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 tr tr tr tr


Number of Questions: 100 Tim tr tr tr tr


e Allotted: 120 minutes
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Testing Timeframe: The midterm exam will only be available starting on Wednesday Week 4 at 1
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2:01 am MT until Saturday Week 4 at 11:59 pm MT.
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1. Exam Coverage tr t


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


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


• Week 4: Urinary System Pathologies tr tr tr tr




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


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


ACID
Type I tr


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


cells and basophils- tr tr


releases histamines based on prior exposure to the allergen. Results to vasodilation,
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bronchoconstriction, hives, edema and anaphylaxis (severe). tr tr tr tr tr


Hay fever, insect bites, food/drug allergies, asthma tr tr tr tr tr tr


Type 2 tr


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


the surface of host cells – blood cell, platelets, tissues – tr tr tr tr tr tr tr tr tr tr


activates the complement system – leads to lysis –
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formation of the membrane attack complex.
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Phagocytosis may occur. tr tr


transfusion reactions, autoimmune hemolytic anemia, Graves Disease, Rh In tr tr tr tr tr tr tr tr


compatibility, MG tr




Type 3 tr


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


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 tr tr tr tr tr




Type 4 tr


Delayed (Cell Meditated)- T-cells (CD4, TH1). Antigen presenting cells tr tr tr tr tr tr tr tr


capture the antigen and present in T helper cells which become sensitized and activ
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ate during subsequent exposure. Upon re-exposure the t cell releases cytokins –
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, activation of immune cells- causes inflammation and tissue damage.
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, Contact dermatitis, TB, chronic transplant rejection, MS tr tr tr tr tr tr




• 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 tr tr tr tr


S/S – tr


Sudden onset wheezing tr


Hives hypotension, tachycardia, dizziness tr tr


Swelling
nausea, vomiting, diarrhea tr tr tr


Shock (severe) tr


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


Fever hypotension, jaundice tr


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




Type 3 -Immune- tr tr


Complex Cause: Autoimmune tr tr tr


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


antigen components, complement, RA, serum sickness, glomerulonephritis, hypers
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ensitivity pneumonitis, TB, MS DMI tr tr tr tr


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


renal involvement Fati tr tr


gue/fever neurological sympotms tr


Joint pain tr


serositis (pericarditis/pleuritis) tr t


Photosensitivity r




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 tr tr tr tr


S/S
Red, itchy rash tr tr


localized swelling tr t


Blisters r


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




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


Epi Antihistamines
Oxygen Corticosteriods
IV fluids tr




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, Airway Management
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r Allergic Rhinitis Treatment
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