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Quiz 6 (Anti Inflammatory) Flashcards

1
Q

Inflammation

A

Body’s response to injury

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2
Q

What is the purpose for inflammation?

A

Intended to be a protective mechanism

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3
Q

What are some clinical signs of inflammation? (3)

A
  1. Redness and heat
  2. Swelling and edema
  3. Pus
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4
Q

What can excessive or prolonged inflammation impair and cause?

A

can impair the healing process and cause pain to the animal

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5
Q

Corticosteroids

A

Hormones produced by the adrenal gland

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6
Q

What are the two types of cortico steroids produced?

A
  1. Mineralocorticoids

2. Glucocorticoid

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7
Q

What do Mineralocorticoids do?

A

regulate mineral levels in the body

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8
Q

what do Glucocorticoids do?

A

exert an anti-inflammatory effect, but also have many other effects in the body

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9
Q

How is the production of corticosteroid regulated?

A

Feedback inhibition mechanism

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10
Q

what are the biologic effects of glucocorticoids in the body?

A
  1. Decrease inflammation
  2. Inhibit scar tissue formation
  3. Suppress the body’s immune system
  4. Affect the cellular blood count
  5. Increase gastric acid secretion and decrease mucus production in GIT
  6. Increase protein breakdown
  7. Can induce parturition
  8. Increase blood glucose levels
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11
Q

What can an overuse of glucocorticoids lead to?

A

disease

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12
Q

How do glucocorticoid drugs differ?

A

Products currently used differ in duration of effect and dosage form available

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13
Q

What is the duration of the effect of short acting glucocorticoids?

What are some examples? (2)

A

biologic effect lasts < 12 hrs.

  1. hydrocortisone
  2. cortisone
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14
Q

What is the duration of the effect of intermediate-acting glucocorticoids?

What are some examples? (3)

A

effect lasts 12-36 hrs.

  1. prednisone (prednisolone)
  2. triamcinolone
  3. methylprednisolone
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15
Q

What is the duration of the effect of Long-acting glucocorticoids?

What are some examples? (3)

A

effect lasts more than 48 hrs.

  1. dexamethasone
  2. betamethasone
  3. flumethasone
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16
Q

What are the dosage forms available with glucocorticoids? (3)

A
  1. topical preparations
  2. oral
  3. injectable products
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17
Q

What are the glucocorticoid parenteral formulations? (3)

A
  1. Aqueous solutions

2. Alcohol solutions

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18
Q

How are aqueous glucocorticoid solutions made?

A

the glucocorticoid is combined with salt and dissolved in water

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19
Q

How are aqueous glucocorticoid solutions administered?

A

can be given in large doses intravenously w/ less risk of an adverse reaction

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20
Q

what are some examples of aqueous glucocorticoid solutions

A
  1. dexamethasone sodium phosphate (Azium),

2. prednisolone sodium succinate (Solu-Delta Cortef)

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21
Q

How are Alcohol glucocorticoid solutions made?

A

glucocorticoid is dissolved in alcohol

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22
Q

What happens when alcohol glucocorticoid solutions are administered IV?

A

adverse reaction

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23
Q

How are glucocorticoid Suspensions made?

A

the glucocorticoid is suspended in a liquid vehicle

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24
Q

What are some examples of glucocorticoids suspension?

A
  1. methylprednisolone acetate (Depo-Medrol)

2. triamcinolone acetonide (Vetalog)

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25
Q

How must glucocorticoid suspensions be stored?

A

store at room temperature

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26
Q

What must happen before use of glucocorticoid suspensions?

A

must be shaken before use

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27
Q

How is glucocorticoid suspension absorbed?

A

absorbed gradually over a period of days

28
Q

what is the administration for glucocorticoid suspension?

A

should never be administered IV

29
Q

Guidelines for safe use of glucocorticoids

A
  1. Use another drug if it can accomplish the same result
  2. Use the smallest dose possible
  3. Avoid continuous use
  4. Be cautious when using glucocorticoids with long-lasting effect
  5. When discontinuing, reduce dose over a period of days
  6. Use may be contraindicated in some patients
30
Q

how do NSAIDS exert their effect?

