GI: GORD + Oesophageal Disorders Flashcards
(90 cards)
1
Q
List oeseophageal disease investigations
A
- Endoscopy:
- Oesophago-gastro-duodenoscopy (OGD) - used in upper GI disease eg dysphagia, dyspepsia, upper GI bleed, coeliac disease
- Radiology-contrast radiology:
- Barium swallow, examines oesophaugs
- Oesophageal pH and manometry
- Oesophageal pH
- Oesophageal manometry
2
Q
Causes of dysphagia
A
- Intrinsic
- Benign stricture
- Malignant stricture
- Oesophageal ring or web
- Foreign body
- Oesophagitis - infective, inflammatory
- Scleroderma (CREST)
- Extrinsic
- Goitre
- Lymphadenopathy
- Enlarged left atrium
- Tongue and mouth
- Tonsilitis
- Motility disorders
- Achalasia
- Scleroderma (CREST)
- Neuromuscular
- Stroke
- GBS
- Myasthenia gravis
- Bulbar palsy (LMN disease)
3
Q
What is GORD?
A
Gastro-oesophageal reflux diease
A common disease caused by reflux of the stomach contents (acid +/- bile) causing troublesome symptoms and/or complications
4
Q
What is the pathophysiology of GORD?
A
Reflux occurs due to:
- More frequent Transient Lower Oesophageal Sphincter Relaxations (TLESRs) and LOJ dysfunction
- Failure of intra-abdominal segment of the oesophagus which acts as a flap valve
- Failure of mucosal rosette formed by folds of the gastric mucosa and the contraction of the crural diaphragm at the LOS
- Reduced oesophageal motility
GORD is when pathological changes have ocurred that allow gastric contents to be in prolonged contact with oeseophagus
5
Q
Risk factors for development of GORD
A
Secondary to..
- Age
- Hiatus hernia
- Smking
- Aclohol
- Increased intra-abdo pressure - obesity, rpegnancy
- Drugs - ant-Ach, ntrates, CCB, TCAs
- Iatrogenic - Hellers myotomy
- Certain foods - fat, chocolate, caffeine (all relax abdo sphincter)
6
Q
What is the main cause of reflux in GORD?
A
LOS relaxes transiently independently of swallow after meals
7
Q
What are oesophageal mucosal defence mechanisms?
A
- Mucus - traps bicarb which acts as a buffer
- Epithelium - structure limits diffusion of H+ into cells
- Sensory mechanisms - pain due to irritation by acid and contraction of longitudinal muscles
8
Q
What are the main causes of GORD?
A
- LOS hypotension
- Hiatus hernia
- Oesophageal dysmotility
- Obesity
- Gastric acid hypersecretion
- Delayed gastric emptying
- Smoking
- Alcohol
- Pregnancy
- Drugs
9
Q
What are the different types of hiatus hernia?
A
- Sliding hiatus hernia
- Rolling hiatus hernia
10
Q
What is a sliding hiatus hernia?
A
The GO junction slides up into the chest. ACid reflux often happens as the LOS becomes less competent in many cases
11
Q
What is a rolling hiatus hernia?
A
The GO junction remains in the abdomen but a bulge of stomach herniates up into the chest alongside the oesophagus. As the GO remains intact, GORD is less common.
12
Q
Which type of hiatus hernia is more commonly associated with GORD?
A
Sliding hiatus hernia
13
Q
What lifestyle factors play a role in the development of GORD?
A
- Smoking
- Alcohol
- Obesity
- Hot beverages
- Caffeine together with patient age and gender.
14
Q
What are symptoms of GORD?
A
- Heartburn - cardinal symptom
- Retrosternal, sometimes gastric.
- Can radiate between shoulder bales/to jaw/back/arms/face
- Worse after eating
- Dyspepsia
- Belching and regurgitation
- Acid brash
- Waterbrash
- Odynophagia
- Nocturnal asthma/Chronic cough
- Laryngitis
- Sinusitis
15
Q
What is dyspepsia?
A
Burning, retrosternal discomfort after meals, lying down, stooping. It can be relieved by antacids
16
Q
What is acid brash?
A
Acid or bile regurgitation
17
Q
What is waterbrash?
A
Markedly increased salivation
18
Q
What is odynophagia?
A
Painful swallowing - can be caused by oesophagitis or ulceration
19
Q
What might your differential diagnosis be for someone presenting with features of GORD?
A
- Oesophagitis from corrosives
- Motility disorder
- Duodenal/Gastric ulcers
- Gastric cancer
- Non-ulcer dyspepsia
- Oesophageal spasm
- Cardiac disease (20% of those admitted to cardiac wards have GORD)
20
Q
If someone presented with features of GORD, what investigations would you consider doing?
A
Primarily clinical diagnosis.
