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EQM351 > Anti-Inflammatory Agents Exam 1 > Flashcards

Anti-Inflammatory Agents Exam 1 Flashcards

1
Q

3 phases of inflammtion:

A
  1. acute inflammation
  2. immune response
  3. chronic inflammation
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2
Q

STUDY THE INFLAMMATORY CASCADE

A
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3
Q

What is one of the biggest side effects of long-term anti-inflammatory use?

A

renal failure and gastric ulcers

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4
Q

What does low dose aspirin control?

A

platelet aggregation

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5
Q

The higher the dose of anti-inflammatories the more ______ _______

A

side effects

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6
Q

Effect of eicosanoids on muscle:

A

-vascular: vasodilation or vasoconstriction
-GI: contraction, colic
-uterus: contraction
-pulmonary: constriction (contraction)

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7
Q

The left side of the inflammatory cascade is only effected by what type of drug?

A

steroidal

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8
Q

The right side of the inflammatory cascade is only effected by what type of drug?

A

non-steroidal

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9
Q

What is the most important mediator of inflammation?

A

prostaglandin

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10
Q

What is the first mediator of inflammation?

A

arachidonic acid

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11
Q

NSAIDs stand for

A

non-steroidal anti-inflammatory drugs

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12
Q

What is activity of NSAIDs mediated by?

A

the inhibition of prostaglandins

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13
Q

During treatment, how is inflammation reduced with NSAIDs?

A

by decreasing the release of mediators from granulocytes, basophils, and mast cells

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14
Q

All NSAIDs are:

A

-analgesic (relieve pain by reducing inflammation)
-anti-inflammatory
-antipyretic
-anti-endotoxic
-anti-thrombotic (inhibit platelet aggregation)
-gastric irritants

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15
Q

NSAIDs can cause ______ problems

A

kidney

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16
Q

Why should NSAIDs not be taken after surgeries?

A

because we need the inflammation to be able to heal

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17
Q

How are NSAIDs different from opioids (pain killers)

A

opioids work on receptors in the brain

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18
Q

NSAIDs used in horses:

A

-flunixin meglumine (banamine)
-phenylbutazone (bute)
-ketoprofen
-naproxen
-firocoxib
-aspirin
-dypirone

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19
Q

Stacking

A

using more than 1 NSAID - increasing chances of side effects, usually done in the case of an emergency

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20
Q

Uses for NSAIDs:

A

-relieving pain
-reducing fever
-counteracting endotoxemia
-reducing excessive blood clotting

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21
Q

Analgesia (reducing pain) process

A

prostaglandin produce pain, by reducing prostaglandins NSAIDs provide pain relief

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22
Q

Anti-pyretic (reducing fever) process:

A

prostaglandins produced during both infection and inflammation cause fever
-fever is a natural mechanism the body uses to fight infection but when it is too high it can cause irreversible brain damage

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23
Q

Counteracting Endotoxemia process

A

endotoxemia is where bacteria toxins reach the bloodstream
-these toxins can be life-threatening
-generally flunixin meglumine is the preferred NSAID for this

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24
Q

Reducing excessive blood clotting process

A

by blocking thromboxane production, NSAIDs help maintain blood flow in situations where excessive blood clotting causes problems

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25
Q

Phenylbutazone

A

-aka bute
-potent pain reliever, antipyretic, and anti-inflammatory

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26
Q

What is bute commonly used for?

A

-lameness resulting from soft tissue injury
-muscle soreness
-bone and joint problems
-laminitis

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27
Q

How can bute be given?

A

IV or PO

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28
Q

How long does it take for bute to start relieving pain/reducing fever?

A

1-2 hours

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29
Q

What should you do for a horse that needs to be on bute for more than a few days?

A

use drugs that protect the GI tract

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30
Q

Drugs that help protect the GI tract while taking NSAIDs

A

-omeprazole
-cimetidine
-ranitidine

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31
Q

Flunixin Meglumine

A

-aka banamine

32
Q

What are the uses for flunixin meglumine?

A

-pain relief in the treatment of colic
-protection from septic/endotoxic shock due to any GI insult
-used as an anti-inflammatory in the treatment of painful conditions of the eye
-may be used to reduce or control fevers due to viral or bacterial infections

33
Q

What can banamine cause?

A

GI ulcers

34
Q

How can banamine be administered?

A

IV or PO

35
Q

What can happen if banamine is given IM?

A

clostridial myositis (C-diff)
anaerobic bacteria

36
Q

How is cortisol produced?

A

produced by the adrenal cortex gland in a negative feedback loop

37
Q

What is cortisol released by?

A

the hypothalamus and pituitary adrenal axis

38
Q

What does cortisol do?

A

-proper glucose metabolism (gluconeogenesis = synthesis of new glucose)
-regulation of blood pressure
-insulin release for blood sugar maintenance
-immune function
-inflammatory response

39
Q

When are cortisol levels naturally higher?

A

in the morning

40
Q

What is the negative feedback loop of cortisol?

