Acute/Chronic inflammation Flashcards
Cells associated with acute and chronic inflammation
Acute:
-Microbes
-Epithelial barriers
-Phagocytes
-NK cells
-Complement
Chronic:
-B lymphocytes -> antibodies
-T lymphocytes -> effector cells
Inflammation defintion
-The reaction of vascularised living tissue to local injury
-In higher animals the reaction of the blood vessels to local injury leads to the accumulation of fluid and cells that characterise inflammation
-Tissues that are not vascularised (e.g. cornea) do not become inflamed according to the classical definitions
Repair defintion
-The replacement of injured tissue
-Either by regeneration if the damaged parenchyma can divide and be replaced
-Or by fibroblastic or glial “scar” tissue
Inflammation/repair for good and bad
+Inflammation and repair can meet a challenge and restore tissue to health
-Inflammation and repair can contribute in different ways to
many tissue diseases such as:
=> rheumatoid arthritis - persistent autoimmune inflammation
=> fibrous bowel adhesions following surgery
=> renal inflammation
What are the 4 signs of inflammation?
Rubor - redness
Tumour - swelling
Calor - heat
Dolor - pain
Features of acute inflammation
-Mediated by innate immune system
-Relatively rapid onset
-Short duration
-Stereotyped response
-Rapid resolution
Vascular changes in acute inflammation
-Transient vasoconstriction of arterioles
-Vasodilatation and increased blood flow
-Slowing of the circulation because of increased permeability of the microvasculature (Stasis)
-Exudation of fluid and plasma proteins (oedema)
What is acute serous inflammation?
-When accumulation of fluid
is the dominant feature of
inflammation
-Observed in a friction blister or a burn
What may acute inflammation be accompanies by?
Exudate:
An inflammatory extravascular fluid that has:
-a high protein concentration
-cellular debris
-specific gravity above 1020
Pus:
-A purulent exudate rich in leucocytes
(mostly neutrophils) and parenchymal cell debris
Exudate vs transudate
Exudate:
-Inflammatory extravascular fluid
-High protein concentration
-Specific gravity above 1020
Transudates:
-Ultrafiltrates of low protein content (mostly albumin)
-Specific gravity less than 1012
Movement of cells into an acute
inflammatory lesion
-Weibel Palade bodies release cell adhesion molecules (P selectin) to endothelial surface
-When stimulated by histamine complement C5a or LPS
-Expression of P/E selectin on endothelium causes neutrophils to slow down
-By interacting with carbohydrate receptors and rolling along endothelium (margination)
-Release of chemokines (e.g. IL-8) attract neutrophils along a concentration gradient in response to stimuli such as LPS (chemotaxis)
-Interaction between integrin molecules on leukocytes and endothelial adhesion molecules (ICAM-1) makes a firmer connection to permit diapedesis (movement across endothelium) and extravasation
What is margination?
-Increased adhesion of inflammatory cells to endothelium and rolling along endothelium
Chemotaxis definition
The unidirectional migration of cells towards a chemokine
What are the 3 main inducers of chemotactic agents for neutrophils?
-Bacterial products
-Components of the complement system, particularly c5a
-Products of the lipoxygenase pathway of arachidonic acid
metabolism, particularly leukotriene B4
What is extravasation?
-Movement of cells into tissues following the chemokine gradient
Accumulative suppurative inflammation naked eye and microscopically
-White areas on surface of appendix represent massive accumulations of pus
-Many neutrophils in inflamed tissues
What are acute inflammations of the lung called?
-Pneumonia
-‘Red hepatisation’ - looks like liver
-Air spaces filled with neutrophils
-Capillaries are dilated and filled with red blood cells (rubor)
-Fibrin also present - coagulation casscade (acute fibrinous inflammation)
What is membranous inflammation?
-Inflammatory membrane forms over tissue
-Historically seen in Diphtheria
-Also seen in pseudomembranous colitis (due to antibiotics)
What follows acute inflammation?
Features of chronic inflammation
-Relatively long duration
-Associated with the presence of lymphocytes and macrophages
-Proliferation of blood vessels and connective tissue
-Not uniform as many factors modify the course and histological appearance
What causes chronic inflammation?
May follow acute inflammation
May begin as a low grade smouldering response:
-Persistent infections by intracellular organisms
-Prolonged exposure to non-degradable substances
-Autoimmune diseases
Histology of chronic inflammation
Infiltration by mononuclear cells
-Macrophages
-Lymphocytes
-Plasma cells
Proliferation of fibroblasts and small blood vessels
-Increased connective tissue and fibrosis
Chronic granulomatous inflammation
-Macrophages are attracted to area of necrosis by chemokines
-Macrophages form spherical mass - early granuloma
-Non infectious cause: Non-caseating (non-infectious) epithelioid granuloma
-Infectious cause: Caseating (infectious) epithelioid granuloma with central necrosis
-Fibroblasts form on granuloma and produce collagen which replace granuloma with scar
Monocyte vs macrophage
-Monocyte (in blood)
-Macrophage (in tissue)
Foreign body granulomas
-Granulomas are rounded, pale pink staining structures
-They form around foreign material, shown in polarised light
What does this image show?
-Pulmonary tuberculosis - granulomatous inflammation
-Caseous necrosis - central right white
What does this image show?
-Foreign body-type multinucleated giant cells surrounding droplets of paraffin oil in the lung
