Pharm test #3 – Flashcards

→Gland is made up of cells arranged in circular follicles (Karch, 564) →The center of each follicle is composed of colloid tissue, in which the thyroid hormones produced by the gland are stored (Karch, 564) →Cells around the follicle are parafollicular cells - produce calcitonin, which affects calcium levels and acts to balance the effects of the parathyroid hormone (Karch, 564) The thyroid gland produces two slightly different thyroid hormones, using IODINE that is found in the diet. 1.) thyroxine or tetraiodothyronine (T4)-4 iodine atoms. Given therapeutically in the synthetic form: levothyroxine 2) Triiodothyronine (T3)-3 iodine atoms, given in teh synthetic form liothyronine. *Thyroid gland produces more T4 than T3, more T4 is released into circulation *T3 is 4x more active than T4 *T4 has a half life of 12 hours and is converted to T3 at the tissue level *T3 has a half-life of about 1 week →The thyroid cells remove iodine from the blood, concentrate it, and prepare it for attachment to tyrosine, an amino acid (Karch, 565) *A person must obtain sufficient amounts of dietary iodine to produce thyroid hormones. →Thyroid hormone regulates the rate of metabolism, affect heat production and body temperature, oxygen consumption and cardiac output, blood volume, enzyme system activity, and metabolism of carbohydrates, fats, and proteins (Karch, 565) →Important regulator of growth and development especially within the reproductive and nervous systems (Karch, 565) →Necessary for growth and development in children including mental development and attainment of sexual maturity (Porth, 785) →Increases the metabolism of all body tissues except the retinas, spleen, testes, and lungs (Porth, 785) →Can increase basal metabolic rate 60%-100% above normal (Porth, 785) -Lipids are mobilized from adipose tissue and the catabolism of cholesterol by the liver is increased. →Rise in oxygen consumptions and production of metabolic end products (Porth, 785) -Absorption of glucose from the GI tract is increased. →Increase in vasodilation (Porth, 785) →Increased blood volume, cardiac output, and ventilation (Porth, 785) →Heart rate and cardiac contractility are enhanced (Porth, 785) →Blood pressure changes little due to vasodilation offsetting increased cardiac output (Porth, 785) →Enhances gastrointestinal function causing increased motility and production of gastrointestinal secretions that often results in diarrhea (Porth, 785) →Increase in appetite and food intake accompanies the higher metabolic rate; at the same time, weight loss occurs because of the increased use of calories (Porth, 785) →Skeletal muscles react more vigorously with increase thyroid hormone and react sluggishly with a drop in thyroid hormone (Porth, 785) →Causes extreme nervousness, anxiety, and difficulty in sleeping (Porth, 785) →Strong interaction between thyroid hormone and the sympathetic nervous system (Porth, 785) •Hyperthyroidism suggest over activity of the sympathetic nervous system - tachycardia, palpitations, sweating, tremor, restlessness, anxiety, diarrhea (Porth, 785)

→Stimulates osteoclasts or bone cells to release calcium from the bone (Karch, 574) →Increases intestinal absorption of calcium (Karch, 574) →Increases calcium resorption from the kidneys (Karch, 574) →Stimulates cells in kidney to produce calcitriol, the active form of vitamin D, which stimulates transport of calcium into the blood (Karch, 574)

→Adrenal medulla is part of the sympathetic nervous system with ganglion that releases norepinephrine and epinephrine, which acts as a backup system for the sympathetic system (Karch, 549) →The adrenal medulla synthesizes corticosteroids - androgens, glucocorticoids, and mineralocorticoids - they affect electrolytes, stimulate protein production, and decrease protein breakdown (Karch, 549) -Adrenal medulla secretes epinephrine and NE and is part of the SNS. -Adrenal cortex secretes 3 types of steroid hormones: 1.) Glucocorticoids (cortisol/hydrocortisone) aid in regulating metabolic functions (blood glucose) of the body and controlling inflammatory response. Essential for survival in stress situations. 2.) Mineralcorticoids (aldosterone) function in sodium, potassium and water balance. promotes sodium retention and potassium excretion. 3.) Adrenal androgens (chief sex hormones). Principally androgens, serve mainly as a source of androgens for women. -Adrenal cortical function is necessary for life.

→The synthesis and release of anterior pituitary hormones are largely regulated by the action of releasing or inhibiting hormones from the HYPOTHALAMUS, which is the coordinating center of the brain for endocrine, behavioral, and autonomic nervous system function. →It is at the level of the hypothalamus that emotion, pain, body temperature, and other neural input are communicated to the endocrine system. →The posterior pituitary hormones: ADH and oxytocin are synthesized in the cell bodies of neurons in the hypothalamus that have axons that travel to the posterior pituitary. →Receives input from virtually all other areas of the brain including the limbic system and the cerebral cortex (Karch, 527) →Able to influence and be influence by emotions and thoughts (Karch, 527) →Acts as a sensor to various electrolytes, chemicals, and hormones in circulation and do not affect other areas of the brain (Karch, 527) →Maintains internal homeostasis by sensing blood chemistries and by stimulating or suppressing endocrine, autonomic, and CNS activity - it can turn the autonomic nervous system on or off (Karch, 527) →Produces and secretes hormones or factors that stimulate the pituitary gland to stimulate or inhibit various endocrine glands throughout the body including growth hormone-releasing hormone (GHRH), somatostatin, dopamine, thyrotropin-releasing hormone (TRH), gonadotropin-releasing hormone (GnRH), corticotropin-releasing hormone (CRH), and prolactin-releasing hormone (PRH). (Karch, 527) → GH secretion is stimulated by GHRH → Thyroid-stimulating hormone TSH is stimulated by TRH → ACTH is stimulated by CRH → Luteinizing hormone (LH) and FSH by GnRH. → Stomatostatin functions as an inhibitory hormone for GH and TSH. → Prolactin secretion is inhibited by dopamine; thus, persons receiving antipsychotic drugs that block dopamine often have increased prolactin levels. → With the exception of GH and prolactin, most of the pituitary hormones are regulated by hypothalamic simulatory hormones. →Produces two inhibiting factors that act as regulators to shut off the production of hormones when levels become too high: growth hormone release-inhibiting factor (somatostatin) and prolactin-inhibiting factor (PIF) (Karch, 527) (website definition) The hypothalamus controls the autonomic nervous system. The autonomic nervous system is the portion of the nervous system responsible for maintaining homeostasis. Thus, damage to the hypothalamus results in severe imbalances in the internal environment. The hypothalamus contains the thirst center, the hunger center and the body's thermostat. Thus, damage to the hypothalamus frequently results in water, glucose and temperature imbalances. The hypothalamus controls the hypophysis (pituitary gland). The hypophysis is the most important endocrine gland in the body and is often referred to as the "master gland". The hyopohysis is referred to as the master gland because it controls most of the other endocrine glands in the body such as the thyroid, adrenal gland, testis and ovaries. By controlling the hypophysis the hypothalamus exerts control over most endocrine glands. The control of the hypophysis by the hypothalamus is the best example in the human body of the big boss nervous system (hypothalamus) controlling the little boss endocrine system (hypophysis). The hypothalamus is the site of emotions and the effect emotions can have on the body.

