Therapeutics Neuro/psych Exam 2- Schizophrenia

Front 1

schizo- lifetime incidence
onset (age)
gender

Back 1

lifetime incidence- 1%

onset- late adolescence/early adulthood- earlier in males

new studies show males > females

Front 2

etiology of schizo (3)

Back 2

Genetic Susceptibility (multiple alleles)- risk increased if have first degree relative with it
environmental (infection in fetus, hypoxia, leads to abnormal neuron migration), maybe SCZ has something to do with dendrite pruning since this usually occurs by midadolescence

Front 3

schizo course of illness (most deterioration when?) and tx efficacy vs. timing (2)

maintenance therapy efficacy

Back 3

 Most deterioration in psychosocial functioning
occurs within the first 5 years- Early treatment predicts better long-term
outcomes
 Majority of patients experience 1+ relapse: Antipsychotic maintenance therapy
significantly reduces the risk of relapse at 1 yr

Front 4

ideal schizo case

Back 4

Initial psychotic episode is quickly detected and treated and further
illness is prevented by prophylactic treatment

Front 5

chronic schizo relapsing case

Back 5

Chronic relapsing condition with each psychotic
exposure decreasing global function

Front 6

Schizo and suicide correlation (% of pt that do it, cause of death)

Back 6

 ~ 30%-40% of people with schizophrenia attempt
suicide at some point in their lifetime
 Suicide is the most common cause of premature
death among patients with schizophrenia

Front 7

6 risk factors for suicide in SCZ patients

Back 7

 Symptoms of depression
 Hallucinations (voices telling patient to commit suicide)
 Substance abuse
 Being unmarried
 Not having a job
 Recent discharge from the hospital

Front 8

definition of psychosis (3)

Back 8

A severe mental disturbance that involves a
profound misinterpretation of perceptions or
loss of contact with reality
 Interferes with the ability to interact
appropriately with others or with the
environment
 Psychotic features/symptoms are present in
various disorders (including mood disorders)

Front 9

definition of psychotic disorder

Back 9

Include psychotic symptoms as a prominent
aspect of their presentation

Front 10

clinical presentation of schizo: 3 types of sx

Back 10

Negative- taking away something
Positive- adding somthing
Cognitive- inability to make decision, decrease mental functionality

Front 11

positive sx =

Back 11

psychotic sx

Front 12

positive sx consist of (4)

4 types of delusions

Back 12

 Hallucinations
 Delusions- fixed false beliefs about things e.g. Persecutory (paranoia), Grandiose, Referential (books/tv sending messages to them), Bizarre (weird **** that can't be true)
 Disorganized speech
 Grossly disorganized or catatonic behavior

Front 13

Negative symptoms (5)

Back 13

 Affective flattening- impaired outward display of emotions
 Alogia (Poverty of
Speech)- Decreased speech
fluency
 Avolition- Lack of motivation or
“drive”
 Anhedonia- Loss of interest or
pleasure
 Asociality- lacking the capacity
for social interaction

Front 14

6 cognitive symptoms of schizo

Back 14

 Poor concentration
 Poor abstraction (can't see deeper meaning in things)
 Memory disturbances
 Inability to plan
 Impaired decision making
 Difficulty executing tasks

Front 15

DSM-IV dx criteria for schizo (sx and durations) (3 portions/criteria)

Back 15

Two or more of the following symptoms, each
persisting for significant portion of at least a 1-
month period (unless treated):
 Delusions
 Hallucinations
 Disorganized speech
 Grossly disorganized or catatonic behavior
 Negative symptoms

Social/occupational dysfunction:
 For a significant portion of the time since onset of the
disorder, one or more major areas of functioning
such as work, interpersonal relations, or self-care are
significantly below the level prior to onset

Continuous signs of the disorder for at least 6 months
 Must include 1+ month of acute symptoms (unless
successfully treated) and may include prodromal or
residual periods

Front 16

DSM IV: Schizoaffective disorder (3)

