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Year 2 Gastro > Upper GI tract > Flashcards

Upper GI tract Flashcards

1
Q

What is the cervical oesophagus?

A

Up to sternal notch

Contains skeletal muscles

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2
Q

What are the anatomical contributions to the lower oesophageal sphincter?

A

3-4cm distal oesophagus within abdomen
Diaphragm surrounds LOS
Intact phrenoesophageal ligament
Angle of His

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3
Q

What is the angle of his?

A

Angle between distal oesophagus and the fundus

Compresses distal oesophagus from lateral to medial

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4
Q

What are the phases of swallowing?

A

Oral
Pharyngeal
Upper oesophageal
Lower oesophageal

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5
Q

How is the motility of the oesophagus measured?

A

Pressure measurements (manometry)

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6
Q

What is the pressure of peristaltic waves?

A

40mmHg

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7
Q

What is the resting pressure of the LOS?

A

20mmHg

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8
Q

What happens to pressure of LOS during receptive relaxation?

A

Decreases by 5mmHg

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9
Q

What is the relaxation of the LOS mediated by?

A

Mediated by inhibitory noncholinergic nonadrenergic neurons of myenteric plexus

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10
Q

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

A

Stricture

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11
Q

What are the functional oesophageal disroders?

A

Hypermobility
Hypomobility
Lack of coordination
GORD

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12
Q

What is odynophagia?

A

Pain on swallowing

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13
Q

What is regurgitation?

A

Return of oesophageal contents from above an obstruction

May be functional or mechanical

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14
Q

What is reflux?

A

Passive return of gastroduodenal contents to the mouth

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15
Q

What is hypermotility of oesophagus called?

A

Achalasia

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16
Q

What causes Achalasia?

A

Loss of ganglion cells in aurebach’s myenteric plexus in LOS wall

decreased inhibitory neuron activity

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17
Q

What diseases is hypermotility seen in?

A

Chagas disease
Protosoa
Amyloid
Sarcome

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18
Q

What is the pathophysoligy of achalasia?

A

Increasing rested pressure of LOS

Receptive relaxation sets in late and is too weak

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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19
Q

What is the disease course of achalasia?

A

Insidious onset
Progressive dilatation (seen on barium swallow)
Pain
Increased risk of oesophageal cancer (28 fold)

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20
Q

What is the treatment of achalasia?

A

Pneumatic Dilatation
Heller’s Myotomy
Dor fundoplication
POEM

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21
Q

What is pneumatic dilatation?

A

Weakens LOS by circumferential stretching and in some cases, tearing of its muscles fibres

71-90% efficacy but many relapses

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22
Q

What is Heller’s myotomy

A

A continuous myotomy performed for 6cm on the oesophagus and 3 cm onto the stomach

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23
Q

What is dor fundoplication?

A

anterior fundus folded over oesophagus and sutured to right side

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24
Q

What is POEM?

A

Peroral endoscopic mytomy

Less invasive

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25
Q

What are the stages of POEM?

A

Mucosal incision
Creation of submucosal tunnel
Myotomy
Closure of mucosal incisons

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26
Q

What does hypomotility cause?

A

Sceroderma

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27
Q

What is scleroderma?

A 
Autoimmune disease
Hypomotility due to neuronal defects
Atrophy of smooth muscle of oesophagus
Peristalsis in the distal portion ceases
Decreases LOS resting pressure 
GORD develops
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28
Q

What does disordered coordination cause?

A

Corkscrew oesophagus

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29
Q

What is the pathophysiology od corkscrew?

A 
Diffues oesophageal spasm
Dysphagia and chest pain
Pressures of 400-500 mmHg
Marked hypertrophy of circular muscle 
Corkscrew seen on barium swallow
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30
Q

Describe anatomy of oesophageal perforations

A

3x area of anatomical constriction:
Cricopharyngeal constriction
Aortic and bronchial
Diaphragmatic

Pathological narrowing:
Cancer, foreign body, physiological dysfunction

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31
Q

Where are iatrogenic oeseophgeal perforations normally?

