Oesophageal + Stomach disorders Flashcards
(76 cards)
1
Q
What is the epithelium of the stomach?
A
columnar epithelium
2
Q
Describe the disease of Achalasia?
(4)
A
- Degenerative loss of ganglia from the Auerbach’s plexus.
- Impaired peristalsis of the oesophagus
- lower oesophageal sphincter is unable to relax
- Overall leads to dilation of the oesophagus.
3
Q
What are the clinical features of Achalasia?
(3)
A
- Progressive dysphagia of BOTH foods and liquids
- Regurgitation of undigested food
- Chest pain, heartburn and weight loss
4
Q
What are the investigations for Achalasia? (2)
A
Gold standard;
1. Oesophageal manometry
* Excessive LOS tone which does not relax on swallowing.
- Barium swallow : expanded oesophagus - ‘Bird’s beak’ appearance
5
Q
What is the first line management of Achalasia
A
Pneumatic balloon dilation
6
Q
What is the gold standard management of Achalasia?
A
If persistent symptoms
* Heller Cardiomyotomy
: a laproscopic procedure where a small cut in made in the lower sphincter to relive the pressure
7
Q
What are the options for management for Achalasia?
A
- First line : Pneumatic balloon dilation
- Second line :
Heller Cardiomyotomy : a laproscopic procedure where a small cut in made in the lower sphincter to relive the pressure - Third line :
Intra-sphincteric injection of botulinum toxin to relax sphincter
8
Q
What is the pathophysiology of Barret’s oesophagus?
(3)
A
- Metaplasia of the lower oesophageal mucosa where normal squamous epithelium is replaced by columnar epithelium
- Occurs through chronic acid exposure, causes chronic irritation and metaplasia.
- This results in an increased risk of oesophageal adenocarcinoma.
9
Q
What are the risk factors associated with Barret’s oesophagus? (4)
A
GORD, Male gender, smoking, haitus hernia
10
Q
How is Barret’s oesphagus diagnosed? (3)
A
- OGD and bisosy
- goblet cells present which indicates indicates metaplasia,
- May progress from metaplasia to dysplasia eventually resulting adenocarcinoma
11
Q
What are the management options of Barrett’s oesophagus (6)
A
- High dose proton pump inhibitor - reduces change of progression to dysplasia or limits region of metaplasia
- Endoscopic surveillance with biopsy
- i ) patients with identified metaplasia need monitoring endoscopies every 3-5 years
- ii ) If dysplasia is identified - Endoplasmic intervention is offered
- Radiofrequency ablation for low grade dysplasia
- Endoscopic muscosal resection
12
Q
What is the definition of GORD?
A
characterised by the reflux of stomach acid and bile into the oesophagus
13
Q
What are the clinical features of GORD? (5)
A
- heartburn
- regurgitation
- chest pain, belching,
- Acid Brash
- odynophagia
14
Q
What are the complications of GORD?
A
- Oesophagitis
- Barrett’s oesophagus
- Oesophageal adenocarcinoma
15
Q
What are the risk factors which cause GORD? (5)
A
- Obesity
- Smoking, alcohol excess
- Haitus hernia
- Drugs which relax the LOS -
- Tricyclic antidepressants, nitrates, CCB, NSAIDs.
16
Q
What drugs increase the risk of GORD and how? (4)
A
Drugs which relax the LOS -
* Tricyclic antidepressants
* nitrates
* CCB
* NSAIDs.
17
Q
Which drugs cause dyspepsia? (3)
A
- NSAIDS
- Bisphosphonates
- Steroids
18
Q
What is the definition of ‘Mallory-Weiss syndrome’
A
- Severe vomiting causes sudden increase in intra-abdominal pressure
- leading to partial thickness laceration, involving mucosa and submucosa but not the muscular layer.
19
Q
What are the risk factors for Mallory Weiss syndrome? (4)
A
- Alcoholism
- bulimia
- hiatal hernia
- hyperemesis gravidarum
20
Q
What are the clinical features of Mallory-Weiss syndrome (4)
A
- Haematemesis following severe vomiting or retching
- Marlena
- Epigastric/back pain
- Signs of haemodynamic instability - hypotension, tachycardia
21
Q
What investigations are indicated in Mallory Weiss syndrome?
