lOMoARcPSD|63525276
Table of Contents
Week 1: Hypersensitivity Reactions
Types I–IV, immune mechanisms, diagnostics, treatment, case studies, review Qs
Week 2: Anemias, CAD & Heart Failure
Anemia classification, iron/B12/folate/ACD, CAD pathophysiology, HF types & staging
Week 3: Pulmonary Pathology
Obstructive vs. restrictive disease, COPD, emphysema vs. bronchitis, PFTs, case studies
Week 4: Urinary Pathology
UTIs, pyelonephritis, renal calculi, acute/chronic renal failure, ARF stages, CKD stages
Week 5: GI & Neurobiological Disorders
GERD, PUD, IBD, cirrhosis; MDD, bipolar, anxiety, schizophrenia — patho to symptoms
Week 6: Endocrine System
HPA axis, thyroid disorders, diabetes T1/T2, PTH disorders, adrenal disorders (Cushing's/Addison's)
Week 7: Neurological & Dermatological
Alzheimer's, Parkinson's, MS, myasthenia gravis, neuropathies, seizures, stroke, skin disorders
Page 2
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Week 1
Hypersensitivity Reactions
Immune mechanisms · Clinical presentations · Diagnostics · Treatment
Core Concept
Hypersensitivity reactions are excessive or misdirected immune responses causing tissue damage. Types I–III
are antibody-mediated; Type IV is T-cell mediated (no antibody involvement). Each type has a distinct
mechanism, onset, and clinical presentation.
Feature Type I Type II Type III Type IV
IgG/IgM → cell Immune complexes
IgE → mast cell surface antigens → deposit in tissues → T-cell mediated; no
Mechanism degranulation cell destruction complement activation antibodies
IgE, mast cells, CD4+/CD8+ T-cells,
basophils, histamine, IgG/IgM, complement, IgG/IgM, complement, macrophages,
Mediators leukotrienes phagocytes, ADCC neutrophils cytokines
Onset Minutes Hours to days Variable (hrs–days) 48–72 hours (delayed)
Anaphylaxis, asthma,
allergic rhinitis, Hemolytic anemia, SLE, post-strep GN, Contact dermatitis,
Examples urticaria Graves' disease serum sickness PPD test, T1DM
Type I — Immediate / IgE-Mediated
Allergen → B-cells produce IgE → IgE binds FcεRI receptors on mast cells
(sensitization). Re-exposure: allergen cross-links IgE → mast cell degranulation →
Mechanism histamine, leukotrienes, prostaglandins released → inflammation.
Histamine (vasodilation, ↑ vascular permeability) · Leukotrienes (bronchoconstriction) ·
Key Mediators Prostaglandins (inflammation)
Respiratory: wheezing, rhinorrhea, sneezing. Skin: urticaria, pruritus, erythema.
S&S; Systemic (anaphylaxis): hypotension, angioedema, laryngospasm.
Examples Anaphylaxis (bee sting, food allergy), allergic rhinitis, asthma, urticaria, eczema
Diagnostics Skin prick test · Serum IgE levels · RAST (Radioallergosorbent Test)
Allergen avoidance · Antihistamines · Corticosteroids · Epinephrine (anaphylaxis) ·
Treatment Desensitization immunotherapy
NR507 Advanced Pathophysiology — Comprehensive Study Guide Page 3
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Type II — Cytotoxic
IgG or IgM antibodies bind antigens on host cell surfaces → complement activation +
Mechanism ADCC + phagocytosis → cell lysis, inflammation, or cellular dysfunction.
Onset Hours to days
Hemolytic Anemia (AIHA)
Autoantibodies bind RBC surface antigens → RBCs destroyed by macrophages via Fc
Mechanism receptors (IgG) or complement lysis (IgM). Spleen/liver are primary effectors.
Fatigue, pallor, jaundice (↑ bilirubin), dark urine (hemoglobinuria), tachycardia,
Signs & Symptoms dyspnea, splenomegaly
Direct Coombs (DAT): detects IgG/C3 on RBCs — most important test. Indirect
Coombs: free antibodies in serum. CBC: ↓ Hgb, ↑ reticulocytes. ↑ LDH, ↓ haptoglobin,
Diagnostics ↑ indirect bilirubin.
Corticosteroids (first-line) · Immunosuppressants (azathioprine) · IVIG · Blood
Treatment transfusion (cautious) · Splenectomy (refractory)
Graves' Disease
TSI autoantibodies mimic TSH → bind TSH receptors → stimulate excess T3/T4
production. Thyroid tissue NOT destroyed — function is altered. NOTE: Type II
Mechanism because antibodies bind to cell surface receptor.
