front 1 total body water | back 1 intracellular fluid and extracellular fluid |
front 2 intracellular fluid | back 2 fluid inside the cells |
front 3 extracellular fluid | back 3 fluid outside the cells intravascular and interstitial and transcellular and cerebrospinal fluids |
front 4 sources of water | back 4 liquids foods cellular metabolism |
front 5 losses of water | back 5 urine feces insensible losses (lungs and skin) |
front 6 balance of water a electrolyets | back 6 thirst mechanism in the hypothalamus antidiuretic hormone aldosterone atrial natriuretic peptide |
front 7 capillary exchange | back 7 filtration diffusion active transport osmosis |
front 8 filtration | back 8 movement of fluid from blood to interstitial spaces hydrostatic pressure (push) osmotic pressure (pull) |
front 9 diffusion | back 9 solutes down their concentration gradient |
front 10 active transport | back 10 solute moved against their concentration gradient using ATP power |
front 11 osmosis | back 11 movement of water down the "water" gradient, toward higher solute concentration |
front 12 edema | back 12 excess fluid on the interstitial compartment causing swelling or enlargement of the tissues localized or general can interfere with venous return, arterial circulation, and cell function in the area |
front 13 causes of edema | back 13 increased capillary hydrostatic pressure loss of plasma proteins obstruction of lymphatic circulation increased capillary permeability |
front 14 effects of edema | back 14 localized swelling pitting edema increased body weight functional impairment of organs or joints pain impaired arterial circulation when sustained poor dental impressions skin susceptible to ulceration |
front 15 dehydration | back 15 insufficient body fluid resulting from inadequate intake or excessive loss of fluid or a combination of both |
front 16 fluid loss | back 16 measured by change in body weight; adjusted for age, body size, and condition |
front 17 isotonic dehydration | back 17 proportionate loss of fluid and electrolytes |
front 18 hypotonic dehydration | back 18 loss of more electrolytes than water, leaving ECF with lower plasma osmolality |
front 19 hypertonic dehydration | back 19 loss of more fluids than electrolytes, leaving ECF with hight plasma osmolality |
front 20 causes of dehydration | back 20 vomiting and diarrhea excessive sweating with loss of sodium and water diabetic ketoacidosis insufficient water intake use of concentrated infant formula |
front 21 direct effects of dehydration | back 21 dry mucous membranes in mouth decreased skin turgor or elasticity lower blood pressure (low blood volume) fatigue increased hematocrit decreasing mental function |
front 22 compensation for dehydration | back 22 increased thirst increased heart rate constricting cutaneous blood vessels produce less urine that is more concentrated |
front 23 third-spacing | back 23 situation in which fluid shifts out of the blood and into a body cavity or tissue; it is no longer available as circulatory fluid can occur with peritonitis or burns |
front 24 sodium imblanaces | back 24 primary cation of ECF active transport with Na+/K+ ATPase in cells maintain high in ECF active secreted in mucus and body secretion forms of NaCl and NaHCO3 in body ingested in with food and fluids; lost in sweat, urine, feces levels controlled by kidneys important for maintain ECF volume involved in nerve conduction and muscle contraction |
front 25 causes of hyponatremia | back 25 Na+ loss: excessive sweating, vomiting, diarrhea use of certain diuretic drugs and low Na+ diet low aldosterone, excess ADH, adrenal insufficiency early chronic renal failure excess H2O intake |
front 26 effects of hyponatremia | back 26 fatigue, muscle cramps, abdominal discomfort, or cramps with nausea and vomiting impaired nerve conduction fluid imbalances between compartments fluid shift into cells brain cells may swell |
front 27 causes of hypernatremia | back 27 ingest large amounts of Na+ high H2O losses insufficient ADH, large volumes of dilute urine loss of thirst mechanism, not drinking watery diarrhea prolonged periods of rapid respiration |
front 28 effects of hypernatremia | back 28 fluid out of cells weakness, agitation firm, subcutaneous tissue increased thirst with dry, rough mucus membranes decreased urine output due to normal ADH secretion |
front 29 potassium imbalance | back 29 primary cation of ICF active transport with Na+/K+ ATPase in cells to maintain low in ECF and high in ICF ingested in with food insulin promotes movement of K+ into cells influenced by acid-base balance abnormal K+ affects contractions of cardiac muscle and causes changes in ECG |
