V - Diseases of the Immune System Flashcards
Type of immunity mediated by neutrophils, macrophages and natural killer cells and includes epithelial barriers of the skin, GIT and respiratory tract.
Innate immunity (natural/native)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.108
Type of immunity mediated by lymphocytes and their products, and is normally silent and responds to the presence of microbes by becoming active, expanding and generating potent mechanisms for neutralizing and eliminating microbes.
Adaptive immunity (acquired/specific)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.108
Type of adaptive immunity mediated by soluble antibody proteins that are produced by B lymphocytes. Effective against extracellular microbes.
Humoral immunity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.109
Type of adaptive immunity mediated by T lymphocytes. Designed to combat cell-associated microbes (e.g. Phagocytosed microbes and microbes in the cytoplasm of infected cells).
Cell-mediated or cellular immunity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.109
Results from activation of TH2 CD4+ helper T cells by environmental antigens, leading to the production of IgE antibodies, which become attached to mast cells.
Type I Hypersensitivity (immediate)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Caused by antibodies that bind to FIXED TISSUE AND CELL ANTIGENS and promote phagocytosis and destruction of the coated cells or trigger pathologic inflammation in tissues.
Type II Hypersensitivity (Antibody-mediated)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Caused by antibodies binding to antigens to form COMPLEXES that circulate and may deposit in vascular beds and stimulate inflammation, secondary to complement activation.
Type III Hypersensitivity (immune complex mediated)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Cell-mediated immune responses in which T lymphocytes cause tissue injury, either by producing cytokines that induce inflammation and activate macrophages, or by directly killing cells.
Type IV Hypersensitivity (T-cell mediated/Delayed)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:SLE
Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Multiple sclerosis
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Transplant rejection
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Anaphylaxis
Type I(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Goodpasture syndrome
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Serum sickness
Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Arthus reaction
Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Autoimmune hemolytic anemia
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Allergies
Type I(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Type I DM
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Tuberculosis
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Bronchial asthma
Type I(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Acute rheumatic fever
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Poststreptococcal glumerulonephritis
Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Polyarteritis nodosa
Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Rheumatoid arthritis
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Inflammatory bowel disease
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Tuberculin reaction
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Reactive arthritis
Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Graves disease
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Acute rheumatic fever
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Myasthenia gravis
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Insulin resistant DM
Type II (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Pernicious anemia
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
A special form of graft rejection occuring in the setting where PREFORMED ANTIDONOR ANTIBODIES are present in the circulation of the host before transplant. Occurs within minutes to a few hours after transplantation.
Hyperacute rejection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.133
Rejection which occurs within days to weeks (but may aslo be months or years) of transplantation in a nonimmunosuppressed host. Caused by both cellular and humoral immune mechanisms.
Acute rejection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.133
Acute rejection most commonly seen within the first months after transplantation, typically accompanied by signs of renal failure. Extensive CD4+ and CD8+ T-cell (MONONUCLEAR) infiltration with edema and mild interstitial hemorrhage.
Acute cellular rejection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.133
Acute rejection caused by antidonor antibodies. May take the form of necrotizing VASCULITIS with endothelial cell necrosis, neutrophilic infiltration, deposition of antibody, complement, and fibrin, and thrombosis.
Acute humoral rejection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.133
Rejection which present clinically months to years after transplantation with a progressive rise in serum creatinine levels. Dominated by arteriosclerosis, interstitial fibrosis and loss of renal parenchyma.
Chronic rejection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.133
A multisystem autoimmune disease which principally affects the skin, kidneys, serosal membranes, joints and heart. Associated with autoantibodies including ANAs.
Systemic Lupus Erythematosus(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.139
SOAP BRAIN MD mnemonic for SLE stands for?
SerositisOral ulcersArthritisPhotosensitivityBloodRenal disorderANA positiveImmunologic disorderNeurologic disorderMalar rashDiscoid rash(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.140
How many symptoms must be present in a patient for her/him to be diagnosed as having SLE?
4 out of 11 symptoms(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.140
A systemic, chronic inflammatory disease affecting many tissues but principally attacking the joints to produce a nonsuppurative proliferative synovitis that frequently progress to destroy articular cartilage and underlying bone with resulting disabling arthritis.
Rheumatoid arthritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.145
Characteristic lesion in RA, formed by proliferating synovial-lining cells admixed with inflammatory cells, granulation tissue and fibrous connective tissue.
Pannus(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.146
Cytokine which plays a central role in the pathogenesis of RA.
TNF(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.146
A clinicopathologic entity with a triad of dry eyes, dry mouth and arthritis.
Sjogren syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.148
Characterized by progressive fibrosis involving the skin, GIT and other tissues. May be a result of activation of fibroblasts by cytokines produced by T cells.
Systemic sclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.149
A vascular disorder characterized by reversible vasospasm of the arteries. Typically the hands turn white due to vasospasm, then blue due to cyanosis, then red due to reactive hyperemia.
Raynaud phenomenon(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.151