nr_507_midterm_exam question and answers

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NR 507 MIDTERM EXAM / NR507 ADVANCED
PATHOPHYSIOLOGY MIDTERM EXAM|| ALL
QUESTIONS AND 100% CORRECT ANSWERS
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VERSION 2024-2025 WITH VERIFIED SOLUTIONS||
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Primary immunodeficiency - ANSWER: -less common and occur in result of
single gene defects (defect on the development of the immune system)
-this could involve antibody deficiencies, B- and T- cell deficiencies, defects in the
phagocytic cells and deficiency of complement
-something is lacking with the immune system


Ex: B-lymphocyte deficiency is one of the most common forms of primary
immunodeficiency


Examples of primary immunodeficiency - ANSWER: -Chronic Granulomatous
Disease of Childhood
-DiGeorge Syndrome
-Familial Mediterranean fever
-Job Syndrome
-Common Variable Immunodeficiency


Secondary Immunodeficiency - ANSWER: -conditions where the immune system
becomes compromised because of a complication of some other physiological
condition or disease
-can be caused by cancer, effect from a drug (chemotherapeutic agents that
suppress immune system), and infections that compromise the immune system

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Ex: Patient with HIV gets pneumocystis carinii


What is is a predominant cause of secondary immune deficiencies worldwide? -
ANSWER: -malnutrition


Examples of secondary immunodeficiency - ANSWER: -Pneumocystis Carinii
-HIV
-PNA
-Sinus infection
-Lung cancer


Hypersensitivity Type I - ANSWER: - allergic reaction
-mediated by IgE
-mast cells are the primary effector cells involved
-inflammation due to mast cell degranulation


Hypersensitivity Type I symptoms - ANSWER: Local: itching, rash
Systemic: wheezing


Hypersensitivity Type I example - ANSWER: Most dangerous form: anaphylactic
reaction -> systemic response -> hypertension -> severe bronchoconstriction


Treatment: epinephrine reverses the effects


Hypersensitivity Type II - ANSWER: -cytotoxic reaction

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-tissue/organ specific
-macrophages are primary effector cells involved
-can cause tissue damage or alter function


Mechanism: Tissue-specific destruction or impairment because of:
1. Antibody binding followed by lysis via complement
2. Antibody binding followed by macrophage phagocytosis
3. Antibody binding followed by neutrophil destruction
4. Antibody-dependent cell (NK)-mediated cytotoxicity
5. Antireceptor antibodies


Hypersensitivity Type II examples - ANSWER: 1. Grave's disease
(hyperthyroidism): altering thyroid function, but does not destroy thyroid tissue


2. Incompatible blood type (ABO incompatibility): cell/tissue damage occurs
-severe transfusion reaction -> transfused erythrocytes destroyed by agglutination
or complement-mediated lysis


3. Drug allergies


4. Hemolytic anemia


Graves disease - ANSWER: -Autoantibodies specific for thyroid tissue impair
receptor for TSH


ABO incompatibility - ANSWER: -Complement damages RBC membrane and
cells lyse

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Hypersensitivity Type III - ANSWER: -NOT organ specific
-antibody binds to soluble antigen outside the cell surface that was released into the
blood of body fluids -> complex is then deposited in the tissues
-organ rejection involved cytotoxicity
-antigens from target cells stimulate T-cells to differentiate into cytotoxic T-cells
-neutrophils are the primary effector cells


Raynaud's phenomenon - ANSWER: -Complex deposited in small peripheral
vessels in cool temperatures leading to vasoconstriction and blocked circulation


Hypersensitivity Type III examples - ANSWER: 1. Rheumatoid arthritis:
antigen/antibodies are deposited in the joints


2. Systemic Lupus Erythematosus (SLE): antigen/antibodies deposit in organs that
cause tissue damage


3. Serum sickness


4. Raynaud's phenomenon


Systemic Lupus Erythematosus (autoimmune response) - ANSWER: -facial rash
confined to cheeks (malar rash)
-discoid rash (raised patches, scaling)
-photosensitivity (rash developed as a result to light exposure)
-oral or nasopharyngeal ulcers
-hematologic disorders