lOMoARcPSD| 62788957
NR507 – Advanced Pathophysiology
Exam Study Guide – Midterm Study Guide
Exam Format: Noncumulative
Question Type: Multiple Choice
Number of Questions: 100
Time Allotted: 120 minutes
Testing Timeframe: The midterm exam will only be available starting on Wednesday Week
4 at 12:01 am MT until Saturday Week 4 at 11:59 pm MT.
1. Exam Coverage
Content Areas:
• Week 1: Immunological Pathologies
• Week 2: Hematological and Cardiovascular Pathologies
• Week 3: Pulmonary Pathologies
• Week 4: Urinary System Pathologies
2. Key Concepts to Study
Alterations in Immunity and Inflammation:
• Pathophysiology of the four types of hypersensitivity reactions
1. Type 1 Reaction: (hypersensitivity reaction)
a. Immediate and primarily driven by IgE antibodies that sensitize mast cells and
basophils.
b. These cells release proinflammatory mediators like histamine, leukotrienes,
prostaglandins, and cytokines in response to allergen exposure.
c. This results in an allergic reaction, anaphylaxis, or atopic disease.
d. Clinical manifestations: vasodilation (drop in blood pressure), bronchial smooth
muscle contraction (respiratory difficulty), and increased mucus production
(obstructing airways).
2. Type 2 Reaction: (cytotoxic hypersensitivity)
a. Mediated by IgG or IgM antibodies. Antibody binds to antigen on cell surface.
b. Immune reactions against a specific cell or tissue that display self-antigens.
, lOMoARcPSD| 62788957
NR507 – Advanced Pathophysiology
c. This attack is mediated by autoantibodies that recognize these altered antigens
on cell surfaces, a process that can result in the destruction of these cells
through various mechanisms.
d. The clinical symptoms manifest according to the tissue or organ where the
altered antigens are expressed.
e. For example, heparin-induced thrombocytopenia (HIT) is a tissue reaction where
the immune system causes your platelets to clot when introduced to heparin,
which puts a client at risk of developing life-threatening blood clots.
f. Precautions such as blood typing and cross-matching are essential to prevent
cytotoxic reactions during procedures like hemolytic transfusions, where the
compatibility of donor and recipient blood is critical to avoid an immune system
attack on the transfused blood cells.
3. Type 3 Reaction: (immune complex-mediated hypersensitivity)
a. Antibodies bind to soluble antigens in the blood, leading to the formation of
immune complexes and eventually deposit in various tissues or blood.
b. Once deposited, these immune complexes activate the complement system and
attract neutrophils, resulting in tissue damage through inflammatory processes.
This type of reaction is systemic rather than organ-specific, and neutrophils are
the main cells involved in the immune response.
c. One of the hallmark complications of Type III hypersensitivity is the development
of autoimmune diseases (e.g., systemic lupus erythematosus, serum sickness,
or Raynaud phenomenon), where the body's inability to clear the immune
complexes effectively leads to a buildup and consequent inflammatory damage.
4. Type 4 Reaction: (delayed-type hypersensitivity)
a. Mediated by T lymphocytes and macrophages and do not become apparent until
days after exposure to the antigen.
b. Upon encountering the antigen, specific T cells are activated and migrate to the
site where the antigen is then processed and presented, leading to localized
epidermal reactions including redness, cellular infiltration, and vesicle formation.
c. In some instances, T cells and macrophages are unable to eliminate the antigen,
prompting them to confine it by forming a granuloma, a collection of immune cells
meant to isolate the antigen. Multiple granulomas can lead to tissue damage
and organ dysfunction.
, lOMoARcPSD| 62788957
NR507 – Advanced Pathophysiology
d. This mechanism of action is involved in the pathogenesis of certain autoimmune
diseases such as rheumatoid arthritis (RA) and type 1 diabetes mellitus.
• Prototype diseases that reflect each of the four types of hypersensitivity (i.e. Type
IV-contact dermatitis) and signs and symptoms
1. Type 1 reaction:
a. Allergic rhinitis, asthma, angioedema, and anaphylaxis
i. Congestion, itchy eyes, sneezing, runny nose, watery eyes, rash/hives,
wheezing, hypotension, swelling, and difficulty breathing
b. Environmental antigens (pollen, insects, tree nuts, and medications). Allergic
reactions can also occur to foods, latex, animal hair, and pet dander.
2. Type 2 reaction:
a. Autoimmune hemolytic anemia, erythroblastosis fetalis, Myasthenia gravis, and
immune thrombocytopenia
b. Graves' disease
i. Production of autoantibodies targeting the thyroid-stimulating hormone
receptor
ii. Headache, bulging eyes, goiter, palpitations, tachycardia, tremors, N/V,
irregular period, muscle weakness, joint pain, anxiety, and weight loss
c. Blood mismatch
i. Fever, chills, SOB (dyspnea), and aches
3. Type 3 Reaction:
a. Systemic lupus erythematosus (SLE)
i. B- and T-cells become overactive, increasing the production of
autoantibodies and activating the complement system and neutrophils
ii. Symptoms: hair loss, light sensitivity, mouth sores, memory loss, anemia,
blood clotting, fatigue, muscle/joint pain, kidney issues, high blood
pressure, fever, and rash
b. Serum sickness and Raynaud phenomenon (a form of serum sickness)
i. Fever, swelling, achy joints, and rash
c. Rheumatoid Arthritis (RA), Serum Sickness, Post-streptococcal
Glomerulonephritis, and certain vasculitides like Polyarteritis Nodosa and
Henoch-Schönlein Purpura (HSP)
4. Type 4 Reaction:
NR507 – Advanced Pathophysiology
Exam Study Guide – Midterm Study Guide
Exam Format: Noncumulative
Question Type: Multiple Choice
Number of Questions: 100
Time Allotted: 120 minutes
Testing Timeframe: The midterm exam will only be available starting on Wednesday Week
4 at 12:01 am MT until Saturday Week 4 at 11:59 pm MT.
