Nurs 6030 exam 2 questions with complete solution.

Are you taking NURS 6030 (Advanced Pathophysiology) and preparing for Exam 2? This comprehensive study guide contains complete questions and solutions covering every advanced topic you'll encounter. From benign vs malignant tumors, oncogenes, tumor suppressor genes, and the Philadelphia chromosome to innate vs adaptive immunity, hypersensitivity reactions (Types I-IV), HIV/AIDS, inflammation, anemia classification (microcytic, macrocytic, normocytic), leukemia, lymphoma, multiple myeloma, hemostasis, and thrombocytopenia – this resource is your all-in-one exam preparation tool. What's Inside – Complete NURS 6030 Exam 2 Domain Coverage: Category Key Concepts & Questions Covered Oncology (Cancer Biology) Benign tumor (encapsulated, well-differentiated cells); Malignant tumor (poorly differentiated, metastasizes); Tumor suppressor genes (product inhibits cell division – both copies must be inactivated); Oncogenes (dominantly expressed, mutated genes giving growth advantage); Proto-oncogenes (normal cellular genes for growth/division); Cancer results from activation of proto-oncogenes to oncogenes + inactivation of tumor suppressor genes; Characteristics of cancer cells (uncontrolled replication, DNA damage doesn't stop division, grows without growth factors); Philadelphia chromosome (associated with leukemia – translocation between q9 and q22) Immunology Basics Innate immunity (non-specific – skin, gastric acid, phagocytes, lysozyme, complement – rapid, inflammatory); Adaptive immunity (specific – requires exposure, slower, includes memory cells – humoral B cell and cellular T cell); Complement system (~30 blood proteins – amplify inflammation, enhance phagocytosis, lyse pathogens); Cytokines (regulators directing immune response, produced by WBCs, vascular epithelium, fibroblasts); Antigen presenting cells (possess MHC II – B cells and macrophages – display antigens to activate T cells) Infectious Disease Microbiome (100 trillion bacteria on skin/digestive tract – digest nutrients, produce vitamin K, inhibit bacterial growth); Virulence (potential to produce disease); Pathogens (virulent organisms); Saprophytes (harmless); Opportunistic (cause disease in immunocompromised hosts); Prions (protein particles without genome – transmissible neurodegenerative diseases, amyloid plaques in brain, no treatment); Virus lifecycle (attachment, penetration, uncoating, replication, assembly/release, latency, oncogenesis); Influenza virus (antigenic shift yearly – two surface proteins); HIV/AIDS (attacks CD4 helper cells – lymphoid areas first, CD4 decline – opportunistic infections, malignancies, wasting – treatment: HAART); Stages of infection (incubation, prodromal, acute, convalescent, resolution) Bacteria, Fungi, Toxins Bacteria (prokaryotic, unicellular – gram positive/negative, attach via pili/fimbriae, biofilm, encapsulation, mutation, enzymes); Fungi (eukaryotic, dimorphic – mold/yeast, require antifungals); Mycosis (fungal infection – can be systemic, opportunistic); Exotoxins (proteins, enzymes, neurotoxins); Endotoxins (lipopolysaccharides from gram-negative cell walls); Bacterial toxins cause excess inflammation Inflammation & Healing Vascular phase (first phase – vasodilation, vascular permeability, WBCs, activation of plasma proteins – goal: prevent infection, begin healing); Cellular phase (second phase – WBCs activated, adhesion molecules cause margination, diapedesis, migration, chemotaxis); Regeneration and repair phase (healing – wound filled with collagen, replaced with scar tissue); Primary intention (clean wound heals easily, no tissue loss); Secondary intention (deep wound requires tissue regeneration); Inflammatory response S/S (pain, heat, redness, swelling – increased temperature, blood flow, phagocyte attack); Plasma protein systems (complement, coagulation, kinin); Opsonization (complement proteins and antibodies coat microorganism for phagocytosis) Hypersensitivity Reactions Type I (allergies – pollen, mold, food, animal hair – IgE binds to mast cells – primary/secondary response, genetic predisposition); Type II (antibody-mediated disorders – antibodies bind to tissue-specific antigens – RBC destruction, glomerulonephritis, Graves' disease); Type III (immune-complex mediated – antigen-antibody complexes form in circulation, deposit in tissues/vessels – vasculitis in lupus); Type IV (T-cell mediated – TB testing, poison ivy) Autoimmunity Complex disorders without single source; Inherit "susceptibility genes"; Change in gene expression rather than sequence; Malfunction of adaptive immunity; Environmental factors trigger Hematology – Anemia Classification Erythropoiesis (kidney/liver sense hypoxia → produce erythropoietin → stem cells in flat bones become erythrocytes); Hematocrit (volume of RBCs in 100mL blood); Hemoglobin (amount of hemoglobin per deciliter); Reticulocyte count (rate of RBC production); MCV (mean corpuscular volume – RBC size); MCH (mean cell hemoglobin – red cell mass); MCHC (mean corpuscular hemoglobin concentration); Anemia (reduction in RBCs or hemoglobin – S/S: fatigue, pallor, weakness, increased HR/RR, SOB, dizziness) Anemia Types by Morphology Microcytic (decreased RBC size); Normocytic (normal RBC size); Macrocytic (increased RBC size); Hypochromic (decreased MCHC); Normochromic (normal MCHC) Specific Anemias Acute blood loss anemia (normocytic/normochromic – decreased BP, increased HR); Chronic blood loss anemia (insufficient building blocks for RBC synthesis); Hemolytic anemia (RBCs destroyed prematurely – congenital or acquired); Macrocytic/normochromic-megaloblastic anemia (large RBCs from defective DNA synthesis – B12 or folate deficiency); Normocytic-normochromic anemia (insufficient RBCs – acute