NURS 5315/ NURS5315 Exam 2 – Advanced Pathophysiology Guide | UTA (Latest 2026/2027 Update) Verified Questions & Answers | Grade A

NURS 5315/ NURS5315 Exam 2 – Advanced Pathophysiology Guide | UTA (Latest 2026/2027 Update) Verified Questions & Answers | Grade A 2026/2027 | GRADED A+ | 100% VERIFIED Question: Antibodies appear _________ days after an antigen invades the body Answer 6-7 Question: Secondary immune response is also known as _________ immune response Answer Anamnestic Question: The pathogenesis of ___________ is related to antibody/antigen complexes which are deposited in tissues/organs and triggers the immune response Answer Lupus Question: ___________ ____________ ________________ is derived from the fatty acids in the plasma membrane. This substance can be produced by neutrophils, monocytes, endothelial cells and platelets. It works in a similar fashion as leukotrienes and causes endothelial cell retraction, increases vascular permeability, activates platelets, and enhances leukocyte adhesion to endothelial cells. Answer Platelet activating factor (PAF) Question: Blood loss, gross or occult, will lead to ____________________ anemia Answer an iron deficiency Question: Colon cancer can cause what type of anemia? Answer Iron deficiency Question: Pernicious anemia is due to lack of Answer intrinsic factor Question: Beefy red tounge, neurologic symptos, paresthesia of handsfeet and loss of sense of position/vibration all symptoms of what Answer pernicious anemia Question: ________________ anemia may result in myocardial damage and poor heart contractility Answer Pernicious Question: Alcohol interferes with ___________ metabolism in the liver and therefore depletes stores Answer folate Question: Severe cheilosis, burning mouth syndrome, dysphagia, flatulence and watery diarrhea all symptoms of ________________________________ anemia Answer folate deficiency Question: Review how prednisone impairs phospholipase A. Answer Corticosteroids inhibit the action of phospholipase A2 thus preventing the formation of prostaglandins, thromboxane A2, prostacyclin and leukotrienes Question: Joint bleeding Answer tissue hematomas large, spontaneous, centrally located ecchymosis bleeding after trauma, surgery, or an injury tends to be delayed Question: symptoms of what hemostasis disorder Answer Coagulopathy hemmorhage hemophilia Question: Epistaxis Answer Oral bleeding GI or GU Bleeding (in the absence of malignancy) Hemoptysis Heavy menses Question: symptoms of what hemostasis disorder Answer Thromobocytopenia hemmorhage Question: Etiology of Thrombocytopenia Answer decrease in total number of platelets Question: hemodilution Answer spleenomegaly HIV Bone marrow failure meds Question: ___________ functions to help with maturation of T-Cells Answer IL2 Question: lymphocytosis results from _________________ infections Answer viral Question: neutrophilia results from _______________ infections Answer bacterial Question: Eosinophilia results from __________________ infections Answer parasitic and allergic reactions Question: Transplant rejection is a ___________________________ response Answer T-Cell mediated Question: Aging does what to T-Cell function Answer activity decreases Question: Clopidogrel works by inhibiting the ______________________________ Answer P2Y12 receptor block ADB from binding to P2Y12 receptor thus allowing cAMP to exert its action and prevent platelet aggregation Question: renal failure can be a cause of ________________________ Answer COX 2 inhibitors they do not cause gastric ulcerations/edema/olatelet dysfunction Question: The ________________ in a CBC test is the best way to determine type of anemia Answer MCV Question: Edema of hands/feet in an infant can be a result of Answer sickle cell anemia/vaso-occlusive crisis Therapeutic interventions for Protein S deficiency Answer Coumadin low molecular weight heparin cannot inhibit _____________________. it can only inhibit clotting factor ___ Answer Thromibin Xa When histamine 1 is stimulated: Answer promote inflammation when histamine 2 is stimulated anti-inflammatory properties location of histamine 1 receptors smooth muscle, bronchi location of histamine 2 receptors gastric mucosa normal phys---gastric acid secretion symptoms associated with flu are a result of release of cytokines hemodilution splenomegaly HIV, bone marrow failure hemolysis medications all can result in what happening to platelets thrombocytopenia Malignant transformation of B-cells which