Special Considerations Flashcards
(35 cards)
When is the peak plasma conc of sidenafil?
What is it metabolized by?
Peak plasma conc at 1 hr so pts instructed to take 1 hr before intercourse
HL 4 hr (effective duration)
Metabolized by CYP3A4
Sildenafil
Viagra
Large ↓ in BP, syncope, lower cardiac perfusion and MI if used with nitrates
Calcium
Combine with vit D supp when osteoporosis meds are taken
Calcium Gluconate (IV)
Safer SC infiltration than CaCl
Calcium Chloride (IV)
Necrosis can occur if spills from blood to tissues so cannot use SC or IM
Calcitriol
1,25 -OH D3
May cause more hypercalcemia than either paricalcitol or doxercalciferol
What happens if PTH is active 3-5 hr/day
osteoblast activity ↑ more than osteoclast
What happens if PTH is active 24 hr/day
osteoclast activity ↑ more than osteoblast → bone loss and ↑ serum Ca2+
Teriparatide
hPTH 1-34
In rodents, LT use causes osteosclerosis and osteosarcomas
Raloxifen
↓ risk of breast ca and endometrial ca but not stroke or embolism
Biphosphonates
Poor intestinal absorption so must take in the AM after overnight fast with nothing but water for the first 30-60 mins after taking
Can cause esophageal erosion so take w/ 8 oz water and do not lay down for 1 hr
Drug holidays after 5 yrs due to atypical femur fx (even tho rare)
Ibandronate
oral or IV
Lack of hip fx reduction data so not considered first line like other biphosphonates
Denosumab
Similar to biphosphonates but more expensive
Inj subcutaneously q6mo (osteoporosis), or q1mo (malignancy)
Salmon Calcitonin
Longer HL than human’s
Cortisol/Glucocorticoids
Diabetogenic when combined with calcineurin inhibitors (must monitor glucose levels closely)
Azathioprine
Avoid combining with ACE
inhibitors – drug interaction → potentiated myelosuppression
ACE inhibitors suppress
erythropoietin
PMT metabolizes 6-MP
FDA
recommends genotyping patient’s for inactive allele of TPMT (bc will accumulate 6-MP)
Patients with inactive allele → ↓ dosage of azathioprine
Mycophenolate Mofetil
Selectively targets lymphocyte population (B- and T-cells) due to:
Lymphocyte population
dependent on de novo purine synthesis pathway (containing IMPDH) for synthesis of guanine nucleotides.
Other cell types can alternatively use purine salvage pathway for synthesis of guanine nucleotides
Mycophenolate preferentially inhibits type II isoform of IMPDH, which is primarily expressed in lymphocytes
This selectivity is thought to make MM less toxic overall compared to azathioprine, methotrexate & glucocorticoids
Calcineurin Inhibitor
Diabetogenic when combined with glucocorticosteriods
Combined with glucocorticosteriods to lower effective/therapeutic dose of cyclosporine
Must closely monitor blood levels
Sirolimus
Thought to be associated with less renal toxicity compared to calcineurin inhibitors
Adalimumab
Humira
Often combined with other traditional DMARD’s (e.g. methotrexate, azathioprine, cyclosporine)
Concurrent therapy with methotrexate to prevent antibody formation against adalimumab
Etanercept
Enbrel
Less immunogenic than other TNF-alpha blocking agents
Often combined with other traditional DMARD’s (e.g. methotrexate, azathioprine, cyclosporine)
Infliximab
Remicade
Often combined with other traditional DMARD’s (e.g. methotrexate, azathioprine, cyclosporine)
Concurrent therapy with methotrexate to prevent antibody formation against infliximab
Rituximab
Often given in conjunction with methotrexate to prevent Ab formation against Rituximab
Tocilizumab
Suppression of IL-6 receptor can lead to induction of CYP2C9, 2C19, 2D6 and 3A4
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Plasma levels of drugs metabolized by these enzymes are typically decreased by tocilizumab
