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30 Cards in this Set

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What are the adverse effects of hypercortisolism?
CUSHINGOID GC

Central fat
'u'phoria
skin thinning
Hair loss/growth (Hypertension)
Infections
Neg Nitrogen Balance
Gonadal dysfunction
Osteroporosis
Insomnia
Delayed wound healing (bruising)

H(igh) - high BP hypertension
G - Gordo (obese)
C - Cataracts
Antagonist at GC receptor
Mifepristone (RU 486)
Antagonist at MC receptor
Spironolactone
Potent Mineralocorticoid analog
Fludrocortisone
DoC for systemic/oral treatment of inflammation as in IBD or severe asthma
Prednisolone
_ or _ are used to cause immunosupression (in graft pts)
Methylprednisolone or dexamethasone
Steroid used to treat allergic rhinitis
fluticasone
Steroid used to treat severe psoriasis
Triamcinolone acetonide
The main glucocorticoid?

Mineralcorticoid?
cortisol

aldosterone
Why can't cortisone and prednisone be used topically?
11 beta hydroxysteroid dehydrogenase is needed to convert these two drugs into their active forms. It is not present in the skin.
Antiinflammatory and immunosuppressive effects on the immune system are cheifly due what type of corticosteroids?
glucocorticoids, not mineralocorticoid
An excess of corticoisteroids results in (hyper/hypotension).
hypertensions - predominately mineralocorticoids, (some gc)
Corticosteroids Decrease the transcription and translation of _, _ and _.

But an increase in trx and trl of _
IL-2, GM-CSF, and TNFaalpha


anti-inflammatory factors -IL10 and IkBalpha.

Overall, immune cell are impaired.
Glucocorticoid receptors are found _.

Mineralocorticoid receptors are found _. What enzyme is present with these that deactivate cortisol?
everywhere


in kidney. 11 beta hydroxysteroid dehydrogenase
turns hydroxyl group into ketone (opposite effect than in skin)
In the indirect mechanism of action, The glucocorticoid/receptor complex binds to _ , which prevents it from going into the nucleus and binding to the _.
nfkappaB

DNA

It prevents nfKappaB from binding to the DNA and triggering transcription
too much/too little glucocorticoids is life threatening. What is this condition called?
too little - Addison's

because of Adrenal insufficiency or abrupt withdrawal of glucocorticoids
Patient presents N/V, abdominal pain, dehydration, weakness. BP is 80/60, blood shows hyponatremia and hyperkalemia. What is this describing?
acute adrenal insufficiency

- due to abrupt withdrawal of glucocorticoids or stress in adrenally compromised pt
How do you diagnose Cushings?
dexamethasone
_ is great for mineralocorticoid replacement
Fludrocortisone
What drug is given to the fetus when delivery is expected prematurely in order to stimulate lung maturation and surfactant production?
BETAmethasone
Hydrocortison is used for
topical therapy (eczema)
What corticosteroids have poor bioavailability and are rapidly metabolized by the liver, minimizing their systemic side effects? These are used in allergies.
Beclomethasone, Budesonide, Fluticasone
What are some unavoidable side effects from corticosteroids?
Insomnia, increased appetite, weight gain.
What are some delayed and insididois side effects of long term corticoisteroids?
atherosclerosis, cataracts
3) Jason is admitted to the hospital for a wide-spread rash. Following oral administration of prednisone his symptoms do not resolve as quickly as expected. Which one of the following is the most likely reason for the delayed effect?
decreased liver function
Decreased NFkappaB activities results in decreased transcription of _ and _ enzymes
Phospholipase A2 (dec LT synthesis)

and

COX 2 (dec PG synthesis)
Decreased transcription of CM-CSF results in decreased proliferation of _
leukocytes
Decreased TNFalpha signal transduction results in _
decreased chemotaxis
Increased IL 10 transciption results in _
suppressing the activity of T helper lymphocytes
Decreased AP-1 activity works (indirectly/directly)
indirectly

AP-1targets genes for collagenase and IL2, (increases extracellular matrix remodeling functions)