Upper GI tract Flashcards

1
Q

Describe the anatomical contributions to the lower oesophageal sphincter

A

3-4 cm distal oesophagus within abdomen
Diaphragm surrounds LOS
An intact phrenoesophageal ligament - The upper limb attaches the esophagus to the superior surface of the diaphragm and the lower limb attaches the cardia region of the stomach to the inferior surface of the diaphragm at the cardiac notch of stomach. The ligament allows independent movement of the diaphragm and esophagus during respiration and swallowing.
Angle of His - acts as a barrier against reflux

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2
Q

Describe the stages of swallowing

A

Stage 0: Oral phase - Chewing & saliva prepare bolus. Both oesophageal sphincters constricted.
Stage 1: Pharyngeal phase - Pharyngeal musculature guides food bolus towards oesophagus. Both oesophageal sphincters open.
Stage 2: Upper oesophageal phase - Upper sphincter closes. Superior circular muscle rings contract & inferior rings dilate. Sequential contractions of longitudinal muscle.
Stage 3: Lower oesophageal phase - Lower sphincter closes as food passes through

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3
Q

How is the motility of the oesophagus measured?

A

Manometry pressure measurements - tube passed through nose down oesophagus to record pressure of the contractions, exposing whether contractility is normal or not.

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4
Q

What are normal pressure measurements in the oesophagus?

A

Peristaltic waves ~ 40 mmHg
LOS resting pressure ~ 20 mmHg
↓<5 mmHg during receptive relaxation - this is mediated by inhibitory noncholinergic nonadrenergic (NCNA) neurons of myenteric plexus

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5
Q

What causes functional disorders of the oesophagus?

A

Absence of a stricture. Caused by either abnormal oesophageal contraction (hypermotility, hypomotility, disordered coordination) or failure of protective mechanisms for reflux (gastrooesophageal reflux disease).

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6
Q

What is dysphagia?

A

Dysphagia is difficulty in swallowing. Localisation important - depends whether distal or the cricopharyngeal sphincter. Types of dysphagia:
For solids or fluids
Intermittent or progressive
Precise or vague in appreciation

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7
Q

What is odynophagia, regurgitation and reflux?

A

Odynophagia is pain on swallowing
Regurgitation refers to return of oesophageal contents from above an obstruction. May be functional or mechanical.
Reflux is passive return of gastroduodenal contents to the mouth.

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8
Q

What is achalasia?

A

Refers to hypermotility. Occurs due to loss of ganglion cells in Aurebach’s myenteric plexus in LOS wall which leads to decreased activity of inhibitory NCNA neurones.

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9
Q

What is the proposed pathophysiology of achalasia?

A

An environmental trigger such as a chronic infectious insult combined with a genetic predisposition and genetic factors (mutations and SNIPs ALADIN, NOS, IL-10 etc) lead to increase in non autoimmune inflammatory infiltrates (increase in Th1, Tregs, Bregs, pDCregs). This leads to extracellular turnover, wound repair mechanisms activating and fibrosis. Conversely, increase in immune cells can trigger an immunosuppressive response leading to loss of immunological tolerance, loss of neurons and eventually humoral response (antinuclear antibodies, antimyenteric antibodies). Causes myenteric neuronal abnormalities, autoimmune myenteric plexitis, vasculitis, absence of peristalsis and decreased relaxation of LOS.

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10
Q

What is secondary achalasia?

A

Caused by other disorders which mimic the symptoms of primary achalasia. These diseases cause oesophageal motor abnormalities: Chagas’ Disease, Protozoa infection, Amyloid/Sarcoma/Eosinophilic Oesophagitis.

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11
Q

What happens in achalasia?

A

Increased resting pressure of LOS, almost 80mmHg. Receptive relaxation sets in late & is too weak - during reflex phase pressure in LOS is markedly ↑er than stomach. Swallowed food collects in oesophagus causing ↑ pressure throughout with dilation of the oesophagus. Propogation of peristaltic waves cease.

