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Mechanisms & Morphology of Cellular Injury, Adaptation & Death -…

- - - - Disruption of biochemical pathways
        
        ATP depletion
        
        DNA damage
        
        Increased permeability of cell membranes
      - Direct membrane injury
        
        Plasma membrane
        
        Indirect membrane injury
        
        Cellular hypoxia
        
        Oncosis
        
        Cyanide poisoning
    - - Interference with lipid metabolism >> lipidosis
      - Lysosomal rupture
      - Influx of Ca ions >> incr enzyme activity
        
        Protein catabolism
        
        Depletion of ATP + potent uncouplers of mito resp.
        
        Membrane damage
        
        Injury to DNA
    - - Swelling
      - Vacuoles
        
        Watery
        
        Fatty
        
        Size
    - - Parenchamous organs
      - Hepatosis
        
        Swelling
        
        Paler
      - Fatty hepatosis
        
        Swelling
        
        Yellow/brown, greasy & floats
      - Nephrosis
  - - - Morph = swelling, vacuolation, blebbing & incr. perm of plasmalemma
      - Cell death >> necrotic changes
        
        Coagulation & shrinkage cytoplasm + nuclear pycnosis >> karyolysis
        
        Cause = release enzymes from lysosomes
      - Cell swelling >> direct/indirect membrane injury
      - Inflammation
      - Pathological
      - Histological features
        
        Equivalent to sub lethally injured cells
        
        Morph changes due to necrosis
        
        Swollen cells : Necrotic cells = severity
    - - Follows cell death - hydrolytic enzyme release from lysosomes >> denaturation & coagulation of cytoplasmic proteins
      - Necrotic tissue
        
        Red = vascular injury or hemorrhage
        
        Inflammatory rection zone >> RBC & WBC
        
        Pale, dull, soft, swollen (early) or sunken (late)
      - Gross features
        
        Liquefactive >> CNS
        
        Caseous >> TB & Caseous lymphadenitis
        
        Coagulative >> pale, dull, soft, swollen
        
        Fat necrosis
        
        Traumatic
        
        = traumatized fat deposits
        
        = exposed to pancreatic enzymes >> free fatty acid release from adipocytes >> saponification & inflammation
        
        Enzymatic
        
        Nutritional = steatitis / yellow fat disease >> ROS formatio & lipid peroxidation
        
        Metabolic fat necrosis
        
        Saponification when free fatty acids release too fast
        
        Gangrene
        
        Dry = desiccation
        
        Wet = 2ary infection w/ saprophytic anaerobic bacteria
        
        Extremities - ergot poisoning & frost bite
        
        Gas = advanced wet >> gas produced by clostridia
    - - No inflammation
      - Physiological process = involution & normal cell turnover
      - Morph = cytoplasmic shrinkage & nuclear pycnosis >> karyorrhexis >> phagocytosed
      - Pathological
        
        Hyperthermia, hypoxia, irradiation
        
        Regression of hyperplasia, malignant neoplasms & pathological atrophy
        
        Elimination of auto-reactive lymphocytes & other cells, cell-mediated immune diseases
        
        Viral infections, toxins & drugs
      - Programmed cell death
      - How = activation of caspases + Bcl2 gene >> denaturation cytosolic & nuclear proteins via complex cascades
- - - - Hypoplasia = failure to reach normal size
      - Miscellaneous disorders
        
        Hamartoma = abnorm overgrowths of tissue normal to location
        
        Choristoma = normal tissue in abnormal areas
        
        Failure of fusion, closure, canalisation, separation
        
        Vestigial remnants, accessory/superbunery tissues. ectopic location
        
        Dysplasia >> hip/renal (dystrophies)
      - Aplasia = failure to grow renew
      - Genetic or environmental >> irreversible changes
      - Agenesis = failure to develop
    - - Hyperplasia = incr size > incr no indiv cells
        
        Physiological = glandular epi of endometrium
        
        Pathological = splenic red pulp in hemolysis
        
        Cause = need incr function
        
        vs Neoplasia >> hard to distinguish - hyperplasia still under control
      - Metaplasia = one type mature (differentiated) cell replaced by another type mature cell - not normal to tissue but same embryonal origin
        
        Metaplastic cells derived from undiff stem cells
        
        Epithelial tiss - chronic irritation >> squamous metaplasia brachial epi (smokers) >> neoplasia
        
        Cause = change in fxnal req
        
        CT - fibroblasts >> chondroblasts &/or osteoblasts e.g. spirocerca lupi
      - Hypertrophy = incr size > incr size indiv cells
        
        Physiological = uterus w/ fetes
        
        Pathological = cardiac aortic stenosis
        
        Cause = incr workload
      - Dysplasia = maladaptive response of cells to chronic injury
        
        Disorderly diff of tissue & cellular atypic >> stratified squamous epi of unpigmented skin exp to UV
        
        Dysplasia >> neoplasia (can)
      - Atrophy = decr size after reaching norm.
        
