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Unit 6

Unit 6. Gordons Functional Health Pattern Activity - Exercise. Blood Disorders. Blood Conditions. Unit objectives: Discuss the components, characteristics and functions of the hematopoietic system. Compare the assessment data and the pathophysiologic bases that occurs in blood disorders

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Unit 6

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  1. Unit 6 Gordons Functional Health Pattern Activity - Exercise Blood Disorders

  2. Blood Conditions • Unit objectives: • Discuss the components, characteristics and functions of the hematopoietic system. • Compare the assessment data and the pathophysiologic bases that occurs in blood disorders • Discuss blood transfusion administration, reactions and management • Describe the various anemia’s in relationship to decreased, increased and hemolysis of erythrocytes • Discuss diagnostic tests, medical management and nursing interventions for the anemia

  3. Blood conditions • Discuss the chronic conditions in which anemia can occur. • Describe sickle cell crisis and its management • Differentiate between DIC and clotting problems • Compare and contrast acute (ALL, ANLL) and chronic (CML, CLL) leukemias, their clinical manifestations and management. • Compare and contrast lymphomas, multiple myeloma, Hodgkin’s and non-Hodgkin’s lymphoma, their diagnostic evaluations, clinical manifestations and management. • Discuss other FHP’s that might relate to hematopoietic problems

  4. Blood Conditions REQUIRED READING: • Smeltzer: Chapter 33

  5. Blood Conditions • A & P review: blood • Hematologic system  blood, bone marrow & reticuloendotheliaL system [REM] • Organs: Peripheral Lymphoid Tissue – sites for antigen processing • Lymph nodes- small organs, < 5 mm in diameter, found throughout body & interconnected w lymph vessels; provide RES & immune functions; receive fluids taken up by lymphatic capillaries from distal tissue sites. Macrophages w/I the node monitor the fluid for foreign particulates & phagocitis them; found in large numbers in abdominal & thoracic areas; called superficial nodes – lying close to the body surface; when inflamed & swollen  palpated & diagnostic • Lymph nodules – modules found in mucosal epithelium lining in resp, GI, and urogenital tracts.

  6. Blood conditions • Central Lymphoid Organs • Spleen – largest lymphoid organ in body; functions  blood-clearing process; assisting in recycling iron by capturing HgB released from destroyed RBC’s, and removing particles from RBC’S w/o destroying the cell itself; the pulp is divided into red zones & white zones ( accumulations of lymphocytes) • Thymus – located in the mediastinum, reaches peak development during childhood; endocrine organ secretes hormones that contributes to maintenance of T-cells.

  7. Blood conditions • Bone marrow – one of largest organs in body, total weight in adult of about 3000 g (comparable to liver); • Visual appearance –red marrow – hematopoietic cells interspaced w sinusoidal capillaries and yellow marrow – large number of adipose cells • Functions: • Stem cells – primitive; self-replicate, all blood cells are derived • An environment for the differentiation and maturation of blood cells • A storage site for large numbers of neutrophils & erythrocytes • Transformation of undifferentiated lymphocytes into mature Hematopoiesis

  8. Blood conditions • Blood  mixture of cells- RBC’s, WBC’s, & platelets, plasma • Functions: supplies oxygen from the lungs & absorbed nutrition from the GI tract to cells’ • Removing waste products from tissues to the kidneys, skin & lungs for excretion • Transporting hormones from their origin in the endocrine glands to other areas of body • Protecting the body from dangerous microorganisms • Promoting homeostasis ( the arrest of bleeding) • Regulating body temperature by heat transfer

  9. Composition of blood • 8% of total body wt is blood; young female has 4-5 L, young male has 5-6 L • Inverse relationship between blood volume & kg of body wt  the less body fat, the more blood per kg of body wt • Arterial blood is bright red because of O2 bound to Hgb & w/I RBC’s. venous blood is darker • Blood is 3-4x more viscous [thick] than water. • Blood is slightly alkaline, pH of 7.35 -745 [neutral pH is 7.0]

  10. Plasma • The liquid portion of the blood, • 55% of blood • 92% water, 7% protein, and < 1% nutrients, metabolic wastes, resp gases, enzymes, hormones, clotting factors, • 45% suspended particles [blood cells & platelets] • Major function is to maintain blood volume • Packed cell volume or hematocrit: the volume or % of the RBC’s in sample –35% to 45% • HcT can be  from loss of plasma (dehydration) or  production of RBC’s (polycythemia) • WBC’s & platelets -1 % of blood volume; form a buff coat or white layer seen at interface of the RBC’s and plasma

