Edapt Pathophysiology Questions Week 1-4 Test Questions with Answers Rated A
1. Characteristics of Systolic HF: B, D, E, G
A. Heart failure with ejection
fraction e50%
B. Heart failure with ejection
fraction d40%
C. Pulmonary congestion with-
out cardiomegaly on chest
X-ray
D. Pulmonary congestion with
cardiomegaly on chest X-ray
E. Increased size of left ventri-
cle
F. Decreased size of left ventri-
cle
G. S3 gallop
H. S4 gallop
2. In a primary care office, a Urticaria, wheezing, vomiting, and diaphoresis
nurse practitioner (NP) assesses Immediate hypersensitivity is mediated by IgE antibodies,
a client who reports taking a which result in an allergy, anaphylaxis, or atopic disease.
new medication 30 minutes be- The NP should expect the client to have a type 1 hypersen-
fore arrival. The NP is concerned sitivity to recent medication use, which can include these
that the client may be having a immediate reactions as clinical manifestations: urticaria,
hypersensitivity reaction. Which wheezing, vomiting, and diaphoresis.
clinical manifestations should Hypertension and bradycardia are not associated with im-
the NP expect mediate hypersensitivity reactions.
Hypertension
Wheezing
Bradycardia
Diaphoresis
Urticaria
Vomiting
, Edapt Pathophysiology Questions Week 1-4 Test Questions with Answers Rated A
3. are the primary ef- Mast cells are the primary ettector cells and responsible for
fector cells and responsible initiating and mediating type 1 hypersensitivity reactions.
for initiating and mediating
hypersensitivity. Characterized by the rapid release of proinflammatory me-
Eosinophils, Neutrophils, Mast diators like histamine, leukotrienes, and cytokines in re-
cells, or T-cells sponse to allergen exposure, mast cells are the primary
Type 1, 2, 3, or 4 ettector cells responsible for initiating and mediating type
1 hypersensitivity reactions.
4. hypersensitivity re- Type 3 hypersensitivity reactions involve the formation of
actions involve the formation immune complexes that can deposit in tissues, leading to
of that can deposit complement activation, inflammation, and tissue destruc-
in tissues, leading to comple- tion.
ment activation, inflammation,
and tissue destruction. Type 3 hypersensitivity reactions involve the formation of
Type 1, 2, 3, or 4 immune complexes that can deposit in tissues, leading to
IgE, IgM, IgG, immune complex- complement activation and inflammation. This process can
es cause tissue damage and is associated with systemic lupus
erythematosus (SLE) and serum sickness.
Type 1 reactions are mediated by IgE antibodies, and type
2 are mediated by IgG or IgM antibodies. Type 4 reactions
are activated by T-helper cells.
5. Highlight the finding(s) the cough, wheezing, SOB, gradual onset, outside, eczema,
nurse practitioner (NP) recog- dog
nizes as risk factors that may
contribute to the client's new di- Allergic rhinitis attacks are related to ongoing exposure to
agnosis of allergic rhinitis. Se- specific ottending agents. The strongest risk factor for de-
lect all that apply. veloping asthma is a history of atopic disease (the client has
eczema, a form of atopic dermatitis). Environmental factors
Camille Rutherford, and allergens—such as high humidity, cold, dry weather,
45-years-old house dust mites, pet fur, and pollen—can place a client at
, Chief Complaint: red, dry, itchy risk for a new diagnosis of allergic asthma.
skin on arms and legs, short- With prior exposure to allergens, Camille was sensitized.
ness of breath, wheezing, and Chronic exposure to allergens mediated IgE antibodies
cough to attach to sensitized cells, and with further exposure,
Medical History: presents with a IgE caused sensitized cells to degranulate. When de-
nonproductive cough, expirato- granulation occurs, inflammatory mediators like histamine,
ry wheezing, and shortness of leukotrienes, and prostaglandins are released to produce
breath upon exertion; reports a several ettects on the body, such as shortness of breath and
gradual onset of these symp- wheezing. Constriction of bronchial smooth muscle also
toms and mentioned that they occurs, which explains her respiratory symptoms: shortness
have been progressively wors- of breath, cough, and wheezing. The NP can diagnose the
ening when walking their dog client with a type I hypersensitivity reaction based on local-
outside ized and systemic symptoms.
Past Medical History: eczema, The client's age and history of hypertension are not risk
hypertension factors.
