NURS 615 exam 3 - Maryville.
1. corticosteroid drugs: prednisone, methylprednisolone, dexamethasone, topical such as hydrocortisone, and then joint
injections for pain
2. MOA of corticosteroids drugs: drugs that suppress inflammation by mimicking glucocorticoid hormones
Inhibit interleikin one, tumor necrosis factor and other cytokines, impairs phagocytosis, impairs lymphocytes, and inhibits tissue
repair
3. indications for cortocosteriod use: Allergy or hypersensitivity, respiratory, shock, rheumatology, neurology, hepatic,
neoplastic... basicly every organ is covered if there is an issue.
4. withdrawal from corticorsteriod symptoms: malaise, myalgia, headache, nausea, fevers, hypotension and relapse
of symptoms (pain, inflammation, ashtma)
5. what must you do with corticosteriods to prevent withdrawal: Must taper them down, you can have possible adrenal
crisis if you do not.
6. corticosteriod considerations: suppression patients response to infections- no live viral vaccines, and have increased
susceptibility to disease.
If used over 6 months: Increase blood glucose, impair immune function (get vaccines) , impair wound healing, GI complaints
(report black tarry stools) , osteoporosis (decreases calcium), anxiety/insomnia, sodium & fluid retention 9monitor weight and
fluid retention)
If on 1gram or more also prescribe PPI (omeprazole) to prevent PUD
contraindicated with active infection and hypersensitivity
7. What are the adverse effects of corticosteroids if administered for six months or more?: The main thing you
want to worry about is osteoporosis
It can also worsen diabetic control
Patients should report any tarry black stools or abdominal pain.
8. NSAIDS: nonsteroidal anti-inflammatory drugs
Ibprofen, aspirin, torsdol, naproxin, Mobic
9. Arachidonic Acid Cascade: Cell membrane º Arachinidonic acid º Cycloxygenerase (COX)º prostaglandin's
Or
Cell membrane º Arachinidonic acid º Lipoxygenaseº Leukotrines
,10. NSAID mechanism of action: • NSAIDs inhibit the enzymes COX I and II • Results in reduction in formation of
prostaglandin precursors and thromboxanes from arachidonic acid
COX1- ibuprofen, naproxen, aspirin, when this is inhibited you are also inhibiting the prostaglandins that protect the stomach
COX2 - celebrex more stomach proctective
11. Drug interactions with NSAIDS: Pretty much anything that is highly protien bound. Do not give together with
ACE inhibitors - counteracts antihypertensive effect BetaBlockers - counteracts
antihypertensive effect lithium - increases lithium levels
Anticoagulants - increases bleeding
Antidiabetics- increases hypoglycemic effect
12. Black box warning for NSAIDS: May cause an increased risk of serious cardiovascular thrombotic events:
•Patients with cardiovascular disease or with risk factors for cardiovascular disease may be a greater risk. **
•Myocardial-infarction
•Stroke which can be fatal.**
•This risk may increase with duration of use.
NSAIDs can also cause an increased risk of serious gastrointestinal adverse effects including •Bleeding**
•Ulceration
•Perforation the stomach or intestines which can be fatal.
•These events can occur at any time during use and without warning symptoms.
•Elderly patients are at greater risk for serious GI events.
13. Tylenol: non opioid, non NSAID analgesic
treatment for mild pain and fever, has no anti- inflammatory properties The main mechanism is performed a
proposed is the inhibition of cox.
And recent findings suggest that it's highly selective cox-2.
Because of its selectivity for cox-2 it does not significantly inhibit the production of pro clotting thromboxanes.
14. Tylenol warnings: Acute overdoses of acetaminophen can cause potentially fatal liver damage.
**The maximum recommended dose is 3 grams in 24 hours.
, NURS 615 exam 3 - Maryville.
