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Phase 1b - Gastroenterology > Upper GI Tract > Flashcards

Upper GI Tract Flashcards

1
Q

What types of muscles make up the trachea?

A
  1. Skeletal muscle
  2. Skeletal muscle / Smooth muscle
  3. Smooth muscle
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2
Q

What are the two sphincters that are at the beginning and end of the trachea?

A
  • Upper oesophageal sphincter
  • Lower oesophageal sphincter
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3
Q

What are these 3 structures?

A
  • Red: Trachea
  • Green: Aorta
  • Purple: Diaphragm
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4
Q

Does the oesophagus extend within abdomen?

A
  • Extends 3-4 cm distal oesophagus within abdomen
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5
Q

What structures make up the phrenoesophageal ligament?

A
  • A seal where the esophagus passes from the thorax into the abdomen through the diaphragmatic hiatus

Formed by the right and left crus of the diaphragm

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6
Q

What is the angle formed between the oesophagus and the stomach (red-dotted line)?

A
  • Angle of His
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7
Q

What are the 4 stages of swallowing?

A
  • Stage 0: Oral phase
  • Stage 1: Pharyngeal phase
  • Stage 2: Upper oesophageal phase
  • Stage 3: Lower oesophageal phase
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8
Q

What happens during “Stage 0: Oral phase” of swallowing?

Stage of food and status of oesophageal sphincters

A
  • Chewing & saliva prepare bolus
  • Both oesophageal sphincters constricted
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9
Q

What happens during “Stage 1: Pharyngeal phase” of swallowing?

Stage of food and status of oesophageal sphincters

A
  • Pharyngeal musculature guides food bolus towards oesophagus
  • UOS opens reflexly
  • LOS opened by vasovagal reflex (receptive relaxation reflex)
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10
Q

What happens during “Stage 2: Upper oesophageal phase” of swallowing?

Status of oesophageal muscles and status of oesophageal sphincters

A
  • UOS closes
  • Superior circular muscle rings contract & inferior rings dilate
  • Sequential contractions of longitudinal muscle
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11
Q

What happens during “Stage 3: Lower oesophageal phase” of swallowing?

Status of oesophageal sphincters

A
  • LOS closes as food passes through
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12
Q

The LOS has a resting pressure ~ 20 mmHg and decreases to ↓< 5 mmHg during receptive relaxation. Which neurones facilitate this change?

A
  • Mediated by inhibitory noncholinergic nonadrenergic (NCNA) neurons of myenteric plexus
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13
Q

Define dysphagia.

A

Difficulty in swallowing

  • Localisation is important – cricopharyngeal sphincter or distal
    • Type of dysphagia
    • For solids or fluids
    • Intermittent or progressive
    • Precise or vague in appreciation
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14
Q

Define odynophagia.

A

Pain on swallowing

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15
Q

Define regurgitation.

A

Return of oesophageal contents from above an obstruction

May be functional or mechanical

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16
Q

Define reflux.

A

Passive return of gastroduodenal contents to the mouth

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17
Q

What are the causes of absence of a stricture?

A
  • Abnormal oesophageal contraction
    • Hypermotility
    • Hypomotility
    • Disordered coordination
  • Failure of protective mechanisms for reflux
    • GastroOesophageal Reflux Disease (GORD)
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18
Q

Outline the pathophysiology of achalasia (oesophageal hypermobility) (3 steps).

A
  1. Loss of ganglion cells in Aurebach’s myenteric plexus in LOS wall
  2. Decreased activity of inhibitory NCNA neurones
  3. Hypermobility
Proposed model of achalasia pathophysiology
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19
Q

What is the primary cause of achalasia (oesophageal hypermobility)?

A

Unkown

Proposed model of achalasia pathophysiology
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20
Q

What is the secondary cause of achalasia (oesophageal hypermobility) (5)?

A
  • Diseases causing oesophageal motor abnormalities similar to 1o achalasia
    • Chagas’ Disease
    • Protozoa infection
    • Amyloid
    • Sarcoma
    • Eosinophilic Oesophagitis
Proposed model of achalasia pathophysiology
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21
Q

What are the pathophysiological effects of acahalasia (oesophageal hypermobility)?

A
  • Increased resting pressure of LOS
  • Receptive relaxation sets in late & is too weak
    • During reflex phase pressure in LOS is markedly higher than stomach
  • Swallowed food collects in oesophagus causing increased pressure throughout with dilation of the oesophagus
  • Propagation of peristaltic waves ceas
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22
Q

What are the symptoms of achalasia (oesophageal hypermobility) (3)?

A
  • Weight loss
  • Trouble swallowing
  • Pain
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23
Q

Outline the disease course of achalasia (oesophageal hypermobility).

A
  • Has insidious onset - symptoms for years prior to seeking help
  • Without treatment → progressive oesophageal dilatation
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24
Q

What is the risk of oesophageal cancer following achalasia (oesophageal hypermobility)?

