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 1- IgE-mediated
Mediated through the binding of IgE to Fc receptors on
mast cells and cross-linking of IgE by antigens that bind to
the Fab portions of IgE. Cross-linking causes mast cell
degranulation and the release of histamines and other
inflammatory substances.
Histamine, acting through the H1 receptor,
contracts bronchial smooth muscle, causing
bronchial constriction; increases vascular
permeability, leading to edema; and increases blood
flow into the affected area, resulting in vasodilation.
Histamine acts on H2 receptors, increasing gastric
acid secretion and decreasing histamine released
from mast cells and basophils.
o Type II- Tissue-specific
Caused by five possible mechanisms: complement-
mediated lysis, opsonization and phagocytosis, neutrophil-
mediated tissue damage, antibody-dependent cell-
mediated cytotoxicity, and modulation of cellular function.
o Type III- Immune complex- mediated
Formation of immune complexes that are deposited in
target tissues, where they activate the complement
cascade, generating chemotactic fragments that attract
neutrophils into the inflammatory site. Neutrophils release
lysosomal enzymes that result in tissue damage.
o Type IV- cell- mediated
Cytotoxic T lymphocytes (T cells), lymphokine- producing
TH1 cells, and activated macrophages.
, 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)
, SLE
Pathophysiology of Systemic Lupus Erythematosus (SLE)
o Production of a large variety of antibodies (autoantibodies)
against self- antigens, including nucleic
acids/erythrocytes/coagulation
proteins/phospholipids/lymphocytes/platelets. Autoantibodies
react with the circulating antigen and form circulating immune
complexes.
Diagnosis of SLE, including the autoantibodies involved
o Labs: positive antibody screening test (ANA), Smith antigen,
and dsDNA. Urinalysis and serum C-reactive protein and
complement levels.
Clinical symptoms of SLE
o Skin (rash/photosensitivity), eyes (keratoconjunctivitis, scleritis,
uveitis, retinopathy), mucus membranes (ulcers), joints
(arthralgias), linings of the viscera (serositis, pleuritis), kidney
(proteinuria), blood (anemia), gut (abdominal pain/vasculitis/
hepatobiliary disease), and neurologic system (seizures or
psychosis). High risk for end-stage renal failure. Cardiovascular
disease is common.
Treatment options for SLE, including treatment during flare-
ups
o Avoid triggers, NSAIDS, hydroxychloroquine, and
corticosteroids are prescribed for FLARE UPS.
Immunosuppressive drugs: methotrexate, cyclophosphamide,
azathioprine, tacrolimus, or mycophenolate mofetil- treatment
for symptoms.
Immunotherapies focus on B-cell depletion
(belimumab/rituximab)
Anifrolumab (anti-type 1 interferon receptor antibody
Ustekinumab (antibody against IL-12-23 P40)- clinical
trials
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 1- IgE-mediated
Mediated through the binding of IgE to Fc receptors on
mast cells and cross-linking of IgE by antigens that bind to
the Fab portions of IgE. Cross-linking causes mast cell
degranulation and the release of histamines and other
inflammatory substances.
Histamine, acting through the H1 receptor,
contracts bronchial smooth muscle, causing
bronchial constriction; increases vascular
permeability, leading to edema; and increases blood
flow into the affected area, resulting in vasodilation.
Histamine acts on H2 receptors, increasing gastric
acid secretion and decreasing histamine released
from mast cells and basophils.
o Type II- Tissue-specific
Caused by five possible mechanisms: complement-
mediated lysis, opsonization and phagocytosis, neutrophil-
mediated tissue damage, antibody-dependent cell-
mediated cytotoxicity, and modulation of cellular function.
o Type III- Immune complex- mediated
Formation of immune complexes that are deposited in
target tissues, where they activate the complement
cascade, generating chemotactic fragments that attract
neutrophils into the inflammatory site. Neutrophils release
lysosomal enzymes that result in tissue damage.
o Type IV- cell- mediated
Cytotoxic T lymphocytes (T cells), lymphokine- producing
TH1 cells, and activated macrophages.
, 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)
, SLE
Pathophysiology of Systemic Lupus Erythematosus (SLE)
o Production of a large variety of antibodies (autoantibodies)
against self- antigens, including nucleic
acids/erythrocytes/coagulation
proteins/phospholipids/lymphocytes/platelets. Autoantibodies
react with the circulating antigen and form circulating immune
complexes.
Diagnosis of SLE, including the autoantibodies involved
o Labs: positive antibody screening test (ANA), Smith antigen,
and dsDNA. Urinalysis and serum C-reactive protein and
complement levels.
Clinical symptoms of SLE
o Skin (rash/photosensitivity), eyes (keratoconjunctivitis, scleritis,
uveitis, retinopathy), mucus membranes (ulcers), joints
(arthralgias), linings of the viscera (serositis, pleuritis), kidney
(proteinuria), blood (anemia), gut (abdominal pain/vasculitis/
hepatobiliary disease), and neurologic system (seizures or
psychosis). High risk for end-stage renal failure. Cardiovascular
disease is common.
Treatment options for SLE, including treatment during flare-
ups
o Avoid triggers, NSAIDS, hydroxychloroquine, and
corticosteroids are prescribed for FLARE UPS.
Immunosuppressive drugs: methotrexate, cyclophosphamide,
azathioprine, tacrolimus, or mycophenolate mofetil- treatment
for symptoms.
Immunotherapies focus on B-cell depletion
(belimumab/rituximab)
Anifrolumab (anti-type 1 interferon receptor antibody
Ustekinumab (antibody against IL-12-23 P40)- clinical
trials
