Nurs 605 Module 15 Flashcards
Describe the mechanism of action for NSAIDs
- Inhibit prostaglandin synthesis; acts directly on the COX enzyme
- Mostly inhibit COX 1
- Important for prostaglandin synthesis including platelets, GI protection, kidney vasodilator prostaglandins
- Reduction of prostaglandins – suppress s/s of inflammation, “resets” thermostat in the hypothalamus= fever reducer; analgesic effects by reducing bradykinin etc.
- Decreased prostaglandins= s/s: GI distubances; ulcer formation due to decreasd mucousal secretion; dyspepsia, nausea/vomting
- Rashes
- Acute kidney injury-can be reversed by stopping the drug
- CV effects- antiplatelet = imcreaed risk of bleeding; raise BP
Describe the mechanism of action for COX 2
- Celecoxib (coxib drugs)
- Inflammatory cells, activates inflammatory cytokines
- Expressed in the kidney
- Mainly responsible for mediators of inflammation
- Inhibtion of COX 2 is mostly irreversible
- s/s: less GI effects in comparison to COX 1 inhibitors
- increasd risk of hypertension, MI
- headache, dizziness, skin rashe, peripheral edema
Describe the mechanism of action for acetaminophen
- Similar to NSAIDs in which they have an anti-inflammatory and fever reduction component; some inhibition of prostaglandins in the CNS
- Chronic or large doses can cause hepatotoxicity
MOA opioids
/s: constipation, dizziness, fall, fractures, potential for misuse- not first choice in OA management
• tramadol can be a potential drug that is a safer option in elderly and those who require greater pain relief
Describe the basic differences in therapy for osteoarthritis vs rheumatoid arthritis.
- Rheumatoid arthritis
- Caused by degenerative joint changes, mostly an autoimmune disease
- Drugs target inflammatory cytokines – antirheumatic drugs (halt the progression of autoimmune inflammatory cytokines); NSAIDs (for symptom relief)
- Immunosuppressants – methotrexate, sulfasalazine
- Glucocorticoids
- Anti TNF 1
- Osteoarthritis
- Most common MSK disorder-can be primary (usually involves elderly) and secondary (due to trauma or other insult to the joint ie) RA)
- Pain, stiffness, discomfort and joint function impairment
- Non pharm vs. pharm
- Non pharm-exercise, weight loss, nutrition, avoidance of repeated trauma to joint
- Exercise and physiotherapy, orthotics, surgery
- Pharm- topical analgesics ie diclofenac
- Acetaminophen-1st line
- NSAIDs
- Opiods- tramadol but no 1st choice in OA management
- Glucosamime, chondroitin -maintenance of cartilage in a joint
- Oral corticosteroids
- Injectable corticosteroids
List comorbidities where NSAIDS and/or COX-2 inhibitors should be avoided.
- Severe renal or hepatic impairment
- Allergies or intolerance
- GI bleeds/active bleeds
- Unstable angina or NTEMI
What is gout
Increased MSU crystals that deposit in joints, bursa, tendons, soft tissue
Common in men >40 years of age
Reduction of serum uric acid=greater preservation of kidneys
Describe the therapeutic options in the treatment of acute gout and the side effects of these agents.
- NSAIDs - effective at reducing pain and reducing inflammation in acute gout attacks
- Naproxen, celecoxib, indomethacin
- Adverse effects greater in older adults with renal dysfunction or impairment
- s/s: GI upset, ulcers, dyspepsia, n/v, tinnitus (in older adult), bleeding
- at risk for GI bleed or ulcer? Can use celecoxib and PPI
- Colchicine – effective within 24 hours of attack
- 1.2mg initially, followed by 0.6mg OD-BID prophylactically and hour later for control
- s/s: abdo cramps, nausea/vomiting, diarrhea – at higher doses
- corticosteroids: short term prednisone appropriate; no tapering needed
- s/s: GI upset, not usually with short term courses
- Combo therapy may be needed if not responding to monotherapy
Describe the therapeutic options in the prevention of gout and the side effects of these agents.
- Xanthane oxidase-allopurinol and febuxostat- inhibits production of uric acid
- Allopurinol
- Use <100mg in those with normal kidney function
- s/s: caution in renal impairment as higher doses can cause allopurinol hypersensitivity syndrome (includes SJS, TEN, rash, dermatitis, fever, vasculitits)
- increased risk = renal impaired, Chinese/Thai descent, thiazide drugs
- febuxostat
- used in those with sever renal impairment
- safe and effective in those who cannot tolerate allopurinol
- s/s: liver function abnormalities, nauseas, diarrhea, arhtlagias, rash
- uricosurics – probenecid, fenofibrate, losartan
- probenecid first line-only through health Canada authority
- fenofibrate and losaratan not approved for gout therapy
- s/s: GI side effects
Formulate a management plan for a patient presenting with an attack of gout.
- Initiating urate therapy early may increase risk of acteu gouty attacks
- Use colchicine and NSAID if needed
- Large amounts of colhcine in addition to CYP 450 inhibitors can be fatal
- Decreased amount of colchicine during this time
- Stop taking colchicine if appropriate
What are the risks for developing osteoporosis?
Age
Gender- female; menopausal
History of fragility fracture
Fragility fracture-fracture from little trauma, either
standing height or walking speed
Corticosteroid use? Prednisone 7.5mg daily x 3 months
Hip/vertebral fracture + >50 years or post menopause = HIGH RISK and should be offered treatment
What are osteoclasts?
secrete bone absorbing enzymes. responsible for breaking down bone
What are osteoblasts?
secretion of collagen to make bone
stiumulates secretion of calcium and phosphorus to make new bone
what are osteocytes?
former osteoblasts-act as sensors and senses damage to skeleton and bone
stimulates break down of bone and creation of bone
What are the steps of bone remodelling?
activation-cytokines and growth factors stimulate activation of osteoclasts
reabsorption-absorption of old bone by osteoclats
reversal-end of absoprtion
formation- obsteoblasts lay out new bone
