Mental Health Exam 2

Monoamine oxidate

enzyme responsible for deactivating monoamine neurotransmitters

dopamine

• monoamines

• movement and coordination , emotions, voluntary judgement, reward signals

• an excitatory neurotransmitter that is responsible for transmitting info about emotional responses, complex movements, and cognition

• responsible for pleasure and reward from behaviors

• its neurotransmission can be affected by stress

• contributes to depression

increased levels of dopamine are associated with

mania and schizophrenia

decreased levels of dopamine are associated with

parkinsons and depression

serotonin

• monoamines

• neurotransmitter is responsible for emotional regulation, sexual behaviors, temperature regulation, sleep, and pain perception

• appetite and aggression

high and low levels of serotonin are associeted with

anxiety

norepinephrine

• monoamines

• excitatory neurotransmitter that is responsible for learning, sleep, memory, mood, and attention

• associated with anxiety and depression

• regulates mood, perception, attention, memory, and sleep-wake

histamine

• monoamines

• neuromodulation

• regulate the release of histamine, glutamate,, serotonin,, and gaba

• alertness and wakefulness

• sleep-wake cycle, psychomotor activity, appetite

• associated with anxiety, depression, and psychosis

GABA (gama amino butyric acid)

• amino acid

• inhibitory neurotransmitter

• modulates other neurotransmitters

• slows down body activity

• promotes neuronal development, improves sleeplessness, and minimizes manifestations of depression

• benzos enhance the binding of GABA to reduce manifestations of anxiety and inducing sleep

glutamate/ aspartate

• amino acid

• excitatory neurotransmitter

• interacts with dopamine to regulate motor, affective, and cognitive functions

• low levels are associated with autism, OCD, depression, and schizophrenia

acetylcholine

• cholinergic

• inhibitory and excitatory properties

• found particularly in skeletal muscles

• regulates sleep-wake cycle

• primary neurotransmitter in muscle functioning

• low levels are associated with neurocognitive disorders (alzheimer’s)

somatostatin

neuromodulator of other neurotransmitters

neurobiology

studies how the functioning of the brain impacts behavior and attempts to answer questions related to mental health

neuroplasticity

the brain’s ability to adapt synaptic connections, particularly in response to stress or learning or after experiencing an injury

anxiolytic (antianxiety): benzodiazepines

• most prescribed med for treating anxiety

• regulate GABA: binds to GABA receptor sites, causing an influx of chloride to enter the neuron, producing a major inhibitory effect

  • this creates a cascading effect when benzos is intoroduced to the brain causing a large amount of dopamine to be released into the limbic system

    • dopamine release increases risk of dependance

• CNS depression

• manifestations are related to CNS depression: sedation, poor concentration, impaired memory, drowsiness

  • next day sedation: a result due to its long half-life

  • paradoxical response: iside effects are observed that are opposite of the intended effect

• fall risk

• toxicity: soltuion is FLUMAZENIL

• no alcohol or other CNS depressants

• SEDATIVE effect is SERIOUS, so plan accordingly

• long-term use creates a tolerance and becomes dependent on the substance

• DO NOT ABRUPTLY DISCONTINUE→ must TAPER

anxiolytic (antianxiety): buspirone

• doesn’t depress CNS

• partial serotonin receptor agonist and weak dopamine receptor antagonist which doesn’t affect GABA receptors

• commonly used to treat anxiety

• no addiction potential

• acts on serotonin receptors causing side effects like sedation, nausea, headaches, and dizziness

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Antidepressants: Monoamine oxidase inhibitors (MAOIs)

• mechanism of action: inhibits the function of the enzyme monoamine oxidase

• Adverse Effects: weight gain, daytime sedation, sexual dysfunction, and insomnia

• avoid eating tyramine rich foods due to the increased risk of hypertensive crisis

