Pathophysiology 1
NRSG 310 Pathophysiology 1 Exam 2 2026 | Immune
Disorders & Reactions | Practice Questions & Verified
Answers
Ch 12 – Immune Disorders
1. List and describe the 4 types of hypersensitivity reactions. Define anaphylaxis and identify
treatments.
Hypersensitivity reactions are exaggerated or inappropriate immune responses that cause tissue damage. Too much
immune reaction
Type I-III are antibody mediated|
• Type I (IgE-mediated): ALLERGIES; This is an immediate allergic reaction where an allergen triggers IgE
antibodies bound to mast cells and basophils, leading to the release of histamine and other inflammatory
mediators. It causes symptoms like itching, swelling, bronchoconstriction, and hypotension. Common examples
include seasonal allergies, asthma, and anaphylaxis
• H1 receptor- RESPIRATORY; responsible for symptom like itching and swelling
• H2 receptors- GI; responsible for GI symptoms
- Always a part of adaptive immune response – IgE binds to surface of mast cells and basophils
releasing histamine and symptoms of allergic reaction
- Treatment: antihistamines – block H1 receptors, corticosteroids, Epinephrine (only for anaphylaxis)
• Anaphylaxis is a life-threatening systemic Type I hypersensitivity reaction. It involves widespread vasodilation,
bronchospasm, and shock. First-line treatment is epinephrine, followed by airway management, antihistamines,
corticosteroids, and IV fluids.
• Type II (Antibody-mediated cytotoxic): TISSUE SPECIFIC; In this reaction, IgG or IgM antibodies target
antigens on cell surfaces, causing destruction through complement activation or phagocytosis. This occurs in
conditions like hemolytic anemia, Myasthenia Gravis disease, Graves' disease, and blood transfusion reactions
autoimmune attacking
Example: Myasthenia Gravis is the autoimmune motor disorder from Ch.12 that IgG antibodies mistakenly bind/attack
acetylcholine receptors leading to muscle weakness.
• Type III (Immune complex-mediated): “ANTIGENS +ANTIBODIES GET MARRIED” -Antigen-antibody
complexes form and deposit in tissues (versus reacting on cell surfaces), activating complement and triggering
inflammation. This leads to diseases like glomerulonephritis, systemic lupus erythematosus (SLE) and serum
sickness.
,Pathophysiology 2
Only type 4 is T-CELL MEDIATED
,Pathophysiology 3
• Type IV (T-cell-mediated delayed): This type does not involve antibodies. Instead, sensitized T cells recognize
antigens and release cytokines that cause inflammation, recruit and activate phagocytosis. It typically develops
over 48–72 hours. Examples include contact dermatitis and the TB skin test.
• GRAFT REJECTION, TB AND CONTACT DERMATITIS (POSION IVY)
Differentiate direct cell-mediated cytotoxicity from delayed-type hypersensitivity.
Cell mediated cytotoxicity involves CD8 T cells that directly kill infected abnormal cells
Delayed type hypersensitivity: delayed 24-72hrs involve the CD4 helper T cells release cytokines that
brings in cytokines for phagocytosis/inflammation
2. Define immunodeficiency and distinguish between primary and secondary
immunodeficiency.
Immunodeficiency: refers to an impaired immune system that fails to defend the body against infections. Clinically, it
presents as frequent, severe, or unusual infections, poor wound healing, chronic diarrhea, and failure to thrive in children.
• Primary immunodeficiency is congenital or genetic. It typically presents in infancy or childhood and may
involve T cells, B cells, phagocytes, or complement. Patients often have recurrent infections early in life.
• Secondary immunodeficiency is acquired later in life due to external factors such as HIV, chemotherapy,
malnutrition, immunosuppressive medications, or aging. It can affect anyone and is often linked to an underlying
condition.
Importantly, immunodeficiency is not the same as autoimmunity. Immunodeficiency results from an underactive
immune system, while autoimmunity results from an overactive immune response against the body’s own tissues.
Alloimmunity – immune reaction towards tissue of another individual example-
, Pathophysiology 4
3. Define autoimmune disease and describe mechanisms that can lead to self-reactive
antibodies.
Autoimmune disease: occurs when the immune system loses its ability to distinguish self from non-self and begins
attacking the body’s own tissues. This loss of self-tolerance leads to the production of self-reactive antibodies or
autoreactive T cells.
Mechanisms that contribute to autoimmunity include:
• Genetic predisposition, particularly related to HLA (human leukocyte antigen) genes
• Molecular mimicry, where a pathogen's antigens resemble host tissue and confuse the immune system
• Defects in T-cell regulation, allowing self-reactive cells to survive
• Environmental triggers, such as infections, medications, or chemicals
Autoimmune diseases can be systemic (like lupus or rheumatoid arthritis) or organ-specific (like Type 1 diabetes or
Hashimoto’s thyroiditis).
HIV
Molecular and Biologic Features of HIV
• Two related forms
• HIV-1 – most associated with infections in US, Europe, and Central Africa
• HIV-2 – mostly found in West Africa
- Spreads more slowly and causes disease more slowly than HIV-1
• Retrovirus
• Genetic material is RNA
• Selectively invades immune cells
• CD4+ T cells, macrophages, and dendritic cells
HIV structure-
Retrovirus
• Single stranded RNA
Contains enzymes:
• Reverse transcriptase – reverse
transcribes ss viral RNA into ds DNA
• Integrase – inserts new viral DNA into our own DNA
• Protease – cuts the polyprotein into individual viral proteins and enzymes
NRSG 310 Pathophysiology 1 Exam 2 2026 | Immune
Disorders & Reactions | Practice Questions & Verified
Answers
Ch 12 – Immune Disorders
1. List and describe the 4 types of hypersensitivity reactions. Define anaphylaxis and identify
treatments.
Hypersensitivity reactions are exaggerated or inappropriate immune responses that cause tissue damage. Too much
immune reaction
Type I-III are antibody mediated|
• Type I (IgE-mediated): ALLERGIES; This is an immediate allergic reaction where an allergen triggers IgE
antibodies bound to mast cells and basophils, leading to the release of histamine and other inflammatory
mediators. It causes symptoms like itching, swelling, bronchoconstriction, and hypotension. Common examples
include seasonal allergies, asthma, and anaphylaxis
• H1 receptor- RESPIRATORY; responsible for symptom like itching and swelling
• H2 receptors- GI; responsible for GI symptoms
- Always a part of adaptive immune response – IgE binds to surface of mast cells and basophils
releasing histamine and symptoms of allergic reaction
- Treatment: antihistamines – block H1 receptors, corticosteroids, Epinephrine (only for anaphylaxis)
• Anaphylaxis is a life-threatening systemic Type I hypersensitivity reaction. It involves widespread vasodilation,
bronchospasm, and shock. First-line treatment is epinephrine, followed by airway management, antihistamines,
corticosteroids, and IV fluids.
• Type II (Antibody-mediated cytotoxic): TISSUE SPECIFIC; In this reaction, IgG or IgM antibodies target
antigens on cell surfaces, causing destruction through complement activation or phagocytosis. This occurs in
conditions like hemolytic anemia, Myasthenia Gravis disease, Graves' disease, and blood transfusion reactions
autoimmune attacking
Example: Myasthenia Gravis is the autoimmune motor disorder from Ch.12 that IgG antibodies mistakenly bind/attack
acetylcholine receptors leading to muscle weakness.
• Type III (Immune complex-mediated): “ANTIGENS +ANTIBODIES GET MARRIED” -Antigen-antibody
complexes form and deposit in tissues (versus reacting on cell surfaces), activating complement and triggering
inflammation. This leads to diseases like glomerulonephritis, systemic lupus erythematosus (SLE) and serum
sickness.
,Pathophysiology 2
Only type 4 is T-CELL MEDIATED
,Pathophysiology 3
• Type IV (T-cell-mediated delayed): This type does not involve antibodies. Instead, sensitized T cells recognize
antigens and release cytokines that cause inflammation, recruit and activate phagocytosis. It typically develops
over 48–72 hours. Examples include contact dermatitis and the TB skin test.
• GRAFT REJECTION, TB AND CONTACT DERMATITIS (POSION IVY)
Differentiate direct cell-mediated cytotoxicity from delayed-type hypersensitivity.
Cell mediated cytotoxicity involves CD8 T cells that directly kill infected abnormal cells
Delayed type hypersensitivity: delayed 24-72hrs involve the CD4 helper T cells release cytokines that
brings in cytokines for phagocytosis/inflammation
2. Define immunodeficiency and distinguish between primary and secondary
immunodeficiency.
Immunodeficiency: refers to an impaired immune system that fails to defend the body against infections. Clinically, it
presents as frequent, severe, or unusual infections, poor wound healing, chronic diarrhea, and failure to thrive in children.
• Primary immunodeficiency is congenital or genetic. It typically presents in infancy or childhood and may
involve T cells, B cells, phagocytes, or complement. Patients often have recurrent infections early in life.
• Secondary immunodeficiency is acquired later in life due to external factors such as HIV, chemotherapy,
malnutrition, immunosuppressive medications, or aging. It can affect anyone and is often linked to an underlying
condition.
Importantly, immunodeficiency is not the same as autoimmunity. Immunodeficiency results from an underactive
immune system, while autoimmunity results from an overactive immune response against the body’s own tissues.
Alloimmunity – immune reaction towards tissue of another individual example-
, Pathophysiology 4
3. Define autoimmune disease and describe mechanisms that can lead to self-reactive
antibodies.
Autoimmune disease: occurs when the immune system loses its ability to distinguish self from non-self and begins
attacking the body’s own tissues. This loss of self-tolerance leads to the production of self-reactive antibodies or
autoreactive T cells.
Mechanisms that contribute to autoimmunity include:
• Genetic predisposition, particularly related to HLA (human leukocyte antigen) genes
• Molecular mimicry, where a pathogen's antigens resemble host tissue and confuse the immune system
• Defects in T-cell regulation, allowing self-reactive cells to survive
• Environmental triggers, such as infections, medications, or chemicals
Autoimmune diseases can be systemic (like lupus or rheumatoid arthritis) or organ-specific (like Type 1 diabetes or
Hashimoto’s thyroiditis).
HIV
Molecular and Biologic Features of HIV
• Two related forms
• HIV-1 – most associated with infections in US, Europe, and Central Africa
• HIV-2 – mostly found in West Africa
- Spreads more slowly and causes disease more slowly than HIV-1
• Retrovirus
• Genetic material is RNA
• Selectively invades immune cells
• CD4+ T cells, macrophages, and dendritic cells
HIV structure-
Retrovirus
• Single stranded RNA
Contains enzymes:
• Reverse transcriptase – reverse
transcribes ss viral RNA into ds DNA
• Integrase – inserts new viral DNA into our own DNA
• Protease – cuts the polyprotein into individual viral proteins and enzymes
