PATH 370: Ch. 10, 11, 13, 14, 15

A 5-year-old patient's parents report loss of appetite and fatigue in their child. The parents also state that the child refuses to walk as a result of pain. The child's most likely diagnosis is: ALL (acute lymphoid leukemia) CLL (chronic lymphoid leukemia) AML (acute myeloid leukemia) CML (chronic myeloid leukemia)

ALL (acute lymphoid leukemia) ALL is primarily a disorder of children with an abrupt onset of bone pain, bruising, fever, and infection. Children may refuse to walk and experience fatigue, loss of appetite, and abdominal pain. In CML, AML, and CLL, children do not complain of pain with walking. Additionally, chronic leukemia is most commonly found in adults.

Which type of leukemia primarily affects children? ALL (acute lymphoid leukemia) CLL (chronic lymphoid leukemia) AML (acute myeloid leukemia) CML (chronic myeloid leukemia)

ALL (acute lymphoid leukemia) ALL is primarily a disorder of children. The peak incidence occurs between the ages of 3 and 7 years. The average age of patients with CLL is about 65 to 70 years. The median age of presentation of AML is 64 years. Average onset of CML is between 40 and 50 years.

In general, the best prognosis for long-term disease-free survival occurs with: ALL (acute lymphoid leukemia). CLL (chronic lymphoid leukemia). AML (acute myeloid leukemia). CML (chronic myeloid leukemia

ALL (acute lymphoid leukemia). ALL is highly curable in the pediatric population with an 85% survival rate in children. The average age of patients with CLL is 65 to 70 years. Median survival rate is less than 8 years. Patients younger than age 60 have a 4-year survival rate of 30% to 40% in AML. CML does not respond well to chemotherapy and carries a long-term survival rate of 50% to 60%.

Which clinical finding is indicative of compartment syndrome? Peripheral edema Absent peripheral pulses Redness and swelling Atrophy of distal tissues

Absent peripheral pulses Compartment syndrome creates an effective absence of arterial circulation to an extremity. Swelling within a cast or tight dressing may contribute to the development of compartment syndrome. Compartment syndrome creates pallor in the affected extremity. Acute arterial occlusion is an emergency, and could result in profound ischemia in the involved limb.

A diagnostic laboratory finding in myeloma is: Bence Jones proteins in the urine. decreased platelet count. increased IgM antibody titer. elevated blood glucose levels.

Bence Jones proteins in the urine. Bence Jones protein in the urine is a common clinical manifestation of plasma cell myeloma. It is also known to accumulate in the kidneys and cause kidney damage. Decreased platelet count is not usually a finding in plasma cell myeloma. IgM is not a factor in plasma cell myeloma. Glucose levels are not directly impacted in plasma cell myeloma.

Which form of leukemia demonstrates the presence of the Philadelphia chromosome? ALL (acute lymphoid leukemia) CLL (chronic lymphoid leukemia) AML (acute myeloid leukemia) CML (chronic myeloid leukemia)

CML (chronic myeloid leukemia) The majority of CML cases are characterized by malignant granulocytes that carry the Philadelphia chromosome. ALL is manifested by the malignant transformation of B cells and some T cells. CLL is associated with T-cell transformation. The Philadelphia chromosome is not seen in CLL. AML is associated with a transformation of a myeloid stem cell.

What is the correct definition of complete remission (CR) of leukemia? CR is the absence of leukemic cells in the blood. CR is less than 5% blasts in marrow and normal CBC values. CR is absence of leukemic cells regardless of CBC values. CR is less than 5% leukemic cells in the blood

CR is less than 5% blasts in marrow and normal CBC values. Complete remission (CR) is a return to normal hematopoiesis. The bone marrow must have less than 5% blasts and must be maintained for at least 4 weeks in order to achieve CR. CR is an absence of leukemic cells, in addition to normal red cell, platelet, and neutrophil counts. CR must include normal hematopoiesis as well as an absence of leukemic cells. CR must include less than 5% blasts in marrow in addition to no detectible neoplastic cells.

The hypersensitivity reaction that does not involve antibody production is type: I. II. III. IV.

IV. Type IV hypersensitivity reactions do not involve antibody production. The principal mediators are lymphocytes, including T helper cells (Th) that mediate the reaction by releasing lymphokines (cytokines) and/or antigen-sensitized cytotoxic T cells (Tc) that can directly kill cells. The other types involve antibody production. Type I involves IgE; type II involves IgM or IgG; type III involves IgG.

The principle Ig mediator of type I hypersensitivity reactions is: IgA. IgG. IgM. IgE.

IgE. Immunoglobulin E (IgE) is the principal antibody mediating type I hypersensitivity reactions. IgA is not the primary Ig mediator of type I hypersensitivity reactions. IgG is involved in type II hypersensitivity reactions. IgM is involved in type II hypersensitivity reactions.

