Key areas 2 Flashcards
Agonist
molecule that binds to a receptor and activates it
agonists and GPCRs
agonists bind to GPCRs and induce conformational change that fully activates the receptor, leading to a robust signaling response.
ie) morphine is a full agonist at opioid receptors
partial agonist
binds to a receptor but activates it less effectively than a full agonist, resulting in weaker response
partial agonists and GPCRs
when bound to GPCRs, partial agonists activate the receptor but produce a lower level of signaling compared to full agonists
Spectrum: no agonist
constitutive activity; baseline
Spectrum: full agonist
maximum signal transduction
Spectrum: silent antagonist
back to baseline, constitutive activity only, same as no agonist
Spectrum: partial agonist
partially enhanced signal transduction
Spectrum: inverse agonist
beyond antagonism; even constitutive activity is blocked
Where is serotonin produced
primarily in raphe nuclei of brainstem
what is the primary effect of serotonin
regulates mood, appetite, sleep, cognition. Involved in feelings of well-being and happiness
disorders linked to serotonin
depression (low levels), anxiety (dysregulation), OCD (implicated)
Where is NorE produced?
locus coeruleus in brainstem and adrenal glands
what is the primary effect of NorE?
plays a role in arousal, attn, stress response, and mood regulation
disorders linked to NorE?
depression (dysregulation), anxiety (overactivity), PTSD (implicated in hyperarousal and stress response)
Where is dopamine produced
several areas including substantia nigra and ventral tegmental area
what is the primary effect of dopamine
regulates mood, motivation, reward, and motor control
what disorders are linked to dopamine
parkinson’s disease, schizophrenia, addiction
where is GABA produced
synthesized throughout the brain, particularly in interneurons
what is the primary effect of GABA
acts as the main inhibitory neurotransmitter, reducing neuronal excitability and promoting relaxation and calmness
what disorders are linked to GABA
anxiety disorders (low gaba=anxiety), epilepsy (dysregulation leads to seizures d/t excessive neuronal activity), and mood disorders (imbalances may contribute to depression and bipolar)
where is glutamate produced?
found throughout the brain, synthesized in neurons from glucose and other precursors
what is the primary effect of glutamate?
primary excitatory neurotransmitter, essential for synaptic plasticity, learning, memory
disorders associated w/ glutamate
alzheimer’s (excessive leads to neurotoxicity and cognitive decline), schizophrenia (imbalances in glutamate signaling), autism (dysregulation may affect synaptic development and function)
spectrum of mood disorders
MDD, dysthymia, bipolar disorders, cyclothymia, SAD, DMDD. Brain areas responsible for controlling feelings are amygdala and orbirofrontal cortex
key neurotransmitters in mood disorders
serotonin, norepinephrine, dopamine
what is the monoamine hypothesis?
theorizes imbalances in certain neurotransmitters, specifically monoamines, play a critical role in development of mood disorders, especially depression and anxiety
Key monoamine: serotonin
influences mood, emotion, sleep, appetite; low levels or dysreg L/T depression and anxiety d/os
key monoamine: norepinephrine
affects arousal, attn, stress response; decrease NorE assoc w/ depressive s/s
key monoamine: dopamine
involved in reward, motivation, mood regulation; low levels can contribute to anhedonia. Dysregulation r/t bipolar and certain anxiety d/os
Unipolar depression
aka MDD. Persistent depressive episodes w/o hx of manic or hypomanic episodes
bipolar depression
episodes of depression that alternate with episodes of mania or hypomania
bipolar I
at least one manic episode which may be preceded or followed by depressive episodes
bipolar II
at least 1 major depressive episode and at least one hypomanic episode, but no full manic episodes
Duration dx criteria for manic episode
distinct period of abnormally and persistently elevated, expansive, or irritable mood lasting at least 1 wk (or any duration if hospitalization is necessary)
dx criteria for manic episode: mood changes
during period of mood disturbance, 3 or more of the following s/s have persisted (4 if mood is only irritable) and represent a noticeable change in bx
1. inflated self-esteem or grandiosity
2. decreased need for sleep
3. hyperverbal or rapid pressured speech
4. flight of ideas or racing thoughts
5. increase in goal directed activities
6. easily distracted
