Lecture 8

1. Compare & Contrast the 4 levels of Anxiety

• Anxiety - apprehension uneasiness, uncertainty, or dread from real or perceived threat

  • Normally anxiety - necessary for survival 

• Fear - reaction to specific danger 

• Peplau & Anxiety: mild, moderate, severe, & panic 

  • Mild symptoms - individually developed coping mechanisms 

  • Severe cases - may experience serious functional impairment 

2. Identify genetic, biological, psychological, & cultural factors that may contribute to anxiety disorders

• GAD Etiology: 

  • Biological/Genetic: 

    • Highly heritable condition 

    • Increased risk for mood & anxiety disorders w/ a 1st degree relative who has GAD & increased risk (7x) for panic disorder w/ a 1st degree relative who has panic disorder

  • Psychological: 

    • Behavioural theory: anxiety is learned from environmental stimuli or behaviours of others (somatic symptoms appear due to the anxiety/fear which may result in the trigger being avoided -> child gets stomach ache due to fear of bullies at school and then they don’t have to go to school)

    • Cognitive theory: dysfunctional thought leads to extreme emotions -> believes they will fail test which causes panic resulting in failing the exam which strengthens their original belief

    • Learning theory: use of defense mechanisms to avoid the unpleasant thoughts

  • Neurobiological: 

    • Emotional processing: limbic system (amygdala & hypothalamus) regulate emotions, behaviour, motivation, & memory

    • Orbitofrontal cortex (OFC): regulate/controls impulses, mood, emotions, behaviour

    • Prefrontal area: executive function (decision making, etc.) 

    • Anxiety disorders are caused by a disruption in the emotional centers of the brain which could alter higher cognitive centers

  • Neurotransmitter pathways: 

    • GABA neurotransmitter dysregulation or underactivity leads to feelings of anxiousness; GABA also impacts the function of several neurotransmitters (norepinephrine, serotonin, & dopamine)

  • Social/Cultural: 

    • Different cultures believe panic attacks are caused by magic or are related to witchcraft 

      • Cambodians believe anxiety is when someone’s “inner wind” &/or blood flow is disturbed

      • In Chinese culture having anxiety is believed to be caused by or related to organ dysfunction (“weak heart”) 

      • South Asian, South America, the Pacific Islands, & Southern European cultures value group harmony & shame or guilt those who deviate from social rules 

  • Environment: 

    • Exposure to traumatic experiences

    • Parenting style they were raised w/ (over protective or critical or under-responsive)

3. Discuss defense mechanisms & consider adaptive & maladaptive uses of each

• Denial: refuse to accept 

• Displacement: transfer or negative emotions on others 

• Rationalization: provide logical reason to justify difficult/unacceptable feelings 

• Projection: recognize unacceptable traits/ impulses in others to avoid recognizing those traits/impulses in self 

• Regression: individual return to an earlier developmental stage 

4. Discuss the foundational characteristics of GAD, OCD, & PTSD 

• DSM-5 for GAD

  • Excessive anxiety & worry about life circumstances for at least 6 months

  • 3 of the following symptoms accompany the worry 

    • Restlessness or feeling on edge 

    • Being easily fatigued 

    • Difficulty concentrating 

    • Sleep disturbances 

    • Irritability 

    • Muscle tension 

  • Pts w/ GAD also tend to display a depressed mood

  • Autonomic nervous system is hypersensitive to various stimuli in anxious people

• DSM-5 for PTSD

  • Must have all of the following symptoms for at least 1 month 

    • At least 1 re-experiencing symptom

      • Flashbacks (w/ physical symptoms like racing heart)

      • Bad dreams 

      • Frightening thoughts 

    • At least 1 avoidance symptom

      • Staying away from places & events/objects which act as reminders of the traumatic experience 

      • Avoiding thoughts/feelings related to the traumatic event 

    • At least 2 arousal & reactivity symptoms 

      • Being easily disconcerted 

      • Feeling tense or “on edge” 

      • Having difficulty sleeping 

      • Having angry outbursts 

    • At least 2 cognition & mood symptoms 

      • Trouble remembering key features of the traumatic event 

      • Negative thoughts about oneself of the world 

      • Distorted feelings like guilt or blame 

      • Loss of interest in enjoyable activities 

• OCD

  • Obsessions: thoughts, impulses, or images that persist & recur, that individual cannot be dismissed from the mind 

