Silly Endocrinopathies

I'm starting to see the light at the end of a very long tunnel - there are only 26 days and 2 exams left before I complete my second year of medical school! I'm more than excited by it!

There is an exam on Tuesday, which covers Gastrointestinal and Endocrine systems. I have so much physiology to learn (especially regarding the endocrine system, hormones have never been my thing!), and a whole lot of pathology to look over (seriously, what's up with all of these silly names for diseases?! Addison's, Cushing's, Conn's, Schmidt's, Wermer's, Sipple's, Sheehan's, Grave's, Hashimoto's, deQuervain's, Plummer Disease..can't we just have names for the diseases that relate to what they are instead of by who discovered the disease and stuck their name on it?)

Here's a little revision what each of those silly names actually mean, for those who are medically inclined:
Addison's: Primary chronic adrenocortical insufficiency, resulting from progressive destruction of the adrenal cortex. Most commonly caused by autoimmune adrenalitis due to Autoimmune Polyendocrine Syndrome Type 1 (APS1) --> characterized by chronic candidiasis and abnormalities of skin, dental enamel, and nails + hypoparathyroidism...or due to Autoimmune Polyendocrine Syndrome Type 2 (APS2) --> adrenal insufficiency + autoimmune thyroiditis + type 1 diabetes mellitus.
   President John F. Kennedy had this disease.
     Symptoms: Progressive weakness and easy fatigability, nausea, vomiting, weight loss, hypotension,
               skin pigmentation (due to increased ACTH and MSH)
     Labs show:
               Low glucocorticoids (decreased glucose and then increased ACTH)
               Low mineralcorticoids (hypotension due hyponatremia, Acidosis due to hyperkalemia).
    *Stressors may precipitate an acute adrenal crisis, which can lead to coma and death without rapid treatment with corticosteroids.
Cushing's: hypercotisolism
     #1 Cause - exogenous glucocorticoid use causes adrenal atrophy.
      Endogenous causes: "Cushing's Disease" = pituitary ACTH tumor --> Increased ACTH
               --> Bilateral Adrenal Hyperplasia
      Endogenous: "Cushing's Syndrome" = adrenal adenoma/carcinoma or nodular hyperplasia
              --> Decreased ACTH --> Contralateral gland atrophy
      Endogenous: "Cushing's Syndrome" = ectopic ACTH tumor (such as small cell carcinoma of the lung)
             --> Increased ACTH --> Bilateral Hyperplasia
     Symptoms: Hypertension & weight gain early; then truncal obesity, moon faces, buffalo hump,
              weakness, diabetes/glucose intolerance, osteoporosis, pink skin striae,
              increased infections, mental disturbances.
Conn's: a solitary adrenal adenoma secretes aldosterone
     Symptoms: hypertension (due to hypernatremia), with or without muscle weakness (due to hypokalemia)
          Increased aldosterone = rental Na retention and K loss --> Increased blood pressure & possible hypokalemia
Schmidt's: an autoimmune polyendocrine syndrome (APS). Also known as "APS Type 2".
     Addison's disease + hypothyroidism + diabetes mellitus type 1
Wermer Syndrome:AKA Multiple Endocrine Neoplasia 1 (MEN1). These are known as the "P" lesions.
     Cause: Gene Mutation - MEN1 mutation (a tumor suppressor gene)
     "P" Lesions:
               Parathyroid - hyperparathyroidism, hypercalcemia
               Pituitary - prolactinoma most common, acromegaly.
               Pancreatic Islets -  gastrinoma or insulinoma
               Peptic Ulcers - from gastrinoma
Sipple Syndrome: AKA Multiple Endocrine Neoplasia 2a (MEN2a).
  "TAP"(Thyroid, Adrenal, Parathyroid)
     Diseases: Medullary Carcinoma of the Thyroid & Pheochromocytoma, plus Parathyroid Hyperplasia.
                *Parathyroid Hyperplasia* is not present in MEN2b.
     Cause: Mutation of RET Oncogene
               Screen family of patient; suggest prophylactic thyroidectomy to those with RET mutation
Sheehan's: Post-partum anterior pituitary necrosis. Relatively common.
     Various Mechanisms, including: shock, DIC (post-partum)
     Hormones Affected: All anterior pituitary hormones will decrease, most notably TSH and ACTH.
Grave's:
     Etiology: Usually affects women in their 20s-40s, 1-2% of entire population.
     Symptoms: Triad: Hyperthyroidism, Opthalmopathy (eye proptosis), & Dermopathy (pretibial leg edema)
     The cause is: Autoimmune --> antibodies to TSH receptor (TSI - "Thyroid Stimulating Immunoglobins")
Hashimoto's: lymphocytic infiltrate with germinal centers & Hurthle cell hyperplasia, maybe fibrosis. Painless.
     Etiology: Women. 45-65 yrs old. Adult Down's Syndrome patients have increased risk.
            Autoimmune assocation (SLE, RA, DM, etc.)
     Symptoms: Painless enlargement of thyroid. Hypothyroidism
            (#1 cause of hypothyroidism is Hashimoto's). Goiter.
     Cause: Antimicrosomal Antibodies (antibodies to thyroid peroxidase), Anti-thyroglobulin antibodies.
     Risks: Small increased risk of developing B-Cell Lymphoma (especially MALT Lymphoma)
DeQuervain's subacute granulomatous thyroiditis:
     Symtpoms: Fever; Painful thyroid enlargement, Self-limited, transient hyperfunction.
     Cause: Viral? (incidence peaks in summer)
     Lab Findings: Giant cells/granulomas in thyroid.
Plummer Syndrome: toxic multinodular goiter (goiter is an enlarged thyroid gland). An autonomous nodule within a long-standing goiter which produces lots of T3/T4, thus producing hyperthyroidism symptoms.
     Symptoms: Hyperthyroidism.


Right. Now that we have that cleared up, I think I can go ahead and continue my never-ending revisions. The GI system is easy enough for me, because the diseases are much more common, but endocrinology is more difficult. Fingers crossed for a good mark on this exam; I'm working towards getting a good final grade in organ systems!