  • aged/strong cheese: swiss and blue cheese

  • cured and processed meat: with nitrate and salt

  • sauces: teriyaki, fish, shrimp, soy

  • dried or overripe fruit: raisins, prunes, avocado, bananas, wine

Antidepressants: tricyclic antidepressants (TCAs)

• mechanism of action: affects serotonin and norepinephrine by blocking their reuptake in presynaptic receptors

• Adverse Effects: blocks cholinergic receptors which result in anticholinergic effects like dry mouth and consftipation

  • risk of orthostatic hypotension

  • may develop a tolerance to anticholinergic effects of TCAs with long-term use

• may take 2-4 weeks to begin to work

Antidepressants: Selective Serotonin Reuptake Inhibitors (SSRIs)

• mechanism of action: affects serotonin by selectively blocking the reuptake of presynaptic receptors

• Adverse Effects: may experience nausea, agitation, and sexual dysfunction

• may take 4-6 weeks to work

Antidepressants: Serotonin Norepinephrine Inhibitors (SNRI)

• mechanism of action: affects serotonin and norepinephrine by selectively blocking the reuptake of presynaptic receptors

• Adverse Effects: may experience nausea, agitation, sexual dysfunction, and appetite suppression

Antidepressant warnings

• Anyone beginning or increasing the dosage of any antidepressants should be watched closely for worsening depression or unusual behavior, including suicide

• client should avoid herbal remedies

• client should avoid taking MAOIs with other TCAs and OTC drugs that contain ephedrine

antipsychotics (neuroleptics)

• used to treat manifestations in schizophrenia and other psychotic-related disorders

• 2 generations of antipsychotics:

  • First generation antipsychotics (FGA): typical

    • work by blocking dopamine receptors

    • very potent dopamine antagonists that can be effective at treating severe manifestations of schizophrenia

    • potency can cause concerning side effects

    • ex: haloperidol, fluphenazine, clozapine, and chlorpromazine ,

  • Second generation antipsychotics (SGA): atypical

    • work by blocking dopamine receptors to a lesser degree and by inhibiting the reuptake of serotonin

    • treats a different profile of manifestions than FGA

    • Three SGAs: aripiprazole, brexpiprazone, and cariprazine are sometimes called third generation antipsychotics (TGA) they are dopamine stabilizers

• long term IM antipsychotic med can be given IM and are depot injections

• adverse effects:

  • anticholinergic manifestations: dry mouth, constipation, blurred vision, and OH

  • can cause enlargement of breast tissue, decreased sex drive, menstrual irregularities, and weight gain

  • SGA: metabolic side effects are more common→ increased blood sugar, increased blood pressure, and increased cholesterol

• teaching

  • med compliance

  • routine labs: blood glucose and lipid levels (SGA)

    • ANC for clozapine

Mood stabilizers: Lithium

• for mood dysregulation disorder like bipolar

• has effect on regulating the reuptake of monoamine neurotransmitters

• the primary med used to treat mood dysregulation

• Adverse effect: diarrhea, nausea, increased thirst, fine hand tremors, weight gain

  • more than half of the clients who discontinue lithium therapy decide to do so beause of the AEs

• incresed sodium levels reduce effectiveness of lithium while low sodium levels increase absorption of lithium and lead to toxicity

• emphasize non-pharm interventions in reducing stress

• bloodwork to check lithium levels (0.6-1.2) every few days to a few weeks

  • initial treatment: 1-2x/week

  • weekly or every 2 weeks until therapeutic which then turns to monthly

• Kidney function should also be monitored

• consume 2-3L of water per day to help kidneys excrete lithium and minimize the risk of lithium toxicity

• avoid excessive sweating

• report all OTC meds, herbals, caffeine

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mood stabilizers: anticonvulsants and SGA aripiprazole (depot injection)

• if lithium is not well tolerated, anticonvulsants like carbamazepine and valproic acid can also be used

  • these inhibit the kindling process, that causes seizure activity to increase in severity and occurence

    • may be linked with episodes that produce mania and explain why this is effective

