ms pharm

Question 1

osteoporosis pharm

Answer 1

bisphosphonates
selective estrogen receptor modulators
hormone therapy: calcitonin - not as effective long term as above classes (used short term though), HRT no longer used d/t r/o blood clots, breast cancer, other cancers)

Question 2

aldendronate

Answer 2

Biphosphates
moa: Bind permanently to surfaces of bones to inhibit osteoclast activity (decrease bone breakdown)
i: Osteoporosis – prevent and treat

Question 3

aldendronate: SE

Answer 3

GI common – n/v/d, esophageal ulcerations – stay upright for 30 min after taking

Question 4

aldendronate: nc

Answer 4

Reduce fractures by 50%
Don’t take with Ca for 2 hrs bc low bioavail
Take with water
Typically 1/wk

Question 5

raloxifene

Answer 5

Selective estrogen receptor modulators (SERMs)
moa: Mimic estrogen by increasing bone density, inhibit bone resorption, increase bone density but not as well as bisphosphonates
i: Post-menopausal osteoporosis – prevent and treat

Question 6

raloxifene: SE

Answer 6

Hot flashes, leg cramping
BB!: stroke

Question 7

raloxifene: nc

Answer 7

Safer than estrogen (HRT)
Reduce risk of spinal fractures by 50%
Must take adequate Ca and vit D replacement to work
d/c at least 72 hr before planned procedures – any prolonged immobile periods, high risk of clot
don’t smoke or drink
don’t use if preg

Question 8

Calcitonin-salmon

Answer 8

moa: Inhibit bone removal by osteoclasts
Slow down bone loss and increase spinal bone density
I: Osteoporosis treatment – not long term
Acute analgesic effect with acute vertebral fractures
Reduce pain in hip fractures

Question 9

Calcitonin-salmon: SE and NC

Answer 9

SE: Intranasal – can cause irritation
nc: Reduce spinal fractures by 30% - must take for at least 5 years to see long term benefit
Expensive, not 1st line

Question 10

prednison

Answer 10

corticosteroid for RA
rapid suppression of inflam
use only when s not controlled with NSAIDs
not best choice long term - usually small doses <10mg/day
usually used in conjunction with DMARDs + NSAIDs

Question 11

biologic agents

Answer 11

newer gen of DMARDs
biologic response modifiers
target parts of immune S that trigger inflam that cause joint and tissue damage
usually given in combo with methotrexate
can increase r/o severe skin or lung infections, skin cancers, serious allergic reactions
v expensive -> creation of biosimilars
work well

Question 12

Methotrexate

Answer 12

DMARD
Antineoplastic, anti-rheumatic
moa: Immunosuppressive
I: 1st line for RA
Cancer therapy – smaller doses

Question 13

Methotrexate: SE

Answer 13

Lots – GI (nva), bone marrow suppression – chemo drug so monitor wbc and rbc, shortened life expectancy
Interfere with metabolism of folate
Toxic to liver (metabolized) – monitor ALT, AST, alk phos
11 BB!:

Question 14

Methotrexate: nc

Answer 14

PO or SQ/IV
Need folate replacement
Only admin 1/week – deadly if daily
NO OH (liver)
Teratogenic – never for preg, 2 forms of BC
Higher r/o infection – contact hcp if s/s (Pneumocystis carinii)
Caution with liver and KD
Aplastic anemia risk when using NSAIDs - CBC

Question 15

Hydroxychloroquine

Answer 15

DMARD
Antimalarial
Anti-rheumatic
moa: Unknown, anti inflam processes – dampen macrophage, t helper cell and inflam cytokine activity
Slow progression of RA hwne used in combo with other DMARDs
I: Used alone or in combo with methotrexate for early/mild RA
SE: Much better tolerated than methotrexate
Retinopathy – rare but report blurry vision or other s/s

Question 16

NSAIDS

Answer 16

review

Question 17

glucocorticoids

Answer 17

review s/s

Question 18

Allopurinol

Answer 18

Moa: Inhibit xanthine oxidase enzyme, which prevents uric acid production
I: gout r/t excess uric acid production, prevention! Prophylactic!

Question 19

Allopurinol: SE

Answer 19

Agranulocytosis - monitor wbc and cbc
Aplastic anemia
Known to cause fatal skin rxns (SJS/TENS)

Question 20

Allopurinol: NC

Answer 20

s/s infection
monitor effectiveness with serum uric acid levels
interact with warfarin (monitor INR) and anti DM (metformin, SLG2 I, GLP1 agonist) – increase effects, monitor for hypogly
see effects after 2-6 wk, continue taking to prevent future flares

Question 21

Colchicine

Answer 21

Moa: Reduce inflam response to deposits or urate crystals in joint; cell mitosis
I: 2nd line gout, flares and prophylaxis
Can be short term

Question 22

Colchicine: SE

Answer 22

Powerful inhibitor of mitosis and can cause short term leukopenia – bone marrow suppression
GI and urinary bleed
CI: any person with severe renal, GI, hepatic, or cardiac disorders or bleeding disorders

Question 23

Colchicine: NC

Answer 23

Stomach flu type s = early s of drug tox, stop taking immediately, v concerned if perfuse v, can cause multiple organ failure and death
PO only

Question 24

Probenecid

Answer 24

Uricosuric agent
Moa: inhibit reabs of uric acid in kidney, promoting excretion
I: Hyperuricemia with gout
Alone or combo with allopurinol when not effective alone

Question 25

Probenecid: SE and NC

Answer 25

SE: GI upset, dizzy or HA, kidney/liver damage, lots of drug interactions
NC: Take with food and drink and plenty of fluids
Report s of kidney problems – hematuria, change in amount of urine, weight gain
Report s of liver issues