lOMoAR cPSD| 67691079
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 CoverageContent 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
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
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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.
Contact dermatitis, TB, chronic transplant rejection, MS
Prototype diseases that reflect each of the four types of hypersensitivity (i.e. Type
IVcontact dermatitis) and signs and symptoms
Type I – Immediate (Anaphylaxis)
Cause: Allergens (food/meds/hay fever, asthma, dermatitis)
Components: IgE, Mast Cells, histamine
S/S –
Sudden onset wheezing
Hives hypotension, tachycardia, dizziness
Swelling nausea, vomiting, diarrhea
Shock (severe)
Type 2 -Cytotoxic (Antibody Mediated)
Cause: receiving incompatible blood type, hemolytic anemia, Graves Disease,
MG
S/S –
Fever hypotension, jaundice
Chills hemoglobinuria Back/flank pain renal
failure/shock (severe)
Type 3 -Immune-Complex
Cause: Autoimmune response
Components – IgG/IgM, antibody-antigen components, complement, RA, serum
sickness, glomerulonephritis, hypersensitivity pneumonitis, TB, MS DMI
S/S-
Butterfly rash (Malar rash) renal involvement
Fatigue/fever neurological sympotms
Joint pain serositis (pericarditis/pleuritis) Photosensitivity
Type 4 – Delayed Type
Cause : skin contact with allergen (poison ivy, nickel, latex)
Components -T cells, cytokins, macrophanges
S/S
Red, itchy rash localized swelling
Blisters
Scaling/thickened skin (with chronic exposure)
Treatment options for diseases under each hypersensitivity category
Type I – Immediate Type (Anaphylaxis)
Anaphylaxis Treatment
, lOMoAR cPSD| 67691079
Epi Antihistamines
Oxygen Corticosteriods
IV fluids Airway Management
Allergic Rhinitis Treatment
Antihistamines (oral and intranasal) Allergy avoidance
Intranasal corticosteriods immunotherapy (allergy shots)
Decongestants
Asthma Treatment (allergic)
Inhaled corticosteroids leukotriene inhibitors (montelukast)
Beta antagonists (albuterol) biologics (omalizumab)
Atopic dermatitis
Emollient and moisturizer antihistamines
Topical corticosteroids avoidance of triggers
Type 2 – Antibody Mediated (Cytotoxic)
Transfusion Reaction
Stop transfusion monitor renal function
IV fluids supportive care
Myasthenia Gravis
Acetylcholinesterase inhibitors (pyridostigmine)
Immunosuppressants
Thymectomy Plasmapheresis or
IVIG for crisis
Graves Disease
Antithyroid drugs (methimazole, PTU) beta blockers
Radioactive ion therapy surgery (thyroidectomy)
Autoimmune hemolytic anemia
Corticosteroids Blood Transfusion
Immunosuppressants Splenectomy
Type 3 -Immune Complex
SLE
NSAIDS immunosuppressants
Hydroxychloroquine biologics (belimumab)
Corticosteroids
RA
NSAIDs biologic agents (TNF inhibitors)
DMARDs (Methotrexate) corticosteroids
Serum sickness
, lOMoAR cPSD| 67691079
Stop exposure to offending agent corticosteroids (severe)
Antihistamines NSAIDs
Post-Strep glomerulonephritis
Supportive care Diuretics
Antihypertensives antibiotics (for underlying
infection)
Type 4 – Delayed Reaction
Contact Dermatitis
Avoid trigger allergen/irritant
Topical corticosteroids
Antihistamines (for itching)
Tuberculosis (Active/Latent) Latent:
isoniazid, rifampin
Active: combination therapy (isoniazid, rifampin, pyrazinamide, and
ethambutol)
Type I Diabetes Mellitus Insulin
replacement
Blood glucose monitoring
Lifestyle management
Multiple Sclerosis
Corticosteroids (acute flares)
Disease modifying therapy (interferons, glatiramer acetate, monoclonal
antibodies)
Graft-host virus
Immunosuppressants (cyclosporin, tacrolimus) Corticosteroids
Pathophysiology of Human Immunodeficiency Virus (HIV)
Targets immune system – CD4 – T helper cells (coordinate immune response)
Enters body through blood, vaginal secretions, semen or breastmilk
Once infected, it uses reverse transcriptase to convert RNA to DNA – can remain
latent or become active producing more virus
Acute infection
clinical latency
AIDS – CD4 count is below 200, opportunistic infections/cancers develop.
Widespread immune dysfunction.
