1. H&E stain
    • Hemotoxylin stains acidic blue (DNA and RNA)
    • Eosin stains basic red (proteins)
  2. Trichrome stain
    • Connective tissue bluish green
    • Muscle reddish brown
  3. Cilia
    • Simple columnar or pseudostratified
    • Basal body underneath
    • For pushing things along
  4. Stratified columnar
    • Looks more like simple
    • Salivary gland
  5. Transitional epithelium
    • Bladder
    • Stratified cuboidal to stratified squamous
  6. Goblet cells
    • Psuedostratified
    • Eject stuff
    • Look for even once cell that spans
  7. Brush border
    • Microvilli
    • Gut
    • Absorb
    • Simple columnar
  8. Stereocilia
    Long and made of actin
  9. Terminal bar
    • Apical junctional complex around the cells
    • Tight junction and adherens/intermediate junction and desmosome
  10. Junctions
    • Basolateral
    • You can see adherens junction/intermediate junction (zonula adherens) but not a tight junction (kissing point/zonula occludens) unless there is fluid trying to get through
    • Desmosome (macula adherens) just at certain points (intermediate filaments)
    • Gap junctions allow limited small flow (no proteins nucleic acids or polysaccharides
    • Basal
    • Hemidesmosome anchors to basement membrane (intermediate filaments) can cause blister if bad
  11. Connective tissue types
    • Loose (lots of cells)
    • Mesenchymal (loose embryonic)
    • Mucous connective tissue (loose in umbilical cord)
    • Dense irregular
    • Dense regular (tendon and ligament)
  12. Connective tissue fibers
    • Collagen
    • Elastic fibers
    • Reticular fibers
  13. Collagen
    • Triple helix quarter staggered and not end to end connected
    • Procollagen has N and C propeptides that are cleaved once triple helix forms
    • Vitamin C required for hydroxylation of proline and lysine
    • Lots of variety
  14. Elastic fiber
    • Made from a random coiling of elastin polypeptides that are desmosine (unique amino acid) linked
    • Fibrillin, when present, tells elastin where to be deposited and without it elastin forms sheets
  15. Reticular fiber
    • Stroma of lymphatic tissue (not exclusively)
    • Type III collagen
    • High sugar content so stain black in silver stain
    • Early wound healing and early development
  16. Cells in connective tissue matrix
    Fribroblasts, macrophages, mast cells, adipocytes, stem cells
  17. Junk in connective tissue
    Fibers, GAGs, proteoglycans, glycoproteins
  18. Leucocytes
    • White blood cells
    • Granulocytes
    • Neutrophil, eosinophil, basophil (order of increasing granularity) all polynuclear
    • Agranulocytes
    • Lymphocyte (large nucleus) and monocyte which differentiates to macrophage (kidney nucleus)
  19. Physiological adaptation
    Response to hormone or other normal chemical substance
  20. Pathological adaptation
    Response to nonlethal but bad stimuli
  21. Hypertrophy
    • Increase in cell size
    • Physiological (reversible) can be building muscle or pregnant uterus
    • Pathological can be in cardiac muscle due to stenotic aortic valves or in stomach due to pyloric stenosis
    • Hypertrophic obesity is mature onset (little increase in cell number)
  22. Hyperplasia
    • Increase in cell number
    • Physiological can be hormonal like breast or regrowing of liver (compensatory)
    • Pathological can also be hormonal but is bad like psorias of skin or hyperplasia of endometrium from hyperestrinism
    • Hyperplastic obesity is juvenile with increase in number
  23. Atrophy
    • Reduction in size and number often
    • Adult tissue reduction
    • Physiological can be return to normal size after physiological hyperplasia/trophy like muscle, uterus, ovary in menopaus
    • Pathological can be localized or generalized like ischemic atrophy due to stenosis like kidney or pressure atrophy like amyloid deposition in cardiomyocytes
  24. Hypoplasia
    • Developmentally smaller organ
    • For some reason the most menopausal endometrium is also hypoplasia
  25. Replicative capacity
    • Continuous-skin, endometrium, bone marrow, GI epithelium, respiratory epithelium
    • Conditional-liver, pancreas, kidney
    • Non dividing-muscle (scar by fibrosis) or brain (scar by cyst)
  26. Metaplasia
    • Change in differentiation (reversible)
    • Can lead to dysplasia
    • Genetic deprogramming of stem cell
    • Pathological, but if you take away stimulus it usually reverts
    • Smoker's lung glandular epithelium to squamous (squamous metaplasia) more resistant but loose cilia
    • Barret's esophagus squamous epithelium to glandular epithelium (glandular metaplasia)
    • Mesenchymal metaplasia is a response to injury in connective tissue with fibroblasts to osteoblasts or chondroblasts
  27. Dysplasia
