Upper GI tract Flashcards

1
Q

Where is the lower oesophageal sphincter (LOS)?

A
  • 3-4 cm distal oesophagus within abdomen
  • An intact phrenoesophageal ligament
  • Angle of His
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What surrounds LOS?

A

Diaphragm surrounds LOS (Lt & Rt crux)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is stage 0?

A

oral phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What happens during stage 0?

A
  1. Chewing & saliva prepare bolus

2. Both oesophageal sphincters constricted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is stage 1?

A

Pharyngeal phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What happens during stage 1?

A
  1. Pharyngeal musculature guides food bolus towards oesophagus
  2. Upper oesophageal sphincter opens reflexly
  3. LOS opened by vasovagal reflex (receptive relaxation reflex)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is stage 2?

A

Upper oesophageal phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What happens during stage 2?

A
  1. Upper sphincter closes
  2. Superior circular muscle rings contract & inferior rings dilate
  3. Sequential contractions of longitudinal muscle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is stage 3?

A

Lower oesophageal phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What happens during stage?

A

Lower sphincter closes as food passes through

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is oesophageal motility determined by?

A

by pressure measurements (manometry)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the pressure of peristaltic waves?

A

40 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the LOS resting pressure?

A

20 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

When does the pressure of LOS decrease? What is it mediated by?

A
  1. ↓<5 mmHg during receptive 
relaxation 


2. Mediated by inhibitory 
noncholinergic nonadrenergic (NCNA) neurons of myenteric plexus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is can functional disorders of oesophagus be caused by?

A
  1. Abnormal oesophageal contraction

2. Failure of protective mechanisms for reflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why might there by abdnormal oesophageal contraction?

A
  • Hypermotility

  • Hypomotility

  • Disordered coordination
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Why could there be Failure of protective mechanisms for reflux?

A

GastroOesophageal Reflux Disease (GORD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is dysphagia?

A

difficulty in swallowing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Why is it important to localise dysphagia?

A

Localisation is important – cricopharyngeal sphincter or distal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the types of dysphagia?

A

-For solids or fluids
-Intermittent or progressive

-Precise or vague in appreciation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is odynophagia?

A

pain on swallowing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is regurgitation?

A

refers to return of oesophageal contents from above an obstruction - may be functional or mechanical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is reflux?

A

passive return of gastroduodenal contents to the mouth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is achalasia?

A

hypermobility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the cause of achalasia?

A
  1. Due to loss of ganglion cells in Aurebach’s myenteric plexus in LOS wall
  2. leads to decreased activity of inhibitory NCNA neurones
    - Cannot relax LOS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the primary and secondary causes of achalasia?

A

• Primary: aetiology unknown
• Secondary
-Diseases causing oesophageal motor abnormalities similar to primary achalasia
•Chagas’ Disease
•Protozoa infection
•Amyloid/Sarcoma/Eosinophilic 
Oesophagitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What happens to the resting pressure of LOS in achalasia?

A

increased

28
Q

What is the result of achalasia?

A
  1. Receptive relaxation sets in late and is too weak
  2. During reflex phase pressure in LOS is 
markedly higher than stomach
    
3. Swallowed food collects in oesophagus causing increased pressure throughout with dilation of the oesophagus 

  3. Propagation of peristaltic waves cease
29
Q

What is the disease course of achalasia?

A
  1. Has insidious onset - symptoms for years 
prior to seeking help
  2. Without treatment: progressive 
oesophageal dilatation of oesophagus
30
Q

What happens to the risk of oesophageal cancer in achalasia?

A
  • increased 28-fold 


- annual incidence only 0.34%

31
Q

What is the treatment of achalasia?

A

pneumatic dilation (PD)

32
Q

How does pneumatic dilation work?

A

PD weakens LOS by circumferential stretching & in some cases, tearing of its muscle fibres 


33
Q

How effective is PD?

A

71 - 90% of patients respond initially but many patients subsequently relapse

34
Q

What are the surgical options for achalasia treatment?

A
  1. Heller’s myotomy

2. Dor fundopilaction

35
Q

What happens in heller’s myotomy?

A

A continuous myotomy performed for 6 cm on the oesophagus & 3 cm onto the stomach

36
Q

What happens in dor fundoplication?

A

anterior fundus folded over oesophagus and sutured to right side of myotomy

37
Q

What are the risk of surgical treatment of achalasia?

A
  • Oesophageal & gastric perforation (10 – 16%) 


* Division of vagus nerve – rare 
•Splenic injury – 1 – 5%

38
Q

What happens in peroral endoscopic myotomy (POEM)?

A
  1. Mucosal incision

  2. Creation of submucosal tunnel
  3. Myotomy

  4. Closure of mucosal incision
39
Q

What is disorder of hypomobility?

A

Scleroderma

40
Q

What is scleroderma?

