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Mental Health > Pharmacology MNTH > Flashcards

Pharmacology MNTH Flashcards

1
Q

Indications for Antipsychotics

A

Manage Psychotic symptoms
(SCZ, Bipolar, etc)

Improve mood, reduce anxiety, reduce sleep disturbance

Antiemetic effect

Pruritis

Preoperative Sedative

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2
Q

Which drug can treat anxiety in autism disorder?

A

Risperidone

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3
Q

Where does the mesolimbic pathway go, and which receptors are there?

Where does the mesocortical pathway go, and what are its receptors?

A

To the nucleus accumbens and increase in DA cause positive psychosis symptoms

To the Prefrontal cortex, and DA hypoactivity causes negative symptoms of psychosis.

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4
Q

A blockade of the D2R will do what?

A

Block the mesocorticomesolimbic Pathway
-Alleviates psychosis symptoms

Block the nigrostriatal pathway
Produce EPS and Tardive dyskinesia

Block the tuberoinfundibular pathway
-Increases prolactin secretion

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5
Q

What action do most typical antipsychotics have vs Atypical?

A

Typical: D2R antagonism

Atypical: D2R antagonism and inverse agonism of 5-HT2A

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6
Q

What are EPS?

Treatment?

A

Extrapyramidal Symptoms

Come from block of D2R in the Nigrostriatal pathway

Dystopia
Parkinson’s-like symptoms
Akathisia (motor restlessness)

The higher potency (typical) antipsychotics will cause more EPS

TD: Antiparkinsonian agents, amantadine, benztropine diphenhydramine

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7
Q

Which potency will have more OFF-target effects in antipsychotics?

A

Low potency. High potency stay at the receptors for longer and can cause EPS or TD. The low potency will cause more off target effects.

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8
Q

What is Tardive Dyskinesia?

How do you treat it?

A

Caused by block of D2R of the nigrostriatal pathway

Fly-catching or worm-like tongue movements

Treat with VMAT inhibitors (valbenazine and deutertrabenazine)

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9
Q

What is neuroleptic malignant syndrome?

A

Resembles severe Parkinsonism with autonomic instability.

Leads to lead-pipe muscle rigidity altered mental status, fever and unstable BP.

Use Dantrolene or bromocriptine

If symptoms last longer than a week then it increases mortality risk

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10
Q

What are the times of onset of these antipsychotic ADRs?

Acute dystopia
Akathisis
Parkinsonism
Neuroleptic malignant syndrome
Personal tremor
Tardive dyskinesia
A 
1-5 days
5-60 days
5-30 days
Weeks to months
Months to years of Tx
Months or year of Tx
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11
Q

What can be used to stop hyperprolactinemia if you can’t switch antipsychotics?

A

Bromocriptine

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12
Q

Chlorpromazine and Thioridazine

A

Typical Antipsychotics

Least potent of the class

Can cause EPS, increase serum TG and cause hyperglycemia

Wide range of CNS, autonomic, and endocrine effects

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13
Q

Fluphenazine

A

Typical Antipsychotic

Oral form has high risk for EPS

Low potential for weight gain, sedation, orthostasis, and antimuscarinic effects

Has injectable long acting form 2-3 weeks

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14
Q

Haloperidol

A

Typical Antipsychotic

Low potential for orthostasis, weight gain, sedation

Higher incidence of EPS

Can be used in acute psychosis

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15
Q

What are newer Atypical Antipsychotics good for generally?

A

Positive symptoms

Cause more metabolic syndrome, CAD, stroke, and HTN

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16
Q

Which are usually first line for psychosis, typical or atypical antipsychotics?

A

Atypical

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17
Q

Which antipsychotics cause the highest risk of developing diabetes?

A

Olanzapine and Clozapine

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18
Q

What needs to be monitored for those on atypical antipsychotics?

A 
A1C
Weight and heigh
BP
Glucose
Lipids
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19
Q

What is the black box warning of atypical antipsychotics?

A

Elderly with dementia-related psychoses are at increased risk of stroke death.

