This quiz, titled 'GLD Ch. 10 T2(Blood)', assesses knowledge on blood components and disorders. It covers topics such as erythrocytes, pancytopenia, capillary structure, vitamin K's role, blood types, and circulatory systems, essential for students in medical or biological studies.
Leucopenia
Neutropenia
Pancytopenia
Erythrocytosis
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Multiple endothelial layers.
A thick layer of smooth muscle.
Two or three epithelial layers.
A single endothelial layer.
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Heparin.
Prothrombin.
Amino acids.
Bilirubin.
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Contains A and B antibodies.
Contains A and B antigens.
Contains A and B antigens.
Contains A and B antigens.
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Pulmonary and systemic circulations
Peripheral and central circulations
Cardiovascular and lymphatic circulations
Cardiopulmonary and peripheral circulations
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Shortened life span of the erythrocytes.
Lower metabolic rate.
Loss of protein and electrolytes.
Smaller amount of recycled iron available.
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A defective gene inherited from both parents
A chronic bacterial infection
Bone marrow depression
An autoimmune reaction
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Hypochromic, microcytic
Normochromic, normocytic
Elongated, sickle-shaped
Megaloblastic or macrocytic nucleated cells
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Persistent hyperbilirubinemia
Increasing acidosis affecting metabolism
Vitamin B12 deficit causing peripheral nerve demyelination
Multiple small vascular occlusions affecting peripheral nerves
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Sickle cell anemia.
Aplastic anemia.
Iron deficiency anemia.
Acute leukemia.
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Chest pain, palpitations
Jaundice, stomatitis
Pallor, dyspnea, and fatigue
Bradycardia, heat intolerance
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Lack of folic acid for DNA synthesis
Frequent microinfarcts in the tissues
Deficit of oxygen for epithelial cell mitosis and metabolism
Elevated bilirubin levels in blood and body fluids
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Pancytopenia
Hypochlorhydria
Leukocytosis
Multiple infarcts
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An immune reaction in the stomach would destroy the vitamin.
Digestive enzymes would destroy the vitamin.
The vitamin irritates the gastric mucosa.
The ingested vitamin would not be absorbed into the blood.
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Decreased production of erythrocytes
Shorter life span of erythrocytes
Abnormal structure of hemoglobin chains
Deficit of folic acid
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Painful joints and skeletal deformity
Abdominal discomfort and splenomegaly
Excessive bleeding and recurrent infections
Palpitations and chest pain
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The red blood cells are abnormally large.
Increased hemolysis of erythrocytes occurs.
Erythrocytes change to sickle shape when hypoxia occurs.
HbS is unable to transport oxygen.
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Most hemoglobin is in the form of HgS
Sickling of erythrocytes occurs with severe hypoxia.
Painful sickling crises with multiple infarctions occur frequently.
A child’s skeletal growth is delayed.
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Several amino acids in the globin chains have been replaced by substitute amino acids.
More than four globin chains are found in the erythrocytes.
The iron molecule is displaced in hemoglobin.
There is failure to synthesize either the alpha or beta chains in the hemoglobin molecule.
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Aplastic anemia
Sickle cell anemia
Thalassemia major
Pernicious anemia
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Vitamin B12.
Intrinsic factor or parietal cells.
Mucus-producing glands.
Hydrochloric acid.
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Increased blood volume.
Frequent infarcts in the coronary circulation.
Congested spleen and bone marrow.
Increased renin and aldosterone secretions.
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Excessive hemolysis.
Leucopenia.
Increased bleeding.
Hemoglobin deficit.
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It is transmitted as an X-linked dominant trait.
There is usually a total lack of factor VIII in the blood.
Males and females can be carriers.
Hematomas and hemarthroses are common.
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Increased thrombocytes and blood clotting
Hemolysis with loss of blood cells
Massive sepsis and hemorrhage
Multiple thrombi and deficit of clotting factors
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Prothrombin
Heparin
Fibrinogen
Vitamin K
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The number of white blood cells is decreased.
Many circulating leukocytes are immature.
Severe anemia interferes with the immune response.
Decreased appetite and nutritional intake reduce natural defenses.
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Deficit of calcium ions
Impaired production of prothrombin and fibrinogen
Decreased platelets
Dysfunctional thrombocytes
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Exposure to radiation.
Certain fungal and protozoal infections.
Familial tendency.
Cigarette smoking.
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Defective erythrocytes that become deformed in shape, causing occlusions.
Excessive lymphocytes that do not mature.
Absence of a clotting factor that helps platelets clump and stick.
A lack of hemoglobin due to iron deficiency.
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Severe chronic kidney disease.
Peripheral vascular disease.
Deficient calcium levels in the long bones.
Excessive bleeding of hematomas.
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Plasma cells.
Granulocytes.
Bone cells.
Lymph nodes.
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Radiation
Chemotherapy
Surgery
Immunotherapy
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Caused by excessive iron intake in the diet.
Results from excessive hemolysis of RBCs.
A metabolic error that leads to excess amounts of hemosiderin, causing damage to organs.
An inherited defect that results in abnormal hemoglobin.
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A defect in one or more genes for hemoglobin.
An abnormal form of heme.
Abnormal liver production of amino acids and iron.
Overproduction of hypochromic, microcytic RBCs.
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Frequent angina attacks.
Certain types of anemia.
Severe chronic bronchitis.
Renal disease.
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It is used as an antidote for warfarin (Coumadin).
The liver requires it to produce prothrombin.
It is a fat-soluble vitamin.
The bone marrow requires it to synthesize hemoglobin.
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The presence of Philadelphia chromosome translocation in cases of acute myelogenous leukemia (AML).
Very low incidence in persons with Down syndrome.
Little evidence of familial incidence.
Transmission as a recessive gene.
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Certain vegetarian diets.
Excessive menstrual flow.
Malabsorption syndromes.
Diabetes mellitus.
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Chronic leukemias are more common in older people.
AML is the most common childhood leukemia.
Exposure to chemicals is not considered a predisposing factor.
Lymphoid tissue produces abnormal leukocytes.
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Thalassemia.
Acute myelogenous leukemia (AML).
Myelodysplastic syndrome.
Multiple myeloma.
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It is produced by the liver.
It increases iron absorption for heme production.
It stimulates production of red blood cells.
Hypoxia stimulates the red bone marrow to produce erythropoietin.
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Bleeding time
Coagulation time
PTT time
Prothrombin time
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It is usually a secondary complication.
It is always initiated by excessive bleeding.
It results in an inability of platelets to adhere.
It is not life threatening.
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Pernicious anemia
Aplastic anemia
Iron deficiency anemia
Sickle cell anemia
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Idiopathic in many cases.
A genetic disorder.
Predisposed by exposure to myelotoxins.
Both A and C.
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Iron deficiency anemia.
Polycythemia.
Disseminated intravascular coagulation.
Hemophilia A.
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