptoms and signs of paranoid psychosis appear for the first time in elderly (female):

paranoid persecutory delusions;

accusative, abusive auditory hallucinations.

Thoughts disorder and negative symptoms are rare.

Good response to medications.

Spontaneous remissions are less likely

Cognitive deficit but intact recall and
visuospatial ability, intact orientation

124
Q

List high, low and deposit forms of Typical antipsichotics

A

Typical antipsychotics:

High potent: Haloperidol (Haldol), Trifluoperazine ( Stelazine ), Fluphenazine ( Madecate ),

High risk of extrapyramidal side effects, hyperprolactinemia.

Less potent: Chlorpromazine ( Largactil ), Thioridazine (Aldazine), Pericyazine Neulactil

Less risk of EP side effects, but more anticholinergic effect.

Depot forms:
Haloperidol Decanoate IM every 4 weeks.
Fluphenazine decanoate IM every 4 weeks.

125
Q

Sedation as adverse effect of atypic antipsychotics - which drugs are high and low risk, whats the management

A

Sedation:

High risk: Olanzapine, Clozapine , Quetiapine,
Low risk: Aripiprazole, Amisulpride , Risperidone,

Management:

Reassure the patient that the degree of sedation is likely to decline over 1 to 2 weeks.
If this does not occur and the degree of sedation is unacceptable to the patient, reduce the dose or change the medication.

126
Q

Risperidone - side effects, doses, management

A

Risperidone:

Common side effects:

Weight gain is one of the most common side effects (4.6 pounds after 10 weeks of treatment) due to increased appetite.
Drowsiness
Dizziness
Nausea

Other side effects:

Parkinsonism
Gynaecomastia (late term side effect). Galactorrhoea. Absence of periods in females. Delay in growth.
Sexual dysfunction.

Risperidone (Risperdal) initial dose 1 mg maximum dose 6 mg

Risperdal Consta IM every two weeks

Indications: positive and negative
symptoms.

127
Q

Hyperprolactinemia - drugs related, management

A

High risk: Amisulpride , Paliperidone, Risperidone, Ziprazidone , all typical antipsychotics.

Low risk: Olanzapine, Quetiapine, Clozapine, Aripiprazole.

Hyperprolactinemia:
Monitor prolactin concentration.
Reduce the dose.
Switch to antipsychotic with low risk.
Or add small dose of Aripiprazole.
Consider Sildenafil (Viagra), Tadalafil.

128
Q

When to add aripiprazole?

A

Aripiprazole atypical antipsychotic causes weight loss and significant reduction in total and low density lipoprotein cholesterol.

Aripiprazole can be added to clozapine. It has beneficial effects.

Alternative option for weight reduction is Metformin. This medication can be used in combination with Clozapine.

Clozapine is used for drug resistant schizophrenia and should not be stopped or changed for other medication unless there are severe side effects such as neutropenia, myocarditis.

Olanzapine is associated with weight gain and metabolic syndrome.

Quetiapine is associated with weight gain.

129
Q

Changing from one antipsychotic to another - recommendations

A

When switching between oral antipsychotics a crossover phase of at least 1 to 2 weeks is recommended, during which the dose of the drug being ceased is reduced and the dose of the new drug is gradually increased

130
Q

The most effective treatment for cannabis addiction

A

Cognitive behavioural therapy and motivational enhancement therapy (aimed at reducing the chances of reexposure and establishing coping mechanisms to resist further use).

There is no evidence to use pharmacotherapy in the management of cannabis abuse disorder.

131
Q

Dysthymic disorder - main feature to diagnose

A

Dysthymic disorder is characterized by mild to moderate symptoms of depression lasting for at least 2 years.

132
Q

What is the projection defense mechanism, and how does it work?

A

Projection is misattribution of undesired thoughts, feelings, or impulses onto another person 🔄
Used when thoughts are unacceptable to express 😡
Lack of insight and acknowledgment of one’s own motivations and feelings 🧠
Example scenario: blaming government for financial problems to protect ego 🏛️💰

Disliking your manager but accusing them of having a grudge against you
Accusing your spouse of being in a bad mood when you are
Blaming your child for weight issues instead of addressing your own self-confidence 🙅‍♂️🔀

133
Q

What is the denial defense mechanism, and how does it work?

