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PATHOLOGY > Week 1(1) Acute Inflammation > Flashcards

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
Q

What are the three (3) subtypes of acute inflammation?

A

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
Q

What is a complication of puralent inflammation?

A

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
Q

What are the systemic effects of inflammation?

A

* fever

*malaise

* decreased appetite

*increased pulse

*leukocytosis

28
Q

More detail of the systemic effects of inflammation (FEVER)

A

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
Q

What is the role of lymphatics in inflammation

A
  • lymph flow is INCREASED to help drain oedema fluid
  • lymph also drains WBC
  • lymph nodes may become inflamed
30
Q

Outcomes of acute inflammation?

A

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
Q

What is GRANULATION TISSUE?

A
  • macrophages, small vessel proliferation, lymphocytes and fibroblasts

PATHOLOGY (17 decks)

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