upper GI Flashcards
What are the upper/middle/lower parts of oesophagus made of muscle wise?
Upper part - skeletal. Middle - skeletal + smooth. Lower - smooth.
What are the contributions to the lower oesophageal sphincter?
- 3-4cm distal oesophagus within abdomen (abdominal oesophagus)
- diaphragm surrounds LOS (contracts against LOS more effective)
- intact phrenoesophageal ligament
- angle of His (normally acute angle between abdominal oesophagus and fundus of stomach - prevents reflux)
What are the phases of swallowing and what happens at each phase?
Stage 0: oral phase - chewing & saliva prepare bolus (both UOS and LOS constricted). Stage 1: pharyngeal phase - guides bolus to oesophagus - UOS opens reflexly & LOS opened by vasovagal reflex (receptive relaxation reflex). Stage 2: upper oesophageal phase - UOS closed and superior circular muscle rings contract & inferior rings dilate - sequential contraction of longitudinal muscle guides bolus down. Stage 3 - lower oesophageal phase - LOS closes as food passes through
What is motility of the oesophagus determined by clinically?
Manometry - measures/records pressure of contractions during swallowing.
What is normal peristaltic wave pressure? Normal LOS resting pressure? When does LOS resting pressure decrease?
Normal peristaltic wave pressure = 40mmHg. Normal LOS resting pressure = 20mmHg. Decreases more than 5mmHg during receptive relaxation of LOS mediated by inhibitory non-cholinergic non-adrenergic neurones (NCNA) of myenteric plexus
What can abnormal oesophageal contraction be divided into?
Hypermotilty, hypomotility, disordered coordination or failure of protective mechanisms for reflux
What is dysphagia? How do we differentiate between types?
Difficulty swallowing. Localisation important (proximal, distal) and type (solids, fluids, both, intermittent/progressive, vague/precise)
What is odynophagia?
Pain when swallowing
What is regurgitation?
Return of oesophgeal contents from above an obstruction
What is reflux?
Return of gastroduodenal contents to the mouth
What is hypermotility (achalasia) due to?
Due to loss of ganglion cells in aurebach’s myenteric plexus in LOS wall thus decreases activity of inhibitory NCNA neurones.
What are causes of secondary achalasia?
Chagas disease (trypanosomiasis), protozoa infection, amyloid/sarcoma/eosinophilic oesophagitis
What is pathophysiology of hypermotility (achalasia)? What does it lead to?
Decreased activity of inhibitory NCNA neurones so increased resting LOS pressure. Receptive relaxation happens too late and is too weak. Because pressure in LOS a lot higher than stomach pressure, swallowed food collects in oesophagus causing increased pressure throughout with dilation of oesophgaus. Loss of peristalsis in distal oesophagus because LOS constricted so food cant pass. Resultant dysphagia, regurgitation, oesophgaitis, weight loss, possible pneumonia due to aspirating oesophageal contents.
What is the disease course of hypermotility (achlasia) and what happens if untreated? Risks?
Insidious, symptoms gradually worsen over years. Untreated can lead to progressive oesophageal dilatation. Risk of oesophgeal cancer high.
What are treatments for achalasia and what do they involve?
- pneumatic dilatation (PD): weakens LOS by by stretching and inflating it. Efficacious but many relapse. Surgical –> 1. heller’s myotomy: continous myotomy on oesophagus and stomach 2. dor fundoplication: anterior fundus sutured to distal oesophagus. Risks - oesophgeal/gastric perforation, division of vagus nerves, splenic injury.
What is hypomotility (scleroderma)? What does it cause? What is it often assoicated with?
Scleroderma is autoimmune disease. Neuronal defects cause atrophy of smooth muscle of oesophagus, peristalsis in distal portion stops, decreasing resting pressure of LOS. Get GORD as a result. Associated with CREST syndrome.
What is treatment for hypomotility (scleroderma)?
Exclude organic obstruction (malignnacy), give prokinetics to improve peristalsis (cisapride) but not very effective (usually peristaltic failure irreversible)
What is disordered coordination of oesophagus and what does it cause?
Disordered coordination of oesophgeal contractions lead to dysphagia and chest pain. Very high pressures of 400-500mmHg. Marked hypertrophy of circular muscle
Why do we see corkscrew oesophagus on barium in disordered coordination?
Marked hypertrophy of circular muscle in oesophagus so corkscrew oesophagus
Treatment for corkscrew oesophagus?
May respond to forceful PD of cardia (pneumatic dilatation but response unpredictable)
What is boerhaave’s syndrome and what does it cause?
Sudden increase in intra-oesophageal pressure with negative intra-thoracic pressure (eg vomitting against closed glotis) causes spontaneous perforation of oesophagus
How can foreign bodies cause oesophgeal perforation?
Swallow foreign bodies (batteries can cause electrical burns), sharp objects, dishwasher tablets etc
How can trauma cause oesophageal perforation? What is seen in presentation?
Penetrating trauma in neck or blunt force in thorax. Can present with dysphagia, blood in saliva, haematemesis, surgical emphysema
What is primary management of oesophageal perforation? What is treatment?
NBM (nil-by-mouth), IV fluids, broad spectrum Abx and antifungals. Surgical emergency because mortality increases if 24h delayed diagnosis. Conservative management (if small contained perforation) - covered metal oesophageal stent. Definitive management: 1. primary repair optimal 2. oesophagectomy - joining stomach to patent oesophagus proximally
Why does LOS close and what increases LOS pressure / decreases LOS pressure?
LOS usually closed as barrier against reflux/gastric juices. LOS pressure increased by acetylcholine, a-adrenergic agonists, hormones. LOS pressure decreased by eating fats, smoking, nitrous oxide.
