PH7.4 | PH7.4 | Anterior Pituitary Hormone Modulators — SDL Guide — Summary & Reflection

KEY TAKEAWAYS

Anterior Pituitary Hormone Modulators — Key Takeaways:

• GH suppression (acromegaly): somatostatin analogues (octreotide LAR/lanreotide — first-line medical) → cabergoline (adjunct) → pegvisomant (refractory; lowers IGF-1, not GH).
• Prolactin suppression (prolactinoma): dopamine agonists first-line — cabergoline preferred (>80% efficacy, weekly dosing, better tolerated); bromocriptine alternative.
• GnRH analogue paradox: pulsatile = stimulates LH/FSH; continuous = downregulates GnRH receptors → suppresses LH/FSH (castration). Clinical uses: prostate cancer, endometriosis, precocious puberty (suppressive); infertility via pump (stimulatory).
• Pegvisomant: GH receptor antagonist — IGF-1 is the monitoring endpoint, NOT GH (GH may rise).
• Cabergoline vs bromocriptine: cabergoline preferred for prolactinoma — less nausea, higher efficacy, weekly dosing.
• Leuprolide flare: initial testosterone surge → add anti-androgen (bicalutamide) for 4 weeks in prostate cancer.

REFLECT

Consider the concept of receptor pharmacodynamics in the context of leuprolide and the GnRH paradox. If you understand why continuous agonist stimulation causes receptor downregulation (and physiological suppression), can you apply this principle elsewhere in pharmacology? Think of one other example where a receptor agonist causes paradoxical suppression through desensitisation. Now consider a patient with endometriosis who asks 'why is this injection making my period worse for the first 2 weeks?' — how would you explain the leuprolide flare in patient-friendly language? Write a 3-sentence patient explanation.