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20
Q

Clozapine

A

Atypical Antipsychotic

Indicated for Tx of people with low threshold for EPS

Not first line because of hematological side effects

Will cause weight gain, myocarditis, diabetes, sedation
Constipation can also lead to deadly small bowel obstruction

Contraindicated when WBC is below 3000 or if Granulocytes are below 1500

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21
Q

Aripiprazole

A

Atypical Antipsychotic

Indicated: SCZ, Bipolar, Autism

Low occurrence of EPS, Low potential for weight gain, sedation, antimuscarinic effects

Partial agonist of D2
Antagonist of 5HT2A

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22
Q

Olanzapine

A

Atypical Antipsychotic

Indications: SCZ, Acute Mania, Maintenance of Bipolar 1

Antagonist of 5HT2A and D2

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23
Q

Quetiapine

A

Atypical Antipsychotic

Indications: SCZ, Acute Bipolar 1, Bipolar Depression

Weak antagonist of D2 and 5HT2A

Least likely to cause EPS (Best for Parkinson patients)***

Increase QT interval***

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24
Q

Risperidone

A

Atypical Antipsychotic

Indications: Maintenance of SCZ 13-17 and adults, Acute manic episodes

Antagonist of 5-HT2A and D2

Will elevate Prolactin

Low likelihood of EPS

Weight Gain, anxiety, vomiting, ED and rhinitis.

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25
Q

How are Antipsychotics metabolized?

A

Through the CYPs in the liver

First pass metabolism is significant.

The drug may last longer than planned because it can hide in adipose tissue (very lipophilic)

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26
Q

What are the three hypotheses for the pathophysiology of MDD?

A

Monoamine hypothesis

Glutamatergic Hypothesis: NMDAR Antagonists

Neurotrophic hypothesis: Depression associated with low BDNF. Tx of depression increases Neuro genesis.

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27
Q

How long does it take for antidepressant effects to work?

Why?

A

6 weeks

Acute treatment activates inhibitory autoreceptors to lower the firing rate of serotonergic and NE neurons.
This may increase suicide risk

With chronicity of Tx, the autoreceptors are downregulated.

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28
Q

What are the general differences between typical and atypical antidepressants?

A

Typical (SSRI, SNRIs, TCA, MOAIs) will inhibit reuptake or degradation of monoamines

Atypical target receptors and/or inhibit reuptake of monoamines

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29
Q

SSRIs

A

Fluoxetine, Sertraline, Citalopram, Paroxetine, Fluvoxamine Escitalopram

Safety during an overdose

Indications: GAD, PTSD, OCD, PMDD, Bulimia

ADR: anxiety nervousness, insomnia, sexual dysfunction, GI effects

  • Specifics: Serotonin Syndrome
  • No Cardio side effects

CYP2D6 metabolized: inhibition of CYPs will cause muscle rigidity and hyperreflexia

Quick withdrawal causes discontinuation syndrome:
- dizziness, HA, nervousness, Nausea, insomnia.

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30
Q

Which SSRIs cause the most discontinuation syndrome and least?

A

Most paroxetine (short 1/2 life)

Least Fluoxetine (Long 1/2 life)

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31
Q

Serotonin Syndrome?

A

Increase of serotonin usually because the CYP is block when using an SSRI or SNRI

Serotonin levels cause muscle rigidity, hyperthermia, hyperreflexia, and autonomic instability.

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32
Q

SNRIs

A

Venlafaxine, Desvenlafaxine, Duloxetine, Levomilnacipran

Indications: MDD, GAD, Stress unrinary incontinence, Fibromyalgia, binge-eating

ADR: Anxiety nervousness, insomnia, sexual dysfunction, increase in BP and autonomic effects due to excess NE

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33
Q

Which SNRI can be used to treat fibromyalgia?

A

Milnacipran

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34
Q

Which SNRI causes Orthostatic hypotension vs dose-related hypertension?

A

Duloxetine

Venlafaxine

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35
Q

Tricyclic Antidepressants

A

Amiltriptyline, nortriptyline, imipramine, desipramine

Not first line- risk of lethal overdose

Indications: MDD, Pain, Enuresis, Insomnia

Affects muscarinic R: Anticholinergic effects, alpha-1 adrenergic R: orthostatic hypotension and sedation, H1 R: Sedative effects and weight gain, Quinidine-like effects on cardiac conduction. Prolonged QTc

Seizure threshold is lowered

Eliminated by hepatic CYPs

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36
Q

What is the most serious ADR of TCA Antidepressants?

A

Prolonged QTc

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37
Q

Monoamine Oxidase Inhibitors

A

Selegiline, tranylcypromine, phenelzine, isocarboxazid

Indication: Depression (transdermal patch)

Avoid tyramine: inhibition of MAOs increases the Bioavailability of tyramine. Will cause a hypertensive crisis
(Transdermal may reduce HTN risk)

Slow CYP acetylators at higher risk for toxicity.

