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BRS Y2 > Upper GI Tract > Flashcards

Upper GI Tract Flashcards

1
Q

What vertebral level does the oesophagus start and end at?

A

Starts at C5 ends at T10

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2
Q

What are some anatomical advantages the LOS has

A

Distal 3-4cm is in the abdomen
Diaphragm surrounds it
Angle of His allows expansion after a heavy meal

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3
Q

What are the 4 phases of swallowing? Describe them briefly

A

Oral phase: chewing and saliva prepare bolus, both sphincters are constricted
Pharyngeal phase: musculature guides bolus to oesophagus, upper sphincter opens reflexly, LOS opened by vasovagal reflex (receptive relaxation reflex)
Upper oesophageal phase: upper sphincter closes, superior muscle rings contract, inferior rings dilate
Lower oesophageal phase: LOS closes as food passes through

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4
Q

What reflex opens the LOS? What is its name?

A

The vasovagal reflex aka receptive relaxation reflex

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5
Q

How is the motility of the oesophagus measures?

A

Manometry

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6
Q

What is the pressure of normal peristaltic waves?

A

40 mmHg

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7
Q

What is the resting pressure of the LOS?

A

20 mmHg

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8
Q

What is the pressure of the LOS when it relaxes?

A

5 mmHg

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9
Q

What mediates the relaxation of the LOS?

A

Inhibitory noncholinergic noradrenergic neurons of the myenteric plexus

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10
Q

Define dysphagia?

A

Difficulty swallowing

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11
Q

How do we describe dysphagia?

A

Is it during solid or fluid intake
Is it intermittent or progressive
Is it precise or vague

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12
Q

What are the 2 localisations for dysphagia?

A

Cricopharyngeal sphincter

Distal

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13
Q

Define odynphagia

A

Pain on swallowing

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14
Q

Define regurgitation and what are the 2 types

A

Return of oesophageal contents from above an obstruction

Can be functional or mechanical

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15
Q

Define reflux

A

Passive return of gastroduodenal contents to the mouth

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16
Q

What is the other name for hypermotility in the oesophagus?

A

Achalasia

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17
Q

Why does achalasia arise?

A

Due to loss of ganglion cells in Aurebach’s myenteric plexus in LOS wall leading to reduced activity of inhibitory NCNA neurones

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18
Q

What are secondary causes of achalasia?

A

Diseases causing oesophageal motor abnormalities eg
Chagas’ Disease
Protozoa infection
Amyloid/Sarcoma/Eosinophilic Oesophagitis

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19
Q

Describe what happens in achalasia?

A

Theres increased resting pressure of the LOS
Receptive relaxation is too weak
In reflex LOS pressure is higher then in the stomach
Swallowed food collects in the oesophagus and there is increased pressure and dilation
Peristaltic waves decrease

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20
Q

What type of onset does achalasia have?

A

Insidious

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21
Q

What happens if achalasia isnt treated?

A

Progressive oesophageal dilation

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22
Q

What does achalasia increase risk of?

A

Oesophageal cancer

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23
Q

What is the main non surgical treatment for achalasia?

A

Pneumatic dilation. it weakens LOS by circumferential stretching & in some cases, tearing of its muscle fibres

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24
Q

What are the surgical treatments for achalasia?

A

Heller’s myotomy= myotomy for 6 cm of oesophagus and 3cm of stomach
Dor fundoplication= the anterior fundus is folded over the oesophagus and sutured to the right side of the myotomy

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25
Q

What type of disease is sclerodoma?

A

Autoimmune

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26
Q

Why does hypomotility arise and what does it lead to?

A

Its due to neuronal defects and leads to atrophy of smooth muscle

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27
Q

What condition develops if there is hypomotility?

A

GORD

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28
Q

How is hypomotility treated?

A

Exclude organic obstruction
Improve force of peristalsis with prokinetics (cisapride)
Once peristaltic failure occurs its usually irreversible

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29
Q

What is corkscrew oesophagus?

A

Diffuse oesophageal spasm and incoordinate contractions leading to dysphagia and chest pain

30
Q

What is the pressure in corkscrew oesophagus?

A

400-500 mmHg

31
Q

Where is hypertrophy in corkscrew oesophagus?

A

In the circular muscle

32
Q

How is corkscrew oesophagus treated?

A

It may be responsive to forceful pneumatic dilation of the cardia

33
Q

What is dysphagia lusoria?

A

Vascular compression of the oesophagus from an aberrant right subclavian artery

34
Q

Describe the path of the right subclavian artery from where it arises to where it goes

A

Arises from the thoracic aorta and goes posterior to the oesophagus

35
Q

How is dysphoria lusoria treated?

A

Surgically

36
Q

What are the 3 areas of constriction in the upper GI tract?

A

Cricopharyngeal constriction
Aortic and bronchial constriction
Diaphragmatic and sphincter constriction

37
Q

What might cause pathological constriction in the upper GI tract?

