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Flashcards in Acute Inflammation Deck (64)
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1
Q

What is acute inflammation?

A

Acute inflammation is a dynamic homeostatic response which maintains the integrity of the organism. It involves a series of protective mechanisms that occur in response to injury.

2
Q

What are the 5 cardinal signs of inflammation?

A
  • Rubor- redness
  • Calor- heat
  • Tumour- swelling
  • Dolor- pain
  • Loss of function
3
Q

What can the cardinal signs of inflammation be explained by?

A

The sequence of pathological events taking place.

4
Q

What are the aetiologies of inflammation?

A

Infection (bacteria/viruses/parasites/fungi etc)
Trauma (even sterile surgery)
Dead tissue (cell necrosis irritates adjacent tissue)
Hypersensitivity

5
Q

Where does acute inflammation take place?

A

Microcirculation

6
Q

What is the microcirculation?

A
  • Capillary beds, fed by arterioles and drained by venules
  • Extracellular space and fluid around it
  • Lymphatic channels and drainage
  • Starling forces control the fluid flux across the membrane
  • Dynamic balance (hydrostatic/colloid osmotic pressures, compartments and physical constants
7
Q

What is the pathogenesis of acute inflammation? (Steps)

A

Changes in the arterial radius (FLOW)
Changes in the permeability of the vessel wall (EXUDATION)
Movement of neutrophils from the vessel to the extravascular space

8
Q

What are the local changes in vessel radius and blood flow?

A
  1. Transient arteriolar constriction (few movements, probably protective)
  2. Local arteriolar dilation (active hyperaemia)
  3. Relaxation of vessel smooth muscle (autonomic NS/mediator derived)
9
Q

What is the triple response?

A

Flush, flare, wheal.

10
Q

What does an increased arteriolar radius cause?

A

Increased blood flow to the local tissue- results in the cardinal redness and heat.

11
Q

What does increased permeability involve?

A

There is an endothelial leak-fluid and protein is not held in the vessel lumen due to an imbalance of Starling forces. It also involves locally produced chemical mediators.

12
Q

What are the effects of increasing permeability?

A

There is a net movement of plasma from the capillaries to the extravascular space. This process is called exudation- the fluid leaked is called the exudate.

13
Q

What is an exudate rich in?

A

Immunoglobulin and fibrinogen.

14
Q

What are the effects of exudation?

A

Oedema- accumulation of fluid in the extravascular space
Explains swelling as a cardinal sign of inflammation- this can lead to a localised loss of function in the affected area. Oedema.

15
Q

Where are plasma, WBC and erythrocytes situated within the vessel during normal laminar flow?

A

Plasma all around, WBC in middle, erythrocytes surrounding them.

16
Q

Where are plasma, WBC and erythrocytes situated within the vessel during inflammation?

A

Plasma remains, WBC extend to the surface, erythrocytes (RBC) move into the middle.

17
Q

What are the phases of neutrophil emigration?

A

When neutrophils migrate from pre-endothelium in the vessel to the extravascular space.

18
Q

What are the phases of neutrophil emigration?

A
  • Margination- neutrophils move to the endothelial aspect of the lumen
  • Pavementing- neutrophils adhere to the endothelium
  • Emigration- neutrophils squeeze between endothelial cells (active process) to the extravascular tissues
19
Q

What are the outcomes of acute inflammation?

A

Resolution
Suppuration (pus formation)
Organisation
Chronic inflammation

20
Q

What is the ideal outcome of acute inflammation?

A
  • Inciting agent is isolated and destroyed (pathogenic destruction)
  • Macrophages move in from the blood and phagocytose debris then leave
  • Epithelial surfaces regenerate
  • Inflammatory exudate filters away
  • Vascular changes return to normal
  • Inflammation resolves
21
Q

What are the benefits of acute inflammation?

A
  • Rapid response to a non-specific insult
  • Cardinal signs and loss of function provide transient protection of the inflamed area
  • Neutrophils destroy organism and denature the antigen for macrophages
  • Plasma proteins localise the process
  • Can be resolved and restored to normal
22
Q

What is inflammation characterised by in terms of nomenclature?

A

-‘itis’ prefix

23
Q

What is inflammation called in the lungs?

A

Pneumonia

24
Q

What is inflammation called in the pleural cavity?

A

Pleurisy

25
Q

What do neutrophils do?

A

Neutrophils are mobile phagocytes- they recognise foreign antigens and move towards them in the chemotaxis process. They then adhere to them. Granules produce oxidants and enzymes which phagocytose and destroy the foreign antigen.

26
Q

What are the consequences of neutrophil action?

A
  • Neutrophils die when the granule is released
  • Produces a soup of fluid/bits of cell organisms/ endogenous proteins = PUS
  • Might extend into other tissues, progressing the inflammation
27
Q

What plasma proteins play a role within acute inflammation?

A

Fibrinogen

Immunoglobulin

28
Q

What does fibrinogen do?

A

Fibrinogen- coagulation factor (forms fibrin, clots the exudate which localises the inflammatory process)

29
Q

What does immunoglobulin do?

A

Immunoglobulin- specific for antigen (humoral immune response).

30
Q

What are the mediators of acute inflammation?