Weight loss (increased appetite), heat intolerance, sweating, tachycardia, anxiety,
Signs & Symptoms tremors, goiter, exophthalmos (unique to Graves'), menstrual irregularities
↓ TSH, ↑ free T4/T3 · TSI (Graves'-specific autoantibodies) · RAIU scan: high diffuse
Diagnostics uptake · TRAb antibodies
Methimazole (preferred) or PTU · Beta-blockers (symptom control) · Radioactive iodine
Treatment (definitive) · Thyroidectomy · Corticosteroids (exophthalmos)
Type III — Immune Complex
Antigen-antibody (IgG/IgM) complexes form in circulation → deposit in tissues
(kidneys, joints, skin, vessels) → complement activation → neutrophil recruitment →
Mechanism neutrophils fail to phagocytose → enzyme release → tissue inflammation and damage.
Kidneys (SLE, PSGN): glomerulonephritis. Joints (RA, SLE): arthritis, swelling. Skin:
Tissue & Outcome rash, purpura. Blood vessels: vasculitis. Lungs: alveolitis, pneumonitis.
Examples SLE · Post-streptococcal glomerulonephritis · Serum sickness · Arthus reaction
SLE Highlights
NR507 Advanced Pathophysiology — Comprehensive Study Guide Page 4
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SLE is primarily Type III (immune complex deposition) but has Type II features
Dual type (autoantibodies target blood cells → cytopenias).
ANA (sensitive screening) · Anti-dsDNA + anti-Sm (specific for SLE) · ↓ C3/C4
Key diagnostics (consumed in complexes) · ↑ ESR/CRP
MSK: arthralgia/arthritis. Skin: malar rash, discoid rash, photosensitivity, alopecia.
Renal: hematuria, proteinuria. Hematologic (Type II): anemia, leukopenia,
S&S; by system thrombocytopenia. CNS: seizures, psychosis.
NSAIDs · Corticosteroids · Immunosuppressives · Antimalarials · Biologics · Sun
Treatment protection
Type IV — Delayed / T-Cell Mediated
Antigen → T-cell sensitization. Re-exposure: CD4+/CD8+ T-cells recruit and activate
macrophages → cytokine release → inflammation and cell death. No antibody
Mechanism involvement — distinguishes from Types I–III.
Onset 48–72 hours (delay due to T-cell recruitment and macrophage activation time)
Examples Contact dermatitis (poison ivy), tuberculin skin test (PPD), Type I Diabetes Mellitus
S&S; (Contact Dermatitis) Redness, intense pruritus, papules/vesicles, peeling/lichenification (chronic)
Treatment Prednisone · Topical hydrocortisone (suppress T-cell activation and cytokine release)
NR507 Advanced Pathophysiology — Comprehensive Study Guide Page 5
Table of Contents
Week 1: Hypersensitivity Reactions
Types I–IV, immune mechanisms, diagnostics, treatment, case studies, review Qs
Week 2: Anemias, CAD & Heart Failure
Anemia classification, iron/B12/folate/ACD, CAD pathophysiology, HF types & staging
Week 3: Pulmonary Pathology
Obstructive vs. restrictive disease, COPD, emphysema vs. bronchitis, PFTs, case studies
Week 4: Urinary Pathology
UTIs, pyelonephritis, renal calculi, acute/chronic renal failure, ARF stages, CKD stages
Week 5: GI & Neurobiological Disorders
GERD, PUD, IBD, cirrhosis; MDD, bipolar, anxiety, schizophrenia — patho to symptoms
Week 6: Endocrine System
HPA axis, thyroid disorders, diabetes T1/T2, PTH disorders, adrenal disorders (Cushing's/Addison's)
Week 7: Neurological & Dermatological
Alzheimer's, Parkinson's, MS, myasthenia gravis, neuropathies, seizures, stroke, skin disorders
Page 2
, lOMoARcPSD|63525276
Week 1
Hypersensitivity Reactions
Immune mechanisms · Clinical presentations · Diagnostics · Treatment
Core Concept
Hypersensitivity reactions are excessive or misdirected immune responses causing tissue damage. Types I–III
are antibody-mediated; Type IV is T-cell mediated (no antibody involvement). Each type has a distinct
mechanism, onset, and clinical presentation.
Feature Type I Type II Type III Type IV
IgG/IgM → cell Immune complexes
IgE → mast cell surface antigens → deposit in tissues → T-cell mediated; no
Mechanism degranulation cell destruction complement activation antibodies
IgE, mast cells, CD4+/CD8+ T-cells,
basophils, histamine, IgG/IgM, complement, IgG/IgM, complement, macrophages,
Mediators leukotrienes phagocytes, ADCC neutrophils cytokines
Onset Minutes Hours to days Variable (hrs–days) 48–72 hours (delayed)
Anaphylaxis, asthma,
allergic rhinitis, Hemolytic anemia, SLE, post-strep GN, Contact dermatitis,
Examples urticaria Graves' disease serum sickness PPD test, T1DM
Type I — Immediate / IgE-Mediated
Allergen → B-cells produce IgE → IgE binds FcεRI receptors on mast cells
(sensitization). Re-exposure: allergen cross-links IgE → mast cell degranulation →
Mechanism histamine, leukotrienes, prostaglandins released → inflammation.
