Exam 2 Study Guide PDF

What is the definition on inflammation? - The reaction of vascularized tissues to cell injury or death. Characterized by the production of inflammatory mediators and the movement of fluid and leukocytes from the vascular into the extravascular tissue 2. What is the purpose of inflam...

What is the definition on inflammation? - The reaction of vascularized tissues to cell injury or death. Characterized by the production of inflammatory mediators and the movement of fluid and leukocytes from the vascular into the extravascular tissue 2. What is the purpose of inflammation? - Minimize or alleviate the effects of the injury, remove the damaged tissue, promote the growth of new tissue 3. What can cause inflammation? - Trauma, surgery, infection, hypoxia, ischemia 4. Who are the first cells on the scene in acute inflammation? - Neutrophils 5. What is acute inflammation? - Self-limited and has a short duration, acute inflammation give your neutrophils and exudate 6. What is chronic inflamation? - Self-perpetuating and may last weeks, months, years, chronic inflammation is an infiltration by mononuclear cells and lymphocytes and you get fibroblasts 7. What is the vascular phase of acute inflammation? - Also known as hemodynamic and is changes in the small blood vessels at the site of injury 8. What is vasodilation? - An increase in capillary pressure, causes an outflow of fluid and it accumulates in the tissue spaces causing swelling, pain and function issues 9. Purpose of vasoconstriction? - Minimize blood loss, help maintain healthy blood flow, blood pressure drop 10. Name the vascular changes that may occur with inflammation. - Immediate transient response: occurs with minor injury - Immediate sustained response: occurs with more serious injury and continues for several days, damages the vessels in the area - Delayed hemodynamic response: Involves an increase in capillary permeability that occurs 4 to 24 hours after injury (sunburn) 11. What is the cellular phase? - Activates inflammation, when white blood cell show up 12. What are the two types of leukocytes in the acute inflammatory response? - Granulocytes( neutrophils, basophils and eosinophils) - Monocytes ( that largest of the white blood cells) 13. What are the Phagocytosis 5 steps - Chemotaxis, adherence plus opsonization, ingestion-receptor activation, digestion- attachment to lysosome, intracellular killing 14. Cardinal signs - Rubor( redness), Tumor (swelling), calor( heat), dolor(pain), functio laesa( loss of function) 15. Systemic signs - Fever, malaise( not feeling well) 16. What is the purpose of inflammatory mediators? - Cause inflammation by increasing body response to the spot of pain 17. What is chemotaxis? - The direct migration of a cell in response to a chemical stimulus, such as a growth factor 18. What are the plasma derived mediators? - The kinin system( cause pain), clotting system( form clots to prevent spread of infection and stop bleeding), complement system ( causes vasodilation) 19. What are the chemical mediators? - Histamine ( released in response to stimuli such as trauma and immune reaction), serotonin (actions similar to histamine) 20. What are the arachadonic acid metabolites? - Prostglandins ( induce inflammation and potential effects of histamine), leukotrine( functions similar to histamine) 21. What is nitric oxide - Produced by a variety of cells and plays multiple roles in inflammation, relaxes smooth muscle of vessels walls, regulates leukocyte movement 22. What are the types of inflammatory exudates? - Serous exudate ( watery fluids low in protein content, result from plasma entering the inflammatory site), hemorrhagic exudates ( occur when there is severe tissue injury that causes damage to blood vessels),membranous exudate ( develop on mucus membrane surfaces), puralent exudates( contain pus), fibrinous exudates ( contain large amounts of fibroses) 23. Granulomous inflammation - Associated with foreign bodies (splinters, sutures) associated with microorganisms that cause ( tuberculosis, syphilis, deep fungal infections) 24. Factors invloved in the bodies protective response - Inflammatory reaction, immune response, tissue repair 25. Most prominent manifestations of inflammation 26. Increased plasma proteins, increased skeletal muscle breakdown, alterations of white blood cells, fever 27. What are the fever patterns? 28. Intermittent ( normal temp between fever), remittent ( remains above normal but fluctuates more than 1 degree in 24 hours), sustained( remains above normal but doesn't fluctuate more than 1 degree in 24 hours), neurogenic(brain and spine trauma) 29. What are fevers dangerous? 30. 