## Histopathology of Achalasia ### Clinical Context The patient presents with classic features of achalasia: dysphagia, regurgitation of undigested food, and endoscopic findings of a dilated esophagus with a narrowed GE junction. The histopathological hallmark is the loss of ganglion cells in the myenteric (Auerbach's) plexus. ### Key Histological Features **Key Point:** Achalasia is characterized by selective degeneration and loss of inhibitory neurons (containing nitric oxide and VIP) in the myenteric plexus, leading to unopposed contraction of the lower esophageal sphincter. **High-Yield:** The myenteric plexus normally contains: - Excitatory neurons (acetylcholine) - Inhibitory neurons (nitric oxide, VIP) In achalasia, loss of inhibitory neurons → unopposed acetylcholine effect → persistent LES contraction. ### Microscopic Findings in Achalasia | Feature | Finding | | --- | --- | | **Ganglion cells** | Markedly reduced or absent | | **Nerve fibers** | Degeneration of inhibitory nerve fibers | | **Muscle fibers** | Initially normal, later hypertrophied | | **Inflammation** | Minimal (unlike secondary achalasia) | | **Fibrosis** | Develops in chronic cases | ### Pathophysiology 1. Loss of inhibitory neurotransmitters (NO, VIP) 2. Unopposed excitatory (cholinergic) activity 3. Persistent LES contraction 4. Failure of LES relaxation with swallowing 5. Progressive esophageal dilation proximal to the narrowed junction **Clinical Pearl:** The diagnosis is confirmed by manometry showing incomplete LES relaxation and elevated resting pressure, but histology showing ganglion cell loss is pathognomonic. **Mnemonic: ACHALASIA** — **A**bsence of **C**ontraction + **H**ypertension of **L**ES + **A**bsent **S**wallowing-induced **I**nhibition + **A**bsent ganglion cells [cite:Robbins 10e Ch 17] 
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