front 30 causes of hypokalemia | back 30 excess losses from diarrhea diuresis associated with certain diuretic drugs excessive aldosterone or glucocorticoids in the body decreased dietary intake treatment of diabetic ketoacidosis with insulin |
front 31 effects of hypokalemia | back 31 cardiac dysrhythmias and abnormal ECG patterns fatigue and muscle weakness paresthesias - pins and needles decreased digestive tract motility impaired renal function, failure to concentrate urine severe deficits, respiratory muscles become weak, shallow respirations |
front 32 causes of hyperkalemia | back 32 renal failure aldosterone deficit use of "potassium-sparing" diuretic durgs leakage of intracellular K+ into ECF in patients with extensive tissue damage displacement of K+ from cells by prolonged or severe acidosis |
front 33 effects of hyperkalemia | back 33 cardiac dysrhythmias and abnormal ECG patterns fatigue and muscle weakness paresthesias - pins and needles nausea |
front 34 calcium imbalance | back 34 divalent cation of ECF ingested in food; stored in bone, excreted in urine and feces balance maintained by PTH and calcitonin Ca2+ and phosphate ions have reciprocal relationship in the ECF |
front 35 causes of hypocalcemia | back 35 hypoparathyroidism malabsorption syndrome deficit serum albumin increased serum pH - alkalosis renal failure |
front 36 effects of hypocalcemia | back 36 muscle twitching, carpopedal spasm, hyperactive reflexes chvostek sign trousseau sign laryngospasm parethesias weak heart contractions |
front 37 causes of hypercalcemia | back 37 neoplasms; malignant bone tumors hyperparathyroidism immobility or decreased stress on bone increased intake of Ca2+ from more vit D intake milk-alkali syndrome |
front 38 effects of hypercalcemia | back 38 depress neuromuscular activity stupor, anorexia, nausea personality changes interferes with ADH in kidneys causing polyuria increased strength of cardiac contractions and dysrhythmias develop may contribute to kidney stones |
front 39 magnesium imbalance | back 39 divalent cation of the ICF 50% stored in bone serum levels linked to K+ and Ca2+ levels imbalances are rare |
front 40 causes of hypomagnesemia | back 40 malabsorption or malnutrition use of diuretics; diabetic ketoacidosis; hyperparathyroidism; hyperaldosteronism |
front 41 effects of hypomagnesemia | back 41 neuromuscular irritability; tremors of chorea; insomnia; personality changes; increased heart rate with arrhythmias |
front 42 cause of hypermagnesemia | back 42 renal failure |
front 43 effects of hypermagnesemia | back 43 depressed neuromuscular function; decreased reflexes; lethargy; cardiac arrhythmias |
front 44 phosphate imbalance | back 44 divalent anion; located in bone functions in bone and tooth mineralization; metabolic processes; phosphate buffer system and removal of H+ through kidneys |
front 45 causes of hypophosphatemia | back 45 malabsorption; diarrhea; excessive use of antacids; alkalosis; hyperparathyroidism |
front 46 effects of hypophosphatemia | back 46 tremors; weak reflexes; paresthesias; confusion and stupor; anorexia; dysphagia; poor blood cell function |
front 47 causes of hyperphosphatemia | back 47 renal failure; tissue damage or chemotherapy that releases intracellular phosphate |
front 48 effects of hyperphosphatemia | back 48 same manifestations as that for hypocalcemia |
front 49 buffer systems | back 49 combination of a weak acid and its alkaline salt; components react with acids or alkali in blood |
front 50 four main buffer pairs | back 50 sodium bicarbonate and carbonic acid phosphate system hemoglobin system protein system |
front 51 bicarbonate - carbonic acid buffer system | back 51 catalyzed by carbonic anhydrase in blood, lungs, kidneys ratio of bicarbonate to carbonic acid must be 20:1 to maintain pH 7.35-7.45 |
front 52 respiratory system | back 52 chemoreceptors detect increase in CO2 or decrease in pH, stimulate increased respiratory rate to drive off more CO2; raises blood pH in alkalosis, respiratory rate reduced and more CO2 retained; lowering blood pH |
front 53 renal system | back 53 exchange Na+ with H+ under influence of aldosterone |
front 54 diagnostic tests for acid-base imbalance | back 54 arterial blood gases base excess or deficit anion gap |
front 55 respiratory acidosis | back 55 increased CO2 from respiratory problems |
front 56 acute causes of respiratory acidosis | back 56 pneumonia; airway obstruction; chest injuries; patient taking opiates |
front 57 chronic causes of respiratory acidosis | back 57 chronic obstructive pulmonary disease like emphysema |
front 58 metabolic acidosis | back 58 decreased availability of bicarbonate ions |
front 59 causes of metabolic acidosis | back 59 excessive bicarbonate loss from diarrhea, nonvolatile acid production high; renal disease or renal failure, H+ not secreted and bicarbonate not reabsorbed |
