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Neoplasias I
Track 1 Lecture 1
| Question | Answer |
|---|---|
| White blood cell (WBC) (or Leukocyte) count in the blood plasma | 5,000 to 10,000 / uL |
| Granulocytes | Neutrophil Eosinophil Basophil |
| Neutrophil Count | 55-65% of all WBCs |
| Eosinophil Count | 1-3% |
| Basophil Count | 0.3-05% |
| Lymphocytes | T Cells B Cells (Plasma Cells) Natural Killer Cells |
| Lymphocyte Count | 20-30% |
| Monocytes | 3-8% |
| If the WBC count is < 5-10,000 it is called what? | LEUKOPENIA |
| How can all WBC Counts be decreased? | Aplastic Anemia Irradiation Chemotherapy Malnutrition |
| Aplastic anemia | is a condition where bone marrow does not produce sufficient new cells to replenish blood cells |
| Lymphopenia is rare or common? | RARE |
| In what disease states or treatments is lymphopenia likely to occur? | 1. Congenital Immunodeficiencies 2. Advanced HIV 3. After glucocorticoid treatment 4. Autoimmune Disease 5. Certain Infections |
| What is the MOST common leukopenia? | Neutropenia (<1500 uL) |
| Agranulocytosis | means SEVERE neutropenia (<200 uL) |
| Aplastic Anemia | All myeloid stem cells affected--monocytes, granulocytes, platelets, erythrocytes--resulting in anemia, agranulocytosis, and thrombocytopenia |
| Thrombocytopenia | is a relative decrease of platelets in blood |
| Neutropenia is caused by? | reduced production or increased removal of neutrophil granulocytes |
| What is the major cause of Neutropenia? | Most cases are DRUG-related |
| Chemotherapeutic drugs are | alkylating agents, antimetabolites |
| What do chemotherapeutics drugs do? | Inhibit the proliferation of neutrophil precursors (and other rapidly dividing cells, ex. intestinal mucosa) |
| What is idiosyncratic depression of bone marrow function? | 1. Direct toxicity to precursor cells 2. Immune-mediated destruction of cells |
| What drugs are responsible for idiosyncratic depression of bone marrow function? | Several Drugs--chloramphenicol, sulfonamides, thiouracyl, phenothiazines |
| What are other causes of neutropenia | 1. Neoplasms involving the bone marrow leukemias/lymphomas 2. Deficiency of Vitamin B12 or Folate 3. Lupus erythematosus (Fely Syndrome) 4. Congenital Neutropenias (rare) |
| Consequences of neutropenia? | Frequent Infections w/ Gram-NEGATIVE bacteria and fungi (respiratory, GI, skin) |
| Tx of neutropenia? | Hematologic Growth Factors (G-CSF) Prophylactic Abx |
| Can neutropenia be fatal? | Yes |
| Leukocytosis | raised white blood cell count (the leukocyte count) above the normal range in the blood. |
| Neoplasm | abnormal mass of tissue as a result of neoplasia |
| Neoplasia | the abnormal proliferation of cells |
| Reactive | become large (inflammatory) |
| Leukocytoses | is the increase in WBCs (aka leukocytes) |
| Leukocytoses can be ______ or _______. | reactive or neoplastic |
| Neutrophilic Leukocytoses occurs in | ACUTE bacterial infections Tissue necrosis (burns, infarction [tissue death]) |
| Eosinophilic Leukocytoses occurs in | Allergic disorder (asthma, hay fever, drug rxn) Parasitic Infxns |
| Lymphocytosis and Monocytosis indicate | CHRONIC immunologic stimulation Viral infxn (hepatitis, infectious mono-nucleosis) Lupus erythematosus Inflammatory Bowel Disease |
| Reactive (Inflammatory) Leukocytosis causes | Endotoxemia Acute infection Hypoxia Exercise Epinephrine Glucocorticoids Chronic infxn or inflammation Tumors Myeloproliferative d/o |
| Endotoxemia Acute infection Hypoxia | Increase leukocytes by increasing release from marrow stores |
| Exercise Epinephrine | Increase leukocytes by decreasing margination |
| Chronic infection or inflammation Tumors Myeloproliferative d/o | Increase leukocytes by increasing the number of marrow precursors |
| Glucocorticoids | Increase leukocytes by decreasing extravasation into tissues |
| Infectious Mononucleosis | a lympho-proliferative disorder |
| Lympho-proliferative disorder | WBC rises to > 15000 cell/uL w/ 60% lymphocytes (absolute lymphocytosis) |
| What is the cause of IM? | Epstein-Barr virus (EBV, a DNA virus) |
| What % of humans become infection with IM? | 90% |
| True or False. The EBV persists for a lifetime in its host. | True |
| What is the pathogenesis of infectious mononucleosis? | Oral Infxn |
| Where does the EBV bind? | It binds to the B-cell receptor in the lymphoid tissues of the OROPHARYNX (typically the tonsils) |
| What happens in the "productive" infxn by EBV? | the virus is released from lysed B cells |