    • Abnormal hyperplasia (sometimes reversible)
    • Can lead to neoplasia
    • Mostly in epithelial cells especially cervix uteri
    • Mild is reversible (from irritation)
    • Carcinoma in situ is when it spans epithelium and is non reversible
  28. Neoplasia
    Uncontrolled growth (irreversible)
  29. Mild cell injury
    Hydropic change due to Na/K pump or hypoxia indicates mild injury (reversible)
  30. Nature of chronic accumulations/injuries
    • Endogenous come from within body like fat, protein etc
    • Exogenous come from outside like carbon
  31. Fatty Liver Disease
    • Hepatic steatosis
    • Fatty liver, acute hepatitis, lipogranulomas, mallory bodies (alcoholic)
    • Can also be caused by obesity, diabetes or metabollic syndromes
    • Decrease fatty acid oxidation and VLDL-TG secretion
    • Increase fatty acid synthesis and influx
    • Mallory bodies are clumps of intermediate fillaments
    • Collagenous bands form around hepatocytes that try and regrow, forming nodules, thus cirrhosis
  32. Coal miner's lung
    • Anthracotisis plus silica plus fibrosis
    • Fibrosis causes more fibroblasts so more cells between alveolus and capillary increases distance and reduces surface area and diffusion
  33. alpha1-AT accumulation
    • Accumulates in liver and inactivates elastase, which destroys lung parenchyme leading to larger air pockets and fewer capilaries (the proteases that do this are inhibited by alcohol and activated by smoking)
    • Fills, spills, and kills hepatocytes
  34. Coagulative necrosis
    • Heart, post myocardial infarct
    • Fresh necrosis has hemorrhage and is soft, but results in fibrotic scar
    • Becomes hypereosinophillic as far as histology goes so it is red
    • Also in kidneys and spleens where they can't regrow
  35. Liquefactive necrosis
    Brain, forms a cyst, ghostlike cell appearance where you can only see outline
  36. Granulomas
    • Caseating
    • Middle is necrotic and soft, looks like cheese
    • Tuberculosis, fungal, cat scratch, leprosy
    • Non caseating
    • middle is many macrophages morphed into one large mutli nuclear body that is still alive
    • Sarcoidosis, beryllosis, crohn's, foreign body
  37. Fat necrosis
    • Pancreatitis (untreatable)
    • Only affects adipose tissue
    • Calcium enters and high pH causes saponification
  38. Tumor necrosis
    Tumor outgrows blood supply and dies in the middle and scars
  39. Cell injury to tipping point
    • Hypoxia, free radicals, nitrogen oxide, lipid peroxidation
    • Accumulates and gets to irreversible point
    • Membrane damage and calcium homeostasis disruption and ATP depletion are key
  40. Calcium ingress
    • Messes up ATPases so you have ATP depletion
    • Leads to other ion fluxes and membrane damage
    • Cell swelling to necrosis
  41. Free radical generation
    • Arginine NOS to NO.
    • O2 oxidases to O2- to OH.
  42. Mechanisms of free radical damage
    • Guanine + OH. to guanine-OH. makes 8 hyrdoxy guanine to cause a mutagenic lesion in DNA
    • Unsatruated fatty acid + OH. to H20 and unsaturated fatty acid radical which binds two oxygen (peroxidation) and then takes an H from another unsaturated fatty acid to make another unsaturated fatty acid radical (propogation)
    • Protein damage to misfold
  43. Antioxidants
    • SOD, super oxide dismutase, makes OH. to H2O2
    • Vitamin C, uric acid, GSH, catalase, glutathione peroxidase, N-Acetyl Cysteine
  44. Reperfusion injury
    • Too much oxygen too fast leads to ROS
    • Increases inflammatory response, which generates free radicals
    • Calcium from fresh blood can get into holes in membrane and wreak havoc
  45. Enzymes released in necrosis
    • Liver AST/ALT
    • Pancrease amylase
    • Heart troponin I
  46. Apoptosis on cellular level
    • No inflammatory response
    • Blebbing, phagocytized by adjacent cells, shrinkage (loss of water) chromatin condensation and DNA fragmentation
  47. Key players in apoptosis
    • Caspases signal apoptosis through cascade and do proteolytic cleavage
    • p53 signals, transcribes BAX, which releases cytochrome C from mitochondria, which activates first caspase
    • There is an extrinsic pathway for apoptosis without p53 but still caspases that uses signal from outside
  48. Necroptosis
    • Looks like necrosis, no blebbing, does spill and no nuclear condensation
    • Apoptotic like pathway without caspases
  49. Utility of apoptosis
    • Physiological
    • Embryonic tissue remodeling
    • Physiological and pathological
    • Removal of activated T cells at end of immune response, elimination of virus infected cells, removal of DNA damaged cells, killing of inflammatory cells in immune privileged sites (eye)
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