Social History: lives at home
with daughter and their dog
6. A 25-year-old presents to the C.
emergency department (ED) Graves' disease is an example of a type 2 hypersensitivity re-
with symptoms of ongoing action in which the immune system produces autoantibod-
weight loss, rapid heart rate, bi- ies, particularly IgG antibodies, that bind to and stimulate
lateral neck swelling, and hand the thyroid-stimulating hormone (TSH) receptor on thyroid
tremors. Family medical histo- follicular cells. This leads to excessive thyroid hormone pro-
ry reveals a history of thyroid duction, hyperthyroidism, and the characteristic symptoms
disorders. Physical examination observed in the client. Cytotoxic antibodies target specific
and laboratory tests confirm the cell surface antigens (in this case, the TSH receptor), result-
diagnosis of Graves' disease. ing in cellular dysfunction rather than cell destruction.
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 dam-
age
C. Production of autoantibodies
targeting the thyroid-stimulat-
ing hormone receptor
D. Formation of immune com-
plexes in the thyroid tissue
7. Pathophysiological processes of 1. Antibodies bind to antigens
a type 3 immune complex hy- 2. Immune complexes form
persensitivity into the correct 3. Complexes deposit in blood vessels or tissues
order. 4. Activation of complement
5. Inflammatory response at the site of deposit
6. Release of lysosomal enzymes and chemical mediators
7. Tissue damage
8. A client presented to the pri- C.
mary care office with a gener- Type 4 hypersensitivity reactions are T cell-mediated de-
alized rash and epidermal blis- layed hypersensitivity reactions, have a delayed onset, and
tering from contact exposure to the rash is often characterized by epidermal blistering.
poison ivy two days ago. What T-cells are central in recruiting other immune cells and
clinical manifestations should causing inflammation in response to an antigen.
the NP consider to differentiate Type 1 hypersensitivity reactions typically involve activating
a type 1 hypersensitivity rash mast cells and basophils, releasing histamine and other in-
from a type 4 hypersensitivity flammatory mediators. This can result in localized erythema
rash? (redness) and the formation of hives or urticaria.
A. Type 1 hypersensitivity rash is
usually associated with contact
dermatitis, while the rash in a
type 4 hypersensitivity reaction
1. Characteristics of Systolic HF: B, D, E, G
A. Heart failure with ejection
fraction e50%
B. Heart failure with ejection
fraction d40%
C. Pulmonary congestion with-
out cardiomegaly on chest
X-ray
D. Pulmonary congestion with
cardiomegaly on chest X-ray
E. Increased size of left ventri-
cle
F. Decreased size of left ventri-
cle
G. S3 gallop
H. S4 gallop
2. In a primary care office, a Urticaria, wheezing, vomiting, and diaphoresis
nurse practitioner (NP) assesses Immediate hypersensitivity is mediated by IgE antibodies,
a client who reports taking a which result in an allergy, anaphylaxis, or atopic disease.
new medication 30 minutes be- The NP should expect the client to have a type 1 hypersen-
fore arrival. The NP is concerned sitivity to recent medication use, which can include these
that the client may be having a immediate reactions as clinical manifestations: urticaria,
hypersensitivity reaction. Which wheezing, vomiting, and diaphoresis.
clinical manifestations should Hypertension and bradycardia are not associated with im-
the NP expect mediate hypersensitivity reactions.
Hypertension
Wheezing
Bradycardia
Diaphoresis
Urticaria
Vomiting
, Edapt Pathophysiology Questions Week 1-4 Test Questions with Answers Rated A
3. are the primary ef- Mast cells are the primary ettector cells and responsible for
fector cells and responsible initiating and mediating type 1 hypersensitivity reactions.
for initiating and mediating
hypersensitivity. Characterized by the rapid release of proinflammatory me-
Eosinophils, Neutrophils, Mast diators like histamine, leukotrienes, and cytokines in re-
cells, or T-cells sponse to allergen exposure, mast cells are the primary
Type 1, 2, 3, or 4 ettector cells responsible for initiating and mediating type
1 hypersensitivity reactions.
