6-16-10 Patho II Blood
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| "cytic" refers to | the morphologic class cell size
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| "chromic" refers to | the Hb content (ex hyperchromic)
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| Anisocytosis is | a person with different size RBCs
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| Poikilocytosis is | RBCs with different shapes
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| Anemia is defined in what two ways? | decreased # of circulating RBCs or in the quality or amount of Hb
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| What are the causes of anemia? | decreased production of RBCs, destruction of RBCs or a combination of both
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| What is the name of the first and second cell types in the production of an RBC? | Hemocytoblast and proerythroblast
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| What takes place in phase 3 of RBC production? | Ejection of nucleus
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| Another name for the RBC stem cell | Hemocytoblast
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| What happens in phase 1 of RBC synthesis | Ribosome synthesis
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| What is another name for the RBC in the committed cell stage | Proerythroblast
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| What happens in phase 2 of RBC synthesis | Hemoglobin accumulation
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| How wide is an average RBC | 7.5 um
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| How thick is an average RBC | 2.0 um
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| When does hypoxemia present asymptomatic | when it happens gradually without greater oxygen demand
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| How does one compensate for anemia | through CV, Resp, and Hematological system. increase reabsorbtion of fluid from extravascular comp., increase vol (with decrease viscosity), increase circulation (more turbulent)
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| What does anemia do to the heart | Causes tachycardia and eventually CHF
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| What are the S/S in ineffective compensated anemia | Dyspnea, tachycardia, dizziness and fatigue at rest
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| Severe or sudden onset of anemia causes | Peripheral vasoconstriction, increase Na H2O retention, decreased urine output
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| Icterus | accumulation of products from broken RBCs
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| Anemia caused by Vit B12 def. causes | myelin degeneration of the nervous system in the spinal cord and peripheral nerves
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| S/S of anemia caused by Vit B12 (10 of them) | paresthesia, extreme weakness, gait disturbances, spasticity and reflex abnormalities, abdominal pain, nausea, vomiting, anorrexia, and low grade fever
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| What is the tx for anemia | palliation of symptoms and correction of underlying cause - blood transfusions, dietary corrections, and admin of vitamins or iron
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| Megaloblastic anemias result from | defective DNA synthesis
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| Megaloblasts results from | def. of vit B12 or folate acid
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| megaloblasts turn into | Macrocytes
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| pernicious anemia is caused by | def Vit B12 that is caused from the lack of the intrinsic factor (IF) in the gastric mucosa (cogenital - atrophy of the gastric mucosa) or after partial or total gastrectomy
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| Chronic atrophic gastritis can be caused by (3 things) | Alcohol, hot tea, smoking
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| 5 vague symptoms of pernicious anemia | infections, mood swings, and renal, CV or GI problems
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| Weakness, fatigue, distal paresthesias, and neurological manifestations occur when Hb level is ? | less than 8 g/dl
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| Neurological manifestations (related to pernicious anemia)are due to | demylination of the lateral and posterior columns of the spinal cord
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| Symptoms that appear when Hb is less than 8g/dl (8 of them) | weakness, fatigue, distal paresthesia, neurological manifestations (ataxia, spasticity, loss of the vibration and position sense), anorexia, abdominal pain, weight loss,and sore tongue
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| Hepato-splenomegaly is diagnosed by (4 things) | clinical manifestations, blood test, bone marrow aspiration and Schilling test
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| Schilling test | measures the urine excretion of administered radioactive cobalamin
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| A positive Schilling test for pernicious anemia is identified by | low urinary excretion of cobalamin
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| If intrinsic factor (IF) is given and cobalamin excretion increases, what does this mean? | It is the secondary confirmation test of the diagnosis of pernicious anemia
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| What happens in 1-3 yrs of untreated pernicious anemia | Death
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| What prevents death in pernicious anemia | Life long administration of Vit B12
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| Folic acid is a component of (3 things) | thymine, adenine, and guanine
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| The daily requir.of folic acid | 50-200ug
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| Three resons for folate acid deficiency | Alcoholism, chronic malnourished, and diets low in vegetables
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| Clinical manifestions of folate anemia are similar to pernicious anemia with the addition of (4 things) | Stomatitis (painful ulcerations of the buccal mucosa and tongue), dysphagia, flatulence, and liquid diarrhea
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| What manifestation is usually not present in folate anemia that is in pernicious anemia | Neurologic manifestations
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| Tx for folate anemia (the 2 doses) | Folate daily - 1 mg normally, 5 mg alcoholics
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| Macrocytic - normochromatic anemias (2 of them) | Pernicious anemia and folate anemia
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| Name microcytic - hypochromatic anemias (3 of them) | Iron def. anemia, porphyrin and Hb synthesis disorders, and globin synthesis disorder
