Glasgow Pharm Flashcards
PGE2/PGI2 Renal
Increase renal blood flow
Decrease ADH induced water reabsorption
Decrease Chloride Reabsorption in Loop of Henle
Increase Renin Release
Adrenocorticosteroids that do not activate MR receptor
Triamcinolone
Betamethasone
Dexamethasone
Due to substitution on D ring.
Enzyme that takes Cortisol to Cortisone
11-Beta-Hydroxysteroid dehydrogenase 2
Synthetic Aldosterone like drug
Fludrocortisone
MR Receptor Antagonists
Spironolactone
eplerenone
Used for aldosterone excess, or cortisol excess.
S/E: hyperkalemia, metabolic acidosis, gynecomastia (esp Spiron), impotence (esp Spiron), and GI.
Spironolactone is a bit of an androgen receptor antagonist.
Fully activated form of Vitamin D
Calcitriol (1, 25-dihydroxy-cholecalciferol)
DHT—dihydrotachysterol
Vitamin D Synthetic derivative
no 1-OH needed for activation; does need liver 25-OH
1-alpha-hydroxycholecalciferol
Doxercalciferol (1-hydroxyvitamin D2)
already has 1-OH group
Does need liver 25-OH
Paricalcitol
Calcitriol Analog
reduces PTH without hypercalcemia
used in chronic renal failure
Analogs used when trying to shut down PTH after get calcium levels where they need to be.
22-oxacalcitriol
Calcitriol Analog
Suppressor of PTH gene expression, limited action on intestine and bone. Used in chronic renal failure, primary hyperparathyroidism. Low affinity for serum binding protein leads to shorter half life than calcitriol.
Sevelamer
Phosphate binding polymer
Cinacalcet
“calcimimetic.” Inhibits PTH secretion by enhancing the sensitivity of the CaSR (calcium receptor in the parathyroid gland). Lowers the concentration of Ca at which PTH secretion is suppressed.
Approved for treatment of secondary hyperparathyroidism due to chronic renal failure.
colchicine
Gout Drug used in Acute Attack when NSAIDs don’t work
interferes with mitotic spindle function
inhibits migration and phagocytic actions of granulocytes
inhibits neutrophil elaboration of inflammatory glycoprotein
NSAIDs used in Acute Gout Attack
naproxen, indomethacin, sulindac
These are your stronger NSAIDs
allopurinol
Used in chronic gout
parent drug and metabolite alloxanthine inhibit
xanthine oxidase, decrease uric acid synthesis
drug interaction: inhibits metabolism of azathioprine, 6-mercaptopurine
can be used with impaired renal function
Since it is a purine, it can interferer with metabolism of other purines like azothiaprine and 6-mercaptopurine which are cancer chemotherapy drugs; therefore back off dose x4
febuxostat
Used in Chronic Gout
nonpurine xanthine oxidase inhibitor
liver function abnormalities, diarrhea, nausea
Does have potential interaction
probenecid
Used in Chronic Gout
uricosuric agent, inhibits uric acid renal tubular reabsorption
developed to inhibit renal tubular secretion of penicillin
multiple drug interactions by blocking renal secretion
Need a functional kidney. Will not work in patients with kidney failure. Effects secretion of many organic ions, thus block elimination of other drugs, too.
rasburicase
Used in Chronic Gout
recombinant urate oxidase that oxidizes uric acid intomsoluble and inactive metabolite allantoin
used to manage plasma uric acid levels in pediatric patients receiving chemotherapy (for leukemia, lymphoma, etc.)
therapeutic efficacy may be limited by production of antibodies against drug
Oxidizes UA. Makes it more soluble
pegloticase
recombinant mammalian uricase coavalently attached to
methoxy plolethylene glycol (mPEG) to prolong
circulating half-life and diminish immunogenic response
treatment of refractory chronic gout
Same as rasburicase, but has pegalated group in order to extend half life
glucocorticoids
prednisone main player in immunosuppresive use of glucocorticoids. Stop cytokine production.
cyclosporine/tacrolimus
inhibits calcineurin phosphatase activity
decrease dephosphorylation of NFAT; therefore decreasing production of IL-2, 4, 6, etc
T-cell selective
renal toxicity due to accumulation in kidney. Tacrolimus not as much.
hyperglycemia with tacrolimus
sirolimus
same family as tacrolimus/cyclosporine
blocks T cell response to cytokines
inhibits a kinase involved in cell-cycle progression
hyperlipidemia as adverse effect
Binds to binding proteins, act on receptor (IL-2) and interfere with IL-2 signal transduction