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Aneesha Flashcards BRS 2 > Upper GI tract > Flashcards

Upper GI tract Flashcards

1
Q

What spinal level does the oesophagus a) originate b) pass through oesophageal hiatus of diaphragm

A

C5
T10

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2
Q

What are 2 ways of dividing the oesophagus?

A
  1. Proximal (upper) 1/3, middle 1/3, distal (lower) 1/3
  2. Cervical (0-18), upper thoracic (18-24), mid thoracic (24-32), lower thoracic oesophagus (32-40)- 0 is level of incisors
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3
Q

What types of epithelium is found in upper oesophagus, then lower oesophagus?

A

Non-keratinising squamous in upper, columnar lower

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4
Q

What types of muscle tissue is found in upper, middle, lower third of oesophagus?

A

Skeletal, skeletal and smooth, smooth

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5
Q

What are the 2 sphincters of the oesophagus?

A

Upper oesophageal sphincter, lower oesophageal sphincter

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6
Q

What muscles are involved in the formation of the upper oesophageal sphincter?

A

Thyropharyngeus, cricopharyngeus

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7
Q

What are the anatomical contributions to the lower oesophageal sphincter?

A

3-4cm of distal oesophagus within the abdomen
Diaphragm surrounds LOS (right and left crus)
Intact phrenoesophageal ligament
Angle of His
((also intraabdominal pressure?))

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8
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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9
Q

What happens during stage 0 of swallowing?

A

Chewing and saliva prepares bolus
Both oesophageal sphincters are closed

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10
Q

What happens during stage 1 of swallowing?

A

Pharyngeal muscle guides food bolus towards oesophagus
UOS opens reflexively
LOS opens by vasovagal reflex (receptive relaxation reflex)

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11
Q

What happens during stage 2 of swallowing?

A

UOS closes
Superior rings of smooth muscle constrict while inferior rings dilate
Sequential contraction of longitudinal muscle

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12
Q

What happens during stage 3 of swallowing?

A

LOS closes as food passes through

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13
Q

How do we determine oesophageal motility?

A

Manometry (pressure measurement)

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14
Q

Oesophageal pressure during peristaltic contractions?

A

40mmHg

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15
Q

a)LOS resting pressure? b)What happens to this during receptive relaxation?

A

a)20mmHg
b) drops below 5mmHg

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16
Q

What neurons mediate receptive relaxations?

A

Non-cholinergic noradrenergic (NCNA) neurons of the myenteric plexus

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17
Q

Name 2 causes of functional disorders of the oesophagus

A

Abnormal oesophageal contractions (hyper motility, hypomotility, disordered co-ordination)

Failure of protective mechanisms for reflux (GORD)

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18
Q

a)What is dysphagia?

b)Name 3 types of dysphagia.

A

a)Difficulty swallowing (localisation is important- cricopharyngeus/ distal oesophagus)

b)solids or fluids, intermittent or progressive, precise or vague in appreciation

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19
Q

What is odynophagia?

A

Pain on swallowing

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20
Q

Difference between regurgitation and reflux?

A

Regurgitation is the return of oesophageal contents from above a mechanical/ functional obstruction, while reflux is passive return of gastroduodenal contents to the mouth

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21
Q

Loss of what type of cells causes achalasia?

A

Ganglion cells in myenteric (Auerbach’s) plexus in LOS wall- this leads to decreased inhibitory NCNA neuronal activity

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22
Q

What are the causes of achalasia?

A

Primary- aetiology unknown
Secondary- Chagas disease, protozoan infection, amyloid/ sarcoid/ eosinophilic oesophagitis

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23
Q

What is seen on barium swallow in achalasia?

A

Bird’s beak

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24
Q

Describe the pathophysiology of achalasia

A

Increased resting pressure of LOS
Receptive relaxation sets in late and is too weak- during reflex phase LOS pressure is markedly higher than in the stomach
Swallowed food accumulates in oesophagus eating to increased pressure throughout and dilatation through oesophagus
Propogation of peristaltic waves cease

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25
Q

Describe the ONSET and disease course of achalasia

A

insidious onset and progressive course- symptoms for years prior to seeking help

without treatment there is progressive dilation of the oesophagus

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26
Q

What does achalasia increase the risk of?

A

Oesophageal cancer

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27
Q

How is achalasia treated non-surgically and how effective is this?

A

Pneumatic dilatation- weakens LOS by circumferential stretching and in some cases tearing of its muscle fibres

71-90% of patients respond initially but then relapse

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28
Q

What surgical treatments are available for achalasia?

