Thought D/O Flashcards
what do you need for dx of schizophrenia
sx last at least 6 months
(2 or more required): there are delusions or hallucinations, disorganized speech, disorganized or catatonic behaviour or negative symptoms
schizophrenia the four “As”
flattening of: affect
ambivalence
autism
loosening of associations
5 subtypes of schizophrenia
- paranoid: delusions and hallucinations are predominate sx
- catatonic: motor sx are predominate
- disorganized: disorganized speech, behavior, or inappropriate effect are predominate
- residual: absence of prominent positive sx, but continuing evidence of disturbance through less severe positive symptoms or negative sx
- undifferentiated: none of the above sx clusters predominate
what substances are associated with psychotic sx the most
cannibus and cocaine
what is the difference between schizophrenia and schizoaffective d/o
schizoaffective d/o is made when mood sx co-occur with + sx
duration of sx are at least 2 weeks of + sx in absence of mood sx and then the mood sx present for a significant portion of total illness duration
difference between schizophrenia and schizophrenoform
schizophreniform d/o lasts less than 6months and is not associated with functional decline
genetics theory of schizophrenia
schizophrenia risk is higher in general population by approximately 12x if the disease is present in one biological parent and by approximately 40x if present in both biological parents (risk remains if child is raised in adoptive home)
monozygotic twins is over three times greater than in dizygotic twins
biological theory of schizophrenia
abnormalities in three chromosomes: X, 22q11, 1q42/11q14
total of 400 genes linked to schizophrenia
biochemical alterations in schizophrenia
dopamine hypothesis suggests that psychotic sx result form excess of DA in brain; this is determined by the effective medications for psychotic sx have antagonists action on the DA type 2 receptor; drugs increase DA are psychotomimetic like cocaine
- DA dysregulation is intrinsic to schizophrenia and predates first psychotic episode
- SE excess is hypothesized to cause both + and - sx
- GABA has been implicated in schizophrenia
- some persons with disease experience a loss of GABA neurons in the hippocampus
- gaba regulates DA so if you have loss of those neurons that produce it it could result in excess of DA neuron activity
Neuropathology in schizophrenia
- gray matter reduction in anterior cingulate, bilateral frontal lobe, hippocampus, amygdala
- enlargement of third ventricle
- reductions in glial cell density and reduced density of callbindin-expressing neurons have been reported
neural circuitry deficits in schizophrenia
neural circuitry deficits may underlie memory alterations
working memory is mediated by cortical network
hypoactivation of dorsolateral prefrontal cortex suggests px mobilizing neuronal resources for memory tasks
hyperactivation indicates greater use cortical resources than general population to perform similar tasks and persons with schizophrenia are less accurate and require more time to complete tasks
brain metabolism in schizophrenia
-presence of mitochondrial dysfunction, including reduced mitochondrial density and volume as well as defective mitochondrial energy in persons with schizophrenia; alterations associated with oxidative stress that induces cell damage
environmental basis of schizophrenia
variety of environmental factors have implicated schziophrenia etiology as well as geographic and demographic incidence variation
risk fx and schizophrenia
- male
- persons living in urban situations rather than rurual environments (likely to have higher rates of cannabis use, social stress, low social connectedness, poverty, and or environmental toxins)
- persons with personal or fx hix of migration
- 2.7x greater than general population for first generation immigrants and 4.5x greater for second generation (socially isolated status, discrimination, biological explanations like vitamin D deficiency)
- higher prevalence in more developed countries and among persons of lower as opposed to higher socioeconomic status
- risk factors are not proven to cause disease; disease arises from many different pathways; these are just known influences on disease development
positive sx of schizophrenia
-hallucinations, delusions
common delusions associated with schizophrenia
-delusions of reference and persecution
most common hallucinations
- most common auditory
- most common threatening or accusatory auditory hallucinations
negative sx in schizophrenia
- flat or blunted affect, thought blocking, poverty of speech, avolition, social w/drawal
- primary are intrinsic to schizophrenia and secondary negative sx reflect external fx like depression or med side effects
cognitive sx in schizophrenia
- memory and attention deficits
- language difficulties,
- problems with executive fx
- px with executive functioning are evidenced by difficulties in: ordering sequential behaviors, establishing goal-directed plans, maintaining task when interrupted, monitoring personal behavior, associated knowledge with required responses
- cognitive impairment is thought to be associated with poor outcomes in social and vocational areas
disorganized sx in schizophrenia
-formal thought d/o, derailment, poverty of sp[eech or bheavioral disorganization
formal thought d/o
lack of progressive goal directed thought processes, includes derailment and poverty of speech
derailment
