NR 283 PATHOPHYSIOLOGY WORKSHEET 4 (Newest 2023/2024) Verified Content

NR 283 PATHOPHYSIOLOGY WORKSHEET 4 (Newest 2023/2024) Verified Content Worksheet 4 NR 283 PATHOPHYSIOLOGY WORKSHEET 4 (Newest 2023/2024) Verified Content 1. Define pathophysiology. - involves the study of functional or physiologic changes in the body that result from disease processes 2. Define homeostasis. - a relatively stable or constant environment in the body, including blood pressure, temperature, and pH, maintained by the various control mechanisms 3. Discuss the terms acute vs chronic. Provide examples. - Acute rejection develops after several weeks when unmatched antigens cause a reaction - Chronic or late rejection occurs after months or years, with gradual degeneration of the blood vessels. 4. Define hypokalemia. Discuss common effects of hypokalemia. - hypokalemia the serum level of potassium is less than 2 mmol per liter or 3.5 mEq per liter - Effects: Cardiac dysrhythmias  cardiac arrest. Hypokalemia interferes with neuromuscular function, and the muscles become less responsive to stimuli, as shown by fatigue and muscle weakness commencing in the legs. Paresthesias such as “pins and needles” develop. decreased appetite (anorexia) and nausea. In people with severe potassium deficits, the respiratory muscles become weak, leading to shallow respirations. In severe cases, renal function is impaired, leading to failure to concentrate the urine, and increased urine output (polyuria) results. 5. Define hyperkalemia. Discuss common effects of hyperkalemia. - hyperkalemia the serum level of potassium is greater than 2.6 mmol per liter or 5 mEq per liter - Effects: The ECG shows typical cardiac dysrhythmias, which may progress to cardiac arrest. Muscle weakness is common, progressing to paralysis as hyperkalemia advances and impairs neuromuscular activity. Fatigue, nausea, and paresthesias are also common. 6. Define hyponatremia. Discuss common effects of hyponatremia. - Hyponatremia refers to a serum sodium concentration below 3.8 to 5 mmol per liter or 135 - Effects: Low sodium levels impair nerve conduction and result in fluid imbalances in the compartments. Manifestations include fatigue, muscle cramps, and abdominal discomfort or cramps with nausea and vomiting. Decreased osmotic pressure in the extracellular compartment may cause a fluid shift into cells, resulting in hypovolemia and decreased blood pressure. The brain cells may swell, causing confusion, headache, weakness, or seizures. 7. Define hypernatremia. Discuss common effects of hypernatremia - Hypernatremia is an excessive sodium level in the blood and extracellular fluids (more than 145 mEq per liter) - Effects: The major effect of hypernatremia is a fluid shift out of the cells owing to the increased osmotic pressure of interstitial or extracellular fluid; this effect is manifested by: Weakness, agitation, firm subcutaneous tissues, increased thirst, with dry, rough mucous membranes, decreased urine output because ADH is secreted - Note that the manifestations can change depending on the cause of the problem: If the cause of hypernatremia is fluid loss caused by lack of ADH, urine output is high. 8. Define hypocalcemia. Discuss common effects of hypocalcemia. - In hypocalcemia, the serum calcium level is less than 2.2 mmol per liter or below 4 mEq per liter - Effects: Low serum calcium levels increase the permeability and excitability of nerve membranes, leading to spontaneous stimulation of skeletal muscle. This leads to muscle twitching, carpopedal spasm (atypical contraction of the fingers), and hyperactive. Chvostek's sign, spasm of the lip or face when the face is tapped in front of the ear, and Trousseau's sign, carpopedal spasm when a blood pressure cuff blocks circulation to the hand, both indicate low serum calcium and tetany, or skeletal muscle spasm. Severe calcium deficits may cause laryngospasm, which obstructs the airway. Paresthesias are common, as are abdominal cramps. Heart contractions become weak owing to insufficient calcium for muscle action, conduction is delayed, arrhythmias develop, and blood pressure drops. 9. Define hypercalcemia. Discuss common effects of hypercalcemia. - In hypercalcemia the serum calcium is greater than 5 mEq per liter or greater than 2.5 mmol per liter - Effects: High serum calcium levels depress neuromuscular activity, leading to muscle weakness, loss of muscle tone, lethargy, and stupor, often with personality changes, anorexia, and nausea. High calcium levels interfere with the function of ADH in the kidneys, resulting in less absorption of water and in polyuria. If hypercalcemia is severe, blood volume drops, renal function decreases, nitrogen wastes accumulate, and cardiac arrest may ensue. Cardiac contractions increase in strength, and dysrhythmias may develop. Effects on bone vary with the cause of hypercalcemia. If excess PTH is the cause, bone density will be decreased, and spontaneous (pathologic) fractures may occur, particularly in the weight-bearing areas, causing bone pain. If intake of calcium is high, PTH levels will be low, and more calcium will be stored in the bone, maintaining bone strength. 