If dysphagia, or >55 yrs with alarm symptoms, or failure to respond to treatment:
- Endoscopy
- 24-hr intramural pH monitoring/impedence +/- manometry
- H. Pylori testing
21
Q
What can endoscopy show in someone with features of GORD?
A
- Oesophagitis
- Hiatus hernia
- Barrett’s oesophagus
Assesses level of inflammation, biopsy for histology and can be used theraputically to dilate stricture.
Results poorly correlate to symptoms though - severe symptoms may have normal endoscopy and histology
22
Q
What is involved in pH monitoring?
A
24-hour ambulatory monitoring uses a pH-sensitive probe positioned in the lower oesophagus and is used to identify acid reflux episodes (pH <4). Catheter and implantable sensors are available; both are insensitive to alkali.
pH is a valuable means of correlating episodes of acid reflux with patient’s symptoms.
Rules out oesphageal dysmotility
23
Q
What is involved in impedance monitoring?
A
Uses a catheter to measure the resistance to flow of ‘alternating current’ in the contents of the oesophagus. Combined with pH it allows assessment of acid, weakly acid, alkaline and gaseous reflux, which is helpful in understanding the symptoms that are produced by a non-acid reflux.
24
Q
What is manometry?
A
Performed by passing a catheter through the nose into the oesophagus and measuring the pressures generated within the oesophagus.
It is used to assess oesophageal motor activity. It is not a primary investigation and should be performed only when the diagnosis has not been achieved by history, barium radiology or endoscopy.
25
What is defined as excessive reflux on pH testing?
pH \< 4 for \> 4% of the time + correlation with symptoms
26
What lifestyle factors would you address when managing someone with GORD?
* **Weight loss**
* **Smoking cessation**
* **Small, regular meals**
* **Avoid eating \< 3 hrs before bed**
* **Raise head of bed**
* **Reduce**
* Hot drinks and alcohol
* Citrus fruits
* Spicy food
* Caffeine
* Chocolate
* **Stop NASIDs, steroids, CCBs, and nitrates**
27
What medications would you consider givign someone who was suffering from GORD?
In order
1. **Antacids** - Gaviscon, magnesium trisilicate mixture
2. **PPI** - lansoprazole, omeprazole
3. **H2 blockers**
28
What drugs would you want to avoid in someone with GORD?
Affecting oesophageal motility
* **Nitrates**
* **Anticholinergics**
* **CCBs**
Causing mucosal damage
* **NSAIDs**
* **K+ Salts**
* **Bisphosphonates**
29
What are antacids?
Eg gaviscon - create a "foam roof" on top of stomach contents
30
What are examples of PPIs?
* **Omeprazole** - 40mg daily/10mg long use (life long unless progression to surgery)
* **Rabeprazole**
* **Lansoprazole**
* **Pantoprazole**
* **Esomeprazole**
31
How do PPIs work?
Work by reducing the acid secretion of parietal cells in the stomach by inhibiting the proton pump. Normally the proton pump exchanges H+ ions in the parietal cells for K+ ions in the stomach lumen, thereby increasing the H+ in the stomach, which forms HCl. By inhibiting this pump, PPI's reduce the HCl in the stomach.
32
What are indications for PPIs?
* **Gastric and duodenal ulcers**
* **H.Pylori eradication**
* **Dspepsia**
* **GORD**
* **Pprevention and treatment of NSAID-associated ulcers**
* **Zollinger-Ellison syndrome.**
33
What are side effects of PPIs?
* **Nausea**
* **Vomiting**
* **Bloating**
* **Abdominal pain**
* **Diarrhoea or constipation**
* **Rarely hepatitis and interstitial nephritis can be seen**
34
Example of a H2 blocker
Ranitidine
35
How do H2 antagonists work?
Paracrine cells in the stomach lining produce histamine in response to gastrin (stimulated by protein ingestion) or ACh (from vagal stimulation) which stimulates the parietal cells to produce gastric acid
H2-receptor antagonists block the receptors on the parietal cells thus inhibiting this action and decreasing acidity.
36
WHat are prokinetic agents?
Eg domperiodne, metoclopramide
Increase gastric emptying by increasing peristalsis
37
How would you manage someone the first time the presented with features of GORD?
* **Lifestyle changes**
* **PPIs**
38
If, when managing someone with PPIs and Lifestyle advice for GORD, they had an incomplete response to PPIs, how would you manage them?
* **Higher dose PPIs**
* **H2 antagonists**
* **Further testing**
39
When would you consider surgery in someone with GORD?
Surgery (open or laparoscopic fundoplication) reserved mainly for:
* **Good response to proton-pump inhibitors (PPIs) but who do not wish to take long-term medical treatment**
* **Refractory GORD**
* **Complications of GORD** eg recurrent pneumonia, bronchiectasis
40
What surgical procedure is used to treat GORD?
