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pr3153 > ic10 schizophrenia and psychosis > Flashcards

ic10 schizophrenia and psychosis Flashcards

1
Q

what is “psychosis” and “schizophrenia”

A

psychosis is an acute and severe episode of being out of touch with reality along with lack of insight

schizophrenia is protracted psychosis (>6m); a syndrome of disorganised and bizarre thoughts, delusions, hallucinations and impaired psychosocial func

hallucinations can be in the form of auditory, visual, tactile, olfactory and gustatory

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2
Q

differentiate between “affective disorders” and “organic disorders”

A

affective disorders are more related to mood while organic disorders are more related to structural deficits or psychologic dysfunc

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3
Q

what are the possible diagnoses related to psychosis sx

A
  1. organic disorders like epilepsy, cerebral lesions (trauma, CVA, trauma), nervous system illness (due to infection, genetic/ congenital), endocrine disorders, metabolic disorders or physiological disturbances affecting the nervous system, iatrogenic causes, psychosis related to alcohol and psychoactive substance misuse, parkinson’s disease, dementia
  2. affective disorders like mania, psychotic depression, post-partum psychosis
  3. schizophrenia, schizotypal personality disorder, delusional disorder (incl psychosis in childhood or adolescence)
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4
Q

what contributes to the etiology of schizophrenia

A
  1. predisposing factors (factors from early life determining vulnerability to precipitating factors) incl genetics, environment in utero, neurodevelopmental effects, personality, physical, psychological and social factors in infancy and early childhood
  2. precipitating factors (events occuring shortly before onset) incl cerebral tumors or injury, drugs/substance induced psychosis, personal misfortune, environment of highly expressed emotion
  3. perpetuating (factors that prolong the course) incl secondary demoralisation, social withdrawal, lack of support or poor socio-economic status or environment, poor adherence to antipsychotics
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5
Q

what are some common substances or drugs that can induce psychosis

A

benzodiazepines, alcohol, barbiturates, antidepressants, corticosteroids, CNS stimulants (amphetamines), hallucinogens (LSD, cannabis, volatiles), BB (propanolol), dopamine agonists (levodopa, bromocriptine)

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6
Q

what is the main idea behind the pathophysiology of schizophrenia

A

abnormality occuring in one of the various NT incl dopamine, 5HT, glutamatergic func

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7
Q

what are the chromosomal regions identified for schizophrenia

A

chromosome 6, 8, 13, 15, 22

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8
Q

categorise the risks of developing schizophrenia based on one’s familial factors

A

if none, approx 1%
if first degree relative, 10%
if second degree relative, 3%
if both parents, 40%
if monozygotic twin, 48%
if dizygotic twin, 12-14%

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9
Q

what is the diagnostic criteria for schizophrenia

A

based on DSM-5 criteria

(A) at least two of the following with each lasting for at least 1m: delusions, hallucinations, disorganised speech, grossly disorganised or catatonic behavior, neg sx

(B) social or occupational dysfunc (relating to work, interpersonal relations, self care)

(C) continuous sx alsting for at least 6m (incl sx lasting for at least 1m in (A) unless successfully treated) (may incl prodromal or residual sx)

(D) schizoaffective or mood disorders excluded

(E) exclude medical disorders and substance use

(F) if hx of pervasive developmental disorder aka delays in development of social and communication skills, must display hallucination or delusions for at least 1m

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10
Q

what are the assessments to be done when wanting to diagnose schizophrenia

A
  1. hx of presenting illness
  2. psychiatric hx (neurosis, psychosis)
  3. substance use hx (incl alcohol, cigarettes, substances)
  4. complete medical and medication hx (allergy, response, supplements)
  5. family, social, occupational, forensic, developmental hx
  6. physical and neurological exam (look for head trauma)
  7. mental state exam (MSE) for accurate diagnosis (look for signs of suicidality or homicidal ideations, repeat upon every interview)
  8. labs and other investigations (vital signs, weight and BMI, RFTs through U/E/Cr, LFTs, TFTs, FBC (rule out anemia, infection), ECG (to rule out QTc prolongation bc c/i), lipid panel, fasting blood glucose, urine toxicology; exclude general medical conditions or substance induced withdrawal sx)
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11
Q