• All adrenocorticol hormones are steroids and are synthesized from acetate and cholesterol. • ALDOSTERONE: principal mineralcorticoid • CORTISOL (hydrocortisone): major glucocorticoid • ANDROGENS: chief sex hormones → Adrenal androgens • Contribute to the pubertal growth of body hair, particularly pubic and axillary hair in women (Porth, 790) • Exert little effect on normal sexual function. DHEA and its sulfate conjugate (DHEAS) contribute to the pubertal growth of body hair, particularly pubic and axillary hair in women. They also may play a role in the steroid hormone economy of the pregnant woman and the fetal-placental unit. DHEAS is used with Addison's disease. → Mineralocorticoids (Aldosterone) • Essential role in regulating potassium and sodium levels and water balance (Porth, 791) • Increased levels of aldosterone promote sodium retention by the distale tubules of the kidneys while increasing urinary losses of potassium. → Glucocorticoids (cortisol) • Necessary function in response to stress and are essential for survival (Porth, 791) • Aid in regulating the metabolic functions of the body and in controlling the inflammatory response (Porth, 791) • Glucose metabolism → Ability to stimulate gluconeogenesis (glucose production) by the liver (Porth, 792) → Decreases glucose use by the tissues • Protein metabolism → Body proteins are broken down and their amino acids are mobilized and transported to the liver, where they are used in the production of glucose (Porth, 792) → Increases plasma protein levels • Fat metabolism → Increases mobilization of fatty acids. Increases use of fatty acids. • Anti-inflammatory action → Increased cortisol blocks inflammation at an early stage by decreasing capillary permeability and stabilizing the lysosomal membranes so that inflammatory mediators are not released (Porth, 792) → Decreases capillary permeability to prevent inflammatory edema → Depresses phagocytosis by WBCs to reduce the release of inflammatory mediators → Suppresses immune response • Causes atrophy of lymphoid tissue • Decreases eosinophils • Decreases antibody formation • Decreases the development of cell-mediated immunity → Large quantities of cortisol are required for an effective anti-inflammatory action - achieved by the administration of pharmacologic rather than physiologic doses of cortisol (Porth, 792) → Suppresses fibroblast activity and thereby lessens scar fomation (Porth, 792) → Inhibits prostaglandin synthesis, which may account for its anti-inflammatory actions (Porth, 792) → Reduces fever • Psychic effect → May contribute to emotional instability • Permissive effect → Facilitates the response of the tissues to humoral and neural influences, such as that of the catecholamines, during trauma and extreme stress.

-Adrenal cortex: cortisol-increases glucose levels, suppresses inflammatory and immune reactions. aldosterone-sodium retention/potassium excretion -Kidney (Juxtaglomerular cells): erythropoietin-stimulates RBC production renin- stimulates increase in BP/vascular volume -Pancreas: insulin/glucagon/somatostatin -Regulation of glucose, fat metabolism (islets of langerhans) -Parathyroid glands: PTH increases serum calcium -Pineal gland: melatonin affects secretion of hypothalamic hormones, particularly gonadotropin-releasing hormone -Placenta: Estrogens/progesterone Maintains fetal growth and development, prepares the body for delivery -Thyroid: thyroid hormone/calcitonin Thyroid hormone: Stimulates BMR Calcitonin: decreases calcium levels

→ Pathophysiology • Primary adrenal insufficiency in which adrenal cortical hormones are deficient and ACTH levels are elevated because of lack of feedback inhibition. • Chronic metabolic disorder that requires lifetime hormone replacement therapy. • All layers of the adrenal cortex are destroyed (Porth, 794) • Autoimmune destruction is the most common cause (Porth, 794) • Before 1950, tuberculosis was the major cause of Addison disease in the United States and Canada, and it continues to be a major cause of the disease in countries where the infection is more prevalent (Porth, 794) • Rare causes include metastatic carcinoma fungal infection (particularly histoplasmosis), cytomegalovirus, amyloid disease, and hemochromatosis (Porth, 794) • Bilateral adrenal hemorrhage may occur in persons taking anticoagulants, during open heart surgery, and during birth or major trauma. • Adrenal insufficiency can be caused by AIDS, in which the adrenal gland is destroyed by a variety of opportunistic infectious agents (Porth, 794) • Drugs (Ketoconazole) that inhibit synthesis or cause excessive breakdown of glucocorticoids can also result in adrenal insufficiency (Porth, 794) • Chronic metabolic disorder that requires lifetime hormone replacement therapy (Porth, 794)

• Increased urinary losses of sodium, chloride, and water, along with decreased excretion of potassium leading to hyponatremia, loss of extracellular fluid, decreased cardiac output, and hyperkalemia (Porth, 794) • Abnormal appetite for salt (Porth, 794) • Orthostatic hypotension, dehydration, weakness, fatigue, cardiovascular collapse, shock, poor stress tolerance, hypoglycemia, lethargy, weakness, fever, gastrointestinal symptoms (e.g. anorexia, nausea, vomiting, diarrhea weight loss) (Porth, 794) • Hyperpigmentation, oral mucous membranes may become bluish-black (Porth, 795). Skin looks bronzed or suntanned in exposed and unexposed arease, and the normal creases and pressure points tend to become expecially dark. • Myalgia, arthralgia and abd pain (10%)

•Hypercortisolism •Pituitary form of Cushing is caused by excess production of ACTH by a tumor of the pituitary gland (Porth, 795)** • Adrenal form of Cushing is caused by benign or malignant adrenal tumor (Porth, 795) • Ectopic Cushing is caused by non-pituitary ACTH-secreting tumor (Porth, 795) • Certain extrapituitary malignant tumors such as small cell carcinoma of the lung may secrete ACTH or, rarely, CRH and produce Cushing's syndrome. • Can also result from long-term therapy with one of the potent pharmacologic preparations of glucocorticoids - this is called iatrogenic Cushing syndrome (Porth, 795)

