Chapter 44: Anti-inflammatory and antigout drugs Flashcards Preview

Lilley: Pharmacology > Chapter 44: Anti-inflammatory and antigout drugs > Flashcards

Flashcards in Chapter 44: Anti-inflammatory and antigout drugs Deck (39)
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1
Q

salicylates

A

aspirin
diflunisal (Dolobid)
salsalate (Salistab)
choline salicylate (Arthropan)

2
Q

Acetic Acid Derivatives

A
diclofenac sodium (Voltaren)
indomethacin (Indocin)
sulindac (Clinoril)
tolmetin (Tolectin)
etodolac (Lodine)
ketorolac (Toradol)
meclofenamate (generic only)
mefenamic acid (Ponstel)
3
Q

Cyclooxygenase-2 Inhibitors

A

celecoxib (Celebrex)

4
Q

Enolic Acid Derivatives

A

nabumetone (Relafen)
meloxicam (Mobic)
piroxicam (Feldene)

5
Q

Propionic Acid Derivatives

A
fenoprofen (Nalfon)
flurbiprofen (Ansaid)
ibuprofen (Motrin, Advil, others)
ketoprofen (Orudis KT)
naproxen (Naprosyn, Aleve)
oxaprozin (Daypro)
6
Q

NSAIDs: FDA-APPROVED

INDICATIONS

A
  • Acute gout
  • Acute gouty arthritis
  • Ankylosing spondylitis
  • Bursitis
  • Fever
  • Juvenile rheumatoid arthritis
  • Mild to moderate pain
  • Osteoarthritis
  • Primary dysmenorrhea
  • Rheumatoid arthritis
  • Tendinitis
  • Various ophthalmic uses
7
Q

NSAIDs relieve pain, headache, and inflammation by

A

blocking
the chemical activity of the enzyme called cyclooxygenase
(COX).

8
Q

This greater enzyme specificity of the COX-2

inhibitors allows for the

A

beneficial antiinflammatory effects
while reducing the prevalence of adverse effects associated with
the nonspecific NSAIDs, such as gastrointestinal ulceration

9
Q

The leukotriene pathway is

A

inhibited by some antiinflammatory

drugs, but not by salicylates.

10
Q

All NSAIDs can be…

A

ulcerogenic and induce gastrointestinal

bleeding due to their activity against tissue COX-1.

11
Q

Aspirin has the unique property

A

irreversible inhibitor of COX-1
receptors within the platelets themselves…

reduced formation of thromboxane A2, a substance that normally
promotes platelet aggregation

12
Q

NSAIDs

are sometimes combined with an opioid

A

They tend to have an opioid-sparing effect when given together
with opioids, because the drugs attack pain using two different
mechanisms. This often allows less opioids to be used

13
Q

NSAIDs show a ceiling effect

A

limits their effectiveness;
that is, any further increase in the dosage beyond a certain
level increases the risk for adverse effects without a corresponding
increase in the therapeutic effect

14
Q

Contraindications to NSAIDs

A

Contraindications to NSAIDs include known drug allergy and
conditions that place the patient at risk for bleeding, such as rhinitis
(risk for epistaxis [nosebleed]), vitamin K deficiency, and
peptic ulcer disease. Patients with documented aspirin allergy
must not receive NSAIDs.

15
Q

adverse effects of the NSAIDs is their effect

on the gastrointestinal tract

A

Symptoms can range from mild
symptoms such as heartburn to the most severe gastrointestinal
complication, gastrointestinal bleeding. Most fatalities associated
with NSAID use are related to gastrointestinal bleeding.

16
Q

black box warning per wilkipedia

A

It is the strongest warning that the FDA requires, and signifies that medical studies indicate that the drug carries a significant risk of serious or even life-threatening adverse effects

17
Q

The drug

misoprostol (Cytotec)

A

has proved successful
in preventing the gastric ulcers and hence gastrointestinal
bleeding that can occur in patients receiving NSAIDs. Misoprostol
is a synthetic prostaglandin E1 analogue that inhibits
gastric acid secretion and also has a cytoprotective component

18
Q

NSAIDs can compromise existing renal function

A

Renal toxicity
can occur in patients who are dehydrated, those with heart failure
or liver dysfunction, and those taking diuretics or angiotensin-
converting enzyme inhibitors.

19
Q

NSAIDs: ADVERSE EFFECTS

A

Cardiovascular
Moderate to severe noncardiogenic pulmonary edema
Gastrointestinal Dyspepsia, heartburn, epigastric distress, nausea, vomiting, anorexia, abdominal pain, gastrointestinal bleeding, mucosal lesions (erosions or ulcerations)
Hematologic Altered hemostasis through effects on platelet function
Hepatic Acute reversible hepatotoxicity
Renal Reduction in creatinine clearance, acute tubular
necrosis with renal failure
Other Skin eruption, sensitivity reactions, tinnitus, hearing
loss

20
Q

salicylism

A

Salicylate toxicity, usually from aspirin

Chronic salicylate intoxication is also
known as salicylism and results from either short-term administration
of high dosages or prolonged therapy with high or even
lower dosages

21
Q

ACUTE OR CHRONIC
SALICYLATE INTOXICATION:
SIGNS AND SYMPTOMS

A

Cardiovascular Increased heart rate
Central nervous Tinnitus, hearing loss, dimness of vision, headache,
dizziness, mental confusion, lassitude,
drowsiness
Gastrointestinal Nausea, vomiting, diarrhea
Metabolic Sweating, thirst, hyperventilation, hypoglycemia
or hyperglycemia

22
Q

The most common manifestations of chronic salicylate

intoxication in adults

A

tinnitus and hearing loss.

children are hyperventilation and central nervous system
(CNS) effects such as dizziness, drowsiness, and behavioral
changes.