Which is not considered to be a risk factor for thrombus formation? Thrombocytopenia Vascular trauma Stasis of blood flow Circulatory shock

Thrombocytopenia Thrombocytopenia is not involved in the development of thrombi. Thrombi may form in the chambers of the heart following a myocardial infarction or damage to the heart valves. Venous stasis can be a risk factor for thrombus formation as a result of the alteration in blood flow to the extremity. Circulatory shock states occur when individual organs may not obtain sufficient blood flow to meet metabolic needs.

Which is not a manifestation of acute arterial obstruction? Pain Purpura Pallor Pulselessness

Purpura Purpura is purple-colored spots on the skin, which are not a manifestation of acute arterial obstruction. Pain is intense, continuous, and unrelated to activity in an acute arterial obstruction. In an acute arterial obstruction, pallor is seen in the involved extremity. Pulselessness may occur in the affected extremity of an acute arterial occlusion, although often a weak pulse may be noted by Doppler.

What is the effect on resistance if the radius of a vessel is halved? Resistance doubles. Resistance decreases by a factor of 16. Resistance decreases by half. Resistance increases by a factor of 16.

Resistance increases by a factor of 16. Doubling the radius of a vessel on the flow of blood results in a 16 times greater blood flow that increases the vessel's resistance by a factor of 16. The resistance is not doubled, it is increased by a factor of 16. The resistance is not decreased when the radius of a vessel is halved.

Which disorder is associated with a type III hypersensitivity mechanism of injury? Systemic lupus erythematosus Graves disease Erythroblastosis fetalis Seasonal allergic rhinitis

Systemic lupus erythematosus Systemic lupus erythematosus is a type III hypersensitivity disorder. Type III hypersensitivity is characterized by antigen-antibody complex deposition into tissues, with consequent activation of complement and a subsequent self-sustaining inflammatory reaction. Graves disease and erythroblastosis fetalis are type II hypersensitivity reactions. Seasonal allergic rhinitis is a type I hypersensitivity reaction.

The only known curative treatment for CML is allogeneic bone marrow transplantation from a suitable donor. True False

True Allogeneic bone marrow transplantation from a suitable donor is the only curative treatment for CML.

Two of the most serious oncology emergencies associated with non-Hodgkin lymphoma are obstruction of the superior vena cava and compression of the spinal cord. True False

True Compression of the spinal cord is one of the two most serious oncology emergencies associated with non-Hodgkin lymphoma.

Hemophilia B is also known as Christmas disease. True False

True Hemophilia B is also known as Christmas disease.

The anemia resulting from a deficiency of either vitamin B12 (cobalamin) or folate is caused by a disruption in DNA synthesis of the blast cells in the bone marrow that produces very large abnormal bone marrow cells called megaloblasts. True False

True Megaloblasts are large abnormal bone marrow cells.

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

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

Which vessel normally demonstrates the most rapid blood flow? An arteriole A capillary A venule The vena cava

The vena cava The vena cava has the most rapid rate of flow. Arterioles don't offer the most rapid blood flow. Capillaries are composed of a single thickness of endothelial cells attached to a protein network called the basement membrane and don't offer the most rapid blood flow. A venule begins where the arteriole ends and doesn't offer the most rapid blood flow.

While in the hospital for management of acute lymphoid leukemia (ALL), a patient develops severe thrombocytopenia. The most appropriate action for this condition is: anticoagulant therapy. chemotherapy. activity restriction. isolation.

activity restriction. Thrombocytopenia can produce a life-threatening hemorrhage. Patients with this condition should be protected from trauma and placed on activity restriction to reduce the risk of bleeding. Anticoagulant therapy in a patient with thrombocytopenia could actually cause the patient more bleeding. Thrombocytopenia is a complication of leukemia and chemotherapy. Chemotherapy is not an appropriate treatment option for thrombocytopenia. Isolation is not effective in managing the risk of hemorrhage.

When systemic vascular resistance is decreased, blood flow: increases. decreases. stays the same. moves to the extremities.

decreases. When SVR is pathologically decreased, the blood is spread over a larger area and blood flow slows dramatically. Individual organs, such as the kidney and brain, may not obtain sufficient blood flow to meet metabolic needs. Blood flow decreases in response to decreases in vascular resistance. When SVR is pathologically decreased, the blood is spread over a larger area and blood flow slows dramatically. Individual organs, such as the kidney and brain, may not obtain sufficient blood flow to meet metabolic needs. Blood flow is not diverted to the extremities when systemic vascular resistance is decreased. However, the vital organs may not have sufficient blood flow to maintain metabolic needs.

Severe combined immunodeficiency (SCID) syndrome is an example of a(n): deficient immune response. excessive immune response. primary acquired immunodeficiency. hypersensitivity reaction.

deficient immune response. SCID syndrome is an example of a deficient immune response in which the immune response is ineffective because of disease-causing genotypes or secondary/acquired dysfunction. An excessive immune response includes disorders in which the immune system is overfunctioning or hyperfunctioning. HIV/AIDS is an example of a primary acquired immunodeficiency disorder. Hypersensitivity reactions are an excessive immune response.

