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Pharmacology > Pharm 20- Glucocorticoids & Immunosuppressants > Flashcards

Pharm 20- Glucocorticoids & Immunosuppressants Flashcards

1
Q

In stress, hypothalamus releases what?

A

Corticotropin-releasing factor

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2
Q

Corticotropin-releasing factor acts on what part of the body?

A

Anterior pituitary

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3
Q

Anterior pituitary releases what?

A

Cortiocotropin (ACTH)

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4
Q

Corticotropin (ACTH) acts on what? Which then releases what?

A

Adrenal Medulla; aldosterone/cortisol/androgens

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5
Q

Whats the classic stress hormone?

A

Glucocorticoids

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6
Q

What do glucocorticoids do?

A

Promote gluconeogenesis, protein catabolism, and lipolysis; which allows critters to respond to overwhelmingly stressful situations

POTENT anti-inflammatory (NOT analgesic)

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7
Q

Glucorticoids result in what physiologically?

A

Vasoconstriction, glucose release

Break down fat and muscle (lipolysis) to produce more glucose and the need for more glyconeogenesis

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8
Q

Why are glucocorticoids insulin antagonists?

A

They inhibit the uptake of glucose by fat and muscle and increase hepatic glucose output

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9
Q

What is an adverse affect of glucocorticoids?

A

Decrease WBC #’s

All are immunosuppressive even as a single dose

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10
Q

Are glucocorticoids catabolic steroids or anabolic steroids? Why?

A

Catabolic steroids; because they involve the breakdown of complex molecules in living organisms to form simpler ones

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11
Q

Anabolic

A

construct molecules from smaller units

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12
Q

Describe the “feedback inhibition” of glucocorticoids.

A

Causes feedback inhibition of further glucocorticoid and thyroid-stimulating hormone production

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13
Q

What’s important to note about discontinuing glucocorticoids, based on the feedback inhibition?

A

Wean off little by little bc instead of having too much you’ll have none

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14
Q

Effects of Glucocorticoids at high doses

A 
Bone density loss
Myopathy
Steroid rage and personality changes
Gastric Ulcers
Diabetogenic
Moon Face & Humpback
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15
Q

What is hyperglucocorticism?

A

Cushing Syndrome

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16
Q

What is hypoglucocorticism?

A

Addison’s Disease

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17
Q

What is the archetypical glucocorticoid?

A

Cortisol, given a value of “1” when comparing anti-inflammatory and salt-retaining properties

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18
Q

What is the half-life of cortisol?

A

1-2 hours

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19
Q

Another name for cortisol?

A

Hydrocortisone

20
Q

List the Glucocorticoids.

A 
Hydrocortisone (Solu-Cortef)
Dexamethasone (Decadron)
Prednisone
Prednisolone
Methylprednisolone (Medrol)
21
Q

Which (Short-acting) glucocorticoids do we care about for bypass?

A

Hydrocortisone
Cortisone
(1-12 hours)

22
Q

When would we use long acting glucocorticoids? Name them.

A

Transplant patient; immunosuppressed for a long time. Bethamethasone, Dexamethasone
(36-55 hours)

23
Q

What are the two general immunosuppressant categories?

A
  1. Induction Drugs: Used at the time of transplanation

2. Maintenance Drugs: Required for long term immunosuppresion

24
Q

What are the 5 Major pharmacological classes of Immunosuppressives

A
  1. Glucocorticoids
  2. Calcineurin Inhibitors
  3. mTOR Inhibitors
  4. Antiproliferative Agents
  5. Monoclonal Antibodies
25
Q

What is a standard component of induction and maintenance? (high doses initially tapering over time)

A

Glucocorticoids

26
Q

What is the drug of choice for moderate rejection episodes?

A

Glucocorticoids

27
Q

What do glucocorticoids suppress?

A

T-lymphocytes

28
Q

Calcineurin Inhibitors

A

Cyclosporin (Sandimmune)

Tacrolimus (Prograf)

29
Q

Calcineurin

A

Major T-cell activator

30
Q

What is the break through drug that allowed transplants to successfully occur?

A

Cyclosporin

31
Q

Describe the side effects of cyclosporin.

A 
Dose-dependent Nephrotoxicity
Immune suppression
Hepatotoxicity
Cardiotoxicity
(patients on these if not balanced well will be coming back for second or third kidney transplants)
32
Q

What’s important to note about monitoring patients on cyclosporin?

A

Cyclosporin levels must be monitored closely

33
Q

How to reduce dosage and side-effects of cyclosporins?

A

Use in combination therapy

34
Q

Tacrolimus

A

Better, safer form of cyclosporin; orders of magnitude more potent than cyclosporins
More efficacious than cyclosporin

35
Q

Describe the toxicity of Tacrolimus.

A

More nephrotoxic/less cardiotoxic than cyclosporins

36
Q

How do mTOR Inhibitors work?

A

Blocking mTOR prevents maturation and proliferation of T-cells

37
Q

mTOR side effects

A

Nephrotoxicity

Delayed wound healing

38
Q

mTOR Inhibitor example

A

Sirolimus (Rapamune); only available orally

39
Q

How to antiproliferative agents work?

A

By preventing proliferation of cells, rapidly dividing cells (like B- and T- lymphocytes) don’t multiply

40
Q

Antiproliferative Agent Examples

A 
Azathioprine (Imuran)
Mycophenolate mofetil (Cellcept)
Mycophenolate sodium (Myfortic)
41
Q

Azathioprine (Imuran)

A

Prototypical “early” immunosuppressant
Works best on acute rather than chronic immunogenic response (Why?)
Numerous and Severe side effects (bone marrow suppression)

42
Q

Mycophenolate Mofetil (Cellcept)

A

Much less severe side-effects than azathioprine; mainly GI and bone-marrow suppression

43
Q

Mycophenolate Sodium (Myfortic)

A

Designed to be a “slower-releasing” and “enterically-pleasing” form of Mycophenolate Mofetil
No real evidence that it is more effective or safer (marketed better)

44
Q

Monoclonal Antibodies

A

Train B lymphocytes to turn into plasma cell and make one antibody against one specific clone antibody.
Contain only one type of antibody that is derived from a single cloned B-lymphocyte

45
Q

Monoclonal Antibodies are directed against what?

A

Single cell-surface protein of target cells

46
Q

Two types of Monoclonal Antibodies

A 
Antithymocyte Antibodies- attacks thymocytes; immune cells
Antilymphocyte antibodies (Othoclone OKT3)

Pharmacology (23 decks)

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