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Identifying suicide risk factors
IS PATH WARM
Ideation
Substance Abuse
Purposelessness
Anger
Trapped
Hopelessness
Withdraw
Anxiety
Recklessness
Mood
Psychosis
Psychosis is a mental health condition characterized by an
“impaired relationship with reality”
Primary symptoms of psychosis
Hallucinations: Sensory experiences without an external stimulus, common auditory
Delusions: Firmly held false and fixed beliefs that are resistant to reasoning
Disorganized Thinking: Incoherent speech and difficulty organizing thoughts
Secondary symptoms of psychosis
Emotional Disturbance: Blunted or inappropriate affect
Behavioral Changes: Agitation or unusual/change in behaviors including
impulsivity, withdrawn, self-care neglect…
Cognitive Impairment: Impact on memory and concentration
SIG(M)ECAPS
S: Changes in sleep patterns (insomnia or hypersomnia)
I: Loss of interest or pleasure in most or all activities
G: Thoughts of worthlessness or guilt
M: Depressed mood
E: Low energy
C: Poor concentration
A: Changes in appetite or weight
P: Psychomotor disturbances (retardation or agitation)
S: Recurrent thoughts about death or suicide
Hamilton depression rating scale
Clinician-rated tool for research & depression severity
Conducted by trained clinician via structured interview
HDRS length, scoring, symptoms
17-24 items, assesses physical and psychological symptoms
Scoring varies by version, requires clinical interpretation
Focuses on sleep, weight loss, and mood
Patient health questionnaire 9
Self-report tool for screening, severity, and progress monitoring
Completed by patient; quick for routine screening
PHQ-9 length, scoring, symptoms
9 items, aligned with DSM depression criteria
Scores 0-27, clear severity cutoffs
Focuses on mood, interest, energy, and self-harm thoughts
Areas of brain implicated by depression
hypothalamus, amygdala, hippocampus, frontal lobe, cerebellum
How does depression affect the hypothalamus?
the hypothalamus is responsible for the circadian rhythm, hunger, thirst, etc
depression causes increased/decreased sleep/appetite and decreased energy/libido
How does depression affect the amygdala
the amygdala is responsible for mediating emotional learning and behavior
depression causes increased amygdala activation, sensitivity to sadness/fear/stress, anxiety, and anhedonia, also causes a decrease in motivation
How does depression affect the hippocampus?
the hippocampus is responsible for learning and memory
depression causes memory impairment, feelings of worthless, hopelessness, and guilt
How does depression affect the frontal lobe
the frontal lobe controls higher level thinking
depression causes depressed mood and problems concetrating
How does depression affect the cerebellum?
the cerebellum is responsible for balance, posture, coordination of voluntary movement, and fine motor skills
depression causes psychomotor retardation/agitation
Biochemical depression theory
deficiency of serotonin, norepinephrine, dopamine, GABA, and glutamate
taking tryptophan produces 5-HT which allows body to produce serotonin
Hypothalamic-pituitary-adrenal (HPA) axis disturbance theory
controls body’s stress response
in depression: HPA axis dysregulation causes prolonged/abdominal cortisol signaling
Causes disrupted sleep and appetite, decreased energy, mood, memory, and concentration
Psychosocial learning theory
Learned helplessness: pattern of giving up after repeated failure or lack of control
Seligman’s experiments
Tested learning theory
dogs exposed to unavoidable stress, later did not make attempt to escape even when escape was possible
Clinical meaning: person may abandon attempts to suceed, cope, or improve, even when help or solutions are available
Psychosocial object loss theory
Depression may be linked to early loss or separation from an important loved one
Physical or emotional separation from a caregiver during the first year of life may disrupt emotional development, may increase vulnerability to depression later in life
Psychosocial cognitive theory
Depression is influenced by negative patterns of thinking
Beck’s cognitive triad
Self: negative expectations about oneself
World/experience: negative interpretation of experiences
Future: negative expectations about the future
Psychosocial anger turned inward theory
Repressed anger is directed towards self instead of outward
After losing or feeling disappointed by an emotionally significant person,
anger toward that person may be redirected inward toward the self. This internalized anger may contribute to guilt, self-blame, low self-worth, and depressive symptoms
Individual Psychotherapy Focus
