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Pot number 2

  • Describing a pot
    • Look at both the front and the back – cut surface (flat) and another surface (the anatomical surface or capsular surface)
  1. Organ (kidney + ureter)
  2. Cut surface and anatomical surface (how it is cut e.g. bisected)
  3. Describe abnormality
    1. Lesions
      1. Creamy
      2. 2-5 mm
      3. On the parenchyma/capsular surface
      4. Obvious blood vessels = hyperaemia
  4. Capsular exudate
  • 2 bisected kidneys showing the cut surface and capsular surface showing a segment of the ureter
    • Autopsy – always strip the surface of the kidney
    • Shows the calaseal (?) system and the pelvis
    • Urine is made in the glomeruli in the cortex of the kidney (that drains to the pelvis)
    • Starts in the outside area and drains into the pelvis
    • Abnormality:
      • Scattered throughout the parenchyma there are multiple creamy/white lesions
      • Fluff on the capsule = exudate
      • Redness due to vascularity (hyperaemia) and vascular congestion
  • Transudate is a serous fluid, but an exudate contains protein and cellular material
  • Vesico-ureteric reflux. Causes a lower urinary tract infection. Organisms make their way
    • Vesico-ureteric valve is between the ureter and the bladder (Look at the urinary system – kidneys, ureters, bladder, urethra)
    • Presents with
      • Dysuria (burning pain when urinating)
      • Fever
      • Loin pain and tenderness (hurts when you palpate kidney area)
  • Creamy lesions are pus, hyperaemia, exudate on outside
  • Diagnosis: acute pyelonephritis (look up where the pyelo part comes from). An infective cause of acute inflammation.
  • More common in females as the urethra is shorter and straighter than in males
  • Normal urine is sterile (shouldn’t get into the bladder) – bacteria in the MSU is abnormal
  • Causes of acute inflammation: CHINPIG in a vascularised tissue. Examples:
    • Burns are especially bad
    • Trauma
    • Infection
    • Immunological
  • Framework for talking about diseases – learn the framework he said. Put pneumonia into the framework
  • Cut yourself – things that happen
  • Think of the things that happen first:
    • Vascular responses
      • Transitory vasoconstriction followed by
      • >Vasodilation
      • >Increased blood flow (redness and heat)
      • >Increased permeability of vessels
    • Cellular responses
  1. Chemotaxis in the blood stream (happens from 1-4)
  2. Margination
  3. Adhesion (involves selectins and integrins)
  4. Migration (diapedesis)
  5. Chemotaxis in the tissue
    • Chemotactic molecules (from mast cells, surface molecules on the bacteria, and leucocytes) are released from the site
  • Normally, red blood cells run in the middle and the leucocytes run near the border
    • Acute inflammation – margination of leucocytes (even more prominent)
  • Exudation causes the blood to get thicker and slower – called “haemostasis” (hydrostatic and osmotic pressure)
  • Surface molecules on the leucocytes interact with surface molecules on the endothelial cells. They roll and then stick.
  • Leucocytes project pseudopodia and migrate through the endothelial wall via diapedesis
  • The leucocytes then follow a chemotactic gradient toward the site of injury
  • Aims of inflammation: clearing the irritant and healing the injured area. But there is some collateral damage. In asthma there is
  • Beneficial effects of exudation
    • Dilution of the irritant
    • Plasma proteins
      • Complement
      • Immunoglobulins (antibodies)
      • Fibrin (as fibrinogen that gets activated in tissue)
    • Nutrients that the cells need to survive
  • Deleterious effects of exudation
    • Swelling can increase pressure in closed spaces, causing pain
    • Spreading microbes
      • Loose tissues that can spread
      • E.g. orbital cellulitis, acute epiglottitis (w/ tracheal component … obstructs airways and you can die)
  • Chemotaxis
    • Definition: Directional movement of a cell in response to a chemical gradient
    • In acute inflammation – we are referring to neutrophils (PMNs – polymorphonuclear leucocytes. They have lobular nuclei)
    • PMNs (lobated nuclei)
  • Neutrophils
  • Basophils
  • Eosinophils
  • Chemotactic molecules
    • Complement products
    • Interleukins (e.g. IL-8)
    • Leucotrienes (LT4)
    • Prostaglandins ??
    • Lysosomal enzymes (released in the process of lysosomes in phagocytosis) – dynamic – as they die, their products from death are chemotactic. [Keeps on recruiting cells. Hopefully it ends in resolution, but not always]
    • Complement
      • Clotting cascade
      • Lots of other branches that do many things
  • (Chronic inflammation – lymphocytes and macrophages)
  • Phagocytosis
    • Takes in the infective particle (although there is some killing that occurs in the extracellular area)
  1. Recognition – opsonisation (coated with a protein that makes it a target). Obviously need to be able to recognise it

Opsonins include antibodies, complement, and surface markers on certain bacteria (as we can recognise self easily, we can easily recognise foreign) (such as antigens and formylmethionine residues)

  1. Engulfment (with pseudopodia)
  2. Intracellular (enzymic) killing (by spamming lysosomes at the phagosome – fusion of the two to form a phagolysosome)

TB stops this happening – uses the cell to reproduce etc.

Pot number 2

  • Lung abscess (a walled-off accumulation of pus)
    • One of the sequelae of acute inflammation
  • Has a “hole” in the lung