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DMPit-Hypothal Axis
Endocrinology Diagnostic Methods
| Question | Answer |
|---|---|
| Growth hormone stimuli | Exercise, hypoglycemia, high protein diet, acute starvation, and oral contraceptives (secondary to estrogen) |
| Causes of GH deficiency | Obesity and corticosteroid therapy |
| Preferred Imaging study for diagnosing pituitary adenoma | MRI |
| Hypersecretion of GH causes | Acromegaly or Pituitary gigantism |
| Normal response of GH to hyperglycemia | Hyperglycemia normally suppresses GH secretion. Hypoglycemia prompt GH release |
| Pituitary Dwarfism causes | Pituitary tumors, Pituitary damage, Pure GH deficiency |
| IGF-1 levels are better than ___ in diagnosing Pituitary Dwarfism | GH; IGF-1 levels are more consistent throughout the day whereas GH has a dirunal variation |
| Where is IGF-1 made? | Synthesized in the liver, influenced by nutritional status of an individual (low levels in malnutrition) |
| Function of IGF-1 | Mediates the effect of GH on skeletal muscle |
| Prolactinomas | the most common disorder involving excess pituitary secretion |
| ACTCH stimlutes what? | glucocorticoid (cortisol is the predominant form) production in the adrenal cortex |
| 2 Major actions of ADH | Alters the permeability of renal collecting tubules to water to keep water in the body, causes vasoconstriction |
| ADH is secreted at what serum osmolality? | 285mOsm/liter |
| How does renal dysfunction affect ADH? | causes decreased response to ADH and results in lower concentrating ability. Nephrogenic Diabetes Insipidus |
| Central Diabetes Insipidus | Hypothalmic origin...ADH production or release is deficient |
| ADH regulation altered by | neoplasm, surgery, trauma, inflammatory destruction of tissue (MI) or idiopathic |
| Diabetes Insipidus diagnosis | come back to |
| ADH deficiency | come back to |
| Primary ADH deficiency | Come back to |
| Nephrogenic DI or psychogenic | come back to |
| Causes of polyuria | hyperglycemia, uremia, hypercalcemia, hypokalemia, diuretic rx, renal dz of sodium or bicarb excretion |
| Psychogenic polydipisia | Compulsive, abnormal intake of fluids causes low concentration diuresis (tubules don't respond to ADH temporarily) |
| SIADH | excessive levels of ADH active material of non-pituitary origin. Low serum sodium levels, urine very concentrated. Look at BUN and Creatinine |
| Normal urine and serum osmolarity | Urine osm<Serum |
| SIADH urin and serum osmolarity | urine osm>serum |
| High serum calacium levels stimulates the thyroid to release | Calcitonin |
| Calcitonin causes | Calcium deposition in bone |
| Low serum calcium stimulates | PTH release |
| PTH causes | Calcium resorption from bone |
| PTH main function | Maintenance of adequate serum calcium levelss |
| alkaline phosphatase (ALP) | an enzyme associatd with osteocyte activity, primarily bone deposition. Elevated in growing kids. In adults, if ALP is high, but liver function is normal, think bone mets. |
| Metaolites of Vit D do what? | enhance PTH's effect on mobilization of skeletal calcium and phosphorus |
| Prolactin's unique feature | Prolactin is a unique hormone in that secretion is not driven by "positive stimulation", instead it has constant production unless suppressed by a specific inhibitory mechanism. |