15. DMARDs (disease modifying anti-rheumatic drugs): Methotrexate
Folic acid antagonist- slows the disease process by inhibiting DNA synthesis and cell reproduction causes hepatotoxicity
leukopenia, anemia
has tons of drug interations
16. Drugs for Gout: allopurinol (Zyloprim), colchicine, and febuxostat (Uloric)
17. Gout patient teaching: Decrease alcohol and organ meat, dish and bacon in diet
18. Allopirinol MOA: Prevents formation of uric acid by inhibiting xanthine oxidase
19. Allopirinol considerations: Monitor renal and liver tests prior to administration, drowsiness/dizzyness can occur
20. Febuxostat (Uloric) MOA: inhibit synthesis of uric acid by inhibiting xanthine oxidase conversion of hypoxanthine &
xanthine to uric acid
21. Febuxostat (Uloric) considerations: **risk of gout flare up when starting febuxostat patient should be concurrently
taking NSAID or colchicine for up to 6 months monitor liver labs
*pts may have vomiting with 40mg daily doses
22. Chochicine MOA: decreases inflammation by decreasing movement of leukocytes into tissues constaining urate cyrstals
23. Cholchicine considerations: for prophylaxis of gout flares in adults **treatment for behcets syndrome (pain, swelling,
redness, associated with gout flares)
**Colchicine always causes diarrhea, other GI symptoms (upset stomach, nausea, abdominal pain) can be decreased if taken with
food
Do not stop abruptly
Decrease dose with hepatic dysfunction
Patient should be educated to recognize and report proximal muscle weakness, myalgia, and neuropathy if taking colchicine.
Contact doctor These can be an adverse effect of colchicine and usually resolve within 3-4 weeks of stopping the medication.
24. Low dose versus high dose of cholchicine: Low dose vs. High dose—low dose has better efficacy with less s/e
25. Uricosuric agents: probenecid (Benemid) & Sulfinpyrazone (Anturane)
26. probenecid (Benemid) & Sulfinpyrazone (Anturane): •probenecid & sulfinpyrazone inhibit renal tubular
reabsorption of urate and therefor increase excretion of uric acid via the kidneys and decrease serum uric acid
•sulfinpyrazone also competitively inhibits platelet aggregation, multiple drug interactions
•not anti-inflammatory
•not for use in acute attacks
1. corticosteroid drugs: prednisone, methylprednisolone, dexamethasone, topical such as hydrocortisone, and then joint
injections for pain
2. MOA of corticosteroids drugs: drugs that suppress inflammation by mimicking glucocorticoid hormones
Inhibit interleikin one, tumor necrosis factor and other cytokines, impairs phagocytosis, impairs lymphocytes, and inhibits tissue
repair
3. indications for cortocosteriod use: Allergy or hypersensitivity, respiratory, shock, rheumatology, neurology, hepatic,
neoplastic... basicly every organ is covered if there is an issue.
4. withdrawal from corticorsteriod symptoms: malaise, myalgia, headache, nausea, fevers, hypotension and relapse
of symptoms (pain, inflammation, ashtma)
5. what must you do with corticosteriods to prevent withdrawal: Must taper them down, you can have possible adrenal
crisis if you do not.
6. corticosteriod considerations: suppression patients response to infections- no live viral vaccines, and have increased
susceptibility to disease.
If used over 6 months: Increase blood glucose, impair immune function (get vaccines) , impair wound healing, GI complaints
(report black tarry stools) , osteoporosis (decreases calcium), anxiety/insomnia, sodium & fluid retention 9monitor weight and
fluid retention)
If on 1gram or more also prescribe PPI (omeprazole) to prevent PUD
contraindicated with active infection and hypersensitivity
7. What are the adverse effects of corticosteroids if administered for six months or more?: The main thing you
want to worry about is osteoporosis
It can also worsen diabetic control
Patients should report any tarry black stools or abdominal pain.