Back 16

 Major Depressive Episode, Manic Episode, or
Mixed Episode concurrent with acute
symptoms of Schizophrenia
 During same period of illness, there have been delusions or hallucinations 2+ weeks in absence of prominent mood symptoms (euthymic)- basically must be 2+ weeks where patient has psychotic sx but no mood disorder
 Mood episode symptoms present for a "substantial" portion of the illness duration

Front 17

CNS diseases to r/o to dx schizo (6)

Back 17

 Huntington’s Disease
 Multiple Sclerosis
 Epilepsy
 Migraines
 CNS infections
 Deafness

Front 18

metabolic disorders to r/o for schizo (3)

Back 18

 Hypoxia
 Hypercarbia
 Hypoglycemia

Front 19

endocrine disorders that can cause psychotic disorders (3)

Back 19

 Hyper/Hypothyroidism
 Hyper/Hypoparathyroidism
 Cushing’s syndrome
 Addison’s disease

Front 20

3 misc. disorders that can cause psychotic sx (3)

Back 20

 Fluid/electrolyte
imbalances
 Hepatic or renal disease
 Systemic lupus
erythematosis

Front 21

substances associated with psychotic sx (9)

Back 21

 Alcohol
 Amphetamines
 THC
 Cocaine
 PCP
 LSD
 Inhalants
 Opioids
 Sedative/Hypnotics

Front 22

substances that cause psychosis with withdrawal (2)

Back 22

 Alcohol
 Sedative/Hypnotics

Front 23

4 DA pathways

Back 23

mesolimbic
mesocortical
nigrostriatal
tuberoinfundibular

Front 24

4 DA pathways and where they go/what they do

Back 24

mesolimbic pathway- brain stem to limbic
mesocortical- brain stem to cortex
nigrostriatal- sub nigra to striatum (motor- EPS sx)
Tuberoinfundibular- hypothalamus to pituitary- inhibits prolactin release

Front 25

Dopamine hypothesis (2)

Back 25

excess of DA activity in mesolimbic: positive sx
deficiency of DA in mesocortical: negative sx/cognitive sx

Front 26

DA antagonism: tx efficacy and cause of adverse effects (4)

Back 26

DA inhibition in mesolimbic is good- but if we block too much DA and it affects other areas in brain- e.g. EPS in nigrostriatal, hyperprolactinemia (tuberoinfundibular)
Minimal improvement of negative sx in mesocortical

Front 27

Ideal Antipsychotic for schizo properties (3)

Back 27

 Decrease DA activity in the mesolimbic
pathway to treat positive symptoms
 Increase DA activity in the mesocortical
pathway to treat negative symptoms
 Maintain adequate DA activity in the nigrostriatal and tuberoinfundibular pathways
to minimize side effects

Front 28

Antipsychotic classes

Back 28

first gen antipsychs
second gen antipsychs

Front 29

first gen antipsychs- how they work
and what types of drug (3)

Back 29

primarily work by blocking D2 receptor

are conventional agents, neuroleptics or typical antipsychotics

Front 30

second gen antipsychs- type of drug
MoA

Back 30

 Atypical antipsychotics
 Dopamine and
serotonin blockade (less EPS sx...not sure why. i think serotonin block counters it). IDK this paper says that it's because the binding to D2 receptors is more transient/not as hard as dopamine

Front 31

comparison of antipsychotic pharmacology

Back 31

chart - did not enter

Front 32

First gen antipsychotics- 2 categories

Back 32

phenothiazines (-zines)
non-phenothiazines

Front 33

phenothiazines (5)

Back 33

 Chlorpromazine (Thorazine®)
 Thioridazine (Mellaril®)
 Perphenazine (Trilafon®)
 Trifluoperazine (Stelazine®)
 Fluphenazine (Prolixin®)

Front 34

non-phenothiazines (5)

Back 34

 Thiothixene (Navane®)
 Haloperidol (Haldol®)
 Loxapine (Loxitane®)
 Molindone (Moban®)
 Pimozide (Orap®) – primarily for Tourette syndrome