A

OGD

More common in presence of diverticula or cancer

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32
Q

What is Boerhaave’s?

A

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

Vomiting against a close glottis

3.1 per 100,000

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33
Q

What foreign bodies cause perforations?

A 
Disk batteries
Magnets
Sharp objects
Dishwasher tablets
Acid/Alkali
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34
Q

What operations can cause perforations?

A

Hiatus hernia repair
Hellers cardiomyotomy
Pulmonary surgery
Thyroid surgery

35
Q

What investigations do you carry our with perforations?

A

CXR
CT
Swallow (gastrograffin)
OGD

36
Q

What is the definitive management with oesophageal perforations?

A

Operative management default

Unless

  • minimal contamination
  • contained
  • unfit

Then conservative management with stent

37
Q

What are the surgical option for oesophageal perforations?

A

Primary repair is optimal

+/- Vascularised pedicle flap
+/- Gastric fundus buttressing
e.g. Dor
Drains ++

38
Q

What would a definitive solution be?

A

Oesophagectomy

With reconstruction at the same time or delayed

39
Q

What are the three mechanism that protect agains reflux?

A

Volume clearance - oesophageal peristalsis reflex
pH clearance
Epithelium - barrier properties

40
Q

What increases LOS pressure?

A 
Acetycholine
Alpha-adrenergic agonists
Hormones
Protein-rich food
Histamine
High intra-abdominal pressure

Inhibits reflux

41
Q

What decreases LOS presuure?

A 
Vasoactive intestinal peptide
Beta-adrenergic agonsists
Hormones
Dopamine
NO
PGI2
PGE2
Chocolate
Acid gastric juice
Fat
Smoking

Promotes reflux

42
Q

Why is sporadic reflux normal?

A

Pressure on full stomach
Swallowing
Transient sphincter opening

43
Q

What does failure of the protective mechanisms result in?

44
Q

What are sliding hiatus hernias?

A

Portion of stomach herniated

Squeezes through diaphragm

45
Q

What is a rolling hiatus hernia?

A

Junction is in place and the stomach herniates alongside the oesophagus

46
Q

How do you investigate GORD?

A

OGD - to exclude cancer
or confirm oesophagitis, peptic stricture and barretts

Oesophageal manometry

24hr oesophageal pH recording

47
Q

What are the treatments for GORD?

A 
Lifestyle changes (weight loss, smoking, EtOH)
PPIs
48
Q

What surgical treatments are available for GORD?

A

Dilation peptic strictres

Laparascopic Nissen’s fundoplication

49
Q

What are the different types of gastritis?

A

erosive and haemorrhagic
Nonerosive, chronic active gastritis
Atrophic (fundal gland) gastritis
Reactive gastritis

50
Q

What are the features of erosive and haemorrhagic gastritis?

A

Numerous causes

Acute ulcer - gastric bleeding and perforation

51
Q

What are the features of Nonerosive, chronic active gastritis?

A

Antrum
Helicobacter pylori
Treat with amoxcillin, clarithromyocin, pantoporzole for 7-14 days

52
Q

What are the features of Atrophic (fundal gland) gastritis?

A

Fundus
Autoantibodies vs parts and products of parietal cells
Parietal cells atrophy
Decreased acid and IF secretion

53
Q

Reactive gastritis

A

Reactive to the acute haemorrhagic gastritis

54
Q

What are methods of mucosal protection?

A

Mucus film
HCO3- secretion
Epithelial barrier (tight junctions, strong apical membrane)
Mucosal blood perfusion (good blood supply can get rid of H+ quickly)

55
Q

What are mechanisms repairing epithelila defects?

A

Migration
Gap closed by cell growth
Acute would healing

56
Q

How does migration repair epithelium?

A

30 mins
Adjacent epithelial cells flatten to close gap
via sideward migration along BM

57
Q

How are ulcer formed?

