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1B Gastroenterology > Upper GI Tract > Flashcards

Upper GI Tract Flashcards

1
Q

what are the boundaries to the oesophagus and what muscle is it composed of?

what are the boundaries of the upper oesophagus?

A
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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 (lt and Rt crux)
  • Intact pharyngoesophageal ligament
  • Angle of his
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3
Q

what is the angle of his?

A

Angle between distal oesophagus and fundus allow expansion and compression from lateral to medial

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4
Q

what are the stages to swallowing?

A
  • Stage 0: oral phase
  • Stage 1 : pharyngeal phase
  • Stage 2: Upper Oesophageal phase
  • Stage 3: lower oesophageal phase
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5
Q

what happens during stage 0 swallowing

A
  • Chewing & saliva prepare bolus
  • Both oesophageal sphincters constricted
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6
Q

what happens during stage 1 swallowing?

A
  • Pharyngeal musculature guides food bolus towards oesophagus
  • Upper oesophageal sphincter opens reflexly
  • LOS opened by vasovagal reflex (receptive relaxation reflex)
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7
Q

what happens during stage 2 swallowing?

A
  • Upper sphincter closes
  • Superior circular muscle rings contract & inferior rings dilate
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8
Q

what happens during stage 3 swallowing?

A
  • Lower sphincter closes as food passes through
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9
Q

what is oesophageal motility determined by?

A
  • determined by pressure measurements (manometry)

Peristaltic waves are about 40 mmHg

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10
Q

what is the resting LOS pressure?

A

20 mmHg

  • Decreased <5 during receptive relaxation
  • Mediated by inhibitory noncholinergic noradrenergic NCNA neurones of myenteric plexus
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11
Q

what are functional disorders of the oesophagus caused by?

A
  • Abnormal oesophageal contraction:
    • Hypermotility
    • Hypomotility
    • Disordered coordination
  • Failure of protective mechanisms for reflux
    • GORD
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12
Q

what is dysphagia?

A

difficulty in swallowing

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13
Q

what are the types of dysphagia?

A

for solids or fluids

intermittent or progressive

precise or vague in appreciation

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14
Q

what is odynophagia?

A

pain on swallowing

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15
Q

what is regurgitation?

A

return of oesophageal contents from above an obstruction

may be functional or mechanical

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16
Q

what is reflux

A

passive return of gastroduodenal contents to the mouth

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17
Q

what is achalasia?

A

due to hypermotility of the oesophagus

  • Due to loss of ganglion cells in Auerbach’s myenteric plexus in LOS wall
    • Decreased activity of inhibitory NCNA neurones
    • Cannot relax oesophageal sphincter
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18
Q

what is the cause of achalasia?

A

Primary – aetiology unknow

Secondary- diseases causing oesophageal motor abnormalities similar to primary achalasia

  • Chagas’ disease
  • Protozoa infection
  • Amyloid/ sarcoma/ eosinophilic oesophagitis
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19
Q

what is the mechanism of hypermotility?

A
  • Increased resting pressure of LOS
  • Receptive relaxation sets in too late & is too weak
    • During reflex phase pressure is LOS is markedly increased than stomach
  • Swallowed food collects in oesophagus = increased pressure with dilation of oesphagus
  • Propagation of peristaltic waves cease
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20
Q

what is the disease course of hypermotility of oesophagus?

A

Disease course:

  • Insidious onset-symptoms for years prior to seeking help
  • Progressive without treatment à progressive oesophageal dilation of oesophagus
  • Weight loss, trouble swallowing, pain
  • Esophagitis
  • Aspiration pneumonia
  • Increased risk oesophageal cancer
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21
Q

what is the treatment of hypermotility of oesophagus?

A

pneumatic dilatation

surgery

peroral endoscopic myotomy

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22
Q

how does Pneumatic dilatation (PD) work in hypermotility?

A
  • PD weakens LOS by circumferential stretching & in some cases tearing of muscle fibres
  • Efficacy of PD high but many patients relapse
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23
Q

what are the options for surgery for hypermotility?

A
  • Heller’s myotomy
    • A continuous myotomy performed for 6cm on oesophagus & 3cm onto the stomach
  • Dor fundoplication
    • Anterior fundus folded over oesophagus and sutures to right side of myotomy
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24
Q

what are the risks of surgery for hypermotility oesophagus?