A

autoimmune disease

41
Q

What does the scleroderma lead to?

A
  1. Hypo mobility in its early stages due to neuronal defects
  2. Lead to atrophy of smooth muscle of oesophagus
  3. Peristalsis in distal portion ultimately ceases altogether
  4. Decreased resting pressure of LOS
  5. Lead of GORD develop (assoicated with CREST syndrome)
42
Q

What is the treatment of scleroderma?

A
  1. Exclude organic obstruction
  2. Improve force of peristalsis with prokinetics (cisapride)
  3. Once peristaltic failure occurs (usually irreversible)_
43
Q

What can cause disorder coordination?

A

Corckscrew oesophagus

44
Q

What does diffuse oesophageal spasm lead to?

A

•Incoordinate contractions
-dysphagia & chest pain 

•Pressures of 400-500 mmHg 
•Marked hypertrophy of circular muscle

45
Q

What is the treatment of corckscrew oesophagus?

A
  • May respond to forceful PD of cardia 


- Results not as predictable as achalasia

46
Q

What vascular anomalies cause dysphagia?

A
  1. Dysphagia lusoria

2. Double aortic arch

47
Q

What is the anatomy of oesophageal perforations?

A
  1. 3x areas of anatomical constriction
    - cricopharyngeal constriction
    - Aortic and bronchial constriction 

    - Diaphragmatic and ‘sphincter’ constriction
  2. Pathological narrowing (cancer, foreign 
body, physiological dysfunction)
48
Q

What are NCNA secreted by?

A

postganglionic non-cholinergic neurons of the enteric nervous system

49
Q

What are NCNAs? What are examples

A
  • hormone that affects ‘nerves’

- vasoactive intestinal peptide (VIP), gastrin release peptide (GRP), and enkephalins

50
Q

What is Chagas’ disease?

A

South American chronic infection with parasite Trypanosoma Cruzi

51
Q

What are the symptoms of achalasia?

A
  1. dyspha- gia (trouble swallowing)
  2. regurgitation of food (not vomiting)
  3. retrosternal pain
  4. weight loss
52
Q

What are the serious complications of achalasia?

A
  1. esophagitis

2. pneumonia, caused by aspiration of esophageal contents (contain- ing bacteria)

53
Q

What are the causes of oesophageal perforation?

A
  1. Iatrogenic (OGD) >50% 

  2. Spontaneous (Boerhaave’s) - 15% 

  3. Foreign body - 12% 

  4. Trauma - 9% 

  5. Intraoperative - 2% 

  6. Malignant - 1%
54
Q

When is the the oesophageal perforation latrogenic?

A

-Usually at OGD

-More common in presence of
diverticula or cancer

55
Q

What is the incidence of latrogenic oesophageal?

A
  1. OGD = 0.03%
  2. Stricture dilatation = 0.1-2% 
3, Sclerotherapy = 1-5% 

  3. Achalasia dilatation = 2-6%
56
Q

What happens in Boerhaave’s?

A
  1. Sudden increase in intra-oesophageal pressure with negative intra thoracic pressure
  2. Vomiting against a closed glottis
    - Massive pressure
57
Q

How common is Boerhaave’s?

A

3.1 per 1,000,000

58
Q

What sort of foreign bodies are found in oesophageal perforations?

A
• Disk batteries growing problem

• Cause electrical burns if impact 
in mucosa 
•Magnets 

•Sharp objects 

•Dishwasher tablets 
•Acid/Alkali
59
Q

What sort of trauma would cause neck oesophageal perforation?

A

penetrating

60
Q

What sort of trauma would cause thorax oesophageal perforation?

A

blunt force

61
Q

Why can it be difficult to diagnose oesophageal perforations- what do you look out for?

A
  • Dysphagia

  • Blood in saliva

  • Haematemesis

  • Surgical empysema
62
Q

What sort surgeries can cause oesophageal perforation?

A

•Hiatus hernia repair

•Hellers Cardiomyotomy 

•Pulmonary surgery 

•Thyroid surgery 


63
Q

When can there be malignant oesophageal perforation?

A
  • Advanced cancers 

  • Radiotherapy 

  • Dilatation 

  • Stenting 

  • Poor prognosis
64
Q

When does the oesophagus start and end?

A

C5-T10 and around 25cm

65
Q

What do you need to make sure when diagnosing a functional disorder of oesophagus?

A

absence of stricture

66
Q

What are some proposed ideas of the model of achalasia pathophysiology?

A
  • environmental trigger
  • Genetic predisposition
    1. Then non autoimmune inflammatory infiltrates
    2. This promotes wound repair and fibrosis
    3. Then loss of immunological tolerance
    4. Then autoimmune so causes apoptosis
    5. Then get humoral response
    6. Then get autoimmune myenteric plexistis/gangolitis vascultisis etc