Asynch 1 Foundational Concepts and Immune System

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24 Terms

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Pathophysiology

change in physiological process inside cell, tissue, or organ

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What are 4 parts of pathophysiology

etiology

pathogenesis

chemical manifestations

treatment implications

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etiology

ideopathic

latrogenic

where disease originates, direct/underlying cause of disease (infectious, congenital, inherited, nutritional)

unknown case

resulting from healthcare treatment/procedure

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pathogenesis

how disease process happens (originate, develop, worsen). describes cellular, tissue, organ system level change, results in changes to structure/function

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chemical manifestations

signs (objective, labs, xrays)/symptoms (subjective, feeling, experience). may change over time

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treatment implications

connecting all 3 of them to see what treatments would be helpful

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epidemiology

study of patterns of disease in populations

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incidence

prevalence

# of cases per year

total # of people in population with condition

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primary prevention

secondary prevention

tertiary prevention

efforts aimed at preventing disease before it occurs

efforts aimed at early identification

efforts aimed at preventing disease-related deterioration

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Plasma membrane

moves things across plasma membrane via exocytosis + endocytosis

active transport via transport proteins (ATP driven pumps, channel)

lipid soluble can go directly across

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why do cells adapt

increase functional demand, ir/reversible cell injury

adapting is normal! adapt to changing environment/stimuli

adapting stops when need has been met

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Atrophy

shrinkage in cell, decrease in workload/support/stimulation, conserve energy/oxygen

disuse, denervation (paralysis), decrease hormone stimulation (menopause), poor nutrition

original cell —>decrease in number

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Hypertrophy

growth in size because of increase workload/support/stimulation, consume more energy/oxygen

physiologic (exercise), genetic, pathologic (increase bp, increase heart pump, increase heart muscle)

original cell —> bigger mass

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Hyperplasia

growth in number of cells due to increased cell proliferation

physiologic (child to adult), compensatory (regeneration of tissue), hormonal (lactate glands), pathologic (cancer)

original cell —> increase number of cells

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Metaplasia

reversible change in cellular type bc of stressor

can progress to irreversible if initial stimuli is not resolved

original cell —> disformed shape

found in epithelial tisue (respiratory tract: smoking, esophagus: acid reflux)

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dysplasia

change in cellular size, shape, organization (progress from metaplasia)

reversuvke uf ubutial stimulus resolves

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Apoptosis

controlled cell death, breaks down cell into cellular components without contaminating surrounding rissue, replace old cells with new

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necrosis

cell death related to injury

caused by hypoxia, unable to synthesize proteins, destruction of cellular membrane

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Inflammation

Nonspecific, predictable response of living tissue to injury, protective process

prepare tissue for immune response, initiate tissue repair

local or systemic, acute or chronic

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causes of injury

physical trauma, presence of foreign body, infection, ischemia, hypoxia

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Stages of inflammation

  1. Initial Insult

  2. Vascular Response: cytokines released, vasodilate, increase permeability

  3. WBC accumulate/migrate: attract wbc, leukocytes squeeze out of the vessel and into tissue, neutrophils arrive

  4. Kill the microbes: neutrophils cause apoptosis, release cytokines, complement system, T cells activate adaptive immune system

  5. Resolution: platelet and clotting factors to stop bleeding, tissue repair


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4 cardinal signs of inflammation

pain (swelling, tightness), warmth (dilation, increase blood flow), redness/erethema (increase blood flow), swelling (increase vascular permeability), loss of function

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chronic inflammation

caused by persistence of original injury/prolonged exposure

involves:

prolonged duration and inflammation (lymphocyte, macrophage)

tissue healing (scar tissue, fibroblasts)

tissue destruction (initial stimulus or immune cells)

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acute vs chronic inflammation

acute: rapid onset, rapid termination. migration of neutrophils, fluids exudate

chronic: post acute inflammation. lymphocyte/macrophage, tissue destruction.