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Pathophys Ch7 test 2
Disorders of the blood cells
| Question | Answer |
|---|---|
| Composition of the blood (connective tissue) | Two main components: 1. Plasma - 55% of blood vol -clear extra cellular fluid; A. Proteins - 7%; B. Water - 92%; C. Solutes- 1%; 2. Formed elements -45% of blood volume; A. Erythrocytes (RBCs)-99%; B. Leukocytes (WBCs)-1%; |
| What are the blood plasma proteins (7%) composed of? | Fibrinogen (5%) - clotting Immunoglobulins (alpha)(15%) - immune reaction Other globulins (beta) (20%)- transport; reactant proteins Albumin (60%) - Transport; plasma osmotic pressure; |
| What is blood plasma water (92%)for? | Transport medium (oxygen) and solvent |
| What solutes are part of the 1% blood plasma? | Amino acids Glucose Electrolytes Lipids Hormones Vitamins Metabolic waste |
| Formed elements -Leukocytes (1%) -WBC - composition | 5% Monocytes - Phagocytosis; immune reactions 30% Lymphocytes - immune reactions 65% Granulocytes |
| Granulocytes (65% of the WBC) are composed of | 97% Neutrophils - Acute inflammatory reactions - Phagocytosis - Digestion of foreign and inflammatory debris 2% Eosinophils - Allergic & antiparasitic reac 1% Basophils - allergic reactions |
| WBCs' role | Active in inflammation and immunity |
| What is the life span of blood cells? | Varies greatly |
| What are two main groups of blood cells? | 1. Myeloid; 2. Lymphoid; Both derived from a primitive progenitor cell. |
| Laboratory assessment of Formed Elements (CBC) | 1. WBC count, WBC differential (% of each type) 2. Platelet count 3. RBC count 4. Hematocrit (HCT= RBC % blood volume) 5. Hemoglobin (HCB=gm pe 100 ml whole blood) 6. Calculation of RBC |
| Calculation of RBC | MCV = HCT/RBC; MCHC= HGB/HCT; MCH= worthless |
| RBC indices | Measurement of red cell size (MCV), hemoglobin content (HGB) and concentration (MCHC) are calculated from blood hemoglobin (HGB), red cell count (RBC), and hematocrit (HCT) |
| What are anemia of hemorrhage due to? | Blood loss |
| What are hemolytic anemia due to? | Red cell destruction |
| What are some anemias due to | insufficient red cell production |
| What does chronic hemorrhage produces first, then what later? | first: produces anemia of hemorrhage; later: causes failed RBC production due to iron deficiency anemia due to RBC production |
| Clinical and pathologic findings in Sickle cell anemia | |
| The blood smear in iron deficiency anemia | the red cells are small (microcytic) and pale(hypochromic) |
| The blood smear in vitamin B12 deficiency | Macrocytic RBCs (Folic acid deficiency also causes red cell macrocytosis) |
| Bone marrow in aplastic anemia | Few bone marrow cells are present. Most of the tissue is fat |
| Polycythemia (Erythrocytosis) definition | Excess RBC in body (body vs blood; All blood specimens are collected from peripheral pool, which is more concentrated than central pool. |
| What is Relative polycythemia | Low plasma volume (dehydration), "stress" polycythemia = apparent polycythemia (total RBC normal) |
| What is Absolute polycythemia | Secondary= lung disease, life at altitude; Primary= overproduction of RBC by marrow= increased total body RBC. A neoplastic state (polycythemia vera) |
| Leukopenia | low white cell count |
| Leukocytosis | high white cell count |
| Lymphadenopathy & Lymphadenitis | conditions of the lymph nodes |
| Malignancies of WBC are according to | Cell type; +/- malignant cells in blood, bone marrow; Plasma cell proliferations: multiple myeloma, Waldenstrom disease |
| Malignancies of WBC according to cell type | Lymphoid (B or T lymphocytes, NK cells) - Leukemia, lymphoma, plasma cells proliferations Myeloid (granulocytes, RBCs, megakaryocytes) - Leukemia, myelodysplasia, myeloproliferative syndromes |
| Malignancies of WBC according to +/- malignant cells in blood, bone marrow | Leukemia: + cells in blood and BM: diffuse, no mass-> Acute (aggressive) or chronic (indolent;) Lymphoma: - cells in blood or BM: discrete mass -> Hodjkin lymphoma and Non-Hodjkin lymphoma-Follicular or diffuse; |
| Bone marrow in Leukemia | The marrow is packed with cells of single type. No fat remains |
| Myeloid malignancies | Acute myeloid leukemia; chronic myeloid leukemia; mylodisplasia; myeloproliferative syndrome |
| Acute myeloid leukemia | is rapidly progressive |
| Chronic myeloid leukemia | is slowly progressive |
| Myelodysplasia | is a preleukemia syndrome |
| Myeloproliferative syndromes | are related to myeloid malignancies |
| The origin of myeloid malignancies - progenitor cells | Each malignancy derives from a particular type of myeloid progenitor cell: -undifferentiated myeloid progenitor; -megakaryocyte progenitor, -erythrocyte progenitor (RBCs), -granulocyte progenitor (granulocytes and monocytes) |
