Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Barry Patho II Mid
6-16-10 Patho II Blood
| Question | Answer |
|---|---|
| "cytic" refers to | the morphologic class cell size |
| "chromic" refers to | the Hb content (ex hyperchromic) |
| Anisocytosis is | a person with different size RBCs |
| Poikilocytosis is | RBCs with different shapes |
| Anemia is defined in what two ways? | decreased # of circulating RBCs or in the quality or amount of Hb |
| What are the causes of anemia? | decreased production of RBCs, destruction of RBCs or a combination of both |
| What is the name of the first and second cell types in the production of an RBC? | Hemocytoblast and proerythroblast |
| What takes place in phase 3 of RBC production? | Ejection of nucleus |
| Another name for the RBC stem cell | Hemocytoblast |
| What happens in phase 1 of RBC synthesis | Ribosome synthesis |
| What is another name for the RBC in the committed cell stage | Proerythroblast |
| What happens in phase 2 of RBC synthesis | Hemoglobin accumulation |
| How wide is an average RBC | 7.5 um |
| How thick is an average RBC | 2.0 um |
| When does hypoxemia present asymptomatic | when it happens gradually without greater oxygen demand |
| 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) |
| What does anemia do to the heart | Causes tachycardia and eventually CHF |
| What are the S/S in ineffective compensated anemia | Dyspnea, tachycardia, dizziness and fatigue at rest |
| Severe or sudden onset of anemia causes | Peripheral vasoconstriction, increase Na H2O retention, decreased urine output |
| Icterus | accumulation of products from broken RBCs |
| Anemia caused by Vit B12 def. causes | myelin degeneration of the nervous system in the spinal cord and peripheral nerves |
| 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 |
| What is the tx for anemia | palliation of symptoms and correction of underlying cause - blood transfusions, dietary corrections, and admin of vitamins or iron |
| Megaloblastic anemias result from | defective DNA synthesis |
| Megaloblasts results from | def. of vit B12 or folate acid |
| megaloblasts turn into | Macrocytes |
| 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 |
| Chronic atrophic gastritis can be caused by (3 things) | Alcohol, hot tea, smoking |
| 5 vague symptoms of pernicious anemia | infections, mood swings, and renal, CV or GI problems |
| Weakness, fatigue, distal paresthesias, and neurological manifestations occur when Hb level is ? | less than 8 g/dl |
| Neurological manifestations (related to pernicious anemia)are due to | demylination of the lateral and posterior columns of the spinal cord |
| 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 |
| Hepato-splenomegaly is diagnosed by (4 things) | clinical manifestations, blood test, bone marrow aspiration and Schilling test |
| Schilling test | measures the urine excretion of administered radioactive cobalamin |
| A positive Schilling test for pernicious anemia is identified by | low urinary excretion of cobalamin |
| 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 |
| What happens in 1-3 yrs of untreated pernicious anemia | Death |
| What prevents death in pernicious anemia | Life long administration of Vit B12 |
| Folic acid is a component of (3 things) | thymine, adenine, and guanine |
| The daily requir.of folic acid | 50-200ug |
| Three resons for folate acid deficiency | Alcoholism, chronic malnourished, and diets low in vegetables |
| 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 |
| What manifestation is usually not present in folate anemia that is in pernicious anemia | Neurologic manifestations |
| Tx for folate anemia (the 2 doses) | Folate daily - 1 mg normally, 5 mg alcoholics |
| Macrocytic - normochromatic anemias (2 of them) | Pernicious anemia and folate anemia |
| Name microcytic - hypochromatic anemias (3 of them) | Iron def. anemia, porphyrin and Hb synthesis disorders, and globin synthesis disorder |
| The most common anemia worldwide | Iron def. anemia |
| 4 causes of iron def. anemias | parasitic infestations, decreased ingestion of Fe (malnutrition), pregnancy, chronic blood loss |
| The mls of daily blood loss that can cause anemia | 2-4 mls (1-2 OF Fe)is sufficient to cause anemia |
| 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 |
| 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 |
| Two lab tests to evaluate Fe anemia | Directly (bone marrow biopsy) or indirectly (serum ferritin, transferrin saturation, or total iron-binding capacity) |
| The most conclusive diagnosis of Fe anemia | an increase of 1-2 g/ml after initiation of Fe therapy |
| Name 5 normocytic - normochromic anemias | Aplastic anemia, posthemorrhage anemia, hemolytic anemia, anemia of chronic inflammation, sickle cell anemia |
| Aplastic anemia results from (2 things) | Bone marrow hypoplasia or aplasia |
| Pancytopenia | where all the series are effected |
| 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) |
