BMS 150 Esophagus Spring 2023 PDF

Part 1: https://ccnm.ca.panopto.com/Panopto/Pages/Vi ewer.aspx?id=4acc4014-903a-4459-805e- afcb00098066 Part 2: https://ccnm.ca.panopto.com/Panopto/Pages/Vi ewer.aspx?id=4fd36ff9-4519-4639-816e- afcb0017200b PHL & PAT Esophagus BMS 150 Week 11  GI: Esophagus Junquiera...

Part 1: https://ccnm.ca.panopto.com/Panopto/Pages/Vi ewer.aspx?id=4acc4014-903a-4459-805e- afcb00098066 Part 2: https://ccnm.ca.panopto.com/Panopto/Pages/Vi ewer.aspx?id=4fd36ff9-4519-4639-816e- afcb0017200b PHL & PAT Esophagus BMS 150 Week 11  GI: Esophagus Junquiera 13th p 299-301 Guyton p 763-766 Boron Chapter 41  Esophagus Collapsible muscular tube about 25cm long Lies posterior to trachea Begins at inferior end of laryngopharynx Passes through inferior aspect of neck to enter mediastinum Pierces diaphragm through esophageal hiatus Ends in superior portion of stomach Esophagus: Histology Mucosa - Epithelium Nonkeratinized stratified squamous epithelium Langerhans cells present - Lamina propria Esophageal cardiac glands in 2 clusters (near pharynx and stomach) - secrete mucous Lymphoid nodules - Muscularis Only a single layer of longitudinally smooth muscle mucosae Submucosa Dense, irregular fibroelastic CT Esophageal glands proper: mucous and serous cells Muscularis externa Outer and inner layers, with variable amounts of skeletal muscle upper 1/3 mostly skeletal, middle 1/3 mixed, lower 1/3 mostly smooth muscle Serosa / adventitia Adventitia until it pierces the diaphragm, then serosa  ç Esophagus: Anatomy Major arteries include thoracic branches of the aorta superiorly Branches of the left ç gastric artery inferiorly Major venous drainage (next slide) via the azygous vein and the portal venous system via the left gastric veins ç ç Esophagus – Anatomy At the lower esophagus, the portal circulation (branches of the left gastric vein) “overlaps” or drains the same area as the systemic venous circulation (esophageal branches à azygous vein) This interface is a pathologically important site of bleeding if the veins rupture Discussed later in liver pathology Muscular anatomy The larynx compresses the esophagus superiorly to some extent Muscles that move the larynx and hyoid upwards and anteriorly to allow swallowing (don’t need to memorize them here) The cricopharyngeus muscle and the rest of the inferior pharyngeal constrictor muscle are the major players in “pushing food down” There’s a “weak spot” just above the cricopharyngeus ç muscle (circled) ç Sometimes an outpouching develops and food “gets stuck” – known as a Zencker Diverticulum  ç Esophagus: Anatomy FYI diagram – note the rich nerve ç plexuses around the esophagus, including ç the vagi and thoracic ç ç sympathetic nerves ç  Esophageal Movements Deglutition (swallowing) § Complex process involving mouth, pharynx and esophagus § Can be divided into: Voluntary stage Pharyngeal stage Esophageal stage  Esophageal Movements Voluntary Stage of swallowing: § After chewing, food is voluntarily squeezed or rolled posteriorly into the pharynx § By pressure of the tongue upward and backward against the palate § From here on, swallowing becomes almost entirely automatic Esophageal Movements Pharyngeal Stage of swallowing: § Reflex controlled by brain stem (medulla) 1.Food in pharynx – tactile stimulation 2.Soft palate pulled upward Good idea – blocks the nasal cavity so food doesn’t get shoved out your nose 3.Palatopharyngeal folds pulled together creates “sagittal slit” for selective action Esophageal Movements 4. Trachea is closed (respiration inhibited) Vocal cords approximated Larynx raises and epiglottis covers vocal cords 5. Relaxation of UES 6. Peristaltic contraction of pharynx  Nervous control of Pharyngeal Stage Swallowing Center - medulla - Sensory input from pharnyx and esophagus - Coordinates activity from vagal nuclei with other centers (e.g., inhibits respiratory center) Pharyngeal Phase - - Food in pharynx ® afferent sensory input via vagus N. / glossopharyngeal N. ® swallowing center ® brain stem nuclei ® efferent