Psychosis Flashcards
Define delirium
a state of acute mental confusion that develops over a short time
-disturbance of attention and awareness of the environment
-change in cognition
-pt usually returns to baseline after cause is removed
high prevalence in hospitalized older adults
a medical emergency
What are the manifestations of delirium?
restlessness
psychomotor agitation
hallucinations
labile emotions
can see hypoactive delirium-drowsy
decreased motor activity
Describe the Confusion Assessment Method (CAM)
Based on 4 cardinal features of delirium
1) acute onset and fluctuation
2) inattention
3) disorganized thinking
4) altered LOC
presence of 1 & 2 and either 3 or 4 =CAM +
What are the common investigations of delirium/confused state?
-infection/sepsis work up
-blood for electrolyte and other imbalances
-brain imaging CT, MRI– stroke, trauma, masses/lesions
-lumbar punctuate (LP)– meningitis or encephalitis
-drug screen
Describe a lumbar puncture for CSF analyses
lie with knees to abdomen and head flexed to the chest (recumbent position) to help vertebrae separate
Physician inserts needle below 3rd lumbar vertebrae– no risk to spinal cord as it ends between 1st and 2nd vertebrae
-assess if pt is able to tolerate position and presence of any contraindications
-ensure specimen is transferred immediately on ice
-apply dressing and position pt per policy
-assess for complications
What are some ways of managing Delirium?
Nonpharmacological:
-reduce stimulation
-increase familiarity
-keep safe
Pharmacotherapy:
-chemical restraint of haloperidol most common in hospital (given IM or IV)
Describe schizophrenia
-genetic component
-neurotransmitter imbalance (overstimulation of DA D2 receptors)
-positive and negative symptoms
Describe positive and negative symptoms
positive symptoms:
-hallucinations
-delusions
-disorganized speech
negative symptoms:
-flat affect
-poverty of speech
-impairment in cognition, including attention, memory and executive functions
How can antipsychotics cause movement disorders similar to Parkinson?
-antipsychotics block D2 receptors
-blocking D2 receptors completely produces extrapyramidal side-effects (EPS) that look like Parkinson
-atypicals don’t block to the same degree
What happens when the specific serotonin receptor (5HT2A) is blocked?
-blocked by atypicals
-reduces EPS and negative symptoms (movement disorders)
What are the three kinds of EPS?
Acute dystonia, Akathisia and drug-induced Parkinsonism
Describe acute dystonia
-muscle spasms of the back, neck, tongue and face
-at onset of treatment
-treatment includes IV anticholinergics that cross the BBB such as benztropine and diphenhydramine
-likely due to rapid and intense change of dopamine D2 receptor antagonism
-occurs more with high potency first gen and even more so if given IM
Describe Akathisia
-restlessness
-onset within 5-60 days
-treatment includes propranolol (no other beta blockers are effective), anticholinergics (benztropine) and switching to a 2nd generation antipsychotic
-likely related to an imbalance between the central dopaminergic and beta2-adrenergic systems
Describe Drug-induced Parkinsonism
-tremors, muscle rigidity, shuffling gait
-onset within 5-30 days
-treatment includes anticholinergic (benztropine) and switching to 2nd gen antipsychotic
-due to an imbalance between dopamine and acetylcholine in the CNS
-should go away when the antipsychotic is stopped or the dose is reduced
Describe Tardive dyskinesia
-unusual tongue and face movements
-onset is months to years after starting meds
-thought to be related to over-sensitivity to dopamine by D2 receptors
-may be permanent even if med is stopped
-treatment includes VMAT2 inhibitors (decrease uptake of dopamine)
-could be caused by neuroleptic-induced dopamine hypersensitivity
What is neuroleptic malignant syndrome (NMS)?
a neurologic emergency caused by abrupt decrease in dopamine levels
-life-threatening
What are the signs and symptoms of NMS?
-confusion
-muscle rigidity
-agitation
-hyperthermia
-seizures
-coma
What is the treatment for NMS?
-discontinue dopamine antagonist therapy (or resume dopamine agonist in case of withdrawal)
-stop potential contributing agents (lithium, etc)
-maintain cardiorespiratory stability and perfusion pressures (antiarrhythmics, IV fluids)
-treat hyperthermia with cooling blankets, ice water gastric lavage and axillary ice packs
-use benzodiazepines to control agitation
-dantrolene (muscle relaxant) for rigidity
What is Rhabdomyolysis (rhabdo)?
a condition that results from the breakdown of skeletal muscle which causes release of myoglobin into the bloodstream
-can obstruct renal tubules and lead to acute kidney injury
-can result from traumatic muscle “crush” injuries such as being trapped under a car but is more common in pts who have experienced a “prolonged lie” where the pt is unable to move for a long time (coma)
What are the lab findings for NMS?
-increased creatine kinase
-increased leukocytosis
-low serum iron
What are the main differences between serotonin syndrome and NMS?
physical exam findings:
SS– hyperreflexia, myoclonus, ocular clonus
NMS– severe rigidity, hyporeflexia
Lab:
SS– no lab findings
NMS– increased creatine kinase, leukocytosis, low serum iron
Course of illness:
SS–within 24 hours of starting therapy and resolves within days
NMS– 1-2 weeks after starting therapy and resolves within 9-14 days
What are some adverse effects of antipsychotics?
-blocking DA– EPS
-muscarinic receptors– dry mouth, blurred vision, urinary retention, constipation
-histamine receptors– sedation
-alpha-1 adrenergic receptors– orthostatic hypotension
What patient/family teaching is needed for antipsychotics?
-knowing how to manage side-effects in advance may improve adherence (may feel numbed)
-make aware of time to therapeutic effect and risk of temptation for self-medication
-risks of taking CNS depressants (ETOH, benzos)
-consider taking at bedtime due to sedation
-avoid activities requiring mental alertness until effects are known
-caffeine and smoking may reduce antipsychotic efficacy for many medications
