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Questions and Answers
What best describes the main function of selectins and integrins in the inflammatory response?
Which of the following characteristics differentiates an exudate from a transudate?
During acute inflammation, which of the following steps occurs first in the recruitment of leukocytes?
What term describes the process by which leukocytes move toward the site of inflammation?
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Which of the following is a common outcome of chronically inflamed tissues?
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What is the primary role of macrophages in chronic inflammation?
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Which of the following best explains the term 'cardinal signs of inflammation'?
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What mechanism leads to increased vascular permeability during the inflammatory response?
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Which type of inflammation is characterized by solid casts or cores of fibrin forming from damaged membranes?
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What is a defining feature of purulent inflammation?
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Which inflammatory condition is specifically associated with the term 'pyo'?
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Which immune cells are first to arrive at the site of acute inflammation?
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In granulomatous inflammation, which type of cell is often formed by the fusion of epithelioid macrophages?
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What type of inflammation is typically associated with irritation from mildly irritating chemicals?
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Which term is used for inflammation of the liver?
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Which cells play a crucial role in amplifying or limiting inflammatory reactions?
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What tissue type is primarily affected in dermatitis?
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Abscesses form as a result of which inflammatory process?
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Which type of inflammation results mainly from inactivated bacteria or low virulence pathogens?
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Kupffer cells are specialized macrophages found in which organ?
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What is the lifespan of neutrophils in tissue during an inflammatory response?
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What type of inflammatory response is characterized by tissue necrosis and examples include pyometra and pyothorax?
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Which mediators primarily induce vasodilation during acute inflammation?
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What is NOT considered one of the cardinal signs of acute inflammation?
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What is a hallmark feature of increased vascular permeability during acute inflammation?
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Which of the following processes is NOT involved in the recruitment of leukocytes during inflammation?
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Which type of inflammatory response occurs during the transitional stage between acute and chronic inflammation?
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What is the primary function of Toll-like receptors in inflammation?
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Eotaxin is especially important for which function in the immune response?
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Which cell type is primarily associated with chronic inflammation?
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Which leukocytes are primarily responsible for phagocytosis during inflammatory reactions?
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What outcome can result from unresolved fibrinous inflammation?
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What is the primary effect of major basic protein (MBP) found in eosinophils?
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Which phase of inflammation involves alterations in vascular caliber and permeability?
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Which of the following best describes peracute inflammation?
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Which cytokine is NOT typically associated with promoting leukocyte recruitment during inflammation?
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What term describes the loss of function associated with inflammation?
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Which term refers to the clear fluid characteristic of serous inflammation?
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Which type of exudate indicates an inflammatory reaction with high protein concentration?
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During acute inflammation, which of the following describes the process of margination?
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Which inflammatory mediator plays a significant role in vascular permeability?
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Which inflammatory pattern is marked by the formation of a pseudomembrane?
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Which leukocyte is primarily involved in the early stages of acute inflammation?
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Which process is primarily responsible for the removal of harmful stimuli during inflammation?
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What is a common outcome of chronic inflammation?
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What type of inflammation is most commonly associated with large molecules like fibrinogen in the extracellular space?
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Which component plays a crucial role in tissue repair following inflammation?
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What is a significant systemic effect of inflammation characterized by increased body temperature?
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What is the primary reason for leukocytosis during inflammatory reactions?
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Which of the following proteins primarily increases in concentration in response to inflammation?
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What characterizes labile tissues in the context of tissue repair?
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Which process occurs as part of the healing response but can lead to scar formation?
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Which factor is NOT known to impair tissue repair?
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What is the main role of acute-phase proteins during inflammation?
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Which type of tissue primarily consists of terminally differentiated non-proliferative cells?
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Which of the following is a systemic symptom related to the actions of cytokines during inflammation?
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What occurs during macrophage activation that aids in eliminating injurious agents?
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How do stable tissues respond to injury compared to labile tissues?
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Which factor is NOT a local characteristic influencing wound healing?
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What is the primary purpose of leukocyte margination during inflammation?
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Which of the following is not a type of selectin involved in the adhesion of leukocytes to the endothelium?
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What role do integrins play in the process of leukocyte adhesion?
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Which of the following factors is considered an exogenous chemoattractant?
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What is the function of opsonins in phagocytosis?
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During phagocytosis, what structure is formed when the plasma membrane engulfs the offending agent?
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What primary mechanism do neutrophils use to kill phagocytosed microbes?
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Which cytokine is known to enhance the expression of adhesion molecules on endothelial cells?
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What is the physiological consequence of defects in leukocyte adhesion?
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What is the process of chemotaxis primarily driven by?
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Which of the following is true about collateral damage caused by leukocytes?
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What is the initial step in phagocytosis?
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How do macrophages contribute to tissue regeneration?
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In which type of disease could leukocyte responses be inappropriately directed against host tissues?
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Which cytokine is NOT primarily produced by activated macrophages?
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What is a key function of chemokines in inflammation?
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Which component of the complement system is known as a powerful chemotactic agent?
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What role does bradykinin play during inflammation?
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What outcome of acute inflammation involves the restoration of normal tissue?
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Which of the following is a mediator that enhances the inflammatory response through endothelial leukocyte adhesion?
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Which process involves the degradation of complement proteins leading to an enzymatic cascade?
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Which statement correctly describes chronic inflammation?
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What is the primary trigger for the systemic acute-phase response?
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Which statement is TRUE about the kinin system in inflammation?
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What is the function of the membrane attack complex (MAC) in the complement system?
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Which inflammatory mediator is responsible for causing platelet aggregation?
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Which outcome of acute inflammation may occur if there is significant tissue destruction?
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What is the role of oxygen-derived free radicals in inflammation?
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What is a characteristic feature of monoclonal gammopathy on serum protein electrophoresis?
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Which condition is most commonly associated with monoclonal gammopathy?
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What is Bence-Jones proteinuria indicative of in animals?
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What leads to hypoglobulinaemia in neonatal animals?
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What is the significance of serum IgG levels in neonatal foals?
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Which test is considered the best agreement with the gold standard for assessing failure of passive transfer?
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What can cause hypoglobulinaemia aside from failure of passive transfer?
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What is the role of serum GGT activity in newborn calves and lambs?
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Which of the following conditions is characterized by defective fusion of phagosomes and lysosomes in phagocytes?
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What primarily ends the acute inflammatory response?
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Which of the following mediates the transition from pro-inflammatory to anti-inflammatory signals during inflammation termination?
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Which cell type is a major source of histamine in inflammatory responses?
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In the context of inflammation, what role do prostaglandins primarily serve?
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What is a key characteristic of leukotrienes in relation to inflammation?
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Which mediator is released by macrophages to help suppress the inflammatory response?
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What is the physiological effect of serotonin during inflammation?
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Which enzyme is responsible for converting arachidonic acid (AA) into prostaglandins?
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Which type of mediators are mainly produced in the liver and require activation to become biologically active?
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What is a significant role of chemokines in the inflammatory process?
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What is the primary function of anti-inflammatory lipid mediators in the context of inflammation?
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Which of the following pathways is used for the synthesis of leukotrienes?
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Which of the following characteristics is NOT true regarding mediators of inflammation?
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What is the primary mechanism by which albumin maintains colloid osmotic pressure in plasma?
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What is a common cause of relative hyperproteinemia in a patient?
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Which protein is primarily responsible for transporting calcium in serum?
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What method is primarily preferred for the quantitation of albumin in veterinary diagnostic laboratories?
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Which type of globulin is primarily associated with immunological functions?
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What potential issue can arise when determining total protein concentration using refractometry?
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Which condition is most commonly associated with hypoproteinemia?
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What is the effect of glucocorticoid therapy on albumin levels in dogs?
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Which component is typically used to measure globulin concentration?
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What adverse effect can occur due to elevated levels of fibrinogen in the plasma?
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What role do alpha globulins primarily serve in the blood?
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In what scenario would hypoalbuminemia most likely be observed?
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What potentially alters the color of a protein sample in refractometry without affecting the protein reading?
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How do proteins separate during serum protein electrophoresis?
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What condition is primarily characterized by a long half-life of albumin, which minimizes the occurrence of hypoalbuminaemia during acute inflammation?
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How might persistently high globulin concentrations indirectly affect albumin production?
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Which mechanism is suggested to play a role in the reduction of albumin levels due to high globulin levels?
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In which scenario would hypoalbuminaemia most likely lead to ascites?
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What is the primary role of acute phase proteins during an inflammatory response?
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What distinguishes major acute phase proteins from moderate acute phase proteins?
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What is a notable characteristic of the polyclonal gammopathy seen in chronic inflammatory diseases?
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Which acute phase protein is known for being a sensitive indicator of inflammation specifically in cattle?
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What distinguishes the acute phase response when inflammation persists over seven days?