what are some non pharmacotx for schizophrenia

A

on individual level: counselling, personal therapy, social skills therapies, sheltered vocational workshops (employment and rehabilitative eg. psychosocial rehabilitative programmes to improve pt’s adaptive func)

on group level: social/ interactive

to target cognitive behavioural: CBT, compliance therapy

to target neurostimulation: electroconvulsive therapy (ECT), repetitive transcranial magnetic stimulation (rTMS)

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12
Q

what to consider for ECT (a non pharmacotx for schizophrenia)

A

electroconvulsive therapy (ECT) is conducted under general anesthesia which is not appropriate for all pts

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13
Q

what are the therapeutic goals for schizophrenia (split into the three main phases of journey of schizophrenia tx)

A
  1. acute stabilisation (minimise threat to self and others, minimise acute sx, improve func, identify appropriate psychosocial interventions, collab with family and caregivers)
  2. stabilisation (minimise or prevent relapse, promote adherence, optimise dose and manage s/e)
  3. stable/ maintenance (improve func and QoL, maintain baseline func, optimise dose and manage s/e, monitor for prodromal sx of relapse, monitor and manage s/e)
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14
Q

what is the general use of an antipsychotic

A

tranquilise without impairing consciousness and without causing paradoxical excitement; in short term can calm disturbed pts

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15
Q

what are the common indications of an antipsychotic, what are other possible uses of antipsychotics

A

schizophrenia, short term adjunct for severe anxiety or psychomotor agitation or violent behaviour, acute mania, adjunct for MDD

other uses incl antiemetic, motor tics and adjunct for choreas and tourettes syndrome, intractable hiccups, irritability assoc w bipolar disorder

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16
Q

what is the use of an antipsychotic specifically for schizophrenia

A

relieve sx of psychosis such as thought disorder, hallucinations and delusions and prevent relapse

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17
Q

what is the importance of tx with an antipsychotic for long term

A

req long term tx after first episode of psychosis and to prevent illness from becoming chronic

higher risk of relapse if withdrawn inappropriately; maintenance therapy can reduce risk of relapse to <30% per year; if w/o maintenance therapy 60-70% relapse within 1 yr and 90% relapse within 2 years

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18
Q

does relapse occur immediately after withdrawal from an antipsychotic

A

no, relapse can be delayed for several weeks after cessation of tx bc adipose tissues act as a depot reservoir since antipsychotics are mostly lipophilic thus will distribute in adipose tissues and will diffuse back into blood stream after cessation of tx

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19
Q

what are some ways to overcome adherence issues

A
  1. IM long acting injections
  2. community psychiatric nurses to conduct home visits to administer LA inj regularly
  3. patient and family/ caregiver education
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20
Q

what are the four dopamine tracts i. which antipsychotics acts on, which tracts are significant for what, and which tracts are responsible for various s/e

A
  1. mesolimbic tract - blockade of dopamine receptors in this tract probably the common moa for all antipsychotics bc overactivity in this tract is responsible for the pos sx of schizophrenia
  2. mesocortical tract - decr dopamine and hypofunc in this region results in neg sx of schizophrenia (thus blockade gives rise to more neg sx)
  3. nigrostriatal tract - regulates body movement (blockade gives rise to EPSE)
  4. tuberoinfundibular tract - regulates prolactin secretion (blockade gives rise to hyperprolactinemia)

*blockade of path 2,3,4 gives rise to s/e

21
Q

relate the effects of antagonism on impt receptors (therapeutic and postulated s/e)

A

D2: antagonism improves pos sx; antagonism causes EPSE, hyperprolactinemia

5HT1A: agonism allows it to act as an anxiolytic (reduce anxiety)

