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Pathophysiology, 5e 5th Edition By Lee-Ellen C. Copstead

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Pathophysiology, 5e 5th Edition By Lee-Ellen C. Copstead

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Pathophysiology, 5e 5th Edition By Lee-Ellen C. Copstead

Chapter 2: Homeostasis and Adaptive Responses to Stressors

Test Bank

 

MULTIPLE CHOICE

 

  1. Indicators that an individual is experiencing high stress include all the following except
a. tachycardia.
b. diaphoresis.
c. increased peripheral resistance.
d. pupil constriction.

 

 

ANS:  D

Pupils dilate during stress from the effects of catecholamines. Tachycardia, diaphoresis, and increased peripheral resistance are indicators of stress and also occur due to catecholamine release.

 

REF:   Pg. 18 | Pg. 21

 

  1. Which is not normally secreted in response to stress?
a. Norepinephrine
b. Cortisol
c. Epinephrine
d. Insulin

 

 

ANS:  D

Insulin secretion is impaired during stress to promote energy from increased blood glucose. Norepinephrine is secreted during stress as a mediator of stress and adaptation. Cortisol is secreted during stress as a mediator of stress and adaptation and stimulates gluconeogenesis in the liver to supply the body with glucose. Epinephrine is secreted during stress as a mediator of stress and adaptation and increases glycogenolysis and the release of glucose from the liver.

 

REF:   Pg. 17

 

  1. Selye’s three phases of the stress response include all the following except
a. allostasis.
b. resistance.
c. alarm.
d. exhaustion.

 

 

ANS:  A

Allostasis is defined as the ability to successfully adapt to challenges. Allostasis may/may not occur in response to stress. Alarm, resistance, and exhaustion are the three phases of the stress response as described by Selye in the general adaptation syndrome.

 

REF:   Pgs. 13-14

 

  1. Many of the responses to stress are attributed to activation of the sympathetic nervous system and are mediated by
a. norepinephrine.
b. cortisol.
c. glucagon.
d. ACTH.

 

 

ANS:  A

Norepinephrine is secreted in response to activation of the sympathetic nervous system during stress by the adrenal medulla. Cortisol is secreted by the adrenal cortex. Glucagon is secreted by the pancreas. ACTH is secreted by the pituitary gland.

 

REF:   Pg. 17

 

  1. The effects of excessive cortisol production include
a. immune suppression.
b. hypoglycemia.
c. anorexia.
d. inflammatory reactions.

 

 

ANS:  A

Cortisol suppresses immune function and inflammation and stimulates appetite. Cortisol leads to hyperglycemia by stimulating gluconeogenesis in the liver.

 

REF:   Pgs. 21-22

 

  1. All the following stress-induced hormones increase blood glucose except
a. aldosterone.
b. cortisol.
c. norepinephrine.
d. epinephrine.

 

 

ANS:  A

Aldosterone results in water and sodium retention and potassium loss in the urine. It does not affect blood glucose. Cortisol is a glucocorticoid secreted by the adrenal cortex. Cortisol stimulates gluconeogenesis in the liver, thus increasing blood glucose. Norepinephrine inhibits insulin secretion, thus increasing blood sugar. Epinephrine increases glucose release from the liver and inhibits insulin secretion, thus increasing blood glucose.

 

REF:   Pgs. 17-19

 

  1. Allostasis is best defined as
a. steady state.
b. a state of equilibrium, of balance within the organism.
c. the process by which the body heals following disease.
d. the overall process of adaptive change necessary to maintain survival and well-being.

 

 

ANS:  D

Allostasis refers to the overall process of adaptive change necessary to maintain survival and well-being.

 

REF:   Pg. 13

 

  1. The primary adaptive purpose of the substances produced in the alarm stage is
a. energy and repair.
b. invoke resting state.
c. produce exhaustion.
d. set a new baseline steady state.

 

 

ANS:  A

These resources are used for energy and as building blocks, especially the amino acids, for the later growth and repair of the organism. The substances do not produce a resting state. The substances can produce exhaustion if they continue, but that is not the adaptive purpose of these. Although a new baseline steady state may result from the stress response that is not the adaptive purpose of the substances produced during the alarm stage.

 

REF:   Pgs. 15-16

 

  1. Persistence of the alarm stage will ultimately result in
a. stress reduction.
b. permanent damage and death.
c. movement into the resistance stage.
d. exhaustion of the sympathetic nervous system.

 

 

ANS:  B

If the alarm stage were to persist, the body would soon suffer undue wear and tear and become subject to permanent damage and even death. Actions taken by the individual during the resistance stage lead to stress reduction. The resistance stage may or may not occur following the alarm stage, based on resource availability. The sympathetic nervous system will continue to function, resulting in continued release of stress hormones.

 

REF:   Pg. 16

 

  1. The effect of stress on the immune system
a. is unknown.
b. has been demonstrated to be non-existent in studies.
c. most often involves enhancement of the immune system.
d. may involve enhancement or impairment the immune system.

 

 

ANS:  D

Many studies demonstrate that long-term stress impairs the immune system, but many researchers identify that short-term stress may enhance the immune system.

 

REF:   Pg. 19

 

MULTIPLE RESPONSE

 

  1. Aldosterone may increase during stress, leading to (Select all that apply.)
a. decreased urinary output.
b. increased blood potassium.
c. increased sodium retention.
d. increased blood volume.
e. decreased blood pressure.

 

 

ANS:  A, C, D

Aldosterone increases water and sodium reabsorption and potassium excretion by the renal distal tubules and collecting ducts, thus leading to decreased urinary output, sodium retention in the body, and increased extracellular fluid volume. Because it leads to potassium excretion, aldosterone leads to decreased blood potassium.

 

REF:   Pg. 18

 

  1. Chronic activation of stress hormones can lead to (Select all that apply.)
a. cardiovascular disease.
b. depression.
c. impaired cognitive function.
d. autoimmune disease.
e. overactive immune function.

 

 

ANS:  A, B, C, D

Excessive cortisol levels promote hypertension, atherosclerosis, and the development of cardiovascular disease. Chronic overactive stress hormones may result in atrophy and death of brain cells. Elevated levels of stress hormones are found in individuals with depressive disorders. Chronic stress leads to immune function impairment, rather than overactive immune function, and has been implicated in autoimmune disorders.

 

REF:   Pgs. 21-22

 

  1. Events which occur during the alarm stage of the stress response include secretion of (Select all that apply.)
a. catecholamines.
b. ACTH.
c. glucocorticoids.
d. immune cytokines.
e. TSH.

 

 

ANS:  A, B, C, D

During the alarm stage, catecholamines (epinephrine, norepinephrine), ACTH, glucocorticoids, and immune cytokines are secreted. TSH is not secreted during the stress response.

 

REF:   Pgs. 14-15

 

 

Chapter 14: Alterations in Hemostasis and Blood Coagulation

Test Bank

 

MULTIPLE CHOICE

 

  1. A normal bleeding time in association with normal platelet count, and increased prothrombin time (PT) and INR, is indicative of
a. vitamin K deficiency.
b. hemophilia B.
c. hemophilia A.
d. idiopathic thrombocytopenia.

 

 

ANS:  A

Vitamin K deficiency should be considered as the cause for bleeding when the PT and INR are increased but other coagulation studies are normal. Hemophilia B results from factor deficiency or the abnormal function of factor IX. Hemophilia A results from factor deficiency or the abnormal function of factor VIII. In idiopathic thrombocytopenia, a decreased platelet count is seen in prolonged bleeding times.