A
  • Oesophageal & gastric perforation
  • Division vagus nerve
  • Splenic injury
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25
Q

how does peroral endoscopic myotomy work? (POEM)

A
  • A) Mucosal incision
  • B) Creating submucosal tunnel
  • C) Myotomy
  • D) Closure of mucosal incision
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26
Q

what is scleroderma

A

immune disease

caused by oesophagus hypomotility

  • hypomotility due to Neuronal defects à smooth muscle atrophy of oesophagus à no peristalsis in smooth muscle à hypomotility à gastroesophageal reflux disease
    • Decreased resting pressure of LOS
    • GERD often associated with CREST syndrome
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27
Q

what is the treatment for scleroderma?

A
  • Exclude organic obstruction
  • Improve force of peristalsis wit prokinetics (cisapride)

Once peristaltic failure occurs à usually irreversible

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28
Q

how can disordered coordination of oesophagus be seen?

A

Diffuse oesophageal spasm

  • Incoordinate contractions à dysphagia & chest pain
  • Pressures 400-500 mmHg
  • Marked hypertrophy of circular muscle
  • Corkscrew oesophagus on barium
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29
Q

what is the treatment for disordered oesophagus coordination?

A
  • May respond to forceful PD of cardia
  • Results not a predictable as achalasia
30
Q

what vascular abnormalities can cause dysphagia?

A
  1. Dysphagia lusoria- aberrant right subclavian artery
    1. Altered by surgical correction
  2. Double aortic arch
31
Q

what are the possible causes of oesophageal perforation?

A
  • Iatrogenic (OGD) >50%
  • Spontaneous (Boerhaave’s) -15%
  • Foreign body
  • Trauma
  • Intraoperative
  • malignant
32
Q

what are the iatrogenic causes of oesophageal perforation?

A
  • usually at OGD
  • more common in presence of diverticula or cancer
  • Incidence
  • OGD
  • stricture dilation
  • sclerotherapy
  • achalasia dilatation
33
Q

what is the mechanism of Boerhaave’s?

A
  • Sudden increase in intra-oesophageal pressure with negative intrathoracic pressure
  • vomiting agaists a closed glottis
34
Q

what objects often cause foreign body oesophageal perforation?

A
  • Disk batteries growing problem
  • cause electrical burns if impact in mucosa
  • magnets
  • sharp objects
  • dishwasher tablets
  • acid/alkali
35
Q

how can trauma cause oesophageal perforation?

A
  • Neck= penetrating
  • Thorax= blunt force
  • Can be difficult to diagnose
  • dysphagia
  • blood in saliva
  • haematemesis
  • surfical empysema
36
Q

what surgery can cause oesophageal perforation?

A
  • hiatus hernia repair
  • Hellers cardiomyotomy
  • pulmonary surgery
  • thyroid surgery
37
Q

what malignancy can cause oesophageal perforation and what is the prognosis?

A
  • Advanced cancers
  • radiotherapy
  • dilatation
  • stenting
  • poor prognosis
38
Q

what is the presentation of oesophageal perforation?

A
  • Pain
  • Fever
  • Dysphagia
  • Emphysema
39
Q

what is the initial management of oesophageal perforation?

A
  • NBM
  • IV Fluid
  • Broad spectrum A/Bs & Antifungals
  • ITU/HDU level care
  • Bloods
  • Tertiary care referral
  • Surgical emergency
    • 2x mortality if 24 hr delay in diagnosis
  • Operative management should be default
40
Q

when should operative management for oesophageal perforation not be used?

A
  • Minimal contamination
  • Contained
  • Unfit
  • In this case = Conservative management with covered metal stent
41
Q

what is the definitive management of oesophageal perforation?

A
  • Primary repair optimal
    • +/- vascularised pedicle flap
    • +/- gastric fundus buttressing (e.g Dor)
    • Drains ++
  • Oesophagostomy- definitive solution
    • Oesophagus joined to stomach
    • With reconstruction or oesophagostomy & delayed reconstruction
42
Q

what are the functions of the stomach?

A
  • Breaks food into smaller particles (acid & pepsin)
  • Holds food, releasing it ina controlled steady rate into duodenum
  • Kills parasites & certain bacteria
43
Q

what is the structure of the stomach?

A

invaginated into mucosa- tubular glands

44
Q

what is mucins in the stomach?

A

gel coating

HCO3- trapped in mucus gel

45
Q

what is the pH in the stomach?

A

epithelial surface = 6-7

lumen = 1-2

46
Q

what are the protective mechanisms against reflux?

