MENTAL HEALTH

Question 1

Vitamin B1 / Thiamine use

Answer 1

Vitamin

For suspected Wernicke’s encephalopathy (vitamin B1 deficiency) (or cerebral beriberi)(oculomotor dysfunction/ vision problems, ataxia/ lack of muscle coordination and control, encephalopathy/ disease affecting brain function like liver encelopathy where the liver cannot filter toxins which results in toxins accumulating in brain and blood)

OR

For Wernicke’s prophylaxis dosing

Lileys: treats a variety of metabolic disorders

peripheral neuritis associated with pellagra (niacin deficiency)

deitary supplement to traet deficiency in cases of malabsorption; such as that induced by alcoholism, cirrhosis, or GI disease

Adverse effects: nausea, restlessness, pulmonary edema, pruritis, urticaria, weakness, sweating, angioedema, cyanosis, and cardiovascular collapse [IV- anaphylaxis, IM- local tenderness]

Interactions: alkaline/ sulfite containing solutions

Peak: 1-2 hr
Elimination half life: 1.2 hr
Duration of action: 24hr

Question 2

Vitamin B1 / Thiamine mechanism of action

Answer 2

water soluble; b complex

required for carbohydrate metabolism and other metabolic pathways

(for metabolism,)

also a key role in the integrity of the peripheral nervous system, cardiovascular system, and GI tract

Question 3

Beriberi

Answer 3

Vitamin B1 deficiency

Common findings in beriberi include brain lesions, polyneuropathy of peripheral nerves, serous effusions (abnormal collections of fluids in body tissue), and cardiac anatomical changes

Lileys: a disease of the peripheral nerves caused by a dietary deficiency of thiamine; symptoms- fatigue, diarrhea, weight loss, edema, heart failure, and disturbed nerve function

Question 4

Folic acid

Answer 4

water soluble vitamin

lexidrug: used for alcohol withdrawal syndrome, anemia, prevent nural tube defect, folate deficiency, methanol toxicity, methotrexate toxicity

MOA: folic acid is necessary for formation of a number of coenzymes in many metabolic systems; maintains erythopoesis; stimulate WBC and platelet production in folate defiency anemia

Question 5

Multivitamin

Answer 5

Vitamin

Multivitamins are used to provide vitamins that are not taken in through the diet. Multivitamins are also used to treat vitamin deficiencies (lack of vitamins) caused by illness, pregnancy, poor nutrition, digestive disorders, and many other conditions.

Question 6

Magnesium sulphate

Answer 6

Electrolyte Replacements

Used for: asthma, COPD, constipation, eclampsia, preterm birth, hypomagnesemia, parenteral nutrition, torsades de pointes

MOA: lexidrug- promotes bowel evacuation by causing osmotic retention of fluid which distends the colon with increased peristaltic activity.

Parenterally- Mg decreases Ach in motor nerve terminals and acts on myocardium by slowing rate of SA node impulse formation and prolomng conduction time

(AE- hypotension, vasodilation)

Mg is necessary for the movement of Ca, NA, and K in and out of cells as well as stabilizing excitable membranes.

AE- Mg toxicity

Question 7

Phosphorus

Answer 7

Electrolyte Replacements

Does the opposite of Ca

(work inversely; if calcium is high, phosphate will be low)

Essential in bone and teeth formation; help regulate calcium

Question 8

Potassium phosphate

Answer 8

Electrolyte Replacements, hypophoshatemia, parenteral, urine acidification

Phosphorus in the form of organic and inorganic phosphate has a variety of important biochemical functions in all organs and tissues; critical role in nucleic acid structure, energy storage and transfer, cell signaling, cell membrane composition and structure, acid base balance, mineral homeostatsis, and bone mineralization.

K is the major cation of intracellular fluid and is essential for the conduction of nerve impulse in heart, brain, and skeletal muscle; contractions of cardiac, skeletal, and smooth muscle, maintenance of normal renal function, acid base balance, carbohydrate metabolism, and gastric secretion.

Question 9

Potassium chloride

Answer 9

Electrolyte Replacements

essential for nerve impulses in heart, brain, and skeletal muscle; contraction of cardiac, skeletal, and smooth muscles; maintenance of renal function, acid base balance, carbohydrate metabolism, and gastric secretion

AE- bradycardia, chest pain, hyperkalemia (abnormal heartbeat, confusion, dizziness, syncope, weakness, SOB, numbeness/ tingling), hyponatremia, abdominal distress

Question 10

dimenhyDRINATE

Answer 10

Used for motion sickness, relieve N & V, vertigo

Histamine H1 antagonist/ anti emetic

AEs: tachycardia, dizziness, drowsiness, excitement, headache, restlessness

Competes with histamine for H1 receptor sites on effector cells in the GI tract, BVs, and respiratory tract; blocks chemoreceptor trigger zone, diminishes vestibular stimulation, and depress labyrinth function through its central anticholinergic activity

Onset: IM- 20-30 min; oral- 15-30 min
Duration: Oral-4-6 hrs

Question 11

Metoclopramide

Answer 11

antiemetic, dopamine antagonist, prokinetic, serotonin 5 HT4 receptor agonist

used to relieve N&V, dyspepsia, migraine, headache

AE- drowsiness, bradycardia, AV block, flushing, HTN, supraventicular tachycardia

MOA: blocks dopamine receptors and (when given in higher doses) also blocks serotonin receptors in chemoreceptor trigger zone of the CNS; enhances the response to Ach of tissues in upper GI tract causing enhanced motility and accelerated gastric emptying without stimulating gastric, biliary, or pancreatic secretions; increases lower esophageal sphincter tone

Onset: 30-60 minutes
Duration: 1-2 hours

Lileys: treat delayed gastric emptying, GERD, antiemetic; contraindicated in pts with seizure disorder, GI obstruction

Question 12

Ondansetron

Answer 12

antiemetic, selective 5 HT3 receptor antagonist

N&V

AE: constipation, headache, QT prolongation, hypersensitivity

MOA: blocks serotonin both peripherally on vagal nerve terminals and centrally in chemoreceptor trigger zone

Onset: 30 minutes

Lileys: Duration: 6-12 hr IV, onset- 15-30 min

Question 13

Benzodiazepines

Answer 13

-PAM

depressants

Recommend symptom-based regimen, using the Clinical Institute Withdrawal Assessment for Alcohol (CIWA-Ar) score.
The recommended goal is to achieve light somnolence OR to achieve minimal to moderate sedation.
CIWA-Ar NOT applicable to mechanical ventilated patients, seizure and post ictal state, and delirious patients and patients with baseline cognitive impairment. Patient must be alert, orientated and able to answer questions.

• If respiratory rate less than 10 breaths/minute, hold benzodiazepines and Notify Authorized Prescriber

_______

Lileys: anxiolytic drugs, scheduled IV controlled substances

exert their anxiolytic effects by depressing activity in the brainstem and the limbic system; believed to increase action of GABA (an inhibitory neurotransmitter; block nerve transmission in the CNS

Used to relieve anxiety, induce sleep, sedate, and prevent seizures

eg: diazepam, lorazepam, alprazolam

interacting drugs:

1. CNS depressants- opiods/ alcohol; additive effects; enhanced CNS depression/ sedatiom
2. Oral contraceptive, antifungals, opiods, valporic acid- inadequate liver elimination of benzo; enhanced benzo effect- CNS depression
3. rifampin- enhanced benzo clearance; reduced effects
4. theophylline- antagonistic effects- reduced sedative effects
5. phenytoin- reduced clearance; digoxin toxicity and phenytoin toxicity

Question 14

Diazepam

Answer 14

longest acting benzodiazepine

indicated for relief of anxiety, management of alcohol withdrawal, reversal of status epilepticus or preoperative sedation; less frequency- relief of muscle spams

diazepam has active matabolites that can accumulate in pts with liver dysfuncion because it is metabolized primarily in the liver. this accumulation can result in additive effects; prolonged sedation, repsiratory depression, or coma.

avoid in pts with major liver compromise

AE: headache, confusion, slurred speech, amnesia, anorexia, drowsiness, dizziness, ataxia, visual changes, hypotension, weight gain or loss, nausea, weakness

PO [onset- 30-60 min, duration- 12-24 hr]

____

Lexidrug: for anxiety, intoxication, NMS, muscle spasm, seizures, serotonin syndrome, substance withdrawal, vertigo, hydroxychloroquine toxicity

MOA: enhance inhibitory effect of GABA which results in a less excitable state

Question 15

chlordiazePOXIDE

Answer 15

benzodiazepine

used for alcohol withdrawal syndrome or anxiety disorder

AE: edema, syncope, abnormal EEG, ataxia, confusion, drowsiness, EPS, constipation, nausea

Monitor and educate pt to report suidcidal ideation or unusaula changes in behaviour

monitor signs of withdrawal in pts being treated for alcohol withdrawal

monitor respiratory and cardiovascuale status (osthostasis), mental status, paradoxical reactions (excitement, stimulation, acute rage), S&S of ethanol withdrawal

long acting benzo

MOA: enhance inhibitory effect of GABA on neurons which results in a less excitable state and stabilization

Question 16

Lorazepam

Answer 16

drug of choice for the elderly, or patients with COPD or severe liver disease

intermediate acting benzodiazepine

PO [onset-30-60 min, duration- 8 hr]

irritating to muscle; must be diluted

IV push- useful in treatment of an acutely agitated pt

Cont infusion- agitated pt who are undergoing mechanical ventilation

used to treat or prevent alcohol withdrawal

has fewer active metabolites and less drug interactions

_________

Lexidrug

used for; anxiety, akathisia, catatonia, intoxication, N&V, mechanical ventilation, NMS, seizures, SS, sun=bstance withdrawal, vertigo

Catatonia is a neuropsychiatric syndrome where an individual becomes very nonreactive to their environment due to an underlying medical condition. Individuals with catatonia often appear withdrawn and unaware of their surroundings; they also may hold odd positions, sit still or stand in the same position for hours, and be unable to speak or eat.

short to intermediete acting benzo (based on HL) binds to benzodiazepine receptors on the postsynaptic GABA neuron within the CNS; enhance inhibitory effect of GABA which results in less excitable state and stabilization

onset: IV- within 10 minutes

Question 17

Chlordiazepoxide and diazepam

Answer 17

should not be used for elderly patients or those with hepatic impairment.

Question 18

Clinical Communication – For the following CIWA-Ar score:

Answer 18

If CIWA-Ar score 0-9, reassess score every 4 hours and PRN
* If CIWA-Ar score 10 or greater, reassess score every 1 hour until score less than 10 on
3 consecutive measurements
* If CIWA-Ar score 20 or greater on 2 measurements, continue benzodiazepines AND notify
Authorized Prescriber to determine if dose adjustment is required
* Reassess need for ongoing CIWA-Ar assessments after 5 days
* If respiratory rate less than 10 breaths/minute, hold benzodiazepines and Notify Authorized Prescriber

Question 19

If CIWA-Ar score 20 or greater – Severe agitation or Moderate agitation

Answer 19

diazepam or LORazepam

Question 20

If CIWA-Ar score cannot be used OR prefer a long acting medication

Answer 20

chlordiazePOXIDE or diazepam

and lorazepam PRN

Hold if respiratory rate is less than 10 breaths per minute

Question 21

anxiety

Answer 21

unpleasant state of mind in which real or imagined dangers are anticipated/ exaggerated

Question 22

bipolar disorder

Answer 22

a major psychological disorder characterized by episodes of mania or hypomania, cycling with depression

Question 23

depression

Answer 23

a mood disorder characterized by exaggerated feelings of sadness, melancholy, dejection, worthlessness, emptiness, and hopelessness that imp[acts a pts life and may be out of proportion to reality

sigs; withdrawal from social contact, loss of appetite, insomnia

Question 24

dystonia

Answer 24

a syndrome of abnormal muscle contraction that produces repetitive involuntary twisting movements and abnormal posturing of the neck, face, trunk, and extremities; often an AE of psychotropic medications

Question 25

extrapyramidal symptoms

Answer 25

S&S that results from pathological changes to the pyramidal portions of the brain.

symptoms; various motion disorders similar to those seen in PD and are an AE associated with the use of antipsychotic drugs

extrapyramidal side effects (EPS) Adverse effects, including akathisia, acute dystonias, pseudoparkinsonism, and tardive dyskinesia, caused by blockage of D2 dopamine receptor sites in the motor areas.

Question 26

GABA/ gamma aminobutyric acid

Answer 26

amino acid in the brain that function to inhibit nerve transmission in the CNS

alteration of GABA in CNS results in relief of anxiety, sedation, and muscle relaxation.

Question 27

hypomania

Answer 27

a less severe and less potentially hazardous form of mania

State in which people have voracious appetites for social engagement, spending, activity, and even indiscriminate sex. During hypomania, constant activity and a reduced need for sleep prevent proper rest.

Question 28

mania

Answer 28

a period of abnormally and persistently expansive/ irritable mood, including persistently increased goal directed activity/ energy

An exaggerated euphoria or irritability.