Takes up to 2 weeks to recover from MAO activity

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38
Q

5-HT2 Receptor Modulators

A

Trazodone

Indications: Major depression, Anxiety disorders

ADRs: Orthostatic hypotension, Prapism, Hepatotoxicity

Trazodone is contraindicated with MAOIs

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39
Q

Atypical Antidepressants

A

Mirtazapine, Bupropion, Amoxapine

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40
Q

Mirtazapine

A

Atypical Antidepressants

ADR: Somnolence (good for insomnia), Increased appetite, weight gain
Not as many sexual effects

Hepatic metabolism with long 1/2 life

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41
Q

Bupropion

A

Atypical Antidepressants

NET, DAT Blocker

Indications: Depression, smoking cessation, ADHD

ADR: anxiety, tachycardia, HTN, irritability, tremor, insomnia, Not commonly associated with sexual effects

Seizures are worst ADR

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42
Q

Should antidepressants should be used with what for Bipolar disorder?

A

Mood-stabilizers

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43
Q

Which antipsychotics are used for acute mania and bipolar depression?

A

Clozapine: Monotherapy or Adunctive, refractory mania

Olanzapine: adjunctive, Bipolar depression

Quetiapine : monotherapy, Bipolar depression

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44
Q

Lithium

A

Bipolar depression, acute mania, prophylaxis

ADR: HA, fatigue, GI disturbances, hypothyroid, Nephrogenic Diabetes Insipidus***** T-wave inversion
80% have ADRs

Neurotoxicity w/ antipsychotic, metronidazole, methyldopa

Eliminated Renally
Caffeine can enhance the renal elimination of lithium

Narrow therapeutic index. Need to stay within .6-1.2 mEq/L. Lower doses used for prophylaxis (600 mg/day), Higher for acute mania (900-1200 mg/day)

Altered Extracellular fluid volume can cause toxicity

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45
Q

Symptoms of lithium toxicity?

A

Ataxia
Slurred speech
Coarse tremors
Confusion

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46
Q

When do you need hemodialysis for lithium toxicity?

A

2.5 mEq/L and moderate-sever neurologic toxicity
More than 4 and renal impairment
More than 5 regardless of clinical status

47
Q

Anticonvulsants

A

Valproate

Carbamazepine

Lamotrigine

48
Q

Valproate

A

Used for bipolar mania not for bipolar depression

ADR: GI, CNS depression, alone is, thrombocytopenia, pancreatitis, teratogenicity

Highly protein-bound, CYP metabolized

49
Q

Carbamazepine

A

Acute Mania

Not first-line agent

INDUCES CYPs

Lower efficacy for biplolar

ADR: Stevens-Johnson syndrome risk, agranulocytosis, aplastic anemia, hepatic failure

HLA-B 1502 and Asian must be screened for Stevens-Johnson syndrome

Acute overdose is potentially lethal above 15 mcg/mL
Ataxia, choreiform movements, diploid, nystagmus, seizures, coma

50
Q

Lamotrigine

A

Maintenance Tx of bipolar 1 disorder and bipolar 2

Low rates of switching to mania, useful to prevent bipolar depression

ADRs: HA, nausea, Rash, Stevens-Johnson syndrome risk

51
Q

What is the remission goal with depression in the STAR*D Trials?

A

Remission for more than 2 months

52
Q

What were the levels of remission for each of the 4 levels

A
  1. 37%
  2. 31%
  3. 14%
    4 13%
53
Q

What is ECT?

A

Electroconvulsive therapy

Electrical current that produces a generalized seizure. Usually unilateral. Few contraindications. Needs 6-12 rounds for remission.

Very safe, even for pregnancy.

54
Q

What is the first line treatment of a delusional disorder?

A

Risperidone

Antipsychotic

55
Q

Which Anxiolytics can cause coma and which don’t?

A

Barbiturates, alcohol

Benzodiazepines and newer hypnotics don’t

56
Q

What are the indications for anxiolytics/anxiety disorder?

A 
GAD
PTSD
Acute Stress Disorder
Panic Disorder
OCD
57
Q

What is the primary treatment for Anxiety disorders?

A

SSRIs
Benzodiazepines
Exposure Therapy

58
Q

Explain the role of BDNF in anxiety

A

The higher the level of BDNF, it is essential for acquisition and extinction of anxiety.

