phar_358_20241002172701 Flashcards

Question

Compare and contrast: BDI vs. BDII - History of depression

Answer 1

BDI: - nil BDII: necessary

Answer 2

Clinican-rated to assess severity of depression

Answer 3

Clinician-rated to assess severity of depression - gold standard for clinical research

Answer 4

Clinician-rated - used in research for screening and assessing severity of mania

Answer 5

Patient-rated. Used to screen for possible BD. Most specific for identifying BDI

Answer 6

1. Delay to diagnosis 2. Misdiagnosis 3. Limited clinical trials

Answer 7

1. Average delay 8-12 years 2. Often patients do not recall hypomanic symptoms 3. More likely to seek help for depression vs. mania

Answer 8

1. Survey found that 73% of BD pts are initially misdiagnosed 2. In 2000 ~30% of pts waiting 10 years for correct dx 3. Most often misdiagnosis = depression - consequences include developing hypo/manic episodes and rapid cycling

Answer 9

1. Heterogenous illness 2. Co-morbidities 3. Manic symptoms --> impaired judgement --> impaired adherence 4. Require longitudinal assessment

Answer 10

1. Eliminate mood episode with complete remission of symptoms, ongoing. "Acute treatment" 2. Prevent recurrences or relapses of mood episodes, ongoing. "Maintenance treatment" 3. Improve quality of life and optimize psychosocial functioning, ongoing 4. Minimize harm to self and others (including prevent suicide, ongoing 5. Maximize adherence and minimize adverse effects of pharmacotherapy, ongoing 6. Identify and minimize risk factors for mood episodes, ongoing 7. Provide care for comorbid psychiatric, substance use or, medical condition, ongoing 8. Provide education to patient and family members, ongoing

Answer 11

1. Response = 1-2 weeks 2. Full clinical benefit = 3-4 weeks

Answer 12

1. Response = 2-4 weeks 2. Full clinical benefit = 6-12 weeks

Answer 13

1. Exercise 2. Adequate sleep 3. Healthy diet 4. Decreased/abstinent substance use 5. Decreased caffeine/nicotine/alcohol

Answer 14

1. Bright light - more for depression 2. Relapse prevention plan 3. Psychoeducation, supportive counselling, biosocial rhythm normalization, psychotherapy (CBT, interpersonal therapy) 4. ECT 5. Collaborative care 6. Case management 7. Medication adherence

Answer 15

1. Lithium 2. Valproic Acid/Divalproex 3. Lamotrigine

Answer 16

1. VPA/Divalproex 2. Lamotrigine 3. Carbamazepine 4. Oxcarbazepine (3 and 4 use is limited by ADEs and drug interactions) 5. Topiramate 6. Gabapentin (5 and 6 rare used as mood stabilizers due to lack of efficacy & poor tolerability)

Answer 17

1. BD - Acute mania treatment - Prophylaxis/maintenance 2. Schizoaffective disorder 3. Unipolar depression - Antidepressant augmentation

Answer 18

1. Interaction with downstream signaling cascades 2. Enhances GABA activity 3. Alters Ca-mediated intracellular functions 4. Decreases CNS adrenergic activity

Answer 19

Can lead to tremors or nausea, can switch to XR if that's the case

Answer 20

False - not bound to plasma proteins

Answer 21

It distributes evenly in the total body water space

Answer 22

12-27 hours (typically call it 24 hours for the sake of calculations)

Answer 23

95% renally It's freely filtered by the glomerulus like Na and K, 80% reabsorbed in the proximal tubules (with sodium)

Answer 24

False - follows linear, dose-proportional PK

Answer 25

1. Hyponatremia 2. Dehydration 3. Renal failure or dysfunction 4. Decreased renal blood flow

Answer 26

1. Acute mania = 1.0-1.2 mmol/L 2. Maintenance therapy = 0.6-1.0 mmol/L 3. Elderly = 0.6-0.8 mmol/L

Answer 27

1. 12 hour post dose level 2. Take is STAT if toxicity or non-adherence is suspected

Answer 28

1. 5-7 days after starting or changing dose, then q weekly until at stabilized dose for 2 weeks, then q monthly for up to 3 months, then at least q 6 months.

Answer 29

Initial is 1-2 times per day then try to go with BID

Answer 30

1. Usually given at night to improve compliance 2. Some trials show decrease in urine volume and decreased renal toxicity with once daily dosing 3. Pts sensitive to peak related side effects may respond to XR formulations 4. When Li changes from multiple daily dosing to once daily dosing, can expect ~10-25% increase in 12h Li level

Answer 31

No. Pts undergoing dialysis should have dose after dialysis

Answer 32

1. Hold dose 2. Repeat plasma level next day 3. Restart therapy when within target range

Answer 33

Because Li PK is linear can do cross multiplication 900mg/0.6mmol/L = Xmg/1.0mmol/L X = 1500mg

Answer 34

1. Pregnancy (contraindicated in 1st trimester anyways) 2. Sodium supplement 3. Hemodialysis 4. Peritoneal dialysis 5. Burns 6. Caffeine

Answer 35

1. Sodium loss 2. NSAIDs 3. Thiazide diuretics 4. ACEis/ARBs

Answer 36

1. Diuretics (e.g., furosemide, chlorthalidone) - Potentially mixed effects 2. NSAIDS - Decrease Li clearance, increasing concentration 3. ACEis 4. Antipsychotics - Risk of additive neurotoxicity 5. Antidepressants - Theoretical risk of serotonin syndrome

Answer 37

1. Increased thirst and urinary frequency (dose-related) 2. Fine tremors to hands/arms (usually symmetric and at high frequency and worse with fine motor activity; dose-related) 3. Headache, sedation, weakness (dose-related) 4. GI upset (nausea, diarrhea) (dose-related) 5. Skin changes (acne, psoriasis) 6. Alopecia 7. Weight gain (avg 4-6 kg in first 2 years)

Answer 38

1. Hypothyroidism 2. Renal injury: interstitial nephritis, renal failure, end stage renal disease 3. Blood dyscrasias (i.e., leukocytosis) 4. Bradycardia or conduction abnormalities 5. Nephrogenic diabetes insipidus - Cannot concentrate urine --> polydipsia, polyuria - Secondary to Li accumulation in collecting tubule - Li interferes with antidiuretic hormone - Volume depletion = Li reabsorption = toxicity

Answer 39

1. Coma with hyper-reflexia 2. Muscle tremor 3. Hyperextension of limbs 4. Pulse irregularities 5. HTN or hypotension 6. ECG changes (T wave depression or inversion) 7. Peripheral circulatory failure 8. Neuroleptic malignant syndrome 9. Epileptic seizures 10. Acute tubular necrosis (renal failure) can occur

Answer 40

1. Decrease 2. Increase 3. Increase 4. Increase 5. Decrease 6. Decrease

Answer 41

1. Drink water, hard candies (should subside) 2. Take with food; can consider ER formulation if doesn't subside 3. Take at bedtime; don't drive 4. Talk to pharmacist or physician for treatment 5. Talk to physician if doesn't subside

Answer 42

1. Seizures - Generalized tonic-clonic (grand mal), partial onset, absence - Has broad-spectrum anti-epileptic activity 2. Bipolar disorder - Acute mania treatment - Maintenance (prophylaxis)

Answer 43

1. Inhibition of voltage-gated Na channels 2. Increasing action of GABA 3. Modulates signal transduction cascades and gene expression 4. May effect neuronal excitation mediated by the NMDA subtype of glutamate receptors 5. Also effects serotonin, dopamine, aspartate, and T-type Ca channels

Answer 44

False, it is bound 85-90% to serum albumin

Answer 45

Hepatically

Answer 46

liver toxicity

Answer 47

12-18 hours

Answer 48

350-700 umol/L

Answer 49

Steady state trough level 3-4 days after initial therapy

Answer 50

1. Hepatic disease - decreased protein binding and clearance. Avoid in hepatic disease b/c unbound conc goes up 2. Renal impairment - no dosage adjustment necessary. 3. Elderly have decreased protein binding and clearance, use lower initial doses