1. Exam Coverage
Content Areas:
• Week 1: Immunological Pathologies
• Week 2: Hematological and Cardiovascular Pathologies
• Week 3: Pulmonary Pathologies
• Week 4: Urinary System Pathologies
2. Key Concepts to Study
Alterations in Immunity and Inflammation:
• Pathophysiology of the four types of hypersensitivity reactions
1. Type 1 Reaction: (hypersensitivity reaction)
a. Immediate and primarily driven by IgE antibodies that sensitize mast cells and
basophils.
b. These cells release proinflammatory mediators like histamine, leukotrienes,
prostaglandins, and cytokines in response to allergen exposure.
c. This results in an allergic reaction, anaphylaxis, or atopic disease.
d. Clinical manifestations: vasodilation (drop in blood pressure), bronchial smooth
muscle contraction (respiratory difficulty), and increased mucus production
(obstructing airways).
2. Type 2 Reaction: (cytotoxic hypersensitivity)
a. Mediated by IgG or IgM antibodies. Antibody binds to antigen on cell surface.
b. Immune reactions against a specific cell or tissue that display self-antigens.
, lOMoARcPSD| 62788957
NR507 – Advanced Pathophysiology
c. This attack is mediated by autoantibodies that recognize these altered antigens
on cell surfaces, a process that can result in the destruction of these cells
through various mechanisms.
d. The clinical symptoms manifest according to the tissue or organ where the
altered antigens are expressed.
e. For example, heparin-induced thrombocytopenia (HIT) is a tissue reaction where
the immune system causes your platelets to clot when introduced to heparin,
which puts a client at risk of developing life-threatening blood clots.
f. Precautions such as blood typing and cross-matching are essential to prevent
cytotoxic reactions during procedures like hemolytic transfusions, where the
compatibility of donor and recipient blood is critical to avoid an immune system
attack on the transfused blood cells.
3. Type 3 Reaction: (immune complex-mediated hypersensitivity)
a. Antibodies bind to soluble antigens in the blood, leading to the formation of
immune complexes and eventually deposit in various tissues or blood.
b. Once deposited, these immune complexes activate the complement system and
attract neutrophils, resulting in tissue damage through inflammatory processes.
This type of reaction is systemic rather than organ-specific, and neutrophils are
the main cells involved in the immune response.
c. One of the hallmark complications of Type III hypersensitivity is the development
of autoimmune diseases (e.g., systemic lupus erythematosus, serum sickness,
or Raynaud phenomenon), where the body's inability to clear the immune
complexes effectively leads to a buildup and consequent inflammatory damage.
4. Type 4 Reaction: (delayed-type hypersensitivity)
a. Mediated by T lymphocytes and macrophages and do not become apparent until
days after exposure to the antigen.
b. Upon encountering the antigen, specific T cells are activated and migrate to the
site where the antigen is then processed and presented, leading to localized
epidermal reactions including redness, cellular infiltration, and vesicle formation.
c. In some instances, T cells and macrophages are unable to eliminate the antigen,
prompting them to confine it by forming a granuloma, a collection of immune cells
meant to isolate the antigen. Multiple granulomas can lead to tissue damage
and organ dysfunction.
, lOMoARcPSD| 62788957
NR507 – Advanced Pathophysiology
d. This mechanism of action is involved in the pathogenesis of certain autoimmune
diseases such as rheumatoid arthritis (RA) and type 1 diabetes mellitus.
• Prototype diseases that reflect each of the four types of hypersensitivity (i.e. Type
IV-contact dermatitis) and signs and symptoms
1. Type 1 reaction:
a. Allergic rhinitis, asthma, angioedema, and anaphylaxis
i. Congestion, itchy eyes, sneezing, runny nose, watery eyes, rash/hives,
wheezing, hypotension, swelling, and difficulty breathing
b. Environmental antigens (pollen, insects, tree nuts, and medications). Allergic
reactions can also occur to foods, latex, animal hair, and pet dander.
2. Type 2 reaction:
a. Autoimmune hemolytic anemia, erythroblastosis fetalis, Myasthenia gravis, and
immune thrombocytopenia
b. Graves' disease
i. Production of autoantibodies targeting the thyroid-stimulating hormone
receptor
ii. Headache, bulging eyes, goiter, palpitations, tachycardia, tremors, N/V,
irregular period, muscle weakness, joint pain, anxiety, and weight loss
c. Blood mismatch
i. Fever, chills, SOB (dyspnea), and aches
3. Type 3 Reaction:
a. Systemic lupus erythematosus (SLE)
i. B- and T-cells become overactive, increasing the production of
autoantibodies and activating the complement system and neutrophils
ii. Symptoms: hair loss, light sensitivity, mouth sores, memory loss, anemia,
blood clotting, fatigue, muscle/joint pain, kidney issues, high blood
pressure, fever, and rash
b. Serum sickness and Raynaud phenomenon (a form of serum sickness)
i. Fever, swelling, achy joints, and rash
c. Rheumatoid Arthritis (RA), Serum Sickness, Post-streptococcal
Glomerulonephritis, and certain vasculitides like Polyarteritis Nodosa and
Henoch-Schönlein Purpura (HSP)
4. Type 4 Reaction:
