MENTAL HEALTH Flashcards

Question

extrapyramidal symptoms

Answer 1

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.

Answer 2

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.

Answer 3

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.

Answer 4

a period of abnormally and persistently expansive/ irritable mood, including persistently increased goal directed activity/ energy An exaggerated euphoria or irritability.

Answer 5

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)

Answer 6

endogenous chemicals that conducts nerve impulses between nerve cells

Answer 7

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

Answer 8

emotional disorder; changes in mood

Answer 9

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

Answer 10

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)

Answer 11

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

Answer 12

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

Answer 13

a drug that stimulate the CNS

Answer 14

process of eliminating a toxic substance from the body

Answer 15

stimulation, excitement, or stupefaction produced by a chemical substance

Answer 16

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

Answer 17

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

Answer 18

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

Answer 19

a neurological disorder characterized by apathy, drowsiness, ataxia, nystagmus, ans ophthalmoplegia caused by thiamine deficiency secondary to alcohol misuse

Answer 20

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

Answer 21

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

Answer 22

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

Answer 23

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

Answer 24

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

Answer 25

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

Answer 26

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

Answer 27

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

Answer 28

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

Answer 29

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

Answer 30

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

Answer 31

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)

Answer 32

distressing motor restlessness

Answer 33

painful muscle spasms

Answer 34

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

Answer 35

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

Answer 36

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

Answer 37

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

Answer 38

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

Answer 39

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

Answer 40

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)

Answer 41

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

Answer 42

excitatory/ inhibitory nicotinic-always excitatory

Answer 43

excitatory/ inhibitory a "feel good" neurotransmitter release enhanced by amphetamines; removal from synapse blocked by tricyclic antidepressants and cocaine

Answer 44

excitatory/ inhibitory a "feel good" neuroransmitter. deficient in PD dopamine neurotransmission increases on schizophrenia

Answer 45

mainly inhibitory plays a role in sleep, appetite, nausea, migraine headache, and regulating mood drugs that BLOCK its uptake relive anxiety and depression.

Answer 46

excitatory/ inhibitory involved in wakefulness, appetite control, and learning, and memory

Answer 47

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

Answer 48

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

Answer 49

drugs is aimed to block dopamine effects

Answer 50

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

Answer 51

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

Answer 52

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

Answer 53

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

Answer 54

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

Answer 55

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

Answer 56

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.

Answer 57

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

Answer 58

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.

Answer 59

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.

Answer 60

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

Answer 61

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.

Answer 62

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

Answer 63

A group of diagnoses related to disturbances in mood.

Answer 64

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

Answer 65

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

Answer 66

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

Answer 67

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.

Answer 68

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.

Answer 69

Any intense and strongly defended irrational suspicion.

Answer 70

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

Answer 71

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

Answer 72

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

Answer 73

selective serotonin reuptake inhibitors (SSRIs)

Answer 74

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

Answer 75

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.

Answer 76

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

Answer 77

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

Answer 78

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.

Answer 79

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.

Answer 80

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

Answer 81

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

Answer 82

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

Answer 83

A form of degen- erative dementia.

Answer 84

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

Answer 85

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.

Answer 86

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

Answer 87

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

Answer 88

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.

Answer 89

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

Answer 90

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 91

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.

Answer 92

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

Answer 93

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).

Answer 94

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.

Answer 95

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.

Answer 96

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)

Answer 97

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.

Answer 98

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

Answer 99

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

Answer 100

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.

Answer 101

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).

Answer 102

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.

Answer 103

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

Answer 104

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).

Answer 105

regulation of mood, sleeo, appetite

Answer 106

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

Answer 107

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

Answer 108

the neurotransmitter responsible for fight or flight response (SNS) adrenergic

Answer 109

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.

Answer 110

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.

Answer 111

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

Answer 112

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

Answer 113

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.

Answer 114

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.

Answer 115

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.

Answer 116

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.

Answer 117

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.

Answer 118

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

Answer 119

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)

Answer 120

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.

Answer 121

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.

Answer 122

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.

Answer 123

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.

Answer 124

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

Answer 125

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.

Answer 126

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.

Answer 127

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.

Answer 128

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.

Answer 129

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.

Answer 130

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).

Answer 131

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.

Answer 132

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

Answer 133

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.

Answer 134

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

Answer 135

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.

Answer 136

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.

Answer 137

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.

Answer 138

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.

Answer 139

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.

Answer 140

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

Answer 141

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.

Answer 142

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.

Answer 143

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.

Answer 144

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)

Answer 145

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

Answer 146

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.

Answer 147

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

Answer 148

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.

Answer 149

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.

Answer 150

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

Answer 151

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.

Answer 152

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.

Answer 153

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.

Answer 154

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.

Answer 155

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.

Answer 156

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.

Answer 157

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

Answer 158

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?

Answer 159

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.

Answer 160

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.

Answer 161

* 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)

Answer 162

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.

Answer 163

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.

Answer 164

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.

Answer 165

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.

Answer 166

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.

Answer 167

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).

MENTAL HEALTH Flashcards

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