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 ACID
Hypersensitivity Reactions (ACID)
Hypersensitivity reactions are exaggerated or inappropriate immune responses that result in
tissue damage. They are classified into four types, remembered by the acronym ACID:
1. A – Type I: Allergic / Anaphylactic (Immediate)
2. C – Type II: Cytotoxic
3. I – Type III: Immune Complex-Mediated
4. D – Type IV: Delayed-Type (Cell-Mediated)
1. Type I: Allergic / Anaphylactic Reaction (Immediate)
Pathophysiology:
Triggered by IgE antibodies against harmless antigens (allergens) like pollen, dust mites,
or certain foods.
Sensitization phase:
1. Allergen enters the body.
2. B cells produce IgE, which binds to mast cells and basophils via Fc receptors.
Activation phase (upon re-exposure):
1. Allergen cross-links IgE on mast cells.
2. Mast cells release histamine, leukotrienes, prostaglandins, and other mediators.
Clinical effects:
, o Vasodilation → hypotension
o Increased vascular permeability → edema
o Smooth muscle contraction → bronchospasm
o Typical manifestations: urticaria, asthma, anaphylaxis
Examples:
Anaphylaxis, hay fever, asthma, food allergies.
2. Type II: Cytotoxic Reaction
Pathophysiology:
Mediated by IgG or IgM antibodies directed against antigens on cell surfaces or the
extracellular matrix.
Mechanisms of tissue damage:
1. Complement activation → cell lysis
2. Opsonization → phagocytosis of targeted cells
3. Antibody-dependent cellular cytotoxicity (ADCC) via NK cells
Clinical consequences: destruction of specific cells expressing the antigen.
Examples:
Hemolytic anemia (autoimmune or drug-induced)
Goodpasture syndrome – antibodies against basement membrane of kidney and lungs
Blood transfusion reactions
Graves disease and myasthenia gravis are antibody-mediated, but not cytotoxic in
classic sense—they alter receptor function.
3. Type III: Immune Complex-Mediated Reaction
Pathophysiology:
Occurs when antigen-antibody complexes (IgG or IgM) are deposited in tissues.
Complement activation → recruitment of neutrophils → tissue damage via enzymes and
reactive oxygen species.
Typically affects blood vessels, glomeruli, and joints.
Examples:
Systemic lupus erythematosus (SLE) – immune complex deposition in kidneys, skin,
joints
Post-streptococcal glomerulonephritis
Serum sickness – reaction to foreign proteins or drugs
Arthus reaction – local immune complex-mediated skin reaction
,Key distinction: In type III, tissue damage is indirect, caused by inflammatory response to
immune complexes, not by direct antibody attack on cells.
4. Type IV: Delayed-Type / Cell-Mediated Reaction
Pathophysiology:
T-cell mediated, not antibody-mediated.
CD4+ T helper 1 (Th1) cells recognize antigens and release cytokines (e.g., IFN-γ,
TNF-α).
Cytokines recruit macrophages → tissue damage.
CD8+ cytotoxic T cells may directly kill antigen-presenting target cells.
Reaction develops over 24–72 hours (“delayed”).
Examples:
Contact dermatitis – poison ivy, nickel allergy
Tuberculin skin test (PPD)
Type 1 diabetes mellitus – T-cell mediated destruction of pancreatic β-cells
Chronic transplant rejection – T-cell attack on graft cells
Summary Table: ACID
Type Mechanism Mediators Time Examples
Histamine,
I (Allergic) IgE + mast cells Minutes Anaphylaxis, asthma
leukotrienes
IgG/IgM + Complement, NK Hemolytic anemia,
II (Cytotoxic) Hours
complement/cells cells transfusion reaction
III (Immune IgG/IgM + antigen Complement,
Hours SLE, serum sickness
Complex) complexes neutrophils
Cytokines, 24–72
IV (Delayed) T cells (CD4+/CD8+) Contact dermatitis, PPD
macrophages hrs
Type I
, Immediate (Anaphylaxis) – uses IgE antibodies – antibodies bind to mast
cells and basophils- releases histamines based on prior exposure to the allergen.
Results to vasodilation, bronchoconstriction, hives, edema and anaphylaxis
(severe).
Hay fever, insect bites, food/drug allergies, asthma
Type 2
Antibody-Mediated (Cytotoxic) -IgG/IgM antibodies – bind to antigens on
the surface of host cells – blood cell, platelets, tissues – activates the complement
system – leads to lysis – formation of the membrane attack complex.
Phagocytosis may occur.
transfusion reactions, autoimmune hemolytic anemia, Graves Disease, Rh
Incompatibility, MG
Type 3
Immune-Complex -IgG/IgM. formation of immune complex that deposit
in the tissues. Activates the complement system – leads to inflammation and
tissue damage.
SLE, RA, serum sickness, vasculitis, glomerulonephritis
Type 4
Delayed (Cell Meditated)- T-cells (CD4, TH1). Antigen presenting cells
capture the antigen and present in T helper cells which become sensitized and
activate during subsequent exposure. Upon re-exposure the t cell releases
cytokins – activation of immune cells- causes inflammation and tissue damage.