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12
Q

Describe disease course of achalasia

A

Has insidious onset - symptoms for years prior to seeking help. If untreated, progressive oesophageal dilatation of oesophagus occurs. Causes a 28-fold increase in risk of oesophageal cancer.

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13
Q

What is a treatment option for achalasia?

A

Pneumatic dilatation. Stent with balloon inserted and balloon then inflated, opening up LOS. 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.

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14
Q

What are surgical treatment options for achalasia?

A

Heller’s Myotomy - A continuous myotomy performed for 6 cm on the oesophagus & 3 cm onto the stomach.
Dor fundoplication – anterior fundus folded over oesophagus and sutured to right side of myotomy

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15
Q

What are the risks of gastric surgery?

A

Oesophageal & gastric perforation (10 – 16%)
Division of vagus nerve – rare
Splenic injury – 1 – 5%

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16
Q

What is scleroderma?

A

An autoimmune disease referring to hypomobility in its early stages due to neuronal defects - atrophy of smooth muscle of oesophagus occurs. Peristalsis in the distal portion ultimately ceases altogether. Decreased resting pressure of LOS means GORD develops and is often associated with CREST syndrome.

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17
Q

What is the treatment for scleroderma?

A

Exclude organic obstruction
Improve force of peristalsis with prokinetics (cisapride)
Once peristaltic failure occurs → usually irreversible

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18
Q

What does corkscrew oesophagus cause?

A

Disordered coordination due to diffuse oesophageal spasm. Incoordinate contractions causes dysphagia & chest pain. Pressures of 400-500 mmHg can occur. Marked hypertrophy of circular muscle.

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19
Q

What is treatment for corkscrew oesophagus?

A

May respond to forceful PD of cardia but results not as predictable as achalasia.

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20
Q

Describe anatomy of oesophageal perforations

A

There are 3 areas of anatomical constrictions: Cricopharyngeal constriction, aortic and bronchial constriction, diaphragmatic and sphincter constriction. However, pathological constrictions can be caused by cancer, foreign body, physiological dysfunction.

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21
Q

Describe aetiology of oesophageal perforation

A
Iatrogenic (OGD) >50% 
Spontaneous (Boerhaave’s) - 15% 
Foreign body - 12%
Trauma - 9% 
Intraoperative - 2%
Malignant - 1%
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22
Q

What causes iatrogenic oesophageal perforation?

A
Usually caused by oesophago-gastro-duodenoscopy. More common in the presence of diverticula or cancer. Incidences:
OGD = 0.03%
Stricture dilatation = 0.1-2%
Sclerotherapy = 1-5%
Achalasia dilatation = 2-6%
23
Q

How does Boerhaave’s cause oesophageal perforation?

A

Sudden increase in intra-oesophageal pressure with negative intra thoracic pressure - essentially perforation caused by vomiting against a closed glottis. Incidence of 3.1 per 1,000,000.

24
Q

How can trauma causing oesophageal perforation present?

A

Penetrating trauma more common in neck while blunt force more common on chest. Can be difficult to diagnose: Symptoms include dysphagia, blood in saliva, haematemesis and surgical emphysema.

25
Q

How does oesophageal perforation present?

A

Pain 95 %
Fever 80 %
Dysphagia 70 %
Emphysema 35 %

26
Q

What investigations are adviced for oesophageal perforation?

A

CXR
CT
Swallow (gastrograffin)
OGD

27
Q

What is primary management for oesophageal perforation?

A

Is a surgical emergency as 2x mortality if 24 hours delay in diagnosis. Initial management includes: NBM (nil by mouth), IV fluids and broad spectrum A/Bs & antifungals.
ITU/HDU level care needed. Bloods (including G&S) collected. Tertiary referral centre escalated.

28
Q

What is definitive management for oesophageal perforation?

