DNP 510 Exam 1 | Questions with 100% Correct Answers

DNP 510 Exam 1 | Questions with 100% Correct Answers What are universal cell components shared across mammalian cells? Nucleus, cytoplasm, organelles (mitochondria, ER/Golgi, lysosomes/peroxisomes), and cytoskeleton. Ch1 Cellular Why can fat-soluble vitamins diffuse across cell membranes and why does this matter clinically? They dissolve in the lipid bilayer (nonpolar), bypassing transporters; excess intake (A, D, E, K) risks toxicity. Ch1 Cellular What role does cholesterol play in membranes? Stabilizes membrane fluidity and integrity; essential for mammalian cells. Ch1 Cellular Differentiate integral vs peripheral membrane proteins. Integral traverse/anchor in bilayer; peripheral loosely attach to surface or cytoskeleton. Ch1 Cellular Name and define three key electrophysiologic properties of cardiac/neuronal membranes. Automaticity (spontaneous firing), excitability (respond to stimuli), conductivity (propagate impulses). Ch1 Cellular. Compare passive vs active transport with one clinical example. Passive: down gradient (facilitated diffusion). Active: ATP-dependent (Na+/K+ ATPase); insulin shifts K+ into cells via pump ↑. Ch1 Cellular Define endocytosis and exocytosis. Endocytosis brings cargo into cell via vesicles; exocytosis fuses vesicles with membrane to secrete cargo. Ch1 Cellular Outline transcription and translation. Transcription: DNA→mRNA in nucleus. Translation: ribosomes synthesize polypeptides from mRNA codons. Ch1 Cellular List protein structural levels with an example of quaternary structure. Primary, secondary (α/β), tertiary, quaternary (e.g., hemoglobin tetramer). Ch1 Cellular Name cell cycle phases and a key checkpoint guardian. G1, S, G2, M; p53 enforces DNA integrity at checkpoints. Ch1 Cellular Match adaptation: atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia. ↓size; ↑size; ↑number; cell type replacement; disordered growth (premalignant). Ch1 Cellular Differentiate apoptosis vs necrosis. Apoptosis: programmed, non-inflammatory; Necrosis: pathologic, membrane rupture, inflammation. Ch1 Cellular List gangrene types and a defining feature of each. Dry (ischemic, mummified), Wet (infection+ischemia, liquefaction), Gas (Clostridium, crepitus). Ch1 Cellular Define epigenetics with examples. Heritable expression changes without DNA sequence change; e.g., DNA methylation, histone modification. Ch1 Cellular What is a SNP and why does it matter? Single nucleotide polymorphism; can alter disease risk/drug response (e.g., MTHFR). Ch1 Cellular Define hemizygous and provide an example. Single allele present (e.g., X-linked genes in XY males). Ch1 Cellular Contrast autosomal vs sex-linked inheritance. Autosomal on non-sex chromosomes; sex-linked on X or Y; transmission patterns differ. Ch1 Cellular What is mosaicism and when does it occur? Post-zygotic mutation leads to genetically distinct cell lines in one individual; seen after mitotic errors. Ch1 Cellular Clinical correlation: why does insulin lower serum potassium? It stimulates Na+/K+ ATPase, moving K+ into cells with glucose. Ch1 Cellular Which molecules primarily mediate platelet adhesion at an injury site? vWF linking subendothelium to platelet GPIb; TXA2 amplifies aggregation. Ch1 Cellular Define paracrine vs autocrine signaling with examples. Paracrine: local cell-to-cell (NO, neurotransmitters). Autocrine: self-signaling (tumor growth factors). Ch1 Cellular What is cellular senescence? Exit to G0/replicative arrest, often telomere-mediated; normal aging or stress response. Ch1 Cellular List major causes of cell injury. Hypoxia/ischemia, toxins, physical agents, radiation, infection, immune reactions, genetic, nutritional. Ch1 Cellular Primary role of lysosomes and peroxisomes? Lysosomes: digestion/recycling. Peroxisomes: detox (ROS), lipid metabolism. Ch1 Cellular Name two organs heavily dependent on oxidative phosphorylation. Heart and brain—high ATP demands. Ch1 Cellular Define totipotent, pluripotent, multipotent, unipotent. Totipotent: all cells incl. placenta; Pluripotent: all body cells; Multipotent: limited lineages; Unipotent: single lineage. Ch1 Cellular What is the clinical significance of membrane glycoproteins/glycolipids? Cell recognition (e.g., immune self, ABO antigens); pathogen attachment sites. Ch1 Cellular Explain why cystic fibrosis causes thick mucus (simplified). Defective CFTR channel → ↓Cl−/H2O