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Pharmacology > Exam #4- MSK > Flashcards

Exam #4- MSK Flashcards

1
Q

difference between aspirin (salicylates) and other agents

A

cox-1 and 2 inhibition

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2
Q

NSAIDs MOA

A

all except Cox-2 selective agents and nonacetylated salicylates inhibit platelet aggregation

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3
Q

cox 2 selective inhibitors (coxibs) MOA

A

inhibit prostaglandin synthesis at sites on inflammation w/o affecting cox-1 (in GI, kidneys, platelets)

cox-2 inhibitors lead to renal toxicities like other traditional NSAIDS

higher rate of thrombotic events r/t cox-2 inhibitors

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4
Q

NSAID effects

A

decreased sensitivity of vessels to bradykinin and histamine

affect t lymphocytes

reverse vasodilation of inflammation

newer NSAIDs= analgesic, anti-inflammatory, and anti-pyretic

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5
Q

indications for use of NSAIDs

A

mild to moderate pain r/t soft tissue athletic injury, dental pain, minor surgery, OA, RA, dysmenorrhea

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6
Q

various MS etiologies for NSAIDs

A

OA as well as localized MS issues

sprains, strains, low back pain, gout

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7
Q

NSAIDs for rheumatic dx

A

not all NSAIDs are FDA approved

most likely effective in RA

psoriatic arthritis

arthritis r/t IBD

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8
Q

aspirin indications

A

acute or LT symptomatic tx of mild-moderate pain, RA, OA

decreased risk of recurrent TIA/CVA in pts who have had TIAs d/t fibrin platelet emboli

decreased risk of death/nonfatal MI w/previous infarction/unstable angina

decreases risk for colorectal cancer

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9
Q

anti-inflammatory effects of aspirin

A

decreases inflammation by inhibiting production of prostaglandins, prostacyclin, and thomboxanes in CNS and peripheral tissues. decreases sensitivity of vessels to bradykinin and histamine, affects t-lymphocytes, and reverses vasodilation of inflammation.

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10
Q

analgesic effect of aspirin

A

pain is relieved when inflammation is decreased and prostaglandins are decreases. salicylates can decrease pain at subcortical sites.

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11
Q

antipyretic effect of aspirin

A

blocks effect of interleukin-1 on hypothalamus (controls temp). also decreases fever by causing vasodilation of peripheral superficial blood vessels.

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12
Q

anti-platelet effects of aspirin

A

comes from blocking COX-1 enzyme and producing thomboxane

aspirin causes IRREVERSIBLE inactivation of cox-1 which decreases production of thomboxane for the life of the patient!!!

why you stop taking ASA week before surgery

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13
Q

other NSAID’s anti-platelet effects

A

have a REVERSIBLE inactivation of cyclooxygenase which ONLY LASTS for the DURATION of the DRUG ACTIVITY

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14
Q

NSAID ADE

A

CNS (HA, tinnitus, dizziness)

CV (fluid retention, HTN, edema, MI, CHF)

GI (abdominal pain, dysplasia, N/V, ulcers, bleeding)

Heme (thrombotcytopenia, neutropenia, aplastic anemia)

hepatic (increased LFTs, liver failure)

pulmonary (asthma)

skin (rashes, pruritus)

renal (renal insufficiency, renal failure, hyperkalemia, proteinuria)

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15
Q

MSK pain

A

start w/ non-drug treatment

RICE

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16
Q

treatment for MSK pain

A

1st-acetaminophen

2nd- NSAIDs

goal of treatment is to limit inflammatory process, protect joint, and relieve pain

non-drug methods are important in ALL uses of NSAIDs- if pt has moderate pain, consider starting NSAIDs at same time as non-drug treatment

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17
Q

drug choices for treatment of MSK pain

A

aspirin: effective and cheap. up to 12 tabs a day needed so compliance be be a problem. salicylcate usually cheaper than NSAIDs.
pharmacokinetics: consider duration of action (frequency of dosing), protein binding (drug interactions), and renal excretion (renal function)

