C1D3: inflammation

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Questions and Answers

How does Platelet-Activating Factor (PAF) enhance both vasodilation and vascular permeability during inflammation, and what is the underlying mechanism that allows these dual effects to occur?

PAF triggers vasodilation by inhibiting the synthesis of vasoconstrictors like endothelin-1 and increases vascular permeability by stimulating the production of vascular endothelial growth factor (VEGF).
PAF causes vasodilation by directly stimulating endothelial cells to release nitric oxide (NO), while increasing vascular permeability by activating histamine receptors on mast cells.
PAF causes vasodilation by suppressing the sympathetic nervous system and increases vascular permeability by enhancing the transcytosis of albumin across endothelial cells.
PAF induces vasodilation by promoting smooth muscle relaxation in blood vessels and increases vascular permeability by disrupting endothelial cell junctions and inducing cytoskeletal changes. (correct)

Cytokines such as TNF-α, IL-1, and IL-6 have both local and systemic effects. Given the role of TNF-α in inflammatory bowel disease (IBD), what is the primary mechanism by which anti-TNF medications alleviate symptoms in conditions like Crohn’s disease and ulcerative colitis?

By blocking TNF-α, which prevents neutrophils from entering the mucosa of the colon, reducing inflammation. (correct)
By directly killing the bacteria that cause inflammation in the gut.
By stimulating the regeneration of damaged endothelial cells in the gut, repairing the intestinal lining.
By enhancing the production of protective mucus in the colon, creating a barrier against inflammatory agents.

Platelet-activating factor (PAF) is a potent mediator involved in inflammation and allergic reactions. Considering the range of PAF's actions, which of the following is the MOST comprehensive description of its effects?

PAF selectively activates B lymphocytes, leading to antibody production and enhanced adaptive immunity.
PAF primarily induces vasoconstriction and decreases vascular permeability to limit the spread of inflammation.
PAF causes vasodilation, increased vascular permeability, leukocyte activation, chemotaxis, and degranulation. (correct)
PAF's main role is to inhibit the complement system, preventing excessive inflammatory responses.

How does procalcitonin (PCT) specifically aid in calcium regulation and bone remodeling during bacterial infections, particularly in cases of osteomyelitis?

PCT is converted to calcitonin, which inhibits osteoclast activity, helping to regulate bone resorption and maintain bone integrity. (C) Signup and view all the answers

During acute inflammation, how does the transmigration of leukocytes across the vascular wall differ between neutrophils and monocytes, and what implications does this have for their respective roles in the inflammatory response?

Neutrophils transmigrate primarily via paracellular migration, rapidly entering the tissue to combat infection, while monocytes utilize transcellular migration to differentiate within the vessel wall, delaying their entry but enhancing their phagocytic capacity. (A) Signup and view all the answers

Considering the vascular and cellular events in acute inflammation, how does the dynamic interplay between vasodilation, increased vascular permeability, and leukocyte recruitment contribute to the cardinal signs of inflammation—redness, heat, swelling, and pain?

Vasodilation increases blood flow leading to redness and heat; increased permeability causes edema leading to swelling; leukocyte recruitment releases inflammatory mediators, sensitizing nerve endings and causing pain. (C) Signup and view all the answers

In an acute inflammatory response, if a patient's aspirated fluid reveals a high protein concentration and a significant number of leukocytes, what can be inferred about the nature of the fluid and the likely underlying pathological process?

The fluid is exudate, suggesting increased vascular permeability due to an inflammatory process, such as infection or tissue injury. (A) Signup and view all the answers

Which of the following scenarios best illustrates the 'double-edged sword' role of macrophages in chronic inflammation?

Macrophages eliminate a persistent bacterial infection but, in the process, release reactive oxygen species and proteases that cause significant damage to surrounding healthy tissue, exacerbating inflammation. (D) Signup and view all the answers

In the context of chronic inflammation, how do alternatively activated macrophages (induced by IL-4 and IL-13) primarily contribute to the resolution phase?

