NR 507 Pathophysiology Final Study guide Completed_100+ Pages | NR507 Pathophysiology Final Study guide Completed- A grade

NR 507 Pathophysiology Final Study guide Completed- Chamberlain College of Nursing Final Study guide REPRODUCTIVE: endometrial cycle and the occurrence of ovulation uterine prolapse polycystic ovarian syndrome (PCOS) testicular cancer and conditions that increase risk symptoms that require evaluation for breast cancer signs of premenstrual dysphoric disorder dysfunctional uterine bleeding pathophysiology of prostate cancer HPV and the development of cervical cancer ENDOCRINE body’s process for adapting to high hormone levels Cushing’s Syndrome causes of hypoparathyroidism lab results that point to primary hypothyroidism pathophysiology of thyroid storm signs of thyrotoxicosis NEUROLOGICAL dermatomes substance release at the synapse Spondylolysis location of the motor and sensory areas of the brain pathophysiology of cerebral infarction and excitotoxins agnosia accumulation of blood in a subarachnoid hemorrhage most common cause of meningitis GENITOURINARY diet and the prevention of prostate cancer Impact of Benign Prostatic Hypertrophy (BPH) on the urinary system GENETICS the role of DNA in genetics transcription effects of genetic mutations Trisomy Down Syndrome Klinefelter syndrome Duchenne muscular dystrophy Neurofibromatosis diseases that have multifactorial traits multifactorial inheritance MUSCULOSKELETAL ions that initiate muscle contraction growth of long bones in children bones belonging to the appendicular skeleton IMMUNITY & INFLAMMATION how vaccines are formed populations at risk for getting systemic fungal infections and parasitic infections systemic manifestations of infection mechanisms responsible for the increase in antimicrobial resistance worldwide functions of normal flora in the body desensitization therapy cells involved in “left shift” in the WBC count differential forms of immunity major histocompatibility class I antigens inflammatory chemicals blocked by anti-inflammatory drugs characteristics of acute phase reactant C-reactive protein DERMATOLOGY process by which a deep pressure ulcer heals complications of the development of contractures during wound healing ACID/BASE causes of respiratory alkalosis molecules that act as buffers in the blood CARDIOVASCULAR most common cardiac valve disease in women when myocardial ischemia may be reversible symptoms of stable angina orthostatic hypotension isolated systolic hypertension results of sustained controlled hypertension the relationship of insulin resistance on the development of primary hypertension defects in the normal secretion of natriuretic hormones and the impact on renal system effects of increased sympathetic nervous system activity due to primary hypertension complications of unstable plaque in the coronary arteries forms of dyslipidemia associated with the development of the fatty streak in atherosclerosis events that initiate the process of atherosclerosis signs and symptoms of increased left atrial and pulmonary venous pressures in left sided heart differences between left and right sided heart failure infective endocarditis PERIPHERAL VASCULAR DISEASE pathophysiology of deep vein thrombosis Vichow’s triad HEMATOLOGY physiological response to hypoxia in anemia populations at the highest risk for developing folate deficiency anemia causes of iron deficiency anemia expected lab test results found in long standing iron deficiency anemia Sickle Cell Anemia causes of aplastic anemia underlying pathophysiologic mechanisms leading to autoimmune hemolytic anemia secondary polycythemia anemia of chronic renal failure FLUIDS & ELECTROLYTES conditions that result in pure water deficit (hypertonic volume depletion) osmoreceptors that stimulate thirst and the release of ADH causes of hypernatremia effects of increased aldosterone dependent edema definition of isotonic principle of capillary oncotic pressure types of fluid compartments in the body PULMONARY most effective measure to prevent pulmonary embolus from developing in patients when the practitioner will note tactile fremitus cause of acute airway obstruction in the patient with chronic bronchitis types of pneumothorax results of the loss of alph-1-antitrypsin in emphysema the result of loss of surfactant in ARDS Characteristics of Cheyne-Stokes respirations SHOCK causes of hypovolemic shock; how the body maintains glucose levels during shock Reproductive: The Menstrual (Ovarian) Cycle: Purpose: Pregnancy and menstrual bleeding (the menses). Starts with Menarche (first menstruation) ends with menopause (cessation of menstrual flow for 1 year). Cycles are anovulatory at first and may vary in length from 10 to 60 days then regular patterns of menstruation and ovulation occur lasting from 21 to 45 days. CYCLE: Commonly accepted cycle average is 28 (27 to 30) days, with rhythmic intervals of 21 to 35 days (Normal). Phases of the Menstrual Cycle: (two phases) 1- the follicular/proliferative phase (postmenstrual) followed by 2- the luteal/secretory phase (premenstrual). Menstruation (menses),the functional