Advanced Pathophysiology Exam 1. Reviewed Questions and Correct Answers (Graded A+).

Advanced Pathophysiology Exam 1 (Latest Update) Questions and Answers (GRADED A) A certain disease is currently found in 1 of every 10 people in the country and 1,000 people contract the disease yearly. The population of the country is 4,500,000. Which of the following statements is correct? a. The prevalence of the disease is 10% and the incidence is .02%. b. The prevalence of the disease is .02% and the incidence is 10%. c. Neither is correct. d. There is insufficient data A In relation to disease development, the term "etiology" refers to which of the following? r of people with the disease b. cause of the disease c. definition of the disease d. outcome of the disease B Which of the following is(are) true about "symptoms"? a. objective and measurable b. the same as "signs" c. both of the above d. neither of the above DIn 1992, there were 980 deaths in a Midwestern city with a population of 1,000,000. At the beginning of that year, 900 cases of AIDS existed in this population. During the year, 250 new cases of AIDS were diagnosed, and 75 people died of the disease in 1992. Using the data given above, what was the incidence rate (per 100,000 population) at the end of 1992 for AIDS? a. 6 b. 25 c. 88 d. 116 B What level of prevention is a blood pressure screening program for high school students who are pregnant? a. primary b. secondary c. tertiary B Mr. Forbes complains of "indigestion" and becomes sweaty and pale. His wife takes him to the Emergency Department at Northwestern Memorial Hospital. A cardiac catheterization 2 days later shows partial blockage of his right coronary artery (RCA). Blockage of the right coronary artery can lead to myocardial cell injury because it results in which of the following? a. bilirubin accumulation in myocardial cells b. alteration in the genetic material of myocardial cells c. reduced energy production in myocardial cells d. activation of the complement system CWhen myocardial cells are injured, the function of the Na-K membrane pump may be impaired. Which of the following may then result? cellular sodium will increase b. extracellular potassium will decrease c. cell volume will decrease d. all of the above A Mr. Forbes is being prepared for open heart surgery when he suffers a myocardial infarction in which a large part of his left ventricle has suffered lethal cell injury. Mr. Forbes' CPK-MB and LDH1, enzymes associated with myocardial cells, are significantly elevated. What is the best explanation for this? a. It is a sign that necrotic myocardial cells have released their cytoplasmic contents into the blood. b. It is a sign of reversible fatty accumulation in the myocardial cells c. It is a sign that the myocardial cells are undergoing hypertrophy. d. None of the above. A If a tissue specimen of myocardial cells were obtained for examination from Mr. Forbes, which of the following findings would indicate irreversible cell injury? a. cellular swelling b. decreased ATP production c. decreased intracellular calcium d. dissolution of nuclear material DThe accumulation of lactic acid that occurs with impaired energy production results from which of the following? a. increased intracellular glucose b. increased anaerobic metabolism c. decreased metabolic rate d. increased oxidative phosphorylation B A mountain climber is stranded at 23,000 feet in the Swiss Alps and has lost all his equipment and supplies in an avalanche. Subsequently, he suffers cell injury due to impaired ATP production. The reason for the decrease in ATP is which of the following? a. enzyme inhibition b. uncoupling c. hypoxia d. none of the above C An elderly patient develops an obstruction in his left middle cerebral artery. The brain tissue supplied by this artery becomes hypoxic. The best explanation for this is which of the following? a. the obstruction results in decreased blood flow b. the obstruction results in decreased hemoglobin in the blood c. while blood flow stays the same, the obstruction reduces oxygen content in the blood d. none of the above explain the reason for the hypoxia AIncreased mobilization and delivery of free fatty acids to liver cells can result in fat accumulation. Which of the following problems results in increased mobilization of free fatty acids? a. anemia b. hepatic toxins c. starvation d. hypoxia C Generalized hypoxia results in a switch to anaerobic metabolism in cells. Anaerobic metabolism results in which of the following? a. decreased lactic acid inside cells b. decreased arterial pH c. more effective ATP production d. increased pH inside cells B There is a disease of the spleen, which results in an excessive destruction of RBCs. This increase in RBC destruction can lead to which of the following? a. hypoxia b. hypobilirubinemia c. an increase in platelets d. all of the above A Your body has developed an increased demand for thyroid hormones. This will lead to ____________ of the thyroid gland. a. atrophyb. hypertrophy c. dysplasia d. metaplasia B You palpate a gangrenous leg and note the presence of crepitus. Crepitus is associated with which of the following? a. wet gangrene b. dry gangrene c. gas gangrene d. all of the above C Direct cell membrane destruction may result from which of the following? a. complement activation b. bacterial enzymes c. free radicals d. all of the above D Which of the following is true regarding apoptosis? a. It occurrence may be physiological or pathological. b. It does not stimulate the inflammatory process. c. It results in phagocytosis of the apoptotic cell. d. all of the above. DInsufficient blood flow to a part of the body is defined as: a. hypoxia. b. hypoxemia. c. necrosis. d. ischemia. D A cellular change, which is often precancerous, is called: a. hyperplasia. b. metaplasia. c. dysplasia. d. hypertrophy. C Which of the following changes is indicative of irreversible cell injury? a. sodium influx into the cytoplasm b. glycolysis (anaerobic metabolism) c. detachment of ribosomes from rough endoplasmic reticulum d. release of lysosomal enzymes D Which of the following best describes reperfusion injury? a. The increased blood pressure in the area of reperfusion causes rupture of small arterioles and release of free radicals.b. The return of blood flow to the area results in a burst of free radical production from neutrophils that accumulated in the area. c. Reperfusion injury results from restoration of the function of the sodium-potassium pump. d. Reperfusion of the area results in apoptosis of the previously ischemic cells. B Which of the following best describes free radicals? a. stable molecules not normally found in the body, but introduced exogenously during ischemia b. unstable molecules that are normal products of oxidative metabolism and are removed by endogenous antioxidants c. stable molecules that have an affinity for iron in the cytoplasm of the cell d. none of the above B The usual fate of apoptotic cells is which of the following? a. metaplastic transformation b. calcification c. hypertrophy d. phagocytosis e. neoplastic transformation D Which of the following statements is true regarding the difference between cell necrosis and apoptosis? a. Apoptosis is a more rapid process. b. Apoptosis is usually initiated by ischemia-induced cell injury. c. Apoptosis is genetically controlled.d. Apoptosis characteristically involves rupture of the cell membrane. C You are a nurse practitioner working in an outpatient clinic. Your patient's echocardiogram shows moderate aortic stenosis (narrowing of the aortic valve). You know that the stenotic valve creates an increased resistance against which the left ventricle contracts. The cellular adaptation most likely to occur in the left ventricle is which of the following? a. atrophy b. hypertrophy c. hyperplasia d. metaplasia B Select the condition that is an example of physiologic hyperplasia. a. breast enlargement during puberty b. endometrial hyperplasia from excessive estrogen stimulation c. prostatic hyperplasia occurring as men age d. none of the above are physiologic A Your patient has a long history of mitral stenosis (narrowing of the mitral valve). As the years go by, the left atrium, which contracts against the increased resistance of the stenotic valve, begins to fail--and output from the left ventricle begins to decline. If the left ventricle were to undergo adaptation, what would it most likely be? a. atrophy. b. hypertrophy. c. hyperplasia. d. metaplasia.A Which of the following is not characteristic of cellular dysplasia? a. variation in size and shape of cells b. small, pale nuclei c. disorderly arrangement of cells d. preneoplastic change B If a normal individual began to take cortisol 100 mgs. every day as a medication, which of the following would result? a. hypertrophy of the adrenal gland b. hyperplasia of the adrenal gland c. atrophy of the adrenal gland d. hypertrophy and hyperplasia of the adrenal gland C If a normal individual began to take thyroid hormone 100 mcgs. every day as a medication, which of the following would result? a. hypertrophy of the thyroid gland b. hyperplasia of the thyroid gland c. atrophy of the thyroid gland d. hypertrophy and hyperplasia of the thyroid gland BChronic alcoholism can result in the development of a fatty liver because it results in which of the following? a. increased production of free fatty acids b. increased conversion of free fatty acids to triglycerides c. decreased oxidation of cholesterol, triglycerides, and phospholipids d. decreased binding of cholesterol, triglycerides, and phospholipids to apoproteins A Which of the following is the primary difference between wet and dry gangrene? a. Infection and inflammation are present in wet gangrene. b. Wet gangrene results from arterial occlusion and dry gangrene from venous stasis. c. Dry gangrene involves the presence of Clostridium perfringens. d. Wet gangrene occurs only in internal organs. E Which of the following components is not involved in apoptosis? a. Bcl-2 b. apaf-1 c. caspase 9 d. cytochrome c e. HLA 2 E Some cancer-causing viruses are able to protect the cells that they transform from undergoing apoptosis by interfering with the action of the apoptosis promoter called:a. TNF-alpha. b. Fas. c. p53. d. IL-2. e. INF-beta. C Which of the following diseases is thought to be related to free radical damage? a. osteoarthritis b. detached retina c. cerebral aneurysm d. cancer D Which of the following enzymes, released from dying cells, may indicate problems in the liver? a. alanine aminotransferase b. aspartate aminotransferase c. alkaline phosphatase d. all of the above e. none of the above D Researchers hypothesize that the disappearance of dopamine-generating cells in the midbrain in Parkinson's Disease may be related to oxidative stress due to a decrease in the amount of glutathione in the midbrain. The best explanation for this theory is which of the following? a. DNA synthesis requires glutathione for optimal development. b. Dopamine synthesis requires glutathione to prevent free radical production.c. Free radicals produced via dopamine synthesis are neutralized by glutathione. d. Glutathione is needed for entry of dopamine into the cerebral circulation. C Which of the following is(are) true regarding aging? a. may involve an increase in autoantibodies b. may result from damage accumulation c. both are true d. neither is true C In theories of aging, cross-linking implies which of the following? a. The lifespan and number of times a cell can replicate are preprogrammed. b. The number of cell doublings is limited. c. There