NUR2063 Exam 3 Focused Review .docx CORRECT EXAM GUIDING POINT FOR AN A+ SCORE

NUR2063 Exam 3 Focused Review .docx CORRECT EXAM GUIDING POINT FOR AN A+ SCORE Ch. 2 Homeostasis, Allostasis, and Adaptive Responses to Stressors Electrolyte pools- bones act as an electrolyte pool and store calcium magnesium, and phosphate ions; shift of electrolytes into electrolyte pools will decrease plasma electrolyte concentration and shift of electrolytes from an electrolyte pool into the extracellular fluid will increase the plasma electrolyte concentration Ch. 7 Neoplasia Metastasis- process by which cancer cells escape their tissue of origin and initiate new colonies of cancer in distant sites Ch. 9 Inflammation and Immunity Passive vs active immunity- Passive: transfer of preformed antibodies against specific antigen from a protected or immunized individual to an unprotected or nonimmunized individual; types: mother to fetus: IgG- can cross placenta, mother to infant: IgA- from breast milk, serotherapy- direct injections of antibodies (human or animal); active: a protected state owing to the body’s immune response as a result of active infection or immunization, types: immunizations- vaccines Immunoglobulins- antibodies; two identical light polypeptide chains joined to identical heavy polypeptide chains by disulfide bonds; five different classes: IgG, IgM, IgA, IgD, & IgE • Ch. 11 Malignant Disorders of White Blood Cells Chronic myeloid leukemia (CML)- characterized by malignant granulocytes that carry the Philadelphia chromosome (Ph+); does not respond well to chemotherapy: poor overall survival time; Blast stage CML- poor prognosis: 3 to 4 months; treatment- bone marrow transplant Age of onset for multiple myeloma- median age 65 years Malignant Disorders of WBCs- may be nonspecific signs & symptoms • Ch. 13 Alterations in Oxygen Transport Anemia- occurs from a manifestation of diseases; a deficit of RBCs; leads to hypoxia Polycythemia- excess of RBCs; increases blood viscosity & volume; leads to hypertension Erythropoietin- is stimulated from the kidney secretion hormone to stimulates RBC production Acute blood loss- type of anemia; may be from trauma or secondary to a disease process; symptoms develop with activity at 20% loss of blood volume (tachycardia and postural drop in BP), and increase in severity with continued blood loss; shock and death can occur with 50% loss of circulating volume; treatment: blood volume replacement therapy with crystalloids, colloids, and fresh whole blood; prognosis: excellent with treatment unless blood loss is severe • Ch. 14 Alterations in Hemostasis and Blood Coagulation Thrombocytopenia causes- 1) bone marrow suppression from chemotherapy, 2) recent immunizations, 3) alcohol ingestion, 4) decreased platelet production, 5) decreased platelet survival, 6) splenic sequestration, & 7) intravascular dilution of circulating platelets from transfusion DIC (Disseminated Intravascular Coagulation)- acquired hemorrhagic syndrome in which clotting, and bleeding occur simultaneously. Widespread clot formation in small vessels; clotting and platelets consumed resulting in bleeding. Causes: trauma, malignancy, burns, shock, and abruptio placentae. Clinical manifestations: fibrinogen level and platelet count decreased, increased bleeding time, elevated PT/INR/aPTT, elevated D-dimer/fibrin split products. Treatment: Removal/correction of underlying cause, support major organs, fresh frozen plasma, packed red blood cells, platelets, or cryoprecipitate, heparin used to minimize further consumption of clotting factors (controversial). • Ch. 15 Alterations in Blood Flow Atherosclerosis is the leading cause of coronary artery/heart disease Ch. 16 Alterations in Blood Pressure Treatment of hypertension- (lifestyle modifications) weight loss, exercise, DASH diet, alcohol moderation, decreased sodium intake; drug therapy affects HR, SVR, and/or stroke volume Long term problems from hypertension- Renal failure, stroke, heart disease, Damage to arterial system and acceleration of atherosclerosis lead to cardiovascular disease, Increased myocardial work results in