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Y2 - BRS - GI > Upper GI Tract > Flashcards

Upper GI Tract Flashcards

1
Q

Oesophagus anatomy:

A

Oesophagus = C5-T10

Consists of the cervical, upper thoracic, mid thoracic, and lower thoracic oesophagi

Cervical oesophagus is between the upper oesophageal sphincter and sternal notch

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2
Q

What is the lower oesophageal sphincter (LOS)and why is it an anatomical advantage?

A

Last 3-4 cm of the oesophagus = within the abdomen = so as diaphragm contracts, intraabdominal pressure increases causing the LOS to clamp shut

An intact phrenoesophageal ligament = extension of the fascia of the inferior surface of the diaphragm, which divides into two limbs
2 limbs = upper limb of diaphragm attached to oesophagus, lower limb attached to cardiac of stomach

Ligament allows for independent movement of diaphragm and oesophagus during respiration and swallowing

Angle of His = acute angle between LOS and fundus of stomach at oesophagogastric junction 
Air in(fundus) stomach compresses lateral to medial  oesophagogastric junction structures - pushing close the gastroesophageal flap valve
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3
Q

What are the 4 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
Upper oesophageal sphincter opens reflexly
LOS opened by vasovagal reflex (receptive relaxation reflex)

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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4
Q

How is it possible to measure the motility of the oesophagus?

How does the motility of the oesophagus change at different parts of the swallowing process?

A

Use pressure measurements (manometry):

When oesophagus contracts for peristalsis - 40mmHg

LOS resting = 20 mmHg, reduces to 5mmHg during receptive relaxation to allow food in

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5
Q

What nerves mediate the relaxation of the LOS?

A

Mediated by inhibitory noncholinergic nonadrenergic (NCNA) neurons of myenteric plexus

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6
Q

What do you eliminate first with functional disorders of the oesophagus?

What are the functional disorders of the oesophagus?

A

Absence of stricture (fibrous, stiff tissue due to exposure to severe inflammation)

Functional disorders can be caused by:
1. Abnormal oesophageal contractions e.g. hypermotility, hypomotility, disordered co-ordination

  1. Failure of protective mechanisms for reflux e.g. Gastro-oesophageal Reflux Disease (GORD)
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7
Q

Describe the terms below:

Dysphagia
Odynophagia
Regurgitation 
Reflux
Dyspepsia
A

Dysphagia = difficulty in swallowing (can be either cricopharyngeal or distal sphincter)

Odynophagia = pain on swallowing

Regurgitation = return of oesophageal contents from above an obstruction (can be functional or mechanical)

Reflux = passive return of gastroduodenal contents to the mouth

Dyspepsia: recurrent epigastric pain, heartburn or symptoms of acid regurgitations, with or without bloating, nausea or vomiting​

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8
Q

What is an example of a hypermotility disorder in the oesophagus and what causes it?

A

Achalasia - loss of ganglion cells in aurebach’s myenteric plexus in LOS wall = decreased activity of the inhibitory NCNA neurones

Results in inability of the LOS to relax –> swallowed food collects in the oesophagus

Unknown primary aetilogy

Secondary = diseases that cause oesphageal motor abnormalities

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9
Q

What can mimic achalasia (display as similar hypermotility problems)?

A

The diseases that show oesophageal abnormalities similar to achalasia are:

Chagas’ disease = parasite
Protozoa infection
Amyloid / Sarcoma / Eosinophilic oesophagitis

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10
Q

What is the mechanism of Achalasia?

A

Increased rested pressure of LOS (e.g. at 80mmHg)

Receptive relaxation sets in late and is too weak (decreases only to 60 mmHg)​

During reflex phase pressure in LOS is markedly higher than stomach

Swallowed food collects in oesophagus

Increases oesophageal pressure

Dilatation of the oesophagus

Peristalsis ceases

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11
Q

What is the disease course of achalasia?

A

Insidious onset - symptoms for years prior to seeking help​

Without treatment = progressive oesophageal dilatation of oesophagus (seen on barium swallow)

Causes weight loss, trouble swallowing and pain.

Can lead to oesophagitis, pneumonia (aspirational pneumonia) and increases risk of oesophageal cancer (28 fold)

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12
Q

How may patients with achalasia present clinically?

A

Presenting with “mega-oesophagus” – an enormous oesophagus with food contents which haven’t been able to reach the stomach

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13
Q

How is achalasia treated?

A

Pneumatic dilation (PD) - inflate a balloon in the LOS, leads to circumferential stretching, which this stretches and sometimes tears muscle fibres leading to weakened LOS​

Efficacy of PD = 71-90% respond initially
Usually relapses though in many patients

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14
Q

What are some surgical treatments for achalasia?

