Pharm - Lithium Flashcards
contraindications associated w/ lithium use
- do NOT use w/ CCBs d/t increased risk of neurotoxicity and significant bradycardia
- withdraw or dc 2+ days before ECT and don’t resume until 2-3 days after last tx
given a pt starting lithium, select the appropriate lab tests and EKG for a given patient
- labs: UA, serum creatinine/BUN, TSH, calcium
- pregnancy test (b/c teratogenic)
- EKG for pts at high risk for CVD or pre-exsisting cardiac condition
expected clinical effect of lithium in acute mania
- up to 80% response in aborting acute manic/hypomanic episode
- 6-8 week delay in antidepressant effects
- prophylactic response in 2/3 of pts
- reduced suicide risk by 8-10 fold
- long term: effective in pts w/ prior episode, hx of euthymia or good function b/w episodes, and w/ family hx of bipolar w/ positive response to lithium
acute side effects of lithium
- dose related and worse at peak concentration times (1-2 hours postdose)
- nausea
- tremor
- polyuria
- weight gain
- loose stool
- cognitive impairment
interventions that can be used to reduce the side effects secondary to lithium
- lower dose
- take smaller doses w/ food
- use extended release products
- once daily dosing at bedtime
most common GI sx related to lithium
- N/V/D
- dyspepsia
measures that can be taken to reduce the GI sx severity
- take w/ food
- lower dose
- use XR dosage forms
- add antiacids or antidiarrheal agents
- for diarrhea switch from tab/cap to a liquid formulation
associated b/w lithium use and nephrogenic diabetes insipidus
- polydipsia w/ polyuria/nocturia in 20-40% of pts
- nocturia is important to monitor for the development of NDI
- first sx of loss of concentrating ability is nocturia
clinical presentation of lithium-induced nephrogenic diabetes insipidus
-low urine specific gravity
-low osmolality polyuria
(>3L/day)
-nocturia and polydipsia
explain the mechanism of lithium inducing nephrogenic diabetes insipidus
-lithium buildup in collecting tubules –> inhibits enzymes that control transport of water/sodium –> cell becomes less responsive to aldosterone/ADH
what is the role of amiloride in the treatment of lithium induced nephrogenic diabetes insipidus
- blocks sodium channels
- lithium can’t buildup in collecting tubules
- this partially restores urinary concentrating ability
- works best early in the disease
describe the clinical presentation of a lithium-induced tremor
- up to 50% of pts - can be a sx of lithium toxicity
- occurs when lithium is started, or dose titrated upwards
- symmetric, limited to hands/UE, releated to dose/serum concentration
- nonprogressive, increased by anxiety, caffeine, emotional/physical stress/fatigue
appropriate management strategies for lithium-induced tremor
- modify aggravating factors
- reduce lithium dose if possible
- obtain lithium levels to r/o toxicity
- change dosage form from long to short acting
- take smaller amount more often
- try different salt (carbonate to citrate)
- add beta blocker when bothersome
monitoring parameters for kidney function at baseline and follow up when starting lithium
- UA and BUN/Cr q 2-3 months for 1st 6 months
- then q 6-12 months
clinical presentation of thyroid disease in a pt using lithium
- lithium concentrates in the thyroid gland
- it interferes w/ TH synthesis
- induces formation of thyroid antibodies
- goiter seen in 40-50% of pts, hypothyroidism in up to 50% (can be asymptomatic)
