Antiinflammatory

Front 1

What is the main use of glucocorticoids in rheumatoid arthritis?

Back 1

To gain control. They can slow the progression of rheumatoid arthritis but can't safely use them chronically.

Front 2

When are glucocorticoids used in rheumatoid arthritis?

Back 2

When other more conservative methods have failed.

Front 3

How do glucocorticoids interfere with glucose?

Back 3

Glucocorticoid refers to the ability to increase hepatic glucose output by hepatic gluconeogenesis, enhanced hepatic glycogen synthesis, and decreased glucose uptake and utilization by muscle and fat causing an anti-insulin effect (*diabetogenic).

Front 4

How do glucocorticoids interfere with lipid metabolism?

Back 4

Enhance lipase activity to increase lipolysis in adipose tissues, increase formation of ketones, decreased lipid formation in liver, and chronically redistributes fat from extremities to face, shoulders, and abdomen (moon face, buffalo hump).

Front 5

How do agents with aldosterone effect electrolytes and water in the body?

Back 5

Enhance sodium reabsorption in exchange for potassium (increases BP), and glucocorticoids enhance water excretion, indirectly antagonizing ADH.

Front 6

True/False: Antiinflammatory steroids can also cause vasoconstriction and thinning of the skin, in addition to stabilizing membranes and serving as a neuromodulator to the extent that some even have anesthetic properties.

Back 6

True.

Front 7

What effects can antiinflammatory steroids have on the blood?

Back 7

May increase Hb and RBC content, change the distribution of lymphocytes out of plasma to lymphoid tissue and increase apoptosis of T cells, directly inhibit mediator release from eosinophils, reduce the number of circulating eosinophils, and change the distribution of neutrophils to increase blood levels.

Front 8

What is the mechanism of action of glucocorticoids?

Back 8

1.Lipocortin is produced which inhibits PLA2 (which decreases LT and PG).
2.Reduce the expression of COX 2 (induced by inflammation).
3. Repress the expression of some of the cytokines that are proinflammatory (TNF alpha, IL-1) and induce COX 2.

Front 9

How are the best antiinflammatory efects obtained?

Back 9

By using PHARMACOLOGICAL doses, which guarantees some adverse effects that become more serious the longer they are used.

Front 10

What is the most common cause of drug-induced osteoporosis?

Back 10

Glucocorticoids.

Front 11

List some of the adverse effects of antiinflammatory steroids.

Back 11

Muscle wasting, peptic ulcers, diabetogenic effects, thin skin, infection exacerbation, and CNS effects like psychosis and depression. Other adverse effects include: occular effects, redistribution of fat, hepatomegaly, acne and hirsutism, and steroid withdraw.

Front 12

List some therapeutic uses for glucocorticoids.

Back 12

Addison's disease, malignancies, septic shock, cerebral edema, asthma, COPD, nephrotic syndrome, ulcerative colitis, rheumatoid arthritis, collagen diseases, lupus erythematosis, inflammatory neuropathies, and organ transplant rejection.

Front 13

Name the four inhaled antiinflammatory aerosols/nasal sprays.

Back 13

beclomethasone, triamcinalone, flunisolide, flutacasone.

Front 14

What is the purpose of ADT (alternate day therapy)?

Back 14

To minimize adrenal cortex supression, to allow GC levels to fall low enough so that ACTH release increases to stimulate adrenals, increasing production and release of cortisol...because we can't survive trauma without it!!!

Front 15

True/False: NSAIDS are more toxic than DMARDS.

Back 15

False. DMARDS are more toxic than NSAIDS.

Front 16

What is the "gold standard" drug in the treatment of rheumatoid arthritis?

Back 16

Methotrexate (drug of choice).

Front 17

This DMARD is also an antimalarial but takes many months to see any benefit and one of the serious side effects include irreversible retinopathy.

Back 17

Hydroxychlorquine.

Front 18

This DMARD is used when patients are unresponse to NSAIDS but has a high incidence of toxicity.

Back 18

Gold.

Front 19

One side effect of this medication is chrysiasis. What drug is it?

Back 19

Gold. Chrysiasis is small deposits of gold crystals in the skin.

Front 20

This DMARD is also a chelating agent that is usually used when gold compounds don't work. It helps to decrease bone destruction in rheumatoid arthritis.

Back 20

Penicillamine.

Front 21

What limits the use of penicillamine?

Back 21

Severe side effects with a greater frequency of side effects than that of the gold compounds. Side effects include: GI effects very frequently, aplastic anemai, agranulocytosis, nephrotoxicity, and allergy problems with a cross allergy to penicillins.

Front 22

Although the mechanism of action for this DMARD is unclear, it is believed to interfere with metalloproteinases that breakdown cartilage.

Back 22

Minocycline.

Front 23

This DMARD inhibits de novo pyrimidine synthesis to produce anti-proliferative effects in lymphocytes and slows the disease progression in rheumatoid arthritis, decreasing pain and joint swelling.

Back 23

Leflunomide.

Front 24

Side effects of this DMARD include alopecia and hepatotoxicity.

Back 24

Leflunomide.

Front 25

This drug can be combined with methotrexate in the treatment of RA to get an increase in the efficacy but no increase in toxicity.

Back 25

Etanercept.

Front 26

Adverse effects of this DMARD include activation of latent TB, pancytopenia, CNS demylinating disorders, and injection site reactions.

Back 26

Etanercept.

Front 27

This drug is always given with methotrexate, is considered a monoclonal antibody to TNFa, poses a greater risk of infection and can cause a SLE-like syndrome.

Back 27

Infliximab

(contraindicated in pt's with moderate to severe heart failure).

Front 28

This over-the-counter topical prep stimulates the release of substance P from afferents in patients with RA and OA.

