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Hormonal Regulation Final Review
Terms in this set (39)
Primary organ of the body concerned with homeostasis; keeping the body's internal environment constant. It also sends hormones to anterior or posterior pituitary gland
Posterior Pituitary gland
Stores ADH and Oxytocin produced in the anterior pituitary. Oxytocin stimulates contraction of uterine smooth muscles and stimulates smoothe muscles lining in milk ducts. Anti-Diuretic Hormone (ADH) aids in the control of blood volume by acting on the kidneys to absorb more water back in the blood. ADH is referred as vasopressin because of its ability to vasoconstrict if plasma levels are extremely elevated. ADH retains water ONLY.
Syndrome of Inappropriate ADH (SIADH)
Water intoxication!!!! High levels of ADH released continually without normal physiological stimuli for release. ADH secretion increases the amount of water reabsorbed by the kidneys. Characterized by decreased urine output, concentrated urine hyperosmolarity (high specific gravity)and s/s of hypovolemia. Blood is diluted. serum osmolarity level is low. May also have confusion, seizures and coma from cell swelling of neurons.
Hyposecretion of ADH or lack of renal response to ADH causes excessive loss of water. Symptoms: polyuria (excreting large volumes of dilute urine), polydypsia (excessive thirst), low specific gravity (dilute urine) , hypernatremia. High specific osmolarity (blood concentrated) and neurological symptoms due to shrinkage and dehydration.
Greek for large extremities. Excess growth hormone caused by a tumor on the pituitary gland usually in the 4th of 5th decade of life. Increased bone density and width of bones enlarge: lower jaws, hands, face,and feet. Course skin and body hair. Increase in blood sugar.
Major target organ for hypothalamus hormones with release of its sex hormones. Hormones produced include growth hormones, thyroid stimulating hormones (TSH), and adrenocorticotropin (ACTH) which controls the release of cortisol form the adrenal gland.
Autoimmune disease in which developed antibodies stimulate TSH production and inappropriately active production of thryoid hormone.Common symptom is exopthalmus: large protruding eyes. Non-reversible overgrowth of connective tissue. Adrenergic stimulation or increased BMR, all metabolic activities are increased; energy expenditures are increased and heat production rises. excessive sweating, tremors, nervousness, thinned hair and skin, tachycardia and palpitations.
Life threatening complication involving : a sudden increase in thyroid hormone, uncontrollable fever 100-106 degrees, significant tachycardia, dysrhythmias, profound diaphoresis, shock, vomiting, dehydration, hyperkinesis, anxiety and confusion.
A medical emergency. A diminished level of consciousness associated with severe hypothyroidism. S&S: hypothermia, hypoventilation, hypotension, and bradycardia. Also have nonpitting, boggy edema around eyes, hands and feet, thickened tongue, hoarseness and slurred speech. Treated with Synthroid a thyroid replacement therapy.
Caused by failure of the normal feedback system. PTH continues to be secreted int he presence of normal levels of calcium. A compensatory response to low levels of calcium in diet. High calcium levels and low Phosphorous levels. too much PTH causes calcium to be removed form the bones into serum (hypercalcemia). S&S: multiple fractures, kyposis and compression fractures, fatigue and weakness, calcium based renal stones, constipation, N/V, anorexia, bone pain and EKG abnormalities.
usually caused by removal of all viable parathyroid tissue during total thyroidectomy. Lack of normal feedback regulation. Too little PTH in spite of calcium level. Low calcium and high phosphorus. Tetany is a major clinical manifestation. Other S&S: laryngeal spasms, carpopedal smasms, seizures and positive Chvostek or Trousseau's sign
Corticosteroid excess resulting from pituitary of adrenal tumor, excess intake of cortisol or corticosteroid drugs. S&S: moon face, purple straie (stretch mark) and buffalo hump. Increased glucocorticoids cause:Thin extremites from breakdown of fat and protein, hyperglycemia, depression to psychosis. increased mineralcorticoids retain water and sodium, too much aldesterone and lose K. Increased sex hormones acne, oily skin and hirsuitism (male patterned hair growth in women)
Chronic adrenal insuffiency caused by destruction of adrenal glands may be autoimmune. Deficient cortisol secretion, may decrease aldosterone and androgen production. Not enough aldostrone so will lose Na and water and increase K. Most S&S will be from hyperkalemia. symptoms vague intil 80-90% adrenal destroyed. Cortisol insuffiency causes diminished gluconeogenesis, decreased liver glycogen and increased sensitivity to insulin. Blood sugar goes down. Chronic fatigue, muscle weakness, salt cravings, anorexia, weight loss,hypoglycemia and hyperpigmentation. Pts become weak dehydrated and unable to maintain BP.
used as a thyroid replacement therapy to treat Myxedema coma. 100-150 mcg/day for LIFE. Increases levels of T3 and T4 because T4 is converted to T3
Used for hyperthyroidism in Graves disease and thyroid storm. Stops the thyroid from making thyroid hormone, Doesn't destroy existing thyroid stores. Preferred treatment during pregnancy and breast feeding, Monitor T3 and T4 levels.
