Nu Patho Study Guide 3 questions with correct answers, Exams of Nursing

Download Nu Patho Study Guide 3 questions with correct answers and more Exams Nursing in PDF only on Docsity! Nu Patho Study Guide 3 1. Know all STDS: pathophysiology, etiology, clinical manifestations, diagnostic tests, treatment, and complications. How is each transmitted during pregnancy to the fetus? Know the different stages of syphilis; what organism causes each STD and is it viral, bacterial etc.? Do you treat both partners and why? What age group has the greatest risk of STDs and why? What causes cervical cancer? - correct answer ✔✔See end 2. Understand the different uterine tumor types. - correct answer ✔✔(p. 821-822, 830-831; 7th ed) Uterine tumor Leiomyomas: p.821: Commonly called Myomas or Uterine Fibroids, are benign smooth muscle tumors in the myometrium. Cause is unknown but size of tumor is related to estrogen, progesterone, growth factor, angiogenesis, and apoptosis. Also possible genetic component. Classified as: Subserous, Submucous, and Intramural based on location within the various layers of the uterine wall. Unlike cancer, cannot proliferate blood flow. Risk Factors: nulliparity, obesity, PCOS, diabetes, black race, and hypertension. Endometrial carcinomas: p. 830: Arise from glandular epithelium of uterine lining. Primary risk factor is prolonged exposure to estrogen without presence of progesterone (known as unopposed estrogen). Other risk factors include obesity, diabetes, gallbladder disease, and hypertension. About 75% endometrial cancers are adenocarcinomas. Clinical manifestation: most common is abnormal vaginal bleeding. Uterine sarcomas: p.830: Rare and arise from mesenchymal tissues of and near uterus including myometrial smooth muscle, endometrial stroma, or adjacent connective tissues. Uterine sarcomas are rare. Can be divided into: endometrial stromal sarcoma, leiomyosarcoma, and adenosarcoma based on the involved tissue types. Lack of epidemiological and treatment data due to low occurrence. Risk factors may include chronic excess estrogen exposure, tamoxifen, and African American race. Symptoms: abnormal uterine bleeding, mass, pelvic pressure/pain, and foul and profuse vaginal discharge Treatment: Total hysterectomy which may include bilateral salpingo-oophorectomy and selective lymphadenectomy followed by radiation therapy or chemotherapy, or both. Two types of histology for uterine cancer: Type I tumors: most common result from estrogen exposure leading to endometrial hyperplasia 3. What is PCOS and what does it cause? Clinical manifestations? Treatment? Causes? Pathophysiology? - correct answer ✔✔(p. 824-826, 6th ed) (p. 810-812, 7th ed) Polycstic Ovary Syndrome remains one of the most common endocrine disturbances affecting women, especially young women. And is a Leading cause of Infertility in the United States. Have to have at least two of the following conditions for diagnosis of PCOS: oligo-ovulation/anovulation, elevated levels of androgens, or clinical signs of hyperandrogenism and polycystic ovaries. Do not need to have polycystic ovaries for diagnosis, and having polycystic ovaries doesn't necessarily mean one has PCOS. Evidence of androgen excess, chronic anovulation, and inappropriate gonadotropin secretion along with a glucose tolerance test help with positive diagnosis of PCOS. Complications of PCOS : Leading Cause of Infertility ; Possible late outcomes of PCOS include: dyslipidemia, diabetes mellitus, cardiovascular disease, hypertension, endometrial hyperplasia and carcinoma. Women with PCOS are at an inncreased risk for gestational DM, pregnancy-induced HTN, preterm birth, and perinatal mortality. Clinical Manifestations: Usually appear within 2 years of puberty but may appear after a variable period of normal menstrual function and, possibl pregnancy. Symptoms are related to anovulation and hyper- androgenism and include; dysfunctional bleeding or amenorrhea, hirsutism, acne, and infertility. See Box 24-4 p.811 for a complete listing of signs and symptoms (with prevelance), summary of hormonal disturbances, and complications of PCOS. Cause: Underlying cause unknown but thought to have a genetic factor making ovaries more susceptible/sensitive to insulin's stimulation of androgen production. Pathophysiology: A Hyperandrogenic state is a cardinal feature in the pathogenesis of PCOS. Insulin stimulates androgen secretion by the ovarian stroma and reduces serum sex hormone-binding globulin 4. What is the difference between primary and secondary amenorrhea and what is compartment II? - correct answer ✔✔(p. 805-807, 7th ed) Amenorrhea is lack of menstruation. Primary amenorrhea is the failure of menarche and the absence of menstruation by age 13 years without the development of secondary sex characteristics or by age 15 regardless of the presence of of secondary sex characteristics. A thorough evaluation is needed. The major clinical manifestation is: absence of 1st menstrual period. The cause of amenorrhea determines whether secondary sex characteristics and height are affected. TX: correction of underlying disorder hormone replacement to induce secondary sex characteristics. (p.805-806) (See fiqure 24-2 on page 806.) Secondary amenorrhea is the absence of menstruation for a time equivalent to three or more cycles in women who have previously menstruated. Pregnancy is the most common condition to rule out prior to further evaluation. Can be caused by dramatic weight loss (malnutrition or excessive exercise). Common during early adolescence and the peri-menopausal period, pregnancy, and lactation. The most common cause is (after pregnancy) are thyroid disorders (hypothyroidism) hyperprolactinemia, HPO interruption 9. Know the male GU anatomy and the function of the glands. - correct answer ✔✔(p. 784-791, 7th ed) male anantomy In men the external genitalia perform the major functions of reproduction. Sperm, are produced in the testes and delivered to the vagina by the penis. The internal male genitalia have a more accessory function. They consist of conducting tubes and fluid-producing glands, all of which aid in the transport of sperm from the testes to the urethral opening of the penis. External Genitalia: Testes: are the essential organs of reproduction. They produce gametes (sperm) and produce sex hormones (androgens and testosterone). They are suspended in the scrotal sac outside of the pelvic cavity because sperm production requires an environment that is 1 or 2 degrees cooler than the body temperature. Its supply lines include the ducts, blood