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
Which drugs are approved for treatment of osteoporisis?
bisphosphonates-first line
desunomab
calcitonin
teriparatide
What are the bisphosophates that show strong evidence for decreasing risk of vetebral and hip fractures?
etidronate
alendronate
risodreante
zolenic acid
What T score must a person have before dx of osteoprosis?
T score,. BMD
<2.5
What is the MOA of bisophonates?
bind to hydroxyapatite
initiates osteoclast apoptosis and inactivation (prevents break down of bone)
What are the side effects of bisosphonates?
common: upper GI effects. acute reaction during IV
uncommon: femoral fractures, osteonecrosis of the jaw, a fib , esophageal cancer
What are contraindications in use of bisophosphnates?
hypocalcemia
renal insufficieny
esophageal concerns
What is the evidence in use of bisphosphonates in post menopausal women with prev. fracture? (ARRs)
ARR hip fracture all bisphosphonates 1.1% ARR etidronate vertebral fracture 5.3% ARR alendronate vertebral fracture 7.0% ARR ritedronate v. fracture 10.9% ARR zolendric acid v fracture 7.6%
Which bisphosphate is the only drug to evidence to PREVENT vertebral fractures in women who have not had a fracture?
alendronate
ARR 1.7%
What is the evidence surrouding men and osteoporisis? who is at risk?
fractures occur in age >70
osteoprosis often undiagnosed
at risk >70, no psyical activity, prev. fragility fracture
What is the evidence surrouding older adults and osteoporsis? older adults >70
under represented
no evidence to prove or support reduction of fractures
What is the relationship between bisphosphonates and individuals on systemic gluticosteroids? What alternative drug can be offered to those on systemic corticosteroids
ind. taking prednison 7.5mg daily x 3 mos =increased risk of osteoprosis
should offer bisphosphonate- alendronate and risedonate
baseline risk ususally comes back within 1 year of stopping corticosteroid
tiperatide can be used as an alternativew
What is the recommended daily dose of calcium and vitamin D in women and men?
calcium: men and women >50 years 1200mg/day men decrease in calcium to 1000mg as they get odler, but women stay the same vitamin D: 600-800IU daily
What is the role of vitamin D in calcium homeostasis?
decreased serum calcium increaess serum PTH which increases calcitrol (active vitamin D)
calcitrol stimulates PTH and calcium absoprtion
What are some other non pharmacological options to decrease risk of osteoporosis?
decrease caffeine intake
decreased alcohol intake
smoking cessation
increase exercise
What is the optimal duration of treatment of biphosphonate therapy?
unknwon
3-5 years in trials, so shoudl be assess after this time frame
What is the MOA of denosumab? when would it be used in osteoporiis?
binds to RANKL and prevents initation and formation of osteoclasts == prevents bone break down
only use in those who cannot tolerate bisphosphonates or non therapeutic
What is the MOA of teriparatide?
responds to decreased plasma calcium and stiumulates production of PTH to reabsorb calcium and stimulate bone formation
What is the relationship between calcium and vitamin d in osteoporosis?
no strong evidence but beneft appears when used in combodniation with biphosphonates
What are the side effects of desonumab?
flatulence
dont use in hypocalemia
arthralgia
exzema
Discuss acetaminophen toxicity
most common toxicity
usally people think actemainipehn is harmelss
over ingestion
What are the phases of acteaminiphon tox and its clinical manifestitaions?
phase 1: asymptomatic, maybe n/v, pallor, malaise, incresing LFTs
pahse 2: upper quadrant pain, n/v, diaphoresis, incrased LFTS
phase 3: jaundice, hepatic failutre, renal failure, coma, death
phase 4: recovery if survival of pahse 3
Describe anticholinergic txocities, what are the common clinical manifestions?
drugs: antihistamines most common, parkinsons, antidepressants, antipsychotis
• Clinical manifestions:
• Dry as a bone- dry axilla
• Red as a beet- skin warm and flushed
• Mad as a hatter- delirium, hallucinations, high pitched cries in infants
• Hot as hades-agitation, hypothermia
• Blind as a bat- dilated pupils
• Stuffed as a pipe- urinary retention, decreased bowel sounds, decreased gastric emptying
