Acute Inflammation 1 Flashcards

1
Q

Define “acute inflammation”.

A

Acute inflammation is a series of protective changes occurring in living tissue as a response to injury.
Maintains integrity of organism.
Is a dynamic homeostatic mechanism
Only occurs in higher organisms.

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2
Q

Name the cardinal signs of inflammation.

A

Rubor - redness, darkening
Calor - heat
Tumor - swelling
Dolor - pain
Loss of function.

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3
Q

List the causes of acute inflammation.

A

Microorganisms
Mechanical
Chemical
Physical
Dead tissue
Hypersensitivity.

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4
Q

Describe how microorganisms can cause acute inflammation.

A

Pathogenic organisms (e.g. bacteria, fungi, parasites etc) cause infection.

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5
Q

Describe the mechanical causes of acute inflammation.

A

Trauma
Injury to tissue
**All injuries, even sterile (e.g. surgery).

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6
Q

Describe the chemical causes of acute inflammation.

A

This refers to the stable environment being disturbed:
Acid or alkali
Bile and urine (e.g. irritation when in inappopriate place e.g. peritoneum)

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7
Q

Describe the physical causes of acute inflammation.

A

(extreme conditions)
Heat (e.g. sunburn)
Cold (e.g. frostbite)
Ionising radiation

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8
Q

Describe how dead tissue causes acute inflammation.

A

Necrosis of cells can irritate adjacent tissue -> causing inflammation.
Necrotic tissue occurs, when the skin sustains an injury (for example).

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9
Q

Describe how hypersensitivity causes acute inflammation.

A

(this is a linkage with acute inflammation)
Involves several classes of reaction.

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10
Q

Describe the process of acute inflammation.

A

Series of microscopic events
Localised to affected tissue
Takes place in the microcirculation
Results in the clinical signs and symptoms of acute inflammation - cardinal signs.

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11
Q

Define “microcirculation”

A

Capillary beds, fed by arterioles and drained by venules.
(Extracellular compartment - fluid and molecules within it)
Lymphatic channels and drainage (tissue fluid)
Starling forces control flow (fluid flux) across membrane.

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12
Q

Describe the dynamic balance of microcirculation.

A

Hydrostatic and colloid oncotic pressure are countering each other.

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13
Q

List the steps in pathogenesis (in acute inflammation).

A

Changes in vessel radius, means that there are changes in the flow.
There are changes in permeability of the vessel wall - exudation of fluid.
Movement of neutrophils from the vessel to the extravascular space - emigration.

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14
Q

Describe the relationship between radius of a blood vessel and the “flow”.

A

Flow is proportional to radius to the power of 4.
I.E. a tiny increase of radius = a large increase of flow.

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15
Q

Define “the triple response”.

A

Flush, flare, wheal.

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16
Q

Describe the flush part of the triple response.

A

The triple response is mediated by histamine, bradykinin (pain) + prostaglandins (released first).
Flush is the initial red colour at the original site.
This comes from vasodilation of venules and capillaries.
**Causes increased blood flow and immune cells to the site of infection.

17
Q

Describe the flare part of the triple response.

A

Flare follows flush.
This is a spreading redness around the original site - caused by vasodilation of surrounding arterioles.

18
Q

Describe the wheal part of the triple response.

A

Wheal is essentially the swelling or enlargement of the area and it follows flare.
There is an exudation of fluid out of the capillary caused by an increase in permeability of the capillary membrane and exudation of fluid.
This causes neutrophils, monocytes and fibrinogen to move into the ECF (oedema)

19
Q

Describe the exudate released.

A

Exudate is a fluid rich in protein - plasma - includes immunoglobulin and fibrinogen.

20
Q

Define an oedema.

A

An oedema is an accumulation of fluid in the extravascular space.
They explain the swelling of tissue in acute inflammation.
Swelling causes pain - reduces function.

21
Q

Define “stasis”.

A

Stasis is when the rate of flow through vessels slows.

22
Q

Describe the phases of emigration of neutrophils.

A

1) Margination - neutrophils move to the endothelial aspect of lumen.
2) Pavementing - neutrophils adhere to endothelium.
3) Emigration - Neutrophils squeeze between endothelial cells (active process) -to extravascular tissues.

23
Q

Define “diapedesis”.

A

Diapedesis is the passage of blood cells through the cells to other tissues.

24
Q

Describe the resolution of acute inflammation to the ideal outcome.

A

The inciting agent is isolated and destroyed.
The macrophages move in from blood and phagocytose debris: they then leave.
Epithelial surfaces regenerate.
The inflammatory exudate filters away
Vascular changes return to normal
Inflammation resolves.

25
Q

Describe the benefits of acute inflammation.

A

-Rapid response to non-specific insult.
-Cardinal signs and loss of function acts as a transient protection of inflamed area.
-Neutrophils destroy organisms and denature antigen for macrophages to phagocytose.
-Plasma proteins localise process (fibrinogenin coagulates and walls off area of inflammation)
Resolution and return to normal.

26
Q

State the 4 outcomes of acute inflammation.

A

Resolution
Suppuration
Organisation
Chronic inflammation

27
Q

Describe in outline, the process of acute inflammation.

A

1) The injury stimulus
2) Necrotic cells irritates adjacent tissue
3) Chemical mediators are released from immune cells
4) Blood vessels dilate (Vasodilation) increasing blood flow to site
OBSERVED - redness and heat.
5) Imbalance of Starling forces causes increased permeability
6) Endothelial leak of fluid and protein = exudation
7) Exudate causes swelling, plasma proteins (Bradykinin - increases sensitivity of nerves).
8) Swelling causes pain causes loss of function.
CONTINUED

28
Q

Describe the effects of increased permeability.

A

Net movement of plasma from capillaries to extravascular space (compartment) = exudation.

Increase in viscosity due to loss of fluid, so rate of flow slows = stasis.

29
Q

Define coagulation.

A

Coagulation is essentially blood clotting.