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Pharm > NSAIDs > Flashcards

NSAIDs Flashcards

1
Q

what does inflammation/pain occur due to?

A

Immune response to injury, infection, and disease processes

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2
Q

What is pain and inflammation regulated by?

A

cytokines and eicosanoids

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3
Q

what do prostaglandins regulate?

A

inflammation and pain response

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4
Q

Role of Eicosanoids:

A
  • Pain
  • Inflammation
  • Fever
  • Thrombus
  • Normal Gastric fx
  • Normal Kidney fx
  • Vascular/Respiratory Regulation
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5
Q

Eicosanoid involvement in kidney disease

A

PGEs are beneficial & helps maintain fx

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6
Q

Eicosanoid involvement in circulatory disease

A

TBXs involved in coagulation cascade

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7
Q

Eicosanoid involvement in heart disease

A

PGEs believed to be involved in atherosclerosis

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8
Q

Eicosanoids Involvement in Cancer

A

certain eicosanoids involved in the development of Colon and other GI tract cancers

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9
Q

Eicosanoids Involvement in Alzheimer’s disease

A

some evidence that chronic inflammation mediated by eicosanoids may be involved in the pathogenesis of this disease

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10
Q

Eicosanoids involvement in uterine disease

A

PGEs involved in dysmenorrhea and child
birth

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11
Q

Eicosanoids Involvement in lung disease

A

Leukotrienes involved in airway constriction
in asthma (NSAIDS have no effect on Leukotrienes)

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12
Q

How is peripheral pain and inflammation treated?

A
  • By blocking prostaglandin PGE production
  • Aspirin and all NSAIDs inhibit Cox enzyme
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13
Q

Two COX isoforms

A

COX-1 (normal function) and COX -2
(emergency)

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14
Q

COX 1

A

specific to the mucosa of gut (stomach) and kidney
 involved in protective layer in the stomach — protects against ulcers
 involved in glomerular filtration— kidney function

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15
Q

COX 2

A

involved in pain, inflammation and fever

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16
Q

COX 2 Specific Inhibitors

A
  • Relatively new
     Celecoxib (Celebrex), Rofecoxib (Vioxx) & Valdecoxib (Bextra):
     Analgesic, anti-pyretic, anti-inflammatory effects, but fewer GI and kidney side effects
     Interferes with ACE-inhibitors, diuretics, warfarin, and lithium
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17
Q

COX-2 inhibitors may….

A

increase clotting and increase HTN and cardiac issues

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18
Q

Uses of NSAIDs

A
  • Mild to moderate pain: ideal for pain from minor sx, musculoskeletal injury, menstruation or simple HA
  • inflammation
  • antipyretic (fever)
  • vascular disorders and prophylaxis of blood clot: inhibition of thromboxanes reduces platelet activation
  • prevention of cancer
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19
Q

How is aspirin unique compared to other NSAIDs

A
  • it irreversibly inhibits platelet aggregation (used in low doses after MI/CVA)
20
Q

Other benefits of aspirin

A
  • anti inflammatory
  • analgesic (mild to mod)
  • anti pyretic
  • not given to children due to Rye’s syndrome
21
Q

What is the #1 problem with conventional NSAIDs

A
  • Gastric Discomfort
     “enteric coating” and co-medication with antacid only marginally successful in preventing dysfunction
     PGEs promote mucous production
     Ulcer (peptic or duodenal) may result (long term use not recommended)
22
Q

What is the #1 problem with conventional NSAIDs

A
  • Gastric Discomfort
     “enteric coating” and co-medication with antacid only marginally successful in preventing dysfunction
     PGEs promote mucous production
     Ulcer (peptic or duodenal) may result (long term use not recommended)
23
Q

Other side effects of NSAIDs

A

 Acute nephritis (in patients with renal disease or who are dehydrated or in shock)
 Reye’s Syndrome: in children (including teens) w/ fever, may exacerbate fever (multiple NSAIDS)  CV shock in people w/ hypersensitivity (Aspirin)
 May prolong healing: inhibits connective tissue remodeling

24
Q

Pain killers taken off the market

A
  • Vioxx
  • Bextra
  • Both COX-2 inhibitors
  • Lead to drugs being required to state the adverse effects on the box cover and include a warning about the risks associated with the entire class of drugs
25
Q

Black Box Warning

A

 Since 2005 the FDA advised manufacturers of
several common pain killers that their labeling would have to include a so-called “black-box warning”
 This warning is to alert patients about the
increased risks of heart attacks and ischemic strokes for patients taking these medications

26
Q

Drugs with black box warnings

A

 Ibuprofen,
 Indomethacin
 Ketoprofen
 Fenoprofen
 Naproxen
 Diclofenac
 Celebrex

27
Q

What is indomethacin useful in treating?