vessels, lymphatic vessels, and nerves of the spermatic cord. The seminiferous tubules constitute the bulk (80%) of testicular volume and are the site of sperm production. The two ends of the seminiferous tubule join through a straight section called the tubulus rectus. Sperm travels through these sections to the central portion of the testis, rete testis, then though the efferent tubules to the epididymis, where the sperm mature. Epididymis: comma shaped structure that curves over the posterior portion of each testis and consists of a single highly packed and markedly coiled duct whose structural function is to conduct sperm from the efferent tubules to the vas deferens. *The duct can become inflamed from infection by microorganisms, causing epididymitis. While sperm is contained in the epididymis (12 days or more), they receive nutrients and testosterone and some biochemical or physiologic mechanism to enhance their capacity for fertilization. The tail of the epididymis is continuous with the vas deferens, a duct with muscular layers capable of powerful p 10. Know the role of the different female hormones involved in menstruation, menopause, ovulation, dysmenorrhea, etc. - correct answer ✔✔Page 780 (7th ed) Table 23-2 Female hormones Menstruation •Leptin: increase sensitivity.....regulatory hormone of appetite and energy metabolism- increases with puberty and menarche • Gonadotropin-releasing hormone (GnRH) is stimulated as a result of feedback mechanisms originating in the dominant follicle, which is determined in the first 5-7 day of the cycle. GnRH is secreted by the hypothalamus and travels to the anterior pituitary, which stimulates luteinizing hormone (LH) and follicle-stimulating hormone (FSH). • Controls Ovarian events of the menstrual cycle • High FSH levels stimulate follicle and ovum maturation (follicular phase) Then a surge of LH causes ovulation which is followed by development of the corpus luteum (luteal phase) • Estrogen— Generic for ( Estradiol, estrone and estriol). Estradiol (E2) most potent and plentiful and is 95% produced by the ovaries. • Early Follicular Phase: estrogen levels low; minute amount of progesterone secreted; GnRH, FSH, and LH levels are low Ovarian follicle develops; endometrium proliferates. • Late Follicular Phase (preovulatory): estrogen levels high; progesterone increases with small surge before ovulation; GnRH, FSH, and LH all surge (LH dominates) Process of ovulation begins; endometrial proliferation complete. • Ovulatory Phase: estrogen levels dip, progesterone levels begin to rise; GnRH, FSH, and LH all fall sharply. Corpus luteum begins to develop; endometrium enters secretory phase. • Early Luteal Phase: estrogen and progesterone levels high, progesterone dominates; GnRH, FSH, and LH all gradually decline. Corpus luteum fully developed; endometrium ready for implantation. • Late Luteal Phase: estrogen and progesterone levels fall sharply; GnRH, FSH, and LH all rise slightly. Corpus luteum regresses; endometrium breaks down; menstruation 11. Know the different parts of the female GU system and the function of each. - correct answer ✔✔(p. 771-776 ,7th ed) female anatomy The function of the female reproductive system is to produce mature ova and, when they are fertilized, protect and nourish them through embryonic and fetal life and expel them at birth. External Genitalia Mons pubis - is a fatty layer of tissue over the pubic symphysis. This cushion of tissue protects the pubic symphysis during sexual intercourse. Labia majora - the principal function is to protect the inner structures of the vulva. It has two folds of skin that arise at the mons pubis and extend back to the fourchette, forming a cleft. The labia majora contains an extensive network of nerve endings making the labia majora highly sensitive to temperature, touch, pressure, and pain. Labia minora - two smaller, thinner folds of skin lie within the labia majora. Anteriorly they form the clitoral hood and frenulum then split to enclose the vestibule and converge near the anus, forming the fourchette. Well supplied with nerves, blood vessels, and sebaceous glands. These glands secrete a bactericidal fluid that has a distinctive odor and lubricates and waterproofs the vulvar skin. Clitoris - a richly innervated, erectile organ that lies anterior between the labia minora. The clitoris is a major site of sexual stimulation and orgasm. It secretes a fluid called smegma, which has a unique odor and may be erotically stimulating to the male. Vestibule - an area protected by the labia minora and contains the external opening of the vagina (introitus). The hymen may cover the introitus. Also contains the urethra (urinary meatus). These structures are lubricated by two pairs of glands: Skene and Bartholin. Skene glands open on each side of the meatus, and Bartholin glands open on each side of the introitus. Secretions from both sets of glands facilitate coitus, and enhances the viability and 12. What occurs with the fetus at each week of gestation? - correct answer ✔✔(p. 768-770 , 7th ed) WEEKS OF GESTATION During embryonic development, the initial reproductive structures of male and female embryos are homologous (the same) and consist of one pair of primary sex organs, or gonads, and two pairs of ducts, the mesonephric ducts (wolffian ducts) and the paramesonephric (mullerian ducts). Both pairs of ducts empty into the urogenital sinus. During the first 7-8 weeks of gestation, both male and female embryos develop an elevated structure called the genital tubercle, which develops into the external reproductive organs under hormonal influence of testosterone or lack there of in females. Male embryos: • 6-7 weeks gestation- the male embryo will differentiate under the influence of testes-determining factor (TDF, stimulating the gonadal development of testes, which in turn produces antimullerian hormone(AMH) and testosterone. Sertoli cells appear and aggregate to form testicular cords. When sertoli cells mature, they will produce inhibin and androgen-binding protein, which is important for spermatogenesis. • 8th week- Leydig cells differentiate and the secretion of testosterone begins. Under the influence of testosterone, the male gonads develop into two testes. The paramesonephric ducts degenerate and the mesonephric ducts develop (Wolffian system) into the vas deferens (tubes that carry sperm from the testes to the urethra.) • Testis (XY) differentiated by 9 weeks gestation. • 9 months gestation- testes have descended into the scrotum. Female embryos: • 6-8 weeks- In the absence