59
Q

What are the three theories of the pathogenesis of Anxiety?

A

Noradrenergic Model: ANS of anxious pts is hypersensitive

GABAa-Receptor Model: Inhibits 5-HT, NE, and DA

Serotonin Model: Lower serotonin function in those with anxiety

60
Q

Are partial agonist for 5-HT1a effective agains GAD or panic disorder?

A

Yes for GAD but not panic disorder.

61
Q

Benzodiazepines

A

Positive Allosteric modulators of GABAa Receptors

Indications: GAD, agoraphobia, Seizures, Insomnia, Operations
(Each one has different uses)

Alprazolam: GAD and Agoraphobia
Diazepam: Status Epilepticus, GAD
Lorazepam: Alcohol withdrawal, GAD

ADR: Drowsiness, Confusion, Ataxia, Seizures, Abuse
—Sudden withdrawal can be fatal.

62
Q

What are the withdrawal symptoms for Benzodiazepines?

A

Anxiety, Insomnia, Tremor, Myoclonus, Delirium, Seizures

63
Q

Barbiturates and Anxiety

A

Linked to fatal overdose

Not first line.

Low doses are positive Allosteric modulators of GABAa

High doses are agonists of GABAa, so they form a loop for themselves (dangerous)

64
Q

Buspirone

A

5-HT1a Receptor Antagonist

Indications: GAD ***especially in elderly

Less abuse potential

CYP metabolized

65
Q

Chloral Hydrate

A

Sedative Drug for Anxiety

Not usually used, schedule 4

Barbiturate-like effects on GABA

Metabolized by hepatic alcohol dehydrogenase

66
Q

Meprobamate

Carisoprodol

A

Anxiety

Schedule 4

Meprobamate causes CNS depression

Carisoprodol has an active metabolite that is meprobamate.

67
Q

What can be used for acute anxiety?

Can you overlap drugs?

A

Benzodiazepines and B-adrenergic antagonists

SSRIs and SNIS, Buspirone have delayed onset, but you can use a benzo first and overlap it with SSRI tx.

68
Q

Transient
Short-Term
Long-term Insomnia

A

Less than tree days: low dose hypnotics for 2-3 nights. No Benzos before big events

3 days to 3 weeks: 7-10 nights of hypnotics

More than 3 weeks: Use sleep hygiene, hypnotics, and identification of other condition

69
Q

What are the ADRs of Hypnotics in Insomnia?

A

Affect sleep quality
Barbiturates>Benzos>Z-drugs

Rebound anxiety, sedation

Can cause rebound insomnia with cessation.

70
Q

Which Benzodiazepines are approved for Insomnia?

A

Flurazepam, ternazepam, quazepam, estazolam

71
Q

Zolpidem, Zaleplon

A

Z-drugs for Insomnia

GABAa agonists

Sedative effects only, and less disruptive of sleep architecture

Less ADRs

72
Q

Besides illicit drugs, what is the next most common used drug?

A

Marijuana

73
Q

What is one of the most common, but one of the most addictive drugs?

A

Nicotine

74
Q

What is a substance use disorder?

A

Maladaptive pattern of substance use despite continued adverse consequences

75
Q

What is the DSM-5 for Substance Use Disorder?

Alcohol
Marijuana
Opioids

A

Problematic pattern of substance use leading to clinically significant impairment or distress. Needs 2 of 11 criteria occurring in a 12-month period

  1. Taken in larger amounts or over longer periods of time
  2. Persistent desire but unable to control use
  3. Great deal of time used to get, use, or recover from effects
  4. Craving
  5. Failure to fulfill obligations
  6. Continued use even with persistent interpersonal problems
  7. Activities given up for use
  8. Recurrent use even with physical hazardous conditions
  9. Continued use even with knowledge that use will cause hurt or problems
  10. Tolerance
  11. Withdrawal

2-3 Mild, 4-5 Moderate, 6+ Severe

76
Q

Can you use lab values to diagnose a SUD?

A

NO

Good to know if drugs are in the system for a withdrawal or intoxication situation.

77
Q

What do substances of abuse do in dopamine pathways?

A

Elevate dopamine in reward circuitry

Increase activity in Ventral Tegmental Area, and Nucleus Accumbens

78
Q

Substance Intoxication Syndrome

A

Substance exerts behavioral or psychological changes on the central nervous system

Reversible, substance-specific.