Answer 51

Macrolides - Clarithromycin - Erythromycin - Telithromycin

Answer 52

Carbapenems - Ertapenem - Imipenem - Meropenem

Answer 53

ASA/salicylates

Answer 54

Lamotrigine

Answer 55

GI 1. NVD CNS 1. Tremors 2. Sedation 3. Ataxia 4. Dizziness

Answer 56

1. Increased transaminases and LDH 2. Hepatotoxicity 3. Pancreatitis

Answer 57

1. Weight gain 2. Menstrual disturbances 3. Alopecia

Answer 58

False - it is teratogenic

Answer 59

1. Seizures - Partial seizures (adjunct), absence seizures (monotherapy), generalized tonic-clonic (monotherapy) 2. BD - Acute bipolar depression - Maintenance in BDI or II

Answer 60

1. Alters signal transduction via: - Binding to the open channel conformation of the voltage-gated Na channels - Reducing release of glutamate (which may be a secondary result of blocking Na channels, rather than an independent effect) 2. Weak 5-HT3 receptor inhibitory effects

Answer 61

1. Phenytoin 2. Carbamazepine 3. Oral contraceptives

Answer 62

Slow titration is very very important. Faster titration can lead to SEVERE skin rashes, such as SJS or necrolysis (leading to end organ failure)

Answer 63

1. Sedation 2. Headaches 3. Nausea 4. Dizziness

Answer 64

1. Dyspepsia 2. Dysmenorrhea 3. Anxiety or emotional lability

Answer 65

1. Risk of SJS (if titrated too quickly) 2. Aseptic meningitis 3. Hepatotoxicity

Answer 66

VPA/DVP - can increase lamotrigine level two-fold or more

Answer 67

Self-monitoring for rash. If any signs of skin abnormalities, STOP taking, and seek medical attention. Don't start any new lotions or creams when starting this med.

Answer 68

1. Seizures - Generalized tonic-clonic (grand mal), partial-onset 2. BD - Acute mania treatment - Maintenance 3. Neuropathic pain (off-label) 4. Trigeminal neuralgia

Answer 69

Signal transduction modulation (decrease repetitive action potential firing) and anti-kindling properties - Blocks voltage-dependent Na channels (at a different recpetor/subunit than VPA) - Blocks NMDA glutamate receptor and decreases [Ca2+] - May depress activity in the nucleus ventralis of the thalamus or decrease synaptic transmission

Answer 70

Carbamazepine stimulates the release of ADH and potentiates its action in promoting reabsorption of water

Answer 71

Hepatically via CYP enzymes (CYP3A4)

Answer 72

It is active and has therapeutic and toxic effects. Is hydrolyzed by CYP1A2

Answer 73

It induces its own metabolism via the epoxide-diol pathway (AUTOINDUCTION)

Answer 74

Both are variable due to autoinduction

Answer 75

Trough within 1 hour prior to dose

Answer 76

1. During auto-induction (every 1-2 weeks until on stable regimen) 2. Steady state trough (after 5 weeks)

Answer 77

1. Hepatic disease - not recommended in pts with decompensated liver disease, dose reduction may be needed in pts with stable liver disease 2. Renal impairment - no dosage adjustment necessary 3. Elderly have decreased hepatic clearance, use initial lower doses and smaller dose increases

Answer 78

1. Initiate slowly due to early long half-life in order to minimize side effects 2. Can initiate with any dosage form 3. Best to give in divided doses, usually Q12H or Q8H, instead of a single dose 4. Dosing best at mealtime

Answer 79

Do a drug interaction check. - Co-administration of CYP3A4 inhibitors and inducers increase and decrease CBZ levels respectively with initiation or dose increase - CBZ induces multiple enzyme systems too

Answer 80

1. Macrolides (clarithromycin, erythromycin, telithromycin) 2. Azoles (itraconazole, fluconazole, ketoconazole) 3. CCBs (diltiazem, verapamil)

Answer 81

1. Cimetidine 2. Grapefruit juice 3. Propoxyphene 4. Quinine

Answer 82

Anticoagulants - warfarin and DOACs

Answer 83

1. GI - NV 2. CNS - sedation 3. CV - tachycardia

Answer 84

1. SIADH/hyponatremia 2. Blood dyscrasias: leukopenia, thrombocytopenia, eosinophilia 3. Rash (10% morbilliform) and hypersensitivity reactions.

Answer 85

**1. Concurrent use with clozapine** 2. History of hepatic disease 3. CVD 4. Blood dyscrasias 5. Bone-marrow depression

Answer 86

1. Risperidone 2. Quetiapine 3. Olanzapine 4. Aripiprazole 5. Lurasidone 6. Asenapine

Answer 87

Atypicals - generally have a lower risk of EPS and hyperprolactinemia. Typicals rarely used in BD

Answer 88

BD patients are more likely to show EPS when treated with comparable doses of antipsychotics compared to patients with psychosis (more likely to go into depression)

Answer 89

1. Avoid AD monotherapy without antimanic agent 2. Use with caution in people with history of AD-induced mania, mixed features, or rapid cycling 3. Ds/c during acute manic episode (taper or abrupt discontinuation if severe mania) 4. Consider tapering off once depression symptoms eliminated for 3-4 months

Answer 90

1. Avoid TCAs > Avoid SNRIs (higher risk of switching) 2. Safest in BDII - Bupropion > sertraline, then fluoxetine or other SSRIs > venlafaxine 3. Paroxetine NOT recommended due to level 2 negative evidence in BDII

Answer 91

1. Risk of aggressive behaviour or violence to others 2. Risk of suicide 3. Degree of insight 4. Ability to adhere to treatment 5. Co-morbidities 6. Substance use 7. Physical conditions & lab tests 8. Most appropriate treatment setting (inpatient vs. outpatient)

Answer 92

1. Antidepressants 2. Stimulants (caffeine, amphetamines) 3. Alcohol 4. Nicotine (gradual discontinuation)

Answer 93

1. Prescribed medication 2. Illicit-drug use/abuse (treat if present) 3. Endocrine disorder 4. Neurological disorder

Answer 94

1. Lithium 2. Quetiapine 3. Divalproex 4. Aripiprazole 5. Paliperidone (dose >6mg) 6. Risperidone

Answer 95

1. Quetiapine + Li/DVP 2. Aripiprazole + Li/DVP 3. Risperidone + Li/DVP 4. Asenapine + Li/DVP

Answer 96

Lithium is preferred over DVP for individuals who display classical euphoric grandiose mania (elated mood in the absence of depressive symptoms), few prior episodes of illness, a mania-depression- euthymia course, and/or those with a family history of BD, especially family history of lithium response

Answer 97

DVP is equally effective in those with classical and dysphoric mania. It is recommended for those with multiple prior episodes, predominant irritable or dysphoric mood and/or comorbid substance abuse or those with a history of head trauma

Answer 98

Some therapeutic response is expected within 1-2 weeks after starting a 1st line agent. If no response is observed within 2 weeks with therapeutic doses of antimanic agents, and other contributing factors are excluded, then switch or add-on strategies should be considered

Answer 99

1. Gabapentin 2. Lamotrigine 3. Omega 3 fatty acids 4. Topiramate

Answer 100

1. Severity of depression 2. Risk of suicide/self-harm behaviour 3. Ability to adhere to treatment 4. Psychosocial support network 5. Ability to function 6. Previous treatments 7. Decided appropriate treatment setting: - Hospital - Outpatient

Answer 101

1. Stimulants 2. Nicotine 3. Caffeine 4. Drugs 5. Alcohol

Answer 102

1. Symptoms due to alcohol/drug use, medications, other treatments 2. General medical conditions

Answer 103

1. Quetiapine 2. Lurasidone + Li/DVP 3. Lithium 4. Lamotrigine 5. Lurasidone (monotherapy) 6. Lamotrigine (adjunct)

Answer 104

Antidepressant monotherapy - Available trials do not support their efficacy - Safety concern = mood switching

Answer 105

1. Reverse cognitive impairment 2. Preserve brain plasticity 3. May lead to improved prognosis and minimization of illness progression

Answer 106

Psychoeducation is the only 1st line psychosocial intervention for maintenance therapy that should be offered to all patients

Answer 107

1. Medications effective in acute phase (usually effective in maintenance phase) - Controversial if antidepressants should be continued 2. History (clinical course, response to previous medications, family history) 3. Psychiatric comorbidities 4. Predominant illness polarity 5. Polarity of most recent illness

Answer 108

1. Stimulants 2. Nicotine 3. Caffeine 4. Drugs 5. Alcohol use

Answer 109

1. Symptoms due to alcohol/drug use, other treatments 2. General medical condition

Answer 110

1. Li 2. Quetiapine 3. DVP 4. Lamotrigine 5. Asenapine 6. Quetiapine + Li/DVP 7. Aripiprazole + Li/DVP 8. Aripiprazole 9. Aripiprazole OM