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Which statement about Serum Amyloid A (SAA) is correct?
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What condition is characterized by the increased production of γ-globulins, often leading to decreased albumin synthesis?
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Which cytokine is NOT typically involved in the stimulation of acute phase proteins?
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What is a common leading cause of hyperglobulinaemia?
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In horses, which acute phase protein is beneficial for monitoring postoperative recovery?
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Study Notes
Inflammation Overview
- Vital host defense mechanism that helps eliminate infections and heal injuries.
- Defined as the response of vascularized tissues to infection and damage, facilitating the movement of defense cells and molecules to affected areas.
- Balances beneficial effects (healing) and detrimental effects (potential tissue injury).
Cardinal Signs of Inflammation
- Four classic signs:
- Rubor (redness)
- Tumor (swelling)
- Calor (heat)
- Dolor (pain)
- Functionality: Reflects early vascular changes during inflammation, with loss of function identified as an additional sign.
Causes of Inflammation
- Stimuli triggering inflammation include infections, tissue necrosis, hypoxia, foreign bodies, and immune reactions (hypersensitivity).
Classification of Inflammation
-
Duration:
- Acute: Rapid onset, lasting minutes to hours.
- Subacute: Transitional phase between acute and chronic inflammation.
- Chronic: Prolonged duration, often resulting from unresolved acute inflammation or slow responses to low-grade injuries.
-
Morphology: Patterns indicate underlying causes of inflammation and include:
- Serous: Thin, clear fluid, seen in conditions like skin blisters.
- Fibrinous: Thick exudate with fibrin, found in peritonitis and pleuritis.
- Suppurative/Purulent: Pus production indicative of abscesses and infections.
- Catarrhal: Mucus-rich exudate, typical in mucous membranes.
- Granulomatous: Chronic inflammation characterized by granulomas, seen in tuberculosis and fungal infections.
Key Cells in Inflammatory Response
- Neutrophils: First responders, short-lived (~24-48 hours), release enzymes, form traps for pathogens.
- Macrophages: Long-lived, crucial for phagocytosis, cytokine production, and tissue repair.
- Mast Cells: Involved in acute and chronic phases, release histamine and other mediators.
- Eosinophils: Active in allergic reactions and parasitic infections, contain toxic granules.
- Lymphocytes: Role in both antibody-mediated and cell-mediated immunity, influence macrophage activity.
Vascular Events in Acute Inflammation
- Vasodilation: Increases blood flow, induced by mediators like histamine.
- Increased Vascular Permeability: Allows plasma proteins and leukocytes to exit circulation, leading to edema.
-
Exudate vs. Transudate:
- Exudate: High protein concentration and cellular debris, indicative of inflammation.
- Transudate: Low protein fluid, usually non-inflammatory.
Leukocyte Recruitment Processes
- Recruitment involves:
- Margination: Leukocytes move closer to vessel walls as blood flow slows.
- Rolling: Leukocytes interact loosely with endothelial cells.
- Firm Adhesion: Strong attachment to endothelium via adhesion molecules.
- Emigration: Movement across endothelial cell layers into tissues.
Phagocytosis
- Process whereby leukocytes engulf and digest pathogens or debris, crucial for resolving inflammation.
Termination of Acute Inflammatory Response
- Involves removal of stimuli, apoptosis of leukocytes, and restoration of tissue homeostasis.
Mediators of Inflammation
- Numerous cellular and plasma-derived mediators, such as cytokines and chemokines, play critical roles in both promoting and regulating the inflammatory response.
Differences Between Acute and Chronic Inflammation
- Acute: Short duration, primarily neutrophilic infiltration, rapid onset.
- Chronic: Long-lasting, characterized by macrophages, lymphocytes, and plasma cells, involves ongoing tissue repair and often results in fibrosis.
Systemic Effects of Inflammation
- Inflammation can have systemic responses, including fever, increased white blood cells, and altered metabolic processes.
Terminology
- Inflammation names often use the suffix “-itis” indicating affected tissues (e.g., Hepatitis, Dermatitis). Exceptions exist (e.g., pneumonia for lung inflammation).### Inflammation Process
- Hemodynamic changes during inflammation lead to leukocyte margination.
- Rolling and adhesion of leukocytes to endothelial cells depend on adhesion molecules augmented by cytokines.
- Adhesion molecules include selectins (L-selectin, E-selectin, P-selectin) and integrins, facilitating leukocyte-endothelial interactions.
