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Midterm Study Guide
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- Chamberlain College Of Nursing
This is a midterm study guide for NR507 Advanced Pathophysiology
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NR507 MidtermHypersensitivity
Type 1: allergic reaction, inflammation causes mast cell degeneration, most
dangerous is anaphylactic reaction systemic response (severe
bronchoconstriction and hypotension), caused by IgE autoantibodies
o Local: itching, rash
o Systemic: wheezing
o Within minutes of exposure, IgE antibodies will bind to pollen
releasing histamines to react
Type 2: cytotoxic reaction that is tissue specific (causing damage to the cell
or the function of the cell is altered), macrophages are primarily involved,
caused by IgG or IgM
o Incompatible blood type is an example of cell/tissue destruction that
occurs. Severe transfusion reaction occurs, and the transfused
erythrocytes are destroyed by agglutination or complement-mediated
lysis.
o Grave’s Disease: known as hyperthyroidism, it does not destroy
tissues, but it does alter their function. Autoantibodies or TS1 target
and bind to TSH receptors in which TS1 mimics TSH and fools TS3
and T4 to over work. This happens even in the absence of TSH
Autoantibody Mediated: caused by IgG autoantibodies
targeting TSH receptors
Stimulatory, Not Cytotoxic: Grave’s disease causes cell
overstimulation not lysis
Common Symptoms: increased metabolism, sweating,
tremors, and bulging eyes (exophthalmos)
o Cytotoxic: Rh+ meets Rh- and destroys the RBCs in new pregnancy,
which then cross the placenta
Type 3: Immune responses in which antigen antibody complexes (immune
complexes) form in the blood (refuse to breakdown) and become abnormal,
while depositing in various tissues. Formed by IgG or IgM.
o Leads to inflammation and then tissue damage. They deposit in small
blood vessels, joints, and kidneys
o Common sites of deposition include kidneys, lungs, skin, and joints
o It could be due to foreign proteins or drugs
o Rheumatoid Arthritis: deposited in joints
o SLE: closely related to autoimmunity-antigen/antibodies deposit in
organs and can cause tissue damage.
, Immune complex formation-> tissue deposition-> inflammatory
response (compliment activation= widespread organ
damage)
Flare Ups: symptoms are different for every person, when
symptoms worsen, they are triggered by stress, infection,
sunlight, hormones, or medications. They range from mild to
severe (joint pain, fatigue, skin rashes, kidney issues, fever, or
chest pain. To avoid flare ups, avoid triggers
Management: Medications (NSAIDS (for mild flare up),
corticosteroids (not long term), immunosuppression
(methotrexate and azathioprine to prevent tissue damage),
antimalarials (hydroxychloroquine), biologics (last case).
Lifestyle support (monitor organ function, sun protection, diet,
and rest)
Recognize that signs and symptoms are widespread
o Can be triggered by an illness (like strep), forming immune
complexes, which can then settle in the kidneys, causing reaction
which recruit neutrophils and macrophages to the site
Differences between type 2 and 3
o Type 2: organ specific, antibody binds to the antigen on the cell
surface
o Type 3: NOT organ specific, antibody binds outside the cell surface
and released into the blood or fluids and the complex is then deposited
in the tissue
Alloimmunity: when and individual’s immune system reacts against
antigens or the tissues of other members of the same species
o Neonatal Disease (Rh- to Rh+ blood)
o Transplant rejection
o Transfusion reaction
Type 4: DELAYED response does NOT involve antigen/antibody
complexes like types 1-3. T Cell Mediated
o Treatment of rash: topical corticosteroids, DO NOT use
antihistamines or epinephrine (because type 4 does not have H1
receptors or mast cells)
o Happens 24 to 72 hours after exposure
Differences between type 1 and 4
o Type 1: immediate hypersensitivity reaction, atopic dermatitis and
characterized by widely distributed lesions
o Type 4: contact dermatitis with lesions only on site of contact
, Type Type 1 Type 2 Type 3 Type 4
Mechanism IgE IgG or IgM Immune T-cell-
antibodies antibodies complexes mediated
bind to bind to (antigen- response
allergens, antigens on antibody) against
causing mast cell surfaces, form, deposit antigens in
cell triggering cell in tissues, and tissues,
degranulation destruction activate releasing
and release of complement cytokines and
histamine recruiting
macrophages
Immune IgE, mast IgG, IgM, IgG, IgM, T-cells
Mediators cells, complement, complement, (CD4+,
basophils, phagocytes neutrophils CD8+),
histamine macrophages
Examples - Allergic - Hemolytic - Systemic - Contact
rhinitis (hay anemia lupus dermatitis
fever) erythematosu (e.g., poison
s (SLE) Ivy)
Immunodeficiency
Primary: since birth, genetic deficiency, over 400 types, something is
lacking in the immune system itself. Most are a result of single gene defects.
For example, B-lymphocyte deficiency
Secondary: complication that is acquired, infections (HIV), medications
(immunosuppressants), chronic disease (cancer), malnutrition (most
common cause worldwide). Management: reduce the cause/ symptoms
Common Variable Immunodeficiency (CVI): defect in antibody
production, leads to increased susceptibility to infections. Due to
encapsulated bacteria or viruses
o Impaired antibody response: low levels of IgG, IgM, and IgA
o Symptoms: increased infections (respiratory), chronic diarrhea or GI
issues, RI, lupus, or thrombocytopenia, lymphadenopathy or
splenomegaly
o Management: immunoglobulin replacement (infusions to boost
immunity), antibodies, manage complications, regular follow-ups for
infection and therapy adjustments
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