NR507 – Advanced Pathophysiology
Exam Study Guide – Midterm Exam
Exam Format : Non-cumulative
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 Friday, Week 8 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 1 (IgE mediated)
▪ Helper T2 cells are activated by an antigen which causes
IL-4 and IL-5 production. High IL-4 levels cause B-cells to
change to IgE producing cells. IgE binds to masts cells in
the plasma membrane. Subsequent exposure, the allergen
triggers mast cell degranulation and the release of
histamine, causing vasodilation, smooth muscle
contraction, and increased vascular permeability.
▪ Mast cells are the primary effector of type 1
reactions.
▪ When a large amount of IgE has bound to mast cells, an
individual is considered sensitized. Subsequent exposures
signal mast cells to degranulate and release mediators.
, ▪ Characterized by rapid release of proinflammatory
mediators (ex: histamines, leukotrienes,
prostaglandins) and cytokines in response to
allergen.
▪ Physical manifestations:
• Vasodilation
• Bronchial smooth muscle contraction
• Mucus production
o Type 2 (Tissue specific)
▪ The symptoms of Type 2 reactions are determined by which
tissue/organ is expressing the antigen.
▪ Macrophages are the primary effector cells of these
reactions
▪ Causes the following reactions:
• Cell to be destroyed by antibody
• Cell destruction via phagocytosis
• Damage to cells by neutrophils triggering
phagocytosis
• Natural killer cells release toxic substances
• Cell wall malfunction without destruction
▪ Complement-mediated
• IgM or IgG binds to tissue-specific antigens,
activating the complement cascade. Formation of the
membrane attack complex (c5-9), results in lysis of
the cell.
▪ Antibody dependent cytotoxicity
• Antibodies bound to antigens activate macrophages,
neutrophils, and NK cells which in turn attack target
cells. Deposits of C3b on target cell’s surface signals
macrophages and NK cells and increased
phagocytosis of target cell.
▪ Anti-receptor antibodies
• Causes the target cell to malfunction instead of
destroying it.
• Autoantibodies cause a change in target cell function
by blocking, overstimulating, or destroying it.
o Example: Grave’s disease
▪ TSIs bind to TSH which stimulates the
thyroid cells to overproduce thyroxine
causing hyperthyroidism.
,o Type 3 (Immune complex mediated)
▪ Immune complexes form in the bloodstream from
circulating antigen and antibody.
• Immune complexes activate complement and
neutrophil cells --> tissue destruction
▪ Type III reactions are not organ specific and result in
vasculitis.
▪ Neutrophils attempt to phagocytose the immune
complexes
▪ During phagocytosis, lysosomal enzymes are released
instead of phagolysosomes to the inflammatory site.
▪ Most common type III reactions are serum sickness and
Raynaud syndrome.
▪ Neutrophils are the primary effector cell
▪ Phenytoin reduces corticosteroid effectiveness
▪ AUTOIMMUNE DISEASES
• Serum Sickness:
o Symptoms include fever, rash, generalized joint
pain, and localized swelling
▪ Type 3 Reaction Sequence:
• Antibodies bind to antigens
• Immune complexes form
• Complexes deposit in blood vessels or tissues
• Activation of complexes
• Inflammatory response @ deposit site
• Release of lysosomal enzymes and chemical
mediators
• Tissue damage
o Type 4 (Cell mediated)
▪ Mediated by T lymphocytes and macrophages
▪ Type 4 occurs through antigens on major histocompatibility
molecules to T cells. Helper T cells produce Helper T1 and
T17 cytokines which activate macrophages and cytotoxic T
lymphocytes.
▪ Reaction occurs 24 to 72 hours post exposure.
▪ Characterized by
• Erythema
• Cellular infiltration
• Vesicles
, ▪ Formation of multiple granulomas can lead to tissue
damage and organ dysfunction
• Granulomas are when T cells and macrophages
cannot destroy offending antigen
▪ Steps to reaction sequence:
• Macrophage presents antigen
• Sensitization of t-lymphocytes
• Release of lymphokines
• Inflammation and lysis of antigen-bearing cells
• Tissue destruction
▪ Some Autoimmune diseases
• Rheumatoid Arthritis
o T cell response to type 2 collagen can lead to
joint damage
• Type 1 Diabetes
o T cell response to antigen on pancreatic beta
cells contributes to beta-cell destruction
• Contact dermatitis
o Eczematous, cutaneous skin condition
o Dryness with pruritus
• Prototype diseases that reflect each of the four types of
hypersensitivity (i.e. Type IV-contact dermatitis) and signs and
symptoms
o Type 1
▪ Anaphylaxis --> flushing, hives, itching, swelling, rash,
N/V, wheezing
• Treatment -> epinephrine, oxygen, IVF,
antihistamines, corticosteroids.
o Type 2
▪ Hemolytic Anemia --> jaundice, thrombocytopenia,
blistering skin, neutropenia, muscular fatigue, double
vision.
• Treatment -> blood transfusion, steroids to reduce
RBC destruction, splenectomy, Rituximab, SC tx, IVIG
o Type 3
▪ Raynaud phenomenon --> pallor, numbness, cyanosis,
gangrene (late sign) of fingers, toes, and nose.