A
- . Endoscopy
- FBC
22
Q
What is the management of Mallory Weiss syndrome?
A
- Supportive management with IV fluids
- IV PPI
- Endoscopic band ligation
23
Q
What is the definition of Boerhaave syndrome?
A
- Spontaneous rupture esophagus - full thickness tear
typically as a result of - Sudden increase in intraesophageal pressure combined with poor esophageal wall integrity.
24
Q
What is the cause of Boerhaave syndrome?
A
- Associated with severe vomiting or retching,
- Leading to a sudden increase in intrathoracic and intraabdominal pressures.
- The increased pressure can cause a rupture in the weakened esophageal wall.
25
What are the risk factors of Boerhaave syndrome?
Oesophagitis, Barrett’s oesophagus, ulcers, stricture dilatation
26
What are the clinical features associated with Boerhaave syndrome?
1. Mackler’s triad : Chest pain, vomiting, subcutaneous emphysema - ‘crunching sound’ over heart beat caused by mediastinal emphysema
2. Severe vomiting
3. Severe chest or abdominal pain localised to epigastric region or back pain,
4. Tachypnea, dyspnea, cyanosis, fever
27
Which investigations are indicated in Boerhaave syndrome?
1. Diagnosis: Avoid endoscopy as this may worsen tear
2. CXR : pleural effusion
3. CT scan : oesophageal wall oedema, mediastinal widening, pneumothorax
28
Boerhaave syndrome : complications? (3)
1. Chemical mediastinitis: gastric contents enter and contaminate the mediastinum
2. Pleural effusion : can rupture the pleural cavity resulting in pleural effusion
3. Sepsis.
29
What is the management of Boerhaave syndrome?
1. V PPI
2. Prophylactic antibiotics
3. Surgical management
30
What is the definition of Oesenophillic oesophagitis?
Allergic reaction to ingested food - results in oesophageal inflammation
31
What are the clinical features of Oesenophillic oesophagitis? (4)
1. Pain and dysphagia
2. Strictures and fibrosis of oesophagus
3. Regurgitation or food impaction
4. Weightloss - result of being off food
32
Oesenophillic oesophagitis : investigations for diagnosis? (2)
1. PPI trail : no improvement with PPI - r/o GORD
2. Endoscopy with oesophageal biopsy - dense eosinophil infiltrate and stricture
33
Oesenophillic oesophagitis : Management (3)
1. Dietary modification - exclude foods assoc with allergies such as egg, nuts, soy etc
2. Topical solution of steroids - fluticasone
3. Surgery - oesophageal dilatation to reduce sx of strictures
34
Oesenophillic oesophagitis : Complications (3)
Strictures, Mallory-weiss tear, Impaction of food which may need endoscopic intervention to remove.
35
What are the two main types of oesophageal cancer and their incidence rates?
1. Squamous cell carcinoma: most common in the developing world
2. Adenocarcinoma: most common in the developed world - US/UK
36
Oesophageal cancer : location and causes of Squamous cell carcinoma?
1. Upper 2/3 of the oesophagus
_Causes :_
1. Smoking
2. Alcohol,
3. Achalasia
37
Oesophageal cancer : location and adenocarcinoma cell carcinoma? (3)
1. Originates in the columnar glandular epithelium - lower 1/3 of the oesophagus
* Causes :
1. GORD or Barrett’s oesophagus, repeated oesophagitis from the acid reflux
* replaces the squamous epithelium with columnar epithelium similar to the intestines this process is called metaplasia, which is better at withstanding acidic environment
38
Oesophageal cancer : clinical features? (3)
1. Dysphagia (most common presenting symptom)
2. Anorexia, weight loss,
3. Vomitting
39
Oesophageal cancer : Investigations for diagnosis? (3)
1. Upper GI endoscopy with biopsy
2. Endoscopic ultrasound for regional staging
3. CT scan can be used for initial staging : Stages according to the TNM system, T for tutor size, N for lymph node metastases, M for distal metastases.
