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Exam (elaborations)

NURS 213 Proctored Exam 5 2024

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Disease process - etiology, pathogenesis, morphologic changes, clinical manifestations, diagnosis, and clinical course immunosenescence - the weakening of both the innate and adaptive immune system with increasing age Multicausality - the combination of internal processes and influences from the environment that cause cell changes with aging physiological reserve - decrease in the ability to repair damage Senescence - progressive loss of ability to replicate over time Apoptosis - genetically programmed cell death. ex ovaries during menopause necrosis - cells die due to stressors infarction - consequence of prolonged ischemia . ex- myocardial infarction gangrene - prolonged ischemia infarction and necrosis then are exposed to bacteria that thrive on dead tissue atrophy - cells revert to smaller size. loss of hormonal stimulation, malnutrition, ischemia, age hypertrophy - increase in cell size physiological- normal with exercise pathological- increase without increase in supportive structures (high bp higher workload for LV) hyperplasia - increase in number of cells. pregnancy stimulates mitotic division of breast gland cells. keloid metaplasia - replacement of one type of tissue into a form that is not normally found there. ex. GERD dysphagia - deranges cell growth, precancerous. ex. cervical plasia seen in pap smear.. anaplasia - cancerous hypoxic cell injury - most common; ischemia, anemia, low oxygen environments, pneumonia, suffocation, airway obstruction free radical cell injury - oxidative phosphorylation, small amount of reactive o2 molecules are byproducts. present in cigarette smoke and toxins. damages the cells DNA. counteract with antioxidants (vitamins A,E,C) Acute inflammation stage 1 - vascular permeability; histamine and bradykinin enable vasodilation, more permeable permitting fluids, WBC, and platelets to travel in. Area is warm and red (erythema) and swollen. acute inflammation stage 2 - cellular chemotaxis; chemical signal attracts more platelets and WBC to site. WBC-cytokines, modulate by activating or inhibiting response. margination- wbc line up acute inflammation stage 3 - systemic response; symptoms throughout body, fever, pain lymphadenopathy, lethargy, etc chonic inflammation - characterized by macrophages; cause tissue damage. granuloma- where macrophages have aggregated and transform into epithelial like cells leading to tubercle. Acute inlammation - characterized by neutrophils; first to site Skin wound healing (3 processes) - 1-inflammation 2-proliferation, fibroblast synthesizes collagen, form granulation tissue. 3-maturation and remodeling exudate - purulent drainage. fluid leaving capillaries is protein rich filtrate containing wbc, microbial organisms, and cellular debris primary intention - -Clean laceration that requires simple re-epithelialization when edges are approximated •Example: Surgical Laceration secondary intention - -A wound with a large gap in tissue -some of the tissue has been gouged out Ex. decubitus ulcer tertiary intention - large gap from missing tissue has been contaminated and needs drainage tube while healing requires skingraft mast cells - release histamine histamine - -inflammatory mediator released from basophils, platelets, and mast cells. -causes vasodilation -sneezing, runny nose, eye tearing are consequences of histamine released in URT -benedryl is antihistamine

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Uploaded on
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