lOMoARcPSD|63525276
Comprehensive Study Guide for
Advanced Pathophysiology (NR507)
Midterm Exam
Alterations in Immunity and Inflammation
Understand the pathophysiology of the four types of hypersensitivity
reactions, prototype diseases exemplifying each type such as type IV-
contact dermatitis, clinical signs and symptoms, and treatment options;
also study the pathophysiology of HIV and systemic lupus erythematosus
(SLE), including diagnostic autoantibodies, clinical symptoms, treatment
approaches, alloimmune phenomena, differences between primary and
secondary immunodeficiencies, and common variable immunodeficiency.
The immune system can respond abnormally, leading to hypersensitivity
reactions that are classified into four types based on their mechanisms:
Type I (Immediate Hypersensitivity): Mediated by IgE antibodies
binding to allergens, leading to mast cell degranulation. Common
diseases include allergic rhinitis, asthma, and anaphylaxis. Treatment
involves antihistamines, corticosteroids, and allergen avoidance.
Type II (Cytotoxic Hypersensitivity): Involves IgG or IgM antibodies
targeting antigens on cell surfaces, causing cell destruction via
complement activation or phagocytosis. Examples include hemolytic
transfusion reactions and autoimmune hemolytic anemia.
Type III (Immune Complex Hypersensitivity): Formation of immune
complexes that deposit in tissues, activating complement and causing
inflammation. Diseases include systemic lupus erythematosus (SLE) and
serum sickness. Treatment may involve immunosuppressants and
corticosteroids.
, lOMoARcPSD|63525276
Type IV (Delayed Hypersensitivity): T-cell mediated responses
causing tissue damage after exposure to antigens. Contact dermatitis
(e.g., poison ivy) and tuberculin skin tests are typical examples.
Management includes corticosteroids and avoiding triggers.
Prototype Diseases & Signs/Symptoms:
Type I:Anaphylaxis, hives, bronchospasm.
Type II:Hemolytic anemia, Goodpasture syndrome.
Type III:SLE, rheumatoid arthritis.
Type IV:Contact dermatitis, graft-versus-host disease.
Pathophysiology of HIV: HIV infects CD4+ T lymphocytes, leading to
progressive immune deficiency. It integrates into host DNA, causing cell
destruction and impairing immune responses. Over time, this results in
AIDS, characterized by opportunistic infections and certain cancers.
Pathophysiology of SLE: An autoimmune disease where autoantibodies
target nuclear antigens, leading to immune complex deposition in tissues
such as skin, joints, kidneys, and heart. Key autoantibodies include anti-
dsDNA, anti-Smith, and ANA. Clinical signs include malar rash, arthritis,
renal impairment, and hematologic abnormalities.
Diagnosis of SLE: Relies on clinical criteria and laboratory findings:
Presence of ANA (antinuclear antibody)
Anti-dsDNA and anti-Smith antibodies
Complement levels (C3, C4) often decreased during active disease
Elevated ESR and CRP as markers of inflammation
Treatment of SLE: Includes NSAIDs for pain, corticosteroids for
inflammation, antimalarials like hydroxychloroquine, immunosuppressants
(e.g., azathioprine), and biologic agents in severe cases. During flare-ups,
corticosteroids are adjusted to control disease activity.
, lOMoARcPSD|63525276
Alloimmune Phenomenon: Occurs when the immune system reacts
against antigens from another individual of the same species, such as in
transfusions, organ transplants, or pregnancy.
Immunodeficiency Types:
Primary (Congenital): Caused by genetic defects affecting immune
components (e.g., severe combined immunodeficiency, common
variable immunodeficiency).
Secondary (Acquired): Result from external factors like HIV infection,
malnutrition, or immunosuppressive therapy.
Common Variable Immunodeficiency (CVID): Characterized by low levels
of immunoglobulins (IgG, IgA, IgM), leading to recurrent infections,
especially respiratory and gastrointestinal. Diagnosis involves measuring
serum immunoglobulin levels and assessing antibody responses.
Hematological Pathologies
Focus on the pathophysiology of various anemia types including
microcytic, macrocytic, normocytic, anemia of chronic disease, folate
deficiency, and sickle cell anemia; understand red blood cell production
and erythropoietin's role, lab markers for anemia diagnosis, risk factors for
different anemia forms, treatment of beta-thalassemia major, and
implications for vaccinating immunocompromised patients.
Anemia Types & Pathophysiology:
Microcytic Anemia: Characterized by small RBCs, commonly caused by
iron deficiency or thalassemia. Iron deficiency impairs hemoglobin
synthesis, leading to reduced hemoglobin content.
Macrocytic Anemia: Larger RBCs due to impaired DNA synthesis, often
from vitamin B12 or folate deficiency. Results in ineffective
erythropoiesis and hemolysis.
