PATHOLOGY
Inflammation and Repair 200 practice questions · 74 study notes
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Questions QUESTION 81
What structural feature determines the division of chemokines into four groups?
QUESTION 82
Which complement fragments act as opsonins when fixed to a microbial wall?
QUESTION 83
Which cytokine produced by dendritic cells and macrophages increases IFN-g production in chronic inflammation?
QUESTION 84
Which event triggers the classical pathway of complement activation?
QUESTION 85
Generation of biologically active IL-1 depends on activation of which structure?
QUESTION 86
Selective COX-2 inhibitors may increase cardiovascular and cerebrovascular risk through impaired endothelial production of which mediator?
QUESTION 87
How does aspirin inhibit prostaglandin synthesis?
QUESTION 88
Proteolytic cleavage of which complement component is the critical step in complement activation?
QUESTION 89
An individual has an inherited deficiency of the terminal complement components. Disseminated infection with which organism is specifically associated with this deficiency?
QUESTION 90
How do the cytokines listed under acute inflammation contribute to chronic inflammatory reactions?
QUESTION 91
Binding to which molecules enables chemokines to be displayed at high concentrations on endothelial surfaces and in the extracellular matrix?
QUESTION 92
Which cells constitutively produce homeostatic chemokines that help maintain tissue architecture?
QUESTION 93
Which drug inhibits leukotriene production and is useful in treating asthma?
QUESTION 94
Microbial lipopolysaccharide triggers complement activation in the absence of antibody. Which pathway is involved?
QUESTION 95
Histologic examination shows a pink meshwork of fibrin exudate overlying the pericardial surface. What is the diagnosis?
QUESTION 96
Which mediator activates protease-activated receptors expressed on platelets and leukocytes?
QUESTION 97
Inherited deficiency of which complement regulatory protein causes hereditary angioedema?
QUESTION 98
Which histologic finding characterizes the margins of an ulcer during its acute stage?
QUESTION 99
What term denotes accumulation of fluid in a mesothelium-lined body cavity?
QUESTION 100
Which complement regulatory protein directly inhibits formation of the membrane attack complex?
QUESTION 101
What is a stated consequence of inherited deficiencies of complement proteins?
QUESTION 102
A patient develops a skin blister after a burn. Which morphologic pattern of inflammation does the accumulated blister fluid represent?
QUESTION 103
Which vascular effects does platelet-activating factor produce at low concentrations?
QUESTION 104
Which combination constitutes the morphologic hallmarks of acute inflammation?
QUESTION 105
During complete resolution of acute inflammation, which route is mainly responsible for resorption of edema fluid?
QUESTION 106
Following acute inflammation, abundant fibrin exudate in the pleural cavity cannot be fully cleared. Which outcome is expected?
QUESTION 107
Mutations in which complement regulatory protein are associated with both hemolytic uremic syndrome and wet macular degeneration?
QUESTION 108
Which process produces the surface defect characteristic of an ulcer?
QUESTION 109
An acute inflammatory response fails to resolve because the injurious agent persists. Which outcome does this favor?
QUESTION 110
Which complication is often increased in diseases of excessive complement activity, such as hemolytic uremic syndrome and paroxysmal nocturnal hemoglobinuria?
QUESTION 111
Which enzyme cleaves high-molecular-weight kininogen to produce bradykinin?
QUESTION 112
What sustains the chronic immune reaction responsible for tissue damage in autoimmune diseases?
QUESTION 113
Which pair of processes accomplishes replacement of damaged tissue with connective tissue during healing in chronic inflammation?
QUESTION 114
A tissue sample contains macrophages that promote angiogenesis, activate fibroblasts, and stimulate collagen synthesis. Which macrophage phenotype best accounts for these effects?
QUESTION 115
Why do macrophages often become the dominant cell population within 48 hours of the onset of an inflammatory reaction?
QUESTION 116
How are long-lived tissue-resident macrophages such as microglia and Kupffer cells mainly replenished?
QUESTION 117
Which macrophage activity establishes a feedback loop essential for cell-mediated defense against many microbes?
QUESTION 118
Which cells dominate most chronic inflammatory reactions?
QUESTION 119
Which cell population may dominate chronic inflammation in autoimmune and other hypersensitivity diseases?
QUESTION 120
Which combination of effector changes enhances the ability of classically activated macrophages to kill ingested organisms?