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| The most common anemia worldwide | Iron def. anemia
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| 4 causes of iron def. anemias | parasitic infestations, decreased ingestion of Fe (malnutrition), pregnancy, chronic blood loss
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| The mls of daily blood loss that can cause anemia | 2-4 mls (1-2 OF Fe)is sufficient to cause anemia
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| The three characteristic stages of the development of iron def. anemia | Stage I = Fe storage depleted but Hb and RBC normal, Stage II = Fe def. causes erythropoiesis, Stage III = small Hb def. cells replace circulating old normal RBC
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| S/S when Fe anemia Hb drops below 7-8g/dl (10 things) | fatigue, weakness, dyspnea, pale skin and mucose membranes, koilonychia nails, glossitis, gastritis, headache, irritability, neuromuscular changes
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| Two lab tests to evaluate Fe anemia | Directly (bone marrow biopsy) or indirectly (serum ferritin, transferrin saturation, or total iron-binding capacity)
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| The most conclusive diagnosis of Fe anemia | an increase of 1-2 g/ml after initiation of Fe therapy
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| Name 5 normocytic - normochromic anemias | Aplastic anemia, posthemorrhage anemia, hemolytic anemia, anemia of chronic inflammation, sickle cell anemia
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| Aplastic anemia results from (2 things) | Bone marrow hypoplasia or aplasia
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| Pancytopenia | where all the series are effected
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| Aplastic anemias are either ? or ? and may be further calssified as ? or ? | Aplastic anemias are either hereditary (fanconi anemia - defect in DNA repair)or acquired which may be further classified as primary (idiopathic 50% of cases with 80% over 50 yrs of age) or secondary (by chemical agents and ionizing radiation)
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| PRCA, what is it and what series does it effect | Pure red cell aplasia, it effects the red series only
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| True / false: PRCA is very common when eating raw chicken on OBT | False, it is very rare
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| Palliative treatment for aplastic anemia (2 things) | Blood transfusions and bone marrow transplant (or pharmacological stimulation of the marrow function)
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| What "ectomy" might take place with aplastic anemia | Splenectomy
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| The most common type of hemolytic anemia with normal Hb | Cogentital hemolytic anemia (or Acholuric jaundice)
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| The cause of cogenital hemolitic anemia | An unknown abnormality of protein in thje RBC membrane that causes increased Na permeability leading to increase ATP consumption and premature death r/t overworked (as well as abnormal RBC shape - spherocyte)
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| What happens to a spherocyte when it circulates through the spleen | adios amigo
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| When (developmental stage) do clinical manifistation of cogenital hemolitic anemia occur | neonatal period or early infancy
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| Tx of cogenital hemolytic anemia | blood exchange transfusion and/or phototherapy
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| What "megaly" is almost always present after infancy (r/t cogenital hemolytic anemia) | Splenomegaly
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| What % of splenectomies occur with cogenital hemolytic anemia | 50%
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| What is the most serious complication during childhood with cogenital hemolitic anemia | Aplastic crisis (RBC production shut down for 10 days from parvovirus B19)
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| Specific test to diagnose cogenital hemolitic anemia | None
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| Clinical cure for cogenital hemolitic anemia | Splenectomy (done after 5 yrs of age)
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| Thing to be evaluated to diagnose cogenital hemolitic anemia (4 things) | Family history, blood smear, osmotic fragility, and autohemolysis
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| Sickle cell anemia is chacaterized by the presents of | Hb S
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| Hb S results from glutamic acid being replaced by | Valine
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| Hb S reacts when subjected to (2 things) | Deoxygenation and dehydration
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| True/False: When Hb S reacts it turns into the shape of a buttermilk biscuit and is soft and fluffy | False, cresent and stiff
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| Sickled cells do what to microcirculation and thereby cause what 3 things | occlude and cause ischemia, pain, infarction
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| T/F: Sickle cells under go hemolysis and sequestration in the liver | False, both hemolysis and sequestration in spleen - only seq. in liver
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| What does sickle cells cause in the bone marrow and sometimes liver | Erythropoiesis - the production of RBC related to decreased O2 delivery to kidneys which secrete erythropoietin
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| Name 4 types of anemic crises | Vasoocclusive, Aplastic, Sequestration, and Hyperhemolytic
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| Vasoocclussive (thrombotic) crisis | crisis which may be spontaneous or precipitated by infections, exposure to cold, decreased PO2, decreased pH, or localized hypoxemia
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| Aplastic crisis | crisis results from RBC with a shorter survival (10-20 days)and a compromised compensatory responce
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| Sequestration crisis | crisis in both the spleen and liver
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| Hyperhemolitic crisis | crisis is unusual but may occur in association with certain drugs and infections
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| The most frequent cause of death in patient with sickle cell | Infection (meningitis and general sepsis)
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| What test confirms the present of Hb S in the blood | Sickle cell solubility test