A

Denial is refusing to experience a situation or fact 🚫
Coping by not accepting reality to avoid unpleasant consequences and pain 😖
Examples include denying health consequences of smoking or refusing to acknowledge a failing business 🚭📉

134
Q

What is the displacement defense mechanism, and how does it work?

A

Displacement is repressing emotions or impulses and redirecting them toward another person or object 🎯
Often due to irrational or socially unacceptable feelings 🙅‍♀️
Examples involve getting mad at a family member for issues unrelated to the true source of frustration 🤬🎯

135
Q

What is the rationalization defense mechanism, and how does it work?

A

Rationalization involves explaining or creating excuses for events or actions 📜
Used to avoid accepting the true cause or reason 🚫
Examples include justifying being late for dinner or cheating on a test 🍽️📝

136
Q

What is the regression defense mechanism, and how does it work?

A

Regression is reverting to behaviors from an earlier age in response to stress or anxiety 🧒🔄
Seeking comfort in familiar, secure actions or habits 🍼📺
Examples involve thumb-sucking in the hospital or resorting to temper tantrums instead of mature parenting 🚼🪣

137
Q

What is the recommended duration of antidepressant therapy for most patients with depression, and when should it be extended?

A

Typically 6 to 12 months of antidepressant therapy for most patients with depression 📆💊
Extend therapy to 3 to 5 years in the following situations:
Two episodes of major depression in 5 years
Three previous episodes of major depression
Depression with psychotic features
Depression with a serious suicidal attempt 🧠💉
Reassess after 3-5 years, and some patients may require lifelong therapy 🔄🩺

138
Q

What is a normal grief reaction, and how long do its symptoms typically last?

A

Symptoms include disruption of daily routine, weight loss, decreased sleep, and appetite 💔
Typically, patients return to normal social functioning within 2 months, but symptoms may last up to one year with waxing and waning 🕰️
Key features: sadness, despair, tearfulness, decreased sleep, decreased appetite, and decreased interest in life and the world 🙁

139
Q

How should grief-related insomnia be managed when red flags are absent?

A

Prescribe a short course of benzodiazepines (< 7 days) for insomnia 🌙💊
Refer the patient to grief counseling to help cope with the loss 🩺🧡
SSRIs are not indicated for depressive symptoms or sleep issues unless a diagnosis of moderate to severe depression is present 🚫
Referral to a psychiatrist is not necessary at this stage 🙅‍♂️
Antipsychotics are not indicated for grief-related auditory and visual hallucinations unless there are psychotic features necessitating treatment 🚫👻

140
Q

What do T-scores indicate in osteoporosis diagnosis, and what is the most appropriate advice for preventing osteoporosis in postmenopausal women without evident bone loss?

A

T-score of -2.5 or less indicates osteoporosis 🦴
T-scores between -1 to -2.5 suggest osteopenia 🦴
T-score of -1 or above is considered normal bone density 🟩
For prevention, maintain a high-calcium diet with a total daily calcium intake of 1300 mg, with diet being the preferred source of calcium 🍽️💊
Encourage patients with low dietary calcium intake to increase their intake of calcium-rich foods instead of supplements 🥛🧀
Limit the dose from a supplement to 500 to 600 mg of elemental calcium daily, ideally achieved from dietary sources 🚫
Bisphosphonates are used for treatment of established osteoporosis or osteopenia, not for prevention 🚫
Calcium supplementation is used when adequate calcium intake cannot be ensured through diet 🚫
Exercise has additional benefits but is not the primary preventive measure 🏋️‍♀️
Exposure to sunlight is necessary for vitamin D production, which aids calcium absorption but is not the primary preventive measure ☀️
Maintain a serum 25-hydroxyvitamin D concentration above 50 nanomol/L in patients taking drug therapy for osteoporosis 🌞

141
Q

How should osteoporosis treatment be monitored, and when should bone mineral density (BMD) measurements be taken?

A

To monitor osteoporosis treatment, use actual BMD values; T-scores and Z-scores are not appropriate 🦴
Measure BMD at the lumbar spine and hip:
2 years after starting treatment
1 to 2 years after a significant change in treatment 📊
Consider more frequent BMD measurement (but not more often than once a year) in patients with severe osteoporosis or high risk of bone loss, including those taking high-dose glucocorticoid therapy ⏳
If BMD is stable or improving, subsequent measurement is not required for at least 2 years; an interval of up to 5 years may be reasonable 📈
If BMD decreases by more than 5% or 0.05 grams/cm2 at any major site, or if a fracture occurs, consider investigation for new or unrecognised risk factors, and check adherence to therapy. A change of therapy may be appropriate. 🚑

142
Q

How should osteoporosis be managed and monitored, especially in patients with fracture risk?