of testosterone there is a loss of the Wolffian system and the two gonads develop into ovaries. • 16-20 weeks- There is rapid mitotic multiplication of germ cells, peak of 6-7 million oogonia. Oogonia are transformed into oocytes throughout the remainder of pregnancy. By birth, only 1-2 million oocyt 13. Understand hypo/hyperglycemia - correct answer ✔✔(p. 743, 747; 7th ed) o 3. Proliferative: neovascularization (angiogenesis) and fibrous tissue formation within the retina or optic disc. Traction of the new vessels on the vitreous humor may cause retinal detachment or hemorrhage into the vitreous humor. Maculopathy is progressive process that may accompany the increased retinal capillary permeability, vessel occlusion, and ischemia. If formation of exudates, edema, or ischemia occurs near the forvea, serious loss of vision may result. Macular ed 17. Why does polyuria and polydipsia and weight loss occur with the onset of diabetes? - correct answer ✔✔(p. 749, 6th ed) (p. 738, 7th ed) Table 22-7 Polyuria - In Type 1 Diabetes Mellitus polyuria is caused because hyperglycemia acts an osmotic diuretic; the amount of glucose filtered by the glomeruli of the kidneys exceeds the amount that can be reabsorbed by the renal tubules; glycosuria results, accompanied by large amounts of water lost in the urine. Polydipsia occurs because of the elevated blood glucose levels, water is osmotically attracted from body cells, resulting in intracellular dehydration and hypothalamus stimulation of thirst. Weight loss occurs because of the fluid loss in osmotic diuresis and the loss of body tissue as fat and proteins are used for energy as a result of the effects of insulin deficiency. 18. Know hyperglycemic hyperosmolar syndrome (HHS)? Know diabetic ketoacidosis? What's the difference? - correct answer ✔✔(p. 744-746, 7th ed) Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS), or hyperglycemic Hyperosmolar state (HHS) is a life-threatening emergency. Precipitated by infections, meds, nonadherence to diabetic Tx, coexisting disease. More common with Type2 diabetes and with chronic pancreatitis. Pathophysiology: HHNKS differs from DKA in the degree of insulin deficiency (more profound in DKA) and the degree of fluid deficiency (more marked in HHNKS). HHNKS: characterized by lack of ketosis. Insulin levels are sufficient to prevent excessive lipolysis but not to use glucose properly. Glucose levels are higher than in DKA because of volume depletion. Clinical manifestations: Glycosuria and polyuria result from extreme glucose elevation. (19g of glucose/hr loss in diuresis). Severe volume depletion, increased serum osmolarity, intracellular dehydration, loss of electrolytes (K+). Neuro changes: stupor, seizure, coma (correlates with the degree of hyperosmolarity, common and sometimes called hyperosmolar hyperglycemic coma). Evaluation and Tx: HHNKS glucose as high as 600mg/dl, near normal bicarb and pH. Serum osmolarity greater than 320mOsm/L. Absent or low ketone levels. Dehydration far more severe than in DKA. (more rapid fluid replacement needed). Deficit in Potassium (extreme), phosphorus and sodium. High risk for infection, sepsis, venous thrombosis. High mortality. Diabetic Ketoacidosis (DKA) (p. 744) Complication of DM. Develops with absolute or relative deficiency of insulin and an increase in insulin counterregulatory hormones. Most common with Type 1 diabetes (can occur in type2). Also in ketosis- prone diabetes (KPD syndrome). Precipitating factors: intercurrent illness, infection, trauma, surgery, MI, interruption of insulin administration. Young or old. Low BMI. Pathophysiology: with relative ins 19. What is hypoparathyroidism? - correct answer ✔✔(p. 733, 7th ed) Hypoparathyroidism: Abnormally low PTH levels are most commonly caused by damage to the parathyroid glands during thyroid surgery. A low serum Ca+ level and a high phosphorous level in the absence of renal failure, intestinal disorders, or nutritional deficiencies suggest hypoparathyroidism. Hypoparathyroidism is also associated with genetic syndromes, including familial hypoparathyroidism and DiGeorge syndrome (velocaridofacial syndrome). Hypomagnesemia also can cause a decrease in PTH secretion and function. Pathophysiology: A lack of circulating PTH causes a depressed serum calcium level and an increased serum phosphate level. In the absence of PTH, the abilities to reabsorb calcium from bone and to regulate calcium reabsorption from the renal tubules is impaired. The phosphaturic effects of PTH are lost, resulting in hyperphosphatemia. The effects of hypomagnesemia are not clearly understood. Once serum magnesium levels return to normal, however, PTH secretion returns to normal, as does peripheral tissues' responsiveness to PTH. Clinical Manifestations: Symptoms associated with hypoparathyroidism are related to hypocalcemia. Hypocalcemia causes a lowering of the threshold for nerve and muscle excitation. This is manifested as muscle spasms, hyperreflexia, tonic-clonic convulsions, laryngeal spasms, and in severe cases, death from asphyxiation. Chvostek and Trousseau signs may be used to evaluate for neuromuscular irritability. Chvostek sign is elicited by tapping the cheek resulting in twitching of the upper lip. Trousseau sign is elicited by sustained inflation of a sphygmomanometer placed on the upper arm to a level above the systolic blood pressure with resultant painful carpal spasm. Other symptoms include dry skin, loss of body and scalp hair, hypoplasia of developing teeth, horizontal r 20. What is Graves disease? Signs and symptoms? Labs? - correct answer ✔✔(p. 736-738, 6th ed) (p. 726-728, 7th ed) Graves disease: Is an autoimmune disease that results in stimulation of the thyroid gland and resultant hyperthyroidism (50-80% of cases of hyperthyroidism). It is more common in women. Characterized as a multisystem syndrome consisting of one or more of the following: hyperthyroidism, diffuse thyroid enlargement (goiter), ophthalmopathy, and pretibial myxedema. Triggers for onset include: stressful life events, recent childbirth, and infection. Genetic and environmental factors play an important role in the development of Graves disease; however the exact cause is unknown. Pathophysiology: Normal regulatory mechanisms are overridden by abnormal immunologic mechanisms. T lymphocytes are sensitized to thyroid antigens and stimulate B cells to produce IgG antibodies that bind to TSH receptors in the thyroid gland and stimulate the synthesis and secretion of excess TH (autoantibodies called thyroid-stimulating immunoglobulins, which