NR 507 Edapt Pathophysiology Week 1-4 Exam
2026/2027 Questions And Answers Graded A+
A 25-year-old presents to the emergency department (ED) with symptoms of
ongoing weight loss, rapid heart rate, bilateral neck swelling, and hand tremors.
Family medical history reveals a history of thyroid disorders. Physical examination
and laboratory tests confirm the diagnosis of Graves' disease. Which mechanism
below best explains the pathophysiology of Graves' disease?
A. Delayed-type hypersensitivity response in the thyroid gland
B. Activation of complement proteins leading to tissue damage
C. Production of autoantibodies targeting the thyroid-stimulating hormone receptor
D. Formation of immune complexes in the thyroid tissue
C.
Graves' disease is an example of a type 2 hypersensitivity reaction in which the
immune system produces autoantibodies, particularly IgG antibodies, that bind to
and stimulate the thyroid-stimulating hormone (TSH) receptor on thyroid follicular
cells. This leads to excessive thyroid hormone production, hyperthyroidism, and
the characteristic symptoms observed in the client. Cytotoxic antibodies target
specific cell surface antigens (in this case, the TSH receptor), resulting in cellular
dysfunction rather than cell destruction.
Pathophysiological processes of a type 3 immune complex hypersensitivity into the
correct order.
1. Antibodies bind to antigens
2. Immune complexes form
,3. Complexes deposit in blood vessels or tissues
4. Activation of complement
5. Inflammatory response at the site of deposit
6. Release of lysosomal enzymes and chemical mediators
7. Tissue damage
A client presented to the primary care office with a generalized rash and epidermal
blistering from contact exposure to poison ivy two days ago. What clinical
manifestations should the NP consider to differentiate a type 1 hypersensitivity
rash from a type 4 hypersensitivity rash?
A. Type 1 hypersensitivity rash is usually associated with contact dermatitis, while
the rash in a type 4 hypersensitivity reaction is commonly seen in allergic
reactions.
B. Type 1 hypersensitivity rash is often localized and erythematous, whereas the
rash in type 4 hypersensitivity is generalized and pruritic.
C. Type 1 hypersensitivity rash often involves hives or urticaria, while a delayed
onset, epidermal blistering rash characterizes a type 4 reaction.
D. Type 1 hypersensitivity rash results from T-cell-mediated inflammation,
whereas the rash in a type 4 hypersensitivity reaction is primarily due to the
activation of mast cells
C.
Type 4 hypersensitivity reactions are T cell-mediated delayed hypersensitivity
reactions, have a delayed onset, and the rash is often characterized by epidermal
blistering. T-cells are central in recruiting other immune cells and causing
inflammation in response to an antigen.
Type 1 hypersensitivity reactions typically involve activating mast cells and
basophils, releasing histamine and other inflammatory mediators. This can result in
localized erythema (redness) and the formation of hives or urticaria.
,Characteristics of Systolic HF:
A. Heart failure with ejection fraction ≥ 50%
B. Heart failure with ejection fraction ≤ 40%
C. Pulmonary congestion without cardiomegaly on chest X-ray
D. Pulmonary congestion with cardiomegaly on chest X-ray
E. Increased size of left ventricle
F. Decreased size of left ventricle
G. S3 gallop
H. S4 gallop
B, D, E, G
In a primary care office, a nurse practitioner (NP) assesses a client who reports
taking a new medication 30 minutes before arrival. The NP is concerned that the
client may be having a hypersensitivity reaction. Which clinical manifestations
should the NP expect
Hypertension
Wheezing
Bradycardia
Diaphoresis
Urticaria
Vomiting
Urticaria, wheezing, vomiting, and diaphoresis
Immediate hypersensitivity is mediated by IgE antibodies, which result in an
allergy, anaphylaxis, or atopic disease. The NP should expect the client to have a
type 1 hypersensitivity to recent medication use, which can include these
, immediate reactions as clinical manifestations: urticaria, wheezing, vomiting, and
diaphoresis.
Hypertension and bradycardia are not associated with immediate hypersensitivity
reactions.
____________ are the primary effector cells and responsible for initiating and
mediating _____________ hypersensitivity.
Eosinophils, Neutrophils, Mast cells, or T-cells
Type 1, 2, 3, or 4
Mast cells are the primary effector cells and responsible for initiating and
mediating type 1 hypersensitivity reactions.
Characterized by the rapid release of proinflammatory mediators like histamine,
leukotrienes, and cytokines in response to allergen exposure, mast cells are the
primary effector cells responsible for initiating and mediating type 1
hypersensitivity reactions.
____________ hypersensitivity reactions involve the formation of _____________
that can deposit in tissues, leading to complement activation, inflammation, and
tissue destruction.
Type 1, 2, 3, or 4
IgE, IgM, IgG, immune complexes
Type 3 hypersensitivity reactions involve the formation of immune complexes that
can deposit in tissues, leading to complement activation, inflammation, and tissue
destruction.