Patients with immunodeficiency disorders are usually first identified because they: run high fevers. have unusually high WBC counts. develop brain infections. develop recurrent infections.

develop recurrent infections. The first clinical indicators of immunodeficiency disorders are the signs and symptoms of infection, and the disorders are often first suspected when an individual has severe recurrent, unusual, or unmanageable infections. High fevers can occur in patients who have an intact immune system. Because of the immune deficiency, patients with immunodeficiency disorders may not demonstrate expected WBC counts with infection. Infections in patients with immunodeficiency disorders can occur anywhere in the body.

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

disseminated intravascular coagulation (DIC). 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.

A laboratory test finding helpful in confirming the diagnosis of iron-deficiency anemia is: elevated total iron-binding capacity. elevated MCHC and MCV. elevated total and indirect bilirubin. positive direct or indirect Coombs test.

elevated total iron-binding capacity. In iron-deficiency anemia, the total iron-binding capacity is elevated. The red cell indices of MCHC and MCV are decreased in iron-deficiency anemia. Total and indirect bilirubin levels are not utilized in diagnosing iron-deficiency anemia. Coombs testing is not utilized in obtaining a diagnosis of iron-deficiency anemia.

The most effective therapy for anemia associated with kidney failure is: iron administration. high-protein diet. erythropoietin administration. vitamin B12 and folate administration.

erythropoietin administration. Therapy in anemia of chronic renal failure consists of dialysis and erythropoietin administration. The use of erythropoietin stimulating agents is to increase hemoglobin values to ensure adequate oxygen-carrying capacity. Iron, folate, and vitamin B12 replacement are initiated if necessary. Iron administration is utilized in iron-deficiency anemia. A high-protein diet is not the treatment of choice in the patient with renal failure, and a high-protein diet may be contraindicated. Vitamin B12 and folate are prone to nutritional anemias and receive replacement to adequate levels if necessary. However, dialysis and erythropoietin are more effective.

The prothrombin time (PT) and INR (international normalized ratio) measure the integrity of: platelet function. extrinsic pathway. intrinsic pathway. fibrinolysis.

extrinsic pathway. 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.

Treatment for hemophilia A includes: heparin administration. factor IX replacement. factor VIII replacement. platelet transfusion.

factor VIII replacement. 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.

The conversion of plasminogen to plasmin results in: clot retraction. fibrinolysis. platelet aggregation. activation of thrombin.

fibrinolysis. 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.

Patients who experience anemic episodes when exposed to certain drugs most likely have: thalassemia. spherocytosis. sickle cell anemia. glucose-6-phosphate dehydrogenase deficiency.

glucose-6-phosphate dehydrogenase deficiency. Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a RBC intracellular defect. Usually this anemia is first recognized during or after an infectious illness or exposure to certain drugs. Thalassemia does not carry a manifestation associated with pharmacologic agents. Spherocytosis is a hereditary anemia with manifestations of jaundice. Episodes of sickle cell anemia are associated with recurrent painful episodes related to organ dysfunction.

The effects of histamine release include: vasoconstriction. bronchodilation. increased vascular permeability. decreased gut permeability.

increased vascular permeability. Histamine release leads to increased vascular permeability, which fosters fluid movement out of capillaries and into tissues leading to the edema common in type I hypersensitivity. Histamine leads to bronchoconstriction, increased gut permeability, and vasodilation (not vasoconstriction).

Venous obstruction leads to edema because it ________ pressure. increases capillary oncotic increases arterial blood decreases tissue increases capillary hydrostatic

increases capillary hydrostatic Increased fluid accumulation in the interstitial space also occurs when the lymphatic flow is impaired or when capillaries become more permeable and "leak" fluid. These pressure gradients lead to edema. Interstitial fluid colloid osmotic pressure increases play a role in edema. Arterial blood pressure does not lead to edema. Decreased tissue pressure does not lead to edema in venous obstruction.

The major cause of death from leukemic disease is: infection. malnutrition. hypovolemic shock. kidney failure.

infection. Infection is the most common cause of death in the immunocompromised patient, because it can become a life-threatening sepsis. Malnutrition can be a side effect of the disease process or the treatment. Hypovolemic shock is not generally associated with leukemic disease. There is no direct connection between kidney failure and death in leukemia, although kidney failure may occur as a result of treatment.

A deficiency of von Willebrand factor impairs: activation of the coagulation cascade. platelet aggregation. platelet adhesion to injured tissue. platelet production.

platelet adhesion to injured tissue. 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.

The megakaryocyte is a precursor to: factor IX. white blood cells. red blood cells. platelets.

platelets. 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.

