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Questions and Answers
Which chemical mediators are known to increase vascular permeability during acute inflammation?
Which chemical mediators are known to increase vascular permeability during acute inflammation?
What is the term for the movement of neutrophils along concentration gradients of chemo-attractants?
What is the term for the movement of neutrophils along concentration gradients of chemo-attractants?
Which of the following mechanisms allows neutrophils to migrate out of blood vessels?
Which of the following mechanisms allows neutrophils to migrate out of blood vessels?
What is the process by which neutrophils recognize and engulf pathogens?
What is the process by which neutrophils recognize and engulf pathogens?
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Which of these factors is NOT a chemical mediator involved in acute inflammation?
Which of these factors is NOT a chemical mediator involved in acute inflammation?
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Which cytokines are implicated in the alteration of adhesion molecules on neutrophils during their migration?
Which cytokines are implicated in the alteration of adhesion molecules on neutrophils during their migration?
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Which of the following substances is a product released on neutrophil death?
Which of the following substances is a product released on neutrophil death?
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What is the role of prostaglandins in the acute inflammatory response?
What is the role of prostaglandins in the acute inflammatory response?
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What role do opsonins play in microbial killing?
What role do opsonins play in microbial killing?
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Which of the following substances is produced during the O2-dependent killing mechanism?
Which of the following substances is produced during the O2-dependent killing mechanism?
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What is the primary causative organism responsible for lobar pneumonia?
What is the primary causative organism responsible for lobar pneumonia?
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Which of the following is a local complication of acute inflammation?
Which of the following is a local complication of acute inflammation?
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What effect do endogenous pyrogens have during acute inflammation?
What effect do endogenous pyrogens have during acute inflammation?
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Which of the following is a characteristic feature of hereditary angio-oedema?
Which of the following is a characteristic feature of hereditary angio-oedema?
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Which acute phase protein is clinically useful to monitor inflammation?
Which acute phase protein is clinically useful to monitor inflammation?
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In cases of acute inflammation in serous cavities, what complication may arise from localized fibrin deposition?
In cases of acute inflammation in serous cavities, what complication may arise from localized fibrin deposition?
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What type of necrosis is typically seen in the center of an abscess?
What type of necrosis is typically seen in the center of an abscess?
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Which outcome represents a complete resolution of acute inflammation?
Which outcome represents a complete resolution of acute inflammation?
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What characterizes the systemic effects of acute inflammation?
What characterizes the systemic effects of acute inflammation?
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What is the outcome when tissue architecture is destroyed during inflammation?
What is the outcome when tissue architecture is destroyed during inflammation?
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Which of the following is NOT a mechanism of O2-independent killing?
Which of the following is NOT a mechanism of O2-independent killing?
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In hereditary angio-oedema, what is the role of C1 inhibitor?
In hereditary angio-oedema, what is the role of C1 inhibitor?
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What can occur when exudate collects in serous cavities?
What can occur when exudate collects in serous cavities?
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What condition can result from a deficiency of α1-antitrypsin?
What condition can result from a deficiency of α1-antitrypsin?
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Study Notes
Acute Inflammation-2
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Objectives include: Chemical mediators (overview), mechanisms of fluid loss and neutrophil emigration, neutrophil action (phagocytosis), local and systemic effects of inflammation, sequelae, and clinical examples.
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Chemical Mediators:
- Cellular Sources: Histamine, serotonin, lysosomal enzymes from mast cells, basophils, platelets; prostaglandins, leukotrienes, platelet-activating factors, activated oxygen species, nitric oxide, cytokines produced by various cells (leukocytes, platelets, endothelial cells, macrophages, lymphocytes).
- Plasma Sources: Factor XII activation (kinin system - bradykinin), Complement system (C3a, C5a), coagulation/fibrinolytic systems, metabolites of arachidonic acid (prostaglandins, leukotrienes), blocked by NSAIDs (e.g., aspirin), cytokines/chemokines from WBCs (interleukins, PAF, TNF-alpha, PDGF, TGF beta)
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Other Inflammatory Mediators:
- Platelets: 5-HT, histamine, ADP.
- Neutrophils: lysosomal constituents, products released on cell death.
- Endothelium: prostacyclin, nitric oxide.
- Plasminogen activators/inhibitors.
- Oxygen-derived free radicals.
- Inactivation of antiproteases, injury to other cells.
Vascular Changes
- Vascular dilatation: Histamine, prostaglandins, nitric oxide are involved.
- Increased vascular permeability: Transient, histamine, bradykinin, leukotrienes (C4, D4, E4).
- Neutrophil emigration: C5a, leukotriene B4, and bacterial products are important mediators.
