NR 507 MIDTERM EXAM NR 507 MIDTERM EXAM
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NR 507 MIDTERM EXAM / NR507 ADVANCED PATHOPHYSIOLOGY MIDTERM EXAM|| ALL
QUESTIONS AND 100% CORRECT ANSWERS ALREADY GRADED A+|| LATEST AND
COMPLETE VERSION 2026 WITH VERIFIED SOLUTIONS|| ASSURED PASS!!!
Primary immunodeficiency - ANS >> -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 - ANS >> -Chronic Granulomatous
Disease of Childhood
-DiGeorge Syndrome
-Familial Mediterranean fever
-Job Syndrome
-Common Variable Immunodeficiency
Secondary Immunodeficiency - ANS >> -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
,NR 507 MIDTERM EXAM NR 507 MIDTERM EXAM
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Ex: Patient with HIV gets pneumocystis carinii
What is is a predominant cause of secondary immune deficiencies worldwide? -
ANS >> -malnutrition
Examples of secondary immunodeficiency - ANS >> -Pneumocystis Carinii
-HIV
-PNA
-Sinus infection
-Lung cancer
Hypersensitivity Type I - ANS >> - allergic reaction
-mediated by Ige
-mast cells are the primary effector cells involved
-inflammation due to mast cell degranulation
Hypersensitivity Type I symptoms - ANS >> Local: itching, rash Systemic:
wheezing
Hypersensitivity Type I example - ANS >> Most dangerous form: anaphylactic
reaction -> systemic response -> hypertension -> severe bronchoconstriction
Treatment: epinephrine reverses the effects
Hypersensitivity Type II - ANS >> -cytotoxic reaction
,NR 507 MIDTERM EXAM NR 507 MIDTERM EXAM
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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. Interreceptor antibodies
Hypersensitivity Type II examples - ANS >> 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 - ANS >> -Autoantibodies specific for thyroid tissue impair
receptor for TSH
ABO incompatibility - ANS >> -Complement damages RBC membrane and cells
lyse
, NR 507 MIDTERM EXAM NR 507 MIDTERM EXAM
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Hypersensitivity Type III - ANS >> -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 - ANS >> -Complex deposited in small peripheral vessels
in cool temperatures leading to vasoconstriction and blocked circulation
Hypersensitivity Type III examples - ANS >> 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) - ANS >> -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
1|Page
NR 507 MIDTERM EXAM / NR507 ADVANCED PATHOPHYSIOLOGY MIDTERM EXAM|| ALL
QUESTIONS AND 100% CORRECT ANSWERS ALREADY GRADED A+|| LATEST AND
COMPLETE VERSION 2026 WITH VERIFIED SOLUTIONS|| ASSURED PASS!!!
Primary immunodeficiency - ANS >> -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 - ANS >> -Chronic Granulomatous
Disease of Childhood
-DiGeorge Syndrome
-Familial Mediterranean fever
-Job Syndrome
-Common Variable Immunodeficiency
Secondary Immunodeficiency - ANS >> -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
,NR 507 MIDTERM EXAM NR 507 MIDTERM EXAM
2|Page
Ex: Patient with HIV gets pneumocystis carinii
What is is a predominant cause of secondary immune deficiencies worldwide? -
ANS >> -malnutrition
Examples of secondary immunodeficiency - ANS >> -Pneumocystis Carinii
-HIV
-PNA
-Sinus infection
-Lung cancer
Hypersensitivity Type I - ANS >> - allergic reaction
-mediated by Ige
-mast cells are the primary effector cells involved
-inflammation due to mast cell degranulation
Hypersensitivity Type I symptoms - ANS >> Local: itching, rash Systemic:
wheezing
Hypersensitivity Type I example - ANS >> Most dangerous form: anaphylactic
reaction -> systemic response -> hypertension -> severe bronchoconstriction
Treatment: epinephrine reverses the effects
Hypersensitivity Type II - ANS >> -cytotoxic reaction
,NR 507 MIDTERM EXAM NR 507 MIDTERM EXAM
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. Interreceptor antibodies
Hypersensitivity Type II examples - ANS >> 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 - ANS >> -Autoantibodies specific for thyroid tissue impair
receptor for TSH
ABO incompatibility - ANS >> -Complement damages RBC membrane and cells
lyse
, NR 507 MIDTERM EXAM NR 507 MIDTERM EXAM
4|Page
Hypersensitivity Type III - ANS >> -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 - ANS >> -Complex deposited in small peripheral vessels
in cool temperatures leading to vasoconstriction and blocked circulation
Hypersensitivity Type III examples - ANS >> 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) - ANS >> -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