  • Compulsions: ritualistic behaviours an individual feels driven to perform in an attempt to reduce anxiety

5. Identify the risk factors & treatment modalities for GAD, OCD, & PTSD 

• OCD risk factors: 

  • When 1st degree family members have OCD there is an increased genetic likelihood of developing OCD 

  • Abnormalities in frontal cortex and subcortical structures *altered serotonin levels 

  • Childhood trauma has been associated w/ OCD

• PTSD risk factors: having bad coping skills, predisposition to traumatic events & hx of trauma (ex. Abuse, car accident, war, natural disaster), & other basic anxiety issues

6. Discuss the nursing process for GAD 

• Nursing diagnoses: 
  

  • Anxiety (moderate, severe, panic) 

  • Fear 

  • Inadequate coping 

  • Reduced diversional activity 

  • Social isolation 

  • Inadequate health maintenance 

  • Post-trauma stress 

  • Decisional conflict 

  • Insomnia 

  • Sleep deprivation 

  • Fatigue 

  • Hopelessness 

  • Chronic low self-esteem 

  • Spiritual distress 

  • Self-care deficit 

  • Reduced skin integrity 

  • Imbalanced nutrition (more or less than body requirements) 
    

• Interventions: 

  • Promotion of self-care activities 

  • Teamwork & safety 

  • Counselling 

  • Pharmacological interventions & education 

  • Integrative therapy (use of herbs, music, physical activity, meditation) 

7. Describe basic-level & advanced-practice interventions for anxiety & related disorder 

• Advanced practice Nursing: 

  • Behaviour therapy - 

    • Modelling (use of role models) 

    • Systematic desensitization (gradually introducing the fear) 

    • Flooding (exposing pt to an undesirable stimuli/trigger) 

    • Response prevention (not allowing the pt to perform their compulsive ritual) 

    • Thought stopping (interrupting the pts negative thoughts) 

    • Stop Now And Plan therapy (for behaviour issues, emotional regulation, self-control, & problem-solving skills)

  • Exposure therapy 

  • Cognitive restructuring (aim is to make sense/examine the event)

Lecture 9 

1. Identify biological, psychological, & sociocultural factors that may contribute to substance & addictive-related disorders 

• Biological: 

  • Reward pathways - substances stimulate cholinergic receptors which result in a release of neurotransmitter (dopamine) which signals a pleasurable reaction 

  • Psychoactive drugs - have similar structures/chemical compositions as neurotransmitters (alter the messaging system in brain)

  • Inheritability - changes in genetic coding (polymorphism) can cause a family pattern of substance abuse; altered molecular mechanisms caused by substances (cocaine alters protein structure of DISC1 gene) predispose users to the development of psychiatric conditions (SZ, MDD, BP)

• Psychological: 

  • Learning theory - enjoyable activities vs activities which cause distress

  • Tolerance/Habituation - increased doses are needed to provide an effect

  • Personality Theory - extroverts using substances socially (frequent usage)

  • Attachment theory - emotional bonds & a supportive environment makes a person less likely to use compared to someone who experienced early vulnerabilities (stress, crises, etc.) or a lack of support system

  • Self-medication hypothesis - maladaptive coping (substance use to cope)

  • Psychodynamics - failure to resolve conflict between I.D, ego, & superego

• Socio-culture factors: 

  • Some cultures have more prevalent substance use as it is more socially acceptable 

  • Religious cultures may strictly prohibit or may distance from substance use/consumption 

2. Discuss the epidemiology & comorbidity of psychoactive substance use 

• Concurrent disorder (CD) is a combination of a psychiatric comorbidity & a substance use disorder. 24% of those w/ an anxiety disorder have a CD, 47% of SZ people have a CD, 27% of people w/ MDD have a CD, & 56% of BP people have a CD. 

• Younger people tend to use drugs more than those over 25

• Medical comorbidities:

  • Deficiency of Thiamine/Vitamin B1

    • Wernick’s (alcoholic) encephalopathy: Acute & reversible condition which manifests as confusion, paralysis of the CN III (nerve used to move eyes), & peripheral neuropathy/lack of coordination 

    • Korsakoff’s syndrome/psychosis: chronic condition w/ a ~20% recovery rate caused by not treating Wernick’s encephalopathy. Involves psychosis, loss of memory, polyneuropathy, hypothermia, & CVS related issues (tachycardia, postural hypotension, syncope, etc.)