input to pharynx Coordination of Swallowing Entire pharyngeal swallowing stage occurs in less than 2 seconds § Only interrupts respiration for a fraction of a usual respiratory cycle Swallowing center inhibits respiratory center of the medulla, halting respiration at any point in its cycle to allow swallowing to proceed Peristaltic waves “push” food down into the stomach (takes more than one) Esophageal Movements Secondary peristalsis § Result from distention of the esophagus by retained food, or by reflux of gastric contents into the esophagus Continue until all the food has emptied into stomach § Initiated by intrinsic neural circuits in myenteric nervous plexus and vagal afferent fibers from esophagus to medulla and back to esophagus through vagal efferent fibers Lower Esophageal Sphincter (LES) 1-2 cm below diaphragm and 2-5cm above juncture with stomach where esophageal circular muscle functions as LES (aka GES) § Normally remains tonic and constricted When a peristaltic wave passes down esophagus, receptive relaxation relaxes the LES ahead of the peristaltic wave to allow easy propulsion of food into stomach § Prevents reflux Esophageal manometry: -Note the high resting pressures of the UES, and the low resting pressures of the LES -Note the higher pressures in the LES after food has passed into the stomach -Relaxation of the LES mainly due to activity of NO- and VIP-secreting branches of the vagus nerve Esophageal Pathology The Esophagus A wide range of common pathologies that run the gamut from benign to deadly § Not to mention the rare stuff… Basic “groups” of pathologies: § Dysphagic/motility diseases Dysphagia = difficulty swallowing § Inflammatory diseases § Metaplastic/neoplastic diseases Done in future lectures § Vascular diseases Done in future lectures Motility/obstructive disorders Nutcracker esophagus § Visceral pain from the esophagus is well-localized, and excess distention cause relatively intense, brief chest pain High-amplitude esophageal contractions Outer longitudinal layer of smooth muscle contracts before the inner circular layer Cause periodic short-lived esophageal obstruction Other motor disorders of esophagus include diffuse esophageal spasm (very common) § result in minor obstruction or chest pain as well § Due to dysfunction of inhibitory nerves Patchy neural degeneration localized to nerve processes noted on histology Motility/obstructive disorders Achalasia § Increased tone of the LES can be due to impaired smooth muscle relaxation If inhibitory neurons do not release VIP or NO after swallowing, the LES won’t relax properly § Achalasia = incomplete LES relaxation, increased LES tone, and aperistalsis of the esophagus § Primary achalasia is idiopathic, caused by failure of distal esophageal inhibitory neurons Degenerative changes in neural innervation, either intrinsic to the esophagus or within the extraesophageal vagus nerve or the dorsal motor nucleus of the vagus, may also occur § Secondary achalasia: diabetic autonomic neuropathy, malignancy Infections (tropical countries) - Trypanosoma cruzi infection causes destruction of the myenteric plexus, failure of peristalsis, and esophageal dilatation, partial or absent lower esophageal sphincter relaxation Motility/obstructive disorders Achalasia § Clinical features: Dysphagia, chest pain, regurgitation Incidence of 1/100,000/year Does not affect mortality – unless malignancy is involved § Treatment: Botox Myotomy Esophageal imaging – barium swallow Diffuse esophageal spasm Achalasia Manometry studies  Motility/obstructive disorders Other causes of dysphagia: Iron-deficiency anemia or chronic reflux disease sometimes causes fibrosis or non-malignant growths that obstruct the esophagus Worsening dysphagia and reflux symptoms in many populations needs to be investigated to ensure that the patient has not developed esophageal cancer § We will cover esophageal malignancies later this semester  Esophagitis Infectious esophagitis § Usually a sign of immunosuppression HSV (small “punched-out” lesions), cytomegalovirus (CMV), or fungal organisms Among fungi, candidiasis is most common, although mucormycosis and aspergillosis may occur § Typically grayish-white pseudomembrane on a tender, erythematous base Autoimmune esophagitis § Crohn’s disease (rare) § Scleroderma – mostly obstructive & regurgitation vs. inflammatory findings, since LES and distal esophagus becomes atrophic and loses functionality § Eosinophilic esophagitis – emerging disease Eosinophilic Esophagitis Esophagitis that is usually distributed throughout the length of the esophagus, with primarily esosinophilic inflammation § > 15 eosinophils/high-power field, much fewer neutrophils and lymphocytes § Marked basal cell hyperplasia and elongation of the submucosal papillae Increasing in incidence and is a disease of both children and adults § Not uncommon – prevalence of ~ 50/100,000  Normal and Eosinphilic esophagitis Brief pathophysiology: Th2 response with an abundance of IL-4, IL-5, and IL-13 in serum and in affected tissue Often a history of atopic illness during or before the GI symptoms No candidate genes identified as of yet – food intolerance/allergies are thought to be major inciting factors  Eosinophilic esophagitis Clinical features: § Kids – nausea and vomiting, small for age, weight loss if severe Heartburn/reflux less prominent in small children, more common in older § Adults – main symptom is dysphagia and food impaction – chest pain can occur as well Heartburn can be present, and is usually resistant to PPIs, though occasionally does respond to PPIs Diagnosis: § Endoscopy § Often IgE levels are elevated Reflux esophagitis Normal histology = stratified squamous epithelium § Resistant to abrasion from foods but is sensitive to acid § Submucosal glands, more abundant in the proximal and distal esophagus, secrete mucin and bicarbonate § Constant lower esophageal sphincter tone prevents reflux of acidic gastric contents Though most people have physiologic occurrence of reflux that is asymptomatic or mildly symptomatic Reflux of gastric contents into the lower esophagus is the most frequent cause of esophagitis § Most common outpatient GI diagnosis in the United States  Reflux esophagitis Caused by reflux of bile and gastric acid into the esophagus § Decreased LES tone or increased abdominal pressure likely contribute to GERD § Aggravating factors include alcohol and tobacco use, obesity, central nervous system depressants, pregnancy, hiatal hernia, delayed gastric emptying, and increased gastric volume  Reflux esophagitis Findings include: § Hyperemia, mild eosinophilic infiltration in less severe cases § Basal zone hyperplasia exceeding 20% of the total epithelial thickness and elongation of lamina propria papillae may be present in more severe cases § Barrett’s esophagus = patches of red, velvety mucosa extending upward from the gastroesophageal junction that alternate with the smooth, pale normal esophageal mucosa Metaplasia looks similar to intestinal glandular epithelium – goblet cells are present – with time many will progress to dysplasia More common with more significant reflux Can be a pre-malignant change, but most do not progress to esophageal cancer – Barrett’s needs to be followed via endoscopy over time Esophagitis images  Reflux esophagitis Clinical features § Dysphagia, heartburn, and, less frequently, regurgitation § Rarely, chronic GERD is punctuated by attacks of severe chest pain that may be mistaken for heart disease Treatment with proton pump inhibitors or H2 histamine receptor antagonists, which reduce gastric acidity, typically provides symptomatic relief § Severity of symptoms is not closely related to the degree of histologic damage but disease duration is § Heartburn that increases in severity and is accompanied by dysphagia is a red flag for esophageal carcinoma More later this semester Food Triggers Coffee and tea Chocolate Spicy food Beer, wine, and other forms of alcohol Fried or greasy foods Mint Tomatoes and tomato-based foods Sweets and high-glycemic index foods