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BRS Flashcards (Y2) > Upper GI Tract > Flashcards

Upper GI Tract Flashcards

1
Q

How long is the oesophagus?

A

Approx. 27 cm

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2
Q

At what level does the oesophagus enter the abdominal region?

A

T10

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3
Q

What are the anatomical contributions to the lower oesophageal sphincter?

A

3-4 cm distal oesophagus within abdomen
Diaphragm surrounds LOS (Lt & Rt crux)
An intact phrenoesophageal ligament
Angle of His - angle at which oesophagus enters stomach

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4
Q

Describe the phases of swallowing

A

Stage 0: Oral phase
- Chewing & saliva prepare bolus
- Both oesophageal sphincters constricted
Stage 1: Pharyngeal phase
- Pharyngeal musculature guides food bolus towards oesophagus
- Upper oesophageal sphincter opens reflexly
- LOS opened by vasovagal reflex (receptive relaxation reflex)
Stage 2: Upper oesophageal phase
- Upper sphincter closes
- Superior circular muscle rings contract & inferior rings dilate
- Sequential contractions of longitudinal muscle
Stage 3: Lower oesophageal phase
- Lower sphincter closes as food passes through

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5
Q

How do you assess oesophageal motility?

A

Manometry - motility is determined by pressure measurements

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6
Q

What is the approximate pressure of peristaltic waves?

A

40 mmHg

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7
Q

What is the resting pressure of the LOS and what is it mediated by?

A

20mmHg
Drops <5mmHg during receptive relaxation
Mediated by inhibitory noncholinergic nonadrenergic neurons (NCNA) of myenteric plexus

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8
Q

What is dysphagia?

A

Difficulty when swallowing

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9
Q

What is important to consider when taking a history of dysphagia?

A

Localisation - cricopharyngeal sphincter or distal
Types of dysphagia:
- Solids or fluids
- Intermittent or progressive (red flag for OC)
- Precise or vague in appreciation

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10
Q

What is odynophagia?

A

Pain on swallowing

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11
Q

What is regurgitation?

A

Return of oesophageal contents from above an obstruction
May be functional or mechanical

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12
Q

What is reflux?

A

Passive return of gastroduodenal contents to the mouth

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13
Q

What is achalasia?

A

A condition characterised by the failure of the LOS to relax plus some abnormality in oesophageal peristalsis

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14
Q

What is the primary cause of achalasia?

A

Unknown

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15
Q

What is the pathophysiology of achalasia?

A

Loss of ganglion cells in Auerbach’s myenteric plexus in LOS wall
Leads to decreased activity of inhibitory NCNA neurons

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16
Q

What are the secondary causes of achalasia?

A

Chagas’ Disease - caused by parasites
Protozoa infections
Amyloid/sarcoma/eosinophilia
Oesophagitis
Diseases cause oesophageal motor abnormalities similar to primary achalasia

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17
Q

When a person with achalasia undertakes a barium swallow, how does the oesophagus appear?

A

Bird’s beak appearance - tapering of distal oesophagus and dilated oesophagus proximal to this

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18
Q

Must a person have a bird beak appearance of their oesophagus in order to be diagnosed with achalasia?

A

No, shouldn’t be used as a diagnostic tool, instead perform manometry
Person can have achalasia with a normal barium swallow
Bird beak appearance is a later stage sign

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19
Q

What is achalasia a risk factor of?

A

squamous oesophageal cancer

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20
Q

What happens when a person with achalasia eats?

A

Increased resting pressure of LOS
During reflex phase, pressure in LOS is much greater than in stomach as receptive relaxation sets in too late (and is too weak)
Swallowed food collects in oesophagus - increases pressure and causes dilation
Propagation of peristaltic waves cease
N.B. three types of achalasia - absence of peristaltic waves is one type

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21
Q

Describe the disease course of achalasia

A

Insidious onset - symptoms can persist for years before seeking help
Without treatment -> progressive oesophageal dilation
Increases oesophageal cancer risk 28x

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22
Q

What is a risk of food build-up in oesophagus?

A

Bacterial overgrowth - people may report a bad smell

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23
Q

is there a cure for achalasia?

A

No, all treatments are palliative and designed to relieve symptoms

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24
Q

How does pneumatic dilatation work?

A

Treatment for achalasia
Weakens LOS by circumferential stretching and in some cases tearing of muscle fibres
Patients receive it every few months
Majority of patients respond initially and then later relapse

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25
Q

What is a risk of pneumatic dilatation?