A 
H. Pylori
Increased gatric juice secretion
Decreased bicarbonate secretion
Decreased cell formation
Decreased blood perfusion
58
Q

What are the clinical outcomes for H. pylori?

A

Asymptomatic or chronic gastritis
Chronic atrophic gastritis/ Intestinal metaplasia
Gastric or duodenal ulcer
Gatric cancer/MALT Lyphomas

59
Q

What is dysphagia?

A

Difficulty in swallowing

60
Q

What is important to distinguish with dysphagia?

A

Localisation

Cricopharyngeal sphincter or distal

61
Q

What are the different types of dysphagia?

A

For solids or fluids
Intermittent or progressive
Precise or vague in appreciation

62
Q

What are the risks of surgical management of achalasia?

A

Oesophageal and gastric perforation (10-16%)

Division of vagus nerve - rare

Splenic injury (1-5%)

63
Q

How would you treat scleroderma?

A

Exclude organic obstruction

Improve force of peristalsis with prokinetics (cisapride)

Once peristaltic failure occurs it is usually irreversible

64
Q

How would you treat corkscrew oesophagus?

A

May respond to forceful PD of cardia

Results not as predictable as achalasia

65
Q

What valvular anomalies can cause dysphagia?

A

Dysphagia Lusoria

Double Aortic Arch

66
Q

Describe the aetiology of oesophageal perforation?

A 
Iatrogenic >50%
Spontaneous - 15%
Foreign body - 12%
Trauma - 9%
Intraoperative - 2%
Malignant - 1%
67
Q

How can trauma cause oesophageal perforation?

A 
Neck = penetrating
Thorax = blunt force
68
Q

What are the symptoms of oesophageal perforation caused by trauma?

A

Dysphagia
Blood in saliva
Haematemesis
Surgical empysema

69
Q

What malignant causes of oesophageal perforation?

A

Advanced cancers
Radiotherapy
Dilatation
Stenting

  • poor prognosis
70
Q

How do oesophageal perforations present?

A

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

71
Q

What is the primary management of oesophageal perforations?

A 
Initial management
• NBM
• IV fluids
• Broad spectrum A/Bs &
Antifungals
• ITU/HDU level care
• Bloods (including G&S)
• Tertiary referral centre
72
Q

What questions should be asked to assess severity of perforation?

A

Is the perforation transmural or intramural?
Where is it & on which side?
How big?
Is leak well defined or diffuse?

73
Q

How is gastric secretion stimulated? (neural)

A

ACh - postganglionic transmitter

of vagal parasympathetic fibres

74
Q

How is gastric secretion stimulated? (endocrine)

A

Gastrin (G cells of antrum)

75
Q

How is gastric secretion stimulated? (paracrine)

A

Histamine (ECL cells & mast

cells of gastric wall)

76
Q

How is gastric secretion inhibited? (endocrine)

A

Secretin (small intestine)

77
Q

How is gastric secretion inhibited? (paracrine)

A

Somatostatin (SIH)

78
Q

How is gastric secretion inhibited? (paracrine + autocrine)

A

PGs (E2 & I2), TGF-α &

adenosine

79
Q

How does closing gaps by cell growth repair epithelium?

A

Stimulated by EGF, TGF-α, IGF-1, GRP & gastrin

80
Q

How does acute wound healing repair epithelium?

A

BM destroyed - attraction of leukocytes &
macrophages; phagocytosis of necrotic cells;
angiogenesis; regeneration of ECM after repair
of BM

epithelial closure by restitution & cell division.

81
Q

What is the primary medical treatment for ulcers?

A

PPI or H2 blocker
Triple Rx (amoxicillin, clarithromycin,
pantoprazole) for 7-14 days)

82
Q

When would you opt for elective surgery for ulcers?

A 
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 [ZollingerEllison syndrome])
• OGD: biopsy all 4 quadrants of ulcer
(rule out malignant ulcer) if refractory
83
Q

What are the surgical indications for ulcers?

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

Year 2 Gastro (10 decks)

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