Question 29

neuroleptic malignant syndrome

Answer 29

an uncommon but serious AE associated with the use of antipsychotic drugs

symptoms includes fever, cardiovascular instability, myoglobinemia (presence in blood of muscle breakdown proteins)

Question 30

neurotransmitters

Answer 30

endogenous chemicals that conducts nerve impulses between nerve cells

Question 31

akathisia

Answer 31

a movement disorder in which there is an inability to sit still; motor restlessness; can occur as an AE of psychotropic meds

Question 32

affective disorders

Answer 32

emotional disorder; changes in mood

Question 33

psychosis

Answer 33

serious mental health disorder that can take several different forms and is associated with being out of touch with reality

an individual is unable to distinguish imaginary from real circumstances and events; includes presence of hallucinations/ delusions

Question 34

serotonin syndrome

Answer 34

a rare of collection of symptoms resulting from elevated levels of the neurotransmitter serotonin

may occur form use of any psychotropic drugs that enhances brain serotonin activity (like antidepressants, buspirone, tramadol)

Question 35

tardive dyskinesia

Answer 35

a serious adverse drug reaction characterized by abnormal and distressing involuntary body movements and muscle tension that is associated with antipsychotic medications

Question 36

addiction

Answer 36

strong psychological or physical dependence on a drug or other psychoactive substance

Question 37

amphetamine

Answer 37

a drug that stimulate the CNS

Question 38

detoxification

Answer 38

process of eliminating a toxic substance from the body

Question 39

intoxication

Answer 39

stimulation, excitement, or stupefaction produced by a chemical substance

Question 40

physical dependence

Answer 40

a condition characterized by physiological reliance on a substance, usually indicated by tolerance to the effects of the substance and development of withdrawal symptoms when use of the substance is terminated

Question 41

psychological dependence

Answer 41

a condition characterized by strong desires to obtain and use a substance

Question 42

substance misuse

Answer 42

the use of mood or bahaviour altering substances in a maladaptive manner that often compromises health, safety, and social and occupational functioning and cause legal problems

Question 43

wernicke’s encelopathy

Answer 43

a neurological disorder characterized by apathy, drowsiness, ataxia, nystagmus, ans ophthalmoplegia

caused by thiamine deficiency secondary to alcohol misuse

Question 44

withdrawal

Answer 44

a substance specific mental health disorder that occurs as a group of symptoms varying in severity following cessation or reduction in use of psychoactive substance that has been taken regularly

Question 45

buspirone hcl

Answer 45

anxiolytic/ miscellaneous drug

agonist activity at both serotonin and dopamine receptors

treat anxiety

lacks sedative properties and dependency potential of benzo

AE: paradoxical anxiety, dizziness, blurred vision, headache, nausea

Interaction- serotonin syndrome/ antidepressant like SSRI

MAOIs- HTN

Question 46

lithium

Answer 46

0.6 to 1.2 mmol/L; best measured 8-12 hrs after las dose; monitor NA levels

both NA and lithium are monovalent positive ions and affect the other

antimanic agent, mood stabilizing drug

used for bipolar disorder, major depressive disorder, postpartum psychosis

AE; cardiac arythmia, bradycardia, abnormal T waves, drowsiness, sedation, ataxia, abnormal gait, confusion, letahrgy, headache,. dyspepsia, nausea, vomiting, tremor, lithium toxicity (weakness, tremor, ataxia, tinnitus, nausea, diarrhea/ vomiting, slurred speech, confusion, lethargy), polyuria, polydipsia

educate pt on proper hydration, report any mood changes, inability to focus, restlessness, abnormal heartbeat, changes in urine, weight gain, advise pt not to drastically change their NA intake

narrow therapeutic range and require blood level monitoring

MOA: thought to potentiate serotonergic neurotransmission

influence re uptake of serotonin and and or norephinepherine

Question 47

tricyclic antidepressants (TCAs)

Answer 47

1st gen

amitriptyline hcl

second line drug therapy for whom SSRIs are inadequate/ or as an adjunct

MOA: corrects imbalnce in the nurotrasmitter concnerations of serotonin and NE at the nrve endings in the CNS; block the presynaptic reuptake of neurotransmitters which make them available for transmission of nerve impulses to adjacent nuron in the brain

used for neuropathic pain, insomnia, rare for depression

contraindications- MAOIs within 14 days, pregnancy, allergy

AE: blocks chollinergic receptors results in undesirable antichollinergic effects; constipation, urinary retention

adrenergic and dopaminergic receptor blockade; disturbance in cardia conduction a dn hypotension

histamine blockage cause sedation

serotonergic blockade- alter seizure threshold, sexual dysfunction

interactions, anticholinergics, MAOIs

Question 48

MAOIs/ monoamine oxidase inhibitors

Answer 48

1st gen

used for PD, atypical depression, mood disorder with phobic trait

interaction: stimulant meds/ tyramine containing substances, sympathomimetic drugs- HTN crisis

selegiline hcl for PD

can potentiate effects of meperidine hcl and is contraindicated

Question 49

SSRI/ selective serotonin reuptake inhibitor

Answer 49

2nd gen

-TINE/ LINE

inhibit serotonin reuptake; which increases the amount of circulating serotonin in the brain

used for depression, bipolar disorder, obesity, eating disorder, OCD, panic attacks, social anxiety disorder, PTSD, alcoholism

contraindicated with MAOIs in the previous 14 days

AE: serotonin syndrome [delirium, agitation, tachycardia, sweating, muscle spasms, hyperreflexia, shivering, tremors; if severe- hyperthermia, seizures, rnhabdomylosis, CKD, cardia dysrhythmias, disseminated intravascular coagulation

interaction; highly bound to albumin (if given with drugs that are also highly bound to protein such as warfarin, phenytoin, they compete for binding sites

Question 50

SNRI/ seronotin norephinephrine reuptake inhibitor

Answer 50

inhibit reuptake of serotonin and NE; which increases the amount of circulating serotonin and NE in the brain

used for depression, bipolar disorder, obesity, eating disorder, OCD, panic attacks, social anxiety disorder, PTSD, alcoholism

contraindicated with MAOIs in the previous 14 days

AE: serotonin syndrome [delirium, agitation, tachycardia, sweating, muscle spasms, hyperreflexia, shivering, tremors; if severe- hyperthermia, seizures, rnhabdomylosis, CKD, cardia dysrhythmias, disseminated intravascular coagulation

interaction; highly bound to albumin (if given with drugs that are also highly bound to protein such as warfarin, phenytoin, they compete for binding sites

Question 51

bupropion

Answer 51

can be used as smoking cessation/ for depression

a weak dopamine and NE reuptake inhibitor/ inhibit reuptake of NE; MOA is dopaminergic and NORADRENERGIC

antidepressant/ dopamine- NE reuptake inhibitor, smoking cessation aid

used for attention deficit/ hyperactivity disorder, BD, MDD, seasonal affective disorder, sexual dysfunction, smoking cessation

AE- activation of mania/ hypomania, CNS stimulation/ neuropsychiatric effects (increased energy, insomnia, agitation, nervousness, anxiety/ panic, pananoia, delusion, hallucination, suicidal or homicidal ideation),ocular effects (acute angle closure glaucoma), seizure, suicidal thinking/ behaviour

Monitor BP, body weight, suicidality, renal/ hepatic function

Nursing: place pt on seizure precautions, assess for risk of suicidal ideation, monitor ECG changes, risk of falls, report depression, nervousness, restlessness, grouchiness, panic attacks, potential for misuse, menstrual chnages, watch fro steven johnson syndrome- red, swollen, blistered or peeling skin

Question 52

trazodone

Answer 52

antidepressant, SSRI, serotonin modulator

used for depression / insomnia, agressive/ agitated behaviour associated with dementia, insomnia, MDD

AE- strong sedative properties, activation of mania/ hypomania, bleeding risk, cardiac arythmias, O hypotension, priapism, serotonin syndrome, suicidal behaviour/ thinking, withdrawal syndrome

inhibits reuptake of serotonin, also significantly blocks histamine 1 and alpha 1 adrenergic receptors

Question 53

fluoxetine

Answer 53

SSRI, antidepressant

used for depression; prototypical SSRI

used for binge eating, BD, body dismorphic disorder, bulimia nervosa, fibromyalgia, MDD, OCD, panic disorderm PTSD, premature ejaculation, social anxiety disorder

AE- activation of mania/ hypomania, bleeding risk, cardiac arythmias, O hypotension, priapism, serotonin syndrome, suicidal behaviour/ thinking, withdrawal syndrome

monitor NA levels, blood glucose, liver/ renal function, ECG for QT prolongation/ ventricular arythmia, monitor for depression, suicidality, changes in behaviour like anxiety, hostility, impulsitivity esp. during the initial 1-2 months of therapy

Nursing- monitor for risk of suicidal ideation, falls, adherance, changes in vision, alcohol use, SS (like dizziness, headache, agitation, fast heartbeat, flushing, tremor, swaeting, sensing things that seem real, upset stomach, severe diarrhea)

inhibit CNS neuron serotonin reuptake, minimal or no effect on reupptake of NE or dopamine

Question 54

mirtazapine

Answer 54

tetracyclic antidepressant, alpha 2 antagonist

promotes the presynaptic relase of both serotonin and NE in the brain

used for depression/ bipolar disorder, headache (chronic tension), panic disorder, MDD, sexual dysfunction associated with SSRIs

AE- activation of mania/ hypomania, drug induced movement disorder, O hypotension, serotonin syndrome, suicidal behaviour/ thinking, withdrawal syndrome, sexual dysfunction, weight gain, hematologic abnormalities, dyslipidemia

monitor CBC, renal/ liver function, check weight, nursing- monitor for risk of suicidal ideation, behavioural changes, infection, weight gain/ SS- hallucination, seizure, abnormal heartbeat, confusion, agitation)

MOA- tetracyclic antidepressant- central presynaptic alpha 2 adrenergic receptor antagonist effects which results in increased release of NE and serotonin; does not inhibit reuptake of S and NE

Question 55

duloxetine

Answer 55

delayed release SNRI

considered an analgesic/ antidepressant/ anxiolytic

used for depression and generalized anxiety disorder; also indicated for pain resulting from diabetic peripheral neuropathy, fibromyalgia, chronic lower back pain, and OA of the knee. stress urinary incontinence, nueropathic pain

interacts with SSRIs AND TRIPTANS (INCREASE RISK FOR SS)

AE- activation of mania/ hypomania, bleeding risk, fragility #, hepatotoxicity, hyponatremia, ocular effects, SS, sexual dysfunction, suicidal thinking/ behaviour, withdrawal syndrome

MOA-potent inhibitor of nuronal serotonin and NE reuptake and a weka inhibitor of dopamine reuptake

onset- 4-6 weeks/ up to 12 weeks

nursing- monitor for changes in BP (O hypotension, syncope), hyperglycemia (confusion, fatigue, flusing, fast breathing, unusual thirst/ hunger, urinating frequently), risk of falls, adherance, mania/ hypomania, SS (dizziness, headache, tremors, hallucinations, flushing, sweating..), signs of steven johnson syndrome (red, swollen, bistered pr peeling skin)

Question 56

akithisia

Answer 56

distressing motor restlessness

Question 57

dystonia

Answer 57

painful muscle spasms

Question 58

conventional antipsychotics

Answer 58

all antipsychotics block dopamine receptors in the brain which decreases dopamine concentration in the CNS

reduce positive symptoms of schizophrenia

AE: NMS (results fro. reduced dopamine activity, causing fever, vital sign instability, cardiac dysrhythmias), extrapyramidal symptoms (involuntary motor symptoms like PD), tardive dyskinisia- involuntary contractions of oral and facial muscles

block dopamine receptors in brain called neostritum but blockade in this area is believed to cause EPS

Question 59

atypical antipsychotic

Answer 59

reduced effect on prolactin levels

also improves negative symptoms of schizophrenia

Atypical (2nd gen)
Risperidone
Olanzapine
Clozapine -AE; agranulocytosis (monitor infection)
PINE

Help control both positive and negative symptoms of schizophrenia

Acts as serotonin and dopamine ANTAGONIST in the body

Question 60

clozapine

Answer 60

atypical antipsychotic/ 2nd gen

more selectively blocks the dopaminergic receptors in the mesolimbic region of the brain

drug of choice in pts with PD because they have a weak dopamine blocking abilities

used for bipolar D, schizoprenia, psychosis in PD, suicidal behaviour in schizoprenia

AE- antichollinergic effects:high for clozapine; blurred vision, tachycardia, constipation, urinary retention

dyslipedemia, EPS, fever, GI hypomotility, hepatic effects, hyperglycemia, myocarditis, NMS, orthostatic hypo, QTc prolongation, sedation, seizures

monitor for bowel function, adherance, CBC, lytes, kidney and live, TSH, ECG, echo for myocarditis, EPS, HBA1c, lipd panel, metal status/ alertness, prolactin, smoking patterns, clozapine concentration, VS, weight, BMI, height

monitor for othostatic hypotension, tach, weight gain, metabolic syndrome (obesiy, dyslepedemia, HTN)

change position slowly, hydration, report dizziness, falls, palpitations, sudden fever, muscle rigidity, seizure, confusion

antagonize dopamine receptors snd serotonin receptors, also antagonizes alpha adrenergic, histamine and chollinergic receptors

Question 61

risperidone

Answer 61

atypical antipsychotic/ 2nd gen

antimanic agent

used for agitation/ agression associated with psychiatric disorders, substance intoxication, dementia, BD, delusional disorder, MDD, OCD, schizoprenia, tourrette syndrome, untington disease, delirium, disruptive behaviour