Identify strengths
Build coping
Identify/address internal conflicts
Understand depression drivers (e.g., stressors)
Cognitive behavioral therapy focus
Reframes negative thoughts about self, world, and future
Targets automatic thought errors: personalization, all-or-nothing thinking, mind-reading, discounting positives
Dialectical behavioral therapy focus
Emotional regulation: Manage intense emotions
Distress tolerance: Cope without worsening crisis-reduce suffering
Interpersonal effectiveness: Build healthier and meaningful relationships
Mindfulness: Stay present and grounded to find inner strength
Group therapy focus
Supports discussion of:
Depressive mood symptoms and recovery: factors that contribute to and maintain depression
Illness impact and consequences: relationships, functioning, coping skills and recurrence prevention
Group therapy nurse responsibilities
During Group: establish group norms, encourage participation, observe and document patient responses
Post Group: ensure to do 1:1 follow-up with your assigned patient who attended a group using the “Clinical Practice Tool”
Family therapy focus
Work with family to: promote communication, improve support, reduce symptoms, promote healing, restore adaptive family functioning
Pt centered care using self management strategies
Support holistic recovery and prevent, recognize, and manage illness episodes early
Build patient confidence and self-management skills
Promote use of evidence-based strategies
Ketamine therapy
Fast-acting Antidepressant (works within hours)
Helps people with severe treatment-resistant depression and suicidal thoughts
Repetitive Transcranial Magnetic Stimulation (rTMS)
non-invasive FDA-approved treatment for depression, especially treatment-resistant depression
~30% of pts achieve remission
rTMS how it works
A magnetic coil is placed on the scalp
The coil delivers repetitive targeted
magnetic pulses to specific brain areas involved in mood regulation
These pulses help modulate dysfunctional brain activity
rTMS schedule
3 to 5 sessions per week
40 mins/session
Usually 4-6 weeks
rTMS side effects
headache, scalp discomfort, facial tingling, and tinnitus
Vagus Nerve Stimulation
invasive, implantable treatment for depression that has not improved with standard treatments, such as medications and therapy
~13-40% of pts improve
~13% achieve remission
VNS how it works
A pulse generator is surgically implanted under the skin of the left chest
A wire connects the generator to the left vagus nerve in the neck
The device sends regular electrical impulses to the vagus nerve
Signals travel to brainstem areas that influence serotonin and norepinephrine pathways, affect limbic and cortical brain regions involved in mood regulation
Deep brain stimulation
invasive, not FDA-approved; remains investigational and is studied only for severe treatment-resistant depression
Goal: Help normalize dysfunctional brain activity
~40% of pts respond to treatment
~26% achieve remission
DBS how it works
Electrodes are surgically implanted deep in targeted brain areas
The electrodes deliver adjustable electrical stimulation
Stimulation helps modulate brain circuits involved in mood, anxiety, and compulsive behaviors
Electroconvulsive therapy
non-invasive treatment for severe depression, especially when medications are ineffective or rapid symptom relief needed
ECT how it works
Electrical stimulus under general anesthesia induces a controlled seizure
Modulates monoamines: ↑ 5-HT, NE, DA
May ↑ GABA and endorphin activity
May support neuroplastic/restorative brain changes, especially hippocampus/amygdala
↑ seizure threshold over repeated treatments
Antidepressants
MAOIs, tricyclics, atypical, SSRIs, SNRIs, herbal agents
MAO
An enzyme found in most body tissues
Main function: Breaks down monoamine:
NE norepinephrine: ↑ blood pressure
EPI epinephrine: ↑ blood pressure
DA dopamine: high levels can ↑ blood pressure
Tyramine: an amino acid that can trigger
↑ norepinephrine release
Why MAO matters:
Breaks down excess tyramine
Helps prevent excessive ↑ NE, EPI, and DA
Helps keep blood pressure from rising too high
how MAOIs work
decrease breakdown of monoamine transmitters
Increase serotonin, dopamine, and norepinephrine levels
May improve depressive symptoms
MAOI nursing considerations & pt education
Tyramine restriction
Watch for signs of hypertensive crisis
Caffeine avoidance
OTC medications: Avoid unapproved cold/allergy products:
sedating antihistamines may ↑ sedation, confusion, & anticholinergic effects;
decongestants may cause hypertensive crisis; dextromethorphan may cause serotonin syndrome