are found in 95% people with Graves disease). Hyperfunction of the thyroid gland is reflected in a dramatically increased iodide uptake and increased rate of hypervascularity and enlargement of the gland (goiter). Increased T3 production leads to long-term hyperstimulation of the thyroid gland. A small number of patients with Graves disease and very high levels of thyroid-stimulating immunoglobulins experience pretibial myxedema (Graves dermopathy), characterized by subcutaneous swelling on the anterior portions of the legs and by indurated and erythematous skin. Thyroid-associated dermopathy is associated with thyrotropin receptor antigens on fibroblasts and recruited T lymphocytes. Manifestations occasionally appear on hands leading to the appearance of clubbed fingers (thyroid acropachy). Clinical Manifestations: Manifestations include: goite 21. What is acromegaly? - correct answer ✔✔(p. 722-724, 7th ed) Acromegaly occurs in adults exposed to continuously excessive levels of GH and concomitant elevation of IGF-1(insulin-like growth factor). In children and adolescents whose epiphyseal plates have not yet closed, the effect of increased GH levels on long bone growth is termed gigantism. The most common cause is a primary autonomous GH-secreting pituitary adenoma. Acromegaly occurs more often in women than men and is diagnosed most often in adults in their forties and fifties, although the disease is usually present for years preceding the diagnosis. Acromegaly is a slowly progressive disease that, if untreated, is associated with a decreased life expectancy. The increased number of deaths associated with acromegaly are caused by cardiac hypertrophy, hypertension, atherosclerosis, and type 2 DM that lead to CAD. Malignancies, including colon, breast, and lung cancer are also more common. Patho: With a GH- secreting adenoma, the usual GH baseline secretion pattern and sleep-related GH peaks are lost, and an unpredictable secretory pattern ensues. With only slight elevations of GH, IGF-1 levels increase, stimulating growth. In children whose epiphyseal plates have not yet closed, the effect of increased GH levels causes excessive skeletal growth, with some growing to 8-9 feet tall. In the adult, epiphyseal closure has occurred and increased amounts of GH and IGF-1 cause connective tissue proliferation and increased cytoplasmic matrix, as well as bony proliferation that results in the characteristic appearance of acromegaly. GH also effects glucose, lipid, and protein metabolism. Hyperglycemia results from GH's inhibition of peripheral glucose uptake and increased hepatic glucose Functions: Conserves sodium, blood volume, and blood pressure. Maintains extracellular volume by acting on distal nephron epithelial cells to increase sodium reabsorption and potassium and hydrogen excretion. Other effects of aldosterone include: enhancement of cardiac muscle contraction, stimulation of ectopic ventricular activity through secondary cardiac pacemakers in the ventricles, stiffening of the blood vessels with increased vascular resistance, decreased fibroinolysis. Pathologically elevated levels of aldosterone have been implicated in the m 26. What is the role of calcitonin? - correct answer ✔✔(p. 709, 6th ed) (p. 702, 7th ed) Table 21-6, Pg. 701 Calcitonin (thyrocalcitonin) acts to lower serum calcium levels by inhibition of bone-resorbing osteoclasts. High levels of calcitonin are required for the bone-resorbing effect to take place yet deficiencies do not lead to hypocalcemia. Consequently, the metabolic effects of calcitonin deficiency or excess do not appear to be significant in humans. Calcitonin is used in the treatment of osteoporosis, osteoarthritis, Paget bone disease, hypercalcemia, osteogenesis imperfect, and metastatic cancer of the bone. The precursor molecule to calcitonin (procalcitonin) is a stress hormone that is elevated in infectious and inflammatory disorders and its measurement can aid in the diagnosis of these serious diseases. Lowers serum phosphate levels May also decrease calcium and phosphorus absorption in GI 27. What is oxytocin? How does it relate to the pituitary gland? - correct answer ✔✔(p. 698-699, 7th ed) Oxytocin: Oxytocin is responsible for contraction of the uterus and milk ejection in women and may effect sperm motility in men. In women, oxytocin is secreted in response to sucking and distention of the female reproductive tract. Stimulated by sucking, this results in increased intramammary pressure and milk expression ('letdown" reflex). Oxytocin functions near the end of labor to enhance the effectiveness of contractions, promote delivery of the placenta, and stimulate postpartum uterine contractions. oxytocin has also been implicated in the behavioral response in the brains response to stress, especially in pregnant and postpartum states. Relationship to pituitary: Oxytocin is secreted by the posterior pituitary. The posterior pituitary can be seen as a storage and releasing site for hormones synthesized in the hypothalamus. The release of oxytocin is mediated by cholinergic and adrenergic neurotransmitters. The major stimulus to release is glutamate, whereas the major inhibitor is GABA. 28. Understand the role of insulin, how does insulin affect potassium. - correct answer ✔✔(p. 114, 704- 706, 7th ed) Role of insulin: Insulin is an anabolic hormone synthesized by the beta cells of the pancreas that circulates freely in the plasma. It promotes the synthesis of proteins, carbs, lipids, and nucleic acids in the liver, muscle, and adipose tissue (see table 20-8) with a net effect to stimulate cellular metabolism. The major consequence of insulin release is to decrease blood glucose as well as stimulate protein and fat synthesis. By binding to its tyrosine-kinase receptor subtype (initiating a series of events) insulin facilitates a 10-20 fold increase rate of glucose uptake into many cells within the body, particularly skeletal and cardiac muscle, liver, and adipose cells (figure 20-16). The sensitivity of the insulin receptor is a key component in maintaining normal cellular function. The brain and red blood cells do not require insulin for glucose transport. Insulin secretion is promoted by increased blood levels of glucose, amino acids (arginine and lysine), serum free fatty acids, and gastrointestinal hormones, and by parasympathetic stimulation of the beta cells. Insulin secretion is diminished in response to low blood glucose levels (hypoglycemia), high levels of insulin (negative feedback to the beta cells), and sympathetic stimulation