NUR 2063 Pathophysiology Rasmussen College Final Exam

1. Explain primary prevention - Preventing"; altering susceptibility or reducing exposure of disease for people 2. Explain secondary prevention - "Screening"; early detection, screening, and management of disease to catch disease early before it spreads 3. Explain tertiary prevention - "Treating" and preventing further complications from a disorder or disease after the person has the condition 4. What are examples of primary prevention? - Vaccinations and Handwashing 5. What are examples of secondary prevention? - PAP smears for STDs, lab work for HBA1C check, mammogram 6. What are examples of tertiary prevention? - Rehab for hip surgery, relearning ADL's after amputation, Wound care after stroke to prevent pressure ulcer 7. What happens to the body during the sympathetic phase of the flight or fight response? - Pupils dilate, salivation inhibited, increase in HR, bronchodilation of airway, increased respirations, glucose release, inhibit GI/GU. 8. What happens to the body during the parasympathetic phase of the flight or light response? - Rest and Digest. Pupils constrict, salivation occurs, decreased HR, bronchoconstriction, decreased respiration, GI/GU systems resume action 9. Explain the role of the nucleus - control center of the cell, where DNA and genes are stored, produces mRNA to help build body proteins 10. Explain the role of the mitochondria - Powerhouse of the cell. Provides energy in ATP, and has its own set of DNA 11. Explain the role of the ribosome - produces RNA to produce proteins through transcriptions of DNA and translation of RNA into a protein 12. Explain the role of the lysosomes - helps breakdown and digest dead cells, organelles, or tissues 13. Explain the role of the rough ER - folded membranes that move proteins around the cell. Has ribosomes attached to it and helps produce proteins for the cell membrane 14. Explain the role of the smooth ER - helps the Liver and kidney cells to detoxify, lipid metabolism, synthesis of hormones, and calcium storage 15. Explain the role of the peroxisome - membrane cells that contain oxidase and catalase to detoxify harmful chemicals, breakdown hydrogen peroxide and filter metabolic wastes 16. Explain the role of the Golgi body - stacked membranes that act as the sorter and packager for proteins from the ER. Helps move things in and out of cell 17. Explain passive immunity - the transfer of preformed antibodies against specific antigens from a protected or immunized individual to an unprotected or non-immunized person. Provides immediate and short-term protection. No memory cells are produced. IgA and IgE. Passes protection 18. What are examples of passive immunity? - mom to fetus through placenta or mom to infant through breast milk. Serotherapy 19. Explain active immunity - a protective state owing to the immune system response as a result of active infection or immunization. It has to be activated in the body and the body has to fight it to have long term immunity 20. What are examples of active immunity? - Vaccinations 21. Explain what edema is - accumulation of fluid in the interstitial space. Leads to tissue swelling 22. What are some causes of edema? - increase in the forces that move fluid from capillaries to interstitial compartments or decrease in the opposite. 23. What are factors that contribute to edema? - Increase in hydrostatic forces in the capillaries that increases the blood volume, increased capillary permeability, CHF, HYPTN, decrease in plasma proteins like albumin (causes liver to hold onto more water- ascites, cirrhosis), blockage of lymph drainage 24. What is a hypersensitivity? - an overreaction to antigens or allergens that is beyond the normal range, leading to damage 25. What is a type 1 hypersensitivity? - anaphylactic. Occurs within 2-30mins of exposure. Can be systemic or localized. Binds to IgE and mast cells that release histamine, leukotrienes, and prostaglandins to create inflammation 26. Mediating Factor for type 1 hypersensitivity - IgE 27. Examples of type 1 hypersensitivity - allergic reaction to dust. someone eats peanuts and breaks out in hives and runny nose 28. How do we treat type 1 hypersensitivity reactions? - antihistamines to block histamine, beta adrenergics to bronchodilator , corticosteroids, to decrease inflammation. IgE therapy, epinephrine given during anaphylaxis through IV or through IM in epipens 29. What are signs and symptoms of a type 1 hypersensitivity reaction? - hives, runny nose, eczema, throat constriction, ,localized edema, wheezing, tachycardia, anaphylaxis. 