5HT2A: antagonism can help improve neg sx

5HT2C: antagonism results in weight gain

H1: antagonism results in sedation, weight gain

M1: antagonism results in memory dysfunc and peripheral anticholinergic

alpha1: antagonism results in orthostasis (postural hypotension), sedation

IKr: antagonism results in QTc prolongation (pro-arrhythmic)

22
Q

what is the postulated hypothetical threshold relating D2 receptor blockade to the various s/e

A

antipsychotic effect threshold: 60%
prolactin threshold: 70%
EPSE threshold: 80%

23
Q

which antipsychotics (typical and atypical) are most likely to have affinity for any of M1, alpha1, H1

A

chlorpromazine: M1, alpha1, H1
clozapine: M1, alpha1, H1
olanzapine: M1, alpha1, H1
quetiapine: H1
risperidone: alpha1, alpha2, H1

24
Q

what is the tx algorithm for schizophrenia

A

confirm diagnosis -> initiate SINGLE FGA/SGA (except clozapine) -> if inadequate or no response, use another SINGLE FGA/SGA (except clozapine) that is not yet prev tried -> if inadequate or no response, use clozapine -> clozapine w augmenting agent that can be FGA/SGA/ECT -> use combi tx (FGA+FGA/SGA+FGA or antipsychotic w ECT)

at any juncture if adequate resp and no intolerable s/e and compliant then continue tx

25
Q

what are the key principles to note for tx of schizophrenia

A
  1. medication selection is individualised based on pt clinical circumstances, past response or failures on antipsychotics, pts needs, efficacy and s/e profiles of tx
  2. pts req compliance to an adequate trial of antipsychotics (excl clozapine) of at least 2-6w at optimal therapeutic dose before considered as non responders; for clozapine, trial req more time of up to 3m to confirm therapeutic response (thus trial for at least 8-10w before adding on another antipsychotic)
  3. manage any intolerable s/e accordingly or switch tx
  4. consider a LA inj if pt prefers or non compliant to PO
  5. consider clozapine in those who are tx resistant (aka failed at least 2 adequate trials of different antipsychotics, one of which is SGA), if started must ensure routine hematological monitoring
26
Q

what are eg. of LA inj for tx of schizophrenia (explain why are decanoates used to create LA products)

A

IM risperidone microspheres, IM paliperidone prolonged release suspension, IM aripiprazole, IM haloperidol decanoate, IM flupenthixol decanoate, IM zuclopenthixol decanoate

drug molecule will have OH group bound to a long aliphatic chain and will form an ester which results in a very large molecule that is easily dissolved in fat and upon injecting into muscles will breakdown into fatty acids and ester bond will break apart to release the parent molecule that is of therapeutic property

27
Q

what are the precautions and c/i to use of antipsychotics

A
  1. epilepsy or risk factors predisposing to seizures
  2. parkinson’s disease
  3. elderly w dementia (bc incr risk of mortality and stroke)
  4. depression
  5. CVD (c/i in QTc prolongation)
  6. myasthenia gravis
  7. hx of jaundice
  8. severe respiratory disease
  9. prostatic hypertrophy
  10. closed angle glaucoma
  11. blood dyscrasia esp for clozapine (bc of clozapine induced agranulocytosis)

*note that ECG is req if physical exam identifies CV risk factors or if there is personal hx of CVD or if pt is being admitted as inpatient and is nave to antipsychotics

28
Q

what are possible adjunctive tx for schizophrenia tx

A
  1. acute agitation (psychiatric emergency)
    if cooperative:
    a) PO lorazepam 1-2mg
    b) PO antipsychotics (haloperidol 2-5mg w pretx ECG, risperidone 1-2mg; quetiapine 50-100mg, olanzapine 5-10mg)

if uncooperative:
a) IM lorazepam 1-2mg
b)IM olanzapine 5-10mg (2nd dose at least 2h after first and third dose at least 4h after second)
c) IM aripiprazole 9.75mg
d) IM haloperidol 2.5-10mg w pretx ECG
e) IM promethazine 25-50mg
f) a + d
g) d + e

