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BRS Phase 1b > Upper GI Tract > Flashcards

Upper GI Tract Flashcards

1
Q

Where does the oesophagus start and end ?

A

Start-C5
End-T10

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2
Q

Name the 2 Oesophageal sphincters ?

A

Lower Oesophageal Sphincter-LOS
Upper Oesophageal Sphincter-UOS

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3
Q

What are the 4 anatomical contributions to the Lower Oesophageal Sphincter ?

A

LOS is more of a physiological sphincter, with a number of contributing anatomical contributions;
1- Distal 3-4cm of oesophagus in abdomen.
2-Diaphragm surrounds the LOS.
3- Intact Phrenoesophageal ligament.
4-Angle of His.

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4
Q

How does the distal 3-4 cm of the oesophagus being in the abdomen contribute to LOS function?

A

If you get an increase in intra-abdominal pressure you get an increase in LOS pressure as well.

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5
Q

How does the diaphragm surrounding the LOS contribute to its function ?

A

The left and right crux act like scissors when the diaphragm contracts, they contract against the sphincter.

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6
Q

What is the role of the phrenoesophageal ligament in the function of the LOS ?

A

You need to have an intact phrenoesophageal ligament, this is an extension of the inferior diaphragmatic fascia, with two limbs one that goes superiorly and attaches to the lower part of the oesophagus the other goes inferiorly and attaches to the cardia of the stomach, this allows individual movement of the diaphragm during respiration and the oesophagus when you swallow.

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7
Q

What is the structure known as ?

A

Angle of His, an acute angle between the abdominal oesophagus and the fundus of the stomach, at the oesophago-gastric junction. This prevents reflux disease by the fundus expanding and combressing the oesophagus when someone has had a large meal.

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8
Q

How many stages are there in normal swallowing?

A

4

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9
Q

What is stage 0 of normal swallowing ?

A

Oral phase - chewing and saliva prepares bolus, both the oesophageal sphincters are constricted

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10
Q

What is stage 1 of normal swallowing ?

A

Pharyngeal phase - pharyngeal musculature guides food bolus towards oesophagus, the UOS opens reflexly. The LOS is opened by vasovagal reflex (receptive relaxation reflex).

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11
Q

What is stage 2 of normal swallowing ?

A

Upper Oesophageal phase - the UOS closes and superior circular muscle rings contract whilst inferior rings dilate, with sequential contractions of longitudinal muscle.

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12
Q

What is stage 3 of normal swallowing ?

A

Lower oesophageal phase - LOS closes as food passes through.

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13
Q

How do you measure normal swallowing ?

A

Manometry, this is where a tube is passed throught he nose down the oesophagus that measures pressure of contractions.

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14
Q

What are normal peristaltic waves ?

A

40mmHg

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15
Q

What is the normal pressure of the LOS ?

A

20mmHg

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16
Q

What happens to the pressure at the LOS during receptive relaxation ?

A

Decreases to <5mmHg this is mediated by inhibitory noncholinergic nonadrenergic NCNC neurons of myenteric plexus.

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17
Q

What are 3 causes of functional oesophageal disorders ?

A
  1. Absence of a stricture.
  2. Abnormal oesophageal contraction.
  3. Failure of protective mechanisms for reflux.
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18
Q

What is an example of Abnormal oesophageal contraction ?

A
  • Hypermotility
  • Hypomotility
  • Disordered Coordination
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19
Q

What is an example of failure of the protective mechanisms for reflux ?

A

GastroOesophageal Reflux disease GORD

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20
Q

What term is used for difficulty in swallowing ?

A

Dysphagia, it is important to localise the dysphagia as well as what type ( to solids or liquids), if it is getting better or worse.

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21
Q

What is the term for pain on swallowing?

A

Odynophagia

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22
Q

What term describes the return of oesophageal contents from above an obstruction?

A

Regurgitation, is it functional or mechanical.

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23
Q

What term describes passive return of gastroduodenal contents into the mouth ?

A

Reflux

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24
Q

Give an example of hypermotility ?

A

Achalasia

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25
Q

What is Achalasia ?

A

Increased resting pressure of LOS, due to loss of ganglion cells in Auerbachs myenteric plexus in LOS walls. Therefore you have a decreased activity of inhibitory NCNA neurones.

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26
Q

What happens in Achalasia ?

A

Receptive relaxation sets in too late and is too weak, so during reflex phase the pressure in the LOS is higher than in the stomach. So swallowed food collects in the oesophagus causing increased pressure throughout, with dilation of the oesophagus. it gets to a point where propagation of peristaltic waves ceases.

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27
Q

What is the disease course of Achalasia ?

A

Insidious onset, without treatment it can lead to progressive oesophageal dilation of the oesophagus. You also have an increased risk of Oesophageal cancer by 28 fold.

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28
Q

What are the treatment options for Achalasia ?