7. engaging in risky bx
manic episode: functional impairment dx criteria
the mood disturbance is sufficiently severe to cause marked impairment in social or occupational functioning or to necessitate hospitalization to prevent harm to self or others, or there are psychotic features
characteristics of med-induced hypomanic episode
- elevated or irritable mood
- increased energy
- decreased need for sleep
- more talkative
5 racing thoughts - impulsivity
-onset occurs shortly after starting or increasing certain meds like antidepressants, stimulants, steroids
management of med-induced hypomania
1) assessment to confirm med-induced and not part of underlying mood d/o
2) med review: figure out what started it
3) dose adjustment/discontinuation
4) monitor for changes in mood or bx during withdrawal or adjustment period
5) supportive care: provide supportive interventions, therapy
6) meds for symptoms: use mood stabilizers or antipsychotics to manage hypomanic s/s esp if causing impairment
7) schedule follow ups to assess stability and adjust as needed
What is NMS
neuroleptic malignant syndrome: potentially life-threatening rxn to antipsychotic meds (neuroleptics). Manifests as a combination of severe s/s like muscle rigidity, fever, altered mental status, autonomic dysregulation, elevated CK
S/s of NMS
-severe muscle rigidity
-high fever
-altered mental status
-autonomic dysreg: increased HR, labile BP, sweating, tachypnea
-elevated CK (indicative of muscle breakdown)
How to manage NMS in OP setting
immediately assess for s/s like muscle rigidity, fever, and altered mental status. obtain detailed med hx, focusing on recent changes in antipsychotic meds or dosages. Contact emergency services. Ensure they are hydrated and in safe environment while waiting for help. Document all findings including s/s, vitals, med hx, condition during visit. Plan for f/u, re-eval need for antipsychotics, consider alt tx w/ lower NMS risk, monitor for s/s recurrence if meds are resumed. Educate pt on warning signs and reporting s/s.
what is tardive dyskinesia
movement disorder caused by long-term use of antipsychotics, particularly typical antipsychotics. Characterized by involuntary repetitive movements, primarily affecting face, tongue, and limbs
common s/s of TD
oral-facial movements: lip smacking, tongue protrusion, facial grimacing. Limb movements: involuntary arm or leg movements like twitching or writhing. Postural changes: abnormal posture or body movements
how to assess for TD?
ask about involuntary movements, when they started, if they’ve worsened. Abnormal involuntary movement scale (AIMS) standardized tool to assess presence and severity of TD; includes questions and observation checklist to rate movements in different body parts.
what is akathisia
inner sense of restlessness and an uncontrollable need to be in constant motion. can occur as side effect of antipsychotic meds, particularly during early tx phases
s/s of akathisia
restlessness, pacing, fidgeting, shifting positions; anxiety and feeling tense or agitated; inability to sit still, may express discomfort when seated for long periods
how do you assess for akathisia
ask about feelings of restlessness, inability to remain still, and any associated anxiety. Rating scales: barnes akathisia rating scale is used to assess severity, includes items to evaluate motor restlessness and subjective feelings of inner restlessness. Observe for fidgeting or restlessness during appt.
Dx criteria for MDD: s/s
5 or more of the following s/s must be present during same 2-wk period and represent change from previous functioning, and at least one of the symptoms must be depressed mood or loss of interest/pleasure
1. depressed mood
2. loss of interest/pleasure
3. significant weight change (5% in 1mos w/o effort)
4. sleep disturbances
5. psychomotor agitation or retardation
6. fatigue or loss of energy
7. feelings of worthlessness or excessive guilt
8. difficulty concentrating
9. recurrent thoughts of death or SI
-functional impairment & not better explained by another mental disorder, and no hx mania or hypomania
Dx criteria for PTSD
1) exposure to trauma
2) re-experienced via nightmares, flashbacks, intrusive thoughts
3) avoidance of certain things, feelings, people, or activities
4) unable to function
5) month (at least)
6) arousal increased, startles easily
OCD dx criteria
presence of obsessions, compulsions, or both which are time-consuming and impair functioning
dx criteria: GAD
excessive worry and anxiety for more days than not for at least 6mos.