AE: activating (akathisia.\/ restlessness)/ sedating effects (drowsiness), angiedema, dyslipidemia, EPS (dystonia, PD, akathisia, tardive dyskinisia), hematologic abnormalities, hyperglycemia, hyperprolactinemia (changes in menstruation, libido, gynecomastia, galactorrhea, erectile/ ejaculatory function), NMS, orthostatic hypotension, QT prolongation, sexual dysfunction, weight gain, TEMPERATURE DYSREGULATION, constipation, N &V, anxiety, dizziness, fatigue

Monitor- adherance, lytes, renal function, liver function, TSH, CBC, EPS symptoms, fall risk, HBA1c, lipid panel, mental status, alerness, metabolic syndrome, prolactin, tarduve dyskenisia, VS, weight, height, BMI

Monitor for psychosis, depression, suicidal ideation (educate pt to report signs od depression, changes in movement, vision, menstruation/ sexual function, dizziness, sudden fever, confusion/ muscle rigidity

antagonizes dopamine receptors, also antagonizes alpha adrenergic and histaminergic receptors

onset: 1-2 weeks with continued improvements over 6-12 weeks

Question 62

liver

Answer 62

produces bile to aid in fat digestion

reception and metabolization of absorbed products from digestion

detoxification of toxic substances received from digestion

storage and release of carbohydrates

production of proteins- primarily plasma proteins such as albumin and clotting factors

Question 63

kidney

Answer 63

filter waste products from the blood in the form of urine (through the nephrons)

reabsorbs water and electrolytes (back into the capillaries /body)and excretes wastes products and acid

Reabsorption into the body
-PCT: 65% K, NA, Mg, Ca, Cl ions, HC03, H20, A.A., urea, glucose
-DL: H20
-AL: ions, HC03
-DCT: ions, HC03, water
-CD: NA, CL, HC03, water, urea

Secretion back into nephron to be excreted
-PCT: urea, uric acid, creatinine, hydrogen ions, drugs, ammonia
-DL: urea
-AL: none
-DCT: H ions, drugs, ammonia
-CD: H ions, drugs, ammonia

regulate blood pH, blood volume, blood pressure, osmolality

produce hormones (erythopoetin, RAAS (renin), calcitrol)

acid base balance by reabsorbing bicarbonate from the urine back to the blood or by secreting hydrogen ions into the urine

Question 64

Mental status examination

Answer 64

the purpose is to evaluate an individual’s current cognitive, affective (emotional), and behavioural functioning. For acutely ill pa- tients, it is not unusual for the mental health clinician to administer MSEs every day. It is the key assessment tool used by all members of the mental health team for ongoing assessment of the patient and to establish treatment effectiveness, as well as certain aspects of recovery.

Appearance observed
Behaviour observed
Speech observed
Mood observed and inquired
Thought observed and inquired
Perception observed and inquired
Cognition inquired
Ideas of Harming Self or Others (inquired)

Question 65

nabilone

Answer 65

antiemetic

used for aggression/ agitation

MOA- a synthetic cannabinoid with antiemetic properties.

antiemetic activity may be due to effect on cannabinoid receptors within the CNS

Question 66

Ach

Answer 66

excitatory/ inhibitory

nicotinic-always excitatory

Question 67

NE

Answer 67

excitatory/ inhibitory

a “feel good” neurotransmitter

release enhanced by amphetamines; removal from synapse blocked by tricyclic antidepressants and cocaine

Question 68

dopamine

Answer 68

excitatory/ inhibitory

a “feel good” neuroransmitter.

deficient in PD

dopamine neurotransmission increases on schizophrenia

Question 69

serotonin

Answer 69

mainly inhibitory

plays a role in sleep, appetite, nausea, migraine headache, and regulating mood

drugs that BLOCK its uptake relive anxiety and depression.

Question 70

histamine

Answer 70

excitatory/ inhibitory

involved in wakefulness, appetite control, and learning, and memory

Question 71

GABA

Answer 71

generally inhibitory

principal inhibitory neurotransmitter in the brain

important in presynaptic inhibition

inhibitory effects augmented by alcohol, antianxiiety drugs of the benzodiazepine class and barbiturates

substances that block its synthesis/ release/ action induce convulsions

Question 72

glutamate

Answer 72

generally excitatory

important in learning and memory

the stroke neurotransmitter

excessive release produces excitotoxicity- neurons stimulated to death; most commonly caused by ischemia due to a blocked vessels

Question 73

huntington disease

Answer 73

drugs is aimed to block dopamine effects

Question 74

Haloperidol

Answer 74

1st gen antipsychotic

used for agitation, BD, delirium, nausea and vomiting in advanced/ terminal illness/ post op, postpartum psychosis, schizoprenia, tourette syndrome

AE: angioedema, EPS, hematologic abnormalities, metabolic syndrom (weight gain, hyperglycemia, HTN), mortality in oA, QTc prolongation, sexual dysfunction, temperature dysregulation, NMS

monitor adherance, CBC, lytes, kidney/ liver function, EPS, fall, HB1A, lipid panel, mental status and aletness, metabolic syndrome hx, ocular exam, prolactin, tardive dyskinesia, weight, height, BMI

nonselectibvely blocks post synaptic dopaminergic receptors in the brain

IM- within 15 minutes

IV- 3-20 minutes

PO- 1-2 weeks

Question 75

delirium

Answer 75

A neurocognitive disturbance charac- terized by inattention, disorganized thinking, altered consciousness, and fluctuations in mental status.

Question 76

delusions

Answer 76

Alterations in thought content (what a person thinks about). Delusions are false fixed beliefs that cannot be corrected by reasoning.

Question 77

dementia

Answer 77

Global deterioration of cogni-
tive functioning (e.g., memory, judgement, ability to think abstractly, orientation). Often progressive and irreversible, depending on the underlying cause.

Question 78

hallucinations

Answer 78

The perception of a sensory experience for which no external stimulus exists (e.g., hearing a voice when no one is speaking).

Question 79

major depressive disorder (MDD)

Answer 79

A history of one or more major depressive episodes without a history of manic or hypomanic episodes.

Question 80

manic episode

Answer 80

Individuals experiencing a
manic episode feel euphoric and energized, do not sleep or eat, and are in perpetual motion. They often take significant risks and engage in hazardous activities.

Question 81

medical assistance in dying (MAiD)

Answer 81

The situation where a person seeks and obtains medical help to end their life.

Question 82

melatonin

Answer 82

A naturally occurring hormone; although it is a popular over-the-counter nutraceutical, there are few data to support its use in the management of insomnia.

Question 83

mental health

Answer 83

A state of well-being in which the individual is able to realize their potential, cope with the normal stresses of life, work pro- ductively and fruitfully, and make a contribu- tion to the community. Psychiatry’s definition is continually evolving since it is shaped by the prevailing culture, societal values, and political climate.

Question 84

mental illness

Answer 84

Alterations in cognition, mood, or behaviour that are coupled with significant distress and impaired functioning.

Question 85

mental status examination (MSE)

Answer 85

Analo- gous to the physical examination in general medicine. The purpose is to evaluate an indi- vidual’s current cognitive, affective (emotion- al), and behavioural functioning.

Question 86

monoamine oxidase inhibitors
(MAOIs)

Answer 86

Group of antidepressant drugs that prevent the destruction of monoamines by inhibiting the action of monoamine oxidase.

Question 87

mood disorders

Answer 87

A group of diagnoses related to disturbances in mood.

Question 88

negative symptoms

Answer 88

The absence of some- thing that should be present but is not (e.g., apathy, lack of motivation, anhedonia, poor thought processes).

Question 89

neuroleptic malignant syndrome (NMS

Answer 89

A
potentially fatal reaction to antipsychotic medications. Symptoms include muscular rigidity, hyperpyrexia, and sometimes oculo- gyric crises.

Question 90

neurotransmitters

Answer 90

Chemicals that transmit signals from one neuron to the next across synapses.

Question 91

panic attack

Answer 91

The sudden onset of extreme ap- prehension or fear, usually associated with feel- ings of impending doom. The feelings of terror present during a panic attack are so severe that normal function is suspended, the perceptual field is severely limited, and misinterpretation of reality may occur.

Question 92

panic disorder (PD)

Answer 92

An anxiety disorder char- acterized by recurring severe panic attacks. It may also effect significant behavioural changes lasting at least a month and ongoing worry about having other attacks.

Question 93

paranoia

Answer 93

Any intense and strongly defended irrational suspicion.

Question 94

personality disorders

Answer 94

Disorders that cause significant challenges in self-identity or self-direction and problems with empathy or intimacy within relationships.

Question 95

post-traumatic stress disorder (PTSD)

Answer 95

An acute emotional response to a traumatic event or situation involving severe environmental stress.

Question 96

positive symptoms

Answer 96

The presence of something that is not normally present (e.g., hallucinations, delusions, bizarre behaviour, paranoia).

Question 97

selective serotonin reuptake inhibitors (SSRIs)

Answer 97

selective serotonin reuptake inhibitors (SSRIs)

Question 98

serotonin–norepinephrine reuptake inhibitor (SNRI)

Answer 98

A drug used to treat generalized anxi- ety disorder (GAD), social anxiety disorder (SAD), and panic disorder (PD).

Question 99

suicidal ideation

Answer 99

Also known as suicidal thoughts. These thoughts can range from a fleeting idea about one’s own death (or about not being here) that does not include the act of killing oneself to a detailed plan, including the final act of killing oneself.

Question 100

suicidal behaviour

Answer 100

Actions that cause self- harm (also referred to as self-injury) initiated with a clear intent to cause bodily harm or death by suicide.

Question 101

stressors

Answer 101

Psychological or physical stimuli that are incompatible with current functioning and require adaptation.

Question 102

sundowning

Answer 102

Also known as sundown syn- drome. Symptoms become more pronounced in the evening. This symptom-exacerbation pattern may occur in people who have either delirium or dementia.

Question 103

tardive dyskinesia (TD or TDK)

Answer 103

A persistent extrapyramidal side effect that usually appears after prolonged treatment and persists even after the medication has been discontinued. TD consists of involuntary tonic muscular contractions that typically involve the tongue, fingers, toes, neck, trunk, or pelvis.

Question 104

addiction

Answer 104

The persistent, compulsive depen- dence on or use of a substance or behaviour despite its negative consequences and the increasing frequency of those consequences.

Question 105

affect

Answer 105

The outward representation of a person’s internal state of being, manifested in facial expression, tone of voice, and body language.

Question 106

akathisia

Answer 106

Psychomotor restlessness evident as pacing or fidgeting, sometimes pronounced and very distressing.

Question 107

Alzheimer’s disease (AD)

Answer 107

A form of degen- erative dementia.

Question 108

anticholinesterase drugs

Answer 108

Drugs that interfere with the action of acetylcholinesterase with the result of elevated levels of the neurotransmitter acetylcholine.

Question 109

anticholinergic-induced delirium

Answer 109

A po- tentially life-threatening medical emergency secondary to use of anticholinergic drugs and characterized by dry mucous membranes; reduced or absent peristalsis; mydriasis; non- reactive pupils; hot, dry, red skin; hyperpyrexia without diaphoresis; tachycardia; agitation; unstable vital signs; worsening of psychotic symptoms; delirium; urinary retention; seizure; and repetitive motor movements.

Question 110

anxiety

Answer 110

A feeling of apprehension, uneasiness, uncertainty, or dread resulting from a real or perceived threat.

Question 111

catatonia

Answer 111

A psychomotor disorder usually involving a lack of movement and communi- cation, but may also altered movements and expression include agitation, confusion, and restlessness.

Question 112

BD

Answer 112

bipolar I disorder A chronic, recurrent illness marked by shifts in mood, energy, and ability to function and in which at least one episode
of mania alternates with major depression. Psy- chosis may accompany the manic episode.

bipolar II disorder A chronic, recurrent illness marked by shifts in mood, energy, and ability to function and in which hypomanic episodes alternate with major depression. Psychosis is not present. Hypomania tends to be euphoric and often increases functioning; depression in this disorder tends to put people at particular risk for suicide.

Question 113

Dopamine and NE

Answer 113

Decreased norepinephrine and serotonin levels are related to depression and suicide, and elevated levels are related to mania and pathological fear.

Abnormalities in dopamine receptors and dopamine transporters are implicated in ADHD, certain addictions, and schizophrenia

Question 114

Dopamine

Answer 114

The neurotransmitters serotonin, dopamine, gamma-aminobutyric acid (GABA), glutamate, and acetylcholine all have an impact on anger and aggression.

Dopamine too, has been linked to aggressive outbursts. There is some indication that this may be based on whether a reward–avoidance pro- cess is present during the dopamine transmission.

Chester et al. (2016) found that individuals with low dopamine systems were more likely to seek external rewards through activities such as thrill-seeking, sub- stance use, and acts of risk and violence

Answer 115

Any medication that crosses the blood–brain barrier may affect sleep and wakefulness through the modulation of these neurotransmitters.

Many of the medications used in psychiatry manipulate these neurotransmitter systems.

For example, amphetamines, which promote wakefulness, increase the release of dopamine and norepinephrine.

Caffeine (methyl- xanthine), which promotes alertness, functions by blocking adenosine.

Question 116

Neurotransmitters

Answer 116

increased amounts of dopamine being released in the brain either directly or indirectly through other neurotransmitters being activated. During this process, prominent physical changes occur in areas of the brain that are critical to judgement, decision making, learning and memory, and behavioural control.

