Inflammation and Healing Flashcards
What are the features of acute inflammation?
- dilation of small vessels leading to an increase in blood flow, 2. increased microvasculature permeability enabling plasma proteins and leukocytes to leave the circulation 3. emigration of leukocytes from the circulation, accumulation at injury site, and activation to eliminate the offending agent
What is the difference between exudate and transudate?
Exudate has a high protein content and implies increased vascular permeability, transudate has a low protein content and normal vascular permeability (mainly fluid)
What is the process of leukocyte migration?
The leukocytes first roll (via selectins), then adhere (via integrins) to endothelium, then transmigrate (via CD31) across the endothelium, pierce the basement membrane, and migrate toward chemoattractants (e.g. TNF, IL-1, chemokines) emanating from the source of injury and are then activated by TLRs and PRRs to phagocytise offending agents
What are the 3 main types of exudate and examples of each?
– Purulent/suppurative: lots of neutrophils and necrotic debris eg. bacterial meningitis, abcess (localised collection of necrosis and neutrophils) – Fibrinous: fibrinogen leaks through the vasculature into the extracellular space and deposits fibrin eg. Acute appendicitis, fibrinous pleuritis, – Serous: effusion of cell-poor fluid eg. Blister
What is the pathogenesis of an abscess?
If an area of tissue necrosis is extensive, and the cause is a pus-forming (pyogenic) bacterium, an acute abscess may form. At this stage, if the bacteria are able to survive, proliferate, and cause necrosis, it may continue to enlarge
What are the local and systemic effects of TNF-alpha and IL-1?
Local effects:
@ vascular endothelium: increase leukocyte adhesion, production of IL-1, chemokines and coagulant, down regulation of anticoagulant
@ leukocytes: activate leukocytes, produce cytokines
@ fibroblasts: proliferation and increased collagen synthesis
Systemic effects: fever, leukocytosis, increase acute-phase proteins, increase sleep, decrease appetite
What are regenerative capacities of Labile, Stable and Permanent cells? and give an example of each
Labile: continuously in the cell cycle e.g. epithelial cells, GIT cells, pluripotent SC in bone marrow
Stable: normally in Go but can be stimulated to proliferate e.g. fibroblasts, liver, kidney, pancreas cells
Permanent: Can’t replicate e.g. neurons of CNS and cardiac muscle
What are the main mediators of acute inflammation?
Vasodilation – Histamine, prostaglandins, NO
- Increased vascular permeability – Histamine, serotonin, bradykinin, leukotrienes
- Endothelial activation – TNF, IL1
- Chemotaxis – Complement components, certain cytokines (chemokines,TNF, IL-1), leukotriene B4
- Tissue damage – Neutrophil granule contents, ROS, NO
- Pain – Prostaglandins, bradykinin
- Fever – IL-1, IL-6, TNF, prostaglandins
What are the 3 outcomes of acute inflammation?
- Resolution: removal of cellular debris and microbes by macrophages, and resorption of oedema fluid by lymphatics, restoration of normal function 2. Fibrosis: connective tissue grows into the area of damage or exudate, converting it into a mass of fibrous tissue, a process also called organisation 3. Chronic inflammation: Acute to chronic transition occurs when the acute inflammatory response cannot be resolved, as a result of either the persistence of the injurious agent or some interference with the normal process of healing.
What is granulation tissue and what is its histological appearance?
Migration and proliferation of fibroblasts and deposition of loose connective tissue, together with the vessels and interspersed leukocytes, form granulation tissue. histologically, it is characterised by proliferation of fibroblasts and new thin-walled, delicate capillaries (angiogenesis), in a loose ECM, often with some inflammatory cells, mainly macrophages
What is the time course for repair and healing?
Repair begins within 24 hours of injury by the emigration of fibroblasts and the induction of fibroblast and endothelial cell proliferation. By 3 to 5 days, the specialized granulation tissue that is characteristic of healing is apparent
What is healing by first intention?
When the injury involves only the epithelial layer, the principal mechanism of repair is epithelial regeneration, there is a clean, thin wound, close edges = less scarring and quicker, better healing
What is healing by second intention?
The inflammatory reaction is more intense, there is development of abundant granulation tissue, accumulation of ECM and formation of a large scar, and wound contraction by the action of myofibroblasts.
What are the 4 patterns of intercellular signalling?
Juxtacrine: Signalling b/w adjacent cells E.g. gap junctions Autocrine: Acts locally on same cell type Paracrine: Acts locally on different cell type Endocrine: produces hormone which enters circulation to a distant site
what are some local and systemic factors which may delay wound healing?
Local: infection, foreign material, blood flow, movement, size/type/location of wound Systemic: nutrition, immune impairment e.g. diabetes, AIDS, corticosteroids
What is this and what are its features?
Neutrophils, exhibit progressive segmentation of their nucleus, lightly stippled granular pink cytoplasmic appearance due to numerous small membrane-bound granules, pink cytoplasm,
What does this depict and what are the 3 features?
Chronic inflammation in the lung, showing all three characteristic histologic features: (1) collection of chronic inflammatory cells (*), (2) destruction of parenchyma (normal alveoli are replaced by spaces lined by cuboidal epithelium, arrowheads ), and (3) replacement by connective tissue (fibrosis, arrows )
What does this depict and what are the features?
acute inflammation of the lung (acute bronchopneumonia), neutrophils fill the alveolar spaces and blood vessels are congested.