23
Q
  • Little or no toxicity: less than 150 mg/kg
  • Mild to moderate toxicity: 150 to 300 mg/kg
  • Severe toxicity: 300 to 500 mg/kg
  • Life-threatening toxicity: over 500 mg/kg
A

A serum salicylate concentration measured 6 hours or
longer after the ingestion may be used in conjunction with the
Done nomogram to estimate the severity of intoxication and
help guide treatment

24
Q

NSAID-induced

hyperkalemia or hyponatremia can also occur.

A

pg 711 ?

25
Q

Ketorolac (Toradol) is somewhat unique

A

some antiinflammatory activity, it is used primarily
for its powerful analgesic effects

indicated for short-term use (up to 5 days)
because of its potential adverse effects
on the kidney and gastrointestinal tract.

26
Q

Celecoxib (Celebrex) was the first COX-2 inhibitor and is the
only one remaining on the market

A

indicated for the treatment
of osteoarthritis, rheumatoid arthritis, acute pain symptoms,
ankylosing spondylitis, and primary dysmenorrhea

27
Q

Gout is caused by the

A

overproduction of uric acid or decreased
uric acid excretion, or both. This overproduction and/or
decreased excretion can often result in hyperuricemia (too
much uric acid in the blood).

28
Q

allopurinol (Zyloprim)

A

relief of gout is the inhibition of the enzyme xanthine oxidase, which thereby prevents uric acid production

purine (DNA/RNA) (DIET) metabolizes…… hypoxanthine
to xanthine and eventually to uric acid.

29
Q

assess and document the duration, onset,
location, and type of inflammation and/or pain the patient
is experiencing as well as any precipitating, exacerbating, or relieving factors.

A

With aspirin, NSAIDs, other antiinflammatory drugs, and

antigout drugs,

30
Q

aspirin triad

A

includes asthma, nasal
polyps, and rhinitis. These conditions are considered to put the
patient at risk for reactions to aspirin

31
Q

allopurinol, assess the integrity of the

skin due to

A

potentially life-threatening skin adverse effects of
exfoliative dermatitis, Stevens-Johnson syndrome, and toxic
epidermal necrolysis. Assess blood counts because of the potential
for aplastic anemia and agranulocytosis

32
Q

NURSING DIAGNOSES pg 716

A
  1. Acute pain related to the disease process or injury to joints
    and other disease-affected areas
  2. Deficient knowledge related to first-time drug therapy for
    treatment of a disease process
  3. Risk for injury related to the effects of the disease and treatment
    on mobility and the performance of ADLs
33
Q

To reduce the risk for

Reye’s syndrome,

A

aspirin or medications that contain aspirin must not be given
to children or teenagers to treat viral illnesses or fever.

34
Q

Some changes noted in elderly patients that effect drug treatment include

A

changes in renal elimination, protein binding, body composition, drug distribution,
drug clearance, and sensitivity to drugs, as well as an increased incidence
of adverse reactions to all types of medications.

35
Q

NSAIDs work by blocking

A

cyclooxygenase, the enzyme responsible for conversion of arachidonic acid into prostaglandins. Decreasing the synthesis of prostaglandins results in decreased pain and inflammation.

36
Q

When teaching a patient about potential side effects of NSAID therapy, the nurse will teach the patient to promptly report which effect?

A

A major side effect of NSAID therapy is gastrointestinal (GI) distress with potential GI bleeding. Black tarry stools are indicative of a GI bleed.

37
Q

The nurse is administering probenecid (Benemid) to a patient with recurrent strep throat. The nurse teaches the patient that the most likely reason for taking this medication is to

A

Besides its use for the treatment of the hyperuricemia associated with gout and gouty arthritis, probenecid also has the ability to delay the renal excretion of penicillin, thus increasing serum levels of penicillin and prolonging its effect.

38
Q

The nurse assesses for therapeutic effects of colchicine based on knowledge that colchicine

A

Colchicine works by decreasing the mobility and migration of leukocytes into joints affected by gout, thus resulting in decreased inflammation.

Colchicine is administered on an hourly basis until pain is resolved or the patient develops diarrhea. Hemorrhagic colitis is a potential life-threatening side effect of colchicine.

39
Q

Patient teaching for a patient receiving allopurinol (Zyloprim) should include which information?

A

Patients taking allopurinol should be informed to increase fluid intake to 3 L per day, avoid hazardous activities if dizziness or drowsiness occurs with the medication, and avoid the use of alcohol and caffeine because these drugs will increase uric acid levels and decrease the levels of allopurinol.