A

Measure bone mineral density (BMD) in patients with significant risk factors for fracture, and in patients 70 years and older.
Calculate absolute fracture risk using online calculators (eg Fracture Risk Assessment Tool [FRAX])
Start osteoporosis drug therapy for patients aged 70 and older with T-scores of –2.5 or less.
Consider treatment for younger patients with declining BMD or high fracture risk; seek specialist advice when needed.
Ensure sufficient calcium and vitamin D intake and advise on fracture prevention.
After a minimal-trauma fracture, assess BMD, and treat if T-score is osteopenic or osteoporotic.
For normal T-scores, investigate other causes of fracture and consider treatment based on fracture site and risk factors.
If BMD measurement isn’t possible, start drug therapy for hip or vertebral fractures, and consider follow-up BMD when available.

143
Q

What are the commonly used drugs for osteoporosis treatment, and what are their advantages and disadvantages?

A

Alendronate: Oral dosing 🩸, Low cost 💰, Can cause or exacerbate upper gastrointestinal tract irritation 😫, Absorption reduced by food, antacids, calcium, magnesium, and iron 🚫, Requires more frequent dosing than intravenous options 📅, Not recommended in severe kidney disease 🚑.
Risedronate: Oral dosing 🩸, Low cost 💰, Enteric-coated formulation available (may have a lower incidence of gastrointestinal adverse effects, and absorption less affected by food, antacids, calcium, magnesium, and iron) 🍽️, Can cause or exacerbate upper gastrointestinal tract irritation 😫, Absorption reduced by food, antacids, calcium, magnesium, and iron 🚫, Requires more frequent dosing than intravenous options 📅, Not recommended in severe kidney disease 🚑, Enteric-coated formulation only available as a weekly dose (non–enteric-coated formulation available as a monthly dose) 🗓️.
Zoledronic Acid: Intravenous administration avoids gastrointestinal adverse effects 💉, Yearly dosing can improve adherence 🗓️, Intravenous administration not acceptable to some patients 🚫, Not recommended in severe kidney disease 🚑, Can cause transient influenza-like symptoms 🤒, Can cause uveitis (uncommon) 👁️, Can cause hypocalcaemia (particularly in patients with impaired kidney function, vitamin D deficiency, or a malabsorption disorder) 🚑.
Denosumab: Subcutaneous administration avoids gastrointestinal adverse effects 💉, Dose adjustment not required in kidney disease 🚑, 6-monthly dosing can improve compliance 🗓️, Subcutaneous dosing not acceptable to some patients 🚫, Adherence to 6-monthly dosing regimen is essential to prevent loss of bone mineral density between doses 📅, Therapy must be either indefinite or replaced by a bisphosphonate if stopped 🔄, Withdrawal or interruption of treatment (dose delayed by more than 4 weeks) is associated with an increased risk of multiple spontaneous vertebral fracture 🦴, Can cause hypocalcaemia (particularly in patients with impaired kidney function, vitamin D deficiency, or a malabsorption disorder) 🚑.

144
Q

What are the suitable regimens for bisphosphonate treatment in osteoporosis, and what precautions should be taken during their administration?

A

Alendronate: 70 mg orally, once weekly on an empty stomach 💊🍽️, Low cost 💰, Limited by upper gastrointestinal irritation 😫, Absorption affected by food, antacids, calcium, magnesium, and iron 🚫, Frequent dosing required 📅, Caution in severe kidney disease 🚑.
Risedronate: 35 mg orally, once weekly on an empty stomach 💊🍽️, Low cost 💰, Enteric-coated formulation available for reduced gastrointestinal adverse effects 🍽️, Can cause or exacerbate upper gastrointestinal tract irritation 😫, Absorption affected by food, antacids, calcium, magnesium, and iron 🚫, Frequent dosing required 📅, Caution in severe kidney disease 🚑, Monthly dosing option available 🗓️.
Zoledronic Acid: 5 mg intravenous infusion once a year 💉, Avoids gastrointestinal adverse effects 💊🍽️, Improves adherence with yearly dosing 📅, Risk of transient influenza-like symptoms 🤒, Risk of uveitis (uncommon) 👁️, Risk of hypocalcaemia, especially with risk factors 🚑.
Denosumab: 60 mg subcutaneously every 6 months 💉🗓️, Increases BMD and reduces fractures 🦴, Need for patient adherence to 6-month regimen 🔄, Considerations upon therapy cessation leading to rapid bone turnover and loss of BMD 📈🦴, Risk of hypocalcaemia, especially with risk factors 🚑, Requires calcium and vitamin D sufficiency 🍽️🌞, Discussion with patients on the importance of adherence and therapy continuation or replacement 🗣️.

