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PMHNP > NMS and EPS > Flashcards

NMS and EPS Flashcards

1
Q

EPS definition and association

A

constellation of disorders relating to movement

associated with exposure to dopamine antagonists

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2
Q

EPS acute manifestation

A

dystonia
akathisia
parkinsonism

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3
Q

EPS chronic manifestation

A

Tardive Dyskinesia

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4
Q

Acute EPS pathophysiology

A

Release of ACH is regulated by release of dopamine

Dopamine inhibits ACH

But when taking D2, the D2 receptors blocked and the ability to inhibit ACH blocked

So more ACH released which leads to the movement sx

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5
Q

Dystonia definition, onset, course, sx

A

Prolonged and unintentional contractions of voluntary and or involuntary muscles

Can occur within hours of 1st dose of antipsych drug

Occasionally chronic presentation

Causes repetitive and twisting movements

Often affects the head and neck

Visuals

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6
Q

Dystonia presentations and name

A

oculogyric crisis
trismus
torticollis
blepharospasm

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7
Q

Dystonia tx prophylaxis

A

anticholinergic (benztropine) in higher risk pt

also if admin 1st dose high potency IM

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8
Q

Dystonia tx acute/urgent

A

options:
Biperiden 5mg
benztropine 1-2mg
diphenhydramine 50mg IM or IV

also consider BZD in oculogyric crisis that doesnt respond to anticholinergic rx

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9
Q

Akathisia definition, onset, risk factor

A

subjective and objective psychomotor restlessness

Patients often unable to remain still: “mounting tension” or irresistible urge to move around

Typically occurs early in treatment with antipsychotics

Risk appears to be higher in antipsychotic-naïve patients started on a new drug

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10
Q

Akathisia tx

A

reduce dose or d/c

1st line tx propranolol 10mg and titrate to response

2nd line: 5HT2A antagonist (mirtazapine, cyproheptadine) and BZD

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11
Q

Akathisia prevention

A

avoid polypharmacy and rapid dose inc with antipsychotics

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12
Q

lower risk drug for akathisia

A

risperidone
olanzapein
ziprasidone
quetiapine

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13
Q

parkinsonism sx, patient profile

A

Drug-induced Parkinsonism is associated with bradykinesia, postural instability, tremor, and rigidity

More common in elderly and female patients

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14
Q

parkinsonism differentiation

A

Differentiating between idiopathic and drug-induced Parkinsonism:

Drug-induced presents as symmetrical akinetic rigidity

Follows the ingestion of an associated medication

Does not respond to anti-Parkinson’s drugs

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15
Q

Parkinsonism tx

A

reduce dose
switch to agent with lower risk
Benztropine (caution in elderly)
Amantadine (useful in elderly r/t anticholinergic)

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16
Q

Tardive Dyskinesia onset, sx, presentation, risk factor, prognosis

A

Onset: months to years and slow

Presents as involuntary movements of lower face, limbs, trunk
Ex: lip smacking/puckering, tongue movements, excessive blinking

May also present with sx similar to EPS, tremor, myoclonus, tourettism

Risk factor: early presence of EPS

Prognosis: may be irreversible

17
Q

Tardive Dyskinesia pathophysiology

A

chronic blockade of D2 receptors leads them to up regulate

upregulation takes time hence why slow onset

now patient is hypersensitive to dopamine which causes involuntary movements

18
Q

Tardive Dyskinesia tx

A

reduce or switch: Little benefit

VMAT2 inhibitor: Valbenazine, deutetrabenazine

modest evidence for clonazepam

Gingko biloba extract

19
Q

AIMS scale

A

Applies to any EPS acute or chronic

Diagnosing EPS

Includes dental status cuz it looks like EPS

Important if they are going to be on antipsychotic therapy

20
Q

antipsychotic AE profile chart

A
21
Q

Neuroleptic Malignant Syndrome and sx

A

Acute side effect of neuroleptic medications

Characterized by:
fever
muscular rigidity
altered level of consciousness
autonomic instability

22
Q

DSM criteria for NMS

A

hyperthermia >38 on 2 separate occasions

CPK >4x ULN

mental status change: delirium, ALOC

Autonomic activation:
tachy >25% inc
diaphoresis
BP inc >25%
BP fluctuation >20 dia or >25 syst
incontinence
pallor
tachypnea >50% inc