A

Exert their effect by blocking enzymes in the inflammatory cascade

31
Q

what is the benefit of NSAIDs over glucocorticoids?

A

Produce fewer side effects

32
Q

what do NSAIDs bind to withing the system?

A

Highly bound to plasma proteins

33
Q

what are some adverse effect on the GI tract?

A

anorexia, diarrhea, melena, ulcer formation

34
Q

why do NSAIDs affect the GI tract?

A

they decreased protective prostaglandin production (PGE, PGI2)

35
Q

what protective abilities do prostaglandins PGE and PGI2 have (4)

A
  1. Decrease volume and acidity of gastric secretions
    2, Increase sodium bicarbinate secreations in the intestines
  2. Increase gastric intestinal mucus productions
  3. Increase turnover and repair of GI epithelia cells
36
Q

what kind of kidney damage can NSAIDs cause?

A

tissue necrosis

37
Q

why do NSAIDs effect the kidey?

A

they decreased protective prostaglandin production (PGE2)

38
Q

what species is phenylbutazone mostly used?

39
Q

what drug forms is phenylbutazone available in?

A

tablet, paste, and injectable forms

40
Q

how does phenylbutazone provide an antiinflammatory response?

A

Inhibits cyclooxygenase

41
Q

what are some adverse effects of phenylbutazone? (4)

A
  1. GI ulceration
  2. renal necrosis
  3. retention of water and sodium
  4. bone marrow suppression
42
Q

which species have a very low tolerance to phenylbutazone?

43
Q

what species is flunixin meglumine mostly used in to relieve severe pain?

44
Q

what form is flunixin meglumine availale in

A

injectable, paste and granules for oral administration

45
Q

what kind of potent properties does flunixin meglumin have?

A

analgesic properties

46
Q

what adverse effect can happen in dogs taking flunixin meglumine?

A

GI ulceration after 3-4 days of use

47
Q

which NSAIDs derive from propionic acid?

A

Ibuprofen, Ketoprofen, Naproxen

48
Q

How does flunixine meglumine provide an antiinflammatory effect?

A

Inhibit cyclooxygenase and lipooxygenase

49
Q

what are some adverse effects in dogs?

A

GI ulceration after days of use

50
Q

what does Acetylsalicylic Acid do when administered?

A

Decreases platelet aggregation by decreasing thromboxane production

51
Q

how is Acetylsalicylic Acid metabolized

A

in the liver by binding it w/ glucuronic acid for elimination

52
Q

why cannot cats metabolized Acetylsalicylic Acid?

A

they do not produce glucuronic acid

53
Q

what is the newest group of NSAID agents referred to as?

A

COX-2 inhibitors

54
Q

how do COX-2 inhibitors provide and antiinflammatory effect?

A

selectively inhibit production of prostaglandins associated w/ inflammation

55
Q

what kind of an effect do COX-2 inhibitors have on the GI and kidney?

A

minimal effect

56
Q

what are somepossible side effects with COX-2 inhibitors? (4)

A
  1. liver disease
  2. renal disease
  3. hematologic abnormalities
  4. serious GI disease reported
57
Q

what kind of effect does acetaminophen have? (2)

A
  1. Provides analgesia

2. fever reducer

58
Q

what kind of effect does not occur with acetaminophen? (2)

A
  1. No GI ulceration

2. no anti-inflammatory effect

59
Q

what does the liver metabolize acetaminophen to?

A

Toxic metabolite

60
Q

how is the toxic metabolite rendered non toxic?

A

binds to glutathione

61
Q

what are some adverse side effect of acetaminophen with overdose? (3)

A
  1. Methemoglobinemia
  2. Heinz body formation
  3. liver tissue destruction
62
Q

what is phenacetin?

what are the concerns?

A

OTC medication

The body will convert this to acetaminophen

63
Q

how does dimethyl sulfoxide provide and antiinflammatory effect?

A

Inactivates superoxide radicals produced during inflammation

64
Q

what other effects does dimethyl sulfoxide have?

A

Penetrates intact skin, can be used as vehicle to carry drugs into body

65
Q

what are the adverse side effects of dimethyl sulfoxide?

A
  1. erythema
  2. edema and itching (w/ topical use)
  3. hemolysis (w/ IV administration)

Pharmacology (9 decks)

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