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Pharmacology Exam 4 > 56 - NSAIDs and Gout > Flashcards

56 - NSAIDs and Gout Flashcards

1
Q

When does inflammation occur?

A

Occurs when immunologically competent cells are activated in response to injurious or noxious stimulus (foreign organisms, antigenic substances, physical injury, etc)

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2
Q

Is inflammation beneficial or deleterious?

A

BOTH - May be beneficial (healing, essential for survival) or deleterious (asthma, rheumatoid arthritis)

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3
Q

What are the classic inflammatory symptoms?

A

REDNESS (rubor)
SWELLING (tumor)
HEAT (calor)
PAIN (dolor)

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4
Q

What cellular and molecular changes do we see during inflammation?

A
  • Transient local vasodilation
  • Increased capillary permeability with exudation
  • Activation of numerous molecular inflammatory mediators
  • Increased stimulation of mast cells
  • Infiltration of leukocytes
  • Activation of phagocytosis
  • Tissue degeneration and fibrosis
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5
Q

What molecular inflammatory mediators will we see?

A
  • Kinins (bradykinin)
  • Neuropeptides (substance P)
  • Vasoactive amines (histamine, 5HT)
  • Arachodonic acid metabolites (cyclooxygenase (prostaglandin, thromboxanes, prostacyclin) and lipoxins and leukotrienes)
  • Cytokines (TNF-alpha)
  • Oxygen free radicals
  • Proteases
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6
Q

What is the general therapeutic strategy of inflammation

A
  • Relief of pain

- Delay or arrest of disease process

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7
Q

What are the typical pharmacologic approaches to inflammation?

A
  • NSAIDs***
  • Glucocorticoids
  • DMARDS
  • Opioids and other analgesics
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8
Q

What are the functions of NSAIDs?

A
  • Analgesia (reduce pain)
  • Antipyretic (reduce fever)
  • Anti-inflammatory
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9
Q

What is the primary target of NSAIDs?

A

Primary target: Prostaglandin production via cyclooxygenases COX-1 and COX-2

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10
Q

Is acetaminophen an NSAID?

A

Acetaminophen is NOT an NSAID

- It does have analgesic and antipyretic properties though

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11
Q

What are the “main players” of inflammatory prostaglandins?

A
  • PGE2

- PGI2

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12
Q

What is the function of PGE2 and PGI2 prostaglandins?

A
  • Increased edema and vascular permeability

- Modulation of lymphocyte function

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13
Q

What do the two COX isozymes do?

A

Convert arachidonic acid to prostaglandins

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14
Q

What are the two COX isozymes?

A

COX-1 and COX-2

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15
Q

What is the function of COX-1?

A
  • Constitutively active and expressed
  • Widely distributed in the body
  • “Housekeeping” function such as synthesizing prostaglandins in the stomach mucosa to protect the stomach lining from gastric acid
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16
Q

What is the function of COX-2?

A
  • Inducible in times of inflammation
  • Functions to produce inflammatory molecules
  • COX-2 is expressed in vascular endothelium (produces PGI2)
  • Renal COX-2 is essential for normal functioning
17
Q

What is the arachidonic acid pathway?

A

A pathway that begins with injury and exposure of cell membrane phospholipids which activates arachidonic acid and ends in two different inflammatory pathways

18
Q

What are the two inflammatory pathways?

A

Pathway 1

  • Airway inflammation
  • Asthma
  • Allergic rhinitis

Pathway 2

  • Inflammation
  • Pain
  • Fever
19
Q

What pathway do COX-1 and COX-2 work on?

A

The inflammation, pain and fever pathway

  • This is also the pathway that NSAIDs work on
  • NSAIDS work by inhibiting COX-1/2 and therefore inhibiting prostaglandin synthesis
20
Q

Reminder of what COX-1 and COX-2 are responsible for again…

A

COX-1

  • GI tract (gastric mucosa)
  • Constitutive
  • Protective

COX-2

  • Inducible
  • Inflammatory
21
Q

NSAIDs are either non-selective or selective. Which ones are in each category?

A

Non-selective

  • Acetylsalicylic Acid (Aspirin)
  • Ibuprofen
  • Indomethacin

COX-2 Selective
- Celecoxib

22
Q

What are the common clinical uses for NSAIDs?

A
  • Pain (analgesic)
  • Fever (antipyretic)
  • Inflammation (arthritis)
  • Antithrombotic
  • Miscellaneous uses
23
Q

Describe the use of NSAIDs for pain (analgesia)

A
  • mild to moderate pain

- alone or in combination (caffeine)

24
Q

Describe the use of NSAIDs for fever (antipyretic)

A
  • aspirin & other PG synthesis inhibitors NOT recommended as fever reducers in children or in viral diseases (acetaminophen can be used)
  • May be used in adults
25
Q

Describe the miscellaneous uses of NSAIDs

A
  • menstrual cramping
  • closure of a patent ductus arteriosus
  • myocardial infarction / stroke (antithrombotic)
  • prevention of colorectal cancer
  • Alzheimer’s disease
26
Q

What NSAID drug interactions exist?

A
  • Displacement of protein binding (pharmacokinetics)
  • Diuretics (makes the effect attenuated, amplified)
  • Anticoagulants (increases effect)
  • GI effects (upset, ulcer, bleeding)
27
Q

How do you decide which NSAIDs to prescribe?

A
  • All NSAIDs (including aspirin) have similar efficacies
  • Clinical use is differentiated based on toxicity and cost-effectiveness

Balance of efficacy, cost-effectiveness, safety and numerous personal factors (eg. other drugs taken, concurrent illness, compliance, insurance, etc.)

28
Q

Which NSAID is the best?

A

Trick question

  • No best NSAID for everyone
  • 1 or 2 best NSAIDs for each individual person
29
Q

What is gout?

A

Metabolic disease characterized by recurrent episodes of acute arthritis due to deposits of monosodium urate (uric acid crystals) in joints and cartilage

30
Q

What are the systemic effects of gout?

A
  • Inflammation results in granulocytic phagocytosis of the crystals
  • Low pH produced by leukocytes lead to increased uric acid crystallization
31
Q

What is gout usually associated with?

A

Usually associated with hyperuricemia – high serum levels of uric acid

32
Q

What causes gout?

A

Increased uric acid levels

Increased production

  • Metabolic imbalance (product of purine metabolism)
  • Increased dietary consumption of purine rich foods
  • Increased tissue destruction (CA chemotherapy

Or decreased excretion by the kidney

33
Q

What are the therapeutic goals of treating gout?

A

** Pain and inflammation control **

Also, terminate attack. prevent future attacks, low purine food diet and limited alcohol consumption

34
Q

What are the agents used to treat acute gout attacks?

A
  • Indomethacin

- Colchicine

35
Q

What are the four agents used prophylactively to prevent future gout attacks?

A

Xanthine oxidase inhibitors to reduce the PRODUCTION of uric acid

  • Allopurinol
  • Febuxostat

Urocosuric agents used to increase the renal EXCRETION of uric acid

  • Probenecid
  • Sulfinpyrazone

Pharmacology Exam 4 (8 decks)

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