NR507 MIDTERM STUDY GUIDE: IMMUNOLOGY,
HEMATOLOGY, CARDIOVASCULAR,
PULMONARY,RENAL | CORRECT QUESTIONS AND
VERIFIED ANSWERS ~ CHAMBERLAIN UNIVERSITY.
NR507 MIDTERM — COMPLETE FILLED-OUT STUDY GUIDE
(Weeks 1–4: Immunology, Hematology, Cardiovascular, Pulmonary, Renal)
WEEK 1 — IMMUNOLOGICAL PATHOLOGIES
Four Types of Hypersensitivity Reactions
Prototype
Type Mechanism Key S/S Treatment
Disease
Allergen
Anaphylaxis
Type I cross-links IgE , allergic Urticaria, Epinephrine,
on mast cells → bronchospasm antihistamines,
(IgE-mediated) rhinitis,
histamine , hypotension steroids
asthma
release
IgG/IgM bind to Hemolytic
Type II cell-surface Hemolysis, Remove trigger,
anemia,
(Antibody-media antigens → Graves hyperthyroidis immunosuppressio
ted cytotoxic) complement m n
disease
activation
Antigen-antibod
Type III Steroids,
y complexes SLE, serum Rash, arthritis,
(Immune-comple deposit in sickness nephritis immunosuppressan
x) tissues → ts
inflammation
Sensitized T
Type IV (Delayed Contact Erythema, Avoid allergen,
cells cause dermatitis, vesicles,
T-cell mediated) topical steroids
tissue damage TB test induration
HIV Pathophysiology
• Virus binds CD4 receptors + CCR5/CXCR4 co-receptors
• Reverse transcription → integration into host genome
• Progressive CD4 destruction → impaired cell-mediated immunity
• Opportunistic infections when CD4 < 200
,
, Systemic Lupus Erythematosus (SLE)
Pathophysiology
• Loss of self-tolerance → autoantibodies form immune complexes
• Complexes deposit in skin, kidneys, joints → complement activation →
inflammation
Diagnosis
• ANA (sensitive)
• Anti-dsDNA (specific, correlates with disease activity)
• Anti-Smith (specific)
• Low complement (C3/C4)
Clinical Symptoms
• Malar rash
• Photosensitivity
• Oral ulcers
• Arthritis
• Nephritis
• Serositis
• Cytopenias
Treatment
• Mild: NSAIDs, hydroxychloroquine
• Moderate: steroids
• Severe: immunosuppressants (azathioprine, mycophenolate)
• Flare: high-dose steroids
Alloimmune Phenomenon
• Immune reaction to non-self antigens from same species
• Examples: transplant rejection, hemolytic disease of newborn
Primary vs. Secondary Immunodeficiency
HEMATOLOGY, CARDIOVASCULAR,
PULMONARY,RENAL | CORRECT QUESTIONS AND
VERIFIED ANSWERS ~ CHAMBERLAIN UNIVERSITY.
NR507 MIDTERM — COMPLETE FILLED-OUT STUDY GUIDE
(Weeks 1–4: Immunology, Hematology, Cardiovascular, Pulmonary, Renal)
WEEK 1 — IMMUNOLOGICAL PATHOLOGIES
Four Types of Hypersensitivity Reactions
Prototype
Type Mechanism Key S/S Treatment
Disease
Allergen
Anaphylaxis
Type I cross-links IgE , allergic Urticaria, Epinephrine,
on mast cells → bronchospasm antihistamines,
(IgE-mediated) rhinitis,
histamine , hypotension steroids
asthma
release
IgG/IgM bind to Hemolytic
Type II cell-surface Hemolysis, Remove trigger,
anemia,
(Antibody-media antigens → Graves hyperthyroidis immunosuppressio
ted cytotoxic) complement m n
disease
activation
Antigen-antibod
Type III Steroids,
y complexes SLE, serum Rash, arthritis,
(Immune-comple deposit in sickness nephritis immunosuppressan
x) tissues → ts
inflammation
Sensitized T
Type IV (Delayed Contact Erythema, Avoid allergen,
cells cause dermatitis, vesicles,
T-cell mediated) topical steroids
tissue damage TB test induration
HIV Pathophysiology
• Virus binds CD4 receptors + CCR5/CXCR4 co-receptors
• Reverse transcription → integration into host genome
• Progressive CD4 destruction → impaired cell-mediated immunity
• Opportunistic infections when CD4 < 200
,
, Systemic Lupus Erythematosus (SLE)
Pathophysiology
• Loss of self-tolerance → autoantibodies form immune complexes
• Complexes deposit in skin, kidneys, joints → complement activation →
inflammation
Diagnosis
• ANA (sensitive)
• Anti-dsDNA (specific, correlates with disease activity)
• Anti-Smith (specific)
• Low complement (C3/C4)
Clinical Symptoms
• Malar rash
• Photosensitivity
• Oral ulcers
• Arthritis
• Nephritis
• Serositis
• Cytopenias
Treatment
• Mild: NSAIDs, hydroxychloroquine
• Moderate: steroids
• Severe: immunosuppressants (azathioprine, mycophenolate)
• Flare: high-dose steroids
Alloimmune Phenomenon
• Immune reaction to non-self antigens from same species
• Examples: transplant rejection, hemolytic disease of newborn
Primary vs. Secondary Immunodeficiency
