Pathology- Acute and Chronic inflammation Flashcards Preview

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Flashcards in Pathology- Acute and Chronic inflammation Deck (22)
1

Acute inflammation

Rapid host response triggering vascular and cellular reaction

2

Vascular reaction to acute inflammation

Vascular changes to maximise movement of plasma proteins to site of injury:
Vasodilation leads to increased blood flow to the area of injury, clinically causing redness and heat (ERYTHEMA). This is induced by histamine and nitric acid.
Increased permeability follows, which leads to fluid leaking into the extravascular tissue. This leads to swelling (OEDEMA)
Together this creates blood stasis, pooling the blood at site of inflammation

3

VASCULAR PERMEABILITY

Endothelial cells of vessel wall triggered to contract increasing inter-endothelial spaces, triggered by histamine, bradykinin, leukotriens, substance P etc. It is the Immediate transient response

4

Endothelial injury

Endothelial injury leading to endothelial cell death, vessel wall is damaged and there is immediate extravascular leakage

5

Transcytosis

Transcytosis leading to increased transport of fluids/proteins through cell channels. Promoted by specific factors triggered by inflammation eg VEGF

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VEGF

Vascular endothelial growth factor (VEGF), is a signal protein produced by cells that stimulates vasculogenesis and angiogenesis. It is part of the system that restores the oxygen supply to tissues when blood circulation is inadequate.

7

Cellular reaction to acute inflammation

Main aim of inflammation is to recruit leucocytes to area of damage. by adhering them to vessel wall
Neutrophils and macrophages ingest and kill bacteria and necrotic cells, as well as promoting repair.
These white blood cells need to be recruited from the vessel lumens.

8

Margination

Red blood cells flow in centre of vessel lumen and WBCs flow peripherally. In stasis, more wcc fall into peripheral flow.

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Rolling

This leads to an increased amount of leucocytes to roll along then edge of the damaged endotehlium. Mediated by selectins.

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Adhesion

The leucocytes finally stop and adhere to the endothelium. Cytokines secreted by by injured cells encourage the adhesion of the leucocytes.

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Transmigration

Leucocyte is then encouraged to pass through endothelium to extravascular space
Chemokines stimulate migration and leucocyte move towards the chemical concentration gradient
(towards site of injury where the chemokines are being produced)
PECAM-1 – platelet endothelial cell adhesion molecule

12

Chemotaxis

Exogenous (bacteria ) and endogenous (cytokines/complement) substances attract the leucocytes towards the area of injury.

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Neutrophils

Neutrophils appear at 6-24 hours, monocytes appear at 24-48hours. Neutrophils are more common in circating blood and respond to chemokines.

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Function of leucocytes

Receptors on the leucocytes recognise foreign microbes
These include:
-Toll like receptors present on cell surface of leucocytes and attach to bacteria products
-G protein coupled receptors recognise N-formymethionyl of bacteria as well as chemokine breakdown
-Opsonin receptors recognoze microbes that have been coated with proteins ( antibodies/complement) or opsonins, thus called opsonization. This targets them for phagocytosis
-Cytokine receptors are present on leucocytes respond to the cytokines produced in response to microbes.

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Phagocytosis

Through these receptors the leucocyte recognises and attaches itself to bacteria or damaged cell
The leucocytes then engulfs the cell/particle
The leucocyte then kills and degrades the offending agent, removing its harmful effects.
This continues until all foreign and damaged products are removed, so healthy cells remain and healing and repair can begin.

16

Chronic inflammation

Persistent infection: microorganisms that are difficult to remove e.g. parasite, mycobacteria.
Immune mediated inflammation: reaction against host tissue leading to auto-immune diseases.
Prolonged exposure to toxic agent : silica, asbestos, lipids (atherosclerosis)
Predominantly show infiltration of mononuclear cells: macrophages, lymphocytes and plasma cells.
( Macrophages destroy damaged cells and promote repair)
Tissue destruction following prolonged inflammatroy reaction
Signs of attempts at healing: connective tissue repair, increased growth of small blood vessels and fibrosis

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Granulomas

Cellular attempt to contain offending agent it cannot eradicate
Strong activation of macrophages and T lymphocytes, leading to injury of normal tissues.
e.g Tuberculosis which leads to caseating lesions in the lungs.

18

Medications

Non-steroidal anti-inflammatories (NSAIDs)
Anti-histamines
Steroids
Targeted biologics against immune response proteins e.g anti TNF

19

Acute appendicitis

Peak age 10-30 years
Central abdominal pain which localises to right iliac fossa; worse on movement; may have nausea/vomiting
Pyrexia, raised HR, raised WCC and CRP
Management – appendicectomy
Complications – perforation leading to peritonitis, abscess formation

20

Septic Arthritis

Red hot swollen joint
Unable to move joint as limited by pain
Pyrexia, tachycardia, raised WCC and CRP
Risk factors: prosthetic joint, recent surgery/trauma to knee, age, RA, Immunodeficiency
Treatment – Joint aspirate, IV antibiotics, sepsis 6

21

Rheumatoid Arthritis

Chronic autoimmune inflammatory condition
Leading to warm swollen, stiff and painful joints.
Vessels also can become involved – Vasculitis, leading to circulatory problems.
Immune systems views host cell as foreign, leading to a chronic inflammatory response.
macrophages, lymphocytes (T cell) and plasma attempt to remove foreign agent. Instead healthy joints are destroyed.
Treatment: Steroids, DMARDs, biologics

22

Peptic Ulcers

Acute inflammatory response e.g. h pylori/excess acid
Necrotic inflammed mucosa falls away and is exposes to stomach acid/ h pylori and does not repair, leading to chronic inflammation
At risk of developing bleed/perforation
Treatment – PPIs / histamine receptor agonist/ antibiotics