of the alpha cells in the islets. Prostaglandin also inhibits insulin secretion. Insulin and Potassium: Insulin also facilitates the intracellular transport of potassium, phosphate, and magnesium. Insulin contributes to the regulation of plasma potassium levels by stimulating the sodium- potassium-APase pump, thereby promoting the movement of potassium into liver and muscle cells simultaneously with glucose transport. Insulin can also be used to treat hyperkalemia; however, dangerously low levels of plasma potassium can result from the administration of 29. What is the role of TSH? Where is it secreted? Know the negative feedback loop - correct answer ✔✔(p. 690-691, 700-702, 7th ed) Role: The effects of TSH on the thyroid include; (1) an immediate increase in the release of stored thyroid hormones, (2) an increase in iodide uptake and oxidation, (3) an increase in thyroid hormone synthesis, and (4) an increase in the synthesis and secretion of prostaglandins by the thyroid. TSH is also important in stimulating the growth and maintenance of the thyroid gland by stimulating thyrocyte hypertrophy and hyperplasia and decreasing apoptosis. Secretion: Thyroid-stimulating hormone (TSH) is a glycoprotein hormone synthesized and stored within the anterior pituitary. TSH is secreted from cells in the anterior pituitary called thyrotrophs (thyrotropic). It circulates to bind with TSH receptor sites located on the outer side of the thyroid cell's plasma membrane. Negative-feedback loop: Negative-feedback is the most common type of feedback system. In Negative- feedback system, plasma levels of one type of hormone influence the level of other types of hormones. Increased anterior pituitary release of TSH stimulates the synthesis and secretion of TH. TSH is inhibited by thyroxin (T4) and to a lesser extent by triiodothyronine (T3). TSH secretion is regulated by TRH primarily in the hypothalamus and by the negative-feedback inhibition from TH. Negative-feedback maintains hormones within physiologic ranges. Lack of negative-feedback inhibition on hormonal release often results in pathologic conditions. The concentration of thyroid hormones (T3 and T4) in the blood regulates the pituitary release of TSH; when T3 and T4 concentrations are low, the production of TSH is increased, and, conversely, when T3 and T4 concentrations are high, TSH production is decreased. 30. Understand the roles of epinephrine and norepinephrine. - correct answer ✔✔(p. 340, 719; 6th ed) (p. 345-346, 710; 7th ed) The adrenal medulla, together with the sympathetic division of the autonomic nervous system, is embryonically derived from neural crest cells. The adrenal medulla functions as a sympathetic ganglion without postganglionic processes. Chromaffin cells (pheochromacytes) are the cells of the adrenal medulla. The major products stored and secreted by the chromaffin cells are the catecholamines epinephrine (adrenaline) and norepinephrine, which are synthesized from the amino acid phenylalanine. Only 30% of circulating epinephrine comes from the adrenal medulla; the other 70% of is released from nerve terminals. The medulla is only a minor source of norepinephrine. Adrenal catecholamines are stored in secretory granules within the chromaffin cells. Physiologic stress to the body (e.g. traumatic injury, hypoxia, hypoglycemia, and many others) triggers release of adrenal catecholamines through acetylcholine (from the preganglionic sympathetic fibers), which depolarizes the chromaffin cells. Depolarization causes exocytosis of the storage granules from the chromaffin cells with release of epinephrine and norepinephrine into the bloodstream; therefore, the catecholamines from the adrenal medulla are hormones and not neurotransmitters. Once released, the catecholamines remain in the plasma for only seconds to minutes. The catecholamines exert their biologic effects after binding to a plasma membrane receptor (alpha-1, alpha- 2, beta-1, or beta-2) in target cells and activating the adenylyl cyclase system. Catecholamines have diverse effects on the entire body. Their release and the body's response have been characterized as the "fight or flight" response. The metabolic effects of catecholamines promote hyperglycemia through a variety of mechanisms and through interference with usu 31. What is parathyroid hormone? What are the effects of PTH? - correct answer ✔✔(p. 711-712, 6th ed) (p. 702-703, 7th ed) The parathyroid glands produce parathyroid hormone (PTH), a regulator of serum calcium. PTH works in concert with vitamin D to increase serum calcium concentration. PTH is regulated primarily by the level of ionized plasma calcium, although how these regulatory mechanisms work is not precisely clear. Calcium also increase intraparathyroid destruction of PRH but apparently does not affect the rate of PRH synthesis. Magnesium and phosphate levels also affect PTH secretion. Hypomagnesemia in persons with normal calcium levels acts as a mild stimulant to PTH secretion. Hypomagnesemia decreases PTH secretion. Hyperphosphatemia leads to hypocalcemia because of calcuim-phosphate precipitation in soft tissue and bone. Alterations in serum phosphate levels therefor may indirectly influence PTH secretion 36. What hormone is linked to obesity and early puberty in females? - correct answer ✔✔(p. 778, 803, 7th ed) (BOX: What's New? Precocious Puberty) OBESITY & EARLY PUBERTY Studies implicate obesity, leptin, ghrelin, and environmental endocrine disruptor chemicals (EDCs) as possible contributors to precocious puberty in girls. Obesity may affect the production and secretion of leptin and ghrelin, powerful communicators of satiety, hunger, metabolic rate, and in timing of puberty. Menarche appears to be related to body weight, especially percentage of body fat (ratio of fat to lean tissue), which may trigger a change in the metabolic rate and lead to hormonal changes associated with early menarche. There is an increased sensitivity to leptin (a regulatory hormone of appetite and energy metabolism) during puberty and, in theory, the adolescent consumes more calories to meet caloric needs of the pubertal growth spurt. The percent of body fat and leptin levels in girls continue to increase, whereas muscle mass increases in boy. 37. Etiology of cervical intraepithelial carcinoma (CIN) and cervical Ca. - correct answer ✔✔(p. 825-826, 7th ed) Cervical cancer is almost exclusively caused by human papillomavirus (HPV) infection. HPV causes both CIN and cervical cancer. Infection with high-risk oncogenic types of HPV (16 & 18) is a necessary