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Upper GI Xavier MachadoTILOs Organs of the gastrointestinal tract: Summarise the structure of gastrointestinal organs and relate these to their functions. 1 Cells of the gastrointestinal tract: Describe the cellular arrangement of tissues throughout the gastrointestinal tract and relate to local function. 2 Gastrooesophageal disorders: Summarise the pathology and pathophysiology of gastrooesophageal disorders. Gastrooesophageal disorders: Describe the clinical features and treatment options of gastrooesophageal disorders.Lecture Timeline Pathophysiology Features Management Anatomy Function DisorderAnatomy Upper GI tract Mouth to major papilla in duodenum Mouth to ileum Mouth to duodenojejunal junction (DJ)Oesophagus Vertical muscular tube Travels through the neck, thorax and abdomen, between the trachea and vertebral bodies Therefore divided into: 1. Cervical 2. Thoracic 3. Abdominal 1 C5 T10 Skeletal Smooth 2 Two sphincters present - prevent entry of air, and reflux of gastric contents Upper oesophageal sphincter 3 Lower oesophageal sphincterOesophagus Upper oesophageal sphincter anatomical, striated muscle sphincter at the junction between the pharynx and oesophagus Swallowing Lower oesophageal sphincter No specific muscle Physiological sphincter, 4 factors: 1 1. Acute angle 2. 3-4cm distal oesophagus within abdomen 2 3. Diaphragm surrounds LOS 4. Intact phrenoesophageal sphincter 3Disorders - oesophagus Disorders of oesophageal contraction Hyper motility Hypo motility Disordered coordination Oesophageal motility Manometry Peristaltic waves = 40 PD weakens LOS by circumferential stretching & in some cases, tearing of its muscle fibres • Efficacy of PD — 71 - 90% of patients respond initially but many patients subsequently relapse LOS resting pressure = 20 (decreased by 5 during receptive relaxation) Meditated by inhibitory noncholinergic nonadrenergic (NCNA) neurons of mesenteric plexus Achalasia Due to loss of ganglion cells in Aurebach’s myenteric plexus in LOS wall • → ↓ed activity of inhibitory NCNA neurones. Primary Aetiology unknown Secondary Diseases causing oesophageal motor abnormalities Chagas’ disease Protozoa infection Amyloid/Sarcoma/Eosinophilic oesophagi’s ↑ed resting pressure of LOS Treatment Pneumatic Dilatation / Surgery some cases, tearing of its musclperformed for 6 cm on the oesophagus & 3 cm onto PD — 71 - 90% of patients responthe stomach but patients subsequently relapserelapDor fundoplication – anterior fundus folded overe fibres • Efficacy of PD — 71 - 90% of patients respond initially but many oesophagus and sutured to right side of myotomy Risk of cancer: 28-fold increase Has insidious onset - symptoms for years prior to seeking help • Without treatment → progressive oesophageal dilatation of oesophagus.Scleroderma Autoimmune ↓ed resting pressure of LOS Hypomotility in its early stages due to neuronal defects → atrophy of smooth muscle of oesophagus Peristalsis in the distal portion ultimately ceases altogether. → gastroesophageal reflux disease develops Treatment Exclude organic obstruction PD weakens LOS by circumferential stretching & in some cases, tearing of its muscle fibres • Efficacy of PD — 71 - 90% of patients respond initially but many paImprove force of persitalsis with pro kinetics (cisapride) Once peristalsic failure occurs, usually irreversibleCorkscrew oesophagus Disordered coordination “Diffuse oesophageal spasm” Incoordinate contractions Dysphagia and chest pain Pressures of 400-500mmHg Marked hypertrophy of circular muscle Corkscrew oesophagus on Barium swallow Treatment May respond to pneumatic dilatation, but not effective oftenOesophageal perforation Aetiology 3 areas where this can happen PD weakens LOS by circumferential stretching & in some cases, tearing of its muscle fibres • Efficacy of PD — 71 - 90% of patients respond initially but many patients subsequently relapserogenic (OGD) >50% Trauma 9% Malignant 1% Spontaneous (Boerhaave’s) 15% Intraoperative 2% Foreign body 12% Iatrogenic Boerhaave’s Foreign Body Trauma Usually at OGD Sudden increase in Disk intra-oesophageal batteries Neck = penetrating More common in pressure Thorax = blunt force PD weakens LOS by circumferentialPD weakens LOS by circumferentialPD weakens LOS by circumferential stretching LOS by circumferential stretching stretching & in some cases, teariclosed glottisn some cases, teari& in some cases, tearing of its muDifficult to diagnoseing of its muscle fibres • of patients respond initially butof patients respond initially butinitially but many patients subsequentlylly but many patients subsequentlyspond patients subsequently relapse patients subsequently relapse robjects relapse 1 aspect ofteral oesophagus Dishwasher tablets Acid/alkali 2 Presentation Investigations Initial Management Conservative Pain CXR Nil By Mouth (NBM) 3 Covered metal stent Fever CT Fluids - why? Broad spec Abx + anti-fungals Surgical PD weakens LOS by circumferential stretching & in some cases, tearing of its muscle fibres • Efficacy of PD— 71 - 90% of patients respond initially but many patients subsequently relapse Emphysema OGD ITU care Repair Tertiary referral Oesophagectomy centre (definitive)Function + dysfunction - Stomach LOS pressure Decreased Increased Transient sphincter opening Function + dysfunction - Stomach Protective Mechanism How? Defect Effect of Defect 1. Volume clearance oesophageal peristalsis reflex Abnormal peristalsis Reduced vol. clearance 2. pH clearance saliva Decrease in buffering capacity of saliva (e.g. smoking) Reduced pH clearance Decrease in saliva production (e.g. sleep) 3. Epithelium barrier properties Defective mucosal protective mechanism (e.g. alcohol) Reduced protective capacity Reflux oesophagitis Epithelial metaplasia CarcinomaGORD A cause of GORD is hernias: Investigations Medical Mx Surgical Mx OGD -> rule out cancer, confirms other conditions Lifestyle changes (weight loss) Dilatation of strictures PD24hr oesophageal pH recordingal stretching & in some cases, tearing of its muscle fibres • Efficacy of PD — 71 - 90% of patients respond initially but many patients subsequently relapse Oesophageal manometry PPIs Nissen’s fundoplicationStomach functions • Breaks food into smaller particles (acid & pepsin) Holds food, releasing it in controlled steady rate into duodenum • Kills parasites & certain bacteriaGastritis Type Site Causes Properties Erosive & haemorrhagic gastritis Local/diffuse Numerous – NSAIDs, alcohol, trauma, Acute ulcer Ischaemia → gastric bleeding & perforation Nonerosive, chronic active gastritis Antrum Helicobacter pylori Triple Therapy – amoxicillin, clarithromycin, pantoprazole Can cause long-term outcomes Atrophic (fundal gland) gastritis Fundus Autoantibodies vs parts + products of Parietal cells parietal cells → Reduction in acid + IF secretion Reactive gastritis Body/Antrum In response to various stimuli (infection, Can cause epithelial metaplasia → carcinoma (if trigger not trauma) addressed/not treated)UlcerUlcer Thank you for listening If you could scan and complete this it would be very helpful