By promoting angiogenesis and fibroblast proliferation, facilitating tissue repair and extracellular matrix remodeling. (B) Signup and view all the answers

In granulomatous inflammation, what is the primary role of epithelioid macrophages in the formation and maintenance of the granuloma?

Forming a physical barrier that walls off the inciting agent, preventing its dissemination and protecting surrounding tissues. (C) Signup and view all the answers

How does the immune response in leprosy differ between tuberculoid and lepromatous forms, and what accounts for these differences?

Tuberculoid leprosy features well-defined granulomas with few bacteria due to an effective Th1 response, while lepromatous leprosy shows poorly formed granulomas with abundant bacteria due to a weak Th1 response. (B) Signup and view all the answers

Which of the following statements best describes the role of neutrophils in chronic inflammation, particularly in conditions like osteomyelitis?

Neutrophils are recruited to sites of chronic bacterial infection where they release enzymes and reactive oxygen species, contributing to tissue damage and perpetuating inflammation. (C) Signup and view all the answers

What distinguishes the granulomas seen in Crohn's disease from those observed in tuberculosis, and how does this distinction aid in diagnosis?

Crohn's disease granulomas are non-caseating and often located in the bowel wall, whereas tuberculosis granulomas are typically caseating and found in the lungs, assisting in diagnosis. (A) Signup and view all the answers

In sarcoidosis, what is the most significant characteristic of the granulomas that differentiates them from other granulomatous diseases, and what implications does this have for diagnosis?

Sarcoidosis granulomas are non-caseating and often accompanied by hilar lymphadenopathy, which, in the absence of other known causes, raises suspicion for sarcoidosis. (A) Signup and view all the answers

Following an acute inflammatory response in a tissue, what specific cellular and molecular processes determine whether the tissue will undergo complete regeneration versus scar formation?

The activation of local stem cells and their differentiation into parenchymal cells, coupled with the availability of intact extracellular matrix scaffolding. (D) Signup and view all the answers

Hepcidin is crucial in regulating iron metabolism during chronic inflammation. What is the primary mechanism by which hepcidin contributes to anemia of chronic disease (ACD)?

By inducing the degradation of ferroportin, which reduces iron absorption from the gut and iron release from macrophages, limiting iron availability for erythropoiesis. (B) Signup and view all the answers

In the context of liver regeneration after acute injury, what distinct roles do the proliferation of remaining hepatocytes and the activation of progenitor cells play, and under what conditions is each process most critical?

Hepatocyte proliferation primarily occurs in mild to moderate injuries where the extracellular matrix is intact, while progenitor cell activation is dominant in severe injuries with significant matrix disruption. (A) Signup and view all the answers

Defects in tissue repair can lead to chronic wounds. How do abnormal levels or activity of matrix metalloproteinases (MMPs) contribute to the pathogenesis of chronic wounds, such as venous leg ulcers?

By leading to excessive degradation of the extracellular matrix, impairing cell migration and preventing the formation of a stable granulation tissue. (C) Signup and view all the answers

Distinguish fibrosis from normal scarring.

Fibrosis causes significant impairment of organ function. (A) Signup and view all the answers

What role does complement C3a play in triggering histamine release, and how does this contribute to the inflammatory response?

C3a stimulates mast cell degranulation, resulting in the release of histamine and other inflammatory mediators. (D) Signup and view all the answers

Which specific cyclooxygenase (COX) enzyme is predominantly responsible for producing prostaglandins that mediate pain sensitization, and what mechanism does it employ?

COX-2 is primarily induced during inflammation and produces prostaglandins that sensitize nociceptors, leading to hyperalgesia. (C) Signup and view all the answers

Leukotriene B4 (LTB4) is a potent chemotactic agent. By what specific mechanism does LTB4 attract immune cells to the site of inflammation?

Binding to specific G protein-coupled receptors on leukocytes, initiating signaling cascades that promote directed migration. (C) Signup and view all the answers

Tumor necrosis factor alpha (TNF-α) often leads to hypotension and shock in severe inflammation. By what primary mechanism does TNF-α induce these systemic effects?

