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Aneesha Flashcards BRS 2 > Upper GI tract > Flashcards

Upper GI tract Flashcards

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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
Describe the ONSET and disease course of achalasia
insidious onset and progressive course- symptoms for years prior to seeking help without treatment there is progressive dilation of the oesophagus
26
What does achalasia increase the risk of?
Oesophageal cancer
27
How is achalasia treated non-surgically and how effective is this?
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
28
What surgical treatments are available for achalasia?
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)
29
What are some risks of surgical treatments for achalasia?
oesophageal and gastric perforation splenic injury division of the vagus nerve (rare)
30
What type of disease is scleroderma?
autoimmune
31
Describe the pathophysiology of scleroderma
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
How is scleroderma treated?
First exclude organic obstruction Increase force of peristalsis with prokinetics (cisapride) Once peristaltic failure occurs- usually irreversible
33
What happens in disordered co-ordication of oesophageal contraction?
Diffuse oesophageal spasm Causes dysphagia and chest pain Pressures of 400-500mmg Marked hypertrophy of circular muscle corkscrew oesophagus on Barium swallow
34
How is corkscrew oesophagus treated?
May respond to forced PD of cardia (results less predictable than in achalasia)
35
What is the anatomy of oesophageal perforation?
Three areas of anatomical constriction (aortic and bronchial, cricopharyngeal, diaphragmatic and sphincter)-ABCD Pathological narrowing- cancer, foreign body, physiological dysfunction
36
What is the aetiology of oesophageal perforation?
ISFTIM Iatrogenic (OGD) Spontaneous (Boerhaave's) Foreign body Trauma Intraoperative Malignant
37
What are iatrogenic causes of oesophageal perforation?
OGD (more common in the presence of diverticula/ cancer) Stricture dilatation Sclerotherapy Achalasia dilatation
38
What is Boerhaave's syndrome?
Sudden increase in oesophageal pressure with negative intrathoracic pressure (e.g. vomiting against a closed glottis)
39
What is the most common oesophageal rupture point in Boerhaave's syndrome?
left posterolateral aspect of distal oesophagus
40
What foreign bodies are commonly implicated in oesophageal rupture?
Disk batteries Magnets Sharp objects Dishwasher tablets Acids/alkali
41
What types of trauma can cause oesophageal rupture?
Neck (penetrating) Thorax (blunt force)
42
What are some indications of oesophageal rupture?
Dysphagia Blood in saliva Haematemesis Surgical emphysema
43
How does oesophageal rupture usually present?
Pain Fever Dyphagia Surgical emphysema
44
What investigations are carried out for oesophageal rupture?
Chest Xray CT OGD Swallow (gastrografin)
45
How is oesophageal perforation treatment managed
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
What can cause increased LOS pressure and what does this lead to?
Anticholinergics, alpha adrenergic agonists, hormones, histamine, high intra-abdominal pressure, protein rich food, PGF 2α Inhibits reflux
47
What can cause decreased LOS pressure and what does this lead to?
VIP, beta adrenergic agonists, hormones, dopamine, PGI2, PGE2, chocolate, fat, smoking, NO, gastric acid juice Promotes reflux
48
What can cause sporadic reflux?
Pressure on a full stomach Swallowing Transient LOS opening
49
What are the 3 protective mechanisms against reflux
1. volume clearance- oesophageal peristalsis reflex 2. pH clearance-saliva 3. epithelial barrier function
50
Give examples of how protective mechanisms against reflux can fail
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
What is a sliding hiatus hernia?
In a sliding hiatus hernia, the stomach distends superiorly through the diaphragm, increasing gastric acid reflux into the distal oesophagus and gastroesophageal junction
52
What is a rolling/paraoesphageal hiatus hernia?
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
What are the investigations for GORD?
OGD (To exclude oesophageal cancer. Oesophagitis, Barrett's oesophagus and peptic stricure confirm) Oesophageal manometry 24 hour oesophageal pH recording
54
How is GORD treated?
Medical- lifestyle changes (weight loss, smoking, EtOH), PPIs Surgical- Dilatation peptic stricure, laparoscopic nissen's fundoplication
55
What are the basic functions of the stomach?
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
What substances are secreted by different regions of the stomach
Cardia and pyloric region- mucus only Body and fundus- mucus, pepsinogen, HCl Antrum- gastrin
57
What are the 4 types of gastritis?
Erosive and haemorrhage gastritis Non-erosive, chronic active gastritis Reactive gastritis Atrophic (fundal gland) gastritis
58
What causes erosive and haemorrhage gastritis and what can it lead to?
Numerous causes Leads to formation of acute ulcer- perforation and bleeding
59
What causes non-erosive, chronic active gastritis?
H. pylori infection
60
What region of the stomach does non-erosive, chronic active gastritis occur in?
Antrum
61
How is non-erosive, chronic active gastritis treated?
Triple Rx (amoxicillin, clarithromycin, pantoprazole) for 7-14 days
62
What region of the stomach does atrophic gastritis occur in?
fundus
63
Explain the pathophysiology of atrophic gastritis
Autoantibodies form and attack parietal cell parts and products Parietal cells atrophy Decrease in HCl and IF
64
What factors stimulate gastric secretion?
Neural- ACh (vagal postganglionic fibres) Endocrine- gastrin (G cells of antrum) Paracrine- histamine (ECL cells and mast cells of gastric wall)
65
What factors inhibit gastric secretion?
Endocrine- secretin (small intestine) Paracrine- somatostatin (SIH) Paracrine and autocrine- PGs (E2 and I2), TGF-α, adenosine
66
What factors contribute to mucosal protection against ulcers?
Mucus film Mucosal blood perfusion HCO3- secretion Epithelial barrier
67
What mechanisms are involved in gastric ulcer healing?
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
What factors contribute towards gastric ulcer formation?
Helicobacter pylori Increased gastric acid secretion Decreased HCO3- secretion Decreased blood perfusion Decreased cell formation
69
What are the possible clinical outcomes of an H. pylori infection?
1. Asymptomatic or chronic gastritis 2. Atrophic gastritis and intestinal metaplasia 3. Gastric/ duodenal ulcer 4. Gastric cancer/ MALT lymphoma
70
What is the primary medical treatment for H. pylori infections?
PPI or H2 blocker Triple Rx (amoxicillin, clarythromycin, pantoprazole for 7-14 days)
71
What are the indications for surgical treatment for peptic ulcers?
Intractability (after medical treatment) Relative- requiring continuous treatment with steroid therapy/ NSAIDs Complications- haemorrhage, obstructions, perforations
72
When would you carry out elective surgery for peptic ulcers?
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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