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Flashcards in Inflam Deck (41):

Acute inflammation definition

- Fundamental response maintaining integrity of organism
- Series of protective changes occurring in living tissue as a response to injury


Causes of acute inflammation

- Micro-organisms, pathogenic organisms
- Mechanical, trauma
- Chemical, upset to stable environment. Acid or alkali, bile or urine in wrong place
- Physical, sunburn, frostbite, ionising radiation
- Hypersensitivity, several classes of reaction


Benefits of acute inflammation

- Rapid response to non-specific insult
- Cardinal signs and loss of function, act as transient protection of inflamed area
- Neutrophils destroy organisms and denature antigen for macrophages
- Plasma proteins localise process
- Resolution and return to normal


Sequence of microvascular change

1. Flush - transient arteriolar constriction
2. Flare - local arteriolar dilatation
3. Wheal - relaxation of vessel smooth muscle


Mechanisms of microvascular change

- Change in the vessel radius which results in increased flow
- Permeability of the vessel is increased to allow for exudation
- Neutrophils move from the vessel to the extracellular space


Sequence of events in exudate formation

- Increased permeability: plasma moves from capillaries to extravascular space
- Exudation
- A fluid rich in protein, plasma with immunoglobulin and fibrinogen is leaked
- Oedema formed, accumulation of fluid in extravascular space
- Swelling of tissue in inflammation, causes pain and reduction in function


How neutrophils get through the capillary beds

- Blood is non-Newtonian fluid
- In laminar flow, bigger molecules are closer to the centre
- In turbulent flow, red cells aggregate in the centre of the lumen and the neutrophils are found near the endothelium
- Neutrophils then adhere to the endothelium and squeeze out of the endothelial cells to extravascular tissues


Local effects of acute inflammation

- Rubor: redness
- Calor: heat
- Tumor: swelling
- Dolor: pain
- Loss of function, you protect it


Immediate systematic effects

- Pyrexia: raised temperature. Endogenous pyrogens from white cells act centrally
- Feeling unwell: Malaise, anorexia, nausea. Abdominal pain and vomiting in children
- Neutrophilia: raised white cell count. Bone marrow releases/produces


Long term systematic effects

- Lymphadenopathy: regional lymph node enlargement
- Weight loss: as inflammation is a catabolic process
- Anaemia


Suppuration features

- Pus formation
-Pyogenic membrane surrounds pus
- Abscess
- Empyema - in a hollow viscus
- Pyaemia


Pus formation

- Dead tissue, organisms, exudate, neutrophils, fibril, red cells, debris


Pyogenic membrane

- Capillary sprouts, neutrophils, fibroblasts
- Walls off the pus



- Collection of pus under pressure
- Single locule, multiloculated: when the pus bursts through the pyogenic membrane and forms new cavities
- 'Points' and discharges
- Collapses - healing and repair



- In a hollow viscus (internal organ)
- Gall bladder
- Pleaural cavity



Discharge into bloodstream


Role of neutrophil

- Mobile phagocytes
- Chemical blast
- Release of granule contents
- Phagocytose and destroy foreign antigen


Mobile phagocytes

- Recognise foreign antigen
- Move towards it - chemotaxis (based on concentration gradient)
- Adhere to organism


Chemical blast

- Granules possess oxidants and enzymes
- Oxidants liberate oxygen and water and they pick up various molecules with charge
- Enzymes catalyse a reaction that picks up specific chemicals, it's a more specific response


Consequences of neutrophil action

- Neutrophils die when granule contents are released
- A 'soup' of fluid with bits of cell, organisms and endogenous proteins called pus is released



- Plasma proteins in inflammation
- Coagulation factor, forms fibrin and clots exudate, localises inflammatory process
- Stack of fibrinogen, some cleave off and active sizes are available, forms fibrin, then a clot
- Increases permeability and acute inflammation, fibrinogen can go to affected site


Immunoglobulins in plasma specific for antigen

- Plasma proteins in inflammation
- Humoral immune response


Types of mediators of acute inflammation

- Molecules on endothelial cell surface membrane
- Molecules released from cells
- In the plasma, fibrinogen and kinins


Molecules on endothelial cell surface membrane

- ICAM-1 on endothelial
- P-selectin on neutrophil surface



- Released from cells
- Makes stuff leakier
- Preformed in mast cells where it's needed - blood vessels, platelets and basophils
- Released as a result of local injury
- Vasodilatation and permeability
- Acts via H1 receptors on endothelial cells



- Released from cells
- When you want it to be less leaky
- Preformed in platelets
- Released when platelets degranulate in coagulation
- Vasoconstriction


Histamines vs. serotonin

- You have a tendency towards histamine or serotonin depending on the situation



- Released from cells
- Many cells (endothelium and leukocytes)
- Many promote histamine effects and inhibit inflammatory cells
- Some promote platelet aggregation and vasconstriction



- Released from cells
- Neutrophils especially
- Vasoactive - dynamic effect on vessels to increase permeability and constrict smooth muscle


Omega-3 polyunsaturated fatty acids

- Released from cells
-Decrease synthesis of arachidonic acid derived inflammatory mediators


Platelet-activating factor (PAF)

- Released from cells
-Cell membrane of activated inflammatory cells
- Reduces permeability by enhancing platelet degranulation at site of injury


Cytokines and chemokines

- Released from cells
- Small molecules produced by macrophages, lymphocytes, endothelium in response to inflammatory stimuli
- Attract inflammatory cells


Nitric oxide

- Released from cells
- Various cells
- Smooth muscle relaxation, anti-platelet, regulate leukocyte recruitment to inflammatory focus


Oxygen free radicals

- Released by neutrophils on phagocytosis
- Amplify other mediator effects


Mediators of inflammation in plasma

- Blood coagulation pathways, clots fibrinogen in exudate
- Fibinrolysis: breaks down fibrin, helps maintain blood supply, vasoactive
- Kinin system: bradykinin pain, built upon the stimulation of the PNS, tells brain there's pain
- Complement cascade: ties inflammation with immune system, active components stimulate increased permeability, chemotaxis, phagocytosis, cell breakdown


Effects of mediators

- Vasodilatation
- Increased permeability
- Neutrophil adhesion
- Chemotaxis
- Itch and pain


Neutrophil adhesion

- Neutrophils and endothelial cells both have mediators on the outside that are compatible which creates the stickiness



- Spread to bloodstream: bacteraemia, septicaemia, toxaemia


Steps in septic shock

- Peripheral vasodilatation: mediators cause vasodilation, loss of systemic vascular resistance (build in pressure)
- Tachycardia: catecholamine released, adrenaline and noradrenaline. Tachycardia tries to maintain cardiac output
- Hypotension
- Pyrexia: bacterial endotoxin released, acts on hypothalamus
- Haemorrhagic skin rash: activation of coagulation


Septic shock can lead to

- Tissue hypoxia
- Loss of cell tissue and organ function
This is because the heart rate is insufficient to maintain cardiac output and there can be reduced perfusion of tissues


4 outcomes of inflammation

1. Resolution
2. Suppuration - pus
3. Organisation - healing
4. Dissemination - sepsis
5. Chronic inflamation