Answer 111

If therapy requires adjustment and no acute mania or depression

Answer 112

1. Discontinue antidepressants 2. Monotherapy --> atypical antipsychotic 3. Combination therapy --> Li/DVP + atypical antipsychotic

Answer 113

Avoid: DVP/VPA, CBZ Small increased risk in 1st trimester: lithium

Answer 114

Lamotrigine

Answer 115

Least studied, but risk appears neutral for quetiapine, risperidone, aripiprazole, olanzapine

Answer 116

Lithium Reduces risk of depressive relapse, serotonin-mediated reduction in impulsivity or aggressive behaviour (e.g., toward triggers) and a non-specific benefit from long-term monitoring provided during therapy with lithium

Answer 117

1. Screening for presence or history of mania 2. Avoiding antidepressant monotherapy 3. Patient education 4. Appropriate dosing 5. Supporting adherence

Answer 118

1. CNS disorders (brain tumor, strokes, head injuries, etc.) 2. Infections (encephalitis, sepsis, HIV, etc.) 3. Electrolyte or metabolic abnormalities (Ca or Na fluctuations) 4. Endocrine or hormonal dysregulation (Addison's disesase, Cushing's, etc.)

Answer 119

1. Alcohol intoxication 2. Drug withdrawal states 3. Antidepressants (MAOIs, TCAs, etc.) 4. DA-augmenting agents (CNS stimulants: amphetamine, cocaine; DA agonists) 5. Marijuana intoxication 6. NE-augmenting agents 7. Steroids (anabolic, cortico, etc.)

Answer 120

1. Bright light therapy 2. Deep brain stimulation 3. Sleep deprivation

Answer 121

A normal emotion under circumstances of threat and is thought to be part of the evolutionary fight or flight reaction of survival.

Answer 122

When it is overwhelming and affecting function and quality of life

Answer 123

1. Psychological - Fear/anxiety, worry, apprehension, difficulty concentrating 2. Somatic (physical) - Increased HR, tremor, sweating, GI upset

Answer 124

Amygdala-centered circuit

Answer 125

Cortico-striato-thalamo-cortical circuit

Answer 126

1. 5HT 2. GABA 3. Glutamate 4. CRF/HPA 5. NE 6. Voltage-gated ion channels

Answer 127

False - despite their names they have no association with GABA, they work on the 𝜶2ẟ subunit of presynaptic N and P/Q voltage-sensitive calcium channel to block release of glutamate when neurotransmission is excessive

Answer 128

Symptoms can be worsened at initial dosing with SNRIs but as β1 receptors downregulate, fear/worry improves long term

Answer 129

1. Gather history 2. Review of systems 3. Rule out anxiety disorders due to general medical conditions or substance use - Review substances used (caffeine, OTC use, herbal medications, recreational substances) 4. Suicidal ideation or intent

Answer 130

1. SSRIs 2. SNRIs 3. TCAs

Answer 131

1. Gabapentin 2. Pregabalin

Answer 132

1. Buspirone 2. Second generation antipsychotics (SGAs)

Answer 133

1. Activating. 2. Risk of seizures, avoid if seizure history, head trauma, bulimia, anorexia, electrolyte disturbances

Answer 134

1. Slow onset, modest efficacy. 2. May be helpful to augment therapy in those with partial response to antidepressants. 3. Avoid if comorbid depression

Answer 135

1. Lower risk for insomnia, agitation, drug interactions compared to other SSRIs. 2. Dose dependent risk of QT prolongation

Answer 136

1. May be useful for comorbid pain. 2. Compared to SSRIs: increased withdrawal symptoms if not tapered, increased insomnia or agitation. 3. Avoid if liver disease or heavy EtOH use.

Answer 137

1. Similar to citalopram, except QT risk is controversial

Answer 138

1. More activating than other SSRIs 2. Self-tapering due to long half-life 3. Drug interactions

Answer 139

1. Withdrawal symptoms if not tapered. 2. Risk for drug interactions due to inhibition of CYP1A2 and CYP2C19

Answer 140

1. Useful for co-morbid insomnia 2. Dose-related anticholinergic effects limit clinical use

Answer 141

1. Anticholinergic; cardiotoxic in overdose 2. Not well tolerated

Answer 142

1. Helpful with comorbid insomnia 2. Lower doses are more sedating 3. May increase appetite and lead to weight gain

Answer 143

1. Compared to other SSRIs, more sedating, less agitation, more constipation, withdrawal symptoms if not tapered. 2. May be associated with greater weight gain. 3. Concern for drug interactions 4. Avoid in pregnancy due to cardiac septal defects

Answer 144

1. Sedation and dizziness are common 2. Weight gain, especially with long-term use

Answer 145

1. Concerns for metabolic ADEs, sedation, EPS

Answer 146

1. Compared to other SSRIs, insomnia, agitation, dizziness

Answer 147

1. Compared to other antidepressants, greater risk for insomnia or agitation as well as increased BP 2. Possible benefit for comorbid pain 3. Few drug interactions 4. Withdrawal symptoms if not tapered 5. Better evidence for psychological symptoms (e.g., ruminative worry of GAD)

Answer 148

Usually in late adolescence or early adulthood - Cases in older adults as well

Answer 149

A combined effect of biological and psychological factors

Answer 150

1. Medications 2. Natural products 3. Medical conditions 4. Medication withdrawal - Alcohol, sedatives, benzos 5. Socioeconomic: poor minority classes 6. Stressful event in susceptible person

Answer 151

1. Antidepressants - bupropion 2. NSAIDs 3. Stimulants 4. Sympathomimetics - pseudoephedrine, phenylepherine

Answer 152

1. Excessive anxiety 2. Worries that are difficult to control 3. Feeling keyed up or on edge 4. Poor concentration 5. Restlessness 6. Irritability 7. Sleep disturbances

Answer 153

1. Fatigue 2. Muscle tension 3. Trembling or shaking 4. Feeling of fullness in throat/chest 5. Sweating 6. Cold, clammy hands

Answer 154

1. 7-item scale 2. Screens for GAD and severity 3. Self-rated 4. Brief (5 mins)

Answer 155

1. 14-item scale 2. Assess severity of anxiety 3. Clinician rated 4. Brief (10-15 mins) 5. Assess response to treatment 6. Need trained rater

Answer 156

1. Decrease severity and duration of anxiety symptoms 2. Improve overall function

Answer 157

1. Remission - With minimal or no anxiety symptoms - No functional impairment - Improve patient QoL

Answer 158

1. Psychotherapy + pharmacotherapy - Psychotherapy is least invasive and safest - Pharm indicated if symptoms severe enough to produce functional disability 2. Treatment plan depends on severity and chronicity of symptoms, age, medication history, and comorbid medical and psychiatric conditions 3. Consider: anticipated ADEs, history of prior response in patient or family member, patient preference, cost

Answer 159

1. Reduce/avoid alcohol, caffeine, nicotine use 2. Avoidance of non-prescription stimulants & medications known to induce anxiety 3. Exercise 4. Psychotherapy +/- counselling (CBT most effective) 5. Relaxation techniques 6. Biofeedback

Answer 160

1.SSRI: - Escitalopram - Paroxetine - Sertraline 2. SNRI: - Duloxetine - Venlafaxine 3. Pregabalin

Answer 161

1. BZD (short-term use) - Alprazolam - Lorazepam - Diazepam 2. Bupropion 3. Buspirone 4. Hydroxyzine

Answer 162

Current data does not provide guidance as to whether it is best to increase to dose, augment, or switch when there has been a partial response to drug therapy

Answer 163

Anticholinergic, sedation

Answer 164

1. 2-4 weeks 2. 12 weeks 3. 12-24 months

Answer 165

1. Bind to the benzodiazepine receptors on the GABA neuron 2. Leads to an increase in the frequency of opening of the chloride channels by increasing binding affinity for the endogenous ligand GABA 3. The shift in chloride ions results in hyperpolarization (a less excitable state) and stabilization

Answer 166

Provides rapid initial relief of anxiety symptoms, but effects may not be significantly different from placebo after 4-6 weeks of treatment

Answer 167

1. Bromazepam 2. Alprazolam 3. Lorazepam 4. Diazepam

Answer 168

False? So, there are no RCTs evaluating its use in GAD, but it is used extensively in clinical practice.