        Quantitative = decr size indiv cells
        
        Cause
        
        Loss hormonal stim
        
        Red blood supp
        
        Loss innervation
        
        Inad nutrition
        
        Red workload
        
        Aging
        
        Reversible
        
        Numerical = decr no indiv cells
        
        May/may not be reversible >> regen capacity of cell type
        
        Involution = physiological >> organ/tissue decr in size i.e. after partutition
- - - - Atherosclerosis = chol accum in walls arteries & arterioles
      - Old haematomas & haemorrhages
      - Histos = cholsterol clefts
    - - Eosinophilic, round droplets varying in size
      - Cause
        
        Excessive production gamma globulins >> retention proteins >> Russell-body plasma cells
        
        Endothelial injury >> prot accum inner wall pulm alveoli, bv walls & basement membs
        
        Diseases = protein leakage due to glomeruli damage >> epi cells of PCT >> proteinuria
    - - Intracell during cell injury OR
      - In hepatocytes
        
        Incr mobilisation
        
        Abnorm cell metab
        
        Lack apoprotein form
        
        Incr intake
      - Lipid storage diseases > accum in lysosomes > genetic deficiency enzyme needed to degrade lipid substate
      - Macrophages > ingest lrg amt lipid = vacuolated = malacia of CNS or necrosis of adipose tissue
  - - - Silica & Asbestos
        
        Chronic alveolitis w/ prog fibrosis of lung parenchyma
        
        Irritate parietal pleura >> neoplasia lining cells >> mesothelioma
      - Trypan blue
        
        Used to treat babesiosis
      - Carbon
        
        Anthracosis = macroph ingest carbon
    - - Haemosiderin
        
        Iron stored in body bound to apoferritin = ferritin >> intracell ferratin aggreg = haemosiderin
        
        Spleen, old haemorrhages, alveoli (animals w/ congestive heart failure)
        
        Yellow/brown aggregates in macros
      - Bile pigments
        
        Green-brown >> Yellow-brown homogenous deposits
        
        Where = Bile canaliculi, hepatocytes & epi cells of PCTs
        
        Cause = hepatic diseases, post-hepatic obstruction to bile flow
        
        Icterus >> accum bilirubin = yellow discoloration of mucous membs
      - Melanin
        
        In cyto of melanocytes & epi cells
        
        Path - cyto of macrophages (= melanophages)
        
        Pseudomelanin
      - Haematoidin
        
        Bright yellow
        
        Sites prev haemorrhage = locally precipitated extracell bilirubin
      - Lipofuscins = from cell memb breakdown
        
        Golen/brown & finely granular
        
        Older individuals = aging pigment
        
        Post-mitotic cell cytoplasm
        
        Atrophic skeletal m cells
        
        Lipofuscinosis of smooth m in intestines >> Vit E/Selenium def >> brown/yellow intestine
        
        Ceroid = variant of lipofuscin, acid-fast & autofluorescent
      - Haematin
        
        Acid haematin = artefactual derivative of haemoglobin in tissues fixed in unbuffered formalin
        
        Blueish/black comp derived from haemoglobin by removal of prot part & oxidation of iron atom
- - - - Paraneoplastic syndrome
        
        Neoplastic cells of some lymphomas + apocrine carcinoma > prod protein > mimics actions PTH > hypercalcaemic calc
      - Primary hyperparathyroidism - rare
      - Vit D poisoning
        
        Incr Vit D >> absorption lrg amts Ca in intestinal lumen
        
        Vit D rodenticides
        
        Calc of lungs, intestinal mucosa, vessel walls & kidneys
      - Secondary hyperparathyroidism - renal/nutritional
      - Chronic renal disease
        
        75% kidney fxn destroyed >> hyperphosphataemia > hypercalcaemia
        
        Extra Ca cant be absorbed >> chronic renal disease = no activation Vit D
        
        Parathyroid stim > PTH release > osteoclasts stim > bone resorption Ca rel > hypercalcemia
        
        Chronic interstitial nephritis = chronic uraemia, Calc cranial IC spaces, endocard LA, gastric mucosa, kidney & alv walls
      - Destruction of bone - rare