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Z YEAR 2 BRS GASTRO > Upper GI Tract 2 > Flashcards

Upper GI Tract 2 Flashcards

1
Q

How do oesophageal perforations present?

A
  1. Pain 95 % 

  2. Fever 80 % 

  3. Dysphagia 70 % 

  4. Emphysema 35 %
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2
Q

What imaging do you fo for oesophageal perforations?

A
  1. CXR 

  2. CT 

  3. Swallow (gastrograffin) 

  4. OGD
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3
Q

What is the initial management of oesophageal perforations?

A
  1. NBM
  2. IV fluids
  3. Broad spectrum A/Bs & 
Antifungals 

  4. ITU/HDU level care 

  5. Bloods (including G&S) 

  6. Tertiary referral centre
  7. Surgical emergency

  8. 2x ↑mortality if 24h delay in
    diagnosis
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4
Q

How do you determine management with questions in an oesophageal perforation?

A
  1. Is the perforation transmural or 
intramural? 

  2. Where is it & on which side?
  3. How big? 

  4. Is leak well defined or diffuse?
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5
Q

When is operative management of an oesophageal perforation not default?

A
  • Minimal contamination
  • Contained

  • Unfit
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6
Q

What is the conservative management of an oesophageal perforation?

A

covered metal stent

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7
Q

What sort of repair is optimal?

A
  • Primary but if not:
    1. +/- Vascularised pedicle flap 
2. +/- Gastric fundus buttressing 
(e.g. Dor) 

    3. Drains ++
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8
Q

What is a definitive solution?

A
  1. Oesophagectomy - definitive solution

2. With reconstruction or oesophagostomy & delayed reconstruction

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9
Q

What state is LOS usually in?

A

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

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10
Q

What is LOS pressure increased by?

A
  1. Acetylcholine
  2. Alpha-adrenergic agonists
  3. Hormones
  4. protein rich food
  5. histamine
  6. high intra-abdominal pressure
  7. PGF2alpha etc
    - Causes Increased pressure in esophageal sphincter
    - Inhibits reflux
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11
Q

What is LOS pressure decreased by?

A
  1. VIP
  2. Beta-adrenergic agonists
  3. Hormones
  4. Dopamine
  5. NO
  6. PGI2 and PGE2
  7. Chocolate
  8. Acid gastric juice
  9. Fat
  10. Smoking
    - Causes decreased pressure in oesophageal sphincter
    - Promotes reflux
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12
Q

Is sporadic reflux normal?

A

Sporadic reflux is normal
• pressure on full stomach

• swallowing

• transient sphincter opening

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13
Q

What are the 3 mechanisms protect following reflux?

A
  1. Volume clearance - oesophageal 
peristalsis reflex 

  2. pH clearance - saliva 

  3. Epithelium - barrier properties
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14
Q

What happens in GORD?

A

failure of protective mechanisms

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15
Q

What can happen in GORD?

A
  1. Decrease sphincter pressure
  2. Transient sphincter opening (air, CO2)
  3. Abnormal peristalsis (decreased volume clearance)
  4. Decreased saliva production (in sleep, xerostomia)
  5. Decreased buffering capacity of saliva (e.g. through smoking)
    - Decreases pH clearance
  6. Hiatus hernia
  7. Defective mucosal protective mechanism (e.g. alcohol)
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16
Q

What do these aspects of GORD lead to?

A
  • reflux esophagitis
  • epithelial metaplasia
  • carcinoma
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17
Q

What is volume clearance?

A

rapid return of reflux volume by oesophageal peristalsis reflex

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18
Q

What is pH clearance?

A

residual gastric juice left behind – pH rises step by step with swallowed saliva buffers residual rfux volume

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19
Q

What is a sliding hiatus hernia?

A
  • Variable association with GORD
  • Most pts with severe stages of GORD have a hernia
  • But most GORD pts don’t have a hernia & many with a hernia don’t have GORD
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20
Q

What is another type of hernia?

A
  • Rolling/paraoesophageal hiatus hernia
  • gastrooesophagel junction in place
  • Emergency surgery
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21
Q

Why do you do OGD?

A

•To exclude cancer


•Oesophagitis, peptic structure & Barretts 
oesophagus confirm ∆

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22
Q

What images do you do in GORD?

A
  • OGD
  • Oesophageal manometry
  • 24hr oesophageal recording.
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23
Q

What medical treatment do you do for GORD?

A
  • Lifestyle changes (wt loss, smoking, EtOH)

* PPIs

24
Q

What surgical treatment do you do for GORD?

A

•Dilatation peptic strictures


•Laparoscopic Nissen’s fundoplication

25
Q

What are the functions of the stomach?