1 degree increase leads to an extra 15 beats per minute of the heart 31. Types of structures of body organs and tissues 32. Parenchymal( tissues contain the functioning of an organ or body part), stromal tissues( consist of supporting connective tissue, blood vessels, nerve fibers) 33. Two types of healing 34. Primary healing ( small, clean wound, papercut) 35. Secondary healing ( great loss of tissue with contaminations, heart surgery) 36. Stages of wound healing 37. Inflammatory response (at the site of the injury the products of thr injury trigger white blood cells to show up), proliferative phase ( focuses on building new tissue, key is fibroblast, make the tissue connect after a cut), maturational/remodeling( development of scars) 38. Classifications of immune deficiency states 39. Primary: congenital or inherited 40. Secondary(acquired later in life): malnutrition, infection, neoplastic disease, immunosupportive therapy 41. Results of alterations of the immune systems 42. Immunodeficiency states, allergic or hypersensitivity reactions, autoimmune disorders, transplantation rejection 43. Four major categories of immune mechanics 44. The complement system, humoral or antibody mediated immunity, cell mediates immunity, phagocytosis 45. Types of immune responses 46. Cell mediated: T-cells (attack invaded cells directly) fungi, viruses, cancer 47. Antibody-mediated= B cells (generate plasma cells that secrete immuniglobins or antibodies) circulating pathogens 48. What is an antigen? 49. Something that causes an immune response 50. Immunogenicity( provoke immune system) reactivity( reacts specifically with provoked cells 51. Types of immunity 52. Natural, active: you produce T,B cells and they respond 53. Natural, passive: antibodies transfer across placenta to fetus 54. Artificial, active: vaccination 55. Artificial, passive: IV injection of antibodies 56. Antibodies 57. IgG( its a girl, most abundant) 58. IgA( makes up 10-15% of antibodies, found in sweat, tears, saliva) 59. IgM(about 5-10% of all antibodies in the blood) 60. IgD(.2% of antibodies, involved in the activation of B cells) 61. IgE(.1% of antibodies, involved in alllergic and hypersensitivity reactions) 62. Disorders that effect your immune system 63. AIDS (HIV virus attacks, damages CD4 cells, immunidieficiency within 2-10 years) 64. Allergic reactions( overactive immunity in response to allergens) 65. Infectious mononucleosis( causes enlargement and abdormal cells) 66. Type 1 hypersensitivity reactions 67. Commonly called allergic reactions, examples: food allergies, hives, exema 68. Type 2 antibody mediated 69. IgM or IgG attack antigens ores or white blood cells, examples: Rh disease, Drug reactions, involves neutrophils, macrophages and IgG,IgM 70. Type 3 immune complex mediated 71. Antigen is not attached to the cells, inflammatory response produces the damage, examples: lupus, serum sickness, Arthur's reaction 72. Type 4 Cell-mediated hypersensitivity 73. Cell mediated: T cells attack antigen examples: Tuberculin test, allergic contact dermatitis 74. Types of transplant reactions 75. Hyperacute reactions: occurs immediately after transplantation 76. Acute rejection: occurs within a few months after transplantation with signs of organ failure 77. Differnece between HIV and AIDS 78. HIV-the virus 79. AIDS- the manifestations of the infections 80. How to diagnose HIV 81. ELISA 82. Western Blot to confirm 83. What are opportunistic infections 84. Respiritory diseases: tuberculosis, pneumonia 85. GI diseases: Thrush, protozoal infections leading to diarrhea 86. Nervous system: AIDS dementia, Toxoplasmosis- caused by a parasite that leads to neurological dysfunction 87. Malignancies: Kaposi Sarcoma affects the endothelial cells that line the blood vessels, painless in early stages, tumors obstruct blood flow 88. Wasting syndrome: involuntary weight loss, chronic weakness, fever 89. What is a positive and negative ion name? 90. Negative (anion) positive ( cations) 91. Functions of body fluids 92. Transport gases, nutrients and waste, take part in metabolism, maintain body function 93. What are the Distribution of body fluids 94. Intracellular compartment( fluid inside the cell, 2/3 of body water, high concentration of potassium) extracellular (contains all the fluid outside the cell, 1/3 of body water, high concentration of sodium) 95. What is the fluid exchange at the capillaries? 96. Four forces control the movement of water between the capillary and interstitial spaces 97. Starlings law of the capillaries 98. Volume reabsorbed=volume filtered 99. When filtration is greater than reabsorbtion? 100. Edema (accumulation of fluid in extracellular spaces) 101. Concerns with edema 102. Increase distance for diffusion of nutrients, impaired function, compression of blood vessels 103. Where does edema develop? 104. Stomach, lungs, heart 105. Water gain/loss 106. 2500ml in 2500mls out 107. Physiological mechanism assisting in regulating body water? 108. Thirst (primary regulator of water intake), ADH (regulator of water output) 109. Ways to lose water 110. Insensible (sweat, breathing), measurable ( urine, vomit, diarrhea) 111. Regulators of sodium? 112. Kidney is the main regulator of sodium( monitors arterial pressure;retains sodium whe arterial pressure is decreased and eliminates it when arterial pressure is increased) 113. What makes us thirsty? 114. Osmoreceptors in the hypothalamus 115. Types of thirst? 116. Hypodispia( can't sense thirst) polydipsia(excessive thirst) 117. Disorders of ADH expression 118. Diabetes insipidus ( when a person loses too much water in their unrine), SIADH(Failure of the negative feedback system that regulates the release and inhibition of ADH) 119. Types of diabetes insipidus 120. Central or neurogenic (occurs because of a defect in the synthesis or release of ADH) nephrogenic diabetes insipidus (occurs because the kidneys do not respond to ADH) 121. Disorders of sodium and water balance 122. The amount of sodium and water change proportionately (isotonically) or disproportionately 123. What is isotonic fluid volume or hypovolemia? 