A
  • Pneumatic dilation - weakens the LOS by circumferential stretching and in some casesmuscle tearing. 71-90% of patients respond initially but many relapse.
  • Heller’s Myotomy - A continuous myotomy carried out on 6cm on the oesophagus and 3 cm onto the stomach, this is a more permanent solution. Involves Dor fundoplication - this is where the anterior fundus is folded over the oesopagus and sutured to the right side of myotomy. Risks include; oesophageal and gastric perforation 10-16%, division of the vagus nerve (rare) and splenic injury 1-5%.
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29
Q

What is an example of Hypomotility ?

A

Scleroderma

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30
Q

What is Scleroderma ?

A

Autoimmune disease - results due to neuronal defects, so you get atrophy od smooth muscle of oesophagus and peristalsis in the distal portion ultimately ceases altogether. The decreased resting pressure of the LOS can develop GORD, which can be associated with CREST syndrome.

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31
Q

What is CREST syndrome ?

A
  • Calcinosis in soft tissue
  • Raynaud’s phenomenon - constriction of peripheral blood vessels, leads to problems with hands.
  • Esophageal problems
  • Scerodactyly- thickening of digits of hands and toes
  • Telengiactasia- dilated or broken blood vessels near the surface of the skin.
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32
Q

What is the treatment for Scleroderma ?

A
  • Exclude organic obstruction
  • Imrove force of peristalsis with prokenetics (cisapride), not very effective.
  • Unfortunately once peristaltic failure occurs it is usually irreversible.
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33
Q

What is an example of Disordered coordination of the Oesophagus ?

A

Corkscrew Oesophagus

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34
Q

What is Corkscrew Oesophagus ?

A

Diffuse oesophageal spasm, presents as dysphagia and chest pain. Pressures can reach 400-500mmHg, with marked hypertrophy of circular muscle. Treatment may involve Pneumatic dilation but results are not predictable/favourable.

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35
Q

Where do you get Oesophageal Perferation ?

A

3 main areas of anatomic constriction;

  1. Cricopharyngeal constriction
  2. Aortic and Bronchial constriction
  3. Diaphragmatic and sphincter constriction
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36
Q

How do you get oesophageal perforations?

A
  • Latrogenic (OGD)>50%
  • Spontaneous (Boerhaave’s) - 15%
  • Foreign Body - 12%
  • Trauma - 9%
  • Intraoperative - 2%
  • Malignant - 1%
37
Q

How do you get Oesophageal perforation latrogenically ?

A

Usually at OGD (Oesophago-Gastro-Duodenoscopy), more common in the presence of diverticula or cancer.

38
Q

How do you get Oesophageal perforation due to Boerhaave’s?

A

Often described as spontaneous perforation, a sudden increase in intra-oesophageal pressure with negative intra thoracic pressure. You are essentially vomiting against a closed glottis. Incidence is 3.1 per 100,000.

Perforation at left posterolateral aspect of the distal oesophagus.

39
Q

What are examples of foreign objects that cause oesophageal perforation?

A

Disk batteries, Magnets, Sharp objects, Dishwasher tablets

40
Q

How do you get oesophageal perforation via trauma ?

A

Neck- penetrating, Thorax- Blunt force. Can be difficult to giagnose, dysphagia, blood in saliva, surgical emphysema, Haematemesis.

surgical emphysema is air under the skin and sound likes crackling when walking on snow.

41
Q

What is the presentation of Oesophageal perforation?

A

Pain, Fever, Dysphagia, Emphysema.

Do CXR, CT, OGD, swallow gastrograffin.

42
Q

What is the management of oesophageal perforation ?

A

It is a surgical emergency, there is a 2X mortality if surgery is delayed by 24 hours. NBM, IV Fluids, Broad spectrum antibiotics. ITU level care. Mangement can be conservative with a metal stent, but primary repair is optimal and oesophagectomy is definitive.

43
Q

What increases LOS pressure and thereby inhibits reflux?

A

Acetylcholine, α-adrenergic agonists, hormones, protein rich food, histamine, high intra-abdominal pressure, Prostaglandin F2α.

44
Q

What decreases LOS pressure and thereby promotes reflux?

A

Vasoactive intestinal peptide VIP, ß-adrenergic agonists, hormones, dopamine, NO, PG12, PGE2 both vasodilator local hormones, chocolate, acid gastric juice, fat, smoking.

45
Q

What causes normal sporadic reflux?

A
  • Pressure on full stomach
  • swallowing
  • transient sphincter opening
46
Q

What are 3 protective mechanisms following reflux?

A
  • Volume clearance - oesophageal peristalsis reflex
  • pH clearance - saliva
  • Epithelium - barrier protects
47
Q

What protective mechanisms fail in GORD?