A

Perforation of oesophagus

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26
Q

What is Heller’s Myotomy and what procedure is often carried out in addition to prevent acid reflux?

A

Continuous myotomy (division of muscle) performed for 6cm of oesophagus and 3cm of stomach
Dor fundoplication is carried out alongside to prevent reflux -> anterior fundus is folded over oesophagus and sutured to the right side of myotomy

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27
Q

What are the risks of Heller’s Myotomy?

A

Oesophageal and gastric perforation
Division of vagus nerve - rare
Splenic injury

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28
Q

What is Scleroderma?

A

Autoimmune disease
Smooth muscle atrophy
Hypomotility in early stages due to neuronal defects
Peristalsis in distal oesophagus ultimately ceases
Decreased resting pressure of LOS
Development of GORD

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29
Q

What condition is Scleroderma often associated with?

A

CREST syndrome

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30
Q

How is Scleroderma treated?

A

Improve force of peristalsis with prokinetics
Exclude organic obstruction
Usually irreversible post peristaltic failure

31
Q

What is diffuse oesophageal spasm?

A

Corkscrew oesophagus on barium swallow
Incoordinate contractions causing dysphagia and chest pain
Marked hypertrophy of circular muscle
Pressures of 400-500mmHg

32
Q

What is a potential treatment of diffuse oesophageal spasm?

A

May respond to forceful pneumatic dilatation
Results not as predictable as achalasia

33
Q

What is the anatomy of oesophageal perforations?

A

Three areas of anatomical constriction:
- cricopharyngeal constriction
- aortic and bronchial constriction
- diaphragmatic and ‘sphincter constriction’

34
Q

What are the causes of oesophageal perforation?

A

Iatrogenic (OGD - endoscopy)
Spontaneous (Boerhaave’s)
Foreign body
Trauma
Intraoperative
Malignant

35
Q

What two muscle form the UOS?

A

Thyropharyngeus (inferior constrictor) and cricopharyngeus muscle

36
Q

What is the term for the weak spot between the muscles of the UOS and what is the clinical significance?

A

Killian’s dehiscence - can also develop a condition called pharyngeal pouch
During OGD, camera can get into ones of these pouches and cause a perforation (usually microscopic)
Can lead to subcutaneous emphysema- air released into layers of neck and chest

37
Q

What are the iatrogenic causes of oesophageal perforation?

A

Usually OGD - common in presence of diverticula or cancer
Stricture dilatation
Sclerotherapy
Achalasia dilatation

38
Q

What is Boerhaave’s oesophageal perforation?

A

Sudden rise in intra-oesophageal pressure with negative intra thoracic pressure
Vomiting against a closed glottis - e.g. due to excess alcohol intake
Perforation in left posterolateral aspect of distal oesophagus

39
Q

List examples of foreign bodies that cause perforation

A

Disk batteries - cause electrical burns if embedded in mucosa
Magnets
Sharp objects
Dishwasher tablets
Acid/alkali

40
Q

What types of trauma can cause oesophageal perforation?

A

Neck - penetrating, e.g. stabbing
Thorax - blunt force - tends to be more dangerous as oesophageal content may leak into mediastinum

Can be difficult to diagnose:
Dysphagia
Blood in saliva
Haematemesis
Surgical (subcutaneous) emphysema

41
Q

How does oesophageal perforation typically present?

A

Pain
Fever
Dysphagia
Emphysema - pneumomediastinum -> borders of mediastinum visible because of air

42
Q

What are the investigations for oesophageal perforation?

A

CXR
CT
Swallow (gastrograffin)
OGD - gold standard but not usually done because of fear of worsening perforation

43
Q

What does this image show?

A

Contrast scan
Air is black
White is contrast - leaking out of oesophagus

44
Q

What is the initial management of oesophageal perforation?

A

Nil-by-mouth
IV fluids
Broad spectrum antibiotics & antifungals (necessary - lots of fungi in oesophagus)
ITU/HDU level care
Bloods (including G&S)
Tertiary referral centre

45
Q

What is the definitive management of oesophageal perforation?

A

Conservative management with covered metal stent (chest drain -> stent -> ITU -> recovery)
Operative - Primary repair (sown up) or oesophagectomy

46
Q

What can cause sporadic reflux?