 

REF:   Pg. 306

 

  1. The final step in clot formation is
a. conversion of prothrombin to thrombin.
b. platelet degranulation and adhesion.
c. conversion of fibrinogen to fibrin.
d. clot retraction.

 

 

ANS:  D

Clot retraction, the final stage of clot formation, occurs when the components of the fibrin clot are compressed or contracted to form a firm clot. Platelets serve as a catalyst in accelerating the conversion of prothrombin to thrombin. Platelet degranulation is not involved in clot formation. The formation of a fibrin clot occurs when fibrinogen is converted to fibrin, usually at the site of an injury.

 

REF:   Pg. 295

 

  1. Dysfunction of which organ would lead to clotting factor deficiency?
a. Liver
b. Kidney
c. Spleen
d. Pancreas

 

 

ANS:  A

The liver is responsible for the synthesis of coagulation factors. A clotting factor deficiency is the result of liver dysfunction. Coagulation does not occur in the kidneys. About 25% of the total number of platelets can be found in the spleen. The pancreas is not a location where coagulation occurs.

 

REF:   Pg. 295

 

  1. The conversion of plasminogen to plasmin results in
a. clot retraction.
b. fibrinolysis.
c. platelet aggregation.
d. activation of thrombin.

 

 

ANS:  B

Fibrinolysis is the process of clot dissolution and occurs when plasminogen activators cleave plasminogen to plasmin. Clot retraction occurs when the components of the fibrin clot are compressed or contracted to form a clot. Factors released from platelets contribute to hemostasis by enhancing vasoconstriction, platelet aggregation, and vessel repair. Platelet aggregation is not the result of plasmin conversion. Thrombin cleaves fibrinogen to form a fibrin clot.

 

REF:   Pg. 297 | Pg. 299

 

  1. Activation of the extrinsic pathway of coagulation is initiated by
a. platelet factors.
b. collagen exposure.
c. tissue thromboplastin.
d. factor VII.

 

 

ANS:  C

The extrinsic pathway of coagulation begins when the vascular wall is traumatized. Tissue factor from injured tissue activates factors which in turn activate and convert into thrombin for clotting. Platelets play a major role in primary hemostasis as well as secondary hemostasis and clot retraction. Platelets accelerate the conversion of prothrombin to thrombin. Platelets adhere to collagen exposed by trauma and initiate degranulation. Factor VII is involved in the extrinsic pathway of coagulation when it is activated by tissue factor following a traumatic injury.

 

REF:   Pgs. 296-297

 

  1. The prothrombin time (PT) and INR (International Normalized Ratio) measure the integrity of
a. platelet function.
b. extrinsic pathway.
c. intrinsic pathway.
d. fibrinolysis.

 

 

ANS:  B

The PT and INR assess the extrinsic pathway of coagulation. Platelet function is measured through a CBC. The aPTT assesses the intrinsic pathway of coagulation. The D-dimer assay reflects fibrinolysis.

 

REF:   Pg. 301

 

  1. The activated partial thromboplastin time (aPTT) is a measure of the integrity of
a. the extrinsic pathway.
b. the intrinsic pathway.
c. factor VIII synthesis.
d. plasminogen.

 

 

ANS:  B

The intrinsic pathway is assessed through the aPTT. The extrinsic pathway is assessed through measurements of the PT and INR. An abnormal factor VIII function results in hemophilia A. The deficiency is verified by factor assay. The aPTT is not utilized to assess the integrity of plasminogen.

 

REF:   Pg. 301

 

  1. A commonly ingested substance associated with prolongation of the bleeding time is
a. acetaminophen.
b. tobacco.
c. caffeine.
d. aspirin.

 

 

ANS:  D

Many drugs are associated with prolonged bleeding times. Aspirin is known to alter normal platelet function. Acetaminophen is not associated with prolongation of bleeding time. Tobacco does not interfere with bleeding times. Caffeine does not interfere with bleeding times.

 

REF:   Pg. 297

 

  1. The megakaryocyte is a precursor to
a. factor IX.
b. white blood cells.
c. red blood cells.
d. platelets.

 

 

ANS:  D

Platelets are produced by bone marrow megakaryocytes. Production falls when the number of megakaryocytes is reduced or when the process of platelet production is ineffective. One major role in the formation of factor IX is the presence of calcium. White blood cells are not formed in response to megakaryocytes. Megakaryocytes are not a precursor to red blood cells.

 

REF:   Pg. 303

 

  1. A cause of thrombocytopenia includes
a. hypoxemia.
b. reduced erythropoietin.
c. chemotherapy.
d. secondary polycythemia.

 

 

ANS:  C

Bone marrow suppression from chemotherapy, recent immunizations, and alcohol ingestion are common causes of platelet production. Underlying systemic diseases may be present related to bleeding problems. Hypoxemia is not directly associated with thrombocytopenia. A reduction in erythropoietin is not associated with alterations in coagulation. Secondary polycythemia is not a cause of thrombocytopenia.

 

REF:   Pg. 302

 

  1. Widespread activation of the clotting cascade secondary to massive trauma is called
a. hemophilia B.
b. disseminated intravascular coagulation (DIC).
c. Hageman disease.
d. idiopathic thrombocytopenia purpura.

 

 

ANS:  B

Widespread clotting in small vessels leads to consumption of the clotting factors and platelets, which in turn leads to bleeding. DIC is either acute or chronic and occurs secondary to malignancy, sepsis, snake bites, trauma, shock, burns, and many other factors. Hemophilia B results from factor deficiency or the abnormal function of factor IX. Massive trauma is unrelated to the development of Hageman disease. Immune thrombocytopenia, formerly called idiopathic thrombocytopenia purpura, is an acquired immune-mediated disorder.

 

REF:   Pg. 306

 

  1. A 3-year-old boy who exhibits prolonged bleeding after minor trauma and a prolonged aPTT, but a normal platelet count, is likely to be diagnosed with
a. hemophilia.
b. liver dysfunction.
c. disseminated intravascular coagulation.
d. thrombocytopenia.

 

 

ANS:  A

Hemophilia is rare, but it is the most common severe inherited coagulation disorder. Prolonged bleeding from a minor trauma is a characteristic manifestation. Liver disease is commonly manifested by a decreased platelet count and prolonged coagulation studies. DIC is more often seen in adults as the result of trauma or sepsis. A very low platelet count is often seen in thrombocytopenia.

 

REF:   Pg. 304

 

  1. Treatment for hemophilia A includes
a. heparin administration.
b. factor IX replacement.
c. factor VIII replacement.
d. platelet transfusion.

 

 

ANS:  C

Factor VIII administration is a common treatment choice for hemophilia A, particularly with dental procedures requiring local anesthesia. Heparin administration is typically highly contraindicated in an individual with a bleeding disorder although in some cases it is given to patients with DIC. Factor IX may be available as a treatment option for hemophilia B. A platelet transfusion is not of benefit in the hemophilia A patient.

 

REF:   Pgs. 304-305

 

  1. Disseminated intravascular coagulation may be treated with heparin therapy to
a. enhance fibrinolysis.
b. inhibit clotting factor consumption.
c. activate platelets.
d. enhance liver synthesis of clotting factors.

 

 

ANS:  B

Although controversial, heparin may be used to minimize further consumption of clotting factors. Fibrinolysis is not enhanced by the use of heparin. The use of heparin does not activate platelets. Heparin is not known to enhance liver synthesis of clotting factors.