  11. RBC’s • Erythrocytes • carry O2 or hemoglobin to the cells & CO 2 back to lungs • Assist with acid-base balance – carbonic anhydrase • Structure: no nucleus, 7.5 um in diameter, depression on flat side  very large surface area, to allow cell to change shape passively as it goes thru capillaries. • Production  erythropoises every minute, more than 100 million RBC’ s are formed to replace of destroyed cells. • Precursor cells, proper microenvironment, & adequate supplies of iron, vit B12, folic acid, protein, pyridoxine & traces of copper • Arise from nucleated cells called hematopoietic stem cells • Immature erythrocytes leave the bone marrow  circulation now called reticulocytes  spleen  undergo conditioning  mature erythrocytes  general circ. Life span 105-120 days •  RBC production when O2 levels ↓ ; during pregnancy or erythropoietin – healthy bone marrow can increase production 6-7 x normal rate

  12. RBC’s • Erythrocytes • Aged erythrocytes  fragile  rupture  release of hemoglobin, “ghost cells”, taken up by macrophages  hemoglobin broken down into heme (iron) goes to liver; porphyrin  liver converts into bilirubin  excreted as bile • Nutritional influences on RBC production • Vit B12 – RBC maturation, nervous system function • Not synthesized in body, must ingest from diet [meat, dairy products]; called extrinsic factor (outside the body), when digested from food, Vit B 12 binds w glycoprotein called intrinsic factor (inside body) in duodenum for absorption in the blood • Folic acid – a B-group vit, • Synthesized by many plants & bacteria; food sources: vegetables & fruit • Iron – essential to hemoglobin production. • Adults 50 mg of Fe per 100 ml of blood; Hgb accounts for 2/3 of iron (essential iron), 1/3 resides in bone marrow, spleen & liver. In Fe deficiency develops these stores are reduced first, followed by a gradual loss in Hgb

  13. Platelets • Platelets (thrombocytes) • Are granular fragments from giant multinucleated cells in red bone marrow (megakaryocytes); takes 5 days to form & live only 7 -10 days • have two roles in homeostasis: • Occlusion of small openings in blood vessels • Provide chemical components leading to coagulation • Substances released from platelet aggregation activate coag factors that provide for a stable clot or plug w fibrin

  14. Role of liver & spleen • Spleen – reservoir for erythrocytes – during severe anemia • Liver – fixed macrophages (Kupffer cells) remove inanimate particulates & bacterial cells; • Production of small quantities of erythropoietin • Synthesis of plasma proteins & clotting factors • Decomposition of Hgb into bilirubin • Storage of iron in form of ferritin

  15. Homeostasis • Normal homeostasis – process that repairs vascular breaks to reduce blood loss while maintaining the flow of blood through vascular system; 3 components: • Blood vessels, the platelets, & coagulation factors • Work in 3 stages: • Vascular phase  vasoconstriction of the vessel occurs • Blood vessels supplying the site constrict (muscular tissue & reflex nervous system reactions, serotonin is released. • Formation of a platelet plug • In circulation, recognize a disruption or alteration in the endothelial lining of blood vessels  become sticky & adhere to one another • Coagulation or formation of a fibrin clot • If bleeding is severe, coagulation factors must join w platelets for form a permanent clot • once clot has served its purpose, it is balanced by fibrinolysis (clot dissolution)

  16. Homeostasis • Clot formation: results in either one or two pathways: table 1, pg 63 a • Extrinsic pathway: initiated when tissue injury occurs outside the vessel i.e.: burn • Damaged tissue releases factor III (tissue thromboplastin) which initiates the clotting cascade to form activated factor X  leads to clot formation • Intrinsic pathway: involves blood itself, i.e.: antigen – antibody reactions & endotoxins; • All factors for this reaction already in blood; pathway starts when factor VII is exposed to a foreign surface  cascade of enzymatic reactions to activate factor X • Activated Factor X is responsible for conversion of prothrombin to thrombin & soluble fibrinogen to insoluble fibrin clot (forms dense interlacing threads to entrap cells)

  17. Fibrinolysis • Blood carries natural anticoagulants – heparin, antithrombin • Clot dissolves: • Plasminogen is required to breakdown fibrin, already in blood & in clot  turns into plasmin  digests the fibrinogen & fibrin