  • increased levels of GABA

  • may require blood seerum concentration levels 12 hours post admin and liver function

  • adverse effects:

    • sedation

    • dry mouth

    • possible weight gain (depends on med) or weight loss (med dependent)

  
  

• outside of acute bipolar episodes, the SGA aripiprazole, as a depot injection, is effective at helping the client remain stable in the maintenance phase of treatment

  • once monthly

  • IM only- gluteal or deltoid

sedative hypnotics

• used to treat the sleep-wake disorder insomnia

• benzodiazepines

• nonbenzodiazepine hypnotic: act on benzodiazepine site of GABA receptor

  • mechanism of action: like benzo but have fewer AEs

• melatonin receptor agonist: usually prescibed to pts who have difficulty falling asleep

• AE: headache, fatigue, dizziness, and nausea

  • more serious: sleep-driving, sleep-walking, amnesia, hallucinations, and suicide idealation

• never take prior to operating a vehicle

• avoid alcohol and other CNS depressants

• often short term treatment

stimulants

• CNS stimulants are primarily used to treat manifestations of ADHD and narcolepsy

• cause presynaptic neuron to release dopamine, serotonin, and norepinephrine. the med also inhibits the reuptake of them

• improvement in reduction of hyperactivity, impulsivity, and inattentiveness

• CNS stimulants to aid in the treatment of certain sleep disorders like narcolepsy

• AE:

  • nausea, dry mouth, heart palpitations, and irritability

  • monitor for decreased appetitie which can lead to weight loss

• teaching

  • emphasize diet considerations

  • avoid caffeine

Serotonin syndrome

• high influx of serotonin

• manifestations:

  • restlessness

  • sweating

  • dilated pupils

  • tachycardia

  • increased BP

  • muscle rigidity and loss of muscle coordination

• interventions

  • vital sign stabilization

  • sedation with benzodiazepines

  • admin of serotonin antagonist med like cyproheptadine

activation syndrome

• set of manifestation which include impulsivity and suicidal idealation that may present after starting and antidepressant

• manifestations: irritability, anxiety, impulsivity, aggressiveness, agitiation, possible increased thoughts of suicide

• interventions

  • awareness of client behaviors

antidepressant discontinuation syndrome (ADDs)

• clinical manifestations that may occur with sudden discontinuation of the antidepressant med which the client has been taking for more than a month

• manifestations

  • difficulty sleeping, anxiety, depression, and flu-like symptoms

  • may report electric-shock-like symptoms

  • if abruptly stopping MAOIs, psychosis may occur

  • manifestations may persist for weeks

• interventions

  • PREVENTION

  • taper off med

Lithium toxicity

• early toxicity:

  • lithium level of greater than 1.5

  • neuro dysfunction like poor coordination, confusion, and sedation

  • gi dyscomfort, nausea, coarse tremors, vomiting, and diarrhea

  • withhold lithium treatment and contact provider

• advanced toxicity: 2.0-2.5

  • seizure and stupor

  • extemely diluted urine, blurred vision, respiratory complications, tinnitus, and jerking motor movements

  • admin urea or mannitol can help increase the rate of kidney excretion

  • if intentional overdose, consult for possible gastric lavage

• Severe toxicity: greater than 2.5

  • rapid deterioration with the advent of a comatose state

  • risk of severe respirator complication, leading to death

  • initiate hemodialysis

agranulocytosis

• potential, life-threatening condition in which the blood has a low number of WBCs

• commonly caused by taking antipsychotics (esp. clozapine)

• manifestations

  • flu-like symptoms

    • fever

    • sore throat

    • fatigue

    • muscle aches

• interventions

  • before beginning clozapine, get a baseline WBC

  • weekly testing is required even after discontinuation of med

neuroleptic malignant syndrome

• a potentially life-threatening reaction to antipsychotic drugs characterized by fever, altered mental status, muscle rigidity, and vital sign instability

