Acute Inflammation Flashcards

1
Q

Define Acute inflammation

A

Response of living tissue to damage. Usually innate, immediate and short duration e.g. minutes/hours/days

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2
Q

List 5 causes of acute inflammation

A
Microbial infection
Hypersensitivity reaction
Physical agents
Chemicals
Tissue necrosis
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3
Q

What are the 5 features of acute inflammation?

A
R-rubor- redness
T-tumor- swelling
C-calor- heat
D-dolor- pain
\+ Loss of function
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4
Q

What causes the main changes in tissue during A.I?

A

Changes in blood flow
Exudation of fluid into tissues
Infiltration of inflammatory cells.

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5
Q

How does blood flow change?

A

Transient vasoconstriction of arterioles
Vasodilatation of arteroiles to increase blood flow
Increased permeability of the vessels
Exudation of protein rish fluid into the tissue
Slowing of circulation - oedema
STASIS- increased viscosity of blood and conc of RBC in vessels

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6
Q

What is the role of histamine?

A

Is released from mast cells in response to stimuli.
e.g. physical damage, immuological response, factors released from neutrophils and platelets.

It causes: vascular dilatation, increase in vascular permeability, pain.

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7
Q

What is Starlings law?

A

Fluid flowing across capillary walls is determined by balance of hydrostatic and colloid osmotic pressure.
Comparing plasma an interstitial fluid.

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8
Q

What happens when you increase hydrostatic pressure?

A

Increased fluid out of the vessel

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9
Q

What happens when you increase the colloid osmotic pressure of interstitium?

A

increase fluid flow out of the vessel

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10
Q

Why does oedema occur?

A

Arteroilar dilatation leads to increase hydrostatic pressure
Increased permeability of vessel walls leads to loss of proteins into interstium.

Results in net flow of fluid out of the vessel into interstitial fluid.

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11
Q

What is the difference between transudate and exudate?

A

Exudate is high protein content- seen in inflammation

Transudate is low protein content. Due to low hydrostatic pressure- e.g. cardiac failure or venous outflow obstruction.

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12
Q

Explain the role of neutrophils

A

Granulocyte WBCs that are polymorphs.
they line up at the edge of the endothelium - Margination.
They then roll along and stick to the endothelium - Adhesion
Finally Emigration though the blood vessel wall

MR.AE

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13
Q

How do neutrophils escape from vessels?

A

Relaxation of interepithelial junctions
Digestion of vascular basement membrane

Chemotaxsis- movement along the concentration gradient of chemoattractants

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14
Q

What is diapedesis?

A

passage of blod cells through the endothelium

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15
Q

How do neutrophils kill?

A

O2 dependent- produces superoxide and hydrogen peroxide

O2 independent- lysozyme and hydrolases, BPI- bacterial permeability increasing protein.

c5a, LTB4, C3b

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16
Q

How does exudate combat injury?

A

Delivers plasma proteins to area of injury e.g. Igs, inflammatory mediators and finbrinogen

Dilutes toxins
Increases lymphatic drainage

17
Q

Which other factors of acute inflammation combat injury?

A

Vasodilatation increases delivery and temperature.

Pain and loss of function enforces rest and reduces chance of damage

18
Q

List the complications of acute inflammation

A

Swelling causes blockage of tubes
Exudate can cause blockage e.g. cardiac tamponade and serositis
Loss of fluid and pain
Systemic: fever - IL-1 and TNFalpha

19
Q

Describe the Acute phase response

A

Loss of appetite, raised pulse rate, altered sleep
increased CRP, alpha antitrypsin, haptoglobin, serum amyloid A and fibrinogen.

SHOCK

20
Q

What happens in resolution of A.I?

A

Changes gradually reverse and vascualr changes stop
Exudate drains into lymph
Neutrophils die and break up
Damaged tissue may regenerate

21
Q

List 3 examples of A.I and their presentation

A

Bacterial meningitis: acute inflammation- vascualr thrombosis and reduce cerebral perfusion
Lobar pneumonia:Alveoli contain exudate, worsening fever, dry cough and SOB
Liver abscess: often caused by ascending cholangitis.

22
Q

Describe presentation of pericarditis

A

Ascites, pleural or pericardial effusion causes cardiac or respiratory impairment
Localised fibrin deposition