Stimulants: Avoid amphetamines and other unapproved stimulants because they ↑ NE & BP
Therapeutic effect: Symptoms improvement may take 2 to 4 weeks or longer
Medication washout: Wait at least 14 days when switching between an MAOI and most antidepressants to prevent serious interactions, including serotonin syndrome. Wait at least 5 weeks after stopping fluoxetine (Prozac®) before starting an MAOI because fluoxetine and its active metabolite, norfluoxetine, remain in the body longer, ↑ risk of serotonin syndrome
Orthostatic hypotension
Photosensitivity: Teach sunblock use and protective clothing when outdoors
MAOI diet rules
Fresh Fast
Fresh foods
Refrigerated dairy
Eggs
Safe grains
Healthy snacks
Fruits
Animal proteins
Salads & veggies
Thirst quenchers
Tricyclics nursing considerations & pt education
Mechanism: Blocks serotonin (5-HT) and norepinephrine (NE) reuptake→
↑ 5HT & ↑ NE
Overdose
Sedation
Falls precautions
Orthostatic hypotension
Nausea/vomiting
Anticholinergic effects
Weight gain
Tapering: Teach gradual tapering to prevent symptoms recurrence, discontinuation symptoms, and cholinergic rebound
Discontinuation syndrome
caused by abruptly stopping of TCAs or tetracyclics medication instead of tapering
Symptoms
Flu-like: headache, muscle aches, sweating
GI: nausea, vomiting, diarrhea
Sleep: insomnia, vivid dreams
Mood: irritability, anxiety, agitation, low mood
Neurologic: dizziness, tremor, confusion
Cholinergic rebound
caused by abruptly stopping an antidepressant with strong anticholinergic effects, especially a TCA, rapidly removes acetylcholine blockade (results in symptoms opposite of SPSS)
Symptoms
Secretions: Runny nose, sweating, increased salivation
GI: Nausea, abdominal cramping, diarrhea
Other: Headache, insomnia, or restlessness
Atypical antidepressants
Atypical antidepressant work in different ways, no single mechanism
Bupropion mechanism
inhibits norepinephrine and dopamine re-uptake, increases both
Maprotiline mechanism
tetracyclic that mainly inhibits NE re-uptake, has TCA like effects
Mirtazapine
increase NE and 5-HT signaling, often sedating
Trazodone
modulates 5-HT signaling - changes/regulates how serotonin communicates between neurons - increases 5-HT, sedating and often used for insomnia
Atypical antidepressants nurse considerations
Safety: Monitor for worsening depression or suicidal thoughts
Delayed effect: may take 2–6 weeks
Dry mouth
Nausea/vomiting
Fall risk
Stopping treatment: Do not stop abruptly
Avoid alcohol/CNS depressants
Drug interactions: Review all medications and follow prescribed washout periods, especially with MAOIs
SSRI common uses
Depression, anxiety, OCD, PTSD
Takes 4-6 weeks to work
SSRI SE
may be activating or sedating depending on meds and pt
Nausea, headache, insomnia/sedation, sexual dysfunction
SSRI nurse considerations
Insomnia
GI effects
Hyponatremia: may cause syndrome of inappropriate antidiuretic hormone secretion (SIADH), leading to water retention and low blood sodium. Watch for headache, weakness, confusion, seizures, or decreased consciousness; monitor sodium as indicated
Anticholinergic effects: Uncommon with most SSRIs
Bleeding risk
Bulimia nervosa: Fluoxetine (Prozac®) is the only FDA approved SSRI
Stopping treatment: Do not stop abruptly
Serotonin syndrome
abrupt onset
rapidly resolving
Cues: myoclonus, tremor, increased reflexes, mydriasis
Neuroleptic malignant syndrome
due to decreased dopamine
gradual onset
prolonged
Cues: diffuse rigidity, decreased reflexes
SNRI common uses
depression, anxiety, fibromyalgia, neuropathic pain
Takes 4-6 weeks to work
SNRI SE
may increase energy and help fatigue
nausea, headache, insomnia, sexual dysfunction, increased HR, BP, and anxiety
St John’s Wort
serotonergic effects
risk of serotonin syndrome, photosensitivity, many drug interactions
St John’s Wort nursing considerations
Avoid with MAOIs/other antidepressants unless prescribed; educate on sunscreen use and review all medications, OTC drugs, herbs, and supplements
Ma huang/Ephendra
cause increased HR and BP, risk of dysrhythmias, stroke, or HTN crisis
Ma huang/Ephendra nurse considerations
Avoid with MAOIs, or other stimulants to prevent risk for dangerous BP elevation/hypertensive crisis
Kava
increased sedation/CNS depression
possible serious liver injury
Kava nurse considerations
Avoid alcohol, opioids, benzodiazepines, & other sedatives; monitor for liver-injury
Ginseng
may potentiate MAOIs
Ginseng nurse considerations
Avoid with MAOIs unless approved; monitor for BP/CNS effects
Brewer’s Yeast
may contain high tyramine
severe increase in BP with MAOIs
Brewer’s Yeast nurse considerations
Avoid with MAOIs to prevent hypertensive crisis