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| What test reveals the amount of Hb S in the RBC | Hb electrophoresis
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| How can prenatal diagnosis of sickle cell be made | Chorionic Villus sample (8-10 wks gestation) or Amniocentesis (15 wks gestation)
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| Treatment of sick cell anemia is aimed at | Prevention (prevent consequences and crisis)
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| 5 triggers of sickle cell crisis | Fever, infection, dehydration, acidosis, and exposure to cold temp
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| Tx for sickle cell (5 of them) | bone marrow transplant, blood transfusion, oral administration of folate, spenectomy, and genetic counseling
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| If both parents have sickle cell trait, what is the % the child will have the disease | 25%
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| Thalassemia (a microcytosis disease) is charactered by the impairment of what | Impaired rate of synthesis of one of the alpha or beta chains
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| What are the 2 major classifications of Thalassemias and the 2 sub classes | Alpha Thalassemia or Beta Thalassemia and then either Minor or Major
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| Both alpha and beta thalassemia are life threatening in children who are (4 things) | weak, failure to thrive, show poor development, and are cardiac compromised
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| An untreated child with thalassemia will die at what age | 5-6 yrs
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| Diagnosis of thalassemia is based on (4 things) | Family history, clinical manifestations, peripheral blood smear (microcytosis), and Hb electrophoresis
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| Tx for thalassemia includes (4 things) | blood transfusions, iron chelation therapy (experimental), spenectomy, and neocyte transfusion (experimental)
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| The definition of polycythemia | excessive production of RBC
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| What type of polycythemia results from hemoconcentration of the blood due to dehydration | The Relative Type (actual absolute RBCs numbers are normal as well as bone marrow function)
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| The Absolute Type of Polycythemia is further classified as | Primary or Secondary
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| The other name for Absolute Primary Polycythemia | Polycythemia Vera (PV)- a neoplastic (cancerous)disorder where RBC mass is self distructive.Also hyperplasia of the bone marrow with inc. platlets and WBC leads to altered Pluripotential
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| Polycythemia cause what to the blood volume and viscosity | They both go up, increasing probabilitiy of thromboembolism and tissue infaction/necrosis
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| Clinical S/S of polycythemia (12 of them) | H/A, hepatomegaly, spenomegaly, drowsiness, delirium, mania, psycotic depression, visual disturbances, GI thrombosis, portal HTN, angina, and chorea
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| How is abosulte polycythemia diagnosed | blood test = increase in absolute RBCs and total blood volume
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| What is the Tx for Absolute polycythemia | phlebotomy Q 3-4 momths, radioactive phosphorus, myelosuppresive drugs (clorambucil)
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| Absolute secondary polycythemia is usually caused by | Secretion of erythropoieten in responce to hypoxemia (high altitude, heavy smoking, CFH, COPD)or cancer (tumors associated with renal, hepatomas, and cerebellular hemangioblastomas
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| Excessive white blood cells is called | Leukocytosis
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| Decreased or ineffective WBCs is called | Leukopenia
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| T/F: leukocytosis and leukopenia usually involve more than one type of WBC in the same individual? | False
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| The physiological causes for leukocytosis are (10 of them) | Infection, strenuous exercise, emotional stress, temp changes, ANESTHESIA, surgery, pregnancy, drugs, hormones, and toxins
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| The pathological causes for leukocytosis include (2 of them) | Malignancies and hematological disorders
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| Causes for leukopenia (4 of them) | Radiation, anaphylactic shock, SLE, and some chemotherapeutical agents
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| WBC count less than ? are at risk for infection | Less than 1000/mm3
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| WBC count less than ? are at risk for life threatening infection | Less than 500/mm3
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| An increase in Granulocytes and Monocytes can be from (2 things) | Infection or myeloprolifrative disorders
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| A decrease in Granulocytes and Monocytes can be from (2 things) | Used up faster than can be made, or depression/suppression of bone marrow
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| Granulocytosis usually refers to | Neutrophilia (which is present in the early stages of infection = above 7500/ul)
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| Neutrophilia in which count is higher than 100,000/ul may cause | Thrombus due to increase in viscosity
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| An increase in the release of immature WBC is called a | Shift to the Left ( the degree of shift is usually related to the serverity of the infection)
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| Neutropenia is a count less than ? and is seen in ? | Less than 2000/ul and is seen in servere prolonged infections
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| Causes for decreased neutrophil production (3 things) | Aplastic anemia, Leukemia, Drug-induced neutropenia
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| Decreased neutrophil life span is related to | Autoimmune disorder (SLE and RA)
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| Abnormal neutrophil distribution and sequestration are caused by (3 things) | Hypersplenism, starvation, and anorexia nervosa
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| Eosinophilia usually occurs in ? and give 6 examples | Allergic reactions - Asthma, hay fever, drug reactions, pemphigus (a blistering autoimmune dz), some types of dermatitis and parasitic invasions
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| Eosinopenia is caused by | migration of eosinophils into sites of inflammation.
