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Which of the following chemical mediators is involved in vasodilation, increased vascular permeability, and pain?
Which of the following chemical mediators is involved in vasodilation, increased vascular permeability, and pain?
What is the primary mechanism of increasing vascular permeability during the acute inflammatory response?
What is the primary mechanism of increasing vascular permeability during the acute inflammatory response?
Which of the following is a characteristic of the vascular phase of the acute inflammatory response?
Which of the following is a characteristic of the vascular phase of the acute inflammatory response?
What is the primary function of neutrophils during the acute inflammatory response?
What is the primary function of neutrophils during the acute inflammatory response?
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Which of the following chemical mediators is involved in chemotaxis and is released by activated inflammatory cells?
Which of the following chemical mediators is involved in chemotaxis and is released by activated inflammatory cells?
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What is the primary benefit of oedema during the acute inflammatory response?
What is the primary benefit of oedema during the acute inflammatory response?
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Which of the following is a systemic complication of acute inflammation?
Which of the following is a systemic complication of acute inflammation?
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What is the primary mechanism of neutrophil migration through the interstitium during the acute inflammatory response?
What is the primary mechanism of neutrophil migration through the interstitium during the acute inflammatory response?
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Which of the following adhesion molecules is involved in the binding of neutrophils to the endothelium during the acute inflammatory response?
Which of the following adhesion molecules is involved in the binding of neutrophils to the endothelium during the acute inflammatory response?
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What is the primary function of chemical mediators during the acute inflammatory response?
What is the primary function of chemical mediators during the acute inflammatory response?
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What is the primary consequence of continued acute inflammation with chronic inflammation?
What is the primary consequence of continued acute inflammation with chronic inflammation?
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What is the role of neutrophils in the process of complete resolution?
What is the role of neutrophils in the process of complete resolution?
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What is the primary complication of bacterial meningitis?
What is the primary complication of bacterial meningitis?
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What is the characteristic of an abscess?
What is the characteristic of an abscess?
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What is the consequence of inflammation of serous cavities?
What is the consequence of inflammation of serous cavities?
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What is the characteristic of hereditary angio-oedema?
What is the characteristic of hereditary angio-oedema?
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What is the result of increased vascular permeability?
What is the result of increased vascular permeability?
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What is the primary role of mediators in the acute phase response?
What is the primary role of mediators in the acute phase response?
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What is the primary mechanism of emphysema development in alpha-1 antitrypsin deficiency?
What is the primary mechanism of emphysema development in alpha-1 antitrypsin deficiency?
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Which of the following is a consequence of intestinal oedema in patients with cutaneous angio-oedema?
Which of the following is a consequence of intestinal oedema in patients with cutaneous angio-oedema?
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What is the inherited defect in chronic granulomatous disease?
What is the inherited defect in chronic granulomatous disease?
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What is the consequence of abnormal alpha-1 antitrypsin protein in the liver?
What is the consequence of abnormal alpha-1 antitrypsin protein in the liver?
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What is the primary mechanism of laryngeal involvement in patients with cutaneous angio-oedema?
What is the primary mechanism of laryngeal involvement in patients with cutaneous angio-oedema?
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What is the characteristic feature of granulomas in chronic granulomatous disease?
What is the characteristic feature of granulomas in chronic granulomatous disease?
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Study Notes
Inflammation
- Inflammation is a rapid response to injury of vascularized living tissue, delivering defensive materials (white blood cells and fluid containing plasma proteins) to the site of injury.
- It is a protective response, but can cause local and systemic complications.
Causes of Inflammation
- Foreign bodies (splinters, dirt, sutures)
- Immune reactions
- Infections (bacterial, viral, parasitic) and microbial toxins
- Trauma (blunt and penetrating)
- Physical and chemical agents (thermal injury, e.g., burns or frostbite, irradiation, environmental chemicals)
Clinical Signs
- Vasodilation of blood vessels (RUBOR)
- Loss of function (enforces rest and reduces the chance of further damage)
Vascular Changes
- Changes in blood flow
- Movement of fluid into tissue (vascular phase)
- Starling's law: fluid movement controlled by the balance between hydrostatic pressure and oncotic pressure
- Increased capillary hydrostatic pressure = increased fluid flow out of vessel
- Increased interstitial oncotic pressure = increased fluid flow out of vessel
Acute Inflammation
- Vasodilation = increased capillary hydrostatic pressure
- Increased vessel permeability = loss of plasma proteins into interstitium (increased interstitial oncotic pressure)
- Net flow of fluid OUT of vessel INTO interstitium
- Oedema (swelling, TUMOUR)
Types of Interstitial Fluid
- Exudate:
- Occurs in inflammation
- Increased vascular permeability
- Protein-rich (delivering proteins to area of injury)
- Transudate:
- Fluid loss due to increased capillary hydrostatic pressure or reduced capillary oncotic pressure
- No change of vascular permeability - therefore less protein present
- Occurs in heart failure, hepatic failure, renal failure - systemic problems
Mechanisms of Increased Vascular Permeability
- Endothelial contraction (gaps between endothelial cells)
- Histamine, leukotrienes
- Endothelial cytoskeleton reorganization (change of shape increases gaps between them)
- Cytokines IL-1 beta, TNF alpha
- Direct injury:
- Chemical, toxic burns
- Leucocyte-dependent injury:
- Enzymes and toxic oxygen species from leucocytes
Neutrophils
- The primary white blood cell involved in acute inflammation
- Trilobed nucleus
- A granulocyte
- Chemotaxis and neutrophil infiltration:
- Stasis causes neutrophils to line up at the edge of blood vessels along the endothelium (MARGINATION)
- Neutrophils then roll along endothelium, sticking to it intermittently (ROLLING)
- Then stick more avidly - use of adhesion molecules (ADHESION)
- Followed by EMIGRATION of neutrophils through blood vessel wall
Adhesion Molecules
- Selectins:
- On endothelial cell surface
- Upregulated by chemical mediators
- Integrins:
- On neutrophil surface
- Bind to receptors on endothelial surface
Inflammatory Infiltrate
- How do neutrophils move through the interstitium?
