Week 1(1) Acute Inflammation Flashcards

1
Q

What are some examples that can potentially cause the body injury?

A

*Trauma *Infection *Heat/Cold *Chemical *Radiation *Infarction

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2
Q

How does the body protect itself from injury BEFORE it occurs?

A

*neural reflexes *fear/fight flight responses *protection against infection - skin barrier -enzymes in saliva - acid in stomach - bacteria in gut - mucus and cilia in gut - marophages in airway

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3
Q

How does the body protect itself from injury AFTER it happens?

A

= INFLAMJMATIOn

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4
Q

What should be happening in the histology slides at the following stages

a. Inflammation

b. Demolition

c. Repair

A

a. Many NEUTROPHILS are present
b. Many MACROPHAGES are present
c. Many BLOOD VESSELS are developing

Note- See Page 4 Lecture 1

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5
Q

What is Inflammation?

A
  • The protective response of living vascularised tissues to injury
  • to eradicate cause and consequences of injury
  • repair or healing (repair=cell regeneration or scars)
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6
Q

Name the IMPORTANT FEATURES of Inflammation

A
  • blood components: cells, proteins
  • blood vessels
  • chemical mediators
  • cellular and extracellular components of CT
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7
Q

What are the two main types of Inflammation?

A

Chronic

OR

Acute

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8
Q

Name the main two types of inflammation and the differeces between each type

A

Acute

  • earliest response
  • lasts days
  • FEATURES = neutrophils, oedematous, exudate, vasodilation, NON-specific

Chronic

  • later response
  • lasts weeks –> months

-FEATURES = macrophages, lymphocytes, plasma cells, often leads to fibrosis (scarring), specific OR non-specific

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9
Q

What causes ACUTE inflammation?

A

* Certain infections

* Trauma

*Burns

*Infaction

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10
Q

What does ACUTE inflammation aim to do?

A

* deliver nutrients, defence cells

*destroy infective agents

*remove debris

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11
Q

Features of ACUTE inflammation

A

1. Vascular response

2. Exudate

3. Variable tissue necrosis

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12
Q

What are the vascular and cellular responses of acute inflammation?

A

* Initial dialation of focal blood vessels increasing blood flow, then blood flow SLOWS

* Vessels become LEAKY and PERMEABLE, permitting the passage of water, salts adn small proteins = EXUDATION

*Circulating NEUTROPHILS are attached to damaged areas and adhere to swollen endothelial cells (MARGINATION) and migrate through BM (EMIGRATION) into damaged areas

* Later, macrophages and lymphocytes migrate to damaged areas.

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13
Q

What is Exudate?

A

Definition - Protein rih fluid and cells that have escaped from blood vessels due to an increase in vascular permeability.

NB - VERY different from transudate

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14
Q

What is the COMPOSITION of exudate?

A

FLUID: nutrients, immunoglobulins. Circulates through vessels and extracellular space

FIBRIN: a network of fibrin prevents migration of micro-organisms and assists migration of neutrophils and macrophages to damaged areas

NEUTROPHILS: MANY OF THESE

MACROPHAGES: Phagocytic and kill bacteria, assist in repair. Have a more important role in chronic inflammation.

LYMPHOCYTES: more frequently found in CHRONIC inflammation

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15
Q

What are the FUNCTIONS of acute inflammatory exudate?

A

* Carries proteins, fluid and cells from local blood vessels into the damaged area

* The compenents of teh exudate are able to destroy the infective causative agent

* Break down and remove damaged material

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16
Q

Chemical mediators of inflammation

A

* may be produced locally by cells at the site of inflammation

* cell-derived mediators

*plasma-dervived mediators

17
Q

What are the cell-derived mediators of inflammation?

A
  • circulating NEUTROPHILS,

MONOCYTES,

PLATELETS and TISSUE

MAST CELLS

MACROPHAGE

and ENDOTHELIAL cells

are all cellular sources of inflammatory mediators

18
Q

What are the plasma-dervived mediators of inflammation?

A

3 Proteins circulating - complement, kinin and coagulation

Complement pathway - once activate complement proteins opsonize patricles e.g. microbes which enhances phagocytosis and destruction

Kinin and coagulation system - Hageman Factor

19
Q

What are NEUTROPHILS and their role?

A

* prodcued in bone marrow

* short life span

*chemical mediators attracts them to the area

*actively phagocytose and destroy bacteria

*release free radicals

*release lusosomal enzymes to break down extracellular matrix

20
Q

How does a neutrophil work?

A
  1. Moves along the endothelium (margination)
  2. Then into tissues (emigration)
  3. Attracted to damaged area (chemotaxis)
21
Q

What stimulates the release of Neutrophilia?

A

Cytokines released from macrophages and neutrophils in an acute inflammatory response circulate in the blood and stimulate increased neutrophil release and increased production of neutrophils in the bone marrow

22
Q

Macrophages - what are they?

A
  • dervived from blood monoytes
  • phagocytic
  • assist in repair
  • important in chronic inflammation and immunity
23
Q

What are the physical signs of acute inflammation?

A

* redness

*heat

*pain

*swelling

24
Q

Why do we have each of the 4 physical (clinical) effects of acute inflammation?

A

Redness: due to vessel dilatation and increased blood flow

Heat: due to vessel dilatation adn increased blood flow

Pain: due to pressure effects on nerve endings and chemical factos

Swelloing: due to accumulation of exudate

25
What are the three (3) subtypes of acute inflammation?
**1.PURALENT:** produces large quantities of pus which consists of neutrophils, necrotic cells and odema, abscesses **2. FIBRINOUS**: More severe injury - greater vascular permeability **3. SEROUS** - outpouring of thin fluid (e.g. blisters)
26
What is a complication of puralent inflammation?
**ABSCESS** \*caused by pyogenic bacteria \*localised area of dead tissue necrosis with live and dead neutrophils \* may become walled off by fibrosis/scar tissue
27
What are the **_systemic_** effects of inflammation?
\* fever \*malaise \* decreased appetite \*increased pulse \*leukocytosis
28
More detail of the systemic effects of inflammation (FEVER)
**_FEVER:_** 1. release of exogenous pyrogens from bacteria, viruses or injured cells stimulate production of *_endogenous pyrogens_* 2. EP stimulate prostaglandin synthesis within the vascular and perivascular cells of the HYPOTHALAMUS 3. these PGs stimulate neurotransmitters to reset body temp at a higher level
29
What is the role of **_lymphatics_** in inflammation
- lymph flow is INCREASED to help drain oedema fluid - lymph also drains WBC - lymph nodes may become inflamed
30
Outcomes of acute inflammation?
**_Resolution_**: retuen of the tissue structure to normal. Cells can be replaced by cells of the same type. Phagocytes clear fluid, leukocytes and dead tissue **_Regeneration (repair):_** variable cell replication adn organisation (scar - formed by **_granulation tissue_**) **_Chronic Inflammation_**: ongoing inflammation and tissue damage proceed at the same time as attempts at healing
31
What is GRANULATION TISSUE?
- macrophages, small vessel proliferation, lymphocytes and fibroblasts