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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
What are the available treatments for achalasia (oesophageal hypermobility) (2)?
* **Pneumatic Dilatation (PD)** * **Surgery** * Heller’s Myotomy * Dor fundoplication
26
Describe Pneumatic Dilatation (PD) for the treatment of achalasia (oesophageal hypermobility).
* PD **weakens LOS by circumferential stretching** & in some cases, tearing of its muscle fibres
27
What is the efficacy of Pneumatic Dilatation (PD) for the treatment of achalasia (oesophageal hypermobility)?
* **71 - 90% of patients respond initially** but many patients subsequently relapse
28
Outline the surgery used to treat achalasia (oesophageal hypermobility).
* **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
29
What are the risks of the surgery used to treat achalasia (oesophageal hypermobility)?
* **Oesophageal & gastric perforation** (10 – 16%) * **Splenic injury** – 1 – 5% * **Division of vagus nerve** – rare
30
What is the cause of scleroderma (oesophageal hypomobility)?
Autoimmune disease
31
Outline the pathophysiology of scleroderma (oesophageal hypomobility) (3).
1. Hypomotility in its early stages due to **neuronal defects** → **atrophy of smooth muscle of oesophagus** 1. **Peristalsis** in the distal portion ultimately **ceases** altogether 1. **Decreased resting pressure of LOS**
32
What are the pathophysiological effects of scleroderma (oesophageal hypomobility)?
* Decreased resting pressure of LOS * → **Gastroesophageal reflux disease develops** ## Footnote Often associated with CREST syndrome
33
What is the treatment available for scleroderma (oesophageal hypomobility)?
* **Exclude organic obstruction** * Improve force of peristalsis with **prokinetics (cisapride)** ## Footnote * Once peristaltic failure occurs → usually irreversible
34
Outline the pathophysiology of corkscrew oesophagus (3).
* Diffuse oesophageal **spasm** * **Incoordinate contractions** * Pressures of 400-500 mmHg * Marked **hypertrophy of circular muscle**
35
How is corkscrew oesophagus diagnosed?
Barium swallowing
36
What are the symptoms of corkscrew oesophagus (2)?
* Dysphagia * Chest pain
37
What treatment is available for corkscrew oesophagus?
* May respond to forceful pneumatic dilation (PD) of cardia ## Footnote Results not as predictable as achalasia
38
What are the 3 areas of anatomical constriction of the oesophagus?
* Cricopharyngeal constriction (larynx) * Aortic and bronchial constriction * Diaphragmatic and 'sphincter' constriction
39
What are the causes of oesophageal perforation (6)?
* Iatrogenic (OGD) >50% * Spontaneous (Boerhaave’s) - 15% * Foreign body - 12% * Trauma - 9% * Intraoperative - 2% * Malignant - 1% ## Footnote * Usually at OesophagoGastroDuodenoscopy (OGD) * More common in presence of diverticula or cancer
40
Outline the pathophysiology of Boerhaave’s syndrome.
* **Sudden increase in intra-oesophageal pressure** with **negative intra thoracic pressure** ## Footnote Vomiting against a closed glottis
41
How common is Boerhaave’s syndrome?
3.1 per 1,000,000
42
What are common foreign bodies that cause oesophageal perforation (5)?
* **Disk batteries** * Cause electrical burns if embeds in mucosa * **Magnets** * **Sharp objects** * **Dishwasher tablets** * **Acid/Alkali**
43
What are the symptoms of oesophageal perforation caused by trauma (4)? ## Footnote Neck = penetrating Thorax = blunt force
* Dysphagia * Blood in saliva * Haematemesis * Surgical empysema
44
How does oesophageal perforation present (4)?
* Pain 95 % * Fever 80 % * Dysphagia 70 % * Emphysema 35 %
45
What investigations are recommended in suspected oesophageal perforation (4)?
* **CXR** * **CT** * Swallow (**gastrograffin**) * OesophagoGastroDuodenoscopy (**OGD**)
46
What is the primary managements of oesophageal perforation (6)?
* **NBM** * **IV fluids** * Broad spectrum **ABx** & **Antifungals** * **ITU**/HDU level care * **Bloods** (including G&S) * Tertiary referral centre * **Surgical emergency** - Oesophagectomy ## Footnote 2x ↑mortality if 24h delay in diagnosis
47
What are the protective mechanisms against reflux?
* **Increased LOS pressure** * **Angle of His** * **Volume clearance** - oesophageal peristalsis reflex * **pH clearance** - saliva * **Epithelium** - barrier properties
48
What does the failure of the protective mechanisms against reflux lead to?
Gastro-oesophageal reflux disease (GORD)
49
What is the diagnosis?