Different substances may produce similar syndromes

79
Q

Explain the general features and the effects of intoxication and withdrawal symptoms for

Sedatives (alcohol, hypnotics)

Stimulants

A

Pupil Dilation:
Intoxication: Stimulants and hallucinogens
Withdrawal: Opioids, Alcohol

Pupil Constiction:
Intoxication: Opioids
Withdrawal: Stimulants

Psychotic Symptoms:
Intoxication: Stimulants, Alcohol, Hallucinogens
Withdrawal: Sedatives and Alcohol

CV Symptoms:
Intoxication: Stimulants
Withdrawal: Sedatives and Alcohol

80
Q

Which drug routedoes not following the finding of higher Cp=higher pharmacological effect?

A

Smoked

81
Q

Explain addiction impulsivity and compulsivity?

A

Impulsivity: Early in drug use and is a risk factor for development of substance use disorder

Compulsivity: Later in addiction and contributes to maintenance of use disorder

82
Q

Name the stages of the addiction cycle

A

Binge/intoxication
-high or reward

Withdrawal/Negative Affect
-withdrawal

Preoccupation/Anticipation
-craving

83
Q

What is a stress-induced relapse

A

Stress signaling induces craving

Drug sought to alleviate stress

84
Q

What is cue-induced relapse

A

Stimuli associated with either positive or negative reinforcement of the drug induces craving

Can cause an induced withdrawal as well

85
Q

What are the receptors of marijuana, and what are their mechanisms?

A

CB1 and CB2, central and peripheral

G coupled (inhibition of adenylyl Cyclase)
Can also inhibit Ca and K channels

Endogenous cannabinoids (anandamide) operate by retrograde signaling to decrease the effect on postsynaptic neuron

86
Q

Why doesn’t cannabis cause respiratory depression?

A

There is an absence of CB1R’s in the Medulla

87
Q

What does THC Agonism of CB1 receptors do?

A 
Relaxes
Hyperphagia (munchies)
Tachycardia
Decreased coordination
Conjunctivitis
Hallucinations
Minor pain control
88
Q

Explain the effect of THC

A

Agonism of CB1R stimulates the amygdala causing a sense of “novelty”

Heavy users have down-regulation of CB1R
Loss of motivation, and reduced IQ

Also causes loss of short-term memory due to imbalances of GABA in hippocampus.

89
Q

What are the symptoms of Cannabis Intoxication

A

Euphoria, sensory intensification, or apathy, fear, distrust, and panic

Increased appetite, hallucinations, dry mouth

Sedation

Tachycardia

Conjunctival congestion

90
Q

What are the symptoms of withdrawal of cannabis use?

Tx?

A 
Restlessness
Irritability
Mild agitation
Insomnia
Sleep EEG
Nausea, cramping
Craving
Pain

No pharm Tx available for all withdrawal
-depression and insomnia may be treated by zolpidem, buspirone, and Gabapentin

91
Q

LSD

A

Partial agonism of 5-HT2A

Effects through serotonin, dopamine, and norepinephrine

Can induce psychosis

Toxicity is rare, cardiovascular collapse observed with very high doses

NO tolerance or withdrawal.

92
Q

Hallucinogen Intoxication Syndrome

A 
Pupillary dilation
Tachycardia
Sweating
Palpitations
Blurring of vision
Tremors

Tx: Counseling, Benzos, antipsychotics

93
Q

MDMA

Intoxication, and withdrawal symptoms

A

Hallucinogen and stimulant (amphetamine)

Increases concentration of serotonin by reversal of SERT function

Marked intracellualr 5-HT depletion for 24 hours after a single dose (causes depressive symptoms after use). Can cause increased aggression during these periods.

ADR:
Acute toxicity: hyperthermia, serotonin syndrome, seizures
Chronic Toxicity: Neurotoxicity

Toxicity: Pupillary dilation, Tachycardia, Sweating, Palpitations, blurring of vision, tremors

94
Q

Phencyclidine

A

PCP

Antagonist of NMDA receptors, induces psychotic symptoms

Causes extreme Violence in intoxication syndromes

Tx: Non-stimulating environment, restraints, acidification of urine, antipsychotics

ADR Toxic events: Cardiovascular toxicity, neurological toxicity, Rhapdomyolysis

Intoxication syndromes: Violence, nystagmus, numbness, ataxia, dysarthria, muscle rigidity, muscle rigidity, seizures or coma

95
Q

What are the therapeutic indications of stimulants?

