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Year 2 Gastro > Upper GI tract > Flashcards

Upper GI tract Flashcards

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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
What are the stages of POEM?
Mucosal incision Creation of submucosal tunnel Myotomy Closure of mucosal incisons
26
What does hypomotility cause?
Sceroderma
27
What is scleroderma?
``` 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 ```
28
What does disordered coordination cause?
Corkscrew oesophagus
29
What is the pathophysiology od corkscrew?
``` Diffues oesophageal spasm Dysphagia and chest pain Pressures of 400-500 mmHg Marked hypertrophy of circular muscle Corkscrew seen on barium swallow ```
30
Describe anatomy of oesophageal perforations
3x area of anatomical constriction: Cricopharyngeal constriction Aortic and bronchial Diaphragmatic Pathological narrowing: Cancer, foreign body, physiological dysfunction
31
Where are iatrogenic oeseophgeal perforations normally?
OGD | More common in presence of diverticula or cancer
32
What is Boerhaave's?
Sudden increase in intra-oesophageal pressure with negative intra thoracic pressure Vomiting against a close glottis 3.1 per 100,000
33
What foreign bodies cause perforations?
``` Disk batteries Magnets Sharp objects Dishwasher tablets Acid/Alkali ```
34
What operations can cause perforations?
Hiatus hernia repair Hellers cardiomyotomy Pulmonary surgery Thyroid surgery
35
What investigations do you carry our with perforations?
CXR CT Swallow (gastrograffin) OGD
36
What is the definitive management with oesophageal perforations?
Operative management default Unless - minimal contamination - contained - unfit Then conservative management with stent
37
What are the surgical option for oesophageal perforations?
Primary repair is optimal | +/- Vascularised pedicle flap +/- Gastric fundus buttressing e.g. Dor Drains ++
38
What would a definitive solution be?
Oesophagectomy With reconstruction at the same time or delayed
39
What are the three mechanism that protect agains reflux?
Volume clearance - oesophageal peristalsis reflex pH clearance Epithelium - barrier properties
40
What increases LOS pressure?
``` Acetycholine Alpha-adrenergic agonists Hormones Protein-rich food Histamine High intra-abdominal pressure ``` Inhibits reflux
41
What decreases LOS presuure?
``` Vasoactive intestinal peptide Beta-adrenergic agonsists Hormones Dopamine NO PGI2 PGE2 Chocolate Acid gastric juice Fat Smoking ``` Promotes reflux
42
Why is sporadic reflux normal?
Pressure on full stomach Swallowing Transient sphincter opening
43
What does failure of the protective mechanisms result in?
GORD
44
What are sliding hiatus hernias?
Portion of stomach herniated | Squeezes through diaphragm
45
What is a rolling hiatus hernia?
Junction is in place and the stomach herniates alongside the oesophagus
46
How do you investigate GORD?
OGD - to exclude cancer or confirm oesophagitis, peptic stricture and barretts Oesophageal manometry 24hr oesophageal pH recording
47
What are the treatments for GORD?
``` Lifestyle changes (weight loss, smoking, EtOH) PPIs ```
48
What surgical treatments are available for GORD?
Dilation peptic strictres | Laparascopic Nissen's fundoplication
49
What are the different types of gastritis?
erosive and haemorrhagic Nonerosive, chronic active gastritis Atrophic (fundal gland) gastritis Reactive gastritis
50
What are the features of erosive and haemorrhagic gastritis?
Numerous causes | Acute ulcer - gastric bleeding and perforation
51
What are the features of Nonerosive, chronic active gastritis?
Antrum Helicobacter pylori Treat with amoxcillin, clarithromyocin, pantoporzole for 7-14 days
52
What are the features of Atrophic (fundal gland) gastritis?
Fundus Autoantibodies vs parts and products of parietal cells Parietal cells atrophy Decreased acid and IF secretion
53
Reactive gastritis