• Altered fat metabolism causes a peculiar deposition of fat characterized by a protruding abdomen; subclavicular fat pads or "buffalo hump" on the back; and a round, plethoric "moon face" (Porth, 795) • Muscle weakness, and the extremities are thin because of the protein breakdown and muscle wasting (Porth, 795) • Skin over the forearms and legs becomes thin, having the appearance of parchment (Porth, 795) • Purple striae, or stretch marks from stretching of the catabolically weakened skin and subcutaneous tissues are distributed over the breast, thighs, and abdomen (Porth, 795) • Osteoporosis may develop because of destruction of bone proteins and alterations in calcium metabolism, resulting in back pain, compression fractures of the vertebrae, and rib fractures. As calcium is mobilized from bone, renal calculi may develope (Porth, 795) • Derangements in glucose metabolism are found in approximately 75% of patients, with clinically overt diabetes mellitus occurring in approximately 20%. • Hypokalemia as a result of excessive potassium excretion and hypertension resulting from sodium retention (Porth, 795) • Inflammatory and immune responses are inhibited, resulting in increased susceptibility to infection (Porth, 795) • Cortisol increase gastric acid secretion, which may provoke gastric ulceration and bleeding (Porth, 795) • Ecchymoses • An accompanying increase in androgen levels causes hirsutism, mild acnes, and menstrual irregularities in women (Porth, 795) • Excess levels of the glucocorticoids may give rise to extreme emotional lability ranging from mild euphoria and absence of normal fatigue to grossly psychotic behavior (Porth, 796)

•Life-threatening, end-stage expression of hypothyroidism (Porth, 788) •The pathophysiology of myxedema coma involves 3 major aspects: i. Carbon dioxide retention and hypoxemia (Porth, 788) ii. Fluid and electrolyte imbalance (Porth, 788) Hyponatremia/Hypoglycemia iii. Hypothermia (Porth, 788) •Occurs most often in elderly women who have chronic hypothyroidism from a spectrum of causes. •Occurs more frequently in winter months suggesting that cold exposure may be a precipitating factor (Porth, 788) •Severely hypothyroid patients are unable to metabolize sedatives, analgesics, and anesthetic drugs, and buildup of these agents may precipitate coma (Porth, 788)

•Coma, hypothermia, cardiovascular collapse, hypoventilation, hyponatremia, hypoglycemia, lactic acidosis (Porth, 788) • Manifestations of hypothyroidism → Coarse, brittle, dry hair → Loss of lateral eyebrows → Pallor → Large tongue → Weight gain → Lethargy and impaired memory → Periorbital edema and puffy face → Deep, coarse voice → Diminished perspiration → Cold intolerance → Slow pulse, enlarged heart → Gastric atrophy → Constipation → Menorrhagia → Muscle weakness → Peripheral edema

•Disease of hyperthyroidism, goiter, ophthalmopathy, or less commonly dermopathy (Porth, 789) • Onset is usually between 20-40 years old and women are five times more likely to develop Graves than men (Porth, 789) • Autoimmune disorder characterized by abnormal stimulation of the thyroid gland by thyroid-stimulating antibodies (TSH-receptor antibodies) that act through the normal TSH receptors (Porth, 789) • May be associated with other autoimmune disorders such as myasthenia gravis and pernicious anema (Porth, 789) • Associated with human leukocyte antigen (HLA)-DR3 and HLA-B8 and a familial tendency is evident (Porth, 789)

•Ophthalmopathy can cause severe eye problems including abnormal positioning of the extraocular muscles resulting in diplopia; involvement of the optic nerve can cause visual loss; corneal ulceration may occure because the lids do not close over the protruding eyeball (Porth, 789) • Hyperthyroidism, goiter, ophthalmopathy, dermopathy (Porth, 789) → Manifestations of hyperthyroidism: • Fine hair • Exopthalmos-bulging eyes • Sweating/heat intolerance • Muscle wasting • Oligomenorrhea • Nervousness/restlessness/emotional instability/insomnia • Tachycardia/palpitations/high output failure • Increased appetite • Weight loss • Fine tremor • Pretibial mysedema

→ Related to the hypometabolic state resulting from thyroid hormone deficiency and myxedematous involvement of body tissues (Porth, 787) → Weakness, fatigue, weight gain despite a loss of appetite, cold intolerance, dry and rough skin, coarse and brittle hair (Porth, 787) → Decreased conversion of carotene to vitamin A leading to high blood levels of carotene causing a yellowish skin color (Porth, 787) → Puffy face with edematous eyelids, thinning of the outer third of the eyebrows (Porth, 787) → Fluid may collect in almost any serous cavity and in the middle ear giving risk to conductive deafness (Porth, 787) → Gastrointestinal motility is decrease producing constipation, flatulence, and abdominal distention (Porth, 787) → Delayed relaxation of deep tendon reflexes and bradycardia are sometimes noted (Porth, 787) → Mental dullness, lethargy, impaired memory (Porth, 787) → Tongue is often enlarge, the voice become hoarse and husky, carpal tunnel is common, muscle impairment with stiffness, cramps, and pain (Porth, 787) → Pericardial or pleural effusion may develop (Porth, 787) → Mucopolysaccharide deposits in the heart cause generalized cardiac dilation, bradycardia, and other signs of altered cardiac function (Porth, 787)

→Related to increase oxygen consumption and use of metabolic fuels associated with the hypermetabolic state as well as the increase in sympathetic nervous system activity that occurs (Porth, 788) →Nervousness, irritability, fatigability, weight loss despite a large appetite, tachycardia, palpitations, shortness of breath, excessive sweating, muscle cramps, heat intolerance, restlessness, fine muscle tremor, exophthalmos or an abnormal retraction of the eyelids, infrequently blinking, thin hair and skin with a silky appearance, atrial fibrillation (Porth, 788)