 

REF:   Pgs. 306-307

 

  1. A deficiency of von Willebrand factor impairs
a. activation of the coagulation cascade.
b. platelet aggregation.
c. platelet adhesion to injured tissue.
d. platelet production.

 

 

ANS:  C

Absence of platelet adhesion at the site of vascular injury and deficient factor VIII activity in the intrinsic coagulation pathway contribute to the bleeding seen in von Willebrand disease. The coagulation cascade is not activated by a deficiency of von Willebrand factor. Platelet aggregation is not related to a deficiency of the von Willebrand factor. von Willebrand factor is necessary for normal adherence of platelets for damaged vascular endothelium.

 

REF:   Pg. 305

 

  1. A patient presents to the physician’s office with pinpoint hemorrhages on the skin. The patient is most likely between the ages of _____ years.
a. 6 months and 2
b. 4 and 7
c. 15 and 18
d. 25 and 45

 

 

ANS:  B

Allergic purpura is most often seen in children between the ages of 4 and 7 years. Allergic purpura is not often seen in infants, teenagers, or adults.

 

REF:   Pgs. 301-302

 

  1. A patient is diagnosed with a tortuous blood vessel of the right hand that bleeds spontaneously. This patient presents with
a. petechiae.
b. purpura.
c. telangiectasia.
d. thrombocytosis.

 

 

ANS:  C

A telangiectasia is a dilated or tortuous small blood vessel found in the skin or mucous membranes that has a tendency to bleed spontaneously or following minor trauma. Petechiae are pinpoint hemorrhages. Purpura is a collection of petechiae. Thrombocytosis is a platelet count above 400,000/mm3.

 

REF:   Pgs. 298-299

 

  1. A newborn has melena, bleeding from the umbilicus, and hematuria. The newborn most likely experiencing
a. vitamin K deficiency bleeding.
b. acquired vitamin K deficiency.
c. von Willebrand disease.
d. disseminated intravascular coagulation.

 

 

ANS:  A

Vitamin K deficiency bleeding is found in newborns and includes melena, bleeding from the umbilicus, and hematuria. Acquired vitamin K deficiency may include gastrointestinal bleeding, ecchymoses, menorrhagia, and hematuria. von Willebrand disease presents as epistaxis, mucosal bleeding, ecchymoses, gastrointestinal bleeding, and menorrhagia. Disseminated intravascular coagulation includes bleeding from orifices, petechiae, and ecchymoses on skin and mucous membranes.

 

REF:   Pg. 305

 

MULTIPLE RESPONSE

 

  1. What is involved in the release of plasminogen activators? (Select all that apply.)
a. Factor X
b. Factor XII
c. HMWK
d. Kallikrein
e. Thrombin

 

 

ANS:  B, C, D, E

Factor XII, HMWK, kallikrein, and thrombin are involved in the release of plasminogen activators. Factor X initiates the common final pathway of coagulation.

 

REF:   Pg. 297

 

  1. Which involves bleeding associated with vascular or platelet defects? (Select all that apply.)
a. Bleeding that occurs immediately after trauma
b. Bleeding that involves skin or mucous membranes
c. Bleeding that is brief in duration
d. Bleeding that is delayed
e. Bleeding into muscles or joints

 

 

ANS:  A, B, C

Bleeding associated with vascular or platelet defects usually occurs immediately after trauma (e.g., dental extraction), involves skin or mucous membranes, and is brief. Delayed bleeding or bleeding into muscles or joints is more typical of a coagulation defect.

 

REF:   Pg. 297

 

  1. Which diseases may be associated with a bleeding problem? (Select all that apply.)
a. Urinary retention
b. Renal failure
c. Cirrhosis
d. Systemic lupus erythematosus
e. Ovarian cancer

 

 

ANS:  B, C, D, E

Renal failure may be associated with a bleeding problem. Liver disease, such as cirrhosis, may be associated with a bleeding problem. Systemic lupus erythematosus may be associated with a bleeding problem. Malignancies, such as ovarian cancer, may be associated with a bleeding problem. Urinary retention is not a disease.

 

REF:   Pg. 297

 

  1. A male patient involved in a motor vehicle accident is brought to the emergency department with acute flank pain. What additional signs of bleeding may the patient exhibit? (Select all that apply.)
a. Hematuria
b. Melena
c. Hematemesis
d. Menorrhagia
e. Hemoptysis

 

 

ANS:  A, B, C, E

Blood in the urine is indicative of a bleeding disorder. Blood in the feces could indicate internal bleeding. Blood in vomit may signify a bleeding disorder. Menorrhea is excessive menstrual bleeding, which would not be seen in the male patient. Bloody sputum is a common symptom of a bleeding disorder.

 

REF:   Pg. 299

 

COMPLETION

 

  1. The ________ is responsible for the synthesis of coagulation factors, with the exception of part of factor VIII.

 

ANS:

liver

The liver is responsible for the synthesis of coagulation factors, with the exception of part of factor VIII.

 

REF:   Pg. 295

 

  1. Hemophilia B is also known as ________ disease.

 

ANS:

Christmas

Hemophilia B is also known as Christmas disease.

 

REF:   Pg. 304

 

Chapter 28: Acute Kidney Injury and Chronic Kidney Disease

Test Bank

 

MULTIPLE CHOICE

 

  1. The oliguric phase of acute tubular necrosis is characterized by
a. fluid excess and electrolyte imbalance.
b. fever and diminishing cognition.
c. sodium retention and potassium loss in the urine.
d. magnesium and phosphorous loss in the urine.

 

 

ANS:  A

The oliguric phase of ATN is characterized by fluid excess and electrolyte imbalance. Fever and diminishing cognition are not typical manifestations of ATN oliguric phase. During this phase sodium is lost in the urine and potassium is not excreted, and magnesium and phosphorous are retained in the body.

 

REF:   Pg. 599

 

  1. Osteoporosis commonly occurs in patients with end-stage renal disease because of
a. hyperparathyroidism.
b. hypercalcemia.
c. excess active vitamin D.
d. phosphorous deficiency.

 

 

ANS:  A

Osteoporosis commonly occurs in patients with end-stage renal disease because of hyperparathyroidism. Hypocalcemia occurs in end-stage renal disease. Insufficient active vitamin D would result in osteoporosis. Phosphate is retained in end-stage renal disease.

 

REF:   Pg. 603

 

  1. Gastrointestinal drainage, perioperative and postoperative hypotension, and hemorrhage may all contribute to renal failure by causing
a. hydronephrosis.
b. acute tubular necrosis.
c. nephrosis.
d. renal inflammation.

 

 

ANS:  B

Gastrointestinal drainage, perioperative and postoperative hypotension, and hemorrhage may all contribute to renal failure by causing acute tubular necrosis. Gastrointestinal drainage, perioperative and postoperative hypotension, and hemorrhage do not cause hydronephrosis, nephrosis, or renal inflammation.

 

REF:   Pgs. 595-596

 

  1. Appropriate therapy for prerenal kidney injury includes
a. fluid administration.
b. potassium supplementation.
c. fluid restriction.
d. protein restriction.

 

 

ANS:  A

Appropriate therapy for prerenal oliguria includes fluid administration; most often prerenal kidney injury is due to fluid volume deficit. Potassium supplements are not appropriate in prerenal oliguria, as potassium is not being excreted. Appropriate therapy for prerenal oliguria includes fluid administration. Protein restriction is not indicated in prerenal oliguria.

