WGU D115 Advanced Pathophysiology
Mechanisms Cheat Sheet for OA Exam
D115 Advanced Pathophysiology —
Mechanisms of Disease
Step-by-step cascades for every major disease · WGU OA Exam Focus
HOW IT STARTS → WHAT BREAKS → WHY SYMPTOMS OCCUR → HOW
TREATMENT WORKS
Unit 2 — Immunity: Mechanisms
,U2 Type I Hypersensitivity (Anaphylaxis)
TRIGGER Allergen exposure (1st time) → sensitization only — no symptoms yet
▼
STEP 1 B cells → IgE antibodies → bind Fc receptors on mast cells & basophils →
Sensitization patient is now primed
▼
STEP 2 Allergen cross-links 2 adjacent IgE molecules → triggers mast cell
degranulation signal
Re-exposure
▼
STEP 3 Mast cells release: Histamine (vasodilation, ↑permeability, bronchoconstriction),
heparin, tryptase
Degranulation
▼
STEP 4 Membrane → arachidonic acid → Leukotrienes (sustained bronchospasm,
Arachidonic mucus) + Prostaglandins
cascade
▼
Massive vasodilation + capillary leak → distributive shock. Airway smooth muscle
OUTCOME
contracts → wheeze/stridor
Epinephrine FIRST: α1→vasoconstriction (↑BP), β2→bronchodilation, β1→↑HR.
Antihistamines only block histamine — they DON'T stop leukotrienes or reverse shock.
, WGU: Why epi, not antihistamines? Epi counteracts ALL mediators + reverses vascular
collapse. Antihistamines = too slow, too narrow.
U2 SLE — Autoimmune / Type III Mechanism
Genetic (HLA-DR3) + UV/viral/drugs → defective apoptotic debris clearance
TRIGGER
▼
STEP 1 Failed clonal deletion → autoreactive B + T cells survive → produce
Tolerance failure
autoantibodies (anti-dsDNA, anti-Smith, ANA)
▼
STEP 2 Autoantibodies + nuclear antigens → circulating immune complexes (Type III
mechanism)
Immune complexes
▼
STEP 3 Complexes deposit in: glomeruli (nephritis), skin (malar rash), joints, serosal surfaces
Deposition
(pleuritis)
▼
Complement activated → C3a/C5a → neutrophils → tissue destruction.
OUTCOME
↓C3/C4 = active disease
Hydroxychloroquine: blocks TLR signaling → ↓autoantibody production. Steroids: suppress
inflammation. Belimumab: blocks BLyS → ↓B cell survival.
WGU: SLE = Type III at its core (immune complexes). Active disease = ↓C3/C4 (complement
consumed). Anti-dsDNA RISES before flares — tracks activity.
Unit 3 — Neuro & Endocrine: Mechanisms
U3 Myasthenia Gravis — NMJ Failure
Mechanisms Cheat Sheet for OA Exam
D115 Advanced Pathophysiology —
Mechanisms of Disease
Step-by-step cascades for every major disease · WGU OA Exam Focus
HOW IT STARTS → WHAT BREAKS → WHY SYMPTOMS OCCUR → HOW
TREATMENT WORKS
Unit 2 — Immunity: Mechanisms
,U2 Type I Hypersensitivity (Anaphylaxis)
TRIGGER Allergen exposure (1st time) → sensitization only — no symptoms yet
▼
STEP 1 B cells → IgE antibodies → bind Fc receptors on mast cells & basophils →
Sensitization patient is now primed
▼
STEP 2 Allergen cross-links 2 adjacent IgE molecules → triggers mast cell
degranulation signal
Re-exposure
▼
STEP 3 Mast cells release: Histamine (vasodilation, ↑permeability, bronchoconstriction),
heparin, tryptase
Degranulation
▼
STEP 4 Membrane → arachidonic acid → Leukotrienes (sustained bronchospasm,
Arachidonic mucus) + Prostaglandins
cascade
▼
Massive vasodilation + capillary leak → distributive shock. Airway smooth muscle
OUTCOME
contracts → wheeze/stridor
Epinephrine FIRST: α1→vasoconstriction (↑BP), β2→bronchodilation, β1→↑HR.
Antihistamines only block histamine — they DON'T stop leukotrienes or reverse shock.
, WGU: Why epi, not antihistamines? Epi counteracts ALL mediators + reverses vascular
collapse. Antihistamines = too slow, too narrow.
U2 SLE — Autoimmune / Type III Mechanism
Genetic (HLA-DR3) + UV/viral/drugs → defective apoptotic debris clearance
TRIGGER
▼
STEP 1 Failed clonal deletion → autoreactive B + T cells survive → produce
Tolerance failure
autoantibodies (anti-dsDNA, anti-Smith, ANA)
▼
STEP 2 Autoantibodies + nuclear antigens → circulating immune complexes (Type III
mechanism)
Immune complexes
▼
STEP 3 Complexes deposit in: glomeruli (nephritis), skin (malar rash), joints, serosal surfaces
Deposition
(pleuritis)
▼
Complement activated → C3a/C5a → neutrophils → tissue destruction.
OUTCOME
↓C3/C4 = active disease
Hydroxychloroquine: blocks TLR signaling → ↓autoantibody production. Steroids: suppress
inflammation. Belimumab: blocks BLyS → ↓B cell survival.
WGU: SLE = Type III at its core (immune complexes). Active disease = ↓C3/C4 (complement
consumed). Anti-dsDNA RISES before flares — tracks activity.
Unit 3 — Neuro & Endocrine: Mechanisms
U3 Myasthenia Gravis — NMJ Failure
