Pathophysiology-Endocrine

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Hypopituitarism

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Decreased secretion of pituitary hormone; 70-90% of anterior pituitary destroyed before symptoms develop; causes: tumors, surgery, lesions, infections, genetic disease; ACTH deficience is most serious deficiency with hypopituitarism

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Hypofunction of Endocrine

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Under secretion; congenital defects, infection, inflammation, autoimmune, neoplasms, altered blood flow to gland, aging, atrophy secondary to drug therapy, defective receptor sites

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Hyperfunction of Endocrine

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Over secretion; excessive hormone production, hyperplasia of gland, tumor

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Growth Hormone

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Somatotropin hormone; necessary for growth and metabolic functions, secreted during lifespan, contributes to growth of epiphyseal plates in long bones, stimulated by: hypoglycemia, fasting, starvation, stress, exercise

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GH Deficiency (Children)

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Short stature: height <5% on growth chart; panhypopituitarism: deficiency of ALL anterior pituitary hormone

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GH Deficiency (adults)

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Two categories: present during childhood; developed during adulthood, usually due to pituitary tumor

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GH Excess (children)

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Tall Stature may be caused by genetic/chromosomal disorder; precocious puberty;gigantism (rare)

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GH Excess (adults)

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Acromegaly; most common cause is adenoma (tumor); enlargement of small bones in hands and feet; enlargment of soft tissues (pronounced brow, nose, jaw); enlarged heart usually leads to death

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Hyperthyroidism

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Excessive thyroid hormone delivery to tissue; causes: autoimmune disorders, excess secretion of TSH from pituitary gland, neoplasms, excessive intake of thyroid medications

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Manifestations of Hyperthyroidism

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Increased metabolism, restlessness, diarrhea, weightloss, heat intolerance

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Grave's Disease

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Antibodies stimulate thyroid hormone via TSH receptors; cause unknown; seen more in women 20-40; goiter and exophthalmos

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Control of Thyroid

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Secretion of thyroid hormone is controlled by hypothalmic-pituitary-thyroid feedback system; TRH controls release of TSH which promotes release of TH from thyroid gland; increased levels of TH inhibit secretion of TRH, thus inhibiting the release of TSH

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Actions of Thyroid Hormone

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Increases metabolism, protein synthesis

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Goiter

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Hyperplasia of thyroid gland

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Hypothyroidism

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Congenital: results in mental retardation (cretinism- disease associated with untreated hypothyroidism) Acquired: thyroidectomy, radiation, antithyroid meds, iodine deficience, autoimmune disorder (Hashimoto's Thyroiditis)

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Manifestations of hypothyroidism

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Decreased metabolic state, weakness/fatigue, weight gain, cold intolerance, dry skin, constipation, mental dullness, lethargy, myxedematous coma

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Thyroid Storm

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life threatening coma, rare, precipitated by: stress, trauma, manipulation; fever, tachycardia, heart failure, angina, agitation, restlessness

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Adrenal Cortex

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Outer portion of the gland, steroid hormones, hormones are all synthesized from cholesterol, cells of the adrenal cortex are stimulatied by ACTH from anterior pituitary

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Hormones of Adrenal Cortex

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Essential for survival; play a role in stress, metabolism, and inflammatory (reduce inflammation) process. Glucocorticoids, Mineralcorticoids, Mineral Corticoids

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Glucocorticoids

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Have direct effects on carbohydrate metabolism; they increase blood glucose concentration by promoting stimulating glucose production (gluconeogenesis) in the liver and decreasing use of glucose in muscle, adipose tissue, and lymphatic tissue; contribute to emotional state

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Cortisol

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most potent occurring glucocorticoid; regulated by the hypothalamus and interior ptuitary gland; ACTH is the main regulator of cortisol secretion

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Mineralcorticoids

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Aldosterone: regulated by RAAS

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Hypothalamus>Pituitary>Adrenal Cortex>Adrenal Medulla

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Hypothalamus (CRH)> Anterior Pituitary (ACTH)> Adrenal Cortex (corticosteroids, mineralcorticoids, androgens)> Adrenal Medulla (catecholemines)

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Adrenal Medulla

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Secretes epinephrine and norepinephrine *disorders of the adrenal cortex or adrenal medulla result in changes in the production of adrenocorticotropic hormone (ACTH)