Study notes Protective functions of inflammation and acute–chronic progression
Inflammation brings circulating host defenses into vascularized tissues affected by infection or injury, allowing elimination of harmful agents and initiation of repair. →
Cardinal signs, stages, and harmful consequences of inflammation
Inflammation produces recognizable external signs and proceeds through a sequence of defensive and reparative steps. Under some circumstances, the reaction itself causes disease. →
Inflammatory reactions: initiation, tissue injury, and impaired defense
Inflammation begins with recognition of microbes or damaged cells by tissue cells. It contributes to tissue injury in several diseases, while inadequate inflammation increases susceptibility to infection. →
Causes of inflammation and transition to tissue repair
Inflammation may be triggered by infection, tissue necrosis, foreign bodies, or immune reactions. After elimination of the offending agents, repair replaces injured tissue. →
Recognition of microbes and damaged cells in inflammation
Inflammation begins when cellular receptors and circulating proteins recognize microbes or necrotic cells. →
Major components and early vascular changes of acute inflammation
Acute inflammation delivers plasma proteins and leukocytes to sites of infection or tissue injury through coordinated vascular and cellular responses. →
Inflammatory fluid leakage, edema, and stasis
Increased microvascular permeability follows vasodilation and allows protein-rich fluid to enter extravascular tissues. →
Lymphatic responses and initial leukocyte recruitment
Acute inflammation increases lymphatic drainage and recruits circulating leukocytes through a sequence of endothelial interactions and tissue migration. →
Selectins in leukocyte rolling and fluid accumulation mechanisms
Selectins mediate early leukocyte attachment to endothelium. The accompanying fluid-formation material contrasts transudates with inflammatory exudates. →
Exudates, transudates, and leukocyte recruitment
Inflammation increases vascular permeability and recruits leukocytes through a sequence of interactions with the endothelium. →
Leukocyte integrin ligands and the dynamics of rolling
Leukocyte adhesion molecules bind specific endothelial ligands. Weak selectin interactions slow leukocytes so that they can recognize additional adhesion molecules. →
Integrin-mediated firm adhesion of leukocytes
Leukocytes stop rolling and attach firmly to endothelium at sites of inflammation through coordinated activation of leukocyte integrins and endothelial integrin ligands. →
Leukocyte diapedesis, chemotaxis, and early inflammatory infiltrates
After adhering to endothelium, leukocytes cross the vessel wall and follow chemical gradients toward injury. The predominant recruited cell changes with time. →
Evolution and exceptions in inflammatory leukocyte infiltrates
Early neutrophil predominance commonly gives way to longer-lasting macrophage infiltration, but the inflammatory stimulus can alter this pattern. →
Phagocytosis and intracellular destruction of microbes
Recruited neutrophils and monocytes are activated by microbial products, necrotic cells, and local cytokines to destroy microbes and clear dead tissue. →
Functional differences between neutrophils and macrophages
Neutrophils and macrophages share phagocytosis, migration into tissues, and chemotaxis, but differ in origin, longevity, and responses to activation. →
Reactive oxygen and nitrogen species in microbial killing
Activated phagocytes generate destructive oxygen- and nitrogen-derived molecules that damage microbial cellular constituents. →
Phagolysosomal killing and leukocyte granule contents
Phagocytosis brings microbes into intracellular compartments where granule enzymes and reactive oxygen and nitrogen species destroy them. →
Neutrophil extracellular traps and leukocyte-mediated tissue injury
Activated leukocytes destroy microbes but can also injure normal tissues through extracellular release of antimicrobial substances. →
Additional inflammatory cells and subsidence of acute inflammation
Besides neutrophils and macrophages, several immune cell types contribute to inflammatory defense and allergic reactions. →
Sources, activation, and control of inflammatory mediators
Chemical mediators initiate and regulate inflammation. They may originate from local cells or from circulating precursors activated at the inflammatory site. →
Histamine and serotonin as vasoactive mediators
Vasoactive amines are preformed mediators that influence vascular responses during inflammation. →
Arachidonic acid metabolism and prostaglandin production
Arachidonic acid supplies lipid mediators that participate in vascular and cellular reactions of acute inflammation. →
Actions of thromboxane, prostacyclin, leukotrienes, and lipoxins
Arachidonic acid metabolites regulate vascular reactions, platelet aggregation, and leukocyte recruitment; some also suppress inflammation. →
Major inflammatory mediators and pharmacologic inhibition of eicosanoids
Inflammatory mediators have overlapping vascular and leukocyte effects. Drugs targeting eicosanoid synthesis can reduce inflammatory symptoms. →
Corticosteroids, leukotriene receptor antagonists, and cytokines