The goal of long term heparin for the management of a deep vein thrombosis is to: relieve edema. prevent clot dislodgement. dissolve the thrombus. prevent further clot formation.

prevent further clot formation. Anticoagulation is utilized in deep vein thrombosis to prevent further clot formation. Heparin does not play a role in edema. Prevention of clot dislodgement is not the goal of therapy with the use of heparin. Heparin is not utilized to dissolve a thrombus.

A serious complication of deep vein thrombosis is: stroke. hypertensive crisis. extremity necrosis. pulmonary embolus.

pulmonary embolus. Deep vein thrombosis is treated aggressively, as it is the most frequent source of pulmonary embolus. Deep vein thrombosis is not the cause of a stroke. Hypertensive crisis is unrelated to deep vein thrombosis. Extremity necrosis could result from prolonged arterial occlusion.

Transfusion reactions involve RBC destruction caused by: donor antigens. recipient antibodies. donor T cells. recipient T cells.

recipient antibodies. The recipient of the blood transfusion has antibodies to the donor's red blood cell (RBC) antigens; the antibodies destroy large numbers of RBC. Donor antigens, donor T, and recipient T cells do not cause transfusion reactions.

The movement of blood through the vascular system is opposed by the force of: viscosity. the vessel length. the vessel radius. resistance.

resistance. The movement of blood through the vascular system is opposed by the force of resistance. Three determinants of resistance are vessel length, vessel radius, and blood viscosity. Viscosity is the thickness of fluid and has an effect on resistance. The length of the vessel does have an effect on the resistance. Vessel radius has an effect on resistance.

Burkitt lymphoma is most closely associated with: Epstein-Barr virus. radiation exposure. immunodeficiency syndromes. history of cigarette smoking.

Epstein-Barr virus. Epstein-Barr virus has been implicated in the development of Burkitt lymphoma. Radiation exposure is a factor in leukemia and lymphoma because of radiation damage. Immunodeficiency syndrome has not been found to be associated with Burkitt lymphoma. Carcinogens found in cigarette smoking are believed to predispose the emergence of malignancies, but are not directly associated with lymphoma.

Seasonal allergic rhinitis is most involved in type II hypersensitivity reactions. True False

False Seasonal allergic rhinitis is most involved in type I hypersensitivity reactions.

Vaccination for pneumococcal pneumonia should be performed before 1 year of age in patients with sickle cell anemia. True False

False Vaccination for pneumococcal pneumonia should be performed before 2 years of age in patients with sickle cell anemia and booster vaccinations given 3 to 5 years later.

Which disorder is considered a primary immunodeficiency disease? HIV/AIDS Malnutrition immunodeficiency Cancer immunodeficiency Radiation immunodeficiency

HIV/AIDS HIV/AIDS is a primary immunodeficiency disease involving destruction of T helper cells. Malnutrition immunodeficiency is a secondary immunodeficiency disorder and leads to T-cell destruction and dysfunction. Cancer immunodeficiency is a secondary immunodeficiency disorder caused by the destruction of rapidly proliferating cells from chemotherapeutic agents. Radiation immunodeficiency is a secondary immunodeficiency disorder caused by the destruction of rapidly proliferating cells from the effects of radiation.

Certain autoimmune diseases are associated with the presence of specific proteins on a person's cells. These proteins are called ________ proteins. complement antibody receptor HLA or MHC TCR or BCR

HLA or MHC Human major histocompatibility complex (MHC) genes located on chromosome 6p21 (also called human leukocyte antigen (HLA) genes) are frequently associated with certain autoimmune disorders. Complement, antibody receptors, and TCR or BCR are not factors in development of autoimmune disease.

Which condition is associated with an elevated reticulocyte count? Renal disease Aplastic anemia Hypertension Hemolytic anemia

Hemolytic anemia Hemolytic anemia is associated with an increased number of circulating reticulocytes or reticulocytosis. Anemia of chronic renal failure is not associated with reticulocytosis. Rather, it occurs from failure of the renal endocrine function. Aplastic anemia is a stem cell disorder that is characterized by pancytopenia, a decrease in red cells, white cells, and platelets. Hypertension is not related to reticulocytosis.

A child with a history of recent strep throat infection develops glomerulonephritis. This is most likely a type _____ hypersensitivity reaction. I II III IV

III Immune complex glomerulonephritis (an inflammatory renal disorder) is an example of a type III hypersensitivity reaction. The circulating immune complex is then deposited in the glomerular capillary wall and mesangium. Glomerulonephritis secondary to strep throat is

The arterial oxygen content (CaO2) for a patient with PaO2 100 mm Hg, SaO2 95%, and hemoglobin 15 g/dL is _____ mL oxygen/dL. 19.4 1909.8 210 21.05

19.4 A hemoglobin level of 15 divided by 100 equals 0.15. Multiply by 1.34 mL and then multiply by saturation on 95%. The result is 19.1% oxyhemoglobin. Then add 0.3% volume dissolved in plasma to get the total content of oxygen/dL. The arterial blood oxygen content is the amount of oxygen carried in the arterial blood. 1909.8 is an incorrect answer if the formula is followed correctly. 210 is incorrect when the formula is applied correctly. 21.05 is an incorrect response if the formula is applied correctly.