Front 35

First gen antipsychotic potency: high potency drugs properties (2)

Back 35

 More potent D2 antagonism (more EPS)
 Less anticholinergic, alpha-antagonism, sedation

Front 36

examples of high potency antipsychotics (5)

Back 36

Haloperidol, fluphenazine, thiothixene,
trifluoperazine, pimozide

Front 37

Moderate Potency FG antipsychotic property

Back 37

Moderate D2 antagonism as well as receptor selectivity- less...AE? (litsen again)

Front 38

relative potency- highest (4)

mod (3)

least (2)

Back 38

least potent- chlorpromazine, thioridazine (phenothiazines)

moderate- Perphenazine, loxapine, molindone

potent-this was on a diff slide

Front 39

FGA oral dosing/max dose

Back 39

what to take away: low potency agent like (chlorpromazine- you need like hundreds of mg to get an effect)

know the relative...like..."ranges". in the tens or hundreds

won't ask "is 30 mg in range for X drug

Front 40

Haloperidol max dose and usual dosage range

Back 40

100 mg is MAX- people used to use these high doses regularly


nowadays very rare to use more than 20 mg of haloperidol due to dose related risk of EPS (range is 2-20)

Front 41

Second gen antipsychotics (10)

Back 41

Clozapine
Risperidone
Olanzapine
Quetiapine
Ziprasidone
ripiprazole (abilify)
paliperidone
iloperidone
asenapine
lurasidone

Front 42

D2 receptor occupancy and EPS/prolectin elevation

Back 42

no subject with D2 occupancy below 78% showed any EPS

72% for prolactin

Front 43

What haloperidol D2 receptor study told us

Back 43

high potency typical antipsychotic
response is possible (but not probable) without
EPS or prolactin elevation with appropriate D2
occupancy, however therapeutic window is narrow and variable

Front 44

Functional interactions b/t 5HT and DA

Back 44

5-HT disinhibition of DA normally- but if you block this then DA can release normally in nigrostriatum

Front 45

D2/5HT2 occupancy of risperidone (and other second gens)

Back 45

...looks like it had almost 100% binding of 5HT2A receptors

Front 46

Exception to 5HT2/D2 effects in second gen antipsychotics (2)

Back 46

Clozapine- advantage- inability to occupy > 70% of D2 binding profile (saturation even at higher doses) - so not much EPS

Quetiapine is similar

Front 47

missed a few slides due to computer dying

time course of response to antipsychotics (4 steps)

Back 47

1-2 weeks- decreased aggression/hostility/normal sleep/appetite

2-3 weeks- improve socialization, mood

2-6 weeks- improvement on psychotic sx "though disorders"

residual sx - fixed delusions or hallucinations

Front 48

Reasons for nonadherence to antipsychs (5)

Back 48

side effects (highest)
didn't like it
thought they didn't need it when they were doing well
didn't work
forgot to take

Front 49

Clinical consequences of D2 blockade (2)

Back 49

hyperprolactinemia
drug induced movement disorders

Front 50

hyperprolactinemia consequences (6)

Back 50

 Amenorrhea
 Dysmenorrhea
 Gynecomastia
 Lactation
 Sexual dysfunction
 Osteoporosis?

Front 51

hyperprolactinemia sx more common with what drugs (3)

Back 51

increased risk with FGAs risperidone and paliperidone

Front 52

drug induced mvmt (2 types and define them, kind of)

Back 52

- Extrapyramidal Symptoms (EPS) includes...
 Dystonia
 Akathisia
 Pseudoparkinsonism
-Tardive Dyskinesia (TD)

Front 53

Dystonia characterized by... (6)

Back 53

sustained muscle contractions
 Torticollis
 Protrusion or twisting of the tongue
 Trismus
 Blepharospasm
 Oculogyric crisis- eyes get rolled up into back of head
 Laryngospasm

Front 54

acute dystonia sx onset

Back 54

Generally occurs within hours to days of
starting antipsychotic or increasing dose

Front 55

risk factors for dystonia (4)

Back 55

 Young Patients
 Males (maybe because we tend to give young muscular...male patients higher doses)
 High Potency FGAs
 Previous Dystonic Reaction

Front 56

tx for dystonia

Back 56

preferred is anticholinergics (benadryl or benztropine)- due to recipricol reactions between Ach and DA. if ineffective or not tolerated can use benzos

Ach suppresses mvmt so if you block it, you get opposite effect.

