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!!!!! BRS YR2 !!!!! > Gastro - Upper GI Tract Disorders > Flashcards

Gastro - Upper GI Tract Disorders Flashcards

1
Q

What 5 sections can the oesophagus be split into?

A

→ cervical oesophagus
→ upper thoracic oesophagus
→ middle thoracic oesophagus
→ lower thoracic oesophagus + oesophageal junction
→ abdominal oesophagus

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2
Q

What parts of the oesophagus are skeletal muscle?

A

cervical oesophagus

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3
Q

What parts of the oesophagus are skeletal + smooth muscle?

A

upper thoracic + middle thoracic

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4
Q

What parts of the oesophagus are smooth muscle?

A

lower thoracic

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5
Q

At what vertebral level is the upper oesophageal sphincter located / does the oesophagus start?

A

C6

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6
Q

Where is the LOS located?

A

3-4 cm distal oesophagus within abdomen

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7
Q

How does the diaphragm support the LOS?

A

→ diaphragm surrounds LOS (around left + right crux)
→ intact phrenoesophageal ligament (one part attaches to the upper part of oesophageal, other one attaches to cardia of stomach

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8
Q

What is the angle of His?

A

→ acute angle between the abdominal oesophagus + fundus of stomach at the oesophageal junction
→ prevents reflux

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9
Q

What are the 4 stages of swallowing?

A

→ stage 0 : oral pahse
→ stage 1 : pharyngeal phase
→ stage 2 : upper oesophageal phase
→ stage 3 : lower oesophageal phase

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10
Q

What does stage 0 involve?

A

Oral phase:
→ Chewing & saliva prepare bolus
→ Both oesophageal sphincters constricted

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11
Q

What does stage 1 involve?

A

Pharyngeal phase:
→ Pharyngeal musculature guides food bolus towards oesophagus
→ Upper oesophageal sphincter opens reflexly
→ LOS opened by vasovagal reflex (receptive relaxation reflex)

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12
Q

What does stage 2 involve?

A

Upper Oesophageal Phase :
→ Upper sphincter closes
→ Superior circular muscle rings contract & inferior rings dilate
→ Sequential contractions of longitudinal muscle

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13
Q

What does stage 3 involve?

A

Lower Oesophageal Phase :
→ Lower sphincter closes as food passes through

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14
Q

How is oesophageal motility is measured?

A

manometry

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15
Q

What is the average normal peristaltic wave pressure?

A

40 mmHg

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16
Q

What is the resting pressure of the LOS?

A

20 mmHg

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17
Q

What happens to the LOS resting pressure during receptive relaxation?

A

decreases by 5 mmHg

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18
Q

What is the decrease in LOS resting pressure mediated by?

A

inhibitory noncholinergic nonadrenergic neurons (NCNA) of the myenteric plexus

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19
Q

What can cause absence of stricture?

A

→ abnormal oesophageal contraction
→ failure of protective reflux mechanisms

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20
Q

What causes abnormal oesophageal contraction?

A

→ hypermotility
→ hypomotility
→ disordered coordination

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21
Q

What is an example of failure of protective reflux mechanisms?

A

GORD (gastrooesophangeal reflex disease)

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22
Q

What is dysphagia?

A

difficulty swallowing

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23
Q

What do you look for when exploring a patient’s dysphagia?

A

→ localisation is important (cricopharyngeal sphincter or distal)
→ solids or fluids?
→ intermittent or progressive
→ precise or vague in appreciation

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24
Q

What is odynophagia?

A

pain in swallowing

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25
Q

What is regurgitation?

A

return of oesophageal contents form above an obstruction (can be functional or mechanical)

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26
Q

What is reflux?

A

passive return of gastroduodenal contents to the mouth

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27
Q

What is Achalasia?

A

hyper motility

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28
Q

What is the cause of Achalasia?

A

→ Due to loss of ganglion cells in Aurebach’s myenteric plexus in LOS wall
→ decreased activity of inhibitory NCNA neurones.

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29
Q

What is the pathophysiology of Achalasia?

A

→ Environmental triggers + genetic predisposition + non autoimmune inflammatory infiltrates = extracellular turnover wound repair fibrosis + loss of immunological tolerance
→ leads to apoptosis of neurones + humoral response
→ leads to myenteric abnormalities etc.

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30
Q

What are the 2 different types of achalasia?

A

→ primary
→ secondary

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31
Q

What other diseases cause similar hypermotility abnormalities?

A

→ Chagas disease
→ protozoa infection
→ amyloid / sarcoma/ eosinophilic oesophagitis

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32
Q

What happens as a result of achalasia?