Which condition enhances lymphatic flow? Increased tissue hydrostatic pressure Increased interstitial fluid colloid osmotic pressure Decreased capillary hydrostatic pressure Increased capillary oncotic pressure

Increased interstitial fluid colloid osmotic pressure Lymphatic flow is controlled by increasing interstitial fluid colloid osmotic pressure and by the stimulation of the contractile fibers (often called lymphatic pumps) as they are stretched. Increasing interstitial fluid colloid osmotic pressure enhances lymphatic flow. Lymphatic flow is not enhanced by decreased capillary hydrostatic pressure. Lymphatic flow is controlled by increases in osmotic pressure, not oncotic pressure.

What is necessary for red blood cell production? Phosphate Iron Magnesium Calcium

Iron Immature red blood cells produce hemoglobin, which is composed of two pairs of polypeptide chains, the globins. Each globin has an attached heme molecule that contains iron. Dietary iron is transported through the plasma on the RBC membrane. Phosphates are not a necessary component of red blood cell production. Magnesium is not a part of the production of red blood cells. Calcium is not involved in red blood cell production.

A low mean corpuscular hemoglobin concentration (MCHC) and mean corpuscular volume (MCV) are characteristic of which type of anemia? Vitamin B12 deficiency Folate deficiency Iron deficiency Erythropoietin deficiency

Iron deficiency Iron-deficiency anemia is characterized by a low hemoglobin concentration and low mean corpuscular volume. Vitamin B12 deficiency anemia is characterized by a high concentration of MCV and a normal level of MCHC. Folate deficiency anemia is characterized by a normal mean corpuscular hemoglobin concentration and a high mean corpuscular volume. Erythropoietin deficiency creates hypoxia from a low hemoglobin level.

Which characteristic is indicative of hemolytic anemia? Increased total iron-binding capacity Increased heart rate Hypovolemia Jaundice

Jaundice Jaundice is a classic clinical manifestation of hemolytic anemia. The total iron-binding capacity in hemolytic anemia is not increased. Hemolytic anemia is not generally associated with an increased heart rate unless there is aplastic crisis associated with infection. Hypovolemia is not an indication of hemolytic anemia.

Dysfunction of which organ would lead to clotting factor deficiency? Liver Kidney Spleen Pancreas

Liver 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.

Renal insufficiency is a common complication of which disease? Chronic myeloid leukemia (CML) Chronic lymphoid leukemia (CLL) Myeloma Hodgkin disease

Myeloma Renal insufficiency is seen in approximately 50% of patients with plasma cell myeloma, because of hyperproteinemia, Bence Jones protein, hypercalcemia, and hyperuricemia. Chronic myeloid leukemia is manifested by splenomegaly. Chronic lymphoid leukemia is a disease that affects lymphoid tissues and bone marrow. Malignancy along lymphatic pathways is more typical of Hodgkin disease.

Which group of clinical findings describes the typical presentation of ALL (acute lymphoid leukemia)? Pain in long bones, infection, fever, bruising Vertebral fracture, hypercalcemia, bone pain Elevated WBC count found on routine examination, asymptomatic Painless enlarged cervical lymph node, fever, weight loss

Pain in long bones, infection, fever, bruising The onset of symptoms of ALL is abrupt and may begin when a child refuses to walk or begins to exhibit loss of appetite, fatigue, or abdominal pain. Bruising, fever, and infection are also common early findings. Vertebral fractures, elevated calcium levels, and bone pain are more frequently associated with plasma cell myeloma. Asymptomatic onset is generally found with CLL and is often found by accident on a routine blood count. Enlarged cervical lymph nodes are seen more commonly in Hodgkin disease.

What laboratory finding is usually found in aplastic anemia? Leukocytosis Thrombocythemia Neutrophilia Pancytopenia

Pancytopenia Aplastic anemia is a stem cell disorder affecting the bone marrow mass. It is usually caused by toxic, radiant, or immunologic injury to the bone marrow stem cells, which causes a decrease in red cells, white cells, and platelets, or pancytopenia. Thrombocythemia causes an increased number of platelets and is not found in aplastic anemia. Leukocytosis indicates a higher white blood count and is not found in aplastic anemia. The presence of neutrophils in laboratory findings does not indicate a diagnosis of aplastic anemia.

A commonly ingested substance associated with prolongation of the bleeding time is: acetaminophen. tobacco. caffeine. aspirin.

aspirin. 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.

