NR507 MIDTERM STUDYGUIDE QUESTIONS AND CORRECT DETAILED ANSWERS WITH RATIONALES

NR507 MIDTERM STUDYGUIDE QUESTIONS AND
CORRECT DETAILED ANSWERS WITH RATIONALES
NR507 – Advanced Pathophysiology
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Exam Study Guide – Midterm Study Guide
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Exam Format: Noncumulative
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Question Type: Multiple Choice vi vi vi vi


Number of Questions: 100 Tim
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e Allotted: 120 minutes
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Testing Timeframe: The midterm exam will only be available starting on Wednesday Week 4 at
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12:01 am MT until Saturday Week 4 at 11:59 pm MT.
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1. Exam Coverage vi


Content Areas:
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• Week 1: Immunological Pathologies vi vi vi


• Week 2: Hematological and Cardiovascular Pathologies
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• Week 3: Pulmonary Pathologies vi vi vi


• Week 4: Urinary System Pathologies vi vi vi vi




2. Key Concepts to Study
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Alterations in Immunity and Inflammation:vi vi vi vi


• Pathophysiology of the four types of hypersensitivity reactions vi vi vi vi vi vi vi vi


ACID
Type I vi


Immediate (Anaphylaxis) – uses IgE antibodies – antibodies bind to mast vi vi vi vi vi vi vi vi vi vi


cells and basophils- vi vi


releases histamines based on prior exposure to the allergen. Results to vasodilatio
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n, bronchoconstriction, hives, edema and anaphylaxis (severe).
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Hay fever, insect bites, food/drug allergies, asthma vi vi vi vi vi vi


Type 2 vi


Antibody-Mediated (Cytotoxic) -IgG/IgM antibodies – bind to antigens on vi vi vi vi vi vi vi vi


the surface of host cells – blood cell, platelets, tissues –
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activates the complement system – leads to lysis –
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formation of the membrane attack complex.vi vi vi vi vi vi


Phagocytosis may occur. vi vi


transfusion reactions, autoimmune hemolytic anemia, Graves Disease, Rh I vi vi vi vi vi vi vi vi


ncompatibility, MG vi




Type 3 vi


Immune-Complex -IgG/IgM. formation of immune complex that deposit vi vi vi vi vi vi vi


in the tissues. Activates the complement system –
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leads to inflammation and tissue damage.
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SLE, RA, serum sickness, vasculitis, glomerulonephritis vi vi vi vi vi




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,Type 4
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Delayed (Cell Meditated)- T-cells (CD4, TH1). Antigen presenting cells
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capture the antigen and present in T helper cells which become sensitized and act
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ivate during subsequent exposure. Upon re-
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exposure the t cell releases cytokins – activation of immune cells-
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causes inflammation and tissue damage.
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, Contact dermatitis, TB, chronic transplant rejection, MS
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• Prototype diseases that reflect each of the four types of hypersensitivity (i.e. Type IV-
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contact dermatitis) and signs and symptoms
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Type I – Immediate (Anaphylaxis)
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Cause: Allergens (food/meds/hay fever, asthma, dermatitis)
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Components: IgE, Mast Cells, histamine vi vi vi vi


S/S – vi


Sudden onset wheezing vi


Hives hypotension, tachycardia, dizziness vi vi


Swelling
nausea, vomiting, diarrhea vi vi v


Shock (severe) i vi


Type 2 -Cytotoxic (Antibody Mediated)
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Cause: receiving incompatible blood type, hemolytic anemia, Graves Disease,
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MG
S/S – vi


Fever hypotension, jaundice vi


Chills hemoglobinuria
Back/flank pain renal failure/shock (severe) vi vi vi




Type 3 -Immune- vi vi


Complex Cause: Autoimmune vi vi


response
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Components – IgG/IgM, antibody- vi vi vi


antigen components, complement, RA, serum sickness, glomerulonephritis, hyper
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sensitivity pneumonitis, TB, MS DMI vi vi vi vi


S/S-
Butterfly rash (Malar rash) vi vi vi


renal involvement Fati vi vi


gue/fever neurological sympotms vi


Joint pain vi


serositis (pericarditis/pleuritis) vi


Photosensitivity vi




Type 4 – Delayed Type
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Cause : skin contact with allergen (poison ivy, nickel, latex) Co
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mponents -T cells, cytokins, macrophanges
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S/S
Red, itchy rash vi vi


localized swelling vi


Blisters vi


Scaling/thickened skin (with chronic exposure) vi vi vi vi




• Treatment options for diseases under each hypersensitivity category
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Type I – Immediate Type (Anaphylaxis)
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Anaphylaxis Treatment vi


Epi Antihistamines
Oxygen Corticosteriods
IV fluids vi




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, Airway Management
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Allergic Rhinitis Treatment
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