  18. Leukocytes (WBC’s) • 5 types _classified according to presence or absence of granules & staining characteristics of their cytoplasm • Myeloid Stem cell  granulocytes 3 types: • Neutrophils – primary cell to respond to an acute inflammatory response, stored primarily in bone marrow • Eosinophils – protect against parasitic infections & modulate IgE – mediated allergic responses. • Basophils – store heparin, histamine • Agranulocytes (WBC w/o cytoplasmic granules) 2 types: • Monocyte – released into circ as a immature phagocytic cell,  liver, transform into macrophage with full phagocytic function • Lymphocytes – some programmed to become T cells & others B cells in bone marrow • B cells function in antibody-mediated immune response to defend the body against invasive types of bacteria,, bacterial toxins & some virus • T cells are bases of cell-mediated immune functions that defend against intracellular pathogens, fungi & virus

  19. Anemia’s • Loss of RBCs • Decreased production of RBCs • Increased destruction of RBCs • Medical management is directed towards correcting or controlling the cause and/or replacement of RBCs • Nursing interventions are directed at managing fatigue, maintaining adequate nutrition and perfusion, complying with prescribed therapy, and monitoring and managing potential complications

  20. Types of Anemia • Anemias of Renal Disease and Chronic Disease • Aplastic • Iron Deficiency • Megaloblastic • Myelodysplastic Syndromes • Hereditary Hemochromatosis • Thalassemia • Sickle Cell • Immune Hemolytic

  21. Anemias 2. Anemia in renal dz – due to decreased production; deficiency of erythropoietin and shortened RBC life span 3. Anemia in chronic disease – due to decreased production, deficiency of erythropoietin and shorten RBC life span 4. Iron-deficiency anemia (chronic, microcytic, hypochromic) a. Pathophysiology – inadequate absorption or excessive loss of iron b. clinical manifestations Lab – low hbg, ↓total RBC, MCV, MCH & MCHC. Mild case may be asymptomatic c. Management/nursing determine cause, iron preparations, diet, preventive education – diet with foods high in iron – organ meats, beans, leafy vegetables, raisins, molasses. Pace/plan activities. 5. Magablastic anemia – caused by deficiencies of vitamin B12 and or folic acid.

  22. Anemias • Aplastic anemia (normochromic normocytic) pancytopenia ↓ RBC,WBC,and Platelets • Pathophysiology – decrease in or damage to marrow stem cells. • Clinical manifestation Lab:↓RBC gradual onset, weakness, dyspnea on exertion, abnormal bleeding when thrombocytopenia present. • Management/nursing bone marrow transplantation, immunosuppressivetherapy, supportive therapy (transfusions), preventive education. Plan/pace activities and avoid trauma.

  23. Anemias 6. Vitamin B12 deficiency (pernicious anemia) • Pathophysiology – faulty absorption from the GI tract, lack of intrinsic factor • Clinical Manifestations Lab - ↓ RBC, WBC, and MCH and  MCV and number of megaloblasts (by bone marrow aspiration). Schilling test SXS – pale, fatigue, weakness, smooth sore red tongue, mild diarrhea, confusion, paresthesia of extremities, difficulty maintaining balance. • Management/nursing preventive education – vegetarians vit B12 administration support during tests care of neuropathy problems • Folic acid deficiency – more commonly seen than Vit deficiency a. Pathophysiology – folic acid deficiency b. Clinical manifestations – Lab – decreased serum folate – schilling test. Sxs – sore red tongue, no neurological manifestations c. Management/Nursing diet – uncooked vegetables, green leafy vegetable, liver, citrus fruits, and yeast folic acid supplementations.

  24. Anemias Hemolytic anemias: • Major hallmarks – shortened RBC life span, abnormal increase in the number of RBC destroyed and failure of the bone marrow to replace destroyed RBCs • Causes trauma, chemical agents and medications, infectious agents, systemic disease, antigen-antibody reactions • Clinical manifestations Lab:  retic count,  indirect bilirubin, ↓haptoglobuin and red cell survival study. SXS – pale, dyspnea, jaundice, cholelithiasis, splenomegaly, hepatomegaly • Management/nursing ID cause and correct maintain fluid and electrolytes balance 02 administrations, preventive education, pace/plan activities