A

→ increased pressure of LOS
→ receptive relaxation sets in late + too weak
→ swallowed food collects in oesophagus causing increased pressure throughout with dilation of the oesophagus
→ cessation of propagation of peristaltic waves

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33
Q

What are the complications that achalasia can lead to?

A

→ pain
→ dysphagia
→ weight loss
→ oesophagitis
→ pneumonia due to aspiration of food
→ 28x increased risk of oesophageal cancer

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34
Q

What is onset like for achalasia?

A

→ insidious onset
→ symptoms for years prior to seeking help

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35
Q

What happens to oesophagus in achalasia without treatment?

A

progressive oesophageal dilation

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36
Q

What is the treatment for achalasia?

A

pneumatic dilation

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37
Q

How does PD treat achalasia?

A

→ endoscopy with wire + deflated balloon
→ when blown up in the LOS, weaken LOS by circumferential stretching & in some cases, tearing of its muscle fibres

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38
Q

What is the efficacy of PD?

A

71 - 90% of patients respond initially but many patients subsequently relapse

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39
Q

What are the surgical treatments for achalasia?

A

→ Heller’s Myotomy
→ Dor Fundoplication

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40
Q

What is Heller’s Myotomy?

A

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

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41
Q

What is Dor Fundoplication?

A

anterior fundus folded over oesophagus and sutured to right side of myotomy

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42
Q

What are the risks of surgery for achalasia?

A

→ Oesophageal & gastric perforation (10 – 16%)
→ Division of vagus nerve – rare
→ Splenic injury – 1 – 5%

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43
Q

What is Scleroderma?

A

→ autoimmune disease
→ hypo motility in early stages due to neuronal defects

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44
Q

What happens in scleroderma?

A

→ hypo motility in early stages leads to atrophy of smooth muscle of oesophagus
→ Peristalsis in the distal portion ultimately ceases altogether
→ increased resting pressure of LOS
→ gastroesophageal reflux disease develops
→ Often associated with CREST syndrome

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45
Q

What is CREST syndrome?

A

→ C = calcinosis (deposits of calcium in soft tissue)
→ R = Raynaud’s phenomenon (constriction of peripheral blood vessels, leads to problems in hands)
→ E = eosophageal dysmotility
→ S = sclerodactyly (thickening of hands + toes)
→ T = telangiectasia (spider veins)

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46
Q

What is the treatment for scleroderma?

A

→ Exclude organic obstruction
→ Improve force of peristalsis with prokinetics (cisapride)
→ Once peristaltic failure occurs → usually irreversible

47
Q

What is corkscrew oesophagus?

A

→ disordered oesophagus coordination
→ diffuse oesophageal spasm

48
Q

What are the symptoms + signs of corkscrew oesophagus?

A

→ inco-ordinate contractions that lead to dysphagia + chest pain
→ Pressures of 400-500 mmHg
→ Marked hypertrophy of circular muscle
→ Corkscrew oesophagus on Barium

49
Q

What is the treatment for corkscrew oesophagus?

A

→ May respond to forceful PD of cardia
→ Results not as predictable as achalasia

50
Q

Where do oesophageal perforations usually occur?

A

at the 3 areas of anatomical constriction

51
Q

What are the 3 areas of anatomical constriction?

A

→ cricopharyngeal constriction
→ aortic + bronchial constriction
→ diaphragmatic + sphincter constriction

52
Q

What are the causes of perforation in Oesophagus?

A

→ Iatrogenic (investigative)(OGD) >50%
→ Spontaneous (Boerhaave’s) - 15%
→ Foreign body - 12%
→ Trauma - 9%
→ Intraoperative - 2%
→ Malignant - 1%

53
Q

What makes perforation more common in an OGD?

A

more common in presence of diverticula or cancer

54
Q

What is a Boerhaave’s perforation?

A

spontaneous oesophageal perforation

55
Q

What causes Boerhaave’s?

A

→ sudden increase in intra-oesophageal pressure with negative intra thoracic pressure
→ causes vomitting against closed glottis

56
Q

What is the incidence of Boerhaave’s like?

A

→ 3.1 out of a million

57
Q

Where is a Boerhaave’s perforation most likely in the oesophagus?

A

Left posterolateral aspect of the distal oesophagus

58
Q

What foreign bodies can cause oesophageal perforation?

A

→ Disk batteries is a growing problem (Cause electrical burns if embeds in mucosa)
→ Magnets
→ Sharp objects
→ Dishwasher tablets
→ Acid/Alkali

59
Q

What types of trauma can cause oesophageal perforation?

