2-10-99

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2-10-99

  1. 1. Endocrine (2-10-99) pituitary: “master gland of the body” called this because it was believed to control all the other glands Disorders of the Pituitary: difficult to spot primary disorders because you often spot the secondary ones first Hormones: ACTH Corticotropin GH Growth Hormone PRL Prolactin TSH Thyrotropin FSH Follicle Stimulating Hormone LH Luteinizing Hormone ACTH: bound by cell surface receptors, which activate cAMP in the adrenals, ACTH stimulates steroidogenesis (of cortisol) has extra adrenal actions stimulates lipolysis in fat cells stimulates amino acid and glucose uptake in muscle stimulates secretion of GH stimulates insulin secretion but - the above are not significant at normal levels ACTH hypersecretion: one result could be hypoglycemia increased cortisol (Cushing’s) if pituitary problem  hyperpigmentation (Cushing’s Disease) Cushing’s Disease – wake up with headaches due to hypoglycemia secretion of ACTH is stimulated by CRF (Corticotropin Releasing Factor) ACTH levels are normally highest in the AM (5-9 AM), lowest in the PM so – a value is ‘OK’ or ‘not OK’ depending on the time of day it is if levels are constant, it’s not normal (loss of the circadian rhythm) lots of things occur in pulses (Circadian rhythms, etc.) WBCs fighting the flu virus typically released in the PM (afternoon/early evening) 30-40X increase phagocytize the viruses and release lysozymes their contents give you nausea and make you feel bad get over it after 3-5 days
  2. 2. dual regulation of ACTH “long loop” cortisol inhibition of ACTH at the pituitary and CRF at the hypothalamus “short loop” ACTH inhibition of CRF at the hypothalamus GH: very popular today may be replacing steroids among athletes as a performance enhancer its anti-aging effects are being researched its secretion is stimulated by GHRF its secretion is inhibited by somatostatin Actions: stimulation of cellular differentiation/growth (both skeletal and soft tissue) promotes islet Beta cell hyperplasia increases lipolysis increases oxidative fatty acid metabolism Note: Release is not the same as activity! Factors Influencing GH Secretion: augmented by: stress (traumatic, surgical, infection)  increased concentration alpha adrenergic agonists beta adrenergic antagonists ** hypoglycemia (fasting) decreased fatty acid levels uremia hepatic cirrhosis estrogens, glucagon, vasopressin inhibited by: emotional deprivation alpha adrenergic blockers (antagonists) beta adrenergic agonists hyperglycemia (ex – insulin-dependent DM) twin studies: you have a 50% chance of getting DM if your twin has it the diabetic twin is smaller than the non-diabetic twin (they think hyperglycemia is the culprit) increased fatty acid levels obesity somatostatin, high doses of cortisol There is an inverse relationship between blood glucose and GH concentration. You can use hyperglycemia to check GH control If you make them hyperglycemic, but the GH does not decrease  BAD sign
  3. 3. Prolactin: inhibited by estrogen during pregnancy once the placenta is delivered, the estrogen decreases, so the lactogenic action of prolactin is expressed TSH: synthesis is stimulated by TRH inhibited by somatostatin and T3 (feedback inhibition) (T3 usually stimulates the other stuff) stimulates the thyroid gland FSH: controlled by gonadotropin releasing hormone (GRH) stimulates gametogenesis (both sexes) males: Sertoli cells females: ?? LH: controlled by GRH males: Leydig cells females: ?? Mechanisms of Pituitary-Hypothalamus Dysfunction: 1) 2) 3) helps you explain to the Pt why the condition is present a biggie in terms of secondary disorders the pituitary suffers from primary disorders like hyperchromatosis (??) Developmental: often associated with cleft palate or other midline deformities the pituitary often fails to grow in these cases Infectious Agents: viral encephalitis  hypothalamus  pituitary acquired “idiopathic” diabetes insipidus may be due to a viral infection pyrogenic abscess  bacteremia  severe headaches and loss of vision (signs of systemic infection) TB, syphilis (rare today) devastating when they do occur Granulomas and Infiltrative: ( cells accumulate a foreign substance) noninfectious granulomas sarcoidosis hemochromatosis myxedema often see hypopituitarism with these
  4. 4. Autoimmune Disorders: lymphocytic hypophysitis  hypopituitarism Ischemia: relatively common in the 1950s due to severe postpartum hemorrhagic or infectious shock Sheehan’s Syndrome: tissue anoxia following postpartum hemorrhage (6-8 weeks later, 3-4 months later) the Pt developed symptoms resembling a loss of pituitary function due to a 40-60% increase in the size of the pituitary gland during pregnancy (due to lactotropic cell hyperplasia) but – in a bony structure (unyielding) hemorrhage  vasospasm cellular edema  increased tissue pressure  decreased circulation in the area (circulation was not re-established)  pituitary necrosis Today: We can rapidly replenish the blood supply following a hemorrhage so that people don’t get Sheehan’s Syndrome. Most Common Cause of Pituitary Dysfunction: Tumor Tumors are the most common cause of hypopituitarism. Tumors are also the most common cause of hyperpituitarism. Hypopituitarism: If acute and complete, this can be life threatening. In its mild form, it can remain undetected for years. We see more cases of it now, possibly due to better detection. It has a wide range of symptoms, with many different presentations. (unlike hyperthyroid, which has one presentation) Disease states are influenced by: The Pt’s age The rapidity of onset of the disorder The extent of impaired hormone secretion The pathologic process involved in the cause How the Pt’s age affects a GH deficiency (Two 40-year-old Pts) #1: Age of onset = 30 fewer clinical consequences (actually, we don’t know the Pt has it) #2: Age of onset = 9 Pt is much shorter
  5. 5. GH deficiency in adults – unknown ‘normal’ is unknown/undefined (just declines in adults) Rapidity of Onset: Ex: 30 lb. Weight gain #1: Over a 10-year period (SLOW) probably won’t notice the cause #2: Over a 10-day period a definite clinical difference TSH deficiency: 30 days vs. 3 years 3 years: The Pt may have adapted to it and not notice the subtle clinical findings There may or may not be a drop in thyroid hormone (it depends on the amount of the deficiency) Extent of Impaired Hormone Secretion: 3% TSH excess vs. 30% TSH excess It’s easier for the body to compensate/adapt for a 3% excess (Innate can handle it) If the 3% excess is caused by a tumor, you get down-regulation of the thyroid receptors Pathologic Process: Speed of progression Extra endocrine manifestations ACTH Deficiency vs. Prolactin Deficiency Hypopituitarism: Many clinical pictures with diverse symptoms. Range from unrecognized to death (panhypopituitarism) Often associated with nuisance Pts. Tired, don’t feel good, … Often describes geriatric Pts, but would b abnormal in a younger Pt. 2nd Quiz in 2 weeks. Lab Dx Midterm on March 1.

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