Ch. 25 - Antiinflammatory Drugs Flashcards
Inflammation
- ) Response to tissue injury & infection
- ) Vascular reaction
- ) Protective mechanism
Infection:
caused by microorganisms –> inflammation
5 Characteristics of Inflammation:
- ) Erythema
- ) Edema
- ) Heat
- ) Pain
- ) Loss of function
Prostaglandins:
- ) Released when cellular injury takes place
2. ) Injection of prostaglandins into body –> inflammatory process
Cyclooxygenase (COX):
COX1 = protects stomach lining & regulates platelets
COX2 = triggers inflammation & pain
Antiinflammatory Agents:
- Nonsteriodal agents
- Steroidal agents
Nonsteriodal Antiinflammatory Drugs (NSAIDS):
Aspirin
-Aspirin like drugs –> inhibit COX2 enzyme
Nonsteriodal Antiinflammatory Drugs (NSAIDS): cont…
Salicylates & Nonsalicylates
1st generation NSAIDs
2nd generation NSAIDs (COX2 inhibitors)
Salicylates (ASA):
Strong prostaglandin inhibitor
—> reduces inflammatory process
Inhibits prostaglandin synthesis
—> COX1 & COX2 enzymes
Acetylsalicylic Acid (ASA) (1):
Antiplatelet drug:
- Decrease platelet aggregation
- Decrease blood clotting
Acetylsalicylic Acid (ASA) (2):
Low doses —> analgesic, antipyretic effect
Higher doses —> anti-inflammatory effect
Acetylsalicylic Acid (ASA) (3):
Most common adverse effects:
1. ) Gastric irritation 2. ) Occult Bleeding
Hypersensitivity to ASA
- ) Tinnitus
- ) Vertigo
- ) Bronchospasm
Tx of Headache (HA) / Fever:
- ) ASA
- ) Acetaminophen
- ) Ibuprofen
Tx of Inflammation / Swelling, Pain, Stiff Joints
NSAIDs = cost more than ASA
Contraindicted:
-allergic to ASA (asa is Aspirin)
Over the Counter (OTC) NSAIDs:
- ) Ibuprofen (Motrin, Advil)
2. ) Naproxen (Aleve)
Rx Drugs that Contain NSAIDs :
- 1st Generation ——————*2ndGeneration
- meloxican (Mobic) ———- celecoxib (Celebrex)
- naproxen (Naprosyn)
- nabumentone (Relafen)
Nursing Process (ASA):
Observe for signs of bleeding:
1. ) Dark Stools 2. ) Bleeding Gums 3. ) Petechiae 4. ) Ecchymosis
Bleeding from an IV site
Client Teaching (ASA) (1):
- ) DO NOT take with:
- Alcohol
- Anticoagulant Drugs
- ) Inform Dentist
- ) d/c 3-7 days before surgery
Client Teaching (ASA) (2):
Do not give to children for virus/flu symptoms
- Reye Syndrome
Client Teaching (ASA) (3):
- ) Take with:
- Food/meals
- Fluids
5.) Enteric coated
Other NSAIDs (1):
indomethacin (Indocin):
- ) Po/ rectal
- ) Arthritis
- ) Strong prostaglandin inhibitor
- ) Highly protein bound
- ) Very irritating to stomach
Other NSAIDs (2):
ketorolac (Toradol):
- ) IM / IV / po
- ) Greater analgesic properties
- ) Short-term pain relief
- ) Opiate level analgesia
SE /Adverse Reactions (1st Generation NSAIDs):
- ) Fewer SE than ASA
- ) GI irrigation (take with food)
- ) Sodium & water retention
- ) Alcohol —> increase gastric irritation
Selective COX2 Inhibitors:
2nd Generation
**Drug of choice for severe arthritis
-Does not inhibit COX1
Ex: Celecoxib (Celebrex)
Corticosteroids:
Steroid
Tx: inflammatory disorders
- Local - Systemic
Corticosteroids (1)
- ) Produced in adrenal cortex
- ) Anti-inflammatory properties (Glucocorticoid)
- ) Salt-retaining properties (Mineralcorticoid)
Corticosteroids (2):
High doses / over long periods —>
-suppress hypothalamic pituitary adrenal hormone production
Corticosteroids (3):
Glucocorticoid properties:
- alter CHO, protein, & lipid metabolism
Corticosteroids (4):
Mineralcorticoid properties:
- Enhance reabsorption of sodium
- increase excretion of potassium & hydrogen ions —> effects fluid / electrolyte
Side Effects:
Fluid retention
Altered glucose levels
Altered fat disposition
moon face , buffalo hump
Corticosteroids (5):
Long term use:
- Wasting of muscle tissue in extremities
- Delayed growth in children
Corticosteroids (6):
- Prevent or suppress inflammatory signs & symptoms
