Well then smarty-britches, what are you going to see with severe (I always want to say EXTREME!!) lithium toxicity (>2.5 mEq/L)?
Impaired consciousness (coma)
impaired renal function
What are the side effects of antipsychotic (neuroleptic) drugs?
(This is a booger of a card, so just read it for information)
laryngeal dyskinesia (laryngospasm → sudden respiratory distress)
opisthonosis and oculogyric crises may occur (we'll discuss this momentarily)
acute dystonia (responds to diphenhydramine)
hypotension (a-adrenergic blockade, direct vasodilation, and direct cardiac depression)
neuroleptic malignant syndrome (NMS)
↑ prolactin levels (Gynecomastia, galactorrhea)
obstructive jaundice (an allergic reaction 2-4 wks p administration)
hypothermia (with chlorpromazine)
↓ seizure threshold
skeletal muscle relaxation
So, what is this opisthonosis junk? (For KNOWLEDGE!!!)
Opisthotonos [ō′pisthot′ənəs]: a prolonged severe spasm of the muscles causing the back to arch acutely, the head to bend back on the neck, the heels to bend back on the legs, and the arms and hands to flex rigidly at the joints. It is related to meningitis.
Alright, then what is that oculogyric crisis business? (For MORE KNOWLEDGE!!!)
Oculogyric crisis [ok′yəlōjī′rik]: a paroxysm in which the eyes are held in a fixed position, usually up and sideways, for minutes or several hours, often occurring in postencephalitic patients with signs of parkinsonism. In some cases, the eyes are held down or sideways, and there may be spasm or closing of the lids. Oculogyric crises may be precipitated by emotional stress and neuroleptic overdose, and patients with the disorder frequently show psychiatric symptoms.
What is this Neuroleptic Malignant Syndrome all the hip kids are talking about nowadays?
hypertonicity of skeletal muscles
ANS instability (alterations in systemic BP, tachycardia, cardiac dysrhythmias)
fluctuating levels of consciousness
Likely R/T dehydration and intercurrent illness in pts treated with antipsychotic drugs.
Hmm... So what is the treatment for NMS?
Treatment is empirical and supportive: Dantrolene (direct-acting muscle relaxant) and bromocriptine or amantadine (dopamine agonists)
Malignant hyperthermia and central anticholinergic syndrome may mimic NMS (NDNMBDs produce flaccid paralysis in NMS pts but NOT in MH pts!)
(S&H p. 424-425)
WHAT IS THE MECHANISM OF ACTION OF DROPERIDOL AND HALOPERIDOL?
MOA thought to be due to the blockade of DA receptors (DA2) in the basal ganglia and limbic portions of the forebrain (blockade of DA receptors in the chemoreceptor trigger zone of the medulla is responsible for the antiemetic effects)
To which class of drugs does DROPERIDOL belong?
Why, butyrophenones (antipsychotics/neuroleptics), of course!
WHAT ARE CLINICAL USES OF DROPERIDOL?
FDA labeled: acute or prophylactic treatment of N/V with surg/diag procedures
Non-FDA labeled: Agitation-psychotic disorder, chemo-induced N/V, benign HA, migraine
WHAT DISEASE IS DROPERIDOL CONTRAINDICATED? WHY? (These all-caps questions were just copied and pasted here. Ask Shores about his syntax and desire to yell at the students...)
Prolongation of QT interval (this is the best answer I could find within the book)
Also: “Of note, since droperidol was approved in 1970, not a single case report has surfaced in which droperidol in doses used for the management of port-operative N/V has been associated with QTc prolongation, cardiac dysrhythmias, or cardiac arrest.” (S&H)
I like this quote because I love this drug. And now you know.
Define epilepsy, please. Thank you.
Recurring disturbance in the normal pattern of neuronal activity.
Must occur more than once to be considered epilepsy, as opposed to a single episodic seizure (e.g., febrile)
FYI: not a mental illness, not a sign of low intelligence, and not contagious.
WHAT ARE THE DRUG INTERACTIONS OF COMMON ANTIEPILEPTIC DRUGS?
(ventilatory depressant, miotic, sedative, and analgesic effects likely exaggerated)
How does levodopa work?
Crosses BBB and converted to DA by aromatic-L-amino-acid decarboxylase; this acts to replenish DA stores in the basal ganglia
What are these Peripheral Decarboxylase Inhibitors?
Carbadopa or benserazide
Administered with levodopa to increase the CNS action of levodopa; think of it as a “fall guy” that takes the metabolic hit while allowing levodopa to escape across the BBB to act on the CNS.
MOA of Selegiline?
MAO-B inhibitor; ↓ catabolism of endogenous DA