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Pathophysiology: Alterations in Immunity and Inflammation
Terms in this set (46)
What is hypersensitivity?
Altered immunologic response to an antigen that results in disease or damage to the host
What is an allergy?
A deleterious effects of hypersensitivity to nonmicrobial environmental antigens.
A disturbance in the immunologic tolerance of self-antigens.
What is immediate hypersensitivity?
Occurs within minutes to hours after antigen exposure.
What is delayed hypersensitivity?
Onset may be within hours but maximum severity often days after exposure.
What is alloimmunity?
An immune response by one individual producing a reaction against antigens of another individual.
What are the 4 types of hypersensitivity?
Type I immediate hypersensitivity
Type II, antibody-mediated disorders
Type III, Immune-complex mediated
Type IV, Cell-mediated immune disorders.
Type I immediate hypersensitivity, IgE mediated hypersensitivity has the immediate reaction of?
Vasodilation, vascular leakage, smooth muscle spasm, and increased glandular secretion.
Type I immediate hypersensitivity, IgE mediated hypersensitivity is caused by?
A rapid immunologic reaction occurring in a previously sensitized individual triggered by the binding of an antigen to IgE antibody on the surface of mast cells.
Binding of an allergen to an IgE antibody causes mast cells to undergo?
Minute quantities of allergen are injected in increasing doses over a prolonged period of time. What is the mechanism of this Type I desensitization?
May induced IgG blocking antibodies which prevent binding to IgE coated mast cells.
Type 2 hypersensitivity - antibody mediated, tissue specific antigens have 3 stimuli. What are they?
Opsonization and phagocytosis
Complement and Fc (antibody) mediated tissue inflammation
Antibody mediated cellular dysfunction.
What is the mechanism of autoimmune hemolytic anemia?
Group of disorders caused when the immune system misidentifies red blood cells (RBCs) as foreign and creates autoantibodies that attack them.
Goodpasture syndrome and pemphigus vulgaris are what type of hypersensitivity?
Type II - Complement and Fc Receptor Mediated tissue injury
Myasthenia gravis and Graves disease are what type of hypersensitivity?
Type II - Antibody mediated cellular dysfunction.
Myasthenia gravis causes progressive weakness by?
Antibodies to the ACh receptor in a synapse binds and inhibits ACh from binding to the receptor.
Graves disease is caused by?
Antibodies against the TSH receptor prevents negative feedback on the thyroid increasing the release of thyroid hormones.
Systemic lupus erythematosus (SLE), poststreptococcal glomerulonephritis are what type of hypersensitivity?
Type III - Immune complex deposition
What antigen is involved in SLE and where does it like to "plant?"
Nuclear antigens plant in the kidney.
Poststreptococcal glomerulonephritis is caused by what antigen and is planted where?
Streptococcal cell wall antigens become planted in glomerular basement membrane.
In serum sickness various proteins deposit where?
Synovium, blood vessels, and kidney.
RA, MS, and T1DM are what kind of hypersensitivity?
Type IV hypersensitivity - T-cell Mediated
RA clinically causes chronic arthritis with inflammation and cartilage destruction. What is the mechanisms and specificity of pathogenic T-cells?
Mechanism of injury: Th17 cytokines; antibodies, immune complexes
Specificity of pathogenic T-cells: Collagen and citrullinated self proteins.
MS clinically causes demyelination of CNS, muscle weakness, and paralysis. What is the mechanism of injury and specificity of pathogenic T-cells.
Mechanism of injury: Th1 and Th17 cytokines, activated macrophages
Specificity of pathogenic T-cells: Protein antigens in myelin.
T1DM, what is the specificity of pathogenic T-cells and mechanism of injury?
Mechanism of injury: Destruction of islet cells by CTLs
Specificity of pathogenic T-cells: Pancreatic islet B-cells
What is peripheral tolerance?
Mature B and T-cells bind a self antigen in the lymph node. They undergo inactivation (anergy), apoptosis, or suppression by regulatory T-cells.
What is central tolerance?
Immature B and T-cells bind to antigens in the primary lymphoid organs, then under go apoptosis, B-cell receptor editing, or the T-cell becomes regulatory.
What are the mechanism of breaking self tolerance due to an infection?
Infections may upregulated the expression of costimulators on APCs presenting self antigens.
Some microbes may express antigens that have the same amino acid sequence as self antigens.
Innate immunity includes 2 lines of defense: ____ and ____.
Natural barriers; inflammation
Physical, mechanical, and biochemical barriers make up what part of innate immunity?
The inflammatory response (second line of defense), triggers what reactions?
Rapid activation of biochemical and cellular processes that are relatively nonspecific
What are the cardinal signs of inflammation?
Redness (rubor), swelling (tumor), heat (calor), pain (dolor), and loss of function.
The vascular response causes blood vessel dilation, which allows what to happen?
Increased vascular permeability.
WBC adherence to the inner walls of vessels and migration through the vessels (diapedesis).
Heat (calor) and redness (rubor) are local manifestations of inflammation. They are caused by?
Vasodilation and increased blood flow.
Swelling (tumor) is a local manifestation of inflammation. It is caused by?
Exudate accumulations and fluid from capillary permeability.
Pain (dolor) from inflammation is due to?
Pressure exerted by exudate accumulations (swelling), prostaglandins, and bradykinins.
Fever, leukocytosis, and increased plasma protein synthesis are signs of?
Systemic manifestations of inflammation
Fever is caused by exogenous ___ and endogenous ___ like ____.
toxins; pyrogens; cytokines like IL-1 and bradykinin
Leukocytosis increases the number of ___ cells causing a left shift.
What are the acute phase reactants from increased plasma protein synthesis?
CRP, fibrinogen, haptoglobin, amyloid A, and ceruloplasmin
Chronic inflammation is characterized by the presence of ____ and ___ in tissue.
A failure of neutrophils and macrophages to destroy a microorganism like listeria, fungi (histoplasmosis coccidiodomycosis), and acid fast baccili (TB), can result in?
What is the composition and purpose of granulomatous inflammation?
Composed of degenerative cellular debris, lymphocytes, and macrophages in an attempt to "wall off" viable organisms.
What are the two subtypes of granulomatous inflammation?
Noncaseating and caseating
A granuloma that lacks central necrosis is an example of what subtype?
TB and fungal infections causing a granuloma with central necrosis is an example of what subtype?
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