Acute Inflammation Flashcards
What is inflammation
a protective response of vascularised tissue that delivers leukocytes and molecules of host defense from cirulation to the site of infection or cell damage to eliminate the offending agent
Suffix that is indicative of inflammation
-itis
Main steps of an inflammatory response - 5 R’s
- Recognition
- Recruitment of leukocytes
- Removal of agent
- Regulation/control of infection
- Repair
Causes of inflammation - PIC AIF
- Physical/ mechanical
- Infection
- Chemical
- Adjacent necrosis - vital reaction
- Immunologic reaction - hypersensitivity, autoimmune
- Foreign material - splinters/ sutures
Acute inflammation - 4
- initial and rapid response
- role in nnate immunity
- may resolve or persist leading to chronic inflammation
- Exhudation of fluids and plasma proteins (oedema) or emigration of leukocytes (neutrophils)
Chronic inflammation - 3
- longer duration
- role in adaptive immunity
- more tissue destruction, lymphocytes and macrophages, proliferation of blood vessels, deposition of connective tissue
Clinical signs of inflammation
- Redness - rubor
- Swelling - tumor
- Heat - calor
- Pain - dalor
- Loss of function - functio laesa
Major components of acute inflammation - DIE
- Dilation of small vessels to increase blood flow
- Increase in permeability of vasculature enabling pp and fluid and leukocytes to leave the circulation
- Emigration of leukocytes from circulation to the site of infection, THEIR ACCUMULAION AND ACTIVATION
Vasculature reactions in acute inflammation - VIER
- vasodilation mediated by histamine and causes erythema and increase in blood flor
- increase in permeability induced by histamine and kinins which produces gaps on the cell by injury and leakage of pp and fluids out of the endothelium
- edema from fluid leakage and escape of pp and leukocytes
- response of lymph nodes and lymphadtics which drain fluids and an increase in immune demand may cause inflammation in this area (lymphadenitis)
How are leukocytes recruited to the site of infection
- loose attachment and rolling on the endothelium mediated by selections
- firm attachment to the endothelium mediated by integrins
- migration through the endothelial spaces
How do leukoctyes remove the offending agent
- phagocytosis
- further destruction by phagolysosome
- destruction is caused by lysosomal enzymes and ROS, NO which is generated from activated leukocytes
- damage to normal tissue can also occur
- termination of inflammatory response by anti inflammatory mediators
examples of anti inflammatory mediators
L-10, TGF-β, lipoxins, and resolvins.
Important mediatiors
- chemotaxis
- phagocytosis
- degranualtion
phagocytosis
- recognition - opsonins (ig and complemet)
- ingestion - phagosomes
- killing/ digestion - phagolysosome and ROS
chemotactic agents
- complement
- bacterial agents
- leukotrines
small specific granules
- collagenases
- lysosome
- lactoferrin
- alkaline phosphatases
- ahesion molecules
large azurophil granules
- cationic proteins
- lysosymes
- acid hydrolases
- myeloperoxidases
- estelases
2 types of cell mediated chemical mediators
preformed and synthesised denovo
specific vs large azurophilic
= specific - antimicrobial activity
= azurophilic - pathogen destruction
preformed
histamine and serotonin
red line
localised capillary oedema
synthesised de novo - CCRANP
-Chemokines
-Cytokines
-ROS
-Arachidonic acid mediators
-NO
-Platelet Activating Factor
Plasma derived
complement and factor XII activation
red flare
diffuse dilatation
weal
raised area from oedema
another name for neutrophils
polymorphonuclear leucocyte
neutrophils will SLAP you
Smaller specicif granules and larger azurophilic granules
Lobated nucleus
Actively mobile
Pus formation
eosinophils responds BRA
Bilobed
Red granules
Allergic reactions, parasitic infections, drug reactions
Basophils nucleus
sometimes obscured by granules
NB
please be careful when doing monocytes and mast cells.. DO NOT mix them up hey
mononuclear phagocytes are SIMDPM
Scavenger cells - remove foreign particles
Immune function = present antigen for development of cell mediated immunity and produce cytokines
Monocytes in blood and macrophages in tissue
Derived from the BM
Phagocytosis and production of inflammatory mediators
May fuse to form multinucleated giant cells
lymphocytes are SRAT +
Single small, round nucleus
Recognize antigens and foreign material
Activate macrophages
T lymphocytes - helper and cytotoxic
- B - Ig
how do lymphocytes activate macrophages
through the release of cytokines and this is performed by t helper cells
Plasma cells say daar say DDTS
Dark round eccentric nucleus wit clock face chromatin
Dark cytoplasm with paranuclear pale hof
Transformed from B cells
Synthesise antibodies
Hallmark of acute inflammation
- dilation of small blood vessels, accumulation of leukocytes and fluids in EXTRAVASCULAR tissue
Morphologic patterns of acute inflammation - 6
Serous - high fluid content = burns and blisters
Fibrinous - high fribrinogen/firbin content = pleural effusion in pneumonia or fibrinous pericarditis
Haemorrhagic - high RBC content = meningococcal septicaemia
Catarrhal - high mucus content = bronchitis
Pseudomembraneous = false membrane of nectrotic debris and inflammation = diphtheria
Suppurative = pus
what is pus
semiliquid substance composed of dead and livind neutrophils, dead digested tissue and fluid exudate
abcess
localised collection of pus
systemic reaction to acute inflammtion- 4
- fever
- weakness, headache, lethargy, hyperaesthesia, loss of appetite
- leukocytosis
- protein synthesis
what is meant by a systemic reaction
how the body response
fever
- bacterial endotoxins, IL-1
- IL-1 acts on themosensory centre and causes formation of prostaglandins
- aspiring blocks the formation of prostaglandin and this reduces temperature
leukocytosis
- increase in WBC count
- neutrophils, lymphocytes and eosinophils
protein synthesis
- IL-10, TNFa
- c-reactive protein, fibrinogen, serum amyloid A complement
Outcome of acute inflammation - 7
Healing by regeneration and repair
Resolution (back to normal)
Tissue destruction and suppuration
Fibrosis
Chronic inflammation
Septicaemia
Death