 

REF:   Pgs. 594-595

 

  1. A patient with renal disease is at risk for developing uremia as the nephrons progressively deteriorate, because
a. the basement membrane becomes increasingly permeable.
b. filtration exceeds secretory and reabsorptive capacity.
c. excessive solute and water are lost in the urine.
d. GFR declines.

 

 

ANS:  D

A patient with renal disease is at risk for developing uremia as his nephrons progressively deteriorate because GFR declines. The basement membrane does not become increasingly permeable. Filtration does not exceed secretory and reabsorptive capacity. Excessive solute and water are not lost in the urine.

 

REF:   Pg. 600

 

  1. The most likely cause of anemia in a patient with end-stage renal disease is
a. insufficient erythropoietin.
b. blood loss secondary to hematuria.
c. vitamin B12 deficiency secondary to deficient intrinsic factor.
d. iron deficiency.

 

 

ANS:  A

The most likely cause of anemia in a patient with end-stage renal disease is insufficient erythropoietin secretion by the kidney, which is necessary for RBC production. Blood loss secondary to hematuria, vitamin B12 deficiency secondary to deficient intrinsic factor, and iron deficiency are not the most likely causes of anemia in a patient with end-stage renal disease.

 

REF:   Pg. 603

 

  1. The most likely cause of acidosis in a patient with end-stage renal disease is
a. insufficient filtration of bicarbonate ions at the glomerulus.
b. excessive production of respiratory and metabolic acids.
c. insufficient metabolic acid excretion due to nephron loss.
d. hypoventilation secondary to uremic central nervous system depression.

 

 

ANS:  C

The most likely cause of acidosis in a patient with end-stage renal disease is insufficient metabolic acid excretion due to nephron loss. Insufficient filtration of bicarbonate at the glomerulus would lead to alkalosis, not acidosis. Excessive production of respiratory acids would lead to respiratory acidosis not metabolic acidosis. The problem is metabolic acids are not excreted. Hypoventilation secondary to uremic CNS depression may occur, but this would lead to respiratory acidosis, not metabolic acidosis.

 

REF:   Pg. 600

 

  1. The most helpful laboratory value in monitoring the progression of declining renal function is
a. serum creatinine.
b. serum potassium.
c. blood urea nitrogen.
d. mental status changes.

 

 

ANS:  A

Serum creatinine is the most stable and accurate reflection of renal function. Serum potassium is affected by many factors and thus not the most helpful value in monitoring the progression of this disease. Blood urea nitrogen is not as stable as serum creatinine; it is affected by muscle breakdown, protein intake, and so forth. Mental status changes can occur due to multiple factors other than renal function.

 

REF:   Pg. 599

 

  1. Appropriate management of end-stage renal disease includes
a. potassium supplementation.
b. a high-protein diet.
c. erythropoietin administration.
d. a high-phosphate diet.

 

 

ANS:  C

Erythropoietin administration is appropriate, as the kidneys are not able to secrete erythropoietin. Potassium is not appropriate, as the kidneys are unable to excrete potassium. A high-protein diet is not appropriate, as the kidneys are unable to excrete urea. A high-phosphate diet is not appropriate, as the kidneys are unable to excrete phosphorous.

 

REF:   Pg. 603

 

  1. What problem is a patient likely to experience in end-stage renal disease?
a. Hypokalemia
b. Polyuria and nocturia
c. Uremia
d. Hematuria

 

 

ANS:  C

Uremia occurs in end-stage renal disease because the kidneys cannot excrete urea, the end product of protein metabolism. Hyperkalemia occurs in end-stage renal disease. Polyuria and nocturia do not occur in end-stage renal disease; the kidneys are unable to excrete urine. Hematuria does not generally occur unless another problem is causing it.

 

REF:   Pgs. 602-603

 

  1. Which intervention has been found to retard the advancement of chronic kidney disease?
a. Calcium supplementation
b. Erythropoietin
c. Insulin
d. ACE inhibitors

 

 

ANS:  D

ACE inhibitors or A-II receptor blockers have been found to retard the advancement of chronic kidney disease by reducing proteinuria. Calcium supplementation, erythropoietin, and insulin have not been found to retard the advancement of chronic kidney disease.

 

REF:   Pg. 605

 

  1. In patients with polycystic kidney disease, renal failure is expected to progress over time as the cystic process destroys more nephrons. At what point will a patient reach end-stage renal disease?
a. Greater than 15%
b. Greater than 25% nephron loss
c. Greater than 50% nephron loss
d. Greater than 90% nephron loss

 

 

ANS:  D

End-stage renal disease occurs when greater than 90% of the nephrons have been lost. End-stage renal disease is possible to predict based on nephron loss. It occurs when greater than 90% (not 15%, 25% or 50%) of the nephrons have been lost.

 

REF:   Pgs. 601-602

 

  1. At his most recent clinic visit, a patient with end-stage renal disease is noted to have edema, congestive signs in the pulmonary system, and a pericardial friction rub. Appropriate therapy at this time would include
a. initiation of dialysis.
b. fluid restriction.
c. antibiotics.
d. phlebotomy.

 

 

ANS:  A

Dialysis is the appropriate therapy at end-stage renal disease. Although fluid restriction may be appropriate at some point in renal failure, it will not correct the identified problems. Antibiotics will not correct the problems identified and may further impair remaining renal function. Phlebotomy will not correct the identified problems.

 

REF:   Pg. 606

 

  1. The most common cause of intrinsic kidney injury is _____ injury.
a. glomerular
b. tubular
c. interstitial
d. vascular

 

 

ANS:  B

Tubular injury (acute tubular necrosis) is the most common cause of acute kidney injury. Glomerular, interstitial, and vascular injury are not the most common causes of acute kidney injury.

 

REF:   Pg. 595

 

  1. One of the most common causes of acute tubular necrosis (ATN) is
a. ischemic conditions.
b. cytotoxic agents.
c. immune reaction.
d. prolonged postrenal kidney injury.

 

 

ANS:  A

Ischemia and nephrotoxic agents are the most common causes of ATN. Cytotoxic agents, immune reaction, and prolonged postrenal kidney injury are not the most common causes of ATN.

 

REF:   Pg. 595

 

  1. The most common cause of ischemic acute tubular necrosis (ATN) in the United States is
a. hypotension.
b. hypovolemia.
c. renal artery stenosis.
d. sepsis.

 

 

ANS:  D

Sepsis is the most common cause of ischemic ATN in the United States. Hypotension, hypovolemia, and renal artery stenosis are not the most common causes of ischemic ATN.

 

REF:   Pg. 595

 

  1. The most common agent resulting in nephrotoxicity and subsequent acute tubular necrosis (ATN) in hospitalized patients is
a. contrast media.
b. antibiotics.
c. cancer chemotherapy.
d. recreational drugs.

 

 

ANS:  A

The most common agent resulting in nephrotoxicity and subsequent ATN is contrast media. Contrast media, cancer chemotherapy, and recreational drugs are not the most common agents resulting in nephrotoxicity and subsequent ATN.

 

REF:   Pgs. 595-596

 

  1. The risk for contrast media–induced acute tubular necrosis (ATN) is highest in
a. a 70-year-old patient with heart failure.
b. a 50-year-old patient post gallbladder surgery.
c. a 12-year-old patient with recurrent bladder infections.
d. a 30-year-old patient with appendicitis.