30. Explain Type 2 Hypersensitivity - The cells attack healthy organs and blood, causing symptoms 31. Mediating factor for type 2 hypersensitivity - cytotoxic- IgM/ IgG 32. Examples of type 2 hypersensitivity - Blood transfusions when wrong blood given, hemolytic disease of newborn, grans disease, myasthenia gravis 33. What is type 3 hypersensitivity? - The igG antibodies are stuck beneath the membranes of cells. Can activate immune responses that can damage tissues. Immune complex 34. Mediating factor type 3 hypersensitivity - immune complexes 35. Examples type 3 hypersensitivity - RA, lupus 36. What is type 4 hypersensitivity? - there is a delayed cell reaction caused by the T cells. Antigens are phagocytized and are sensitized to receptors on the t cell. Reexposure causes the memory cells to release destructive cytokines. 37. Mediating factor type 4 hypersensitivity - delayed cell mediated 38. Examples type 4 hypersensitivity - TB test, contact dermatitis 39. Characteristics of benign tumors - Localized growth that is curable. They more closely resemble the original tissue type, they grow slowly, have little vascularity, rarely necrotic, and usually have similar function to the original cells. Can be fatal depending on the location (brain, heart,etc), usually grows at the original areas of the body. Encapsulated 40. Characteristics of malignant tumors - usually cancerous. They ignore growth controlling signals and replicate despite signals from the environment. They can escape signals and can die. they can also display different functions poorly or not at all related to the tissue. Greater degree of differentiation means that it is more aggressive. Can move around with a poor prognosis. Anaplasia, metastasis 41. S/S of peptic ulcer disease - epigastric burning pain that is usually relieved by food or antacids (gastric ulcers present on empty stomach but can be after food, duodenal ulcers present 2-3 hours after food and is relieved by food). Can also be life threatening as GI bleeding can occur without warning and cause a drop in H/H and dark tarry stools and hematemesis 42. What is H.pylori? - has a key role in promoting both gastric and duodenal ulcer formation and thrives in acidic areas. It slows down ulcer healing and can reoccur frequently, and taking it away can help ulcers heal 43. What is a functional bowel obstruction? - problem with the act of the bowel actually moving, such as things that inhibit movement from surgery, medications, opioids, low fiber diets that can slow motility or shut off the GI system from the SNS stimulation 44. What is a mechanical bowel obstruction? - blockage of the bowel inhibiting movement. adhesions, hernia, tumors, impacted feces, volvus or twisting of the intestines, intussusception 45. adhesions - bands of scar tissue joining two surfaces that are normally separated in the bowel 46. hernia - Protrusion of bowel through the wall of the cavity that normally contains it 47. volvus - twisting of the bowel 48. Intusseption - telescoping of the intestines 49. S/S of appendicitis - Periumbilical pain, RLQ pain, presence of a positive McBurneys point and rebound tenderness when one presses on the belly button and hip region and when the pressure is removed, the client has pain, nausea, vomiting, fever, diarrhea, RLQ tenderness, systemic signs of infection. 50. how to assess appendicitis - McBurney's point technique when pressing on the belly button and RLQ hip region and removing the pressure causes intense pain, indicates positive appendicitis. Rebound tenderness= positive 51. rebound tenderness - pain that increases when pressure (as from a hand) is removed-in appendicitis 52. S/S of liver disease - hepatocellular failure (jaundice, decreased clotting, hypoalbuminemia, decreased vitamin D and K) and portal hypertension (GI congestion due to blockage of blood, more esophageal or gastric varies, hemorrhoids, enlarged spleen,) 53. what is jaundice? - green yellow staining of tissues from increased level of bilirubin as the liver cannot metabolize extra bilirubin. Found on eyes, skin, and mouth. present