→ Actions • (ATI) Thyroid hormones are a synthetic form of thyroxine (T4) that increase metabolic rate, protein synthesis, CO, renal perfusion, oxygen use, body temperature, blood volume, and growth processes. • Increase the metabolic rate of body tissues, increasing oxygen consumption, respiration, heart rate, growth and maturation, and the metabolism of fats, carbohydrates, and proteins (Karch, 568) • Indicated for replacement therapy in hypothyroid states, treatment of myxedema coma, suppression of TSH in the treatment and prevention of goiters, management of thyroid cancer (Karch, 568) • Used with antithyroid drugs to treat thyroid toxicity, prevent goiter formation during thyroid overstimulation, and treat thyroid overstimulation during pregnancy (Karch, 568) → Adverse effects • Skin reactions and loss of hair are sometimes seen especially during the first few months of treatment in children (Karch, 570) • Symptoms of hyperthyroidism may occur as the drug dose is regulated (Karch, 570) • Overmedication can result in signs of hyperthyroidism (anxiety, tachycardia, palpitations, altered appetite, abd cramping, heat intolerance, fever diaphoresis, weight loss, and menstrual irregularities) • Less predictable effects are associated with cardiac stimulation (arrhythmias, hypertension), central nervous system effects (anxiety, sleeplessness, headache), and difficulty swallowing (Karch, 570) → Drug-to-drug interaction • Decreased absorption of thyroid hormones occurs when they are taken concurrently with cholestyramine - take 2 hours apart (Karch, 570) • Effectiveness of oral anticoagulants (Coumadin) is increased if they are combined with thyroid hormone (Karch, 570) • Decreased effectiveness of digitalis glycosides can occur - monitor digitalis levels (Karch, 570) • Theophylline clearance is decreased in hypothyroid states - monitor theophylline levels (Karch, 570) • Antacids • Iron • Calcium • Sucralfate • Antiseizure/antidepressants: carbamazepine (Tegretol), phenytoin (Dilantin), Phenobarbital, and sertraline (Zoloft). → Contraindications • During acute thyrotoxicosis or during/following acute myocardial infarction because the thyroid hormones could exacerbate these conditions (Karch, 5769) • During lactation because the drug enters breast milk and could suppress the infant's thyroid production (Karch, 5769) • With hypoadrenal conditions (e.g. Addison) (Karch, 570) • Pregnancy Risk A be cautious. • Use cautiously in patients with cardiovascular problems: HTN, angina pectoris, ischemic heart dz. → Time for therapeutic effect • 1-3 weeks orally (Karch, 570) • 24-48 hours IV (Karch, 570) → Signs and symptoms of overdose • See signs and symptoms of hyperthyroidism - e.g. tachycardia, hypertension, anxiety, skin rash (Karch, 570) → Take daily on an empty stomach (before breakfast)

→Uses: Grave's dz, producing a euthryoid state before thyroid removal, as an adjunct to irradiation of the thyroid gland, in the emergency tx of thyrotoxicosis. → Actions • (ATI) blocks synthesis of thyroid hormones; prevents the oxidation of iodide; and blocks conversion of T4 to T3. • Lowers thyroid hormone levels by preventing the formation of thyroid hormone in the thyroid cells, which lowers the serum levels of thyroid hormone (Karch, 572) • Partially inhibit the conversion of T4 to T3 at the cellular level (Karch, 572) → Adverse effects • Effects of thyroid suppression - drowsiness, lethargy, bradycardia, nausea, skin rash, depression, edema, cold intolerance, dry skin, menorrhagia (Karch, 573) • Agranulocytosis • Nausea, vomiting, GI complaints (Karch, 573) → Drug-to-drug interaction • Increased risk for bleeding when taken with oral anticoagulants (Karch, 573) • Digoxin • Changes in serum levels of theophylline, metoprolol, propranolol, and digitalis may lead to changes in the effects as the patient moves from hyperthyroid to euthyroid (Karch, 573) → Contraindications • During pregnancy because of the risk of adverse effects on the fetus and the development cretinism (Karch, 573) Pregnancy Risk Category D • During lactation because of the risk of antithyroid activity in the infant including the development of a neonatal goiter (Karch, 573) • Use caution with bone marrow suppression and immunosuppression. → Time for therapeutic effect • Varies per patient (Karch, 572-573) Someimtes takes 1-2 weeks (ATI) → Signs and symptoms of overdose • See signs and symptoms of hypothyroidism - e.g. bradycardia, lethargy, fatigue, drowsiness (Karch, 573)

•Hormones produced by the anterior pituitary control body growth and metabolism (GH), function of the thyroid gland (TSH), glucocorticoid hormone levels (ACTH), function of the gonads (FSH and LH), and breast growth and milk production (prolactin). Melanocyte-stimulating hormone (MSH), which is involved in the control of pigmentation of the skin, is produced by the pars intermedia of the pituitary gland.

→ Adverse effects •Breakthrough bleeding, menstrual irregularities, dysmenorrhea, amenorrhea, changes in libido (Karch, 626) •Fluid retention, electrolyte disturbances, headache, dizziness, mental changes, weight changes, edema (Karch, 626) •Nausea, vomiting, abdominal cramps, bloating, colitis (Karch, 626) •Acute pancreatitis, cholestatic jaundice, hepatic adenoma (Karch, 626) →Drug-to-drug interactions •If given in combination with drugs that enhance hepatic metabolism (e.g. barbiturates, rifampin, tetracyclines, phenytoin), serum estrogen levels may decrease (Karch, 626) •Increased therapeutic and toxic effects of corticosteroids (Karch, 627) •Smoking while taking estrogens because the combination with nicotine increases the risk for development of thrombi and emboli (Karch, 627) •Grapefruit juice can inhibit the metabolism of estradiols, leading to increased serum levels (Karch, 627) •St. John's wort can affect the metabolism of estrogens and can make estrogen-containing contraceptives less effective (Karch, 627) •Additional herbal and alternative interactions box 40.6 (Karch, 627) →Nursing responsibilities •Administer with food if GI upset is severe (Karch, 630) •Provide analgesic for relief of headache (Karch, 630) •Strongly urge the patient to stop smoking to reduce the risk of thromboemboli (Karch, 630) •Encourage the use of small, frequent meals to assist with nausea and vomiting (Karch, 630) •Monitor for swelling and changes in vision or fit of contact lenses to monitor for fluid retention and fluid changes (Karch, 630) •Arrange for at least an annual physical examination, including pelvic examination, Pap smear, and breast examination to reduce the risk of adverse effects and to monitor drug effects (Karch, 630) •Assess the patient periodically for changes in perfusion or signs of vessel occlusion because of the risk of thromboemboli (Karch, 630) •Monitor liver function periodically for the patient on long-term therapy to evaluate liver function and ensure discontinuation of the drug at any sign of hepatic dysfunction (Karch, 630) •Offer support and reassurance to deal with the drug and drug effects (Karch, 630) →Lab tests to monitor •Monitor liver function for the patient on long-term therapy to evaluate liver function and discontinue the drug at any sign of hepatic dysfunction (Karch, 630) •PT, INR →Contraindications •In the presence of any known allergies (Karch, 626) •In patients with idiopathic vaginal bleeding, breast cancer, or any estrogen-dependent cancer, all of which can be exacerbated by the drug (Karch, 626) •With a history of thromboembolic disorders, including cerebrovascular accident or heavy smokers because of increased risk of thrombus and embolus (Karch, 626) •With hepatic dysfunction because of the effects of estrogen on liver function (Karch, 626) •Contraindicated during pregnancy due to the risk of serious fetal defects (Karch, 626) •Avoided during breast-feeding because of possible effects on the neonate (Karch, 626) •In patients with metabolic bone disease because of the bone-conserving effect of estrogen, which could exacerbate the disease (Karch, 626) •In renal insufficiency, could interfere with renal excretion of the drug and increase risk for potential adverse effects on fluid and electrolyte imbalance (Karch, 626) •With hepatic impairment, could alter the metabolism of the drug and increase risk for adverse effects including those on the liver and GI tract (Karch, 626) →Assessment •Assess for contraindications or cautions: history of allergy to any sex hormone or component of the drug product to avoid hypersensitivity reactions (Karch, 628) •Assess current status related to pregnancy and lactation due to adverse effects on the fetus and neonate (Karch, 628) •Assess hepatic dysfunction that might interfere with drug metabolism (Karch, 628) •Assess cardiovascular disease, breast or genital cancer, renal disease, or metabolic bone disease, which could be exacerbated by estrogen use (Karch, 628) •Assess for history of thromboembolism or smoking, which may increase the patient's risk for embolic conditions (Karch, 628) •Assess for idiopathic vaginal bleeding or pelvic disease, could represent an underlying problem t