is oxygen toxicity. d. Cell permeability decreases. D Etiology Causative factors in a particular disease Iatrogenic produced by treatmentEpidemiology risk factors and distribution in populations Incidence number of new cases Prevalence number of existing cases both new and old clinical manifestations signs, symptoms, and diagnostic criteria how are symptoms and signs different symptoms are what the patient reports signs are objective or measurable outcomes cure, remission, chronicity, or death primary prevention Efforts to prevent an injury or illness from ever dary prevention -focuses on early identification of individuals or communities experiencing illness, providing treatment, and conducting activities that are geared to prevent worsening health status -examples: communicable disease screening and case finding; early detection and treatment of diabetes; exercise programs for older adult clients who are frail Tertiary prevention -aims to prevent the long-term consequences of a chronic illness or disability and to support optimal functioning -examples: prevention of pressure ulcers as complication of a spinal cord injury; promoting independence for the client who has traumatic brain injury Atrophy Decrease or shrinkage in cellular size.Most common in skeletal muscle, heart, secondary sex organs, and brain. Physiologic atrophy occurs with early development. Ex. Thymus gland gets physiologic atrophy during childhood. pathologic atrophy occurs as a result of decreases in workload, pressure, use, blood supply, nutrition, hormonal stimulation, and nervous stimulation hypertrophy Increase in the size of the cells that increase the size of the affected organ. Heart and kidneys (responsive to enlargement) and skeletal ologic hypertrophy occurs with increased demand, stimulation of hormones, and growth factors. Ex. Pregnancy causes hormone induced hypertrophy of the uterus, in skeletal muscle occurs as a response to heavy workload. pathologic hypertrophy results from chronic hemodynamic overload. Ex. Hypertension or heart valve dysfunction. Hypertrophic cells have increased accumulation of ER, plasma membrane, myofilaments, mitochondria (not cellular fluid). Nucleus is also hypertrophic with increased DNA synthesis. Triggers for cardiac hypertrophy include mechanical signals (stretch) and trophic signals (growth factors and vasoactive agents). Hyperplasia increase in number of cells in an organ/tissue as a response to injury that results from an increased rate of cellular division compensatory Physiologic hyperplasia is an adaptive mechanism that enables certain organs to regenerate. Occurs in skin, intestines, hepatocytes, bone marrow, and fibroblasts. Ex. Is when skin gets callus in response to mechanical stimulus. Hormonal physiologic hyperplasia Hormonal occurs mainly from estrogen dependent organs such as uterus and breasts.Ex- after ovulation estrogen stimulates endometrium to grow/thicken for fertilized ovum. Pathologic hyperplasiahe abnormal proliferation of normal cells and can occur as a response to excessive hormonal stimulation or the effects of growth factors on target cells. These cells have enlargement of the nucleus, clumping of chromatin (package and protect DNA), and the presence of one or more large nucleoli. Ex. Benign prostatic hyperplasia (BPH) and endometriosis-both the result of hormonal imbalance. Metaplasia reversible replacement of one mature cell type (epithelial or mesenchymal) by another, sometimes less differentiated, cell type. Cause of metaplasia develops from reprogramming of stem cells. Found in association with tissue damage, repair, and regeneration. pathophysiology of metaplasia Adaptive replacement cell may be more suitable to the changed conditions in the surrounding environment. Ex. GERD damages squamous epithelium of the esophagus, cells are replaced by glandular epithelium which may tolerate the acid better. Not always beneficial. Ex. Smoking causes changes in bronchi cells, which don't have cilia or secrete mucus, causing loss of protective mechanism. What is the significance of metaplasia Can be reversed if stimulus is removed. If continues, can cause malignant transformation. Dysplasia abnormal changes in the size, shape, and organization of mature cells. mostly found in epithelia Significance of dysplasiacan be reversed if it does not involve the entire epithelium. When dysplastic changes penetrate the basement membrane it is considered a preinvasive neoplasm (carcinoma in situ) mechanisms of cell injury ATP depletion, mitochondrial damage, accumulation of oxygen and oxygen-derived free radicals membrane damage protein folding defects DNA damage defects calcium level alterations reperfusion injury injury to tissue that occurs after blood flow is restored restoration of needed oxygen is accompanied by oxidative stress with the generation of toxic oxygen radicals which damage cellular membranes and mitochndria What helps reperfusion injury? antioxidants and anti-inflammatory drugs examples of cell injury ischemic and hypoxic injury ischemia-reperfusion injury oxidative stress or accumulation of oxygen-derived free radicals induced injury chemical injuryCell injury: ATP depletion loss of mitochondrial ATP and decreased ATP synthesis results include: cellular swelling decreased protein synthesis decreased membrane transport lipogenesis all changes that contribute to loss of integrity of the plasma membrane Cell injury: Oxygen and oxygen-derived free radicals lack of oxygen is key in progression of cell injury in ischemia (reduced blood supply) activated oxygen species (free radicals) cause destruction of cell membranes and cell structure Cell Injury: Intracellular calcium and loss of calcium steady state Normally intracellular cytosolic calcium concentrations are very low; ischemia and certain