NR507 – ADVANCED PATHOPHYSIOLOGY MIDTERM
LATEST STUDY GUIDE
Exam 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
o Type I – Immediate (IgE-mediated)
▪ Patho: Allergen → IgE production → binds mast cells → re-
exposure → histamine release
▪ Onset: Minutes
▪ Examples: Anaphylaxis, Allergic Rhinitis
▪ Symptoms: Urticaria, bronchospasm, hypotension
▪ Treatment: Epinephrine, antihistamines, corticosteroids
o Type II – Cytotoxic (antibody-mediated)
▪ Patho: IgG/IgM antibodies target cell surface antigens →
cell destruction
▪ Examples: Hemolytic Anemia, Graves Disease
▪ Symptoms: Depends on organ (e.g., anemia,
hyperthyroidism)
, ▪ Treatment: Immunosuppressants, corticosteroids
o Type III – Immune Complex
▪ Patho: Antigen-antibody complexes deposit in tissues and
create inflammation
▪ Examples: Lupus, Post-streptococcal Glomerulonephritis
▪ Symptoms: Vasculitis, arthritis, nephritis
▪ Treatment: anti-inflammatories, immunosuppressants
o Type IV – delayed (T-cell mediated)
▪ Patho: Sensitized T cells > cytokine release > macrophage
activation
▪ Onset: 24-72 hours
▪ Examples: contact dermatitis, tuberculosis (PPD test)
▪ Treatment: corticosteroids, avoidance of trigger
• Prototype diseases that reflect each of the four types of
hypersensitivity (i.e. Type IV-contact dermatitis) and signs and
symptoms
• Treatment options for diseases under each hypersensitivity category
• Pathophysiology of Human Immunodeficiency Virus (HIV)
o HIV targets CD4+ T helper cells
o Virus enters via gp120 binding, then uses reverse transcriptase
to integrate into host DNA
o Leads to progressive destruction of CD4 cells
o Causes immunosuppression > opportunistic infections
o Key Stages
▪ Acute infection: flu like symptoms
▪ Clinical latency
▪ AIDS (CD4 <200)
• Pathophysiology of Systemic Lupus Erythematosus (SLE)
o Autoimmune disease with loss of self-tolerance
o Production of autoantibodies against nuclear components
o Formation of immune complexes > deposition in tissues
o Causes multisystem inflammation
• Diagnosis of SLE, including autoantibodies involved
o ANA (antinuclear antibody) – sensitive
o Anti-dsDNA – specific, correlates with disease activity
o Anti-Smith antibody – highly specific
o Complement levels (decreased C3, C4)
• Clinical symptoms of SLE
o Malar (butterfly rash)
, o Photosensitivity
o Arthritis
o Renal Involvement (lupus nephritis)
o Fatigue, fever
o Hematologic abnormalities
• Treatment options for SLE including treatment during flare-ups
o Baseline
▪ NSAIDS
▪ Antimalarials (hydroxychloroquine)
o Moderate-Severe
▪ Corticosteroids
▪ Immunosuppressants (methotrexate)
o Flare Ups
▪ High dose corticosteroids
▪ Possible biologics
• Alloimmune phenomenon
o Immune response against antigens from another individual of
the same species
o Examples: blood transfusion reactions, organ transplant
rejections, hemolytic disease of the newborn
• Differentiation between primary and secondary immunodeficiency
including causes
Feature Primary Secondary
Cause Genetic Acquired
Onset Early Life Any age
Example Common Variable HIV, chemo
Immunodeficienc
y
o
• Common variable immunodeficiency
o Patho: impaired B cell differentiation > decreased
immunoglobulins
o Leads to: recurrent infections (Esp respiratory)
o Symptoms: sinusitis, pneumonia, GI infections
o Treatment: IV immunoglobulin (IVIG)
Hematological Pathologies:
• Pathophysiology of microcytic, macrocytic, and normocytic anemias
• Pathophysiology of anemia of chronic disease