•Various forms of HRT have been associated with increased risks of breast and cervical cancer. •The newer drugs used have shown to be associated with only a possible increase in risk of breast and cervical cancer, but with long-term use, they are associated with an increased risk of cardiovascular events. • Estrogen receptor modulators-have anitestrogen effects on the breast and may remove the cancer risk. However, these drugs may be less reliable in the management of menopausal symptoms. • In 2002 the Women's Health initiative was stopped when it was found that women using HRT for 5 or more years had an increased incidence of cardiovascular dz and stroke, as well as blood clots, gallstones, and ovarian cancer. • A complete family history and personal history of cancer and CAD risk factors should be completed to help the patient balance the benefits vs. the risks of this therapy. • The current recommendation of the U.S. Preventative Services Task Force is that women should feel comfortable taking HRT to reduce the symptoms for short-term therapy (less than 5 years). • Long-term use provides decreased risk of osteoporosis and related fractures, possibly reduced risk of dementia, and a reduction in risk of colon cancer. The negative aspects of this therapy include a definite but small increased risk for heart disease, stroke, and breast cancer.

→ Therapeutic uses • Used as contraceptives, most effectively in combination with estrogens (Karch, 624) • Used to treat primary and secondary amenorrhea and functional uterine bleeding and as part of fertility programs (Karch, 624) • Useful in treating specific cancers with specific receptor-site sensitivity (Karch, 624) → Adverse effects • Dermal patch includes systemic effects as well as local skin irritation (Karch, 626) • Vaginal gel use is associated with headache, nervousness, constipation, breast enlargement, and perineal pain (Karch, 626) • Intrauterine systems are associated with abdominal pain, endometriosis, abortion, PID, and expulsion of the intrauterine device (Karch, 626) • Vaginal use is associated with local irritation and swelling

→Normal • Doderlein bacilli metabolize glycogen and produce lactic acid maintaining vaginal pH between 3.8 and 4.5 (Porth, 1042) • Many different species of bacteria • Dominated by species that produce lactic acid • Vaginal pH 3.8-4.2 • Protect against infections • Normal flora can be disrupted by: → Abnormal estrogen levels, post menopause → Antibiotics →Abnormal • Candida albicans, Trichomonas vaginalis and bacteria are most common causes of vaginitis (Porth, 1042)

→Breast tissue, body hair, skin elasticity, and subcutaneous fat decreases (Porth, 1058) →Ovaries and uterus diminish in size (Porth, 1058) →Cervix and vagina become pale and friable (Porth, 1058) →Vaginal dryness, urinary stress incontinence, urgency, nocturia, vaginitis, and urinary tract infection (Porth, 1058) →May have painful or traumatic intercourse (Porth, 1058) →Significant vasomotor instability secondary to the decrease in estrogens and relative increase in other hormones including FSH, LH, GnRH, dehydroepiandrosterone, and androstenedione (Porth, 1058) →Instability may give risk to hot flashes, palpitations, dizziness, and headaches as the blood vessels dilate (Porth, 1058) →Irritability, anxiety, and depression may occur as a result of uncontrollable and unpredictable events (Porth, 1058) →Insomnia →Osteoporosis due to an imbalance in bone remodeling (Porth, 1058) →Increased risk for cardiovascular disease, which is the leading cause of death for women after menopause (Porth, 1058) r/t the loss of estrogen and progesterone effects on the body. →With perimenopause, changes occur in cardiovascular lipid profile: total cholesterol increases, HDL cholesterol decreases and LDL cholesterol increases.

→Asymptomatic approximately half of the time and may be discovered during routine pelvic examination (Porth, 1049) → Menorrhagia (excessive menstrual bleeding), anemia, urinary frequency, rectal pressure/constipation, abdominal distention, and infrequently pain (Porth, 1049) → Signs & symptoms cause menorrhagia (excessive bleeding) leading to: (slides) • Anemia • Rectal pressure from tumor further leads to → Constipation & → Urinary frequency & → Abdominal distention

→5%-10% of all breast cancers are hereditary, with genetic mutations causing up to 80% of breast cancers in women younger than 50 years of age (Porth, 1062) →BRCA1 is known to be involved in tumor suppression - with a mutation in BRCA1, a woman has a lifetime risk of 60%-85% for breast cancer and an increased risk of ovarian cancer (Porth, 1062) →BRCA 1 is a mutation on chromosome 17 and BRCA 2 is on chromosome 13. →BRCA2 is similar to BRCA1 (Porth, 1062) →Inherited alterations in these genes are indicated in hereditary cases of breast and ovarian cancer →Genes code for proteins that help repair DNA after it has mutated →Mutation make cancer more likely →13.2 percent of women in the general population will develop breast cancer, compared with estimates of 36 to 85 percent of women with an altered BRCA1 or BRCA2 gene. →Risk for ovarian cancer for women in the general population indicate that 1.7 percent will get ovarian cancer, compared with 16 to 60 percent of women with altered BRCA1 or BRCA2 genes →Increased incidence of breast and/or ovarian cancer is associated with BRCA1 or BRCA2 →Highest in families with a history of multiple cases of breast cancer, cases of both breast and ovarian cancer, one or more family members with two primary cancers or an Ashkenazi (Eastern European) Jewish background. →Men with an altered BRCA1 or BRCA2 gene also have an increased risk of breast cancer (primarily if the alteration is in BRCA2), and possibly prostate cancer

