NURS 5140 Advanced Pathophysiology Final Exam 2026

NURS 5140 Advanced Pathophysiology Final Exam 2026 Primary intervention - -removes risk factors, so diseases do not occur Examples of primary interventions - -immunizations, seat belts, helmets Secondary interventions - -detecting disease when still curable Examples of secondary interventions - -pap smears, routine blood screens, chemotherapy Tertiary interventions - -preventing further deterioration or reducing complications of disease Examples of tertiary interventions - -beta blockers following MI, chemo, radiation Homeostasis - -property of a system in which variables are regulated so that internal conditions remain stable and relatively constant; examples include the stability of the human body's environment in response to changes in external conditions Mitochondria - -cellular powerhouse; cellular respiration; convert ingested substances to ATP (cellular metabolism) Endoplasmic reticulum - -protein synthesis and fat metabolism Ribosomes - -site of protein synthesis Golgi apparatus - -packages and modifies proteins from the ER for secretion; produces lysosomes; predominant in secretory cells Lysosomes and peroxisomes - -cellular digestion Cytoskeleton - -filaments and microtubules maintain cell shape; permit movement Types of injurious stimuli (cellular) - -hypoxia, chemical/toxic agents, physical agents, microorganisms and immunologic reactions, genetic defects, nutritional imbalances How does hypoxia affect cells? - -causes cellular swelling, local or generalized release of lactic acid How do chemical/toxic agents affect cells? - -damage cell membrane NURS 5140 NURS 5140 Types of adaptive immunity - -humoral, cell-mediated Humoral immunity - -utilizes circulating antibodies produced by B-lymphocytes Primary response of humoral immunity - -(1) antigen phagocytosed by macrophage, (2) antigen presenting cells, (3) antigen delivered to B cells, (4) B cells enlarge and differentiate into: antibody producing plasma cells, memory B cells Secondary response of humoral immunity - -memory B cells respond to subsequent antigen exposure in a more rapid and powerful way Cell-mediated immunity - -exposure to antigen presented by macrophages cause antigen-specific T-cell differentiation and proliferation in the lymphoid tissue; activated T-cells continually cycle from lymph to blood to lymph, able to directly respond to an antigen and destroy the target cell Where do B lymphocytes mature? - -bone marrow Where to T lymphocytes mature? - -thymus What are the major components of innate immunity? - -epithelial barriers, phagocytic cells (neutrophils, macrophages), NK cells, plasma proteins, inflammatory response Natural killer (NK) cells - -T-cells; play role in both adaptive and innate immunity; identify viruses, infections (non-self cells) Complement system - -amplifies the antigen-antibody reaction; includes 9 interacting components (proteins); effects include: opsonization, agglutination, neutralization, chemotaxis, mast cell and basophil activation, general inflammatory effects Basophils - -innate immunity; release histamine Mast cells - -secrete histamine; prompted to degranulate during activation Macrophages - -"pac man"; consume bacteria, cell debris/waste; serve as apcs Neutrophils - -release interleukins (cytokines) to signal other immune cells to travel to injured area during chemotaxis Toll-like receptors - -sense damage; release chemical mediators that initiate inflammatory response; found particularly in endothelial layer of capillary beds Antigen-presenting cells (apcs) - -include macrophages, dendritic cells, Langerhans cells, activated B-cells; (1) engulf foreign particles, (2) present fragment of antigens on their own surfaces to be recognized by T cells NURS 5140 NURS 5140 T cells - -response to intracellular pathogens; recognize self B cells - -act as antibody making factories HIV - -retrovirus that attacks CD4+ T lymphocytes; enveloped virus that replicates in a host cell through the process of reverse transcription Primary infection phase of HIV - -viral replication/load, CD4+ T-cells decrease; S/S manifest about 1 month after exposure Latency phase of HIV - -controls viral replication; gradual decrease leading to extremely low levels of CD4+ T cells; no s/s of illness AIDS - -CD4+ 200 cells u/L; AIDS-defining illness (e.g., wasting syndrome) Myasthenia gravis - -disorder of transmission at neuromuscular junction; affects communication between neuron and muscle (r/t loss of acetylcholine receptors) S/s of myasthenia gravis - -muscle weakness, fatigue, difficulty chewing/swallow, respiratory dysfunction Causes of myasthenia gravis - -autoimmune origin; thymus abnormalities often present Myasthenic crisis - -weakness to the point where respiration isn't effective (progressive weakness of respiratory muscles, can't clear secretions, etc.) Diagnostic tests for myasthenia gravis - -physical exam, anticholinesterase test Treatment for myasthenia gravis - -immunosuppressants, corticosteroids, IV igg, plasmaphoresis, thymectomy Guillain-Barre syndrome - -rapid-onset weakness of the limbs as a result of an acute polyneuropathy (disorder affecting the peripheral nervous system) S/s of guillain-barre - -ascending paralysis, change in sensation or pain, symmetrical and progressive weakness Ischemic stroke - -caused by interruption of blood flow in a cerebral vessel Hemorrhagic stroke - -caused by bleeding into the brain usually from a blood vessel rupture caused by HTN, aneurysm, arteriovenous malformations, head injury, or blood dyscrasias TIA - -focal neurological deficit lasting less than 1 hour; zone of penumbra without central infarction NURS 5140 NURS 5140 Zone of Penumbra - -area that's been affected by ischemic event, but isn't completely dead; if blood flow can be restored quickly, area can be saed Traumatic brain injury - -caused when an external force traumatically injures the brain; can be classified based on severity, mechanism, or other features Causes of TBI - -focal impact on the head, sudden acceleration/deceleration within the cranium, or a complex combination of both movement and sudden impact Diffuse brain injury - -multifocal brain injury Types of diffuse brain injury - -diffuse axonal injury (widespread damage to white matter), ischemic brain injury, vascular injury, swelling (increase ICP), concussion Causes of diffuse brain injury - -hypoxia, meningitis, damage to blood vessels, acceleration/deceleration injuries Where is CSF produced? - -chorioplexus and ventricular walls Functions of CSF - -surrounds the spinal cord, fills ventricles within the brain ("shock absorber"), circulates nutrients, removes waste products Conditions involving CSF - -brain herniation, hydrocephalus, meningitis, TBI Early s/s of Alzheimer's - -difficult remembering recent conversations, names or events; apathy and depression Later s/s of Alzheimer's - -impaired communication, poor judgment, disorientation, confusion, behavior changes, difficulty speaking/swallowing/walking Plaques - -deposits of protein fragments (beta-amyloid) seen in cortex of patients with Alzheimer's; interfere with intracellular signaling/communication at synapses Tangles - -twisted strands of tau protein seen in cortex of patients with Alzheimer's; cause the disintegration of microtubules, inhibiting transport of nutrients between neurons Screening/diagnostic tests for Alzheimer's - -detailed medical history, mental status testing, physical and neuro exam, blood tests, brain imaging; autopsy is only true diagnostic test Wintrobe's classification of rbcs - -microcytic (small cell): MCV 80 fl Normocytic (normal): MCV 80-100 fl Macrocytic (large): MCV 100 fl