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 ACID
Hypersensitivity Reactions (ACID)
Hypersensitivity reactions are exaggerated or inappropriate immune responses that result in
tissue damage. They are classified into four types, remembered by the acronym ACID:
1. A – Type I: Allergic / Anaphylactic (Immediate)
2. C – Type II: Cytotoxic
3. I – Type III: Immune Complex-Mediated
4. D – Type IV: Delayed-Type (Cell-Mediated)
1. Type I: Allergic / Anaphylactic Reaction (Immediate)
Pathophysiology:
Triggered by IgE antibodies against harmless antigens (allergens) like pollen, dust mites,
or certain foods.
Sensitization phase:
1. Allergen enters the body.
2. B cells produce IgE, which binds to mast cells and basophils via Fc receptors.
Activation phase (upon re-exposure):
1. Allergen cross-links IgE on mast cells.
2. Mast cells release histamine, leukotrienes, prostaglandins, and other mediators.
Clinical effects:
, o Vasodilation → hypotension
o Increased vascular permeability → edema
o Smooth muscle contraction → bronchospasm
o Typical manifestations: urticaria, asthma, anaphylaxis
Examples:
Anaphylaxis, hay fever, asthma, food allergies.
2. Type II: Cytotoxic Reaction
Pathophysiology:
Mediated by IgG or IgM antibodies directed against antigens on cell surfaces or the
extracellular matrix.
Mechanisms of tissue damage:
1. Complement activation → cell lysis
2. Opsonization → phagocytosis of targeted cells
3. Antibody-dependent cellular cytotoxicity (ADCC) via NK cells
Clinical consequences: destruction of specific cells expressing the antigen.
Examples:
Hemolytic anemia (autoimmune or drug-induced)
Goodpasture syndrome – antibodies against basement membrane of kidney and lungs
Blood transfusion reactions
Graves disease and myasthenia gravis are antibody-mediated, but not cytotoxic in
classic sense—they alter receptor function.
3. Type III: Immune Complex-Mediated Reaction
Pathophysiology:
Occurs when antigen-antibody complexes (IgG or IgM) are deposited in tissues.
Complement activation → recruitment of neutrophils → tissue damage via enzymes and
reactive oxygen species.
Typically affects blood vessels, glomeruli, and joints.
Examples:
Systemic lupus erythematosus (SLE) – immune complex deposition in kidneys, skin,
joints
Post-streptococcal glomerulonephritis
Serum sickness – reaction to foreign proteins or drugs
Arthus reaction – local immune complex-mediated skin reaction
,Key distinction: In type III, tissue damage is indirect, caused by inflammatory response to
immune complexes, not by direct antibody attack on cells.
4. Type IV: Delayed-Type / Cell-Mediated Reaction
Pathophysiology:
T-cell mediated, not antibody-mediated.
CD4+ T helper 1 (Th1) cells recognize antigens and release cytokines (e.g., IFN-γ,
TNF-α).
Cytokines recruit macrophages → tissue damage.
CD8+ cytotoxic T cells may directly kill antigen-presenting target cells.
Reaction develops over 24–72 hours (“delayed”).
Examples:
Contact dermatitis – poison ivy, nickel allergy
Tuberculin skin test (PPD)
Type 1 diabetes mellitus – T-cell mediated destruction of pancreatic β-cells
Chronic transplant rejection – T-cell attack on graft cells
Summary Table: ACID
Type Mechanism Mediators Time Examples
Histamine,
I (Allergic) IgE + mast cells Minutes Anaphylaxis, asthma
leukotrienes
IgG/IgM + Complement, NK Hemolytic anemia,
II (Cytotoxic) Hours
complement/cells cells transfusion reaction
III (Immune IgG/IgM + antigen Complement,
Hours SLE, serum sickness
Complex) complexes neutrophils
Cytokines, 24–72
IV (Delayed) T cells (CD4+/CD8+) Contact dermatitis, PPD
macrophages hrs
Type I
, Immediate (Anaphylaxis) – uses IgE antibodies – antibodies bind to mast
cells and basophils- releases histamines based on prior exposure to the allergen.
Results to vasodilation, bronchoconstriction, hives, edema and anaphylaxis
(severe).
Hay fever, insect bites, food/drug allergies, asthma
Type 2
Antibody-Mediated (Cytotoxic) -IgG/IgM antibodies – bind to antigens on
the surface of host cells – blood cell, platelets, tissues – activates the complement
system – leads to lysis – formation of the membrane attack complex.
Phagocytosis may occur.
transfusion reactions, autoimmune hemolytic anemia, Graves Disease, Rh
Incompatibility, MG
Type 3
Immune-Complex -IgG/IgM. formation of immune complex that deposit
in the tissues. Activates the complement system – leads to inflammation and
tissue damage.
SLE, RA, serum sickness, vasculitis, glomerulonephritis
Type 4
Delayed (Cell Meditated)- T-cells (CD4, TH1). Antigen presenting cells
capture the antigen and present in T helper cells which become sensitized and
activate during subsequent exposure. Upon re-exposure the t cell releases
cytokins – activation of immune cells- causes inflammation and tissue damage.
