NR 507 MIDTERM EXAM / NR507 ADVANCED PATH
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OPHYSIOLOGY MIDTERM EXAM|| ALL QUESTION p p p p
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Primary immunodeficiency - ANSWER: -
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less common and occur in result ofsingle gene defects (defect on the development o
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f the immune system)
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-this could involve antibody deficiencies, B- and T-
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cell deficiencies, defects in thephagocytic cells and deficiency of complement
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-something is lacking with the immune system p p p p p p
Ex: B- p
lymphocyte deficiency is one of the most common forms of primaryimmunodefici
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ency
Examples of primary immunodeficiency - ANSWER: -
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Chronic GranulomatousDisease of Childhood
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-DiGeorge Syndrome p
-Familial Mediterranean fever p p
-Job Syndrome p
-Common Variable Immunodeficiency p p
Secondary Immunodeficiency - ANSWER: - p p p p
conditions where the immune systembecomes compromised because of a complicatio
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n of some other physiological condition or disease
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-
can be caused by cancer, effect from a drug (chemotherapeutic agents that suppress
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immune system), and infections that compromise the immune system
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Ex: Patient with HIV gets pneumocystis carinii
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What is is a predominant cause of secondary immune deficiencies worldwide? -
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ANSWER: -malnutrition
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Examples of secondary immunodeficiency - ANSWER: -Pneumocystis Carinii
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-HIV
-PNA
-Sinus infectionp
-Lung cancer p
Hypersensitivity Type I - ANSWER: - allergic reaction p p p p p p p
-mediated by IgE p p
-mast cells are the primary effector cells involved
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-inflammation due to mast cell degranulationp p p p p
Hypersensitivity Type I symptoms - p p p p
ANSWER: Local: itching, rashSystemic: wheezing
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Hypersensitivity Type I example - p p p p
ANSWER: Most dangerous form: anaphylacticreaction -> systemic response -
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> hypertension -> severe bronchoconstriction
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Treatment: epinephrine reverses the effects
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Hypersensitivity Type II - ANSWER: -cytotoxic reaction p p p p p p
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-tissue/organ specific p
-macrophages are primary effector cells involvedp p p p p
-can cause tissue damage or alter function
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Mechanism: Tissue-specific destruction or impairment because of:
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1. Antibody binding followed by lysis via complement
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2. Antibody binding followed by macrophage phagocytosis
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3. Antibody binding followed by neutrophil destruction
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4. Antibody-dependent cell (NK)-mediated cytotoxicity p p p
5. Antireceptor antibodies p
Hypersensitivity Type II examples - p p p p
ANSWER: 1. Grave's disease (hyperthyroidism): altering thyroid function, but do
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es not destroy thyroid tissue
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2. Incompatible blood type (ABO incompatibility): cell/tissue damage occurs
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-severe transfusion reaction -
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> transfused erythrocytes destroyed by agglutinationor complement-mediated lysis
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3. Drug allergies p
4. Hemolytic anemia p
Graves disease - ANSWER: -
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Autoantibodies specific for thyroid tissue impairreceptor for TSH
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ABO incompatibility - ANSWER: -
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Complement damages RBC membrane andcells lyse
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Hypersensitivity Type III - ANSWER: -NOT organ specific p p p p p p p
-
antibody binds to soluble antigen outside the cell surface that was released into theblo
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od of body fluids -> complex is then deposited in the tissues
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-organ rejection involved cytotoxicity
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-antigens from target cells stimulate T-cells to differentiate into cytotoxic T-cells
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-neutrophils are the primary effector cells p p p p p
Raynaud's phenomenon - ANSWER: - p p p p
Complex deposited in small peripheral vessels in cool temperatures leading to vasoco
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nstriction and blocked circulation p p p
Hypersensitivity Type III examples - p p p p
ANSWER: 1. Rheumatoid arthritis:antigen/antibodies are deposited in the joints
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2. Systemic Lupus Erythematosus (SLE): antigen/antibodies deposit in organs thatc
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ause tissue damage
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3. Serum sickness p
4. Raynaud's phenomenon p
Systemic Lupus Erythematosus (autoimmune response) - ANSWER: -
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facial rashconfined to cheeks (malar rash)
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-discoid rash (raised patches, scaling)
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-photosensitivity (rash developed as a result to light exposure)p p p p p p p p
-oral or nasopharyngeal ulcers
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-hematologic disorders p