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 CoverageContent 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
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
, lOMoAR cPSD| 67691079
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.
Contact dermatitis, TB, chronic transplant rejection, MS
Prototype diseases that reflect each of the four types of hypersensitivity (i.e. Type
IVcontact dermatitis) and signs and symptoms
Type I – Immediate (Anaphylaxis)
Cause: Allergens (food/meds/hay fever, asthma, dermatitis)
Components: IgE, Mast Cells, histamine
S/S –
Sudden onset wheezing
Hives hypotension, tachycardia, dizziness
Swelling nausea, vomiting, diarrhea
Shock (severe)
Type 2 -Cytotoxic (Antibody Mediated)
Cause: receiving incompatible blood type, hemolytic anemia, Graves Disease,
MG
S/S –
Fever hypotension, jaundice
Chills hemoglobinuria Back/flank pain renal
failure/shock (severe)
Type 3 -Immune-Complex
Cause: Autoimmune response
Components – IgG/IgM, antibody-antigen components, complement, RA, serum
sickness, glomerulonephritis, hypersensitivity pneumonitis, TB, MS DMI
S/S-
Butterfly rash (Malar rash) renal involvement
Fatigue/fever neurological sympotms
Joint pain serositis (pericarditis/pleuritis) Photosensitivity
Type 4 – Delayed Type
Cause : skin contact with allergen (poison ivy, nickel, latex)
Components -T cells, cytokins, macrophanges
S/S
Red, itchy rash localized swelling
Blisters
Scaling/thickened skin (with chronic exposure)
Treatment options for diseases under each hypersensitivity category
Type I – Immediate Type (Anaphylaxis)
Anaphylaxis Treatment
, lOMoAR cPSD| 67691079
Epi Antihistamines
Oxygen Corticosteriods
IV fluids Airway Management
Allergic Rhinitis Treatment
Antihistamines (oral and intranasal) Allergy avoidance
Intranasal corticosteriods immunotherapy (allergy shots)
Decongestants
Asthma Treatment (allergic)
Inhaled corticosteroids leukotriene inhibitors (montelukast)
Beta antagonists (albuterol) biologics (omalizumab)
Atopic dermatitis
Emollient and moisturizer antihistamines
Topical corticosteroids avoidance of triggers
Type 2 – Antibody Mediated (Cytotoxic)
Transfusion Reaction
Stop transfusion monitor renal function
IV fluids supportive care
Myasthenia Gravis
Acetylcholinesterase inhibitors (pyridostigmine)
Immunosuppressants
Thymectomy Plasmapheresis or
IVIG for crisis
Graves Disease
Antithyroid drugs (methimazole, PTU) beta blockers
Radioactive ion therapy surgery (thyroidectomy)
Autoimmune hemolytic anemia
Corticosteroids Blood Transfusion
Immunosuppressants Splenectomy
Type 3 -Immune Complex
SLE
NSAIDS immunosuppressants
Hydroxychloroquine biologics (belimumab)
Corticosteroids
RA
NSAIDs biologic agents (TNF inhibitors)
DMARDs (Methotrexate) corticosteroids
Serum sickness
, lOMoAR cPSD| 67691079
Stop exposure to offending agent corticosteroids (severe)
Antihistamines NSAIDs
Post-Strep glomerulonephritis
Supportive care Diuretics
Antihypertensives antibiotics (for underlying
infection)
Type 4 – Delayed Reaction
Contact Dermatitis
Avoid trigger allergen/irritant
Topical corticosteroids
Antihistamines (for itching)
Tuberculosis (Active/Latent) Latent:
isoniazid, rifampin
Active: combination therapy (isoniazid, rifampin, pyrazinamide, and
ethambutol)
Type I Diabetes Mellitus Insulin
replacement
Blood glucose monitoring
Lifestyle management
Multiple Sclerosis
Corticosteroids (acute flares)
Disease modifying therapy (interferons, glatiramer acetate, monoclonal
antibodies)
Graft-host virus
Immunosuppressants (cyclosporin, tacrolimus) Corticosteroids
Pathophysiology of Human Immunodeficiency Virus (HIV)
Targets immune system – CD4 – T helper cells (coordinate immune response)
Enters body through blood, vaginal secretions, semen or breastmilk
Once infected, it uses reverse transcriptase to convert RNA to DNA – can remain
latent or become active producing more virus
Acute infection
clinical latency
AIDS – CD4 count is below 200, opportunistic infections/cancers develop.
Widespread immune dysfunction.