Histamine (vasodilation, ↑ vascular permeability) · Leukotrienes (bronchoconstriction) ·
Key Mediators Prostaglandins (inflammation)
Respiratory: wheezing, rhinorrhea, sneezing. Skin: urticaria, pruritus, erythema.
S&S; Systemic (anaphylaxis): hypotension, angioedema, laryngospasm.
Examples Anaphylaxis (bee sting, food allergy), allergic rhinitis, asthma, urticaria, eczema
Diagnostics Skin prick test · Serum IgE levels · RAST (Radioallergosorbent Test)
Allergen avoidance · Antihistamines · Corticosteroids · Epinephrine (anaphylaxis) ·
Treatment Desensitization immunotherapy
NR507 Advanced Pathophysiology — Comprehensive Study Guide Page 3
, lOMoARcPSD|63525276
Type II — Cytotoxic
IgG or IgM antibodies bind antigens on host cell surfaces → complement activation +
Mechanism ADCC + phagocytosis → cell lysis, inflammation, or cellular dysfunction.
Onset Hours to days
Hemolytic Anemia (AIHA)
Autoantibodies bind RBC surface antigens → RBCs destroyed by macrophages via Fc
Mechanism receptors (IgG) or complement lysis (IgM). Spleen/liver are primary effectors.
Fatigue, pallor, jaundice (↑ bilirubin), dark urine (hemoglobinuria), tachycardia,
Signs & Symptoms dyspnea, splenomegaly
Direct Coombs (DAT): detects IgG/C3 on RBCs — most important test. Indirect
Coombs: free antibodies in serum. CBC: ↓ Hgb, ↑ reticulocytes. ↑ LDH, ↓ haptoglobin,
Diagnostics ↑ indirect bilirubin.
Corticosteroids (first-line) · Immunosuppressants (azathioprine) · IVIG · Blood
Treatment transfusion (cautious) · Splenectomy (refractory)
Graves' Disease
TSI autoantibodies mimic TSH → bind TSH receptors → stimulate excess T3/T4
production. Thyroid tissue NOT destroyed — function is altered. NOTE: Type II
Mechanism because antibodies bind to cell surface receptor.
Weight loss (increased appetite), heat intolerance, sweating, tachycardia, anxiety,
Signs & Symptoms tremors, goiter, exophthalmos (unique to Graves'), menstrual irregularities
↓ TSH, ↑ free T4/T3 · TSI (Graves'-specific autoantibodies) · RAIU scan: high diffuse
Diagnostics uptake · TRAb antibodies
Methimazole (preferred) or PTU · Beta-blockers (symptom control) · Radioactive iodine
Treatment (definitive) · Thyroidectomy · Corticosteroids (exophthalmos)
Type III — Immune Complex
Antigen-antibody (IgG/IgM) complexes form in circulation → deposit in tissues
(kidneys, joints, skin, vessels) → complement activation → neutrophil recruitment →
Mechanism neutrophils fail to phagocytose → enzyme release → tissue inflammation and damage.
Kidneys (SLE, PSGN): glomerulonephritis. Joints (RA, SLE): arthritis, swelling. Skin:
Tissue & Outcome rash, purpura. Blood vessels: vasculitis. Lungs: alveolitis, pneumonitis.
Examples SLE · Post-streptococcal glomerulonephritis · Serum sickness · Arthus reaction
SLE Highlights
NR507 Advanced Pathophysiology — Comprehensive Study Guide Page 4
, lOMoARcPSD|63525276
SLE is primarily Type III (immune complex deposition) but has Type II features
Dual type (autoantibodies target blood cells → cytopenias).
ANA (sensitive screening) · Anti-dsDNA + anti-Sm (specific for SLE) · ↓ C3/C4
Key diagnostics (consumed in complexes) · ↑ ESR/CRP
MSK: arthralgia/arthritis. Skin: malar rash, discoid rash, photosensitivity, alopecia.
Renal: hematuria, proteinuria. Hematologic (Type II): anemia, leukopenia,
S&S; by system thrombocytopenia. CNS: seizures, psychosis.
NSAIDs · Corticosteroids · Immunosuppressives · Antimalarials · Biologics · Sun
Treatment protection
Type IV — Delayed / T-Cell Mediated
Antigen → T-cell sensitization. Re-exposure: CD4+/CD8+ T-cells recruit and activate
macrophages → cytokine release → inflammation and cell death. No antibody
Mechanism involvement — distinguishes from Types I–III.
Onset 48–72 hours (delay due to T-cell recruitment and macrophage activation time)
Examples Contact dermatitis (poison ivy), tuberculin skin test (PPD), Type I Diabetes Mellitus
S&S; (Contact Dermatitis) Redness, intense pruritus, papules/vesicles, peeling/lichenification (chronic)
Treatment Prednisone · Topical hydrocortisone (suppress T-cell activation and cytokine release)
NR507 Advanced Pathophysiology — Comprehensive Study Guide Page 5