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Congenital Adrenal Hyperplasia

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Autosomal recessive trait; deficiency in cortisol synthesis; increased levels of ACTH and adrenal hyperplasia; may have Na loss; may have enlarged genitalia

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Cushing's Syndrome

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Chronic disorder in which hyperfunction of the adrenal cortex produces excessive amounts of circulating cortisol or ACTH; more common in females 30-50; Patho: Pituitary tumor (ACTH excess causes excess adrenal hormone), adrenal cortex tumor (stimulate corticoids/mineralcorticoids),long term glucocorticoid therapy

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Manifestations of Cushing's

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BOHEMI: Buffalo hump, obesity, hairy, emotional, moonface, increase susceptibility; SSSS-sugar, salt, sex, stria..sugar causes liver to release glucogen, salt-excess aldosterone, decreased libido, stretch marks

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Addison's Disease

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Chronic deficiency of cortisol, aldosterone, adrenal androgens; more common in women

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Pathophysiology of Addison's

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autoimmune destruction of adrenal; cancer, fungal, cytomegalovirus; bilateral adrenal hemorrhage from anticoagulant therapy; ACTH def. from pituitary tumor/surgery/irradiation; abrupt withdrawal from long-term high-dose steroid therapy

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Manifestations of Addison's

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slow onset; hyponatremia, hyperkalemia, fluid volume loss, hypotension, hypoglycemia, hyperpigmentation *opposit man. of Cushing's

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Addisonian Crisis

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life threatening response to acute adrenal insufficiency; primary symptoms are high fever, weakness, abdominal pain, severe hypotension, circulatory collapse, shock, coma; treat-rapid fluid replacement and glucocorticoids

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Energy Metabolism (Alpha Cells)

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Alpha- Glucogen: stimulates breakdown of glycogen in the liver (glycogenolysis), formation of carbs in liver (glyconeogenesis) and the breakdown of lipids; primary function is to increase blood glucose levels; acts when blood glucose levels falls below app. 70mg/dl

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Energy Metabolsism (Beta cells)

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Insulin- transports glucose into cells and transports potassium; decreases blood glucose levels by assisting glucose into the cells; release is regulated by blood glucose levels- levels rise within minutes of eating; inhibit breakdown of stored fat

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Energy Metabolism (Delta cells)

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Somatostatin-inhibits production of glucagon and insulin

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Glycogenolysis

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breakdown of glycogen stores to produce glucose

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Glyconeogenesis

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formation of glycogen in the liver from non-carbohydrate sources such as amino acids and lactates

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Catecholamines

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help to maintain blood glucose levels during periods of stress by inhibiting insulinrelease and promoting glycogenolysis

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Growth Hormone (blood glucose regulation)

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increases level of blood glucose by decreasing cellular uptake of glucose

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Glucocorticoid Hormone (Glucose level relation)

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Increase blood glucose levels by stimulating gluconeogenesis

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Glucose for Cellular Metabolism

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all organs require insulin for glucose uptake except brain, liver, intestines, and renal tubules

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Diabetes Mellitus

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Leading cause of renal failure; contributes to CAD

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Type I DM

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autoimmune reaction that destroys beta cells; beta cells of pancreas no longer produce insulin (absolute deficiency); genetic/environmental

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Type II DM

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Inadequate or insufficient amount of insulin secretion; enough insulin to prevent ketones

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Hyperglycemia

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Polyuria, Polydipsia, Polyphagia, glycosuria, dry/flushed skin, fruity breath, Kussmaul respirations, vision problems, fatiques, parethesias, skin infection

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Diabetic Ketoacidosis

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Ketone production by the liver exceeds cellular use and renal excretion; blood glucose>250 mg/dL-600; pH <7.3

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Hyperglycemic Hyperosmolar Nonketotic Syndrome

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serum osmolality >340; blood glucose >600

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Hypoglycemia

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excess insulin in blood; error in insulin dose; failure to eat; increased exercise; rapid onset; altered cerebral function

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Somogyi Effect

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Combination of hypoglycemia during night with rebound morning rise

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Dawn Phenomenon

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rise in glucose between 4am and 8am; thought to be related to nocturnal increase in GH