blood loss or impaired production – aplastic anemia); Aplastic anemia (pancytopenia – chemo/radiation, chemicals, viral illness, idiopathic – rapid death from infection or bleeding – treatment: bone marrow/stem cell transplant); Pernicious anemia (B12 deficiency – missing intrinsic factor – antibodies to parietal cells or intrinsic factor – requires B12 injections); Folic acid deficiency (megaloblastic anemia – increased MCV, decreased serum folic acid – NO neurological symptoms – causes: malnutrition, malabsorption, alcoholism); Iron deficiency anemia (microcytic, hypochromic – MOST COMMON anemia – causes: nutritional deficiency, blood loss – S/S: brittle/thin/concave nails, glossitis – treatment: replace iron) Sickle Cell Anemia Inherited hemolytic anemia (recessive); Abnormal hemoglobin, decreased O2; Triggers: hypoxia, dehydration, acidosis, cold, stress, illness; Heterozygous = less severe; Homozygous recessive = jaundice, splenic damage, vessel occlusion, pain, infarction, growth retardation; No cure – prevent sickling episodes, transfusions Polycythemia Excess RBCs; Relative (loss of plasma volume); Primary (polycythemia vera – neoplastic, nonmalignant increase in RBCs, increased WBCs/platelets/splenomegaly – ruddy appearance, high BP, pruritus – hypercoagulable → organ ischemia); Secondary (response to chronic hypoxia – smoking, COPD, heart disease, high altitude) White Blood Cell Disorders Granulocytosis (response to bacterial infection); Lymphocytosis (response to viral infection); Segmented neutrophils ("segs" – mature); Banded neutrophils ("bands" – immature); "Shift to the left" (increased bands released from bone marrow during prolonged/severe infection); Leukopenia (abnormally low WBC count – never normal); Neutropenia (low neutrophils – severe/prolonged infection, viral); Agranulocytosis (virtual absence of neutrophils – radiation or sepsis); Lymphocytopenia (reduced lymphocytes – cancer, radiation, chemo, immune deficiency) Leukemia Malignancy of WBCs in bone marrow and blood; Overcrowds marrow → decreased production of normal cells; Genetic translocations (Philadelphia chromosome most common – between q9 and q22); Classification: by cell origin (myeloid or lymphoid) and rate of progression (acute – immature blast cells, rapid progression; chronic – more differentiated, slower progression) Lymphoma & Multiple Myeloma Hodgkin lymphoma (B cell origin – large abnormal Reed-Sternberg cells); Non-Hodgkin lymphoma (T or B cell origin – lacking Reed-Sternberg cells – worse prognosis); Lymphoma (neoplasm of lymph tissue); Multiple myeloma (proliferation of malignant plasma cells in bone marrow – unregulated M-protein production – increased cytokines → increased bone resorption – S/S: hypercalcemia, bone pain/lesions, pathologic fractures, renal failure) Hemostasis & Coagulation Steps of hemostasis (vasoconstriction, platelet plug formation, sequential activation of clotting factors, fibrin meshwork); Virchow's triad (risk factors for thrombi: 1) injury to blood vessel, 2) abnormalities to blood flow, 3) hypercoagulability of blood); Vitamin K deficiency (associated with abnormal bleeding) Thrombocytopenia Low platelet count; Causes: decreased production by bone marrow or decreased platelet survival; Type I heparin-induced thrombocytopenia (benign, non-immune – mild reduction 1-4 days after dose); Type II heparin-induced thrombocytopenia (serious, immune-mediated – 30-50% reduction 5-14 days after heparin exposure); Pathophysiology of HIT (heparin binds with PF4 → forms immune complex with IgG → platelet aggregation → thrombus formation; macrophages destroy too many platelets) Key Questions & Answers You'll Master: Question Correct Answer Benign tumor characteristics Encapsulated new growth of well-differentiated cells Malignant tumor characteristics Poorly differentiated cells with ability to metastasize Both copies of a tumor suppressor gene must be inactivated to contribute to cancer? TRUE Philadelphia chromosome is associated with which cancer? Leukemia What does HIV/AIDS attack/destroy? CD4 helper cells What property of cancer cells makes them more susceptible to NK cell attack? Reduced cell surface proteins, Class I MHC antigen Inflammatory response includes what? Increased temperature, blood flow, phagocyte attack – S/S: pain, heat, redness, swelling What is opsonization? Complement proteins and antibodies coat microorganism for phagocytosis What causes vitamin B12 deficiency? Pernicious anemia (missing intrinsic factor), antibodies to parietal cells, poor absorption, vegan diet Most common anemia? Iron deficiency anemia (microcytic, hypochromic) What is a "shift to the left"? Increased "bands" (immature neutrophils) released from bone marrow during prolonged/severe infection What are the 3 risk factors for thrombi (Virchow's triad)? Injury to blood vessel, abnormalities to blood flow, hypercoagulability of blood What vitamin deficiency is associated with abnormal bleeding? Vitamin K deficiency Type II heparin-induced thrombocytopenia is what kind of reaction? Serious, immune-mediated – 30-50% reduction 5-14 days after heparin exposure Why This Guide Works: Complete solutions – Every question answered with detailed explanations Exam-style Q&A – Mirrors actual NURS 6030 Exam 2 format Comprehensive coverage – Oncology, immunology, infectious disease, hematology, inflammation Clinical correlations – Real-world applications for nursing practice Memory aids – Anemia classifications, hypersensitivity types, Virchow's triad Perfect for: NURS 6030 Advanced Pathophysiology students Graduate nursing programs (NP, CNS, CNM, CRNA) Medical students and physician assistant programs NCLEX-RN and graduate-level nursing exams Anyone needing comprehensive pathophysiology review for Exam 2