 

 

ANS:  A

This patient with the highest risk has two risk factors for contrast media–induced ATN: age over 70 and co-existing heart failure. The other patients have no risk factors for contrast media–induced ATN.

 

REF:   Pg. 596

 

  1. If acute tubular necrosis (ATN) does not resolve and continued tubular dysfunction ensues, the patient will then experience
a. oliguria and sodium retention.
b. infections and sepsis.
c. magnesium and phosphorus loss in urine.
d. polyuria and sodium wasting.

 

 

ANS:  D

If ATN does not resolve, the high blood urea nitrogen (BUN) creates osmotic diuresis; the urine is high in sodium content. Oliguria and sodium retention, infections and sepsis, and magnesium and phosphorous loss in the urine do not result from tubular necrosis and tubular dysfunction.

 

REF:   Pg. 600

 

  1. One of the most frequent causes of chronic kidney disease is
a. hypertension.
b. glomerulonephritis.
c. chronic pyelonephritis.
d. polycystic kidney disease.

 

 

ANS:  A

Hypertension and diabetes are the most common causes of chronic kidney disease. Although glomerulonephritis, chronic pyelonephritis, and polycystic kidney disease can result in CKD, hypertension and diabetes are the most common causes of chronic kidney disease.

 

REF:   Pg. 601

 

  1. The patient most at risk for post-renal acute kidney injury is a(n)
a. elderly patient with hypertrophy of the prostate.
b. middle-aged woman with bladder infection.
c. young child with reflux at the ureterovesical junction.
d. patient who has both hypertension and diabetes.

 

 

ANS:  A

Post-renal acute kidney injury is caused by obstruction in the urinary tract below the level of the kidneys. Elderly men with prostatic hypertrophy are at risk for urinary retention. Bladder infection generally does not obstruct urine flow. Ureterovesical junction reflux is likely to cause pyelonephritis, but not obstruction. Diabetes and hypertension result in intra-renal disease.

 

REF:   Pgs. 594-595

 

  1. The defining characteristic of severe acute kidney injury is
a. proteinuria.
b. oliguria.
c. hematuria.
d. diuresis.

 

 

ANS:  B

Acute kidney injury is defined by oliguria or anuria. Proteinuria, hematuria, and diuresis are not defining characteristics of severe acute kidney injury.

 

REF:   Pg. 599

 

  1. A primary laboratory finding in end-stage chronic renal disease is
a. decreased blood urea nitrogen (BUN).
b. decreased serum sodium.
c. metabolic alkalosis.
d. increased serum creatinine.

 

 

ANS:  D

End-stage chronic renal disease causes increased serum creatinine and blood urea nitrogen, because the dysfunctional kidneys are not able to excrete these metabolic waste products. Chronic renal failure causes increased blood urea nitrogen. Hyponatremia is not a primary laboratory finding in end-stage chronic renal disease. Metabolic alkalosis is not common with end-stage chronic renal disease.

 

REF:   Pg. 602 | Pg. 606

 

  1. The condition associated with end-stage chronic renal disease that is the most immediately life threatening is
a. azotemia.
b. increased creatinine.
c. hypertension.
d. hyperkalemia.

 

 

ANS:  D

Hyperkalemia from decreased renal excretion of potassium can cause dysrhythmias and cardiac arrest. While azotemia, increased creatinine, and hypertension are consequences of end-stage chronic renal disease, they usually are not acutely life threatening.

 

REF:   Pg. 603

 

  1. Renal insufficiency occurs when _____ of the nephrons are not functional.
a. 25%
b. 50%
c. 75% to 90%
d. more than 90%

 

 

ANS:  C

In renal insufficiency, 75% to 90% of the nephrons are not functional. When 25% to 50% of nephrons are not functional, it is decreased renal reserve. When 90% of nephrons are not functional, it is end-stage renal disease.

 

REF:   Pg. 602

 

  1. The effect on the renal tubules during the postoliguric phase of acute tubular necrosis involves
a. reconstruction of the basement membrane.
b. blocking the tubule lumens by dead cells.
c. making the glomeruli patent again.
d. regeneration of the renal tubular epithelium.

 

 

ANS:  D

During the postoliguric phase of acute tubular necrosis, the renal tubular epithelium is regenerating. Disruption of basement membranes is not characteristic of acute tubular necrosis. Blockage of the tubule lumens would cause oliguria. The glomeruli are not clogged during acute tubular necrosis.

 

REF:   Pg. 600

 

  1. Prerenal acute kidney injury may be caused by
a. severe hypotension.
b. glomerulonephritis.
c. bilateral kidney stones.
d. acute tubular necrosis.

 

 

ANS:  A

Prerenal acute kidney injury occurs when blood flow to the kidneys is compromised. Severe hypotension from heart failure, hypovolemia, or shock is a leading cause. Glomerulonephritis does not cause prerenal acute kidney injury, because the glomeruli are located within the kidneys. Bilateral kidney stones do not cause prerenal acute kidney injury, because they are located distal to the nephrons. Acute tubular necrosis does not cause prerenal acute kidney injury, because the renal tubules are located within the kidneys.

 

REF:   Pg. 594

 

  1. Postrenal acute kidney injury may be caused by
a. severe hypotension.
b. glomerulonephritis.
c. bilateral kidney stones.
d. acute tubular necrosis.

 

 

ANS:  C

Bilateral kidney stones can cause postrenal acute kidney injury due to obstruction of normal outflow of urine from the kidneys. Severe hypotension causes prerenal acute kidney injury. Glomerulonephritis does not cause postrenal acute kidney injury, because the glomeruli are located within the kidneys. Acute tubular necrosis does not cause postrenal acute kidney injury, because the renal tubules are located within the kidneys.

 

REF:   Pg. 595

 

  1. Individuals with end-stage chronic renal disease are at risk for renal osteodystrophy and spontaneous bone fractures, because
a. excess potassium leaches calcium from bone.
b. erythropoietin secretion is impaired.
c. urea causes demineralization of bone.
d. they are deficient in active vitamin D.

 

 

ANS:  D

Vitamin D, required for calcium absorption in the digestive tract, is activated in the kidneys. With chronic renal failure, vitamin D is not activated. Hyperkalemia does not influence bone mineralization. Erythropoietin is important for red blood cell production. Urea does not cause renal osteodystrophy.

 

REF:   Pgs. 602-603 | Pg. 605

 

  1. Anemia in people who have end-stage chronic renal disease is caused by
a. chronic loss of blood in the urine.
b. poor appetite, with lack of iron intake.
c. decreased secretion of erythropoietin.
d. increased secretion of aldosterone.

 

 

ANS:  C

Decreased secretion of erythropoietin is the major cause of anemia in end-stage chronic renal disease. Hematuria is not a characteristic of end-stage chronic renal disease. Iron deficiency does not cause the anemia in end-stage chronic renal disease. Aldosterone levels do not contribute to anemia.

 

REF:   Pg. 603

 

  1. A patient being treated for acute tubular necrosis (ATN) develops mild polyuria. The nurse responds to questions about why this occurring by stating
a. “Since he was oliguric for so long, he probably has rebound polyuria. As long as his blood pressure is stable, he is not hypovolemic, so I would not worry.”
b. “I am glad you noticed this change. It happened so gradually that we did not see it. We should call the doctor and get him to measure ADH.”
c. “His renal tubules are recovering, so he is making more urine, but he is not able to concentrate urine well, because he is not fully recovered.”
d. “We had better measure his blood sugar. He may have developed diabetes, and what you see is osmotic diuresis from glucose in the urine.”