The Philadelphia chromosome is a balanced chromosome translocation that forms a new gene called: bcr-abl. Rb. p53. ARA-c.

bcr-abl. bcr-abl is the translocation of chromosomes 9 and 22, which are known as the Philadelphia chromosome. Rb is a retinoblastoma protein, which is not associated with the Philadelphia chromosome. p53 is a tumor suppressor not associated with the Philadelphia chromosome. ARA-c is a chemotherapeutic agent used to treat leukemia.

Most carbon dioxide is transported in the bloodstream as: carboxyhemoglobin. bicarbonate ion. dissolved carbon dioxide. carbonic acid.

bicarbonate ion. Approximately 90% of the CO2 in the arterial blood and 60% of the CO2 in the venous blood are transported as bicarbonate. Carbon dioxide is not transported as carboxyhemoglobin. Some of the remaining carbon dioxide binds with protein to form carbaminohemoglobin for CO2 transport, but dissolved carbon dioxide is not the primary means of bloodstream transportation. Carbonic acid is disassociated into hydrogen and bicarbonate ions for elimination by the lungs and kidneys.

Excessive red cell lysis can be detected by measuring the serum: hemoglobin. methemoglobin. bilirubin. erythropoietin.

bilirubin. Any condition causing increased red cell destruction increases the total load of bilirubin to be cleared, which leads to increased serum bilirubin levels and possible jaundice. Red cell destruction does not lead to changes in the hemoglobin level. Methemoglobin is formed when iron of the hemoglobin molecule is oxidized to the ferric state. Erythropoietin is secreted in response to hypoxia.

Velocity of blood flow is measured in: centimeters per second. millimeters per minute. yards per hour. kilometers per minute.

centimeters per second. Velocity of blood flow is measured in centimeters per second. Millimeters per minute is the not the measurement of the velocity of blood flow. Yards per hour is not a measurement of velocity. The velocity of blood flow is not measured in kilometers per minute.

A cause of thrombocytopenia includes: hypoxemia. reduced erythropoietin. chemotherapy. secondary polycythemia.

chemotherapy. Bone marrow suppression from chemotherapy, recent immunizations, and alcohol ingestion are common causes of platelet production. Underlying systemic diseases may be presently 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.

The final step in clot formation is: conversion of prothrombin to thrombin. platelet degranulation and adhesion. conversion of fibrinogen to fibrin. clot retraction.

clot retraction. 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.

Red blood cells differ from other cell types in the body, because they: contain cytoplasmic proteins. have no cytoplasmic organelles. have a longer life span. contain glycolytic enzymes.

have no cytoplasmic organelles. Red blood cells have no cytoplasmic organelles, nucleus, mitochondria, or ribosomes. Therefore, RBCs cannot synthesize protein or carry out oxidative reactions. Red blood cells are not capable of synthesizing protein because of their lack of organelles. Red blood cells live for 80 to 120 days in the circulation and then die and are replaced. Red blood cells do not contain glycolytic enzymes.

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: hemophilia. liver dysfunction. disseminated intravascular coagulation. thrombocytopenia.

hemophilia. 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.

An important mediator of a type I hypersensitivity reaction is: complement. antigen-antibody immune complexes. T cells. histamine.

histamine. Histamine mediates type I hypersensitivity reactions. Complement mediates type II hypersensitivity reactions. Antigen-antibody immune complexes mediate type III hypersensitivity reactions. T cells mediate type IV hypersensitivity reactions.

When a patient is struck in the eye by a baseball, the result is redness and swelling. This increase in blood flow to a localized area is called: autoregulation. edema. hyperemia. hypoxia.

hyperemia. Hyperemia is a local increase in blood flow. Autoregulation is the ability of blood vessels within organs to maintain a constant blood flow. Edema is the swelling that results from hyperemia. Hypoxia is an insufficient supply of oxygen.

Risk factors for atherosclerosis include: female gender. hyperlipidemia. high-protein diet. low-fiber diet.

hyperlipidemia. Hyperlipidemia is a modifiable risk factor associated with atherosclerosis. Men have a higher incidence of atherosclerosis earlier in life than women. A high-protein diet is not associated with atherosclerosis. Dietary fats do play a role as a modifiable risk factor. A low-fiber diet is not a risk factor for atherosclerosis.

Myasthenia gravis is a type II hypersensitivity disorder that involves: impaired muscle function. symptoms of hyperthyroidism. symptoms of arthritis or polyarthralgia. symptoms of glomerular disease.

impaired muscle function. Myasthenia gravis involves muscle weakness caused by loss of acetylcholine stimulation at the motor end-plate. Symptoms of hyperthyroidism occur in Graves disease. Symptoms of arthritis or polyarthralgia occur in systemic lupus erythematosus, a type II hypersensitivity disorder. Glomerular disease can occur in type III hypersensitivity disorders.

