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BRS YEAR 2 > Upper Gi Tract > Flashcards

Upper Gi Tract Flashcards

1
Q

Landmarks of oesophagus trachea and aorta

A

Oesophagus approximately 25cm long - C5/6 to T10, where it enters the diaphragm, progressing from skeletal to smooth muscle

Trachea lies anterior to oesophagus

Aorta lies on left hand side of oesophagus

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2
Q

Perfusion of thoracic and abdominal part as well as drainage

A
  • Thoracic part supplied by branches of aorta, superior supplied by branches of the thyroid artery (from the thyrocervical trunk)
  • Abdominal part supplied by left gastric artery and inferior phrenic artery
  • Drainage from thoracic part is the azygous vein (systemic), but also has portal vein
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3
Q

Anatomy of lower oesophagus

A

Phrenoesophageal ligament upper and lower limbs anchor oesophagus to the diaphragm

The Lower Oesophageal sphincter is surrounded by the diaphragm

The angle of His is the angle between the peritoneum of the stomach and the oesophagus

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4
Q

Swallowing phases

A
  • Stage 0 - Oral phaseChewing and Saliva prepare the bolusBoth oesophageal sphincters are constricted
  • Stage 1 - Pharyngeal phaseBolus guided to upper sphincter by pharyngeal musculatureUpper oesophageal sphincter opens reflexivelyLOS opened by vasovagal reflex
  • Stage 2 - Upper oesophageal phaseUpper sphincter closesSuperior circular muscle rings contract, inferior rings dilateSequential contractions of longitudinal muscle
  • Stage 3 - Lower oesophageal phaseLower oesophageal sphincter closes as food passes
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5
Q

Motility

A
  • Determined by pressure managements (manometry)
  • Peristaltic waves ~40mmHG
  • Resting pressure of lower sphincter ~ 20mmHg
    This goes down by less than 5mmHg during receptive relaxation
    This is mediated by inhibitory noncholinergic nonadrenergic neurones (NCNA) of the myenteric plexus
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6
Q

Functional disorders of oesophagus

A
  1. Absence of a stricture
    Caused by abnormal oesophageal contraction, as a result of disordered coordination, hyper OR hypomotility
  2. Failure of protective mechanisms for reflux
    Gastrooesophageal Reflux Disorder (GORD)
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7
Q

Dysphagia

A

Difficulty swallowing
Localisation is important - upper (cricopharyngeal) or lower (distal) sphincter

Types:

  • For fluids or solids
  • Intermittent or progressive
  • Precise or vague in appreciation
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8
Q

Odynophagia

A

Pain when swallowing

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9
Q

Regurgitation

A

Return of oesophageal contents from above an obstruction
May be functional or mechanical

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10
Q

Reflux

A

Passive return of gastroduodenal contents to mouth

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11
Q

Hypermotility achalasia

A

Achalasia - a condition in which the muscles of the lower part of theoesophagus fail to relax, preventing food from passing into the stomach.

Occurs as a result of loss of ganglion cells in Auerbach’s myenteric plexus in the LOS wall causing decreased activity of inhibitory NCNA neurones

  • Primary - cause unknown
  • Secondary - known disease with similar oesophageal motor abnormalities, e.g.:
  • Chagas’ disease
  • Protozoa infection
  • Amyloid / sarcoma / eosinophilic oesophagitis
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12
Q

Pathophysiology of achalasia

A

Increased resting pressure of LOS
Receptive relaxation is late and too weak
During reflex phase pressure in LOS is much higher than in stomach
Swallowed food collects in oesophagus causing increased pressure throughout with dilation of oesophagus
Propagation of peristaltic waves

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13
Q

Progression of achalasia

A
  • Insidious onset, people have symptoms for years before seeking help
  • Without treatment, there is a progressive dilation of the oesophagus
  • Risk of oesophageal cancer increased 28 fold, but incidence rate is only 0.34%
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14
Q

Treatment of achalasia

A
  • Pneumatic dilation (PD)
    Weakens the LOS by circumferential stretching, and sometimes tearing of its muscle fibres
    71-90% of patients initially respond, but many subsequently relapse
  • Surgery
  • Heller’s Myotomy: a continuous myotomy performed for 6cm on oesophagus and 3cm onto stomach
  • Dor Fundoplication - anterior fundus folded over oesophagus and sutured to right side of myotomy
    Risks:
    -Oesophageal & gastric perforation (10-16%)
    -Division of vagus nerve (rare)
    -Splenic injury (1-5%)
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15
Q

