NURS 6501 Week 5 Quiz Advanced Pathophysiology –Walden University Questions And Answers Up, Exams of Nursing

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Nurs601ADVANCED

PATHOPHYSIOLOGY

Exam 3

A certain disease is currently found in 1 of every 10 people in the country and 1, 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? a.number 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 - D In 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 - C When myocardial cells are injured, the function of the Na-K membrane pump may be impaired. Which of the following may then result? a.intracellular 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 - D The 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?

b. It does not stimulate the inflammatory process. c. It results in phagocytosis of the apoptotic cell. d. all of the above. - D Insufficient 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 - B Chronic alcoholism can result in the development of a fatty liver because it results in which of the following?

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 treatment Epidemiology - 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 occurring. secondary 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 muscle. physiologic 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 hyperplasia - he 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.

• 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 emphysema radiation 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)

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 fetus example 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 cytoplasm detachment 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 p Epstein-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:

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 > 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 arrest clinical 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

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)/ (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 edema - decreased 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 develop normal ranges of pH, PaCO2, and HCO3 - 7.35 - 7. 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 acidosis clinical manifestations of metabolic acidosis - drowsiness/coma decreased BP bradycardia nausea/vomiting diarrhea abdominal pain deep rapid respirations headache diagnostics of metabolic acidosis - HCO3 < pH <7. etiology of metabolic alkalosis - - addtion of bicarbonate to the body