- Chemotaxis:
- Movement along a chemical gradient of chemoattractants
- Rearrangement of neutrophil cytoskeleton
- Pseudopod formation
- Chemotaxis:
What Do Neutrophils Do?
- Phagocytosis:
- Phagosomes fuse with lysosomes
- Produce secondary phagolysosomes
How Do Inflammatory Cells Limit Damage?
- Removal of toxins and pathogenic organisms
- Removal of necrotic tissue
- Release of chemical mediators stimulates and regulates further inflammation
- Stimulates pain (encourages rest and limits risk of further damage)
Why Is Acute Inflammation Effective?
- Vascular phase:
- Exudation of fluid into interstitium (oedema)
- Dilute toxin effect
- Cellular phase:
- Infiltration of neutrophils
- Kills pathogens
How Does Oedema Limit Damage?
- Dilutes toxins
- Delivers plasma proteins to area of injury
- Fibrin (mesh limits spread of toxin)
- Inflammatory mediators - stimulates and regulates further inflammation
- Immunoglobulins - regulates the process
- Increased lymphatic draining from area of injury
Chemical Mediators
- A vast array of chemicals that contribute to the inflammatory process
- Overlapping functions
- Varying chemical structures
- Some circulate in an inactive state in blood
- Released by:
- Activated inflammatory cells
- Platelets
- Endothelial cells
Chemical Mediators at Each Step
- Vasodilation:
- Histamine, serotonin, prostaglandins, nitric oxide
- Increased vascular permeability:
- Histamine, bradykinins, leukotrienes, C3a, and C5a
- Chemotaxis:
- C5a, LTB4, TNF-alpha, IL-1 beta, IL8, bacterial peptides
- Fever:
- Prostaglandins, IL-1 beta, TNF-alpha, IL-6
- Pain:
- Bradykinin, substance P, prostaglandins
Local Complications
- Swelling:
- Blockage of nearby tubes and ducts (bile duct/intestines)
- Exudate:
- Compression of organs
- E.g. complete resolution, abscess, chronic inflammation, and fibrous repair
Complete Resolution
- All changes gradually reverse:
- Resolution is absolutely vital
- Neutrophils no longer marginate
- Vascular permeability returns to normal
- Vessel calibre
- Therefore:
- Exudate drains away via lymphatics
- Fibrin is degraded
- Neutrophils die, break up, and get phagocytosed
- Damaged tissue may be able to regenerate, if architecture is preserved
- Mediators are diluted/inactivated/degraded
Clinical Examples
- Appendicitis:
- Blocked lumen (commonly faecolith)
- Accumulation of bacteria, increased pressure, reduced blood flow
- Pneumonia:
- Many causative organisms
- Signs and symptoms: shortness of breath, fever, cough, sputum production, chest pain
- Risk factors: smoking, pre-existing lung condition (COPD, asthma, malignancy)
- Bacterial meningitis:
- Inflammation of the meninges
- Caused by a variety of pathogens
- Clinical signs: neck stiffness, fever, photophobia, altered mental state
- Rapidly fatal
Abscess
- An accumulation of dead and dying neutrophils
- With associated liquefactive necrosis
- Causes compression of surrounding structures and nerves:
- Pain, blockage of ducts
Inflammation of Serous Cavities
- Variety of causes:
- Exudate pours into serous cavity:
- Ascites - abdominal distension
- Pleural effusion - shortness of breath
- Pericardial effusion - cardiac impairment
- Exudate pours into serous cavity:
Disorders of Acute Inflammation
- Rare disorders
- Illustrate the complex mechanisms of acute inflammation
- Hereditary angio-oedema:
- Autosomal dominant condition
- Inherited deficiency of C1-esterase inhibitor
- Patients have attacks of non-itchy cutaneous angio-oedema
- Recurrent abdominal pain due to intestinal oedema
- Family history of sudden death due to laryngeal involvement
- Alpha-1 antitrypsin deficiency:
- Autosomal recessive disorder
- Varying levels of severity
- Low levels of alpha-1 antitrypsin
- Patients develop emphysema
- Liver disease also occurs
- Chronic granulomatous disease:
- Genetic condition
- Phagocytes are unable to generate the free radical superoxide
- Bacteria are phagocytosed but phagocytes cannot kill them
- Results in many chronic infections in the first year of life
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Description
This quiz covers the basics of inflammation, a response to injury in vascularized living tissue. It involves the delivery of defensive materials to the site of injury and is controlled by various mediators.