145
Q

What are the effects of glucocorticoids on bone mineral density (BMD), and how can glucocorticoid-induced osteoporosis be prevented and managed?

A

Effects of Glucocorticoids on BMD: Reduce bone formation, increase bone resorption, affect osteoblast function, hinder intestinal calcium absorption, cause osteocyte dysfunction, lead to hypercalciuria, and suppress gonadal function 🦴📉.
Fracture Risk with Glucocorticoids: Increased fracture risk regardless of BMD, higher risk compared to non-users with similar BMD 🦴📈.
Factors Affecting Bone Loss: Highest bone loss rate in the initial 3 to 6 months, dose and duration-dependent bone loss, prednis(ol)one dose ≥ 7.5 mg/day or equivalent associated with highest risk, increased risk even with low doses (≥ 2.5 mg/day) 📆.
Prevention and Management: Assess fracture risk, measure BMD, ensure sufficient calcium and vitamin D intake, optimize other fracture risk factors, advise on minimal-trauma fracture prevention 📊🍽️🌞.
Treatment Options: Bisphosphonates (first-line), Denosumab, Teriparatide (strict eligibility criteria), Estrogen therapy (for postmenopausal women) 💊🦴.
Monitoring: Consider BMD measurement every 12 to 24 months initially, with less frequent monitoring if stable and acceptable results 📏🔄.

146
Q

What is transient osteoporosis of pregnancy, and how does it manifest?

A

Definition: Rare demineralizing condition, primarily affecting the hip, but can impact other joints. Mechanism unknown 🤰🦴.
Distinguishing Factors: Differentiate from physiological bone mass loss during pregnancy and lactation. Presents in the third trimester with severe atraumatic anterolateral groin pain, anterior thigh radiation, acute or insidious onset 🚼🤕.
Bone Mineral Density: Hip BMD significantly reduced compared to lumbar spine 📏.
Resolution: Self-limiting, typically resolves 2 to 6 months postpartum 🔄.
Management: Requires specialist assessment and management 👩‍⚕️.

147
Q

What are common symptoms associated with thyroid dysfunction (hyper AND hypo)?

A

Decreased Libido

Psychosis

148
Q

What are the general rules for the approval of ECT on involuntary patients?

A

Mental Health Tribunal authorizes ECT for involuntary patients, forensic patients, those under supervision, or with a community treatment order.
Approval requires patient’s incapacity to give informed consent and the opinion of two medical practitioners (at least one being a psychiatrist).
The medical practitioners must consider the patient’s clinical condition, treatment history, and alternative treatments.
ECT approval aims to prevent serious mental or physical deterioration. ⚖️🧠🏥

149
Q

When can authorized psychiatrists administer ECT without tribunal approval?

A

Authorized psychiatrists can perform ECT without tribunal approval in life-saving emergencies for involuntary patients, those under supervision, or forensic patients.
ECT is administered when necessary to save a person’s life or prevent irreparable harm.
Following emergency ECT, authorized psychiatrists must report the procedure to the tribunal. 🆘⚡🏨

150
Q

What are the recommendations for the use of emergency ECT?

A

Emergency ECT should be avoided when possible and not administered without a second opinion.
Practical discussions with the chief psychiatrist or their representative are encouraged.
Unlike other medical procedures, consent from relatives, administrators, colleagues, or seniors is not required for involuntary patients. 🚫👥💬

151
Q

What does an MMSE score indicate in terms of dementia?

A

An MMSE score of 21-24 suggests mild dementia, and a patient with this score may have mild functional dependence. 🧠📊👴

An MMSE score between 10 and 20 is associated with moderate Alzheimer’s disease and indicates more immediate dependency on daily activities. Patients may have difficulty with tasks like driving, hygiene, and shopping. 🧠📊🚗🧼🛒

Severe dementia, with MMSE scores under 10, is associated with total dependence and the need for constant supervision. It’s marked by motor impairments (like gait and balance issues), incontinence, and myoclonus. 🧠📊👴🚶‍♀️🚽🙅‍♀️

152
Q

What are the symptoms and mechanisms of anticholinergic toxicity?

