Gastro - Upper GI tract Flashcards

1
Q

What are the 4 stages of swallowing and describe what happens at each stage?

A

Stage 0 - oral phase:

- Chewing and saliva prepare bolus
- Both oesophageal sphincters are constricted

Stage 1 - Pharyngeal phase:

- Pharyngeal musculature guids food bolus towards oesophagus 
- Upper oesophageal sphincter opens
- LOS opened by vasovagal reflex

Stage 2 - Upper oesophageal phase:

- Upper sphincter closes
- Superior circular muscle rings contract & inferior rings dilate

Stage 3 - Lower oesophageal phase:
- Lower sphincter closes as bolus passes through

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2
Q

What is the effect of a functional disorder of the oesophagus?

A

Absence of a stricture - dysphagia

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3
Q

What are the causes of functional disorders of the oesophagus?

A

Abnormal oesophageal contraction:
- Hypermotility
- Hypomotility
- Disordered coordination
Failure of protective mechanisms for reflux:
- GastroOesophageal reflux disease (GORD)

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4
Q

What is dysphagia?

A

Difficulty swallowing

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5
Q

What is odynophagia?

A

Pain on swallowing

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6
Q

What is regurgitation?

A

Return of oesophageal contents from above an obstruction

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7
Q

What is reflux?

A

Passive return of gastroduodenal contents to mouth

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8
Q

Describe the mechanism of achalasia?

A
  • Loss of ganglion cells in Aurebach’s myenteric plexus in LOS wall
  • This leads to reduced activity of inhibitory NCNA neurones
  • This means the LOS cannot relax/dilate
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9
Q

Describe pneumatic dilatation

A
  • A pneumatic dilator is placed in the oesophagus
  • A balloon is then placed in the LOS and is inflated
  • Once complete inflation has occurred, everything is removed and flow is restored in the oesophagus
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10
Q

What is a Heller’s myotomy?

A

A surgical procedure:
cut the muscle 6cm on the oesophagus and 3cm onto the stomach to remove the stricture then wrap the fundus of the stomach around the exposed mucosa

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11
Q

What is a peroral endoscopic myotomy?

A
  • A muscosal incision in made on the inisde of the oesophagus
  • The creation of a submucosal tunnel occurrs
  • Then a myotomy occurs, where as much muscle required, is removed
  • Then the mucosal incision is closed up endoscopically
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12
Q

How does hypomotility occurr?

A

Neuronal defects result in muscle atrophy of oesophagus, therefore no peristalsis in smooth muscle and hence hypomotility - sphincter pressure is too low

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13
Q

Describe disordered coordination of the oesophagus

A
  • Incooardinate contractions of the ring muscles in the oesophagus results in corkscrew oesophagus
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14
Q

What vascular anomalies can cause dysphagia and why?

A

Dysphagia Lusoria:

  • Abberant right subclavian artery wraps around behind the oesophagus
  • This applies pressure on it and makes it hard to swallow

Double aortic arch:
- The presence of a left and right arch that form a loop around the oesophagus can result in pressure making it difficult to swallow

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15
Q

What is the primary management for oesophageal perforations?

A

Initial:

  • NBM
  • IV fluids
  • Broad sprectrum antibiotics and antifungals
  • ITU/HDU level care
  • Bloods

Surgical emergency

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16
Q

What is an oesophagectomy ?

A

When the main oesophagus is removed and the stomach is stretched and attached to the first viable part of the oesophagus

17
Q

Describe a sliding hiatus hernia

A

Part of the stomach pushes through the diaphragm

18
Q

State and describe the different types of gastritis

A
  • Erosive and haemorrhagic gastritits:
    • Acute ulcer - gastric bleeding and perforation
  • Nonerosive, chronic active gastritis:
    • Antrum
    • Infection from helicobacter pylori
  • Atrophic (fundal gland) gastritis:
    • Fundus
    • Autoantibodies destroy parts of pairetal cells and products of them, causing parietal cell atrophy
    • This results in lower acid levels which can result in G cell hyperplasia and potentially cancer
  • Reactive gastritis
19
Q

How is gastric secretion regulated?

A

Stimulation:

- Neural:
    - ACh: postganglionic transmitter of vagal parasympathetic fibres
- Endocrine:
    - Gastrin (G cells of antrum)
- Paracrine:
    - Histamine (ECL cells and mast cells of gastric wall)

Inhibition:

- Endocrine:
    - Secretin (small intestine)
- Paracrine:
    - Somatostatin (SIH)
- Paracrine & autocrine:
    - PGs (E2 & I2), TGF-alpha & adenosine
20
Q

How is mucosal protection acheived?

A
  1. Mucus film :
    • Produced by epithelium
    • Protective barier
  2. Bicarbonate secretion:
    • Produced by prostaglandins
    • Maintain pH
  3. Epithelial barrier:
    • Apical layer is strong
    • Can expel H+ ions
  4. Mucosal blood perfusion:
    • Good blood supply
    • Can easily remove H+ ions
21
Q

What can occur during epithelial repair and wound healing?

A

Rapid restitution through migration:
- The endothelial cells can flatten and spread across the area of damage/exposure

Can cover defect through cell division

If basement membrane is destroyed:
- Acute wound healing required through normal healing cascade of white cells

22
Q

How does H. Pylori affect the stomach?

A

The bacteria produced urease which converts urea and H20 into CO2 and NH3 which neutralises gastric acid

23
Q

What are the treatments for ulcers?

A

PPI’s (Proton pump inhibitors)
H2 blockers

Surgery in extreme cases