23
Q

NMS DDX and key difference

A
24
Q

NMS etiology

A

not well understood

Thinking is that a dopamine antagonist can lead to a hypothalamic dopamine blockade

this Can cause hyperthermia and autonomic dysfunction

That leads to cascade of other sx
1. Vasomotor sx
2. Issues with sympathetic nervous system
3. ALOC

Not many build on to each other
1. Hyperthermia leads to inc sweating which leads to dehydration which can lead to kidney complications

Supported by inc rate of NMS in those initiating antipsychotics

25
Q

NMS risk factors modifiable

A
  • High Temperature
  • Low Iron
  • Dehydration
  • Restraint
  • Medication with D2 antagonistic activity
    (IV or IM administration associated with greater risk)
26
Q

NMS risk factors not modifiable

A
  • Advanced Age
  • Personal or Family History of Catatonia
  • Concurrent Medical Conditions
27
Q

NMS risk factor drugs: antipsychotics

A

Antipsychotic Drugs

Atypical:
* Clozapine, olanzapine, risperidone, quetiapine, aripiprazole, paliperidone, asenapine, ziprasidone

Typical:
* Haloperidol, fluphenazine, thioridazine, chlorpromazine, prochlorperazine, loxapine, periciazine, trifluoperazine, flupentixol, zuclopentixol, methotrimeprazine

SGAs are more associated with EPS and NMS but SGAs implicated too

Clozapine: may present differently (less
rigidity/tremors)

28
Q

NMS risk factor drugs: others

A

Other Drugs

Mood Stabilizers
* Lithium, carbamazepine

Antidepressants
* Paroxetine, sertraline, amitriptyline

Antiemetics
* Metoclopramide

Evidence for the role of these drugs in NMS is limited

29
Q

management of NMS: first

A

1st: D/c suspected agent
dont wait for lab results

30
Q

NMS staging based treatment

A

Basically it is 1-5

1 looks like typical EPS and you may be able to get away with switching the agent

3 looks like proper NMS and will need to d/c the agent

31
Q

NMS mgmt supportive care

A

note there is an aspiration risk

note that an antipyretic may not work

32
Q

NMS mgmt pharmacotherapy: supportive

A

Agitation
* Benzodiazepines can be used to control agitation

Blood Pressure Control
* NMS is associated with severe and labile HTN
* Beta blockers such as labetalol and DHP calcium channel blockers such as amlodipine have been used

VTE
* Use heparin as necessary for VTE prophylaxis

33
Q

NMS mgmt pharmacotherapy: treatment

A

Three main agents:
1. Dantrolene
2. Bromocriptine
3. Amantadine

limited data

34
Q

Dantrolene

A

Mechanism: peripheral skeletal muscle relaxant
* Directly decreases rigidity and hyperthermia

  • Most useful in cases with severe hyperthermia and rigidity

Dosing
* 1-2.5mg/kg IV initially, followed by 1mg/kg every six hours

Adverse effects
* Anaphylaxis, hepatotoxicity, flushing, heart failure, tachycardia

35
Q

Bromocriptine

A

Mechanism: Dopamine agonist
* Displaces dopamine antagonist drugs from D2 receptors

Dosing
* 2.5mg every 8-12 hours via NG tube

Adverse effects
* Hypotension, GI ulcer, psychosis

36
Q

Amantadine

A

Mechanism: Dopamine agonist
* Displaces dopamine antagonist drugs from D2 receptors

Dosing
* 200-400mg daily in 2-3 divided doses

Adverse effects
* Orthostatic hypotension, agitation, UTI, nausea

37
Q

Reinitiating antipsychotics after NMS

A

note future risk of NMS episodes
–30% possibly

wait 2 wks before resuming rx

start low with rx that is low potency and titrate slowlyt

38
Q

thermoregulation in schizophrenia

A

Dysregulation is common

Different baseline

Abn daily range

Impaired compensation to heat but more effective compensation to cold

May be cuz of dx or rx but don’t know

Good to counsel patients
1. May have poor access to air conditioning

PMHNP (26 decks)

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