The patient is a 12-year-old boy diagnosed with acute lymphoid leukemia (ALL). As part of treatment, the patient must undergo several weeks of chemotherapy. The most serious complication of chemotherapy is: vomiting. anemia. alopecia. infection.

infection. Infection is the most troublesome complication of chemotherapy for the immunosuppressed patient, and infection is a major cause of death in a leukemic patient. Nausea and vomiting are common findings in the treatment phase. While anemia is a common complication of the disease and treatment, it is not as serious as immunosuppression. Alopecia is an unfortunate side effect of chemotherapy, but is not a life-threatening complication.

Disseminated intravascular coagulation may be treated with heparin therapy to: enhance fibrinolysis. inhibit clotting factor consumption. activate platelets. enhance liver synthesis of clotting factors.

inhibit clotting factor consumption. 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.

Clinical manifestations of chronic arterial obstruction include: edema. intermittent claudication. decreased pressure proximal to the obstruction. distal hyperemia.

intermittent claudication. Arterial thrombosis is usually manifested by intermittent claudication (pain with activity) in the affected limb that improves with rest. Venous obstructions are manifested by edema. Ischemia can occur distal to the point of the occlusion. An increase in blood flow causes hyperemia, which is located in the area proximal to the obstruction.

Pernicious anemia is caused by a lack of: iron. intrinsic factor. folate. erythropoietin.

intrinsic factor. The fundamental defect causing pernicious anemia is the lack of intrinsic factor. Without it, vitamin B12 cannot be absorbed. Iron deficiency does not lead to pernicious anemia. Rather, it is the most common cause of anemia and is the result of unavailability of iron for hemoglobin synthesis. Pernicious anemia and folate deficiency are similar in etiology. Both are caused by a disruption in DNA synthesis of blast cells in bone marrow. Erythropoietin is necessary for the production of red cells.

The cause of the most common form of anemia is: acute bleeding. iron deficiency. protein malnutrition. chronic disease.

iron deficiency. Iron deficiency is the most common nutritional deficiency in the world and the most common cause of anemia. Acute blood loss anemia is the result of trauma or disease processes and is highly treatable. Plasma proteins formed in the liver are an essential factor in regulating blood volume. It is important to determine the underlying cause of the anemia so that treatment and control are effective.

The primary source of erythropoietin is provided by the: bone marrow. kidney. lung. liver.

kidney. Erythropoietin is a hormone that is secreted into the bloodstream by the kidney. Bone marrow is not responsible for the production of erythropoietin. Hypoxia from low hemoglobin levels causes a decrease in tissue oxygen tension in the kidney, thereby releasing the hormone erythropoietin. The liver is not associated with erythropoietin production.

A primary effector cell of the type I hypersensitivity response is: monocytes. mast cells. neutrophils. cytotoxic cells.

mast cells. Mast cells are a primary effector cell of the type I hypersensitivity response. Monocytes, neutrophils, and cytotoxic cells are not primary effectors of the type I hypersensitivity response.

The most appropriate treatment for secondary polycythemia is: volume expansion with saline. measured to improve oxygenation. phlebotomy. chemotherapy.

measured to improve oxygenation. Secondary polycythemia is because of chronic hypoxemia with a resultant increase in erythropoietin production. The goal of treatment is aimed at measures to reduce hypoxemia and improve oxygenation by implementing oxygen therapy. IV fluids may be used to treat relative polycythemia, because it is related to dehydration. Phlebotomy or increases in laboratory studies do not have an effect on secondary polycythemia. Polycythemia is not treated with chemotherapeutic agents.

Thalassemia may be confused with iron-deficiency anemia, because they are both: hyperchromic. microcytic. genetic. responsive to iron therapy.

microcytic. Both thalassemia and iron-deficiency anemia reveal hypochromic, microcytic red cells. Thalassemia and iron-deficiency red cells are hypochromic. Genetics play a role in thalassemia, and are found primarily in Asian individuals. Iron-deficiency anemia is responsive to iron therapy, but thalassemia patients have increased iron absorption.

A 58-year-old woman is seen in the clinic for reports of severe back pain. Her chest x-ray demonstrates generalized bone demineralization and compression fracture. Blood studies demonstrate elevated calcium levels. The most likely diagnosis is: leukemia. myeloma. Hodgkin disease. back trauma.

myeloma. A diagnosis of plasma cell myeloma is confirmed by the presence of hypercalcemia, which can contribute to the compression fracture. Patients with leukemia diagnoses do not exhibit bone demineralization or elevated calcium levels. Lymphadenopathy is a more common manifestation of Hodgkin disease. Compression fractures can be the result of back trauma, but not in the presence of the other radiographic and laboratory results.