Reactive to the acute haemorrhagic gastritis
54
What are methods of mucosal protection?
Mucus film HCO3- secretion Epithelial barrier (tight junctions, strong apical membrane) Mucosal blood perfusion (good blood supply can get rid of H+ quickly)
55
What are mechanisms repairing epithelila defects?
Migration Gap closed by cell growth Acute would healing
56
How does migration repair epithelium?
30 mins Adjacent epithelial cells flatten to close gap via sideward migration along BM
57
How are ulcer formed?
``` H. Pylori Increased gatric juice secretion Decreased bicarbonate secretion Decreased cell formation Decreased blood perfusion ```
58
What are the clinical outcomes for H. pylori?
Asymptomatic or chronic gastritis Chronic atrophic gastritis/ Intestinal metaplasia Gastric or duodenal ulcer Gatric cancer/MALT Lyphomas
59
What is dysphagia?
Difficulty in swallowing
60
What is important to distinguish with dysphagia?
Localisation | Cricopharyngeal sphincter or distal
61
What are the different types of dysphagia?
For solids or fluids Intermittent or progressive Precise or vague in appreciation
62
What are the risks of surgical management of achalasia?
Oesophageal and gastric perforation (10-16%) Division of vagus nerve - rare Splenic injury (1-5%)
63
How would you treat scleroderma?
Exclude organic obstruction Improve force of peristalsis with prokinetics (cisapride) Once peristaltic failure occurs it is usually irreversible
64
How would you treat corkscrew oesophagus?
May respond to forceful PD of cardia | Results not as predictable as achalasia
65
What valvular anomalies can cause dysphagia?
Dysphagia Lusoria | Double Aortic Arch
66
Describe the aetiology of oesophageal perforation?
``` Iatrogenic >50% Spontaneous - 15% Foreign body - 12% Trauma - 9% Intraoperative - 2% Malignant - 1% ```
67
How can trauma cause oesophageal perforation?
``` Neck = penetrating Thorax = blunt force ```
68
What are the symptoms of oesophageal perforation caused by trauma?
Dysphagia Blood in saliva Haematemesis Surgical empysema
69
What malignant causes of oesophageal perforation?
Advanced cancers Radiotherapy Dilatation Stenting - poor prognosis
70
How do oesophageal perforations present?
Pain 95 % Fever 80 % Dysphagia 70 % Emphysema 35 %
71
What is the primary management of oesophageal perforations?
``` Initial management • NBM • IV fluids • Broad spectrum A/Bs & Antifungals • ITU/HDU level care • Bloods (including G&S) • Tertiary referral centre ```
72
What questions should be asked to assess severity of perforation?
Is the perforation transmural or intramural? Where is it & on which side? How big? Is leak well defined or diffuse?
73
How is gastric secretion stimulated? (neural)
ACh - postganglionic transmitter | of vagal parasympathetic fibres
74
How is gastric secretion stimulated? (endocrine)
Gastrin (G cells of antrum)
75
How is gastric secretion stimulated? (paracrine)
Histamine (ECL cells & mast | cells of gastric wall)
76
How is gastric secretion inhibited? (endocrine)
Secretin (small intestine)
77
How is gastric secretion inhibited? (paracrine)
Somatostatin (SIH)
78
How is gastric secretion inhibited? (paracrine + autocrine)
PGs (E2 & I2), TGF-α & | adenosine
79
How does closing gaps by cell growth repair epithelium?
Stimulated by EGF, TGF-α, IGF-1, GRP & gastrin
80
How does acute wound healing repair epithelium?
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
What is the primary medical treatment for ulcers?
PPI or H2 blocker Triple Rx (amoxicillin, clarithromycin, pantoprazole) for 7-14 days)
82
When would you opt for elective surgery for ulcers?
``` 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
What are the surgical indications for ulcers?
``` Intractability (after medical therapy) • Haemorrhage • Obstruction • Perforation • Relative: continuous requirement of steroid therapy/NSAIDs ```

Year 2 Gastro (10 decks)

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