chemicals can cause an increase in cytosolic Ca concentrations sustained levels of Ca continue to increase with damage to plasma membrane Ca causes intracellular damage by activating enzymes Cellular events that occur with ischemia-hypoxic injury -Decrease in oxygen reaching the cell -decrease in ATP production within mitochondria -failed NA+/K pump -Na, Ca enter cell, K leaves -organelle swelling -protein synthesis stops-ATP via oxidative phosphorylation declines, glycolysis increases -glycogen stores depleated -lactic acid produced -decrease in intracellular Ph declines -rupture of lysosomes -autodigestion of the cell contents and membrane Deleterious effects of free radicals on cells -unstable compounds with an unpaired electron in outer ring -anxious to "mate" with other substances affinity for lipid substances (there is a phospholipid bilayer membrane around cell) -combine avidly with cell and organelle membranes -lipid peroxidation - dissolution of the membrane -"drills a hole" examples o diseases linked to oxygen-derived free radicals aging atherosclerosis brain disorders Cancer Cardiac myopathy Diabetes Eye disorders inflammatory disorders iron overload emphysemaradiation injury reperfusion injury rheumatoid arthritis sleep apnea Burns Most types of cellular accumulations occur as a result of what 4 mechanisms 1 - insufficient removal of normal substance because of altered packaging/transport 2-abnormal substance (result of mutated gene) accumulated because of deficits in protein folding, transport, or abnormal degredation 3 - endogenous substance not effectively catabolized because of lack of vital lysosomal enzyme 4 - harmful exogenous materials such as heavy metals, dusts, microorganisms that accumulate because of inhalation, ingestion, or infection normal substances that cause cell accumulation water protein lipid carbs abnormal substances that cause cell accumulation -endogenous: product of abnormal metabolism synthesis -exogenous: infectious agent or material pathophysiology of reperfusion injury-generation of highly reactive oxygen intermediates (oxidative stress) -these radicals cause further membrane damage and mitochondrial calcium overload what does reperfusion cause -causes creation of free radicals, pH alterations, inflammatory signaling, osmotic changes, gap junction changes, calcium overload, apoptosis 7 possible mechanisms of fatty accumulation -increased movement of free fatty acids into the liver -Failure of metabolic process that converts fatty acids to phospholipids resulting in the preferential conversion of the fatty acids to triglycerides -increased synthesis of triglycerides from fatty acids -decreased synthesis of apoproteins (lipid acceptors) -failure of lipids to bind with apoproteins and form lipoproteins -failure of mechanisms that transport lipoproteins out of the cell -direct damage to the ER by free radicals released by alcohol's toxic effects pathogenesis of bilirubin -released when RBCs break down -released into blood (unconjugated) -fat-soluble, cannot be elimintated through urine -unconjugated is taken up in the liver cells, bound to glucuronic acid, becomes conjugated bilirubin -can now be eliminated through the kidney -some becomes part of bile, some is eliminated in urine and feces giving yellow and brown color (bilirubin is a pigment)What is jaundice caused by excess bilirubin what is excess bilirubin caused by -diseases that cause destruction of RBC (hemolytic jaundice) -Diseases affecting the metabolism and excretion of bilirubin in the liver -diseases that can obstruct the common bile duct (gallstones/pancreatic tumors) Effects of free cytosolic calcium -normally removed by ATP dependent calcium pumps -If abnormal permeability of calcium ion channels, direct damage to membranes, or depletion of ATP (i.e. hypoxic injury) -then calcium level increases -if not buffered or pumped out, uncontrolled enzyme activation takes place -leading to: phosphorylation of protein and chromatin fragmentation, membrane damage, cytoskeletal disassembly (damage), nucleus chromatin damage -often final pathway in many causes of cell death pyknosis in some cells the nucleus shrinks and becomes a small dense (clumped together) mass of genetic material. The pyknotic nucleus eventually dissolves (by karyolysis) karyorrhexias a degenerative cellular process involving fragmentation of the nucleus and the breakup of the chromatin into unstructured granuleskaryolysis nuclear dissolution and lysis of chromatin from the action of hydrolytic enzymes. Result of the action of hydrolytic lysosomal enzymes on DNA Liquefactive necrosis brain infarct, bacterial infections; wet gangrene type of necrosis which results in a transformation of the tissue into a liquid viscous mass. coagulative necrosis primarily occurs in kidneys, heart, and adrenal glands results from hypoxia caused by severe ischemia or chemical injury most common usually replaced by scar/fibrous tissue caseous necrosis commonly results from tuberculous pulmonary infection combination of coagulative and liquefactive the dead cells disintegrate but the debris is not digest completely by hydrolases tissues appear soft and granular and resemble clumped cheese Fat necrosis occurs in the breast, pancreas, and other abdominal structures cellular dissolution caused by powerful enzymes called lipasesbreak down triglycerides releasing free fatty acids which combine with calcium, magnesium, and sodium ions, creating soaps necrotic tissue appears opaque and chalk white Gangrenous necrosis refers to death of tissue and results from severe hypoxic injury commonly occurring becasuse of arteriosclerosis especially in lower leg with hypoxia and subsequent bacterial invasion, the tissues undergo necrosis dry gangrene an area that is free of infection and in which the line