A

Most patients need surgery after a PD

  1. Heller’s Myotomy - a continuous myotomy (cutting muscle) performed for 6 cm on the oesophagus & 3 cm onto the stomach
  2. Dor fundoplication – anterior fundus folded over oesophagus and sutured to right side of myotomy
    Take fundus of stomach and wrap around mucosal defect then stitch to the other side to provide protection
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15
Q

What are some risks with the surgical treatments to treat achalasia?

A

Risks =

Oesophageal & gastric perforation (10 – 16%)​ = difficult to cut through only stomach muscle

Division of vagus nerve – rare​

Splenic injury – 1 – 5% = stomach right against spleen, spleen may bleed in splenic injury

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16
Q

What are some endoscopic ways to treat achalasia?

A

POEM - Peroral endoscopic myotomy

Endoscope enters dilated oesophagus - mucosal incision to get under mucosa

Create submucosal tunnel

Myotomy (cutting of muscle)

Closure of mucosal incision

Less invasive but less effective that classic surgical interventions

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17
Q

What is an example of a hypomotility disorder in the oesophagus and what causes it?

A

Scleroderma = autoimmune disease

Secondary due to neruonal defects - atrophy of smooth muscle cells (SMC) of oesophagus

Initially causes hypomotility

Later, peristalsis in distal portion ceases almost all together

Lowered resting pressure of LOS (to 0 mmHg instead of usual 20 mmHg) = reflux disease e.g. GORD (gastro-oesophageal reflux disease)

Often associated with CREST syndrome

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18
Q

What is the treatment for scleroderma?

A

Exclude organic obstruction
Improve force of peristalsis with prokinetics

Usually hard to restore peristalsis once gone (peristalsis failure), may need surgery to remove oesophagus altogether and replace with stomach

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19
Q

How does scleroderma present clinically?

A

Diffuse oesophageal spasm = uncoordinated contractions of the oesophagus

Presents as difficulty swallowing (dysphagia), chest pain, and/or regurgitation

Pressures of 400-500 mmHg

Barium swallow x-ray shows a corkscrew oesophagus (due to marked hypertrophy of oesophageal circular muscles)

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20
Q

How can a ‘corkscrew oesophagus’ be treated?

A

May respond to forceful PD of cardia​

Results not as predictable as achalasia

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21
Q

What are some vascular anomalies that can cause dysphagia?

A

Dysphagia Lusoria = right subclavian artery goes behind oesophagus and constricts it against the trachea - treat with surgical correction​

Double aortic arch = constriction of oesophagus against trachea - move subclavian where it belongs and stitch it in place

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22
Q

What is the anatomy of oesophageal perforations?

A

There are 3 anatomical areas of constriction injuries to oesphagus. Oesophageal perforations (hole/ rupture) occur usually at one of these 3 places:​

Cricoharyngeal constriction​ (commonest place to occur)

Aortic and bronchial constriction​

Diaphragmatic and sphincter constriction

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23
Q

What are the common causes of oesophageal perforations?

A

Most injuries to oesophagus caused by endoscopy (Oesophago-Gastro-Duodenoscopy - OGD) - >50%

Can also get a spontaneous rupture (Boerhaave’s) - 12%

Or a foreign body​ - 9%

Trauma - 9%​

Intraoperative - 2%​

Malignant - 1%

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24
Q

What leads to a spontaneous rupture (Boerhaave’s)?

A

Sudden increase in intra-oesophageal pressure combined with negative intra thoracic pressure​

Vomiting against a closed glottis​

Left posterolateral aspect of the distal oesophagus (most common place) tears​

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25
Q

How can foreign bodies cause oesophageal perforations?

A

Disk batteries are a growing problem​ - cause electrical burns if impact in mucosa​

Magnets​

Sharp objects​

Dishwasher tablets​

Acid/Alkali

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26
Q

How can trauma cause oesophageal perforations?

Why are trauma perforations sometimes difficult to diagnose?

A 
Neck = penetrating (stabbing)​
Thorax = blunt force

Trauma is more difficult to diagnose as it can present as:

Dysphagia​
Blood in saliva​
Haematemesis​
Surgical emphysema (leakage of air)​

27
Q

In what kind of intra-operative surgeries can oesophageal perforations occur?

A

Hiatus hernia repair​
Hellers Cardiomyotomy​
Pulmonary surgery​
Thyroid surgery

[Can perforate oesophagus when operating for something else]

28
Q

How can malignancy cause oesophageal perforations?