 

 

ANS:  C

You have recognized the postoliguric phase of acute tubular necrosis. He does not have rebound polyuria. The polyuria is part of acute tubular necrosis and is not an ADH problem. The polyuria is part of acute tubular necrosis and is not an osmotic diuresis.

 

REF:   Pg. 600

 

  1. A patient injured severely in a motor vehicle accident is hospitalized with acute kidney injury as well as multiple broken bones and lacerations. When family members ask what is meant by the term ‘prerenal,’ the nurse responds
a. “The doctors are not sure what caused your husband’s acute kidney injury, but they are working to help him recover.”
b. “Your husband’s kidney injury did not start in the kidney itself, but rather in the blood flow to the kidney.”
c. “Your husband’s kidney injury is only the beginning of the problems that are expected, so they are being vigilant.”
d. “Acute kidney injury is a new term for what people used to call acute renal failure.”

 

 

ANS:  B

The problem that triggers prerenal acute kidney injury occurs before the blood circulates to the kidney. Hypovolemia is a common cause of prerenal acute kidney injury. Providing the patient’s family with specific information is most effective. Telling the family that you don’t know what caused the injury does not alleviate anxiety in the family member. Speculating about the patient’s future without a clear prognosis causes anxiety in the patient. It is best to provide the family with specific information regarding the patient’s diagnosis and prognosis instead of offering general comments.

 

REF:   Pg. 594

 

MULTIPLE RESPONSE

 

  1. Signs of late chronic renal failure include (Select all that apply.)
a. high-serum potassium levels.
b. high-serum calcium.
c. high-serum phosphorous.
d. high–blood urea nitrogen.
e. anemia.

 

 

ANS:  A, C, D, E

In late chronic renal failure high serum potassium and phosphorous levels are due to inability of the kidneys to excrete these elements. Blood urea also increases due to inability of the kidneys to excrete urea. Anemia occurs due to loss of erythropoietin secretion. The serum calcium is low in chronic renal failure because of the high serum phosphorous.

 

REF:   Pgs. 602-603

 

  1. The diet for a patient with chronic kidney disease (CKD) should include (Select all that apply.)
a. high carbohydrates and fats.
b. low sodium and potassium.
c. high protein.
d. low phosphorous.
e. high calorie.

 

 

ANS:  A, D, E

Patients with CKD are often malnourished especially at later stages. Patients require high carbohydrates and fats to maintain nutritional status. Sodium must be limited due to fluid retention and potassium must be limited due to failure of kidneys to excrete potassium. Low phosphorous is necessary to prevent further hypocalcemia. High calories are needed to maintain energy needs. In general protein must be limited, as the kidneys cannot excrete urea, the end product of protein metabolism.

 

REF:   Pg. 605

 

  1. Acute tubular necrosis can occur from (Select all that apply.)
a. increased ammonia levels from liver failure.
b. contrast dyes used for radiologic studies.
c. ischemia due to hypovolemia.
d. antibiotics that are nephrotoxic.

 

 

ANS:  B, C, D

Radiocontrast media used for radiologic studies occasionally can be nephrotoxic, causing acute tubular necrosis. Ischemia due to hypovolemia is an important cause of acute tubular necrosis. Certain antibiotics, including aminoglycosides, are nephrotoxic and can be a direct cause of acute tubular necrosis. Liver failure with elevated ammonia levels causes toxicity to the central nervous system but does not cause acute tubular necrosis.

 

REF:   Pgs. 595-596

 

  1. When a patient misses two dialysis sessions numerous electrolyte imbalances resulted. The patient will likely demonstrate (Select all that apply.)
a. lethargy due to metabolic acidosis and increased BUN.
b. skeletal muscle weakness and possible cardiac dysrhythmias due to hyperkalemia.
c. positive Chvostek and Trousseau signs due to hypomagnesemia.
d. weight gain of several pounds since her last dialysis session due to hypernatremia.
e. deep rapid breathing due to compensatory mechanism for metabolic acidosis.

 

 

ANS:  A, B, E

A person who needs dialysis and has missed two sessions will have metabolic acidosis and increased BUN, which cause lethargy; deep rapid breathing, which is a compensatory mechanism for metabolic acidosis; and hyperkalemia, which causes skeletal muscle weakness and cardiac dysrhythmias. Hypomagnesemia will not occur in this situation. Although the individual will gain several pounds of fluid without dialysis, the weight gain is due to extracellular fluid volume excess rather than to hypernatremia.

 

REF:   Pg. 603

 

COMPLETION

 

  1. The best intervention for acute kidney injury (AKI) is ________.

 

ANS:

prevention

The best intervention for acute kidney injury is prevention.

 

REF:   Pg. 604

 

  1. ________ is both a cause of chronic kidney disease and a result of chronic kidney disease.

 

ANS:

Hypertension

Hypertension is both a cause of chronic kidney disease and a result of chronic kidney disease.

 

REF:   Pg. 601

 

 

 

Chapter 42: Alterations in Metabolism and Nutrition

Test Bank

 

MULTIPLE CHOICE

 

  1. When released into the circulation, fatty acids are bound to ________ for assimilation into tissue.
a. serum IgG
b. total protein
c. albumin
d. creatinine

 

 

ANS:  C

When released into circulation, the fatty acids, bound to albumin, are quickly assimilated into tissue. Fatty acids are not bound to serum IgG for release into the tissue. Total protein is not bound to fatty acids for release into the circulation. Creatinine does not play a role in the release of fatty acids into tissue.

 

REF:   Pg. 845

 

  1. The metabolic response to physiologic stress is characterized by
a. loss of somatic protein.
b. preservation of visceral protein.
c. body weight less than 80% of ideal.
d. stress-induced protein catabolism.

 

 

ANS:  D

During times of disease, stress, fever, or starvation or during the release of certain hormones such as thyroid hormone and cortisol, catabolism dominates the body’s metabolic processes. Loss of somatic protein does not occur in response to physiologic stress. Tissue wasting associated with catabolism may lead to cellular injury. Body weight less than 80% of ideal is not characteristic of a metabolic response to stress.

 

REF:   Pg. 841

 

  1. Starvation is associated with
a. loss of visceral protein.
b. low serum albumin levels.
c. loss of somatic fat and protein.
d. generalized edema.

 

 

ANS:  C

With physiologic stress, conservation of lean body mass does not occur. The metabolic rate increases rather than decreases, and a high sustained rate of catabolism (breakdown of protein to meet energy needs) results. Adipose is not well used for energy. Starvation is associated with protein being used as an energy source. Low serum albumin levels are not associated with starvation. Retention of fluid and sodium occurs in the immediate phase of stress on the body.

 

REF:   Pg. 848

 

  1. What patient is most at risk for severe protein malnutrition?
a. A postsurgical patient who has been NPO for 3 days
b. A postburn patient who has a deep partial-thickness burn
c. A febrile patient who has had a temperature of 102.6° F for 3 days
d. An immobile patient who has been in skeletal traction for 1 week

 

 

ANS:  B

A burn is an extreme stressor that results in significant hypermetabolism. The energy needs of a burn patient increase 50% to 100% from the basal metabolic requirement. Burn wounds increase the negative nitrogen balance and burns leak soluble proteins from the wound. The postoperative energy requirement can increase from 10% to 35% above BMR. A combination of increased need with decreased intake can have a major impact on wound healing. The metabolic response to fever is both anabolic and catabolic, which greatly increases nutrient requirements. An effect of immobilization is nitrogen loss as tissue mass is decreased from diffuse atrophy.

