General pathology lecture 4 cellular adaptation

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  • Diminished function but not dead.
  • Glucocorticoids, thyroid hormone and TNF stim proteosome-mediated protein degradation; insulin opposes
  • Kidney: atrophy via renal artery stenosis. NB: decrease in cortex (most metabolically active cells)
  • Hormonal: Breast at puberty; breast and uterus during pregnancy Compensatory: regeneration of liver after partial hepatectomy NB; hyperplasia regresses if stim removed; difference with cancer
  • Lft: normal thyroid gland: rings of epithelial cells surrounding colloid. Rt: hyperplasia/hypertrophy of Graves d; note epithelial projections into colloid.
  • Hypertrophy
  • Middle = normal heart; left = hypertrophied heart due to hypertension; rt = dilated heart due to inability to adapt to continued stress
  • Squamous thought to be more durable cell type Squamous epithelium don’t  mucus Acid reflux  col to squamous metaplasia (Barrett esophagus) Connective tissue metaplasia = formation of bone, cart, or adipose tissue in tissues that normally don’t contain them
  • General pathology lecture 4 cellular adaptation

    1. 1. CELLULAR ADAPTATION Lecture 4
    2. 2. Normal +Stress Adapted cell Cell - StressStress = ?Increased/decreased workload * skeletal muscle and body building * cardiac muscle and hypertension * skeletal muscle disuse (limb immobilization)Increased/decreased stimulation
    3. 3. Adapted CellCellular adaptations to stress 1. Hyperplasia (more cells) 2. Hypertrophy (bigger cells) 3. Atrophy (smaller cells)
    4. 4. 3. Atrophy (smaller cells) 1. Physiologic During development: i.e. notochord; thyroglossal duct2. Pathologic (local or generalized) via * disuse * Loss of endocrine stimulation * denervation * Aging * ischemia * Pressure
    5. 5. Atrophy (Mechanism)Reduction in structural components Decreased number of mito, myofilaments, ER via proteolysis (lysosomal proteases; ubiquitin- proteosome system) Increase in number of autophagic vacuoles Residual bodies (i.e. lipofuscin  brown atrophy)
    6. 6. ATROPHY-THYMUS GLAND
    7. 7. ATROPHY-LIVER
    8. 8. CORTICAL ATROPHY
    9. 9. Normal Artophied Brain atrophy
    10. 10. Muscle fiber atrophy. The number of cells is the same as before theatrophy occurred, but the size of some fibers is reduced. This is aresponse to injury by "downsizing" to conserve the cell. In this case,innervation of the small fibers in the center was lost. This is a trichrome
    11. 11. DISUSE ATROPHY (Poliomyelitis)
    12. 12. ATROPHY in OSTEOPOROSIS
    13. 13. HYPOPLASIA-GAS INSUFFICIENCY
    14. 14. Hyperplasia (more cells)1. Physiologic * Hormonal (breast/uterus in pregnancy) * Compensatory (liver after partial hepatectomy)2. Pathologic Excessive hormone/GF stimulation of target tissue * Endometrial hyperplasia (x’s estrogen)
    15. 15. Hyperplasia (Mechanism)Cell proliferation via increased production of TRANSCRIPTION FACTORS due to * Increased production of GF * Increased levels of GF receptors * Activation of intracellular signaling
    16. 16. HYPERPLASIA-PROSTATE GLAND
    17. 17. Thyroid hyperplasia
    18. 18. HYPERPLASIA-UTERUS
    19. 19. Adapted Cell2. Hypertrophy (larger cells) * Not due to swelling * Increased synthesis of structural components * Results in larger organ
    20. 20. HYPERTROPHY OF SMOOTH MUSCLE IN ASTHMA
    21. 21. CARDIAC HYPERTROPHY Myocardial hypertrophy. - Cross-section of the heart of a patient with long- standing hypertension - Shows pronounced, concentric left ventricular hypertrophy
    22. 22. Hypertrophy (Heart)
    23. 23. QuestionWhich term is most likely to fit thedescription of the uterus duringpregnancy? A. hyperplasia B. hypertrophy C. aplasia D. dysplasia E. metaplasia
    24. 24. Metaplasia (Mechanism)Reprogramming 1. of stem cells present in normal tissues 2. of undifferentiated mesenchymal cells in connective tissueMediated by signals from cytokines, Growth FactorLeading to induction of specific transcriptionfactors
    25. 25. METAPLASIA-ESOPHAGUS
    26. 26. 4. Metaplasia **One adult cell type replaces another**ReversibleColumnar to squamous epithelium (most common epithelial -type ofmetaplasia)Chronic irritation i.e. (in trachea and bronchi of smokers)Vit A deficiency squamous metaplasia in respiratory epithelium
    27. 27. Photomicrograph of the junction of normal epithelium(1) with hyperplastic transitional epithelium (2).
    28. 28. Photomicrograph of the trachea from a smoker. Note that the columnarciliated epithelium has been replaced by squamous epithelium.
    29. 29. METAPLASIA-LUNGS
    30. 30. DYSPLASIA-Left• Cellular dysplasia refers to an alteration in the size, shape and organization of the cellular components of a tissue.• It is established that dysplasia is a preneoplastic lesion, in the sence that, it is a necessary stage in the multi-step cellular evolution to cancer.
    31. 31. DYSPLASIA
    32. 32. DYSPLASIA-CERVIX
    33. 33. QuestionWhich of the following best describes thephenomenon of epithelial dysplasia?A. an increase in thickness of the epithelium because of increased number of cellsB. a decrease in thickness of the epithelium owing to decrease in the number of dividing cellsC. an irregular proliferation and maturation of cells throughout the layers of the epitheliumD. an increase in the thickness of the epithelium owing to enlargement of the component cellsE. absence of epithelium because of lack of cell proliferation
    34. 34. MUSCULAR DYSTROPHY
    35. 35. Muscular Dystrophy• What Is Muscular Dystrophy? Muscular dystrophy is a disease in which the muscles of the body get weaker and weaker and slowly stop working because of a lack of a certain protein (see the relationship to genetics?)• Can be passed on by one or both parents, depending on the form of MD (therefore is autosomal dominant and recessive)
    36. 36. ANAPLASIA
    37. 37. • Next Meeting:• Study Inflammation and Repair

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