Back 28

Capsaicin.

Front 29

This drug inhibits the synthesis of uric acid in the treatment of gout.

Back 29

Allopurinol

Front 30

These two drugs increase the urinary excretion of uric acid in the treatment of gout.

Back 30

Probenicid and sulfinyrazone.

Front 31

This drug inhibits leukocyte migration and phagocytosis in the treatment of gout.

Back 31

Colchicine.

Front 32

These drugs relieve symptoms of pain and inflammation associated with gout.

Back 32

NSAIDs.

Front 33

These two types of medicines are used to treat an acute gout attack and for prophylactic therapy.

Back 33

Colchicine and NSAIDs.

Front 34

Adverse effects of this drug include hair loss, BMD, peripheral neuritis (when given IV) and diarrhea which is severe enough it often limits it's use.

Back 34

Colchicine.

Front 35

Acute overdose of what drug can cause burning throat pain, bloody diarrhea, CV shock, renal failure, CNS depression, and can be fatal?

Back 35

Colchicine.

Front 36

This drug can cause potential mutagenesis and teratogenesis, agranulocytosis and aplastic anemia in patient's with chronic toxicity.

Back 36

Colchicine.

Front 37

This group of drugs are as effective as colchicine and produce effects quicker but their prophylactic use is limitied by the risk of chronic adverse effects.

Back 37

NSAIDs.

Front 38

How do NSAIDs work?

Back 38

They inhibit prostaglandin synthesis!

Front 39

What are the three A's of NSAIDs?

Back 39

Analgesic
Antipyretic
Antiinflammatory.

Front 40

This NSAID is used for relief from acute gout attacks and works quickly but it's GI and CNS side effects are significant.

Back 40

Indomethacin.

Front 41

This NSAID is used for relief from acute gout attacks but it has serious hematological side effects, like aplastic anemia, when used chronically.

Back 41

Phenylbutazone.

Front 42

These are used systemically in resistant acute cases when colchicine or NSAIDs don't work or can't be given.

Back 42

Adrenal corticosteroids.

Front 43

This drug doesn't relieve an acute gout attack but is used to treat gouty nephropathy, chronic tophaceous gout, and renal urate stones.

Back 43

Allopurinol.

Front 44

Before initiating therapy with this drug, you must wait for an acute gout attack to resolve and make sure patient is on colchicine or an NSAID because this drug may produce acute gout attacks during initial treatment.

Back 44

Allopurinol.

Front 45

This drug should be used after acute gout attacks, when allopurinol is not tolerated, and when evidence of tophi appears.

Back 45

Probenecid.

Front 46

This drug is hazardous if urinary concentration of urates is high and is contraindicated if urine flow is low or if pt. has a history of renal calculi.

Back 46

Probenecid.

Front 47

If urinary urates are greater than 600mg daily, what is preferred?

Back 47

Allopurinol.

Front 48

If the amount of urates in the urine are <600 mg daily, then what agents should be used?

Back 48

Uricosuric agents.

Front 49

True/False: Concurrent therapy of allopurinol and a uricosuric agent may decrease the effectiveness of each other.

Back 49

True.

Front 50

Is aspirin an NSAID?

Back 50

Yes.

Front 51

Non-selective NSAIDs tend to produce more GI related problems because what is significantly inhibited?

Back 51

COX 1.

Front 52

This NSAID prolongs bleeding times and can interfere with uric acid elimination and aggravate gout.

Back 52

Aspirin.

Front 53

What are the GI effects of aspirin related to?

Back 53

Secondary to decreased prostaglandins that regulate acid secretion, mucin and bicarb production.

Front 54

Mild aspirin toxicity, also known as salicylism, can cause?

Back 54

Headache, dizziness, TINNITUS, hearing loss, drowsiness, NVD, confusion, and sweating.

Front 55

Acute, severe salicylate poisoning can cause?

Back 55

Dehydration, hyperthermia, CNS effects (irritability, psychosis, convulsions and coma), CV collapse, and even death as a result of respiratory failure.

Front 56

Aspirin should be avoided in children with viral illnesses because of the risk of?

Back 56

Reyes syndrome.

Front 57

This non-selective COX inhibitor has no antipyretic effect.

Back 57

Diflusinal.

Front 58

This is one of the most toxic NSAIDs and one of its special uses is to close a patent ductus arteriosus in neonates.

Back 58

Indomethacin.

Front 59

CNS effects are most likely with this NSAID.

Back 59

Indomethacin.

Front 60

This NSAID is extensively used but its use may negate the cardioprotective effects of aspirin by antagonizing irreversible platelet inhibition.

Back 60

Ibuprofen.

Front 61

This prodrug is the only NON-acid NSAID and its long half-life allows for once a day dosing.

Back 61

Nabumetone.

Front 62

This NSAID has a long half-life due to enterohepatic cycling.

Back 62

Piroxicam.

Front 63

This is the only COX 2 inhibitor still on the market due to the increased incidence of MI's associated with the other COX 2 inhibitors.

Back 63

Celecoxib.

Front 64

This is a PGE1 analog that decreases gastric acid production and stimulates bicarb and mucin production decreasing the GI effects of NSAIDs so often given in combination with NSAIDs.

Back 64

Misoprostol.

Front 65

True/False: Acetaminophen is a NSAID.

Back 65

False. No significant antiinflammatory effects.

Front 66

When should acetaminophen be used instead of other NSAIDs?

Back 66

When aspirin can't be used, in kids with viral infections, in patients on anticoagulants, and in patients on uricosurics.

Front 67

What are the signs and symptoms of actue acetominophen toxicity?

Back 67

NV, anorexia, abdominal pain, hepatic necrosis, possible kidney necrosis, and severe hypoglycemia.