40
Oesophageal cancer : Management (2)
1. Surgical resection
2. Oesophagectomy with adjuvant chemotherapy
41
H.pylori : Associated diseases? (4)
1. Gastritis
2. Peptic ulcer disease
3. Gastric cancer,
4. B-cell lymphoma of MALT fissure,
42
H.pylori : Pathophysiology of disease (2)
H-Pylori has 2 main mechanisms to survive in the acidic gastric environment
1. Secrete urease which converts urea into ammonia -> alkalisation of the acidic environment -> H. Pylori are better able to survive
2. Release bacterial cytotoxin such as cytotoxin A which causes epithelial cell death and exposes the underlying mucosal layers to gastric acid -> this in turn can lead to ulcer formation.
43
H.pylori : Investigations for diagnosis? (4)
**1. FIRST LINE :**
Urea breath test - not to be performed within 4 weeks of treatment with antibiotic or PPI - can also be used to check for H. Pylori eradication
2. Rapid urease test - biosy sample is mixed with urea and PH indicator, colour change if H pylori urease activity
3. Stool antigen test
4. Gastric biospy
44
H.pylori : Guidance before investigation for diagnosis?
Urea breath test should not be performed
* <4 weeks after antibiotic therapy
* <2 weeks after PPI use
45
H.pylori : Management? (2)
PPI + Amoxicillin + Clarithromycin/Metronodizole (7 day course)
If allergic to penicillin; PPI + Clarithromycin +Metronidazole
46
Which is the test recommended to confirm H.pylori eradication?
Urea breath test - only test recommended
47
Peptic Ulcer : What are the two types? (2)
Gastric ulcers - form in the lesser curvature of the antrum
Duodenal ulcers - develop right after the pyloric sphincter
48
Peptic ulcer : Causes (3)
1. H. Pylori : secretes proteases which damages mucosa
2. NSAIDs : inhibit cyclooxyrgenase which synthesises prostaglandins, lower levels of prostaglandins leaves the mucosa susceptible to damage
3. Zollinger Ellinson syndrome (Gastrinoma) : neuroendocrine Timor which secretes an abnormal levels of gastrin, this stimulate parietal cells to release excess HCL.
49
Gastric ulcer : Clinical features
1. Increased pain on eating, thus assoc with weightloss
50
Gastric ulcer : Complications
1. Erode into the left gastric artery leading to a haemorrhage
51
Duodenal ulcer : Clinical features
1. Pain decreases on eating, thus assoc with weight gain
52
Duodenal ulcer : Complications (3)
1. Erodes on the posterior wall of the duodenum eroding into the gastroduadenal artery
2. Referred pain in the shoulder : Perforation, air can collect under the diaphragm, irritating the phrenic nerve.
3. If close to pyloric sphincter - can lead to oedema and gastric outlet obstruction
53
Peptic ulcer : investigations for diagnosis?
1. Upper endoscopy
54
Peptic ulcer : Management (4)
1. Dietary and lifestyle adjustments
2. PPI and H2 receptor antagonist : reduce stomach acid production
3. Eradication of H.Pylori + Antibiotic therapy
4. Endoscopic therapy : if high risk of bleeding, consider endoscopic haemostatic clips
55
Gastric cancer : Adenocarcinoma - histology/cause?
Adenocarcinoma - most common type of GI cancer
Histology : Arises from the columnar epithelium
Cause : is H. Pylori bacteria which causes chronic gastritis resulting in metaplasia
56
Gastric cancer : Risk factors
**Blood group A**: Individuals with blood group A have been found to have a higher risk of developing gastric cancer
**Pernicious anaemia**: Pernicious anaemia is an autoimmune condition that results in vitamin B12 deficiency due to impaired absorption in the stomach.
This condition causes chronic inflammation and atrophy of the gastric mucosa, which can eventually lead to gastric cancer.
**H. pylori infection:** It is well established that chronic infection with H. pylori, a gram-negative bacterium that colonises the stomach lining, significantly increases the risk of gastric cancer
**Smoking**: Smoking is a significant risk factor for many types of cancers including gastric cancer
57
Gastric cancer : MALT Lymphoma
Origin : Gastric cancer arising from Lymphoid tissue associated with mucous membrane - part of the immune system found in the gastrointestinal tract.