| Myeloproliferative malignancies w/ their progenitor cells | Primary myelofibrosis with myeloid metaplasia (undiff); Malignant thrombocytopenia (megakar); Polycythemia vera(eryth); Chronic myeloid leukemia (granulo & mono); *All the above lead to myelofibrosis; Myelodysplasia (gran)-> Acute myeloid leukemia |
| Acute myeloid (myelogenous) leukemia)blood smear | AML shows immature myeloid cells (malignant myeloblasts) |
| Myelofibrosis blood smear | Marrow is completely replaced by alignant fibrous tissue. No normal marrow elements remain. |
| Lymphoid malignancies | Lymphoid leukemia (malignant lymphocytes in blood); Lymphoma(no malignant lymphocytes in the blood); Plasma cell proliferations (most are malignant) |
| The peripheral blood in chronic lymphocytic leukemia (blood smear) | All of the white cells are lymphocytes and no granulocytes are present |
| Hodgkin disease aka Hodgkin's lymphoma is | A cancer originating from WBC (lymphocytes)named after Thomas Hodgkin, who first described abnormalities in the lymph system in 1832 |
| How is Hodgkin lymphoma characterized | By the orderly spread of disease from one lymph node group to another and by development of systemic symptoms with advanced disease |
| Hodgkin's microscopic findings | Multi-nucleated Reed-Sternberg cells(RS cells) are the characteristic histopathologic finding |
| How is Hodgkin's lymphoma treated | Radiation therapy, chemotherapy or hematopoietic stem cell transplantation |
| Hodgkin's choice of treatment depends on what? | age and sex of patient and the stage, bulk, and histological subtype of the disease |
| The Hodgkin's disease occurrence shows two peaks: | 1. young adulthood (15-35) 2. ppl over 55 yrs old |
| What is the survival rate in Hodgkin's lymphoma | The overall 5 yr relative survival is 83.9% Since many patients are young they often live 40 yrs or more after treatment |
| Radiation treatments and some chemotherapy drugs to treat Hodgkin's pose what risks? | Risks of causing potential fatal secondary cancers, heart disease, and lung disease 40yrs later. Modern treatments greatly minimize the chances of these late effects |
| Who has an increased risk to develop HL (Hodgkin's Lymphoma)? | Patients with history of infectious mononucleosis because of Epstein-Barr virus (EBV) - the reason is largely unknown |
| Photos with patients having nodular sclerosis Hodgkin disease are showing what | Marked enlargements of the cervical lymph nodes (cervical lymphadenopathy) |
| What is multiple myeloma/Kahler's disease? | Is a cancer of plasma cells (WBC normally responsible for producing antibodies) |
| What happens in multiple myeloma? | Collections of abnormal plasma cells accumulate in the bone marrow, where they interfere with the production of normal blood cells. Most cases of myeloma also feature the production of a paraprotein - an abnormal antibody which can cause kidney problems |
| what else is encountered in multiple myeloma? | Bone lesions and hypercalcemia |
| How is multiple myeloma diagnosed? | Blood tests(serum protein electrophoresis, serum free kappa/lambda chain assay); Bone marrow examination, urine protein electrophoresis, and X-rays of commonly involved bones. Myeloma is generally thought to be incurable but highly treatable. |
| How would remissions of multiple myeloma may be induced | May be induced with: steroids, chemotherapy, proteasome inhibitors, immunomodulary drugs (IMiDs)such as thalidomide or lenalidomide, and stemcells transplants. Radiation therapy is sometimes used to reduce pain from bone lesions. |
| Multiple myeloma develops in whom and what is the incidence? | More common in med than women- unknown reasons; Twice as common in African-Americans than European-Americans; Myeloma develops in 1-4 per 100,000 ppl per yr |
| What is the survival rate in multiple myeloma? | With conventional treatment, median survival is 3-4 years, which may be extended to 5-7 yrs or longer with advanced treatment. It is the second most common hematological malignancy in the US(after Hodgkin's lymphoma), and constitutes 1% of all cancers. |
| Disorders of the Spleen and Thymus | Spleenomegaly; Hypersplenism; Thymic hyperplasia; Thymoma; |
| What is Spleenomegaly? | It is an enlargement of the spleen and it is one of the four cardinal signs of hypersplenism |
| What happens in Spleenomegaly? | Some reduction in the number of circulating blood cells affecting granulocytes, erythrocytes, or platelets in any combination; it is a compensatory proliferative response in the bone marrow. |
| How can abnormalities of splenomegaly can be corrected? | by splenectomy |
| What is splenomegaly associated with? | usually associated with increased workload(such as in hemolytic anemia), which suggests that it is a response to hyperfunction -Associated with any disease as it is involved in cells being destroyed in the spleen |