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18
Q

pt variables to consider for MSK pain treatment

A

medical conditions/comorbidities- especially renal and liver function, CV dx

age- geriatrics more likely to have ADE. avoid in kids d/t reye’s syndrome

ability to comply w/dosing schedules, reliability of pt to report ADE

cost: generic vs. brand name

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19
Q

pathophysiology of osteoarthritis

A

degeneration of articular cartilage

body tries to repair-compensates- hypertrophy at articular margins

forms spurs and thickened synovial membrane

constant low levels of inflammation

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20
Q

non-drug treatment of osteoarthritis

A

exercise with rest periods and weight loss

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21
Q

drug treatment for osteoarthritis

A

TYLENOL

NSAIDs, cox-2 inhibitors, intraarticular injection of steroids

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22
Q

pathophysiology of gout

A

inflammatory response to precipitation of urate crystals in tissues

distal joints usually affected

crystal can occur in any tissue

present as TOPHACEOUSGOUT or urate nephropathy if crystallization is in RENAL MEDULLA

tophi= urate crystals in joint

acute gouty arthritis superimposed on tophaceous gout

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23
Q

goal of treatment for gout

A

decreased s/s of acute attack, decreased risk of recurrent attacks, decreased urate levels

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24
Q

drugs for gout

A

inflammation and pain- NSAIDs, colchicine, glucocorticoids

prevent inflammatory response to crystals- colchicine NSAIDs

inhibit urate formation- allopurinol, febuxostat or increased urate excretion (probenecid)

acute management- NSAIDs, corticosteroids, colchicine

**tx of hyperuricemia AFTER acute attack is over (or you’ll make it worse)

preventative therapy: 1st line= colchicine

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25
Q

colchicine MOA

A

decreases deposition of uric acid and inflammatory response

no effect on uric acid metabolism

not an analgesic- need to use NSAIDs as well

can be used for acute attacks, but doses needed leads to diarrhea

lower doses used to prevent attacks w/hx of attacks

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26
Q

ADE of colchicine

A

N/V/D, abdominal pain

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27
Q

drug interactions of colchicine

A

enhanced effects of CNS depressants and sympathomimetic agents, can interfere w/ vitamin B12 absorption

increased colchicine toxicity w/use of clarithromycin, erythromycin, and grapefruit juice

cyclosporine levels are increased

28
Q

monitoring for colchicine

A

1st time users- monitor weekly for s/s of toxicity

vitamin B12, LFTs

29
Q

MOA of xanthine oxidase inhibitors

A

decreases uric acid production by inhibiting xanthine oxidase

30
Q

allopurinol and febuxostat

A

newer xanthine oxidase inhibitors

both decrease the concentration of less soluble uric acid which decreases uric acid crystals in joints and tissues

used for chronic gout

HOLD these drugs 1-2 weeks after acute attack

31
Q

allopurinol MOA

A

prevents uric acid synthesis by xanthine

decreased uric acid production

does not promote uric acid secretion

32
Q

acute attacks are more common during EARLY therapy, so what should you gie?

A

allopurinol WITH colchicine to prevent acute attack

33
Q

CI of allopurinol

A

prior severe reaction

34
Q

warnings/ADE of allopurinol

A

colchicine given concurrently 1st 3-6 months to decrease risk of attack

can cause hepatotoxicity, hypersensitivity (SJS), dose reduce in impaired renal function, monitor renal function, bone marrow suppression, risk of skin rash increases w/ pts getting amoxicillin or ampicillin

35
Q

drug interactions with allopurinol

A

oral anti-coags (coumadin)

hypoglycemics

theophylline

uricosurics decrease the effect of allopurinol

monitor renal function w/ thiazides

36
Q

monitoring for allopurinol

A

baseline CBC, platelets, serum uric acid levels, renal function

37
Q

MOA of febuxostat

A

inhibits xanthine oxidase

38
Q

ADE of febuxostat

A

LFT abnormalities, nausea, joint pain, rash

monitor LFTs

increase in gout attacks w/start of therapy

prophylactic tx w/NSAID or colchicine needed

higher rate of MI and stroke- monitor for CV events

39
Q

MOA of uricosuric drugs

A

inhibit SECRETION of many weak acids (penicillin, methotrexate) and also inhiits reabsorption of uric acid

used for chronic gout- not acute

can precipitate acute gout attack in early phase of use so give w/colchicine or indomethicin

