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General Surgery > Upper GI > Flashcards

Upper GI Flashcards

1
Q

What are the most common symptoms of GORD?

A

Acidic taste in the mouth
Regurgitation
Heartburn

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2
Q

What are some factors that can increase the likelihood of GORD?

A
  1. Hiatus hernia
  2. Obesity
  3. Zollinger - Ellison syndrome (increases gastric acidity due to increased gastrin production)
  4. Hypercalcaemia
  5. Scleroderma and systemic sclerosis (can cause oesophageal dysmotility)
  6. Drugs: prednislone , NSAIDS, bisphosphonates
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3
Q

What are the stages of management of GORD?

A
  1. Full dose PPI for 4 weeks

2. Test and treat for H Pylori

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4
Q

What are the testing options for H Pylori?

A
  1. Carbon 13 urea breath test
  2. Stool antigen test
  3. Gastric biopsy at endoscopy
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5
Q

How do you treat someone who has had a positive test for H Pylori?

A 
Triple therapy for 7 days with:
1. PPI
2. Amoxicillin
3. Clarithromycin or metronidazole
If symptomatic then retest
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6
Q

How do you treat someone who has had a positive test for H Pylori and who is penicillin alergic?

A

Triple therapy for 7 days with:

  1. PPI
  2. Clarithromycin
  3. Metronidazole
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7
Q

What symptoms would make you think of oesophageal cancer and make you consider an urgent referral (within 2 weeks)?

A
  1. Dysphagia at any age
  2. New onset upper GI pain or discomfort in people over 55 years
  3. New or worsening GI pain with weight loss or iron deficiency anaemia
  4. Vomiting for more than 4 weeks
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8
Q

What is barrett’s oesophagus?

A

Metaplasia of the stratified squamous epithelium that usually lines the oesophagus by columnar epithelium due to persistent reflux of acid or bile.

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9
Q

What is the danger of barrett’s oesophagus?

A

It increases the risk of oesophageal adenocarcinoma

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10
Q

What is eosinophillic oesophagitis

A

An allergic inflammatory condition of the oesophagus that involves eosinophillic infiltration of the oesophageal lining.
Symptoms are difficulty swallowing, food impaction, reguritation or vomiting.
It is more common in people with allergic diseases such as coliac disease and asthma.

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11
Q

What is the most common endoscopic finding in allergic oesophagitis?

A

Corrugated oesophagus

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12
Q

What are the treatment options for allergic oesophagitis?

A

Corticosterioids, chromoglycate, montelukast

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13
Q

What are the risk factors for squamous cell cancers of the oesophagus?

A

Smoking, alcohol, HPV, oesophagitis

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14
Q

What is the main risk factor for adenocarcinoma of the oesophagus?

A

Barretts oesophagus

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15
Q

What is the most common way for oesophageal cancer to present?

A

Dysphagia due to tumour obstruction

Also general symptoms of malignancy such as amaemia and weight loss

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16
Q

What type of cancer makes up 90% of oral cancers?

A

Squamous cell carcinoma

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17
Q

What surgical option can be used to treat GORD and in which patients would you consider this?

A

Nissen fundoplication

You would consider this in young patients with severe/unresponsive GORD

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18
Q

How can you manage barretts oesophagus?

A
  1. Surveillance 2. Optimise PPI dose
  2. Endoscopic mucosal resection
  3. Radiofrequency ablation
  4. Argon
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19
Q

What are the symptoms of gastroparesis?

A

Feeling of fullness, nausea, vomiting (especially undigested food) , weight loss and upper abdominal pain

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20
Q

What is gastroparesis?

A

Partial paralysis of the stomach due to vagus nerve damage. This causes food to remain in the stomach for longer than normal.

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21
Q

What are some of the causes of gastroparesis?

A

Autonomic neuropathy due to diabetes mellitus
Cannabis
Iatrogenic damage to the vagus nerve fro example during surgery
Medication such as opiates or anticholinergics
Systemic diseases such as systemic sclerosis
Deficiency of chloride, sodium or zinc as these are needed for gastric acid production

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22
Q

How do you investigate suspected gastroparesis?

