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46 Cards in this Set
- Front
- Back
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When would you use glucocorticoids?
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-endocrine conditions (if you aren't producing cortisol)
-for dx and evaluation (to suppress ACTH and see if the body was able to have a normal rxn or not) |
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Primary insufficiency:
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problem with adrenal cortex destruction
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Adison's disease is a type of...
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primary insufficiency
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Secondary insufficiency:
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glucocorticoid levels are too low
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Why would you use glucocorticoids for its anti-inflammatory efx?
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Allergic disorder
RA |
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Why would you use glucocorticoids for its immunosuppressant efx?
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autoimmune disorder
collagen disorders |
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How can glucocorticoids be administered?
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systemically (oral) for short term
injected intra-articularly, or epidural systemically long term (controversial) region/organ specific i.e. nasal spray |
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Specific drugs that are glucocorticoids:
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prednisone
dexamethasone dexasone |
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Glucocorticoids can be identical to:
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endogenous hormones
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Glucocorticoids can be synthetic analogs of:
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cortisol
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Adverse efx of glucocorticoids:
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breakdown of supportive tissue
bone loss muscle wasting |
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PT considerations for glucocorticoids:
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watch amount of mm. work, risk for injury
watch for pressure ulcers, shear forces watch for fractures watch for change in glucose levels watch for change in endurance levels |
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Primary steroid of mineralocorticoids
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aldosterone
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Primary function of mineralocorticoids:
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maintain fluid and electolyte balance
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Mineralocorticoids affects kidneys to increase _____ & _____ reabsorption and _____ excretion.
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Na and water
K |
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How does the body stimulate release of mineralocorticoids?
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increased angiotensin II
increased plasma K increased ACTH |
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The process of K+ going into the nephron lumen is called:
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secretion
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The process of Na+ going back into the blood stream is called:
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reabsorption
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The net effect of aldosterone:
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potassium excretion
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Adverse efx of aldosterone:
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HTN
peripheral edema weight gain hypokalemia (water and sodium retention) cardiovasc changes (hypertrophy, fibrosis) |
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Adverse efx of aldosterone anatagonist:
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hyperkalemia
GI disturbances |
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Suffixes for aldosterone antagonists:
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-tone
-none |
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ACTH
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adrenocorticotropic hormone
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CRH
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corticotropin releasing hormone
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What controls synthesis of cortisol?
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CRH and ACTH
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2 ways in which cortisol is released:
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when stressed
upon waking (circadian) |
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Primary fx of cortisol:
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regulate glucose, lipid, protein metabolism
control body's ability to deal with stress |
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Secondary fx of cortisol:
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decrease inflammation
suppress immune system |
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Glucocorticoid suffixes:
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-sone
-olone |
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Sx of Cushing Syndrome:
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round, puffy face
trunk/back fat deposition muscle wasting in extremities osteoporosis increased body hair glucose intolerance |
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The sodium/potassium pump is on which side?
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blood stream side
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2 phases of increasing Na permeability:
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non-nuclear
nuclear |
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Aldosterone antagonists do what?
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increase Na and water excretion
increase K+ retention |
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Aldosterone antagonists are AKA...
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K+ sparing diuretics
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When would you use an aldosterone antagonist?
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to tx HTN, heart failure
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Primary fx of adrenocorticosteriod antagonists:
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inhibit adrenocorticosteroid production
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2 ways adrenocorticosteroid antagonists work:
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block a specific enzyme
directly suppress adrenal gland |
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Renin comes from:
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kidneys
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Renin converts what to what?
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agiotensinogen to angiotensin I
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Angiotensin converting enzyme comes from:
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lungs, other tissues
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Antiotensin converting enzyme converts what to what?
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angiotensin I to angiotensin II
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Angiotensin II increases _____.
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aldosterone release
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Angiotensin II maintains BP by:
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peripheral vessel constriction
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Spironolactone
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aldosterone antagonist (competitive)
may interfere with endogenous sex hormones and can cause CNS efx |
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Primary adverse effect of adrenal steroids:
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breakdown of supporting tissues
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Secondary adverse effects of adrenal steroids:
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water and sodium retention
immune suppression toxicity |