layer of the endometrium disintegrates and is discharged through the vagina. Follicular/proliferative phase: GnRH and a balance between activin and inhibin from the granulosa cells contribute to the rise of FSH levels, which stimulates several follicles. The pulsatile secretion of FSH from the anterior pituitary gland rescues a dominant ovarian follicle from apoptosis by days 5 to 7 of the cycle. Together estrogen and FSH increase FSH receptors in the granulosa cells of the primary follicleà making them more sensitive to FSH. FSH and estrogen combine to induce production of LH receptors on the granulosa cells, promoting LH stimulation to combine with FSH stimulation causing a more rapid secretion of follicular estrogen. As estrogen levels increase, FSH levels drop because of an increase in inhibin-B secreted by the granulosa cells in the dominant follicle. This drop in FSH level decreases the growth of less-developed follicles. Estrogen causes cells of the endometrium to proliferate and stimulates production of LH. A surge in both FSH and LH levels is required for final follicular growth and ovulation. An increase in stromal tissue in the late follicular phase is associated with a rise in androgen levels. Androgen production enhances the process of follicle atresia. Luteal/secretory phase (premenstrual): Ovulation is the release of an ovum from a mature follicle and marks the beginning of the luteal/secretory phase of the menstrual cycle. Ovarian follicle begins its transformation a corpus luteum (hence luteal phase) (see Fig. 24.8, A) Pulsatile secretion of LH from the anterior pituitary stimulates the corpus luteum to secrete progesterone, which in turn initiates the secretory phase of endometrial development. Glands from the endometrium start to secrete a thin glycogen-containing fluid (the secretory phase). If conception occurs, the nutrient-laden endometrium is ready for implantation. Human chorionic gonadotropin (HCG) is secreted 3 days after fertilization by the blastocytes and maintains the corpus luteum once implantation occurs at about day 6 or 7. HCG can be detected in maternal blood and urine 8 to 10 days after ovulation. If conception and implantation do not occur, the corpus luteum degenerates and STOPS production of progesterone and estrogen. Without progesterone or estrogen to maintain it, the endometrium becomes ischemic (“blood-starved”) and disintegrates, hence the name ischemic/menstrual phase. Menstruation then occurs, marking the beginning of another cycle. Ovulation Occurs: Ovulatory cycles- minimum length of 24 to 26.5 days: Primary ovarian follicle requires 10 to 12.5 days to develop, and the luteal phase appears relatively fixed at 14 days (±3 days). Menstrual blood flow usually lasts 3 to 7 days, but it may last as long as 8 days or stop after 1 to 2 days and still be considered within normal limits. Bleeding is consistently scant to heavy and varies from 30 to 80 mL, with most blood loss occurring during the first 3 days of menses. Menstrual discharge consists of blood, mucus, and desquamated endometrial tissue and does not clot under normal circumstances. It is usually dark and produces a characteristic musty odor on oxidation. Environmental factors such as severe emotional stress, illness, malnutrition, obesity, and seasonal variation may affect the length of the menstrual cycle. Uterine prolapse: is descent of the cervix or entire uterus into the vaginal canal (Fig. 25.11). In severe cases the uterus falls completely through the vagina and protrudes from the introitus. Symptoms of other pelvic floor disorders also may be present. Polycystic ovary syndrome (PCOS): is the most common cause of anovulation and ovulatory dysfunction in women. PCOS is defined as having at least two of the following three features: -irregular ovulation, -elevated levels of androgens (e.g., testosterone), and -the appearance of polycystic ovaries on ultrasound. Polycystic ovaries do not have to be present to diagnose PCOS, and conversely their presence alone does not establish the diagnosis. (2 out of 3 need to be present). PCOS is associated with metabolic dysfunction, including dyslipidemia, insulin resistance, and obesity. Cause of PCOS is unknown, a genetic basis is suspected. Symptoms are related to anovulation, hyperandrogenism, and insulin resistance and include dysfunctional bleeding or amenorrhea, hirsutism, acne, acanthosis nigricans, and infertility. Goals of treatment include reversing signs and symptoms of androgen excess, instituting cyclic menstruation, restoring fertility, and ameliorating any associated metabolic or endocrine, or both, disturbances. First-line treatment of PCOS includes combined oral contraceptives (COCs) for management of symptoms (e.g., hirsutism, acne) and to establish regular menses. For those women with PCOS who are overweight or obese, lifestyle modifications, including regular exercise and weight loss, also are considered first-line treatments. Women with insulin resistance, or those women who do not respond to contraceptive therapy, may benefit from the insulin sensitizer metformin. If COCs are not