infiltrate the bone marrow, bone and other soft tissues Multiple myeloma Uncontrolled proliferation of malignant leukocytes which blocks the growth of healthy blood cells Leukemia Antigen antibody complexes bind to the Fc receptors on platelets which leads to their destruction in the spleen. Immune thrombocytopenic purpura They assess for the presence of antibodies to HIV The test can be completed on urine, saliva, or serum; however, the most accurate results are obtained from testing the serum. Together the tests have a sensitivity and specificity of 99% at 12 weeks post-exposure. The 3rd generation immunoassay This test is designed to detect antibodies to HIV and to detect the presence of the P24 antigen. Remember this is part of the HIV's viral proteins. The P24 antigen can be detected as early as ten days post-infection 4th generation combination immunoassay Factor VIII Deficiency, A mutation, the altered or msising protein cannot participate in the clotting cascade process. This results in reduced coagulation ability and prolonged bleeding Hemophilia A Factor IX deficiency, x-linked recessive trait, varied degrees of severity Hemophilia B/Christmas Disease characterized by undifferentiated or immature cells, usually a blast cell, and the onset of disease is abrupt and rapid with a short survival time Acute leukemia the predominant cell is more differentiated but does not function normally, with a relatively slow progression Chronic leukemia excessive production of lymphocytes Lymphocytic leukemia excessive production of granulocytes Myelogenous leukemia HIV EIA (3rd generation immunoassay) can use urine, saliva, or serum (most accurate), need to wait until 12 weeks post exposure to see antibodies, 99% accurate 4th generation immunoassay- "gold standard" measures P24 antigen can test 10 days post exposure Mast cell Cellular bags of granules located in loose connective tisssue close to blood vessels. Activation initiates inflammatory process. Histamine Causes vasodilation, increases vascular permeability, increases blood flow to the site of injury- causes erythema and swelling. Cytokines Soluble factors that contribute to the regulation of innate or adaptive resistance by affecting other neighboring cells. Can be pro-inflammatory or anti-inflammatory. Can react quickly or be more delayed. Leukotrines Released when mast cells degranulate, prolong the inflammatory process. Cause vasodilation, attract neutrophils, monocytes, and t of inhibition for singular. Prostaglandins Released when mast cells degranulate, are produced by the arachidonic pathway. Cause vasodilation, platelet aggregation at site of injury, pain, and fever. Chemotactic factors Biochemical substance that attracts leukocyte to the site of inflammation Neutrophils Predominant leukocyte at work during the early stages of acute inflammation Monocytes Become macrophages when entering the tissue, responsible for presenting antigens to the CD4 cell which triggers T cell immunity and B-cell immunity. Releases additional cytokines IL1, IL6, TNF. Cytokine IL1 function Causes fever, activates phagocytes & lymphocytes and also increases the release of IL6a Cytokine IL6 function Stimulates production of acute phase reactants and promotes growth and stimulation of RBCs Cytokine TNF function Causes fever, increases synthesis of proinflammatory proteins by liver, causes muscle wasting, induces thrombosis Cytokine growth factor function Promotes production and maturation of neutrophils Complement Functions include bacterial lysis, vasodilation and increased vascular permeability, triggers mast cell degranulation, chemotaxis, and opsonization. Kinin Converted to bradykinin which is responsible for pain and chemotaxis, and it increases vascular permeability and vasodilation. Coagulation cascade Factor XII activates kinin. Function is to form fibrin mesh to stop bleeding and trap micro organisms. COX1 Prostaglandin of arachidonic pathway. Provides gastroprotection, platelet aggregation, fluid/electrolyte balance COX2 Prostaglandin of arachidonic pathway. Responsible for pain, fever, renal protection, tissue repair, reproduction development. COX2 inhibitors- clinical implications Protect gastric mucosa- prevent ulcers and bleeding. Removed from market r/t cardiac events except for Celebrex. Can impair renal function , monitor labs. Arachidonic pathway purpose Synthesis of prostaglandins Non-selective NSAIDS Inhibit COX1 and COX2, risk for gastric ulceration, GI bleeds, edema, renal