A
  • Molecules on endothelial cell surface membrane
  • Molecules released from the cells
  • Molecules in plasma
  • Molecules in the cells
31
Q

How do molecules on the endothelial cell surface membrane mediate acute inflammation?

A
  • Sticky- adhesion molecules appear on endothelial cells to make neutrophils stick
  • P-selectin interacts with the neutrophil surface
32
Q

What molecules are released from cells to mediate the inflammatory response?

A
Histamine 
Seratonin 
Prostaglandins
Cytokines 
Nitric oxide 
Oxygen free radicals
33
Q

How does histamine work?

A

Histamine is preformed in most cells beside vessels/platelets/basophils. It is released as a result of local injury, is IgE mediated, and causes vasodilation and an increased permeability.

34
Q

How does serotonin work?

A

Preformed in platelets, released when platelets deregulate in coagulation, vasoconstriction.

35
Q

How do prostaglandins work?

A

These include many cells, many promote histamine effects and inhibit inflammatory cells, thromboxane A2 promotes platelet aggregation and vasodilation, latter effectiveness of NSAIDs.

36
Q

How do cytokines work?

A

These are small molecules produced by macrophages and lymphocytes in response to inflammatory stimuli, have pro-inflammatory and anti-inflammatory effects, can stimulate intracellular pathways and signalling.

37
Q

How does nitric oxide work?

A

Nitric oxide is released from various cells, has a key role in relaxation of smooth muscle, anti-platelet, and regulation of leukocyte recruitment to inflammatory focus.

38
Q

How do oxygen free radicals work?

A

Released by neutrophils on phagocytosis, amplify other mediator effects.

39
Q

How do molecules inside the cells mediate an inflammatory response?

A
  • Pattern associated molecular patterns- microbial antigen, genetically hard-wired to recognise, innate and adaptive immunity
  • Danger associated molecular patterns- substances released in response to a stimulus
  • Stimulate pattern recognition receptors on the cell membrane
  • Activate inflammatory response
40
Q

What are the 4 enzyme cascade interactions?

A
  • Blood Coagulation Pathway-clots fibrinogen in exudate, interacts widely with other systems.
  • Fibrinolysis- breaks down protein/fibrin
  • Kinin System (Bradykinin=pain)
  • Complement Cascade-ties inflammation with the immune system
41
Q

What are the overall effects of inflammatory mediators?

A
  • Vasodilation / vasoconstriction
  • Altered permeability
  • Neutrophil adhesion
  • Chemotaxis
  • Itch and pain
  • Positive and negative effects
  • Dynamic balance
  • Favours and inhibits acute inflammation
  • Relative to need
42
Q

What are the immediate systemic effects of inflammation?

A

Pyrexia- raised temperature (endogenous pyrogens from white cells act centrally).

Malaise- feeling unwell (malaise/anorexia/nausea), abdominal pain and vomiting in children

Neutrophilia- raised count of white blood cells (shows immune response of bone marrow release)

43
Q

What are the long-term systemic effects of inflammation?

A

Lymphadenopathy- regional lymph node enlargement (immune response)

Weight loss- catabolic process

Anaemia

44
Q

What is the process of pus formation called?

A

Suppuration

45
Q

What does pus contain?

A

Dead tissue, organisms, exudate, neutrophils, fibrin, red blood cells, debris.

46
Q

What is the membrane surrounding pus called?

A

Pyogenic membrane

47
Q

What is an abscess?

A

An abscess is pus under pressure.

48
Q

Are abscesses always at a single location?

A

No- they can be singular or multi-located.

49
Q

What does collapse of an abscess lead to?

A

Healing and repair.

50
Q

What is pus called in a hollow cavity?

A

Empyema.

51
Q

What is pus discharge to the bloodstream called?

A

Pyaemia.

52
Q

What is organisation a characteristic of?

A

Granulation tissue.

53
Q

What does organisation involve?

A

Involves healing and repair, leading to fibrosis and the formation of a new scar.

54
Q

What is granulation tissue?

A

Universal patch repair kit for all injuries.

55
Q

What is the granulation tissue composed of?

A

New capillaries (angiogenesis)
Fibroblasts/collagen
Macrophages

56
Q

What is dissemination?

A

Pathogenic spread into the bloodstream.

57
Q

What is a patient subject to dissemination referred to as?

A

Septic.

58
Q

What is bacteraemia?

A

Presence of bacteria in the blood.

59
Q

What is septicaemia?

A

Growth of bacteria in the blood.

60
Q

What is toxaemia?

A

Presence of toxic products in the blood.

61
Q

What are the systemic effects of septic infection?

A

Shock- inability to perfuse tissues.

Peripheral vasodilation, tachycardia, hypotension, pyrexia, haemorrhagic skin rash.

62
Q

What is the pathogenesis of septic infection?

A

Bacterial endotoxin causes systemic release of chemical mediators- cause vascular response but heart has to compensate for this.

63
Q

What is the outcome of septic shock?

A

Often fatal- especially in elderly who are less able to compensate
Major cell death (tissue hypoxia)
Haemorrhage
Needs rapid clinical intervention

64
Q

In summary, what are the outcomes of acute inflammation?

A
Resolution 
Suppuration 
Organisation
Dissemination 
Chronic inflammation