A

Conservative management with covered metal stent fine for perforations that haven’t leaked. Operative management should be default: Primary repair optional but oesophagectomy is the definitive solution.

29
Q

How does the LOS inhibit reflux?

A

Usually at high pressure and closed to act as a barrier against reflux of gastric juice (pepsin + HCl). Increased pressure at sphincter can be caused by ACh, alpha-adrenergic agonists, hormones, protein-rich food, histamine, high intra-abdominal pressure.

30
Q

What factors promote reflux?

A

Decreased pressure in esophageal sphincter promotes reflux. Can be caused by VIP, beta-adrenergic agonists, hormones, dopamine, NO, PGI2, PGE2, chocolate, acid, fat and smoking.

31
Q

What causes sporadic reflux?

A

Pressure on full stomach
Swallowing
Transient sphincter opening

32
Q

What are protective mechanisms against reflux?

A

Volume clearance - oesophageal peristalsis reflex where transient sphincter opening cause LOS pressure to drastically rise.
pH clearance - saliva
Epithelium - barrier properties

33
Q

What is GORD?

A

A failure of protective mechanisms against reflux. Factors lead to reflux esophagitis causing epithelial metaplasia and carcinoma.

34
Q

What factors lead to reflux esophagitis?

A
  1. Decrease in sphincter pressure
  2. Increased transient sphincter opening
  3. Decrease in saliva production (in sleep, xerostomia) reducing pH clearance
  4. Reduced buffering capacity of saliva through e.g. smoking which reduces pH clearance.
  5. Abnormal peristalsis reducing volume clearance
  6. Hiatus hernia
  7. Defective mucosal protective mechanism e.g. due to alcohol
35
Q

Define sliding hiatus hernia

A

The gastro-oesophageal junction (GOJ), the abdominal part of the oesophagus, and frequently the cardia of the stomach move or ‘slides’ upwards through the diaphragmatic hiatus into the thorax.

36
Q

Define rolling hiatus hernia

A

An upward movement of the gastric fundus occurs to lie alongside a normally positioned GOJ, which creates a ‘bubble’ of stomach in the thorax. This is a true hernia with a peritoneal sac.

37
Q

What investigations are done for GORD?

A

OGD - To exclude cancer or confirm oesophagitis, peptic stricture & Barretts oesophagus
Oesophageal manometry
24-hr oesophageal pH recording

38
Q

What are medical and surgical recommendations for GORD?

A

Medical: Lifestyle changes (wt loss, smoking, EtOH) and PPIs
Surgical: Dilatation peptic strictures and Laparoscopic Nissen’s fundoplication

39
Q

What are the functions of the stomach and what does each region produce?

A
  1. Breaks food into smaller particles (acid & pepsin)
  2. Holds food, releasing it in controlled steady rate into duodenum
  3. Kills parasites & certain bacteria

Cardia & Pyloric Region: Mucus only
Body & Fundus: Mucus, HCl, pepsinogen
Antrum: Gastrin

40
Q

What is the presentation and location of different types of gastritis?

A
  1. Erosive and haemorrhagic gastritis - presents as acute ulcer (gastric bleeding and perforation)
  2. Nonerosive, chronic active gastritis - occurs at the antrum caused by Helicobacter Pylori (treated with amoxicillin, clarithromycin, pantoprazole)
  3. Atrophic gastritis - occurs at fundus caused by autoantibodies against parts of and products of parietal cells causing parietal cell atrophy. Decreased acid and IF secretion.
  4. Reactive gastritis
41
Q

What are causes of erosive and haemorrhagic gastritis?

A

NSAIDs, Alcohol, Multi-organ failure/burns, Trauma, Ischaemia

42
Q

Describe how chronic active gastritis causes problems

A

Increased gastrin secretion and normal/increased acid secretion leads to reactive gastritic causing epithelial metaplasia and carcinoma.