Used for growth hormone deficiency. Promotes protein deposits that are essential for growth. Increases metabolism of fatty acids and decreases glucose utilization increasing blood sugar.
Antidiuretic hormone. Used to normalize urinary water excretion in patients with DI (LIFELONG treatment). Use caution with patients with CAD or PVD because of its powerful vasoconstriction. Prevents clot by putting water back in the blood. used on children for wetting the bed at night
Used to treat Addison's disease. Corticosteriod replacement therapy.
Disorder of carbohydrates, proteins, fats metabolism resulting from an imbalance between insulin availability and insulin need. it can represent an absolute insulin deficiency, impaired release of insulin, inadequate or defective insulin receptor or the production of inactive insulin.
Type 1 diabetes
Auto immune destruction of pancreatic cells where auto-antibodies build up in the blood and attack pancreatic beta cells. It's characterized by an absolute lack of insulin, and elevation of blood glucose and a breakdown of body fats and proteins. They are prone to ketoacidiosis. They require exogenous insulin replacement to control blood glucose levels and prevent ketosis.
Type 2 diabetes
A condition of fasting hyperglycemia that occurs despite the availability of available insulin. Caused by factors contributing to inadequate insulin secretion because the pancreas gives out, insulin resistance -a defect in the response of peripheral tissues to insulin and increased hepatic glucose production.
Diabetes Ketoacidosis (DKA)
Prone in type 1.Continued insulin deficiency results in breakdown of body tissue. Both protein and fat are metabolized. As fat stores are metabolized . Fatty acids are produced resulting in transformation of ketoacids in the liver. Major problems are hyperglycemia which leads to osmotic diuresis, dehydration, and crtical loss of electrolytes. ketosisi leads to metabolic acidosis that can progress to coma. May have kussmal breathing (deep and labored), ketouria and fruity smelling breath form acetone formation during ketosis. Warning signs are glucose level above 240 and ketones in urine.
Hyperglycemia, Hyperosmolar, Nonketotic Coma (HHNK)
Prone in type 2. Characterized by extreme hyperglycemia (800-2000) and hypermoslality >350. Combined with osmolar diuresis, eventually leads to hyperosmolar dehydration which can lead to altered consciousness and coma. If an ketoacidosis it is much less severe than DKA because they do have some insulin. No kusmall breathing or metabolic acidosis. Can occur in people on TPN.
Nerve degeneration results in tingling sensation in the fingers and toes, pain, and loss of sensation.
renal failure caused by glomerular lesions, renal vascular atherosclerosis and renal tubular alterations from glycogen and fatty changes. early manifestations are proteinuria and hypertension. As a loss of functioning nephrons progresses, patients develop renal insufficiency and uremia, Patients may require dialysis or renal transplantation.
Leading cause of blindness in US. Damage to retina resulting from lack of oxygen with hypoxia, scarring and microaneurysm formation occurs.
Rapid acting insulin
Onset: 10-30 minutes peak: 1-3 hours Duration: 3-5 hours Cannot be administered more than 5 minutes before meals.
Ex: Lispro (Humalog),Novolog (Aspart) and Apidra (Glulisine)
Short acting insulin
Onset: 30 mins- 1 hour Peak: 2-4 hours Duration: 6-8 hours
Commonly used also used to control witha sliding scale. The only form of insulin given IV. Unmodified human insulin Ex: Humulin R., Novolin R., Exubera
Onset: 1-2 hours, Peak: 6-12 hr Duration: 18-24 hrs "cloudy"
Only longer acting insulin can be mixed with short acting. injected twice daily to provide control between meals and at night Ex: NPH, Lente, Humulin N, Novolin N
24 hour coverage: Lantus (Glargine) avoids peaks and valleys onset 1 hours Levemir (Detemir) onset 3-4 hours Peak 3-4 hrs duration 12-24 hours.
Oral agents to lower plasma glucose levels for type 2 DM only Causes the pancreas to secrete more insulin ex: Glucotrol (Glipizide)
Decrease the liver's glucose production and decrease glucose absorption in the GI tract Ex: Glucophage (Metformin)
Alpha glucosidase inhibitors
Work in the intestines to delay absorption of carbohydrates from the gut Precose (Acarbose) Glyset (Miglitol)
Lowers blood glucose by improving tissue response to insulin. Decrease insulin resistance (make the cells more sensitive to insulin, so less insulin is needed to move glucose) Ex: Avandia
Lower glucose levels by stimulating release of insulin from the pancrease. Must eat within 30 minutes. Ex: Prandin
Increases incretin hormones, increases insulin secretin, decreases Glucagon secretion (Januvia)
Improve beta cell responsiveness; Adjuvant therapy for type 2 diabetics who are taking a Biguanide or Sulfonyurea. Not oral but SQ injection. Ex: Exenatide (Byetta))
Complements the effect of insulin as a supplement to insulin. Not a form of insulin. May be used in the management of Type 1 and Type 2. SQ injection never in arm.
Combination Oral Antidiabetic Agents
Combination products or fixed combination Common in type 2 diabetes management Ex: Glucovance, a sulfonamide and a biguanide
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