Answer 169

1. Alprazolam 2. Lorazepam 3. Bromazepam (maybe, t1/2 is 8-30h which is a huge variation)

Answer 170

1. Clonazepam 2. Diazepam

Answer 171

1. 1-2h 2. 1-2h 3. 20-60 min 4. 30-60 min 5. 30-60 min

Answer 172

1. Ataxia 2. Dizziness/lightheadedness 3. Sedation and residual daytime sleepiness 4. Psychomotor impairment 5. Agitation, irritability, confusion

Answer 173

1. Anterograde amnesia 2. Depression 3. Confusion 4. Bizarre behaviour 5. Hallucination 6. Respiratory depression

Answer 174

1. Psychological and physical dependence may develop with long-term use 2. Risk of dependence increases with higher dose and/or longer use 3. Risk further increased with history of AUD or other SUD or personality disorders 4. Withdrawal symptoms can occur following discontinuation of therapy with as little as one week of use

Answer 175

Lorazepam, oxazepam, temazepam Preferred in elderly and liver dysfunction due to no active metabolites

Answer 176

Pro: - Good choice for tapering as less risk of withdrawal (i.e., diazepam, clonazepam) Con: - More daytime sedation

Answer 177

Pro: - Better hypnotic and sedative properties Cons: - More rebound anxiety - Inter-dose withdrawal - Anterograde amnesia

Answer 178

1. Sweating 2. Tremor 3. Nausea 4. Vomiting 5. Rebound anxiety 6. Increased heart rate 7. Insomnia 8. Agitation 9. Twitching 10. Visual/tactile hallucinations 11. SEIZURES (onset within 1-2 days after BZD stopped)

Answer 179

Diazepam Decrease dose by 10-20% q1-2 weeks

Answer 180

1. SUD (concurrent use with opioids may cause profound respiratory depression, coma, or death) 2. Sleep apnea 3. COPD 4. Elderly 5. CNS depression 6. Pregnancy (floppy infant syndrome; possible teratogen) 7. Clozapine-use

Answer 181

alcohol, opioids, barbiturates

Answer 182

Flumazenil

Answer 183

Reverses hypnotic-sedative effect of BZD but clinically use is limited due to risk of causing seizures in BZD dependent patients

Answer 184

Recurrent unexpected panic attacks with at least 1 of the attacks being followed by a month or longer of at least 1 of the following: - Constant concern about having another attack - Being anxious about the implications of the attack or its consequences (e.g., losing control, having a heart attack) - Maladaptive change in behaviour designed to avoid having panic attacks

Answer 185

1. Tempermental (i.e., learned behaviours) 2. Personality types 3. Environmental 4. Genetic and physiological 5. Medications

Answer 186

1. Other anxiety disorders 2. Depression 3. Bipolar disorder 4. AUD 5. Higher rates of suicide atempts and suicidal ideation 6. Medical comorbidities

Answer 187

1. Depersonalization 2. Derealization 3. Fear of losing control 4. Fear of going crazy 5. Fear of dying

Answer 188

1. Abdominal distress 2. Chest pain 3. Chills 4. Dizziness 5. Feeling of choking 6. Hot flashes 7. Palpitations 8. Nausea 9. Paresthesias 10. Shortness of breath 11. Sweating 12. Tachycardia 13. Trembling or shaking

Answer 189

1. Panic attacks vary in frequency and intensity 2. 1/3 of pts achieve remission 3. 1/5 of pts have unremitting & chronic course 4. Most pts require long-term treatment to achieve remission, prevent relapse, and reduce risks associated with co-morbidity

Answer 190

1. Long duration of illness 2. Comorbidity with personality, mood, other anxiety disorders 3. Excessive sensitivity to physical symptoms of anxiety

Answer 191

1. Panic Disorder Severity Scale (PDSS) 2. Panic and Agoraphobia Scale (PAS)

Answer 192

CBT. Types: - Applied relaxation - Exposure through imagery - Panic managment - Breathing retraining - Cognitive restructuring

Answer 193

1. Effectiveness comparable to pharmacotherapy 2. Limited by lack of availability of trained professionals 3. Studies indicate 8-15 sessions needed

Answer 194

SSRIs: 1. Citalopram 2. Escitalopram 3. Fluoxetine 4. Fluvoxamine 5. Paroxetine 6. Sertraline SNRIs: 1. Duloxetine 2. Venlafaxine

Answer 195

TCAs: 1. Clomipramine 2. Imipramine BZDs: 1. Alprazolam 2. Clonazepam

Answer 196

MAOI: Phenelzine

Answer 197

False - they are not, because the onset of BZDs will typically occur after the panic attack

Answer 198

1. Most pts with PD are hypersensitive to medication ADEs at initation and this can lead to activation (early worsening of anxiety, agitation, irritability) 2. Reduction of panic attack frequency, anticipatory anxiety, and avoidance may start within first 3-4 weeks 3. For pts with significant avoidance, full remission may take up to 6 months or longer

Answer 199

Onset within hours for autonomic symptoms of anxiety, full benefit may take 4-6 weeks

Answer 200

1. 1-3 months (alter treatment if no response after 6-8 weeks) 2. 12 months 3. 4-6 months (taper slowly to reduce risk of relapse)

Answer 201

1. Older adults may show concern about disability due to declining sensory functioning (sensory, hearing) or embarrassment about one's appearance (e.g., tremor from Parkinson's disease) or functioning due to medical conditions (e.g., urinary incontinence) 2. Associated with increased rates of school dropouts; and decreased well-being, employment, workplace productivity, SES, and QoL 3. Associated with being single, unmarried, divorced and not having children 4. Only ~50% of pts with SAD seek treatment and usually only after 15-20 years of symptoms 5. Unemployment is a strong predictor of persistence of SAD

Answer 202

1. Tempermental 2. Environmental 3. Genetic and physiological

Answer 203

1. Females report greater number of social fears and comorbid depressive, bipolar, and anxiety disorders 2. Males are more likely to fear dating, have oppositional defiant disorder or conduct disorder, and use alcohol or recreational drugs to relieve symptoms of disorder 3. Chronic social isolation may lead to MDD 4. Comorbid MDD higher in older adults 5. Substances may be used to self-medicate for social fears but symptoms of intoxication or withdrawal may be a source of further social fear 6. 70-80% have history of concurrent anxiety, depression, and SUD

Answer 204

1. Fears 2. Feared situations 3. Physical symptoms 4. Types

Answer 205

1. Scrutinized by others 2. Embarrassment 3. Humiliation

Answer 206

1. Public speaking 2. Eating or drinking in front of others 3. Interacting with authority figures 4. Talking with strangers 5. Use of public washrooms

Answer 207

1. Blushing 2. "Butterflies in stomach" 3. Diarrhea 4. Sweating 5. Tachycardia 6. Trembling

Answer 208

1. Generalized: fear and avoidance of a wide range of social situations 2. Nongeneralized: fear is limited to one or two situations

Answer 209

1. Liebowitz Social Anxiety Scale 2. Social Phobia Inventory (SPIN)

Answer 210

1. CBT - education, exposure, cognitive restructuring - Treatment for at least 12 weeks - Individual treatment more effective than group therapy - Similar efficacy to pharmacotherapy for acute treatment - Effects may last for 6-12+ months 2. Social Skills Training

Answer 211

1. CBT 2. SSRIs - Escitalopram - Fluoxetine - Fluvoxamine - Paroxetine - Sertraline 3. SNRIs - Venlafaxine 4. Pregabalin

Answer 212

Beta-blockers, such as atenolol and propranolol

Answer 213

1. 6-8 weeks 2. 1+ years (continue for 1 year or longer after response attained) 3. 3-4 months

Answer 214

Women 2x more than men

Answer 215

Insufficient glucocorticoid signaling at the time of trauma results in unopposed sympathetic nervous system activation that enhances the consolidation of the traumatic memory

Answer 216

1. Re-experiencing the event with distressing recollections, dreams, flashbacks, psychological, and physical distress 2. Persistent avoidance of stimuli that might invite memories or experiences of the trauma 3. Increased arousal