The main systems that seem to be involved in substance use are the endorphin, catecholamine (especially dopamine), serotonin, endo- cannabinoid, and GABA systems. Cocaine, amphetamines, and lesser stimulants increase levels of norepinephrine, serotonin, and dopamine. Opioid drugs act on endorphin receptors with a secondary effect on do- pamine. Alcohol and other CNS depressants will act on GABA receptors and, as a result, increase the bioavailability of glutamate, norepineph- rine, and dopamine. Hallucinogens act to varying degrees on serotonin, whereas cannabis acts on endocannabinoids

Question 117

The chemical structure of many psychoactive drugs is similar to that of neurotransmitters. The similarity in structure allows them to be recognized by neurons and to alter normal brain messaging. This leads to five distinct chemical processes that influence the CNS and change behaviour, which are termed pharmacodynamic interactions:

Answer 117

Blocking the reuptake of a neurotransmitter back into the axon
terminal, allowing more of the neurotransmitter to be available for
binding, thus enhancing the message (cocaine)

• Pushing more neurotransmitters out of the storage vesicles into the
  synaptic cleft, increasing the opportunity for binding and thus en-
  hancing the message (amphetamines)
• Enhancing the binding to the neurotransmitters to further enhance
  binding to the receptor site to enhance the message (diazepam)
• Blocking the enzyme from breaking down the drug in the synap- tic cleft, allowing more neurotransmitters to bind to their receptors to enhance the message (monoamine oxidase inhibitors [MAOIs], which are antidepressants, such as phenelzine [Nardil] and tranyl-
  cypromine [Parnate])
• Mimicking neurotransmitters and binding directly to receptor sites,
  but not allowing a message to be transmitted (naloxone).

Question 118

NMS

Answer 118

Neuroleptic malignant syndrome (NMS) occurs in about 0.2% to 1% of people who have taken conventional antipsychotic medications, although it can occur with atypical medication as well. Acute reduction in brain dopamine activity plays a role in its development. NMS is a life-threatening medical emergency and is fatal in about 10% of cases. It can occur any time during treatment.
NMS is characterized by reduced consciousness, increased muscle tone (muscular rigidity), and autonomic dysfunction, including hyper- pyrexia, labile hypertension, tachycardia, tachypnea, diaphoresis, and drooling. Treatment consists of early detection, discontinuation of the antipsychotic, management of fluid balance, temperature reduction, and monitoring for complications. Mild cases of NMS may be treated with benzodiazepines, vitamins E and B6, or bromocriptine.

Question 119

EPS

Answer 119

Conventional antipsychotic medication are antagonists at the dopamine D2 receptor site in both the limbic and the motor centres. This blockage of dopamine D2 receptor sites in the motor areas causes extrapyramidal side effects, which include akathisia, acute dystonias, pseudo-parkinsonism, and TD. The symptoms of EPS are debilitating, can interfere with social functioning and communication, motor tasks, and ADLs (D’Souza & Hoo- ten, 2020). EPS is often associated with poor quality of life and adherence to medication, which may result in disease relapse and rehospitalization (D’Souza & Hooten, 2020). Other adverse reactions include ACh effects, orthostasis, photosensitivity, and lowered seizure threshold.
Conventional antipsychotic medications are becoming less com- mon in the treatment of schizophrenia because of their minimal impact on negative symptoms and their adverse effects. However, conventional antipsychotic medications are effective in treating positive symptoms, are much less expensive than atypical medications, and come in a depot (long- acting) injectable form. (Note: Risperidone, an atypical antipsychotic med- ication, is also available in a depot form [Risperdal Consta].) For people who respond to them and can tolerate their adverse effects, conventional antipsychotic medications can remain an appropriate choice (CAMH, 2021), especially when metabolic syndrome or cost is a concern.

Question 120

EPS 2

Answer 120

Low potency = high sedation + high ACh + low EPSs

High potency = low sedation + low ACh + high EPSs

Conventional antipsychotic medication must be used cautiously in people with seizure disorders, as they can lower the seizure threshold. Three of the more common EPSs are acute dystonia (acute sustained contraction of muscles, usually of the head and neck), akathisia (psy- chomotor restlessness evident as pacing or fidgeting, sometimes pro- nounced and very distressing to patients), and pseudo-parkinsonism (a medication-induced, temporary constellation of symptoms associ- ated with Parkinson’s disease: tremor, reduced accessory movements, impaired gait, and stiffening of muscles).
EPSs can usually be minimized by lowering dosages of antipsychotic medications or adding antiparkinson medication, especially centrally act- ing ACh medications such as trihexyphenidyl and benztropine mesylate. Diphenhydramine hydrochloride (Benadryl) is also useful. Lorazepam, a benzodiazepine, may be helpful in reducing akathisia.
Unfortunately, antiparkinson medications can cause significant ACh adverse effects and worsen the ACh adverse effects of conven- tional antipsychotic medication and other ACh medications. These adverse effects include ACh syndrome, which is seen in the peripheral nervous system (tachycardia, hyperthermia, hypertension, dry skin, urinary retention, functional ileus) and central nervous system (my- driasis, hallucinations, delirium, seizures, and, in some cases, coma)

Question 121

Tardive dyskinesia (TD)

Answer 121

is a persistent EPS that usually appears af- ter prolonged treatment and persists even after the medication has been discontinued. TD is evidenced by involuntary tonic muscular contrac- tions that typically involve the tongue, fingers, toes, neck, trunk, or pelvis. This potentially serious EPS is most frequently seen in women and older persons and affects up to 50% of individuals receiving long- term, high-dose therapy. TD varies from mild to moderate and can be disfiguring or incapacitating; a common presentation is a “guppy like” mouth movement sometimes accompanied by tongue protrusion. Its appearance can contribute to the stigmatization of people with mental illness and antipsychotic medications.
Early symptoms of TD are fasciculations of the tongue (described as looking like a bag of worms) or constant smacking of the lips. These symptoms can progress into uncontrollable biting, chewing, or sucking motions; an open mouth; and lateral movements of the jaw. No reliable treatment exists for TD.

Question 122

Agranulocytosis

Answer 122

A potentially dangerous blood dyscrasia (disease/ disorder of the body/ blood)

low number of graniulocytes ( a type of WBC) in the blood

(a rare occurrence, but a possibility the nurse should be aware of): symptoms include sore throat, fever, malaise, and mouth sores; any flulike symptoms should be carefully evaluated

common in clozapine

Question 123

Anticholinergic-induced delirium

Answer 123

dry mucous membranes; reduced or absent peristalsis; mydriasis; nonreactive pupils; hot, dry, red skin; hyperpyrexia without diaphoresis; tachycardia; agitation; unstable vital signs; worsening of symptoms of psychosis; delirium; urinary retention; seizure; repetitive motor movements

Question 124

atypical antipsychotics

Answer 124

potential first choice because they treat both the positive and the negative symp- toms of schizophrenia. Furthermore, they produce minimal to no extra- pyramidal side effects (EPSs) or tardive dyskinesia (TD) in most people, although these effects may still occur for some patients. Adverse effects tend to be significantly less, resulting in greater adherence to treatment.

Atypical antipsychotic medications include risperidone (Risperdal), lurasidone (Latuda), olanzapine (Zyprexa), paliperidone (Invega), que- tiapine (Seroquel), ziprasidone (Zeldox).

One significant disadvantage of the atypical medication, with the ex- ception of ziprasidone and aripiprazole, is metabolic syndrome, which includes weight gain, dyslipidemia, and altered glucose metabolism, a significant concern due to increased risk for diabetes, hyperten- sion, and atherosclerotic heart disease (McDaid & Smyth, 2015). An additional disadvantage of atypical antipsychotic medications is cost: they are more expensive than conventional antipsychotic medication. Table 15.7 lists the classifications, routes, and adverse-effect profiles of the antipsychotic medications.

Question 125

Atypical antipsychotic subset

Answer 125

A subset of the atypical antipsychotic medications are those medi- cations referred to as third generation antipsychotic medications. These medications include aripiprazole (Abilify) and brexpiprazole (Rex- ulti). They can be described as dopamine system stabilizers that act by reducing dopamine activity in some brain regions while increasing it in others. Aripiprazole and brexpiprazole act as D2 partial agonists (meaning that they attach to the D2 receptor without fully activating it, reducing the effective level of dopamine activity).

Question 126

Conventional Antipsychotic Medication

Answer 126

Conventional antipsychotic medication are antagonists at the dopamine D2 receptor site in both the limbic and the motor centres. This blockage of dopamine D2 receptor sites in the motor areas causes extrapyramidal side effects, which include akathisia, acute dystonias, pseudo-parkinsonism, and TD. The symptoms of EPS are debilitating, can interfere with social functioning and communication, motor tasks, and ADLs (D’Souza & Hoo- ten, 2020). EPS is often associated with poor quality of life and adherence to medication, which may result in disease relapse and rehospitalization (D’Souza & Hooten, 2020). Other adverse reactions include ACh effects, orthostasis, photosensitivity, and lowered seizure threshold.

Question 127

Dopamine theory

Answer 127

The dopamine theory of schizophrenia is de- rived from the study of the action of the first antipsychotic medications, collectively known as conventional (or first-generation) antipsychotic medication (e.g., haloperidol and chlorpromazine). These medications block the activity of dopamine D2 receptors in the brain, limiting the activity of dopamine and reducing some of the symptoms of schizo- phrenia. However, because the dopamine-blocking medications do not alleviate all symptoms of schizophrenia, it is recognized that other neurochemicals are involved in generating the symptoms of schizophrenia. Amphetamines, cocaine, methylphenidate (Ritalin), and levodopa increase the activity of dopamine in the brain and, in biologically susceptible people, may precipitate the onset of schizophrenia. If schizophrenia is already present, these substances may also exacerbate its symptoms. Almost any drug of abuse, particularly marijuana, can increase the risk for schizophrenia in biologically vulnerable individuals

Question 128

Other neurochemical hypotheses.

Answer 128

A newer class of medications, collectively known as atypical (or second-generation) antipsychotic medications, block serotonin as well as dopamine, which suggests that serotonin may play a role in schizophrenia as well. A better under- standing of how atypical medications modulate the expression and tar- geting of 5-hydroxytryptamine 2A (5-HT2A) and its receptors would likely lead to a better understanding of schizophrenia.
Researchers have long been aware that phenylcyclohexyl piperidine (PCP) induces a state closely resembling schizophrenia. This obser- vation led to interest in the N-methyl-D-aspartate (NMDA) receptor complex and the possible role of glutamate in the pathophysiology of schizophrenia.
Glutamate, dopamine, and serotonin act synergistically in neuro- transmission, and thus glutamate may also play a role in causing psy- chosis (Andreou et al., 2015). Neurotransmission by another calming neurotransmitter, gamma-aminobutyric acid (GABA), is also impaired in schizophrenia (Frankle et al., 2015). Kesby et al. (2018) suggest, “ex- cessive dopamine signalling in the associative striatum may directly lead to symptoms of psychosis by compromising the integration of cor- tical inputs” (p. 4).

Question 129

serotonin

Answer 129

regulation of mood, sleeo, appetite

Question 130

dopamine

Answer 130

primary neurotransmitter in the reward center

when a person experience pleasure, a surge of dopamine is released from the nucleus accumbens, which is a cluster of nerves near the hypothalamus (bran’s reward center)

regulates movement, pleasure, reward

Question 131

acetylcholine

Answer 131

primary neurotransmitter of the parasympathetic nervous system (rest and digest)

regulates movement

Question 132

norepinephrine

Answer 132

the neurotransmitter responsible for fight or flight response (SNS)

adrenergic

Question 133

Antidepressant Drugs

Answer 133

Antidepressant drugs can positively alter poor self-concept, degree of withdrawal, vegetative signs of depression, and activity level. Target symptoms include:
* Sleep disturbance
* Appetite disturbance (decreased or increased)
* Fatigue
* Decreased sex drive
* Psychomotor retardation or agitation
* Diurnal variations in mood (often worse in the morning) * Impaired concentration or forgetfulness
* Anhedonia

A drawback of antidepressant drugs is that improvement in mood may take 1 to 3 weeks or longer. If a patient is acutely suicidal, electro- convulsive therapy.

The goal of antidepressant therapy is the complete remission of symptoms. Often the first antidepressant prescribed is not the one that will ultimately bring about remission; aggressive treatment helps in finding the proper treatment. An adequate trial for the treatment of depression is 3 months. Individuals experiencing their first depres- sive episode are maintained on antidepressants for 6 to 9 months af- ter symptoms of depression remit. Some people may have multiple episodes of depression or may have a chronic form (similar to the chronicity of diabetes) and benefit from indefinite antidepressant therapy.

Question 134

Neurobiology of Depression and the Effect of Antidepressants

Answer 134

The imbalance of certain neurotransmitters (serotonin and norepinephrine) contributes to depression in certain parts of the brain.
Prefrontal cortex: regulates role in executive functions and emotional control and memory.
Limbic system: regulates activities such as emotions, physical and sexual drives, and the stress response, as well as processing,
learning, and memory (amygdala, hypothalamus, hippocampus).
Anterior cingulate cortex: regulates heart rate and blood pressure. Other functions include decision making, emotional regulation, error detection, preparation for tasks, and executive functions.

Antidepressants may precipitate a psychotic episode in a person with schizophrenia or a manic episode in a patient with bipolar dis- order. Patients with bipolar disorder often receive a mood-stabilizing drug along with an antidepressant.

