Exam 1 Study Material
STEPs framework
You are expected to choose meds using:
Safety: contraindications, interactions, comorbidities, overdose risk
Tolerability: short and long-term side effects
Efficacy: evidence for the condition and symptom target
Practicality: cost, adherence likelihood, monitoring burden, access
Pharmacokinetics vs pharmacodynamics (test language)
Pharmacokinetics (PK): what the body does to the drug (absorption, distribution,
metabolism, excretion)
Pharmacodynamics (PD): what the drug does to the body (receptors, enzymes,
channels, second messengers)
CYP450 logic (the core rule they keep using)
Inducer of an enzyme → decreases level of a drug that is a substrate of that enzyme
Inhibitor → increases substrate level
Example: Escitalopram is a CYP3A4 substrate. Add a 3A4 inducer → escitalopram levels
decrease, effect can drop, patient can relapse.
If a question says “X is a substrate” and asks “what happens if you add an inducer?” the answer
is almost always “levels drop” unless it’s a trick with prodrugs.
Schizophrenia / Psychosis / Antipsychotics
Acute psychosis and agitation: what the PMHNP does first
If the patient can’t or won’t take PO, use IM antipsychotic options.
IM olanzapine and IM haloperidol, and when using IM haloperidol, give benztropine
or diphenhydramine for EPS coverage.
High-yield clinical reasoning: in acute agitation, you choose what works fastest and is feasible
(practicality), while reducing immediate harm (safety).
Ex. IM Haloperidol + Lorazepam
Typical vs atypical antipsychotics: what gets tested
, Typical (FGA) core adverse effect pattern
FGA adverse effects including:
EPS
Tardive dyskinesia
Hyperprolactinemia
Anticholinergic effects
NMS
QTc prolongation
Seizure threshold lowering
Cardiac dysrhythmias
Sedation
Interpretation: FGAs are “movement side effect heavy.” High potency FGAs are especially
associated with EPS.
Atypical (SGA) core adverse effect pattern
SGAs still can cause EPS/TD, but the big board-style risk is usually metabolic syndrome.
EPS: recognize the subtype, then choose the correct intervention
Acute dystonia
Onset: often early after starting or dose increase (Days to weeks)
Presentation: painful muscle spasm, neck/jaw/eyes (oculogyric crisis), tongue
First-line treatment: benztropine or diphenhydramine
Akathisia (Can occur within days)
Presentation: inner restlessness, pacing, “can’t sit still”
First-line treatment in the slides: propranolol (they also mention benzos as an option)
High-yield mistake: calling it “anxiety” and increasing the antipsychotic dose makes it
worse.
Frequent SE of Aripiprazole
Pseudo-parkinsonism (drug-induced parkinsonism)
STEPs framework
You are expected to choose meds using:
Safety: contraindications, interactions, comorbidities, overdose risk
Tolerability: short and long-term side effects
Efficacy: evidence for the condition and symptom target
Practicality: cost, adherence likelihood, monitoring burden, access
Pharmacokinetics vs pharmacodynamics (test language)
Pharmacokinetics (PK): what the body does to the drug (absorption, distribution,
metabolism, excretion)
Pharmacodynamics (PD): what the drug does to the body (receptors, enzymes,
channels, second messengers)
CYP450 logic (the core rule they keep using)
Inducer of an enzyme → decreases level of a drug that is a substrate of that enzyme
Inhibitor → increases substrate level
Example: Escitalopram is a CYP3A4 substrate. Add a 3A4 inducer → escitalopram levels
decrease, effect can drop, patient can relapse.
If a question says “X is a substrate” and asks “what happens if you add an inducer?” the answer
is almost always “levels drop” unless it’s a trick with prodrugs.
Schizophrenia / Psychosis / Antipsychotics
Acute psychosis and agitation: what the PMHNP does first
If the patient can’t or won’t take PO, use IM antipsychotic options.
IM olanzapine and IM haloperidol, and when using IM haloperidol, give benztropine
or diphenhydramine for EPS coverage.
High-yield clinical reasoning: in acute agitation, you choose what works fastest and is feasible
(practicality), while reducing immediate harm (safety).
Ex. IM Haloperidol + Lorazepam
Typical vs atypical antipsychotics: what gets tested
, Typical (FGA) core adverse effect pattern
FGA adverse effects including:
EPS
Tardive dyskinesia
Hyperprolactinemia
Anticholinergic effects
NMS
QTc prolongation
Seizure threshold lowering
Cardiac dysrhythmias
Sedation
Interpretation: FGAs are “movement side effect heavy.” High potency FGAs are especially
associated with EPS.
Atypical (SGA) core adverse effect pattern
SGAs still can cause EPS/TD, but the big board-style risk is usually metabolic syndrome.
EPS: recognize the subtype, then choose the correct intervention
Acute dystonia
Onset: often early after starting or dose increase (Days to weeks)
Presentation: painful muscle spasm, neck/jaw/eyes (oculogyric crisis), tongue
First-line treatment: benztropine or diphenhydramine
Akathisia (Can occur within days)
Presentation: inner restlessness, pacing, “can’t sit still”
First-line treatment in the slides: propranolol (they also mention benzos as an option)
High-yield mistake: calling it “anxiety” and increasing the antipsychotic dose makes it
worse.
Frequent SE of Aripiprazole
Pseudo-parkinsonism (drug-induced parkinsonism)
