Mehl. extrapyramidal side effects + neuroleptic Flashcards
Extrapyramidal side-effects = The name for the movement disorders associated with anti-psychotic use.
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“Rule of 4s”?
After a patient is started on an antipsychotic, a general trend is seen in terms of the onset of particular symptoms.
The time frame is not strict/rigid; use it as a general trend – i.e., acute dystonia wouldn’t just start at 4 months; tardive dyskinesia wouldn’t occur as early as 2 weeks.
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Acute dystonia at 4 hours. CP?
torticollis, oculogyric crisis, muscle rigidity without fever.
torticollis, oculogyric crisis, muscle rigidity without fever. when?
Acute dystonia at 4 hours.
Torticollis = ?
stiff / crooked neck.
stiff / crooked neck.?
Torticollis
Oculogyric crisis=?
= weird eye movements (don’t confuse with tongue movements of tardive dyskinesia).
= weird eye movements (don’t confuse with tongue movements of tardive dyskinesia).?
- Oculogyric crisis
Muscle rigidity without…?
Muscle rigidity without fever = acute dystonia.
…………..= acute dystonia.
Muscle rigidity without fever = acute dystonia.
Muscle rigidity with fever = …?
neuroleptic malignant syndrome.
………….. = neuroleptic malignant syndrome.
Muscle rigidity with fever
Treat acute dystonia with (muscarinic receptor antagonists, which decrease muscle tone) ….?
Treat acute dystonia with benztropine or trihexyphenidyl
(muscarinic receptor antagonists, which decrease muscle tone)
Treat acute dystonia with <..> OR 1st generation H1 blocker???2
1st generation H1 blocker (diphenhydramine or chlorpheniramine).
1st generation H1 blocker (diphenhydramine or chlorpheniramine). The latter have nasty anti-cholinergic (anti-muscarinic) side-effects that are actually what we want when we’re treating acute dystonia. Maybe 2/3 of acute dystonia Tx Qs will have benztropine as the answer; ~1/3 will have one of the 1st gen H1 blockers as correct.
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Akathisia at 4 days ->?
restlessness.
Akathisia at 4 days -> restlessness. Tx?
Treat with propranolol (beta-blockade).
Treat with propranolol (beta-blockade).??
Akathisia at 4 days -> restlessness.
Parkinsonism at 4 weeks ->?
akinesia / bradykinesia.
Parkinsonism at 4 weeks -> akinesia / bradykinesia. Tx?
Treat with amantadine.
Tardive dyskinesia at 4 months ->?
abnormal facial movements (notably tongue).
abnormal facial movements (notably tongue).?
Tardive dyskinesia at 4 month
Risk is greater with typicals compared to atypicals, what CP to occur??
Tardive dyskinesia at 4 month
Risk is greater with typicals compared to atypicals, but TD can be seen in the latter on NBME.
Tardive Tx?
stop the typical and give an atypical.
Couple of weird Psych NBME Qs on TD:
- Patient on atypical + gets TD; Tx?
stop the atypical and give another atypical. (Just stop the drug and switch to yet another atypical.)
Couple of weird Psych NBME Qs on TD:
Patient on typical for 15 years and has no problems whatsoever (i.e., does not have TD); patient asks the psychiatrist what can be done to decrease his risk of developing TD?
The correct answer is “stop the typical and give an atypical”; wrong answer is “maintain current drug regimen.”
Apparently even if the patient has been on a typical long term without an issue, switching to an atypical still confers a reduction of risk of TD.
What can do metoclopramide?
Metoclopramide (D2 antagonist used as anti-emetic / pro-kinetic) can also cause EPS side-effects and prolong QT interval, same as the anti-psychotics.
There is 2CK Psych Q where they give Parkinsonism in patient on metoclopramide, and the next best step is “discontinue metoclopramide.”
Neuroleptic malignant syndrome (NMS). definition?
Muscle rigidity and fever following commencement of anti-psychotic.
Muscle rigidity and fever following commencement of anti-psychotic.?
Neuroleptic malignant syndrome (NMS)
NMS. The fever will usually be 103+ F, as per my observation on NBME exams.
This is because mere anti- cholinergic side-effects can sometimes give low-grade fever (i.e., hot, red, dry patient).
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Mechanism for NMS?
the ryanodine channel, which allows calcium to move from the sarcoplasmic reticulum into the cytosol, gets stuck open, so incr. calcium moves into the cytoplasm. The cell then needs to use a lot of ATP to pump the calcium back into the sarcoplasmic reticulum. This generates heat -> fever.
This mechanism for NSM secondary to anti-psychotic administration is the same as ……
Same as malignant hyperthermia (MH) due to succinylcholine (nicotinic neuromuscular blocking agent used during surgery).
Neuroleptic malignant syndrome (NMS), Tx?
Tx is dantrolene, which closes the ryanodine channe
NBME will sometimes give vignette of NMS or MH, and then the answer for Tx is “decreases sarcoplasmic calcium release.”
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In theory, bromocriptine (D2 agonist) can be used in the setting of NMS only as an alternative to dantrolene, but I haven’t seen NBME assess this. This is more a pedantic Q students will ask sometimes.
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