precursor to development of the precancerous cell changes, known as dysplasia, of the cervix that leads to invasive cancer. Precancerous dysplasia, also called cervical intraepithelial carcinoma (CIN) and cervical carcinoma in situ (CIS), is a more advanced form of the cell changes. These cell changes can be detected non-invasively through examination of the cervical cells. The cells can be destroyed to prevent cancer development if dysplasia can be detected early. There are 2 main types of cells of the cervix: squamous epithelial cells and columnar epithelial cells. Squamous epithelial cells in older women cover the portions of the cervix that protrude into the vagina, and columnar epithelial cells line the inner portions of the cervical canal. The line where the two cells types meet, known as the transformation zone, is very vulnerable to the oncogenic effects of HPV. Certain gene polymorphisms on the genes that control epidermal growth factor increase the risk that HPV infection will lead to invasive cancer. Anything that affects the integrity of the immune system may affect the later risk of cervical cancer including poor nutrition and chronic stress. HIV infection greatly increases the risk that women infected with HPV will develop cervical cancer, and women with HIV should be screened for cervical cancer more frequently than women without HIV. Like other cancers, cervical cancer requires the accumulation of genetic alterations for carcinogenesis to occur. However, the discrete tumor suppressor gene locations have yet to be identified. Several chromosome regions with recurrent loss of heterozy 38. Etiology of epididymitis. Complications? - correct answer ✔✔(p. 897, 7th ed) Etiology: Epididymitis, or inflammation of the epididymis, generally occurs in sexually active young males (younger than 35 years) and is rare before puberty in young men the usual cause is a sexually transmitted microorganism, such as N. gonorrhoeae or C. trachomatis. Men who practice unprotected anal intercourse may acquire sexually transmitted epididymitis because of Escherichia coli, Haemophilus influenzae, tuberculosis (especially in regions where incidence of pulmonary tuberculosis is high), Cryptococcus, or Brucella. In men older than 35 years, enterobacteriaceae (intestinal bacteria) and Pseudomonas aeruginosa associated with urinary tract infections and prostatitis also may cause epididymitis. Besides an infectious etiology, epididymitis may result from a chemical inflammation caused by the reflux of sterile urine into the ejaculatory ducts. It is associated with urethral strictures, congenital posterior valves, and excessive physical straining in which increased abdominal pressure is transmitted to the bladder. Chemical epididymitis is usually self-limiting and does not require evaluation or intervention unless it persists. The pathogenic microorganism usually reaches the epididymis by ascending the vasa deferentia from an already infected urethra or bladder. The presence of bacteria initiates the inflammatory response, causing symptoms of bacterial epididymitis. Epididymitis caused by heavy lifting or straining results from reflux or urine from the bladder into the vas deferens and epididymis. Urine is extremely irritating to the epididymis and initiates an inflammatory response called chemical epididymitis. Acute, severe pain is typically the main symptom. Antibiotic therapy for the infection itself is necessary. Analgesics, ice and scrotal elevation can provide symptomatic relief. Bed re 39. Sexually transmitted diseases in teenage girls-why are they more susceptible? - correct answer ✔✔(p. 919, 7th ed) TEENAGE GIRLS Adolescents have the greatest risk for STI exposure and infection due to high risk-taking behavior (unprotected sex). Adolescent women may have a physiologically increased susceptibility to infection because of increased cervical immaturity and lack of immunity. Rates of gonorrhea, chlamydia, vaginitis, cervical condyloma, genital warts, and PID are highest in adolescents and young women and decline exponentially with increasing age . 40. Know pathophysiology, etiology, clinical manifestations, diagnostics, treatment and complications of endometriosis. - correct answer ✔✔(p. 823-825, 7th ed) Endometriosis Etiology: Ectopic responds to the hormonal fluctuations of the menstrual cycle. i. Cause of endometriosis is not known but there are 3 theories 1. Sampson: caused by implantation of endometrial cells during retrograde menstruation in which menstrual fluids move through the fallopian tubes and into the pelvic cavity. It is known to happen in all women but not all women develop endometriosis. 2. Impaired cellular and humoral immunity, alterations in cytokines and growth factor signaling have been identified. 3. Possible autoimmune response is suspectedcausing body to tolerate ectopic implantation of endometrial cells ii. A genetic predisposition to endometriosis has been documented. Pathophysiology: can occur throughout the body but generally occur in the pelvic and abdominal cavities. iii. Most common sites of implantation: ovaries, uterine ligaments, rectovaginal septum, peritoneum. 1. Other sites: sigmoid colon, small intestines, rectum appendix, bladder, uterus, vulva, vagina lymph nodes, extremities, pleural cavity, lungs laparotomy scar, and hernia sacs. iv. Cyclic changes depend on the blood supply of the implants and the presence of glandular and stromal cells. 1. If sufficient blood supply, ectopic endometrium proliferates and breaks down, and bleeds with normal menstrual cycles causing inflammationtriggering cellular inflammatory mediators (cytokines/chemokines) leading to fibrosis, scarring, adhesions and pain. Clinical Manifestations: can mimic other disease processes(i.e., PID, IBS, ovarian cyst) v. Symptoms are variable in frequency and severity and include 1. Primarily infertility, pain 2. Dysmenorrhea-not related to the degree of endometriosis 3. Dyschezia(pain on defecation): occurs w/bleeding of ectopic endometrium in the rectosigmoid musculature and subsequent fib 41. Know how protein hormones are transmitted in the blood. - correct answer ✔✔(p. 691, 7th ed) Protein hormones (peptide hormones) are water soluble and circulate in free (unbound) forms throughout the body. Most water soluble hormones activate G protein-linked receptors. Water soluble hormones act as first messengers, binding to receptors on the cell's plasma membrane. The signals initiated by hormone-receptor binding are then transmitted into the cell by the action of the second Nephrogenic DI is