Wilkes NSG 530 Exam 1 2026/2027 | Advanced Pathophysiology | Complete Q&A | Cellular Injury, Genetics, Hypersensitivity & Fluid Balance | Verified Answers with Rationales

INSTANT PDF DOWNLOAD—This comprehensive study guide is specifically designed for Wilkes University graduate nursing students preparing for NSG 530 Advanced Pathophysiology Exam 1 for the 2026/2027 academic year. Based on verified exam materials from top-selling student resources, this resource contains expertly verified practice questions and 100% correct answers with detailed rationales to help you master core advanced pathophysiology concepts and achieve a top score (Grade A+). This comprehensive guide covers all major topics tested on NSG 530 Exam 1 : Cellular Biology & Injury : Hypoxic injury is the single most common cause of cellular injury, resulting from insufficient oxygen reaching tissues; ischemia is the most common cause of hypoxia . Na+/K+ ATPase pump failure during hypoxic injury leads to intracellular sodium accumulation and cellular swelling . Reperfusion injury occurs when oxygen is reintroduced to ischemic tissue, causing reactive oxygen species formation . Cellular adaptations include atrophy (decreased cell size), hypertrophy (increased cell size), hyperplasia (increased cell number), and metaplasia (reversible cell type change) . Fluid & Electrolyte Balance : Isotonic alterations occur when total body water changes are proportional to electrolyte changes . Hypertonic alterations (increased ECF osmolality) cause cells to shrink from water loss; hypotonic alterations cause cells to swell . Edema results from filtration exceeding reabsorption via five mechanisms: increased capillary hydrostatic pressure, decreased plasma oncotic pressure, increased capillary permeability, lymphatic obstruction, and increased tissue oncotic pressure . Hyperkalemia is the most concerning electrolyte imbalance in chronic renal failure due to impaired potassium excretion . Genetics & Chromosomal Disorders : Meiosis involves homologous chromosome pairing with crossing over, producing genetic recombination . Cri du Chat syndrome results from deletion of the short arm of chromosome 5, characterized by cat-like cry, microcephaly, and intellectual disability . Turner syndrome (45,XO) presents with short stature, webbed neck, widely spaced nipples, and sterility . Fragile X syndrome (CGG repeats 200) is the second most common genetic cause of intellectual disability . Cystic fibrosis is an autosomal recessive disorder caused by CFTR gene mutation leading to thickened secretions . Duchenne muscular dystrophy is X-linked recessive with dystrophin deficiency causing progressive muscle degeneration . Huntington disease is autosomal dominant with trinucleotide repeat expansion and late onset (40s) . Hypersensitivity Reactions : Type I (IgE-mediated) involves IgE binding to mast cells, causing histamine release and anaphylaxis . Type II (cytotoxic) includes Graves disease (antibodies stimulate TSH receptor, causing hyperthyroidism), Rh incompatibility (phagocytosis in spleen), and transfusion reactions (alloimmunity) . Type III involves soluble antigen-antibody immune complexes depositing in tissues with complement activation . Type IV is T-cell mediated (delayed hypersensitivity) with Th1 cells attacking cellular targets . Immunoglobulins & Immune Response : IgG is the most abundant immunoglobulin and crosses the placenta; IgE mediates allergic reactions; IgM is produced during primary response; IgA is most abundant in body secretions . Innate immunity provides first-line defense; adaptive immunity provides specific, memory-based responses . Neutrophils are the primary phagocytes in early inflammation; macrophages are longer-acting phagocytes; eosinophils defend against parasites; mast cells release histamine; natural killer cells eliminate virus-infected cells . Inflammation & Cell Death : IL-1 is the primary mediator of fever during inflammation . Diapedesis describes leukocyte movement through endothelial walls . Necrosis involves dissolution of nuclear material and release of cytoplasmic contents (CPK-MB, LDH1 elevation indicates myocardial cell necrosis) . Apoptosis is programmed cell death without inflammation . Epidemiology : Incidence measures new cases over time; prevalence measures total existing cases at a point in time . Etiology refers to the cause of disease . Secondary prevention includes screening programs (e.g., blood pressure screening in pregnant high school students) . Sample Questions Include : "A certain disease is currently found in 1 of every 10 people in the country and 1,000 people contract the disease yearly. The population is 4,500,000. Which statement is correct?" → The prevalence of the disease is 10% and the incidence is 0.02% (Prevalence = 1/10 = 10%; Incidence = 1,000/4,500,000 = 0.00022 = 0.02%) "When antibodies are formed against Rh antigens, how are blood cells destroyed?" → Phagocytosis in the spleen (Rh antibodies cause splenic macrophages to remove RBCs) "What is the most common cause of cellular injury?" → Hypoxia "What is the primary mechanism of cellular swelling during hypoxic injury?" → Failure of the Na+/K+ ATPase pump (intracellular sodium accumulation draws water into cell) "Which electrolyte imbalance is most likely in chronic renal failure?" → Hyperkalemia (impaired potassium excretion) "What level of prevention is a blood pressure screening program for pregnant high school students?" → Secondary prevention (early detection of disease) "What is the most common cause of tissue damage in type III hypersensitivity?" → Complement activation (immune complexes activate complement, causing inflammation) "Which type of immunity prevents a neonate from infection due to maternal antibodies in breast milk?" → Passive immunity (antibodies received from another source) "What finding indicates irreversible cell injury?" → Dissolution of nuclear material (necrosis with nuclear breakdown) All questions include complete rationales based on current evidence-based practice, pathophysiology standards, and Wilkes University curriculum requirements . 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