A

→ neck = penetrating
→ thorax = blunt force

60
Q

What are the main symptoms of oesophageal perforation caused by trauma?

A

→ dysphagia
→ blood in slaiva
→ haematemesis (vomitting blood)
→ surgical emphysema (air under the skin with crackling sensation when touched

61
Q

What symptoms does oesophageal perforation generally present with?

A

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

62
Q

What investigations are needed to diagnose oesophageal perforation?

A

→ chest x-ray
→ CT scan
→ swallow (gastrogaffin contrast)
→ OGD (however could make things far worse)

63
Q

What is the urgency of oesophageal perforation?

A

→ surgical emergency
→ 2x increased mortality if there’s 24 hour delay in diagnosis

64
Q

What is given as initial management for oesophageal perforation?

A

→ NBM (nil by mouth)
→ IV fluids
→ broad spectrum antibiotics
→ antifungals
→ intensive unit level of care
→ should be referred to a tertiary referral centre
→ blood (including G&S)

65
Q

How can oesophageal perforations be conservatively managed?

A

covered metal stent

66
Q

What is the operative management for oesophageal perforation?

A

→ primary repair of perforation is optimal
→ oesophagectomy is a definite solution (stomach is joined to whatever’s left of oesophagus)

67
Q

How does the LOS protect against reflux?

A

usually closed as barrier against reflux of harmful gastric juice (pepsin & HCl)8

68
Q

What increases LOS pressure ?

A

→ acetylene choline
→ a-adrenergic agonists
→ hormones
→ protein-rich food
→ histamines
→ high intra-abdominal pressure
→ PGF, etc.

69
Q

How does increased LOS pressure affect reflux?

A

→ increased pressure in oesophageal sphincter
→ inhibits reflux

70
Q

What decreases LOS pressure?

A

→ VIP
→ beta-adrenergic agonists
→ hormones
→ dopamine
→ Nitric Oxide
→ PG12
→ PGE2
→ chocolate
→ acid gastric juice
→ fat
→ smoking

71
Q

How does decreased LOS pressure affect reflux?

A

→ decreased pressure in oesophageal sphincter
→ promotes reflux

72
Q

What can cause normal sporadic reflux?

A

→ pressur eon full stomach
→ swallowing
→ transient sphincter opening

73
Q

What are the 3 main mechanisms that protect against reflux?

A

→ volume clearance - oesophageal peristalsis reflex
→ pH clearance - saliva
→ epithelium - barrier properties

74
Q

What can cause failure of protective measures against GORD?

A

→ decrease in sphincter pressure
→ increase in transient sphincter opening
→ decrease in saliva production
→ abnormal peristalsis + decreased volume clearance
→ decreased buffering capacity of saliva + decreased pH clearance
→ hiatus hernia
→ defective mucosal protective mechanisms

75
Q

How can GORD cause carcinoma?

A

→ reflux oesophagitis
→ epithelial metaplasia
→ carcinoma

76
Q

What are the 2 forms of hiatus hernia?

A

→ sliding hiatus hernia
→ rolling / paraoesophageal hiatus hernia

77
Q

What is a sliding hiatus hernia?

A

stomach herniates up into the?????

78
Q

What is a rolling/paraoesophageal hiatus hernia?

A

portion of the stomach henriates from under hiatus in the diaphragm

79
Q

What investigations must be undertaken for GORD?

A

→ OGD

→ oesophageal manometry

→ 24 hour oesophageal pH monitoring

80
Q

Why are these investigations done for GORD?

A

→ to exclude cancer

→ to confirm peptic strictures, Barret’s oesophagus, oesophagitis

81
Q

How can GORD be managed conservatively?

A

→ lifestyle chnages (weight loss, stop smoking, etc.)

→ PPIs

82
Q

What are the surgical interventions for GORD?

A

→ dilation peptic strictures

→ laparascopic Nissen’s fundoplication

83
Q

What are the functions of the stomach?

A

→ breaks food into smaller particles (acid + pepsin)

→ holds food, releasing it at acontrolled + steady rate into duodenum

→ kills parasites + certain bacteria

84
Q

What are the different regions of the stomach?

A

→ antrum

→ pyloric region

→ cardia

→ body

→ fundus

85
Q

What regions of the stomach produce mucus only?

A

cardia + pyloric regions

86
Q

What regions of the stomach produce mucus, HCl + pepsinogen?

A

body + fundus

87
Q

What is regions of the stomahc produce gastrin?

A

antrum

88
Q

What are the 4 different types of gastritis?

A

→ erosive + haemorrhagic

→ non-erosive chronic active

→ atrophic (fundal gland)

→ reactive

89
Q

What can cause erosive + haemorrhagic gastritis?