A

 RA and JRA
 Anklosing Spondylitis
 Gout
 OA of hips
 Heterotopic ossification

28
Q

Side effects of indomethacin

A

same as other NSAIDs but somewhat more frequent

29
Q

Analgesic AND antipyretic effects =

A

NSAIDs

30
Q

Does acetaminophen have anti-inflammatory effect?

A

NOPE
also doesnt have anti-coagulant effects

31
Q

Acetaminophen is NOT associated with…

A

GI tract irritation or upset, Reye’s syndrome or kidney toxicity
** Now recommended by Rheumaology Associations for OA

32
Q

What can acetaminophen be toxic to?

A

the liver
- can cause liver necrosis

33
Q

acetaminophen MOA

A

 Not clear – weakly inhibits COX enzyme blocking
prostaglandin release, but appears to work more in CNS, not peripher

34
Q

What is RA

A

 A chronic, systemic, auto-immune disease
 Involves multiple systems, but characterized by
synovitis and destruction of articular tissue
 Pain, stiffness, inflammation of synovial joints
 Marked by exacerbation & remission
 Progressive: leading to severe joint destruction and erosion

35
Q

Difference between RA and OA

A

RA is bilateral and typically effects hips and hands

36
Q

Immune System and RA

A

 Autoimmune response to unknown antigen (virus or susceptible genetic trait)
 The antibodies are produced against antigens in
connective tissue
 Macrophages, T and B-lymphocytes involved

37
Q

Arthrogenic Mediators

A

 cytokines (growth factors, interleukins)
 eicosanoids (prostaglandins, leukotrienes)
 enzymes (protease and collagenase)

38
Q

Pathophysiology of RA

A

 Athrogenic mediators result in articular cartilage & bone destruction: cytokines, eicosanoids, collagenases and proteases

39
Q

pathophysiology of RA - cytokines

A

overgrowth of synovium

40
Q

pathophysiology of RA - Eicosanoids

A

pain, swelling, chemo- attraction, increase blood
flow and vascular permeability

41
Q

Pathophysiology of RA - collagenases and proteases

A

destroy cartilage and bone

42
Q

Goals of Drug therapy

A
  1. Decrease Pain - this is done by decreasing overall joint inflammation
  2. Arrest the disease process - (arrest or prevent physical deformities) - this is accomplished only through the disease modifying anti- rheumatic drugs (DMARDs)
    *** however, few of the agents currently available halt the disease process
43
Q

How Drugs are Used for RA:

A
  1. Staged control of pain and disease progression
  2. NSAIDs are used exclusively for mild symptoms
  3. Glucocorticoids are only used: to control acute exacerbation, local injection of a severe joint, severe/progressive form of RA
  4. DMARDs are used independently or together
  5. Most common is methotrexate in combination with a TNF inhibitor
44
Q

Upside down drug pyramid for RA

A

DMARDs, COX 2, NSAIDs
anti-metabolites
glucocorticoids

45
Q

Osteoarthritis

A

 Intrinsic defect in the cartilage or secondary to
a trauma or overuse
 Primary: no apparent cause
 Secondary: trauma, infection, metabolic dx
 Typically occurs in larger joints, but also in DIP
of fingers
 Genetic component and associated with obesity

46
Q

NSAIDs vs Acetaminophen in OA

A

Inflammation is not a primary concern in
OA
 NSAIDS may have a slight benefit for the
small inflammatory component of OA, but this may be over-shadowed by GI problems
 Acetaminophen is better tolerated and
produces the same analgesic effect

47
Q

Viscosupplementation for OA

A
  • Goal: change consistency of synovial fluid
  • Hyaluronan: increases synovial joint fluid consistency and limits progression of erosion

Pharm (12 decks)

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