→ Adverse effects • Acne, edema, hirsutism (increased hair distribution), deepening of the voice, oily skin, oily hair, weight gain, decrease in breast size, testicular atrophy (Karch, 643) • In boys or men: acne, priapism (erect penis or clitoris does not return to flaccid state), increased facial and body hair, and penile enlargement. Premature epiphyseal closure: may reduce mature height. • Hypercholesterolemia: decrease HDL and increase LDL. • Increase growth in prostate cancer; do not give to patients with prostate cancer. • Polycythemia • Edema from salt and water retention. • Flushing, sweating, vaginitis, nervousness, emotional lability (Karch, 643) • Headache, dizziness, sleep disorders, fatigue, rash, altered serum electrolytes (Karch, 643) • Hepatocellular cancer (Karch, 643) • In women: irregularity/cessation of menses, hirsutism, weight gain, acne, lowering of voice, growth of clitoris, vaginitis, and baldness. • High abuse potential. → Drug-to-drug interactions • None listed in Karch • ATI: oral anticoagulants (monitor PT/INR), insulins/antidiabetic agents, other hepatotoxic medications (monitor liver enzymes and assess for jaundice). → Nursing responsibilities • Remove an old dermal system before applying a new system to clean, dry, intact skin to ensure accurate administration and decrease risk of toxic levels (Karch, 643) • Monitor patient response carefully when beginning therapy so that the dose can be adjusted accordingly (Karch, 643) • Monitor liver function periodically with long-term therapy, and arrange to discontinue the drug at any sign of hepatic dysfunction (Karch, 643) • Inject into large muscle and rotate injection sites. • Monitor signs of masculinity in women. • Advise clients to use barrier method of birth control. • Reduce cholesterol in diet → Lab tests to monitor • Thyroid function may decrease (Karch, 643) • Creatinine and creatinine clearance may increase (Karch, 643) • Monitor Hct and Hgb for polycythemia • PSA • Liver enzymes, and cholesterol • Altered lab results may continue for two weeks after discontinuing therapy (Karch, 643)

→ Adverse effects •In prepubertal males, virilization (e.g. phallic enlargement, hirsutism, increased skin pigmentation) (Karch, 644) • Postpubertal males, inhibition of testicular function, gynecomastia, testicular atrophy, priapism (painful, and continual erection), baldness, change in libido (increased or decreased) (Karch, 644) • Women may experience hirsutism, hoarseness, deepening of the voice, clitoral enlargement, baldness, menstrual irregularities (Karch, 644) • Serum electrolyte changes, liver dysfunction (including life-threatening hepatitis), insomnia, weight gain (Karch, 644) • Cardiomyopathy, hepatic carcinoma, personality changes, sexual dysfunction (Karch, 644) → Drug-to-drug interactions • Oral anticoagulants (Karch, 645) • Decreased need for antidiabetic agents (Karch, 645) • Cause a lack of effectiveness for lipid-lowering agents (Karch, 645) → Nursing responsibilities • Administer with food if GI effects are severe to relieve GI distress (Karch, 647) • Monitor endocrine function, hepatic function, and serum electrolytes before and periodically during therapy so that dose can be adjusted appropriately and severe adverse effects can be avoided (Karch, 647) • Arrange for radiographs of the long bones of children every three to six months so that the drug can be discontinued if bone growth reaches the norm for the child's age (Karch, 647) → Lab tests to monitor • Monitor endocrine function, hepatic function, and serum electrolytes before and periodically during therapy so that dose can be adjusted appropriately and severe adverse effects can be avoided (Karch, 647)

→ Mechanism of action • Phosphodiesterace type 5 (PDE5) receptor inhibitor (Karch, 648) • Selective inhibitors of cyclic guanosine monophosphate (cGMP) (Karch, 648) • Act to increase nitrous oxide levels in the corpus cavernosum (Karch, 648) Augments the effects of nitric oxide released during sexual stimulation, resulting in enhanced blood flow to the corpus cavernosum and penile erection. • Nitrous oxide activates the enzyme cGMP, which causes smooth muscle relaxation, allowing the flow of blood into the corpus cavernosum (Karch, 648) • Prevent breakdown of cGMP by phosphodiesterase, leading to increased cGMP levels and prolonged smooth muscle relaxation, promoting flow of blood into the corpus cavernosum (Karch, 648) → Adverse effects • Headache, flushing, dyspepsia, urinary tract infection, diarrhea, dizziness, possible optic neuropathy, possible eighth cranial nerve toxicity and loss of hearing, rash (Karch, 649) • MI, sudden death • Priapism-notify provider if erection lasts more than 4 hrs → Drug-to-drug interactions • Cannot be taken in combination with any organic nitrates or alpha-adrenergic blockers - serious cardiovascular effects, including death have occurred (Karch, 649) NITROGLYCERIN, and ISOSORBIDE DINITRATE can lead to fatal hypotension • Increased vardenafil or tadalafil levels and effects if PDE5 inhibitors are taken with ketoconazole, itraconazole, or erythromycin (Karch, 649-650) • Grapefruit juice

...

→ Risk factors • African American men have the highest reported incidence rate at all ages (Porth, 1026) • Asians and Native American men have the lowest rate (Porth, 1026) • Disease of aging; incidence increases rapidly after 50 years of age; 85% of all prostate cancers are diagnosed in men older than 65 years of age (Porth, 1026) • Men who have an affected first-degree relative and an affected second-degree relative have an eightfold increase in risk (Porth, 1026) • Increased dietary fats may alter the production of sex hormones and growth factors and increase the risk of prostate cancer (Porth, 1026) • Family hx-both autosomal chromosomes and the X chromosome have genes that have been linked to the possible inheritance risk • Race-African Americans > Caucasians > Asians; • Diet-high fat, red meat consumption Japanese American men > risk than native Japanese men • Other: heavy metal exposure, STDs, vasectomy → Metastasis • Invasion of the urinary bladder is less frequent and occurs later in the clinical course (Porth, 1027). Spread to bladder neck and urinary bladder. • Metastasis to the lung reflects lymphatic spread through the thoracic duct and dissemination from the prostatic venous plexus to the inferior vena cava (Porth, 1027) • Bony metastases particularly to the vertebral column, ribs, and pelvis, produce pain that often presents as a first sign of the disease (Porth, 1027). Bone early, occasionally without significant lymphadenopathy. • Mechanical theory: direct through lymphatics and venous spaces into the lower lumbar spine; first theory of how prostate cancer is spread. • Seed & soil: certain tissue factors must be present for preferential growth in certain tissue such as the bone. Lung, liver, and adrenal metastasis have been reported. • Doubling time early on is 2-4 years; slow.