A

“Hot as a hare” 🌡️
Mechanism: ↑ Body temperature due to reduced sweating.
“Dry as a bone” 💧
Mechanism: Reduced secretions from mucous membranes and sweat glands.
“Red as a beet” 🍅
Mechanism: Flushed skin due to superficial vasodilation from increased body heat.
“Blind as a bat” 🦇
Mechanism: Cycloplegia and mydriasis caused by the paralysis of the ciliary muscle and iris sphincter.
“Mad as a hatter” 🎩
Mechanism: Altered mental status due to the drug permeating the blood-brain barrier and affecting CNS pathways.
“Full as a flask” 🧳
Mechanism: Constipation and urinary retention from decreased intestinal smooth muscle contraction, detrusor contraction, and internal urethral sphincter relaxation.
“Fast as a fiddle” 🏃
Mechanism: Tachycardia resulting from decreased vagal tone at the sinoatrial node.

Mechanism:
“Widespread, competitive blockade of muscarinic acetylcholine receptors” 🧪
Common Causes:
“Overdose of medications with anticholinergic properties (e.g., diphenhydramine)” 💊

153
Q

DDx between serotoninergic and cholinergic syndromes, lithium toxicity and neuroleptic malignant sydrome?

A

Serotoninergic has often GI symptoms (nausea) + neuromuscular hyperactivity. It is
characterized by a triad of mental status changes, autonomic dysregulation, and neuromuscular hyperactivity.

Anticholinergic toxicity is characterized by hyperthermia, delirium, dilated pupils, dry mucous membranes, urinary

Neuroleptic malignant syndrome is characterized by hyperactive vital signs (eg, hyperthermia, tachycardia), altered mental status, and rigidity that develops in the context of antipsychotic use. The absence of an inciting medication, this patient’s hyperreflexia,
and the overall clinical picture make serotonin syndrome more likely

Acute toxicity from lithium (used to treat bipolar disorder) can cause neurologic findings, including confusion and ataxia.
However, acute toxicity typically also causes gastrointestinal symptoms (eg, nausea/vomiting, diarrhea), and hyperthermia and urinary
retention are not expected.

154
Q

What is the first-line treatment for cognitive symptoms of AD, and what improvements can it offer?

A

The first-line treatment for cognitive symptoms of AD is a cholinesterase inhibitor. These drugs can improve the quality of life and cognitive function, including memory, language, thought, and reasoning. 🧠📖
However, it’s important to note that cholinesterase inhibitors do not alter the disease course in any type of dementia. They primarily provide symptomatic relief. 📊

155
Q

What are the cholinesterase inhibitors effective in patients with mild to moderate AD, and how do they function?

A

Cholinesterase inhibitors effective in patients with mild to moderate AD include donepezil, galantamine, and rivastigmine. 🩹
These medications function by increasing the availability of acetylcholine, a neurotransmitter, in the brain. This can help enhance cognitive function in AD patients. 🧪

156
Q

What is the medication for severe AD, and how do they function?

A

Memantine is an NMDA receptor antagonist approved for moderate to severe dementia, specifically in AD. 🧪
It functions by modulating glutamate activity in the brain, which can be beneficial in advanced stages of the disease. 🧠

157
Q

What is the role of amantadine in treating AD, and why is it not considered a first-line treatment?

A

Amantadine is thought to possess dopaminergic and NMDA receptor antagonist properties and is frequently used in the treatment of Parkinson’s disease. 🦠🧠
However, the evidence of its benefit in the treatment of AD is limited, and it is not considered a first-line treatment in this patient. 📉🚫

158
Q

Which drugs are recommended for monotherapy in bipolar depression, and why is antidepressant monotherapy not advised?

A

Recommended monotherapy drugs for bipolar depression: Lamotrigine, lithium, lurasidone, olanzapine, and quetiapine 💊
Antidepressant monotherapy should be avoided as it can induce mania or rapid cycling ⚠️

159
Q

Why is monotherapy alone often ineffective for bipolar depression?

A

Monotherapy alone is often ineffective or only partially effective for bipolar depression, necessitating combination therapy 📉
Combination therapy involves using an antidepressant along with one of the following drugs to prevent manic switch: lithium, lurasidone, olanzapine, quetiapine, or sodium valproate.