heart failure, Glomerular damage results in kidney failure, Affects microcirculation of the eyes, Increased pressure in cerebral vasculature can result in hemorrhage Modifiable vs nonmodifiable risk factors for hypertension- modifiable: dietary factors, sedentary lifestyle, obesity/weight gain, metabolic syndrome, elevated blood glucose levels/diabetes, elevated total cholesterol, alcohol & smoking; nonmodifiable: family history, age, ethnicity/genetics • Ch. 18 Alterations in Cardiac Function Coronary artery disease: characterized by insufficient delivery of oxygenated blood to the myocardium caused by atherosclerotic coronary arteries; known risk factor: atherosclerosis How to determine causes of acute coronary syndrome: associated with acute changes in plaque morphology and thrombosis; evidence of acute ischemia on ECG- STEMI-candidates for acute reperfusion therapy; no ST elevation on ECG- non-STEMI- candidates for antiplatelet drugs; treatment: reperfusion diagnosis and prognosis: diagnosis: Signs and symptoms, Electrocardiographic changes, Elevations of specific marker proteins in the blood, Severe crushing, excruciating chest pain that may radiate to the arm, shoulder, jaw, or back, Accompanied by nausea, vomiting, diaphoresis (sweating), shortness of breath, prognosis: difficult to determine b/c of many different factors; After 18 to 24 hours: area of infarction becomes paler than surrounding tissues, 5 to 7 days: turns yellowish and soft with a rim of red vascular connective tissue, At 1 to 2 weeks: necrotic tissue progressively degraded and cleared away; infarcted myocardium weakened and susceptible to rupture, By 6 weeks: necrotic tissue replaced by tough fibrous scar tissue Unstable angina pectoris vs stable angina- angina pectoris: chest pain associated with intermittent myocardial ischemia; stable angina: most common; also called classic; chronic occlusion of a coronary vessel; chronic syndromes with slow progression because of chronic obstruction from stable atherosclerotic plaques; unstable/crescendo angina pectoris: acute/partial occlusion; plaque distribution and thrombus formation and results in unstable angina or MI; acute coronary syndrome (ACS) associated with acute changes in plaque morphology and thrombosis; abrupt and can be life-threatening (non-STEMI) Myocardial ischemia- acute occlusion: plaque distribution and thrombus formation and results in unstable angina or MI; may be caused by conditions that reduce coronary blood flow or increase myocardial demands for oxygen; may by uncommonly caused by: coronary vasospasm, hypoxemia, & low perfusion pressure from volume depletion or shock • Ch. 19 Heart Failure & Dysrhythmias: Common Sequelae of Cardiac Diseases Left and right sided heart failure including treatment: left-sided: backward effects, which result in accumulation of blood within the pulmonary circulation, pulmonary congestion, and edema; forward effects, which result in insufficient CO with diminished delivery of oxygen & nutrients to peripheral tissues & organs; right-sided: backward effects, caused by congestion in the systemic venous system; forward effects cause low output to left ventricle leading to low CO; treatment: Aimed at improving CO while minimizing congestive symptoms and cardiac workload, Obtained by manipulating preload, afterload, and contractility, Reduce preload—reduces intravascular volume with diuretics and ACE inhibitors, modify fluid and salt intake, Improve CO—digitalis, Inhibit SNS effects—β-blockers, Improve contractility—digitalis or other cardiac glycoside, β agonists (not for long-term use), Reduce effects of Ang II—ACE inhibitors and ARBs, Pacemakers: synchronize ventricular contraction Treatment of myocardial infarction- Aimed at improving CO while minimizing congestive symptoms and cardiac workload, Obtained by manipulating preload, afterload, and contractility, Reduce preload—reduces intravascular volume with diuretics and ACE inhibitors, modify fluid and salt intake, Improve CO—digitalis, Inhibit SNS effects—β-blockers, Improve contractility— digitalis or other cardiac glycoside, β agonists (not for long-term