• manifestations

  • fever

  • encephalopathy

  • vital sign instability

  • elevated creatine kinase

  • rigidity of muscles

• interventions

  • immediate discontinuation

  • monitor fluid and electrolytes

  • initating cooling measures

  • cardiac monitoring

  • consider starting a dopaminergic agent (bromocriptine) or a skeletal muscle relaxing med like dantrolene

extrapyramidal symptoms (EPS)

• a set of manifestations caused by blocking dopamine in the midbrain to the brainstem

• manifestations

  • acute dystonia: muscle rigidity or spasms caused by the use of antipsychotics

  • akathisia: feelings of severe restlessness not relieved by movement caused by the use of antipsychotics

  • pseudoparkinsonism: clinical presentation in which manifestations appear to mimic those of parkinsonism

  • tardive dyskinesia: abnormal involuntary movements that are caused by the use of antipsychotic meds

  • additonal manifestations:includes increased manifestations of anxiety and sometimes even pain

• symptom management and interventions

  • can be relieved by anticholinergic drugs like benzotropine or benedryl

  • if td is experienced, and antichol drugs aren’t working consider valbenazine

  • monitor if eps does not resolve after antipsychotic med has been administered

  • administer the abnormal involuntary movement scale (AIMS), and evidence-based assessment of the level of tardive dyskinesia based on client’s abnormal movement

alcohol withdrawal

• long term use of CNS depressant

• adaptation respnse results from prolonged alcohol consumption results in decreased GABA and increased glutamate functioning

• tolerance

• alcohol withdrawal

  • CNS excitation

• the brain must now function without alcohol

• brain adapted to function with decreased inhibitory and increased excitatory functioning

• excessive amounts of glutamate cause CNS excitation

  • increased HR, inreased BP, n/v, increased seizure risk, hallucinations

  • benzodiazepines are used to bring the brain and body back into a state of balance

opiate overdose

• when consumed long-term, they create a sense of euphoria, which trigger the brain’s adaptation

• acute opiate intoxication: reduced levels of norepinephrine cause drowsiness and pain relief

• chronic exporsure alter neuron function and cause the release of large amounts of norepinephrine

  • adaptive reponse to prolonged consumption result in the down-regulation of opiate receptors, resulting in desensitization of receptor signaling, and upregulation of opiate metabolism

  • withdrawal results in a surge of norepinephrine reslease which manifests as muscle aches and severe discomfort

    • muscle aches, goose flesh, gi discomfort, and sweating

    • gi discomfort to the pointn of severe vomitting and diarrhea, which results in dehydration and severe electrolte imbalances

• interventions

  • admin an opiate replacement like methadone or buprenorphine

  • opiate toxicity: naloxone which reverses respiratory depression, coma, etc

    • monitor for nausea, vomiting, tachycardia, diaphoresis, and returing respiratory depression

    • monitor VS every 5 to 15 minutes for several hours after admin and have emergency equipment available in the event of a full withdrawal

Bowlby Model

Phase 1 = Shock – numbness or protest; the reality of loss is not recognized.

Phase 2 = Yearning/Protest – disequilibrium – weeping, anger, despair

Phase 3  = Despair & disorganization when trying to fill the space for the loss and longing for the loved one, and coming to a place of acceptance of the loss. Consider the sense of hopelessness, despair, questioning, and anger that occurs when trying to make sense of life while still desiring or yearning for the loved one.

Phase 4 = Reorganization occurs as the individual gains acceptance of the current life without the loved one and makes sense of what a new normal way of living will be

Kubler ross model

Denial – Protects the individual against the psychological pain of reality

Anger – Reality sets in – Usually an elevated level of anxiety occurs.  Confusion or inability to function independently. Somatic complaints are common.

Bargaining: ask God/Spiritual power for a second chance or more time “ If only I could…”  “If only I had…”

Depression – mourns for what is lost  - feelings of helplessness or hopelessness – watch for regression, withdrawal, and social isolation

Acceptance – methods of coping are established – less preoccupied with the loss and interest in other aspects of life