 

REF:   Pg. 854

 

  1. Which hormone promotes protein synthesis?
a. Glucagon
b. Epinephrine
c. Cortisol
d. Testosterone

 

 

ANS:  D

Hormones that also promote protein synthesis include growth hormone, especially during growth spurts; testosterone in specific reproductive organs during puberty; and thyroid hormone indirectly, by increasing the metabolic rate. Glucagon stimulates protein breakdown with amino acids. Epinephrine is not associated with protein synthesis. Cortisol increases protein catabolism.

 

REF:   Pg. 846

 

  1. Which condition is associated with an increase in basal metabolic rate?
a. Aging
b. Fever
c. Obesity
d. Starvation

 

 

ANS:  B

Fever is a factor in increasing basal metabolic rate. The aging process decreases the metabolic rate. Calorie-restricted diets and reduced muscle-mass decrease basal metabolic rate. Starvation is associated with a reduction in the basal metabolic rate.

 

REF:   Pg. 853

 

  1. The process of metabolizing proteins to provide energy is called
a. glycogenolysis.
b. glycolysis.
c. gluconeogenesis.
d. proteolysis.

 

 

ANS:  C

Gluconeogenesis is the process by which glucose is formed from non-carbohydrate sources. Glycogenolysis is the breakdown of glycogen to form glucose. Glycolysis is the metabolic sequence that converts glucose to pyruvate. The process of metabolizing proteins to provide energy is not known as proteolysis.

 

REF:   Pgs. 843-844

 

  1. Acute physiologic stress is associated with
a. preferential use of glycogen.
b. catabolism of body proteins.
c. decreased basal metabolic rate.
d. conservation of body energy stores.

 

 

ANS:  B

With physiologic stress, two phases of catabolism occur. The immediate phase of catabolism is characterized by increased sympathetic nervous system stimulation with release of glucagon, glucocorticoids, and catecholamines. The adaptive phase occurs if the sympathetic nervous system response can selectively keep up with the stressors present. An increased production of insulin occurs with immediate physiologic stress. Acute physiologic stress is associated with an increase in basal metabolic rate. In catabolism, an energy deficit is created and alternative mechanisms of glucose production are required.

 

REF:   Pgs. 848-849

 

  1. A patient with a fever of 3° F above normal would be expected to have increased energy expenditure of
a. 3%.
b. 15%.
c. 21%.
d. 50%.

 

 

ANS:  C

Fever increases metabolic needs by 7% for each 1° F increase (13% for each 1° C increase). Energy expenditure is increased by 15% to 30% in trauma patients. The energy needs of a burn patient increase by 50% to 100%.

 

REF:   Pg. 853

 

  1. The main source of energy for the body comes from
a. proteins.
b. fats.
c. carbohydrates.
d. water.

 

 

ANS:  C

Carbohydrates are the main source of energy for the body. Proteins are broken down into amino acids. Fats are the most concentrated form of energy. Water is not the main source of energy for the body.

 

REF:   Pg. 843

 

  1. During times of fasting, the body uses ________ as a source of energy.
a. protein
b. fat
c. carbohydrates
d. glucagon

 

 

ANS:  B

During times of fasting, the body reverts to the breakdown and use of fats as its energy source. Protein is not used as a source of energy during fasting. Carbohydrates are not an energy source during fasting. The body does not use glucagon as a source of energy during fasting.

 

REF:   Pg. 845

 

  1. A body mass index of 25.5 is considered to be
a. morbidly obese.
b. normal.
c. overweight.
d. obese.

 

 

ANS:  C

Overweight is defined with a BMI of 25 to 29.9 kg/m2. Morbid obesity is a BMI of 40 kg/m2 or more. Normal body weight is BMI less than 25. Obesity is defined as a BMI greater than 30 kg/m2.

 

REF:   Pg. 846

 

  1. Malnutrition affecting the respiratory system can lead to
a. increased respiratory function.
b. increased surfactant release.
c. increased vital capacity.
d. respiratory failure.

 

 

ANS:  D

If vital capacity and muscle strength fall below 50% of predicted norms, respiratory failure is probable owing to retention of carbon dioxide. Respiratory muscle function is decreased as a result of protein loss. In malnutrition, surfactant stability is decreased. Malnourished patients often suffer from decreased vital capacity.

 

REF:   Pg. 851

 

  1. The postoperative energy requirement can increase ____ above BMR.
a. 7%.
b. 10% to 35%.
c. 15% to 30%.
d. 50%.

 

 

ANS:  B

The postoperative energy requirement can increase from 10% to 35% above basal metabolic rate. Fever increases metabolic needs by 7% for each increase of 1 degree. Energy expenditure is increased by 15% to 30% in trauma patients. The energy needs of a burn patient increase 50% to 100% from basal metabolic requirement.

 

REF:   Pg. 853

 

  1. The nutritional effects of cancer can be severe and result in
a. malnutrition.
b. anorexia.
c. cachexia.
d. catabolism.

 

 

ANS:  C

The nutritional effects of cancer can be severe and result in what is commonly termed cancer cachexia. The cause of cachexia is inadequate nutritional intake relative to energy requirements and increased anaerobic glycolysis. The nutritional deficits associated with cancer are not known as malnutrition. A major cause of cachexia is anorexia associated with the malignancy and with the treatment. Catabolism is the degradative phase of metabolism and is not caused by cancer.

 

REF:   Pg. 854

 

  1. An immobile patient should be treated with an extra ________ grams of protein daily.
a. 2 to 4
b. 4 to 6
c. 7 to 9
d. 10 to 15

 

 

ANS:  D

An effect of immobilization is nitrogen loss as tissue mass is decreased from disuse atrophy. This loss can total 2 to 3 g/kg per day and require up to 10 to 15 g of protein to replenish the daily loss. Immobility is associated with muscle atrophy and bone demineralization. Patients should be given an extra 10 to 15 grams of protein. Patients require up to 10 to 15 grams of protein to replenish daily loss. Ten to fifteen grams of protein are required daily in the immobile patient.

 

REF:   Pg. 854

 

  1. The metabolic response to fever is
a. anabolic.
b. catabolic.
c. both anabolic and catabolic.
d. related to gluconeogenesis.

 

 

ANS:  C

The metabolic response to fever is both anabolic and catabolic, which greatly increases nutrient requirements. The metabolic response to fever is both anabolic and catabolic, which greatly increases nutrient requirements. The metabolic response to fever is not catabolic only. Gluconeogenesis is increased in trauma patients.

 

REF:   Pg. 853

 

MULTIPLE RESPONSE

 

  1. Which patient is at highest risk for severe negative nitrogen balance? (Select all that apply.)
a. Postsurgical patient
b. Postburn patient
c. Posttrauma patient
d. Postsepsis patient

 

 

ANS:  B, C

Negative nitrogen balance is increased by catabolism and by the use of amino acids to form stress proteins. In addition, burn wounds directly contribute to protein loss, because soluble proteins leak from the wound and proteolysis is activated. Because trauma is a sudden stress, catabolism is much greater than anabolism because the body has not had enough time to replenish the proteins lost. This dominance of catabolism results in excessive negative nitrogen balance and significant loss of skeletal muscle. Nitrogen loss through wounds can be large and create a greater need for increased protein intake. Catabolism is a protective mechanism that provides needed substrates for activation of the immune response to infection, such as in the postsepsis patient.

