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73 Cards in this Set
- Front
- Back
two mains mechanisms for cell death
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cell necrosis and apoptosis
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Cell necrosis
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irreversible change in cellular architecture, manifested by:
nuclear pyknosis, karyolysis karyorrhexis nuclear permeability to vital dyes such as trypan blue |
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Apoptosis
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physiological cell death,
programmed cell death |
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3 main manifestations of disease following cell injury
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inflammation
repair neoplasia |
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4 sequelae of inflammation
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granuloma
abscess chronic inflammation repair |
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2 sequelae of post inflammatory repair
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regeneration, leading to tissue restitution
Fibrosis leading to scar |
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3 sequelae to chronic inflammation
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resolution
organ failure Fibrosis leading to scar |
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2 sources of fibrosis
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post inflammatory repair
post inflammatory chronic inflammation |
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6 principal types of cellular agents of injury
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genetic, nutritional, physical (e.g., hypoxia, radiation), chemical, immune and infectious
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How radiation causes injury
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Direct: macromolecules ionized (most susceptible in S and G1)
Indirect: water or solute molecules are ionized and produce free radicals |
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What cells i liver metabolize alcohol
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centrilobular hepatocytes
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What liver cells metabolize alcohol to
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acetaldehyde
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Effect of acetaldehyde
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impaired fatty acid oxidation, causing fatty liver
inhibition of microtubule-directed protein traffic out of hepatocytes, leading to accumulation of ER and balooned hepatocytes synthesis of abnormal cytokeratin filmanets (Mallory bodies) that attract neutrophils stimlation of lipocytes in the space of Disse to becoome myofibroblasts that synthesis collagen |
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Sequelae of alcoholism
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alcoholic hepatitis, which leads to:
- progressive fibrosis - regeneration of hepatocytes as nodules that lead to cirrhosis |
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Type of infiltrating cell in actue inflammatory response
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neutrophils
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type of infiltrating cell in parasitic infections
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eosinophils
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type of infiltrating cell in drug toxicity
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eosinophil
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type of infiltrating cell in allergy
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eosinophil
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type of infiltrating cell in viral infections
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lymphocytes
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type of infiltrating cell in chronic inflammation
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lymphocytes and plasma cells
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Type of infiltrating cell in granuloma
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closely apposed macrophages that deal with agents that are not readily degraded
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Response to bacteria
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acute inflammation with neutrophils
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Response to viruses
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cytopathic changes in infected cells
or lymphocyte attack |
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Response to fungi, parasites
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granuloma formation
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four ways for substances to enter cell
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passive diffusion
active tansport enzyme carriers (microfilaments) pino or phagocytosis |
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Cell's four defenses against injury
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Vascular space
extracellular space cell structure and differentiation Capacity for division |
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postmitotic - def and example
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remain in G phase; once divided that's it
heart and nerve |
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intermitotic - def and example
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constantly dividing
intentinal epithelium, skin, bone marrow |
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reverting postmitotic - def and example
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usually resting, but capable of division after injury; quiescent for long periods
hepatocytes, renal tubular epithelium |
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pyknosis
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condensation of chromatin
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karyolysis
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dissuolution of chromatin and nuclear membrane
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karyorrhexis
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breakdown of nucleus into clumbs
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atrophy
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decrease in size and/or number of cells
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hypertrophy
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increase in size of cells or tissue
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hyperplasia
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increase in number of cells
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metaplasia
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change from one mature cell population to another (e.g. bronchial pseudostratified columnar to squamous)
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neoplasia
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new growth
includes benign and malignant |
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benign vs metastatic
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limited vs. unlimited growth potential
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most diseases can be considered examples of:
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inflammation
repair neoplasia |
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cause of splenic infarct
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endocarditis
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repair mechanism after coagulative necrosis for postmitotic cells
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fibrosis
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color of amyloid in H&E
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pink
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primary sites of adenocarcinoma
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pancreas, lungs, colon
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bacteria in facial abscess
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actinomycetes
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bacteria in pharyngitis
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streptococcus
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bacteria in pneumonia
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pneumococcus pneumoniae
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bacteria in bacterial meningitis
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meningococcus
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bacteria in pyelonephritis
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escherichia coli
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bacteria in syphilis
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spirochetes
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bacteria in lymphogranuloma venerium
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chlamydiae
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bacteria in osteomyelitis
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staphylococcus
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bacteria in TB
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mycobacteria?
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fungus in meningitis
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crytococcus
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fungus in oral thrush
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candida
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fungus in pneumonia
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aspergillus
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fungus in athlete's foot
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dermatophytes
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virus in polio
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enterovirus
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virus in encephalitis
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herpes
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virus in stomatitis
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herpes simplex
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virus in shingles
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herpes zoster
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virus in measles
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rubeola
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virus in hepatitis
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hepatitis virus
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dysplasia
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cancer precursor
abnormal arrangement or appearance |
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anaplasia
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bad dysplasia
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invasion
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tumor grew through the Basement membrane
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are changes in RER reversible or irreversible
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reversible
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are changes in nuclear chromatin reversible or irreversible
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reversible
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are changes in cell surface reversible or irreversible
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reversible
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are changes in membrane reversible or irreversible
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irreversible
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are changes in mitochondria reversible or irreversible
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irreversible
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are changes in lysosomal Ca++ reversible or irreversible
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irreversible
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Traits of necrosis
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Eosinophilia (denatured protein)
swelling (permeability altered) Glass cytoplasm (loss of glycogen) Vacuolated cytoplasm (loss of organelles) Nuclear decay (pyknosis, karyorrhexis, karyolysis) Inflammation |
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is inflammation characteristic of apoptosis? necrosis?
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necrosis only
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