uricosurics are SULFONAMIDES- so watch for allergies

40
Q

probenecid

A

uricosuric agent (tubular blocking agents)

decreases uric acid by peeing it out

inhibits tubular reabsorption of urate

uricosuric agent of choice

you’re putting these crystals out in your urine increased risk of kidney stones

increased effectiveness of penicillin (keeps in bloodstream longer)

action is blocked by aspirin

41
Q

CI of probenecid

A

blood disorders, kidney stones, high dose ASA therapy

42
Q

warnings for probenecid

A

can exacerbate/prolong acute gout (so give w/colchicine to decrease risk)

do not use w/ASA

caution in pts with PUD

43
Q

monitoring for probenecid

A

BASELINE serum uric acid levels, monitor Q2-3 months

44
Q

osteoporosis

A

occurs when BONE RESORPTION EXCEEDS BONE FORMATION

net loss of bone tissue

45
Q

risk factors for osteoporosis

A

post menopausal white women

hx of fractures as adults

hx of fragility fracture in family

body weight <127 pounds

smokers

PO steroids for >3 months

estrogen deficiency at early age

dementia

poor health

recent falls

decreased calcium intake (lifelong)

low physical activity (para and quads)

ETOH>2 drinks/day

anorexia

46
Q

bisphosphonates

A

fosamax and reclast

47
Q

MOA of bisphosphonates

A

taken on an empty stomach

needs to sit up for 1 hour after taking

decreases osteoclastic bone resorption which increases bone mass

decreases risk of fracture w/osteoporosis

bisphosphonates preferred tx for post-menopasual osteoporotic women

48
Q

ADE of bisphosphonates

A

severe bone, joint, and muscle pain

serious: osteonecrosis of jaw

49
Q

CI of bisphosphonates

A

hypocalcemia (if they don’t have calcium, they won’t be able to form new bone anyway)

renal insufficiency

unable to stand or sit upright 30-60 minutes after taking

esophageal abnormalities

increase in fracture risk in pts on PPI for 1 year or more (because of decreased absorption of calcium)

50
Q

calcitonin

A

2nd line treatment for osteoporosis

51
Q

MOA of calcitonin

A

decreases bone resorption

used when can’t tolerate bisphosphonates and compression vertebral fractures

52
Q

unique property of calcitonin

A

reduces pain r/t osteoporosis fracture (especially vertebral)

53
Q

MOA of SERM (evista)

A

increases bone density without increased endometrial cancer risk and decreased LDL

destroyed in GI tract so given parenteral/intranasal

54
Q

ADE of SERM (evista)

A

risk of VTE comparable to estrogen

hot flashes, leg cramps, increased VTE

55
Q

CI of SERM (evista)

A

avoid in hx of DVT/PE

calcitonin allergy

56
Q

MOA of parathyroid hormone (teriparatide)

A

increases spinal bone density and decreases vertebral fracture risk

1st approved treatment to stimulate bone formation

PTH is primary regulator of calcium and phosphate metabolism in bone and kidneys

daily admin stimulates new bone formation

57
Q

indication of parathyroid hormone (teriparatide)

A

reserved for pts at HIGH risk of fracture or cannot tolerate other osteoporosis therapies

58
Q

precautions for parathyroid hormone (teriparatide)

A

pts w/ increased risk of osteosarcoma (paget’s dx, high alkaline phosphate, hx bone cancer, bone mets, hypercalcemia)

59
Q

ADE of parathyroid hormone (teriparatide)

A

nausea, dizziness, cramps, injection site pain

60
Q

hormone therapy

A

estrogen-progestogen therapy is NOT therapy of choice for treatment of osteoporosis d/t increased VTE, breast cancer, and CV dx

61
Q

muscle relaxants in geriatrics

A

caution= more susceptible to sedative effects of muscle relaxers, increased risk of falls

62
Q

muscle relaxants in peds

A

safety not established in kids <12 yo

63
Q

muscle relaxants in pregnant/lactating patients

A

safety not established

64
Q

what to remember about baclofen

A

it is a GABA receptor stimulant for muscle spasm caused by CNS dx

inhibits reflexes at SPINAL LEVEL

65
Q

valium

A

only benzo indicated for muscle spasm

Pharmacology (3 decks)

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