  1. catatonia
    a) benzodiazepines (PO/IM lorazepam)
  2. depressive sx and/or neg sx of chronic schizophrenia
    a) antidepressants
29
Q

which antipsychotics have long half life

A

haloperidol (12-36h), olanzapine (21-54h), risperidone (3-20h)

30
Q

what are the general PK characteristics of antipsychotics

A

most have Tmax 1-3hr (rapidly absorbed, fast onset) except olanzapine, aripiprazole, brexpiprazole

most have long half life thus can be consolidated into QD dosing (but consider risk of hypotension and seizures) except chlorpromazine, amisulpride, clozapine, quetiapine, sulpiride, ziprasidone

administering lurasidone/ ziprasidone with food can incr F

31
Q

what are the initial starting dose, maintenance dose and max dose for PO (haloperidol, clozapine, olanzapine, quetiapine, risperidone)

A

haloperidol: 0.5-3mg or 3-5mg if severe sx; MD 5-15mg; max 20mg

clozapine: 12.5mg ON/BD on day 1 f/b 25-50mg ON on day 2 f/b 25-50mg increment; MD 200-450mg; max 900mg

olanzapine: 10mg/d; MD 5-20mg; max 20mg

quetiapine: 25mg BD f/b incr 50-100mg/d; MD 150-500mg; max 800mg

risperidone: 2mg/d in one or two divided doses; MD 2-6mg; max 16mg

32
Q

compare the dosing for LA inj (haloperidol decanoate, risperidone, paliperidone prolonged release suspension)

A

haloperidol: 50-300mg/4w

risperidone: 25-37.5mg/2w (to supplement with PO during first 3w)

paliperidone: inj q3m

33
Q

which s/e is consistent throughout ALL typical antipsychotics

A

EPSE and hyperprolactinemia

34
Q

which s/e is consistent throughout clozapine and olanzapine

A

drug induced diabetes, drug induced weight gain

35
Q

what should you supplement with when starting IM LA inj risperidone

A

supplement with PO during first 3w

36
Q

what are the s/e of antipsychotics and what is the onset and what are the risks for each s/e and how to manage each s/e

A
  1. [EPSE] dystonia: muscle spasm; mins if IV vs hrs if PO; high potency antipsychotics, naive to neuroleptics, young males; IM anticholinergics
  2. [EPSE] pseudo-parkinsonism: tremors, rigidity, salivation, bradykinesia, bradyphrenia; days or weeks; elderly women, prev neurological damage; reduce dose or switch to SGA, anticholinergics PRN
  3. [EPSE] akathisia: restlessness; hrs to weeks; high potency antipsychotics (risp > olan > quet/ cloz); reduce dose or switch to SGA, low dose lorazepam or clonazepam PRN, propanolol 20mg TDS
  4. [EPSE] tardive dyskinesia: orofacial movement, pelvic thrusting; months or years and 50% irreversible; FGA > SGA, worsen with anticholinergic drugs; discontinue anticholinergics, reduce dose or switch to SGA, valbenazine 40-80mg/d (a reversible inhibitor of VMAT2), clonazepam or lorazepam PRN
  5. hyperprolactinemia: amenorrhea, decr libido, gynaecomastia, breast swelling and pain; FGA/ pali/ risp > other SGAs; reduce FGA dose, switch to aripirprazole, dopamine agonist (bromocriptine)
  6. [metabolic] weight gain, DM, lipid incr; high risk for olan and clon, moderate risk for quet and risp, low risk for ari and lura and zip and halo; lifestyle modification through diet and exercise, treat DM, switch to lower risk agents (ari, lura, zip, halo)
  7. [CV] orthostatic hypotension: switch to low risk agents (olan, ari), get up slowly
  8. [CV] QTc prolongation: risk from high doses, IV halo; switch to low risk agents (olan)
  9. [CV] VTE/PE: risk from low potency and FGA; prevent, monitor and treat emergent DVT
  10. [CNS] sedation: switch to lower risk agents (olan, ari)
  11. [CNS] seizure: switch to high potency agent (halo)
  12. [CNS] neruroleptic malignant syndrome (NMS): muscle rigidity, fever, autonomic dysfunc (incr PR, labile BP, diaphoresis), altered consciousness, incr CK; risk from high potency antipsychotics, onset hrs to 3d (within 30d); IV dantrolene 50mg TDS, PO dopamine agonist (bromocriptine), switch to SGA
  13. [CNS] psychogenic polydipsia
  14. [CNS] temp dysregulation
  15. [hepatic] incr LFTs, jaundice: switch to lower risk (SGAs apart from olan, quet)
  16. [ophthalmic] high risk for chlor, quet; eye exam q6m for pts on quet
  17. [dermatological] rash, photosensitivity, pigmentation: high risk for chlor; protective clothing, sunscreen, consider switching
  18. [hematologic] decr WBC count, agranulocytosis, decr absolute neutrophil count; high risk clozapine; discontinue if severe (WBC <3x10^9 or ANC <1.5x10^9)