front 60 respiratory alkalosis | back 60 hyperventilation caused by anxiety, high fever, or aspirin overdose re-breathing expired air in a paper bag can help retain CO2 to lower blood pH |
front 61 metabolic alkalosis | back 61 early stage of vomiting, hypokalemia, excessive antacid intake |
front 62 compensation of acid-base imbalance | back 62 the cause of the imbalance determines the first change in the ratio compensation is assessed by subsequent change in second part of the ratio |
front 63 decompensation | back 63 life-threatening condition the kidneys and lungs cannot compensate serum pH moves out of normal range can result from confounding factors involved such as infection or dehydration |
front 64 first line of defense | back 64 nonspecific mechanical barrier skin, mucous membranes body secretions |
front 65 second line of defense | back 65 nonspecific types of inflammation and phagocytosis |
front 66 third line of defense | back 66 specific defense mechanism stimulates production of unique antibodies or sensitized lymphocytes |
front 67 inflammation causes | back 67 direct, physical damage caustic chemicals ischemia or infarction allergic reactions extreme temperatures foreign bodies infection |
front 68 basic steps of inflammatory process | back 68 injury to capillaries and tissue cells bradykinin released from injured cells that activates pain receptors sensation of pain stimulates mast cell and basophils to release histamine bradykinin and histamine cause capillary dilation, increased blood flow and permeability break in the skin allows bacteria to enter tissue neutrophils and macrophages phagocytize bacteria |
front 69 review of normal capillary exchange | back 69 pre-capillary sphincters regulate blood flow to capillary beds movement of fluid and solutes based on net hydrostatic pressure and relative osmotic pressures of blood and interstitial fluid |
front 70 arterial end | back 70 fluid pushed out due to high hydrostatic pressure in capillary and low hydrostatic pressure of interstitial space |
front 71 venous end | back 71 fluid drawn in due to higher osmotic pressure of blood than that of the interstitial fluid |
front 72 capillary exchange with inflammation | back 72 injured cells release chemical mediators that cause vasodilation chemical mediators also increase capillary permeability protein, water, electrolytes leave capillary, from exudate leukocytes leave capillary and move to site of injury to begin phagocytosis of foreign material |
front 73 vascular response in acute inflammation | back 73 due to chemical mediators released in response to damage cause local vasodilation and increased capillary permeability redness and warmth |
front 74 immediate action in vascular response of acute inflammation | back 74 histamine from mast cell granules; kinins and complement system from plasma protein activation |
front 75 later effects in vascular response of acute inflammation | back 75 leukotrienes and prostaglandins synthesized from arachidonic acid in mast cells |
front 76 cellular response of acute inflammation | back 76 white blood cells attracted by chemotaxis mast cells release chemotactic factors neutrophils attracted to injury site phagocytosis of foreign matter |
front 77 exudate | back 77 collection of interstitial fluid formed in inflamed area |
front 78 serous exudate | back 78 watery, fluid with protein and white blood cells |
front 79 fibrinous exudate | back 79 thick and sticky; high cell and fibrin content; increases risk of scar tissue |
front 80 purulent exudate | back 80 thick, yellowish green; leukocytes, cell debris, microbes, bacterial infection; pus |
front 81 abscess exudate | back 81 localize pocket of purulent exudate in solid tissue |
front 82 hemorrhagic exudate | back 82 blood vessels damaged |
front 83 general manifestations of acute inflammation | back 83 mild fever, malaise, fatigue, headache, anorexia |
front 84 cause of fever | back 84 release of pyrogens from macrophages, signaling hypothalamus to reset internal thermostat to hight temperature |
front 85 leukocytosis | back 85 increased number of white blood cells, especially neutrophils |
front 86 differential count | back 86 proportion of each type of white blood cell altered, depending on cause |
front 87 plasma proteins | back 87 increased fibrinogen and prothronmbin |
front 88 erythrocyte sedimentation rate | back 88 elevated plasma proteins increase the rate at which red blood cells settle in a sample |
front 89 c-reactive protein | back 89 a protein not normally found in blood, appears with acute inflammation and necrosis within 24 to 48 hours |
front 90 cell enzymes | back 90 released from necrotic cells and enter tissue fluids and blood; specific enzymes may indicate the site of inflammation |
