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30 Cards in this Set

  • Front
  • Back
pathology?
-study etiology & pathogenesis of disease
principles of diagnosis?
clinical history, physical examination, laboratory tests, specific exams, treatment-specific or symptomatic
dx tests & procedures?
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
ct scan?
bone & gastrointestinal tract
mri scan?
abnormalities in tissue surrounded by bone, lesions in spinal cord or base of skull
cell injury?
hypoxia, physical, chemical agents, medicines, infection, immune rx, agian
-the consequence of cell injury depends on the type of injury, its duration/severatiiy
types of cell injury?
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)
cellular adaptation?
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
injury repair?
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
wound healing?
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
inflammaion?
-a protective response to cell injury
-many infectious or non infectious factors may cause inflammation
-redness, swelling, warming pain
acute inflammation?
-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
acute inflammation results?
-complete resolution replaced by connective tissue
-abscess formation
-progression to chronic, or spread to whole body (septicemia)
chronic inflammation causes?
persistent infection, prolonged or recurrent exposure to inflammatory agents or autoimmune response
morphologic patterns?
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
systemic reaction of inflammation?
1. fever: pryogen produced from WBC in response to infection or toxic response
2. leukocytosis: usually in bact infection & leukocyopenia in virus infection
edema?
-accumulation of fld in interstitial tissues
-can be pitting or non-pitting
-according to the positions of fld accumulation: subcutanous edema, pulmonary edema ect
fld balance of capillary circulation?
fld balance between both sides of capillaries 3 factors:
1. hydrostatic pressure
2. colloid osmatic pressure
3. capillary endothelium permeability
edema pathogenesis?
-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
thrombus/hrombosis?
intravascular clot/he condition of clot formation & obstruction
attached
embolus/embolism?
a clot detached & carried in cardiovascular system
-other substances like fat, cancer cells, ect can also become emboli/the obstruction of the bld vessel
pathogenesis of thrombosis?
1. endothelial injury
2. alteration in normal bld flow
3. hypercoagulation
endothelial injury?
may be caused by inflammation or hypertension, such as injury results in exposure of subendoththelial collagen, adhesion of platelets, activation of other clotting factors
alteration in normal bld flow?
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
hypercoagulability?
bld has become thicker
-genetics, surgery, labor, ect
thrombosis effects?
-pos: stop bleeding
-neg: cause obstruction in vessel
embolism pathogenesis?
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
circulation of embolus?
-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
pulmonary emolism?
-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
systemic embolism?
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