Front 57

missed slides up until tx of induced akathisia

Back 57

--

Front 58

tx of akathisia (2 things to do to current regiment, 3 meds to add)

Back 58

 Lower the antipsychotic dose
 Switch to an SGA
 Add medication for akathisia- beta blocker (propranolol, nadolol, metoprolol) OR benzo but avoid if substance abuse ( i think beta blockers better).

Anticholinergic not effective

Front 59

Pseudoparkinsonism (drug induced) sx (3)

Back 59

similar sx to parkinson's
bradykinesia
resting tremor
cogwheel type rigidity

Front 60

Pseudoparkinsonism incidence and in what drugs

Back 60

occurs in 10-40% of pt treated with FGAs

Front 61

pseudoparkinsonism onset

Back 61

Onset typically 1-3 months
after antipsychotic initiated
 May see as early as 1 week

Front 62

risk factors of pseudoparkinsonism (4)

Back 62

 High potency FGAs
 High dose antipsychotics
 Over 40 years of age
 Females

Front 63

second generation antipsychotics- drugs that cause it more (besides FGAs)

Back 63

Of SGAs, risperidone & paliperidone have higher
risk, particularly at higher doses

Front 64

tx of pseudoparkinsonism (3)

Back 64

 Lower the dose of antipsychotic
 Switch to an SGA
 Add antiparkinsonian medication (anticholinergics- preferred- benztropine/trihexypenidyl) or amantidine is alternative

Front 65

clinical characteristics of tardive dyskinesia (2)

Back 65

 Abnormal, involuntary movements that are
potentially irreversible
 Movements are usually choreic (jerky), athetoid (wavy) or
choreoathetoid (combo): May include chewing, tongue protrusion, lip
smacking, puckering, involuntary movements of the
trunk or limbs, etc.

Front 66

onset of TD

Back 66

may be 3 mo to years after tx

Front 67

TD: why is the onset so long?

Back 67

DA hypersensitivity due to long term blockade- something happens in brain that tries to compensate for blockade and gives receptors that are hypersensitive

Front 68

risk factors for tardive dyskinesia (8)

Back 68

 Age- Elderly (3-5X)
 Long duration of treatment
 FGAs > SGAs
 Gender: Female
 Race: African Americans (2X)
 Affective (Mood) disorders
 Refractory Psychosis
 Early EPS

Front 69

TD in FGA vs. SGA (3)

Back 69

 Difficult to assess due to short duration of trials and 10 years of FGAs on market until TD recognized as a
problem so most everyone had been exposed to FGA at some point
 True risk with SGAs limited due to inability to tease out those not exposed to FGAs
 Reported mean annual incidence of TD
(excluding elderly)
-5.4% with haloperidol
-0.8% with SGAs

Front 70

tx?? of TD (more like how to manage) (3)

antipsychotic drug of choice for severe TD

Back 70

best tx if PREVENTION- monitor with AIMS continuously for ANY emergence of mvmts

d/c AP if possible- to prevent from getting worse (may not get better) ALTHOUGH sometimes you may not be able to d/c successfully because taking them off the blocker can sometimes make TD worse (more DA hitting receptors)
if cna't d/c- switch to SGA or clozapine (drug of choice if severe TD)

Front 71

agents that have been studied for TD and results (4)

Back 71

vit E
melatonin
Acetylcholinesterase inhibitors
branched chain amino acids

not rec'd; no evidence

Front 72

metabolic risk in schizophrenia (primary concern with SGAs) (3)

Back 72

already increased risk with schizo disease state due to:

prevalence of smoking (nicotine may stimulate cognition so may be self medicating), diabetes, CV disease
higher risk of obesity due to ****** nutritional habits and sedentary lifestyle

meds can exacerbate these issues

Front 73

antipsychotics and weight gain (high/moderate/low risk)

Back 73

clozapine is the worst
olanzapine
then quetiapine/risperidone (moderate weight effects)
low risk: abilify, ziprazidone? lorasidone?