Cytokines and Chemokines
- Macrophages, mast cells, and endothelial cells produce cytokines (e.g., TNF, IL-1) in response to injury or infection.
- TNF and IL-1 enhance the expression of adhesion molecules on endothelial cells.
- Chemokines attract leukocytes through a chemical gradient, guiding them to sites of infection.
Leukocyte Function
- Phagocytosis occurs in three steps: recognition, engulfment, and killing of pathogens.
- Opsonization facilitates phagocytosis, primarily through IgG antibodies and complement components (e.g., C3b).
- Engulfed materials form phagosomes that merge with lysosomes for degradation of pathogens.
Phagocytosis Mechanism
- Recognition involves attachment of pathogens to leukocyte receptors.
- Engulfment creates a phagosome, which combines with lysosomes for microbial killing.
- Reactive oxygen and nitrogen species, along with lysosomal enzymes, carry out the degradation.
Macrophage Role
- Macrophages contribute to tissue repair and regeneration by releasing growth factors.
- They can both intensify and limit the inflammatory response by secreting various mediators.
Potential for Damage
- Prolonged inflammatory responses can cause additional tissue damage.
- Autoimmune diseases occur when inflammation is misdirected against host tissues.
- Allergic reactions involve excessive responses to non-harmful substances.
Defects in Leukocyte Function
- Inherited defects, such as leukocyte adhesion deficiencies, increase infection risks.
- Bovine Leukocyte Adhesion Deficiency (BLAD) leads to recurrent infections and is caused by a mutation in the CD18 gene.
- Chédiak-Higashi syndrome impairs phagocytic function due to defective phagosome-lysosome fusion.
Resolution of Inflammation
- Inflammation subsides as mediators have short half-lives and are actively degraded.
- Active termination mechanisms include a shift from pro-inflammatory to anti-inflammatory mediators.
Mediators of Inflammation
- Mediators can be cell-derived or plasma-derived and are crucial in regulating inflammation.
- Cell-derived mediators include vasoactive amines (histamine and serotonin) and arachidonic acid metabolites (eicosanoids).
Key Mediators
- Histamine, released by mast cells, causes vasodilation and increased permeability.
- Prostaglandins influence vascular responses; key types include PGE2, PGD2, PGF2α, PGI2, and TxA2.
- Leukotrienes are produced by leukocytes, acting as chemoattractants and mediators in inflammatory responses.
Cytokines and Chemokines
- TNF and IL-1 are pivotal pro-inflammatory cytokines produced by activated macrophages.
- They activate endothelial cells and leukocytes, inducing systemic acute-phase responses.
Other Inflammatory Mediators
- Platelet-activating factor (PAF) initiates platelet aggregation and has wide inflammatory effects.
- Reactive oxygen species amplify inflammatory responses by increasing chemokine and cytokine production.
Plasma Protein-Derived Mediators
- The complement system, kinin system, and coagulation system play distinct roles in inflammation and immune responses.
- Complement proteins (C3a, C5a) are crucial for increasing permeability and chemotaxis.
Outcomes of Acute Inflammation
- Complete resolution restores normal tissue after mild or limited injury.
- Healing occurs through fibrosis when substantial tissue damage prevents regeneration.
- Chronic inflammation arises from persistent injury or ineffectiveness of healing processes.
Chronic Inflammation
- Characterized by prolonged inflammation, chronic inflammation often results from persistent infections or immune-mediated diseases.
- Histological features include infiltration of mononuclear cells and attempts at healing through fibrosis and angiogenesis.
Systemic Effects of Inflammation
- Fever and leukocytosis are common responses during acute inflammation.
- Acute-phase proteins such as C-reactive protein (CRP) increase in concentration and act as opsonins.
Tissue Repair
- Tissue regeneration and repair mechanisms are intertwined with inflammation and occur shortly after injury.
- Regeneration succeeds when damaged tissues can restore normal function without significant scarring.### Tissue Repair and Regeneration
- Injured tissues may develop structural issues like fibrosis if unable to fully restore or regenerate.
- Tissue repair capability is primarily influenced by the proliferative capacity of the cells.
- The cell cycle regulates cell proliferation via growth factors and interactions with the extracellular matrix.
- Labile tissues continuously lose and replace cells.
- Stable tissues exist in resting phases but can proliferate in response to injury.
- Permanent tissues consist of non-proliferative, terminally differentiated cells.
Scar Formation
- Repair involves connective tissue deposition and scar formation if regeneration is not possible.
