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Anything missing w Addison Disease? - goodman
#1
Autoinmune destruction of the Adrenal Glands, evidenced by lymphocytic infiltration and progressive atrophy of the adrenal cortex.
THINGS TO REMEMBER
Conn Disease
Primary Aldosteronism. Caractherized by episodic weakness, paresthesias, transient paralysis, tetany + diastolic hypertension
Primary Aldosteronism (HYPERALDOSTERONISM) due to an aldosterone-producing adenoma. S/S: Hypertension and Headache.
Lab Finding are Hyperkalemia and Hypernatremia. Metabolic Alkalosis is commnon. ALDOSTERONE HIGH. RENIN LEVELS ARE LOW.
↑ of the Aldosterone which can be cause by adrenal hyperplasia or an adenoma. Hypertension and Hypokalemia are typically finding
NSTx is Spironolactone (Aldosterone receptor antagonists) in bilateral adrenal hyperplasia case. If unilateral Surgery is Tx of choice

Syndrome of Hypocortisolism, chronic weakness, menstrual disturbances, skin melanosis, hypotension, hyponatremia and K+ ↑
The areola and vagina have bluish-black discoloration (HYPERPIGMENTATION). Non-Anion Gap METABOLIC ACIDOSIS
ECG changes (↓ voltage and prolonged PR) EEG (slowing of alpha Rhytm)
Hypoaldosteronism. Non-Anion Gap METABOLIC ACIDOSIS. No Aldosterone. (lossing Na in the URINE)
Hypotension, Hyponatremia, Hyperkalemia, Hyperpigmentation + Non-Anion Gap Metabolic Acidosis
Distinguish from Secundary Hypoaldosteronism or Hypocortisolism in which has NO hyperpigmentation (Pituitary ACTH production ↓Wink
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