Chronic Inflammation Flashcards
Chronic inflammation
Prolonged inflammation with assocatiated repair Delayed onset Variable duration days->years Variable appearances Limits damage - initiates repair Can cause debilitating symptoms
How does chronic inflammation a rise
1 – Takes over from acute inflammation - If resolution not possible with acute inflammation
2 – Develops alongside acute inflammation - Severe/persistent irritation
3 – Arises “de novo” - Without preceding acute inflammation Eg autoimmune conditions Rheumatoid arthritis/Inflammatory Bowel Disease…
Appearance can vary - it depends on the type of cell types present in the tissue
Macrophage
In circulation its in its immature state - monocytes
Once it enters tissue spaces becomes a macrophage
They have abundant foamy cytoplasm (phagolysosme) and they are large cells
Macrophage sometimes described as having a slipper shaped nucleus - because they are inconsistent and unreliable - can look like anything (i.e. a cancer cell) - therefore need to do immunochemistry to see what type of cell it is
e.g. in lung macrophages phagocytose carbon and them accumulate them in their cytoplasm - gives off black appearance
Function - Phagocytosis
Re moval of pathogen/necrosis/debris + Antigen presentation to immune system
Inflammatory Mediators - Synthesis and release of many mediators Controls and regulates inflammatory response
Lymphocytes
Very large nucleus that fills up most of the small cell (slightly larger than RBC) - very little cytoplasm - in histology you cant even see cytoplasm
Function - depends on type -
T cell - variety of types -
Helper T cell - assist other inflammatory cells - CD4
Cytotoxic T cell - destroy pathogens - CD8
B cell - mature into plasma cells produces antibodies and neutralise pathogens
Not possible to distinguish between T and B cell using H+E stain
Plasma cells
Plasma cells can be seen - has a nucleus near the edge of the cell (eccentric nucleus)
the chromatin has shrunk into spherical balls in a circle (clock faced chromatin)
has a paler area near nucleus on H+E (peri-nuclear clearing) - which is the Golgi
These are fully differentiated B lymphocyte which produces antibodies
Eosinophils
Has a Bi-lobed nucleus
Cytoplasm stains (under H+E) as bright red and granular
Red granules in cytoplasm are full of chemical mediators e.g. histamine, NO, prostaglandins
In allergic reactions, then eosinophils release the chemical mediators = symptoms of allergic action (hypersensitivity) - seen in parasitic infection
Fibroblasts/myofibrilblasts
They are taken to site of wound repair
Produce and secret and lay down collagen
forming the reparation process that reconstructs tissues
Myofibirls also contain actin filaments that then allow the cell to contract - contracting the wound to bring it together
Giant cells
Multinucleate cells
Brought about by the fusion of multiple macrophage that increase effectivity of phagocytosis
3 different types of giant cells:
Foreign body great cell - 1 big cytoplasm and nuclei are in a random order
Langhans giant cell - 1 big cytoplasm, nuclei line up along periphery of cell - important in TB
Touton gaint cell - nuclei line up in a little circle in the middle - seen in fat necrosis
Cell types in chronic inflammation
Generally non-specific
Proportion of cell types can indicate a diagnosis
E.g. Rheumatoid arthritis = mainly plasma cells
Chronic gastritis = mainly lymphocytes
Leishmaniasis (protozoal infection) = mainly macrophages
Effects of chronic inflammation
Fibrosis - Deposition of collagen Eg chronic cholecystitis, liver cirrhosis
Impaired Function - Eg inflammatory bowel disease
Rarely = increased function (eg thyrotoxicosis in Graves’ Disease)
Atrophy - Eg atrophic gastritis
Stimulation of immune response - Antigen
Fibrosis
Repeated obstruction of bile duct by gall stones which gives rise to acute inflammation
Repeated bouts of acute inflammation -> chronic inflammation (chronic inflammation rising in conjunction with acute inflammation
Fibrosis of gall bladder wall (thickened and pale)
Impaired function
Idiopathic Inflammatory Bowel Disease:
Crohn’s Disease & Ulcerative Colitis
Abdominal pain, Altered bowel motion, Weight loss, Rectal bleeding
Crohn’s Disease - Can affect all of GI tract (mouth -> anus)
Discontinuous patches of inflammation “skip lesions”
Inflammation affects full thickness of bowel wall “transmural” -> strictures/fistulae
Can sometimes find granulomata
Less likely to have rectal bleeding
Ulcerative Colitis Affects large bowel only Continuous inflammation Inflammation affects superficial bowel wall only Mucosa and submucosa No granulomata More likely to have rectal bleeding
Cirrhosis
- both impaired function and fibrosis -End stage damage to liver
Alcohol Hepatitis Drugs & toxins Fatty liver disease
Fibrosis and attempted regeneration
Nodules of liver - is the livers attempt to regenerate liver tissue but it’s prevented duct to the build up of fibres inbetween the hepatocytes
Granulomatous inflammation
A specific type of chronic inflammation
Chronic Inflammation + Granuloma
Granuloma - a collection of epithelia histiocytes (macrophages that look like epithelial cells - with surrounding lymphocytes
Causes of granulomatous inflammation
Foreign body reaction
Infections - specifically infections that are hard to destroy e.g. mycobacterium - mycobacterium Tb and leprosy -
Hard to breakdown due to a thick cell wall, and mycolic acids present on outside of celll - both of which resist phagocytosis
Mycobacterium granuloma:
- epithelia histocytes lymphocytes in a circle and in the middle (with H+E stain) a pink amorphologous mass of caseous necrosis
Finally idiopathic (we dont know) - Crohn’s Disease Non-caseating granulomata in GI tract Sarcoidosis (multiple well formed granulomas form in) Non-caseating granulomata In lymph nodes, lungs, skin - presents with a dry cough and skin lumps