of demarcation between live and dead tissue is apparent tissue becomes dry and shrunken - mummified wet gangrene often malodorous and the line of demarcation between live and dead tissue is unclear until the infection is arrested gas gangrene wet gangrene caused by clostridium perfringes, an organisms that produces gas within the destroyed tissue. This accumulation of gas produces a distinctive sound on palpation of the area called crepitus systemic manifestations of cellular injury fever increased heart rateincrease in number of leukocytes pain presence of cellular enzymes in extracellular fluid lactate dehydrogenase CK AST ALT ALP amylase aldolase tropinins cellular processes involved in necrosis -caused by an injurious agent, or -cells are induced to commit suicide -a disorganized sequence of events that stimulates the inflammatory process -cellular changes after cell death and process of cellular autodigestion -membrane integrity is lost and necrotic tissue leaks out causing inflammation in the surrounding tissue apoptosis -event that results in cell death -quiet, organized, programmed process resulting in elimination of individual cells Example of physiologic apoptosis removal of webbing between fingers in human fetusexample of pathologic apoptosis AIDS when the HIV induces T-cell apoptosis T/F Apoptosis is associated with inflammation False What is apoptosis initiated by activation of capase enzymes what is necrosis initiated by ischemia toxins physical stimuli what is the time course for apoptosis 12 - 24 hours what is the time course for necrosis 20 - 30 minutes cell characteristics of apoptosis shrinkage of the cell condensation of the cytoplasmdetachment of cell from ECM membrane budding phagocytosis by neighboring cells nuclear DNA fragmentation activation of capases and DNAses cell characteristics of necrosis cell swelling and rupture of cell membrane clumping of nuclear chromatin swelling of intracellular organelles calcium and other electrolyte overload what are the three mechanisms of apoptosis intrinsic or mitochondrial pathway extrinsic or death receptor pathway apoptosis inducing factor Apoptosis - mitochondrial pathway -healthy cell - protein Bcl-2 on surface - inhibits apoptosis -internal damage to cell -protein Bax migrates to the surface of the mitochondria where it inhibits protective effect of Bcl-2 -inserts self into outer mitochondrial membrane punching holes in it -cytochrome c leaks out -cytochrome c binds to the protein Apaf-1 -complexes aggregate to form apoptosomes -bind to and activate caspase-9-cleaves and activates other caspases (executioner ones) -digestion of structural proteins in the cytoplasm -degradation of chromosomal DNA -phagocytosis of the cell Apoptosis death-receptor pathway -Fas and TNF receptor are integral membrane proteins with their receptor domains exposed at the surface of the cell -binding of the complementary death activator (FasL and TNF) transmits a signal to the cytoplasm -actiavation of caspase 8 -initiates cascade of caspase activation -phagocytosis of cell apoptosis-inducing -neurons have another way to self-destruct that does not use caspases -AIF is a protein that is normally located in the intermembrane space of mitochondria -when cell receives death signal, AIF: -released from mitochondria -migrates to nucleus -binds to DNA -triggers destruction of the DNA and cell death relationship of apoptosis to cancer some viruses associated with cancers use tricks to prevent apoptosis of the cells that they have performed -HPV produces protein E6 that binds and inactivates apoptosis promoter p53Epstein-Barr Virus - produces protein similar to Bcl-2 as well as a protein that increases the production of Bcl-2. Both inhibiting apoptosis relationship of apoptosis to AIDS -immune response to a foreign invader - proliferation of lymphocytes (T and B cells) -when their job is done they are removed via apoptosis leaving a small population of memory cells define aging and its relationship to cellular function/structure and genetic and environemental factors -aging is the progressive loss of tissues overtime -senescence is a process of permanent proliferative arrest on cells in response to various stressors -senescent cells accumulate - tissue dysfunction -cellular changes of aging include: -atrophy -decreased function -loss of cells (maybe apoptosis) -free radicals damage tissues during aging -DNA is vulnerable to breaks, deletions, and additions -movement of intracellular and Extracellular substances decreases with age causes of hypovolemia - loss of fluids from anywhere (thoracentisis, paracentisis, vomiting, diarrhea, hemorrhage, suction) - Third spacing (burns, ascites) - diseases with polyuria (polyuria > oliguria > anuria > renal failure) clinical manifestations of hypovolemia-Thirst -Dry mucous membranes -Decreased skin turgor/delay return/tenting -Hypotension, tachycardia -Weight loss -Decreased urine output, concentrated urine -Restless, drowsy, confused, dizzy, weak total body water -usually expressed as a percentage of body weight -varies based on body type, sex, and age -female normal build 50% water -male normal build 60% water causes of hypervolemia Heart failure Kidney disease Cirrhosis Overdose of sodium concentrated fluids Fluid shifts in burns Prolonged use of corticosteroids Severe stress Hyperaldosteronism weight gain manifestations of hypervolemia-Edema pitting -pulmonary congestion -circulatory overload( bounding pulses, jugular vein distention, elevated blood pressure - weight gain hypernatremia occurs when serum sodium levels exceed 145 mEq/L and causes hypertonicity hypovolemic hypernatremia occurs where there is loss of body sodium accompanied by a relatively greater loss of body water causes: loop diuretics, osmotic diuresis (ie from hyperglycemia related