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Host And Defense - Exam 3 > Smith - Prostanoids And Anti-Inflammatory Drugs > Flashcards

Smith - Prostanoids And Anti-Inflammatory Drugs Flashcards

1
Q

Acute inflammation is what?

A

Body’s normal protective response to an injury, irritation, or even surgery

Protective response

Eliminate initial cause of cell injury, clear out necrotic cells and damaged tissues

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2
Q

What are 5 signs of acute inflammation?

LPHaRTS

A

Loss of function

Pain

Heat

Redness

Tenderness

Swelling

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3
Q

What are some non-selective NSAIDS?

A

Aspirin
Ibuprofen
Acetominophen
Naproxen

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4
Q

What are NSAIDS?

A

Nonsteroidal anti-inflammatory drugs

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5
Q

What do NSAIDS do?

A

Inhibit cyclooxygenase enzymes

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6
Q

What is an example of a selective NSAID?

A

COX2 - Celecoxib

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7
Q

What are glucocorticoids?

A

Inhibit phospholipase A2

  • Prednisone
  • Cortisone
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8
Q

What are DMARDs?

A

Disease modifying anti-rheumatic drugs

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9
Q

What are the 2 types of DMARDs?

A

Traditional (non-biologic)

Biologic

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10
Q

Where do a lot of our inflammatory mediators originate from?

A

Breakdown of arachidonic acid

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11
Q

T/F - Glucocorticoids affect the pain process flow at a higher level than the NSAIDS target.

A

TRUE

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12
Q

What are eicosanoids?

A

Oxygenation products of poly-unsaturated long-chain FAs

  • G-coupled proteins
  • Auto and paracrine fxs
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13
Q

What are prostanoids?

A

Sub-class of eicosanoids

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14
Q

What are 3 prostanoids?

A

Prostaglandins
-Mediate inflammatory and anaphylactic rxns

Thromboxanes
-Mediate vasoconstriction

Prostacyclins
-Active in resolution phase of inflammation

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15
Q

Prostanoids have major effects on what?

A

Smooth muscle

Platelets and blood cells

Nerve terminals

Endocrine organs

Adipose tissue

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16
Q

Aspirin and other NSAIDs provide non-specific ___________ of the cyclooxygenase (COX) enzymes.

A

Inhibition

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17
Q

T/F - Non-selective COX inhibitors have both positive (anti-inflammatory) and adverse effects (upset stomach)

A

TRUE

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18
Q

Tell me about COX-1.

A

Constitutive (platelets, kidney, GI)

Inhibition by classic NSAIDS increases risk for GI ulceration

19
Q

Tell me about COX-2.

A

Constitutive in kidney
-Inducible elsewhere by hormones, GFs, and inflammatory mediators

Inhibition by NSAIDs or by selective Coxibs

COX-2 selective inhibitors do NOT inhibit platelet aggregation or cause GI upset/ulceration

20
Q

Tell me about Aspirin.

A

Only NSAID that inhibits both COXs in an IRREVERSIBLE manner

21
Q

Tell me more about Aspirin.

A

Nonselective COX-1 and COX-2 inhibition

Anti-platelet aggregation effects

Rarely used for anti-inflammatory purposes (Dose for those effects is way too high)

22
Q

What are contraindications of Aspirin?

A

NSAID allergies

Avoid children with viral-induced illness (REYE SYNDROME)

Gout, hemophilia, blood thinners, ACE inhibitors, pregnancy near term

23
Q

Tell me about Ibuprofen.

A

Analgesic and antipyretic and antinflammatory

Interferes with the antiplatelet effect of low-dose aspirin

24
Q

Tell me about Naproxen.

A

Same as most other NSAIDs, but available in slow-release formulation (Aleve)

25
Q

When does a fever get to be too high?

A

103 degrees F

26
Q

What are some adverse effects common to all NSAIDs?

A 
CNS - headache
Cardiovascular - Edema
*GI - Pain, dysplasia, nausea, vomiting, ulcers, bleeding
Hematologic
Hepatic
Pulmonary - asthma
Skin - rashes
Renal insufficiency
REYE SYNDROME
27
Q

Tell me about Celecoxib (Celebrex).

