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ATTH 5100 > Drugs To Treat Inflammation > Flashcards

Drugs To Treat Inflammation Flashcards

1
Q

What is acute inflammation?

A
  • rapid onset following injury
  • vascular: initial phase that leads to swelling and pain
  • cellular: cellular changes involving blood flow
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2
Q

What role does cryotherapy have with acute inflammation?

A

Does not completely stop inflammation, just helps to keep it under control (similar to what medications do)

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3
Q

What are the cardinal signs of acute inflammation?

A
  • swelling
  • heat
  • redness
  • altered function
  • pain
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4
Q

What are the signs of infection and not just inflammation?

A
  • redness is more prevalent (large areas of redness)
  • circle of redness or streaks of red going down the limb
  • growing redness
  • heat - excessively warm and red
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5
Q

What is chronic inflammation?

A
  • continued exposure to an offending element
  • activation of macrophages and lymphocytes
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6
Q

2 primary mediators of vasodilation:

A
  • histamine
  • bradykinin
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7
Q

Tissue damage activates ______ and causes release of ______ ______.

A
  • nociceptors
  • chemical mediators
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8
Q

Where is cyclooxygenase 1 (COX-1) found and what does it do?

A
  • found in virtually all tissues, significant in GI system
  • housekeeping functions
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9
Q

Where is cyclooxygenase 2 (COX-2) found and what does it do?

A
  • produced in the brain, kidneys, blood vessel walls
  • induced in inflammatory response
  • involved in maintaining normal functions
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10
Q

3 chemical mediators in the cyclooxygenase (COX) pathway:

A
  • thromboxane A2
  • prostacyclin (PGI2)
  • prostaglandins
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11
Q

What does thromboxane A2 do?

A
  • increases platelet aggregation
  • vasoconstriction
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12
Q

What does prostacyclin (PGI2) do?

A
  • decreases platelet aggregation
  • vasodilation
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13
Q

What does prostaglandins do during normal functions?

A
  • protects gastric mucosa
  • increases renal blood flow
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14
Q

What does prostaglandins do during the inflammatory response?

A
  • increase blood flow
  • produce erythema
  • initiate chemotaxis
  • mediate pain response
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15
Q

What are the 2 pathways created by arachidonic acid?

A
  • COX (prostaglandins, prostacyclin, thromboxane)
  • lipoxygenase (leukotrienes)
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16
Q

How does membrane-bound arachidonic acid turn into arachidonic acid?

A

With phospholipase A2

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17
Q

Anti-inflammatory drugs function to inhibit _____ ______ _______.

A

Arachidonic acid cascade

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18
Q

2 categories of anti-inflammatory drugs:

A
  • non-steroidal anti-inflammatory drugs (NSAIDs)
  • corticosteroids
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19
Q

Corticosteroids act at what point?

A

Phospholipase A2

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20
Q

NSAIDs inhibit at what point?

A

COX

21
Q

4 types/potential actions of anti-inflammatory drugs:

A
  • anti-inflammatory
  • anti-pyretic
  • analgesic
  • anti-platelet
22
Q

NSAIDs work to inhibit the _____ enzyme and decrease formation of ________ _______ metabolites. Decreased ______ production leads to anti-inflammatory effect.

A
  • COX
  • arachidonic acid
  • prostaglandin
23
Q

NSAIDs inhibit ______ and ______ synthesis.

A
  • prostaglandin
  • thromboxane
24
Q

NSAIDs affect pain pathway in 3 ways:

A
  • prostaglandin reduces activation at nociceptor neurons
  • decrease recruitment of leukocytes
  • NSAIDs in brain prevent prostaglandins, which cause pain
25
Q

Primary therapeutic effect of NSAIDs:

A
  • MSK pain/inflammation relief
  • less effective than opioid but fewer ADEs
  • coadministration of NSAID with opioid: reduce opioid dose needed
26
Q

Non MSK examples of therapeutic effects from NSAIDs:

A
  • menstrual pain is only hollow viscera pain treated successfully
  • NSAID plus antiemetic to treat migraine headache
  • Ketorolac can produce analgesia equivalent of morphine to treat diabetic neuralgia
27
Q

Describe the pharmacokinetics of NSAIDs:

A
  • absorption: reach plasma concentration in 2-3 hours (food/antacids may delay absorption - suggested due to gastric disruption)
  • distribution: sufficient CNS concentration to be effective
  • metabolism: first pass metabolism, reduced bioavailability
  • excretion: primarily renal excretion
28
Q

Indications for NSAIDs:

A
  • mild and moderate pain
  • fever
  • headaches
  • reduce swelling
  • inflammatory conditions
  • menstrual pain
  • arthritis
  • rheumatic conditions
29
Q