2026/2027 Questions And Answers Graded A+
A 25-year-old presents to the emergency department (ED) with symptoms of
ongoing weight loss, rapid heart rate, bilateral neck swelling, and hand tremors.
Family medical history reveals a history of thyroid disorders. Physical examination
and laboratory tests confirm the diagnosis of Graves' disease. Which mechanism
below best explains the pathophysiology of Graves' disease?
A. Delayed-type hypersensitivity response in the thyroid gland
B. Activation of complement proteins leading to tissue damage
C. Production of autoantibodies targeting the thyroid-stimulating hormone receptor
D. Formation of immune complexes in the thyroid tissue
C.
Graves' disease is an example of a type 2 hypersensitivity reaction in which the
immune system produces autoantibodies, particularly IgG antibodies, that bind to
and stimulate the thyroid-stimulating hormone (TSH) receptor on thyroid follicular
cells. This leads to excessive thyroid hormone production, hyperthyroidism, and
the characteristic symptoms observed in the client. Cytotoxic antibodies target
specific cell surface antigens (in this case, the TSH receptor), resulting in cellular
dysfunction rather than cell destruction.
Pathophysiological processes of a type 3 immune complex hypersensitivity into the
correct order.
1. Antibodies bind to antigens
2. Immune complexes form
,3. Complexes deposit in blood vessels or tissues
4. Activation of complement
5. Inflammatory response at the site of deposit
6. Release of lysosomal enzymes and chemical mediators
7. Tissue damage
A client presented to the primary care office with a generalized rash and epidermal
blistering from contact exposure to poison ivy two days ago. What clinical
manifestations should the NP consider to differentiate a type 1 hypersensitivity
rash from a type 4 hypersensitivity rash?
A. Type 1 hypersensitivity rash is usually associated with contact dermatitis, while
the rash in a type 4 hypersensitivity reaction is commonly seen in allergic
reactions.
B. Type 1 hypersensitivity rash is often localized and erythematous, whereas the
rash in type 4 hypersensitivity is generalized and pruritic.
C. Type 1 hypersensitivity rash often involves hives or urticaria, while a delayed
onset, epidermal blistering rash characterizes a type 4 reaction.
D. Type 1 hypersensitivity rash results from T-cell-mediated inflammation,
whereas the rash in a type 4 hypersensitivity reaction is primarily due to the
activation of mast cells
C.
Type 4 hypersensitivity reactions are T cell-mediated delayed hypersensitivity
reactions, have a delayed onset, and the rash is often characterized by epidermal
blistering. T-cells are central in recruiting other immune cells and causing
inflammation in response to an antigen.
Type 1 hypersensitivity reactions typically involve activating mast cells and
basophils, releasing histamine and other inflammatory mediators. This can result in
localized erythema (redness) and the formation of hives or urticaria.
,Characteristics of Systolic HF:
A. Heart failure with ejection fraction ≥ 50%
B. Heart failure with ejection fraction ≤ 40%
C. Pulmonary congestion without cardiomegaly on chest X-ray
D. Pulmonary congestion with cardiomegaly on chest X-ray
E. Increased size of left ventricle
F. Decreased size of left ventricle
G. S3 gallop
H. S4 gallop
B, D, E, G
In a primary care office, a nurse practitioner (NP) assesses a client who reports
taking a new medication 30 minutes before arrival. The NP is concerned that the
client may be having a hypersensitivity reaction. Which clinical manifestations
should the NP expect
Hypertension
Wheezing
Bradycardia
Diaphoresis
Urticaria
Vomiting
Urticaria, wheezing, vomiting, and diaphoresis
Immediate hypersensitivity is mediated by IgE antibodies, which result in an
allergy, anaphylaxis, or atopic disease. The NP should expect the client to have a
type 1 hypersensitivity to recent medication use, which can include these
, immediate reactions as clinical manifestations: urticaria, wheezing, vomiting, and
diaphoresis.
Hypertension and bradycardia are not associated with immediate hypersensitivity
reactions.
____________ are the primary effector cells and responsible for initiating and
mediating _____________ hypersensitivity.
Eosinophils, Neutrophils, Mast cells, or T-cells
Type 1, 2, 3, or 4
Mast cells are the primary effector cells and responsible for initiating and
mediating type 1 hypersensitivity reactions.
Characterized by the rapid release of proinflammatory mediators like histamine,
leukotrienes, and cytokines in response to allergen exposure, mast cells are the
primary effector cells responsible for initiating and mediating type 1
hypersensitivity reactions.
____________ hypersensitivity reactions involve the formation of _____________
that can deposit in tissues, leading to complement activation, inflammation, and
tissue destruction.
Type 1, 2, 3, or 4
IgE, IgM, IgG, immune complexes
Type 3 hypersensitivity reactions involve the formation of immune complexes that
can deposit in tissues, leading to complement activation, inflammation, and tissue
destruction.