Answer 217

1. MDD 2. SUD and AUD 3. Anxiety disorders (GAD) 4. Personality dysfunction 5. Bipolar 6. Psychosis

Answer 218

1. CVD 2. Respiratory disorders 3. Autoimmune disorders

Answer 219

False - obviously there are

Answer 220

1. Cognitive Processing Therapy 2. Prolonged Exposure Therapy 3. Eye Movement Desensitization & Reprocessing

Answer 221

1. 30-50% of pts have residual symptoms 2. High drop out rates 3. Resources

Answer 222

1. Symptom reduction 2. Improve sleep, QoL, participation in non-pharm treatment 3. Minimize ADEs and comorbidities

Answer 223

SSRIs: 1. Fluoxetine 2. Paroxetine 3. Sertraline SNRIs: 1. Venlafaxine Prazosin (for trauma related nightmares and to improve sleep)

Answer 224

Benzos such as alprazolam and clonazepam

Answer 225

1. 2-8 weeks 2. 12 weeks+ 3. 12-24 months

Answer 226

Females affected slightly more than males

Answer 227

1. Serotonin neurotransmission 2. Dopamine transmission (especially in cases with co-morbid tics and Tourette's) 3. Glutamate

Answer 228

1. PANDAS (Pediatric Autoimmune Neuropsychiatric Disorder Associated with Streptococcal Infections) 2. Pregnancy 3. Tempermental 4. Environmental 5. Genetics

Answer 229

1. Males more likely to have comorbidities 2. Suicidal thoughts occur at some point in ~50% of patients with OCD, suicide attempts are reported in 25% of patients with OCD 3. MDD and bipolar 4. Anxiety disorder 5. Tic disorder 6. A triad of OCD, tic disorder, and attention-deficit/hyperactivity disorder can also be seen in children 7. Body dysmorphic disorder, trichotillomania, excoriation occuring more likely in pts with OCD than other disorders

Answer 230

1. Good social and occupational adjustment 2. Presence of precipitating event 3. Episodic nature of the symptoms

Answer 231

1. Acting on compulsions 2. Childhood onset 3. Bizarre compulsions 4. Need for hospitalization 5. Comorbid depression 6. Comorbid personality disorder 7. Delusional beliefs

Answer 232

1. Fear of contamination 2. Unwanted sexual or aggressive thoughts 3. Doubts (e.g., left door unlocked) 4. Concerns about throwing away something valuable 5. Need for symmetry

Answer 233

1. Washing, cleaning 2. Checking, praying, "undoing actions," asking for reassurance 3. Repeated checking behaviours 4. Hoarding 5. Ordering, arranging, balancing, straightening until "just right"

Answer 234

Yale-Brown Obsessive Compulsive Scale (Y-BOCS) - Clinician-rated

Answer 235

1. CBT - Found to be as effective as pharmacotherapy - Stronger effects on compulsions vs. obsessions 2. Deep Brain Stimulation (DBS) - Surgically implanted device 3. Radio Frequency Wave Surgery - Destroy small amount of brain tissue in the corticostriatal circuit

Answer 236

SSRIs: 1. Escitalopram 2. Fluoxetine 3. Fluvoxamine 4. Paroxetine 5. Sertraline SNRI: 1. Venlafaxine Adjunct: 1. Aripiprazole 2. Risperidone

Answer 237

Clomipramine

Answer 238

Monitor weekly x 4 weeks then biweekly. Once stable, monitor q1-2 months

Answer 239

1. 2-4 weeks 2. 10-12 weeks 3. 1-2 years

Answer 240

1. Chlorpromazine 2. Flupent(h)ixol 3. Fluphenazine 4. Haloperidol 5. Loxapine 6. Methotrimeprazine 7. Perphenazine 8. Pimozide 9. Trifluoperazine 10. Zuclopenthixol

Answer 241

1. Asenapine 2. Clozapine 3. Lurasidone 4. Olanzapine 5. Paliperidone 6. Quetiapine 7. Risperidone 8. Ziprasidone

Answer 242

1. Aripiprazole 2. Brexpiprazole 3. Cariprazine

Answer 243

A complex syndrome of disorganized bizarre thoughts, hallucinations, delusions, inappropriate affect, and impaired social functioning

Answer 244

Presence of gross impairment of reality testing (e.g., lose touch with reality) as evidenced by delusions, hallucinations, markedly incoherent speech, or disorganized and agitated behaviour without apparent awareness on the part of the patient of the incomprehensibility of their behaviour

Answer 245

Hallucinations or delusions development during or within 1 month of substance use/withdrawal

Answer 246

1. Immigrant ethnic groups 2. Perinatal/early childhood (hypoxia, maternal infection/stress/malnutrition) 3. Urban upbringing 4. Cannabis use 5. Life stress

Answer 247

1. Decreased access to care, poor diet 2. Decreased exercise 3. Increased obesity/diabetes 4. Increased smoking 60-90% 5. SUD 6. Increased CVD - doubles in first year 7. Suicide

Answer 248

1. Decreased motivational drive from AP 2. Adverse effects 3. Poor insight into illness 4. Personal attitudes towards treatment 5. Stigma 6. Financial constraints 7. Homelessness 8. Substance use 9. Lack of support 10. Ethnic minority 11. Weak therapeutic alliance

Answer 249

1. Dopamine dysregulation is the key theory underlying the pathophysiology of the disease 2. Serotonin dysregulation also contributes - Modulates dopamine 3. Glutamate and GABA also have a role - Less clearly understood

Answer 250

1. Nigrostriatal 2. Mesolimbic 3. Mesocortical 4. Tuberoinfundibular

Answer 251

1. Motor coordination 2. Posture control

Answer 252

Movement disorders (EPS)

Answer 253

1. Pleasure 2. Reward 3. Desire 4. Response to stimuli 5. Motivational behaviour

Answer 254

Mesolimbic

Answer 255

Relief of psychosis (positive symptoms)

Answer 256

1. Cognition 2. Motivation 3. Communication 4. Social function 5. Emotional response 6. Problem solving

Answer 257

Mesocortical

Answer 258

1. Akathisia? 2. Treatment of negative symptoms and depression? (possibly through 5HT2A blockade)

Answer 259

Regulates prolactin release

Answer 260

1. Hyperprolactinemia 2. Gynecomastia 3. Galactorrhea 4. Amenorrhea 5. Hirsutism 6. Weight gain 7. Osteoporosis 8. Sexual dysfunction 9. ED

Answer 261

1. Often recognized retrospectively after the diagnosis has been made 2. Reclusive adolescence without close friends (e.g., not involved in school actitivies or teams) 3. Not functioning well in occupational, social, and personal activities 4. Markedly peculiar behaviour, abnormal affects, unusual speech, bizarre ideas and strange 5. Perceptual experiences: - Preoccupation w/ religion; magical thinking; excessive writing without meaning; sensitivity and irritability when touched by others; unusual sensitivity to stimuli

Answer 262

Positive = added experiences Negative = loss of experiences (sense of emotion seems to be blunted)

Answer 263

1. Hallucinations (most commonly auditory or visual) 2. Suspiciousness/paranoia 3. Delusions 4. Disturbed thought content 5. Bizarre or disorganized behaviour (involuntary movements, mannerisms, catatonia) 6. Thought disorder (e.g., tangential speech; thought blocking)

Answer 264

1. Apathy 2. Social indifference 3. Loss of emotional connectedness 4. Loss of motivation (avolition) 5. Alogia (poverty of speech) 6. Flat affect 7. Poor self care 8. Psychomotor retardation

Answer 265

1. Memory impairment 2. Poor concentration 3. Impaired executive function: planning, problem solving

Answer 266

1. Dysphoria 2. Depression 3. Excitement 4. Mania

Answer 267

1. Fixed beliefs that are not amenable to change in light of conflicting evidence 2. Common themes: - Persecutory - Referential - Somatic - Religious - Grandiose

Answer 268

1. Perception-like experiences that occur without an external stimuli 2. Vivid and clear with the full force and impact of normal perceptions and not under voluntary control 3. May occur in any sensory modality but auditory are most common in schizo

Answer 269

1. Usually inferred from the individual's speech 2. Loose associations

Answer 270

1. May manifest in a variety of ways, ranging from a childlike "silliness" to unpredictable agitation 2. Problems may be noted in any form of goal-directed behaviour, leading to difficulties in performing activities of daily living

Answer 271

1. Marked decrease in reactivity to the environment 2. Ranges from resistance to instructions (negativism); to maintain a rigid, inappropriate or bizarre posture; to a complete lack of verbal and motor responses (mutism and stupor) 3. Can also include purposeless and excessive motor activity without obvious cause (catatonic excitement) 4. Other features are repeated stereotyped movements, staring, grimacing, mutism, and the echoing of speech

