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Musculoskeletal Exam 1 > Pharmacology - Anti Inflammatory Drugs > Flashcards

Pharmacology - Anti Inflammatory Drugs Flashcards

1
Q

What are the 4 class of anti-inflammatory drugs?

A

1) Corticosteroids
2) Topical Agents
3) NSAIDs
4) Monoclonal Antibodies

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2
Q

Cortisol is responsible for the redistribution of what?

A

Neutrophils (moves to plasma and then can’t get out), lymphocytes, monocytes, eosinophils, and basophils

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3
Q

What does cortisol cause a decrease in the release from macrophages?

A

Decreases release of TNFa, IL1, metalloproteinase, and plasminogen factor

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4
Q

What does cortisol cause a decrease in synthesis of?

A
  • A decrease in synthesis of prostaglandins, leukotrienes, thromboxane, and histamines from mast cells.
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5
Q

What Cox does cortisol decrease the expression of?

A
  • It decreases the expression of COX2
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6
Q

What are 4 synthetic corticosteroids?

A

1) Prednisone
2) Triamcinolone
3) Dextametasone
4) Fludrocortisone

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7
Q

How are synthetic corticosteroids different from natural corticosteroids?

A
  • Higher affinity for mineral corticoids and glucocorticoid receptors
  • Protein binding affinity, rate of elimination, and metabolic products.
    Basically it prolongs it
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8
Q

What corticosteroid has the highest salt-retaining activity and is essentially equivalent to aldosterone?

A
  • Fludrocortisone
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9
Q

What drugs have the highest anti inflammatory activity?

A
  • Betamethasone, Desamethasone, and Fludrocortisone.
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10
Q

What are the clinical indication for use of corticosteroids?

A
  • Arthritis (Osteoarthritis, Rheumatoid arthritis, and Psoriatic arthritis)
  • Bursitis and tenosynovitis
  • Asthma
  • Temporal arteritis (Giant cell arteritis)
  • Dermatitis
  • Inflammatory bowel disease (chrohn’s and UC)
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11
Q

What are the adverse effects of corticosteroids?

What are some contraindication?

A
  • Na+ retention and hypertension.
  • Hypokalemia
  • Osteoporosis
  • Infections
  • Hyperglycemia, glycosuria, and peptic ulcers
  • Contraindications: peptic ulcers, hypertension, osteoporosis, and heart failure
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12
Q

Why is use of glucocosteroids assist in infection spread?

A
  • due to immune system supression.
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13
Q

Why do NSAIDs cause kidney failure?

A
  • Because of lower levels of prostacyclin in the afferent arterioles.
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14
Q

What 3 classes to NSAIDs fall into?

A
  • Anti-inflammatory, anti-pyretic, and analgesics
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15
Q

What are some adverse affects with long term NSAID use.

A

-Increase in bleeding time, dyspepsia, subepithelial damage and hemorrhage, GASTRIC MUCOSAL EROSION, FRANK ULCERATION, and GASTRIC MUCOSAL NECROSIS

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16
Q

What is NSAIDs effects on the blood vessels?

A
  • decrease the blood vessels’ sensitivity to bradykinin and histamine
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17
Q

What are the 3 traditional classifications of NSAIDs

A
  • Aspirin and other traditional NSAIDs
  • Acetaminophen
  • COX2 - selective
18
Q

In the Mode of action for Aspirin, what is irreversible inhibited and what does that lead to?

A
  • COX1 and COX2 are irreversible inhibited leading to inhibition of prostaglandins, thromboxanes, and prostacyclins.
19
Q

In the mode of action of aspirin what effect is there on energy production?

A

decrease in NADPH oxidase which is responsible for neutrophil oxidative burst (aka energy to engulf stuff)

20
Q

Aspirin inhibition of this leads to increased aspirin-triggered lipoxins?

A

-COX2

21
Q

What are aspirins clinical uses?

A
  • decreases incidence of transient ischemic attacks
  • unstable angina and coronary artery thrombosis
  • ANALGESIC: synergistic with opioids and has been used in combination with morphine, etc. against cancer pain.
22
Q

What are some adverse effects of Aspirin use?