Causing widespread vasodilation and increasing vascular permeability, leading to fluid loss and reduced blood pressure. (B) Signup and view all the answers

How does Serum Amyloid A (SAA) promote transport of cholesterol, and in what context does this contribute to disease?

By binding to high-density lipoprotein (HDL) and altering its function, which may deliver cholesterol to immune cells or damaged tissues. (C) Signup and view all the answers

How do hereditary angioedema (HAE) and ACE inhibitors both relate to bradykinin, and what clinical symptoms can result?

HAE causes increased bradykinin production due to C1 inhibitor deficiency, while ACE inhibitors decrease bradykinin degradation, both leading to angioedema and cough. (B) Signup and view all the answers

What key role does Factor XII (Hageman factor) play in initiating the kinin cascade?

Activating prekallikrein into kallikrein, which then cleaves HMWK to produce bradykinin. (C) Signup and view all the answers

How do adhesion molecules, selectins and integrins, facilitate leukocyte recruitment during acute inflammation.

Selectins mediate rolling, while integrins mediate tight binding. (B) Signup and view all the answers

In granulomatous diseases, what is the most important distinction between caseating and non-caseating granulomas, and what does this distinction imply about the underlying pathology?

Caseating granulomas exhibit central necrosis and are often found in tuberculosis, while non-caseating granulomas lack this necrosis and are commonly seen in sarcoidosis. (D) Signup and view all the answers

Following ischemic stroke in the brain, what determines whether the damaged neural tissue will undergo glial scarring versus partial neuronal regeneration in the penumbral region?

The activation of microglia and astrocytes in the affected area, which can either promote inflammation and scarring or support neurogenesis. (C) Signup and view all the answers

Which of the following factors primarily determines the extent of fibrinogen production during an acute inflammatory response?

Liver (C) Signup and view all the answers

Which of the following processes helps prevent the formation of clots?

Transferrin (B) Signup and view all the answers

Given the complex interplay between clotting and inflammation, which of the following statements accurately explains Factor VII’s (Hageman factor) interaction with the Kinin-Kallikrein system?

Factor VII directly activates prekallikrein into kallikrein, which then leads to the cleavage of HMWK into bradykinin, amplifying vasodilation and inflammation. (A) Signup and view all the answers

Given the contrasting functions of thromboxane A2 (TXA2) and prostacyclin (PGI2) in regulating platelet aggregation, what mechanism helps regulate hemostasis?

TXA2 promotes, and PGI2 inhibits platelet aggregation (A) Signup and view all the answers

How does the combined effect of vasodilation, increased vascular permeability, and increased expression of endothelial cell adhesion molecules facilitate chemotaxis during inflammation, specifically considering the function of chemokines?

Vasodilation decreases blood flow, while increased permeability and endothelial cell expression enable immune cell extravasation and chemotaxis by chemokines toward the inflammatory site. (D) Signup and view all the answers

Given the overlapping roles of histamine and platelet-activating factor (PAF), what key distinction characterizes PAF's effect on vasodilation and vascular permeability compared to histamine, and why is this significant in pathological conditions?

PAF has stronger vasodilation and vascular permeability effects than histamine, contributing to severe outcomes in allergic reactions and sepsis. (D) Signup and view all the answers

Considering the interplay of cyclooxygenase (COX) enzymes in prostaglandin synthesis, what accounts for the gastroprotective effects of COX-1, and how does selective inhibition of COX-2 impact this balance?

COX-1 synthesizes prostaglandins that stimulate mucus and bicarbonate secretion in the stomach, while selective COX-2 inhibitors reduce inflammation without compromising this protection. (B) Signup and view all the answers

Given the distinct roles of lipoxygenases (LOX) in leukotriene synthesis, how does the inhibition of 5-LOX affect the inflammatory response, specifically in conditions like asthma, compared to the use of leukotriene receptor antagonists?

5-LOX inhibition blocks the synthesis of all leukotrienes, reducing both bronchoconstriction and leukocyte recruitment, while receptor antagonists only block specific leukotrienes, allowing other inflammatory effects to persist. (D) Signup and view all the answers

Considering the role of Tumor Necrosis Factor alpha (TNF-α) in systemic inflammation, which of the following mechanisms best explains how TNF-α contributes to hypotension and shock during severe infections, particularly in sepsis?