- Macrophages play a pivotal role in repair by clearing harmful agents and releasing growth factors that promote cell proliferation.
- Key repair processes include inflammation, angiogenesis, granulation tissue formation, and connective tissue remodeling.
Factors Impairing Tissue Repair
- Local and systemic factors affecting wound healing include:
- Local infections
- Metabolic diseases
- Nutritional deficiencies
- Glucocorticoids (steroids)
- Mechanical issues
- Poor tissue perfusion
- Presence of foreign bodies
- Wound characteristics (size, location, type)
Plasma Proteins
- Plasma and serum proteins, primarily albumin and globulins, are maintained within narrow ranges in healthy animals.
- Functions of plasma proteins include:
- Nutritional support
- Maintaining colloid osmotic pressure
- Involvement in immune response, inflammation, and clotting
- Regulation of acid-base balance
Age-Related Changes
- In mammals, plasma protein levels are low at birth, rise after colostrum absorption, drop within a few weeks, and normalize by six months.
Albumin
- Comprises 35-50% of total serum protein; synthesized by the liver; regulated by cytokines like IL-1.
- Half-life varies: ~8 days in dogs, ~19 days in horses, ~2-3 weeks in cattle.
- Responsible for ~75% of plasma's colloidal osmotic activity.
- Functions include:
- Colloid osmotic pressure maintenance
- Transport of small, soluble substances
- Calcium transport (~40% of serum calcium)
- Serving as an amino acid source
- Acts as an antioxidant and buffer
- Identified as a negative acute phase protein
Globulins
- A diverse protein group, separated into three main categories by serum protein electrophoresis: alpha, beta, gamma.
- Alpha-globulins: liver-produced, function as transport proteins and anti-inflammatory agents.
- Beta-globulins: include transport proteins and immunoglobulins (IgM, IgA); synthesized by liver and plasma cells.
- Gamma-globulins: primarily consist of IgG antibodies produced by B lymphocytes.
Protein Measurement Techniques
- Total Protein Evaluation: Refractometry measures total solids in plasma or serum, affected by glucose, urea, sodium levels, and turbidity.
- Albumin Quantification: Bromcresol green dye-binding method is common but can yield false results; serum protein electrophoresis is an alternative.
- Globulin Measurement: Derived from the total protein minus albumin; electrophoresis separates globulin fractions.
Protein Abnormalities (Dysproteinemias)
- Hyperproteinemia: Increased total protein concentration, commonly due to dehydration or inflammatory disease.
- Hypoproteinemia: Decreased protein levels arising from conditions such as burns, gastrointestinal disease, or excessive fluid dilution.
-
Albumin Abnormalities:
- Hyperalbuminaemia: Often related to dehydration.
- Hypoalbuminaemia: Associated with malnutrition, chronic disease, or excessive fluid losses.
-
Globulin Abnormalities:
- Hyperglobulinaemia: Frequently linked to dehydration or increased inflammatory activity.
- Hypoglobulinaemia: Often results from conditions like hemorrhage or protein-losing enteropathies; common in neonates due to passive transfer failure.
Failure of Passive Transfer
- Neonates are born with minimal immunoglobulins; proper colostrum ingestion is essential for protection.
- Serum IgG levels indicate transfer success: >8 g/L is adequate, 2-8 g/L indicates partial failure, and <2 g/L indicates complete failure.
- Various tests are available to assess passive transfer, including glutaraldehyde coagulation, zinc sulfate turbidity, and serum GGT activity.
Acute Phase Proteins (APPs)
- APPs increase in response to inflammation, crucial for immune response and recovery.
- Divided into major and moderate APPs based on their production rate and peak response time.
- Most APPs are derived from liver and respond to cytokines such as IL-1 and TNF.
- Significant in various species, with specific APPs that show characteristic responses.
Gammopathies
- Polyclonal gammopathy: Features broad peaks of diverse immunoglobulin types, indicating chronic inflammation or liver disease.
- Monoclonal gammopathy: Narrow peaks from a single clone of neoplastic cells, reflecting conditions like cancer.
- Hypoglobulinemia often accompanies hypoalbuminemia, indicating potential underlying pathologies.
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Description
Explore the key concepts of inflammation and repair in veterinary anatomy and clinical pathology. This quiz is based on foundational texts, including Robbins Basic Pathology and the Pathologic Basis of Veterinary Disease. Test your understanding and deepen your knowledge in this crucial area of veterinary medicine.