A

Gastric emptying studies - a nuclear study

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23
Q

What are the treatment options available for gastroparesis?

A
  • Removal of precipitating factors such as medication
  • Smaller meals that are easily digestable
  • Metclopramide (D2 receptor antagonist) increasing contractility and resting tone within the GI tract. Metclopramide also helps to improve the symptoms of nausea and vomiting.
  • Pro motility agents such as camicinal
  • Implantable gastric pacemaker (in refactory cases where are least two years of medical management has failed)
  • Sleeve gastrectomy (a procedure in which all or part of the affected portion of the stomach is removed)
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24
Q

What is oesophageal achalasia?

A

A failure of the smooth muscle fibres to relax which causes the oesophageal sphincter to remain closed and fail to open when needed. The most common type os primary achalasia, which has no known underlying cause and is due to a failure of distal oesophageal inhibitory neurones leading to a hypertensive, non relaxed oesophaeal sphincter.

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25
Q

What are the common symptoms of achalasia?

A 
Dysphagia
Regurgitation of undigested food
Chest pain behind the sternum
Weight loss 
(There is a risk of aspiration of saliva and food into the lungs)
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26
Q

What are the specific tests that you would order if you suspected a diagnosis of achalasia?

A

Barium swallow

Oesophageal manometry

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27
Q

What would you see on a barium swallow if the patient had achalsia?

A
  • Absence of normal peristaltic movement
  • Acute tapering at the lower oesophageal sphincter
  • Narrowing at the gastro oesophageal junction (birds beak appearance)
  • Oesophagus may become dilated over time.
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28
Q

What is oesophageal manometry?

A

A catheter is inserted through the nose and the patient is instructed to swallow. The probe then measures muscle contractions int he oesophagus during swallowing.

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29
Q

What will the results of oesophageal manometry testing be in achalasia?

A
  • Manometry will show failure of the lower sphincter to relax and will also reveal a lack of functional peristalsis.
  • Increased pressure of lower oesophageal sphincter
  • Increase in intra oesophageal pressure when compared to gastric pressure.
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30
Q

What are the treatment options available in achalasia?

A
  1. Lifestyle - eat slowly, drink water, avoid eating before bed time and avoid lying flat soon after meals. PPIs are also used to prevent damage by reflux.
  2. Medication - Sublingual nifedipine (calcium channel blocker), nitrates such as nitroglycerin
  3. Botox injected into the sphincter to paralyse the muscles which are holding it shut. (only really for people who can’t have surgery as the effect is temporary and it may make surgery more challenging.
  4. Balloon dilation (the muscle fibres are stretched and torn by the forceful inflation of a balloon)
  5. Surgery (heller myotomy) helps 90% of patients with achalasia
31
Q

Haematemesis after a night of vomiting.

A

Mallory - Weiss tear. This usually stops after 24 - 48 hours but sometimes requires endoscopic exploration/treatment.

32
Q

What is the difference between a mallory weiss tear and boerhaave syndrome?

A

A mallory weiss tear is a tear of the mucosa and submucosa but not the muscular layer. In boerhave syndrome the muscular layer is also torn (oesophagea rupture)

33
Q

What is the treatment of a mallory weiss tear?

A
  • Usually supportive treatment
  • Occacionaly cauterization or injection of epinephrine is required.
  • Very rarely embolization of the arteries is required.
34
Q

Haematemesis followed by excrutiating retrosternal and upper abdominal pain which occurs after a night of vomiting. On examination you hear subcutaneous emphysema. The blood pressure is 90/45 and the HR is 120.

A

Boerhaave syndrome/Oesophageal rupture. This is sue to a sudden increase in intraoesophageal pressure. The tear usually occurs in the left postero lateral aspect of the distal oesophagus and is associated with a high level of morbidity and mortality.
Macklers triad is chest pain, vomiting and subcutaneous emphysema.

35
Q

What investigations are required if you suspect oesophageal rupture?

A

Chest X Ray (air in the mediastimun)
Chest CT
Water soluable contrast esophagram. This reveals the location and the extent of extravasation of contrast. Water soluable contrast is used as the spillage of barium into the mediastinum would be danger and cause an inflammatory response.

36
Q

What is the most common cause of oesohageal perforation?