to uncontrolled diabetes or mannitol), GI losses, failure of kidneys to concentrate urine Euvolemic hypernatremia most common occurs when there is a loss of free water with a near normal sodium concentration causes: inadequate water intake, excessive sweating, fever with hyperventilation and water loss from burns, vomiting, diarrhea, diabetes insipidus hypervolemic hypernatremia rare occurs when there is increased TBW and greater increase in total body sodium level, resulting in hypervolemia causes: infusion of hypertonic saline solutions, over-secretion of ACTH or aldosterone (cushing syndrome)signs of hypernatremia weakness lethargy muscle twitching hyperreflexia due to shrinking of brain cells and alterations in membrane potential labs of hypernatremia hematocrit and plasma protein levels are elevated with water loss sodium >145 hyponatremia develops when the serum sodium concentration decreases to less than 135 mEq/L most common electrolyte disorder in hospitalized individuals occurs when there is a loss of sodium, inadequate intake of sodium, or dilution of sodium by water excess excessive diuretic therapy hyponatremia ECF effects extracellular volume contraction and hypovolemia hyponatremia ICF effects increased intracellular water, edema, brain cell swelling, irritability, depression, confusion, systemic cellular edema (weakness, anorexia, nausea, diarrhea)hypovolemic hyponatremia with pure sodium loss is accompanied by loss of ECF with symptoms of hypotension, tachycardia, decreased urine output hypervolemic hyponatremia weight gain, edema, ascites, jugular vein distention labs of hyponatremia hematocrit and plasma protein level may be elevated with pure sodium deficits Sodium < 135 hyperkalemia greater than 5.0 mEq/L caused by excess dietary or IV intake decreased renal loss renal failure K+ sparing diuretics hypoaldosteronism shift from ICF to ECF metabolic acidosis cell injury severe hyperkalemia depresses the ST segment prolongs the PR interval and widens QRS complex (loss of atrial activity) causing VFIB or cardiac arrestclinical manifestations of hyperkalemia Muscle weakness (cells in relative or absolute refractory period) Flaccid, dilated heart (heart in relative or absolute refractory period) ECG abnormal Ventricular fibrillation Digital numbness and tingling hypokalemida less than 3.5 mEq/L caused by decreased intake starvation anorexia nervosa increased renal loss K+ losing diuretics hyperaldosternoism vomiting diarrhea shift from ECF to ICF metabolic acidosis insulin admin clinical manifestations of hypokalemia - Fatigue - Muscle weakness, leg cramps - Nausea, vomiting, paralytic ileus - Soft, flabby muscles - Paresthesias, decreased reflexes- Weak, irregular pulse - Polyuria - Hyperglycemia hypocalcemia less than 8.5 mg/dL serum level caused by inadequate intestinal absorpition, depostion of ionized calcium into bone or soft tissue, blood admin, decrease in PTH and vit D levels, nutritional deficiences occur with inadequate calcium sources, alkalosis, elevated calcitonin level manifestations of hypocalcemia increased neuromuscular activity tingling muscle spasms intestinal cramping hyperactive bowel sounds osteoporosis fractures severe: convulsions, tetany, prolonged QT, cardiac arrest Chvostek sign or Trousseau sign chvostek Abnormal spasm of the facial muscles in response to a light tapping of the facial nerve. Noted in clients with hyPOcalcemia Trousseau's signA sign of hypocalcemia . Carpal spasm caused by inflating a blood pressure cuff above the client's systolic pressure and leaving it in place for 3 minutes. hypercalcemia greater than 10.5 mg/dL caused by hyperparathyroidism bone metastases with calcium resorption from breast, renal, and cervical cancer sarcoidosis excess vit D tumors that produce PTH calcium containing antacids clinical manifestations of hypercalcemia fatigue weakness lethargy anorexia nausea constipation impaired renal function kidney stones dysrhythmias bradycardia cardiac arrest bone pain osteoporosisfractures calculation of water def the difference between ideal TBW and current TBW = weight in kg x (0.4 F) (0.5 M) (0.6 infants) calculation for ideal TBW (current Na X TBW)/140 calculation for water deficit ((current Na X TBW)/140) - TBW calculation for water excess the difference between current TBW and ideal TBW water excess = weight (kg) x (0.5 F) x (1 - (Na/125)) (0.6 M) (0.7 infants) normal body fluid osmolality 280 - 294 mOsm/Kgosmolality determined by the total solute concentration in a fluid compartment Calculation for serum osmolality OSM = 2 X [sodium concentration] + [glucose concentration/18] + [BUN/2.8] Pseudohyponatremia shift of H2O from ICF to ECF Sosm is hypertonic (>280) due to presence of another effective osmol Mannitol, prostate resection, hyperglycemia artifact of hyperlipidemia/hyperproteinemia (multiple myeloma) (calculated Na will appear low) hyponatremia with hypotonicity "true hyponatremia" most common form usually caused by renal water excretion in the presence of continued water intake calculation for corrected serum sodium G= (pt. glucose - 100)/100(1.6 mEq/L x G) + (serum sodium) Examples of edema caused by decreased capillary oncotic pressure -cirrhosis, malnutrition (decreased synthesis of plasma proteins) -nephrotic syndrome (increased loss of plasma proteins) -Increased plasma Na and H2O retention (dilution of plasma proteins) examples of edema caused by increased capillary permeability -burns -inflammation -neoplastic disease -allergic reactions -infection loss of plasma proteins to interstitial space leading to increased tissue oncotic pressure examples of edema caused by increased capillary hydrostatic pressure -venous obstruction -salt and water retention -heart failure fluid movement into tissue leading to edema how does lymph obstruction cause