Acute Inflammation Flashcards

1
Q

Define acute inflammation

A

Immediate & early response to injury (transient- last short time)

To deliver leukocytes to site of injury

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2
Q

What is ‘itis’ vs ‘osis’ at the end of conditions

A

itis= Inflammation of
osis= Is a disease/condition

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3
Q

What are the 5 causes of inflammation

A

Infections
Hypersensitivity reactions
Physical agents e.g. trauma
Necrosis
Chemicals

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4
Q

What are bacterial exotoxins

A

Chemical released by bacteria stimulating inflammation

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5
Q

What are bacterial endotoxins

A

Associated in cell walls which get released and stimulate inflammation

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6
Q

What is hypersensitivity

A

Excess immune response due to altered immunological state

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7
Q

How does physical agents and chemicals cause inflammation

A

Tissue damage provokes inflammatory response

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8
Q

How does tissue necrosis trigger inflammation

A

Dead tissue releases peptides which trigger inflammatory response

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9
Q

What are the Cardinal signs of acute inflammation (diagnostic features)

A

Redness(rubor)
Heat (calor)
Swelling (tumour)
Pain (dolar)
Loss of function (functio laesa)

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10
Q

What is redness and heat caused by in inflammation

A

Dilation of blood vessels leading to increased blood flow and increased vessel permeability

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11
Q

What causes pain in inflammation

A

Distortion of tissue and release of chemical mediators-
Prostaglandins & Bradykinins

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12
Q

What is swelling caused by in inflammation

A

Accumulation of fluid & increased inflammatory cells migrating to the area

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13
Q

What are the 6 stages of inflammation

A
  1. Chemical mediator release
  2. Vasodilation
  3. Increased vascular permeability
  4. Fluid accumulation
  5. Cellular recruitment (neutrophils)
  6. Phagocytosis
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14
Q

What are the 2 major components of early inflammation

A

Vascular changes (change in vessel calibre)
Cellular events (forms cellular exudate)

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15
Q

How does the vascular calibre change in acute inflammation

A

initial transient constriction then vasodilation occurs

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16
Q

What is exudation

A

Vascular permeability increases which increases net flow of fluid out of the vessels

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17
Q

What processes are involved in forming cellular exudate

A

Margination
Adhesion
Emigration

To accumulate neutrophil polymorphs

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18
Q

What is margination

A

Neutrophils marginate out by inflammation site losing intravascular fluid to slow flow of blood to site

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19
Q

What is adhesion

A

Neutrophils adhere to vascular endothelium
-interaction between paired adhesion molecules on neutrophils and endothelial surface

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20
Q

What is emigration

A

Neutrophils pass between endothelial cells through basil lamina and into the adventitia

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21
Q

What are the components of cellular exudate

A

Cells (endothelial & inflammatory)
Chemical agents (Cytokines, complements, histamine & prostaglandins)

22
Q

What are the early chemical mediators of inflammation

A

Histamine & Thrombin & Neutrophils

23
Q

What chemical mediators of inflammation are released by cells

A

Histamine
Lysosomal compounds
Leukotrienes
Prostaglandins
Serotonin
Chemokines

24
Q

What does histamine cause

A

Vascular dilation and increased permeability

(Released by mast cells)

25
What do lysosomal compounds cause
Increasing vascular permeability and stimulated histamine release from mast cells (released by neutrophils)
26
What do leukotrienes cause
Vasoactive properties (made in neutrophils)
27
What do prostaglandins do
Increase vascular permeability and cause platelet aggregation
28
What does serotonin do
Vasoconstrictor (released by platelets)
29
What do chemokines do
Attract more WBC to site of infection -Common one is Il-8 which attracts neutrophils
30
What are the enzyme cascade systems in plasma
Coagulation system Kinins Fibrinolytic system Complement System
31
What are some Inflammation benefits
Entry of antibodies Dilution of toxins Drug transport Stimulates immune response
32
What are harmful effects of inflammation
Digestion of normal tissue Swelling can compromise airways and cause brain damage Can cause anaphylaxis if inappropriate
33
What are systematic manifestations of acute inflammation
Fever Malaise Loss of appetite Nausea
34
What are outcomes of acute inflammation
Resolution Suppuration Scarring/fibrosis Chronic inflammation
35
What is resolution of acute inflammation
Everything goes back to normal with mininal tissue damage and good vascular drainage to remove fluid & debris
36
What is suppuration
The formation of pus -Mixture of neutrophils (dead & alive), debris & bacteria -Walled off pus forma and abcess
37
What causes scarring/fibrosis
New capillaries lead to more macrophages proliferating more fibroblasts
38
What types of skin healing are there
By primary intention By secondary intention
39
What is healing by primary intention
2 edges of wound brought together an fibrin joins weakly at edges -Over time epidermal re-growth and collagen synthesis makes stronger join
40
What is healing by secondary intention
Tissue defect filled by granulation tissue and epithelial re-growth occurs over surface -Fibrous scar forms contracting over time
41
How does acute inflammation progress to chronic
If causative agent is not removed, cellular exudate changes lymphocytes, plasma cells and macrophages replace neutrophils
42
What are macroscopic signs of chronic inflammation
Chronic ulcer Chronic abscess cavity Fibrosis/tissue thickening
43
what do the cells of chronic inflammation look like
Lymphocytes- Small circular purple dots Plasma cells- fried eggs Macrophages- Big and blobby Eosinophils- Tomato with sunglasses
44
What do lymphocytes do in chronic inflammation
B- turn into plasma cells then produce antibodies T - Killer T cells (CD8+) – cytotoxic function. Helper T cells (CD4+) – Activate killer T and plasma cells
45
What are macrophages good at
Eating things i.e. phagocytosis -Not killed in the process like neutrophils Produce cytokines
46
what do cytokines do in chronic inflammation
Small proteins which enhance cell mediated immunity and antibody response - cell signalling and promote apoptosis
47
What is a granuloma
Collection of histocytes -stationary phagocytic cell present in connective tissue
48
what are giant cells
Macrophages collide (potentially when both trying to eat same particle) producing huge multi-nucleated cells
49
What 3 types of giant cells are there
Foreign body type Langhans Touton type
50
What are foreign body type giant cells
Have random nuclei scattering
51
What are Langhans giant cells
Has a horseshoe nucleus often seen in TB
52
What are touton type giant cells
Lipid breakdown with neat circle of cells