10. Define normal serum pH, normal CO2, and normal HCO3-. - Normal pH: 7.36-7.45 - Normal CO2: 95-100% 23-29 - Normal HCO3: 22-26 11. Define Trisomy 21. List five clinical manifestations of Trisomy 21. - Trisomy 21: the most common form of Down Syndrome, caused by an extra copy of chromosomes number 21 - Flattened face - Small head - Short neck - Protruding tongue - Upward slanting eye lids (palpebral fissures) - Unusually shaped or small ears - Poor muscle tone - Broad, short hands with a single crease in the palm - Relatively short fingers and small hands and feet - Excessive flexibility - Tiny white spots on the colored part (iris) of the eye called Brushfield's spots - Short height - Infants with Down syndrome may be average size, but typically they grow slowly and remain shorter than other children the same age. 12. Define amniocentesis. What is the purpose of this test? - Amniocentesis is a procedure in which amniotic fluid is removed from the uterus for testing or treatment. Amniotic fluid is the fluid that surrounds and protects a baby during pregnancy. This fluid contains fetal cells and various chemicals produced by the baby. Purpose: - Genetic testing: genetic amniocentesis involves taking a sample of amniotic fluid and testing it for certain conditions, such as Down syndrome. - Fetal lung testing: fetal lung maturity testing involves taking a sample of amniotic fluid and testing it to determine whether the baby's lungs are mature enough for birth. - Diagnosis of fetal infection: occasionally, amniocentesis is used to evaluate a baby for infection or other illness. The procedure also can be done to evaluate the severity of anemia in babies who have Rh sensitization: an uncommon condition in which a mother's immune system produces antibodies against a specific protein on the surface of the baby's blood cells. - Treatment: if you accumulate too much amniotic fluid during pregnancy, amniocentesis might be done to drain excess amniotic fluid from your uterus. 13. Discuss the inflammatory response. What is the purpose of the inflammatory response, what effects are seen due to the inflammatory response, why are these effects seen? - Inflammatory response: a response triggered by damage to living tissues. The inflammatory response is a defense mechanism that evolved in higher organisms to protect them from infection and injury. - Its purpose is to localize and eliminate the injurious agent and to remove damaged tissue components so that the body can begin to heal. The response consists of changes in blood flow, an increase in permeability of blood vessels, and the migration of fluid, proteins, and white blood cells (leukocytes) from the circulation to the site of tissue damage. An inflammatory response that lasts only a few days is called acute inflammation, while a response of longer duration is referred to as chronic inflammation. 14. Discuss Universal Precautions. - Universal precautions: provide the basic guidelines by which all blood, body fluids, and wastes are considered “infected” in any client regardless of the client's apparent condition. There are two levels, one general for all individuals, and one specific to known infections at specific sites in the body, for example, the intestines. Gloves and appropriate protective apparel are then used to reduce the transmission of organisms in either direction, that is, from patient to caregiver and from caregiver to patient. Guidelines have been established for the disposal of such potentially dangerous items as needles, tissue, and waste materials. The CDC can be consulted for appropriate and up-to-date information. - Ex: Contaminated food or water or carrier food handlers, window of time, infected travelers 15. Define leukocyte, thrombocyte, erythrocyte, pancytopenia, leukocytosis, leukopenia, thrombocytopenia, and polycythemia vera. - Leukocyte: Neutrophils: Phagocytosis of microorganisms Basophils: Release of histamine leading to inflammation Eosinophils: Numbers are increased in allergic responses - Thrombocyte: platelet - Erythrocyte: a red blood cell that (in humans) is typically a biconcave disc without a nucleus. Erythrocytes contain the pigment hemoglobin, which imparts the red color to blood, and transport oxygen and carbon dioxide to and from the tissues. - Pancytopenia: decrease in all blood cells, erythrocytes, leukocytes, and thrombocytes - Leukocytosis: increased numbers of white blood cells, especially neutrophils - Leukopenia: fewer leukocytes in the blood - Thrombocytopenia: abnormally low number of thrombocytes or platelets. - Polycythemia vera (primary): a condition in which there is an increased production of erythrocytes and other cells in the bone marrow. It is considered a neoplastic disorder. Serum erythropoietin levels are low. 16. Discuss Tinea (tinea capitis, tinea corporis, and tinea pedis). Include the pathophysiology, risk factors, clinical manifestations and treatment. - Tinea capitis: is an infection of the scalp that is common in school-aged children. The infection may result from Microsporum canis, transmitted by cats and dogs, or by Trichophyton tonsurans, transmitted by humans. It manifests as a circular bald patch as hair is broken off above the scalp. Erythema or scaling may be apparent. Oral antifungal agents such as griseofulvin are recommended. - Tinea corporis: is a fungal infection of the body, particularly the non hairy parts. The lesion is a round, erythematous ring of vesicles or papules with a clear center (ringworm) scattered over the body. Pruritus or a burning sensation may be present. Topical antifungal medications such as tolnaftate or ketoconazole are effective. - Tinea pedis: or athlete's foot, involves the feet, particularly the toes. Trichophyton mentagrophytes or Trichophyton rubrum are the usual causative organisms. This condition may be associated with swimming pools and gymnasia if appropriate precautions are not in place (e.g., wearing sandals, changing to clean, dry socks). The organisms may be normal flora that become opportunists or that spread easily from lesions under conditions of excessive warmth and moisture. The skin between the toes becomes inflamed and macerated, with painful and pruritic fissures. The feet may have a foul odor. Secondary bacterial infection is common, adding to the inflammation and necrosis. Topical tolnaftate is usually effective. 