43
Q

Describe how atrophic fundal gland gastritis leads to carcinoma, carcinoid and pernicious anaemia

A

Reduction in pepsinogen, acid secretion and IF secretion occurs as autoantibodies target gastrin receptor, carbonic anhydrase, H+/K+ ATPase pump and IF. Decreased acid secretion causes increased gastrin secretion and G-cell hyperplasia as well as ECL-cell hyperplasia. Epithelial metaplasia leads to carcinoma while ECL-cell hyperplasia leads to carcinoid. Reduced IF secretion causes decreased cobalamine absorption leading to cobalamine deficiency and pernicious anaemia in the long-term.

44
Q

What chemicals stimulate gastric secretion?

A

Neural
ACh - postganglionic transmitter of vagal parasympathetic fibres
Endocrine
Gastrin (G cells of antrum)
Paracrine
Histamine (ECL cells & mast cells of gastric wall).

45
Q

What chemicals inhibit gastric secretion?

A
Endocrine 
Secretin (small intestine)
Paracrine 
Somatostatin (SIH) 
Paracrine & autocrine  
PGs (E2 & I2), TGF-α & adenosine
46
Q

How does gastric mucosal protection work?

A

Presence of mucus film and bicarbonate secretion by epithalial cells have a buffering affect on the H+ present in gastric lumen. Salivary epidermal growth factor also contributes to protecting epithelial surface.

47
Q

What are the mechanisms for repairing epithelial defects?

A
  1. Migration - Adjacent epithelial cells flatten to close gap via sideward migration along basement membrane
  2. Gap closed by cell growth - Stimulated by EGF, TGF-α, IGF-1, GRP & gastrin
  3. Acute wound healing: BM destroyed - attraction of leukocytes & macrophages; phagocytosis of necrotic cells; angiogenesis; regeneration of ECM after repair of BM
  4. Epithelial closure by restitution & cell division
48
Q

What factors cause formation of a gastric ulcer?

A

Helicobacter pylori, increase gastric juice secretion, decreased bicarbonate secretion, decreased cell formation, decreased blood perfusion

49
Q

What factors contribute to a barrier disturbance of gastric epithelium?

A

H. pylori infection causes gastritis and drugs such as indomethacin, diclofenac and acetylsalicyclic acid + smoking cause decrease in prostaglandin synthesis. This decreases mucosal protection and barrier disturbance occurs.

50
Q

What causes increased chemical aggression leading to gastric ulcer formation?

A

H.pylori infection, psychogenic components, smoking and neuroendocrine tumour of myenteric plexus such as gastrinoma all cause increased H+ secretion and increased pepsinogen secretion. Stress (shock, burns, operation) and psychogenic components also lead to decreased blood perfusion and together these factors lead to chemical aggression. Oxygen radicals from gastritis and bile salts + pancreatic enzymes also contribute. Smoking decreases blood perfusion.

51
Q

What are the clinical outcomes of a H.pylori infection?

A

80% leads to asymptomatic/chronic gastritis. 15-20% develop into chronic atrophic gastritis, intestinal metaplasia or gastric/duodenal ulcer. Less than 1% leads to gastric cancer or MALT lymphoma.

52
Q

What is medical treatment for gastric ulcer?

A
  1. PPI or H2 blocker

2. Triple Rx (amoxicillin, clarithromycin, pantoprazole) for 7-14 days)

53
Q

What are surgical indications for a gastric ulcer?

A

Intractability (after medical therapy)
Relative: continuous requirement of steroid therapy/NSAIDs
Complications: Haemorrhage, Obstruction, Perforation

54
Q

What is the course adviced if medication doesn’t work?

A
  1. Rare - most uncomplicated ulcers heal within 12 weeks
  2. If don’t, change medication, observe additional 12 weeks
  3. Check serum gastrin (antral G-cell hyperplasia or gastrinoma [Zollinger-Ellison syndrome])
  4. OGD: biopsy all 4 quadrants of ulcer (rule out malignant ulcer) if refractory.