A

Iatrogenic - for example during endoscopy.

37
Q

What is the treatment of boorhave syndrome?

A

Antibiotics to prevent mediastinitis and sepsis and surgical repair of the perforation.

38
Q

What would your management be of a patient who was having an oesophageal variceal bleed.

A
  1. ABCDE (Airway protection, Oxygen, IV access (2 large bore cannulas, IV fuids)
  2. Activate major haemmorhage protocol - blood transfusion, platelets if actively bleeding, prothrombin in patients on warfarin.
  3. Endoscopy should be offered immediately to all unstable patients immediately after resuscitation. Endoscopy should be performed on all patients within 24 hours of admission.
39
Q

What are the endoscopic treatment options for patients who have a variceal bleed?

A
  1. Terlipressin at presentation (should be stopped after definitive haemostasis has been achieved)
  2. Band ligation
  3. TIPS if bleeding is not controlled by band ligation
    4
40
Q

What two risk scoring systems are used to calculate the risk of variceal haemorrhage? What are the looking at specifically and when are they calculated?

A
  1. Blatchford score - calculated prior to endoscopy, it is used to identify low risk patients who do not require any intervention. This is based on clinical and laboratory parameters including: Blood urea, haemaglobin, BP and co morbiditys.
  2. Rockwall score - used to identify patients who are at risk of ongoing bleeding and death. It is used before and after endoscopy and provides independant risk factors which can predict the risk of mortality and re bleeding. It includes age, evidence of shock, comorbidity, diagnosis and major endoscopic findings.
41
Q

What co morbidities are taken into consideration when assessing the risk to a patient of an upper GI bleed?

A

Cardiac failure, IHD (2 points in rockwall score)

Renal failure, liver failure, disseminated malignancy (3 points)

42
Q

When is the rockwall assessment performed on a patient that has had an upper GI bleed?

A

After endoscopy (endoscopy findings make up part of the score)

43
Q

When is the blatchford assessment performed on a patient that has had an upper GI bleed?

A

First assessment of the patient

44
Q

What bloods would be most important to get in a patient who has had an upper GI bleed?

A

FBC (haemoglobin, platelets)
U & E (renal function)
Group and save/cross match
Coagulation

45
Q

If a patient has had an upper GI bleed and has a blatchford score of 0 - 1 (meaning they are low risk) what are the next steps?

A

If no clinical concern then patient can be discharged without endoscopy and with a review of potential causative drugs and followed up in the community.

46
Q

If a patient has had an upper GI bleed and has a blatchford score of 2 -5 (meaning they are indeterminate risk) what are the next steps?

A
  1. Monitor
  2. If significant bleeding or stigmata the consider IV omeprazole infusion
  3. If known cirrhosis give terlipressin
  4. Consider reversal of coagulopathy
  5. Reassess after 12 - 24 hours to consider need for endoscopy
47
Q

If a patient has had an upper GI bleed and has a blatchford score of over 6 (meaning they are high risk) what are the next steps?

A
  1. Monitor
  2. If significant bleeding or stigmata the consider IV omeprazole infusion
  3. If known cirrhosis give terlipressin
  4. Consider reversal of coagulopathy
  5. In patient endoscopy
    Discuss with senior team ASAP
48
Q

What is the diagnosit criteria for dyspepsia?

A 
One or more of:
1. Postprandial fullness
2. Early satiety 
3. Epigastric pain
4. Epigastric burning 
AND
5. No evidence of structural disease that is likely to explain the symptoms
49
Q

What are the three main organic causes for dyspepsia?

A
  1. Peptic ulcer disease
  2. Drugs (NSAIDs, COX2 Inhibitors)
  3. Gastric cancer
    These make up around 25% of dyspepsia. The remaining 75% of cases are functional.
50
Q

What is the difference in symptoms between dyspepsia and GORD?

A

Heartburn and reflux more common in GORD

51
Q

What would red flag symptoms be in someone presenting with a history of dyspepsia?

A 
Dysphagia
Evidence of GI blood loss (eg anaemia)
Persistent vomiting
Weight loss
Upper abdominal mass 
(If any of these are present then refer to gastroenterologist)
52
Q

What are the first line treatment for dyspepsia?

