Unit 2: Addison's vs Cushing's Disease Flashcards
Addison’s and Cushing’s are r/t what hormone in the pituitary gland?
Acth!
What is released in response to Acth?
Cortisol → glucose regulation
Aldosterone → F&E balance, Na+ reabsorption
Decreased Acth =
Addison’s Disease
(“ADD” steroids)
Increased Acth =
Cushing’s Disease
(“CUSHION” of steroids)
If we don’t have enough Acth, we don’t have enough cortisol, which would cause glucose levels to…
DECREASE → HYPOglycemia!
If we don’t have enough Acth, we don’t have enough Aldosterone, which would cause fluid and Na+ levels to ______ and K+ levels to ______
DECREASE → HYPOvolemia + HYPOnatremia
INCREASE → HYPERkalemia
(Na+ excretion causes K+ retention–just an inverse relationship thing w/ the kidneys, don’t fret about the patho)
Primary Addison’s = issue with
Secondary Addison’s = issue with
Primary → Adrenal glands
Secondary → Pituitary/cessation of LT steroids
What’s the Diagnostic test to distinguish Addison’s Disease?
Acth Stimulation (Provocative) Test
-give Acth
-measure cortisol levels at 30 min + 1 hr
(Think: Hyposecretion → want to INDUCE (or provocate) a response
Acth Stimulation (Provocative) Test
Primary or Secondary Addison’s
Cortisol levels are absent or very decreased
PRIMARY Addison’s (adrenal issue)
gave Acth → adrenal glands didn’t respond
Acth Stimulation (Provocative) Test
Primary or Secondary Addison’s
Cortisol levels are increased
SECONDARY Addison’s (pituitary issue)
gave Acth → adrenal glands responded
When Acute Adrenal Insufficiency (Addison’s) occurs, WHAT DO?!
3 Main Priorities
Hypotension + Hyperkalemia = DEATH RISK!
1. Hormone replacement (for F&E Mx)
2. Hyperkalemia Mx
3. Hypoglycemia Mx
What’s that drug that makes you poop potassium called? What else can we do to decrease K+
Kayexalate!
Insulin + D50
If we have too much Acth, we have too much cortisol, which would cause glucose levels to…
INCREASE → HYPERglycemia
If we have too much Acth, we have too much Aldosterone, which would cause fluid and Na+ levels to ______ and K+ levels to ______
INCREASE → HYPERvolemia + HYPERnatremia
DECREASE → HYPOkalemia
(Again, inverse relationship: Na+ retention causes K+ excretion–just what it iiiis)
If we have too much Acth, we have too much Aldosterone resulting in FVO. What might happen to our calcium levels as a dilutional consequence?
HYPOcalcemia!
Cushing Disease = issue of
Cushing Syndrome = issue of
Cushing Disease = issue of Pituitary (tumor)
Cushing Syndrome = issue of steroid therapy (too much)
We know glucocorticoids (steroids) cause all sorts of LT issues, so what happens in Cushing’s Disease?
Increased body fat (wt gain, truncal obesity, moon face, buffalo hump)
Decreased muscle mass (thin limbs, osteoporosis, fragile skin + capillaries)
Decreased immunity (low WBC + lymph count, small spleen)
Increased Androgen production (acne, altered menses, hirtuism)
If Cushing’s is due to a pituitary problem, will Acth levels be increased/decreased?
INCREASED Acth
(negative feedback loop MALFUNCTION!)
If Cushing’s is due to an adrenal problem, will Acth levels be increased/decreased?
DECREASED Acth
(negative feedback loop: increased end-product = decreased start-product)
What Diagnostic test can we use to determine Cushing’s Disease?
Dexamethasone SUPPRESSION Test
-give steroids
-test 24-hr urine for cortisol
(Think: Hypersecretion → want to INHIBIT (or suppress) a response)
Dexamethasone Suppression Test
What response would indicate Cushing’s disease?
INCREASED Cortisol levels
(Normal response: decreased cortisol levels)
Nutrition restriction r/t Cushing’s Disease
Restrict fluids
Restrict Na+
Increased Cortisol levels inhibit gastric mucus production, so what should we do?
PUD prophylaxis! (PPIs, Antacids)
Avoid NSAIDs
Increased Cortisol levels cause issues with bones and skin integrity, so what should we do?
Fall precautions, mobility aids, VitD
Barrier creams/lotion, avoid tape
Drug therapy for Cushing’s Disease
Steroidogenesis Inhibitors
ADRs of Steroidogenesis Inhibitors
Wt loss
Increased U/O → dehydration