used and pregnancy is not desired, progesterone therapy is recommended to oppose estrogen's effects on the endometrium and as a mean - - - - - - -- - -- -- - - - - - - - - - - -- - - - - - - - - - - - - -- TYPES OF PNEUMOTHORAX o Pneumothorax- presence of air or gas in the pleural space caused by a rupture in the visceral pleura or the parietal pleura and chest wall o Diagnosed with chest radiographs, ultrasound, and CT. o Types  Primary (Spontaneous) Pneumothorax • Often caused by spontaneous rupture of blebs  Secondary (Traumatic) Pneumothorax • Caused by chest trauma (rib fracture, stab, bullet)  Iatrogenic Pneumothorax • Commonly caused by transthoracic needle aspiration o Spontaneous or Traumatic and present as open or tension  Open Pneumothorax (Communicating pneumothorax) • Air pressure in the pleural space equals barometric pressure because air that is drawn into the pleural space during inspiration is forced back out during expiration  Tension Pneumothorax • Site of pleural rupture acts as a one-way valve, permitting air to enter on inspiration, but prevents air escape by closing during expiration Pneumothorax is the presence of air or gas in the pleural space caused by a rupture in the visceral pleura (which surrounds the lungs) or the parietal pleura and chest wall. As air separates the visceral and parietal pleurae, it destroys the negative pressure of the pleural space. This disrupts the state of equilibrium that normally exists between elastic recoil forces of the lung and chest wall. No longer held in check by the recoil forces of the chest wall, the lung fulfills its tendency to recoil by collapsing toward the hilum. Primary Pneumothorax: occurs unexpectedly in healthy individuals (usually men) between ages 20 and 40 years, is most often caused by the spontaneous rupture of blebs (blister-like formations) on the visceral pleura, although there may be underlying pleural disease with emphysema-like changes. Secondary (traumatic) pneumothorax: can be caused by chest trauma, such as a rib fracture, stab or bullet wounds, or a surgical procedure that tears the pleura; rupture of a bleb or bulla (larger vesicle) as occurs in COPD; or mechanical ventilation, particularly if it includes positive end-expiratory pressure (PEEP). Clinical manifestations of spontaneous or secondary pneumothorax begin with sudden pleural pain, tachypnea, and possibly mild dyspnea. Iatrogenic pneumothorax: most commonly caused by transthoracic needle aspiration. Open pneumothorax (communicating pneumothorax): air pressure in the pleural space equals barometric pressure because air that is drawn into the pleural space during inspiration (through the damaged chest wall and parietal pleura or through the lungs and damaged visceral pleura) is forced back out during expiration. Tension pneumothorax: the site of pleural rupture acts as a one-way valve, permitting air to enter on inspiration, but preventing its escape by closing during expiration. As more and more air enters the pleural space, air pressure in the pneumothorax begins to exceed barometric pressure. The pathophysiologic effects of tension pneumothorax are life threatening. Air pressure in the pleural space pushes against the already recoiled lung, causing compression atelectasis, and against the mediastinum, compressing and displacing the heart and great vessels. Tension pneumothorax may be complicated by severe hypoxemia, tracheal deviation away from the affected lung, and hypotension (low blood pressure) Results of the loss of alph-1- antitrypsin in emphysema Primary emphysema, which accounts for 1% to 3% of all cases of emphysema, is commonly linked to an inherited deficiency of the enzyme α1-antitrypsin.94 Normally α1-antitrypsin inhibits the action of many proteolytic enzymes (enzymes that break down proteins). Individuals who have α1-antitrypsin deficiency (an autosomal recessive trait) have an increased likelihood of developing emphysema, because proteolysis in lung tissues is not inhibited. Homozygous individuals have a 70% to 80% likelihood of developing lung disease. (Mechanisms of genetic inheritance are described in Chapter 4.) Persons with α1-antitrypsin deficiency who smoke are even more susceptible to emphysema than those with the deficiency alone. α1-Antitrypsin deficiency is suggested in nonsmokers and individuals who develop emphysema before age 40 years (or in their early forties). Alpha-1 antitrypsin deficiency is an inherited disorder that may cause lung disease and liver disease. The signs and symptoms of the condition and the age at which they appear vary among individuals. People with alpha-1 antitrypsin deficiency usually develop the first signs and symptoms of lung disease between ages 20 and 50. The earliest symptoms are shortness of breath following mild activity, reduced ability to exercise, and wheezing. Other signs and symptoms can include unintentional weight loss, recurring respiratory infections, fatigue, and rapid heartbeat upon standing. Affected individuals often develop emphysema, which is a lung disease caused by damage to the small air sacs in the lungs (alveoli). Characteristic features of emphysema include difficulty breathing, a hacking cough, and a barrel-shaped chest. Smoking or exposure to tobacco smoke accelerates the appearance of emphysema symptoms and damage to the lungs. About 10 percent of infants with alpha-1 antitrypsin deficiency develop liver disease, which often causes yellowing of the skin and whites of the eyes (jaundice). Approximately 15 percent of adults with alpha-1 antitrypsin deficiency develop liver damage (cirrhosis) due to the formation of scar tissue in the liver. Signs of cirrhosis include a swollen abdomen, swollen feet or legs, and jaundice. Individuals with alpha-1 antitrypsin deficiency are also at risk of developing a type of liver cancer called hepatocellular carcinoma. In rare cases, people with alpha-1 antitrypsin deficiency develop a skin condition called panniculitis, which is characterized by hardened skin with painful lumps or patches. Panniculitis varies in severity and can occur at any age. Symptoms related to the lung: • Shortness of breath. • Wheezing. • Chronic bronchitis, which is cough and sputum (phlegm) production that lasts for a long time. • Recurring chest colds. • Less exercise tolerance. • Year-round allergies. • Bronchiectasis. The result of loss of surfactant in ARDS Surfactant impairment results from decreased production or inactivation of surfactant, which is necessary to reduce surface tension in the alveoli and thus prevent lung collapse during expiration. Surfactant impairment can occur because of premature birth, acute respiratory distress syndrome, anesthesia, or mechanical ventilation. As the alveoli increase in size, the surfactant becomes more spread out over the surface of the liquid. This increases surface tension effectively slowing the rate of expansion of the alveoli. Surfactant reduces surface tension more readily when the alveoli are smaller because the surfactant is more concentrated. When there is not enough surfactant the tiny alveoli collapse with each breath, and as they collapse damaged cells collect in the airway causing further affect in breathing. Characteristics of Cheyne-Stokes respirations Alternating periods of deep and shallow breathing. Apnea lasting 15 to 60 seconds is followed by ventilations that increase in volume until a peak is reached, after which ventilation (tidal volume) decreases again to apnea. Cheyne-Stokes respirations result from any condition that slows the blood flow to the brainstem, which in turn slows impulses sending information to the respiratory centers of the brainstem. Neurologic impairment above the brainstem is also a contributing factor. Usually seen in comatose individuals having disease nervous centers respirations. HYPOVOLEMIC SHOCK: Hypovolemic shock is caused by a drastic decrease in whole blood (hemorrhage), plasma (burns), or interstitial fluid (diaphoresis, DM, emesis, or diuresis). Blood loss causes hypovolemia directly, “relative” hypovolemia is caused by indirect fluid loss such as interstitial fluid loss (plasma from intravascular to extravascular space). Hypovolemia is offset at first by compensatory mechanisms such as increased heart rate and SVR (due to catecholamine release from the adrenal gland). This increases CO and tissue perfusion pressures. The liver and spleen then add to blood volume by disgorging stored red blood cells and plasma previously stored. In the kidneys renin stimulates the release of aldosterone and retention of Na, therefore ^ H20 retention. ADH (vasopressin) from the posterior pituitary gland ^ H20 retention. As shock worsens the ADH in plasma decreases. Hypovolemic shock results in compensatory vasoconstriction and ^ SVR and afterload in order to improve BP and perfusion to core vital organs. With continued blood loss the compensatory mechanism fails, resulting in decreased tissue perfusion. Nutrient delivery to the cells and cellular metabolism then fails. Prompt control of hemorrhage is the treatment of choice, followed by replacement of fluids. Clinical manifestations of hypovolemic shock: ^SVR, poor skin turgor, ^ thirst, oliguria, low systemic and pulmonary preloads, and rapid heart rate. HOW THE BODY MAINTAINS GLUCOSE LEVELS DURING SHOCK: Impaired glucose during shock can be caused by either impaired glucose delivery or impaired glucose uptake by the cells. In septic and anaphylactic shock, glucose metabolism may be increased or disrupted due to fever or bacteria. Compensatory mechanisms can also lead to decreased glucose uptake and use by cells. High serum levels of cortisol, growth hormone, and catecholamines account for hyperglycemia and insulin resistance, tachycardia, ^ SVR, and ^ cardiac contractility. Cells shift to glycogenolysis, gluconeogenesis, and lipolysis to generate fuel for survival. Except in the liver, kidneys, and muscles, the body’s cells have extremely limited stores of glycogen. The body stores can only fuel the metabolism for about 10 hours. Depletion of fat and glycogen stores is not itself a cause of organ failure, but the energy costs of glycogenolysis and lipolysis are considerable and contribute to the cellular failure.