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UNMC Patho II exam 2
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UNMC Patho II exam 2
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UNMC Patho II exam 2Immunity - ANS-Function of immune system is to protect body from invasion by foreign
antigens to identify and destroy potentially harmful cells.
Exaggerated immune response - ANS--Against environmental antigens, allergy
-Too much of an IR
Misdirected IR against host's own cell - ANS-Autoimmunity
Isoimmunity - ANS-Directed against beneficial foreign tissues
Body's IS reacts against tissues of usually the same species
-Transplanted tissue
-Blood transfusion
Immune deficiency - ANS-Deficient immune response
Hypersenstivity - ANS--An exaggerated and inappropriate immune response
-A pathologic IR
Autoimmunity - ANS-Breakdown of "code of recognition"
Body's immune system begins to recognize self-antigens as foreign
Development of autoimmune response may be r/t - ANS-Genetics, exposure to antigens
from drugs/infections
Type I hypersenstivity - ANS-IgE mediated allergic reaction/anaphylaxis
Type II hypersensitivity - ANS-Tissue specific, blood transfusion reaction
Type III hypersensitivity - ANS--Immune complex mediated reaction
-AG-AB complexes form and deposit in tissues
Type IV hypersensitivity - ANS-Cell mediated reactions, involve t-cells, macrophages
Allergy/anaphylaxis - ANS-Rapid, immediate hypersensitivity reaction upon re-exposure
to an antigen
Allergy/anaphylaxis systemic reaction - ANS--bronchial constriction
,-Laryngeal edema
-Skin-itching, erythema
-GI-abd cramps, N/V, diarrhea
-Increased secretions from mucus membranes
-Increased vasculature permeability and increased vasodilation
-May see hypovolemic shock
allergy/anaphylaxis is r/t what? - ANS-Release of histamine and leukotrienes
allergy secondary response leads to IgE attaching to mast cell--> - ANS-leads to mast
cell degranulation, capillary vasodilation, and increased capillary permeability
Systemic lupus erythematous(SLE) - ANS--Chronic, autoimmune, multisystem
inflammatory disease
-Type 3 hypersensitivty
-AG-AB comlexes form and deposit in vessel walls
SLE characteristics - ANS-Increased in females
Onset 20-40 years
Genetic predisposition
SLE clinical manifestations - ANS--Arthritis of peripheral joints
-Vasculitis
-Photosensitivty
-Renal disease
-Anemia
-CV disease-pericarditis
Rheumatoid arthritis - ANS-Autoimmune inflammatory joint disease characterized by
destruction of the synovial membrane
-Type 3 and 4 hypersensitivity
-Autoantibodies IgG and IgM
In RA, normal AB become: - ANS-Autoantibodies
-IgM, IgG and attack antigen on cell membrane
Early RA s/s - ANS--Synovitis
-Systemic manifestations of inflammation including fever, weakness, fatigue
Later RA manifestations - ANS--Tenderness, stiff joints
, -Joint pain is better later in the day
RA late manifestations - ANS--Pain
-Deformity
-Loss of function
-Ulnar drift
-Rhematoid nodules
Primary immune deficiences - ANS--Congenital immune deficiencies
-Genetic: immune cells improperly developed
secondary immune deficiencies - ANS--Acquired
-Burns
-Trauma
-Stress
-Physiologic conditions: pregnancy, infancy, elderly, chronic illness, malnutrition
-Iatrogenic: from med tx
The type of hypersensitivity where antigen/antibody complexes form and are deposited
in tissue is what? - ANS-Type 3
Clinical manifestations r/t release of histamine include all of the following except:
a. vomit/diarrhea
b. itching/erythema
c. bronchial dilation
d. increased vasculature permeability - ANS-c. bronchial dilation
-Bronchial constriction actually occurs
Renal failure lab values - ANS--Creatinine increased
-BUN increased
-H+ increased-metabolic acidosis
-Hyponatremia due to Na+ dilution
-Hyperkalemia
-Hyperphosphatemia
-Hypocalcemia
-Anemia due to decreased erythropoetin synthesis
Viral RNA is converted to DNA with help of what 3 enzymes? - ANS--Reverse
transcriptase
-Integrase
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