secretion → dehydrated, thick secretions. Ch1 Cellular Which transport best describes glucose via GLUT4? Facilitated diffusion (insulin-regulated translocation). Ch1 Cellular Name a key antioxidant and its mechanism. Vitamin E protects membranes by inhibiting lipid peroxidation (free radical chain breaking). Ch1 Cellular What organelle is central to apoptosis initiation? Mitochondria (cytochrome c release → caspase cascade). Ch1 Cellular Identify primary vs secondary protein structure bonds. Primary: peptide bonds; Secondary: hydrogen bonds (α-helix/β-sheet). Ch1 Cellular What are telomeres and clinical relevance? Chromosome ends; shortening → replicative aging; telomerase up in cancers. Ch1 Cellular Give an example of metaplasia relevance. Barrett esophagus: squamous → columnar due to chronic acid; premalignant. Ch1 Cellular Which vitamin deficiency impairs collagen hydroxylation? Vitamin C (ascorbate) deficiency → scurvy, poor wound healing. Ch1 Cellular Differentiate innate vs adaptive immunity in speed and specificity. Innate: rapid, non-specific; Adaptive: slower initial, specific with memory. Ch2 Immunity Name key innate cellular players. Neutrophils, macrophages, dendritic cells, NK cells, eosinophils, basophils. Ch2 Immunity What triggers mast cell degranulation? IgE cross-linking by antigen; also complement (C3a/C5a) and direct triggers. Ch2 Immunity List major immunoglobulin classes and a key role for each. IgM (primary), IgG (secondary, placenta), IgA (mucosal), IgE (allergy/parasites), IgD (B-cell receptor). Ch2 Immunity Define antigen vs epitope. Antigen: molecule recognized by immune system; epitope: specific recognized site. Ch2 Immunity Type I hypersensitivity mediators and acute management. Histamine, leukotrienes → vasodilation/bronchoconstriction; treat with epinephrine, antihistamines, steroids. Ch2 Immunity Give one example each for hypersensitivity II, III, IV. II: hemolytic transfusion; III: SLE; IV: contact dermatitis/TB PPD. Ch2 Immunity How do vaccines create immunity? Present antigen safely → adaptive response and memory B/T cells. Ch2 Immunity Active vs passive immunity with example. Active: vaccine or infection; Passive: IVIG or maternal IgG across placenta. Ch2 Immunity SLE key labs and manifestations. ANA+, anti-dsDNA/anti-Sm; malar rash, photosensitivity, serositis, cytopenias, renal. Ch2 Immunity HIV: primary target cell and effect on immunity. CD4+ T helper cells; depletion → opportunistic infections and malignancies. Ch2 Immunity Define acute retroviral syndrome timing and symptoms. 2-4 weeks post-exposure; fever, rash, pharyngitis, lymphadenopathy; high viral load. Ch2 Immunity Name two primary immunodeficiencies. X-linked agammaglobulinemia (B-cell), SCID (T/B severe). Ch2 Immunity Which organisms are common in neutropenia? Bacterial (Gram− rods, Staph), fungal (Candida, Aspergillus). Ch2 Immunity Describe complement's major outcomes. Opsonization (C3b), chemotaxis (C5a), MAC lysis (C5b-9). Ch2 Immunity What is tolerance and how can it fail? Immune non-response to self; failure → autoimmunity (e.g., SLE). Ch2 Immunity Name 3 differences between bacterial and viral pathogens clinically. Bacteria: leukocytosis/neutrophils, local purulence; Viruses: lymphocytosis, systemic prodrome. Ch2 Immunity Define immunogenicity factors. Foreignness, size, complexity, dose, route, adjuvants. Ch2 Immunity Why might chronic steroid therapy predispose to infection? Immunosuppression: ↓ cytokines, lymphocyte function, neutrophil migration defects. Ch2 Immunity What is an adjuvant in vaccines? Substance that enhances immune response (e.g., alum). Ch2 Immunity Explain isotype switching. B cells switch heavy chain constant region (e.g., IgM→IgG) under T-cell cytokine help. Ch2 Immunity Which hypersensitivity often underlies asthma? Type I (IgE-mediated) hypersensitivity. Ch2 Immunity What lab suggests classic bacterial infection vs viral? Neutrophilia with left shift vs lymphocytosis. Ch2 Immunity Define opsonization and a key opsonin. Coating pathogens to enhance phagocytosis; C3b and IgG are major opsonins. Ch2 Immunity Why are asplenic patients at risk for sepsis by encapsulated organisms? Loss of splenic clearance of opsonized encapsulated bacteria (S. pneumoniae, H. influenzae, N. meningitidis). Ch2 Immunity What is clonal selection? Antigen-specific lymphocytes proliferate upon activation, expanding that clone. Ch2 Immunity