Question 135

Norepinephrine (NE) and the Noradrenergic System:

Answer 135

plays a major role in mood and emotional behaviour as well as energy, drive, anxiety, focus, and metabolism.

Question 136

Serotonin (5-HT) and the Serotonergic System: i

Answer 136

involved in the regulation of pain, depression, pleasure, anxiety, panic arousal, sleep cycle, carbohydrate craving, and premenstrual syndrome.

Question 137

Medications for Depression

Answer 137

Medications for depression include the selective serotonin reuptake inhibitors (SSRIs), serotonin–norepinephrine reuptake inhibitors (SNRIs), serotonin antagonist and reuptake inhibitors (SARIs), norepinephrine–dopamine reuptake inhibitor (NDRI), noradrenergic and specific serotonergic antidepressants (NaSSAs), tricyclic antidepressants (TCAs), and monoamine oxidase inhibitors (MAOIs).

They all work equally well and are chosen by their safety profile and side effects.* All have a delayed response, a discontinuation syndrome, and a Black Box Warning for suicide.

Question 138

Selective serotonin reuptake inhibitors.

Answer 138

The SSRIs are recom- mended as first-line therapy for most types of depression. Essential- ly, the SSRIs selectively block the neuronal uptake of serotonin (e.g., 5-HT, 5-HT1 receptors), which increases the availability of serotonin in the synaptic cleft.

SSRI antidepressant drugs have a relatively low adverse-effect pro- file compared with the older antidepressants (tricyclics—discussed lat- er in this chapter); blurred vision, or urinary retention, making it easier for patients to take these medications as prescribed. Adherence to the medication regimen is a crucial step toward recovery or remission of symptoms. The SSRIs are effective in depression with anxiety features and in depression with psychomotor agitation.
Because the SSRIs cause relatively few adverse effects and have low cardiotoxicity, they are less dangerous than older antidepressants when taken in overdose. The SSRIs, SNRIs, and atypical antidepressants have a low lethality risk in suicide attempts, whereas the tricyclic antidepressants (TCAs) have a very high potential for lethality with overdose.

Indications. The SSRIs have a broad base of clinical use. In addi- tion to their use in treating depressive disorders, the SSRIs have been prescribed with success to treat some anxiety disorders, in particular, obsessive-compulsive disorder and panic disorder (see Chapter 12). Fluoxetine has been found to be effective in treating some women who suffer from late luteal phase dysphoric disorder and bulimia nervosa.

Common adverse reactions. Drugs that selectively enhance synap- tic serotonin within the CNS may induce agitation, anxiety, sleep dis- turbance, tremor, sexual dysfunction (primarily anorgasmia), or tension headache. The effect of the SSRIs on sexual performance may be the most significant undesirable outcome reported by patients.

Potential toxic effects. One rare and life-threatening event associ- ated with SSRIs is serotonin syndrome. This syndrome is thought to be related to overactivation of the central serotonin receptors, caused by either too high a dose or interaction with other drugs, including non-prescription medication like St. John’s wort. Symptoms include abdominal pain, diarrhea, sweating, fever, tachycardia, elevated blood pressure, altered mental state (delirium), myoclonus (muscle spasms), increased motor activity, irritability, hostility, and mood change. Severe manifestations can induce hyperpyrexia (excessively high fever), car- diovascular shock, or death.
The risk of this syndrome seems to be greatest when an SSRI is ad- ministered in combination with a second serotonin-enhancing agent, such as a monoamine oxidase inhibitor (MAOI). A patient should dis- continue all SSRIs for 2 to 5 weeks before starting an MAOI.

Question 139

Serotonin–norepinephrine reuptake inhibitors.

Answer 139

The SNRIs inhibit the reuptake of both serotonin and norepinephrine. Pharmacological adverse effects are similar to those of the SSRIs, although the SSRIs may be tolerated better. The SNRIs are indicated for MDD.

SNRIs are medications that increase both serotonin and norepinephrine levels in the brain. Venlafaxine (Effexor XR) and desvenlafaxine (Pristiq) are effective inhibitors of neuronal serotonin and norepinephrine reup- take and weak inhibitors of dopamine reuptake. Thus these neurotrans- mitters will accumulate in the synapse. Venlafaxine has the dual mech- anism of working as an SSRI at lower doses (75 mg/day), affecting the reuptake of serotonin, and as an SNRI at higher doses (150–225 mg/day), affecting the reuptake of both serotonin and norepinephrine.
Duloxetine (Cymbalta) affects norepinephrine and serotonin reuptake equally. Thus it has a greater noradrenergic effect than does venlafaxine at lower doses. This SNRI is indicated for acute and maintenance treatment of major depressive disorder, for acute treatment of GAD, for managing fibromyalgia, and for managing neuropathic pain associated with diabetic peripheral neuropathy. In fact, many SNRIs, as with the TCAs, have thera- peutic effects on neuropathic pain. The common underlying mechanism of neuropathic pain is nerve injury or dysfunction. The mechanism by which TCAs and SNRIs reduce neuropathic pain is through activation of the descending norepinephrine and serotonin pathways to the spinal cord, thereby limiting pain signals ascending to the brain.

Question 140

Tricyclic antidepressants.

Answer 140

The TCAs inhibit the reuptake of nor- epinephrine and serotonin by the presynaptic neurons in the CNS, increasing the amount of time norepinephrine and serotonin are available to the postsynaptic receptors. This increase in norepineph- rine and serotonin in the brain is believed to be responsible for mood elevations.
Indications. The sedative effects of the TCAs are attributed to the blockage of histamine receptors (Burchum & Rosenthal, 2019). Pa- tients must take therapeutic doses of TCAs for 10 to 14 days or longer before they begin to work; full effects may not be seen for 4 to 8 weeks, but an effect on some symptoms of depression, such as insomnia and anorexia, may be noted earlier. Choosing a TCA for a patient is based on what has worked for the patient or a family member in the past and the drug’s adverse effects for that patient.
A stimulating TCA, such as desipramine (Desipramine), may be best for a patient who is lethargic and fatigued. If a more sedating ef- fect is needed for agitation or restlessness, drugs such as amitriptyline (Elavil) and doxepin (Sinequan) may be more appropriate choices. Re- gardless of which TCA is given, the initial dose should always be low and increased gradually.
Common adverse reactions. The chemical structure of the TCAs closely resembles that of antipsychotic medications, and the anticholinergic actions are similar (e.g., dry mouth, blurred vision, tachycardia, constipation, urinary retention, esophageal reflux). These adverse effects are more common and more severe in patients taking antidepressants than in patients taking antipsychotic medica- tions. They usually are not serious and are often transitory, but uri- nary retention and severe constipation warrant immediate medical attention. Weight gain is also a common complaint among people taking TCAs.
The α-adrenergic blockade of the TCAs can produce postural-or- thostatic hypotension and tachycardia. Postural hypotension can lead to dizziness and increase the risk for falls.
Administering the total daily dose of TCA at night is beneficial for two reasons: (1) most TCAs have sedative effects and thereby aid sleep, and (2) the minor adverse effects occur while the individual is sleeping, which increases adherence to drug therapy.
Potential toxic effects. The most serious effects of the TCAs are cardiovascular: dysrhythmias, tachycardia, myocardial infarction, and heart block have been reported. Because the cardiac adverse effects are so serious, TCA use is considered a risk in older persons and patients with cardiac disease. Patients should have a thorough cardiac workup before beginning TCA therapy.
Adverse drug interactions. A few of the more common medi- cations usually not given while TCAs are being used are MAOIs, phenothiazines, barbiturates, disulfiram, oral contraceptives (or other estrogen preparations), anticoagulants, some antihyperten- sives, benzodiazepines, and alcohol. A patient who is taking any of these medications along with a TCA should have medical clearance because some of the reactions can be fatal.
Contraindications. People who have recently had a myocardial infarction (or other cardiovascular problems), those with narrow-angle glaucoma or a history of seizures, and women who are pregnant should not be treated with TCAs, except with extreme caution and careful monitoring.

Question 141

Tricyclic Antidepressants (TCAs) teaching

Answer 141

The patient and family should be told that mood elevation may take from 7 to 28 days. Up to 6 to 8 weeks may be required for the full effect to be reached and for major depressive symptoms to subside.
* The family should reinforce this information frequently to the family mem- ber with depression, who may have trouble remembering and may respond to ongoing reassurance.
* The patient should be reassured that drowsiness, dizziness, and hypoten- sion usually subside after the first few weeks.
* The patient should be cautioned to be careful when working around ma- chines, driving cars, and crossing streets because of possible altered re- flexes, drowsiness, or dizziness.
* Alcohol can block the effects of antidepressants. The patient should be told to refrain from drinking.
* If possible, the patient should take the full dose at bedtime to reduce the experience of adverse effects during the day.
* If the bedtime dose (or the once-a-day dose) is missed, the patient should take the dose within 3 hours; otherwise, the patient should wait until the usual medi- cation time on the next day. The patient should not double the dose.
* Suddenly stopping TCAs can cause nausea, altered heartbeat, nightmares, and cold sweats within 2 to 4 days. The patient should call the primary care provider or take one dose of the TCA until the primary care provider can be contacted.

Question 142

Monoamine oxidase inhibitors.

Answer 142

The enzyme monoamine oxidase is responsible for inactivating, or breaking down, certain monoamine neurotransmitters in the brain, such as norepinephrine, serotonin, do- pamine, and tyramine. When a person ingests an MAOI, these amines do not get inactivated, and there is an increase of neurotransmitters available for synaptic release in the brain. The increase in norepineph- rine, serotonin, and dopamine is the desired effect because it results in mood elevation. The increase in tyramine, on the other hand, poses a problem. When the level of tyramine increases, and it is not inactivated by monoamine oxidase, high blood pressure, hypertensive crisis, and eventually cerebrovascular accident can occur. Therefore people taking these drugs must reduce or eliminate their intake of foods and drugs that contain high amounts of tyramine.

Foods That Contain Tyramine: avocado, banana, fermented, smoked, aged meats, fermented sausages like peperoni/ salami, dried/ cured fish, all cheeses, yeast extract, beer, wine, chrimp pastes, soy sauce.

Indications. MAOIs are particularly effective for people with atypical depression (characterized by mood reactivity, oversleeping, and overeating), along with panic disorder, social phobia, generalized anxiety disorder, obsessive-compulsive disorder, post-traumatic stress disorder, and bulimia. The MAOIs commonly used in Canada at pres- ent are phenelzine (Nardil) and tranylcypromine sulphate (Parnate).
Common adverse reactions. Some common and troublesome long-term adverse effects of the MAOIs are orthostatic hypotension, weight gain, edema, change in cardiac rate and rhythm, constipation, urinary hesitancy, sexual dysfunction, vertigo, overactivity, muscle twitching, hypomanic and manic behaviour, insomnia, weakness, and fatigue.
Potential toxic effects. The most serious reaction to the MAOIs is an increase in blood pressure, with the possible development of in- tracranial hemorrhage, hyperpyrexia, convulsions, coma, and death. Therefore routine monitoring of blood pressure, especially during the first 6 weeks of treatment, is necessary.
Because many drugs, foods, and beverages can cause an increase in blood pressure in patients taking MAOIs, hypertensive crisis is a constant concern. The hypertensive crisis usually occurs within 15 to 90 minutes of ingestion of the contraindicated substance. Early symptoms include ir- ritability, anxiety, flushing, sweating, and a severe headache. The patient then becomes anxious, restless, and develops a fever. Eventually the fever becomes severe, seizures ensue, and coma or death is possible.
When a hypertensive crisis is suspected, immediate medical atten- tion is crucial. If ingestion is recent, gastric lavage and charcoal may be helpful. Pyrexia is treated with hypothermic blankets or ice packs. Fluid therapy is essential, particularly with hyperthermia. A short- acting antihypertensive agent such as nitroprusside, nitroglycerine, or phentolamine may be used. Intravenous benzodiazepines are useful for agitation and seizure control.