RhoGAM (an Rh antibody) would be appropriate in an Rh-_____ woman with an _____ Rh-_____ antibody titer carrying an Rh-_____ fetus. negative; positive; positive positive; negative; negative negative; negative; positive negative; negative; negative

negative; negative; positive If a woman is Rh-negative, RhoGAM is administered for prevention of Rh-positive antibodies. Erythroblastosis fetalis develops during pregnancy when an Rh-negative mother is sensitized to her fetus's Rh-positive red cell group antigens because of exposure during her current or a previous pregnancy. RhoGAM contains antibodies against Rh antigens on fetal blood cells and is given to the mother to destroy fetal cells that may be present in her circulation before her immune system becomes activated and begins to produce anti-Rh antibodies. RhoGAM is not effective if the mother already has a positive antibody titer for fetal Rh antigens. An Rh-positive woman with negative Rh antibody titer carrying Rh-negative fetus does not require RhoGAM because the mother is Rh-positive and the fetus is Rh-negative.

The strength of the bond between oxygen and hemoglobin is known as the: Bohr effect. oxygen-hemoglobin affinity. dissociation curve. hemoglobin synthesis.

oxygen-hemoglobin affinity. The strength of the bond between oxygen and hemoglobin is called the oxygen-hemoglobin affinity. Hemoglobin saturation is higher when oxygen infinity is increased, and saturation is lower when affinity is decreased. The Bohr effect occurs when the oxyhemoglobin dissociation curve experiences a shift resulting from changes in PCO2 and H+ concentration. The dissociation curve describes the relationship between the partial pressure of oxygen and hemoglobin saturation. Hemoglobin synthesis occurs in the immature red cell.

The most common primary immune deficiency that affects only B cells is: DiGeorge. Bruton agammaglobulinemia. Wiskott-Aldrich. selective IgA.

selective IgA. The most common B-cell primary immunodeficiency disorder is selective IgA deficiency. This disorder affects 1:2000 persons. DiGeorge is a T-cell primary immune deficiency. Bruton agammaglobulinemia is not the most common primary immune deficiency affecting B cells; frequency of disease is 1:250,000 males. Females are carriers. Wiskott-Aldrich affects both T cells and B cells.

An increase in hemoglobin affinity for oxygen occurs with: hyperthermia. shift to the right. elevated PCO2. shift to the left.

shift to the left. An increase in oxygen affinity is known as a shift to the left on the dissociation curve. Hyperthermia does not have an effect on the hemoglobin affinity. Elevation in PCO2 is seen with changes in pH. A decrease in the oxygen affinity is associated with a shift to the right on the oxyhemoglobin dissociation curve.

Autologous stem cell transplantation is a procedure in which: there is a high rejection rate. stem cells are transferred to the patient from an HLA-matched donor. stem cells are transferred to the patient from an identical twin. stem cells are harvested from the patient and then returned to the same patient.

stem cells are harvested from the patient and then returned to the same patient. In autologous transplantation, the stem cells are collected from the patient's own blood and then stored and reinfused in the same patient after chemotherapy and radiation. The use of autologous transplants eliminates the problem of graft-versus-host disease. Transplant from a closely matched donor is known as allogeneic transplant. In autologous transplant, stem cells are used from the patient's own blood.

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

telangiectasia. A telangiectasia is a dilated or tortuous small blood vessel found in the skin or mucous membranes that have 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.

Blood flow throughout the periphery is regulated by: cardiac output. the autonomic nervous system. velocity. hemodynamics.

the autonomic nervous system. Blood flow throughout the periphery is controlled by central mechanisms that are mediated by the autonomic nervous system, the venous and thoracic pumps, and intrinsic autoregulatory mechanisms. Cardiac output does not control peripheral blood flow. Velocity is the measure of distance traveled in a given interval. Hemodynamics is the principle that governs the quantity of blood passing by a given point at a certain period.

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

the intrinsic pathway. 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.

Activation of the extrinsic pathway of coagulation is initiated by: platelet factors. collagen exposure. tissue thromboplastin. factor VII.

tissue thromboplastin. 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.

Tissues are able to autoregulate their rate of blood flow by controlling: perfusion pressure. arterial blood pressure. vascular resistance. venous return to the heart.

vascular resistance. Systemic vascular resistance is used to determine the resistance of vessels, diseases, or drug therapies that affect vessels. Any condition that increases vascular resistance requires more work for the heart to overcome the resistance and eject blood volume. Blood moves from an area of higher pressure to an area of lower pressure. The arterial and arteriolar walls with their muscular media coats provide the high-pressure end of the gradient. Seeking a lower pressure, blood moves toward the venous system. The thinner, more pliable walls of the venous bed furnish the low-pressure portion of the pressure gradient.

Peripheral edema is a result of: arterial insufficiency. venous thrombosis. hypertension. atherosclerosis.

venous thrombosis. In the venous system, thrombosis alters venous return, impairing removal of metabolic wastes and producing edema. In arterial obstruction, distal flow results in ischemia. Hypertension does not cause peripheral edema. Atherosclerosis is not directly associated with peripheral edema.

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

vitamin K deficiency bleeding. 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.

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

vitamin K deficiency. 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.