  25. Anemias Inherited hemolytic anemias • Herditary spherocytosis (congenital hemolytic jaundice, congenital sphereocytic anemia). Inherited as a simple medelian dominant trait a. clinical manifestations – anemia, jaundice, splenomegaly b. Management/nursing – splenectomy, O2 adm, blood transfusion • Sickle Cell anemia a. Pathophysiology – inheritance of the sickle hemoglobin gene (Hbs) b. Clinical manifestations – anemia, jaundice. c. preventive education – avoid infections, cold temps. supportive care – hydration, avoid high attitudes, folic acid d. Sickle Cell Crisis – (occlusion of microcirculation) clinical manifestations – severe pain, fever, and leukocytosis management/nursing – control of pain, IV fluids, transfusions, O2 therapy.

  26. Anemias 3. Thalassemia (Mediterranean anemia, cooley’s anemia) Characteristics – hypochromia, microcytosis, hemolysis, variable degrees of anemia • Classified (according to affected globin chain) • a-thalassemia – mild form • b-thalassemia – more common form • Thalassemia minor – asymptomatic • Thalassemia major (cooley’s anemia) – severe anemia, marked hemolysis of erythorytes, jaundice. TX – splenomegaly, transfusions.

  27. Anemias 4. Glucose-6-Phosphate Dehydrogenase Deficiency (G6PD) • Pathophysiology – a genetic defect of the RBC • Clinical manifestations Lab – G6PD may be asymptomatic, jaundiced, pallor, increased reticulocyte, Heins bodies • Management/Nursing – preventive education, rest, fluids & nutritious diet, transfusions 5. Acquired Hemolytic Anemias Immune hemolytic anemia as a result from exposure of the RBC to antibodies. a. Clinical manifestation – fatigue, dyspnea, jaundice, splenomegaly b. Management/nursing – ID causative agent, corticosteroids, blood transfusions, spleenectomy, immunosuppressive agents.

  28. Polycythemia • Polycythemia Vera is a proliferative disorder in which myeloid stem cells escape normal control mechanisms • RBC, WBC, and platelet counts are elevated • Secondary Polycythemia is caused by excessive production of erythropoietin • May occur as response to hypoxia or neoplasms • Medical management is removal of cause or therapeutic phlebotomy

  29. Leukopenia and Neutropenia • Leukopenia is condition of fewer WBCs than normal, results from neutropenia or lymphopenia • Neutropenia results from decreased production or increased destruction of neutrophils • Medical management varies depending on cause • Nursing management is towards preventing and managing infections

  30. Leukocytosis and Leukemias • Leukocytosis is an increased level of WBCs • Leukemia is a neoplastic proliferation of one particular cell • Acute and Chronic Myeloid Leukemia • Acute and Chronic Lymphocytic Leukemia • Agnogenic Myeloid Metaplasia

  31. Leukemia • Is a malignant ds of the blood-forming organs. • 8% of all human cancers • Most common in children & young adults – 80% are lymphatic; 20% nonlymphatic; adults are opposite • Cause unknown • Risk factors: genetic factors; exposure to ionizing radiation & chemicals (benzene); medications ( alkylating agents); congenital abnormalities (Down’s syndrome); presence & infection w human T-cell leukemia virus type 1 [HTLV-1]

  32. Leukemia • Pathophysiology: uncontrolled proliferation of leukocytes  lack of control  normal bone marrow to be replaced by immature & undifferentiated leukocytes (blast cells)  circulate in blood & infiltrate blood forming organs (liver spleen, lymph nodes) • Classification: acute leukemia's are classified according to their morphologic characteristics & histo-chemical staining of blast cells  indicates the % of immature cells in bone marrow

  33. Acute leukemia • Acute = 50% of the marrow cells must be immature; two major forms: lymphocytic & nonlymphocytic leukemia • Clonal disorders  a single lymphocyte stem cell undergoes transformation  divide slowly & take longer to synthesize DNA (blast phase leaving WBC’s undifferentiated or blasts  block cell precursors & compete w normal cellular proliferation “blocking out” the marrow & cause other cell lines to stop production  causing pancytopenia ( a reduction in all cellular components) • Acute lymphoblastic leukemia (ALL) • Most common in children (median age 11 yrs), acute course—initial symptoms & w/o tx die 3-6 months, males > females, more common in European – Americans

