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30 Cards in this Set
- Front
- Back
pathology?
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-study etiology & pathogenesis of disease
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principles of diagnosis?
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clinical history, physical examination, laboratory tests, specific exams, treatment-specific or symptomatic
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dx tests & procedures?
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1. clinical lab tests-concentration of various constitutes in bld, urine, other body flds
2. cytologica & histological exams 3. endoscopy-visual & biopsy 4. xray-different amount of rays absorbed by different density of tissue, low density-black, high density-white 5. test of electrical activity-ECG, EEG, EMG 6. ultra sound-different echoes 7. ct scan & mri |
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ct scan?
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bone & gastrointestinal tract
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mri scan?
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abnormalities in tissue surrounded by bone, lesions in spinal cord or base of skull
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cell injury?
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hypoxia, physical, chemical agents, medicines, infection, immune rx, agian
-the consequence of cell injury depends on the type of injury, its duration/severatiiy |
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types of cell injury?
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1. reversible injury-nonlethal injury like cell swelling & fatty changes, may be reversible
2. necrosis-common type of cell death after exogenous stimuli, main changes: digestion of cells by enzymes & denaturation of protein 3. apoptosis-normals cells have life span & are programmed to die naturally, changes can be physiologic (menstruation) or pathologic (viral infections) |
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cellular adaptation?
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cell adapt to change in their environment to escape injury
1. atrophy-shrinkage of cells by loss of cellular substances like muscular atrophy in paralysis 2. hypertrophy:increase of size of cell, hyperplasia: increase of cell number 3. metaplasia-the type of cell is replaced by another type because of a reversible change of adaptation |
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injury repair?
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1. regeneration by parenchymal cells of same type: most tissues have regenerative ability except nervous cells in brain/spinal cord
2. replaced by connective tissue or fibroplasia: process includes migration/proliferation of fibroblasts, deposition of matrix, formation of new bld vessels, maturation & organization of scar |
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wound healing?
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1. primary union: such as clean surgical incision of skin, healed by original tissue in about 2 weeks
2. 2ndary union: more extensive loss of cells/tissue, abundant granulation tissue grows & large scar formation |
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inflammaion?
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-a protective response to cell injury
-many infectious or non infectious factors may cause inflammation -redness, swelling, warming pain |
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acute inflammation?
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-immediate & early response to injurious agent
-vascular dilation, increased premeability, fld excudates, edema -leukocytes migrate & perform phagocytos -chemical mediators like pgs, histamine, ect release to make vascular dilation |
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acute inflammation results?
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-complete resolution replaced by connective tissue
-abscess formation -progression to chronic, or spread to whole body (septicemia) |
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chronic inflammation causes?
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persistent infection, prolonged or recurrent exposure to inflammatory agents or autoimmune response
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morphologic patterns?
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1. serous inflammation: serous fld is derived from serum or secreted by mesothelial cells lining the peritoneal, plural, & pericardial cavities, skin blister from burn or pleural infusion
2. fibrinous inflammation: with greater change of vascular permeability, larger molecules like fibrin can leak out-bact. dysentery 3. suppurative or purulent inflammation: production of large amount of pus, bact. infection produces inflammation 4. ulcers: local defect of the surface of tissue or organ |
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systemic reaction of inflammation?
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1. fever: pryogen produced from WBC in response to infection or toxic response
2. leukocytosis: usually in bact infection & leukocyopenia in virus infection |
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edema?
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-accumulation of fld in interstitial tissues
-can be pitting or non-pitting -according to the positions of fld accumulation: subcutanous edema, pulmonary edema ect |
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fld balance of capillary circulation?
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fld balance between both sides of capillaries 3 factors:
1. hydrostatic pressure 2. colloid osmatic pressure 3. capillary endothelium permeability |
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edema pathogenesis?
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-low plasma proteins:hepatic or renal disease, malnutrion
-increased hydrostatic pressure: congestive ht failure -increased capillary permeabililty: inflammatory or angioneurotic edema -lymphatic obstruction: following surgery, breast edema |
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thrombus/hrombosis?
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intravascular clot/he condition of clot formation & obstruction
attached |
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embolus/embolism?
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a clot detached & carried in cardiovascular system
-other substances like fat, cancer cells, ect can also become emboli/the obstruction of the bld vessel |
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pathogenesis of thrombosis?
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1. endothelial injury
2. alteration in normal bld flow 3. hypercoagulation |
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endothelial injury?
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may be caused by inflammation or hypertension, such as injury results in exposure of subendoththelial collagen, adhesion of platelets, activation of other clotting factors
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alteration in normal bld flow?
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stasis of bld flow can disrupt laminar flow & bring platelets into contact /endothelium & promote endothelia cell activation to stimulate clotting system, eg-thrombus formation in L atrium in mitral stenosis
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hypercoagulability?
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bld has become thicker
-genetics, surgery, labor, ect |
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thrombosis effects?
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-pos: stop bleeding
-neg: cause obstruction in vessel |
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embolism pathogenesis?
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1. thromboembolism: 99% of all embolie are part of dislodged thrombus
1% from 2. fat embolus: after bone fracture 3. gas bubble w/in circulation 4. amniotic fld embolism: complication of labor |
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circulation of embolus?
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-movement of an embolus usually along w/bld flow in bld circulaiton
-a clot from large viens or R ht usually lodge in pulmonary trunck or its branches, which causes pulmonary embolism -clot from L ht or large artiery |
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pulmonary emolism?
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-90% emboli from deep view in low extremity
-silent when obstruction is small, medium size may result in pulmonary hemorrhae, R ht failure, sudden death |
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systemic embolism?
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most from intracardiac mural thrombi, remainders from aortic anerurysms, atherosclerotic plaques
-systems depend on size of embolus & site of vessel -s/s: cerebral thrombosis, local pain, redness, swelling, ect. -most history of ht disease |