| PRCA, what is it and what series does it effect | Pure red cell aplasia, it effects the red series only |
| True / false: PRCA is very common when eating raw chicken on OBT | False, it is very rare |
| Palliative treatment for aplastic anemia (2 things) | Blood transfusions and bone marrow transplant (or pharmacological stimulation of the marrow function) |
| What "ectomy" might take place with aplastic anemia | Splenectomy |
| The most common type of hemolytic anemia with normal Hb | Cogentital hemolytic anemia (or Acholuric jaundice) |
| 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) |
| What happens to a spherocyte when it circulates through the spleen | adios amigo |
| When (developmental stage) do clinical manifistation of cogenital hemolitic anemia occur | neonatal period or early infancy |
| Tx of cogenital hemolytic anemia | blood exchange transfusion and/or phototherapy |
| What "megaly" is almost always present after infancy (r/t cogenital hemolytic anemia) | Splenomegaly |
| What % of splenectomies occur with cogenital hemolytic anemia | 50% |
| What is the most serious complication during childhood with cogenital hemolitic anemia | Aplastic crisis (RBC production shut down for 10 days from parvovirus B19) |
| Specific test to diagnose cogenital hemolitic anemia | None |
| Clinical cure for cogenital hemolitic anemia | Splenectomy (done after 5 yrs of age) |
| Thing to be evaluated to diagnose cogenital hemolitic anemia (4 things) | Family history, blood smear, osmotic fragility, and autohemolysis |
| Sickle cell anemia is chacaterized by the presents of | Hb S |
| Hb S results from glutamic acid being replaced by | Valine |
| Hb S reacts when subjected to (2 things) | Deoxygenation and dehydration |
| True/False: When Hb S reacts it turns into the shape of a buttermilk biscuit and is soft and fluffy | False, cresent and stiff |
| Sickled cells do what to microcirculation and thereby cause what 3 things | occlude and cause ischemia, pain, infarction |
| T/F: Sickle cells under go hemolysis and sequestration in the liver | False, both hemolysis and sequestration in spleen - only seq. in liver |
| 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 |
| Name 4 types of anemic crises | Vasoocclusive, Aplastic, Sequestration, and Hyperhemolytic |
| Vasoocclussive (thrombotic) crisis | crisis which may be spontaneous or precipitated by infections, exposure to cold, decreased PO2, decreased pH, or localized hypoxemia |
| Aplastic crisis | crisis results from RBC with a shorter survival (10-20 days)and a compromised compensatory responce |
| Sequestration crisis | crisis in both the spleen and liver |
| Hyperhemolitic crisis | crisis is unusual but may occur in association with certain drugs and infections |
| The most frequent cause of death in patient with sickle cell | Infection (meningitis and general sepsis) |
| What test confirms the present of Hb S in the blood | Sickle cell solubility test |
| What test reveals the amount of Hb S in the RBC | Hb electrophoresis |
| How can prenatal diagnosis of sickle cell be made | Chorionic Villus sample (8-10 wks gestation) or Amniocentesis (15 wks gestation) |
| Treatment of sick cell anemia is aimed at | Prevention (prevent consequences and crisis) |
| 5 triggers of sickle cell crisis | Fever, infection, dehydration, acidosis, and exposure to cold temp |
| Tx for sickle cell (5 of them) | bone marrow transplant, blood transfusion, oral administration of folate, spenectomy, and genetic counseling |
| If both parents have sickle cell trait, what is the % the child will have the disease | 25% |
| Thalassemia (a microcytosis disease) is charactered by the impairment of what | Impaired rate of synthesis of one of the alpha or beta chains |
| What are the 2 major classifications of Thalassemias and the 2 sub classes | Alpha Thalassemia or Beta Thalassemia and then either Minor or Major |
| 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 |
| An untreated child with thalassemia will die at what age | 5-6 yrs |
| Diagnosis of thalassemia is based on (4 things) | Family history, clinical manifestations, peripheral blood smear (microcytosis), and Hb electrophoresis |
| Tx for thalassemia includes (4 things) | blood transfusions, iron chelation therapy (experimental), spenectomy, and neocyte transfusion (experimental) |
| The definition of polycythemia | excessive production of RBC |
| 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) |
| The Absolute Type of Polycythemia is further classified as | Primary or Secondary |
| 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 |
| Polycythemia cause what to the blood volume and viscosity | They both go up, increasing probabilitiy of thromboembolism and tissue infaction/necrosis |
| 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 |
| How is abosulte polycythemia diagnosed | blood test = increase in absolute RBCs and total blood volume |
