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of cortisol by adrenals for stress response ○TSH deficiency → TH regulates metabolism ○GH deficiency → promotes growth, promotes protein synthesis, carbohydrate metabolism ○ Hyperpituitarism ■Causes: primary adenoma- caused by a benign slow growing anterior pituitary adenoma-- visual disturbances often begin in one eye & progress to the other (blurry vision)■Hypersecretion of GH, FSH, & LH is common ■Increased tumor size causes headache, fatigue, neck pain or stiffness, & seizures
■Gonadotropic hyposecretion results in menstrual irregularity, decreased libido, & receding secondary sex characteristics in both men & women. ■GH secreting pituitary adenoma effects in children & adults ●In children → gigantism ●In adults → acromegaly ■ Treatment●Goal of treatment is to protect the individual from effects of tumor growth & to control hormone hypersecretion while minimizing damage to appropriately secreting portions of the pituitary●Children (gigantism) - surgical removal of adenoma●Adults (acromegaly) - surgical removal of adenoma, radiation therapy, pharmacologic therapy (somatostatin), growth hormone receptor antagonist●Alterations in growth hormones○ Acromegaly■Results from continuous exposure to high levels of growth hormone (GH) & insulin-like growth factor 1 (IGF-1). It is almost always caused by GH-secreting pituitary adenoma (hyperpituitarism)■ Pathophysiology● Hyperpituitarism ●Increased growth hormone (GH) causes acromegaly ●Hyperglycemia results → Diabetes mellitus occurs when the pancreas cannot secrete enough insulin to offset the effects of GH ●Excessive levels of GH & IGF-1 also affect the cardiovascular system → HTN & left ventricular heart failure are seen in ⅓-½ of persons with acromegaly ●Can cause mild hyperphosphatemia●Hypopituitarism can occur as the adenoma gets larger due to compression of surrounding hormone secreting cells●Hyperprolactinemia can occur in 30%-40% of persons with acromegaly ■Clinical Manifestations●Usually occurs in adults 40-59 years●Slowly progressive disease & if untreated it is associated with a decreased life expectancy ●Increase in connective tissue and extracellular matrix
○Gradual onset ○Enlarged tongue, interstitial edema, overactive sebaceous & sweat glands, coarse skin & body hair ○Bone proliferation of vertebrae ○Enlargement of small bones of hands, feet, face, and skull, broad nose, protruding lower jaw, slanting forehead ○Nerves may be entrapped by bony or soft tissue growth leading to peripheral nerve damage ■Weakness, muscular atrophy, foot drop, sensory changes in hands ○Barrel-chested appearance & increased cartilage in joints○ Gigantism■ Pathophysiology● Hyperptiuitarism ●In children → gigantism ●Bone growth d/t non-closure of epiphyseal plates ■Clinical Manifestations●Excessive skeletal growth (8-9 feet) ○ Dwarfism■ Pathophysiology● Hypopituitarism ●Growth hormone deficiency ■Clinical Manifestations●Short stature, dwarfism ●In adults- osteoporosis, reduced lean body mass- notadequate protein ●