A 
Advanced cancers​
Radiotherapy​
Dilatation​
Stenting​
Poor prognosis
29
Q

How do oesophageal perforations present and how are they investigated / examined?

A

Presentation = pain, fever, dysphagia, emphysema

Investigations =

CXR - can see mediastinal air as air escapes the oesophagus OR increased opacity across chest due to abdominal contents escaping the oesophagus and into the chest (e.g. gastric juices, fluids etc.)

CT - can see uncontained fluid outside the eosopaghus

Swallow (gastrograffin)​

OGD

2x increased mortality if 24h delay in diagnosis

30
Q

What is the primary management of oesophageal perforations?

A

Initially:
Pain management

NBM - nothing by mouth = withhold food and fluids but can’t stop them from swallowing saliva

Broad spectrum antibiotics and antifungals​

ITU/HDU level care​

Bloods (including G&S)​

Tertiary referral centre

31
Q

What questions need to be asked before surgical management of oesophageal perforations?

A

Is the perforation transmural or intramural?​

Where is it & on which side?​

How big?​

Is leak well defined or diffuse?​

32
Q

What is the definitive management of oesophageal perforations?

A

Always manage immediately, not conservatively because once damage is done, difficult to reverse

Therefore operative management should be default, unless-: minimal contamination​, perforation and contents are contained​, or patient is unfit ​for surgery

​Conservative management = covered metal stent

33
Q

What is a primary repair of an oesophageal perforation?

What is the definitive solution of an oesophageal perforation?

A

Primary repair of an acute or sudden injury is often done within 24 hours of the injury. This is usually a direct surgery to fix the injury​

Primary repair is optimal​ =
Vascularised pedicle flap​
Gastric fundus buttressing (e.g. Dor)​
Or chest drains placed in

Definitive solution = oesophagectomy with reconstruction or oesophagostomy and delayed reconstruction​

34
Q

What are the stomach’s protective mechanisms against reflux?

A

Increased LOS pressure = LOS usually closed as barrier against reflux​ of harmful gastric juice (pepsin & HCl)

LOS pressure increased by (inhibits reflex): acetylcholine (Ach), alpha-adrenergic agonists, hormones,​ protein-rich food, histamine,​ high intra-abdominal pressure, PGF2 etc.​

LOS pressure is decreased (promotes reflux): VIP, beta-adrenergic agonists, hormones, dopamine, nitrogen oxide (NO), PGI2, PGE2, chocolate, acid gastric juice,​ fat, smoking, etc.

35
Q

What is sporadic reflux?

A

Normal reflux day to day due to:
Pressure on full stomach
Swallowing
Transient sphincter opening

36
Q

What are the mechanisms of the oesophagus if reflux does occur?

A

Volume clearance: oesophageal peristalsis reflex​

pH clearance - saliva​

Epithelium - barrier properties

37
Q

What is GORD?

A

Failure of the stomach’s protective mechanisms

GORD can be caused by:

Decreased LOS pressure (resting pressure less than 10 mmHg)​

Frequent Transient sphincter opening (air, CO2)​

Decreased volume clearance due to abnormal peristalsis​

Decreased pH clearance due to decreased Saliva production (in sleep, xerostomia)

Decreased Buffering capacity of saliva (e. g. through smoking)​

Hiatus hernia​

Defective mucosal protective mechanism (e. g. alcohol)​

​

38
Q

What risk factors can predispose a person to develop GORD?

A

Anything that decreases volume clearance e.g. abnormal peristalsis predisposes to GORD

Alcohol abuse = muscosal integrity damage = abnormal pH clearance = oesophagitis = predisposition to GORD

Smoking = decreased buffering capacity of saliva

Hiatus hernia

Pregnancy

Obesity

39
Q

How can a patient with GORD present clinically?

A

Heartburn + retrosternal chest pain​

Unpleasant sour taste in the mouth and nausea ​

Swallowing problems (dysphagia)​

Belching or water brash (excess salivation in the mouth).

40
Q

What is the typical treatment for GORD?

A

Treatment = PPI / H2 blocker​

Weight loss, sleep at an incline and don’t eat 2 hours before sleeping

41
Q

What is a sliding hiatus hernia?

A

Portion of stomach herniated - squeezes through diaphragm

At the gastro-oesophageal junction, the abdominal part of the oesophagus, and frequently the cardia of the stomach moves or ‘slides’ upwards through the diaphragmatic hiatus into the thorax

People with severe GORD usually have sliding hiatus hernia

80%

42
Q

What is a rolling / para-oesophageal hiatus hernia?

A

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

​20%

43
Q

What are the risk factors of a hiatus hernia?