17. Discuss pediculosis. Include the pathophysiology, risk factors, clinical manifestations and treatment. - Pediculosis: (lice) can take three forms in humans. Pediculus humanus corporis is the body louse, Pediculus pubis is the pubic louse, and Pediculus humanus capitis is the head louse (cooties). Lice are small, brownish parasites that feed off human blood (humans are hosts only to human lice, not to animal lice) and cannot survive for long without the human host. - Female lice lay eggs on hair shafts, cementing the egg firmly to the hair close to the scalp. The egg, or nit, appears as a small, whitish shell attached to a hair. After hatching, the louse bites the human host, sucking blood for its survival. The site of each bite is demonstrated by a macule or papule, which is highly pruritic owing to the mite saliva. The excoriations that result from scratching and the visible nits provide evidence of infestation; the adult lice usually are not visible. - Treatment: Topical permethrin, malathion, or pyrethrin is used to treat lice, although resistance to these drugs is widespread. A fine-toothed comb can be used to remove empty nits from the hair. Clothing, linen, and the surrounding area need to be carefully cleaned to prevent reinfection. 18. Discuss benign vs malignant tumors. Provide 5 characteristics of benign tumors and 5 characteristics of malignant tumors. - Benign tumor: slow growing, capsulated, non-invasive, do not metastasize, well differentiated, “oma” - Malignant tumor: fast growing, non-capsulated, invasive and infiltrated, metastasize, poorly differentiated, “carcinoma or sarcoma” 19. Define the following: a. Rales: a bubbly or crackling sound in the lungs caused by air mixing with fluid in the airways b. Rhonchi: are continuous low pitched, rattling lung sounds that often resemble snoring. Obstruction or secretions in larger airways are frequent causes of rhonchi. They can be heard in patients with chronic obstructive pulmonary disease (COPD), bronchiectasis, pneumonia, chronic bronchitis, or cystic fibrosis. c. Stridor: an abnormal high-pitched, crowing sound caused by obstruction in the trachea or larynx d. Wheezing: musical high-pitched sounds caused by narrowed airways (asthma), can be inspiratory or expiratory, keep HOB elevated and patient in bed for safety e. Dyspnea: difficulty breathing f. Orthopnea: difficult or labored breathing when recumbent that is usually relieved by an upright position g. Paroxysmal nocturnal dyspnea: refers to attacks of severe shortness of breath and coughing that generally occur at night. It usually awakens the person from sleep, and may be quite frightening h. Hemoptysis: frothy sputum containing streaks of blood, usually bright red; spitting up blood i. Hypercapnia: increased level of carbon dioxide (CO2) in the blood j. Clubbing: sometimes toes result from chronic hypoxia associated with respiratory or cardiovascular diseases. Clubbing is a painless, firm, fibrotic enlargement at the end of the digit k. Eupnea: normal, regular, quiet breathing l. Apnea: lack of breathing m. Hypoxemia: insufficient oxygen in the arterial blood n. Cyanosis: as the bluish or purplish discoloration of the skin or mucous membranes due to the tissues near the skin surface having low oxygen saturation 20. Discuss cystic fibrosis. Include the pathophysiology, risk factors, clinical manifestations and treatment. - Cystic fibrosis: sometimes called mucoviscidosis, is a genetic disorder. Several mutations to the CFTR gene have been identified and relate to a protein involved in chloride ion transport in the cell membrane. This defect in the exocrine glands causes abnormally thick secretions, such as tenacious mucus. The primary effects of cystic fibrosis are seen in the lungs and the pancreas, where the sticky mucus obstructs the passages; other tissues are affected less frequently. Usually several areas in the body are affected in an individual. The severity of the effects varies among individuals. Risk factors: - Most common for Caucasians of northern European descent - CF gene Signs and symptoms: - Signs such as meconium ileus may appear at birth - Salty skin may be noticed by a mother when kissing a newborn with cystic fibrosis. This may lead to a sweat test and the diagnosis of cystic fibrosis. In some cases, the diagnosis may be delayed a few months or several years. - The signs of malabsorption may become apparent during the first year of life, with steatorrhea (bulky, fatty, foul stools), abdominal distention, and failure to gain weight. These signs indicate a lack of the pancreatic enzymes and bile needed to digest food and absorb nutrients. Fats and the fat-soluble vitamins (vitamins A, D, E, and K) are affected Treatment: - Replacement therapy for pancreatic enzymes - Intensive chest physiotherapy - Immediate aggressive treatment for infections 21. Discuss asthma. Include the pathophysiology, risk factors, clinical manifestations and treatment. - A lung disorder, asthma may result from an allergic response in the bronchial mucosa that interferes with airflow. Frequently a triad of atopic conditions including hay fever, eczema, and asthma occurs in family histories Risk factor: - Having a blood relative (such as a parent or sibling) with asthma - Having another allergic condition, such as atopic dermatitis or allergic rhinitis (hay fever) - Being overweight - Being a smoker - Exposure to secondhand smoke - Exposure to exhaust fumes or other types of pollution - Exposure to occupational triggers, such as chemicals used in farming, hairdressing and manufacturing Clinical manifestations: - Shortness of breath - Chest tightness or pain - Trouble sleeping caused by shortness of breath, coughing or wheezing - A whistling or wheezing sound when exhaling (wheezing is a common sign of asthma in children) - Coughing or wheezing attacks that are worsened by a respiratory virus, such as a cold or the flu Treatment: - Prevention and long-term control are key in stopping asthma attacks before they start. Treatment usually involves learning to recognize your triggers, taking steps to avoid them and