A
  • AIRWAY HYPERACTIVITY in asthmatic patients. Susceptible patients may also be reactive to indomethacin, naproxen, mefenamate, and phenylbutazone.
  • REYE syndrome: may affect certain children under a certain age.
23
Q

What NSAIDs are members of the propionic acid derivatives?

A

-IBUPROFEN, naproxen, ketoprofen, flurbiprofen

24
Q

What are some clinical uses for propionic acid derivatives?

A
  • Ibuprofen for arthritis

- a. spondylitis, gout, primary dysmenorrhea

25
Q

Why would naproxen be favored over aspirin?

A
  • Naproxen has a half-life 20x greater than aspirin. **
  • Naproxen directly inhibits leukocyte function
  • Causes less severe adverse effects than aspirin.
26
Q

What are members of the acetic acid derivative class of NSAIDs?

A

INDOMETHACIN, sulindac, etodolac, diclofenac, and ketorolac

27
Q

What is the mode of action of acetic acid derivatives?

A
  • decreases the availability of arachidonic acid in addition to COX inhibition–> other eicosanoids are affected
28
Q

What is Indometacin a direct inhibitor of. What is its clinical use?

A
  • direct inhibitor of neutrophil motility***, but is less tolerated.
  • Used in promoting closure of patent ductus arteriosus.***
29
Q

What is Diclofenac mode of action? What is its main clinical use?

A
  • decreases intrcellular concentration of arachidonic acid

- used widely in renal stone-associated pain

30
Q

What is Ketorolac’s main clinical use?

A
  • Strong analgesic properties, used in post-surgical patients.
31
Q

What drugs are part of Fenamate derivatives?
What does it antagonize?
Compare it to aspirin?
What are it’s uses?

A
  • mefenamate and meclofenamate
  • Antagonize prostanoid receptors
  • Less anti-inflammatory activity and higher adverse effects than aspirin
  • Mefenamate- primary dysmenorrhea
  • Meclofenamate - used for arthritis
32
Q

What is piroxicam’s clinical use?

What does it inhibit?

A
  • As efficacious as aspirin, naproxen, and ibuprofen against arthritis and is tolerated better.
  • Inhibits collagenase, proteoglycanase, and oxidative burst
33
Q

What is the use of Nabumetone?

A
  • A prodrug that is more selective for COX2 and has less GI disturbances
34
Q

What is the difference of Acetaminophen and other NSAID?

A
  • unlike other NSAIDS acetaminophen is devoid of anti-inflammatory activity, but has a lower toxicity profile.
35
Q

What is acetaminophen’s clinical efficacy?

A

Comparable analgesic and antipyretic effects as other NSAIDs

36
Q

What type of toxicity might result from acetaminophen overuse?

A

May cause kidney and liver toxicities. The CYP 2E1 and CYP3A4 mediate toxicity via release of N-Acetyl-benzoquinone imine.

37
Q

What is Celecoxib’s efficacy in treating clinical issues?

A
  • similar efficacy in treating osteoarthritis, rheumatoid arthritis, primary dysmenorrhea but causes less GI side effects than other NSAIDs.
  • also approved for familial adenomatous polyposis
38
Q

What are the toxicity dangers from celecoxib?

A
  • Higher risk of cardiovascular toxicity (heart attack and stroke)** than other NSAIDS
39
Q

Name 3 types of drugs that are antibodies against TNFa?

A
  • Adalimumab (RA)***, Etanercept (RA and psoriatic arthritis), and Infliximab (RA, UC, and Crohn’s, ankylosing spondylitis, and psoriatic arthritis). They work by suppressing IL-1, IL-6, and adhesion molecules involved in leukocytes migration (lymphoma risk)
40
Q

What is the MOA and the clinical use of Abatacept?

A
  • blocks T-cell activation with subsequence decrease in TNFa. It is approved for use in patient with sever resistant rheumatoid arthritis.
41
Q

Glance over D-F

A

s

42
Q

If patient has ankylosing spondylitis what treaments are available?

A

Short term - prostaglandin

Long term - Don’t use corticosteroids

Musculoskeletal Exam 1 (11 decks)

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