  34. Acute Leukemia • Acute adult nonlymphatic leukemia (AANLL) – more common in adults, (median age 67 yrs), also called acute myeloid leukemia (AML) • involves the rapid accumulation of hematopoietic stem cells, (differentiate into monocytes, granulocytes, RBC’s, and platelets) • History: questions – exposure to radiation, chemicals, viruses, & medications, occupation? Power plant or serving in military • S&S: sudden onset of high fever, signs of abnormal bleeding [bleeding gums, long menses, petechiae,  bruising, nose bleeds],  fatigue & malaise, wt loss, night sweats & chills, c/o abd or bone pain, appear acutely ill, dyspnic, & pale, enlarged liver &lymph nodes; CNS involvement – HA, vomiting & papilledema, blurred vision, meningeal irritation, intracranial hemorrhage,  chemo does not pass the blood brain barrier • psychosocial assessment  pts, families are shocked & fearful

  35. Acute leukemia • Neutropenic precautions- neutrophils < 2000 mm3, necessary in prevention & limiting infections (chart 33-9, page 898) • Bone marrow transplant – BMT is the administration of 500-700 ml of marrow aspirated from the pelvic bones of the patient during a remission (autologous transplant) – most common; (allogeneic transplant) – compatible donor – usually a parent or sibling. • Transfusion of RBC’s & platelets – may be required until the BM produces mature cells • Radiation TX – adjunct to chemo when leukemic cells infiltrate the CNS, skin, large mediastinal mass

  36. Chronic Leukemia • Chronic lymphatic leukemia (CLL) –involves lymphocytes, (cells that circulate among the blood, lymph nodes, lymphatic & lymphoid organs); characterized by an uncontrollable spread of abnormal, small lymphocytes (early B lymphocytes) • 33% of new leukemia cases annually in US are dx as CLL. • Least malignant form & progresses more slowly than others, sometimes takes as long as 15 yrs (WBC produced are more mature & better to defend body against infection)

  37. Chronic Leukemia • Causes: unknown, several risk factors:  families, suggesting heredity issues, possible genetic predisposition, immunologic defects – ataxia-telangiectasia (vascular lesions formed by dilation of a group of small vessels, birthmarks) • Men > woman, and over the age of 50 • S&S: same as all types of leukemia;  anemia, thrombocytopenia, & leucopenia; hx of malaise & enlarged nodes, fever  susceptible to opportunistic fungal, viral & bacterial infections, lost wt, any bleeding, family hx of CLL, pale, enlarged liver or spleen, skin has macular or nodular infiltrates

  38. Chronic Leukemia • Chronic myelogenous leukemia or chronic granulocytic leukemia – characterized by abnormal overgrowth of myeloblasts (all granulocytic precursors) • Gradual onset, WBC’s more mature • Two phases: insidious chronic phase – originates in the pluripotent stem cell w an initial finding of hyper cellular marrow w a majority of normal cells; after approx 4 yrs.  enters a blast crises or acute phase. • Causes: 90% of pts have the abnormal Philadelphia chromosome – thought to be induced by radiation or carcinogenic chemicals; unidentified virus • Occurs more commonly in young-to middle aged adults; 25 -60 yrs of age; slightly more men than women

  39. The Lymphomas • Neoplasms of cells of lymphoid origin • Hodgkin’s Disease • Non-Hodgkin’s Disease • Multiple Myeloma

  40. Lymphoma’s • Originating from the lymphatic system, lymphoma is most common tumor of lymphoid system; primary (thymus or BM) or secondary tissue ( lymph nodes, spleen, tonsils)-most arise from secondary • Major subdivisions are: Hodgkin’s lymphoma / Hodgkin's Disease (HD); Non – Hodgkin’s lymphoma (NHL) • 55,000 cases dx annually

  41. Hodgkin’s Disease • In 1832, Hodgkin described a ds w enlarged lymph nodes starting in the neck & spreading throughout the body & bx showed a distinctive large cell – called the Reed-Sternberg cell – when the cell is absent the ds is classified as NHL • Incidence – 7500 new cases per yr, slightly more males than females, strikes in young adult hood (ages 15 to 38) & a second peak later in life > 50, worse prognosis • Etiology – exact cause unknown, researchers suspect an infectious component, ie: Epstein-Barr virus (organ transplant recipients/ immunodeficiency ds, hx of mononucleosis (2-3x), some studies show genetic predisposition (Jews)