Contraindications. The use of MAOIs may be contraindicated with each of the following:
* Cerebrovascular disease
* Hypertension and congestive heart failure
* Liver disease
* Consumption of foods containing tyramine, tryptophan, and dopa-
mine
* Use of certain medications like narcotics, stimulants, tricyclic antidepressants
* Recurrent or severe headaches
* Surgery in the previous 10 to 14 days
* Age younger than 16 years

Question 143

Electroconvulsive Therapy (ECT)

Answer 143

is a procedure in which electrical currents are passed through the brain, intentionally triggering a brief seizure. ECT seems to cause changes in brain chemistry that can quick- ly reverse symptoms of certain mental illnesses. It often works when other treatments are unsuccessful. However, despite being a highly ef- fective somatic (physical) treatment for psychiatric disorders, ECT has a bad reputation. This may be due to media portrayals of patients being restrained on a gurney while having a full-blown seizure induced. Giv- en the current sophistication of anesthetic and paralytic agents, ECT is actually not dramatic at all.
Indications. ECT is an effective acute treatment for non-responsive depression (Van de Velde et al., 2020). Psychotic illnesses are the second most common indication for ECT. For drug-resistant patients with psy- chosis, a combination of ECT and antipsychotic medication has resulted in sustained improvement about 80% of the time. Depression associated with bipolar disorder remits in about 50% of the cases after ECT.
While medication is generally the first line of treatment, ECT may be a primary treatment in the following cases:
* When a patient is experiencing intense suicidal ideation, and there
is a need for a rapid, definitive response
* When a patient is severely malnourished, exhausted, and dehydrat-
ed due to lengthy depression (after rehydration)
* If previous medication trials have not successfully treated the illness
* If the patient chooses
* When there is marked agitation, marked vegetative symptoms, or
catatonia
* For major depression with psychotic features
* In pregnant people
* For people with rapid cycling mood swings (four or more in one year)

Question 144

Transcranial magnetic stimulation (TMS)

Answer 144

s a non-invasive treatment modality that uses magnetic resonance imaging (MRI)–strength mag- netic pulses to stimulate focal areas of the cerebral cortex (Figure 13.6).
Indications. In 2002 Canada approved the use of TMS for patients who have been unresponsive to at least one antidepressant. Research- ers suggest that TMS be used to enhance cognitive function in healthy, non-depressed individuals (Clark & Parasuraman, 2013).
Risk factors. The only absolute contraindication to this procedure is the presence of metal in the area of stimulation. Cochlear implants, brain stimulators, or medication pumps are examples of metals that could interfere with the procedures (Camprodon et al., 2016).
Procedure. Outpatient treatment with TMS takes about 30 min- utes and is typically ordered for 5 days a week for 4 to 6 weeks. Pa- tients are awake and alert during the procedure. An electromagnet is placed on the patient’s scalp, and short, magnetic pulses pass into the prefrontal cortex of the brain (see Figure 13.6). These pulses are similar to those used by MRI scanners but are more focused. The pulses cause electrical charges to flow and induce neurons to fire or become active. During TMS, patients feel a slight tapping or knocking in the head, contraction of the scalp, and tightening of the jaw.
Potential adverse reactions. After the procedure, patients may ex- perience a headache and lightheadedness. No neurological deficits or memory problems have been noted. Seizures are a rare complication of TMS. Most of the common adverse effects of TMS are mild and include scalp tingling and discomfort at the administration site.

Question 145

Nerve Stimulation

Answer 145

The use of vagus nerve stimulation (VNS) originated as a treatment for epilepsy. VNS is approved in Canada for treatment-resistant de- pression (TRD). Clinicians noted that while VNS decreased seizures, it also appeared to improve mood in a population that normally experi- ences increased rates of depression. The theory behind VNS relates to the action of the vagus nerve, the longest cranial nerve, which extends from the brainstem to organs in the neck, chest, and abdomen. Re- searchers believe that electrical stimulation of the vagus nerve results in boosting the level of neurotransmitters, thereby improving mood and also improving the action of antidepressants.

Question 146

Serotonin Modulator and Stimulator

Answer 146

Vortioxetine (Trintellix) is a serotonin modulator and stimulator. It affects many different serotonin receptors by inhibiting serotonin reuptake like the SSRIs, activating 5-HT1A receptors like buspirone, acting as a partial agonist at 5-HT1B receptor, and blocking 5-HT3, 5-HT1D, and 5-HT7 re- ceptors. Geriatric patients may experience an improvement of cognitive deficits independent of its anti-depressant properties. Common adverse effects include constipation, nausea, and vomiting. More serious side ef- fects are hyponatremia and, rarely, induction of hypomania or mania.

Question 147

Serotonin and Norepinephrine Disinhibitors

Answer 147

The class of drugs described as serotonin and norepinephrine disin- hibitors (SNDIs) is represented by only one drug, mirtazapine (Rem- eron). This unique drug increases norepinephrine, dopamine, and se- rotonin transmission by acting as an antagonist at central presynaptic α2-adrenergic receptors. The normal function of these receptors is to inhibit neurotransmitter release when norepinephrine binds to them. Thus any drug that prevents noradrenaline from binding to these re- ceptors will potentiate neurotransmitter release. This is why this drug is called a disinhibitor. Mirtazapine tends to have a more rapid onset of effect than do single neurotransmitter anti-depressant drugs, and this may be because it can simultaneously affect several neurotransmitter systems. Mirtazapine is a potent antagonist of 5-HT2C receptors, which may account for its anti-anxiety and anti-depressant effects, as these receptors, when activated by serotonin, typically inhibit norepineph- rine and dopamine release. In addition, this drug acts as an antago- nist at 5-HT2A and 5-HT3 receptors, activation of which are thought to mediate sexual dysfunction and nausea. Thus these effects are less likely to occur, and this is an advantage compared to other drugs used in depression. Mirtazapine is also a potent H1-receptor antagonist, which accounts for drowsiness and increased appetite resulting in weight gain being the most common adverse effects. Patients may also experience orthostatic hypotension and the occasional occurrence of anti-cholinergic adverse effects. When discontinuing use of any anti- depressant drug, but particularly SSRIs or SNRIs, patients should be weaned gradually over several weeks rather than abruptly due to the risk of discontinuation symptoms such as dizziness, agitation, anxi- ety, sleeping difficulties, nausea, excessive sweating, and fatigue. These symptoms do not indicate that an addiction has developed. Most peo- ple taking anti-depressant drugs never develop a “craving” or feel the need to increase the dose. What these symptoms do indicate is that the brain has adapted to drug-induced changes in neurotransmitter levels. These symptoms typically resolve within 4 to 6 weeks after discontinu- ation of the drug. However, if the symptoms persist beyond this time frame, there is the potential that depression is still present and that the drugs are still needed.

Question 148

Lithium Carbonate

Answer 148

Although the efficacy of lithium carbonate (Carbolith, Lithane, Lith- max) as a “mood stabilizer” in patients with bipolar disorders has been established for many years (Lithium is still a first-line option in the treatment of patients with bipolar disorder, Yatham et al., 2018), its mechanism of action is still far from understood. While it was origi- nally believed to exert its clinical effects via a non-specific disruption of neurotransmission, recent evidence suggests that it may be enhancing neuroprotective pathways and decreasing neuronal injury and death (Forlenza et al., 2014). One target that may play a key role in mediat- ing the effects of lithium is glycogen synthase kinase 3ß (GSK3ß). This enzyme can affect a number of neuroprotective pathways, and its inhi- bition by lithium appears to trigger those that bring about a clinical re- sponse. In addition, lithium appears to increase levels of BDNF, which is thought to be neuroprotective. Another target affected by lithium is inositol monophosphatase 1, an enzyme involved in the phospha- tidylinositol second messenger pathway. Lithium has been shown to inhibit inositol monophosphatase activity, resulting in a disruption of the entire signalling pathway. This is thought to lead to less intracellular signalling from receptor activation and to lessen the risk of neuronal cell death by improving mitochondrial health. Lastly, there is evidence that lithium decreases excitatory neurotransmission by decreasing glu- tamate release and acting as an antagonist at certain glutamate recep- tors. Excessive glutamate release can lead to neuronal injury and death, and so these effects are thought to prevent neuronal harm that may arise from excessive glutamatergic activity (Malhi & Outhred, 2016).
While it is not known exactly how lithium works, many of its ad- verse effects are thought to arise from the fact that it mimics the role of sodium in neurons and thus alters the electrical properties of neuronal membranes. By altering electrical conductivity, lithium represents a po- tential threat to all body functions regulated by electrical currents. Fore- most among these functions is cardiac contraction; lithium can induce, although not commonly, sinus bradycardia. Overdose causes extreme al- teration of cerebral conductivity, which can lead to convulsions. Changes in nerve and muscle conduction can commonly lead to tremor at thera- peutic doses or to more extreme motor dysfunction with overdose.
Lithium commonly induces polyuria (the output of large volumes of urine) as a consequence of decreasing the effectiveness of vasopres- sin on renal function. Long-term use of lithium can result in thyroid gland enlargement (goiter) and, possibly, hypothyroidism in some pa- tients. In addition, hyponatremia can increase the risk of lithium toxic- ity because increased kidney reabsorption of sodium leads to increased reabsorption of lithium as well.

Primarily because of its effects on electrical conductivity, lithium has a low therapeutic index. The therapeutic index is a measure of overall drug safety with respect to the risk for overdose or toxicity. It can be expressed as the ratio between the median lethal dose and the median effective dose. A low therapeutic index means that the dose of the drug that can cause death is not that much greater than the dose re- quired for therapeutic effectiveness. This risk mandates that the blood level of lithium be monitored on a regular basis to ensure that the drug is not accumulating and rising to dangerous levels. See Table 11.3 for a list of some of the adverse and toxic effects of lithium. Chapter 14 con- tains a more in-depth discussion of lithium carbonate treatment and specific dose-related adverse and toxic effects, nursing implications, and the patient teaching plan.

AE- tremor, ataxia, convulsions, confusion, N&V, du=iarrhea, arythmias, POLYURIA, POLYDIPSIA, edema, goiter, hypothyroidism

Question 149

Other Drugs Used to Treat Bipolar Disorders

Answer 149

These drugs work through several different mechanisms but all share the common property of decreasing neuronal excitability. The major modes of action for these drugs include (1) inhibition of sodium channel activity, (2) inhibition of calcium channel activity, (3) enhancement of GABAergic neuro- transmission pathways, and (4) inhibition of glutamatergic neurotrans- mission pathways. Although some drugs work almost exclusively via a single one of these mechanisms, a number of the drugs in this group work through a combination of these effects. Three drugs used in the treatment of seizure disorders, valproate (Depakene), carbamazepine (Tegretol), and lamotrigine (Lamictal, Lamotrigine), have displayed ef- ficacy in the treatment of bipolar disorder and, in the context of this disease, are considered to be mood stabilizers. It is thought that their ability to re-establish a balance between excitatory and inhibitory neu- ronal pathways has a stabilizing effect on mood.

Question 150

Carbamazepine

Answer 150

The primary mechanism of action of carbamazepine is to inhibit neu- ronal sodium channels during depolarization events, hence reducing neuronal excitability. Interestingly, this blocking action is greater in neurons that fire frequently and repetitively, and so the drug is effec- tive at reducing inappropriate excitability. Because of this mechanistic characteristic, carbamazepine does not have as strong of an effect on neurons that are behaving normally and is therefore less likely to af- fect normal neuronal function. Common adverse effects include an- ticholinergic effects (e.g., dry mouth, constipation, urinary retention, blurred vision), orthostatic hypotension, sedation, and ataxia. Rash may occur in 10% of patients (Sadock et al., 2015). Recommended baseline laboratory work includes liver function tests, complete blood count (CBC), electrocardiogram, and electrolyte levels. Blood levels are monitored to avoid toxicity, but there are no established therapeutic blood levels for carbamazepine in the treatment of bipolar disorder.

Question 151

Valproate

Answer 151

As with carbamazepine, valproate also displays efficacy in treating bi- polar disorders. Valproate works through a number of the mechanisms listed earlier. It blocks both sodium and calcium channels and may el- evate GABA levels by inhibiting the enzyme that normally degrades this neurotransmitter. Common adverse effects include tremor, weight gain, and sedation. More rarely occurring but serious adverse effects include thrombocytopenia, pancreatitis, and hepatic failure. In addi- tion, this drug has been demonstrated to be a potent teratogen. Because of its potential to cause hepatotoxicity, baseline levels are established for liver function indicators and a CBC is obtained before an individual is started on this medication. These measurements are then repeated periodically. In addition, the level of the drug in the blood is monitored to ensure that it stays within the recommended therapeutic range.

Question 152

Lamotrigine

Answer 152

Lamotrigine (Lamictal) is perhaps the most effective drug for main- tenance therapy of bipolar disorder, but it is not as effective in acute mania. Lamotrigine is best known for its abil- ity to treat the depressive phase of bipolar disorder, with less risk of causing a switch into mania when compared to anti-depressant drugs. It inhibits neuronal sodium and calcium channels and modulates the release of the excitatory neurotransmitters glutamate and aspartate. Patients should promptly report any rashes, which could be a sign of life-threatening Stevens–Johnson syndrome. This risk can be minimized by slow titration to therapeutic doses.

Question 153

Other Anti-seizure Drugs

Answer 153

Because these drugs work by inhibiting neuronal excitability, they have found a home in the treatment of other disorders. Along with their use with bipolar disorders (as discussed above), some of these drugs show efficacy in treating neuropathic pain, anxiety, and migraines.
Other anti-seizure drugs used as mood stabilizers are gabapentin (Neurontin), topiramate (Topamax), and oxcarbazepine (Trileptal). None of them have Health Canada approval as mood stabilizers, and studies have not provided strong support for their use as primary treat- ments for bipolar disorders. However, they are used for their calming effects during mania. Chapter 14 offers a more detailed discussion of these medications.

Question 154

Mild anxiety

Answer 154

Mild anxiety, which occurs in the normal experience of everyday liv- ing, allows an individual to perceive reality in sharp focus. A person experiencing a mild level of anxiety sees, hears, and grasps more infor- mation, and problem solving becomes more effective. Physical symp- toms may include slight discomfort, restlessness, irritability, or mild tension-relieving behaviours (e.g., nail biting, foot or finger tapping, fidgeting, wringing of hands).

Question 155

Moderate Anxiety

Answer 155

As anxiety increases, the perceptual field narrows, and some details are excluded from observation. The person experiencing moderate anxiety sees, hears, and grasps less information and may demonstrate selective inattention, in which only certain things in the environment are seen or heard unless they are pointed out. While the person’s ability to think clearly is hampered, learning and problem solving can still take place, although not at an optimal level. Physical symptoms of moderate anxiety include tension, pounding heart, increased pulse and respiratory rate, perspiration, and mild somatic symptoms (gastric discomfort, headache, urinary urgency). Voice tremors and shaking may be noticed. Mild or moderate anxiety levels can be constructive because anxiety may signal that something in the person’s life needs attention or is dangerous.