use), Reduce effects of Ang II— ACE inhibitors and ARBs, Pacemakers: synchronize ventricular contraction • Ch. 20 Shock Shock- imbalance between oxygen supply & oxygen requirements at the cellular level; common factor among all types is hypoperfusion and impaired cellular oxygen utilization (impaired tissue perfusion & inadequate cellular oxygenation) s/s: decreased cardiac output, increased HR, increased RR, cool, clammy skin, altered LOC/confusion, decreased capillary refill, decreased kidney perfusion, decreased urinary output; impaired tissue oxygenation leads to cellular dysfunction & cellular hypoxia; GOAL is to treat the underlying cause of the shock Cardiogenic shock- inadequate cardiac output despite sufficient vascular volume; usually the result of severe ventricular dysfunction associated with MI Obstructive shock- circulatory blockage, such as a large pulmonary embolus, cardiac tamponade, and tension pneumothorax; disrupts cardiac output; results from mechanical obstructions that prevent effective cardiac filling and stroke volume Hypovolemic shock- loss of blood volume as a result of hemorrhage or excessive loss of extracellular fluids; results from inadequate circulation blood volume precipitated by hemorrhage, burns, or leakage of fluid into interstitial spaces; most common cause: external hemorrhage Anaphylactic shock- result of excessive mast cell degranulation mediated by IgE antibodies in response to antigen Septic shock including usual cause- response from severe inflammatory response to infection; characterized by release of immune mediators resulting in widespread inflammation; common causes: gram-negative & gram-positive bacteria, fungal infections Reperfusion injury- ischemic cells may produce oxygen-free radicals when oxygen supplies are restored Ch. 21 Respiratory Function & Alterations in Gas Exchange Hypoventilation vs hyperventilation in relation to carbon dioxide- hypoventilation: air delivered to alveoli is insufficient to provide O2 and remove CO2 (increased amount of CO2 in the blood); hypoxemia; hyperventilation: increase of air entering the alveoli leads to hypocapnia (decreased amount of CO2 in the blood) Hypoxemia: deficient blood oxygen as measured by low arterial O2 and low hemoglobin saturation Hypoxia: a decrease in tissue oxygenation; treatment: increase O2 in the blood to correct hypoxia; i.e. blood transfusion, iron intake, etc. Acute respiratory failure: state of disturbed gas exchange; low PaO2 on room air; clinical manifestations: hypoxemia, hypercapnia, headache, dyspnea, confusion, decreased level of consciousness, agitation, dizziness, restlessness; GOAL is to provide adequate oxygenation (PaO2 needs to go up); pH will be corrected as well Causes of embolisms: (undissolved, detached material) types: blood clot, malignant neoplasms or tumors, fat emboli, amniotic fluid, air, foreign bodies, septic, parasites, collection of bacteria/infectious exudate; causes: venous stasis/sluggish blood flow, hypercoagulability, & damage to the venous wall (intimal injury) Initial symptoms of malignancies: Normal blood gas values: pH: 7.35-7.45, PaCO2: 35-45, HCO3: 22-26, PaO2: 80-11 • Ch. 22 Obstructive Pulmonary Disorders Asthma S/S- wheezing (lower respiratory tract), feeling of tightness in chest, dyspnea (SOB), cough (dry or productive) & increased sputum production, hyperinflated chest, & decreased breath sounds; severe attack s/s: use of accessory muscles of respiration, intercostal retractions, distant breath sounds with inspiratory wheezing, orthopnea, agitation, tachypnea, tachycardia Exercise induced asthma- bronchospasm (narrow) often occurs within 3 minutes after the end of exercise Bronchitis- both chronic or acute is inflammation of the upper airway; acute: acute inflammation of the trachea & bronchi; s/s: cough, low-grade fever, substernal chest discomfort, sore throat, postnasal drip, fatigue; treatment: no treatment for viral, antibiotic therapy for bacterial; chronic: chronic inflammation & swelling of the bronchial mucosa resulting in scarring; s/s: SOB dyspnea on exertion, excessive sputum, chronic cough; treatment: medications, low-dose O2 therapy; asthmatic bronchitis: swelling of bronchial mucosa in children associated with obstruction, respiratory distress, & wheezing s/s of COPD: Type A COPD- emphysema “pink puffer”- use of accessory muscles, pursed-lip breathing, cough (minimal or absent), digital clubbing, barrel chest; Type B COPD- chronic bronchitis “blue bloater”- s/s: listed above Both types of COPD (chronic bronchitis & emphysema) are manifested by SOB (dyspnea on exertion Ch. 23 Restrictive Pulmonary Disorders Acute respiratory distress syndrome (ARDS) findings- characteristics-injury to alveoli from a wide variety of disorders, changes in alveolar diameter, injury to pulmonary circulation, atelectasis & decrease in lung compliance from lack of surfactant, fibrosis (hyaline membrane), diffuse, fluffy alveolar infiltrates, disruptions in O2 transport & utilization (severs hypoxemia); Auscultation of lung fields- crackles & rhonchi are heard, accessory muscles used to breathe. Common findings in this type of injury include: (1) severe hypoxemia caused by intrapulmonary shunting of blood; (2) a decrease in lung compliance; (3) a decrease in FRC; (4) diffuse, fluffy alveolar infiltrates on the chest radiograph; and (5) noncardiogenic pulmonary edema. Tension pneumothorax- (accumulation of air in the pleural space) traumatic origin, results from penetrating or nonpenetrating injury, may also be from iatrogenic causes, medical emergency; pathogenesis- results from buildup of air under pressure in pleural space, air enters pleural space during inspiration but cannot escape during expiration, lung on ipsilateral (same) side collapses and forces mediastinum toward contralateral (opposite) side, & decreases venous return & cardiac output Risk factors for pneumonia- elderly, those with a diminished gag reflex, seriously ill, hospitalized patients, hypoxic patients, immune-compromised patients Mycobacterium tuberculosis transmission- acid-fast aerobic bacillus, infects lungs and lymph nodes (airborne precautions); inhalation of small droplets containing bacteria; droplets expelled through cough, sneeze, or talking Ch. 26 Renal Function Glomerulus- the site of fluid filtration from the blood to the nephron tubule. Formed by a capillary tuft; outer layer is called parietal layer, inner layer called podocytes; basement of membrane prevents plasma proteins, erythrocytes, leukocytes, and platelets from passing through. Ch. 27 Intrarenal Disorders Signs and symptoms of kidney cancer- abnormal urinalysis findings, costovertebral angle pain, anemia, malnutrition, bone & mineral disorders, fluid & electrolyte imbalances, hypertension & cardiovascular disease, metabolic acidosis, depression Glomerulonephritis- acute, chronic, & crescentic- immune response to a variety of potential triggers, produce inflammation in glomeruli which results in lysosomal degradation of the basement membrane & GFR may fall as a result of contraction of mesangial cells resulting in decreased surface area for filtration • Ch. 28: Acute Kidney Injury and Chronic Kidney Disease Phases of acute kidney injury: prodromal: normal or declining urine output; oliguric: oliguria and progressive uremia, decreased GFR, hypovolemia; postoliguric: termination of oliguric phase represents renal recovery, urine volume increases (diuresis), tubular function improves fluid volume deficit until kidneys recover Causes of prerenal, intrarenal, and post renal kidney injury- prerenal: renal perfusion; post renal: urine flow distal to the kidney; intrarenal/intrinsic: circumstances within the kidney blood vessels, tubules, glomeruli, or interstitium electrolytes affected by kidney disease- retained potassium, phosphorus, magnesium Purpose of dialysis: used for ATN & CKD in stage 5 in order to remove metabolic wastes and correct fluid & electrolyte abnormalities; development of uremia or hyperkalemia unresponsive to other treatments; types: hemodialysis, peritoneal dialysis, & continuous renal replacement therapy Assessing for kidney disease- sudden reduction in kidney function producing an accumulation of waste materials causing: Disruptions in fluid, electrolyte, and acid-base balances, Retention of nitrogenous waste products, Increased serum creatinine, & Decreased glomerular filtration rate (GFR) Causes of acute tubular necrosis: nephrotoxic insult (contrast media) & ischemic insults (sepsis) Ch. 29 Disorders of the Lower Urinary Tract Treatment of patients with neurogenic bladder: Lifestyle changes: weight loss, reducing caffeine intake, and avoiding constipation, Behavioral, pharmaceutical, and surgical options, Pelvic floor muscle training (for urge incontinence), Bladder training, Medication: anticholinergic agents (e.g., oxybutynin), vaginal or oral estrogen, and alpha-adrenergic blockers (e.g., prazosin) s/s of cystitis: frequency, urgency, dysuria, nocturia, suprapubic pain, and cloudy urine; older adults: delirium & new-onset incontinence; children: fever, irritability, poor feeding, vomiting, & diarrhea Ch. 31 Alterations in Male Genital and Reproductive Function Complications of cryptorchidism- hidden testes, completely descended, external to the canal or located in a position other than the scrotum; treatment: orchiopexy, human chorionic gonadotropin, increase incidence of malignancy and leads to infertility if untreated Ch. 36 Gastrointestinal Disorders Mallory-weiss syndrome- bleeding caused by a tear in mucosa or submucosa of the cardia or lower portion of esophagus; cause: forceful/prolonged vomiting; manifestations: vomiting of blood and passing of large amounts of blood rectally after an episode of forceful vomiting, epigastric or back pain; treatment: blood transfusion, control of active bleeding (vasopressin infusion, Gelfoam embolization), surgical intervention Causes of acute gastritis- (inflammation of the stomach lining); precipitated by ingestion of irritating substances such as: alcohol & aspirin, NSAIDs, viral, bacteria, autoimmune Peptic ulcer disease- disorders of the upper GI tract caused by action of acid and pepsin; injury to the mucosa of the esophagus, stomach, or duodenum; causes: NSAIDs, stress (glucocorticoids), smoking, genetics, H. pylori; treatment: Encourage healing of the injured mucosa by reducing gastric acidity, Prevent recurrence, H. pylori antibiotics, H2 antagonists, Proton pump inhibitors, Sucralfate (forms protective coating over injured mucosa), Smoking cessation, Avoidance of ASA and NSAIDs, Stress reduction, Avoid irritating foods that exacerbate symptoms; i.e., Caffeinated beverages & Alcohol Complications of Crohn’s disease and Ulcerative colitis Management of esophageal varices- (underlying condition should be reversed) performing fluid resuscitation, correcting the coagulopathy, and stopping further bleeding, drugs that can effectively lower portal pressure by dilating alternative collateral pathways, reducing splanchnic blood flow, or both, esophageal varices. S/S of bowel obstruction- fecal impaction, adhesions, hernia, tumors, volvulus, intussusception • Ch. 37 Alterations in Function of the Gallbladder and Exocrine Pancreas How does pancreatic cancer rate in mortality? Ranks 4th among death from all malignancies Endocrine vs exocrine functions of pancreas- which is more? Endocrine: secretes hormones into blood (insulin, glucagon, somatostatin); Exocrine: secretes >1 L of digestive juice into duodenum every 24 hours (exocrine is more) • Ch. 38 Liver Diseases Causes of ascites- inappropriate pressure gradient across the pleura, with the intraabdominal accumulation of sodium, water, and protein. Other causes include: malignancy, infection, pancreatitis, hypothyroidism, vasculitis, nephrosis, cardiac failure, constrictive pericarditis, Budd- Chiari syndrome, & portal vein thrombosis Hepatic encephalopathy causes- exact cause is unknown; Precipitated by conditions that increase protein metabolism (GI hemorrhage and increased protein consumption), and by conditions that further impair hepatocyte function • Ch. 40 Disorders of the Endocrine Function Cushing syndrome- the diagnosis reserved for pituitary-dependent conditions; term is used to describe the clinical features of hypercortisolism, regardless of cause; primary: disease of the adrenal