tracking your breathing to make sure your daily asthma medications are keeping symptoms under control. In case of an asthma flare-up, you may need to use a quick-relief inhaler, such as albuterol 22. Discuss chronic obstructive pulmonary disease (COPD). Be specific about chronic bronchitis vs emphysema. Include the pathophysiology, risk factors, clinical manifestations and treatment. - COPD is a disease that affects the lungs, causing reduced airflow, which makes it hard to breathe. It is also progressive, which means it worsens over time. COPD can include emphysema, chronic bronchitis, or both. - In emphysema, the walls between many of the air sacs are damaged. As a result, the air sacs lose their shape and become floppy. This damage also can destroy the walls of the air sacs, leading to fewer and larger air sacs instead of many tiny ones. If this happens, the amount of gas exchange in the lungs is reduced - In chronic bronchitis, the lining of the airways stays constantly irritated and inflamed, and this causes the lining to swell. Lots of thick mucus forms in the airways, making it hard to breathe - Cigarette smoking is the most common cause of COPD, but there are also other potential causes, including long-term exposure to: Secondhand cigarette smoke, Air pollutants / chemical fumes in the home and workplace, Dust - In COPD, less air flows in and out of the airways because of one or more of the following: The airways and air sacs lose their elastic quality. The walls between many of the air sacs are destroyed. The walls of the airways become thick and inflamed. The airways make more mucus than usual and can become clogged Treatment: smoking cessation, medications (bronchodilators, inhaled steroids, combination inhalers, oral steroids, phosphodiesterase-4 inhibitors, theophylline, antibiotics, lung therapies) 23. Discuss pulmonary edema. Include the pathophysiology, risk factors, clinical manifestation. Pulmonary edema: Fluid collecting in alveoli and interstitial area - Can result from many primary conditions - Reduces amount of oxygen diffusing into blood - Interferes with lung expansion May develop when: - Inflammation in lungs is present (increases permeability of capillaries) - Plasma protein levels are low (decreases osmotic pressure of plasma) - Pulmonary hypertension develops. Signs and symptoms - Cough, orthopnea, rales—in mild cases - Hemoptysis - Frothy, blood-tinged sputum Treatment - Treat causative factors. - Supportive care - Possibility of positive-pressure mechanical ventilation 24. Discuss pulmonary embolus. Include the pathophysiology, risk factors, clinical manifestations. Pulmonary embolus: - Blood clot or mass that obstructs pulmonary artery or any of its branches - Effect of embolus depends on material, size, and location - Small pulmonary emboli might be “silent” unless they involve a large area of lung. - Large emboli may cause sudden death. - 90% of pulmonary emboli originate from deep vein thromboses in legs; are preventable Signs and symptoms - Transient chest pain, cough, dyspnea—small emboli - Larger emboli—increased chest pain with coughing or deep breathing; tachypnea and dyspnea develop suddenly (Later—hemoptysis and fever), (Hypoxia—causes anxiety, restlessness, pallor, tachycardia) - Massive emboli- (severe crushing chest pain, low blood pressure, rapid weak pulse, loss of consciousness) Prevention - Health teaching prior to surgery - Antiembolic stockings - Exercise to prevent thrombosis - Use of anticoagulant drugs Diagnosis - Radiography, lung scan, MRI, pulmonary angiography Treatment - Assessment of risk factors - Prolonged bed rest and compression stockings - Surgically Inserted filter into vena cava (some cases) - Heparin or streptokinase - Mechanical ventilation - Embolectomy 25. How is Vitamin K synthesized? What would a Vitamin K deficiency do to a person’s ability to clot? - Decreases the body’s ability to clot, causing bleeding 26. Blood loss is associated with which anemia? - Iron deficiency 27. Discuss iron deficiency anemia. Include pathophysiology and clinical manifestations. - iron deficiency anemia is a common type of anemia — a condition in which blood lacks adequate healthy red blood cells. Red blood cells carry oxygen to the body's tissues. As the name implies, iron deficiency anemia is due to insufficient iron. Without enough iron your body can't produce enough of a substance in red blood cells that enables them to carry oxygen (hemoglobin). As a result, iron deficiency anemia may leave you tired and short of breath. Signs and symptoms: - Extreme fatigue - Weakness - Pale skin - Chest pain, fast heartbeat or shortness of breath - Headache, dizziness or lightheadedness - Cold hands and feet - Inflammation or soreness of your tongue - Brittle nails - Unusual cravings for non-nutritive substances, such as ice, dirt or starch - Poor appetite, especially in infants and children with iron deficiency anemia 28. Discuss pernicious anemia. Include pathophysiology and clinical manifestations. - Patho: In pernicious anemia vitamin B12 is unavailable owing to a lack of intrinsic factor, a substance responsible for intestinal absorption of the vitamin. In a healthy person, intrinsic factor is produced by the parietal cells of the stomach, the cells that also secrete hydrochloric acid. Intrinsic factor forms a complex with dietary vitamin B12 in the stomach. The complex remains intact, preventing degradation of the vitamin by intestinal juices, until it reaches the ileum of the small intestine, where the vitamin is released and absorbed into the body. - Symptoms of pernicious anemia include fatigue, weakness, waxy pallor, shortness of breath, rapid heartbeat, unsteady gait, smooth tongue, gastrointestinal disturbances, and neurological problems. Weight loss, depressed mood, and memory loss are common in affected persons. Levels of the substances homocysteine and methylmalonic acid typically are high in persons with pernicious anemia, while gastric secretions lack hydrochloric acid (achlorhydria). The anemia may become severe before the disorder is diagnosed, since the vitamin deficiency develops very gradually. 