A
  • LOS usually closed as barrier against reflux of harmful gastic juice (pepsin & HCL)
  • LOS pressure changes change reflux
  • Sporadic reflux is normal
    • Pressure on full stomach
    • Swallowing
    • Transient sphincter opening
  • 3 mechanisms pretect following reflux
    • Volume clearance -oesophageal peristalsis reflex
    • pH clearance- saliva
    • epithelium- barrier properties
47
Q

what does failure of protective mechanisms against reflux cause?

A

GORD

48
Q

what hernias can GORD cause?

A

sliding hiatus hernia (squeezing through diaphragm)

rolling hiatus hernia

49
Q

what can causes reflux?

A

decrease sphincter pressure

transient sphincter opening

decreased saliva production and decreased buffering capacity of saliva -> decreased pH clearance

abnormal peristalsis -> decreased vol clearance

hiatus hernia

defective mucosal protective mechanism (e.g alcohol)

50
Q

what is the treatment for GORD?

A
  • Medical
    • Lifestyle changes (weight loss, smoking, EtOH)
    • PPis
  • Surgical
    • Dilatation peptic strictures
    • Laproscopic Nissen’s fundoplication
51
Q

what are the types of gastritis?

A
  1. erosive and haemorrhagic
  2. nonerosive, chronic active
  3. atrophic (fundal)
  4. reactive
52
Q

what are the causes of erosive and haemorrhagic gastritis?

A

NSAIDS

alcohol

multi-organ failure -> ischamia

burns

trauma

53
Q

what is the consequence of erosive and hemorrhagic gastritis?

A

acute ulcer-causing gastric bleeding and perforation

54
Q

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

A

in the antrum

caused by helicobacter pylori

55
Q

what is reactive gastritis caused by?

A

chronic active gastritis and erosive/ haemorrhagic gastritis

56
Q

what are the effects of chronic active gastritis?

A

increased gastrin

acid secretion normal or increased

causes gastric and duodenal ulcer

57
Q

what are the consequences of reactive gastritis and atrophic gastritis?

A

epithelial metaplasia = carcinoma

58
Q

what happens in atrophic gastritis?

A
  • Fundus (fundal gland)
  • Autoantibodies vs parts & products of parietal cells
  • Patietal cell atrophy
  • Decrease acid & IF secretion
59
Q

what is the overall paths of gastritis?

A
60
Q

what is stimulatory on gastric secretion?

A
  • Neural= Ach- postganglionic transmitter of vagal parasympathetic fibres
  • Endocrine= gastric (G cells of antrum)
  • Paracrine= histamine (ECL cells & mast cells of gastric wall)
61
Q

what can inhibit gastric secretion?

A
  • Endocrine= secretin (small intestine)
  • Paracrine= somatostatin (SIH)
  • Paracrine & autocrine= PGs (E2 & I2), TGF-alpha & adenosine
62
Q

what protection is there from gastric acid?

A
63
Q

what are the mechanisms repairing endothelial defects?

A
  1. Migration
    1. Adjecent epithelial cells flatten to close gap via sideward migration along BM
  2. Gap closed by cell growth
    1. Stimulated by EGF, TGF-alpha, IGF-1, GRP & gastrin
  3. Acute wound healing
    1. BM destroyed- attraction of leukocytes & macrophages
      1. Phagocytosis of necrotic cells
      2. Angiogenesis
      3. Regeneration of ECM after repair of BM

b. Epithelial closure by restitution and cell division

64
Q

how is an ulcer formed?

A
65
Q

what are the H.Pylori outcomes?

A
  1. Asymptomatic or chronic gastritis
  2. Chronic atrophic gastritis or intestinal metaplasia
  3. Gastric or duodenal ulcers
  4. Gastric cancer/ MALT lymphoma
66
Q
A
67
Q

what factors does H.Pylori have associated with virulence?

A
  1. urease
    1. neutralize gastric acid
    2. gastric mucosal injury (by ammonia)
  2. exotoxins
    1. vacuolating toxin
    2. gastric mucosal injury
  3. secretory enzymes
    1. mucinase, protease, lipase
    2. gastric mucosal injury
68
Q

what are the treatments for an ulcer?

A

Primarily medical

  • PPI or H2 blocker
  • Triple Rx (amoxicillin, clarithromycin, pantopraxole for 7-14 days)
69
Q

when is surgery used for an ulcer?

A
  • Rare- most uncomplicated ulcers heal within 12 weeks
  • In 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 if refractory
    • Rule out malignant ulcer
70
Q

what are indications for surgery in an ulcer?

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

1B Gastroenterology (12 decks)

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