Question 156

Severe anxiety

Answer 156

The perceptual field of a person experiencing severe anxiety is greatly reduced. A person with severe anxiety may focus on one particular de- tail or many scattered details and has difficulty noticing their environ- ment, even when it is pointed out by another. Learning and problem solving are not possible at this level, and the person may be dazed and confused. Behaviour becomes automatic (e.g., wringing hands, pacing) and is aimed at reducing or relieving anxiety. Somatic symptoms such as headache, nausea, dizziness, and insomnia often increase; trembling and a pounding heart are common; and the person may hyperventilate and experience a sense of impending doom or dread

Question 157

Panic

Answer 157

Panic, the most extreme level of anxiety, results in noticeably disturbed behaviour. Someone in a state of panic is unable to process what is going on in the environment and may lose touch with reality, even experienc- ing hallucinations, or false sensory perceptions (e.g., seeing people or objects not really there). Physical manifestations may include pacing, running, shouting, screaming, or withdrawal, and actions may become erratic, uncoordinated, and impulsive. These sorts of automatic behav- iours are used to reduce or relieve anxiety, although such efforts may be ineffective. Acute panic may lead to exhaustion.

Question 158

Panic Disorder

Answer 158

Panic disorder is an anxiety disorder characterized by recurring severe panic attacks. It may also effect significant behavioural changes last- ing at least a month and ongoing worry about having other attacks. A panic attack is the sudden onset of extreme apprehension or fear, usu- ally associated with feelings of impending doom. The feelings of terror present during a panic attack are so severe that normal function is
suspended, the perceptual field is extremely limited, severe personality disorganization is evident, and misinterpretation of reality may occur.

People experiencing panic attacks may believe that they are losing their minds or having a heart attack since the attacks are often accom- panied by highly uncomfortable physical symptoms such as palpita- tions, chest pain, breathing difficulties, nausea, a choking feeling, chills, and hot flashes. Typically, panic attacks occur within 10 minutes “out of the blue” (i.e., suddenly, and not necessarily in response to stress), are extremely intense, last a matter of minutes, and then subside. Table 12.3 outlines a generic nursing care plan for PD

Question 159

Agoraphobia

Answer 159

When individuals actively avoid situations from which escape might be difficult or embarrassing or in which help might not be available if panic-like symptoms were to occur, they may be diagnosed with agoraphobia.

Question 160

Phobias

Answer 160

A phobia is a persistent, irrational fear of a specific object, activity, or situation that leads to a desire for avoidance or to actual avoidance of the object, activity, or situation despite the awareness and reassurance that it is not dangerous.

Specific phobias, which are more intense, cause impaired daily functioning and last at least half a year. They are characterized by the experience of high levels of anxiety or fear in response to specific objects or situations, such as dogs, spiders, heights, storms, water, blood, closed spaces, tunnels, and bridges. Specific pho- bias are common and usually do not cause sufferers much difficulty because they can contrive to avoid the feared object.

Question 161

Social phobia, also called social anxiety disorder (SAD)

Answer 161

is charac- terized by severe anxiety or fear provoked by exposure to a social or performance situation (e.g., fear of being scrutinized, saying something that sounds foolish in public, not being able to answer questions in a classroom, eating in public, performing on stage). Fear of public speak- ing is the most common social phobia.

Question 162

Generalized Anxiety Disorder

Answer 162

is an anxiety reaction characterized by persistent and exaggerated apprehension and tension. Worry is the major concern in GAD. The individual’s beliefs about worry are then linked to beliefs about themself, such as having the inability to control anxiety and fear, that if they worry significantly about an upcoming issue it will be prevented, or that worrying is a valued part of their personal identity.

The individual with GAD also displays many of the following symptoms:
* Restlessness
* Fatigue
* Poor concentration
* Irritability
* Tension
* Sleep disturbance

The individual’s anxiety is out of proportion to the true impact of the event or situation about which they worry. Examples of concerns typical of GAD include inadequacy in interpersonal relationships, job responsibilities, finances, the health of family members, household chores, and lateness for appointments. Sleep disturbance is common because the individual pores over the day’s events and real or imagined mistakes, reviews past problems, and anticipates future difficulties. Decision making becomes difficult, owing to poor concentration and dread of making a mistake.

Question 163

Substance-Induced Anxiety Disorder

Answer 163

Substance-induced anxiety disorder is characterized by symptoms of anx- iety, panic attacks, obsessions, and compulsions that develop with the use of a substance or within a month of discontinuing use of the substance.

Question 164

Anxiety Due to Nonpsychiatric Medical Conditions

Answer 164

Respiratory
Chronic obstructive pulmonary disease
Pulmonary embolism
Asthma
Hypoxia
Pulmonary edema

Cardiovascular
Angina pectoris
Arrhythmias
Congestive heart failure
Hypertension
Hypotension
Mitral valve prolapse

Endocrine
Hyperthyroidism
Hypoglycemia
Pheochromocytoma
Carcinoid syndrome
Hypercortisolism

Neurological
Delirium
Essential tremor
Complex partial seizures
Parkinson disease
Akathisia
Otoneurological disorders
Postconcussion syndrome

Metabolic
Hypercalcemia
Hyperkalemia
Hyponatremia
Porphyria

Question 165

Illness Anxiety Disorder

Answer 165

Previously known as hypochondriasis, illness anxiety disorder results in the misinterpretation of physical sensations as evidence of a serious illness. Illness anxiety can be quite obsessive as thoughts about illness may be intrusive and hard to dismiss even when patients realize that their fears are unrealistic (Lebel et al., 2020). People with this disorder experience extreme worry and fear about the possibility of having a disease. Even normal body changes, such as a change in heart rate or abdominal cramps, can be seen as red flags for serious illness and im- minent death.

Question 166

Conversion Disorder

Answer 166

Conversion disorder (also known as functional neurological symptom disorder) manifests itself as neurological symptoms in the absence of
a neurological diagnosis. Conversion disorder is marked by the presence of deficits in voluntary motor or sensory functions, including paralysis, blindness, movement disorder, gait disorder, numbness, paresthesia (tingling or burning sensations), loss of hearing, or seizures resembling epilepsy.

Conversion disorder is a clinical problem that requires the appli- cation of multiple perspectives, namely, biological, psychological, and social, to fully understand the symptoms of individual patients. Experiences of childhood physical or sexual abuse are common among pa- tients with conversion disorder, and comorbid psychiatric conditions include depression, anxiety, PTSD, other somatic disorders, and personality disorders. Patients with conversion disorder symptoms may be found to have “no neurological disorder” by the neurologist and “no psychiatric disorder” by the psychiatrist, thus adding to the complexity of treatment planning.

Question 167

OBSESSIVE-COMPULSIVE DISORDERS

Answer 167

Obsessions are defined as thoughts, impulses, or images that persist and recur and cannot be dismissed from the mind. Obsessions often seem senseless to the individual who experiences them (ego-dystonic), and their presence causes severe anxiety.
Compulsions are ritualistic behaviours or thoughts an individual feels compelled to perform in an attempt to reduce anxiety. Performing the compulsive act temporarily reduces high levels of anxiety. Primary gain is achieved by compulsive rituals, but because the relief is only temporary, the compulsive act must be repeated again and again until it feels “just right”

Common types of obsessions include losing control, harm, contamination, perfectionism, sexual, and religious. There are also common categories of compul- sions: washing and cleaning, checking, repeating, and mental com- pulsions.

At the pathological end of the continuum are obsessive-compulsive symptoms that typically involve issues of contamination, fear of losing control, need for symmetry, unwanted thoughts of a sexual nature, and recurrent feelings of doubt. Pathological obsessions or compulsions cause marked distress to individuals, who often feel humiliation and shame for these behaviours. The rituals are time consuming and in- terfere with normal routines, social activities, and relationships with others. Severe OCD consumes so much of the individual’s mental pro- cesses that the performance of cognitive tasks may be impaired.

Question 168

Acute Stress Disorder

Answer 168

Acute stress disorder occurs within 1 month of a highly traumatic event, such as those that precipitate PTSD. To be diagnosed with acute stress disorder, the individual must display at least three dissociative symptoms either during or after the traumatic event, including a sub- jective sense of numbing, detachment, or absence of emotional re- sponsiveness; a reduction in awareness of surroundings; derealization (a sense of unreality related to the environment); depersonalization (a sense of unreality or self-estrangement); or dissociative amnesia (loss of memory)

Question 169

Post-Traumatic Stress Disorder

Answer 169

PTSD is an acute emotional response to a traumatic event or situation involving severe environmental stress.

The individual with PTSD persistently re-experiences a traumatic event that involved threatened or actual death or serious injury to self or others, and to which the person responded with intense fear, help- lessness, or horror. PTSD may present after any traumatic event that is outside the range of usual experience, such as military combat, de- tention as a prisoner of war, natural disasters (e.g., floods, tornadoes, earthquakes), human disasters (e.g., plane and train accidents), crime- related events (e.g., sexual abuse, bombing, assault, mugging, rape, be- ing taken hostage), or diagnosis of a life-threatening illness.

The major features of PTSD are:
* Persistent re-experiencing of the trauma through recurrent intru-
sive recollections of the event, dreams about the event, and flash- backs—dissociative experiences during which the event is relived (i.e., the person behaves as though they are experiencing the event in the present)
* Persistent avoidance of stimuli associated with the trauma, causing the individual to avoid talking about the trauma or avoid activities, people, or places that rouse memories of the trauma
* Persistent numbing of general responsiveness, as evidenced by the individual’s feeling empty inside or feeling disconnected from others
* Persistent symptoms of increased arousal, as evidenced by irritabil- ity, difficulty sleeping, difficulty concentrating, hypervigilance, or exaggerated startle response

Question 170

DISSOCIATIVE DISORDERS

Answer 170

Dissociative disorders are a group of disorders precipitated by signifi- cant adverse experiences or traumas and resulting in the unconscious altering of mind–body connections. Dissociation is an unconscious defence mechanism that protects the individual against overwhelming anxiety and stress through an emotional separation; however, this sep- aration results in disturbances in memory, consciousness, self-identity, and perception.
Patients with dissociative disorders are able to assess a situation re- alistically, rather than for what they want it to be or fear that it might be. They do not have hallucinations or delusions (meaning that they have “intact reality testing”), but they may have flashbacks or see images that are triggered by current events that are related to the past trauma. Mild, fleeting dissociative experiences are relatively common to all of us; for example, we may be listening to someone and suddenly realize that we have not heard part or all of what was said. These common experiences are distinctly different from the processes of pathological dissociation.

Symptoms of dissociation may be either positive or negative. Posi- tive symptoms refer to unwanted additions to mental activity, such as flashbacks; negative symptoms refer to deficits, such as memory prob- lems or the inability to sense or control different parts of the body.

Question 171

Depersonalization/Derealization Disorder

Answer 171

Depersonalization/derealization disorder may cause a person to feel mechanical, dreamy, or detached from the body. Some people suffer episodes of these problems that come and go, while others have epi- sodes that begin with stressors and eventually become constant. People with this disorder may experience episodes of depersonalization or de- realization or both. When experiencing depersonalization, individuals feel as though they are observers of their own body or mental process- es—there is an internal feeling of disconnect. Similarly, with derealiza- tion, there is a recurring feeling that one’s surroundings are unreal or distant—an external or outside feeling of disconnect. These feelings are not consciously controlled by the patients with dissociative disorders and are reported to be very distressing to those who experience them

Question 172

Dissociative Amnesia

Answer 172

Dissociative amnesia is marked by the inability to recall important autobiographical information, often of a traumatic or stressful nature, that is too pervasive to be explained by ordinary forgetfulness. While autobiographical memory is available (i.e., stored within the brain), the information is not accessible (i.e., the memory cannot be retrieved). When memories are stored, information about the situation (retrieval cues) is also stored. This additional information can be about the envi- ronment (smell, place, colour) or about a feeling (happy, sad, mad) or about an activity at the time (walking, crying, sitting, studying). Seeing or thinking about these retrieval cues helps us recall the memory. For example, have you ever got up from watching television and gone into the kitchen to do something but then forgotten what you were going to do once you got to the kitchen? But then you go back and sit down in front of the television and you remember? You have just accessed a memory using a retrieval cue.

Question 173

Dissociative Identity Disorder

Answer 173

The essential feature of DID is the presence of two or more distinct personality states that alternately and recurrently take control of be- haviour. It is believed that severe sexual, physical, or psychological trauma in childhood predisposes an individual to the development of DID. Each alternate personality (alter), or subpersonality, has its own pattern of perceiving, relating to, and thinking about the self and the environment. Each alter is a complex unit with its own mem- ories, behaviour patterns, and social relationships that dictate how the person acts when that personality is dominant. If the original or primary personality is religious and moralistic, the subpersonality or subpersonalities are often pleasure seeking and nonconforming. The alters may also behave as individuals of a different sex, race, or religion.
DID appears to be associated with two dissociative identity states (alternate personalities): (1) a state in which the individual blocks ac- cess and responses to traumatic memories so as to be able to func- tion daily and (2) a state fixated on traumatic memories. The primary personality, or host, is usually not aware of the subpersonalities and is perplexed by lost time and unexplained events. Experiences such as finding unfamiliar clothing in the closet, being called a different name by a stranger, and not having childhood memories are characteristic of DID. Subpersonalities are often aware of the existence of each other to some degree. Transition from one personality to another occurs during times of stress and may range from a dramatic to a barely noticeable event. Some patients experience the transition when awakening. Shifts may last from minutes to months, although shorter periods are more common.

