The PATH 3610: Principles of Disease Quiz assesses knowledge on the mechanisms of inflammation, focusing on processes like vascular permeability, neutrophil activity, and the role of fibrinogen. It is ideal for students preparing for medical exams, enhancing understanding of disease pathology.
Diapedesis
Phagocytosis
Margination
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Enlarged endothelial pores
Digestive enzymes
Increased phagocytic ability
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True
False
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It is an insoluble polymer
It is one of the constituents of scar tissue
It is formed from fibrinogen, through the action of thrombin
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Phagocytosis of microorganisms
Secretion of complement components
Production of endogenous pyrogen
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Reflex neural mechanisms
The effects of kinins
Release of chemical mediators by damaged cells
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Monocyte
Plasma cell
Macrophage
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True
False
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Emesis
Diapedesis
Chemotaxis
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True
False
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Albumin
Plasma proteins
Antibody
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Passive immunity
The secondary immune response
The primary immune response
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Anergy
Self tolerance
Immunogenicity
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Spleen and tonsils
Peripheral lymph nodes
Thymus and bone marrow
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The B cell response to antigen
The T cell response to antigen
Both of the above
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Are found only in certain tissues of the body
Secrete cytokines which can influence both T and B cell function
Express immunoglobulins on their surfaces
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Reactive
Edematous
Hypertrophic
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Humoral immunity
Cell-mediated immunity
Macrophage function
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Serum chemistry
The body reaction to infectious disease
Antigen-antibody reactions in a laboratory setting
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Antigens
Haptens
Pathogens
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Bound to mast cell surfaces
Directed against specific antigens on cell surfaces
Bound to antigen to form free immune complexes
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Excessive lymphocyte clonal deletion during embryonic development
Excessive suppressor T-cell activity
Reaction against slightly altered tissue components
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Role as a defense mechanism
Specificity
Ability to fight infectious disease
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True
False
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Specific antibody production occurs more rapidly
Peak antibody levels are earlier and lower
higher levels of IgM are produced
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Mast cell degranulation and mediator release
Smooth muscle contraction
The development of vasoconstriction
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True
False
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Immediate hypersensitivity
Delayed type hypersensitivity
Complement activation
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True
False
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Blood poisoning with toxins
Spread of bacteria and their toxins via the bloodstream
Bacterial toxins in the bloodstream
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Arachidonic acid metabolites
Vasoactive amines (histamine and serotonin)
Cytokines
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True
False
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Enhanced
Nonspecific
Decreased
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Opsonization
Phagocytosis
Exocytosis
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Hyperemia
Congestion
Erythema
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Become plasma cells and begin secreting antibody
Undergo clonal expansion to produce a large number of plasma cells
Produce cytokines to recruit more B cells
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Both helper and cytotoxic T cells
CD8+ cells
CD4+ cells, macrophages and dendritic cells in lymph nodes
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Antibodies on the T cell surface
The T cell receptor
Macrophage presentation of the antigen
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Inflammatory response
Immune response
Innate defense mechanisms
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T Cells
B Cells
Macrophages
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Complement
Opsonins
Immune complexes
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Result from both radiation and chemotherapy, due to injury to neutrophils
Result from therapy with corticosteroids
Increase the risk of hypersensitivity reactions
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Macrophages
Dendritic cells
Natural killer cells
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Fibrinoid necrosis of small vessels (necrotizing vasculitis)
Complement activation
Deposition of immune complexes in vessel walls
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The Arthus reaction
The tuberculin reaction
Transplant rejection
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Neutrophil
Lymphocyte
Macrophage
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Similar cell types
Lower albumin levels
Greater numbers of cells
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Formation of pus
increased movement of fluid and proteins out of vessels due to increased permeability
Collection of fluid in body cavities
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