Acute Inflammation Flashcards

1
Q

Some causes of inflammation:

A
  • Infection
  • Hypersensitivity
  • Trauma
  • Chemicals
  • Necrosis
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2
Q

Hypersensitivity:

A

Excess immune response due to altered state of immunological responsiveness

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3
Q

Cardinal signals of acute inflammation

A

Redness - dial action of vessels
Heat - increased blood flow
Swelling - accumulation of fluid

Pain - due to distortion of tissue (chemical mediators released e.g. prostaglandins)

Loss of function

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4
Q

6 stages of inflammation:

A

• Release of chemical mediators
•Vasodilatation
•Increased vascular permeability
•Fluid accumulation
•Cellular recruitment
•Phagocytosis

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5
Q

Functions of neutrophils:

A

They can move via:
• Contracting microtubules
• Chemotaxis

They can stick to opsonised microorganisms:
• When bacteria encounter immunoglobulins or complement components, neutrophils can bind to them

They are Phagocytes

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6
Q

What allows neutrophils to marginate?

A
  • Loss of intravascular fluid
  • Slowing of flow to the site
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7
Q

Adhesion

A

Neutrophils adhere to vascular endothelium

Caused by interaction between paired adhesion molecules on the neutrophil and endothelial surfaces

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8
Q

Emigration

A

When neutrophils pass between endothelial cells through basal lamina and into adventitia

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9
Q

Chemical agents in acute inflammation (4)

A

Cytokines
Complement
Histamine
Prostaglandins

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10
Q

Role of PAF:

A

Docks with corresponding receptor on neutrophil and promotes expression molecules allowing firm neutrophil adhesion to endothelial surface

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11
Q

Function of histamine

A

Causes vascular dilation and permeability

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12
Q

What do prostaglandins cause?

A

Some cause increased vacular permeability, some cause platelet aggregation

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13
Q

Chemokines

A

Family of chemicals which attract more white blood cells to site of inflammation

Eg IL-8 attracts neutrophils

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14
Q

Benefits of inflammation:

A

•Dilution of toxins
•Entry of antibodies
•Stimulation of immune response

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15
Q

Harmful effects of inflammation

A

Digestion of normal tissue
Swelling
Inappropriate inflammatory response

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16
Q

What is resolution?

A

Everything is back to normal

Ideal conditions include:
•Good regenerative capacity
•Minimal tissue damage/cell death
•Quick elimination of the causative agent
•Good vascular drainage to remove fluid and debris

17
Q

What makes up the organisation state after acute inflammation?

A

Formation of granulation tissue

Can occur with substantial amounts of tissue loss, or large amounts of fibrin

New capillaries, leading to more macrophages, leading to proliferation of fibroblasts, leading to fibrosis and/or scarring

18
Q

What is suppuration?

A

Formation of pus:
- Mix of neutrophils, debris, bacteria etc

If it gets walled off, can form abscess

19
Q

Difference in healing outcomes in different tissue types:

A

Bone - Replaced by stronger lamellar bone

Liver - Can get complete healing unless architecture is damaged then there is scarring

Kidney - Epithelium can regenerate, architecture can’t

Smooth muscle - Only vascular smooth muscle can regenerate other smooth muscle is replaced by scar tissue

Neural tissue - Does not repair well, peripheral nerves may regrow but recovery is variable

20
Q

What predisposes progression from acute to chronic inflammation?

A

If causative agent is not removed

The cellular exudate starts to change:
• Neutrophils are replaced with lymphocytes, plasma cells, macrophages

21
Q

When might you get primary chronic inflammation?

A

Acute inflammation fails to resolve

Collection of pus, abscess formation and walling off with granulation and fibrous tissue

Presence of foreign material:

Recurring cycles of acute inflammation then healing

22
Q

What cells are involved in chronic inflammation?

A

Lymphocytes (Small purple dots):

Plasma cells (Fried eggs):

Macrophages (Bigger blobby ones)

Sometimes eosinophils (Tomatoes with sunglasses)

23
Q

What is granulomatous inflammation?

A

A collection of histiocytes

Examples of conditions:
•Tuberculosis
•Sarcoidosis
•Crohn’s disease

24
Q

Primary and Secondary healing (skin):

A

Primary intention:
•Two edges of the wound can be brought together
•Fibrin joins the edges together weakly
•Over time, epidermal regrowth and collagen synthesis makes a stronger join

Secondary intention:
•Tissue defect filled in by granulation tissue
•Epithelial regrowth over the surface
•Fibrous scar forms and contracts over time

25
Q

Role of lymphocytes in chronic inflammation:

A

B cells turn into plasma cells and produce immunoglobins/antibodies

T killer cells are cytotoxic and recruit other cells

Helper T cells activate killer T cells and plasma cells