• Treatment -> lifestyle changes (dressing warmly,
avoiding cold, managing stress), limiting caffeine and
alcohol, CCBs, PDE5 inhibitors
Exam Study Guide – Midterm Exam
Exam Format : Non-cumulative
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 Friday, Week 8 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 1 (IgE mediated)
▪ Helper T2 cells are activated by an antigen which causes
IL-4 and IL-5 production. High IL-4 levels cause B-cells to
change to IgE producing cells. IgE binds to masts cells in
the plasma membrane. Subsequent exposure, the allergen
triggers mast cell degranulation and the release of
histamine, causing vasodilation, smooth muscle
contraction, and increased vascular permeability.
▪ Mast cells are the primary effector of type 1
reactions.
▪ When a large amount of IgE has bound to mast cells, an
individual is considered sensitized. Subsequent exposures
signal mast cells to degranulate and release mediators.
, ▪ Characterized by rapid release of proinflammatory
mediators (ex: histamines, leukotrienes,
prostaglandins) and cytokines in response to
allergen.
▪ Physical manifestations:
• Vasodilation
• Bronchial smooth muscle contraction
• Mucus production
o Type 2 (Tissue specific)
▪ The symptoms of Type 2 reactions are determined by which
tissue/organ is expressing the antigen.
▪ Macrophages are the primary effector cells of these
reactions
▪ Causes the following reactions:
• Cell to be destroyed by antibody
• Cell destruction via phagocytosis
• Damage to cells by neutrophils triggering
phagocytosis
• Natural killer cells release toxic substances
• Cell wall malfunction without destruction
▪ Complement-mediated
• IgM or IgG binds to tissue-specific antigens,
activating the complement cascade. Formation of the
membrane attack complex (c5-9), results in lysis of
the cell.
▪ Antibody dependent cytotoxicity
• Antibodies bound to antigens activate macrophages,
neutrophils, and NK cells which in turn attack target
cells. Deposits of C3b on target cell’s surface signals
macrophages and NK cells and increased
phagocytosis of target cell.
▪ Anti-receptor antibodies
• Causes the target cell to malfunction instead of
destroying it.
• Autoantibodies cause a change in target cell function
by blocking, overstimulating, or destroying it.
o Example: Grave’s disease
▪ TSIs bind to TSH which stimulates the
thyroid cells to overproduce thyroxine
causing hyperthyroidism.
,o Type 3 (Immune complex mediated)
▪ Immune complexes form in the bloodstream from
circulating antigen and antibody.
• Immune complexes activate complement and
neutrophil cells --> tissue destruction
▪ Type III reactions are not organ specific and result in
vasculitis.
▪ Neutrophils attempt to phagocytose the immune
complexes
▪ During phagocytosis, lysosomal enzymes are released
instead of phagolysosomes to the inflammatory site.
▪ Most common type III reactions are serum sickness and
Raynaud syndrome.
▪ Neutrophils are the primary effector cell
▪ Phenytoin reduces corticosteroid effectiveness
▪ AUTOIMMUNE DISEASES
• Serum Sickness:
o Symptoms include fever, rash, generalized joint
pain, and localized swelling
▪ Type 3 Reaction Sequence:
• Antibodies bind to antigens
• Immune complexes form
• Complexes deposit in blood vessels or tissues
• Activation of complexes
• Inflammatory response @ deposit site
• Release of lysosomal enzymes and chemical
mediators
• Tissue damage
o Type 4 (Cell mediated)
▪ Mediated by T lymphocytes and macrophages
▪ Type 4 occurs through antigens on major histocompatibility
molecules to T cells. Helper T cells produce Helper T1 and
T17 cytokines which activate macrophages and cytotoxic T
lymphocytes.
▪ Reaction occurs 24 to 72 hours post exposure.
▪ Characterized by
• Erythema
• Cellular infiltration
• Vesicles
, ▪ Formation of multiple granulomas can lead to tissue
damage and organ dysfunction
• Granulomas are when T cells and macrophages
cannot destroy offending antigen
▪ Steps to reaction sequence:
• Macrophage presents antigen
• Sensitization of t-lymphocytes
• Release of lymphokines
• Inflammation and lysis of antigen-bearing cells
• Tissue destruction
▪ Some Autoimmune diseases
• Rheumatoid Arthritis
o T cell response to type 2 collagen can lead to
joint damage
• Type 1 Diabetes
o T cell response to antigen on pancreatic beta
cells contributes to beta-cell destruction
• Contact dermatitis
o Eczematous, cutaneous skin condition
o Dryness with pruritus
• Prototype diseases that reflect each of the four types of
hypersensitivity (i.e. Type IV-contact dermatitis) and signs and
symptoms
o Type 1
▪ Anaphylaxis --> flushing, hives, itching, swelling, rash,
N/V, wheezing
• Treatment -> epinephrine, oxygen, IVF,
antihistamines, corticosteroids.
o Type 2
▪ Hemolytic Anemia --> jaundice, thrombocytopenia,
blistering skin, neutropenia, muscular fatigue, double
vision.
• Treatment -> blood transfusion, steroids to reduce
RBC destruction, splenectomy, Rituximab, SC tx, IVIG
o Type 3
▪ Raynaud phenomenon --> pallor, numbness, cyanosis,
gangrene (late sign) of fingers, toes, and nose.
• Treatment -> lifestyle changes (dressing warmly,
avoiding cold, managing stress), limiting caffeine and
alcohol, CCBs, PDE5 inhibitors