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| Specific examples of eosinophilia (6 of them) | Cushing syndrome, surgery, shock, trauma, burns, or mental distress
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| Basophilia is very rare but may be seen in | Myeloproliferative disorder
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| Basopenia is seen in (3 things) | Hyperthyroidism, acute infections, and long-term steroid therapy
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| Monocytosis is commonly seen | in the late recovery stages of bacterial infections (when phagocytosis is needed)along with leukopenia, also seen during chronic infections like TB and SBE
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| Monocytopenia is rare and has been identified with (2 things) | Hairy cell leukemia and prednisone therapy
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| Lymphocytosis is typical of what type of infection | Viral (rare in bacterial infections), it is also present in antigen reactions
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| Lymphocytopenia is associated with ? (5 things) and is very serious problem in cases with? | Neoplasms, immune deficiencies, radiation, chemo, and viruses. Serious in cases with AIDS
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| Leukemia is | a clonal (originating from same ancestor), malignant disorder that decreases production and function of normal hemapoietic (blood producing)cells
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| Leukemias are classified | Acute or chronic and as Myeloid or Lymphoid
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| Acute leukemias are those classified by | Undifferenitiated or immature cell (usually a blast cell)with rapid onset and short survival time
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| In Chronic leukemias the predominant cell is | apperently mature but does not function normally (longer survival period than acute)
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| Clinical manifestations of acute leukemia are | Related to bone marrow depression such as fatigue, bleeding, fever (the early sign), infection (oral, resp, lower colon, GU, and skin), anorexia, decreased sweet/sour taste, weight loss, loss of muscle, neurological issues (H/A, vomiting, papilledema
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| Diagnosis of leukemia is done by | Blood test and bone marrow biopsy
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| Treatment for Acute Leukemia is | Chemotherapy (tx of choice), bone marrow transplant, supportive care, immunotherapy agents
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| Treatment for chronic leukemia includes | bone marrow transplant and chemotherapy
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| Multiple myeloma is what type of cancer | B cell cancer
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| Multiple myeloma cells produce large amount of | one class of immunoglobulins - usually IgG - known as M protein
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| M protein causes | infiltration and destruction of organs (particularly bones)
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| Diagnosis of Multiple Myeloma is made by | Radiographic, lab studies, and biopsy of the lesion
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| Treatment of multiple myeloma includes (4 things) | Chemo, Radiation, Plasmapheresis, and bone marrow transplant
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| Malignant Lymphomas involve the proliferation of (2 things) | Lymphocytes and histiocytes (and their precursors and derivatives)
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| Malignant Lymphomas are found in what tissue | Lymphoid tissue
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| Malignant lymphomas are classified as (3 of them) | Lymphoid leukemia (B cell origin), Non-Hodgkin lymphoma (T cell origin), and Hodgkin disease
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| Hodgkin Disease is characterized by the presence of | the Reed-Sternburge cells, lymphadenopathy, enlarged lymph nodes in different locations, fever, night sweats, and wt loss
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| Hodgkin disease is diagnosed by | simple CXR, lymphangiography, and biopsy of enlarged lymph nodes
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| Treatment for Hodgkin disease includes | Radiotherapy and chemotherapy with important success
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| What is different in the clinical findings between Hodgkin and Non-Hodgkin diseases | There are no Reed-Sternberg cells in Non-Hodgkin disease
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| What are the differences in the S/S and treatments of Hodgkin and Non-Hodgkin diseases | None
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