Front 74

Antipsychotics- other metabolic abnormalities (2)

Back 74

lipid abnormalities- nt sure if related to weight gain
glucose dysregulation/diabetes- even without weight gain

Front 75

drugs that cause the most lipid issues and the least (2 ea)

Back 75

Clozapine and olanzapine are reported to cause the
most weight gain and also have the most reports
regarding increased triglyceride levels
 Aripiprazole and ziprasidone have minimal to no
effect on weight & lipids

Front 76

onset of AP diabetes

Back 76

 Most cases of new onset diabetes developed
within 6 months after starting the antipsychotic

Front 77

huge chart of metabolic stuff

best and worst

Back 77

olanzapine/clozapine- worst in temrs of metabolic ****

asenapine, aripriprazole, ziprasidone, lurasidone best

Front 78

SGAs; metabolic monitoring: baseline (6)

Back 78

personal/family hx
weight
waist circ
BP
fasting plasma glucose
fasting lipid profile

Front 79

SGAs: weight monitoring freq

Back 79

monthly for first 3 months then quarterly

Front 80

SGAs waist circ monitoring freq

Back 80

yearly

Front 81

SGAs BP monitoring; when to monitor

Back 81

at 3 months (and that's it?)

Front 82

glucose and lipid monitoring

Back 82

glucose: baseline, 3 mo, yearly
lipids: baseline, 3 mo, q5 years

Front 83

QTc prolongation- warnings on which drugs (2 SGA and 3 FGA)

Back 83

thioridazine- BBW
and mesoridazine (removed- active metabolite of thiridazine)

these were FGAs

and haloperidol IV at high doses-->ECG monitoring if IV
SGAs: ziprasidone and iloperidone- labeled warning

Front 84

comparative QTc prolonging effects for SGAs- idk listen again

Back 84

thioridazine

oral haloperidol NBD
and other SGAs also
lurazidone actually has low QTc prolongation even though it looks high on chart

in particular abilify has really low risk-good choice in pt with long qtc

Front 85

normal QTc

Back 85

360-440 ms (higher in women by 20 ms)

Front 86

risk factors for QTc prolongation (5)

Back 86

Cardiac disease, electrolyte imbalance, bradycardia,
elderly, on concomitant QTc-prolonging drugs

Front 87

for pt with risk factors for QTc what must you do before giving antipsychotics

when to d/c them and how to deal with it in terms of further tx of their psych issues (2)

Back 87

 Recommend baseline ECG for at-risk patients
 Discontinue antipsychotics if QTc >500 msec
 Consider reinitiating therapy with lower risk agent
(e.g. aripiprazole, olanzapine??)

Front 88

possible side effects based on pharmacology for APs (4)

Back 88

Anticholinergic side effects- specific ones on slide
H1 antagonism- sedation/weight
5-HT2c antagonism - weight gain
 Alpha-1 antagonsim
 Orthostatic hypotension, dizziness, sedation

Front 89

most sedating

worst anticholinergic

(2)

most prolactin releasing (3)

Back 89

--

clozapine worst for anticholinergic (well, all side effects that are not DA related)

chlorpromazine- also anticholinergic

Both are most sedating

haloperidol, CPZ, risperidone?? (

Front 90

counseling points: which drugs must be taken with food and why (2)

Back 90

ziprasidone and lurasidone

decrease in BA without food

Front 91

counseling points: orthostasis- which drug and how to counter this

Back 91

iloperidone
must titrate slowly (1 wk schedule)

CPZ, CLZ too????