*for hyperprolactinemia, metabolic and CVD, CNS switch to low risk agents
for hyperprolactinemia: ari
for metabolic: ari, lura
for orthostatic hypotension: ari/ olan
for QTc: olan
for sedation: ari
for jaundice: risp

*for seizures switch to high potency: halo

37
Q

differentiate between the various EPSE

A

dystonia: muscle spams

pseudo-parkinsonism: tremors, rigidity, bradykinesia, bradyphrenia, salivation

akathisia: restlessness

tardive dyskinesia: orofacial movements, pelvic thrusting, choreiform hand movements

38
Q

what are the s/sx of NMS and what can be used to treat NMS

A

NMS is neuroleptic malignant syndrome

the s/sx incl fever, muscle rigidity, autonomic dysfunction (incr PR, labile BP, diaphoresis), altered consciousness, incr CK

give IV dantrolene, PO dopamine agonist (bromocriptine), switch to SGA

39
Q

what are the monitoring parameters and how often should each parameter be monitored

A
  1. BMI: every visit for 6m f/b q3m when stabilised
  2. waist circumference: every visit for 6m f/b q12m
  3. fasting blood glucose: low risk q12m; high risk 3m after initiating f/b q12m
  4. lipid panel: low risk q2-5yr, high risk 3m after initiating f/b q6m
  5. plasma prolactin: at baseline
  6. BP: 3m after start f/b q12m
  7. EPSE exam: q1w for 2w (or until stabilised dose) f/b low risk q6m/q12m (FGA/SGA), high risk q3m/q12m (FGA/SGA)
  8. ECG for risperidone (repeat if risk/ sx of QTc prolongation)
  9. WBC and ANC for clozapine (q1w for 18w f/b q1m)
40
Q

what are the considerations for various special populations with regards to use of antipsychotics (pregnancy, breastfeeding, renal impairment, hepatic impairment, elderly)

A
  1. pregnancy: give olan, cloza and monitor for gestational DM
  2. breastfeeding: give olan, quet (if on cloza alr then continue but do not breastfeed)
  3. renal impairment: PO ari (avoid ami and sulpiride)
  4. hepatic impairment: ami, sulpiride
  5. elderly: avoid drugs with high propensity of alpha1 block due to postural hypotension or anticholinergic s/e and start low go slow, avoid long half life
41
Q

what are the kinds of ddi (general classification)

A

PD ddi (pharmacological effects, physiological effects)

PK ddi (phase 1 rxn - hydrolysis, oxidation, reduction; phase 2 rxn - coupling rxns like glucoronidation)

42
Q

which kind of rxn does cyp affect

A

phase 1 rxn (PK ddi)

43
Q

what are the cyp interactions involving psychiatric drugs

A

1A2 substrates: theophylline, amiodarone, warfarin-R, clozapine, agomelatin, chlorpromazine