pattern of speech in which person’s ideas slip off track onto another unrelated or obliquely related topic; derailment is known as loosening of associations
poverty of speech
inability to start or take part in conversation particularly small talk
behavioral disorganization
ranges from inappropriate affect to attire inappropriate to season or activity; often accompanies formal thought d/o; pronounced during illness exacerbations; presence associated wit poorer outcomes
motor sx in schizophrenia
rarely do we see catatonic sx now adays; if we do it can involve echolalia, echopraxia, waxy flexibility, automatic obedience
echolalia
repeating words
echopraxia
imitating or repeating of another’s actions
waxy flexibility
you can move someones extremety and it will stay there until you move it again
automatic obedience
the pt will comply to all suggestions; mechanically follows directions
neurological hard signs
hard signs indicate impaired relex, sensory or motor fx and are localized to a particular brain region; include hypoalgesia, impaired olfactory functioning and oculomotor abnormalities
neurological soft signs
soft sogns do not implicate a specific brain reagion
they include grimacing, increased blink rates, px with sequencing motor tasks, asterognosis, difficulties with smooth alternation movements
clozapine
has highest anticholinergic activity; muscarinergic agonist
- alpha 1 and 2 antagonism
- beta antagonism
- DA antagonsim
- used last resort/failures to other meds
- APA recommend trial if pt have no response to a 6-wk trial of tow other antipsychgotics and or have persistent suicidal ideation or hostility/agression
- trial should be at least 6 months
- sedation; wt gain; hypersalivation; risk of seizures; agranulocytosis/highest risk during first 6 months of tx (usually reversible once dc med and should not try med again);
- check WBC before and each wk for 6 months; then every 2 weeks after for duration of tx; wkly for one month after dcing med
- advise pts to report tachycardia, sedation during dose titration as well as sx of infection like sore throat, fever, weakness, lethargy
risperidone
- DA postsynaptic antagonsim; SA antagonism, A1 ang A2 and H1 antagonism
- potent 5HT2a and moderate D2 antagonsim
- SE: drowsiness, orthostatic hypotension, wt gain, high risk of prolactin increase (breast tenderness, enlargement, decrease sexual interest/libido, menstrual cycle disruption in women, and retrograde ejaculation in men
- dosage related increases in EPS; most effective dose 4-8mg/day; elderly persons or others experiencing orthostatic hypotension may benifit from BID dosing
paliperidone and risperidone consta
- paliperidone is the major active metabolite in resperidone in an ER form
- side effects and efficacy similar to risperidone
- risperidone consta consists of microspheres delivered intramuscularly and released over time; usual dosage is 25-50mg IM every 2 wks
olanzapine
- antagonist action at D1, 2, 3, 4; 5HT2a, 2c; H1 and A1 and M1, 2, 3, 5
- moderate affinity for 5HT2a, 2c and 3 receptors
- superior to haloperidol for negative and neurocognitive sx and is effective for positive sx
- effective in tx TD associated with other agents
- 5mg PO/day for elderly
- IM: 2.5-10mg
- SE: sedation, wt gain, metabolic effects; DM/hyperglycemia may not be dose-dependent
quetiapine
- weak D1, 2 antagonsim; 5HT21a, 2a, 2c, 6 antagonism; H1 and A1, 2a, 2c antagonsim
- occupies fewer SE receptors and does not saturate the receptors even at high doses
- 400-800 mg/day and can be given once daily or divided
aripiprazole
- partial agonist activity at D2 and 3 and 5HT1a nd 5HT2a
- moderately inhibits SE reuptake
- improves number of + and - sx
- SE: agitation, nausea, insomnia; minimal increases in wt and cholesterol and unlikely to be associated with hyperprolactemia or prolongation of QTc interval
- takes two weeks for pt to achieve therapuetic plasma level
asenapine
- antagonist at D2, greater affinity at 5HT2a, almost no affinity for M1
- SE: nausea, anxiety, agitation, dizziness, sedation,
- use in caution w/ those w/ hx of leukopenia or neutropenia, cardiac arrhythmias and seizures
- do not use in combination w/ CNS depressants or alcohol
- may potentiate effects of antihypertensive meds through a1 antagonism
comparing first generation and second generation antipsychotics
- generally EPS sx are greater w/ risperidone and olanzapine and less with quetiapine and aripiprazole
- wt gain appears to be substantial w/ olanzapine and clozapine and moderate with risperidone and quetiapine, least with ziprasidone and aripiprazole
- rates of DM induction highest w/ olanzapine and clozapine and lowest w/ ziprasidone and aripiprazole
EPS sx
- acute: Parkinsonism, dystonia, akathisia, neuroleptic malignant syndrome
- can occur in first days or wks of tx and are dose dependent and are reversible if meds are reduced or dced
- chronic EPS is TD which occurs after months or years of meds and may be irreversible even in absence of meds
Parkinsonism sx medication induced
- bradykinesia, tremor, rigidity, akinesia
- need to distinguish from negative sx
- difference: usually parkinsonain sx respond to reducing med or to addition of anticholinergic med,
trihexyphenidyl
synthetic antispasmodic, direct inhibiting effect on PSN as well as relaxant upon smooth muscle
- rxs 6-10 mg/day divided doses best given w/out food
- SE dry mouth, nausea, blurred vision, dizziness, often more common in elderly
- need to monitor for increased IOP, closed angle glaucoma common
benzotropine
- anticholinergic and antihistamine
- 1 to 2 mg twice or three times daily.
