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
TYPE 1- Mechanism:
•Initiated by allergen exposure
•Immune components include: IgE antibodies, mast cells, basophils
•Process: First exposure: allergen stimulates B-cells to produce IgE. IgE
binds to FceRI receptors on mast cells/basophils (sensitization). Re-exposure:
cross-linking of IgE which causes mast cell degranulation. Release of histamine,
prostaglandins, leukotrienes that leads to inflammation
-Onset: rapid (minutes after exposure)
TYPE 2- ·Mechanism:
• Initiated by: IgG or IgM antibodies binding to antigens on host cell
surfaces
, ·Onset: hours to days
TYPE 3- Mechanism: ·Initiated by: Formation of antigen-antibody (IgG or IgM)
complexes in circulation
-Onset: can vary depending on the type and amount of antigen exposed to
TYPE 4- Mechanism: Initiated by: T-cell mediated immune response (CD4+ or
CD8+), No antibody involvement, Activation of macrophages and cytotoxic T-cells
leads to inflammation and cell death
-Onset: 48-72 hours after exposure
• Prototype diseases that reflect each of the four types of hypersensitivity (i.e.
Type IV-contact dermatitis) and signs and symptoms
-TYPE 1: anaphylaxis, allergic rhinitis, asthma, urticaria (hives), eczema
-TYPE 2: hemolytic anemia, graves disease, Myasthenia gravis
-TYPE 3: SLE, post streptococcal glomerulonephritis, serum sickness, arthus
reaction
-TYPE 4: contact dermatitis, tuberculin skin test, type 1 DM
• Treatment options for diseases under each hypersensitivity category
-TYPE 1: Avoidance of allergen, Antihistamines, Corticosteroids, Epinephrine,
Desensitization immunotherapy
-TYPE 2:
-TYPE 3:
-TYPE 4:
• Pathophysiology of Human Immunodeficiency Virus (HIV)
- an RNA retrovirus that primarily infects and destroys CD4+ helper T cells (although
it can also infect macrophages and dendritic cells). Retroviruses like HIV use
reverse transcriptase, allowing the virus to copy RNA into DNA and replicate inside
the host’s cells. The attack on CD4+ helper T cells decreases CD4+ levels, leading to
a deficient immune response.
• Pathophysiology of Systemic Lupus Erythematosus (SLE)
- one of the most common, complex, and serious of the autoimmune disorders. It
can affect any organ in the body. SLE is characterized by the production of a large
variety of antibodies (autoantibodies) against self-antigens, including nucleic acids,
erythrocytes, coagulation proteins, phospholipids, lymphocytes, platelets, and
many other self-components.
• Diagnosis of SLE, including autoantibodies involved
, - antinuclear antibody (ANA) lab test, thorough medical history, full physical exam
• Clinical symptoms of SLE
- fatigue, fever, weight loss, musculoskeletal system (joint pain, swelling, muscle
weakness), integumentary system (rash, photosensitivity, lesions), renal system
(lupus nephritis and proteinuria), hematologic system (pancytopenia), neurologic
system (headache, seizure, inflammation), and cardiovascular system
(inflammation, atherosclerosis
• Treatment options for SLE including treatment during flare-ups
- •Medications: Nonsteroidal Anti-Inflammatory Drugs (NSAIDs), Corticosteroids,
Immunosuppressive agents, Antimalarials, Biologics
•Lifestyle and support: Regular monitoring, Sun protection, Healthy lifestyle
• Alloimmune phenomenon
- occurs when the immune system of one individual produces an immunologic
reaction against tissues of another individual. Alloantigens (isoantigens) are
nonself-antigens from members of the same species. No two individuals have
exactly the same antigens on their tissues; therefore the introduction of one
individual’s tissues and cells into another will result in a strong immune response to
the foreign antigens. Alloimmunity can be observed during immunologic reactions
to blood transfusions, fetal tissues, or transplanted tissue.
• Differentiation between primary and secondary immunodeficiency including
causes
- Primary (congenital) immune deficiency is caused by a genetic defect, whereas
secondary (acquired) immune deficiency is caused by another condition, such as
cancer, infection, or normal physiologic changes, such as aging
• Common variable immunodeficiency
- the most common symptomatic primary immune deficiency. There are two peak
ages of onset, one before the age of 10 and another between 30 and 40 years of age.
As the name implies, the presentation is very heterogeneous. It is characterized by
hypogammaglobulinemia, but the particular class of antibody that is decreased
varies. Although B-cell numbers are normal, most individuals have low amounts of
IgG, which may or may not be accompanied by decreased levels of IgA and IgM.