**Open/Laproscopic Nissen fundoplication** - aim to increase resting LOS pressure.
Stomach fundus is sutured around lower oesophagus - means that when the stomach contracts the oeseophagus is sealed off
41
Side effects of a nissen fundoplication
Dysphagia, difficulty to belch/vomit, gas bloating, excess flatulance, diarrhoea
42
What are complications of GORD?
* **Oesophagitis**
* **Ulcers**
* **Benign stricture** - repeated damage to oesophagus, scar tissue builds up and narrows (dysphagia worse for solids and liquids)
* **Iron-deficiency**
* **Barrett's oesophagus**
* Gastric volcus can occur when a hiatus hernia turns in on itself and causes comple oesphageal obstruction. Presents with chest pain, vomiting, dysphasia.
43
What is barrett's oesophagus?
A condition in which part of the normal oesophageal squamous epithelium is replaced by metaplastic columnar mucosa to form a segment of ‘columnar-lined oesophagus’ (CLO). It is a complication of gastro-oesophageal reflux disease and there is almost always a hiatus hernia present.
Affects distal 1/3rd of oesophagus
Major risk is progression to adneocarcinoma (all patients with confirmed Barrett's must undergo regular routine endoscopy)
44
What are risk factors for the development of barrett's oesophagus?
* GORD!!!!!!
* **\>50 years old**
* **Obesity**
* **Male**
* **Caucasian**
* **FH of Barrett's oesophagus**
45
How would you investigate for barrett's oesophagus?
Endoscopy + Biopsy
46
How is barrett's oesophagus classified?
Prague classification:
* **Length of circumferential CLO (C measurement)**
* **Maximum length (M measurement**) - the distance from the top of the gastric folds to the most proximal tongue of the columnar mucosa.
47
What would you look for on endoscopic investigation in someone with barrett's oesophagus?
* **Proximal displacement of the squamocolumnar mucosal junction**
* **Biopsies demonstrating columnar lining above the proximal gastric folds**
48
How would you manage a patient with confirmed barrett's oesophagus?
Screening
* **Dysplasia \< 3cm oesophagus** - discharge
* **Dysplasia \> 3 cm** - 2-3 yearly endoscopy
Dysplasia detercted
* **Low grade** - examine again after 6 months
* **High grade dysplasia/intramural carcinoma** - consider endoscopic resection/radiofrequency ablation
49
What is achalasia?
An oesophageal motor disorder of unknown aetiology, characterised by oesophageal aperistalsis and insufficient lower oesophageal sphincter (LOS) relaxation in response to swallowing.
Rare!
50
Risk factors for achlasia
Autoimmune disease
HLA class 2 antigens
Herpes and measles
51
What weird tropic parasite disease is linked to secondary cause of achlasia?
Chaga's disease
52
What is the pathophysiology of achalasia?
Inflammatory destruction of inhibitory nitrinergic neurons in the oesophageal myenteric (Auerbach) plexus results in loss of peristalsis and incomplete lower oesophageal sphincter relaxation.
Histopathology shows inflammation of the myenteric plexus of the oesophagus with reduction of ganglion cell numbers. Cholinergic innervation appears to be preserved.
Insufficient LOS relaxation in response to swallowing. Distal obstruction to oesophagus.
53
What are symptoms of achalasia?
Tend to be slow, progressive symptoms:
* **Dysphagia** - solids ***_and_*** liquids at the same time, slowly progressive
* **Regurgitation + retrosternal cramps**
* **Dyspespia**
* **Weight loss**
* **Chest pain**
* **Chest infections eg aspiration pneumonia**
54
Why do individuals with achalasia get recurrent chest infections?
Aspiration caused by regurgitation
55
If you suspected achalasia, what investigations would you do?
* **Upper GI endoscopy** to rule out malignancy
* **Barium swallow** - often done with flurosocpy
* **Manometry** - failure of relacation and reduced peristalsis
* **X-ray** - widened mediastinum, aspiration pneumonia
* **CT**
* Radionucleotide oesophageal emptying studies used to montor response to treatment
56
Why would you perform upper GI endoscopy in someone presenting with symptoms of achalasia?
To exclude malignancy - should be done for any cause of new onset dysphagia
57
What might you find on Barium swallow in someone with Achalasia?
* **Loss of peristalsis and delayed oesophageal emptying**
* **Dilated oesophagus that tapers to a beak-like narrowing at GOJ**
* **May be proximal oesophagus dilatation**
58
What might be found on investigation using manometry when investigating for achalasia?
* **Incomplete relaxation of the LOS with wet swallows and oesophageal aperistalsis** - most important diagnostically
* **High resting LO pressure**
* **Swallows followed by simultaneous contraction waves, typically low-amplitude**
59
Why might you do a CT in someone with achalasia?
Check for malignancy
60
Why might you do a CXR in someone with suspected achalasia?