edemadecreased transport of capillary filtered protein leading to increased tissue oncotic pressure leading to edema how does sodium and water retention contribute to edema if the depletion of the intravascular volume stimulates the renin-angiotensin-aldosterone system, the increase in sodium retention and water also adds to edema by further increasing hydrostatic pressure localized edema limited swelling to site of trauma ex sprained finger, injury, cerebral edema, pulmonary edema, pleural effusion, ascites generalized edema is an excessive accumulation of fluid in the interstitial space throughout the body and occurs as a result of conditions such as cardiac, renal or liver failure dependent edema Swelling in the part of the body closest to the ground, caused by collection of fluid in the tissues; a possible sign of congestive heart failure. problems with edema -accumulation of fluid increases distance for nutrients, oxygen, and wastes to move between capillaries and cells in the tissues -diminishes capillary blood flow leading to ischemia -wounds heal more slowly -risk for pressure ulcers increases -edematous fluid is trapped in third space, dehydration can developnormal ranges of pH, PaCO2, and HCO3 7.35 - 7.45 35 - 45 22 - 26 etiology of metabolic acidosis -primary loss of bicarbonate from the body (usually GI or renal) -an increase in the production or addition of metabolic acids (not carbonic acid) -decrease in acid excretion causes of metabolic acidosis related to increased non-carbonic acids (elevated anion gap) -overproduction of ketoacidosis (diabetes, alcohol excess, stavation -lactic acidosis (shock) -ingestions -advanced renal failure -distal renal tubule acidosis causes of metabolic acidosis related to bicarbonate loss (normal anion gap) -diarrhea -uterosigmoidoscopy -early renal failure -proximal renal tubule acidosisclinical manifestations of metabolic acidosis drowsiness/coma decreased BP bradycardia nausea/vomiting diarrhea abdominal pain deep rapid respirations headache diagnostics of metabolic acidosis HCO3 <22 pH <7.36 etiology of metabolic alkalosis -addtion of bicarbonate to the body -hypochloremic metabolic alkalosis (vomitting or GI suctioning with depletion of ECF sodium, chloride, and potassium. Kidneys increase bicarb reabsorption) -loss of hydrogen ions -hydrogen and chloride depletion (prolonged vomiting, GI suctioning) -excessive bicarbonate intake -hyperaldosteronism with hypokalemia -diuretic therapy clinical manifestations of metabolic alkalosis dizzinesstachycardia nausea/vomiting anorexia muscle cramps tetany hypoventilation (slow and shallow) seizures tingling weakness hyperactive reflexes diagnostics metabolic alkalosis HCO3 > 26 pH > 7.44 etiology respiratory acidosis -alveolar hypoventilation -respiratory depression (brainstem trauma, oversedation) -paralysis of the respiratory muscles -disorders of the chest wall -kyphoscoliosis, pickwickian syndrome, flail chest -disorders of the lung parenchyma (pneumonitis, pulmonary edema) -airway obstruction -COPD clinical manifestations of respiratory acidosisinitial: -headache -restlessness -blurred vision -apprehension Later: -lethargy -muscle twitching -tremors -convulsions -coma (neurological symptoms because CO2 crosses BBB) -RR rapid at first then depressed diagnostics of respiratory acidosis PaCO2 > 45 pH < 7.36 etiology of respiratory alkalosis -alveolar hyperventilation and hypocapnia -hypoxemia (high altitudes) -hypermetabolic states (fever, anemia, thyrotoxicosis) -early salicylate intoxication -anxiety or panic disorder -improper use of mechanical ventilators -could occur secondary to metabolic acidosis following hyperventilationclinical manifestations of respiratory alkalosis dizziness confusion tingling convulsions coma deep and rapid respirations carpopedal spasm and other symptoms of hypocalcemia diagnostics of respiratory alkalosis PaCO2 < 35 pH > 7.44 what is the anion gap Concentration of anions (Cl and HCO3) to cations (Na and K) in the ECF, by rule, the concentrations should be relatively equal relationship of anion gap and metabolic acidosis -metabolic acidosis is characterized as either normal anion gap metabolic acidosis or elevated anion gap metabolic acidosis -MA elevated gap - we know abnormal anions -MA normal gap - we know that the cause is loss of bicarbonate What are the causes of elevated anion gap in metabolic acidosisP - paraldehyde L - lactic acidosis U - uremia M - Methanol S - Salicylates E - Ethanol E - Ethylene Glycol D - DKA S - Starvation calculate the anion gap AG = (Na + K) - (Cl + HCO3) relationship between metabolic alkalosis and hydrogen -bicarb generation is coupled with hydrogen secretion -increase in bicarb can be due to loss of hydrogen ions - usually from GI losses or shift from ECF to ICF explain buffers in metabolic acidosis -buffer systems compensate for excess acid and attempt to maintain pH. -H+ into cell, K+ out -acidosis severe then buffers depleted cannot compensate and pH continues to decrease -there is also an increase in Ca because acidosis decreases the amount of Ca bound to albumin What is compensation in ABG's -metabolic (renal) and respiratory (pulmonary) counter adjustments to try to fix pH imbalance in ABG'sex. metabolic alkalosis means high bicarb, respiratory will try to compensate by retaining CO2 into blood partial compensation systemic arterial blood pH is still lower than 7.35 example - respiratory acidosis, renal system tries to balance by reabsorbing bicarb (bc high bicarb will raise pH) but is not enough to reach WDL full compensation pH is normal, pCO2 and HCO3 are abnormal 3 pathophysiolgical types of AKI prerenal intrarenal (intrinsic) postrenal nonoliguria vs oliguria vs anuria nonoliguria - daily volume >500 oliguria - daily volume <500 anuria <100 prerenal AKI