Why do hiatus hernia occur?

A 
Male 
Obesity
Age
Pregnancy 
Genetic predisposition

Occur due to widening of the diaphragmatic hiatus from either pulling up of the stomach (e.g. due to oesophageal shortening) or pushing up the stomach (e.g. due to increased intra-abdominal pressure)

This compromises the LOS function = loss of anti-reflux barrier is lost = GORD

44
Q

How can GORD be investigated?

How do GORD symptoms overlap with cancer symptoms?

A

OGD - to exclude other causes​ e.g.
Cancer
Oesophagitis - inflammed oesophagus
Peptic stricture - narrowing of the oesophagus when erosions/ ulcers heal and form fibrotic scars​
Barretts​ oesophagus - metaplasia from recurrent exposure to stomach acid
etc.

Oesophageal manometry​ - to rule out functional oesophageal disorders e.g. achalasia or diffuse oesophageal spasm (corkscrew oesophagus)

24-hr oesophageal pH recording​

GORD and cancer can both present with: unintended weight loss, iron deficiency anaemia, anorexia (not being able or wanting to eat), odynophagia (painful swallowing), and upper gastrointestinal bleeding

45
Q

What are the treatment options / recommendations for GORD?

A

Medical​ =
Lifestyle changes (wt loss, smoking, EtOH)​
PPIs​

Surgical​ =
Dilatation of peptic strictures (top RHS)​
Laparoscopic Nissen’s fundoplication - dissection and closure of hiatus and then gastric fundus is wrapped around oesophagus which strengthens the LOS

46
Q

What is gastritis?

How do acute and chronic gastritis differ?

A

Gastritis = inflammation of gastric mucosa

Acute = neutrophil infiltration
Chronic = lymphocyte and plasma cell infiltration
47
Q

What are the 4 different types of gastritis?

A

Erosive & haemorrhagic (acute) gastritis = imbalance between mucosal defences and acidic environment​ due to:

Non-erosive, chronic active gastritis = occurs in antrum but can spread to body and is the most common type of gastritis​

Atrophic gastritis/ autoimmune chronic gastritis = in fundus, autoantibodies against parts & products of parietal cells (gastrin receptors, H+/K+ ATPase on parietal cells) and intrinsic factor:

Reactive gastritis​

48
Q

What are the causes of erosive and haemorrhagic (Acute) gastritis?

A

Erosive & haemorrhagic (acute) gastritis = imbalance between mucosal defences and acidic environment​ due to:
- NSAIDS (decreased prostaglandins)
- Alcohol
- Stress: multi-organ failure or sepsis or burns, trauma (endoscope) and ischaemia (vasculitis)​
Usually start with gastric erosions, which are lesions in the gastric mucosa, and these can lead to acute ulcers which are likely to cause gastric bleeding & perforation​

49
Q

What are the causes of non-erosive, chronic active gastritis?

A

Non-erosive, chronic active gastritis = occurs in antrum but can spread to body and is the most common type of gastritis​, caused by:
- Most commonly H. Pylori infection - leads to high levels of gastrin, which increases H+ secretion by parietal cells, so pH of gastric acid decreases ​
Leads to formation of chronic gastric ulcers​

50
Q

What happens in atrophic gastritis/ autoimmune chronic gastritis?

A

Atrophic gastritis/ autoimmune chronic gastritis = in fundus, autoantibodies against parts & products of parietal cells (gastrin receptors, H+/K+ ATPase on parietal cells) and intrinsic factor:

Causes parietal cell atrophy = reduced acid secretion

This can cause G cell (releases gastrin to stimulate HCl) hyperplasia, then metaplasia and possibly cancer

Increased secretion of gastrin = increased risk of neuroendocrine tumour and reduced IF = risk of pernicious anaemia

Also causes reduced serum pepsinogen (as low HCl)​

51
Q

How is gastric secretion regulated?

A

Neural ACh

Endocrine Gastrin (G cells of antrum)

Paracrine Histamine (ECL cells & mast cells of gastric wall)

Endocrine Secretin (small intestine)

Paracrine Somatostatin (SIH)

Paracrine & autocrine PGs (E2 & I2), TGF-α & adenosine

52
Q

What increases gastric secretion?

A

Neural ACh: postganglionic transmitters of vagal parasympathetic fibres binds to M1 receptors and increase gastric secretion​

Endocrine Gastrin (G cells of antrum): stimulates histamine release from enterochromaffin-like (ECL) cells (found in lamina propia)​

Paracrine Histamine (ECL cells & mast cells of gastric wall): histamine binds to H2 receptor on parietal receptors to increase HCl production​

53
Q

What decreases gastric secretion?