LATEST STUDY GUIDE
Exam 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
o Type I – Immediate (IgE-mediated)
▪ Patho: Allergen → IgE production → binds mast cells → re-
exposure → histamine release
▪ Onset: Minutes
▪ Examples: Anaphylaxis, Allergic Rhinitis
▪ Symptoms: Urticaria, bronchospasm, hypotension
▪ Treatment: Epinephrine, antihistamines, corticosteroids
o Type II – Cytotoxic (antibody-mediated)
▪ Patho: IgG/IgM antibodies target cell surface antigens →
cell destruction
▪ Examples: Hemolytic Anemia, Graves Disease
▪ Symptoms: Depends on organ (e.g., anemia,
hyperthyroidism)
, ▪ Treatment: Immunosuppressants, corticosteroids
o Type III – Immune Complex
▪ Patho: Antigen-antibody complexes deposit in tissues and
create inflammation
▪ Examples: Lupus, Post-streptococcal Glomerulonephritis
▪ Symptoms: Vasculitis, arthritis, nephritis
▪ Treatment: anti-inflammatories, immunosuppressants
o Type IV – delayed (T-cell mediated)
▪ Patho: Sensitized T cells > cytokine release > macrophage
activation
▪ Onset: 24-72 hours
▪ Examples: contact dermatitis, tuberculosis (PPD test)
▪ Treatment: corticosteroids, avoidance of trigger
• Prototype diseases that reflect each of the four types of
hypersensitivity (i.e. Type IV-contact dermatitis) and signs and
symptoms
• Treatment options for diseases under each hypersensitivity category
• Pathophysiology of Human Immunodeficiency Virus (HIV)
o HIV targets CD4+ T helper cells
o Virus enters via gp120 binding, then uses reverse transcriptase
to integrate into host DNA
o Leads to progressive destruction of CD4 cells
o Causes immunosuppression > opportunistic infections
o Key Stages
▪ Acute infection: flu like symptoms
▪ Clinical latency
▪ AIDS (CD4 <200)
• Pathophysiology of Systemic Lupus Erythematosus (SLE)
o Autoimmune disease with loss of self-tolerance
o Production of autoantibodies against nuclear components
o Formation of immune complexes > deposition in tissues
o Causes multisystem inflammation
• Diagnosis of SLE, including autoantibodies involved
o ANA (antinuclear antibody) – sensitive
o Anti-dsDNA – specific, correlates with disease activity
o Anti-Smith antibody – highly specific
o Complement levels (decreased C3, C4)
• Clinical symptoms of SLE
o Malar (butterfly rash)
, o Photosensitivity
o Arthritis
o Renal Involvement (lupus nephritis)
o Fatigue, fever
o Hematologic abnormalities
• Treatment options for SLE including treatment during flare-ups
o Baseline
▪ NSAIDS
▪ Antimalarials (hydroxychloroquine)
o Moderate-Severe
▪ Corticosteroids
▪ Immunosuppressants (methotrexate)
o Flare Ups
▪ High dose corticosteroids
▪ Possible biologics
• Alloimmune phenomenon
o Immune response against antigens from another individual of
the same species
o Examples: blood transfusion reactions, organ transplant
rejections, hemolytic disease of the newborn
• Differentiation between primary and secondary immunodeficiency
including causes
Feature Primary Secondary
Cause Genetic Acquired
Onset Early Life Any age
Example Common Variable HIV, chemo
Immunodeficienc
y
o
• Common variable immunodeficiency
o Patho: impaired B cell differentiation > decreased
immunoglobulins
o Leads to: recurrent infections (Esp respiratory)
o Symptoms: sinusitis, pneumonia, GI infections
o Treatment: IV immunoglobulin (IVIG)
Hematological Pathologies:
• Pathophysiology of microcytic, macrocytic, and normocytic anemias
• Pathophysiology of anemia of chronic disease