1A2 inhibitors: fluvoxamine, ciprofloxacin, clarithromycin

2C8 substrates: paclitaxel, rosiglitazone

2C8 inhibitos: gemfibrozil

2C9 substrates: warfarin-S, SU (glipizide), PHT

2C9 inhibitors: amiodarone, fluconazole

2C19 substrates: omeprazole, warfarin-R, SU (tolbutamide)

2C19 inhibitors: omeprazole, fluvoxamine, meclobemide, voriconazole, fluoxetinem ticlopidine

2D6 substrates: risp, olan, ari, brexpiprazole, metoprolol, opioids (tramadol, codeine, oxycodone)

2D6 inhibitors: fluoxetine, paroxetine, duloxetin, bupropion

3A4 substrates: simvastatin, lovastatin, nifedipine, diltiazem, amlodipine, tacrolimus, cyclosporin, risp, quet, ari, brexpiprazole, lurasidone, PB, midazolam, ergotamine

3A4 inhibitors: clarithromycin, protease inhibitors (ritonavir), grapefruit, itra/keto/voriconazole

3A4 inducers: rifampicin, st john’s wort, CBZ, PHT

44
Q

what are the psychiatric drugs that have few cyp interactions

A

midazolam, escitalopram, venlafaxine, desvenlafaxine, vortioxetine

45
Q

what are the clinically significant interactions specifically with antipsychotics

A
  1. CNS depressants (alcohol, opioids) can lead to additive CNS effects
  2. drugs with antimuscarinics, antihistaminic, alpha1-adrenergic blockade, dopamine blockade can have additive s/e
  3. dopamine augmenting agents (levodopa, bromocriptine) can cause mutual antag with antipsychotics
  4. 5HT augmenting agents can cause antag 5HT2A which further decr dopamine and worsen EPSE
  5. antihypertensives can incr hypotensive effects
  6. adrenaline
  7. TCAs can incr toxicity
  8. Lithium
  9. 1A2 inducers (rifampicin, PB, PHT, smoking) can decr chlorpromazine, clozapine, olanzapine, haloperidol
  10. 1A2 inhibitors (fluvoxamine, ciprofloxacin, clarithromycin, isoniazid, ketoconzaole) can incr chlorpromazine, clozapine, olanzapine
  11. 2D6 inducer (rifampicin, PB, PHT, CBZ) can decr chlorpromazine, clozapine, halo, risp, ari
  12. 2D6 inhibitors (fluoxetine, paroxetine, bupropion, duloxetine) can incr chlor, ari, olan, halo, risp
  13. 3A4 inducers (CBZ, PHT, stjohns, rifampicin) decr quet, risp, ari
  14. 3A4 inhibitors (ritonavir, clarithromycin, grapefruit, ketoconazole, fluvoxamine, ciprofloxacin) incr quet, risp, ari
  15. CBZ can cause agranulocytosis with clozapine
46
Q

how might therapeutic outcomes be monitored

A
  1. mental state exam (MSE)
  2. monitor for s/e (metabolic parameters like BP, BMI, FBG, lipids etc and EPSE)
  3. pt’s self assessment
47
Q

what is considered early improvement vs late improvement in terms of therapeutic outcomes

A

early improvement: first week decr agitation, aggression and hostility; in 2-4w decr paranoia, hallucinations, bizarre behaviours with improved thought organisation

late improvement: 6-12w decr in delusions and improvement in neg sx, 3-6m cognitive sx may improve with SGA (cloza, risp)

48
Q

generally compare the types of s/e between the antipsychotics

A

FGA vs SGA: FGA has more muscle s/e (EPSE) while SGA has more metabolic s/e except ari, lurasidone

among SGA: -ines (clozapine, olanzapine, quetiapine) have more sedation and weight gain

49
Q

generally compare eg. of formulations of antipsychotics

A

PO: immediate release, oral dispersible, oral solution, oral extended release

IM: IM short acting (haloperidol, olanzapine), IM long acting (haloperidol decanoate)

pr3153 (18 decks)

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