29. Differentiate angina from myocardial infarction with regard to its cause and the characteristics of pain associated with it. - Angina: Intermittent chest pain or discomfort due to transient, reversible, myocardial ischemia; not quite infarction. Angina is chest pain that goes away during rest. - myocardial infarction is a heart attack cause by a blood clot 30. Discuss myocardial infarction. Include the pathophysiology, risk factors, clinical manifestations and treatment. Patho: A heart attack occurs when the flow of blood to the heart is blocked, most often by a build-up of fat, cholesterol and other substances, which form a plaque in the arteries that feed the heart (coronary arteries). The interrupted blood flow can damage or destroy part of the heart muscle. Risk factors: age (men age 45 or older, women age 55 and older) - Tobacco - High blood pressure - High blood cholesterol or triglyceride levels - Diabetes - Family history of heart attack - Lack of physical activity - Obesity - Stress - Illegal drug use - Preeclampsia - Autoimmune condition such as rheumatoid arthritis or lupus Signs and symptoms: - Pressure, tightness, pain, or a squeezing or aching sensation in your chest or arms that may spread to your neck, jaw or back - Nausea, indigestion, heartburn or abdominal pain - Shortness of breath - Cold sweat - Fatigue - Lightheadedness or sudden dizziness Treatment: - Restore blood flow quickly - Medications (aspirin, thrombolytics, antiplatelet agents, blood-thinning medications, pain relievers, nitroglycerin, beta blockers, ACE inhibitors) - Surgical (coronary angioplasty and stenting, coronary artery bypass surgery) 31. Which laboratory test is used to help diagnose a myocardial infarction? - EKG - simple, painless test that detects and records the heart's electrical activity. The test shows how fast the heart is beating and its rhythm (steady or irregular). An EKG also records the strength and timing of electrical signals as they pass through each part of the heart. - can show signs of heart damage due to coronary heart disease (CHD) and signs of a previous or current heart attack 32. Discuss Hepatitis A, Hepatitis B, and Hepatitis C. How are they transmitted? A: ingestion of fecal matter - Travelers - Sex contacts of infected persons - Household members or caregivers of infected persons - Men who have sex with men - Users of certain illegal drugs - Persons with clotting- factor disorders B: contact with infectious blood, semen, other body fluids - Infants born to infected mothers - Sex partners of infected persons - Persons with multiple sex partners - STDs - Men who have sex with men - Injection drug users - Household contacts of infected persons - Healthcare and public safety workers exposed to blood on the job - Hemodialysis patients - Travelers C: contact with blood of an infected person - Injection drug users - Recipients of clotting factor concentrates before 1987 - Blood transfusions before 1992 - Long term hemodialysis - Unknown exposers to HCV - HIV - Infants born to infected mothers 33. Discuss appendicitis. Include the pathophysiology, risk factors, clinical manifestations and treatment. - Appendicitis patho: The development of appendicitis usually follows a pattern that correlates with the clinical signs, although variations may occur because of the altered location of the appendix or underlying factors. o Obstruction of the appendiceal lumen by a fecalith, gallstone, or foreign material or from twisting or spasm is commonly an initiating factor. o Fluid builds up inside the appendix and microorganisms proliferate. o The appendiceal wall becomes inflamed and purulent exudate forms. The appendix is swollen. Blood vessels in the wall are compressed. o The increasing congestion and pressure within the appendix leads to ischemia and necrosis of the wall, resulting in increased permeability. o Bacteria and toxins escape through the wall into the surrounding area. This breakout of bacteria leads to abscess formation or localized bacterial peritonitis. o An abscess may develop when the adjacent omentum temporarily walls off the inflamed area by adhering to the appendiceal surface. In some cases, the inflammation and pain subside temporarily but then recur. o Localized infection or peritonitis develops around the appendix and may spread along the peritoneal membranes. o Increasing pressure inside the appendix causes increased necrosis and gangrene in the wall (infection in necrotic tissue). The wall of the appendix appears blackish. o If the appendix ruptures or perforates, it releases its contents into the peritoneal cavity. This leads to generalized peritonitis, which may be life threatening. Risk factors: age (10-30), infection, trauma to the appendix Signs and symptoms: - General periumbilical pain related to the inflammation and stretching of the appendiceal wall occurs initially. - Nausea and vomiting are common. - Pain becomes more severe and localized in the lower right quadrant (LRQ) of the abdomen - Lower right quadrant tenderness develops (classically at McBurney's point, midway between the umbilicus and the iliac crest). Localized pain results from involvement of the parietal peritoneum over the appendix. The location of the appendix does vary among individuals, and this can be diagnostically misleading. - If rupture occurs, the pain usually subsides temporarily as the pressure is relieved. - Pain recurs as a steady, severe abdominal pain as peritonitis develops. - Low-grade fever and leukocytosis occur as inflammation develops. - Signs indicating the onset of peritonitis include a rigid “board like” abdomen, tachycardia, and