A

Normal
Pressure on full stomach
Swallowing
Transient sphincter opening

47
Q

What three mechanisms protect the oesophagus from reflux?

A

Volume clearance - oesophageal peristalsis reflex
pH clearance - saliva
Epithelium barrier properties

48
Q

How may protective mechanisms against reflux fail?

A

Sphincter pressure decreases, e.g. due to medication
Abnormal peristalsis
Decreased saliva production
Transient sphincter opening (air, CO2)
Buffering capacity of saliva decreases (e.g. through smoking)
Hiatus hernia
Defective mucosal protective mechanism (due to alcohol consumption)

49
Q

What is chronic acid reflux a risk factor for?

A

Oesophageal adenocarcinoma

50
Q

What is a hernia?

A

A hernia is a protrusion of a viscus (organ) because of a defect in the walls of its containing cavity into an abnormal position

51
Q

What does this image show?

A

Sliding hiatus hernia
Loss of LOS

52
Q

What does this image show?

A

Rolling hiatus hernia
Implication for surgery - can strangulate

53
Q

What do these images show?

A

Sliding hiatus hernia

54
Q

What does this image show?

A

Rolling hiatus hernia

55
Q

What are the investigations for GORD (done in secondary care)?

A

OGD - exclude cancer, can confirm oesophagitis, peptic stricture, Barrett’s oesophagus
Oesophageal manometry
24-hr oesophageal pH recording

56
Q

What are the medical and surgical interventions for GORD?

A

Medical:
Lifestyle changes (weight loss, smoking, alcohol)
PPIs
Surgical:
Dilatation peptic strictures
Laparoscopic Nissen’s fundoplication

57
Q

What are the functions of the stomach?

A

Breaks food into smaller particles (acid & pepsin)
Holds food - releases it in a controlled steady rate into duodenum
Kills parasites and certain bacteria

58
Q

What substances are produced in the cardia & pyloric region?

A

Mucus only

59
Q

What substances are produced in the body & fundus of the stomach?

A

Mucus, HCl and pepsinogen

60
Q

Where is gastric produced?

A

In the antrum of the stomach

61
Q

Label this image

A
62
Q

What are the different types and causes of gastritis?

A
63
Q

What are the neural, endocrine and paracrine stimulants of acid secretion?

A

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

64
Q

What are the autocrine, endocrine and paracrine inhibitors of acid secretion?

A

Endocrine - secretin from small intestine
Paracrine - somatostatin
Paracrine and autocrine - PGs, TGF-alpha, adenosine

65
Q

What factors contribute to mucosal protection from ulcers?

A

Mucus film
HCO3- secretion stimulated by prostaglandins
Epithelial barrier
Mucosal blood perfusion

66
Q

What are the different mechanisms for repairing epithelial defects (ulcers)?

A

Migration:
- Adjacent cell flattens - closes gap via sideward migration along BM
Gap closed by cell growth:
- Stimulated by EGF, TGF-alpha, IGF-1, GRP and gastrin
Acute wound healing:
- BM destroyed - immune cell infiltration, phagocytosis of necrotic cells, angiogenesis and regeneration of ECM after BM repair
- Epithelial closure by restitution and cell division

67
Q

What is the biggest causes of ulcer formation and what are the steps?

A

H.Pylori
Increase gastric acid secretion
Decrease carbonate ion secretion
Decreases cell formation
Decreases blood perfusion

68
Q

Label the images

A
69
Q

What does a CLO test test for?

A

H.Pylori
Campylobacter-like organism

70
Q

What are the primary medical treatments for ulcers?

A

CLO negative: PPI or H2 blocker
CLO positive: Triple Rx - amoxicillin, clarithromycin, pantoprazole - 7-14 days

71
Q

What is Zollinger-Ellison Syndrome?

A

Gastrinoma - tumour producing high levels of gastrin
Multiple ulcers throughout stomach and duodenum

72
Q

What are the elective surgical investigations for ulcers?

A

Rare - most ulcers heal within 12 weeks
If not, change medication and observe for additional 12 weeks
Check serum gastrin (gastrinoma - Zollinger-Ellison Syndrome)
OGD - biopsy all four quadrants of ulcer to rule out malignancy

73
Q

What are the surgical indications for ulcers?

A

Intractability after medical therapy (not responsive)
Continuous requirement of steroid/NSAID therapy
Complications e.g. haemorrhage, obstruction and perforation

BRS Flashcards (Y2) (79 decks)

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