A

Heller’s myectomy (continuous myectomy for 6cm on oesophagus and 3cm on abdomen) and dor fundoplication (anterior fundus is folded over oesophagus and sutured to right side of myectomy)

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29
Q

What are some risks of surgical treatments for achalasia?

A

oesophageal and gastric perforation
splenic injury
division of the vagus nerve (rare)

30
Q

What type of disease is scleroderma?

A

autoimmune

31
Q

Describe the pathophysiology of scleroderma

A

Initial hypomotility is caused by neuronal defects–> atrophy of smooth muscle of oesophagus
Peristalsis in distal portion eventually ceases altogether
Resting pressure of LOS decreases
GORD develops, often associated with crest syndrome

32
Q

How is scleroderma treated?

A

First exclude organic obstruction
Increase force of peristalsis with prokinetics (cisapride)
Once peristaltic failure occurs- usually irreversible

33
Q

What happens in disordered co-ordication of oesophageal contraction?

A

Diffuse oesophageal spasm
Causes dysphagia and chest pain
Pressures of 400-500mmg
Marked hypertrophy of circular muscle
corkscrew oesophagus on Barium swallow

34
Q

How is corkscrew oesophagus treated?

A

May respond to forced PD of cardia (results less predictable than in achalasia)

35
Q

What is the anatomy of oesophageal perforation?

A

Three areas of anatomical constriction (aortic and bronchial, cricopharyngeal, diaphragmatic and sphincter)-ABCD

Pathological narrowing- cancer, foreign body, physiological dysfunction

36
Q

What is the aetiology of oesophageal perforation?

A

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

37
Q

What are iatrogenic causes of oesophageal perforation?

A

OGD (more common in the presence of diverticula/ cancer)
Stricture dilatation
Sclerotherapy
Achalasia dilatation

38
Q

What is Boerhaave’s syndrome?

A

Sudden increase in oesophageal pressure with negative intrathoracic pressure (e.g. vomiting against a closed glottis)

39
Q

What is the most common oesophageal rupture point in Boerhaave’s syndrome?

A

left posterolateral aspect of distal oesophagus

40
Q

What foreign bodies are commonly implicated in oesophageal rupture?

A

Disk batteries
Magnets
Sharp objects
Dishwasher tablets
Acids/alkali

41
Q

What types of trauma can cause oesophageal rupture?

A

Neck (penetrating)
Thorax (blunt force)

42
Q

What are some indications of oesophageal rupture?

A

Dysphagia
Blood in saliva
Haematemesis
Surgical emphysema

43
Q

How does oesophageal rupture usually present?

A

Pain
Fever
Dyphagia
Surgical emphysema

44
Q

What investigations are carried out for oesophageal rupture?

A

Chest Xray
CT
OGD
Swallow (gastrografin)

45
Q

How is oesophageal perforation treatment managed

A

It’s a surgical emergency (*2 increased risk of mortality if treatment is delayed 24hrs

initial management- NBM, IV fluids, broad spectrum antibiotics, antifungals, treatment on ICU/HDU in tertiary referral centre, bloods (including group and save)

conservative management with metal stent

operative management- primary management is first line, oesophagectomy is definitive solution

46
Q

What can cause increased LOS pressure and what does this lead to?

A

Anticholinergics, alpha adrenergic agonists, hormones, histamine, high intra-abdominal pressure, protein rich food, PGF 2α

Inhibits reflux

47
Q

What can cause decreased LOS pressure and what does this lead to?

A

VIP, beta adrenergic agonists, hormones, dopamine, PGI2, PGE2, chocolate, fat, smoking, NO, gastric acid juice

Promotes reflux

48
Q

What can cause sporadic reflux?

A

Pressure on a full stomach
Swallowing
Transient LOS opening

49
Q

What are the 3 protective mechanisms against reflux

A
  1. volume clearance- oesophageal peristalsis reflex
  2. pH clearance-saliva
  3. epithelial barrier function
50
Q

Give examples of how protective mechanisms against reflux can fail

A

Decreased sphincter pressure
Increased transient sphincter opening (Air, CO2)
Decreased saliva production (sleep, xerostomia) or decreased buffering capacity of saliva (smoking)
Abnormal peristalsis (decreased volume clearance)
Defective mucosal protective mechanism (alcohol)
Hiatus hernia

51
Q

What is a sliding hiatus hernia?

