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ESA 2 > MOD 2.1 - Acute Inflammation > Flashcards

MOD 2.1 - Acute Inflammation Flashcards

1
Q

What are the causes of acute inflammation? (5)

A
  • Microbial infections e.g. Pyogenic organisms (staphylococcus)
  • Hypersensitivity reactions (acute)
  • Physical agents e.g. Heat
  • Chemicals
  • Tissue necrosis
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2
Q

What are the clinical features of acute inflammation?

A
  • Rubor (redness)
  • Tumor (swelling)
  • Dolor (pain and loss of function)
  • Calor (heat)
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3
Q

What are the two phases of acute inflammation?

A
  • Vascular

- Cellular

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4
Q

Describe the changes in blood flow during the vascular phase

A
  • Transient vasoconstriction of Arterioles
  • Vasodilation of Arterioles and capillaries
  • Increased permeability of blood vessels
  • Stasis
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5
Q

What happens as a result of vasodilation of Arterioles and capillaries during the vascular phase?

A

Increases blood flow which leads to heat and redness

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6
Q

What happens as a result of an increased permeability of blood vessels during the vascular phase?

A
  • Exudation (seeping) of protein rich fluid into tissues from plasma
  • Slowing of circulation which leads to swelling
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7
Q

What is stasis?

A

The stoppage or slowing of blood flow

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8
Q

What happens as a result of stasis during the vascular phase?

A

Increased concentration of red blood cells which increases blood viscosity

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9
Q

Give an example of a chemical mediator of changes in blood flow

A

Histamine - released as an early response (first 1/2 hour)

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10
Q

What causes a release of histamine and what is it released from?

A
  • Released as a response to stimuli e.g. Physical damage or immunologic reactions
  • Released from mast cells, basophils and platelets
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11
Q

Describe the changes of histamine (3)

A
  • Vascular dilation
  • Transient increase in vascular permeability
  • Pain
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12
Q

What is acute inflammation?

A

The response of living tissue to injury that is initiated to limit tissue damage

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13
Q

What are the chemical mediators for a persistent response?

A

Non-specific, there’s lots of different types

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14
Q

What are the determining factors of fluid flow?

A

Hydrostatic and colloid osmotic pressure comparing plasma and interstitial fluid

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15
Q

What happens as a result of an increase in hydrostatic pressure?

A

There is an increase in movement of fluid out of the vessel

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16
Q

What happens as a result in an increase in osmotic colloid pressure?

A

There is an increase in flow out pressure therefore increasing the protein concentration in the interstitium

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17
Q

What happens due to an increase in vascular permeability?

A
  • Increases concentration of protein in the interstitium therefore causing an outward net flow of fluid
  • Leads to oedema (exudate)
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18
Q

What is oedema and what are the two types?

A
  • An increase of fluid in tissue spaces

- Transudate and Exudate

19
Q

Describe Transudate oedema

A

The protein content of the oedema fluid is THE SAME AS the protein content of the plasma

20
Q

Describe exudate oedema

A

The protein content of the oedema fluid is HIGHER than the protein content of the plasma

21
Q

What are the mechanisms of vascular leakage? (5)

A
  • Endothelial contraction (forms gaps between cells)
  • Cytoskeletal reorganisation (forms gaps between cells)
  • Direct injury e.g. Toxic burns, chemicals
  • Leukocyte dependent injury (enzymatic/ toxic O2 species)
  • Increased Transcytosis (movement of macromolecules across a membrane)
22
Q

Describe the cellular phase of acute inflammation

A

Infiltration of polymorphs (multi lobed nuclei) to the inflamed area

23
Q

What are the four steps in the infiltration of neutrophils?

A
  • Margination
  • Rolling
  • Adhesion
  • Emigration
24
Q

What happens during the Margination step of neutrophil infiltration?

A

Neutrophils line up at peripheries of blood vessels

25
Q

What happens during the rolling step of neutrophil infiltration?

A

Neutrophils adhere loosely to endothelium

26
Q

What happens during the adhesion step of neutrophil infiltration?