Mechanisms of Vascular Leakage
- Endothelial contraction --> gaps (histamine, leukotrienes)
- Cytoskeletal reorganization --> gaps (cytokines IL-1 and TNF)
- Direct injury (toxic burns, chemicals)
- Leukocyte-dependent injury (toxic oxygen species and enzymes)
- Increased transcytosis (channels across endothelial cytoplasm - VEGF)
Mechanisms of Neutrophil Migration
- Neutrophil adhesion and emigration: binding of complementary adhesion molecules on endothelial and neutrophil surfaces.
- Chemical mediators change surface expression or avidity of adhesion molecules: Selectins, Immunoglobulins, Integrins.
How do Neutrophils Escape from Vessels?
- Relaxation of inter-endothelial cell junctions.
- Digestion of vascular basement membrane.
- Movement: Diapedesis and emigration; chemotaxis.
Chemotaxis
- Movement along concentration gradients of chemo-attractants.
- Receptor-ligand binding.
- Rearrangement of the cytoskeleton.
- Production of pseudopods.
Phagocytosis
- Contact, Recognition, Internalization, Cytoskeletal changes.
Microbial Killing
- Recognition facilitated by opsonins (e.g., C3b receptors on phagocytes).
- Phagocytes recognize organisms coated with immunoglobulin or complement.
- Phagosomes fuse with lysosomes to form secondary lysosomes with killing mechanisms.
Killing Mechanisms
- O2-dependent: production of superoxide and hydrogen peroxide, H2O2- myeloperoxidase dependent systems- producing HOCl, myeloperoxidase independent killing is less effective
- O2-independent: lysozyme and hydrolases, bactericidal permeability increasing protein (BPI), cationic proteins (defensins), major basic protein (MBP) in eosinophils.
Complications of Acute Inflammation
- Local: rubor, calor, dolor, tumor (swelling, blockage of tubes, exudate, loss of fluid, pain, functional loss)
- Systemic: acute phase response (decreased appetite, altered sleep, raised heart rate, changes in plasma protein concentrations like CRP, 1 antitrypsin, haptoglobin, fibrinogen, serum amyloid A protein), spread of microorganisms and toxins ->shock
Resolution
- Mediators of acute inflammation have short half-lives and may be inactivated by degradation, dilution or inhibition.
- Gradual reversal of changes: vascular changes stop; neutrophil margination stops, permeability & vessel caliber return normal; exudate drains via lymphatics, fibrin degraded, neutrophils die. Damaged tissue regenerates if tissue architecture wasn't destroyed.
Clinical Examples (Lobar Pneumonia)
- Causative organism: Streptococcus pneumoniae.
- Risk factors: young adults in confined spaces, alcoholics.
- Clinical course: worsening fever, prostration, hypoxemia, dry cough, fairly sudden improvement when antibodies appear.
Clinical Examples (Skin Blisters)
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Causes: heat, sunlight, chemicals
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Predominant features: pain, exudate (clear collection of fluid from the epithelium).
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Inflammatory cells are relatively few, so exudate is clear unless bacterial infection develops.
Clinical Examples (Abscesses)
- Solid tissue
- Inflammatory exudate separates tissue
- Liquefactive necrosis in center
- High pressure causes pain
- Potential tissue damage and compression of adjacent structures
Clinical Examples (Hepatic Abscess)
- Image presented.
Clinical Examples (Acute Inflammation in Serous Cavities)
- Exudate pours into cavities (ascites, pleural or pericardial effusion)
- Respiratory or cardiac impairment
- Localized fibrin deposition
Clinical Examples (Pericarditis)
- Image presented.
Clinical Examples (Hereditary Angioedema)
- Recurrent episodes of swelling (limbs, face, intestinal tract, airways).
- Deficiency in C1 inhibitor. C1 cleaves C2 and C4 to form C3. C1 inhibitor also inhibits Bradykinin. Uninhibited bradykinin increases endothelial permeability causing edema.
- Treated with C1 inhibitor infusions or fresh frozen plasma.
Clinical Examples (α₁-Antitrypsin Deficiency)
- α₁-antitrypsin inhibits elastase.
- Without inhibition, elastase breaks down lung/liver tissue, causing emphysema and liver sclerosis.
Clinical Examples (Chronic Granulomatous Disease)
- Recessive sex-linked trait, Immune phagocytes not working properly.
- Granulomas form as an attempt to contain bacteria.
- Individuals often have infections in the lungs, skin, lymph nodes, liver, and intestines.
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Description
Explore the complexities of acute inflammation in this quiz, covering key chemical mediators, mechanisms of fluid loss, and the role of neutrophils in phagocytosis. Learn about local and systemic effects, sequelae, and relevant clinical examples. Test your understanding of inflammatory responses and mediators.