What is sporadic reflux?
Normal reflux (due to transient sphincter opening)
What are the 3 mechanisms that protect following reflux?
- volume clearance (oesophageal peristalsis clears reflux contents) 2. pH clearance (saliva counteracts low pH), epithelium barrier properties
What can cause failure of protective mechanisms following reflux?
- increased frequency of sphincter opening (fizzy drinks, air, CO2). 2. decreased volume clearance (abnormal peristalsis) 3. decreased pH clearance (not enough saliva) or decreased buffering capacity of saliva (smoking,) 4. hiatus hernia (abnormal exit of tissue/organ through wall of cavity) 5. defective mucosal epithelium (alcohol).
What can reflux oesophagitis lead to?
Epithelial metaplasia –> dysplasia –> carcinoma
What are the 2 types of hiatus hernia and what happens in each?
- sliding hiatus hernia (contributes to GORD) - whole stomach slides up so distal oesophagus within chest. 2. rolling/paraoesophageal hernia - distal oesophagus held in place by ligaments but portion of stomach slides up on side.
Why is rolling hernia an emergency?
Anything below hernia can get strangulated (blood flow compromised) causing ischaemia, death and perforation
What investigations are used for GORD and why?
OGD (to exclude cancer, see oesophagitis, peptic stricture, barret’s), manometry, 24h oesophageal pH recording (see if actually reflux)
What is treatment for GORD? When is surgery appropriate/ what type?
Medical : lifestyle change (weight loss, smoking) & PPIs. Surgery if dilatation of peptic strictures - laparoscopic nissens fundoplication (bit of fundus taken and wrapped around LOS)
What are the functions of the stomach?
- breaks food into smaller particles (acid & pepsin) 2. holds food releasing it steadily into duodenum 3. kills parasites and bacteria.
What is produced in cardia, pylorus, body, fundus, antrum?
Cardia & pylorus - mucus only. Body & fundus - mucus, HCL, pepsinogen. Antrum - gastrin
What is erosive & haemorrhagic gastritis caused by? What does it cause? Where can it happen?
Gastric bleeding and perforation in gastric wall. NSAIDS, trauma, ischaemia. Anywhere in stomach and can cause acute ulcers
What is non-erosive chronic gastritis? Where can it happen? What is the usual cause?
Only in antrum. Usually helicobacter pylori.
How is helicobacter pylori infection treated?
3x abx (amoxicillin, clarithromycin, pantoprazole) for 7-14 days
What is atrophic (fundal) gastritis? Where does it happen? What is the pathophysiology and the consequences?
only fundus. Autoantibodies against parts/products of parietal cells so parietal cell atrophy & dec acid & IF production. Less acid production so G-cell (gastrin) hyperplasia -> epithelial hyperplasia –> carcinoma. ECL-cell hyperplasia –> carcinoid (neuroendocrine tumours). Due to dec IF vtiamin B12 cobalamin deficiency (decreased absorbance)
What are the types of gastritis?
Erosive & haemorrhagic, non-erosive chronic gastritis, atrophic (fundal) gastritis, reactive gastritis
What causes stimulation of gastric secretion?
- neural - Ach (post-ganglionic transmitter of vagal PNS fibres) 2. endocrine - gastrin (G cells of antrum) 3. paracrine (histamine (ECL))
What causes inhibition of gastric secretion?
- endocrine - secretin. 2. paracrine & autocrine - PGs (E2 & I2), TGF-a & adenosine. 3. paracrine - somatostatin
What do parietal cells produce? What do ECF cells produce? What do chief cells produce?
Parietal cells make H+. ECF cells make histamine. Chief cells make pepsinogen
What are protective mechanisms against ulcers?
- mucus film protects against acid & pepsin 2. epithelial cells produce bicarbonate to buffer protons (need prostaglandins for bicarbonate production - decrease with NSAIDS) 3. good mucosal blood perfusion - if H+ gets through taken away with blood supply (ischaemia - lack of blood flow)
What are mechanisms repairing epithelial defects for ulcers?
- migration - adjacent epithelial cells flatten to close gap along base of membranae 2. gap closed by cell growth (stimulated by EGF, TFG-a, IGF-1, GRP & gastrin) 3. acute wound healing - BM destroyed attracts leukocytes, macrophgeas leading to phagocytosis of necrotis cells, angiogenesis and regeneration of ECM. 4. epithelial closure by restitution & wound healing
What causes ulcer formation and why? i
increased chemical aggression - H, pylori, increased gastric juice production, decrease in bicarbonate secretion, decrease in cell formation, ischaemia. H. pylori disturbs barrier function & invades mucosal barrier. NSAIDs decrease PG syntehsis needed for bicarbonate production & inhibition of acid secretion. Smoking causes barrier disrubance. Streess (trauma, surgery, psychogenic, smoking) cause increased hydrogen secretion & pepsinogen secretion
What are some clinical outcomes of ulcers?
H.pylori mostly asymptomatic. Can get chronic atrophic gastritis intestinal metaplasia. Can get gastric/duodenal cancer. Can get gastric cancer & MALT lymphoma
What is treatment for ulcers?
- medical - PPI or H2 blocker. Triple Abx for helicobacter pylori.
What do we do if ulcer don’t heal within 12 weeks?
Change meds and observe for 12 weeks. Check serum gastrin (antral G cell hyperplasia or gastrinoma - zollinger ellisons). OGF - biopsy of 4 quadrants of ulcer to rule out malignancy
What are surgical indications for ulcers?
Intractability after medical therapy, contrinuous requirement of steroids/NSAIDs, complications (haemorrhage, obstruction, perforation)