A

Neutrophils stick fully to endothelium

27
Q

What happens during the emigration step of neutrophil infiltration?

A

Neutrophils emigrate through vessel wall

28
Q

How do neutrophils escape from vessels?

A
  • Interendothelial cell junctions relax
  • Neutrophils digest basement membrane
  • Chemotaxis - neutrophils move along concentration gradients of chemoattractants e.g. C5a
29
Q

What is the significance of dolor?

A
  • Loss of function enforces rest and reduces the chance of further damage
30
Q

What is the role of Serotonin in acute inflammation?

A

Role is the same as Histamine i.e. stimulates vasodilation and the transient increase in membrane permeability.

Also stimulates fibroblasts for tissue repair

31
Q

What is the role of bradykinin in acute inflammation?

A
  • Produces pain

- Increases vascular permeability

32
Q

What is the role of leukotrienes in acute inflammation?

A
  • Mediation of leukocyte accumulation

significant in asthma

33
Q

What is the role of opsonins in acute inflammation?

A

Coat foreign materials and make them easy to phagocytose

34
Q

What is the process of a neutrophil capturing and killing a bacterium?

A
  • Summoned to the place of injury via chemotaxis
  • Become activated by increasing metabolism
  • Margination (Stick to the endothelial surface)
  • Diapedesis (Crawl through the endothelium)
  • Recognition-attachment (Recognise the bacterium and attach to it
  • Phagocytosis
35
Q

Why is clotted blood chemotactic?

A
  • Blood clots are made up of a mesh of Thrombin and Fibrin Degredation Products
  • Both of which are chemotactic
36
Q

What is diapedesis?

A
  • Digestion of the basement membrane by collagenase produced by Leucocytes (neutrophils)
  • Allows neutrophils to move into extravascular space
  • Can then move towards target by pulling themselves along collagen fibres of other tissues
37
Q

What is degranulation and when does it occur?

A
  • The movement and fusion of the granules of a neutrophil towards a phagosome during phagocytosis, after which bactericidal substances are injected into the particle.
  • Occurs before the particle is completely enclosed in the phagosome
38
Q

What is the function of a complement?

A
  • Formation of a tube (called the membrane attack complex)
  • Tube punches holes in bacteria
  • Causes bacteria to die
39
Q

Give FOUR examples of local complications of acute inflammation

A
  • Damage to normal tissue
  • Pain and loss of function
  • Obstruction of tubes e.g. fallopian tubes due to swelling from exudate
  • Loss of fluid e.g. from a surface wound
40
Q

Give FOUR systemic effects of acute inflammation

A
  • Fever
  • Leucocytosis (increased number of leucocytes in circulation)
  • The acute phase response (Change in levels of certain plasma proteins due to a change in protein synthesis in the liver)
  • Shock (large drop in blood pressure due to widespread vasodilation and increase in vascular permeability with exudation)
41
Q

Give FOUR examples of exudate

A
  • Pus/abscess - white as is rich in neutrophils, typical of chemotactic bacteria
  • Haemorrhagic - enough RBCs to seem bloody. Typical of significant vascular damage from destructive infections/exudate from malignant tumours
  • Serous exudate - contains plasma proteins and is typical in blisters e.g. from burns
  • Fibrinous exudate - rich in fibrin, common from cuts to the skin
42
Q

What is hereditary angio-oedema?

A
  • Inherited (autosomal dominant) deficiency of C1- esterase inhibitor (a component of the compliment system)
  • Rapid oedema of dermis, subcutaneous tissue, mucosa etc.
  • Recurrent abdominal pain is also a symptom
43
Q

What is Alpha1-antitrypsin deficiency?

A
  • An autosomal recessive disorder with varying levels of severity
  • low levels of alpha-1 antitrypsin which deactivates enzymes released from neutrophils at the site of inflammation
44
Q

What is chronic granulomatous disease?

A
  • Genetic condition where phagocytes are unable to generate the free radical superoxide
  • Phagocytes can’t kill bacteria as they can’t generate an oxygen burst

ESA 2 (63 decks)

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