## Pathophysiology of Pheochromocytoma Crisis **Key Point:** Pheochromocytoma causes uncontrolled release of catecholamines (epinephrine and norepinephrine) from the adrenal medulla, leading to unopposed α-adrenergic receptor activation. ### Sympathetic Receptor Activation Pattern | Receptor | Tissue | Effect | Manifestation | |----------|--------|--------|----------------| | α₁-adrenergic | Vascular smooth muscle | Vasoconstriction | Hypertension, severe | | α₁-adrenergic | Pupil dilator | Mydriasis | Dilated pupils | | α₂-adrenergic | Presynaptic terminals | Feedback inhibition | Reduced further release | | β₁-adrenergic | Heart | Increased contractility, HR | Tachycardia, palpitations | | β₂-adrenergic | Bronchi, vessels | Bronchodilation, vasodilation | Mild counterbalance | **High-Yield:** In pheochromocytoma crisis, the **massive catecholamine surge overwhelms negative feedback mechanisms**, resulting in unopposed α-adrenergic effects that dominate the clinical picture. The severe hypertension, profuse diaphoresis (α₁ activation of sweat glands), and tremor (β₂ activation of skeletal muscle) are hallmark features. ### Clinical Pearl The **hypertensive crisis** in pheochromocytoma is primarily driven by α-adrenergic vasoconstriction. β-adrenergic effects (tachycardia, tremor) are secondary and less dangerous than the α-mediated hypertension. This is why **α-blockade (phenoxybenzamine) is initiated BEFORE β-blockade** in preoperative preparation — blocking β first can paradoxically worsen hypertension due to unopposed α effects. ### Why This Is the Best Answer The clinical triad of **severe hypertension + profuse sweating + tremor** directly reflects unopposed α-adrenergic receptor activation. The patient's elevated metanephrines confirm massive catecholamine release, and the sympathetic manifestations are proportional to the degree of α-receptor stimulation. [cite:Harrison 21e Ch 405]
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