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NR507 ADVANCED PATHOPHYSIOLOGY MIDTERM EXAM QUESTIONS & CORRECT ANSWERS GRADED A+||

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NR507 ADVANCED PATHOPHYSIOLOGY MIDTERM EXAM QUESTIONS & CORRECT ANSWERS GRADED A+||

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HOSMERIT



NR507 ADVANCED PATHOPHYSIOLOGY MIDTERM
EXAM QUESTIONS & CORRECT ANSWERS GRADED
A+|| 2024-2025

Primary immunodeficiency - ANSWER: -less common and occur in result ofsingle gene defects
(defect on the development of the immune system)
-this could involve antibody deficiencies, B- and T- cell deficiencies, defects in thephagocytic
cells and deficiency of complement
-something is lacking with the immune system


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


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


Secondary Immunodeficiency - ANSWER: -conditions where the immune systembecomes
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




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, rashSystemic: wheezing

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


Treatment: epinephrine reverses the effects


Hypersensitivity Type II - ANSWER: -cytotoxic reaction


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


Mechanism: Tissue-specific destruction or impairment because of:
- Antibody binding followed by lysis via complement
- Antibody binding followed by macrophage phagocytosis
- Antibody binding followed by neutrophil destruction
- Antibody-dependent cell (NK)-mediated cytotoxicity

, - Antireceptor antibodies


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


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


- Drug allergies


- Hemolytic anemia


Graves disease - ANSWER: -Autoantibodies specific for thyroid tissue impairreceptor for TSH


ABO incompatibility - ANSWER: -Complement damages RBC membrane andcells lyse




Hypersensitivity Type III - ANSWER: -NOT organ specific
-antibody binds to soluble antigen outside the cell surface that was released into theblood 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

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