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19 Cards in this Set
- Front
- Back
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what are the causes and symptoms of Cushings disease?
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anterior pituitary tumor - overproduces ACTH
stimulates the adrenal gland to overproduce cortisol, resulting in Cushing's syndrome causes buffalo hump, moon facies, violaceous stria, truncal obesity, HPTN, hyperglycemia, osteoporosis, poor wound healing (decreased collagen and tissue) |
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What are the labs seen in Polycystic Ovarian Syndrome? Menopause?
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POS - hi LH, androstenedione, testosterone, estrone.
low FSH, LH:FSH ration of 2:1 Menopause - low progesterone, low estrogen hi LH, FSH. FSH:LH 2:1 |
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What is the cause of Diabetes Insipidus?
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head trauma wherein the posterior pituitary or hypothalamus are damaged
results in ADH deficiency secondary to decreased secretion by the posterior pituitary causes polyuria and p olydipsia nephrogenic diabetes insipidus is due to lack of kidney response to ADH - similar symptoms |
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What causes Cushings syndrome?
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ANY increase in glucocorticoids: adrenal adenoma/carcinoma (increased cortisol), Cushings Dx (ACTH adenoma), small cell lung carcinoma (paraneoplastic production of ACTH), prolonged glucocorticoids
screen with 24 hour urinary cortisol. confirm with dexamethasone suppression test |
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What is a pheochromocytoma?
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tumor of the adrenal medulla
excess NE and epi (intra medulla) or without epi (extra medulla) screen - 24 hour urinary catecholamines better - 24 hour urinary metanephrines and normetanephrines best - 24 hour urinary VMA (fina metabolite of both epi/NE) |
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What is the typical cause of Addison's disease?
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usually autoimmune, but can be due to Mycobacterium tuberculosis or Histoplasma capsulatum
results in decreased aldosterone production - excess Na excreted, excess K retention. excess production of POMC - ACTH and MSH - hyperpigmented |
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What is the difference between primary and secondary hyper/hypothyroidisms?
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primary hyper - damage to thyroid causing high T3/4, low TSH
secondary hyper - damage to pituitary causing high TSH, high T3/4 primary hypo - problem with thyroid causing low T3/4, high Tsh secondary hypo - problem in pituitary causing low TSH, low T3/4 |
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What is Hashimoto's thyroiditis?
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Tcell disorder with anti-thyroid antibodies and/or anti-thyroglobulin antibodies that result in the destruction of the thyroid gland
hypothyroid symptoms develop treat with levothyroxine |
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What is DeQuervain's thyroiditis?
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sub-acute thyroiditis, granulomatous thyroiditis
viral etiology - follows URI malaise, fever, and upper respiratory complaints - thyroid becomes enlarged and tender with pain radiation to jaws, face and ears hyperthyroid followed by hypo NSAIDs |
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What is follicular adenoma?
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benign thyroid tumor.
single, palpable thyroid nodule - often hyperthyrid. 1 nodule - usually functional - produce increased levels of thyroid hormone |
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what are the 4 thyroid carcinomas?
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papillary - most common - best prognosis - prior radiotherapy of the neck - finger like projections
follicular - middle aged - poorer prognosis anaplastic - elderly = already mets at diagnosis - very aggressive w very bad prognosis medullary - tumor of parafollicular C cells (normally manufacture calcitonin to encourage Ca deposition into bone) - produces high calcitonin - hypocalcemia |
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What are the roles of the parathyroid gland
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activates osteoclasts - increases bone demineralization and increasing serum Ca
increases renal tubular reabsorption of Ca - increases serum Ca increases Vit D conversion to 1,25 in kidneys - increases serum Ca, serum phosphorus (decreases overall) increases renal phophate excretion - decreases serum phosphate increases GI absoprption of Ca - increases serum Ca |
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What is the difference in primary and secondary hyperparathyroidism?
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primary - pathology of parathyroid gland - hi PTH, hi Ca, lo PO4
secondary - due to low calcium with resulting response of activity by parathyroid gland ex: chronic renal failure - kidney does respond to PTH, and will not reabsorb Ca, allowing for loss of Ca in urine. makes even more PTH - hi PTH, lo Ca, hi PO4. |
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What is the primary cause of hypoparathyroidism?
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acidental removal during thyroidectomy
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How does chronic renal failure result in renal osteodystrophy?
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1) decreased phosphate excretion - hi PO4 - binds ionized Ca in serum - Ca precipitates out of serum - HYPOCALCEMIA - increases PTH - bone demineralization - renal osteodystrophy
2) decreased active vitamin D production - HYPOCALCEMIA - increased PTH - bone demineralization - renal osteodystrophy |
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What are the symptoms of Type 1 DM?
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juvenile onset (2-12)
ketoacidosis risk (lack of insulin + stress allows for extreme overactivation of hormone sensitive lipase - explosive lipolysis) - ab pain, deydration, met acid HLA-DR3 and DR2 Anti-islet cell Abs destroy beta-islet cells that produce insulin Lean body habitus - cause increase in hormone sensitive lipase - fat breakdown and decreased glucose and AA uptake by tissue |
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What are the symptoms of Type 2 DM
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very common
hyperosmolar nonketotic coma risk (if untreated, glucose levels can reach enormous levels causing the blood to be very hyperosmolar - causing water to be drawn into the vasculature, dessicating the brain and causing eventual coma) no HLA connection, No autoantibodies Obese body habitus (excess carbs ingested leads to increased demands on pancreas for insulin - leading to Type 2 DM - the excess carbs serve to allow for weight gain) insulin production may be high, normal, or low depending on stage |
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What is MODY?
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maturity onset diabetes of the young
due to a defect in glucokinase - prevents cells from being able to adequately phosphorylate glucose that is made available. The glucose cannot be used and is released back into the serum causing HYPERGLYCEMIA |
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What are the tissues involved with the 3 different multiple endocrine neoplasias (MEN)?
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MEN 1 - Wermers Syndrome - Adrenal cortex, Pituitary, Parathyroid, Pancreas
MEN 2A - Sipple's syndrome - adrenal medulla, Thyroid medulla, Parathyroid MEN 2B - MEN type 3 - Adrenal medulla, Thyroid medulla, Mucosal neuromas, Marfanoid features |