Cause :
Chronic H.pylori infection - triggers excessive B cell proliferation which increases likelihood of mutation into a lymphoma
58
Gastric cancer : Carcinoid Tumor
Origin cancer : Gastric cancer arising from neuroendocrine G-cells in the stomach.
59
Gastric cancer : Investigations for diagnosis?
1. Gastro-duoadenoscopy with biopsy - signet ring cells present
2. CT scan - staging
60
Gastric cancer : Management
Partial or complete gastrectomy with chemotherapy
61
2WW criteria for Oesophageal and Stomach cancer : criteria
Urgent Endoscopy within 2 weeks for the following;
* All patients with dysphafia
* All patients with upper abdominal mass consistent with stomach cancer
* Patients >55 with weightloss and
- Upper abdominal pain
- Reflux
- Dyspepsia
62
Mx of dyspepsia - without red flag sx
This can be summarised at a step-wise approach
* 1. Review medications for possible causes of dyspepsia
* 2. Lifestyle advice
* 3. **Trial of full-dose proton pump inhibitor for one month OR a 'test and treat' approach for H. pylori**
* if symptoms persist after either of the above approaches then the alternative approach should be tried
63
Non urgent endoscopy criteria?
1. Haematemesis
2. Treatment resistent dyspepsia
3. Upper abdomina pain with
- Low Hb
- Raised platelets
4. N+V with weightloss,dyspepsia, upper abdopain
64
PPI : Mechanism of action?
MOA : irreversible blockage of H+/K+ ATPase of gastric parietal cells
65
PPI : Side effects?
1. Hyponatremia (Low Na+)
2. Hypomagnesaemia (Low Mg2+)
3. Osteoporosis - increases risk of fractures
4. Microscopic colitis - can present as chronic diarrhea
5. Increased risk of C.diff infections
66
Clostridium Difficile : Pathophysiology of disease?
* Anaerobic Gram+ rod common in hospital setting
1. Anaerobic G+ rod which produces an exotoxin which target intestinal epithelial cell and cause inflammation of the intestinal tissue
2. Results in a syndrome called pseudomembranous colitis.
*** Transmission- via faecal oral route**
67
Clostridium Difficile : Risk factors?
1. Broadspectrum antibiotics : suppression of normal gut flora by broad spectrum antibiotics ( **Clindamycin** and 2/3rd gen cephalosplorins such as cefexime
2. PPI (Omeprazole)
68
Clostridium Difficile : Clinical features?
1. Diarrhea
2. Abdominal pain
3. Raised WCC count - the higher the WCC + any assoc systemic features the more severe the disease
69
Clostridium Difficile : Investigations for diagnosis?
Stool sample : C.diff toxin
70
Clostridium Difficile : Management of first episode
1. Review and stop current antibiotic therapy
* First episode of C.diff infection
2. First line : Oral vancomycin for 10 days
3. Second line.: Oral fidaxomicin
4. Third line therapy : Oral vancomycin +/- IV metronidazole
71
Clostridium Difficile : Management of second episode
Recurrent episode - recurrent infection in 20% of patients
1. Within 12 weeks since last infection - oral fidaxomicin
2. After 12 weeks since last infection - oral vancomycin or fidaxomicin
72
Acute upper GI bleed : Clinical features
1. Haematemesis - bright red or occasional coffee ground
2. Meleaena - black, tarry stool
3. Raised urea
73
Acute upper GI bleed : Causes
1. Oesophageal varices
2. Oesophagitis
3. Mallory weiss tear
4. Peptic ulcer perforation
74
Acute upper GI bleed : Prevention measures
1. Propanolol - reduced rebleeding and mortality
2. Endoscopic bind ligation - primary prevention of patient with liver cirrhosis and medium-large oesophageal varices
75
Acute upper GI bleed : Management
1. GBS score - raised urea, low Hb, reduced BP
2. Rockall score - used after endoscopy, to assess risk of rebleeding and mortality
3. Blood transfusion
4. Endoscopy within 24 hours
76
Variceal bleed : Management
1. Telipressin and prophylactic antibiotics
2. Band litigation