> Before adding an andidepressant, its possible to attempt an increase the dose of the antipsychotic firslt

160
Q

What should be considered when using antidepressants in bipolar depression, and how should patients be monitored?

A

When using an antidepressant in bipolar depression, closely monitor patients for signs of emerging hypomania or mania, which is more common in young people 👀
Response to treatment is typically noticeable after at least 1 week, with full benefits taking 4 to 6 weeks or longer ⏳
If an acceptable response is achieved, continue combination therapy for 1 to 2 months after recovery from the depressive episode, followed by gradual reduction and discontinuation of the antidepressant. Continue with the other drug as monotherapy for at least 6 to 12 months to prevent relapse. Assess the need for bipolar disorder prophylaxis after this period ⚙️
Note that discontinuing the antidepressant may not always be possible if the patient is prone to recurrent depressive episodes 🔄

161
Q

What precautions should be taken with certain medications in bipolar depression treatment?

A

Avoid paroxetine in young people due to an increased risk of suicidal thoughts, behaviors, and other serious adverse events associated with its use ❌

162
Q

When should prophylaxis be considered in bipolar disorder treatment, and what factors are involved in the decision?

A

Prophylaxis should be evaluated on a case-by-case basis, involving shared decision-making with the patient and the treating psychiatrist 🧑‍⚕️🤝
Consider prophylaxis if the patient has had either:
2 or more episodes of mania or depression 🔄
Mood episodes that significantly impaired their function, with or without psychotic features 📉🧠
Benefits and harms of treatment should be discussed with the patient to make an informed decision 🗣️

163
Q

What medications are typically used for prophylaxis in bipolar disorder, and how should dosing be adjusted?

A

f there was a sufficient response to the drug used for acute therapy, use the same drug for prophylaxis 🔄
The effective dose or target blood concentration may be lower than when the drug was used for acute treatment 🎯

164
Q

What are the first-line and third-line therapy options for bipolar disorder prophylaxis?

A

First-line therapy for prophylaxis: Lithium 💊
Third-line therapy options for prophylaxis: Carbamazepine, Olanzapine 💡

165
Q

How long should prophylaxis for bipolar disorder typically last, and what factors influence the duration?

A

Prophylaxis may be time-limited (3 to 5 years) or indefinite, depending on factors such as the patient’s history of recurrences, response to treatment, patient age, and treatment tolerability 📅🤔

166
Q

What family history factors may be associated with anorexia nervosa and bulimic disorder?

A

Anorexia nervosa may be associated with a family history of leanness or athleticism 🏃‍♂️🧬
Bulimic eating disorders are associated with a personal or family history of obesity 🍔🧬
Sexual abuse is a significant risk factor for the development of eating disorders and various other psychiatric disturbances 🚫🤕

167
Q

Derailment, tangenciality - diferentiation

A

The scenario describes a typical example of ‘tangentiality’. Tangentiality occurs when one idea connects to the next with one word or phrase, but the thoughts become confusing because they go off on a tangent and end in a different subject. In the above example the word ‘food’ ends in another comment about food unrelated to the previous sentence. The word ‘food’ is the only connection. Loosening of association (derailment), on the other hand, happens when one idea does not connect to the next at all.

Following are sentences told by patients in real situations. The first two are examples of derailment (loosening of association), while the third is ‘tangentiality’:

The next day when I’d be going out you know, I took control. Like uh, I put bleach on my hair …
The traffic is rumbling along the main road. They are going to the north. Why do girls always play pantomime heroes?
I think someone has infiltrated my copies of the cases. We’ve got to case the joint. I don’t believe in joints, but they do hold your body together.

168
Q

What drug class is contraindicated in cocaine intoxication

A

Beta blockers should not be used in the treatment of cocaine-induced cardiovascular symptoms and complications owing to the fact that beta blockers may result in unopposed alpha-adrenergic stimulation, resulting in coronary vasoconstriction and end-organ ischemia.

169
Q

Without treatment, how long does a depressive episode last?

A

Without treatment, an episode of major depressive disorder in adults lasts from 6 months to 18 months (average 8 months). The course of the disease in adolescents appears to be different from that of adults. Although there is no solid evidence, it is suggested that major depression in adolescents may last from 2 weeks to many years.

170
Q
A

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