A

Cancer, foreign body and physiological dysfunction

38
Q

What is the most common cause of oesophageal perforation?

A

Latrogenic from OGD (over 50% of perforation is due to this)

39
Q

What are some other causes of oesophageal perforation?

A 
Spontaneous (boerhaave's)
Foreign bodies
Trauma
Intraoperative
Malignant
40
Q

What is Boerhaave’s?

A

A cause of oesophageal perforation:
Sudden increase in in intra-oesophageal pressure with negative intra thoracic pressure
Results in vomiting against a closed glottis

41
Q

How does oesophageal perforation present?

A

Pain
Fever
Dysphagia
Emphysema

42
Q

How is oesophageal perforation diagnosed?

A

CXR
CT
Swallow
OGD

43
Q

How is oesophageal perforation managed?

A

Operative management is default unless there is minimal contamination
Primary management is NDM, IV fluids, broad spectrum antibiotics/antifungals, bloods

44
Q

How is oesophageal perforation managed conservatively?

A

Via covered metal stent

45
Q

How is surgical management of oesophageal perforation done?

A

Primary repair with a vascularised pedicle flap is optimal

Oesophagectomy is a definitive solution with reconstruction

46
Q

How does LOS act as a barrier against reflex?

A

it is closed to prevent contents from the stomach coming back up

47
Q

When does sporadic reflux occur?

A

When theres pressure on full stomach
When swallowing
When the transient sphincter is opening

48
Q

What are the protective mechanisms after reflux?

A 
Volume clearance= oesophageal peristalsis reflux 
pH clearance (saliva)
Epithelium, it has barrier properties
49
Q

What does failure of protective mechanisms cause?

A

GORD

Sliding or rolling hiatus hernia

50
Q

What does non surgical management of GORD involve?

A 
OGD to exclude cancer
Oesophageal manometry 
24 hr oesophageal pH recording 
Lifestyle changes eg weight loss, smoking etc
PPIs
51
Q

What does surgical management of GORD involve?

A

Dilation peptic strictures

Laparoscopic Nissen’s fundoplication

52
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

53
Q

What does the cardia and pylorus of the stomach produce?

A

Mucus only

54
Q

What does the body and fundus of the stomach produce?

A

Mucus, Hcl, pepsinogen

55
Q

What does the antrum of the stomach produce?

A

Gastrin

56
Q

How much acid does the stomach produce everyday?

A

2L

57
Q

What is the pH of the stomach at the epithelial and lumen?

A 
Epithelium= 6-7
Lumen= 1-2
58
Q

What is erosive and haemorrhagic gastritis?

A

When an acute ulcer causes gastric bleeding and perforation

59
Q

What is nonerosive, chronic gastritis? What stomach region is it associated with?

A

Associated with the antrum

Due to helicobacter pylori

60
Q

What is atrophic gastritis? What stomach region is it associated with?

A

Associated with the fundus
Autoantibodies attack parts and products of parietal cells causing parietal atrophy leading to reduced acid and IF secretion

61
Q

What are the 4 types of gastritis?

A

Erosive and haemorrhagic
Nonerosive, chronic
Atrophic
Reactive

62
Q

Where does stimulation come from when regulating gastric secretion?

A

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

63
Q

Where does inhibition come from when regulating gastric secretion?

A

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

64
Q

What are the 3 mechanisms that repair epithelial defects from ulcers?

A

Migration
Gap closed by cell growth
Acute wound healing

65
Q

What is migration in relation to repairing epithelial defects?

A

Adjacent epithelial cells flatten to close gap via sideward migration along the basement membrane

66
Q

What is gap closed cell growth in relation to repairing epithelial defects stimulated by?

A

EGF, TGF-α, IGF-1, GRP & gastrin

67
Q

What is acute wound healing in relation to repairing epithelial defects?

A

BM destroyed and epithelial closure by restitution & cell division

68
Q

What are some mechanisms by which the basement membrane may be destroyed?

A

Leukocytes & macrophages; phagocytosis of necrotic cells; angiogenesis; regeneration of ECM after repair of BM

69
Q

What are some reasons ulcers form?

A 
Infection by helicobacter pylori 
Increased secretion of gastric juice 
Reduced HCO3- secretion 
Reduced cell formation
Reduced blood perfusion
70
Q

What are some of the clinical outcomes of infection by h pylori? How common are they?

A

Asymptomatic or chronic gastritis (80%)
Chronic atrophic gastritis intestinal metaplasia (15-20%)
Gastric or duodenal ulcer (15-20%)
Gastric cancer/MALT lymphoma (< 1%)

71
Q

How are ulcers treated?

A

Primarily via PPI or H2 blocker and triple antibiotics for 7-14 days
They are rarely managed surgically as they usually heal by themselves in 12 weeks

BRS Y2 (85 decks)

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