  42. Hodgkin’s Disease • Pathophysiology – painless progressive enlargement of LN, caused by a proliferation of lymphocytes, histiocytes, eosinophils & Reed – Sternberg giant cells. • Progressive & fatal if not treated, but one of the most curable w tx (5yr survival rate > 90%) • S &S- often are asymptomatic & present w painless lymphadenopathy – • . Nonproductive cough –X-ray shows a mediastinal mass in 50% of pts; • freq noc sweats & fever > 38 *C • Dx: LN & bone marrow bx, Chest - X-ray; CT of thoracic, abd & pelvis & staging laparotomy

  43. Hodgkin’s Disease • Staging: HD is divided into stages according to the microscopic appearance of involved LN, the extent & severity & prognosis

  44. Hodgkin’s Disease • Tx- begins w accurate classification & staging • Radiation is used for early less extensive ds • Stage 2 is combination of radiation & chemo used for IIB, and III A & B, • combo chemo for stage 4

  45. Non-Hodgkin’s Lymphoma • AKA – malignant lymphoma; comprises a group of malignancies w a common origin in the lymphoid cells’ characterized by random proliferation of lymphocytes • Ranges from aggressive, rapidly fatal to indolent nodular varieties • Less promising prognosis than HD • ACS – estimates 55,000 new cases annually, & 25,000 related deaths; average age at dx is in 50’s • 7 x more common than HD • Between 1973 & 1992, a 75% increase in NHL • 60 X more common in pts w AIDS • 6th most common cause of cancer • Men > woman;  in whites than other races

  46. Non-Hodgkin’s Lymphoma • Pathophysiology – an abnormal proliferation of neoplastic lymphocytes – • S&S – localized or generalized lymphadenopathy ( cervical, axillary, inguinal & femoral), swelling is painless, nodes have gradually enlarged over months or years; can be diffuse s&s – B symptoms ( noc sweats, fever & wt loss, 1/3 have hepatomegaly or splenomegaly • Labs: CBC. ESR & peripheral smear,  LDH in advance stages, uric acid, Ca, • LN bx done for adenopathy > 3 weeks; B symptoms not attributed to other causes, abnormal blood tests, Xray– shows possible extranodular involvement, CT of abd & pelvis • Disease staging

  47. Non-Hodgkin’s Lymphoma • Medical Management – tx is based on classification of the cell & staging of ds. The ds process may be slow enough that tx is saved until ds takes a more aggressive path. • Stage 1-11 radiation alone may be curative • Intermediate-high grade lymphomas receive combo chemo; • combination chemo & radiation tx is done to produce tumor shrinkage & remission

  48. Nursing Management • History & Physical- • Any hx of HIV?, organ transplant, autoimmune ds, c/o painless enlarged LN? fever, noc sweats, wt loss, weakness & malaise, cough, dyspnea & chest pain (occur 20%  indicates lung involvement) • LN  palpate chains infraclavicular, iliac, femoral sites (involved nodes are painless, firm & rubbery in consistency)& abdomen signs of hepatosplenomegaly? & ascites? Skin lesions that look like nodules (20% of cases), • Psychosocial assessment – dx of cancer is devastating, more common in older adult, effects retirement plans  may lead to feelings of loss, grief, & anger.

  49. Oncology • Approx 1.2 – 1.3 million new cancers are dx each year • Over 500,000 cancer deaths/ yr • NCI = National Cancer Institute estimate 8.4 live today w a hx of cancer • Terminology: • Tumor – lump, mass, or swelling (lay public use as a synonym for cancer) • Neoplasm – (Greek neos = new, plasis = molding); abnormal mass of tissue serves no useful purpose & may harm the host organism • Benign – usually a harmless growth that does not spread or invade other tissues, does occupy space • Malignant – harmful mass, capable of invasion of other tissues & metastasis (spread) to distant organs • Cancer – used to refer to malignant neoplasms; ds of the cell in which normal mechanisms of control of growth & proliferation are altered, its invasive, spreads directly to surrounding tissue and to new sites • Oncology – refers to the medical specialty that deals w the dx, tx & study of cancer

  50. Oncology • Mortality rate = the # of deaths caused by cancer that occurs in a population in a given yr; expressed as # of deaths due to cancer per 100,000 persons. • Common misconceptions: • Cancer is one disease --- cancer is many diseases • The change from a normal cell to neoplastic cells is a process not a single event or a single alteration in cells; clinical manifestations are only the final stages in the natural history of cancer

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