Cellular Response Flashcards
Aspects of disease process
Etiology
Pathogenesis
Morphologic changes
Clinical manifestation
Refers to the sequence of cellular, biochemical and molecular event that follow the exposure of cells or tissue to an injurious agent
Pathogenesis
Able to handle physiologic demands maintaining a steady state
Homeostasis
Nutrient deprivation triggers an adaptive cellular response
Autphagy
Refers to an increase in the size of cells
Hypertrophy
Activation of signal transduction pathway in hypertrophy
PI3K or AKT pathway
Downstream of signaling G protein coupled receptors
Transcription factors involve in hypertrophy
GAT4
NFAT
MEF2
Hypertrophy is limited by
Vascular supply
Oxidative capabilities
Altered protein synthesis and degradation
Cytoskeleton alterations
Physiologic atrophy examples
Notochord and thyroglossal duct
Common causes of atrophy
Decease workload Loss of innervation Diminished blood supply Inadequate nutrition Loss of endocrine stimulation Pressure
Mechanism of atrophy
Ubiquitin Proteasome pathway
Glucocorticoid
Cytokines like TNF
example of epithelial metaplasia
Columnar to squamous
Stones in the excretory duct
Vitamin A deficiency
Cigarettes smoking
Squamous it columnar
Barrert’s esophagus
Connective tissue metaplasia
Myositis oasificans
Hallmarks of reversible cell injury
Depletion of ATP
Cellular swelling
Causes of cell injury
Oxygen deprivation Physical agents Chemical agents Infectious agents Immunologic reactions Genetic derangement Nutritional imbalances
Morphologic alterations in cell injury
Nonfunctional
Ultrastructural
Light microscopic
gross morphologic
Morphologic changes in Necrosis
Increased eosinophil Glassy homogenous appearance Vacoulated cytoplasm \+myelin figures Calcination of fat cells Nuclear changes
Architecture of dead tissues is preserved
Coagulative necrosis
Digestion of the dead cells resulting in transformation of th tissue into a liquid viscous mass
Liquefactive necrosis
Seen in tuberculous infection
Caseous necrosis
Seen in immune reaction of blood vessels
Fibrinoid vessels
Decreased in scavenging ROS may lead to excess of these free radicals
Oxidative stress
How are free radicals generated
Reduction oxidation rxn Absorption of radiant energy Rapid burst of ROS Enzymatic metabolism Transition metals Nitric oxide
Predominant anti apoptitic proteins
Bcl 2
Bcl x
Pro apoptitic proteins
Bax
Bak
Cytochrome C binds to APAF 1 to trigger what
Caspase 9
Cellular aging
Accumulation of DNA damage
Replicative senescence
Defective protein homeostasis
Nutrient sensing system
