pathology overview

• hypertrophy: increase in size of cell, caused by increased growth factors or hormones. pathological: cardiac muscle. physiological: uterus in pregnancy
• atrophy: decrease in cell size or number. caused by decreased nutrients or stimulation, can involve autophagy and decreased protein synthesis
• hyperplasia: increased number of cells, caused by increased growth factor or hormones. pathological: benign prostatic hyperplasia. physiological: breast in pregnancy
• metaplasia: change in phenotype, caused by chronic irritation
• atrophy can progress to apoptosis
• reversible cell injury

  decreased oxygen phosphorylation, ATP depletion, cellular swelling, decreased membrane integrity, protein synthesis defects, cytoskeletal and DNA damage, membrane blebbing, ribosomes deattachment, chromatin clumping
• necrosis


  always pathological, membrane damage, enzyme leakage, digestion of protein, inflammation, caused by hypoxia or injury or infection, ER lysis, increased eosinophilia, glassy and motheaten cytoplasm, pyknosis, karohexis, karolysis
• apoptosis 


  cell shrinkage, chromatin condensation, eosinophilic cytoplasm, blebbing of cytoplasm, and caspase cascade
• coagulative necrosis

  caused by hypoxia, proteins are denatured, pale and firm cooked appearance, nuclear ghosts, glassy and faded cytoplasm
• liquefactive necrosis

  caused by ischaemia or infection, enzyme dissolution, semi liquid appearance and possible cavity
• gangrenous necrosis

  coagulative necrosis or bacterial and liquefaction
• caseous necrosis

  tuberculosis, granulomatis inflammation, no original architechture, proteinaceous mass
• fat necrosis

  digestion by pancreatic lipases, fatty acids and calcium
• inflammation features


  vasodilation, increased vascular permeability, emigration of leukocytes, neutrophils
• chemical mediators of inflammation

  histamines and prostaglandins cause vasodilation, histamines and complement cause increased vascular permeability, TFN and complement cause chemotaxis, and prostaglandins cause fever and pain
• transudate

  low protein (mostly albumin) content, and no increased vascular permeability
• exudate


  increased protein and debris, increase in vascular permeability
• effusion: joint and pleural fluid
• asciles: in peritoneal cavity
• pus: purulent exudate, rich in neutrophils
• granulomas

  macrophages (activated by IFN-y) group together and form giant cells, may have central necrosis and have a central core of epitheliod macrophages, surrounded by lymphocytes, rim of fibrous tissue, can be caused by foreign body or immune system (tuberculosis)
• chronic inflammation

  fibrous scar tissue, tissue destruction , granulomas, macrophages and lymphocytes
• primary intention

  neutrophils, granulation tissue, fibrous scar
• secondary intention

  myofibroblasts compact down, lots of scarring
• repair by healing


  angiogenesis, fibroblast proliferation (forms granulation tissue), ECM and collagen, connective tissue remodelling
• ulcer

  granulation tissue, oedema, new capillaries
• granulation tissue in ulcers

  scaffold for tissue growth, scarring takes time due to the cross linking of collagen
• abnormalities in wound repair

  wound dehiscence, excess repair (hypertrophic scars or keloids), exuberant granulation tissue, wound contraction
• influences of wound healing

  infection and necrotic tissue, poor tissue perfusion, mechanical factors, hormones, diabetes
• dysplasia

  disordered growth, loss of architechtural orientation, bigger and darker nuclei, crowd neighbour cells
• management of cancer

  surgery, radiotherapy, cytotoxic chemotherapy, immunotherapy
• tumour staging

  extend of spread, tumour, nodes, metastases, suggests prognosis
• tumour grading

  differentiation and prognosis
• anaplasia

  pleomorphism, increased nuclei, loss of polarity, abnormal mitoses, poor differentiation
• benign tumour

  may be encapsulated, no haemorrhage or necrosis, well differentiated
• aetiology of cancer

  genetics (familial or sporadic case), environment (infections or lifestyle), aquired conditions (inflammation, immunodeficiences, precursors)
• malignant tumour

  invasive margins, necrosis and haemorrhage, desmoplasia, poorly differentiated, cellular pleomorphism and hyperchromatism
• local. clinical effects

  local: compression, invasion, ulceration, destruction