A
  • Breaks food into smaller particles (acid & pepsin) 

  • Holds food, releasing it in controlled steady rate into duodenum 

  • Kills parasites & certain bacteria
26
Q

What does the cardiac and pyloric region of the stomach secrete?

A

Mucus only

27
Q

What does the body and fundus region of the stomach. secrete?

A

Mucus, HCl, pepsinogen

28
Q

What does the antrum region of the stomach secrete?

A

Gastrin

29
Q

What invaginates into mucose?

A

tubular glands

30
Q

How much acid is produced. by the stomach?

A
  • 2L/day

* 150mM H+ (3 mill x that in blood)

31
Q

What is mucins?

A
  • Mucins = gel coating

* HCO3- trapped in mucus gel

32
Q

What is the pH at the epithelial surface of the stomach?

A

6-7

33
Q

What is the pH at the lumen of the stomach?

A

1-2

34
Q

What are the different types of gastritis?

A
  1. Erosive & haemorrhagic gastritis
  2. Nonerosive, chronic active gastritis
  3. Atrophic (fundal gland) gastritis
  4. Reactive gastritis
35
Q

What causes Erosive & haemorrhagic gastritis?

A

•Numerous causes: NASAIDs, trauma, sichaemia


•Acute ulcer – gastric bleeding & 
perforation

36
Q

Where is / what causes Nonerosive, chronic active gastritis?

A

• Antrum 

• Helicobacter pylori - Triple Rx
(amoxicillin, clarithromycin, pantoprazole) for 7-14/7

37
Q

What causes Atrophic (fundal gland) gastritis?

A

•Autoantibodies vs parts & products of parietal cells 

•Parietal cells atrophy

•↓acid & IF secretion

38
Q

What is the neural stimulation of gastric secretion?

A

ACh - postganglionic transmitter

of vagal parasympathetic fibres

39
Q

What is the endocrine stimulation of gastric secretion?

A

Gastrin (G cells of antrum)

40
Q

What is the paracrine stimulation of gastric secretion?

A

Histamine (ECL cells & mast

cells of gastric wall)

41
Q

What is the endocrine inhibition of gastric inhibition?

A

Secretin (small intestine)

42
Q

What is the paracrine inihitbition of gastric secretion?

A

Somatostatin (SIH)

43
Q

What is the paracrine and autocrine inhibition of gastric secretion?

A

PGs (E2 & I2), TGF-α & adenosine

44
Q

What are the mechanisms of repairing epithelial defects?

A
  1. migration
  2. gap closed by cell growth
  3. acute wound healing
45
Q

What is migration?

A

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

46
Q

How is the gap closed by cell growth?

A

Stimulated by

  1. EGF
  2. TGF-α
  3. IGF-1
  4. GRP
  5. gastrin
47
Q

How does acute wound healing take place?

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

  2. epithelial closure by restitution & cell division
48
Q

What is >80% of clinical outcomes of H. pylori?

A

asymptomatic or chronic gastritis

49
Q

What is <1% of clinical outcomes of H. pylori?

A
  • chronic atrophic gastritis
  • intestinal metaplasia
  • gastric or duodenal ulcer
50
Q

What is 15-20% of clinical outcomes of H. pylori?

A
  • Gastric cancer

- MALT lymphoma

51
Q

What are the primary medical treatments for ulcers?

A
  1. PPI or H2 blocker

2. Triple Rx (amxoicillin, clarithromycin, pantoprazole) for 7-14 days

52
Q

What are the elective surgical treatments for ulcers?

A
  1. Rare: most uncomplicated ulcers health within 12 weeks
  2. If dont, change medication and observe additional 12 weeks
  3. Check serum gastrin (antral G. cell hyperplasia of gastrinoma (zollinger-ellison syndrome)
  4. OGD: biopsy all 4 quadrants of ulcer (rule out malignant ulcer) if refractory
53
Q

What are the surgical indications for ulcer treatment?

A
  1. Intractability (after medical therapy)
  2. Haemorrhage
  3. Obstruction
  4. Perforation
  5. Relative: continuous requirement of steroid therapy / NSAIDs
54
Q

What are the methods of mucosal protection?

A
  1. Mucus film
  2. HCO3- secretion (changes in pH)
  3. Epithelial barrier (tight junctions) - can expel H+
  4. Mucosal blood perfusion
55
Q

What contributes to ulcer formation?

A
  1. H Pylori
  2. Increased secretion of gastric juice
  3. Decrease HCO3- secretion
  4. Decrease cell formation
  5. Decreased blood perfusion

Z YEAR 2 BRS GASTRO (15 decks)

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