A

Endocrine Secretin (small intestine): stimulates pancreatic bicarbonate secretion (effect potentiated by CCK) and inhibition of gastric acid secretion​

Paracrine Somatostatin (SIH): inhibits gastric secretion​

Paracrine & autocrine PGs (E2 & I2), TGF-α & adenosine: prostaglandins inhibits gastric secretion

54
Q

How is the stomach mucosa protected from the stomach acid?

A

Methods of mucosal protection: =

Thick mucus film produced by epithelium which acts as a protective barrier​

HCO3- from prostaglandins neutralises acid (allows for buffering)​

Epithelial barrier regulated by EGF​ (epidermal growth factor)

High mucosal blood perfusion so can get rid of H+ ions and bring HCO3-​

​

55
Q

What do protaglandins promote?

A

Prostaglandins are small signalling molecules which stimulate:​

Mucus and bicarbonate secretion​

vasodilate the nearby blood vessels allowing more blood to flow to the area​

promote new epithelial cell growth​

also inhibit acid secretion.​

56
Q

What are gastric ulcers?

What is peptic ulcer disease (PUPD)?

A

Chronic lesions in areas exposed to excess gastric acid and peptic juices

PUD arises due to decreased mucosal protection against gastric acid

57
Q

What are some mechanisms to repair epithelial defects to reduce ulcer formations?

A

Migration​ =
Adjacent epithelial cells flatten to close gap​ via sideward migration along Basement Membrane​ (BM)

Gap closed by cell growth​ =
Cover gap through cell division​
Stimulated by EGF, TGF-α, IGF-1, GRP & gastrin​

Acute wound healing​ =
If BM destroyed: attraction of leukocytes & macrophages; phagocytosis of necrotic cells; angiogenesis; regeneration of extracellular matric after repair​ of BM​
Epithelial closure by restitution & cell division

58
Q

How can H. pylori cause gastric and duodenal ulcers?

A

H. pylori colonise gastric mucosa and:​

  • Produce ureases - neutralise gastric acid, which can cause gastric mucosal injury​

[Urease catalyses the conversion of urea into ammonia and carbon dioxide. Ammonia is basic and will neutralise acid, forming a very thin buffer layer surrounding H. pylori.​]

  • Has outer proteins (adhesions) and liposaccharides which allow them to adhere to host cells​
  • Flagella allows bacterial motility and chemotaxis​
  • Secrete enzymes e.g. proteases, lipases and mucinase which cause gastric mucosal injury​
  • Secrete exotoxins e.g. vacuolating toxins (vacA) and effectors like cagA which also cause gastric mucosal injury ​

​

59
Q

What are the treatment options for ulcers?

A

Primarily medical​ =
PPI or H2 blocker (reduce acid in stomach)​
H. pylori: Triple therapy (amoxicillin, clarithromycin, pantoprazole) for 7-14 days​

Surgical interventions =
Very Rare - most uncomplicated ulcers heal​ within 12 weeks​
If don’t, change medication, observe​ for an additional 12 weeks​
Check serum gastrin (antral G-cell​ hyperplasia or gastrinoma [Zollinger-​Ellison syndrome])​

OGD: biopsy all 4 quadrants of ulcer​ (rule out malignant ulcer) if refractory​

60
Q

What are the surgical indications for ulcers?

A 
Intractability (after medical therapy)
• Haemorrhage
• Obstruction
• Perforation
• Relative: continuous requirement of
steroid therapy/NSAIDs
61
Q

What are the complications of ulcers?

A

Haemorrhage - ulcer erodes into an artery​

Obstruction - chronic inflammation causes scarring and fibrosis​

Perforation - burned through mucosa and gastric contents leak outside​

62
Q

What is Zollinger-Ellison syndrome?

How do we test for Zollinger-Ellison syndrome?

A

Zollinger- Ellison syndrome = a gastrinoma = neuroendocrine tumour that is typically located in the duodenal wall or pancreas, and secretes lots of gastrin

Excess gastrin stimulates parietal cells to release excess hydrochloric acid (HCl), overwhelming normal defense mechanisms and allowing ulcers to develop

Test: do secretin test- upon giving secretin the gastrin levels should decrease, but in ZE this doesn’t happen ​

63
Q

What is Antral G-cell hyperplasia?

A

Antral G-cell hyperplasia = pseudo-Zollinger Ellison Syndrome where there is high gastrin levels associated with increase in the number of G cells but an absence of gastrinoma in the pancreas or duodenum​

Y2 - BRS - GI (14 decks)

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