Anxiety and worry are associated w/ 3 or more of the following s/s: restlessness, easily fatigued, difficulty concentrating, irritability, muscle tension, sleep disturbance
dx criteria: schizophrenia
2 or more of the following s/s must be present for a significant portion of 1mos, at least one of them must be one of the first 3 symptoms listed:
1) delusions
2) hallucinations
3) disorganized thinking
4) grossly disorganized or abnormal motor bx
5) negative s/s
-level of functioning is impaired, continuous signs of disturbance persist x6mos, and this 6mos perion must include at least 1mos of symptoms that meet the above s/s characteristics
positive s/s in schizophrenia
hallucinations, delusions, disorganized thinking, disorganized/abnormal motor bx
negative s/s of schizophrenia
blunted affect, avolition, anhedonia, alogia, social withdrawal
differences b/t pos and neg s/s
pos = bx or experiences not typically present in healthy individuals. neg = reduction or absence of normal emotional and bx functions
therapeutic drug monitoring (TDM) for antipsychotics
1) baseline med hx, MH hx, current meds, wt, ht, vitals, labs (CBC, LFTs, kidney function, bmp)
2) regular monitoring: regularly assess s/s, s/e, functioning. vitals–monitor bp, hr, wt, esp for metabolic s/e
3) blood levels: clozapine monitor for agranulocytosis, monitor weekly x 1st 6mos, then q2wks if stable. can monitor for risperidone and abilify if needed.
4) metabolic monitoring: wt, fasting glucose, lipids. metabolic syndrome.
5) neurological monitoring: monitor for s/s EPS or TD
6) adherence monitoring: assess through self-report or pill counts or electronic monitoring devices
7) adjustment based on results
antipsychotic key teaching points: understanding the med
explain purpose: used to tx psychosis s/s like delusions, hallucinations, disorganized thinking. Discuss specific med prescribed, class, how it works.
antipsychotic key teaching points: expected benefits
highlight potential benefits like reduced s/s, improved functioning, enhanced quality of life. Set realistic expectations about timeline, may need weeks to work.
antipsychotic key teaching points: common s/e
drowsiness or sedation, wt gain, metabolic changes (increased BG, cholesterol), EPS (tremors, rigidity), TD (long-term risk). Emphasize importance of reporting s/e to provider
antipsychotic key teaching points: importance of adherence
stress importance of taking med as prescribed, even if s/s improve or if there are side effects. discuss risks of stopping meds suddenly, including potential relapse or worsening of s/s
antipsychotic key teaching points: monitoring & f/u
need for regular f/u appts to monitor effectiveness and s/e. Discuss lab work which may be needed, like blood tests for clozapine
antipsychotic key teaching points: lifestyle considerations
healthy lifestyle choices! regular exercise, healthy eating to manage wt, avoiding alc and rec drugs. Discuss strats to manage potential st gain and metabolic changes
antipsychotic key teaching points: emergency situations
educate about NMS s/s, severe allergic rxns, significant changes in mental status or bx
antipsychotic key teaching points: support systems
encourage involvement of family members in tx process to provide support. Discuss resources for support like therapy, groups, educational materials
antipsychotic key teaching points: coping strategies
provide info on coping and resources for managing stress and anxiety which may be comorbid.
general guidelines for switching antipsychotics
-assess need for switching
-choose new med
-plan transition
-taper old med
-initiate and titrate new med
-monitor closely
-document
-keep pt involved
-crisis management
powerpoint guidelines for switching antipsychotics
-switching b/t 2 agents w/ similar pharmacology is usually fast, easy, and w/ few complications (ie quetiapine to olanzapine)
-same class of drug can be done over 7 days
-switching from one class to another can take longer (pine to a done or done to a pine)
why does switching classes take longer?
-binding characteristics are different
-pines have more anticholinergic and antihistamine actions
-pines have more alpha1 antagonist properties
