NURS611/ NURS 650/ NURS 651 Advanced Pathophysiology Exam 1 (Latest 2026/2027 Update) | Complete Exam Questions with Verified Answers and Detailed Rationales | Cellular Adaptation, Genetics, Immunity, Neoplasia, Fluid & Electrolytes, Acid-Base, Inflammati

INSTANT PDF DOWNLOAD This comprehensive EXAM resource for Advanced Pathophysiology Exam 1 covers Weeks 1-4 content including Cellular Function, Genetics, Immunity, and Neoplasia for the 2026/2027 academic year. It features exam-style clinical scenario questions with verified answers and detailed rationales . Based on official course exam blueprints from multiple graduate nursing programs (NURS 611, NURS 650, NURS 651, UTMB 5355), this resource covers essential topics tested on the first examination . Exam 1 Topics Covered: Cellular Adaptation and Injury: Atrophy (shrinkage in cell size), Hypertrophy (increase in cell size - NOT number), Hyperplasia (increase in cell number), Metaplasia (reversible change of one adult cell type to another), Dysplasia (abnormal changes in size, shape, and organization of mature cells - pre-malignant), Anaplasia (cancerous, undifferentiated cells) . Hypoxia causes decreased ATP → failure of sodium-potassium pump → cellular swelling . Clinical onset is later in life for autosomal dominant disorders while earlier for autosomal recessive disorders . Genetics and Inheritance Patterns: Autosomal dominant (50% chance, each generation affected, examples: Huntington's disease, neurofibromatosis, achondroplasia, familial hypercholesterolemia) . Autosomal recessive (25% of offspring from two carrier parents affected, skips generations, examples: Tay-Sachs, cystic fibrosis, sickle cell anemia, PKU) . X-linked recessive (males more often affected, examples: Hemophilia A, Duchenne muscular dystrophy) . Mitochondrial inheritance (only passed on by females, all mitochondria from mother, can appear in every generation, examples: Leber's hereditary optic neuropathy) . Carrier testing determines whether prospective parents are carriers of specific disorders; prenatal testing assesses fetus health status; preimplantation genetic diagnosis removes a cell from an early embryo to test for genetic defects before implantation . Spontaneous mutations can cause disorders even when parents are not carriers . Neoplasia and Carcinogenesis: Tumors are either benign (similar to cell of origin, slow-growing) or malignant (dissimilar from cell of origin, rapid-growing) . Malignant tumors are either carcinomas (arising in epithelium, most common, spread via lymphatic system) or sarcomas (arising in connective or muscle tissue, spread via bloodstream) . Regulatory genes include proto-oncogenes (normal cellular genes encoding regulatory proteins), oncogenes (altered proto-oncogenes that transform normal cells into neoplastic cells), and tumor suppressor genes (anti-oncogenes that prevent damaged DNA from proliferating) . The p53 gene normally halts cell division, stimulates repair enzymes, and commands mutated cells to self-destruct; it is the most frequently altered gene in human tumors . Carcinogenesis is a multi-step, multi-factorial process consisting of at least three phases: Initiation (irreversible DNA mutation), Promotion/Conversion (promoters enhance development of initiated cells), and Progression (development into biologically malignant cell population with potential metastasis) . Immunology and Inflammation: The five types of immunity include: Natural/Innate immunity (includes inflammation process and NK cells, no memory, broadly specific), Adaptive immunity (cell-mediated immunity, humoral immunity, acquired immunity, passive acquired immunity) . Cell-mediated immunity is carried out by T cells, while humoral immunity is controlled by activated B cells and antibodies . NK cells (Natural Killer cells) come from the lymphoid stem cell line, are part of the innate immune system, and kill via cell lysis or apoptosis without need for specific antigen receptors . Antigen-presenting cells (APCs) include dendritic cells and macrophages; they engulf pathogens and present antigen fragments on MHC II molecules to helper T cells . Fluid and Electrolyte Balance, Acid-Base Disorders: Lipohyalinosis of small penetrating arteries occurs in chronic hypertension, predisposing to intracerebral hemorrhage . In metabolic acidosis (decreased pH, decreased HCO3), the body compensates by respiratory alkalosis (decreased PaCO2 via Kussmaul breathing) . Ascites in liver disease is driven by portal hypertension (increased hydrostatic pressure) plus reduced oncotic pressure from hypoalbuminemia . Central diabetes insipidus: polyuria, low urine osmolality, hypernatremia that corrects with desmopressin administration . Renal compensation for chronic respiratory acidosis occurs via increased bicarbonate reabsorption and ammoniagenesis producing more NH4+ for acid excretion .