A
  1. hypothalamus (in brain) signals the release of corticotropin releasing hormone
  2. this gets sent to the pituitary and signals the release of adrino-corticotropic hormone
  3. This gets send to the adrenal gland (top of kidneys) and signals the release of cortisol
  4. Cortisol than signals the hypothalamus to either shut off or release more cortisol and the loop begins again
41
Q

What does the adrenal gland release?

A

-cortisol
-epinephrine (adrenaline)

42
Q

Cortisol

A

-called the stress hormone
-its levels increase in fight or flight responses (quick burst of energy for survival reasons, heightened memory functions, burst of increased immunity, lower sensitivity to pain, helps maintain homeostasis)

43
Q

What happens when one has prolonged levels of cortisol in the blood stream (chronic stress)?

A

-impaired cognitive performance
-suppressed thyroid function
-blood sugar imbalances such as hyperglycemia
-decreased bone density
-break down of muscle tissue, muscle wasting
-higher blood pressure
-increased fat deposits
-lowered immunity and inflammatory responses in the body

44
Q

What lowers stress and cortisol levels?

A

exercise

45
Q

Metabolic effects of cortisol

A

-carbohydrate, protein, and fat metabolism
-increase serum glucose
-stimulate insulin release and lipogenesis (fat deposits)

46
Q

Metabolism

A

cells doing their jobs to survive

47
Q

Catabolism

A

breaking down

48
Q

Catabolic effects of cortisol

A

-supraphysiologic amounts of steroids lead to decreased muscle mass and weakness
-osteoporosis (bone breaking down)

49
Q

Anabolism

A

building up

50
Q

What anti-inflammatory effects does cortisol have?

A

effects on concentration, distribution, and function of peripheral leukocytes
-reduced prostaglandin, leukotriene, etc.

51
Q

What immunosuppressive effects does cortisol have?

A

inhibit functions of macrophages and antigen-presenting cells
-inhibit ability of macrophage to phagocytose and kill microorganisms

52
Q

What does cortisol reduce the production of?

A

antibodies

53
Q

PPID/Cushings

A

the excessive circulating glucocorticoids
-the pituitary continues to secrete cortisol even if triggered to shut off/there are already too high levels

54
Q

Cushings symptoms

A

-fat deposition
-obesity
-excessive hair
-poor wound healing
-osteoporosis
-insulin resistance
-laminitis

55
Q

When do horses usually get cushings?

A

when they get older

56
Q

Uses for synthetic coricosteroids

A

-allergies: hives, heaves
-auto-immune disorders
-traumatic brain injuries
-recurrent uveitis (blindness)
-joints
-other inflammatory disorders

57
Q

What are short and medium acting steroids?

A

-cortisone
-hydrocortisone
-prednisone (don’t use in horses)
-prednisolone
-meprednisone

58
Q

What are long acting steroids?

A

-dexamethasone
-betamethasone

59
Q

Formulations of steroids (how they can be given)

A

-PO
-IV
-IM
-aerosol

60
Q

What steroid helps decrease brain swelling in traumatic brain injuries?

A

cortisol

61
Q

When do severe side effects occur with steroid use?

A

with long-term administration of the drug

62
Q

How should a horse stop taking a steroid drug?

A

withdrawing slowly and tapering the dosage and prolonging the interval between doses

63
Q

Side effects of steroid

A

-suppressed immune response (if not the desired effect)
-polyuria,polydipsia (excessive urinating and drinking)
-cause or worsen gastric ulcers
-laminitis

64
Q

In what horses should steroids not be used?

A

in horses with cushings

65
Q

Steroids mimic what natural hormone?

A

cortisol

66
Q

Process of steroids acting on the body

A

when they are given, CRH and CTRH are no longer being produced (the cortisol negative feedback loop is shut down), so it must be tapered down to allow the body to start naturally producing cortisol again (by activating the hypothalamus pituitary adrenal axis (HPA))

67
Q

What does chronic administration of steroids suppress?

A

the pituitary release of ACTH, GH, TSH, and LH

68
Q

What types of fat does steroids increase?

A

-visceral
-facial
-nuchal
-supraclavicular

69
Q

Why does osteoporosis occur from steroid use?

A

antagonizes effects of vitamin D on calcium absorption

70
Q

When is dexamethasone used in higher doses?

A

-in emergencies
-anaphylactic reactions
-spinal chord trauma
-shock
-any CNS trauma (helps shrink the brain)

71
Q

When is dexamethasone used in lower doses?

A

-treat allergic reactions: heaves, hives, itching
-inflammatory diseases: arthritis

72
Q

Why do horses not receive prednisone?

A

they do not absorb it

73
Q

When choosing a short term steroid what should you use for horses?

A

prednisolone

74
Q

What is fluticasone used for?

A

to control heaves

75
Q

How is fluticasone given?

A

as aerosol (nebulizer or air mask)
-more localized effects so less chance of side effects

76
Q

What is triamcinolone used for?

A

join injections

77
Q

What is Methyl-prednisolone used for?

A

SI injections

EQM351 (28 decks)

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