→ Risk factors • Cryptorchidism, genetic factors, and disorders of testicular development (Karch, 1022). Patients with a hx of crytochidism have a 10-40x higher risk of testis cancer. • The risk is higher for abdominal undescended testis vs. inguinal location. • Strongest association is with cryptorchid or undescended testis (Karch, 1022) • Genetic predisposition also appears to be important (Karch, 1022) • Family clustering of the disorder has been described, although a well-defined pattern of inheritance has not been established (Karch, 1022) • Men with disorders of testicular development, including Klinefelter syndrome and testicular feminization, have a higher risk of germ cell tumors (Karch, 1022) → Metastasis • Testicular cancer can spread when the tumor may be barely palpable (Porth, 1022) • Higher incidence of metastasis the more undifferentiated the cell type, especially choriocarcinoma. • Common sites especially for nonseminomas: bone, lung, brain and lymph nodes. S&S: back pain, cough & hemoptysis, preceded or coincided with dizziness, welling of the lower extremities (lymph blockage), bone pain. • Approximately 10% of men present with symptoms related to metastatic disease (Porth, 1022) • Signs of metastatic spread including swelling of the lower extremities, back pain, neck mass, cough, hemoptysis, or dizziness (Porth, 1022)

• Most commonly causative organisms for infection and inflammation: • Chlamydia trachomatis • E. coli • Pseudomonas • Klebsiella • Proteus • Orchitis-common complication of mumps, scarlet fever or PNA

→ Definition • Infection of the testes (Porth, 1021) • Inflammatory process; more commonly spontaneous or due to trauma to the groin. • Can be due to pumps, scarlet fever or PNA. → Signs and symptoms • Can be precipitated by a primary infection in the genitourinary tract, or the infection can be spread to the testes through the epididymis, bloodstream, or lymphatics (Porth, 1021) • Can be a complication of a systemic infection (e.g. parotitis, scarlet fever, pneumonia, etc...) (Porth, 1021) • Sudden onset (Porth, 1021) • Fever, painful enlargement of the testes, small hemorrhages into the tunica albuginea, no urinary symptoms (Porth, 1021) • Symptoms last 7-10 days (Porth, 1021)

→ Definition • Inflammation of the epididymis (the elongated cordlike structure that is located along the posterior border of the testis - transport and storage of sperm) (Porth, 1021) • Can be caused by sexually transmitted diseases: Chlamydia/gonnorhea...Older men pseudomonas → Signs and symptoms • Unilateral pain and swelling accompanied by erythema and edema of the overlying scrotal skin that develops over a period of 24-48 hours (Porth, 1021) • Initially, the swelling and induration are limited to the epididymis. The distinction between the testis and epididymis becomes less evident as the inflammation progresses and the testis and epididymis become one mass (Porth, 1021) • Tenderness over the groin or in the lower abdomen (Porth, 1021) • Symptoms of lower urinary tract infection, such as fever, frequency, urgency, and dysuria may be present (Porth, 1021) • Whether urethral discharge is present depends on the organism causing the infection - usually accompanies gonorrheal infections, is less common in chlamydial infections, and is less common in infections caused by gram-negative organisms (Porth, 1021)

→ Testicular torsion • Twisting of the spermatic cord that suspends the testis (Porth, 1020) • Extravaginal torsion occurs in fetuses or neonates and is less common (Porth, 1020) → Occurs when the testicle and fascial tunicae that surround it rotate around the spermatic cord at a level well above the tunica vaginalis (Porth, 1020) → Probably occurs during fetal or neonatal descent of the testes before the tunica adheres to the scrotal wall (Porth, 1020) • Intravaginal torsion involves twisting of the spermatic cord within the tunica vaginalis (Porth, 1021) → True surgical emergency (Porth, 1021) → Can occur at any age, but is more common during adolescence (Porth, 1021) → Occurs in the absence of any precipitating event and is thought to be due to abnormal fixation of the testis within the tunica vaginalis, allowing the testis to twist, especially during periods of testicular growth such as puberty (Porth, 1021) • Must be differentiated from epididymitis, orchitis, and trauma (Porth, 1021) → On physical exam, testicle is often high in the scrotum and in an abnormal orientation (Porth, 1021) → Swelling and redness depends on the duration of symptoms (Porth, 1021) → Cremasteric reflex is frequently absent (normally elicited by stroking the medial aspect of the thigh and observing testicular retraction) (Porth, 1021) → Color Doppler is increasingly used in evaluated of suspected testicular torsion (Porth, 1021)

A. Tx of breast cancers

D. Cardiomyopathy and liver cancers

C. Debilitation and severe weight loss

B. The corpus cavernosum does not fill with blood to allow for penile erection

C. Organic nitrates

A. Sexual stimulation of the penis Onset is 15-30 minutes

D. Increase nitrous oxide levels in the corpus cavernosum, causing vascular relaxation and promoting blood flow into the corpus cavernosum.

A. Hisutism B. Deepening of the voice D. Acne

b, d, e, f B. X-rays of the long bones every 3-6 months so the drug can be stopped when the bone size is appropriate for age D. Learn to cope with an altered body image. E. Regular monitoring of liver function tests F. Monitoring for the development of edema

B. Breakthrough bleeding

A. Acting to block the release of FSH and LH, preventing follicle development

B. The risk for potentially dangerous thromboembolic episodes increases

B. Stimulate milk "let down" in the lactating woman

C. I may not be able to wear my contact lenses while taking these pills, or I might have to be fitted for a new pair.

1. b, c, e, f B. Retaining calcium in the bones C. maintaining the secondary female sex characteristics. E. Stimulating the uterus to increase the changes of conception. F. Relaxing blood vessels

3. a, b, d, e A. Monitoring fetal heart rate during labor B. Regulation of drug delivery between contractions D. Monitoring of maternal blood pressure periodically during and after administration E. Close monitoring of maternal blood loss following delivery

B. Iodine found in the diet

C. Suppress the hypothalamic release of TRH

C. Hyperthyroidism

B. Myxedma

B. Around the clock to assure therapeutic levels

C. A regulator of Calcium

B. Alendronate

2. a, b, d A. Increased body temp B. Thickening of the tongue D. Loss of hair

-needed for growth and maturation of the female reproductive tract and secondary sex characteristics -Block bone resorption and reduce LDL levels. -(At high levels) Estrogens suppress the release of FSH needed for conception.

-Contraception -Relief of postmenopausal symptoms such as hot flashes/mood changes -Prevention of postmenopausal osteoporosis -Tx of dysfunctional uterine bleeding and endometriosis -Tx of prostate cancer Routes: oral, transdermal, intravaginal

-Hx of heart dz -breast or estrogen dependent cancer -undiagnosed abnormal vaginal bleeding -clients with a hx/risk for thromboembolic disease

B. Isosorbide dinitrate (Isodrdil) organic nitrate that is used to manage angina pain. If taken with Viagra can lead to fatal hypotension.

-Warfarin (Coumadin) -Phenytoin (Dilantin) -Corticosteroids -Tamoxifen -Smoking

-Instruct clients to take medication at the same time each day -Apply estrogen patches to the skin of the trunk -Inject IM forms deep in a large muscle mass. Rotate injection sites -Instruct clients to report symptoms of menstrual changes, dysmenorrhea, amenorrhea, breakthrough bleeding, and/or breast changes -Encourage clients to perform monthly breast self-examinations and schedule annual gynecologic and breast examinations with the primary care provider. -Advise the client to report swelling or redness in the legs, shortness of breath, or chest pain. -D/C prior to knee or hip surgery or any surgical procedures that may cause extensive mobilization.

