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NSAIDs > Anti-Inflammatory Corticosteroids > Flashcards

Anti-Inflammatory Corticosteroids Flashcards

1
Q

What is hydrocortisone’s:

• Anti-inflammatory activity

A

1

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2
Q

What is hydrocortisone’s:• Topical activity

A

1

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3
Q

What is hydrocortisone’s:• Salt retaining activity

A

1

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4
Q

What is hydrocortisone’s:• Potency

A

20

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5
Q

What is hydrocortisone’s:• Routes of administration?

A

oral, injectable, topical

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6
Q

What is prednisone’s • Anti-inflammatory activity

A

4

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7
Q

What is prednisone’s • Topical activity

A

0

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8
Q

What is prednisone’s • Salt retaining activity

A

0.3

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9
Q

What is prednisone’s • Potency

A

5

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10
Q

What is prednisone’s • Routes of administration?

A

oral

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11
Q

What is metylprednisolone’s topical activity

A

5

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12
Q

What is metylprednisolone’s salt retaining activity

A

5

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13
Q

What is metylprednisolone’s potency

A

0

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14
Q

What is metylprednisolone’s routes of administration

A

Oral and injectable

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15
Q

What is metylprednisolone’s anti-inflammatory activity

A

Four

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16
Q

What is Triamcinolone’s:

• Anti-inflammatory activity

A

5

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17
Q

What is Triamcinolone’s:• Topical activity

A

5^3

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18
Q

What is Triamcinolone’s: • Salt retaining activity

A

0

19
Q

What is Triamcinolone’s: • Potency

A

4

20
Q

What is Triamcinolone’s: • Routes of administration?

A

oral, injectable, topical

21
Q

What is Dexamethasone’s:

• Anti-inflammatory activity

A

30

22
Q

What is Dexamethasone’s: • Topical activity

A

10

23
Q

What is Dexamethasone’s: • Salt retaining activity

A

0

24
Q

What is Dexamethasone’s: • Potency

A

0.75

25
Q

What is Dexamethasone’s: • Routes of administration?

A

oral, injectable, topical

26
Q

What are the 5 corticosteroid drugs that Dr. French would like us to know?

A

Hydrocortisone, prednisone, methylprednisolone, triamcinolone, dexamethasone

27
Q

What’s the goofy pneumonic I use to keep track of the 5 corticosteroid drugs I should know about?

A 
H - Hyper (Hydrocortisone)
P - Pigs (Prednisone)
M - Mangle (Methylprednisolone)
T - Tomatoes (Triamcinolone)
D - Dramatically (Dexamethasone)
28
Q

Which of the 5 drugs we are supposed to know are able to be used topically?

A

H, T, D (Hydrocortisone, Triamcinolone, Dexamethasone). All of these drugs have a 0 in the salt retaining category, which has to do with Mineralocorticoid activity

29
Q

Where in the pathway of prostaglandin and leukotriene synthesis do Glucocortocoids work?

A

UPSTREAM, they inhibit phospholipase A2, which inhibits the production of Arachidonic Acid, the precursor to both leukotrienes and prostaglandins

30
Q

What is the primary gland affected by chronic GC use?

A

Adrenal gland. With chronic GC use you can get adrenal atrophy and Iatrogenic Cushing’s

31
Q

What are the main scary/concerning side effects in mineralocorticoids?

A

Hypertension, Hypokalemia (low potassium) Metabolic Alkalosis

32
Q

What are the PHYSIOLOGIC (not pharmocologic) Metabolic effects of Glucocorticoids?

A

Carbohydrates, Protein, Fat (increase gluconeogenesis and blood glucose, leading to increased insulin), (decreased protein synthesis as a result of more amino acids made into glucose), (increased lipolysis in the periphery and a resultant increase in free fatty acids)

33
Q

What is the PHARMACOLOGIC Metabolic effects of excess GC use?

A

Carbohydrate, Protein, Fats, Sodium reabsorption (diabetes like state), (muscle wasting and skin/connective tissue atrophy), (increased lipogenesis centrally leading to centripetal obesity seen in moon facies, buffalo hump), (sodium-fluid retention, hypertension, hypokalemia, metabolic alkalosis) ALL THIS LEADING TO IATROGENIC CUSHINGS DISEASE

34
Q

What adverse effect can GC use have on the fluid retention system on the body?

A

Can lead to sodium reabsorption at kidney and thus fluid retention (normally helps increase blood volume and blood pressure). IN EXCESS, you see hypertenstion, hypokalemia (body getting rid of K to compete with increased Na) and metabolic alkalosis

35
Q

What is GC effect on vascular events systemically?

A

reduced vasodilators (prostaglandins), decreased fluid exudation

36
Q

What is the GC effect on cellular events?

A

overall decrease in accumulation-activation of inflammatory and immune cells

37
Q

What is the GC systemic effec on inflammatory and immune mediator production?

A

overall DECREASE in production of inflammatory mediators

38
Q

For a GC chemical to properly work, what Carbon need have an OH group?

A

11’. The 11-Carbon position needs to have an OH. If it doesn’t, it first needs to be metabolized into having the OH at that position (it is likely an 11-KETO)

39
Q

can you use GC in pregnancy without affecting fetus

A

yes, depending on agent (needs to avoid fetal enzyme)

40
Q

why is prednisone so commonly prescribed?

A

Oral administration, and 5:1 GC:MC action

41
Q

which of the GC’s we are supposed to know is the most potent anti-inflammatory?

A

Daxamethasone

42
Q

How are GC’s usually used in RA treatment?

A

As the “bridge” between NSAID and DMARD use. Use as low dose therapy

43
Q

What is the primary clinical benefit to the alternate day glucocorticoid regimen?

A

Minimizes clucocorticoid block of ACTH release which can significantly reduce adrenal atrophy

NSAIDs (2 decks)

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