Hypomobility scleroderma

A

Scleroderma - autoimmune disease

  • Hypomotility in its early stages as a result of neuronal defects causes atrophy of the oesophageal smooth muscle
  • Ultimately peristalsis in the distal oesophagus stops entirely, which causes:
  • Decreased resting pressure of LOS
  • GORD develops (this is often associated with CREST syndrome, a less severe form of scleroderma)
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16
Q

Treatment of hypomobility scleroderma

A
  • Exclude organic obstruction
  • Improve force of peristalsis with prokinetics (cisapride)
  • When peristaltic failure occurs this is usually irreversible
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17
Q

Disordered coordination -corkscrew oesophagus

A

Diffuse oesophageal spasms:

  • Incoordinate contractions causing dysphagia and chest pain
  • Pressures reaching 400-500mmHg
  • Marked hypertrophy of circular muscle
  • Will appear as a corkscrew oesophagus in a Barium study
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18
Q

Treatment of corkscrew oesophagus

A

May respond to forceful PD of cardia, but results are less predictable than achalasia

19
Q

Oesophageal perforation

A

Anatomy: 3 areas of oesophageal perforations
Pathological narrowing, could be due to cancer, foreign bodies, physiological dysfunction

##

20
Q

Aetiology of Oesophageal perforation

A
  • Iatrogenic (OGD) >50%
  • Spontaneous (Boerhaave’s) - 15%
  • Foreign body - 12%
  • Trauma - 9%
  • Intraoperative - 2%
  • Malignant - 1%
21
Q

Iatrogenic

A

Usually at OGD, more common in the presence of diverticula or cancer

Incidence:

  • OesophagoGastroDuodenoscopy (OGD) = 0.03%
  • Stricture dilation = 0.1-2%
  • Sclerotherapy = 1-5%
  • Achalasia dilation = 2-6%
22
Q

Boerhaave’s

A
  • Sudden increase in intra-oesophageal pressure with negative intra thoracic pressure
  • Vomiting against a closed glottis
  • Incidence rate = 3.1 per 1,000,000
  • Transmural laceration, most frequently at left posterolateral aspect of the distal oesophagus
23
Q

Foreign Body

A

Common problems:

  • Disc batteries - can cause electrical burns if embedded in mucosa (growing problem)
  • Magnets
  • Sharp objects
  • Dishwasher tablets
  • Acid / alkali
24
Q

Trauma

A

Locations:

  1. Neck - penetration injury
  2. Thorax - blunt force

Difficult to diagnose, some symptoms are:

  • Dysphagia
  • Blood in saliva
  • Haematemesis
  • Surgical emphysema
25
Q

Primary Management of an Oesophageal Perforation

A

Surgical EMERGENCY - mortality rate double if there is a 24 hour delay in diagnosis

26
Q

Presentation of eosphgeal perforation

A
  • Pain - 95%
  • Fever - 80%
  • Dysphagia - 75%
  • Emphysema - 35%
27
Q

Investigations of oesophagus perforation

A
  • Chest X-ray
  • CT (with gastrogaffin)
  • OGD (Oesophagogastroduodenoscopy)
28
Q

Management for oesophageal perforation

A
  • Initial
    • Nil by mouth
    • IV fluids
    • Broad spectrum antibiotics and antifungals
  • After
    • ITU/HDU care
    • Bloods including G&S (group and save)
    • Tertiary referral centre
  • Definitive management
    • Conservative management - cover with metal stent
    • Operative management should be default, ideally primary repair
      Oesophagectomy is also a definitive solution
29
Q

Stomach function

A

Functions:

  • Breaks food into smaller particles (via acid and pepsin)
  • Holds food, releasing it in a controlled steady rate into the duodenum
  • Kills parasites and certain bacteria

Location of secretion glands in stomach:

  • Cardia & Pyloric regions - Mucous only
  • Body and Fundus - Mucous, HCl, pepsinogen
  • Antrum - Gastrin
30
Q

Protective mechanisms against reflux

A

LOS is usually closed to prevent reflux of gastric juice (pepsin and HCl)

31
Q

What impacts pressure of LOS

A

Increases:

  • Acetylcholine
  • Alpha-adrenergic agonists
  • Hormones
  • Protein-rich food
  • Histamine
  • High intra-abdominal pressure
  • PGF2a

These may inhibit reflux

Decreases:

  • VIP
  • Beta-adrenergic agonists
  • Hormones
  • Dopamine
  • Nitric Oxide
  • PGI2
  • PGE2
  • Chocolate
  • Acidic gastric juice
  • Fat
  • Smoking

These may promote reflux

32
Q

Sporadic reflux

A

entirely normal and can be result of:
- Pressure on a full stomach
- Swallowing
- Transient sphincter opening

33
Q

protective mechanisms following reflux:

A

Volume clearance (oesophageal peristalsis reflex)
- pH clearance via saliva
- Epithelial barrier properties

34
Q

Failure of protective mechanisms - GORD

A
  • Reduced volume clearance
  • caused by abnormal peristalsis
  • Reduced pH clearance
  • caused by reduced saliva production, e.g. xerostomia or sleeping
  • also caused by reduced buffering capacity of saliva, e.g. as a result of smoking
  • Others:
  • Decreased sphincter pressure
  • Increased transient sphincter opening
  • Hiatus hernia
  • Defective Mucosal protective mechanism (e.g. from drinking alcohol)

ALL of the above result in reflux esophagitis, which can lead to epithelial metaplasia (Barrett’s oesophagus) and potentially carcinoma

35
Q

Investigations for gord

A
  • Oesophagogastroduodenoscopy
    Helps to exclude cancer, and confirm oesophagitis, peptic stricture or Barrett’s oesophagus
  • Oesophageal manometry
  • 24 hour oesophageal pH recording
36
Q

Prescription for GORD

A

Medical:

  • Lifestyle changes ( weight loss, smoking, reduce alcohol intake)
  • Proton Pump Inhibitors

Surgical

  • Dilatation peptic strictures
  • Laparoscopic Nissen’s fundoplication
37
Q

Gastritis types

A

Types:

  • Erosive & haemorrhagic
    • Numerous causes
    • Acute ulcers - cause gastric bleeding and perforation
  • Nonerosive, chronic activeOccurs in the antrumMay be with H pylori, in which case prescribe amoxicillin, clarithromycin, pantoprazole for 7-14 / 7
  • Atrophic (fundal gland)Occurs in the fundusAutoantibodies against parts and products of parietal cells, results in parietal cell atrophyDecreased acid and IF secretion
  • Reactive
38
Q

Stomach and ulcers

A

Mucosal protection of Basal membrane

  • Mucus film - prevents pepsin and H+ reaching surface epithelium
  • HCO3- Secretion - neutralises H+, acts as a buffer
    pH of gastric juice = 1
    pH near the surface epithelium of the stomach = 7
  • Epithelial barrier - permeability and barrier integrity regulated by epidermal growth factor in saliva
  • Mucosal blood perfusion allows H+ to enter the blood supply
39
Q

Epithelial repair & wound healing

A

Wound healing involves:

  1. Granulation
  2. Angiogenesis
  3. Restitution of basal membrane
40
Q

Mechanisms repairing epithelial defects:

A
  • MigrationAdjacent epithelial cells flatten to close gap via sideward migration along basal membrane
  • Gap closed by cell growthThis is stimulated by EGF, TGF-a, IGF-1, GRP, Gastrin
  • Acute wound healingBasal membrane destroyed - attracts leukocytes & macrophages; necrotic cells phagocytosed, angiogenesis occurs, regeneration of extracellular matric after BM repairEpithelium closed by restitution and cell division
41
Q

Regulation of gastric secretion

A
  • Stimulation
    • Neural
    • ACh - postganglionic transmitter of vagal parasympathetic fibres
    • Endocrine
    • Gastrin - G cells of antrum
    • Paracrine
    • Histamine (Enterochromaffin-like cells & Mast cells of gastric wall)
  • Inhibition
    • Endocrine
    • Secretin (small intestine)
    • Paracrine
    • Somatostatin (SIH)
    • Paracrine & Autocrine
    • Prostaglandins (E2 & I2), TGF-a, adenosine
42
Q

Ulcer formation

A

Presence of H pylori near the wound may result in an ulcer

This is increased in likelihood by:

  • Increased secretion of gastric juice
  • Decreased HCO3- secretion
  • Reduced cell formation
  • Reduced blood perfusion

Outcomes of H pylori infections:

  • Asymptomatic or chronic gastritis - >80%
  • Chronic atrophic gastritis, intestinal metaplasia, gastric or duodenal ulcer - 15-20%
  • Gastric cancer, MALT lymphoma <1%
43
Q

Ulcer treatment

A

Mainly medical:

  • PPI or H2 blocker
  • Amoxicillin, clarithromycin & pantoprazole for 7-14 days

Elective surgery:

Rare, as most uncomplicated ulcers heal within 12 weeks, but if this doesn’t occur, change the medication and observe for 12 more weeks.

Check serum gastrin (antral G-cell hyperplasia or gastrinoma [Zollinger-Ellison] syndrome)

OGD: biopsy all 4 quadrants of the ulcer if refractory to rule out malignancy

44
Q

Surgical indications for ulcer treatment and complications

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

BRS YEAR 2 (47 decks)

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