front 91 potential complications of acute inflammation | back 91 ulcers, local complications, infections, skeletal muscle spasms |
front 92 chronic inflammation | back 92 develops from unresolved acute episode less swelling and exudate more lymphocytes, macrophages, and fibroblasts more tissue destruction more collagen production |
front 93 complications of chronic inflammation | back 93 arthritis in joints deep ulcers that may perforate the viscera extensive scar tissue |
front 94 aspirin | back 94 acetylsalicylic acid decreases prostaglandin synthesis at site of inflammation; reduces pain and fever never for children some people are allergic gastrointestinal distress and interferes with blood clotting |
front 95 acetaminophen | back 95 tylenol or paracetamol analgesic, antipyretic, not anti-inflammatory |
front 96 NSAIDS | back 96 analgesic, antipyretic, anti-inflammatory ibuprofen some are allergic, delays blood clotting, risk of gastrointestinal distress and gastric ulcers |
front 97 NSAID COX-2 inhibitor | back 97 anti-inflammatory; analgesic similar negative effects as aspirin and NSAIDS edema/increased blood pressure |
front 98 corticosteroids | back 98 anti-inflammatory drugs decrease capillary permeability; enhancement of epinephrine and norepinephrine to stabilize vasculature reduce number of leukocytes and mast cells at site, decreasing release of histamine and prostaglandins |
front 99 adverse effects of corticosteroids | back 99 atrophy of lymphoid tissue; catabolic effects on tissues; delayed healing; delayed growth in children; retention of sodium and water leading to high BP and edema |
front 100 anti-inflammatory herbs and spices | back 100 turmeric black pepper ginger root rosemary |
front 101 RICE | back 101 rest ice compression elevation |
front 102 first aid measures | back 102 RICE mold, moderate exercise can help blood flow elevation and compression can help mediate swelling |
front 103 types of healing | back 103 resolution regeneration replacement healing by first intention healing by second intention |
front 104 resolution | back 104 minimal tissue damage; damaged cells recover and tissue returns to normal after a short period |
front 105 regeneration | back 105 cells of damaged tissue can undergo mitosis; damaged tissue replaced by identical cells generated by cells |
front 106 replacement | back 106 extensive tissue damage, cells not capable of mitosis; replaced by connective tissue |
front 107 healing by first intention | back 107 clean wound, no necrotic tissue, edges held together with minimal gap and minimal scar |
front 108 healing by second intention | back 108 large wound, more inflammation, longer healing period, more scarring |
front 109 healing process | back 109 blood clot forms and seals area inflammation develops in surrounding area granulation tissue grows into gap epithelial cells undergo mitosis fibroblasts and connective tissue cells enter area scar tissue remains |
front 110 factors promoting healing | back 110 youth good nutrition adequate hemoglobin effective circulation clean, undisturbed wound no infection |
front 111 factors delaying healing | back 111 advanced age; reduced mitosis poor nutrition, dehydration anemia circulatory problems certain chronic diseases irritation infection chemotherapy treatment prolonged use of glucocorticoids |
front 112 complications due to scar formation | back 112 loss of function contractures and obstruction adhesions hypertrophic scar tissue ulcerations |
front 113 burn | back 113 a thermal or non-thermal injury that causing acute inflammation and tissue destruction |
front 114 classification of burns | back 114 classified by depth of skin damage and percentage of body surface area involved |
front 115 first-degree burn | back 115 superficial burn damage to epidermis heals without scar; sunburn, mild scald |
front 116 second-degree burn | back 116 partial thickness burn destruction of epidermis and part of dermis red, edematous, blistered, hypersensitivity easily infected; cause scarring |
front 117 third-degree burn | back 117 destruction of all skin layers wound coagulated and charred damaged tissue shrinks causing pressure on edematous tissue beneath escharotomy requires skin grafting for healing |
front 118 effects of burn injury | back 118 shock respiratory problems pain infection metabolic needs |
front 119 healing of burns | back 119 immediate covering; nonstick dressing large areas - stretch skin graft synthetic or biosynthetic substitutes goal to minimize scar tissue formation physiotherapy and occupational therapy to reduce effects of scar tissue |
front 120 burns in children | back 120 growth of children effected during hyper-metabolism of burn recovery thin skin easily burned in hot water for baths additional surgery for grafts required to accommodate growth |