Inflammatory responses can be reduced by suppressing mediator production or blocking mediator receptors. Cytokines coordinate immune and inflammatory reactions. →
TNF and IL-1: production and leukocyte recruitment
Tumor necrosis factor (TNF) and interleukin-1 (IL-1) promote leukocyte adhesion to endothelium and migration through vessels during inflammation. →
Local and systemic actions of TNF and IL-1
Tumor necrosis factor (TNF) and interleukin-1 (IL-1) support leukocyte recruitment and activation, produce systemic inflammatory responses, and provide therapeutic targets in chronic inflammation. →
Inflammatory cytokines: sources and principal actions
Cytokines coordinate systemic inflammatory responses, leukocyte recruitment, and macrophage activation. Their roles overlap between acute and chronic inflammation. →
Chemokines and other cytokines in acute inflammation
Chemokines direct leukocyte movement during inflammation and maintain the normal anatomical distribution of cells within tissues. →
Complement activation: pathways and convergence on C3
The complement system comprises soluble proteins and membrane receptors involved mainly in antimicrobial defense and pathological inflammatory reactions. →
Complement effector functions and membrane attack complex
Following C3 cleavage, complement activation produces mediators of inflammation, opsonins for phagocytosis, and a membrane attack complex that lyses cells. →
Complement regulation and diseases caused by regulatory defects
Complement regulators protect normal host tissues by limiting active complement fragments and removing deposited fragments. Failure of this protection can cause tissue injury. →
Complement activation, functions, and disease
Complement supports host defense, but its activation on host tissues or inadequate regulation can contribute to disease. →
Other inflammatory mediators: PAF, coagulation receptors, kinins, and neuropeptides
Several additional mediator systems influence vascular responses, platelet activation, pain, and inflammatory signaling, although some of their roles remain uncertain. →
Acute inflammation: morphology and serous exudates
Acute inflammatory reactions share vascular and cellular changes, while their specific morphologic patterns can help identify the underlying cause. →
Fibrinous inflammation, purulent inflammation, and abscesses
Acute inflammation can produce fibrin-rich exudates or pus. The composition and subsequent fate of these exudates determine their morphologic appearance and consequences. →
Morphology of inflammatory exudates, abscesses, and ulcers
Inflammatory lesions differ in their exudates, distribution of tissue necrosis, cellular composition, and subsequent repair. →
Outcomes of acute inflammation and the chronic inflammatory response
Acute inflammation typically ends in resolution, connective tissue replacement, or progression to chronic inflammation. The outcome depends partly on the injury, affected tissue, and host response. →
Causes and disease associations of chronic inflammation
Chronic inflammation can arise from persistent infection, inappropriate immune responses, or prolonged exposure to harmful substances. →
Chronic inflammation: morphology and outcomes
Chronic inflammation combines inflammatory cell infiltration, tissue destruction, and attempts at repair. →
Macrophages: functions, tissue locations, and origins
Macrophages are professional phagocytes with roles in host defense, inflammation, and repair. Their circulating counterparts are monocytes. →
Classical and alternative macrophage activation
Macrophages follow two major activation pathways, classical and alternative, according to the activating signals they receive. →
Macrophage functions and persistence in chronic inflammation
Activated macrophages help eliminate injurious agents and initiate repair, while also causing much of the tissue injury in chronic inflammation. →
Lymphocytes and macrophage populations in chronic inflammation
Lymphocytes amplify chronic inflammation, while macrophages differ in their developmental origins and activation-dependent functions. →
T-cell subsets and lymphocyte–macrophage feedback in chronic inflammation
CD4 T-cell subsets produce distinct cytokines that shape inflammation. Reciprocal interactions between lymphocytes and macrophages sustain chronic inflammatory reactions. →
Tertiary lymphoid organs and other cells in chronic inflammation
Chronic inflammatory reactions may contain organized lymphoid structures, eosinophils, and persistent neutrophilic infiltrates. →
Granulomatous inflammation: formation and morphology
Granulomatous inflammation is a form of chronic inflammation characterized by collections of activated macrophages, often accompanied by T lymphocytes and sometimes central necrosis. →
Evaluation of granulomas and systemic inflammatory responses
Granulomas narrow the possible causes of inflammation, while cytokines can produce systemic reactions even when inflammation is localized. →
Fever, inflammatory leukocytosis, and granulomatous reactions
Systemic inflammatory responses include fever and changes in circulating leukocytes. The target passage also describes granulomatous findings in tuberculosis and leprosy. →
Tissue reactions in selected granulomatous diseases