-Dermal patch: systemic/local skin irritation -Vaginal gel: headache, nervousness, constipation, breast enlargement, and perineal pain. -Venous thromboembolism -Loss of vision/diplopia -Migraine headache -Rash -Acne -Cholasma -Alopecia -Breakthrough bleeding -Spotting -Amenorrhea -Fluid retention -Edema -Increase in weight *Intrauterine systems are associated with: abd pain, endometriosis, abortion, PID, and expulsion of the intrauterine device.

-Thyroid hormone (T4) thyroxine by using iodine found in the diet. Thyroid cells remove iodine from the blood, concentrate it, and prepare it for attachment to tyrosine. -T4 is the major hormone secreted by the thyroid follicles -Has 4 bound iodine atoms -(T3)-Triiodothyronine -most T3 is formed at the target tissues by conversion of T4 to T3. -Has 3 bound iodine atoms -T3 is 10x more active -Calcitonin Polypeptide hormone produced by parafollicular of C-cells of the thyroid gland. Lowers blood Ca+ levels. Inhibits osteoclast activity and bone resorption. Stimulates Ca+ reuptake and incorporation into bone matrix.

-Has chief cells which secrete PTH. -PTH release is triggered by falling calcium levels and inhibited by hypercalcemia in blood. -PTH release stimulates: 1) osteoclasts to digest some of the bony matrix and release ionic calcium and phosphates to the blood. 2) enhances resorption of Ca and exretment of phosphate by the kidneys. 3) increases absorption of Ca by the intestinal mucosal cells (via activation of vitamin d)

nervous tissue-SNS -helps us cope with stressful situations -Hormones: catecholamines (epinephrine and norepinephrine) mimic SNS activation

glandular tissue from embryonic mesoderm -helps us cope with stressful situations -Steroid hormones called corticosteroids are synthesized from cholesterol by the adrenal cortex. -Mineralcorticoids: aldosterone-stimulated by renin-angiotensin mechanism (activated by decreasing blood volume or BP) elevated K+, or low Na+ levels and ACTH. Inhibited by increased blood volume and pressure, increased Na+ and decreased blood K+ levels. Aldosterone increases blood levels of Na+ and decreases blood levels of K+. Addison's disease results from low levels of aldosterone. -Glucocorticoids: cortisol Stimulated by ACTH Promotes gluconeogenesis and hyperglycemia; mobilize fats for energy metabolism; stimulate protein catabolism; assists body to resist stressors; causes vasoconstriction and increase in BP; depress inflammatory and immune response. Increase in cortisol results in Cushing's syndrome and decrease in cortisol is seen with Addison's disease. -Gonadocorticoids: chiefly androgens, converted to testosterone or estrogens after release Stimulated by ACTH

-Glucocorticoid excess (cortisol) -may be cuased by ACTH-releasing pituitary tumor (cushing's disease) o rby ACTH releasing malignancy of the lungs, pancreas, or kidneys; or by a tumor of the adrenal cortex. -Most often results from the clinical administration of pharmacological doses of glucocorticoid drugs. Characterized by: -persistent hyperglycemia (steroid diabetes) -dramatic loses in muscle and bone protein -water and salt retention -leading to HTN and edema Signs and symptoms: swollen moon face, fat stomach, and buffalo hump, tendency to bruise easily, and poor wound healing.

-hyposecretory disorder of the adrenal cortex -Usually involves deficits in both glucocorticoids (cortisol) and mineralcorticoids (aldosterone) S&S: -weight loss, hyponatremia/hyperkalemia -Severe dehydration and hypotension

-Hyperthyroidism -the serum of patients with this condition often has abnormal antibodies that mimic TSH and continuously stimulate TH release. -Believed to be autoimmune dz Symptoms: -Exophthalmos, protrusion of the eyeballs, may occur if the tissue behind the eye becomes edmatous and then fibrous. -elevated metabolic rate -sweating -rapid/irregular heartbeat -nervousness/weightloss

Full-blown hypothyroid syndrome in adults. Symptoms: -low metabolic rate -feeling chilled -constipation -thick/dry skin/ puffy eyes -edema -lethargy -mental sluggishness/not retardation If myxedema results from lack of iodine, the thyroid gland enlarges and protrudes, a condition called endemic or colloidal goiter. The follicle cells produce colloid but cannot iodinate it or make functional hormones. The pituitary gland secretes increasing amounts of TSH in a futile attempt to stimulate the thyroid to produce TH, but the only result is that the follicles accumulate more and more unusuable colloid.

A. ADH

(Adrenal cortex) Aldosterone-mineralcorticoid Cortisol-Glucocorticoid Androgens-Gonadocorticoids

-asymptomatic 1/2 the time -Menorrhagia (excessive menstrual bleeding), anemia, urinary frequency, rectal pressure/constipation, abdominal distention, and infrequently pain -Fibroids may increase in size during pregnancy or with exogenous estrogen stimulation (oral contraceptive use or menopausal estrogen replacement therapy) -Sometimes interference with pregnancy, but rare

mutation on chromosome 17 known to be involved with tumor suppression with BRCA-1 woman has a lifetime risk of 60-85% for breast cancer and an increased risk of ovarian cancer

Orchitis

1st is usually: bone lung, liver and sometimes adrenal metastasis

Brain, Bone, Lung, lymph nodes

-Bone pain/lower back pain -Urgency, frequency, nocturia, hesitancy, dysuria, hematuria, blood in ejaculate -SOB -Pathologic fractures -DVT in lower extremities -Lower extremity lymphadenopathy -Supraclavicular adenopathy

-through lymphatics and venous spaces to lower lumber spine

-tissue factors must be present to allow growth in tissues

arise from testicular epithelium

arise from embyronic tissues

True

Cryptorchid or undescended testis

Klinefelter's syndrome and testicular feminization

-swelling of lower extremities -Back pain -Neck mass -Cough -Hemoptysis -Dizziness

Orchitis is an infection of the testes Epididymitis is an inflammation of the epididymis

ORCHITIS

Epididymitis

orchitis

35 UTIs

-Fever, frequency, urgency, dysuria, tenderness over groin, lower abd -unilateral pain and swelling accompanied by erythemia and edema of overlying scrotal skin that develops over a period of 1-2 days

Twisting of the spermatic cord that suspends the testis Extravaginal: Occurs when the testicle and fascial tunicae that surround it rotate around the spermatic cord at a level well ABOVE the TUNICA VAGINALIS. Intravaginal: Involves twisting of the spermatic cord WITHIN the tunica vaginalis. *True surgical emergency *Occurs during periods of testicular growth. Esp. Puberty.