124. Water and electrolytes are lost in isotonic proportions 125. Causes are high salt intake, manifestations are increased thirst and dry mucous membrane 126. Isotonic fluid volume excess or hyperbole is? 127. water and sodium intake or retention is disproportionate 128. Sodium needed per day? 129. 500 mg per day 130. Why's is sodium so important to the body? 131. Maintains the serum osmolality, plays a role in acid-base balance, involved in the transmission of electrical impulses, maintains cell integrity with the sodium- potassium pump 132. What is hyponatremia? 133. Low sodium 134. Types of hyponatremia? 135. Hypertonic hyponatremia( osmotic shift of water due to elevated blood glucose) 136. Hypovolemic hypotonic hyponatremia( most common: ECF is lost by excess sweating, vomiting, diarrhea) 137. Normovolemic hypotonic hyponatremia( most commonly associated with SIADH, result of post op, High ADH) 138. Hypervolemic hypotonic hyponatremia(least common) 139. Hypernatrimia is what? 140. Causes(either too much sodium in or too muc water out) 141. Euvolemic( water from ICF pulled to ECF) 142. Hypovolemic( water loss is greater than sodium loss) 143. Hypervolemic(addition of a hypertonic solution containing both sodium and water) 144. Potassium distribution and regulation 145. Intracellular concentration of 140 to 150 mEq/L 146. Extracellular concentration of 3.5 to 5.0 mEq/L 147. What is hypokalemia? 148. Low potassium (plasma potassium levels below 3.5 mEq/L) 149. Inadequate potassium intake 150. What is Hyperkalemia? 151. Increase in potassium 152. Kidneys not eliminating potassium 153. What does Vitamin D do? 154. Acts top sustain normal plasma levels of calcium and phosphate by increasing thier absorption from the intestine 155. What does calcitonin do? 156. Acts on the kidney and bone to remove calcium from the extracellular circulation 157. Why does parathyroid hormone get released? 158. Drop in serum calcium levels 159. Increase in serum phosphorus will also increase PTH secretion 160. 3 forms of ECF calcium 161. Protein bound 162. Complexed 163. Ionized (50% of ECF calcium is present in the ionized form) 164. Causes of Hypocalcemia 165. Impaired ability to mobilize calcium from bone stores 166. Abnormal losses of calcium from the kidney 167. Symptoms of hypocalcemia 168. Increased neuromuscular excitability 169. Cardiovascular effect 170. Nerve cells less sensitive to stimuli 171. How do you get hyperkalcemia? 172. Increased intestinal absorption 173. Increased bone resorption 174. Decreased elimination 175. Symptoms of hypercalcemia? 176. Changes in neural excitability 177. Exposure of the kidneys to high concentrations of calcium 178. Role of phosphate in the body 179. Plays a major role in bone formation 180. Essential to certain metabolic processes 181. Necessary for delivery of oxygen by the red blood cells 182. Needed for normal function of other blood cells( white blood cells and platelets) 183. Causes of hypoposphatemia (low phosphate) 184. Insufficient intestinal absorption 185. Renal losses 186. Malnutrition 187. Causes of hyperphosphatemia (high phophate) 188. Failure of the kidneys to excrete excess phosphate 189. Rapid redistribution of intracelular phophate to the ECF compartment 190. Excessive intake of phosphate 191. Magnesium balance 192. Essential to all reactions that require ATP 193. Regulation at the kidney level 194. Ingested in the diet 195. Absorbed from the intestine 196. Excreted by the kidneys 197. Causes of Hypomagnesemia (low magnesium) 198. Serum level less than 1.8% 199. Hypertension, tachycardia 200. Causes of hypermagnesemia 201. Excessive intake, decreased exercretion 202. Acidosis and alkalosis number 203. Acidosis (\7.45) 204. 2 types of acids 205. Volatile: leave your body through the lungs 206. Non-volatile: leaves body through kidneys (breakdown of meat proteins, incomplete glucose metabolism, incomplete lipid metabolism) 207. Acid-Base disorders events 208. Primary- initiating event 209. Compensatory event- an attempt to correct the change in pH 210. Metabolic- involves bicarbonate 211. Respiratory- involves CO2 91. What is metabolic acidosis 212. Metabolic acidosis ( primary deficit of bicarbonate and a decrease in pH 92. Causes of metabolic acidosis 213. Decrease of kidney function 214. Increase bicarbonate loss 93. Manifestations of metabolic acidosis 215. Increased respiration 216. Hyperkalemia 94. What is metabolic alkalosis 217. Caused by an increase in pH due to an increase in bicarbonate ions 95. Causes of metabolic alkalosis 218. Loss of acids(vomiting), increased bicarbonate retention 96. What is respiratory acidosis 219. An increase in CO2, an increase in carbonic acid, decrease in pH 97. Causes of respiratory acidosis 220. Acute- always accompanied by low oxygen 221. Acute respiratory failure associated with severe drop in pH with little change in bicarbonate (not getting enough oxygen) 98. What is respiratory alkalosis 222. A decrease in CO2, deficit in carbonic acid, increase in pH 99. Causes of respiratory alkalosis 223. Panic attacks, fever, excessive stress