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42 Cards in this Set
- Front
- Back
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Q. Hypertrophy?
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an increase in size and function of the cell. It is an adaptive response
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Q. Necrosis or Oncosis?
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common after ischemia, chemical injury; cell swelling
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Q. Hypoxia:
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inadequate oxygenation
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Q. Ischemia
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the loss of blood supply
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Q. Apoptosis?
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is the programmed death of the cell. Cell shrinkage.
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Q. Mitochondrial permeability transition?
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leakage of Cytochrome C into the cytosol
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Q. Karyorrhexis?
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fragmentation of the nucleus with scattering of the pieces in the cytoplasm
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Q. Karyopyknosis?
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A cytologic condition caused by shrinkage of the nucleus of a cell with the condensation of the chromatin into structureless masses, as in superficial or cornified cells of stratified squamous epithelium
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Q. Karyolysis?
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dissolution of a cell nucleus
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Q. liquefactive necrosis?
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Enzymatic digestion results in (characteristic of bacterial infection, and stroke)
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Q. Coagulative necrosis?
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Denaturation of proteins results in (characteristic of hypoxic death- ischemia)
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Q. Types of coagulative necrosis?
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Gangrenous necrosis
Caseous necrosis: is coagulation necrosis in tuberculosis Fibrinoid necrosis Fat necrosis |
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Q. Hyperplasia?
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is an increase in the number of cells in an organ or tissue, accompanied by an volume.
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Q. Type of pathological hyperplasia?
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Papilommavirus (HPV)
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Q. Metaplasia?
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is a reversible change in which one adult cell type (epithelial or mesenchymal) is replaced by another adult cell type
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Q. Steatosis?
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abnormal accumulation of triglycerides within parenchymal cells; liver, heart, muscle, kidney
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Q. Atherosclerosis?
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Atherosclerotic plaque - smooth muscle cells; macrophages, foamy cells, lipid vacuoles.
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Q. Xanthomes?
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clusters of foamy cells in subepithelial connective tissue of skin, tendons (“yellow tumors”)
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Q. Xanthelasma?
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clusters of foamy macrophages on the eyelids
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Q. Cholesterolosis?
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accumulation of foamy macrophages in the lamina propria of gall bladder
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Q. AAT?
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controls activation of enzymes in the blood stream
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Q. Metastatic calcifications - deposition of Ca+2 in vital tissue; hypercalcemia Caused by?
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Vitamin D intoxication
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Q. Acute inflammation is accumlation of what?
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Neutrophils
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Q. Chronic inflammation is accumulation of what?
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Macrophages and lymphocytes
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Q. Caseuous necrosis is typically seen in what?
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Tuberculosis
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Q. Hydrogen peroxide (H2O2): H2O2 is produced within the?
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phagolysosome
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Q. Hypochlorous acid (HOCl): major component, catalyzed by?
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myeloperoxidase (MPO
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Q. Sources of histamine and what they cause?
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Source: Mast Cells
Cause: vasodilation and increased permeability of postcapillary venules |
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Q. Serotonin does what?
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Increase permeability of vessels
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Q. Nitric Oxide does what?
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Reduces leukocyte recruitment
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Q. NEUROPETIDES?
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transmission of pain, regulation of B/P, stimulation of secretion by immune and endocrine cells, increase vascular permeability
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Q. A localized collection of pus in a cavity formed by the disintegration of tissue
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Abscess
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Q. Paroxysmal nocturnal hemoglobinuria: what does this cause? What do we see in the night?
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Cause Hemolytic anemia.
Respirotory acidosis at night. |
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Q. Bradykinin does what for inflammation?
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vascular permeability, vasodilation, contraction of smooth muscles, pain
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Q. Thrombin: Which clotting fator? Does what to fibrinogen?
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Clotting factor 2.
Changes fibrinogen to fibrin. |
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Q. Ulcer?
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loss of surface epithelium
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Q. Fistula?
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abnormal communication between two organs
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Q. Chronic inflammation accumulation has two antibody?
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Macrophages are activated by lymphocytes
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Q. Characteristics of granlomatous inflammation?
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macrophages, Lymphocytes, Multinucleated giant cells
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Q. PGE2 is involved?
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Pain
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Q. Protooncogenes?
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are genes involved in normal growth control pathways. They are stimulated by growth factors to induce cell proliferation.
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Q. In the injured area this will start the deposition of collagen in 3-5 days and continue for several weeks?
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Fibroblasts
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