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PoD > Inflam > Flashcards

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

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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
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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
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4
Q

Sequence of microvascular change

A
  1. Flush - transient arteriolar constriction
  2. Flare - local arteriolar dilatation
  3. Wheal - relaxation of vessel smooth muscle
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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
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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
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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
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8
Q

Local effects of acute inflammation

A
  • Rubor: redness
  • Calor: heat
  • Tumor: swelling
  • Dolor: pain
  • Loss of function, you protect it
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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
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10
Q

Long term systematic effects

A
  • Lymphadenopathy: regional lymph node enlargement
  • Weight loss: as inflammation is a catabolic process
  • Anaemia
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11
Q

Suppuration features

A
  • Pus formation
  • Pyogenic membrane surrounds pus
  • Abscess
  • Empyema - in a hollow viscus
  • Pyaemia
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12
Q

Pus formation

A
  • Dead tissue, organisms, exudate, neutrophils, fibril, red cells, debris
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13
Q

Pyogenic membrane

A
  • Capillary sprouts, neutrophils, fibroblasts

- Walls off the pus

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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
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15
Q

Empyema

A
  • In a hollow viscus (internal organ)
  • Gall bladder
  • Pleaural cavity
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16
Q

Pyaemia

A

Discharge into bloodstream

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

PoD (33 decks)

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