Front 92

counseling points: SL tablet

Back 92

asenapine- should not eat or drink within 10 min of taking med

Front 93

Clozapine benefits (3)

Back 93

 Most effective antipsychotic
 Decreased risk of suicidal behavior & aggression
 Relatively low risk of EPS

Front 94

Black box warnings for clozapine (4)

Back 94

agranulocytosis, seizures,
myocarditis, orthostatic hypotension

Front 95

4 AE of clozapine

Back 95

 Constipation: can be severe and even life-threatening- usually started on bowel regimen too
 Sedation
 Adverse metabolic effects
 Sialorrhea (really awful drooling)- no dry mouth!!! hile clozapine is a muscarinic antagonist at the M1, M2, M3, and M5 receptors, clozapine is a full agonist at the M4 subset. Because M4 is highly expressed in the salivary gland, its M4 agonist activity is thought to be responsible for the hypersalivation

Front 96

clozapine- it has so many side effects- what about efficacy?

Back 96

clearly superior in reducing sx so still the best drug we have

Front 97

Clozapine: Agranulocytosis incidence (2) post and premarketing

Back 97

 Premarketing research incidence of 1-2%
 Postmarketing data indicates incidence only 0.38%
with 0.012% being fatal- maybe because we monitor so closely

Front 98

monitoring for agranulocytosis/clozapine (4)

Back 98

 WBC/ANC baseline and weekly x 6 months
 Then every 2 weeks x 6 months
 After 12 months patient can go to monthly monitoring if no drops in WBC/ANC
 Perform WBC/ANC for at least 4 weeks after discontinuation

(have to submit to national registry)

Front 99

clozapine myocarditis- incidence and onset/sx

Back 99

again, low incidence
usually occurs within 3 weeks of starting therapy
sx similar to CHF- fatigue, CP, fluid overload

Front 100

clozapine seizures (2)

Back 100

 All antipsychotics can lower seizure threshold;
seizure incidence 0.1-1.5%
 Clozapine associated with higher incidence than
other antipsychotics at usual therapeutic doses

Front 101

clozapine seizures- how to avoid

Back 101

titrate by doubling dose every few days when initiating

Front 102

Neuroleptic malignant syndrome (NMS)- incidence

Back 102

occurs in 0.5-1% pt on AP

Front 103

NMS sx (6)

Back 103

body temp increase
mental status changes
tachy
diaphoresis
labile BP
"lead pipe" rigidity

Front 104

NMS- hard to distinguish from...

severity of this syndrome
tx options (3)

Back 104

similar to serotonin syndrome
may be fatal if not tx and AP not d/ced
tx primarily supportive care, bromocriptine (D2 agonist?), dantrolene

Front 105

Long acting decanoate antipsychotics- PO overlap required in...(2)

rec'd in...(2)

Back 105

required in risperidone and aripriprazole

rec'd in haloperidol and fluphenazine

Front 106

LAI options (6)

Back 106

haloperidol
fluphenazine
risperidone
paliperidone
olanzapine
aripriprazole

Front 107

risperidone LAI (2) what kind of technology, release profile and implications

Back 107

 Microsphere technology
 Takes a long time to release...so Need to overlap with oral risperidone medication for 3 weeks (at least 2 injections before effects kick in)

Front 108

paliperidone therapeutic advantage (3)

Back 108

therapeutic advantage over risperdal and Consta

 No need for oral medication overlap
 Monthly vs. every 2 week injections
 No refrigeration or reconstitution needed

Front 109

Olanzapine (zyprexa) LAI major issue

what is it
onset
risk mitigation strategy (2 things the pt has to do/can't do)
restrictions

Back 109

post injection delirium sedation syndrome

 Symptoms of olanzapine overdose
 94% of reactions within 3 hrs of administration
 Risk Evaluation and Mitigation Strategy (REMS):
patients must be observed for 3 hrs after EVERY
injection; should not drive on day of injection
 Restricted distribution: prescriber, healthcare facility,
patient, and pharmacy must all be enrolled with
drug company