cortex, secondary: hyperfunction of anterior pituitary ACTH-secreting cells, tertiary: hypothalamic dysfunction or injury; clinical manifestations: purple striae, ecchymoses, moon face and ruddy complexion, impaired wound healing and immune response, thin, fragile skin, fine hair, hypertension & hyperglycemia Ch. 41 Diabetes Mellitus s/s of type 1 diabetes- polyuria (increased urination), polydipsia (thirst), & polyphagia (hunger) Difference between type 1 and type 2 diabetes: Type 1: Makes NO insulin; insulin deficiency; Type 2: insulin resistance; more insulin is needed but less glucose is actually used • Ch. 44 Acute Disorders of the Brain Function Ischemia- inadequate blood flow through the arterial system, producing tissue hypoxia Hypoxia- a reduction in oxygen at the tissue level that may lead to failure of aerobic production of adenosine triphosphate; decrease in tissue oxygenation Traumatic brain injury- injuries of the brain tissues sustained as a consequence of trauma. It is characterized according to severity, location of injury, and mechanism of injury; Types: mild, moderate, and severe; Primary injury: concussion (mild traumatic brain injury MTBI), contusion, and intracranial hematoma Diagnosing a stroke- transient ischemic attack can be an early warning sign that a stroke is about to occur. Meningitis vs encephalitis etiology- meningitis: inflammation of meninges caused by streptococcus pneumoniae; encephalitis: inflammation or infection of brain tissue caused by West Nile Virus, Herpes Simplex virus, & Western equine encephalitis Causes of increased intracranial pressure- space-occupying lesions, vasogenic or cytotoxic edema, or with obstruction or excessive production of CSF; eye movements (CN III, IV, & VI) may be impaired; nystagmus, dysconjugate movement & ocular palsies may be present Reflexes related to brainstem function- pupil reflex (CN II & III) PEERLA • Ch. 45 Chronic Disorders of Neurologic Function Dementia- progressive deterioration and continuing decline of memory and other cognitive changes Cerebral palsy- diverse group of crippling syndromes that appear during childhood and involve permanent, nonprogressive damage to motor control areas of the brain which control voluntary & involuntary muscle movements; there is no cure Seizures- (transient neurologic event of paroxysmal abnormal or excessive cortical electrical discharges that occurs in the brain); causes: cerebral injury, lesions, metabolic/nutritional disorders, idiopathic; 2 most common diagnostic procedures for seizures: electroencephalograms & clinical symptoms Parkinson’s disease- dopamine deficiency in the basal ganglia associated with motor impairment; Lewy bodies; difficulty initiating and controlling movements results in akinesia, tremor, & rigidity; s/s: general lack of movement, loss of facial expression, drooling, propulsive (shuffling) gait, and absent arm swing; there is no cure Nerves affected with multiple sclerosis- CNS; optic and oculomotor nerves and spinal nerve tracts spinal cord injuries- mechanisms of injury: hyperflexion, hyperextension, & compression; secondary injury may result from hemorrhage, swelling, ischemia, inflammation treatment of spinal cord injuries- appropriate stabilization of spinal vertebrae, neurogenic shock, high-dose methylprednisolone, intensive rehabilitation Status epilepticus- a continuing series of seizures without a period of recovery between episodes that can be life threatening and lead to brain damage. Greatest occurrence is tonic- clonic seizures. • Ch. 51 Alterations in Musculoskeletal Function: Trauma, Infection, & Disease Osteoporosis- most common metabolic disease; occurs when rate of bone resorption is greater than bone formation; etiology: estrogen deficiencies, poor calcium intake, and disuse; treatment: calcium and Vitamin D supplements, exercise, bisphosphates, recombinant human parathyroid hormone Ch. 53 Alterations in the Integumentary System Pressure injuries- localized areas of cellular necrosis resulting from a prolonged pressure between any bony prominence and an external object such as a bed or wheelchair (4 stages)