Pathology inflammation 2 Flashcards
Continually dividing cells
Undifferentiated stem cells divide by mitosis and then differentiate and replace cells that were lost due to tissue destruction
e.g. skin cells
Outcome: resolution- minimal tissue damage
Healing and repair of tissue loss
- Continuously dividing/mitotic/labile cells (skin)
- Quiescent/facultative mitotic/stable cells (liver)
- Non-dividing/post-mitotic permanent cells (neuron)
Quiescent, facultative mitotic cells
Cells do not divide regularly but can be stimulated to divide if necessary to replace cells lost by tissue damage e.g. liver cells
Outcome: Regeneration, can be limisted
Non Dividing cells post mitotic cells (permanent cells)
No capacity to divide and regenerate under any circumstances. E.g. Neurons
Outcome: replacement of parenchymal tissue with connective tissue leads to loss of functional capacity
Healing - by first intention
the process involved when the wound is clean, free of foreign material an necrotic tissue and the edges are close together
Healing by second intention
the situation where there is a large break in the tissue more inflammation a longer healing period and more scar tissue
cells participating in Healing wounds
Leukocytes (WBC)
-PMNs
Connective tissue cells
Epithelial cells - undergo mitosis and extend across the wound
-macrophages: stay longer at the site of healing and produce many cytokines, growth factors and mediators
-other connective tissue: Myofiboblast-hybrid properties of smooth muscle cells and fiboblasts
-Angioblast- precursors to blood vessesls
-Fibroblasts - produce most of the extracellular matrix
Healing process
- Blood clots forms and seals the area
- Inflammation develops
- phagocytes, monocytes, macrophages remove cellular debris
- Granulation tissue grows into the gap
- tissue is fragile
- Epithelial cells undergo mitosis and extend across the wound
- fibrolasts enter the area and produce collagen (a protein that is the basic component of scar tissue and provides strength of repair)
- Fibroblasts and macrophages produce cytokines to attract more fibroblasts
- Fibroblasts stimulate epithelial cell proliferation and migration and promote development of new blood vessels
- cross linking and shortening of collagen fibers promotes formation of tight strong scar
- capillaries in the area decrease
- scar tissue is not normal functional tissue
Factors promoting healing
Youth Good nutrition Adequate hemogloblin Effective circulation clean wound no foreign bodies no complications small wound site of wound
Factors delaying healing
advanced age poor nutrition anemia poor circulation presence of other disorders (diabetes) Irritation or excessive mobility infection, foreign materials large sized wound
Complications of healing
- loss of function
- deficient star formation
- excessive scar formation
- infection
Complication of healing -excess scar formation
Keloids-overgrowth of scar tissue with excessive collagen
Contracture-fixation and deformity of the joint
Adhesions-bands of scar tissue that join two normally separated surfaces, e.g. intestine
Complications of wound healing - Infection
May develop in an inflamed tissue because microorganisms can more easily penetrate when the barrier is damaged and the blood supply is impaired
Classification of inflammation
- Duration- How long is it?
- Etiology-What caused it?
- Location-where is it?
- Morphology (pathology) - what does it look like?
Classification of inflammation
Duration - how long is it
Etiology - what caused it?
Location - where is it?
Morphology (pathology) - what does it look like?
Acute inflammation
Process initiated by local vessels near injured tissue
Vessels alter permeability of walls to allow emigration of leukocytes into the area
Leaukocytes migrate along a chemotactic gradient to reach site of injury where they attempt to repair and remove stimulus
Cascade of biochemical events propagates the response involving vascular system, immune system, cells
self regulation of the inflammatory response concludes acute inflammation
removal of stimuli stops the response of the inflammatory process
inflammatory response requires constant stimuli to propagate the process
Outcomes - resolution, abscess formation, chronic inflammation
Chronic Inflammation
May represent prolonged acute inflammation or persistence of causative agents
Not necessarily characterized by classic signs and symptoms of acute inflammation
onset - delayed
Duration-months, years
Outcomes - tissue destruction, fibrosis
Etiology of inflammation
Infections - bacteria, viruses, protozoa, fungi, helminthis (worms)
Chemical - organic or inorganic, industrial, medicinal
Physical - foreign bodies, heat, irradiation, trauma
Immune
Often the etiology is multifactoral
Location of Inflammation
Localized (e.g. sprain)
Systematic (widespread,e.g. sepsis often begins as localized)
Morphology of Inflammation
- serous
- Fibrinous
- Purulent
- Ulcerative
- Pseudomembranous
- Chronic
- Granulomatous
Serous Inflammation
Mildest form of inflammation
Characterized by clear fluid
Occurs in early stages of inflammation, typcal in viral infections, arthritis, burns
Generally self-limiting
Generally resolves easily and without consequence
Fibrinous inflammation
Exudate is rich in fibrin (protein)
Indicative of a more severe inflammation
Seen in bacterial infections, strep throat, bacterial pneumonia, bacterial pericarditis
Does not resolve as easily
Leads to growth of fibrous tissue (scarring) in the parenchyma
Consequence loss of function
Purulent inflammtion
Typically caused by pus-forming bacteria such as sraphylococci and streptococci
Pus can accumulate on the mucosa or skin or in internal organs
Abscess - localized collection of pus
Ulcerative inflammation
Inflammation of body surfaces or mucosa
Leads to ulceration or necrosis of epithelial lining
Ulcer- defect involving the epithelium, can also extend into the connective tissue
E.g.peptic ulcer in stomach
Pseudomembranous inflammation
Combination of ulcerative, fibrinous and purulent inflammation
exudate of fibrin, pus, cellular debris and mucous forms a pseudomembrane on the surface of ulcers
E.g. Diphteria - pseudemembranes form on the throat, can be scraped away to expose ulcerated defects that bleed
Chronic inflammation
Exudate contains monocytes, lymphocytes, macrophages, plasma cells
Secretory products of chronic inflammatory cells stimulate proliferation of fibroblasts and perpetuate inflammation by constantly recruiting new inflammatory cells
Loss of parenchyma is accompanied by scarring
May lead to loss of function
E.g. scarring of Fallopian tubes associated with pelvic inlfammatory disease can lead to infertility
E.g. Fibrosis associated with chronic lung disease can impair passage of oxygen in to lungs
Functional consequences can lead to many serious symptoms
Granulomatous inflammation
special form of chronic inflammation that is not preceded by acute inflammation
T-lymphocytes and macrophages accumulate at the site of injury
Lymphocytes release cytokines that transform macrophages into epithelioid cells
Epithelioid cells fuse with one another to form multinucleated giant cells
Multinucleated giant cells epithelioid cells and lymphocytes aggregate into nodules called granulomas
Granulomas destroy tissue and persist for a long time
E.g. syphilis, tuberculosis
Granuloma consists of
Lymphocytes
Epithelioid cells (macrophages)
Multinucleated giant cells
Clinical correlations of inflammation
Clinical findings of inflammation
- fever-elevation in body temperature that exceeds 37 degrees celsius
- caused by pyrogenic cytokines; interleukin 1 (IL-1) and tumour necrosis factor (TNF)
- Leukocytosis - increase in circulating WBCs
- Constitutional symptoms - non-specific, include fatigue, weakness, depression, malaise, lack of appetite, achiness etc.
Inflammatory disorders
Immune disorders infections injuries arthritis Cancer