Look for oseophageal dilatation
61
Slow onset dysphagia for solids and liquids suggets...
Motility disorder (achalasia)
62
How would you manage someone with achalasia?
* **Initial management -\> Medications** -\> Nitrates, CCBs
* **Surgical fitness assessment**
* **Fit for surgery** - Pneumatic dilatation, Lapro cardiomyotomy (aka Heller's myotomy), botulinum toxin injection (inhibits Ach release- improves 2/3rds of cases for approx 6 months with repeated treatment), gastrotomy 3rd line
* **Not fit for surgery** - Nitrates, CCB, Botulinum toxin A, Gastrostomy
63
Explain pharmacological management of achlasia
Nitrates
CCBs eg nifedipine, verapamil - taken prior to meals, max effect is 30mins - 2 hours
Relax LOJ
64
What is involved in pneumatic dilatation?
It involves the mechanical dilation of the lower oesophageal sphincter using a balloon with a sufficiently forceful mechanical stretch to rupture the muscle fibres. The balloon is inserted endoscopically or by a combined endoscopic-radiological approach.
65
What is involved in a laproscopic cardiomyotomy?
The abdominal approach involves sequentially, division of the peritoneum over the oesophagus, mobilization of the right and left margins of the oesophagus, and exposure of 5cm of oesophagus below the phreno-oesophageal membrane.
After identification of the anterior vagus nerve, a vertical myotomy is performed lateral to it along the oesophagus.
66
What are complications of achalasia?
* **Aspiration pneumonia and lung disease**
* **Increased risk of oesophageal SCC**
67
What is diffuse oesophageal spasm?
A severe form of oesophageal dysmotility that can sometimes produce retrosternal chest pain and dysphagia. It can accompany GORD
68
What is the most common cause of oesophageal stricture?
Benign stricture secondary to reflux
69
What can cause benign oesophageal strictures?
* **Reflux**
* **Ingestion of corrosives**
* **After radiotherapy**
* **After sclerosis of varices**
* **Following prolonged nasogastric intubation.**
70
What organisms most commonly cause oesophageal infection?
* **Candida**
* **Herpes simplex**
* **Cytomegalovirus**
* **Tuberculosis.**
71
Where can oesophageal diverticula occur?
* **Immediately above the UOS** - pharyngeal pouch
* **Near the middle of the oesophagus**
* **Just above the LOS** - epiphrenic diverticulum
72
What is a mallory-Weiss tear?
This is a linear mucosal tear occurring at the oesophagogastric junction and produced by a sudden increase in intra-abdominal pressure. It often occurs after a bout of coughing or retching and is classically seen after alcoholic ‘dry heaves’.
73
What are causes of oesophageal rupture?
* **Iatrogenic** - endoscopy/biopsy/dilatation
* **Trauma** - penetrating/foreign body
* **Carcinoma**
* **Boerhaave syndrome**
* **Corrosive ingestion**
74
What is Boerhaave syndrome?
Rupture due to violent vomiting
75
What are features of oesophageal rupture?
* **Odynophagia**
* **Tachypnoea**
* **Dyspnoea**
* **Shock**
* **Surgical emphysema**
76
What surgical option is used to treat achalasia?
Heller's cardiomyotomy
77
What does odynophagia suggest?
Inflammation - oesophagitis
78
Short history of progressive dustphagia, initially solids and then liquids is suggestive of...
Mechanical stricture - urgent OGD needed to look for malignant stricture
79
Aetiology of oesphageal perforation
OGD (increased risk if dilatation or biopsy done) (IATROGENIC COUNTS FOR 80%)
Foreign body
Trauma
Post-emesis
Cancer (oesophageal)
80
Signs of oesophageal perforation
Chest pain
Shock
Surgical emphysema of neck/chest - "crackling sensation"
81
Investigations oesophageal perforation
CXR - mediastinal surgical emphysema, air/fluid in pleural cavity
82
83
What is a phrayngeal pouch/zenker/s diverticulum?
Protrusion of mucosa and submucosa between 2 parts of the inferior pharyngeal constrictor msucle (this area of weakness if called Killian's dehiscence)
84
Presentation of pharyngeal pouch
Regurgitation
Bulging or gurgling of neck
Halitosis
Globus sensation
85
Investigations pharyngeal pouch
Barium swallow
86
Management of pharyngeal pouch
Surgical excision of pouch plus repair of defect in inferior constrictor.
87
What is plummer vinson syndrome?
RARE condition where there is upper oesophageal web in associateion with iron deficiency anaemia and dysphagia
Generally occurs in post menopausal women
Risk of SCC
88
Presentation plummer vinson
Dysphagia, those of irone defieincy anaemia (koiloychias and glossitis)
89
Investigations plummer vinson
Barium swallow
OGD
90