A

COX-2 selective inhibitor

Analgesic, antipyretic, and anti-inflammatory, like Aspirin

No effect on platelet aggregation

10-20x more selective for COX-2 than COX-1

  • Lower GI adverse effects
  • No cardioprotective effects
  • Increased risk of edema, hypertension, MI, and stroke
28
Q

Tell me about acetaminophen (Tylenol).

A

NON-ASPIRIN pain reliever
-Central-action effect on hypothalamus to cause vasodilation and sweating (reduces fever)
—Analgesic mechanism thru elevation of the pain threshold

29
Q

Tell me more about acetaminophen.

A

Alternative to NSAIDs in pts with allergies, ulcers, bleeding problems, or taking blood thinners (warfarin)

Adverse effects
-Rash, chest pain, bone marrow suppression
—Contraindicated for pts with liver disease and insufficiency due to alcoholism

30
Q

T/F - Acetaminophen is NOT an NSAID.

A

TRUE

31
Q

T/F - Acetominophen should NOT be taken as an anti-inflammatory drug.

A

TRUE

32
Q

Tell me about glucocorticoids.

A

Steroid hormones

Prevents conversion of membrane phospholipids to arachidonic acid by inhibiting the phospholipase A2 enzyme
-Decrease inflammation

33
Q

What are the short to medium-acting glucocorticoids? 3 of them

A

Hydrocortisone

Cortisone

Prednisone

34
Q

What is the long-acting glucocorticoid?

A

Dexamethasone

35
Q

What is a major side effect of overdosing on acetominophen?

A

Hepatotoxicity

-Days->weeks->liver failure->death

36
Q

Tell me about prednisone.

A

Blocks phospholipase A2, and thus shuts down immune responses

Used for

  • Asthma
  • COPD
  • Crohn’s
37
Q

Tell me about non-biologic DMARDs

A

Suppress the progression of the disease by acting against the underlying immunological abnormalities

38
Q

What are 2 non-biologic DMARDs?

A

Methotrexate

Azathioprine

39
Q

What are the main adverse effects of glucocortcoid use?

A

Bone weakening

Skin thinning

Heart risks

Cataracts and glaucoma

40
Q

What is the 1st line DMARD for rheumatoid arthritis?

A

Methotrexate

Inhibits transformylase and thymidylate synthetase enzymes

Adverse:
-Nausea, GI ulcers, stomatitis, hepatotoxicity
—CONTRAINDICATED IN PREGNANCY
—RISK OF LIFE-THREATENING EFFECTS IF TAKING NSAIDS SUCH AS ASPIRIN, NAPROXEN, OR OTHER SALICYLATES.

41
Q

Tell me about azathioprine.

A

PRODRUG that acts thru main metabolite, 6-thioguanine
-Suppresses DNA synthesis and production of rapidly proliferating cells (B and T cell fxs)

Used for:
-rheumatoid arthritis

Adverse:
-Bone marrow suppression, GI upset, increased infection risk, increased lymphoma risk

42
Q

Tell me what the two biologic DMARDs are. (Larger molecules than non-biologics).

A

Proteins produced by recombinant DNA tech:

-T-Cell modulators
—Abatacept

  • TNFalpha-blocking agents
  • Adalimumab
43
Q

Tell me about abatacept.

A

Acts as fusion protein to prevent activation of T-cells

Use:
-Rheumatoid arthritis for those that are not responding well to anti-TNFalpha therapy

Adverse:
-Increased risk of lymphomas, infections, congestive heart failure, lupus-like syndrome

MONTLY COST: $3500-$3800

44
Q

Tell me about adalimumab.

A

Prevents ligand from binding TNFalpha receptor

Use:
-Rheumatoid arthritis, psoriasis, refractory asthma

Adverse:
-Increased risk of lymphomas, infections, lupus-like syndrome

5 different TNFalpha inhibitors

  • Infliximab
  • Adalimumab
  • Certolizumab pegol
  • Golimumab
  • Etanercept (This one is a circulating receptor fusion protein)

Host And Defense - Exam 3 (15 decks)

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