hypotension. Treatment: Surgical removal of the appendix and administration of antimicrobial drugs are the standard treatment 34. Discuss Crohn’s disease vs ulcerative colitis. Include the pathophysiology, risk factors, clinical manifestations and treatment. - Crohn's disease and ulcerative colitis are chronic inflammatory bowel diseases, the causes of which are unknown - A genetic factor appears to be involved because there is a high familial incidence and inflammatory bowel - Patho: Crohn's disease may affect any area of the digestive tract, but occurs most frequently in the small intestine, particularly the terminal ileum and sometimes the ascending colon. Inflammation occurs in a characteristic distribution called “skip lesions,” with affected segments clearly separated by areas of normal tissue. - Patho for Ulcerative Colitis: The mucosa and submucosa are inflamed, commencing at the base of the crypts of Lieberkühn (mucus-secreting goblet cells). The tissue becomes edematous and friable, and ulcerations develop. In an attempt to heal, granulation tissue forms, but it is vascular and fragile and bleeds easily. When the ulcers coalesce, large areas of the mucosa become denuded, but there are residual “bridges” of intact mucosa over the ulcers. This tissue destruction interferes with the absorption of fluid and electrolytes in the colon. Signs and symptoms for Crohn’s: Exacerbations are marked by diarrhea with cramping abdominal pain. The stool is typically soft or semi-formed. Melena may occur if the ulcers erode blood vessels. Pain and tenderness are often centered in the right lower quadrant. Anorexia, weight loss, anemia, and fatigue are associated with malabsorption and malnutrition. Children experience delayed growth and sexual maturation resulting from lack of adequate protein and vitamins, particularly fat-soluble vitamins A and D. Treatment with glucocorticoids also hampers growth. In addition, many psychological implications are characteristic of this type of chronic illness. Signs and symptoms for ulcerative colitis: Diarrhea is present, consisting of frequent watery stools marked by the presence of blood and mucus and accompanied by cramping pain. During severe exacerbations, blood and mucus alone may be passed frequently, day or night, accompanied by tenesmus (persistent spasms of the rectum associated with a need to defecate). Rectal bleeding may be considerable and contributes to severe iron deficiency anemia. Fever and weight loss may be present. - There are many similarities between Crohn's disease and ulcerative colitis, and there may be an overlap in their clinical presentation in some individuals. Both diseases occur in males and females. Crohn's disease often develops during adolescence, whereas ulcerative colitis more frequently appears in the second or third decade. These diseases are characterized by remissions and exacerbations as well as considerable diversity in the severity of clinical effects. Crohn’s: terminal ileum, sometimes colon. Transmural, all layers, skip lesions. Loose, semi formed, granuloma, fistula, fissure, abscess Ulcerative colitis: colon, rectum. Mucosa only and continuous diffuse. Frequent, watery, with blood and mucus. 35. Discuss GERD. Include the pathophysiology, risk factors, clinical manifestations and treatment. - Gastroesophageal reflux disease (GERD) is a chronic digestive disease. GERD occurs when stomach acid or, occasionally, stomach content, flows back into your food pipe (esophagus). The backwash (reflux) irritates the lining of your esophagus and causes GERD. GERD signs and symptoms include: - A burning sensation in your chest (heartburn), sometimes spreading to your throat, along with a sour taste in your mouth - Chest pain - Difficulty swallowing (dysphagia) - Dry cough - Hoarseness or sore throat - Regurgitation of food or sour liquid (acid reflux) - Sensation of a lump in your throat - Both acid reflux and heartburn are common digestive conditions that many people experience from time to time. When these signs and symptoms occur at least twice each week or interfere with your daily life, or when your doctor can see damage to your esophagus, you may be diagnosed with GERD. - Most people can manage the discomfort of GERD with lifestyle changes and over-the-counter medications. But some people with GERD may need stronger medications, or even surgery, to reduce symptoms. 36. Define frank blood, occult blood, and melena. - Frank blood: clear, watery damage. - Occult blood: Blood in the feces that is not visually apparent - Melena: Blood is the feces that is apparent. 37. Discuss cystitis vs pyelonephritis. Include the pathophysiology, risk factors, clinical manifestations and treatment. - Cystitis: inflammation of the urinary bladder. Risk factors include frequent bladder infections and it often presents as painful urination. Treatment includes antibiotic and anti-inflammatory drugs. - Pyelonephritis: inflammation of the substance of the kidney. Risk factors are also frequent bladder infections or a bladder infection that is untreated. Clinical manifestations are tenderness of the lower back and painful urination. Treatment includes antibacterial and anti-inflammatory drugs. 38. Discuss acute post-streptococcal glomerulonephritis. Include the pathophysiology, risk factors, clinical manifestations, diagnosis, and treatment. - This is a disease that presents after an infection of streptococcus bacteria. It is when blood cells are found in the urine and plasma proteins as well. Symptoms are pink or cola-colored urine, foamy urine, and hypertension. Diagnosis is an APSGN test. Treatment includes antibacterial drugs. 