A

ADHD
Narcolepsy
Anorexiant (obesity)
Obstruction/sleep apnea

96
Q

Explain nicotine MOA

A

Agonists of neuronal nicotinic Acetyl cholinergic receptors

16/17 subtypes of the receptors are expressed in the autonomic ganglia and CNS

97
Q

Explain how low doses and high doses of nicotine affect the body generally

Adrenal medulla

Neuromuscular junction

A

Low doses: euphoria, arousal, relaxation
High doses: tremors, convulsions

Small doses stimulate ganglionic cells, large block them

Adrenal medulla: small evoke discharge of catecholamines, large doses prevent release due to spinach ice nerve stimulation

Neuromuscular junction: stimulation is rapidly obscured by paralysis (toxic doses)

98
Q

Explain the different kinds of nicotinic receptors nicotine affects

A

Mechanoreceptors: skin, mesenteric, tongue, lung

Chemoreceptors: carotid body

Thermal receptors: skin and tongue

Pain receptors

99
Q

What are the physiological effects of nicotine?

A

Respiratory Depression

Sympathomimetic: vasoconstriction, tachycardia, HTN

Parasympathomimetic: GI tract and urinary. Increased bowel activity and urination

100
Q

Acute Nicotine Toxicity

Tx

A 
Central stimulation (convulsion, coma, respiratory arrest
- diazepam

Respiratory paralysis
-Mechanical Ventilation

HTN and arrhythmia
-Atropine

101
Q

How does nicotine affect metabolism?

A

Metabolized by CYP2D6

They induce expression of CYP1A2 (caffeine) and CYP2E1 (alcohol)

102
Q

Nicotine Withdrawal

Tx

A

Irritability, impatience, anxiety, restlessness, increased HR, increased appetite

Tx:
Replacement therapy
Bupropion
Varenicline (chantix)

Rimonabant (CB1 inverse agonist) not approved in US

103
Q

Cocaine MOA

A

Blockade of catecholamines neurotransmitter reuptake

Increased dopamine concentrations in reward circuitry

104
Q

What are the physiological effects of cocaine?

A

Stimulant effects: excitement, euphoria, decrease fatigue
Higher doses: Seziure, CV complications

Behavioral risks: trauma while intoxicated, promiscuous sexual activity

Chronic cocaine use: reduced sexual drive, anxiety, violence

105
Q

Acute Cocaine Toxicity

Tx

A

Seizure,
Hyperthermia
Chest Pain
Psych complaints

TD: Benzos

106
Q

Explain metabolism and testing of cocaine

How long does the euphoria last

A

Hydrolysis by tissue esterases
- makes benzoylecgonine metabolite

Urine test can see it for up to 10 days

Snorting: 15-30 min
Smoking 5-10 min

107
Q

Cocaine: Tolerance and Withdrawal

Tx

A

Chronic users experience less euphoric effects

Withdrawal symptoms: dysphoria, sleepiness, craving, bradycardia. For 1-3 weeks

Tx: psycotherapy, behavioral treatments. Can use antidepressants or modafinil for relapse

108
Q

Amphetamines: MOA

A

Elevation of extracellular dopamine

Depletion of DA stores occurs due to inhibition of VMAT and reverse transport of dopamine by the DA transporter

Effects and toxicities are from increased DA and NE signaling

109
Q

Physiological Effects of Amphetamine

A

Performance enhancing

Increased NE and DA

Wakefulness, improved attention, increased Resp rate, suppressed foo intake signaling, CV increased BP heart rate slows reflexively (reflex bradycardia)
Smooth muscle contraction increases (difficult urinating)

110
Q

Amphetamine Intoxication

Tx

A

Euphoria, Insomnia, increased wakefulness, decreased appetite, aggression, anxiety, tachycardia, HTN, Tremors

Benzos for seizures

111
Q

Amphetamine: Withdrawal

Tx

A

Depression, Altered mental status, Drug craving, sleep disturbances, fatigue

Supportive therapy. NO TCA for depression

112
Q

Methamphetamine

A

Brief, intense euphoric effect (rush or flash)

Causes prolonged insomnia and extremely irritable and paranoid state

Long-lasting effects of discontinued use
-depression, fatigue, anergic, cognitive impairments

113
Q

Mehylphenidate

A

ADHD

Low dopamine release, diminished reward in children

DDIs with CYP450: Warfarin, phenytoin, phenobarbital, TCA

ADR: GI discomfort, anorexia, insomnia, fever

Mental Health (6 decks)

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