1|Page
NR 507 MIDTERM EXAM / NR507 ADVANCED
PATHOPHYSIOLOGY MIDTERM EXAM|| ALL
QUESTIONS AND 100% CORRECT ANSWERS
ALREADY GRADED A+|| LATEST AND COMPLETE
VERSION 2024-2025 WITH VERIFIED SOLUTIONS||
ASSURED PASS!!!
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
,2|Page
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
,3|Page
-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
, 4|Page
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
NR 507 MIDTERM EXAM / NR507 ADVANCED
PATHOPHYSIOLOGY MIDTERM EXAM|| ALL
QUESTIONS AND 100% CORRECT ANSWERS
ALREADY GRADED A+|| LATEST AND COMPLETE
VERSION 2024-2025 WITH VERIFIED SOLUTIONS||
ASSURED PASS!!!
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
,2|Page
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
,3|Page
-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
, 4|Page
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
