PATHOLOGY
Inflammation and Repair 203 practice questions · 74 study notes
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Questions QUESTION 161
Which transcription factor increases in response to hypoxia and regulates VEGF production at an injury site?
QUESTION 162
A patient with scurvy has poor wound healing and bleeds easily. Which collagen-related process requires the deficient vitamin as a cofactor?
QUESTION 163
Which cytokine is the most important for synthesis and deposition of connective tissue proteins during scar formation?
QUESTION 164
Which pair constitutes the major components of the basement membrane?
QUESTION 165
A well-apposed surgical skin incision heals by epithelial regeneration with minimal scarring. Which type of healing does this represent?
QUESTION 166
Which molecules mediate cellular attachment to laminin and fibronectin and link the intracellular cytoskeleton to the extracellular environment?
QUESTION 167
Which structural feature is critical for regeneration of epithelial tissue because it provides a scaffold for tissue renewal?
QUESTION 168
During maturation of newly formed capillaries in a healing wound, which cells are recruited alongside the endothelial tubes?
QUESTION 169
Which growth factor is identified as the most important regulator of angiogenesis during tissue repair, stimulating endothelial cell migration and proliferation?
QUESTION 170
Which substances specifically inhibit matrix metalloproteinases during scar remodeling?
QUESTION 171
Which extracellular matrix protein is the major component of both interstitial matrix and scar tissue?
QUESTION 172
At 3 months after a well-sutured skin wound, wound strength may recover to what proportion of normal skin strength?
QUESTION 173
When does remodeling of deposited connective tissue into a stable fibrous scar begin after injury?
QUESTION 174
Which change in collagen type occurs as a healing wound undergoes remodeling?
QUESTION 175
A healing wound contains cells derived from fibroblasts that express smooth muscle actin and pull the wound margins toward the center. Which cells are these?
QUESTION 176
Glucocorticoids may impair postsurgical wound healing by inhibiting production of which cytokine that promotes collagen deposition?
QUESTION 177
Which nutritional deficiency is explicitly associated with inhibited collagen synthesis and delayed wound healing?
QUESTION 178
Reticulin present in early scars is composed of which type of collagen?
QUESTION 179
Which mediators antagonize the inflammatory actions of arachidonic acid metabolites described in the source?
QUESTION 180
Following a serious burn, exaggerated wound contraction causes deformity and restricts joint movement. Which complication has developed?
QUESTION 181
Which material do neutrophils extrude to form extracellular nets that trap and destroy microbes?
QUESTION 182
Which adhesion molecules mediate loose attachment and rolling of leukocytes on endothelium?
QUESTION 183
Which vascular event directly produces edema in acute inflammation?
QUESTION 184
Which cell type is described as abundant in hypertrophic scars?
QUESTION 185
Which cytokine is identified as the major cytokine involved in fibrosis?
QUESTION 186
A localized inflammatory lesion contains pus composed of dead cells, neutrophils, and microbes. What is this lesion called?
QUESTION 187
Which combination accounts for necrosis and failure to heal in diabetic foot ulcers?
QUESTION 188
When injury persists during an acute inflammatory response, what outcome is described?
QUESTION 189
A bedridden patient develops skin ulceration with underlying tissue necrosis where tissue has been compressed against bone for a prolonged period. What is the diagnosis?
QUESTION 190
In the five R's of the inflammatory response, which step immediately follows removal of the injurious agent?
QUESTION 191
Which cells replace neutrophils later in the inflammatory infiltrate and differentiate into macrophages in tissues?
QUESTION 192
A patient's scar grows beyond the boundaries of the original wound and does not regress. What is this lesion called?
QUESTION 193
An elderly patient with severe varicose veins develops a leg ulcer attributed to chronic venous hypertension. Which type of ulcer is this?
QUESTION 194
How do TNF and IL-1 produce fever during inflammation?
QUESTION 195
Which cellular change characterizes granulomatous inflammation?
QUESTION 196
Which tissue is listed as containing continuously dividing cells?
QUESTION 197
A patient develops a cutaneous keloid after wound healing. Which process accounts for this lesion?
QUESTION 198
How does binding of immunoglobulins and acute-phase proteins to red cell membranes increase ESR during inflammation?
QUESTION 199
Which mediator is identified as a potent fibrogenic agent in tissue repair?
QUESTION 200
An injured tissue retains cells capable of proliferation, but its structural framework is damaged and cannot support regeneration. Which repair outcome is expected?
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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