A
  • Increased 28-fold
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25
Q

What are the available treatments for achalasia (oesophageal hypermobility) (2)?

A
  • Pneumatic Dilatation (PD)
  • Surgery
    • Heller’s Myotomy
    • Dor fundoplication
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26
Q

Describe Pneumatic Dilatation (PD) for the treatment of achalasia (oesophageal hypermobility).

A
  • PD weakens LOS by circumferential stretching & in some cases, tearing of its muscle fibres
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27
Q

What is the efficacy of Pneumatic Dilatation (PD) for the treatment of achalasia (oesophageal hypermobility)?

A
  • 71 - 90% of patients respond initially but many patients subsequently relapse
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28
Q

Outline the surgery used to treat achalasia (oesophageal hypermobility).

A
  • Heller’s Myotomy - A continuous myotomy performed for 6 cm on the oesophagus & 3 cm onto the stomach
  • Dor fundoplication – anterior fundus folded over oesophagus and sutured to right side of myotomy
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29
Q

What are the risks of the surgery used to treat achalasia (oesophageal hypermobility)?

A
  • Oesophageal & gastric perforation (10 – 16%)
  • Splenic injury – 1 – 5%
  • Division of vagus nerve – rare
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30
Q

What is the cause of scleroderma (oesophageal hypomobility)?

A

Autoimmune disease

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31
Q

Outline the pathophysiology of scleroderma (oesophageal hypomobility) (3).

A
  1. Hypomotility in its early stages due to neuronal defects → atrophy of smooth muscle of oesophagus
  2. Peristalsis in the distal portion ultimately ceases altogether
  3. Decreased resting pressure of LOS
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32
Q

What are the pathophysiological effects of scleroderma (oesophageal hypomobility)?

A
  • Decreased resting pressure of LOS
  • → Gastroesophageal reflux disease develops

Often associated with CREST syndrome

33
Q

What is the treatment available for scleroderma (oesophageal hypomobility)?

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

  • Once peristaltic failure occurs → usually irreversible
34
Q

Outline the pathophysiology of corkscrew oesophagus (3).

A
  • Diffuse oesophageal spasm
  • Incoordinate contractions
    • Pressures of 400-500 mmHg
  • Marked hypertrophy of circular muscle
35
Q

How is corkscrew oesophagus diagnosed?

A

Barium swallowing

36
Q

What are the symptoms of corkscrew oesophagus (2)?

A
  • Dysphagia
  • Chest pain
37
Q

What treatment is available for corkscrew oesophagus?

A
  • May respond to forceful pneumatic dilation (PD) of cardia

Results not as predictable as achalasia

38
Q

What are the 3 areas of anatomical constriction of the oesophagus?

A
  • Cricopharyngeal constriction (larynx)
  • Aortic and bronchial constriction
  • Diaphragmatic and ‘sphincter’ constriction
39
Q

What are the causes of oesophageal perforation (6)?

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

  • Usually at OesophagoGastroDuodenoscopy (OGD)
    • More common in presence of diverticula or cancer
40
Q

Outline the pathophysiology of Boerhaave’s syndrome.

A
  • Sudden increase in intra-oesophageal pressure with negative intra thoracic pressure

Vomiting against a closed glottis

41
Q

How common is Boerhaave’s syndrome?

A

3.1 per 1,000,000

42
Q

What are common foreign bodies that cause oesophageal perforation (5)?

A
  • Disk batteries
    • Cause electrical burns if embeds in mucosa
  • Magnets
  • Sharp objects
  • Dishwasher tablets
  • Acid/Alkali
43
Q

What are the symptoms of oesophageal perforation caused by trauma (4)?

Neck = penetrating
Thorax = blunt force

A
  • Dysphagia
  • Blood in saliva
  • Haematemesis
  • Surgical empysema
44
Q

How does oesophageal perforation present (4)?

A
  • Pain 95 %
  • Fever 80 %
  • Dysphagia 70 %
  • Emphysema 35 %
45
Q

What investigations are recommended in suspected oesophageal perforation (4)?

A
  • CXR
  • CT
  • Swallow (gastrograffin)
  • OesophagoGastroDuodenoscopy (OGD)
46
Q

What is the primary managements of oesophageal perforation (6)?

A
  • NBM
  • IV fluids
  • Broad spectrum ABx & Antifungals
  • ITU/HDU level care
  • Bloods (including G&S)
  • Tertiary referral centre
    • Surgical emergency - Oesophagectomy

2x ↑mortality if 24h delay in diagnosis

47
Q

What are the protective mechanisms against reflux?

A
  • Increased LOS pressure
  • Angle of His
  • Volume clearance - oesophageal peristalsis reflex
  • pH clearance - saliva
  • Epithelium - barrier properties
48
Q

What does the failure of the protective mechanisms against reflux lead to?

A

Gastro-oesophageal reflux disease (GORD)

49
Q

What is the diagnosis?