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
TYPE 1- Mechanism:
•Initiated by allergen exposure
•Immune components include: IgE antibodies, mast cells, basophils
•Process: First exposure: allergen stimulates B-cells to produce IgE. IgE
binds to FceRI receptors on mast cells/basophils (sensitization). Re-exposure:
cross-linking of IgE which causes mast cell degranulation. Release of histamine,
prostaglandins, leukotrienes that leads to inflammation
-Onset: rapid (minutes after exposure)
TYPE 2- ·Mechanism:
• Initiated by: IgG or IgM antibodies binding to antigens on host cell
surfaces
, ·Onset: hours to days
TYPE 3- Mechanism: ·Initiated by: Formation of antigen-antibody (IgG or IgM)
complexes in circulation
-Onset: can vary depending on the type and amount of antigen exposed to
TYPE 4- Mechanism: Initiated by: T-cell mediated immune response (CD4+ or
CD8+), No antibody involvement, Activation of macrophages and cytotoxic T-cells
leads to inflammation and cell death
-Onset: 48-72 hours after exposure
• Prototype diseases that reflect each of the four types of hypersensitivity (i.e.
Type IV-contact dermatitis) and signs and symptoms
-TYPE 1: anaphylaxis, allergic rhinitis, asthma, urticaria (hives), eczema
-TYPE 2: hemolytic anemia, graves disease, Myasthenia gravis
-TYPE 3: SLE, post streptococcal glomerulonephritis, serum sickness, arthus
reaction
-TYPE 4: contact dermatitis, tuberculin skin test, type 1 DM
• Treatment options for diseases under each hypersensitivity category
-TYPE 1: Avoidance of allergen, Antihistamines, Corticosteroids, Epinephrine,
Desensitization immunotherapy
-TYPE 2:
-TYPE 3:
-TYPE 4:
• Pathophysiology of Human Immunodeficiency Virus (HIV)
- an RNA retrovirus that primarily infects and destroys CD4+ helper T cells (although
it can also infect macrophages and dendritic cells). Retroviruses like HIV use
reverse transcriptase, allowing the virus to copy RNA into DNA and replicate inside
the host’s cells. The attack on CD4+ helper T cells decreases CD4+ levels, leading to
a deficient immune response.
• Pathophysiology of Systemic Lupus Erythematosus (SLE)
- one of the most common, complex, and serious of the autoimmune disorders. It
can affect any organ in the body. SLE is characterized by the production of a large
variety of antibodies (autoantibodies) against self-antigens, including nucleic acids,
erythrocytes, coagulation proteins, phospholipids, lymphocytes, platelets, and
many other self-components.
• Diagnosis of SLE, including autoantibodies involved
, - antinuclear antibody (ANA) lab test, thorough medical history, full physical exam
• Clinical symptoms of SLE
- fatigue, fever, weight loss, musculoskeletal system (joint pain, swelling, muscle
weakness), integumentary system (rash, photosensitivity, lesions), renal system
(lupus nephritis and proteinuria), hematologic system (pancytopenia), neurologic
system (headache, seizure, inflammation), and cardiovascular system
(inflammation, atherosclerosis
• Treatment options for SLE including treatment during flare-ups
- •Medications: Nonsteroidal Anti-Inflammatory Drugs (NSAIDs), Corticosteroids,
Immunosuppressive agents, Antimalarials, Biologics
•Lifestyle and support: Regular monitoring, Sun protection, Healthy lifestyle
• Alloimmune phenomenon
- occurs when the immune system of one individual produces an immunologic
reaction against tissues of another individual. Alloantigens (isoantigens) are
nonself-antigens from members of the same species. No two individuals have
exactly the same antigens on their tissues; therefore the introduction of one
individual’s tissues and cells into another will result in a strong immune response to
the foreign antigens. Alloimmunity can be observed during immunologic reactions
to blood transfusions, fetal tissues, or transplanted tissue.
• Differentiation between primary and secondary immunodeficiency including
causes
- Primary (congenital) immune deficiency is caused by a genetic defect, whereas
secondary (acquired) immune deficiency is caused by another condition, such as
cancer, infection, or normal physiologic changes, such as aging
• Common variable immunodeficiency
- the most common symptomatic primary immune deficiency. There are two peak
ages of onset, one before the age of 10 and another between 30 and 40 years of age.
As the name implies, the presentation is very heterogeneous. It is characterized by
hypogammaglobulinemia, but the particular class of antibody that is decreased
varies. Although B-cell numbers are normal, most individuals have low amounts of
IgG, which may or may not be accompanied by decreased levels of IgA and IgM.