  • Fetal Alcohol Spectrum Disorder: caused by exposure to alcohol in womb; results in impaired learning, birth defects, increased risk of childhood leukemia, etc. 

  • Other Health Issues: Liver Cirrhosis, Gastritis, pancreatitis, Alcoholic Hepatitis, & Hep B & C & HIV (due to needle sharing)

3. List substances used in Canada & how they affect the brain 

• CNS Depressants: increases GABA which inhibits brain activity resulting in a calming effect -> ↓ CNS, HR, BP, anxiety, & processing speed

  • Alcohol, Tranquilizers/Sedatives (Benzos & Barbiturates), Opioids/Fentanyl (natural & synthetic analgesics) (Morphine & Heroin), Cannabis/Marijuana (CS depressant properties), & Inhalants (gas & solvents like Nitrous Oxide, Chloroform, & Acetone) 

  • Treat overdoses w/ Naloxone & withdrawals w/ Methadone 

• CNS Stimulants: inhibit the reuptake of dopamine, serotonin, & norepinephrine which increase CNS & PNS activity -> ↑ CNS, HR, BP, & alertness

  • Caffeine, Nicotine/Tobacco, Amphetamines (Adderall), Cocaine & Crack, & Hallucinogens (cause alter perceptions) such as LSD, psilocybin (shrooms), PCP & Cannabis/Marijuana (b/c of the THC) 

4. Discuss the 4 pillar drug strategy & provide examples 

• Prevention of substance abuse 

• Reduce harm caused by substances (overdoses, infections, spread of communicable diseases)

• Treatment for the harm caused by substances

• Enforce the avoidance of drugs 

Lecture 10 

1. Discuss etiology, clinical manifestations, comorbidity of anger, aggression, & violence 

• Anger: a subjective, emotional response to frustration of desires, threat to one’s needs 

• Aggression: an emotion that results in a verbal or physical attack 

• Rage: an uncontrollable, violent state of anger where a person is unable to think logically

• Violence: the intent to harm (e.g., psychological, physical, & emotional abuse, damage to property, & suicide/self-harm) 

• Biological: 

  • Neurological (temporal & frontal lobes & the limbic system (prefrontal cortex))

    • These areas are responsible for cognition & emotional processing & for memory & emotion control, lesions here can lead to antisocial behaviour 

    • Pt’s at risk include those w/ brain tumors, dementia, epilepsy, or those who have had a stroke 

  • Neurochemical 

    • Serotonin & dopamine can have inhibitory & stimulating effects on aggressive behaviour (it depends on the brain region & where the specific receptors being effected) 

    • GABA receptor modulators can enhance aggression

• Psychological: 

  • Behaviour theory (learned response) - emotions are a learned response to environmental stimuli so when induviduals precieve a threat anger & aggression are triggered

  • Locus of Control (personal power) 

    • Positive/internal LOC - feel good, empowered, control, decision making, results is reduced anger 

    • Rejection/external LOC - devalued, disrespected, powerless, leads to anger & aggression 

  • Social factors 

    • Social learning theory - imitate those around you (ex. If a child grows up seeing their parents abusive relationship, when the child is older & in their own relationship they have a strong likelihood or repeating the abuse)

    • Cultural variations - in different culture people are conditioned to react differently to various conditions & they may also have different triggers

• Comorbidities:

  • Hx of violence (best predictor)

  • Limited coping skills (lack of assertiveness or the use of intimidation)

  • Demographic: Males (females have more oxytocin which reduced the amygdalas response to negative stimuli), age 14-24, low socioeconomic status or economic inequalities, Hx of family violence, subtsnace abuse, inadequate support system, prison time

  • Psychotic behaviours, delusions, hyperactivity, impulsiveness (BP, BPD), PTSD, MDD, & anxiety 

• Signs/Symptoms: ridgid posture, pacing, hyperactivity, clenched jaw or fists; impaired functioning (difficulty w/ simple tasks or being unable to preform a task the way they previously could); poor cognitive functioning; mood is tense, angry, impatient; impulsive; self-harm

2. Explore the nursing process & effective de-escalation techniques for managing a potentially aggressive pt

• Assessment; hx of violence, trauma, psychosis; coping skills; disorders including cognition inhibition; physical appearance (clenched fists, anger, yelling/shouting, avoiding eye contact, threats, self-harm, alertness)

• Diagnosis: 

  • Ineffective coping 

  • Stress overload 

  • Risk for self-directed violence 

  • Risk for other-directed violence 

• Outcomes: 

  • Ensure safety 

  • Maintain therapeutic relationship 

  • Engage w/ social supports 

  • Promote effective coping skills 

• Implementation: 

  • Maintain a non-aggrecive posture 

  • Speak slow, clear, & calm 

  • Keep safe distance & avoid touching agitated pt

  • Assess & remove stressors/triggers 

  • De-escalate 

  • Pharmacological interventions

  • Health teaching/promotion (coping skills)

  • Milieu Management - aim is to provide an environment which encourages healthier ways of thinking/behaving 

    • Short term is used to help a pt regain composure (put in time out in either their own bedroom or a therapeutic room)

    • Long term consists of a structured supportive environment where pts follow a consistent way of living & are encouraged to participate in activities

  • Last resort of restraints or seclusion 

3. Discuss restraints & some of the rules surrounding them (including documentation) 

• Advocate for the least restraint possible

• Inform client of their rights & explain why the are being restrained 

• Review the conditions which lead to use of restraints 

• Review the response from client 

• Document strategies used before having to resort to restraints & must document use of restraints, what type is being used, & continue to monitor & update document 

Lecture 12 

1. Discuss early stress response theories 

• Walter Cannon (father of modern stress research) 

  • Homeostasis 

  • Flight-or-fight response - sympathetic nervous system kicks in resulting in ↑ HR, BR, cardiac output, RR, pupil dilation, & ↓ serotonin 

• Hans Selye 

  • General Adaptation Syndrome (GAS)

    • Alarm/Acute stress stage (flight-or-fight occurs) 

    • Resistance/Adaptation stage (cortisol levels remain in blood for extended period of time & parasympathetic nervous system kicks in to counteract the flight-or-fight) 

    • Exhaustion stage (energy reserve depletes - possible for a psychiatric disorder to develop)

  • Body prepares for stress/threats the body perceives in different ways depending on sex (females have more oxytocin which reduces aggression/decrease stress) 

• Neurotransmitter: ↑ cortisol production impairs serotonin receptor sites (therefore preventing the brain’s ability to use serotonin) 

• Immune system: the nervous system interacts w/ the immune system during the Alarm stage of GAS, this negatively affects the body’s health
  

  • High resting heart rate 

  • Heart disease 

  • Platelet aggregation 

  • Reactive high BP 

  • High triglycerides 

  • renal/hepatic problems 

  • Glucose intolerance 

  • Chronic muscle tension 

  • Hyperventilation 

  • Digestive problems chronic anxiety/anger 
    

2. Describe mediators of the stress response 

• Physical stressors such as homelessness, natural disasters, living in a war zone or dangerous area

• Psychological stressors such as grief, fighting amongst family & friends, divorce, job loss, school grades, performance pressure 

• Personal temperament or perception of stress 

• Social supports such as support groups, cultural views of stress, spirituality & religious consultation/guidance 

3. Identify & describe holistic approaches to stress management 

• Deep breathing exercises 

• Progressive muscle relaxation 

• Relaxation response (chemicals released when peak state of relaxation is met; they slow RR & HR)

• Reduction of caffeine 

• Meditation 

• Guided imagery 

• Biofeedback (regulate & control body function to improve physical performance)

• Physical exercise & outdoor activity 

• Cognitive reframing (change in the perception - e.g., “I can do it”)

• Journaling 

• Humour 

4. List Thomas Holmes & Richard Rahe well-being strategies 

• Health sustaining habits (such as medical compliance, proper diet, & rest) 

• Life satisfaction measures (hobbies, work, pets, spiritual solace, arts, & nature) 

• Social supports (talking w/ family & friends, support groups)

• Effective & healthy responses to stress (exercise/working out, yoga, medication, guided imagery, etc.)

5. Differentiate among the 3 types of crisis & 4 phases of crisis 

• Maturational - a new developmental stage is reached 

  • Old coping skills are no longer effective 

  • Leads to increased tension & anxiety 

  • E.x., marriage, birth, pregnancy, divorce, new job 

• Situational - arise from new events 

  • External, often unanticipated (though not always)

  • E.x., job loss, sudden death/illness, injury 

• Adventitious - unplanned/accidental/disaster 

  • Crime of violence, national disaster, natural disaster, war 

• Crisis Stage 1: initial threat or triggering event 

  • Increase of psychological tension (brief, unnoticed) 

• Crisis Stage 2: escalation 

  • Further increase of psychological tension (acknowledged) 

• Crisis Stage 3: crisis 

  • Psychological distress (anxiety, discomfort) 

• Crisis Stage 4: personality disorganization 

  • Severe psychological tension, disorganization, symptoms, unbalance, CRISIS

6. Identify modalities of crisis intervention 

• Crisis lines; mobile teams; urgent care clinics; in-hospital emergency psychiatric care (including medical & other interventions)

7. Discuss the effects of Serious Mental Illness (SMI) on daily functioning, interpersonal relationships, & QOL

• Having a SMI can cause other mental illnesses like depression & suicidal ideation 

• There are social issues such has stigma, isolation, loneliness, & victimization 

• Economic challenges such as unemployment, poverty, housing instability, & caregiver burden 

• Issues in the SMI treatment also exist such as poor insight, problems w/ adherence, inadequate treatment, adverse effects of medication, residual symptoms, relapse, & chronicity

8. Discuss concepts of rehabilitation & recovery 

• Rehabilitation: 

  • Training/providing services (ex. help patients learn to live with their illness)

  • Managing patient's deficits

  • Process used by practitioner to facilitate recovery of a pt 

• Recovery: 

  • Achieving goals to overcome the challenges of illness/disability - deeply personal 

  • Leading increasingly productive & meaningful lives 

  • Hopeful, empowering, & strengths-focused 

  • A process consumer/survivor undertake - self/patient driven 

9. Discuss 5 evidence-informed practices for the care of SMI pts 
   

• Assertive community treatment (ACT) 

• Cognitive behavioural therapy (CBT)

• Cognitive enhancement therapy (CET) 

• Family support & partnership 

• Social skills training 

• Supportive psychotherapy 

• Vocational rehabilitation & related services
  

10. Explain the role of the nurse on the care of a person w/ SMI

• Assessment: MSE, social supports, physical health, adherence to treatment 

• Diagnosis: 

• Interventions: 

  • Empowering, whole-person approaches 

  • Motivational interviewing 

  • Emphasizing quality-of-life issues 

  • Developing & maintaining relationships 

  • Supportive psychotherapy 

  • Reality checking for psychosis 

  • Activities that increase skill & comfort w/ socialization 

  • Education & support groups for patients & families 

  • Harm reduction & abstinence for comorbid substance use

Medications: 

• Alzheimer’s: 

  • 1st line of treatment is acetylcholinesterase inhibitors or anti-cholinesterase 

    • Prevents the breakdown of the chemical messenger acetylcholine-ɑ. Keeping the level of acetylcholine high, communication via nerve cells is supported. 

    • Donepezil (Aricept) & Rivastigmine (Exelon) 

    • Side effects: nausea, vomiting, diarrhea, urinary incontinence, dizziness, headache, rash (when using Galantamine (Reminyl))

  • N-Methyl-D-Aspartate (NMDA) Receptor Antagonist 

    • Regulates (decreases) activity of glutamate-ɑ neurotransmitter. Aids in the role of information processing, storage, & retrieval. Memantine-ɑ (Namenda) is the drug of choice as it best maintains pt’s Ca level. 

    • Side effects: nausea, vomiting, diarrhea, anorexia, transient bradycardia (sudden decreased HR), falls

  • Namzaric is the trade name for a mixture of both Donepezil & Memantine 

• MDD 

  • Dopamine reuptake inhibition side effects: decreased depression, psychomotor activation, & antiparkinsonian effects 

  • Serotonin antagonists (block action of serotonin receptors) side effects: reduced depression, reduced suicidal behaviour, antipsychotics effects, hypotension, & ejaculatory dysfunction

  • Serotonin reuptake inhibitors side effects: reduced depression, anti-anxiety effects, GI disturbances, & sexual dysfunction 

