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49 Cards in this Set
- Front
- Back
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pathology
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-Bridge between basic science and clinical practice
-“study of suffering” -causes of diseases-“etiology” |
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pathogenesis
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-signs and symptoms of patient
-physiologic mechanism |
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Hypertrophy
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Increase in protein synthesis/ organelles
Increase in size of cells Increase in organ/tissue size |
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Hyperplasia
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-proliferation of cells within organ/tissue
-Increase in NUMBER of cells Increase in size of organ/tissue |
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Aplasia
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-defective development resulting in the absence of all/ part of organ
-Failure of cell production Agenesis or absence of an organ:fetus Loss of precursor cells:adults |
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Hypoplasia
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-underdevelopment/ incomplete development of tissue/ organ
-Decrease in cell production |
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atrophy
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-partial/complete wasting away of a part of the body
-Decrease in mass of preexisting cells -Smaller tissue/organ -Most common causes: disuse poor nutrition lack of oxygen lack of endocrine stimulation aging injury of the nerves |
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Metaplasia
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-Replacement of one tissue by another tissue
-if original cell cant withstand env't- change to dif. form |
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Squamous metaplasia
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benign change in epithelial linings of certain organs
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cartilaginous metaplasia
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occurs in normal tendons
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myeloid metaplasia
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bone marrow undergoes fibrosis
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Hypoxic cell injury
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-Complete lack of oxygen/ decreased oxygen
-Anoxia or hypoxia Causes: ischemia anemia carbon monoxide poisoning decrease tissue perfusion poorly-oxygenated blood |
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ischemia
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restriction of blood supply
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Early stage Hypoxic cell injury
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-Decrease in production of ATP
-Changes in cell membrane -Cellular swelling endoplasmic reticulum mitochondria -Ribosomes disaggregate -Failure of protein synthesis -Clumping of chromatin |
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Late stage Hypoxic cell injury
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Cell membrane damage
myelin blebs cell blebs |
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karyorrhexis
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nuclear fragmentation occurs within 1 or 2 days after injury then the nucleous dissapears
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pyknosis
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a degenerative state of cell nucleous (nucleous shrinkage)
-increase basophilia |
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Cell Death
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-Irreversible damage to the cell membranes
-Calcium influx -Mitochondria calcifies -Release of cellular enzymes lab exams for AST, ALT, CKMB, LDH -Most vulnerable cells: neurons |
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free radicals
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-highly reactive, unstable species, interactive lipids, proteins, carbs
-derived form oxygen |
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Free radicals: superoxide and hydroxyl radicals
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Seen in:
normal metabolism oxygen toxicity ionizing radiation UV light drugs/chemicals ischemia |
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Mechanisms to detoxify free radicals
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-Glutathione
-Catalase -Superoxide dismutase -Vitamin A, C, E -Cysteine,glutathione, selenium, ceruloplasmin -Spontaneous decay |
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Chemical Injury
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Carbon tetrachloride and liver damage
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Necrosis
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-sum of all the reactions seen in an injured tissue, leading to its death
-denaturation of proteins -enzymatic digestion of organelles and other cytoplasmic components |
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autolysis –
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destruction of cell through its own cell’s enzymes
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Heterolysis –
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extrinsic factors
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Coagulative necrosis
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- accidental cell death by ischemia or infarction (bl. supply inadquate)- denature of cytoplasmic proteins
-Interruption of the blood supply -Poor collateral circulation heart kidney -Characteristic nuclear changes pyknosis karyorrhexis karyolysis disappearance of a nuclei |
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pyknosis
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condensation of chromatin (cell death)
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karyolysis
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complete dissolution of chromatin by ?DNAase
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Liquefactive necrosis
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-focal bacterial/ fungal infections
- cell digested by hydrolytic enzymes- results: soft lesion of puss and remains of necrotic tissue which is removed by WBC and left is fluid filled space -Enzymes liquefy the tissue Brain Suppurative infections Bacteria |
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Caseous necrosis
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-biological tissue death
-Coagulative + liquefactive -“cheese - like” -Part of granulomatous inflammation -Classic picture: Tuberculosis |
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Gangrenous necrosis
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-superimposed infection
-Interuption of the blood supply to the lower extremities or bowels -Wet type: complicated by liquefactive necrosis -Dry type: complicated by coagulative necrosis |
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Fibrinoid necrosis
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- death by accumulation of proteinacous material in tissue (fibrin)
-Immune-mediated vascular damage -Protein – like material in the blood vessel walls |
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Fat necrosis
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-formation of Ca soaps when fat is hydrolyzed into glycerol and fatty acids
-Traumatic fat necrosis – after injury Breast -Enzymatic fat necrosis – after inflammation Pancreas |
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APOPTOSIS
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-occurs when cell dies through activation of internal suicide program "programmed cell death"
-Removal of cells -Prevents neoplastic transformation (cell changes manifested from lots)- found in protein 53 which blocks DNA activity so no changes in the nucleous -“falling away from” Useful in Eliminating unwanted cells around tissues -mainly seen in embryogensis |
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Genes affecting apoptosis
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Inhibits:
bcl-2 Facilitates: bax p53 |
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bcl-2
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inhibits apoptosis by regulating mitochondrial function
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bax -
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facilitates apoptosis
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p53 -
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decreases transciption of bcl-2 and increases transcription of bax thus facilitates apoptosis
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Morphological features in apoptosis
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Involves small clusters of cells only
No inflammatory cells Cell membrane blebs (after many changes in the last stage, the cell membrane starts to bubble-cytoplasm shrinks and sometimes nucles disapears) Cytoplasmic shrinkage Chromatin condensation Phagocytosis of apoptotic bodies |
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fatty change
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-accumulation of intracellular parenchymal triglycerides
- occures inliver, heart, kidney due to alcoholism, diabetes, malnutrition obesity and poisen -increased transport -decrease mobilization -decreased use -overproduction |
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Hyaline change
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-Accumulations of proteinaceous materials
-Homogenous, glassy, eosinophilic appearance in H and E stains |
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Exogenous pigments
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-Pulmonary accumulations of carbon, silica and iron dust
-Tissue accumulation of lead (Plumbism) -Tissue accumulation of Silver causing grey discoloration of skin and conjunctivae (Argyria) -Sometimes these pigments cause cell injurty |
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bilirubin
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catabolic by product of heme moiety of hemo and myo
-jaundice |
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Hemosiderosis
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- Fe containing pigment (ferritin)
-Hemosiderin in tissue macrophages -NO tissue damage -No organ damage - iron overload disorder resulting in accumulation of hemosiderin |
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hemochromatosis
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Hemosiderin in parenchymal cells
Tissue damage Scarring Hereditary: Hfe gene on Chromosome 6 “bronze diabetes” Secondary: blood transfusions |
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Lipofuscin
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-yellowish, fat-soluble pigment; an end-product of membrane lipid peroxidation
-referred to as wear-and-tear pigment -accumulates in the elderly esp. in hepatocytes and myocardial cells -Brown atrophy - combination of atrophy and lipofuscin deposition |
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Hemosdrerin-
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granular brown substance composed of ferric oxide; left from the breakdown of hemoglobin
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Hypercalcemia
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“metastatic calcification”
-caused by increased level of calcium;occures in high serum calcium levels; occurs in any organ and normal tissue during periods of hypercalcium (don’t need any pathogenic tissue) |
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“dystrophic calcification”
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-Previously damages tissues
-may occur at any serum calcium level; usually occures in previous injured tissue tuberculosis scarred heart valves |