Front 110

abilify LAI- oral overlap?

dose adjustments/metabolism issues (2)

Back 110

need to overlap with oral med for 2 weeks
must be dose adjusted for presence of 2D6/3A4 inhibitors or in pt who are 2D6 oor metabolizers
avoid use with concomitant 3A4 inducers

Front 111

important pharmacodynamic interactions of APs (3)

Back 111

 Clozapine + carbamazepine = ↑ risk blood
dyscrasias
 Clozapine/iloperidone/quetiapine/
chlorpromazine + antiphypertensives = ↑ risk
orthostasis
 QTc prolongation- Ziprasidone, thioridazine, IV haloperidol, TCAs,
citalopram

Front 112

metabolism pathways of atypical antipsychotics

3A4 (3)

2D6 (3)

no CYPs (2)

1A2- (3)

Back 112

3A4- Q, ARI, LUR

2D6- ARI, RIS, ILO

no CYPS- PALI, ZIP

1A2- CLZ, OLAN, ASEN

Front 113

Important PK interactions of antipsychotics: CYP1A2 interactions (inducers and inhibitors)

Back 113

 Inducers: cigarette smoking, carbamazepine,
omeprazole (weak to moderate)
 Inhibitors: fluvoxamine, fluoxetine (moderate),
ciprofloxacin

Front 114

omfg details of CYP1A2 mediated interactions of atypical psych meds-didn't really talk about

Back 114

 Fluvoxamine + CLZ = ↑ CLZ level three- to four-fold
 Fluvoxamine + OLZ/ASEN = ↑ antipsychotic levels
 Fluoxetine + CLZ = ↑ CLZ level ≈ 50%
 Cigarette smoking + OLZ/CLZ = ↓ OLZ/CLZ levels
 CBZ + OLZ/CLZ = ↓ OLZ/CLZ levels

Front 115

CYP2D6 mediated interactions (3) inhibitors; what listen again; more details on slide she didn't go over

additional substrates metabolized by 2D6 (2)

Back 115

 Additional substrates that are also metabolized by 2D6?? idk: haloperidol, phenothiazines
 Inducers: none known
 Inhibitors: fluoxetine, paroxetine, bupropion

Front 116

CYP3A4 mediated interactions

additional substrates (1)
inducers (3)
inhibitors (**** ton)

Back 116

 Additional substrates: haloperidol
 Inducers: CBZ, OXC, phenytoin
 Inhibitors: nefazodone, ketaconazole, itraconazole,
ritonavir, erythromycin, clarithromycin, cimetidine,
grapefruit juice

Front 117

avoid what drug with QTP- one she specifically mentioned

Back 117

QTP + pneytoin = 5-fold increase in QTP CLEARANCE- significant-->avoid this combo

Front 118

lurasidone CI with which drug(s)

Back 118

strong 3A4 inhibitors

Front 119

Pregnancy and APs- risk for teratogenicity is greatest when

Back 119

 Risk of teratogenesis from medication is
greatest during embryogenesis (3rd-8th week
of gestation)

Front 120

preferred APs in pregnancy (2)

Back 120

 Haloperidol???

Clozapine is pregnancy category B, all others
are category C (except lurasidone is now cat B?)
 Generally more data with typical antipsychotics

Front 121

AP risk/FDA alert for newborn

Back 121

EPS and withdrawal sx in newborn- but still safer to use than to now use

Front 122

AP in elderly- major issue (3)

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Elderly patients with dementia related psychosis treated with antipsychotic drugs are at an increased risk of death compared to placebo

majority of deaths cauesd by CV and infectious (pneumo) reasons

SO- NO SAFE AP in elderly pt with dementia- in both FGA or SGA

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akathisia risk factors (4)

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 High potency FGAs
 Commonly reported with aripiprazole
 High doses
 Rapid dose escalation