4. hypersensitivity re- Type 3 hypersensitivity reactions involve the formation of
actions involve the formation immune complexes that can deposit in tissues, leading to
of that can deposit complement activation, inflammation, and tissue destruc-
in tissues, leading to comple- tion.
ment activation, inflammation,
and tissue destruction. Type 3 hypersensitivity reactions involve the formation of
Type 1, 2, 3, or 4 immune complexes that can deposit in tissues, leading to
IgE, IgM, IgG, immune complex- complement activation and inflammation. This process can
es cause tissue damage and is associated with systemic lupus
erythematosus (SLE) and serum sickness.
Type 1 reactions are mediated by IgE antibodies, and type
2 are mediated by IgG or IgM antibodies. Type 4 reactions
are activated by T-helper cells.
5. Highlight the finding(s) the cough, wheezing, SOB, gradual onset, outside, eczema,
nurse practitioner (NP) recog- dog
nizes as risk factors that may
contribute to the client's new di- Allergic rhinitis attacks are related to ongoing exposure to
agnosis of allergic rhinitis. Se- specific ottending agents. The strongest risk factor for de-
lect all that apply. veloping asthma is a history of atopic disease (the client has
eczema, a form of atopic dermatitis). Environmental factors
Camille Rutherford, and allergens—such as high humidity, cold, dry weather,
45-years-old house dust mites, pet fur, and pollen—can place a client at
, Chief Complaint: red, dry, itchy risk for a new diagnosis of allergic asthma.
skin on arms and legs, short- With prior exposure to allergens, Camille was sensitized.
ness of breath, wheezing, and Chronic exposure to allergens mediated IgE antibodies
cough to attach to sensitized cells, and with further exposure,
Medical History: presents with a IgE caused sensitized cells to degranulate. When de-
nonproductive cough, expirato- granulation occurs, inflammatory mediators like histamine,
ry wheezing, and shortness of leukotrienes, and prostaglandins are released to produce
breath upon exertion; reports a several ettects on the body, such as shortness of breath and
gradual onset of these symp- wheezing. Constriction of bronchial smooth muscle also
toms and mentioned that they occurs, which explains her respiratory symptoms: shortness
have been progressively wors- of breath, cough, and wheezing. The NP can diagnose the
ening when walking their dog client with a type I hypersensitivity reaction based on local-
outside ized and systemic symptoms.
Past Medical History: eczema, The client's age and history of hypertension are not risk
hypertension factors.
Social History: lives at home
with daughter and their dog
6. A 25-year-old presents to the C.
emergency department (ED) Graves' disease is an example of a type 2 hypersensitivity re-
with symptoms of ongoing action in which the immune system produces autoantibod-
weight loss, rapid heart rate, bi- ies, particularly IgG antibodies, that bind to and stimulate
lateral neck swelling, and hand the thyroid-stimulating hormone (TSH) receptor on thyroid
tremors. Family medical histo- follicular cells. This leads to excessive thyroid hormone pro-
ry reveals a history of thyroid duction, hyperthyroidism, and the characteristic symptoms
disorders. Physical examination observed in the client. Cytotoxic antibodies target specific
and laboratory tests confirm the cell surface antigens (in this case, the TSH receptor), result-
diagnosis of Graves' disease. ing in cellular dysfunction rather than cell destruction.
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 dam-
age
C. Production of autoantibodies
targeting the thyroid-stimulat-
ing hormone receptor
D. Formation of immune com-
plexes in the thyroid tissue
7. Pathophysiological processes of 1. Antibodies bind to antigens
a type 3 immune complex hy- 2. Immune complexes form
persensitivity into the correct 3. Complexes deposit in blood vessels or tissues
order. 4. Activation of complement
5. Inflammatory response at the site of deposit
6. Release of lysosomal enzymes and chemical mediators
7. Tissue damage
8. A client presented to the pri- C.
mary care office with a gener- Type 4 hypersensitivity reactions are T cell-mediated de-
alized rash and epidermal blis- layed hypersensitivity reactions, have a delayed onset, and
tering from contact exposure to the rash is often characterized by epidermal blistering.
poison ivy two days ago. What T-cells are central in recruiting other immune cells and
clinical manifestations should causing inflammation in response to an antigen.
the NP consider to differentiate Type 1 hypersensitivity reactions typically involve activating
a type 1 hypersensitivity rash mast cells and basophils, releasing histamine and other in-
from a type 4 hypersensitivity flammatory mediators. This can result in localized erythema
rash? (redness) and the formation of hives or urticaria.
A. Type 1 hypersensitivity rash is
usually associated with contact
dermatitis, while the rash in a
type 4 hypersensitivity reaction
