Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pharmacology > Exam #4- MSK > Flashcards

Exam #4- MSK Flashcards

(65 cards)

Start Studying
1
Q

difference between aspirin (salicylates) and other agents

A

cox-1 and 2 inhibition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

NSAIDs MOA

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

various MS etiologies for NSAIDs

A

OA as well as localized MS issues

sprains, strains, low back pain, gout

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

NSAIDs for rheumatic dx

A

not all NSAIDs are FDA approved

most likely effective in RA

psoriatic arthritis

arthritis r/t IBD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

MSK pain

A

start w/ non-drug treatment

RICE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

non-drug treatment of osteoarthritis

A

exercise with rest periods and weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

drug treatment for osteoarthritis

A

TYLENOL

NSAIDs, cox-2 inhibitors, intraarticular injection of steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

goal of treatment for gout

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
colchicine MOA
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
26
ADE of colchicine
N/V/D, abdominal pain
27
drug interactions of colchicine
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
monitoring for colchicine
1st time users- monitor weekly for s/s of toxicity vitamin B12, LFTs
29
MOA of xanthine oxidase inhibitors
decreases uric acid production by inhibiting xanthine oxidase
30
allopurinol and febuxostat
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
allopurinol MOA
prevents uric acid synthesis by xanthine decreased uric acid production **does not promote uric acid secretion**
32
acute attacks are more common during EARLY therapy, so what should you gie?
allopurinol WITH colchicine to prevent acute attack
33
CI of allopurinol
prior severe reaction
34
warnings/ADE of allopurinol
**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
drug interactions with allopurinol
oral anti-coags (coumadin) hypoglycemics theophylline uricosurics decrease the effect of allopurinol monitor renal function w/ thiazides
36
monitoring for allopurinol
baseline CBC, platelets, serum uric acid levels, renal function
37
MOA of febuxostat
inhibits xanthine oxidase
38
ADE of febuxostat
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
MOA of uricosuric drugs
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
probenecid
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
CI of probenecid
blood disorders, kidney stones, high dose ASA therapy
42
warnings for probenecid
can exacerbate/prolong acute gout (so give w/colchicine to decrease risk) **do not use w/ASA** caution in pts with PUD
43
monitoring for probenecid
BASELINE serum uric acid levels, monitor Q2-3 months
44
osteoporosis
occurs when BONE RESORPTION EXCEEDS BONE FORMATION **net loss of bone tissue**
45
risk factors for osteoporosis
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
bisphosphonates
fosamax and reclast
47
MOA of bisphosphonates
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
ADE of bisphosphonates
severe bone, joint, and muscle pain serious: **osteonecrosis of jaw**
49
CI of bisphosphonates
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
calcitonin
2nd line treatment for osteoporosis
51
MOA of calcitonin
decreases bone resorption used when can't tolerate bisphosphonates and compression vertebral fractures
52
unique property of calcitonin
**reduces pain r/t osteoporosis fracture** (especially vertebral)
53
MOA of SERM (evista)
increases bone density without increased endometrial cancer risk and decreased LDL destroyed in GI tract so given parenteral/intranasal
54
ADE of SERM (evista)
**risk of VTE comparable to estrogen** hot flashes, leg cramps, increased VTE
55
CI of SERM (evista)
avoid in hx of DVT/PE calcitonin allergy
56
MOA of parathyroid hormone (teriparatide)
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
indication of parathyroid hormone (teriparatide)
**reserved for pts at HIGH risk of fracture or cannot tolerate other osteoporosis therapies**
58
precautions for parathyroid hormone (teriparatide)
pts w/ increased risk of osteosarcoma (paget's dx, high alkaline phosphate, hx bone cancer, bone mets, hypercalcemia)
59
ADE of parathyroid hormone (teriparatide)
nausea, dizziness, cramps, injection site pain
60
hormone therapy
estrogen-progestogen therapy is NOT therapy of choice for treatment of osteoporosis d/t increased VTE, breast cancer, and CV dx
61
muscle relaxants in geriatrics
caution= more susceptible to sedative effects of muscle relaxers, increased risk of falls
62
muscle relaxants in peds
safety not established in kids <12 yo
63
muscle relaxants in pregnant/lactating patients
safety not established
64
what to remember about baclofen
it is a GABA receptor stimulant for muscle spasm caused by CNS dx inhibits reflexes at SPINAL LEVEL
65
valium
only benzo indicated for muscle spasm

Pharmacology (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions