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Lecture title - Acute inflammation

49 important questions on Lecture title - Acute inflammation

What do words associated with inflammation end in?

-itis

What are the purposes of inflammation?

1. To localise and eliminate of causative agent
2. To limit tissue injury
3. To restore tissue to normality
4. To destroy, dilute, or wall off the injurious agent

What factors determine the type of inflammation?

1. Time course (rapid, progressive?)
2. Cellular components involved

What are the classical signs of inflammation?

1. Redness (rubor) - red appearance of inflamed tissue
2. Heat (calor) - increase in temperature in peripheral sites only
3. Swelling (tumour)
4. Pain (dolor)
5. Loss of function (functio laesa)- conscious reflex inhibition of movement in the inflamed area

What are the underlying mechanisms of the classical signs of inflammation?

Four classical signs of inflammation are caused by rapid vascular response and characteristic cellular events

What is the main purpose of the classical signs of inflammation?

To bring elements of the immune system to injurious site

How do cells in the tissue, like macrophages, elicit an inflammatory reaction?

1. Cells of injured tissue recognise microbes and damaged cells
2. Mediators are released in response
3. Mediators trigger the vascular and cellular reactions of inflammation

What are the possible vascular responses to acute inflammation?

1. Changes in vessel calibre (vasoconstriction, vasodilation), which changes the vascular flow
3. Changes in vascular permeability

What are the cellular events that follow acute inflammation?

1. Leucocyte emigration
2. Phagocytosis

Explain the process of changes in vessel calibre and vascular flow after an injury (acute inflammation)

1. Vasoconstriction only for a few seconds to stop bleeding
2. Local vasodilation in the arterioles first, then the capillary beds
3. Opening of the arterioles and the capillary beds increase local blood flow by 10 times and also increases hydrostatic pressure
4. This causes redness and heat in the area of injury

How long does vasodilation after vasoconstriction for an acute injury last for?

15 mins to hours

What is the purpose of increasing vascular permeability?

The purpose of increasing vascular permeability is to deliver a protein-rich fluid called exudate to the interstitium of the injury. Exudate contains immunoglobulins and coagulation factors. The delivery of exudate to the interstitium of the injury is enabled by eliciting contraction of endothelial intracellular proteins with chemical inflammatory mediators, which creates temporary gaps to increase fenestration from the blood vessels to the surrounding tissues.

Compare the characteristics of a blood vessel normally vs. during acute inflammation

Normally
1. High hydrostatic pressure at arteriolar end, low hydrostatic pressure at venous end
2. Transudate (low protein) fluid pushed out (due to high hydrostatic pressure at arteriolar end)
3. Fluid moves back into the capillaries with no fluid accumulation in tissues
Acute Inflammation
1. Increased capillary hydrostatic pressure (both arteriolar and venous ends)
2. Escape of exudate fluid (high protein) and plasma proteins
3. Increased outflow of fluid from capillaries due to increased osmotic pressure = accumulation of fluid in interstitial tissue = oedema (swelling due to excess fluid buildup)

Explain how circulation is slowed from responses to acute inflammation

Due to the increased permeability of microvasculature, exudate (protein-rich fluid) escapes to the extravascular tissues. This increases the RBC concentration, which increases the viscosity of the blood. The packed blood in small vessels causes stasis, which overall slows blood flow and forces cells to flow and adhere to the vascular epithelium.

What is peripheral leucocyte margination?

Peripheral leucocyte margination is the pushing out of leucocytes (WBCs) to the vascular epithelium instead of the centre of the vessel due to the thick RBC packed blood filling up the blood vessels.

Explain the three steps of leucocyte emigration

1. Margination - leucocytes/WBCs at the walls of vessels
2. Adhesion - leucocytes adhere to endothelial cells
3. Emigration - leucocytes pass through the endothelial cells and basal lamina and migrate into adventitia (outermost layer of blood vessel wall)

What is the role of cytokines for leukocyte migration through endothelium?

Cytokines promote migration of leukocytes by promoting expression of ligands (selectins, integrins) on the endothelium.

What are the signs of acute inflammation?

Changes in vessel calibre and vascular flow -> rubor, calor
Changes in vascular permeability -> tumour, dolor
Leucocyte emigration -> tumour, dolor

What are the three steps of phagocytosis for acute inflammation?

1. Recognition and attachment - microbes bind to phagocyte receptors
2. Engulfment - microbes are ingested by phagocytic membranes surrounding the microbes
3. Killing or degradation - degradation by lysosome

What is the main purpose of phagocytosis for acute inflammation?

Neutrophils and monocytes ingest debris and foreign particles at the injury site.

Explain what oxygen-independent killing/degradation (acute inflammation) is and the roles of lysozyme and lactoferrin in this process.

Killing of microbes with the use of enzymes and proteins in the absence of oxygen.
1. Lysozyme - hydrolyses bonds in bacterial cell wall
2. Lactoferrin - chelates/binds to iron required for bacterial growth

Explain and list the methods of oxygen-dependent killing/degradation (acute inflammation)

1. Conversion of O₂ --> superoxide --> H₂O₂ (hydrogen peroxide) by NADPH oxidase
2. In neutrophils, MPO (myeloperoxidase) produces hypochlorite (HOCl) from H₂O₂ and Cl-
3. Reactive oxygen species (ROS) and nitric oxide (NOS) kill the bacterias

Define chemical mediators of inflammation

Chemicals released from injured tissue that spread outwards into uninjured areas for inflammatory response.

List the chemical mediators of acute inflammation that causes vasodilation

Histamine, prostaglandin, platelet-activating factor, complement

List the chemical mediators of acute inflammation that causes pain

Prostaglandins, kinins

List the chemical mediators of acute inflammation that causes increased vascular permeability

Histamine, leukotrienes, platelet-activating factor, kinins

Where is histamine stored?

Mast cells, basophils, eosinophils (immune cells)

What is the role of histamine in acute inflammation?

Histamine is a quick-acting, early mediator that dilates blood vessels and increases vascular permeability.

What counteracts histamine?

Anti-histamine (prevents binding of histamine to its receptors)

Where is serotonin stored?

Platelets

What is the role of serotonin in acute inflammation?

Potent vasoconstrictor

What are prostaglandins and leukotrienes and how are they produced?

Prostaglandins and leukotrienes are long chain fatty acids produced by neutrophils and mast cells using arachidonic acid from membrane phospholipids.

What does prostaglandin and leukotriene do in terms of inflammation?

Causes vasodilation and increased vascular permeability

How is prostaglandin and leukotriene inhibited?

Anti-inflammatory drugs (like aspirin and NSAID) inhibit prostaglandin production

What produces and releases cytokines?

Activated lymphocytes and macrophages

List the major cytokines that appear in acute inflammation with their roles

TNF, IL-1 = increases expression of adhesion molecules on endothelial cells
IL-6 = signals for production of acute phase proteins
Chemokines = chemo-attractants to recruit cytokines

What is the overall role of cytokines for acute inflammation?

Vasoactive (affect diameter of vessels) and chemotactic (migration of immune cells to inflammation)

What produces and releases platelet activating factor (PAF)?

Mast cells and neutrophils

What does platelet activating factor (PAF) do in terms of acute inflammation?

Vasodilation, increases vascular permeability, platelet aggregation, facilitates leucocyte adhesion to endothelium

Are PAF antagonists useful against platelet activating factor (PAF)?

What does C5a and C3a (complements) do in terms of acute inflammation?

Chemotaxsis, opsonisation (tagging bacteria with opsonins for easier recognition), triggers release of histamine from mast cells

What activates the kinin system?

Coagulation factor XII

What does bradykinin (from the kinin system) do for acute inflammation?

Increases vascular permeability, chemical mediator of pain

What is acute inflammation an initial response to?

Acute inflammation is an initial response to tissue injury

What happens to the blood vessels for acute inflammation?

Vasodilation

What is the predominant cell in acute inflammation?

Neutrophil polymorph

What are the possible outcomes of acute inflammation

Resolution, suppuration (abscess formation), healing, progress to chronic inflammation

Why does acute inflammation progress to chronic inflammation?

Acute inflammation progresses to chronic inflammation if the agent causing the injury or the infection is persistent. Usually seen in chronic infections, persistent injury, autoimmune diseases, and allergic diseases.

Under which conditions would the outcome of acute inflammation be fibrosis (scarring)?

If the damage is excessive, scarring occurs even after the tissue has healed, losing the tissue function.

The question on the page originate from the summary of the following study material:

FM2004

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