impairment ASA Blocks COX1 and COX2, also inhibits Thromboxane A2 and prostaglandins Corticosteroids Inhibit phospholipase A2, preventing formation of prostaglandins, thromboxane A2, prostacyclin, and leukotrines Thromboxane Vasoconstriction, platelet aggregation Prostacyclin Vasodilation, platelet aggregation (most effective one) Type 1 hypersensitivity E. Immediate response to allergen, food, meds, pollen, asthma, allergic reactions P. IgE binds with antigen at 1st exposure. Antigen binds with this complex at 2nd exposure. Inflammatory cascade initiates. C.M. Urticaria, rhinitis, conjunctivitis, angioedema, anaphylaxis Atopic disorders Genetic Type 1 hypersensitivity, asthma, hay fever, eczema, urticaria Type 2 hypersensitivity E. Antibodies directed against fixed antigens on the plasma membrane of cells C.M. Varies depending on alloimmune or autoimmune Alloimmunity and example of hypersensitivity When an individuals immune system reacts against antigens on the tissues of other members of the same species Blood transfusions- causes clumping and lysis of RBC- fever, nausea, chills, low back pain, dark urine, hives, itching, SOB Rh incompatibility- hemolytic disease of newborn with jaundice, give Rhogam within 72 hours of birth (Rh- mother with Rh+ child) Autoimmunity and example of hypersensitivity A breakdown of tolerance in which the bodies immune system begins to recognize self-antigens as foreign. Graves Disease- autoantibodies form against thyroid cells- bind to thyroid cells and mimic action of TSH, increases secretion of thyroxine Myasthenia Gravis- autoantibodies against acetylcholine bind to the post synaptic receptors and inhibit synaptic transmission of acetylcholine. Leads to muscle weakness and paralysis (mind to ground) Guillain-Barre' syndrome- antibodies bind with myelin sheath of the peripheral nervous system, triggering the immune response. Causes demyelination of the peripheral nerves and a rapidly progressive, ascending paralysis (ground to brain) Type III hypersensitivity Widespread immune and inflammatory response not specified for any cell or tissue. SLE, RA Antibodies are formed against and bind to circulating antigens, antigen-antibody complex deposits in vessel walls or tissue. Causes cellular and tissue damage. IgG and IgM response, spread via circulation- not specific to a cell or tissue- widespread damage. Type IV hypersensitivity T-cell lymphocyte mediated reaction that does not require antibody activation. Delayed response- 24-72 hours. Contact dermatitis- poison ivy, topical drugs, chemicals such as nickel or formaldehyde. Antigens too small to cause a reaction bind to proteins, response includes rash, red bumps, itching, and blisters. Reactive tuberculin test- PPD cause and induration in 24-72 if person was previously exposed to tuberculin antigen Solid organ transplant rejection- 11-14 days after 1st exposure, 5-6 days after 2nd exposure, results in mononuclear infiltration, decreased circulation, and tissue necrosis. Systemic Lupus Erythematosus E. Primarily women aged 20-40, Type III hypersensitivity. Antibodies are formed against DNA Genetic, leads to tissue damage. Exacerbated by infections, UV light, estrogen, meds, stress Diagnosed by serum ANA C.M. Butterfly rash (cheeks), photosensitivity, nonerosive arthritis of at least 2 peripheral joints, inflammation of serous sacs, proteinuria, seizures, anemia, leukopenia, thrombocytopenia Rheumatoid Arthritis E. Primarily women 30-50, systemic autoimmune disease Progressive, irreversible leads to deformity and disability Tx includes PT, NSAIDS, corticosteroids C.M. Joint inflammation, pain, destruction of synovial membrane, widespread symmetrical joint swelling, erythema joints warm to touch, loss of function, morning stiffness- improves with movement, weight loss, weakness, anorexia -Osis or -philia Elevated count of blood cells -penia Low count of blood cells Leukocytosis Increase in number of total WBC Leukopenia Decrease in number of total WBC Neutrophilia- definition and causes Elevated neutrophil count From bacterial infections, inflammation, and necrotic tissue Neutropenia- definition and causes Decreased # of neutrophils From liver disease, viral infections, drugs Eosinophilia- definition and causes Increased # of eosinophils From allergic reactions and parasitic infections Eosinopenia- definition and causes Decreased # of eosinophils From pancytopenia and steroid use Basophilia- definition and causes Increased # of basophils