with liver disease 54. What is ascites? - pathological accumulation of fluid in the peritoneal cavity due to the loss of albumin in the liver, causing fluid to be free amongst the cells. It can cause a lot of pain in the abdomen, and it must be drained with a parenthesis 55. What is hepatic encephalopathy? - neuropsychiatric syndrome from too much ammonia in the blood as the liver cannot break it down. Dementia=ammonia and psychotic symptoms common along with jerking 56. What is portal hypertension? - Increased pressure in the portal venous system from a build-up of portal vein pressure due to progressive hepatic fibrosis which increases hepatic resistance 57. What is esophageal varices? - a complication of portal hypertension resulting from alcoholism or hepatitis. Causes the vessels in the esophagus to become dilated and bleed, and the rupturing can be forceful enough for one to bleed out 58. How do we treat esophageal varices? - reduce the hypertension, banding the varices to prevent rupturing and bleeding by cutting of the flow with a band 59. What role does albumin play in the blood? - Albumin helps keep fluid in the blood stream and in cells so it does not leak into other tissues. It can also carry other substances in the body 60. What happens to albumin during liver failure? - leads to low albumin levels, causing edema in the extremities and buildup of fluid in abdomen called ascites from fluid leaking through the cells and vessels into the tissues 61. Three functions of the kidneys - elimination, excretion, regulation 62. Explain elimination - discharge of waste (urine) from the body 63. Explain Excretion - removal of organic wastes from the blood 64. Explain regulation - regulating blood volume, ion concentration, blood pH and nutrients 65. Manifestations of renal disorders - Pain: usually in the back-flank area, felt at the CVA angle when one palpates with a closed fist and it causes the client tenderness. Pain upon micturition 66. What are abnormal urinalysis findings? - dark, strong smelling urine could denote decreased renal function, infection or dehydration, cloudy urine could denote infection or high WBC count. Ketones or glucose suggest diabetes, and proteinuria 67. Normal GFR - 125 mL/min 68. Normal urine output per hour - 30 mL/hr 69. What is polycystic kidney disease? - a congenital abnormality of the kidney that is genetically transmitted, and it results in fluid filled cysts on one or both kidneys that can lead to renal failure, needing dialysis, or kidney transplantation 70. What causes polycystic kidney disease? - genetics 71. Explain nephron - in the kidney and helps to filter blood and remove waste products. The kidney has 1-2 million of them 72. Explain hematuria - blood found in the urine not due to menstruation 73. Explain proteinuria - protein found in the urine 74. What is nephrolithiasis? - kidney stones that obstruct the ureters and kidneys. Usually made of calcium and can cause urinary stasis and pain 75. What is pyleonephritis? - infected and inflamed kidney, usually caused by from the lower urinary tract that ascends 76. Explain how to assess for pyelonephritis - Percussion at the CVA noting tenderness, pain when urinating, low GFR, concentrated urine with things in urine 77. s/s of pyelonephritis - CVA tenderness most common, fever, chills, N/V, anorexia or not willing to eat, flank pain 78. What is cystitis? - inflammation of the bladder (UTI) 79. How to prevent pyelonephritis - remove catheters as early as possible to prevent infection as it can spread 80. s/s of acute kidney injury (AKI) - low urine output, concentrated urine, low GFR, high BUN/CRE, sudden reduction in kidney function 81. 3 Causes of AKI - Prerenal, intrarenal, postrenal 82. explain pre renal causes of AKI - disruption in renal perfusion and blood flow. It can cause low blood pressure, low blood volume, heart failure, renal artery obstruction, fever, vomiting, diarrhea, burns that lead to dehydration, Drugs such as ACE inhibitors or angiotensin 2 blockers, NSAIDs that can drop the blood pressure or cause bleeding 83. Explain intrarenal causes of AKI - damage or disruptions within the kidney blood vessels, tubules, or glomeruli. It can cause reduced blood supply within the kidneys, toxic injury with medications, chemo, and contrast medias, renal inflammation, or prolonged prostate/ stones/ in the post renal stage 84. Explain postrenal causes of AKI - caused by an obstruction in the urinary collecting system, urethra, bladder, or ureters due to stone, tumor, or enlarged prostate that results in elevated pressure in the Bowman's capsule that impedes glomerular filtration. Prolonged injury can lead to intrinsic injury and irreversible damage 85. Examples of prerenal causes of AKI - low BP, hypovolemia, heart failure, renal artery occlusion, fever, vomiting, diarrhea, burns leading to dehydration, NSAIDs, and antihypertensives that drop the BP 86. Examples of intrarenal causes of AKI - chemo, contrast dye, prolonged kidney stones in the post renal stage 87. Examples of postrenal causes of AKI - renal stones, enlarged prostate, tumor in the urethra 88. What is compartment syndrome? - Damage to nerves and vasculature of an extremity due to compression. if untreated it can cause edema, increased pressure, reduced capillary flow, ischemia and necrosis 89. What must be done in compartment syndrome? - fasciotomy to reduce pressure in the area 90. What are the 5 P's for compartment syndrome? - Pain paralysis paresthesia pallor pulselessness 91. What are pressure ulcers? - localized area of cellular necrosis resulting from pressure between any boney prominence and with an external object 92. Which populations are most likely to have a pressure ulcer? - elderly, bedridden patients, incontinent patients, those who are malnourished, bad hygiene, those with paralysis 93. Risk factors for pressure ulcers - poor nutrition, aging, immobility, sensory loss, bowel and bladder incontinence 94. Most common places to find pressure ulcers - buttocks, coccyx, heels, elbows, back of head, shoulders 95. stage 1 pressure ulcer - Intact skin with non blanching redness 96. stage 2 pressure ulcer - partial thickness skin loss involving the epidermis or dermis or both 97. stage 3 pressure ulcer - full thickness tissue loss with visible fat 98. stage 4 pressure ulcer - full thickness tissue loss with exposed bone, muscle or tendon 99. How can we prevent pressure ulcers - turning patients every 2 hours who are bedridden. Appropriate nutrition and hydration. float heels off bed, clean linens, doing incontinence care, movement of patients 100. What are electrolyte reservoirs? - where electrolytes are found at an abundance, usually in the bones 101. Which electrolytes are stored in the bones? - calcium, phosphate, magnesium 102. What is osteomyelitis? - severe pyogenic infection of bone and local tissues. the organism reaches the blood adjacent to soft tissue or directly into it. if not managed, necrotic bone can separate the bone into dead segments 103. Causes of osteomyelitis - burns, sinus disease, trauma, tumors, periodontal infection and pressure ulcers, open fractures, penetration of wounds, surgical contamination or use of metal screws 104. What is osteoporosis? - occurs when the rate of bone resorption is greater than bone formation. The bones end up becoming fragile and light 105. Who is most likely to get osteoporosis? - women age 60-80 that are caucasian 106. What are the causes of osteoporosis? - estrogen deficiency, poor calcium intake and disuse of supplements 107. S/S of osteoporosis - short stature, muscle wasting, back spasms and difficulty bending. bones will be porous and have holes in them, more fragile 108. How do we diagnoses osteoporosis? - bone mineral density scan with levels being -1.0 to -2.5 109. How do we treat osteoporosis? - calcium and vitamin D supplements, exercise, human parathyroid hormone, supplemental estrogen 110. What is rickets? - defective mineralization of both bone and growth plate cartilage in children 111. What causes rickets? - Vitamin D deficiency 112. Which population is affected by rickets? - children 113. S/S of Rickets - bowleg, knock kneed, beading of ribs, improper formation of teeth, long ends of the bones, pelvis deformities 114. What is osteomalacia? - a rare condition of the adult bone associated with vitamin D deficiency, resulting in decalcification and softening of bone. 115. Which population is affected with osteomalacia? - adults 116. What causes osteomalacia? - Low vitamin D in adults 117. What is osteoarthritis? - local degenerative disorder associated with aging and wear and tear from repetitive stress. Characterized by loss of articular