| What is the Tx for Absolute polycythemia | phlebotomy Q 3-4 momths, radioactive phosphorus, myelosuppresive drugs (clorambucil) |
| 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 |
| Excessive white blood cells is called | Leukocytosis |
| Decreased or ineffective WBCs is called | Leukopenia |
| T/F: leukocytosis and leukopenia usually involve more than one type of WBC in the same individual? | False |
| The physiological causes for leukocytosis are (10 of them) | Infection, strenuous exercise, emotional stress, temp changes, ANESTHESIA, surgery, pregnancy, drugs, hormones, and toxins |
| The pathological causes for leukocytosis include (2 of them) | Malignancies and hematological disorders |
| Causes for leukopenia (4 of them) | Radiation, anaphylactic shock, SLE, and some chemotherapeutical agents |
| WBC count less than ? are at risk for infection | Less than 1000/mm3 |
| WBC count less than ? are at risk for life threatening infection | Less than 500/mm3 |
| An increase in Granulocytes and Monocytes can be from (2 things) | Infection or myeloprolifrative disorders |
| A decrease in Granulocytes and Monocytes can be from (2 things) | Used up faster than can be made, or depression/suppression of bone marrow |
| Granulocytosis usually refers to | Neutrophilia (which is present in the early stages of infection = above 7500/ul) |
| Neutrophilia in which count is higher than 100,000/ul may cause | Thrombus due to increase in viscosity |
| 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) |
| Neutropenia is a count less than ? and is seen in ? | Less than 2000/ul and is seen in servere prolonged infections |
| Causes for decreased neutrophil production (3 things) | Aplastic anemia, Leukemia, Drug-induced neutropenia |
| Decreased neutrophil life span is related to | Autoimmune disorder (SLE and RA) |
| Abnormal neutrophil distribution and sequestration are caused by (3 things) | Hypersplenism, starvation, and anorexia nervosa |
| 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 |
| Eosinopenia is caused by | migration of eosinophils into sites of inflammation. |
| Specific examples of eosinophilia (6 of them) | Cushing syndrome, surgery, shock, trauma, burns, or mental distress |
| Basophilia is very rare but may be seen in | Myeloproliferative disorder |
| Basopenia is seen in (3 things) | Hyperthyroidism, acute infections, and long-term steroid therapy |
| 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 |
| Monocytopenia is rare and has been identified with (2 things) | Hairy cell leukemia and prednisone therapy |
| Lymphocytosis is typical of what type of infection | Viral (rare in bacterial infections), it is also present in antigen reactions |
| 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 |
| Leukemia is | a clonal (originating from same ancestor), malignant disorder that decreases production and function of normal hemapoietic (blood producing)cells |
| Leukemias are classified | Acute or chronic and as Myeloid or Lymphoid |
| Acute leukemias are those classified by | Undifferenitiated or immature cell (usually a blast cell)with rapid onset and short survival time |
| In Chronic leukemias the predominant cell is | apperently mature but does not function normally (longer survival period than acute) |
| 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 |
| Diagnosis of leukemia is done by | Blood test and bone marrow biopsy |
| Treatment for Acute Leukemia is | Chemotherapy (tx of choice), bone marrow transplant, supportive care, immunotherapy agents |
| Treatment for chronic leukemia includes | bone marrow transplant and chemotherapy |
| Multiple myeloma is what type of cancer | B cell cancer |
| Multiple myeloma cells produce large amount of | one class of immunoglobulins - usually IgG - known as M protein |
| M protein causes | infiltration and destruction of organs (particularly bones) |
| Diagnosis of Multiple Myeloma is made by | Radiographic, lab studies, and biopsy of the lesion |
| Treatment of multiple myeloma includes (4 things) | Chemo, Radiation, Plasmapheresis, and bone marrow transplant |
| Malignant Lymphomas involve the proliferation of (2 things) | Lymphocytes and histiocytes (and their precursors and derivatives) |
| Malignant Lymphomas are found in what tissue | Lymphoid tissue |
| Malignant lymphomas are classified as (3 of them) | Lymphoid leukemia (B cell origin), Non-Hodgkin lymphoma (T cell origin), and Hodgkin disease |
| 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 |
| Hodgkin disease is diagnosed by | simple CXR, lymphangiography, and biopsy of enlarged lymph nodes |
| Treatment for Hodgkin disease includes | Radiotherapy and chemotherapy with important success |
| What is different in the clinical findings between Hodgkin and Non-Hodgkin diseases | There are no Reed-Sternberg cells in Non-Hodgkin disease |
| What are the differences in the S/S and treatments of Hodgkin and Non-Hodgkin diseases | None |
Created by:
smorrissey1
Popular Physiology sets