  • Norepinephrine reuptake inhibitors side effects: reduced depression, tremors, tachycardia, erectile/ejaculatory dysfunction (priapism = prolonged erection w/ lack of appropriate stimulation), postural hypotension, dizziness, reflex tachycardia (when BP decreases HR increases in an attempt to accommodate), memory dysfunction

  • 1st line of treatment SSRIs

    • Citalopram (Celexa), Escitalopram (Cipralex & Lexapro), Fluoxetine (Prozac), Fluvoxamine (Luvox), Paroxamine (Paxil), Sertraline (Zoloft) 

    • Side effects: upset/agitated GI tract, insomnia (recommended to take in AM), drowsiness (recommended to take in PM), anticholinergic effects (constipation, urinary retention, dry mouth, blurred vision), sexual dysfunction (impairment of desire, arousal, &/or orgasm & ejaculation) & serotonin syndrome

  • Also 1st line agents SNRIs

    • Venlafaxin (Effexor XR), Duloxetine (Cymbalta), & Desvenlafaxine (Pristiq) 

    • Side effects: hypotension in high dosages (due to increased sympathetic nervous system simulation), otherwise the same as SSRIs, though SNRIs tend to have less GI related side effects and have more frequent neurological side effects; SNRIs also have more sexual dysfunction related side effects. 

  • Also 1st line agents NDRIs

    • Bupropion (Wellbutrin & Zyban)

    • Side effects: insomnia, dry mouth, agitation, constipation; increased risk of seizures w/ higher dose, sexual dysfunction (much less frequent than w/ other meds)

  • Serotonin Modulator/Stimulator

    • Thought to interfere with the action of serotonin receptors

    • Trintellix (Vortioxetine) & Vilazodone (Viibryd)

    • Side effects: nausea, constipation, & vomiting 

  • 2nd line of defense, 1st generation (typical) TCAs

    • Amitriptyline (Elavil & Vanatrip), Clomipramine (Anafranil), Desipramine (Norpramin), Doxepin (Silenor), Mirtazapine, Nortriptyline (Aventyl & Pamelor), Imipramine (Tofranil), & Trimipramine (Surmontil)

    • Side effects: constipation, dry mouth, drowsiness, dizziness, urinary retention, blurred vision, high risk for suicide, tachycardia, orthostatic hypotension, seizures, increased appetite, & weight gain

  • 2nd line of defence, 1st generation (typical) MAOI

    • Moclobemide (Amira, Aurorix, Clobemix, Depnil, & Manerix), Phenelzine (Nardil), and Tranylcypromine (Parnate)

    • Side effects: dizziness/lightheadedness, dry mouth, nausea, diarrhea, constipation, drowsiness, insomnia, hypotension, high risk for suicide, seizures, weight gain, hypertensive crisis (when consuming foods containing tyramine - chocolate, fermented foods, cheese, alcohol, picked vegetables)

• Bipolar

  • 1st line of treatment is Lithium 

    • Mood stabilizer which can take 1-3 weeks for effects start to work 

    • Appropriate blood level is 0.6-1.2meq/L (>1.5meq/L results in diarrhea, twitching/tremors, & vomiting) 

    • Side effects: upset GI tract (helps to take dose w/ food), fine hand tremor, weight gain (caused by fluid retention), renal toxicity, increased negative side effects (when taken with a high salt diet)

      • More salt = less blood lithium (increases side effects of BD)

      • More water = more blood lithium (increase side effects of lithium)

  • Anticonvulsants 

    • Inhibit Na channels, Ca channels, glutamatergic neurotransmitter, & enhance GABA system 

    • Gabapentin (Horizant, Gralise, & Neurontin)

    • Carbamazepine (Tegretol): 

      • Agitation & acute mania 

      • Side effects: anticholinergic effects (urinary retention, orthostatic hypotension, dry mouth), bone marrow suppression, hematological disease, leukopenia, neutropenia, thrombocytopenia, increased hepatic metabolism (due to increased liver enzymes), & may cause leukopenia & anemia 

    • Valproate (Epival) 

      • For acute mania

      • Side effects: drowsiness, weight gain, tremors, hallucinations

      • Rare: thrombocytopenia, hepatotoxicity, pancreatitis, & hepatic failure (nursing considerations include monitoring liver function & drug serum level)

    • Lamotrigine (Lamictal)

