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20 Cards in this Set

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Adrenal Insufficiency:
AKA
Presentation
Addison's Syndrome

Specific: Volume depletion, hyperkalemia, hyperpigmentation

General: fatigue, weakness, weight loss, GI complaints, low BP

PRESENTATION IS VARIABLE
Primary vs Secondary AI
GC function
MC function ([Na+], [K+], blood volume)
ACTH levels (pigmentation)
Pituitary function
Primary:
Lose GC
Lose MC (sodium + volume loss; potassium retention)
High ACTH (lack negative feedback; hyperpigmentation)
Normal pituitary fn

Secondary:
Loss GC
MC okay (no hyperkalemia)
LOW ACTH (no hyperpigmentation)
Hypopituitarism
Why does primary AI result in hyperpigmentation?
ACTH receptor and alpha-MSH receptors come from same receptor line
When tons of ACTH, ACTH will bind alpha-MSH receptors
Autoimmune adrenalitis:
Effects
Antibodies Present
Affiliated Syndromes
Major cause of AI

Adrenal Ab's (21-OHase Ab)

May be part of polyglandular autoimmune syndrome

PRIMARY AI
Polyglandular Autoimmune Syndromes:
Type I vs Type II
Type I:
APECED
Autoimmune polyendocrinopathy
Chronic mucocutaneous candidiasis
Ectodermal dysplasia (abnormal development of the skin, hair, nails, teeth, or sweat glands)

Results in hypopara, AI, and hypogonadism

Type 2:
HLA-related
Affects multiple endocrine systems, most commonly AI, thyroid, and DM I

PRIMARY AI
Cause of AI in undeveloped countries
Tb
Fungal
CMV
HIV

PRIMARY AI
Waterhouse-Friederichson Syndrome is an example of ___________ which can result in _____.
Adrenal hemorrhage (in pts with meningococcal sepsis) and can result in AI

(Clues of adrenal hemorrhage: hypotn, shock, abdominal/flank pain, fever, DROP IN Hg)

PRIMARY AI
Metastatic Causes of AI (cancer types)
BrCa
Lung Ca

PRIMARY AI
What drugs interfere with adrenal function?
Ketoconazole (antifungal)
Etomidate (anesthetic)

PRIMARY AI
Congenital Adrenal Hyperplasia:
Relevance to AI
Impaired production of cortisol

PRIMARY AI
Adrenoleukodystrophy:
Relevance to AI
Defect in oxidation of FA's in peroxisomes-->elevated serum levels of long chain FA's-->accumulation in cell membranes

leads to PRIMARY AI
Familial Glucocorticoid Deficiency
Defect in MCR-2 (Melanocortin Receptor--an ACTH receptor), can't make cortisol
Can make ACTH
Zona glomerulosa not affected, so can make MC

PRIMARY AI
Causes of Secondary AI
EXOGENOUS GLUCOCORTICOIDS
(Suppress HPA axis, adrenals atrophy)

Pituitary/CNS tumors (visual changes, thunderclap tumors)
Hemorrhage into tumors
SHEEHAN'S SYNDROME
Cortrosyn stimulation testing:
Describe
Normal values?
How would results vary based on time since onset of secondary AI?
Cortrosyn stimulation testing (CST):
Large dose of ACTH (CST) then measure cortisol
normal peak >18-20

If primary AI, will have below 18-20
NOT GOOD FOR SECONDARY AI OF RECENT ONSET bc they'll look nrml (non-atrophied zona fasciculata

If it's been a while from onset, shouldn't get an increase in cortisol (atrophy!)
How would you screen for secondary AI?
Insulin tolerance:
Hypoglycemia = stress-->stimulates HPA
Give IV insulin to induce hypoglycemia (<45 gm/dl)

(not that safe, use one below)
OR

Metyrapone testing (blocks last step in cortisol synthesis):

Normally 11-deoxy cortisol low but if block it's conversion to cortisol, cortisol levels will fall, inc'd CRH, inc'd ACTH, inc'd 11-deoxy cortisol
(11-DOC)

If have a problem in pit gland, give metyrapone at bedtime, measure in morning CRH would be low, 11-DOC doesn't go up
How do ACTH levels vary with primary/secondary AI?
If primary AI, ACTH HIGH

If secondary AI, low or inappropriately nl
Glucocorticoids:
Use
AE's
Examples (include MC affinity)
Use: Treat AI

AE's: signs of Cushing's, problems when steroids are withdrawn (can take a year to recover!)

Prednisone
Cortisol, Cortisone (binds MC)
Dexameth (doesn't bind MC as much affinity as Cortisol)
Fludrocortisone:
Mechanism
Use
Fludrocortisone; potent synthetic MC
Use: Primary AI (need to stimulate MC's)

Note: some GC drugs have MC props at high doses
Traditional dosing of glucocorticoid replacement is based on ________.
Circadian rhythms and daily fluctuations of cortisol levels

So higher dose in AM, lower dose in PM

(no good method for biochemical monitoring so if pt feels good, dose is okay)
What is adrenal crisis?
Causes?
Treatment?
More prominent in Primary or Secondary AI? Why?
Presentation of AI as hypotensive shock unresponsive to fluid resuscitation and pressors

Could be due to loss of HPA fn, abrupt withdrawal of HPA Suppression tx
Omission of adrenal replacement tx in known AI
Failure to increase adrenal replacement when necessary for acute stress (Surgery, Illness)

More common in primary Ai bc of combined GC and MC deficiencies

Tx:
Stress dose steroids for serious illness or sx, doses tapered as pt improves (2-4x usual dose of steroids)

Pts should wear Medic-alert bracelet!