| What happens in the "latent" infxn by EBV? | The EBV integrates into the GENOME B-cells become activated, then proliferate and disseminate in the circulation |
| The infected B cells disseminate into circulation and secrete what? | Antibodies--such as the HEREOPHILIC anti-SHEEP RBC antibodies use for diagnosis of IM |
| What is more common--productive or latent--infection of B cells by EBV? | latent (nonproductive) infxn |
| In HEALTHY individuals the immune response is directed against what? | 1. Infected B cells via NK and cytotoxic T lymphocytes 2. The EBV via IgM and IgG antibodies |
| The REACTIVE proliferation of cytotoxic T cells in response to the EBV infection causes what? | 1. Enlargement of lymph nodes (Lymphadenitis) 2. Enlargement of spleen (splenomegaly) |
| In Infectious Mononucleosis, EBV disappears from the blood BUT what can survive the immune response | B cells with latent infection |
| The latent infected B cells can still | shed the EBV for years and transmit it to other people |
| Does a person have to be symptomatic to transmitted IM to another person? | No |
| EBV is involved in a number of malignancies, in particular which kind? | several types of B-cell lymphoma |
| It is most likely occurring in hosts with? | Defective Cellular Immunity like AIDS, Bone Marrow Transplant Recipients |
| Lymphoma caused by EBV is the result of what? | Proliferation of LATENTLY infected cells that progress (through several steps) to EBV-associated B-cell NEOPLASMS |
| B-cell NEOPLASM examples | Burkitt Lymphoma non-Hodgkin Lymphoma Hodgkin Disease |
| The reactive proliferation of cytoxtic T cells causes inflammation of | several organs |
| How long is the incubation period for Infectious Mononucleosis | 4-8 WEEKS |
| After the incubation period, the initial symptoms and signs appear | symptoms= malaise, anorexia, chills signs= fever, pharyngitis, lymphadenopathy |
| What are the major alteration involved in IM? | Blood Lymph Nodes Spleen Liver CNS |
| Lymph node enlargement is mainly present where? | 1. Cervical area 2. axillary 3. groin area |
| Spleen Enlargement | Up to 3x its normal size--hepatitis w/ hepatomegaly and jaundice |
| What % of the cases of IM involve CNS, severe form | 1% |
| How long does acute illness last? | 3-6 weeks, but lethargy may persist longer |
| EBV Pathogensis | Epithelial cells of the oropharynx are the portals of EBV infection. |
| EBV Pathogensis | EBV invades B lymphocytes by means of their CD21 receptors |
| WBC cells return to normal at | 4 weeks |
| How long to heterophile antibodies remain? | 9 MONTHS |
| What is the tx for EBV infection (IM)? | Supportive and Symtomatic Bed Rest and Aspirin |
| What is the ATYPICAL presentation of Infectious Mononucleosis? | 1. Fatigue and lymphadenopathy w/o fever (leukemia?) 2. Fever w/o lymphadenopathy 3. Hepatitis 4. Febrile Rash (Rubella?) |
| What is diagnosis based on in IM? | 1. Lymphocytosis w/ atypical lymphocytes in the blood 2. Positive HETEROPHILE antibody rxn ("monospot"test) 3. Specific anti-EBV antigens |
| Infected B lymphocytes spread the infection throughout the | reticuloendothelial system (e.g., liver, spleen, and peripheral lymph nodes) |
| EBV infection of B lymphocytes results in | a humoral and cellular response to the virus |
| EBV initiates | B lymphocyte proliferation (plasma cells) and immortalization (memory B lymphocyte) without the role of T-helper cells |
| EBV is a B-cell mitogen that can cause | many B lymphocytes to become antibody-producing plasma cells. |
| Many of the antibody-producing plasma cells produce antibodies that do not react with EBV antigens | Some of the plasma cells produce antibodies that react with red blood cells from other mammals such as cattle and sheep. This humoral immune response, called the heterophile response, is the basis for the serologic tests used to screen for IM |
| Other plasma cells produce antibodies that react with EBV antigens | can be used to confirm a diagnosis of infectious mononucleosis |
| As with many viral infections | the T lymphocyte response is essential in the control of EBV infection; natural killer (NK) cells and predominantly CD8 cytotoxic T cells control proliferating B lymphocytes infected with EBV |
| Reactive (Inflammatory) Lymphadenitis | swollen lymph nodes that are palpable or visible |
| Acute Lymphadenitis | red, tender to the touch |
| Chronic Lymphadenitis | not sensitive to the the touch |
| Acute Lymphadenitis | cellular infiltration and edema |
| Acute Lymphadenitis occurs in response to | infection, wounds (nodes contain microbes or foreign matter) |