Sliding Hiatus Hernia
50
What is the diagnosis?
Rolling / Paraoesophageal Hiatus Hernia
51
What investigations are recommended in suspected gastro-oesophageal reflux disease (GORD) (3)?
* **OesophagoGastroDuodenoscopy (OGD)** * To exclude: Cancer * To confirm: Oesophagitis / Peptic stricture / Barretts oesophagus * **Oesophageal manometry** * **24-hr oesophageal pH recording**
52
What treatments are available for gastro-oesophageal reflux disease (GORD) (2M / 2S)?
* Medical * **Lifestyle changes** (wt loss, smoking, EtOH) * **PPIs** * Surgical * **Dilatation peptic strictures** * **Laparoscopic Nissen’s fundoplication**
53
What are the functions of the stomach (3)?
* **Breaks food into smaller particles** (acid & pepsin) * **Holds food, releasing it in controlled steady rate** into duodenum * **Kills parasites & certain bacteria**
54
What is found in the cardia & pyloric region of the stomach to assist with its functions (1)?
Mucus
55
What is found in the body & fundus of the stomach to assist with its functions (3)?
* Mucus * HCl * Pepsinogen
56
What is found in the antrum of the stomach to assist with its functions (1)?
Gastrin
57
What are the 4 main forms of gastritis?
* Erosive & haemorrhagic gastritis * Nonerosive, chronic active gastritis * Atrophic (fundal gland) gastritis * Reactive gastritis
58
What is the main cause (numerous causes) of erosive & haemorrhagic gastritis?
* **Acute ulcer** - gastric bleeding & perforation
59
What is the main cause of nonerosive, chronic active gastritis?
* **Helicobacter pylori** infection in the **antrum** of the stomach
60
What is the main cause of atrophic (fundal gland) gastritis?
* **Autoantibodies** vs parts & products of parietal cells in the **fundus** of the stomach ## Footnote * Parietal cells atrophy * ↓acid & IF secretion
61
What are the 3 forms of stimulations of gastric secretions?
* Neural * Endocrine * Paracrine
62
Describe the neural stimulation of gastric secretion.
* **ACh** from **postganglionic transmitter** of **vagal parasympathetic fibres**
63
Describe the endocrine stimulation of gastric secretion.
* **Gastrin** from **G cells** of **antrum**
64
Describe the paracrine stimulation of gastric secretion.
* **Histamine** from **ECL cells** & **mast cells** of **gastric wall**
65
What are the 3 forms of inhibition of gastric secretions?
* Endocrine * Paracrine * Paracrine & Autocrine
66
Describe the endocrine inhibition of gastric secretion.
* **Secretin** from the **small intestine**
67
Describe the paracrine inhibition of gastric secretion.
**Somatostatin**
68
Describe the paracrine & autocrine inhibition of gastric secretion (4).
* PGE2 * PGI2 * TGF-α * Adenosine
69
How does the stomach protect itself from its acid (4)?
* Mucus film * HCO3- secretion * Epithelial barrier * Mucosal blood perfusion
70
What mechanisms repairing epithelial defects are in place in the stomach (3)?
* Migration * Gap closed by cell growth * Acute wound healing
71
How is 'migration' used as a repairing mechanism in the epithelial defects in the stomach?
* **Adjacent epithelial cells flatten** to close gap via sideward migration along Basal membrane
72
What factors stimulate the cell growth that closes the gap in epithelial defects in the stomach (5)?
* EGF * TGF-α * IGF-1 * GRP * Gastrin
73
How is 'acute wound healing' used as a repairing mechanism in the epithelial defects in the stomach (6 steps)?
1. Basal membrane **(BM) destroyed** 1. Attraction of **leukocytes** & **macrophages** 1. **Phagocytosis of necrotic cells** 1. **Angiogenesis** 1. **Regeneration of ECM** after repair of BM 1. **Epithelial closure by restitution** & cell division
74
What happens when repairing mechanism in the epithelial defects fail?
Ulcers form
75
What are the possible outcomes of a Helicobacter pylori infection?
76
Outline the pathophysiology of a Helicobacter pylori infection leading to an ulcer (5 steps).
77
What is the primary treatment of an ulcer (2)?
Primarily medical * **PPI** or **H2 blocker** * **Triple Rx** (amoxicillin, clarithromycin, pantoprazole) for 7-14 days
78
What are the surgical indications for the treatment of an ulcer (3)?
* **Intractability** (after medical therapy) * Relative: **continuous requirement of steroid therapy/NSAIDs** * **Complications:** * Haemorrhage * Obstruction * Perforation

Phase 1b - Gastroenterology (13 decks)

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