From allergic reactions Monocytosis- definition and causes Increased # of monocytes From TB infection or during recovery from an infection Monocytopenia- definition and causes Decreased # of monocytes From steroid use of HIV infection Lymphocytosis- definition and causes Increased # of lymphocytes From viral infections, lymphoma, or leukemia Lymphocytopenia- definition and causes Decreased # of lymphocytes From AIDS, chemotherapy, or steroid use Which antibodies and antigens do each blood type have A has A antigen and B antibodies B has B antigen and A antibodies AB has AB antigens, and no antibodies O has no antigens, but A and B antibodies What is the etiology, incubation, and mode of transmission for influenza Comes from one of three types- A, B, C Transmitted via aerosol Incubation is 1-4 days (usually 2) What is the etiology, incubation, and mode of transmission for measles Initial infection and viral replication occur locally in tracheal and bronchial epithelial cells. After 2-4 days, local lymphatic tissues are infected. Virus is disseminated to various organs, and rash appears. Transmitted by respiratory droplets, either airborne or on surfaces up to 2 hours Incubated 7-14 days (average 10-12 days) What is the etiology, incubation, and mode of transmission for HIV Virus enters bloodstream and begins seeking out the CD4 (T-helper cells). The virus fuses to CD4 cells and integrates with host's DNA. More CD4 cells become infected, and eventually rupture. Overall CD4 count is reduced, leaving patient susceptible to opportunist infections. Transmitted via bodily fluids-blood borne. Incubates as long as 10 years in untreated individuals. Discuss some clinical implications of solid organ transplant rejection rejection is an immune response, mostly T-cell mediated. Slow process, Type 4 hypersensitivity Patients are highly susceptible to infections r/t use of immunosuppressants Describe the role of HLA in solid organ rejections HLA is typed and matched on donor and recipient to decrease risk of rejection HLA is targeted response for rejection clinical manifestations of influenza fever, sore throat, myalgias, headache, nasal discharge, weakness and severe fatigue, cough and other respiratory symptoms, tachycardia, red, watery eyes, pharyngitis clinical implications of influenza prevention is key- vaccinate at 6+ months, annual diagnosed by rapid swab treat with antivirals- Tamiflu clinical manifestations of measles fever 104, lasts 4-7 days, malaise, anorexia, 3c's- conjunctivitis, cough, coryza (inflammation of mucous membrane of nose), photophobia, periorbital edema, myalgias, Koplik spots (bluish-gray specks on red base, on buccal mucosa), rash- begins at hairline, spreads in 48 hours Clinical implications of measeles One of most contagious infectious diseases, lasts 7-10 days Educate parents on importance of vaccination Immune globulin can be administered within 6 days of exposure Can be fatal for HIV patients Immunocompromised may have no rash Need serologic testing per CDC Tx is supportive- rehydration, Vit A Antiretroviral medications Used to impede viral replication of HIV virus, come in 6 classes 1. Nucleoside reverse transcriptase inhibitors 2. Non-nucleoside reverse transcriptase inhibitors 3. Protease inhibitors 4. CCR5 inhibitors- inhibits binding to CCR3 5. Fusion inhibitor- inhibits fusion between HIV and cell membrane 6. Integrate inhibitor- inhibits viral integrate enzyme Effects of genetic mutation of CCR5 cell receptor Some people of European descent carry the CCR5 delta32 mutation. The mutation makes a person functionally resistant to the HIV virus, and might be a cure for those individuals Describe the difference between HIV and AIDS, and clinical implications CD4 count 200 is HIV, If the CD4 count drops below 200 and an AIDS defining illness occurs then the patient is said to have AIDS. Once they have progressed, they will always have AIDS, even if CD4 count goes up. AIDS defining illnesses: PCP, toxoplasmosis, progressive multi focal leukoencephalopathy, disseminated MAC, Kaposki's sarcoma, lymphoma, TB, esophageal or tracheal candida infection, invasive cervical cancer, CMV infection, and histoplasmosis What are CM that indicate a compromised immune system in a person with HIV Thrush, cervical dysphasia, cervical carcinoma in situ, fever of 38.5 (101.3) or greater X 1 month, oral hairy leukoplakia, herpes zoster, immune thrombocytopenia purpura (ITP), PID, peripheral neuropathy, vaginal yeast