Acute inflammation Flashcards
what are the general features of inflammation
*Response of vascular tissue to infections and damaged tissues that brings cells and immune cells of the host from the circulation to where they are needed in order to eliminate the offending agents
protective response ,essential to survival and not always harmful
What are the main steps of inflammatory response ? - 5 R’s
- Recognition of injurious agent( invading agent)
* epithelial cells ,tissue macrophages ,dendritic cells ,leukocytes and other cell types which express receptors that sense the damage of microbes - REcruitment of leukocytes
- Removal of agent by leukocytes
- regulation of the response
5.Resolution (repair)
either
*elimination of noxious stimuli by decline of the reaction and repair of the damaged tissue complete resolution or scaring by fibrosis
*persistent injury resulting in chronic inflammation
What are the causes of inflammation -7
*Exogenous causes 1.Mechanical injury
2.Chemical injury
3.Physical injury
4Infective agent eg bacteria
- ENDOGENOUS CAUSES
5. Adjecent necrosis
6. Immunological reaction eg hyposensitivity
7. foreign material eg splinter and sutures
t/f Causes of inflammation are similar to causes of cell injury
true
t/f ; Inflammation can be classified according to site
true :
tissue involved + suffix -itis eg appendicitis
Discuss the two types of inflammation :
Acute and chronic
*Acute inflammation {AI) and Chronic inflammation (CI)
1AI; initial ,rapid response (hrs to days) whereas CI has a longer duration
AI exudation(leaking ) of fluids and plasma proteins (edema) into tissue and emigration of leukocytes ( neutrophils) whereas with CI there is more tissue destruction ,lymphocytes and macrophages ,and proliferation of blood vessels ,deposition o connective .
AI plays a role in the innate immunity whereas CI plays a role in the Adaptive immunity
AI may resolve or persist and lead to ci
What are the clinical signs of inflammation
- Rubor -redness
- calor -heat
- dolor-pain
- tumor -swelling
- functio laesa-loss of function
what are the major components of acute inflammation
- Dialation of small vessels leading to an increase in blood flow
- Increased permeability of the vasculature to allow plasma proteins and leukocytes to leave circulation
- Emigration of the leukocytes from circulation ,their accumulation and their activation
discuss the vascular reaction in acute inflammation
- Vasodialation
* Induced histamine
* Cause of erythema(redness) - Incraeased vascular permeability
* Induced by histamine and kinins
* produce gaps in-between epithelial cells
* to allow increased passage of fluid through the endothelium
3.Edema from fluid leakage and escape of plasma proteins and leukocytes
- Response of lymph nodes
* due to drainage of fluids by lymphatics
* leads to reactive lymphadenitis ,show redness and swelling
Discuss the emigration of leukocytes to the site of inflammation
- Multi-steps
* Loose attachment and rolling on endothelium mediated by selectins
* Firm attachment to endothelium mediated by integrins
* Migration through endothelial spaces
- Expression mediators promoted by cytokines
- Neutrophils initially predominate followed by macrophages
Discuss leukocyte activation and removal of offending agent
- Leukocytes eliminate microbes and dead cells by phagocytosis and further destroyed by phagolysosomes
- The invader is then destroyed by free radicles generated by activated leukocytes and lysosomal enzymes
- Microbes are eliminated by neutrophils ,excluding nuclear content ,enzymes and free radicles(ROS)
Damage to normal tissue can occur
*Inflammation is terminated by anti-inflammatory mediators
What are the 3 important mediators of inflammation
- Chemotaxis :The movement o WBC to an attracting stimuli
- Chemotaxic agents are :
- Bacterial products
- Complement protein C5a
- Lipoxygenase pathway of the arachidonic acid metabolism components eg leukotriene
- Phagocytosis
* Recognition is mediated by opsonins(immunoglobulins ,complement )
* killing of microbes is done through phagolysosomes ,oxygen free radicle - Degranulation
* Lysosomal granules
- small specific granules eg lactoferrin ,lysozome ect
* large azurophile granules eg acid hydrolases
What are the effects of histamine
- Localised capillary dilation
- Red flare-redness
- Weal -raised area from edema (swelling)
Discuss the morphology of neutrophils
- Smaller specific granules and larger azurophil granule
- lobated nucleus
- First to arrive and has a short life
- Activily mobile
- orms part of the pus
discuss the unction of eosinophils
- has two lobes
- red granules
- active in allergic conditions ,warms ,parasites
discuss the function of basophils and mast cells
release heparin and histamine and play a role in hypersensitivity where anaphylaxis can result
Discuss the function of mononuclear phagocytes
- scavenger cells( clean up foreign matter
- Immune function: presents antigens to CD4 cells for t helper cell production and activation
- in circulation they are monocytes but are macrophages in tissue
- they are derived from bone marrow
- phagocytosis and production of inflammatory mediators
- May use to form multinucleated giant cells
discuss he unction of lymphocytes
- single ,round nucleus
- recognition of foreign material and antigens
- they activate macrophages
Discuss the function of plasma cells
- dark, eccentric nucleus ,chromatin has a clock face ,dark cytoplasm, paranuclear pale
- transformed b cells
- synthesis of AB
List the 6 morphological patterns of acute inflammation
- Serous inflammation : High fluid content eg blisters
- Frbrinous inflammation : High fibrinogen /fibrin content eg pleural effusion in pneumonia
- Haemorrhagic -high red blood cell content eg meningococcal septicemia
- Catarrhal - high mucus content eg bronchitis
- pseudomembranous - false membrane of necrotic debris and inflammation eg diphtheria
- Suppurative -pus ; semiliquid substance composed of dead and living neutrophils ,dead digested tissue and fluid exudate
what is the systemic reaction to acute inflammation
Fever
Bacterial endotoxins, IL-1
IL-1 acts on thermosensory centre and causes formation of prostaglandins
Aspirin blocks prostaglandin formation, reducing temperature
Headache, lethargy, weakness, hyperaesthesia, loss of appetite
Leucocytosis
Increase white cell count
Neutrophils, lymphocytes, eosinophils
Protein synthesis
IL-1 and TNFα
C-reactive protein, fibrinogen, serum amyloid A complement
What are the outcomes of acute inflammation
*Resolution : repair
*Tissue destruction and suppuration
*Healing by regeneration
*fibrosis
*chronic inflammation
*septicaemia
death