 

REF:   Pg. 854

 

  1. Which are effects of malnutrition on the cardiovascular system? (Select all that apply.)
a. Primary cardiomyopathy
b. Increased oxygen demand
c. Increased cardiac output
d. Atrophy of cardiac muscle
e. Decreased cardiac output

 

 

ANS:  A, D, E

Malnutrition can cause deficiencies in thiamine and selenium which lead to primary cardiomyopathy. A decrease in heart size and atrophy of cardiac muscle could result in decreased cardiac output. Protein-energy malnutrition as seen in an acutely ill patient can result in visceral protein loss and decreases in myocardial function. A decrease in heart size and atrophy of cardiac muscle could result in decreased cardiac output. In compensation, the cardiac muscle fibers lengthen in response to increased workload. This compensation, together with a decreased oxygen demand secondary to decreased intake, curtails the development of cardiac failure. Decreased cardiac output is the result of cardiac muscle atrophy in malnutrition.

 

REF:   Pg. 850

 

 

Chapter 54: Burn Injuries

Test Bank

 

MULTIPLE CHOICE

 

  1. It is true that second-degree, superficial partial-thickness burns
a. are less painful than third-degree burns.
b. involve only the epidermis.
c. usually heal in 7 to 21 days.
d. are rarely associated with scar formation.

 

 

ANS:  C

Second-degree, superficial partial-thickness burns usually heal in 7 to 21 days. Second-degree burns are more painful than third-degree burns, involve damage to the dermis, and can be associated with scar formation.

 

REF:   Pg. 1093

 

  1. The first priority when rescuing a burned individual is
a. establishing a patent airway.
b. removing his or her clothing.
c. eliminating the source of the burn.
d. covering the wounds with wet sheets.

 

 

ANS:  C

The first priority in rescuing a burned individual is eliminating the source of the burn. The next priority is to establish a patent airway. Removing the clothing is not recommended; however, dry, clean sheets or dressings should be placed over the burns. Covering the wound is not advised, as this may cause hypothermia.

 

REF:   Pg. 1095

 

  1. Burn shock is the direct result of
a. hypovolemia.
b. cardiac depression.
c. infection.
d. increased capillary permeability.

 

 

ANS:  D

Burn shock results from systemic capillary permeability with leakage of fluids throughout all tissues; the result is massive edema. Hypovolemia is not the direct cause of burn shock. Burn shock does not result from cardiac depression or infection.

 

REF:   Pgs. 1096-1097

 

  1. Electrical injury may cause extensive damage to low-resistance tissues, particularly
a. bone and muscle.
b. nerves and blood vessels.
c. epidermis.
d. dermis and subcutaneous tissue.

 

 

ANS:  B

Electrical injury may cause extensive damage to low-resistance tissues, particularly nerves and blood vessels. Bone and muscle, and dermis and subcutaneous tissue, are not low-resistance tissues. Skin is a high-resistance tissue.

 

REF:   Pg. 1105

 

  1. The time between the end of burn shock and closure of the burn to less than 20% of total body surface area is called the ________ phase.
a. postshock
b. rehabilitation
c. critical
d. emergent

 

 

ANS:  D

The time between the end of burn shock and closure of the burn to less than 20% of total body surface area is called the emergent phase. Postshock is not a phase of burn wound healing. The rehabilitation phase begins when the burn size is reduced to less than 20% TBSA and the patient is able to assume self-care. There is not a critical phase of burn wound healing.

 

REF:   Pg. 1100

 

  1. The primary aim of burn wound management is to prevent
a. trauma to burned tissue.
b. microbial colonization of the wound.
c. the wound from drying out.
d. premature wound closure.

 

 

ANS:  B

The primary aim of burn wound management is to prevent microbial colonization of the wound. A goal of wound management is to minimize further destruction of viable tissue. It is not possible to prevent the trauma after injury, since it has already occurred. Keeping the wound dry is not a primary aim of burn wound management. Preventing premature wound closure is not a goal of burn wound management.

 

REF:   Pg. 1100

 

  1. The third element essential to survival after major burn injury is
a. excision of the burn followed by skin grafting.
b. frequent wound debridement to encourage wound healing.
c. hyperbaric oxygen therapy.
d. continuous topical antibiotic therapy.

 

 

ANS:  A

The third element essential to survival after major burn injury is excision of the burn followed by skin grafting. Frequent wound debridement, hyperbaric oxygen therapy, and continuous topical antibiotic therapy are not the third element essential to survival after major burn injury.

 

REF:   Pg. 1100

 

  1. The most common cause of burn injuries in children is
a. house fires.
b. cigarette burns.
c. scalding with hot water.
d. contact with chemical agents.

 

 

ANS:  C

The most common cause of burn injuries in children is scalding with hot water. House fires, cigarette burns, and contact with chemical agents are not the most common causes of burn injuries in children.

 

REF:   Pg. 1091

 

  1. The goal of nutritional support of the burned individual is to
a. limit the glucose available to infectious organisms.
b. create a positive nitrogen balance.
c. protect the kidney from excessive protein intake.
d. avoid hyperlipidemia.

 

 

ANS:  B

The goal of nutritional support of the burned individual is to create a positive nitrogen balance. Limiting the glucose available to infectious organisms, protecting the kidney from excessive protein intake, and avoiding hyperlipidemia are not the goals of nutritional support of the burn patient.

 

REF:   Pg. 1100

 

  1. A necessary intervention when managing burns associated with automobile airbag injury include
a. irrigation with water.
b. application of steroid cream.
c. IV infusion of antibiotics.
d. debridement of skin.

 

 

ANS:  A

Management of burns associated with automobile airbag injury is irrigation with copious amounts of water. Application of steroid cream, IV antibiotics, and debridement are not necessary for airbag burns.

 

REF:   Pg. 1107

 

  1. The majority of electrical burns in children are caused by
a. playing with electrical outlets.
b. playing with defective electrical cords.
c. biting on extension cords.
d. putting fingers in electrical sockets.

 

 

ANS:  C

The majority of electrical burns in children are caused by biting on extension cords. Playing with electrical outlets, playing with defective electrical cords, and putting fingers in electrical sockets are not the causes of the majority of electrical burns in children.

 

REF:   Pg. 1105

 

  1. It is true that covering a burn with cool wet sheets
a. promotes comfort.
b. facilitates healing.
c. prevents fluid loss.
d. promotes hypothermia.

 

 

ANS:  D

Cool wet sheets quickly become cold wet sheets that promote hypothermia as the skin’s ability to regulate body temperature is lost. Although cool wet sheets may initially promote comfort, they may be the cause of hypothermia the longer the sheets remain in contact with the burned skin. Cool wet sheets do not facilitate burn healing or prevent fluid loss.

 

REF:   Pg. 1096

 

  1. The immediate management of a thermal burn victim once the fire has been extinguished is to
a. cover with blankets to prevent shock.
b. monitor for signs of respiratory impairment.
c. apply lubricant to the burn area.
d. start an IV line.

 

 

ANS:  B

Excessive heat to the respiratory tract could result in obstruction; therefore, respiratory status is the main priority. Do not cover with blankets, as this will prevent underlying heat from escaping. Do not apply anything but water to a burn. An IV line may be started after management of respiratory status.

 

REF:   Pg. 1096