| What are other common causes of splenomegaly? | Congestion - due to portal hypertension and infiltration by leukemias and lymphomas |
| What would show signs of portal hypertension? | enlarged spleen and caput medusa |
| What is thymic hyperplasia? | enlargement of the thymus and it is not always a disease state. |
| In what life stage does thalamus usually peaks? | peaks during adolescence, and atrophies in the following decades |
| What can thymic hyperplasia be associated with | Myastenia gravis; MRI can be used to distinguish it from thymoma; |
| What is Thymoma? | is a tumor originating from the epithelial cells of the thymus; it is an uncommon tumor. |
| What is thymoma best known for | best known for its association with the neuromuscular disorder myasthenia gravis; found in 15% of patients with myasthenia gravis; |
| Once diagnosed, how can thymoma be treated? | it may be removed surgically; in rare cases of malignant tumor, chemotherapy may be used. |
| what symptoms are associated with thymoma? | a third of all ppl have symptoms caused by compression of the surrounding organs by an expansive mass: - superior vena cava syndrome, dyphalgia (diff swallowing), cough, or chest pain |
| how is this tumor (thymoma) discovered | one-third of the patients have their tumors discovered because they have an associated autoimmune disorder- most common of those conditions is myasthenia gravis (MG) |
| MG vs thymoma condition rate | 10%-15% of patients with MG have a thymoma; 30-45% of patients with thymoma have MG |
| What are other autoimmune conditions associated with thymoma? | pure red cell aplasia, and Good's syndrome (thymoma with combined immunodeficiency and hypogammaglobulinemia) |
| How is thymoma diagnosted? | 1/3 to 1/2 of all ppl with thymoma have no symptoms at all, and the mass is identified on a chest X-ray or CT/CAT scan performed for an unrelated problem-incidental finding |
| Other reported diseases associated with Thymoma | acute pericarditis, Addson's disease, agranulocytosis, alopecia areata, ulcerative colitis, cushing's disease, hemolytic anemia, myocarditis, pernicious anemia, rheumatoid arthritis, systemic lupus eryth.,thyroidis |
| what happens when thymoma is suspected? | A CT/CAT scan is generally performed to estimate the sixe and the extent of the tumor; the lesion is sampled with a CT-guided needle biopsy; the diagnosis is made via histologic examination |
| What can be indicated of a malignancy in regards to thymoma? | increased vascular enhancement on CT scans, as can be pleural deposits |
| How is the final tumor classification and staging accomplished pathologically? | after formal surgical removal of the thymic tumor. |
| What are the selected laboratory tests in Thymoma to look for associated problems or possible tumor spread? | full blood count; protein electrophoresis, antibodies to the acetylcholine receptor (indicative of MG); electrolytes; liver enzymes; and renal function. |
| What are the three principal histological types of thymoma and depending on the appearance of the cells by microscopy? | Type A- if the epithelial cells have an oval or fusiform shape(less lymphocyte count); Type B-if they have epitheloid shape- this type has 3 subtypes:-B1 (lymphocyte rich), B2(cortical), B3(epithelial); Type AB - if tumor has combin. of both cell types |
| That is the mainstay of treatment for thymoma? | -Surgery; -if tumor is invasive and large -> preop chemotherapy and radiation to decrease size and improve resectability before surgery; -When tumor is an early stage no further therapy is necessary; |
| Thymomas treatments in adults vs children | In adults- removal of the thymus does not appear to induce immune deficiency; In children - post op immunity may be abnormal and vaccinations for several infectious are recommended |
| What would invasive thymoma require? | additional treatment with radiotherapy and -chemotherapy(cyclophosphamide, doxorubicin, and cisplatin; -invasive thymomas uncommonly can also metastasize, generally to pleura, bones, liver, or brain in approx. 7% of cases |
| What is the prognosis of thymoma in regards to stages (I,II,III, IV)? | Prognosis is much worse for stage III and IV as compared to stage I and II tumors. Pts with stage III and IV tumors may survive for several yrs with appropriate oncological management. |
| Patients who have undergone thymectomy should be warned of what? | Possible severe side effects after yellow fever vaccination- probably caused by inadequate T-cell response to live attenuated yellow fever vaccine. -Deaths have been reported |
| Who is affected by thymoma? | Men and women- equally affected; typical age at diagnosis is 30-40, however case have been described in every age grp, including children. |
Created by:
adrianaww
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