Answer 272

Poverty of speech; e.g., talks little, uses few words

Answer 273

Reduced range of emotions (perception, experience and expression); e.g., feels numb or empty inside, recalls few emotional experiences, good or bad

Answer 274

Reduced social drive and interaction; e.g., little sexual interest, few friends, little interest in spending time with (or little time spent with) friends

Answer 275

Reduced ability to experience pleasure; e.g., finds previous hobbies or interests unpleasurable

Answer 276

Reduced desire, motivation, persistence; e.g., reduced ability to undertake and complete everyday tasks; may have poor personal hygiene

Answer 277

1. Substance use 2. Smoking (big craving for cigarette) 3. Suicidality (leading cause of premature death in pts with schizo)

Answer 278

1. Clinical psychiatric history 2. Mental status exam 3. Family/social history 4. Medical history 5. Physical exam

Answer 279

1. CBC, serum electrolytes, glucose, BUN, SCr, Ca, Mg, P, LFTs, TSH 2. Screen for syphilis, Hep C, HIV (high risk pts) 3. ECG 4. Urinalysis and urine toxicology screen 5. Blood levels of medications 6. If appropriate: - CXR - CT scan/MRI of head - Lumbar puncture - Sleep deprived EEG

Answer 280

1. Amphetamine & cocaine use & withdrawal 2. Bupropion 3. Caffeine 4. Cannabis 5. Chloroquine 6. Efavirenz 7. Ketamine 8. Steroids

Answer 281

PANSS (Positive and Negative Syndrome Scale)

Answer 282

1. Prevent harm to pt and to others (esp in acutely agitated state) 2. Improve pt functioning 3. Decrease the intensity and duration of active psychotic symptoms 4. Optimize medications/treatments to obtain clinical response 5. Minimize adverse effects to therapy 6. Prevention of relapse 7. Promote adherence 8. Patient/family education

Answer 283

1. Exercise, healthy diet, adequate sleep 2. Decrease substance use 3. Decrease caffeine/nicotine/alcohol 4. Support service interventions to increase medication adherence, individualize based on pts' needs 5. Establish trusting therapeutic relationship; include patients in treatment decisions (shared decision making) when possible 6. Community-case management (multidisciplinary team), vocational and occupational rehab techniques, CBT

Answer 284

1. D2 2. 5HT2A 3. Muscarinic 4. 𝜶1 5. H1

Answer 285

1. D2 receptor antagonism 2. "Dirty pharmacology" - mixed receptor affinity at alpha, muscarinic, histamine receptors

Answer 286

1. D2 receptor antagonism 2. 5HT2A/2C antagonism 3. "Dirty pharmacology" - mixed receptor affinity at alpha, muscarinic, histamine receptors

Answer 287

1. D2 receptor partial agonism 2. 5HT2A antagonism 3. 5HT1A&2C partial agonism

Answer 288

Movement adverse effects

Answer 289

Metabolic adverse effects

Answer 290

1. Antipsychotic effect 2. Improve positive symptoms

Answer 291

1. EPS* 2. Parkinsonism* 3. Akathisia 4. Dystonic reactions 5. Tardive dyskinesia 6. Elevated prolactin: gyno, amenorrhea, impotence, osteoporosis* 7. Sexual dysfunction 8. Worsening of negative symptoms*

Answer 292

Antipsychotic effect - Theoretically improve negative symptoms through increased dopamine release in mesocortical pathway

Answer 293

Anxiolytic

Answer 294

1. Hypotension 2. Sedation 3. Sexual dysfunction

Answer 295

Mesolimbic

Answer 296

Mesocortical

Answer 297

1. Postural hypotension 2. Dizziness 3. Reflex tachycardia 4. Sedation* 5. Incontinence 6. Drooling

Answer 298

Sexual dysfunction

Answer 299

1. Dry mouth 2. Blurred vision 3. Constipation 4. Urinary retention 5. Confusion/memory disturbances

Answer 300

1. Sedation 2. Drowsiness 3. Postural hypotension 4. Weight gain

Answer 301

Pro: - Weaker anticholinergic effects Con: - Higher risk of movement disorders

Answer 302

1. Haloperidol 2. Fluphenazine 3. Perphenazine 4. Flupenthixol

Answer 303

Pro: - Lower risk of movement disorders Cons: - Stronger anticholinergic effects - Highly sedating

Answer 304

1. Chlorpromazine 2. Methotrimeprazine

Answer 305

1. Developed based on different receptor activity (esp. 5HT2A/2C) in addition to D2 blockade 2. Decreased risk of movement disorders but increased metabolic ADEs

Answer 306

1. High affinity for D2, 5HT2, and alpha-adrenergic receptors 2. Lower affinity to alpha-2 and H1 receptors 3. NO affinity for muscarinic receptors (no anticholinergic side effects)

Answer 307

1. Headache 2. Sedation 3. Weight gain (although risk vs. other SGAs) 4. Orthostatic hypotension 5. Rhinitis 6. Anxiety 7. Increased prolactin/sexual dysfunction (more vs. other SGAs)** 8. EPS (more vs. SGAs; less vs. haloperidol)** 9. Possible risk of QT prolongation

Answer 308

risperidone

Answer 309

1. Headache 2. Orthostatic hypotension (less vs. risperidone) 3. EPS 4. Insomnia (more vs. risperidone) or somnolence 5. Weight gain (less vs. risperidone) 6. Increased prolactin/sexual dysfunction (similar to risperidone)** 7. Anxiety 8. Rhinitis 9. Possible risk of QT prolongation

Answer 310

metabolic ADEs

Answer 311

1. WEIGHT GAIN (>10lbs or ≥7% of baseline weight)** 2. Dizziness 3. Sedation 4. Anticholinergic effects 5. Increased liver enzymes 6. Orthostatic hypotension 7. Increased risk of T2DM, dyslipidemia (more vs. others) 8. EPS (especially akathisia); dose-dependent 9. Possible risk of QT prolongation

Answer 312

1. Smoking! (CYP1A2) 2. Pharmacodynamic interactions with drugs of similar actions, 1A2 inhibitors/inducers

Answer 313

1. Insomnia (histamine blocking med, causes sedation) 2. Bipolar 3. Depression 4. Anxiety

Answer 314

1. Headache, dizziness 2. Sedation/somnolence 3. Orthostatic hypotension 4. Conditional risk of QT prolongation 5. Weight gain 6. Increased liver enzymes 7. Increased risk of T2DM and dyslipidemia** 8. May reduce thyroid hormone levels

Answer 315

Meals with ≥500kcal to maximize absorption and therapeutic effect (a good amount of food needed when taking this med)

Answer 316

1. Considered to be weight neutral** 2. Less hyperglycemia/hyperlipidemia vs. other SGA 3. EPS 4. Dizziness 5. Sedation or insomnia 6. Dyspepsia, nausea, constipation 7. Orthostatic hypotension 8. Conditional risk of QT prolongation**

Answer 317

Contraindicated in patients with: 1. QT prolongation 2. Recent MI 3. Uncompensated HF 4. Concurrent QT prolonging drugs

Answer 318

1. Headache, dizziness 2. Drowsiness or insomnia 3. EPS 4. Akathisia (restless, agitation) 5. Suicidal ideation 6. Mouth numbness x 1 hr post dose (oral hypoesthesia)** 7. Orthostatic hypotension 8. Minimal effect on weight, glucose, lipids 9. Increased prolactin 10. Possible risk for QT prolongation

Answer 319

1. Lurasidone 2. Asenapine 3. Ziprasidone

Answer 320

1. Metabolic and movement ADEs 2. High rates of akathisia (aripiprazole > brexpiprazole)

Answer 321

1. Acts as a partial agonist at the 5HT1A and D2 and antagonist at 5HT2A (+ additional receptor effects) 2. Referred to as a "dopamine system stabilizer" - "Goldilocks Principle" - In high levels of dopamine production (positive symptoms) it acts as an antagonist - In low levels of dopamine production (negative symptoms) it acts as an agonist

Answer 322

False - it is long (75h), thus do not increase dose faster than q2weeks

Answer 323

1. Headache 2. GI complaints (e.g., nausea) 3. Insomnia or sedation (more often activating vs. sedating) 4. Akathisia (less so with brexpiprazole)*** 5. Some anxiety 6. Minimal weight gain 7. EPS 8. Orthostatic hypotension 9. Suicidal behaviour 10. Possible risk of QT prolongation