A
  • Decreases sphincter pressure.
  • Increased transient sphincter opening.
  • Abnormal peristalsis leading to reduced volume clearance.
  • Decreased volume clearance due to decreased saliva production e.g. in sleep and xerostomia, as well as decrased buffering capacity of saliva e.g. smoking.
  • Hiatus Hernia
  • Defective mucosal protective mechanism, e.g. alcohol.

All of these factors lead to Reflux esophagitis and can lead to epithelial metaplasia and possibly carcinoma.

48
Q

What type of hernia is this?

A

Sliding hiatus hernia

49
Q

What type of hernia is this?

A

Rolling Hiatus hernia

50
Q

How do you diagnose & treat GORD?

A
  • Diagnosis - OGD to exclude cancer, oesophagitis, peptic stricture, Barrets oesophagus. As well as Oesophageal monometry and possibly 24hr oesophageal ph recording.
  • Treatment - Non surgical; Lifestyle changes e.g. wt loss, smoking, EtOh, as well as PPI’s. Surgical involves Dilation peptic strictures, Laparoscopic Nissen’s fundoplication.
51
Q

What does the Cardia and Pyloric region of the stomach produce?

A

Mucus only.

52
Q

What do the Body&Fundus of the stomach produce?

A

Mucus, HCl, Pepsin.

53
Q

What does the Antrum produce?

A

Gastrin.

54
Q

What are the 4 main types of Gastritis?

A
  • Erosive & haemorrhagic gastritis
  • Nonerosive, chronic active gastritis
  • Atrophic (fundal gland) gastritis
  • Reactive gastritis
55
Q

What are the causes of Erosive & haemorrhagic gastritis?

A

NSAIDs, alcohol, multiorgan failure, burns, trauma, ischaemia. This can happen anywhere in the stomach and lead Acute Ulcer formation which leads to gastric bleeding and perforation.

56
Q

What type of gastritis can Helicobacter pylori lead to ?

A

Nonerosive, chronic active gastritis in the Antrum. Treated with triple dose of antibiotics (amoxicillin, clarithromycin, pantoprazole) for 7-14 days.

57
Q

How can chroic active antral gastritis lead to reactive gastritis?

A

Icreased gastrin production causes normal/increased acid secretion which forms chronic gastric & duodenal ulcer formation which leads to reactive gastritis that can develop into epithelial metaplasia and carcinoma.

58
Q

What happens in Atrophic gastritis ?

A

Occurs in the Fundus, Autoantibodies attack parts/products of parietal cells this lease to parietal cells atrophy. This causes decreases acid secretion & IF Secretion, leading to carcinod/carcinoma formation and Pernicious anaemia respectively.

59
Q

What stimulates Gastric secretion ?

A
  • Neural - ACh, postganglionic transmitter of vagal parasympathetic fibres.
  • Endocrine - Gastrin, from G cells of antrum.
  • Paracrine - Histamine from ECL cells & mast cells of gastric wall.
60
Q

What inhibits gastric secretion ?

A
  • Endocrine - Secretin, from small intestine.
  • Paracrine - Somatostatin.
  • Paracrine & Autocrine - PGs (E2 & I2) TGF-alpha and adenosine.
61
Q

What are 4 mechanisms for Mucosal protection ?

A
62
Q

What are the mechanisms for Epithelial repair and wound healing ?

A
  1. Migration - Adjacent epithelial cells flatten to close th egap via sideward migration along the basement membrane.
  2. Gap closed by cell growth - Stimulated by EGF, TGF-alpha, IGF-1, GRP & gastrin.
  3. Acute wound healing - Basement membrane destroyed, so leukocytes and macrophages are attracted in order to phagocytose necrotic cells; angiogenesis; regeneration of ECM after repair of BM. Restitution and cell division leads to epithelial closure.
63
Q

Why do you get ulcers?

A
  • Helicobacter pylori
  • increased secretion of gastric juices
  • decreased carbonate secretion & therefore decreased mucosal protection dur to inhibition of prostaglandin synthese by NSAIDs.
  • decreased cell formation
  • decreased blood perfusion due to stress, smoking, psychogenic components.
64
Q

What are the consequences of H.Pylori?

A
  • Asymptomatic >80%
  • Chronic atrophic gastritis/ Intestinal metaplasia 15-20%
  • Gastric/ Duodenal ulcer 15-20%
  • Gastric cancer, MALT lymphoma<1%
65
Q

What are the treatments for H.Pylori ?

A
  • Primarily medical- PPI or H2 blocker, Triple Rx (amoxicillin, clarithromycin, pantoprazole) for 7-14 days).
  • Elective Surgical Rx, Rare - most uncomplicated ulcers heal within 12 weeks. If don’t, change medication, observe 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.
  • Surgical indications; Intractability (after medical therapy), Relative: continuous requirement of steroid therapy/NSAIDs. Complications; Haemorrhage, Obstruction, Perforation.
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BRS Phase 1b (80 decks)

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