Question 174

Mood disorders

Answer 174

(also called affective disorders) are a group of psychiatric disorders including depression and bipolar disorder.

Question 175

Major depressive disorder (MDD)

Answer 175

MDD, or major depression, is characterized by a persistently depressed mood lasting for a minimum of 2 weeks. The length of a depressive episode may vary.

h edition (DSM-5): Diagnostic Criteria for Major Depressive Disorder.
The diagnosis for MDD may include one of the following specifiers to describe the most recent episode of depression:
* Psychotic features. Indicates the presence of disorganized think-
ing, delusions (e.g., delusions of guilt or of being punished for sins, somatic delusions of horrible disease or body rotting, delusions of poverty or going bankrupt), or hallucinations (usually auditory, voices berating person for sins).
* Melancholic features. This outdated term indicates a severe form of endogenous depression (not attributable to environmental stress- ors) characterized by severe apathy, weight loss, profound guilt, symptoms that are worse in the morning, early morning awaken- ing, and often suicidal ideation.
* Atypical features. Refers to dominant vegetative symptoms (e.g., overeating, oversleeping). Onset is younger, psychomotor activities are slow, and anxiety is often an accompanying problem, which may cause misdiagnosis.
* Catatonic features. Marked by non-responsiveness, extreme psycho- motor retardation (may seem paralyzed), withdrawal, and negativity.
* Postpartum onset. Indicates onset within 4 weeks after childbirth. It is common for psychotic features to accompany this depression. Severe ruminations or delusional thoughts about the infant signify
increased risk of harm to the infant.

Question 176

Disruptive mood dysregulation disorder

Answer 176

is a disorder characterized by severe and recurrent temper outbursts that are inconsistent with developmental level.

The basic symptoms of disruptive mood dysregulation disorder are constant and severe irritability and anger in individuals between the ages of 6 and 18. Onset is before age 10.

Question 177

Persistent depressive disorder (dysthymia)

Answer 177

is diagnosed when feel- ings of depression occur most of the day, for the majority of days. These low-level depressive feelings last at least 2 years in adults and 1 year in children and adolescents. In addition to depressed mood, individuals with this disorder have at least two of the following: decreased appetite or overeating, insomnia or hypersomnia, low energy, poor self-esteem, difficulty thinking, and hopelessness.

Question 178

Premenstrual Dysphoric Disorder

Answer 178

It refers to a cluster of symptoms that occur in the last week before the onset of a menstrual period. Premen- strual dysphoric disorder causes problems severe enough to interfere with the ability to work or interact with others. Symptoms include mood swings, irritability, depression, anxiety, feeling overwhelmed, and difficulty concentrating. Other physical manifestations include lack of energy, overeating, hypersomnia or insomnia, breast tender- ness, aching, bloating, and weight gain. Symptoms decrease signifi- cantly or disappear with the onset of menstruation.

Question 179

Substance/medication-induced depressive disorder

Answer 179

is a depressive disorder, such as MDD, that is a result of prolonged use of or withdraw- al from drugs and alcohol. The depressive symptoms last longer than the expected length of physiological effects, intoxication, or withdrawal of the substance. The person with this diagnosis would not experience depressive symptoms in the absence of drug or alcohol use or with- drawal. Symptoms appear within 1 month of use. Once the substance is removed, depressive symptoms usually remit within a few days to several weeks.

Question 180

Depressive disorder due to another medical condition

Answer 180

may be caused by disorders that affect the body’s systems or from long-term ill- nesses that cause ongoing pain. The depressive symptoms are the same as the diagnostic criteria for the depressive disorders. It is important to review medications being used for the medical condition to rule out them being the causative agents.

Question 181

Medical Conditions and Substances or Medications Associated With Major Depressive Disorder

Answer 181

Central nervous system depressants:
Alcohol, barbiturates, benzodiazepines, clonidine

Central nervous system medications: amantadine, bromocriptine, levodopa, phenothiazines, phenytoin

Psychostimulants: Amphetamines

Systemic medications: Corticosteroids, digoxin, diltiazem, enalapril, ethionamide, isotretinoin, mefloquine, methyldopa, metoclopramide, quinolones, reserpine, statins, thiazides, vincristine

Question 182

Suicide ideation questions

Answer 182

Patients diagnosed with MDD should always be evaluated for suicidal ideation. Risk for suicide is increased when depression is accompanied by hopelessness, substance use problems, a recent loss or separation, a history of past suicide attempts, or acute suicidal ideation. The following state- ments and questions help set the stage for assessing suicide potential:
* You have said you are depressed. Tell me what that is like for you. * When you feel depressed, what thoughts go through your mind? * Have you gone so far as to think about taking your own life?
* Do you have a suicide plan?
* Do you have the means to carry out your plan?
* Is there anything that would prevent you from carrying out your plan?

Question 183

Depressive disorders Key Assessment Findings

Answer 183

depressed mood and anhedonia (loss of ability to experience joy or pleasure in living) are the key symptoms of depression. Almost 97% of people with depression have anhedonia. Anxiety, a common symptom in depression, is seen in about 60% to 90% of patients with depres- sion. Psychomotor agitation may be evidenced by constant pacing and
wringing of hands. The slowed movements of psychomotor retardation, however, are more common. Somatic complaints (e.g., headaches, mal- aise, backaches) are also common. Vegetative signs of depression, alterations in those activities necessary to support physical life and growth (e.g., change in bowel movements and eating habits, sleep distur- bances, lack of interest in sex), are universally present.

Question 184

Lithium carbonate.

Answer 184

Lithium carbonate (LiCO3 or Li+) is effective in the treatment of bipolar I acute and recurrent manic and depressive epi- sodes. Onset of action is usually within 10 to 21 days. Because the onset of action is so slow, it is usually supplemented in the early phases of treatment by atypical antipsychotics, anticonvulsants, or antianxiety medications.

Indications. Lithium is particularly effective in reducing:
* Elation, grandiosity, and expansiveness
* Flight of ideas
* Irritability and manipulation
* Anxiety
To a lesser extent, lithium controls:
* Insomnia
* Psychomotor agitation
* Threatening or assaultive behaviour * Distractibility
* Hypersexuality
* Paranoia

Therapeutic and toxic levels. There is a small window between the therapeutic and toxic levels of lithium. Lithium must reach therapeutic blood levels to be effective. This usually takes 7 to 14 days, or longer for some patients. Blood serum levels should reach 0.6 to 1.2 mEq/L.

Lithium levels should be measured at least 5 days after beginning lithium therapy and after any dosage change, until the therapeutic level has been reached. Blood levels are determined every month. After 6 months to a year of stability, it is common to measure blood levels every 3 months. Blood should be drawn in the morning, 10 to 12 hours after the last dose of lithium is taken. For older adult patients, the prin- ciple of start low and go slow still applies.

Lithium therapy is generally contraindicated in patients with cardiovascular disease, brain damage, renal disease, thyroid disease, or myasthenia gravis. Whenever possible, lithium is not given to people who are pregnant because it may harm the fetus. The fear of becoming pregnant and the wish to become pregnant are both major concerns for many patients taking lithium. Lithium use is also contraindicated in breastfeeding people and in children younger than 12 years of age.

Question 185

Anticonvulsant drugs are thought to be:

Answer 185

• Superior for continuously cycling patients
• More effective when there is no family history of bipolar disorder
• Effective at dampening affective swings in schizoaffective patients
• Effective at diminishing impulsive and aggressive behaviour in
  some non-psychotic patients
• Helpful in cases of alcohol and benzodiazepine withdrawal
• Beneficial in controlling mania (within 2 weeks) and depression
  (within 3 weeks or longer)

Question 186

Valproate
Divalproex sodium (Epival)

Answer 186

anticonvulsant

Valproate (available as divalproex sodium [Epival] and valproic acid [Depakene]) has surpassed lithium in treating acute mania. Valproate is also helpful in preventing future manic episodes. Although serious complications are rare, it is important to monitor liver function and platelet count periodically. Divalproex doses can cause drowsiness and dizziness and increase thoughts of sui- cide; therefore mood, ideations, and behaviour should be monitored on a regular basis. Therapeutic serum levels that range from 50 to 100 mcg/ mL and 50 to 125 mcg/mL for mania should be monitored to prevent toxicity and overdose (Burchum & Rosenthal, 2019). Symptoms of cen- tral nervous system toxicity can include confusion, fatigue, dizziness, hallucinations, headache, and ataxia.

Question 187

Carbamazepine

Answer 187

Some patients with treatment-resistant bipolar disorder improve after taking carbamazepine (Tegretol) and lithium, or carbamazepine and an antipsychotic. Carbamazepine seems to work better in patients with rapid cycling and in severely paranoid, angry pa- tients experiencing manias rather than in euphoric, overactive, overly friendly patients experiencing manias. It is thought to also be more effective in dysphoric patients experiencing manias.
Liver enzymes should be monitored at least weekly for the first 8 weeks of treatment because the drug can increase levels of liver en- zymes that can speed its own metabolism. In some instances this can cause bone marrow suppression and liver inflammation. Complete blood counts should also be done periodically since carbamazepine is known to cause leukopenia and aplastic anemia.

Question 188

Lamotrigine

Answer 188

Lamotrigine (Lamictal) is a first-line treatment for bipolar depression and is approved for acute and maintenance therapy. Lamotrigine is generally well tolerated but has one serious, though rare, dermatological reaction: a potentially life-threatening rash. Pa- tients should be instructed to seek immediate medical attention if a rash appears, although most are likely benign.
Adverse drug reactions (ADRs), as indicated by the Canadian Net- work for Mood and Anxiety Treatments (CANMAT), that require pa- tient safety monitoring are:
* Both valproic acid and carbamazepine may cause blood dyscrasias,
hepatotoxicity, and teratogenicity.
* Carbamazepine has also been linked to hyponatremia and serious
dermatological adverse effects.
* Valproic acid has been associated with polycystic ovary syndrome, weight gain, acute pancreatitis, and hyperammonemic encephalopathy. * The severe ADRs associated with lamotrigine are dermatological,
namely Stevens–Johnson syndrome.
* Drug interactions such as lamotrigine–valproic acid and carbam-
azepine–hormonal contraceptives are also important to be aware of.

Question 189

Electroconvulsive Therapy

Answer 189

ECT is used to subdue severe manic behaviour, especially in patients with treatment-resistant mania and in those with rapid cycling (i.e., those who experience four or more episodes of illness per year).
ECT seems to be far more effective than medication-based ther- apy for treatment-resistant bipolar depression (Fornaro et al., 2020). Depressive episodes, particularly those with severe, catatonic, or treat- ment-resistant depression, are an indication for this treatment.

Question 190

Other treatment for mania

Answer 190

anti anxiety; Diazepam (Valium), clonazepam (Rivotril), and lorazepam (Ativan) are antianxiety (anxiolytic) drugs useful in the treatment of acute mania in some patients who are resistant to other treatments. These drugs are also effective in managing the psychomo- tor agitation seen in mania. They should be avoided, however, in pa- tients with a history of substance use.

atypical antipsychotics; Many of the second-generation antipsychotics are approved for acute mania. In addition to showing sedative properties during the early phase of treatment (help with in- somnia, anxiety, agitation), the second-generation antipsychotics seem to have mood-stabilizing properties. Most evidence supports the use of olanzapine (Zyprexa) or risperidone (Risperdal).

Support groups

Health Teaching and Health Promotion; Patients and families need information about bipolar disorder, with particular emphasis on its chronic and highly recurrent nature. In ad- dition, patients and families need to be taught the warning signs and symptoms of impending episodes. For example, changes in sleep pat- terns are especially important because they usually precede, accompa- ny, or precipitate mania.

psychotherapy; Pharmacotherapy and psychiatric mental health care and management are essential in the treatment of acute manic attacks and during the continuation and maintenance phases of bipolar disorder. Individuals with bipolar disorder must deal with the psychosocial consequences of their past episodes and their vulnerability to experiencing future epi- sodes. They also have to face the burden of long-term treatments that may involve unpleasant adverse effects. Many patients have strained in- terpersonal relationships, marital and family problems, academic and occupational problems, and legal or other social difficulties. Psycho- therapy can help them work through these difficulties, decrease some of the psychic distress, and increase self-esteem. Psychotherapeutic treatments can also help patients improve their functioning between episodes and attempt to decrease the frequency of future episodes.

Question 191

Milieu Management

Answer 191

Control of hyperactive behaviour during the acute phase almost always includes immediate treatment with an antipsychotic medication. How- ever, when a person is dangerously out of control, use of a seclusion room or restraints may also be required. A seclusion room provides comfort and relief to many patients who are unable to control their own behaviour. Seclusion serves the following purposes:
* Reduces overwhelming environmental stimuli
* Protects a person from injuring themself or others, including staff * Prevents destruction of personal property or property of others
Seclusion is warranted when documented data collected by the nursing and medical staff reflect the following points:
* Substantial risk of harm to others or self is clear.
* The person is unable to control their actions.
* Problematic behaviour has been sustained (continues or escalates
despite other measures).
* Other measures have failed (e.g., setting limits beginning with ver-
bal de-escalation or using chemical restraints).