Inflam Flashcards
1
Q
Acute inflammation definition
A
- Fundamental response maintaining integrity of organism
- Series of protective changes occurring in living tissue as a response to injury
2
Q
Causes of acute inflammation
A
- 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
3
Q
Benefits of acute inflammation
A
- 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
4
Q
Sequence of microvascular change
A
- Flush - transient arteriolar constriction
- Flare - local arteriolar dilatation
- Wheal - relaxation of vessel smooth muscle
5
Q
Mechanisms of microvascular change
A
- 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
6
Q
Sequence of events in exudate formation
A
- 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
7
Q
How neutrophils get through the capillary beds
A
- 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
8
Q
Local effects of acute inflammation
A
- Rubor: redness
- Calor: heat
- Tumor: swelling
- Dolor: pain
- Loss of function, you protect it
9
Q
Immediate systematic effects
A
- 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
10
Q
Long term systematic effects
A
- Lymphadenopathy: regional lymph node enlargement
- Weight loss: as inflammation is a catabolic process
- Anaemia
11
Q
Suppuration features
A
- Pus formation
- Pyogenic membrane surrounds pus
- Abscess
- Empyema - in a hollow viscus
- Pyaemia
12
Q
Pus formation
A
- Dead tissue, organisms, exudate, neutrophils, fibril, red cells, debris
13
Q
Pyogenic membrane
A
- Capillary sprouts, neutrophils, fibroblasts
- Walls off the pus
14
Q
Abscess
A
- 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
15
Q
Empyema
A
- In a hollow viscus (internal organ)
- Gall bladder
- Pleaural cavity
16
Q
Pyaemia
A
Discharge into bloodstream
17
Q
Role of neutrophil
A
- Mobile phagocytes
- Chemical blast
- Release of granule contents
- Phagocytose and destroy foreign antigen
18
Q
Mobile phagocytes
A
- Recognise foreign antigen
- Move towards it - chemotaxis (based on concentration gradient)
- Adhere to organism
19
Q
Chemical blast
A
- 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
20
Q
Consequences of neutrophil action
A
- Neutrophils die when granule contents are released
- A ‘soup’ of fluid with bits of cell, organisms and endogenous proteins called pus is released
21
Q
Fibrinogen
A
- 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
22
Q
Immunoglobulins in plasma specific for antigen
A
- Plasma proteins in inflammation
- Humoral immune response
23
Q
Types of mediators of acute inflammation
A
- Molecules on endothelial cell surface membrane
- Molecules released from cells
- In the plasma, fibrinogen and kinins
24
Q
Molecules on endothelial cell surface membrane
A
- ICAM-1 on endothelial
- P-selectin on neutrophil surface
25
Q
Histamines
A
- 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
26
Q
Serotonin
A
- Released from cells
- When you want it to be less leaky
- Preformed in platelets
- Released when platelets degranulate in coagulation
- Vasoconstriction
27
Q
Histamines vs. serotonin
A
- You have a tendency towards histamine or serotonin depending on the situation
28
Q
Prostaglandins
A
- Released from cells
- Many cells (endothelium and leukocytes)
- Many promote histamine effects and inhibit inflammatory cells
- Some promote platelet aggregation and vasconstriction
29
Q
Leukotrienes
A
- Released from cells
- Neutrophils especially
- Vasoactive - dynamic effect on vessels to increase permeability and constrict smooth muscle
30
Q
Omega-3 polyunsaturated fatty acids
A
- Released from cells
- Decrease synthesis of arachidonic acid derived inflammatory mediators
31
Q
Platelet-activating factor (PAF)
A
- Released from cells
- Cell membrane of activated inflammatory cells
- Reduces permeability by enhancing platelet degranulation at site of injury
32
Q
Cytokines and chemokines
A
- Released from cells
- Small molecules produced by macrophages, lymphocytes, endothelium in response to inflammatory stimuli
- Attract inflammatory cells
33
Q
Nitric oxide
A
- Released from cells
- Various cells
- Smooth muscle relaxation, anti-platelet, regulate leukocyte recruitment to inflammatory focus
34
Q
Oxygen free radicals
A
- Released by neutrophils on phagocytosis
- Amplify other mediator effects
35
Q
Mediators of inflammation in plasma
A
- 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
36
Q
Effects of mediators
A
- Vasodilatation
- Increased permeability
- Neutrophil adhesion
- Chemotaxis
- Itch and pain
37
Q
Neutrophil adhesion
A
- Neutrophils and endothelial cells both have mediators on the outside that are compatible which creates the stickiness
38
Q
Dissemination
A
- Spread to bloodstream: bacteraemia, septicaemia, toxaemia
39
Q
Steps in septic shock
A
- 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
40
Q
Septic shock can lead to
A
- 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
41
Q
4 outcomes of inflammation
A
- Resolution
- Suppuration - pus
- Organisation - healing
- Dissemination - sepsis
- Chronic inflamation