Answer 324

1. High affinity partial agonist at D3 + D2 receptors 2. At low doses --> higher affinity for D3 than D2 3. Lower affinity for D2 than aripiprazole and brexpiprazole 4. High affinity partial agonist at 5HT1A 5. Antagonist at 5HT2A, 5HT2B

Answer 325

1. D3 antagonist --> block activity of somatodendritic D3 receptors 2. D3 partial agonist --> antagonist at high levels of DA, agonist at low levels of DA 3. Prefrontal cortex --> theoretically may improve negative symptoms and cognitive impairment

Answer 326

1. Mood 2. Cognition 3. Addictive behaviours 4. Reward behaviours (in animal models)

Answer 327

implications in improving negative symptoms of schizo

Answer 328

1. May be effective for the treatment of acute exacerbations and prevention of relapse after acute exacerbations - More direct comparative evidence needed 2. May have implications for negative symptoms of schizo due to D3 partial agonism 3. Safety? - Limited by short duration of trials - Long-term withdrawal design trial included enriched population

Answer 329

Each AP has many complex pharmacologic actions, only some of which are shared with other APs

Answer 330

1. FGA appear to have comparable efficacy to SGA - except for clozapine 2. Individual studies have shown higher discontinuation rates due to both adverse effects and lack of treatment effect with FGA 3. Major issue with FGA is significant EPS - particularly in younger pts 4. Pts with early psychosis have been shown to be more at risk for EPS and develop it at lower doses than those with a long history of psychosis/AP treatment 5. Conflicting evidence for whether risk of relapse is higher with FGA compared to SGA 6. Due to the significant increased risk of EPS with FGA, SGA are the preferred agents for the treatment of pts with early psychosis**

Answer 331

Tailor the AP most appropriate to the pt based on symptomatology, ADEs, DIs, cost, and convenience

Answer 332

1. First episode psychosis destroys 10-12cc of brain tissue 2. Each subsequent psychotic episode will destroy more brain tissue --> clinical deterioration, treatment resistance, functional disability 3. Think of the approach to treatment of schizophrenia after the first episode of psychosis as just as critical as secondary prevention after a myocardial infarction

Answer 333

1. If oral medications are effective and tolerated, may continue with oral therapy or switch to long-acting injectable depot to improve adherence (given q2-4 weeks) 2. May be considered if a patient relapses due to non-adherence or if patient prefers injection

Answer 334

1. Decrease risk of relapse 2. Decrease hospitalization 3. Decrease patient/caregiver burden 4. Increase interactions with healthcare team/rapport 5. Increase adherence

Answer 335

1. Aripiprazole 2. Paliperidone

Answer 336

1. Earlier treatment of symptoms 2. Need for greater attention to the physical care of people with schizophrenia due to the reduced lifespan 3. Greater emphasis on recovery and the need to provide personalized care rather than focusing primarily on symptomatic management

Answer 337

1. Early detection & treatment can decrease depression, increase mood/cognitive scores, and increase overall function at 10 years 2. First 2-5 years of illness are critical to offset future disability and improve outcomes; longer duration of untreated psychosis results in decreased response to treatment

Answer 338

1. No particular AP or class found to be clinically superior in 1st episode population 2. Usually SGA (compared to FGA: decreased AE, decreased discontinuation, & equal efficacy) 3. Choose agent based on AE profile & use lowest effective dose 4. Using a long-acting antipsychotic injection may decrease relapse vs oral therapy

Answer 339

1. Controversial; minimum 18 months 2. Indefinite therapy reasonable

Answer 340

4-6 weeks @ optimally tolerated dose

Answer 341

1. First, screen for nonadherence, substance use, drug interactions, - Neither constitute AP treatment failure 2. Second, increase or change AP, trial x 6-8 weeks to determine effect

Answer 342

1. Symptoms fluctuate over lifetime; target therapy to symptoms 2. Non-psychotic symptoms such as mood changes may also be present and necessitate treatment with non-AP medications 3. Maintenance treatment contributes to relapse prevention and decrease hospitalization rates but does not eliminate risk of relapse 4. Risk of re-hospitalization or death increased when the duration of AP treatment prior to discontinuation gets longer; may relate to AP-induced neurologic changes

Answer 343

1. Psychosis persists with abstinence 2. Symptoms do not align with type/amount of substance used 3. Family hx of psychosis; 4. Typical positive symptoms of schizophrenia - e.g. auditory hallucinations 5. Presence of negative/cognitive symptoms

Answer 344

No evidence of benefit for one AP over another for psychosis and SUD Clozapine preferred limited data

Answer 345

1. Stigma is common 2. Patients often conceal one or both conditions 3. Patients often fear being imprisoned, being forced to take psychiatric meds, or having children taken away 4. Create a confidential and private setting for discussions; 5. Preserve continuity of care 6. Provide user-friendly resources

Answer 346

≥2 positive symptoms of moderate severity or 1 positive symptom of severe severity, after ≥2 adequate AP trials

Answer 347

1. Orally for minimum 6 wks at ≥ midpoint of licensed dose range 2. Long-acting injection: at least 6 weeks at steady state

Answer 348

1. Confirm adherence 2. Screen for substance use 3. Review for drug interactions 4. Assess dose

Answer 349

1. Clozapine; response rate of 30-60% but often underprescribed due to fear of ADE, lack of familiarity 2. Delaying clozapine initiation may decrease response

Answer 350

1. Noradrenergic 2. Serotonergic 3. Mesolimbic subtypes 4. Dopamine subtypes (D1, D2, D4)

Answer 351

1. D4 2. 5HT2A 3. 𝜶1 4. M1

Answer 352

1. Tardive dyskinesia (mixed evidence) 2. BD 3. Schizoaffective disorder 4. Psychosis in pts with Parkinsons disease

Answer 353

1. Constipation 2. Blurred vision 3. Dizziness 4. Drooling** 5. Weight gain 6. Increased cholesterol and/or blood sugar 7. Tachycardia and orthostatic hypotension

Answer 354

1. Agranulocytosis* 2. Myocarditis* 3. Cardiomyopathy 4. Constipation* 5. Seizures 6. Neuroleptic Malignant Syndrome

Answer 355

Clozapine-induced agranulocytosis - To detect potentially reversible agranulocytosis - Requires monitoring of CBC with differential

Answer 356

months to years

Answer 357

1. Orthostatic blood pressure changes 2. Fatigue and decreased exercise tolerance 3. Chest pain/discomfort/pressure 4. Palpitations with increased heart rate 5. Shortness of breath 6. Peripheral edema 7. Fever

Answer 358

1. High sensitivity troponin T 2. CRP

Answer 359

If hematological monitoring (CBC with diff - neutrophils) can be guaranteed AND patient is actively registered with a clozapine registry (has a clozapine pin #)

Answer 360

1. AA-Clozapine (SHA pref) 2. GEN-Clozapine 3. CLOZARIL

Answer 361

1. Registration (of pt, physician, testing lab, pharmacy) 2. Maintenance (of national database that monitors blood work) 3. Identification (of status of all approved suppliers of clozapine)

Answer 362

1. Weekly blood tests for the first 6 months - High risk period 2. Change to once every 2 weeks if "green light" has been maintained during the first 6 months of therapy and patient is clinically stable 3. Change to once every 4 weeks if "green light" for another 6 months 4. Monitoring MUST continue for as long as the pt is on clozapine and even for 4 weeks after stopping

Answer 363

1. Monitoring freq does not have to be modified if therapy is interrupted for 3 days or less but dosing needs to be re-titrated if miss >48 hours 2. Hematological testing should be resumed weekly for an additional 6 weeks if therapy is disrupted for more than 3 days (Important to assess adherence)

Answer 364

≥2.0 x 10^9/L

Answer 365

1.5 x 10^9/L < ANC < 2.0 x 10^9/L

Answer 366

First red zone --> ANC < 1.5 x 10^9/L Consider protective isolation when: ANC < 0.5 x 10^9/L

Answer 367

1. Must stop and cannot ever restart therapy if total WBC <2.0 x 10^9 or ANC <1.5 x 10^9 from clozapine therapy 2. Must be communicated with clozapine registry 3. Will require weekly CBC x 4 weeks when stopped - Likely would be done more frequently than weekly when pt is neutropenic (pt would be hospitalized)

Answer 368

False - quantity of clozapine dispensed must be limited to the frequency of clozapine blood work

Answer 369

Because once daily dosing is very sedating

Answer 370

Smoking (chemicals from the tar specifically) induces CYP1A2 which reduces clozapine levels up to 40%, reducing its effects