39. Discuss nephrotic syndrome. Include the pathophysiology, risk factors, clinical manifestations and treatment. - A disease that commonly affects children age 2-6. There is an abnormality in the glomerular capillaries and increased permeability that allows large amounts of plasma protein, primarily albumin, to escape into the filtrate. This results in marked hypoalbuminemia with decreased plasma osmotic pressure and subsequent generalized edema. - Risk factors are simply being a younger child. Clinical manifestations include Urinalysis indicates marked proteinuria, lipiduria and casts (fatty, epithelial, and hyaline). Cells may be present with certain primary diseases. Urine is often frothy. The most notable signs are swelling and weight gain with pallor. - Treatment includes glucocorticoids such as prednisone are prescribed to reduce the inflammation in the kidney. Angiotensin-converting enzyme inhibitor drugs, such as ramipril, may decrease protein loss in the urine. Antihypertensive and antilipemic therapy may be required in some individuals 40. Discuss Wilm’s tumor. Include the pathophysiology, risk factors, clinical manifestations and treatment. - Wilm’s tumor is an abdominal tumor that often develops in younger children. It grows slowly and often goes unnoticed because it does not cause any pain. - Treatment is surgery and radiation. 41. Discuss the negative feedback loop. - A reaction that causes a decrease in function. It occurs in response to stimulus. Often it causes the output of a system to be lessened 42. Discuss type 1 dm, type 2 dm, and gestational diabetes. Include the pathophysiology, risk factors, clinical manifestations and treatment. - Type 1: Happens when a person’s body does not make insulin and causes the blood sugar of the body to become very high. Risk factors are genetics. This disease often causes the affected to urinate frequently, lose weight, lose their appetite, and become very thirsty. There is no cure, but the disease is manageable with insulin shots. - Type 2: Happens when the body does not create enough insulin to regulate blood sugar. Often caused by obesity. Shows as a constant thirst, frequent urination, and sometimes weight gain. Can be treated with insulin shots, sometimes subsides after weight loss. Gestational: happens during pregnancy when the body is trying to regulate blood sugar to both the mother and baby. Can be treated with some drugs, exercise, and weight loss. 43. Discuss signs and symptoms of hyperglycemia and hypoglycemia. - Hyperglycemia: Dehydration, loss of consciousness. - Hypoglycemia: Seizures, loss of conciousness 44. Discuss Syndrome of Inappropriate Antidiuretic hormone vs Diabetes Insipidus. Include the pathophysiology, who’s at risk, and clinical manifestations. - Inappropriate ADH: Causes a retention of fluid. This is sometimes caused by certain thyroid disorders. - Diabetes insipidus: Not enough ADH. May be genetic or caused by electrolyte imbalance or drugs 45. Discuss hypoparathyroidism vs hyperparathyroidism. Describe the pathophysiology and clinical manifestations. - Hypoparathyroidism is a congenital lack of the four parathyroid glands, following surgery or radiation in the neck region, or because of an autoimmune disease. It leads to hypocalcemia, or low serum calcium levels. - Hyperparathyroidism may be caused by an adenoma, hyperplasia, or secondary to renal failure. It causes hypercalcemia, or high serum calcium levels. 46. Discuss acromegaly, gigantism, and dwarfism. Include the pathophysiology, who’s at risk, and clinical manifestations. - Acromegaly: An excess of growth hormone in adults. Causes the bones to become denser and to become harder to move. - Gigantism: This is caused by an excess of growth hormone secreted by the thyroid gland. People at risk are those with thyroid disorders and it is presented by someone who has grown in excess. - Dwarfism: This is a genetic disorder where the person does not grow to an expected height. It is a dominant trait. 47. Discuss hyperthyroidism vs hypothyroidism. Include the pathophysiology, risk factors, clinical manifestations and treatment. - Hyperthyroidism: When the thyroid is overworking itself. This causes the patient to lose weight quickly and to have bigger appetite. Risk factors are genetics or injury to the thyroid gland or any thyroid defect. Treatment are thyroid suppressing drugs. - Hypothyroidism: When the thyroid is not working enough. Risk factors are commonly pre-existing diseases that damage the thyroid. This creates a slow metabolism and causes weight gain. It is easily treatable with doses of the thyroid hormone. 48. Discuss osteoporosis. Include the pathophysiology, risk factors, clinical manifestations and treatment. - This is a common metabolic bone disorder characterized by a decrease in bone mass and density, combined with loss of bone matrix and mineralization. - Risk factors are genetics, old age, women are at higher risk, and a vitamin D deficit. Often, signs include new fractures and pain in the joints. - Treatment is to include more vitamin D in the diet. 49. Discuss osteoarthritis. Include the pathophysiology, risk factors, clinical manifestations and treatment. - This is a degenerative joint disease that causes pain and discomfort in the joints. Cartilage begins to break down, then it becomes rough and worn. Eventually, after more breakdown, there is no cartilage left in the joints and it is only bone rubbing together. - Risk factors include obesity and aging. It begins with pain on weight bearing joints and movement. - Treatment is to try and relieve any unnecessary stress on the joints. 50. Discuss rheumatoid arthritis. Include the pathophysiology, risk factors, clinical manifestations and treatment. - RA is an autoimmune disorder that causes systemic inflammation throughout the body. Remissions and exacerbations lead to progressive damage to the joints. - Risk factors include genetics, and a predisposition to many viral infections. At first, RA is insidious, and turns into aching and stiffness. - Treatment includes a mix between resting the joints and pain control. 