4 routes of administration for NSAIDs:

A
  • oral
  • topical
  • injection
  • rectal
30
Q

List some common NSAIDs:

A
  • aspirin and other salicylates
  • other non selective NSAIDs (ibuprofen, naproxen, diclofenac, ketorolac (Toradol))
  • COX-2 selective inhibitors (celecoxib (celebrex), Vioxx)
31
Q

Adverse effects of NSAIDs:

A
  • gastrointestinal
  • renal toxicity
  • cardiovascular
  • liver toxicity
32
Q

Describe possible GI symptoms from NSAIDs:

A
  • dark, tarry stools
  • indigestion
  • nausea, vomiting
  • abdominal pain
33
Q

How to minimize GI symptoms from NSAIDs:

A
  • take with food or milk
  • use of antacids, proton-pump inhibitors
  • enteric-coated aspirin
  • misoprostol: prostaglandin substitute
34
Q

Describe potential renal adverse effects from taking NSAIDs.

A
  • prostaglandins help regulate renal blood flow. Decreasing them can decrease renal blood flow, causing impaired kidney function
  • use with caution in elderly and patients with conditions such as heart failure and kidney disease
35
Q

Describe potential cardiovascular side effects of taking NSAIDs:

A
  • increased bleeding time (aspirin and non-selective COX inhibitors)
  • increased incidence of heart attack and stroke (selective COX-2 inhibitors)
36
Q

_______ toxicity has lower incidence with NSAID use than ______ toxicity.

A
  • liver
  • renal
37
Q

Drug interactions with NSAIDs:

A
  • aspirin and non selective NSAIDs with NSAIDs decrease effects of anti-hypertensive agents
  • ibuprofen interferes with the cardio protective effect of aspirin
  • agents that increase the risk of GI side effects
38
Q

Therapeutic guidelines for NSAIDs:

A
  • use the lowest dose for the shortest duration of therapy
  • selection of NSAID
  • avoid concomitant use with alcohol, aspirin or other salicylates, other NSAIDs, corticosteroids, anticoagulants.
  • take with food
39
Q

What is the risk of giving NSAIDs to kids

A
  • risk with kids getting Reye’s syndrome (can be fatal if not recognized) - reaction to aspirin in kids
  • do not give aspirin to kids (last choice is baby/children’s aspirin)
40
Q

Endogenous corticosteroids are produced by the _______ _____. An example of these are _________.

A
  • adrenal cortex
  • glucocorticoids
41
Q

After approximately 7 days of taking systemic corticosteroids (oral), what do you need to do stop taking them?

A

Need to wean them off because your body has stopped producing it

42
Q

What are the functions of exogenous corticosteroids?

A
  • inhibit inflammatory response to injury
  • suppress allergic disease by releasing histamine
  • large doses inhibit ACTH release from pituitary gland
43
Q

Mechanisms of action for corticosteroids:

A
  • lower leukocytes migration
  • reverse capillary permeability
  • inhibit factors of inflammatory response
  • decrease vasoactive factors; decrease fibroblast activity at site
  • diminish secretion of lipolytic and proteolytic enzymes
  • suppress vascular changes responsible for inflammation
44
Q

Indications for short-term use of corticosteroids:

A
  • pain
  • reduce swelling
  • inflammatory conditions
  • arthritis
  • rheumatic conditions
  • skin conditions
  • asthma
45
Q

Routes of administration for corticosteroids:

A
  • inhalation
  • topical (to avoid systemic effects of oral medication)
  • local injections
  • oral
  • intramuscular
46
Q

With corticosteroids, the greatest risks come with what routes of administration?

A
  • oral
  • injections (tendon and joints)
47
Q

Risk of multiple corticosteroid injections:

A

Can have degenerative impact on tissues, tendons, and joint surfaces

48
Q

Adverse effects of corticosteroids:

A
  • hypertension
  • increased blood glucose (short term impact is important for diabetics)
  • fat redistribution
  • osteoporosis
  • suppression of growth in children
  • myopathy
  • cataracts, glaucoma
  • CNS adverse effects
  • immunosuppressive
  • peptic ulcer disease (only with oral version)
  • agitation and irritability
  • sleepiness
  • weight gain
  • avascular necrosis or osteoporosis (esp. of femoral head)
49
Q

Therapeutic guidelines for corticosteroids:

A
  • use the lowest dose possible for the shortest duration of time
  • should be considered a bridge treatment
  • generally used when other interventions have been unsuccessful
  • do not abruptly discontinue corticosteroid

ATTH 5100 (13 decks)

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