infections, Kaposi sarcoma, presence of any opportunistic infections. Should be treated with prophylactic antibiotics HIV EIA 3rd generation immunoassay, can use urine, saliva, or serum (best), 99% accuracy test at 12 weeks post-exposure 4th generation immunoassay "gold standard" can test 10 days post exposure can result negative, positive with HIV antibody, or positive without HIV antibody PCP- pneumocystitis jiroveci pneumonia fungus butterfly infiltrates on CXR CM- worsening dyspnea, fatigue, night sweats, weight loss, poor appetite Tx- Bactrim MAC- mycobacterium avium complex AFB- leads to systemic infection, grows slow- thick cell wall hard to penetrate CM- fever, night sweats, anorexia, weight loss, lymphadenopathy Tx- clarithromycin and ethambutol for 6-12 months CMV- cytomegalovirus herpes virus greatest risk for CD4 50 (ensure eye exams) CM- fever, myalgia, cervical lymphadenopathy, mild hepatitis, retinal detachment, vision loss, blindness Tx- resistant to medications, no prevention how is coagulation cascade altered by warfarin blocks Proteins S and C blocks Vit K enzyme to prevent carboxylation, decreasing amount of functional K to be used in Vit K dependent coagulation factors how does low molecular weight heparin affect coagulation cascade inhibits factor Xa and prevents formation of prothrombinase complex and consequently thrombin how do direct thrombin inhibitors alter coagulation cascade prevent activation of fibrinogen and XIII give CM and an example of coagulopathy hemorrhage CM- joint bleeding, tissue hematomas, large spontaneous central ecchymosis, delayed bleeding after surgery, trauma or injury DIC give CM and example of thrombocytopenia hemorrhage CM- mucosal bleeding, epistaxis, GI or GU bleed, oral bleeding, hemoptysis, heavy menses, immediate bleeding after trauma, possible petechiae ITP what are causes of thrombocytopenia post-op hemodilution (nadir 2-4 days), splenomegaly, HIV, bone marrow failure, hemolysis, multiple medications Primary Immune Thrombocytopenic Purpura- patho and CM immune mediated destruction of platelets- primary or secondary (caused by another etiology) CM- petechiae, purpura, easy bruising, epistaxis, gingival bleeding, menorrhagia CM vary with age- worse in elderly Heparin Induced Thrombocytopenia- patho and CM immune system destruction of platelets initiated by heparin Type 1- mild, 2 days post heparin admin, return to normal with continued administration Type 2- severe, drug reaction which destroys platelets risks- female, heparin use 1 week, post-op thromboprophylaxis CM0 unexplained drop in platelets 5-10 days post admin (can be up to 2 weeks post), some will have rapid onset discuss hemophilia A affects 1 in 5-10K males sex linked recessive disease, deficient in factor VIII normal platelets and PT, prolonged PTT, decreased factor VIII CM: knee, elbow, and ankle bleeds, GI bleeds discuss hemophilia B affects 1 in 20-30K males Christmas disease- deficient in factor IX normal platelets and PT, prolonged PTT, decreased factor IX CM: knee, elbow, and ankle bleeds, GI bleeds discuss DIC activation of the coagulation system causes widespread intravascular fibrin deposition, fibrinolytic products attempt to break down fibrin- adhere to platelets to prevent adhesion. coagulation products are eventually consumed and bleeding occurs. may cause organ failure r/t micro-thrombi triggers: malignancy, sepsis, infection, ob complications, trauma, Sx, ARDS, rhabdo, venomous snake bites CM: oozing, bleeding from all puncture sites, bleeds from all body cavities, prolonged PT/PTT, elevated d-dimer, platelet count 100,000 discuss Vitamin K deficiency CM: easy bruising, oozing from nose or gums, excessive wound bleeding, menorrhagia discuss liver disease all factors of clotting can be affected Hageman deficiency deficiency of factor XII- rare genetic disorder asymptomatic, causes prolonged clotting test with no clinical bleeding or risk present causes of thrombus Triad of Virchow- injury to blood vessels, abnormality in blood flow, hypercoagulability some medications increase risks discuss macrocytic, microcytic, and normocytic anemias classified by size of RBC macrolytic- MCV 100, includes pernicious and folic acid anemias, can be caused by ETOH microlytic- MCV 80, folic acid anemia normolytic- MCV 80-100 (normal range), sickle cell is an example Pathophysiology and clinical implications of pernicious anemia A Vitamin B12 deficient leads to fewer RBCs- intrinsic factor is lacking- RBCs get