A

Sliding Hiatus Hernia

50
Q

What is the diagnosis?

A

Rolling / Paraoesophageal Hiatus Hernia

51
Q

What investigations are recommended in suspected gastro-oesophageal reflux disease (GORD) (3)?

A
  • OesophagoGastroDuodenoscopy (OGD)
    • To exclude: Cancer
    • To confirm: Oesophagitis / Peptic stricture / Barretts oesophagus
  • Oesophageal manometry
  • 24-hr oesophageal pH recording
52
Q

What treatments are available for gastro-oesophageal reflux disease (GORD) (2M / 2S)?

A
  • Medical
    • Lifestyle changes (wt loss, smoking, EtOH)
    • PPIs
  • Surgical
    • Dilatation peptic strictures
    • Laparoscopic Nissen’s fundoplication
53
Q

What are the functions of the stomach (3)?

A
  • Breaks food into smaller particles (acid & pepsin)
  • Holds food, releasing it in controlled steady rate into duodenum
  • Kills parasites & certain bacteria
54
Q

What is found in the cardia & pyloric region of the stomach to assist with its functions (1)?

A

Mucus

55
Q

What is found in the body & fundus of the stomach to assist with its functions (3)?

A
  • Mucus
  • HCl
  • Pepsinogen
56
Q

What is found in the antrum of the stomach to assist with its functions (1)?

A

Gastrin

57
Q

What are the 4 main forms of gastritis?

A
  • Erosive & haemorrhagic gastritis
  • Nonerosive, chronic active gastritis
  • Atrophic (fundal gland) gastritis
  • Reactive gastritis
58
Q

What is the main cause (numerous causes) of erosive & haemorrhagic gastritis?

A
  • Acute ulcer - gastric bleeding & perforation
59
Q

What is the main cause of nonerosive, chronic active gastritis?

A
  • Helicobacter pylori infection in the antrum of the stomach
60
Q

What is the main cause of atrophic (fundal gland) gastritis?

A
  • Autoantibodies vs parts & products of parietal cells in the fundus of the stomach

  • Parietal cells atrophy
  • ↓acid & IF secretion
61
Q

What are the 3 forms of stimulations of gastric secretions?

A
  • Neural
  • Endocrine
  • Paracrine
62
Q

Describe the neural stimulation of gastric secretion.

A
  • ACh from postganglionic transmitter of vagal parasympathetic fibres
63
Q

Describe the endocrine stimulation of gastric secretion.

A
  • Gastrin from G cells of antrum
64
Q

Describe the paracrine stimulation of gastric secretion.

A
  • Histamine from ECL cells & mast cells of gastric wall
65
Q

What are the 3 forms of inhibition of gastric secretions?

A
  • Endocrine
  • Paracrine
  • Paracrine & Autocrine
66
Q

Describe the endocrine inhibition of gastric secretion.

A
  • Secretin from the small intestine
67
Q

Describe the paracrine inhibition of gastric secretion.

A

Somatostatin

68
Q

Describe the paracrine & autocrine inhibition of gastric secretion (4).

A
  • PGE2
  • PGI2
  • TGF-α
  • Adenosine
69
Q

How does the stomach protect itself from its acid (4)?

A
  • Mucus film
  • HCO3- secretion
  • Epithelial barrier
  • Mucosal blood perfusion
70
Q

What mechanisms repairing epithelial defects are in place in the stomach (3)?

A
  • Migration
  • Gap closed by cell growth
  • Acute wound healing
71
Q

How is ‘migration’ used as a repairing mechanism in the epithelial defects in the stomach?

A
  • Adjacent epithelial cells flatten to close gap via sideward migration along Basal membrane
72
Q

What factors stimulate the cell growth that closes the gap in epithelial defects in the stomach (5)?

A
  • EGF
  • TGF-α
  • IGF-1
  • GRP
  • Gastrin
73
Q

How is ‘acute wound healing’ used as a repairing mechanism in the epithelial defects in the stomach (6 steps)?

A
  1. Basal membrane (BM) destroyed
  2. Attraction of leukocytes & macrophages
  3. Phagocytosis of necrotic cells
  4. Angiogenesis
  5. Regeneration of ECM after repair of BM
  6. Epithelial closure by restitution & cell division
74
Q

What happens when repairing mechanism in the epithelial defects fail?

A

Ulcers form

75
Q

What are the possible outcomes of a Helicobacter pylori infection?

A
76
Q

Outline the pathophysiology of a Helicobacter pylori infection leading to an ulcer (5 steps).

A
77
Q

What is the primary treatment of an ulcer (2)?

A

Primarily medical
* PPI or H2 blocker
* Triple Rx (amoxicillin, clarithromycin, pantoprazole) for 7-14 days

78
Q

What are the surgical indications for the treatment of an ulcer (3)?

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

Phase 1b - Gastroenterology (13 decks)

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