🩸 Dysmenorrhea Prostaglandin Mechanism Simulator
This simulator models the synthesis of prostaglandins by the endometrium that causes uterine contractions in primary dysmenorrhea, and the effect of NSAIDs at different times of administration to block this process.
Endometrial Breakdown Triggers the Dysmenorrhea Cascade
Falling progesterone destabilizes the endometrium at menses onset.
- Menses: Cycle phase (Day 1 onset)
- Progesterone drop: Trigger (Late luteal phase)
- Lysosome release: Tissue event (Membrane breakdown)
- ~50–90%: Affected women (Report dysmenorrhea)
Why shedding starts the pain pathway
Placeholder: falling hormones destabilize endometrial cell membranes, freeing arachidonic acid.
Arachidonic Acid to Prostaglandin via COX Enzymes
COX-1 and COX-2 convert arachidonic acid into PGF2α and PGE2.
- COX-1/COX-2: Key enzyme (Cyclooxygenase)
- PGF2α: Main mediator (Vasoconstrictor)
- Arachidonic acid: Precursor (Membrane phospholipid)
- Day 1–2: Peak levels (Of menstruation)
Synthesis pathway placeholder
Placeholder: phospholipase A2 frees arachidonic acid, COX oxidizes it into prostaglandin precursors.
Prostaglandins Drive Hypercontractile Uterine Spasm
High PGF2α causes sustained myometrial contraction and ischemia.
- >150 mmHg: Pressure rise (Vs. ~80 normal)
- >4–5/10min: Contraction freq (Hypercontractility)
- Uterine ischemia: Result (Reduced blood flow)
- Cramping pain: Symptom (Pelvic/lower back)
Spasm mechanism placeholder
Placeholder: prostaglandins bind myometrial receptors, driving vasoconstriction and painful contractions.
NSAIDs Inhibit COX to Cut Prostaglandin Output
NSAIDs block the COX active site, reducing new prostaglandin synthesis.
- NSAIDs: Drug class (Ibuprofen, naproxen)
- COX active site: Target (Competitive inhibition)
- ↓PG synthesis: Effect (Not existing PG)
- ~30–60 min: Onset (Oral absorption)
Blockade mechanism placeholder
Placeholder: NSAIDs occupy the COX enzyme pocket, preventing further arachidonic acid conversion.
Why Early Dosing Improves Pain Relief Outcomes
Dosing before pain onset blocks synthesis before prostaglandins accumulate.
- Pre-onset: Best timing (1–2 days before)
- Lower relief: Late dosing (PG already high)
- ~70–90%: Relief rate (With early NSAID use)
- Scheduled dosing: Strategy (Not as-needed only)
Timing dependence placeholder
Placeholder: earlier NSAID timing prevents the prostaglandin surge rather than reversing it.
Placeholder: start NSAIDs before pain begins for the strongest relief effect.
This simulator models the synthesis of prostaglandins by the endometrium that causes uterine contractions in primary dysmenorrhea, and the effect of NSAIDs at different times of administration to block this process.
2D · HTML5 Canvas 2D · 60 FPS target · runs fully client-side, no install