big, but not mature Macrocytic Typical at age 60 as 10 years of B12 is stored in body Risk factors and CM of pernicious anemia Risk: vegan, gastrectomy, atrophy of gastric mucosa r/t autoimmune disease CM: beefy red tongue, weakness, fatigue, loss of appetite, weight loss, neurological symptoms- parenthesis of hands/feet, loss of sense of position and vibration Pathophysiology and clinical implications of folate deficient anemia Folic acid is required for RBC synthesis, when lacking, cell continues to grow- but not mature, will get large and be destroyed in the bone marrow Monitor nutritional status of patients, elderly are easily malnourished ETOH dependent may need supplementation Risk factors and CM of folate deficient anemia Risk: malnourished, alcoholic CM: beefy red tongue, weakness, fatigue, loss of appetite, weight loss Risk factors and CM of iron deficient anemia Risk: PUD, excessive menstruation, occult GI bleed, inadequate dietary intake, Meds with GI bleed risk CM: fatigue, hypoxia, SOB, pale tissues, glossitis, spoon shaped nails Pathophysiology and clinical implications of iron deficient anemia Microcytic Iron is necessary for production of hgb. Iron stores are depleted and less hgb is produced, results in small RBCs Most common worldwide, usially from chronic blood loss or pregnancy, more common in women Risk factors and CM of anemia of chronic disease AIDS, RA, CKD, chronic hepatitis, lupus 2nd most common, chronic disease leads to body's inability to use iron stores Risk factors and CM of sickle cell anemia African descent, Mediterranean, middle eastern, or Indian descent, familial history Pain during crisis Pathophysiology and clinical implications of sickle cell anemia Lack of O2 causes hgb S molecules to transform to sickle shape, treat with 0.45% NaCl to rehydrate cell and reverse shape change Autosomal recessive- can carry trait or active form. Define acute leukemia Rapid onset- aggressive accumulation of immature cells, causes overproduction of leukocytes by the bone marrow, causes overcrowding, prevents formation of normal blood cells Chronic leukemia Gradual onset, cells appear normal but do not function appropriately and accumulate Lymphocytic leukemia Excessive production of lymphocytes Myelogenous leukemia Excessive production of granulocytes Multiple myeloma pathophysiology and CM Chromosomal abnormality that leads to production of malignant plasma cells, cells secrete antibodies which are deposited in organs (mostly bones) and grow malignant tumors, 3 yr life span Vertebrae, skull, ribs and pelvis most frequently affected CM: hypercalcemia, recurrent infections, renal failure Risk factors for multiple myeloma African descent Males more common Around 6th decade of life Etiology and pathophysiology of Hodgkin's Lymphoma Malignant neoplasms of cells called CM of Hodgkin's Lymphoma Large painless lump/mass- usually on neck, eosinophilia, fever, weight loss, night sweats, pruritus, adenopathy, thrombocytosis, leukocytosis, mediastinal or abdominal mass Epidemiology of Hodgkin's Lymphoma Possibly Epstein Barr, unknown Etiology and Epidemiology of Non-Hodgkin's Lymphoma Malignant transformation of lymphocytes, no Reed-Sternberg cells Caused by immunosuppression, AIDS, Hep C, EBV, post transplantation CM of Non-Hodgkin's Lymphoma Generalized lymphadenopathy Late stages bring fever, night sweats, weight loss Acute Lymphocytic Leukemia (ALL) Marked by 30% lymphoblasts in blood or marrow Most common in children Survival rate decreases with age CM: fever, pallor, bleeding, fatigue, lymphadenopathy, infection, joint pain, splenomegaly, hepatomegaly, night sweats, weight loss, anemia, thrombocytopenia, petechiae, ecchymosis Acute Myelogenous Leukemia (AML) Marked by proliferation of immature myeloid cells, decreased apoptosis, and lack of cellular differentiation Most common in adults Remission is inversely related to age CM: fever, pallor, bleeding, fatigue, lymphadenopathy, infection, joint pain, splenomegaly, hepatomegaly, night sweats, weight loss, anemia, thrombocytopenia, petechiae, ecchymosis Chronic Lymphocytic Leukemia (CLL) Malignant transformation of B-lymphocytes Increased occurrence over 40 Survival 10yrs or longer CM: suppression of humoral immunity, increased infections Chronic Myelogenous Leukemia (CML) Presence of Philadelphia chromosome Increased occurrence over 40 Bone marrow transplant may be curative CM: splenomegal (most common), hepatomegaly, hyperuricemia, infection, fever, weight loss