- Common side effects include dry month, blurred vision, and urinary retention.
- Patients prescribed benztropine along with phenothiazines, haloperidol, or tricyclic antidepressants should be instructed to promptly report gastrointestinal complaints, fever, or heat intolerance, as the administration of these medications concomitantly has been associated with paralytic ileus and hyperthermia, which have been fatal in some individuals.
- Benztropine is also associated with glaucoma.
dystonia
- involves spastic contraction of muscle groups (commonly neck, eyes, torso) sudden, dramatic, frightening
- 10% of pts with antipsychotic meds
- responds quickly to IM benztropine or benadryl
- APA recoomend oral maintenance with anticholinergic antyiparkinsonian meds for pts who experience dystonia in past
akathisia
- marked by sensations of restlessness, pacying, inability to sit still
- occurs in up to 30% of pts tx with antipsychotics
- increased motor activity must be differentiated from agitation accompanying psychosis
- it may respond to reduction in antipsychotic or to adding anticholinergic or antiparkinsonian meds
Lorazepam
- benzotropine anxiolytic CNS depressant
- SE drowsiness muscle weakness
- CI pts with glaucoma; dosage should be reduced 50% in elderly
- not recommended for long term use; not rx to women child bearing
Neuroleptic malignant syndrome
-rare but potentially fatal form of acute EPS
-appears to be a reaction to acute dopamine depletion
-reported with virtually all D2 receptor antagonists, (risperidone, clozapine, ziprasidone)
-risks: increased dose of antipsychotic, abrupt w/drawal of dopamine antagonist, dehydration, electrolyte imbalance, and concurrent use of lithium and tricyclic antidepressants
-sx: fevere, skeletal muscle rigidity, altered mental status, autonomic dysfunction, creatinine phosphokinase and WBC elevated, rhabdomyolysis, DIC, renal faluire,
-tx: discontinuing med, dopamine agonists given,
dantrolene sodium reduces fever and muscle rigidity
urine alkalinization w/ high volumes of crystalloids may prevent renal failure, however, hemodialysis is sometimes required
recovery may take several weeks
can rx antipsycho again but gradual and w/ diff med
TD
movement d/o associated w/ chronic antipsych tx and advanced age
- common concern in pts w/ antipsych meds
- process of dopamine metabolism generates free radicals, excessive production of free radicals destabilizes neuronal membrane in the extrapyramidal system which regulates repetitive rhythmical activities of both voluntary and involuntary natures
- characterized by rapid, writhing, involuntary movements of orofacial region, limbs, and or trunk
- lip smacking, puckering, chewing, jaw clenching, tongue protrusion, licking lips,
- tx: stop med, can try diff med, lowest dose possible
prodromal period of schizophrenia
- schizophrenia is often preceded by year of prodromal period which shows a premorbid functioning decline that is problematic, continues untile emergence of psychotic sx; may last only weeks but usually is between 2-5 years
- sx: sleep px, poor concentration, social w/drawal, + sx, suspiciousness, ideas of reference
first psychotic episode
- may be insidious or acute
- occur between 15-45 years old
- phases:
1. acute: florid psychosis—for example, delusions, hallucinations, thought disorder
2. recover: 6-18month period following acute psychosis
3. stable: period when - and residual sx remain but less severe - first 5 years are known as the early course and may be associated with additional deterioration that tapers off by 5-10 years post dx
physical health promotion and outcomes of schizophrenia
- higher mortality and morbidity than general population
- DM, cardiovascular disease, obesity, smoking, sedentary lifestyle, poor diet