Granulomatous diseases differ in their causes, inflammatory cell composition, and patterns of necrosis. →
Acute-phase proteins and systemic manifestations of inflammation
Systemic inflammation alters blood cell counts, induces hepatic plasma protein synthesis, and produces metabolic and constitutional effects. →
Septic shock, systemic inflammatory response syndrome, and tissue repair
Severe systemic inflammation can cause widespread abnormalities, while repair restores tissue architecture and function through regeneration and scar formation. →
Proliferative capacity and tissue regeneration
A tissue's ability to repair injury depends partly on the proliferative capacity of its cells and the preservation of its supporting framework. →
Growth signals and stem cells in tissue regeneration
Regeneration combines proliferation of surviving cells with the production of mature cells from stem cells. →
Tissue regeneration and growth factors in repair
Regeneration depends on the tissue involved, its capacity for cell proliferation, and preservation of the supporting tissue structure. →
Repair growth factors and the importance of the liver framework
Growth factors support repair through effects on fibroblasts, keratinocytes, blood vessels, and extracellular matrix. Liver regeneration also depends on preservation of tissue structure. →
Mechanisms of liver regeneration and repair by scarring
The liver regenerates through residual hepatocyte proliferation or stem cell repopulation, with the dominant mechanism determined by the injury. →
Early stages of skin wound healing and granulation tissue
Skin wounds progress through hemostasis, inflammation, and cell proliferation before remodeling produces a fibrous scar. →
Scar remodeling, wound union, and angiogenesis
Later wound repair reorganizes deposited connective tissue, while new vessel formation supports healing and has wider roles in ischemia and tumor growth. →
Angiogenesis and early connective tissue deposition in wound healing
Repair involves new vessel formation, fibroblast recruitment, and deposition of extracellular matrix (ECM), followed by maturation into a scar. →
Extracellular matrix functions, forms, and contribution to fibrosis
The extracellular matrix (ECM) regulates cell behavior and supplies the structural scaffold needed for regeneration. Persistent injury can instead lead to replacement of normal tissue by connective tissue. →
Structural and adhesive proteins of the extracellular matrix
Extracellular matrix (ECM) components provide tensile strength, recoil, resistance to compression, and attachment sites that support wound repair. →
Integrin signaling and fibroblast activity in scar formation
Cells interact with the extracellular matrix (ECM) through integrins. During wound repair, fibroblasts and myofibroblasts migrate, contract the wound, and synthesize connective tissue proteins. →
Collagen accumulation, scar remodeling, and matrix degradation
Scar maturation reflects the balance between extracellular matrix (ECM) synthesis and degradation. Remodeling strengthens the wound while reducing scar size. →
Morphology of healing tissue and factors delaying wound repair
Granulation tissue develops at an injury site and progresses toward a collagen-rich scar. Infection, metabolic disease, nutritional deficiency, and glucocorticoids can interfere with repair. →
Impaired wound healing and chronic ulcers
Local mechanical factors, inadequate perfusion, and foreign material can impair tissue repair. Chronic ulcers illustrate several distinct mechanisms of healing failure. →
Wound dehiscence, excessive scarring, and contractures
Abnormal repair may produce wound rupture, excessive scar tissue, or exaggerated wound contraction. →
Organ fibrosis and the basic inflammatory response
Fibrosis in chronic disease shares mechanisms with cutaneous scar formation. Inflammation coordinates recognition and removal of injury, followed by regulation and repair. →
Acute inflammatory vascular changes and leukocyte recruitment
Inflammation changes vascular flow and permeability and recruits circulating leukocytes into affected tissues through a sequence of endothelial interactions. →
Leukocyte killing, inflammatory mediators, and morphologic patterns
Leukocytes eliminate microbes and debris using mechanisms that can also injure normal tissue. Inflammatory mediators coordinate these responses, which produce recognizable morphologic patterns. →
Chronic inflammation, systemic effects, and tissue regeneration
Persistent inflammatory stimuli produce chronic cellular responses and scarring. Inflammation also has systemic effects, while tissue regeneration depends on the proliferative capacity of surviving cells. →
Scar formation, wound healing, and C-reactive protein
Repair by scarring replaces injured tissue with connective tissue when regeneration cannot occur. The passage also describes factors affecting wound healing and the significance of C-reactive protein in inflammation. →
Mechanism and causes of an elevated erythrocyte sedimentation rate
The erythrocyte sedimentation rate (ESR) increases when red cells aggregate and sediment more rapidly. This passage explains how inflammatory proteins promote aggregation and lists conditions associated with elevated ESR. →
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