| Where is acute lymphadenitis located? | 1. cervical region-teeth or tonsils 2. Axillary or inguinal-extremeties 3. Mesenteric lymph nodes-bowels, appendicitis |
| In types of infection are acute lymphadenitis more GENERALIZED? | Viral infections Bacteremia |
| Chronic Lymphadenitis is commonly located where? | Inguinal and axillary regions |
| Chronic Lympadenitis is due to | repeated stimuli |
| What signals malignancy in lymphadenitis? | large, hard growing lymph nodes |
| Neoplastic proliferation of WBCs (tumors) can be divided into 3 broad categories | 1. Lymphoid neoplasms 2. Myeloid neoplasms 3. Histiocytic neoplasms |
| The classifcation of lymphomas and leukemias--into Myeloid or Lymphoid--reflect | the usual TISSUE DISTRIBUTION of the disease at the time of clinical presentation |
| What are the pathogenetic factors involved in neoplastic proliferation of WBCs | 1. Chromosomal translocation and oncogenes 2. Inherited genetic factors 3. Viruses 4. Other--infections (HIV), irradiation, chemotherapy |
| Chromosomal translocations and oncogenes | inhierent "genetic instability" is due to mistakes during the formation of variable gene segments of Ig's and receptors |
| Inherited genetic factors | down syndrome predisposed one to leukemia |
| VIruses | Epstein Barr Virus--lymphoma |
| What are the two groups of lymphomas? | 1. Hodgkin Lymphoma 2. Non-hodgkin Lymphoma |
| What distinguishes the two since they both most commonly arise in the lymphoid tissues? | Hodgkin lymphoma are set apart by the distinctive neoplastic REED STERNBERG GIANT CELLS |
| Malignant Lymphomas | Solid tumors originating from lymphoid tissue cells |
| What is the cause of Hodgkin Lymphoma? | unknown |
| How many new cases in the US are there of HL each year? (in young adults and over 50) | 7,300 |
| How many deaths are there each year due to HL? (in young adults and over 50) | 1,400 |
| Where does Hodgkin Lymphoma originate from? | A single lymph node (either cervical or mediastinal) |
| mediastinum | is an undelineated group of structures in the thorax, surrounded by loose connective tissue. It is the central compartment of the thoracic cavity. |
| What is characteristic of Hodgkin Lymphoma? | Reed-SternBerg Cells, with "mirror-image" nuclei: significant diagnosis (from lymph node biopsy) |
| What are the clinical features of HL? | Fever, chills, sweats |
| What is a unique symptoms of Hodgkin Lymphoma? | pain in affected lymph node after alcohol |
| What are other clinical features of HL? | Depressed cellular immunity, anergy (lack of immunity to an antigen) |
| How does advanced stage Hodgkins Lymphoma present? | Liver, Lung, GI become involved, the tumors can be demonstrated by a CT scan |
| What is the therapy for Hodgkins Lymphoma? | Curable w/ radiation and chemotherapy |
| The treatment and prognosis of HL depend on what? | 1. Stage (I-IV) of the disease |
| What is the overall 5-year survival rate for HL? | 85% |
| The survivors of HL are at risk for what? | Other Malignancies |
| Non-Hodgkin Lymphomas | a group of heterogenous (T and B cell) Lymphomas that contain any kind of lymphoma BUT Hodgkins Lymphoma |
| What is the most aggressive form of Non-HL? | DIFFUSE large B-cell lymphoma |
| What is the cause of Non-HL? | Cause is unknown but EBV, immunosuppression may contriibute and H. pylori may play a role in stomach tumors |
| What % of all cancers in the US are related to Non-HL? | 4% of all cancers |
| How many new cases each year are there of Non-HL | 56,000 |
| How many deaths each year are attributed to Non-HL | 19,000 |
| What does the manifestation of Non-HL depend on? | Depends on the Non-HL type and stage |
| Non-HL presents usually as | painless, superficial lymphadenopathy |
| Non-HL spreads to | GI Lung Liver Testes Bone Marrow |
| Humoral immunity (B lympocytes, antibodies) is | usually depressed in NON-HL |
| What tools are used to diagnosis Non-HL | Bone Marrow Biopsy CT scan MRI Bone scans |
| What does therapy for NON-HL depend on? | Histologic type and stage |
| How is early stage Non-HL treated? | Localized radiation |
| How is late stage Non-HL treated? | Combination chemotherapy and radiation |
| What is the overall 5-year cure rate for Non-HL? | 30-60% |
| What is an Rx used to treat Non-HL | RITUXIMAB |
| Rituximab | is a MONOCLONAL ANTIBODY against B-cell antigens (CD 20) |
| Leukemias | neoplasm derived from hematopoietic cells |
| What is leukemia? | Diffuse replacement of bone marrow with immature neoplastic cells |
| How many new cases in the US each year and how many deaths from leukemia each year? | 35,000/22,500 |