A

In a sliding hiatus hernia, the stomach distends superiorly through the diaphragm, increasing gastric acid reflux into the distal oesophagus and gastroesophageal junction

52
Q

What is a rolling/paraoesphageal hiatus hernia?

A

In a rolling hiatus hernia the gastroesophageal junction is intact, and the herniated portion of the stomach lies alongside the oesophagus
surgical emergency due to risk of hernia strangulation
In barium swallow can see fundus containing barium alongside oesophagus

53
Q

What are the investigations for GORD?

A

OGD (To exclude oesophageal cancer. Oesophagitis, Barrett’s oesophagus and peptic stricure confirm)
Oesophageal manometry
24 hour oesophageal pH recording

54
Q

How is GORD treated?

A

Medical- lifestyle changes (weight loss, smoking, EtOH), PPIs
Surgical- Dilatation peptic stricure, laparoscopic nissen’s fundoplication

55
Q

What are the basic functions of the stomach?

A

Breaks food down into smaller particles (pepsin, stomach acid)
Holds food and releases in a steady, controlled stream into the duodenum
Kills parasites and some bacteria

56
Q

What substances are secreted by different regions of the stomach

A

Cardia and pyloric region- mucus only
Body and fundus- mucus, pepsinogen, HCl
Antrum- gastrin

57
Q

What are the 4 types of gastritis?

A

Erosive and haemorrhage gastritis
Non-erosive, chronic active gastritis
Reactive gastritis
Atrophic (fundal gland) gastritis

58
Q

What causes erosive and haemorrhage gastritis and what can it lead to?

A

Numerous causes
Leads to formation of acute ulcer- perforation and bleeding

59
Q

What causes non-erosive, chronic active gastritis?

A

H. pylori infection

60
Q

What region of the stomach does non-erosive, chronic active gastritis occur in?

A

Antrum

61
Q

How is non-erosive, chronic active gastritis treated?

A

Triple Rx (amoxicillin, clarithromycin, pantoprazole) for 7-14 days

62
Q

What region of the stomach does atrophic gastritis occur in?

A

fundus

63
Q

Explain the pathophysiology of atrophic gastritis

A

Autoantibodies form and attack parietal cell parts and products
Parietal cells atrophy
Decrease in HCl and IF

64
Q

What factors stimulate gastric secretion?

A

Neural- ACh (vagal postganglionic fibres)
Endocrine- gastrin (G cells of antrum)
Paracrine- histamine (ECL cells and mast cells of gastric wall)

65
Q

What factors inhibit gastric secretion?

A

Endocrine- secretin (small intestine)
Paracrine- somatostatin (SIH)
Paracrine and autocrine- PGs (E2 and I2), TGF-α, adenosine

66
Q

What factors contribute to mucosal protection against ulcers?

A

Mucus film
Mucosal blood perfusion
HCO3- secretion
Epithelial barrier

67
Q

What mechanisms are involved in gastric ulcer healing?

A

Migration- adjacent cells flatten and migrate sideways along BM to close gap
Gap closed by cell growth- stimulated by EGF, TGF-α, IGF-1, GRP and gastrin
Acute wound healing- BM destroyed, attraction of leukocytes and neutrophils, phacytosis of necrotic cells, angiogenesis, BM repaired, ECM regenerated

68
Q

What factors contribute towards gastric ulcer formation?

A

Helicobacter pylori
Increased gastric acid secretion
Decreased HCO3- secretion
Decreased blood perfusion
Decreased cell formation

69
Q

What are the possible clinical outcomes of an H. pylori infection?

A
  1. Asymptomatic or chronic gastritis
  2. Atrophic gastritis and intestinal metaplasia
  3. Gastric/ duodenal ulcer
  4. Gastric cancer/ MALT lymphoma
70
Q

What is the primary medical treatment for H. pylori infections?

A

PPI or H2 blocker
Triple Rx (amoxicillin, clarythromycin, pantoprazole for 7-14 days)

71
Q

What are the indications for surgical treatment for peptic ulcers?

A

Intractability (after medical treatment)
Relative- requiring continuous treatment with steroid therapy/ NSAIDs
Complications- haemorrhage, obstructions, perforations

72
Q

When would you carry out elective surgery for peptic ulcers?

A

Rare - most uncomplicated ulcers heal within 12 weeks
If don’t, change medication, observe additional 12 weeks
Check serum gastrin (antral G-cell hyperplasia or gastrinoma [Zollinger-Ellison syndrome])
OGD: biopsy all 4 quadrants of ulcer (rule out malignant ulcer) if refractory

Aneesha Flashcards BRS 2 (47 decks)

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