Chapter 13 - Antiinflammatories Flashcards

1
Q

Inflammation

A

Protective mechanism that is designed to remove or neutralize the underlying cause of injury (physical, chemical, or biologic)

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2
Q

What are the 5 cardinal signs of inflammation?

A

1) Redness 2) Heat 3) Swelling/Edema 4) Pain 5) Loss of function

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3
Q

The two larger groups of antiinflammatory drugs used to reduce pain and discomfort

A

Steroidal antiinflammatory drugs and NSAIDs

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4
Q

Nociceptor

A

Pain receptor

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5
Q

Transduction

A

Conversion of physical change into a pain nerve signal

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6
Q

Pain pathway

A

Painful stimulus at nociceptor -> transduction -> transmission of pain along sensory nerves to the spinal cord -> modification and modulation of pain as it ascends spinal cord -> perception of pain signals the brain

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7
Q

Arachidonic Acid Cascade/Pathway

A

One of the principal mechanisms by which inflammatory mediators are generalized

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8
Q

What does the arachidonic acid cascade create?

A

Eicosanois -> enzymatically generates prostaglandins, leukotrienes and other inflammatory mediators

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9
Q

When trauma occurs to cell membranes what enzyme is activated?

A

Phospholipase

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10
Q

Phospholipase converts phospholipid molecules (that make up the cellular membrane) into what?

A

Arachidonic acid

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11
Q

What 2 enzymes may then act on Arachidonic acid?

A

Cyclooxygenase enzymes (COX) or Lipoxygenase enzymes

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12
Q

What do COX enzymes produce when they act on arachidonic acid?

A

Protaglandins and thromboxanes

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13
Q

What do Lipoxygenase enzymes produce when they act on arachidonic acid?

A

Leukotrienes

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14
Q

How do corticosteroids (specifically glucocorticoids) reduce inflammation?

A

By blocking the action of Phospholipase in the early portion of the pathway and reducing production of most of the inflammatory mediators (also blocks COX)

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15
Q

How do NSAIDs reduce inflammation?

A

NSAIDs inhibit COX (and to varying degrees) lipoxygenase - decreasing production of prostaglandins, leukotrienes and thromboxane) reducing inflammatory mediators, therefore decreasing the inflammatory effect of other inflammatory mediators (histamine, kinins, substance p and superoxide radicals)

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16
Q

Mineralcorticoids

A

Affect the minerals in the body (Na, K and other lytes) involved with water and electrolyte balance but have little to no antiinflammatory effect

17
Q

Aldosterone

A

Mineralcorticoid hormone

18
Q

What is aldosterones primary effect and use?

A

Increase the sodium retained in the body - Hypoadrenocorticism (Addisons)

19
Q

What is Desoxycorticosterone Pivalate?

A

Percoten-V - mineralcorticoid, mimics effects of aldosterone and used to treat animals with addisons disease

20
Q

Where are glucocorticoid receptors found in the body?

A

Found on ALL cells in the body, but Liver is primary systemic target for many glucocorticoid effects

21
Q

What are the two natural glucocorticoids and what produces them?

A

1) Cortisol 2) Cortisone - Adrenal gland

22
Q

How long do short-acting glucocorticoids exert their biologic activity on the body?

A

less than 12 hours (Hydrocortisone/cortisone)

23
Q

How long do intermediate-acting glucocorticoids exert their biologic activity on the body?

A

12 to 36 hours (prednisone/prednisolone/methylprednisolone/Triamcinolone)

24
Q

How long do long-acting glucocorticoids exert their biologic activity on the body?

A

48 hours or longer (Dexamethasone/Betamethasone/Flumethasone and Idoflupredone)

25
Q

“Low” doses of glucocorticoids used to achieve normal physiology (addisons) are referred to as ____ doses.

A

Physiologic

26
Q

“Medium” doses of glucocorticoids Supraphysiologc doses are referred to as ____ doses.

A

Antiinflammatory

27
Q

“High” doses of glucocorticoids are referred to as ____ doses.

A

Immunosuppressive