51. Discuss Duchenne’s muscular dystrophy. Include the pathophysiology, risk factors, clinical manifestations and treatment. - MD is a group of inherited disorders characterized by degeneration of skeletal muscle. A metabolic defect, a deficit of dystrophin leads to degeneration and necrosis of the cell. - Early signs appear at around 3 years of age, when motor weakness and regression become apparent in the child. Initial weakness in the pelvic girdle causes a waddling gait and difficulty with climbing stairs or attaining an upright position. - There are currently no treatments for MD. 52. Discuss a sprain vs a strain. - A sprain is an overstretching or tearing of ligaments. – - A strain is stretching or tearing of muscle. 53. Discuss bursitis. Include the pathophysiology, risk factors, clinical manifestations and treatment. - an inflammation of the bursae associated with bones, muscles, tendons, and ligaments of various joints. - The most common causes of this inflammation are repetitive motions or positions that physically irritate the bursae at a specific joint. Bursitis is primarily diagnosed by physical examination in which the joint appears swollen, red, achy, or stiff and pain with joint motion. - The first step in treatment involves rest, application of cold compresses, and pain relievers. 54. Discuss vegetative state. - This is when a person is in a comatose state and has no brain activity. They also require assistive devices to breath for them and circulate blood. 55. Discuss the criteria for brain death. - lack of responses to stimuli, EEG changes, and decreased perfusion in the brain 56. Define aphasia and dysarthria. - Aphasia: loss of the ability to communicate, speak coherently, or understand speech. - Dysarthria: a condition in which the muscles you use for speech are weak or you have difficulty controlling them 57. Discuss increased intracranial pressure. Include the pathophysiology, risk factors, clinical manifestations and treatment. - Pressure of the brain stem or cerebral cortex. - Signs include decreased level of consciousness, vomiting, and headache. - Treatment includes anti-inflammatory drugs. 58. Discuss papilledema. What causes this? - A condition in which increased pressure in or around the brain causes the part of the optic nerve inside the eye to swell 59. Discuss Transient Ischemia Attacks. Include the pathophysiology, risk factors, clinical manifestations and treatment. - A transient ischemic attack (TIA) results from a temporary localized reduction of blood flow in the brain. - A TIA may be caused by partial occlusion of an artery, caused by atherosclerosis, or from a small embolus, a vascular spasm, or local loss of autoregulation. Intermittent short episodes of impaired function, such as muscle weakness in an arm or leg, visual disturbances, or numbness and paresthesia in the face, may occur. Risk factors are hypertension, obesity, and high cholesterol. - Treatment is to find the cause to prevent further or permanent brain damage. 60. Discuss types of CVAs. Include the pathophysiology, risk factors, clinical manifestations and treatment. - Infarction of the brain tissue due to lack of blood. This sometimes causes necrosis of the tissues. - Risk factors include unhealthy diet and plaque buildup in the arteries. Signs of strokes are loss of function on one side of the body, inability to speak, and confusion. - Treatment is often surgery, but the best way to treat a stroke is to catch it before it is able to happen. 61. Discuss partial vs generalized seizures. Include the pathophysiology, risk factors, clinical manifestations and treatment. - Partial seizures only effect on hemisphere of the brain, while generalized seizures affect both. Partial seizures, depending on which hemisphere they are on, may present differently. Risk factors include brain injuries, diseases that affect the brain. - Clinical manifestations are involuntary movements or abnormal sensations. Some stimulating drugs may help prevent some seizures. 62. Discuss Parkinson’s disease. Include the pathophysiology, risk factors, and clinical manifestation. - Disease of the central nervous system. Risk factors include genetics and immunological factors. Degeneration of the CNS causes tremors. 63. Discuss Multiple Sclerosis. Include the pathophysiology, risk factors, clinical manifestations and treatment. - A progressive demyelination of the brain, spinal cord, and neurons. This is most commonly seen in people age 20-40 and women, it is also believed to have genetic, immunologic, and environmental factors. Blurred vision is often an early sign of MS. Later on, it becomes harder to breath, articulate, and see. There is no treatment at this time, though some drugs seem to decrease the frequency of exacerbations. 64. Discuss cerebral palsy. Include the pathophysiology, risk factors, and clinical manifestations. - A group of disorders marked by some degree of motor impairment, caused by genetic mutations, abnormal fetal formation of functional brain areas, infection, or brain damage in the perinatal period. Risk factors include hypoxia or ischemia is the major cause of brain damage; it may occur prenatally, perinatally, or postnatally. Sometimes the signs are evident at birth, but often it is not until several months after birth that the symptoms are seen. Symptoms include intellectual impairment, slow motor skills, seizures, and visual problems 65. Discuss Reye’s syndrome. Include the pathophysiology, risk factors, and clinical manifestations. - Diseases that affects children given aspirin with a viral infection. The major pathological changes occur in the brain and liver. The brain function is severely impaired, while the liver enlarges and becomes fatty leading to acute failure. Initial signs and symptoms are lethargy, headache and vomiting, but can progress to disorientation, hyperventilation, stupor, and coma.