associated with an insensitivity of the renal collecting tubules to ADH. The nephrogenic from of DI can be genetic of acquired. This from of DI is often idiopathic, although several genetic abnormalities that the affect the vasopressin receptor have been noted. One of the best described is a mutation in the gene that codes for aquaporin-2, which if one of four water transport channels in the renal tubule. Acquired nephrogenic DI is generally related to disorders and drugs that damage the renal tubules or inhibit the generation of cAMP in the tubules. These disorders include pyelonephritis, amyloidosis, destructive uropathies, polycystic disease, and intrinsic renal disease, all of which lead to irreversible DI. Dipsogenic: This form occurs when 45. Know pituitary tumors and clinical manifestations of each. - correct answer ✔✔(p. 733, 735-736; 6th ed) (p. 722, 724; 7th ed) Pituitary Adenomas (Hyperpituitarism): (722) usually benign, slow growing tumors that arise from cells of the anterior pituitary, most commonly those that secrete GH and prolactin. Very common in the population with prevalence rates estimated about 17%. The pathogenesis of pituitary adenomas includes hypothalamic and intrapituitary factors, which include altered expression of the pituitary cycle genes, activation of pituitary selective oncoprotiens, or loss of pituitary suppressor factors. The vast majority of pituitary tumors are microadenomas that are hormonally silent and do not pose significant hazards to the individual. These are usually found on high resolution MRI accidentally. Primary pituitary carcinomas are rare, representing 0.2% of all pituitary tumors. Pathophysiology: local expansions of pituitary adenomas may cause both neurological and secretory defects. Adenoma tissue secretes the hormone of the cell type from it arose, without regard to physiological needs and without benefit of regulatory feedback mechanisms. Clinical Manifestations: related to tumor growth and hormone hypersecretion or hyposecretion. Effects from tumor size increase include nonspecific complaints of headache and fatigue. Visual changes produced by pressure on the optic chiasm-visual field impairment and temporary blindness. If the tumor infiltrates to other cranial nerves, neurologic function is affected. Pituitary adenomas arise from hormone producing cells and are most often associated with increased secretion of GH and prolactin. Pressure produced by growing pituitary adenomas is also associated with decreased function of neighboring anterior pituitary hormones. GH hyposecretion will cause menstrual irregularities in woman, decreased libido, and receding secondary sex characte Gonorrhea? - correct answer ✔✔BACTERIAL Gonorrhea Pathology: Local or systemic. Manifestations: Uncomplicated-urethral infections in men and urogenital infections in women. Men will have sudden onset of painful urination or purulent penile discharge or both within a week of infection. Women's symptoms will manifest within 10days or within 1 to 2 days after the next menstrual period. Initially asymptomatic, symptoms appear after spread to the upper reproductive tract. Symptoms include, dysuria, increased vaginal discharge, abnormal menses, dyspareunia, lower abd pain and fever. Complicated- prostatitis, epididymitis, lymphangitis, and urethral stricture in men and salpingitis, PID, and bartholinitis in women. Diagnosis: direct culture is preferred. Physical exam may disclose cervical friability and erythema and mucopurulent discharge from the cervical os. Abdominal palpation bilateral lower quadrant tenderness and rebound tenderness. Treatment: quickly becoming antibiotic resistant. Multidrug therapy is recommended. (Ceftriaxone IM and azithromycin or doxycycline po) Complications: PID, sterility and disseminated infection. Transmission to fetus: If passed to the fetus the infection usually manifests as an eye infection and develops 1-12 days after birth. Syphilis (923) - correct answer ✔✔BACTERIAL Syphilis (923) Pathology: systemic shortly after infection. Etiology: transmission through minor abrasions during sexual intercourse but can occur extragenitally as well. Caused by treponema pallidum. Manifestations: (chart page923) *stage 1- primary: chancre at the site. Microorganisms drain in to adjacent lymph node and stimulate immune responses. *stage2-secondary: systemic spread to all body systems. *stage3-latent: minimal symptoms or the development of skin lesions, silent infection. *stage4-tertiary: the most severe stage, with destruction of bone, skin and soft and neurologic tissues. Noninfectious disease. Significant morbidity and mortality occur. Cardiovascular complications. Diagnosis: darkfield microscopy and serologic testing. During latent stage CSF can be tested. Treatment: injectable PCN, sexual partners are also treated Transmission to fetus: congenital syphilis contributes to prematurity of the newborn with bone marrow depression, CNS involvement, renal failure and intrauterine growth retardation. Transmission to fetus declines with each subsequent pregnancy, but can be transmitted as early as the ninth week of gestation. Chancroid (925) - correct answer ✔✔BACTERIAL Chancroid (925) Pathology: lesions are usually found throughout the genital regions, most commonly on the foreskin in men and the labia, clitoris or fouchette in women. Initially the papule enlarges, it then erodes into a soft, circumscribed ulcer with superficial exudate. Manifestations: - Women are generally asymptomatic and men develop inflamed, painful genital ulcers and inguinal buboes (swollen inflamed lymph node) - Incubation period 1-14days. 3-10 day incubation period. Women generally asymptomatic but can have dysuria, dyspareunia, vaginal discharge, pain on defecation, or rectal bleeding. A vesicopustule lesion forms and erodes into soft ulcer with a necrotic base, surrounding erythema, and a ragged, and serpiginous border. Unilateral painful, local lymphadenopathy presents primarily in men. Inguinal buboes (abscess) develop and fill with exudate. Lesions spread through autoinoculation. Diagnosis: easily confused with other genital ulcers. Chacrodial ulcers are painful, tender and nonindurated. Culture specimens positive for h. ducreyi. Treatment: single dose therapy with injected ceftriaxone or oral azithromycin in BOTH partners. Granuloma Inguinale (donovanosis) (928) - correct answer ✔✔BACTERIAL Granuloma Inguinale (donovanosis) (928) Pathology: Rare. Bacteria are gram negative and survive within macrophages. And is progressively destructive if untreated. Manifestations: localized nodules coalesce to form granulomas and ulcers on the penis in men and labia in women. Diagnosis: tissue smears or biopsy from lesions containing DONOVAN BODIES (bacteria filled vacuole Treatment: Long term treatment w/ doxycycline, azithromycin, cipro, erythromycin, or trimethoprim- sulfamethoxazole. Treat all sexual partners. Relapse can occur 6-18 months later despite effective initial therapy. Complications: secondary infections to other areas. Pseudobuboes. transported to the dorsal root where it remains latent until reactivated. Can be reactivated by stress, menstruation, sun exposure. Etiology: transmitted through genital skin or mucosal contact with a person who is shedding the virus. Manifestations: lesions initially appear as groups of vesicles, at the site of infection, that progress to ulceration with pain, lymphadenopathy, and fever. Individuals are contagious during outbreaks and episodes of asymptomatic viral shedding. Diagnosis: viral cultures can be done, but CDC recommends serologic testing. Treatment: Acyclovir reduces symptoms but does not cure the disease. Complications: lifelong with initial outbreak and subsequent outbreaks. Transmission to fetus: does pass from mother to fetus, so mother should have C-section to prevent transfer. HPV (934) - correct answer ✔✔VIRAL HPV (934) Pathology: DNA virus. Transmission occurs through sexual contact. The initial infection follows trauma to the epithelium that allows the virus to reach and infect the basal cells of the epithelium. The cells then proliferate and may form a warty growth or cancer. May appear after 2-3 months or may not be noticed for years. Manifestations: associated with cervical dysplasia and cancer as well as condylomata acuminata (warts). The high-risk strains that produce cancer do not produce warts. Warts are highly contagious. (Velvety cauliflower-like lesions occur in the genital and anal areas, vagina and cervix and are painless.) Diagnosis: testing is available Treatment: vaccine now available. Warts can be removed but not cured. Pap tests ever 3 years. Complications: CANCER Transmission to fetus: Warts can be transferred to infant at birth causing laryngeal papillomas. Symptoms include, stridor, hoarseness, abnormal cry, and cough and resp distress. Can be infected in utero and by passage through an infected birth canal. Molluscum Contagiosum (937) - correct answer ✔✔VIRAL Molluscum Contagiosum (937) Pathology: benign viral infection of the skin. : transmitted by skin-to-skin contact in children and adults on the face, hands, lower abdomen or genitalia. Can be transmitted by sexual contact or from wet surfaces, towels, equipment, etc. Etiology: The virus is taken into epithelial cells by phagocytosis and replicates within the cytoplasm, where it produces superficial cytoplasmic inclusion and cellular hyperplasia. Manifestations: Incubation of 2-7 weeks. Then small white or flesh colored, round or oval dome shaped papules appear. The surface has a characteristic central umbilication where a thick, cream core material can be expressed. Diagnosis: appearance alone Treatment: heal spontaneously after several months but are contagious until completely healed. Can use cryotherapy, silver nitrate, topical creams or curettage. Trichomoniasis (937) - correct answer ✔✔PARASITIC Trichomoniasis (937) Pathology: parasitic protozoan that adheres to and damages squamous epithelial cells. (Women- vaginal and urethral tissue not the cervical canal. Men- urethra, epididymis and rarely the prostate) Etiology: t. vaginalis, common cause of sexually transmitted diseases and urethritis. Induces a marked inflammatory response in the vagina causing copious discharge. Manifestations: causes vaginitis in women and urethritis in men. Women have a copious amount of malodorous, gray-green discharge with pruritus and sometime "strawberry spots" visible on the vaginal walls and cervix. Increased pH. Men usually are asymptomatic. Diagnosis: microscopic or laboratory confirmation of the presence of the trichomonads in vaginal secretions or urine provide a def diagnosis. Symptoms and Hx are not enough. Treatment: metronidazole for both partners. Scabies (938) - correct answer ✔✔PARASITIC Scabies (938) Pathology: hands between fingers and on the flexor surfaces of the wrists and the extensor surfaces of the elbows. The groin is a common location for sexually transmitted scabies. Lesions can occur on the penile shaft, glans, scrotum or buttocks. Etiology: can be spread by skin-to-skin contact or sexual contact. Common in nursing homes, child care facilities, and prisons. Manifestations: intense pruritus, ESP at night. S shaped burrow with a tiny vesicle at one end. Diagnosis: microscopic identification of the mite, eggs, or feces is recommended. Treatment: topical permethrin. Pediculosis Pubis (CRaBs) (939) - correct answer ✔✔PARASITIC Pediculosis Pubis (CRaBs) (939) Pathology: one of three species of lice that infect humans. 25-30 day life cycle. They depend on blood for nutrition. Etiology: caused by crab louse, p. pubis. Either from sexual contact or contact with infected bed linens or clothing. Can live on objects (towels) for a several days. Highly contagious. Manifestations: mild and severe pruritus. Diagnosis: lice are visible to the naked eye (grayish with claws to attach to pubic hair) Treatment: topical over the counter pediculicides (permethrin cream rinse or lindane lotion.) Second line treatment is malathioin lotion kept on body for 8-12 hours. Sexual partners should be treated regardless of symptoms. Complications: secondary infections from excessive scratching. Hepatitis B Virus - correct answer ✔✔Hepatitis B Virus Pathology: Sexually transmitted. Passes through the blood stream to the liver, where it infects liver cells and multiplies. Etiology: needle puncture, blood transfusion, cuts in the skin, and contact with infected body fluids. Can remain outside body in a dry environment for 1 week and survive. Can only be killed with bleach or VERY high temps. Manifestations: may start with rash, urticarial, polyarthralgias, arthritis, anorexia, nausea, vomiting, headache, fever, jaundice, and moderate liver enlargement with tenderness AND chronic liver disease, hepatocellular cancer.( Mild illness to severe infection) Diagnosis: serologic testing. Treatment: immunization (three injection serious beginning at birth) Supportive care and relief of symptoms. Transmission to fetus: high risk, unless receive immunoglobulin and vaccination within 12 hours of birth. AIDS - correct answer ✔✔Bad Deal!