Answer 371

Reduces the risk of suicide in pts with schizophrenia or schizoaffective disorder

Answer 372

No consistent evidence to support use of high dose AP, switching APs, or AP polypharmacy

Answer 373

Hypothesized pathways among basal ganglia and other structures of the CNS

Answer 374

1. Occur very suddenly (potentially after 1st dose) 2. Tends to be early, but can extend out to any time 3. Most likely in 3-6 weeks then heavy drop off 4. Mostly 6 weeks onward 5. Starts 3 months later for the most part

Answer 375

1. Within 30 days 2. After months or years of treatment, esp if develops after drug dose is decreased or discontinued

Answer 376

Respond to antiparkinsonian drugs (except akathisia which may be mediated by alternate mechanism and thus responds to other treatments)

Answer 377

1. Valbenzaine and deutetrabenazine are FDA only - No other meds or strats have proven efficacy in clinical trials 2. PREVENTION IS KEY

Answer 378

1. Torsions and spasms of muscle groups 2. Mostly affects muscles of the head and neck 3. Examples: oculogyric crisis, trismus, laryngospasm, torti/retro/antero-collis, tortiplevis, blepharospasm

Answer 379

1. Anxiety 2. Fear 3. Panic 4. Dysphoria 5. Repetitive meaningless thoughts

Answer 380

1. Acute (usually within 24-48 hours of the first dose) 2. 90% occur within 1st week of treatment

Answer 381

1. Young males, antipsychotic naive, high potency FGA 2. Rapid dose increase 3. Prior dystonic reaction 4. Hypocalcemia, hyperthyroidism 5. Dehydration 6. Recent cocaine use

Answer 382

1. Acute, painful, spasmodic 2. Oculogyria may be recurrent 3. Acute laryngeal/pharyngeal dystonia may be life-threatening

Answer 383

1. 1st line = IM benzotropine 2. IM diphenhydramine 3. Sublingual lorazepam

Answer 384

1. EPS Rating Scale (ESRS) 2. Simpson Angus EPS Scale (SAS)

Answer 385

Ants in the pants type of restlessness

Answer 386

1. Motor restlessness 2. Fidgeting 3. Pacing 4. Rocking 5. Swinging of legs, 6. Trunk rocking forward and backward 7. Crossing and uncrossing legs 8. Inability to lie still 9. Shifting from foot to foot 10. Respiratory: dyspnea or breathing discomfort

Answer 387

1. Restlessness 2. Intense urge to move 3. Irritability 4. Agitation 5. Violent outbursts 6. Dysphoria 7. Feeling “wound up” or “antsy” 8. Sensation of skin crawling

Answer 388

1. Acute to insidious (hours - days) 2. 90% occur within first 6 weeks of treatment

Answer 389

1. Elderly female, young adults 2. High caffeine intake 3. High potency FGAs 4. Lower risk with SGAs 5. Genetic predisposition 6. Anxiety 7. Mood disorder 8. Microcytic anemia, low ferritin 9. Concurrent SSRI use

Answer 390

1. May continue throughout entire treatment 2. Increases risk of tardive dyskinesia 3. May contribute to suicide and violence

Answer 391

1. Reduce dose or change antipsychotic 2. Benzodiazepines 3. Beta-blockers (propranolol 10-20mg BID) 4. Mirtazapine 7.5- 15mg qHS

Answer 392

Barnes Akathisia Rating Scale (BARS)

Answer 393

1. Tremor: “pill-rolling” type 2. Cogwheel rigidity 3. Bradykinesia: mask-like facial expression, diminished/absent arm swing, shuffling gait, stooped posture, slowness of movement

Answer 394

1. Slowed thinking 2. Fatigue 3. Cognitive impairment 4. Drowsiness

Answer 395

1. Acute to insidious 2. 90% occur within first 6 weeks of treatment

Answer 396

1. Elderly females 2. High potency FGA (low risk with SGA and TGA) 3. Increased dose of antipsychotic 4. Multiple antipsychotics concurrently 5. Discontinuation of anticholinergics 6. Concurrent neurological disorder 7. HIV infection 8. Family history of Parkinson's disease

Answer 397

1. Reduce dose or change antipsychotic 2. Antiparkinsonian drug (benztropine, diphenhydramine, procyclidine, trihexyphenidyl)

Answer 398

ESRS or SAS (same rating scale as acute dystonia)

Answer 399

Pisa = leaning to one side Rabbit = fine tremor of lower lip

Answer 400

Pisa = can be acute or tardive Rabbit = after months of therapy

Answer 401

Pisa = elderly pts, compromised brain function, dementia Rabbit = elderly patients

Answer 402

Same for both: Antiparkinsonian drugs (benztropine, procyclidine, trihexyphenidyl)

Answer 403

Involuntary abnormal movements of body - Can co-exist with Parkinsonism and akathisia

Answer 404

1. Cognitive impairment 2. Distress (talking, swallowing, eating) 3. Embarrassment

Answer 405

1. After 3 or more months of therapy in adults (earlier in elderly) 2. Common early sign is rapid flicking movement of tongue (fly catcher tongue)

Answer 406

1. Over 40 years old 2. Female 3. History of severe EPS early in treatment 4. Chronic use of antipsychotics (FGAs more than SGA/TGAs), metoclopramide 5. Chronic use of high doses of dopamine agonists in treatment of Parkinson’s disease 6. Presence of mood component 7. Diabetes 8. Cognitive impairment 9. Alcohol and drug abuse

Answer 407

1. Persistent** 2. Discontinuation of antipsychotic early increases chance of remission 3. Spontaneous remission in 14-24% after 5 years

Answer 408

1. Valbenazine and deutetrabenazine (not available in Canada) 2. Switch to SGA or TGA (? Clozapine or quetiapine) 3. ? Pyridoxine, clonazepam, tetrabenazine, vitamin E, levetiracetam

Answer 409

AIMS (Abnormal Involuntary Movement Scale)

Answer 410

1. Sustained muscle contraction of face, jaw, tongue, eyes, neck, limbs, back or trunk (e.g. blepharospasm, laryngeal dystonia)

Answer 411

Persistent symptoms of akathisia following dose decrease or withdrawal of antipsychotic

Answer 412

Months or years of therapy (Tardive akathisia can be after med withdrawal)

Answer 413

1. Young male 2. Genetic predisposition 3. Neurologic disorder 4. Coexisting tardive dyskinesia 5. Akathisia

Answer 414

1. Persistent 2. Discontinuation of AP early increases chance of remission

Answer 415

1. Switch to SGA or TGA (? Clozapine) Possible treatments: 1. High dose tetrabenazine or trihexyphenidyl 2. Botox

Answer 416

1. Switch to SGA or TGA 2. Anticholinergics 3. Benzodiazepines 4. Beta-blockers (propranolol)

Answer 417

1. Acute, life-threatening EPS that can occur with any AP 2. Rare, idiosyncratic reaction 3. Severe muscle rigidity, fever (>39C), altered mental status, autonomic instability, elevated WBC and creatine kinase 4. Mortality 10%

Answer 418

1. Anytime 2. Often early in treatment

Answer 419

1. STOP antipsychotic immediately!!! 2. Supportive care 3. Consider bromocriptine 4. Dantrolene sometimes used for malignant hyperthermia

Answer 420

1. Pharmacists are uniquely positioned to assess patients with schizophrenia for medication-related issues and provide clinical care and support. 2. Pharmacists can ensure that patients and their families receive important information about medications including how best to take them to optimize the benefits. 3. Pharmacists can identify possible contraindications, drug interactions, and ADEs to optimize tx 4. Pharmacists can play a vital role by providing psychoeducation, simplifying dosing regimens, using adherence aids such as blister packs, using automated-refill features, and promoting the use of LAIAs. 5. Smoking is the single largest preventable cause of lowered life expectancy in the mental health population. Pharmacists have a role in engaging patients in successfully reducing/quitting smoking.

Answer 421

1. Clozapine 2. Olanzapine

Answer 422

1. Haloperidol 2. Risperidone 3. Zuclopenthixol 4. Aripiprazole 5. Chlorpromazine 6. Clozapine

Answer 423

1. Chlorpromazine 2. Haloperidol

Answer 424

1. Haloperidol 2. Quetiapine 3. Risperidone 4. Ziprasidone 5. Clozapine

phar_358_20241002172701 Flashcards

(496 cards)