      • Depressive episodes 

      • Side effects: Steven-Johnson Syndrome (life-threatening rash) (nursing action to teach pt to avoid using Valproic acid or carbamazepine in conjunction w/ this med)

  • Antipsychotics for BP

    • Olanzapine (Zyprexa) or Risperidone (Risperdal) 

      • Sedation & mood-stabilizing effects for acute mania

      • Side effects: weight gain, increased blood glucose, risk for metabolic syndrome 

  • Anxiolytic AKA anti-anxiety for BP 

    • Diazepam, clonazepam, lorazepam 

      • For short-term acute mania relief 

      • Side effects: reduce agitation/anxiety 

• Psychosis 

  • Conventional/Typical Antipsychotics (1st generation) 

    • Chlorpromazine (Thorazine), Flupentixol (Depixol & Fluanxol), Fluphenazine Decanoate (Modecate, Modiren, Prolixin, & RhoFluphenazine), Haloperidol (Haldol), Loxapine (Loxitane & Adasuve), Pimozide (Orap), & Zuclopenthixol (Cisordinol & Clopixol).

    • Side effects: sedation, constipation, dry mouth, weight gain, Extrapyramidal Movement Disorders/EPS (pseudoparkinsonism, acute dystonia, & akathisia), urinary retention

    • Rare: hyperprolactinemia (menstrual irregularities) in women, gynecomastia in men & galactorrhea in both

  • Atypical Antipsychotics (2nd & 3rd generation)

    • Aripiprazole (Abilify), Asenapine (Saphris), Lurasidone (Latuda), Olanzapine (Zyprexa), Paliperidone (Invega), Quetiapine (Seroquel),  Risperidone (Risperdal), & Ziprasidone (Zeldox)

    • Side effects: weight gain, sedation, dizziness, constipation, dry mouth, urinary retention, orthostatic hypotension, falls, increased risk of diabetes, & higher doses can cause EPS (pseudoparkinsonism, acute dystonia, & akathisia)

    • Clozapine (Clozaril): 

      • Most effective than any other agent at treating both positive, negative, & cognitive symptoms

      • Side effects: agranulocytosis (0.8% of pts), increased sedation & hypersalivation 

  • Dangerous side effects of antipsychotics (stop meds when any occur):

    • Tardive dyskinesia - repetitive, involuntary movements including frequent blinking, brow arching, grimacing, lip smacking which may be irreversible 

      • Occur w/ persistent EPS or prolong treatment of APs, (even when treatment is D/C) 

    • Anticholinergic toxicity - dry mucous membrane, non-reactive pupils, hot & dry red skin, tachycardia, agitation, unstable VS, seizures.

      • *Induced delirium, older adult at risk or use of multiple APs 

    • Neuroleptic malignant syndrome (NMS) - reduce consciousness, muscle rigidity, hyperthermia, increase pulse & respiration, diaphoresis, drooling. Early detection is important, stop the medication

      • Reduction in brain dopamine activity. Rare but potentially fatal. 

    • Agranulocytosis - fever, malaise, flu like symptoms - blood work -> watch for leukopenia or granulocytosis

      • Absence of granulocytes 

    • Pseudoparkinsonism - rigidity, mask like face, shuffling gait 

    • Acute dystonia - acute progressive stiffness & twitching of muscles 

    • Akathisia - motor restlessness (patient unable to sit or stand still) often misdiagnosed as psychotic agitation - increase dose of antipsychotic 

• GAD 

  • Benzodiazepines 

    • Enhance the inhibitory effects by targeting GABA receptors

    • Clonazepam (Rivotril), Lorazepam (Ativan), & Diazepam (Valium) (anything ending in “pam”)

    • Most effective benzos have the following side effects: somatic & autonomic symptoms like muscle tension, dry mouth, & increased sweat production

    • Common side effects: drowsiness, dizziness, reduced concentration, retrograde amnesia, physical dependence (w/d upon discontinuation), high addiction potential, & increased falls risk (elderly)

      • Monitor for: talkativeness, emotional release, excitement, & excessive movement 

  • Hypnotics: Zopiclone (Imovane) - faster onset

  • Melatonin receptor agonists: Busprione hydrochloride (Bustab) - less sedative effect but provides short term relief 

  • Beta Blockers: Atenolol (Tenormin)