Comprehensive Study Guide for
Advanced Pathophysiology (NR507)
Midterm Exam
Alterations in Immunity and Inflammation
Understand the pathophysiology of the four types of hypersensitivity
reactions, prototype diseases exemplifying each type such as type IV-
contact dermatitis, clinical signs and symptoms, and treatment options;
also study the pathophysiology of HIV and systemic lupus erythematosus
(SLE), including diagnostic autoantibodies, clinical symptoms, treatment
approaches, alloimmune phenomena, differences between primary and
secondary immunodeficiencies, and common variable immunodeficiency.
The immune system can respond abnormally, leading to hypersensitivity
reactions that are classified into four types based on their mechanisms:
Type I (Immediate Hypersensitivity): Mediated by IgE antibodies
binding to allergens, leading to mast cell degranulation. Common
diseases include allergic rhinitis, asthma, and anaphylaxis. Treatment
involves antihistamines, corticosteroids, and allergen avoidance.
Type II (Cytotoxic Hypersensitivity): Involves IgG or IgM antibodies
targeting antigens on cell surfaces, causing cell destruction via
complement activation or phagocytosis. Examples include hemolytic
transfusion reactions and autoimmune hemolytic anemia.
Type III (Immune Complex Hypersensitivity): Formation of immune
complexes that deposit in tissues, activating complement and causing
inflammation. Diseases include systemic lupus erythematosus (SLE) and
serum sickness. Treatment may involve immunosuppressants and
corticosteroids.
, lOMoARcPSD|63525276
Type IV (Delayed Hypersensitivity): T-cell mediated responses
causing tissue damage after exposure to antigens. Contact dermatitis
(e.g., poison ivy) and tuberculin skin tests are typical examples.
Management includes corticosteroids and avoiding triggers.
Prototype Diseases & Signs/Symptoms:
Type I:Anaphylaxis, hives, bronchospasm.
Type II:Hemolytic anemia, Goodpasture syndrome.
Type III:SLE, rheumatoid arthritis.
Type IV:Contact dermatitis, graft-versus-host disease.
Pathophysiology of HIV: HIV infects CD4+ T lymphocytes, leading to
progressive immune deficiency. It integrates into host DNA, causing cell
destruction and impairing immune responses. Over time, this results in
AIDS, characterized by opportunistic infections and certain cancers.
Pathophysiology of SLE: An autoimmune disease where autoantibodies
target nuclear antigens, leading to immune complex deposition in tissues
such as skin, joints, kidneys, and heart. Key autoantibodies include anti-
dsDNA, anti-Smith, and ANA. Clinical signs include malar rash, arthritis,
renal impairment, and hematologic abnormalities.
Diagnosis of SLE: Relies on clinical criteria and laboratory findings:
Presence of ANA (antinuclear antibody)
Anti-dsDNA and anti-Smith antibodies
Complement levels (C3, C4) often decreased during active disease
Elevated ESR and CRP as markers of inflammation
Treatment of SLE: Includes NSAIDs for pain, corticosteroids for
inflammation, antimalarials like hydroxychloroquine, immunosuppressants
(e.g., azathioprine), and biologic agents in severe cases. During flare-ups,
corticosteroids are adjusted to control disease activity.
, lOMoARcPSD|63525276
Alloimmune Phenomenon: Occurs when the immune system reacts
against antigens from another individual of the same species, such as in
transfusions, organ transplants, or pregnancy.
Immunodeficiency Types:
Primary (Congenital): Caused by genetic defects affecting immune
components (e.g., severe combined immunodeficiency, common
variable immunodeficiency).
Secondary (Acquired): Result from external factors like HIV infection,
malnutrition, or immunosuppressive therapy.
Common Variable Immunodeficiency (CVID): Characterized by low levels
of immunoglobulins (IgG, IgA, IgM), leading to recurrent infections,
especially respiratory and gastrointestinal. Diagnosis involves measuring
serum immunoglobulin levels and assessing antibody responses.
Hematological Pathologies
Focus on the pathophysiology of various anemia types including
microcytic, macrocytic, normocytic, anemia of chronic disease, folate
deficiency, and sickle cell anemia; understand red blood cell production
and erythropoietin's role, lab markers for anemia diagnosis, risk factors for
different anemia forms, treatment of beta-thalassemia major, and
implications for vaccinating immunocompromised patients.
Anemia Types & Pathophysiology:
Microcytic Anemia: Characterized by small RBCs, commonly caused by
iron deficiency or thalassemia. Iron deficiency impairs hemoglobin
synthesis, leading to reduced hemoglobin content.
Macrocytic Anemia: Larger RBCs due to impaired DNA synthesis, often
from vitamin B12 or folate deficiency. Results in ineffective
erythropoiesis and hemolysis.