- Underlying cause of S/S may still remain
- May mask disease S/S
Corticosteroids (7):
Po, IM, IV, SQ, topical
-Adm DIRECTLY into inflamed site
Ex: joint, skin
*Avoid systemic side effects
Examples:
- ) betamethasone (Celestone) = po, IM, IV
- ) dexamethasone (Decadron) = po
- ) Hydrocortisone (Cortef) = po, SQ, IM, IV
- ) Solu-cortef = (IM, IV)
- ) prednisone = po
- ) prednisolone = po, IM, IV
Avoid Abrupt D/C of Drug —>
Adrenal insufficiency
- Fatal if untreated
- Medical Emergency
D/C drug gradually
Corticosteroids^:
Protect from infection altered response to wound healing
Nursing Dx:
Excess fluid volume r/t fluid rentention secondary to effect of corticosteroid
Disease-Modifying Antirheumatic Drugs:
DMARDs
-Gold therapy = Chrysotherapy
Gold Therapy (1):
Use:
1. ) Stop progression of rheumatoid arthritis 2. ) Prevents deformities
Gold Therapy (2):
Action:
3. ) Depress migration of leukocytes 4. ) Suppress prostaglandins
Gold Therapy (3):
Palliative = not curative
Results:
* may take up to mos (IV) * may take 3-6mos (PO)
auranofin (Ridaura):
Po, Gold sakt
Common SE:
1. ) Skin Problems 2. ) Blood Dyscarsias 3. ) GI Irritation
Nursing Process Health Teaching:
- ) Dental hygiene
- ) Adhere to scheduled blood tests
- ) Metallic taste / pruritus —> early symptom of possible gold toxicity
Nursing Process:
- ) Avoid direct sunlight
2. ) Assess improvement in joint pain & motion
Gout:
1.) Inflammatory condition
2.) Chronic metabolic disease —>
Hyperuricemia (abnormally elevated amounts of uric acid in blood
Gout – Hyperuricemia (1):
D/T:
- ) Decreases renal elimination of uric acid
- ) Increase uric acid production
Gout – Hyperuricemia (2):
- ) Uric acid precipitates as crystals (tophi) –>
4. ) Deposit on tissues & joints –> gouty arthritis
Gouty Arthritis (1):
- ) Inflammation at site of crystal deposits (tophi)
- ) Acte joint pain
- ) Most susceptible site —> Metatarsophalangeal joint of great toe
Gouty Arthritis (2):
- ) Metatarsal bone
2. ) Phalanges
Gouty Arthritis (3):
- ) Increase fluid intake —>
- Promotes uric acid excretion
- Prevents renal calculi
- ) Avoid foods high in purine
- alcohol
Anti-inflammatory Gout Drugs:
Colchine:
- ) Inhibits migration of leukocytes to inflamed site
- ) Alleviates acute symptoms
- take at first sign of attack
Colchicine (1):
DOES NOT:
- ) Inhibit uric acid synthesis
- ) Promote uric acid excretion
Colchicine (2):
Common SE = gastric irritation
High doses = n/v, diarrhea, abdominal pain
Management:
After acute attack is over:
- ) Begin therapy to control hyperuricemia
- ) Reduce serum urate levels to
Uric Acid Inhibitor:
allopurinol (Zyloprim)
- Prevents formation of uric acid in body
allopurinol (Zyloprim) (1):
- ) Interferes w/ conversion of purines to uric acid —–>
- ) Inhibits enzyme xanthine oxidase —->
- ) Good for clients w/ renal obstruction d/t uric acid secretions
allopurinol (Zyloprim) (2):
- ) Prevents attack
5. ) Increase fluid intake —> promote diuresis & alkalization of urine
Uricosurics:
probenecid (Benemid)
- Increases urinary excretion of uric acid
- Prevents reabsorption in renal tubules
probenecid (Benemid):
- ) Initially increases concentration of uric acid in urine —-> @ risk: KIDNEY STONES
- ) Drink large amounts of water
- ) ASA decreases the effect of probenecid
Nursing Process – Nsg Dx:
Impaired skin integrity r/t inflammation of great toe
Acute pain r/t tissue swelling
Client Teaching (1):
- ) Initiate tx at first sign of attack
- ) Avoid certain foods
- ) Encourage fluids
- ) DO NOT use ASA while taking probenecid
Client Teaching (2):
allopurinol (Zyloprim)
*Monitor lab tests = renal, liver function, CBC
Client Teaching:
Annual eye exams
Report:
- Anorexia, n/v, diarrhea, stomatitis - Dizziness, rash, pruritis, metallic taste