etiologies -hypovolemia -hemorrhagic blood loss (trauma, GI bleeding, complications of childbirth) -loss of plasma volume (burns, peritonitis)-water and electrolyte losses (severe vomiting, diarrhea, obstruction, diabetes, diuretics) -hypotension or hypoperfusion -septic shock -cardiac failure -massive pulmonary embolism -stenosis -increased intraabdominal pressure intrarenal AKI etiologies -acute tubular necrosis -glomerulopathies -acute interstitial necrosis (tumors or toxins) -vascular damage -malignant HTN, vasculitis -coagulation defects -renal artery/vein occlusion -bilateral acute pyelonephritis postrenal AKI etiologies -obstructive uropathies (usually bilateral - fibrosis) -ureteral destruction (edema, tumors, stones, clots) -bladder neck obstruction (enlarged prostate) -neurogenic bladder how does urinary sediment differentiate prerenal, intrarenal (glomerulonephritis), intrarenal (ATN), and postrenal AKInormal - bland prerenal - bland intrarenal (G) - active (hallmark) intrarenal (ATN) - muddy brown casts, renal tubular epithelial cells postrenal - bland We have an expert-written solution to this problem! how does urine sodium differentiate prerenal, intrarenal (glomerulonephritis), intrarenal (ATN), and postrenal AKI normal - 20 mEq/L prerenal - <10 mEq/L intrarenal (G) - <20 mEq/L intrarenal (ATN) - >40 mEq/L postrenal - usually low how does urine osmolality differentiate prerenal, intrarenal (glomerulonephritis), intrarenal (ATN) normal - 300 - 900 mOsm prerenal - > 500 mOsm (high) intrarenal (G) - > 500 mOsm intrarenal (ATN) - <300 mOsm postrenal - how does proteinuria differentiate prerenal, intrarenal (glomerulonephritis), intrarenal (ATN), and postrenal AKI normal - 0 - 20 mg/dL prerenal - 5 - 20 mg/dLintrarenal (G) - > 100 mg/dL presence of proteinuria intrarenal (ATN) - 5-20 mg/dL postrenal - 5-20 mg/dL how does specific gravity differentiate prerenal, intrarenal (ATN) normal - 1.00 - 1.03 prerenal - >1.020 intrarenal (ATN) - 1.010 - 1.012 (low) how does BUN/Cr ratio differentiate prerenal, intrarenal (glomerulonephritis), intrarenal (ATN), and postrenal AKI normal - 10 - 20:1 prerenal - >20:1 intrarenal (G) - 10 - 20:1 intrarenal (ATN) - 10 - 20:1 postrenal - >20:1 glomerulonephritis injury to the glomeruli typically from systemic disease usually immunologic in etiology what distinguishes glomerulonephritis from pre-renal AKI azotemia (BUN and Cr will be elevated active urinary sediment proteinuriaacute tubular necrosis damage to the renal tubules due to presence of toxins in the urine or to ischemia most common cause of hospital acquired ARF distinguish ATN from prerenal UA: granular muddy brown casts no significant increase in protein urine sodium is >20 (FE NA >3%) FeUrea is elevated BUN/CR is normal does not respond to volume replacement GFR the filtration of plasma per unit of time the sum of the filtration rate of all the functioning nephrons normal value - 90 - 120 Creatinine derived from the metabolism of muscle and from dietary meat intake freely filtered in the glomerulus and is not reabsorbed 0.6-1.2 T/F if GFR, muscle mass, and diet are stable, the creatinine concentration in the body should remain stableT steady state T/F If the GFR decreases the serum creatinine levels will decrease as well False a small increase in creatinine from baseline signifies a significant fall in GFR renal autoregulation the ability of the nephrons to adjust their own blood flow and GFR without external (nervous or hormonal) control helps keep GFR constant example: BP increases - afferent arterioles constrict preventing an increase in glomerular blood flow and filtration pressure myogenic autoregulation If BP decreases/increases - arteriole relax/contract and will compensate to increase/decrease Renal blood flow tubuloglomerular feedback mechanism by which glomerulus receives feedback on the status of the downstream tubular fluid and adjusts filtration to regulate the composition of the fluid, stabilize its own performance, and compensate for fluctuation in systemic blood pressure macula densa cells of diatal tubule in JGA sense changes in flow rate - intiates signal to compensate changes in afferent arteriolar resistance and GFR identify and rank the major causes of CKD1 - diabetes mellitus - causing diabetic nephropathy 2 - hypertension 3 - glomerulonephritis 4 - cystic kidney disease CKD Chronic kidney disease (rising BUN and serum creatinine levels affect many body systems) GFR <60 for at least 3 months Stage 1 CKD GFR >90 symptoms - usually none, HTN common stage 2 CKD GFR 60-89 increased PTH, early bone disease, increased plasma creatinine in urea symptoms - subtle HTN stage 3 CKD GFR 30-59 erythropoeitin deficiency, anemia, increased plasma creatinine in urea symptoms - mild HTN stage 4 CKDGFR 15-29 increase in triglycerides, metabolic acidosis, hyperkalemia, salt and water retention, increased plasma creatinine in urea symptoms - moderate HTN, hyperphosphatemia, anemia stage 5 CKD GFR <15 end stage, kidney failure uremia symptoms - severe HTN, hyperphosphatemia, anemia renal osteodystrophy decrease in renal function, decrease in vitamin D, which will decrease serum calcium and increase serum phosphorus - PT gland is stimulated to release PTH and elevated PTH causes bone disease kidneys and anemia the kidneys can sense hypoxia/anemia, and incrase endogenous erythropoietin production, which acts in the bone marrow to produce new RBCs if the kidney is failing, this does not work - anemia - kidneys cannot compensate by producing erythropoietin and cannot make new RBCs signs and symptoms and abnormal labs of nephrotic syndrome proteinuria >3.5g/day hypoalbuminemia <3.5g edema - reatining Na/H20 - causes low albumin hypercholestorlemialipiduria vit d deficiency hypothyroidism urine sediment contains large amount of proteins