A
  1. Lifestyle factors (eg obesity)
  2. PPI/H2 receptor antagonist
  3. If persistent then H pylori test and treat if positive
  4. If it is still persistent after eradication and the patient is younger than 55 then consider referral.
53
Q

What are the two main causes of peptic ulcer disease?

A
  1. H Pylori (90% of duodenal ulcers and 60% of gastric ulcers)
  2. NSAIDS
54
Q

Describe the structure of the H Pylori bacteria

A

Gram negative, microareophillic, flagellated bacteria

55
Q

When do people become infected with H pylori?

A

Acquired in infancy through oral - oral or faecal oral spread. The consequences of the infection do not become apparant until later in life.

56
Q

What are the risks of H pylori?

A 
Peptic ulcer disease (20 - 40%)
Gastric cancer (1%)
57
Q

What types of gastric cancer are associated with H pylori?

A

Gastric adenocarcinoma

Low grade B cell gastric lymphoma (MALT)

58
Q

Does H pylori increase of decrease the pH of its microenvironment?

A

Increases (less acidic)

59
Q

How do you treat peptic ulcer disease?

A
  1. Everyone should be on a PPI
  2. Everyone should be tested for H Pylori
    If +ve then eradicate and confirm.
  3. Withdraw NSAIDS
  4. Lifestyle
  5. Rarely surgery
60
Q

What are the main complications that can arise with peptic ulcers?

A

Anaemia
Bleeding
Perforation
Gastric outlet/Duodenal obstruction leading to a fibrotic scar

61
Q

What follow up is required after treatment of a duodenal ulcer?

A

No follow up required unless ongoing symptoms

62
Q

What follow up is required after treatment of a gastric ulcer?

A

Follow up endoscopy at 6 - 8 weeks to ensure healing and no malignancy

63
Q

Severe epigastric pain radiating to the back during/after a meal is characteristic of what?

A

Gastric ulcer. This is because gastric acid production is increased in response to food and hence then ulcer is aggravated.

64
Q

Severe epigastric pain radiating to the back before a meal that is relieved by eating is characteristic of what?

A

Duodenal ulcer. Eating closes the pyloric sphincter and therefore there is no acid reaching the duodenum.

65
Q

What type of cancer does achalasia increase the risk of?

A

Sqaumous cell cancer of the oesophagus

66
Q

What are the symptoms of systemic sclerosis?

A 
CREST syndrome
Calcinosis 
Raynauds phenomenum
Esophageal dysmotility 
Sclerodactyly 
Telangactasia
67
Q

What are the symptoms of a pharyngeal pouch?

A

Episodic dysphagia and haliotosis with occasional regurgitation

68
Q

What is plummer vinson syndrome?

A

A rare disease that consists of

  1. Dysphagia
  2. Iron deficient anaemia
  3. Glossitis
  4. Cheilosis
  5. Oesophageal web
69
Q

What is atrophic gastritis?

A

A process of chronic inflammation of the stomach mucosa that lea to the loss of gastric glandular cells and their eventual replacement with intestinal and fibrous tissue. This leads to impaired secretion of hydrochloric acid, pepsin and intrinsic factor which can result in problems with digestion and cause megalosblastic anaemia (lack of B12) and iron deficiency

70
Q

What are the causes of atrophic gastritis?

A
  • Autoimmune
    Anti parietal and anti intrinsic factor antibodies (causes pernicious anaemia)
  • H Pylori
  • Chemical eg due to NSAIDS, alcohol or bile reflux
71
Q

What does chronic gastritis increase the risk of?

A

Gastric Adenocarcinoma

72
Q

What conditions increase your risk of developing gastric adenocarcinoma?

A

Pernicious anaemia

Hederitary nonopolyposis colorectal cancer/Lynch syndrome

73
Q

What is Hederitary nonopolyposis colorectal cancer/Lynch syndrome ?

A

An autosomal dominant genetic condition that has a high risk of colon cancer (80% risk), endometrial cancer (80% risk), ovarian cancer, gastric cancer. The increased risk is due to the inheritance of mutations that impair DNA mismatch repair mechanisms.

General Surgery (10 decks)

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