A

→ NSAIDs

→ alcohol

→ multi-organ-failure

→ burns

→ trauma

→ ischaemia

90
Q

What is the general progression of erosive + haemorrhagic gastritis?

A

acute ulcer → bleeding perforation

acute ulcer → reactive gastritis → epithelial metaplasia → carcinoma

91
Q

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

A

helicobacter pylori infection

92
Q

What part of the stomach does non-erosive chronic active gastritis affect?

A

antrum

93
Q

How does non-erosive chronic active gastritis progress?

A

→ increased gastrin production → increased acid secretion → chronic gastric + duodenal ulcer → reactive gastritis → epithelial metaplasia → carcinoma

94
Q

What is the treatment for non-erosive chronic active gastritis?

A

triple Rx - amoxicillin, clarithromycin, pantoprazole for 7-14 days

95
Q

What causes atrophic (fundal gland) gastritis?

A

autoantibodies vs parts + products of the parietal cells

96
Q

What part of the stomach does atrophic gastrtis affect?

A

fundus + its parietal cells

97
Q

What is the progression of atrophic gastritis?

A

→ parietal cell atrophy → decreased acid production + IF secretion

→ can result in carcinoids, carcinomas or pernicious anemia

98
Q

What is pernicious anemia?

A

→ autoimmune condition that affects your stomach

→ lack of IF goes hand-in-hand with folate + Vitamin B12 deficiency

99
Q

How is gastrin secretion stimulated?

A

→ neurally : Ach - postganglionic transmitter of vagal parasympathetic fibres

→ endocrine : Gastrin - G cells of the antrum

→ paracrine : histamine - ECL cells + mast cells of the gastric wall

100
Q

How is gastrin secretion inhibited?

A

→ endocrine : secretin - small intestine

→ paracrine : somatostatin - SIH

→ paracrine + autocrine : PGs (E2 and I2), TGF-alpha + adenosine

101
Q

What are the 4 forms of mucosal protection the sotmach lining has?

A

→ mucus film

→ bicarbonate secretion

→ epithelial barrier

→ mucosal blood perfusion

102
Q

What is the mucus film + how does it protect?

A

epithelial cells produce mucus, mucus layer protects epithelium from pepsin + H+ ions

103
Q

How does the bicarbonate secretion protect?

A

produced by epithelial cells + propgated by prostaglandins, buffers the hydrogen, therefore neutralising the acid

104
Q

How does the epithelial barrier protect?

A

phsyical barrier with tight junctions, prevents entry of hydrogen ions

105
Q

How do mucosal blood perfusion protect?

A

bloof perfusion (basolateral sodium + hydrogen exchange) will mitigate any hydrogen ions that do slip through the barrier

106
Q

What 3 mechanisms repair the epithelium if it does get breached?

A

→ migration

→ gap closed by cell growth

→ acute wound healing

107
Q

What is the mechanism of migration + how does it help repair the epithelium?

A

adjacent epithelial cells flatten to close gap via sideward migration along the BM

108
Q

How does gap closed by cell growth work?

A

cell growth is simulated by EGF, TGF-alpha, IGF-1, GRP, gastrin

109
Q

How does acute wound healing occur?

A

when BM is destroyed:

→ attraction of leukocytes + macrophages

→ phagocytosis of necrotic cells

→ angiogensis

→ regeneration of ECM after repair of BM

→ epithelial closure by resitiution + cell division

110
Q

What can cause the formation of ulcers?

A

→ helicobacter pylori

→ increased gastric juice secretion

→ decreased bicarbonate secretion

→ decreased cell formation in BM

→ decreased blood perfusion

111
Q

What are the 4 clinical outcomes of helicobacter pylori infection?

A

→ 80% = asymptomatic or chronic gastritis

→ 15%-20% = chronic atrophic gastritis, intestinal metaplasia, gastric or duodenal ulcers

→ 1% = gastric cancer, MALT lymphoma

112
Q

What is the primary medical treatment of ulcers?

A

→ PPIs or H2 blocker

→ triple rx (amoxicillin, pantoprazole, clarithromycin) for 7-14 days

113
Q

What is the procedure after primary medical treatment?

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 [Zollinger-Ellison syndrome])
  • OGD: biopsy all 4 quadrants of ulcer (rule out malignant ulcer) if refractory
114
Q

What are the indications that ulcers need to be treated surgically?

A
  • Intractability (after medical therapy)
  • Relative: continuous requirement of steroid therapy/NSAIDs
  • Complications e.g. Haemorrhage, Obstruction, Perforation

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