8. NSAIDS: nonsteroidal anti-inflammatory drugs
Ibprofen, aspirin, torsdol, naproxin, Mobic
9. Arachidonic Acid Cascade: Cell membrane º Arachinidonic acid º Cycloxygenerase (COX)º prostaglandin's
Or
Cell membrane º Arachinidonic acid º Lipoxygenaseº Leukotrines
,10. NSAID mechanism of action: • NSAIDs inhibit the enzymes COX I and II • Results in reduction in formation of
prostaglandin precursors and thromboxanes from arachidonic acid
COX1- ibuprofen, naproxen, aspirin, when this is inhibited you are also inhibiting the prostaglandins that protect the stomach
COX2 - celebrex more stomach proctective
11. Drug interactions with NSAIDS: Pretty much anything that is highly protien bound. Do not give together with
ACE inhibitors - counteracts antihypertensive effect BetaBlockers - counteracts
antihypertensive effect lithium - increases lithium levels
Anticoagulants - increases bleeding
Antidiabetics- increases hypoglycemic effect
12. Black box warning for NSAIDS: May cause an increased risk of serious cardiovascular thrombotic events:
•Patients with cardiovascular disease or with risk factors for cardiovascular disease may be a greater risk. **
•Myocardial-infarction
•Stroke which can be fatal.**
•This risk may increase with duration of use.
NSAIDs can also cause an increased risk of serious gastrointestinal adverse effects including •Bleeding**
•Ulceration
•Perforation the stomach or intestines which can be fatal.
•These events can occur at any time during use and without warning symptoms.
•Elderly patients are at greater risk for serious GI events.
13. Tylenol: non opioid, non NSAID analgesic
treatment for mild pain and fever, has no anti- inflammatory properties The main mechanism is performed a
proposed is the inhibition of cox.
And recent findings suggest that it's highly selective cox-2.
Because of its selectivity for cox-2 it does not significantly inhibit the production of pro clotting thromboxanes.
14. Tylenol warnings: Acute overdoses of acetaminophen can cause potentially fatal liver damage.
**The maximum recommended dose is 3 grams in 24 hours.
, NURS 615 exam 3 - Maryville.
15. DMARDs (disease modifying anti-rheumatic drugs): Methotrexate
Folic acid antagonist- slows the disease process by inhibiting DNA synthesis and cell reproduction causes hepatotoxicity
leukopenia, anemia
has tons of drug interations
16. Drugs for Gout: allopurinol (Zyloprim), colchicine, and febuxostat (Uloric)
17. Gout patient teaching: Decrease alcohol and organ meat, dish and bacon in diet
18. Allopirinol MOA: Prevents formation of uric acid by inhibiting xanthine oxidase
19. Allopirinol considerations: Monitor renal and liver tests prior to administration, drowsiness/dizzyness can occur
20. Febuxostat (Uloric) MOA: inhibit synthesis of uric acid by inhibiting xanthine oxidase conversion of hypoxanthine &
xanthine to uric acid
21. Febuxostat (Uloric) considerations: **risk of gout flare up when starting febuxostat patient should be concurrently
taking NSAID or colchicine for up to 6 months monitor liver labs
*pts may have vomiting with 40mg daily doses
22. Chochicine MOA: decreases inflammation by decreasing movement of leukocytes into tissues constaining urate cyrstals
23. Cholchicine considerations: for prophylaxis of gout flares in adults **treatment for behcets syndrome (pain, swelling,
redness, associated with gout flares)
**Colchicine always causes diarrhea, other GI symptoms (upset stomach, nausea, abdominal pain) can be decreased if taken with
food
Do not stop abruptly
Decrease dose with hepatic dysfunction
Patient should be educated to recognize and report proximal muscle weakness, myalgia, and neuropathy if taking colchicine.
Contact doctor These can be an adverse effect of colchicine and usually resolve within 3-4 weeks of stopping the medication.
24. Low dose versus high dose of cholchicine: Low dose vs. High dose—low dose has better efficacy with less s/e
25. Uricosuric agents: probenecid (Benemid) & Sulfinpyrazone (Anturane)
26. probenecid (Benemid) & Sulfinpyrazone (Anturane): •probenecid & sulfinpyrazone inhibit renal tubular
reabsorption of urate and therefor increase excretion of uric acid via the kidneys and decrease serum uric acid
•sulfinpyrazone also competitively inhibits platelet aggregation, multiple drug interactions
•not anti-inflammatory
•not for use in acute attacks
