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Lithium
MOA: Exact mechanism is unknown, but it is thought to alter neuronal sodium transport and influence the reuptake of serotonin and/or norepinephrine. Inhibits phosphoinositol recycling in the neurons, which affects mood
suicide
What does lithium reduce the risk of?
Bipolar disorder, mania
Along with schizoaffective disorder, what are two of the indications for lithium?
hyperparathyroidism, hypermagnesemia, nephrogenic, thirst, hypothyroidism, tremor, narrow
Lithium ADRs
-Endocrine: ______________, hypercalcemia, ____________, sodium depletion, AVP/ADH resistance (________ diabetes insipidus), increased ______, and _______________
-Neurologic: _______ is common, headache, seizures, sedation
-GI: nausea, vomiting, diarrhea, weight gain
-Cardiac: edema, arrhythmias, and EKG changes
-Heme: leukocytosis
-_______ therapeutic index
EKG, thyroid, CBC, 1.5, >
Lithium Monitoring
-Prior to initiating therapy, a basic ____, chemistries, _______ function, beta-hCG, and ____ should be performed.
-Levels should be checked after 5 days, then every 2-3 days until therapeutic. Monitor every 4-8 weeks after. Therapeutic range is 0.8-1.2. Levels may be toxic if > ____. EKG performed on initiation if _ 50 years old
Ebstein, increase, thiazides, Verapamil
Lithium Drug Interactions and Contraindications
-Pregnancy → associated with _______ anomaly if taken during the first trimester
-Severe renal disease → may ________ lithium levels
-Blood level is increased by dehydration, _______, tetracyclines, NSAIDs, ACEIs, and loop diuretics
-Blood level decreased by bronchodilators, _________, theophylline, and carbonic anhydrase inhibitors
Lamotrigine
MOA: Blocks Na and Ca channels, decreases presynaptic glutamate release. Inhibits glutamate’s effect on the NMDA receptor, reducing neuronal activity
dizziness, nausea, SJS
Lamotrigine ADRs
-__________, ataxia, _______, tremor, headache, ____, diplopia, and drug interactions
Valproic Acid
MOA: Potentiates GABA-mediated CNS inhibition, inhibits glutamate and NMDA receptors, increases refractory period of voltage-gated sodium channels, modulates Ca channels
drowsiness, alopecia, gain, hepatic, pancreatitis, neural tube, headache
Valproic Acid ADRs
-Common: __________ (sedation), nausea, tremor, hair loss (_______), weight _____, hepatotoxicity, and inhibition of ______ drug metabolism
-GI: ____________, hepatotoxicity, nausea, vomiting, weight changes
-Teratogenic: Valproate has the highest risk of birth defects of any antiepileptic drug. _______ _____ defects (like spina bifida) are the most common abnormalities seen after using valproate.
-Neurologic: ___________, sedation, tremor, ataxia, tinnitus, nystagmus, increased suicidality
-Nephro: hyponatremia due to SIADH
Liver enzymes
What should be monitored while the pt is on valproate?
Carbamazepine
MOA: Stabilizes neuronal membranes and stops seizure propagation by blocking voltage-gated sodium channels
dizziness, nausea, hepatotoxicity, depression, SIADH, SJS, Asians, agranulocytosis, craniofacial, heart failure
Carbamazepine ADRs
-Common: __________, drowsiness, ataxia, ________, vomiting
-GI: nausea, vomiting, anorexia, _____________ (monitor LFTs)
-Neurological: dizziness, ataxia, diplopia, CNS ___________, cognitive dysfunction
-Hyponatremia (causes _______)
-____ (test for HLA-B*1502), which is a genetic susceptibility marker in _______ associated with an increased risk of developing SJS
-Blood dyscrasias: ____________, aplastic anemia, thrombocytopenia
-Teratogenic potential: _________ abnormalities (cleft lip/palate), spina bifida, CV malformation, hypospadias
-Cardiac: Can exacerbate ______ ________
lupus, CBC
Monitoring Carbamazepine
-Watch for signs of drug induced _____
-Monitor LFTs and ___