TNF-α promotes vasodilation and increases vascular permeability, leading to fluid leakage from blood vessels and reduced blood pressure, culminating in hypotension and potential shock. (C) Signup and view all the answers

Given the complexity of the kinin-kallikrein system, how does Factor XIIa (activated Hageman factor) initiate the kinin cascade, and what is the direct outcome of this activation in the context of inflammation and coagulation?

Factor XIIa activates prekallikrein to kallikrein, which then cleaves HMWK to release bradykinin, initiating vasodilation, increased permeability, and pain, while also activating the clotting cascade. (A) Signup and view all the answers

In cases of severe bacterial infections leading to sepsis, how does procalcitonin (PCT) elevation correlate with disease progression, and what mechanism allows PCT to serve as a more specific marker for bacterial infections compared to other acute phase reactants?

PCT is produced by multiple tissues during bacterial infections and is less influenced by non-infectious inflammatory processes, making it a more specific indicator for bacterial infections and the severity of sepsis. (A) Signup and view all the answers

Given the contrasting roles of positive and negative acute phase reactants during inflammation, how does the decrease in albumin levels contribute to edema, and what is the underlying mechanism that links reduced albumin synthesis to changes in vascular fluid dynamics?

Reduced albumin synthesis lowers plasma oncotic pressure, causing fluid to shift from the intravascular space into the interstitial space, resulting in edema due to increased hydrostatic pressure. (C) Signup and view all the answers

Considering the role of hepcidin in iron metabolism during chronic inflammation, what is the primary mechanism by which elevated hepcidin leads to anemia of chronic disease (ACD), and how does this affect iron availability for both the host and invading pathogens?

Elevated hepcidin binds to ferroportin, causing its internalization and degradation, which inhibits iron release from macrophages and enterocytes, thus reducing iron availability for erythropoiesis and limiting iron access to pathogens. (D) Signup and view all the answers

Given the importance of leukocyte recruitment in acute inflammation, how does the combined effect of vasodilation, increased vascular permeability, and increased expression of endothelial cell adhesion molecules facilitate chemotaxis, specifically considering the function of chemokines?

Vasodilation slows blood flow, enabling leukocytes to marginate and bind to adhesion molecules, while increased vascular permeability allows chemokines to create a concentration gradient that guides leukocytes to the site of injury. (C) Signup and view all the answers

Following an acute inflammatory response in a tissue, what specific cellular and molecular processes determine whether the tissue will undergo complete regeneration versus scar formation, and how do these processes differ in labile, stable, and permanent tissues?

Complete regeneration relies on the survival of the extracellular matrix (ECM) scaffold and the proliferative capacity of resident cells, which is high in labile tissues, moderate in stable tissues, and absent in permanent tissues, whereas scar formation occurs when the ECM is destroyed and replaced by collagen. (D) Signup and view all the answers

Given the complex interplay between clotting and inflammation, which of the following statements accurately explains the connection between Hageman factor (Factor XII) and the Kinin-Kallikrein system, and what are the implications for vascular permeability and pain?

Hageman factor initiates the intrinsic coagulation pathway and activates prekallikrein to kallikrein, which then cleaves high-molecular-weight kininogen (HMWK) to bradykinin, increasing vascular permeability and causing pain. (D) Signup and view all the answers

Granulomatous diseases are characterized by distinct immune responses. Which of the following statements accurately describes the immune cell composition and functional differences between caseating and non-caseating granulomas, and what implications do these differences have for disease progression?

Caseating granulomas feature amorphous, necrotic centers indicative of cell-mediated immunity against intracellular pathogens, while non-caseating granulomas lack this necrosis and often form in response to non-degradable foreign substances or dysregulated immune responses. (B) Signup and view all the answers

Considering the multiple roles of macrophages in chronic inflammation, how do classically activated macrophages (M1) and alternatively activated macrophages (M2) contribute differently to the progression or resolution of chronic inflammatory conditions involving fibrosis?