| Leukemia is the MOST PREVALENT MALIGANCY in what age group? | children and the leading cause of CANCER DEATH (40%) in 1-14 year olds |
| What is the cause of leukemia | Unknown More frequent after irradiation, chemotherapy Chemicals (benzene, others) Chromosomal translocations are a frequent cause |
| Acute Leukemia | Proliferation of STEMS CELLS or PRECURSOR CELLS |
| ALL | Acute Lymphoblastic (or Lymphocytic) Leukemia |
| ALL | most common leukemia in children (2-4 yrs. old) |
| Where does ALL typically originate from? | pre-B-CELLS |
| AML is aka | Acute Myelogenous Leukemia |
| AML is a | a heterogenous group of WBC neoplasias |
| In what age group does AML usually occur? | occurs mostly in adults, increasing w/ age |
| AML is associated with | Down's Syndrome Toxin Exposure |
| What are the common clinical features of ALL and AML? | S/Sx due to depressed bone marrow functiosn (anemia, thrombocytopenia) |
| S/Sx of AML and ALL | sudden onset of fatigue, fever, bone pain, bleeding (gums, nose) |
| AML and ALL individuals present with | 1. infections (due to neutropenia) 2. generalized lymphadenopathy, spenomegaly 3. CNS symptoms--mainly in ALL (headache, vomiting, palsies)--indicating meningeal spread |
| How high is the WBC count in AML and ALL patients? | 100,000 uL and above which is called leukostasis |
| Leukostasis | is caused by occlusion of pulmonary and cerebral vessels |
| Leukostasis is most commonly seen in leukemia and is characterized by | abnormal intravascular leukocyte aggregation and clumping. The brain and lungs are the two most commonly affected organs. |
| Occluded microcirculation resulting from leukostasis is different from leukocyte infiltration into organs and causes | local hypoxemia and hemorrage manifesting as headache, blurred vision, transient ischemic attacks, cerebrovascular accidents and dyspnea |
| What is used to diagnosis AML and ALL | 1. blood and bone marrow cells 2. CT scans to locate other sites 3. Lumbar puncture in ALL to check for CNS involvement |
| What is the treatment for AML and ALL | Chemotherapy 1. Induction-initial chemotherapy 2. Intensification or consolidation to further reduce the number of leukemic cells 3. Maintenance therapy--to maintain remission (up to 2 YEARS for ALL) |
| What is the treatment for CNS involvement (occurs mostly in children w/ALL)? | requires high-dose chemotherapy to surmount the blood-brain barrier |
| What is an example of high dose chemotherapy tx for CNS involvement in ALL? | HDML: high dose methotrexate followed "leucovorin rescue" |
| What is a more dangerous tx in CNS involvement tx for ALL | irradiation |
| What may follow the treatment with chemotherapy | Tumor Lysis Syndrome |
| What is Tumor Lysis Syndrome | Hyperkalemia Hypocalcemia Acidosis Hyperuricemia |
| Tumor Lysis Syndrome can be life-threatening? T or F. | True |
| What it the treatment for Tumor Lysis Syndrome? | 1. Hydration 2. Control of Electrolytes 3. Allopurinol (for hyperuricemia) |
| What is supportive therapy for ALL and AML | Transfusions Antibiotics |
| What is the prognosis for ALL | In children--80% cure w/ chemotherapy In adults--30-40% disease-free survival |
| What is the prognosis for AML? | More difficult to treat Only 15-30% remain disease free for 5 years |
| What is an option for younger patients with AML and ALL who do NOT respond to chemotherapy | Bone Marrow Transplantation |
| Which of one, AML or ALL, occurs mostly in adults? | AML |
| How is HL distinguished from Non-HL? | HL 1. Reed-SternBerg Cells 2. Distinctive clincal features: FEVER 3. Stereotypical Pattern of Spread |
| HL is a tumor of | B-Cell origin |
| ALL | acute leukemia derived from proliferation of lymphoblasts (immature lymphocytes) |
| AML | acute leukemia derived from proliferation of immature "myeloid" cells derived from myeloid stem cells |
| Lymph nodes of the thorax | Lymph nodes of the lungs Mediastinal lymph nodes |
| Lymph nodes of the lungs | flows subsequently to the mediastinal lymph nodes |
| Mediastinal lymph nodes | consist of several lymph node groups, especially along the trachea (5 groups), along the esophagus and between the lung and the diaphragm. |
| The mediastinal lymph nodes along the esophagus are in tight connection | with the abdominal lymph nodes along the esophagus and the stomach. |
| That fact facilitates spreading of tumors cells through these lymphatics in cases of cancers of the | stomach and particularly of the esophagus |
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