M1 macrophages produce high levels of pro-inflammatory cytokines, leading to tissue destruction and perpetuating the inflammatory cycle, while M2 macrophages promote tissue repair via collagen synthesis and angiogenesis, which can contribute to fibrosis if unregulated. (B) Signup and view all the answers

Given the complexity of tissue repair mechanisms, how does the balance between matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) affect the progression of chronic wounds, and what therapeutic strategies can be employed to restore this balance?

Abnormal MMP activity in chronic wounds leads to excessive degradation of extracellular matrix (ECM) components, impairing tissue remodeling and angiogenesis, which can be addressed by using MMP inhibitors and promoting TIMP expression. (D) Signup and view all the answers

Following ischemic stroke in the brain, what molecular and cellular factors determine whether the damaged neural tissue in the penumbral region will undergo glial scarring versus partial neuronal regeneration, and how can these factors be therapeutically manipulated?

Glial scarring results from the activation of astrocytes and the deposition of extracellular matrix (ECM) proteins, inhibiting axonal growth, while neuronal regeneration is facilitated by neurotrophic factors, stem cell differentiation, and ECM remodeling. (B) Signup and view all the answers

In the context of infections with Mycobacterium tuberculosis (TB), what specific aspects of the immune response lead to the formation of caseating granulomas, and how do these necrotic structures contribute to either controlling or exacerbating the infection?

Caseating granulomas are formed due to the combined effects of persistent macrophage activation, T cell-mediated cytotoxicity, and the release of lytic enzymes, leading to intracellular killing of the bacteria that releases mycobacterial lipids that result in central necrosis. (C) Signup and view all the answers

Given the importance of cytokines in chronic inflammation, how do the actions of IL-1, IL-6, and TNF-α synergistically perpetuate inflammation and tissue damage in rheumatoid arthritis (RA), and what signaling pathways are most critical in mediating these effects?

IL-1, IL-6, and TNF-α promote the production of autoantibodies and the activation of T cells, fostering the release of proteases that degrade cartilage and bone in joints, mediated by NF-κB and JAK-STAT pathways. (C) Signup and view all the answers

Considering the different types of tissue and their regenerative capacities, what is the primary mechanism by which the liver is able to regenerate after partial hepatectomy, and which cell types are most critical in this regeneration process?

The liver regenerates by the proliferation of remaining mature hepatocytes and the activation of hepatic progenitor cells (also known as oval cells), stimulated by growth factors (HGF and TGF-α) and cytokines. (D) Signup and view all the answers

Given the various causes of chronic inflammation, how does prolonged exposure to silica particles induce pulmonary fibrosis, and what role do macrophages play in this pathological process?

Silica particles are phagocytosed by macrophages, leading to their activation and the release of pro-inflammatory and pro-fibrotic mediators, such as TGF-β, which stimulates fibroblast proliferation and collagen production in the lungs. (C) Signup and view all the answers

Following tissue injury, what specific interactions between growth factors, cytokines, and extracellular matrix (ECM) components drive the process of angiogenesis, and how are these interactions dysregulated in chronic wounds?

Angiogenesis is driven by increased expression of ECM by fibroblasts and activation of VEGF, and it increases levels of HIF-1α, which increases the release of MMP to remodel perivascular ECM proteins and stimulate capillary sprouting only in areas where the inflammation response is activated. (D) Signup and view all the answers

Flashcards

Histamine

A protein found in mast cells, basophils, and platelets that causes vasodilation, increased vascular permeability, and endothelial activation.

Prostaglandins

Proteins produced by mast cells and leukocytes that cause vasodilation, pain, and fever.

Leukotrienes

Proteins secreted by mast cells and leukocytes that cause increased vascular permeability, chemotaxis, leukocyte adhesion, and activation.

Cytokines (TNF, IL-1, IL-6)

Cytokines produced by macrophages, endothelial cells, and mast cells that cause endothelial activation locally and fever, metabolic abnormalities, and hypotension systemically.