Upper GI Diseases Flashcards

1
Q

What catagories (+ examples) of pathology can cause Dysphagia?

A
  1. Neuromuscular: - mainly affects 1st and/or 2nd phase of swallowing
    • Muscular - e.g. muscular dystrophy, myasthenia gravis, weakened muscles / impaired coordination (elderly)
    • Neurological - e.g. stroke, Parkinson’s, multiple sclerosis
  2. Narrowing of Oesophagus: - mainly affects the 3rd phase of swallowing
    • Cancers e.g. oropharyngeal cancer, oesophageal cancer, mediastinal masses
    • GORD - scars from stomach acid cause stricture
    • Schatzki rings - thickenings of mucosa or muscle
      • A-ring = above squamocolumnar junction (oesophagus/stomach junction)
      • B-ring = found at the squamocolumnar junction
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2
Q

What are some common complications of Dysphagia?

A
  1. Choking
  2. Pulmonary aspiration –> subsequent aspiration pneumonia
  3. Malnutrition - either due to ↓ consumption or vomiting of consumed food
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3
Q

Is Barrett’s oesophagus?:

  1. Neoplasia
  2. Premalignant
  3. Dysplasia
  4. Malignant
  5. Metaplasia
A

2 + 5 (premalignant + metaplasia)

  • Barrett’s ↑ risk of oesophageal cancer by ~ 50 times (risk of cancer is still relatively low i.e. 3 per 1000 - this is higher is dysplasia is present)
  • Metaplasia = cellular adaptation to a stimulus which causes change from one mature cell type to another
    • E.g. Barrett’s - stratified squamous epithelium (oesophageal) –> simple columnar epithelium (stomach)
  • Dysplasia = replacement a mature cell type with a less mature cell type + loss of cell uniformity and tissue organisation (varying severities)
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4
Q

Define Barrett’s Oesophagus?

A

Define:

  • Pre-malignant condition which involves, asymptomatic replacement of normal squamous epithelium of the oesophagus by metaplastic columnar epithelium, clearly visible endoscopically >1cm above gastro-oesophageal junction and confirmed histo-pathologically from biopsies
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5
Q

What course of progression does Barrett’s follow?

A

Oesophagitis –> metaplasia –> dysplasia –> adenocarcinoma (most likely form of cancer)

  • Progression from Barrett’s (metaplasia) to adenocarcinoma occurs in 1-2% of cases over 25-30 years of having Barrett’s
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6
Q

What are some risk factors for Barrett’s?

A
  1. GORD - 5-10% of GORD pts develop Barrett’s
  2. Men > women
  3. Caucasian
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7
Q

What 2 things are protective of the progression from Barrett’s to Oesophageal cancer?

A
  1. NSAIDs
  2. Helicobacter Pylori
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8
Q

Patient presents with dysphagia, anorexia, vomiting, weight loss + Hx of GORD, smoking + alcohol excess.

What are they at risk of?

A

Oesophageal Cancer

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9
Q

Patient presents with dysphagia, odynophagia (painful swallowing) + Hx of heartburn.

No weight loss + appears systemically well.

What are they at risk of?

A

Oesophagitis

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10
Q

Patient presents with dysphagia, systemically unwell and Hx of steroid inhalers + HIV.

What are they at risk of?

A

Oesophageal Candidiasis

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11
Q

Barrett’s Oesophagus is classified based on length of affected segment. What are the classifications?

A
  • Short segment = < 3cm
  • Long segment = > 3cm
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12
Q

What investigations might you do in a patient you suspect of having Barrett’s Oesophagus?

A
  1. Endoscopy (specifically OGD) + histological biopsy
    • Histological confirmation of endoscopically visible columnarisation/metaplasia of oesophagus = gold standard diagnosis
    • Histological confirmation is via prescence of goblet cells in oesophageal epithelium biopsy - this is termed intestinal metaplasia (turning into intestine like)
  2. Endoscopic ultrasound:
    • If high-grade dysplasia / cancer found on surveillance endoscopy –> endoscopic ultrasound needed to evaluate resectability
  3. Surveillance endoscopies:
    • Involves repeat endoscopies - duration of gap depends on grade of dysplasia, length of affected oesophagus etc.
  4. FBC:
    • ↑ WCC - indicates inflammatory cause
    • ↓ Hb - anaemia, could be due to lack of nutrition (deficiencies) or bleeding
  5. CXR:
    • Can identify other oesophageal pathology e.g. mediastinal masses causing dysphagia
  6. ECG:
    • To eliminate cardiac arrhythmias as cause of chest pain
  7. U+Es:
    • Confirm good renal function in case contrast CT is needed
  8. LFTs:
    • Deranged LFTs could imply liver metastases if cancer is a concern
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13
Q

Patient presents with dysphagia of both solids + liquids, heartburn, feels like they are coughing food and sometimes describe it as going down the wrong pipe.

What are they likely to have?

A

Achalasia

  • Achalasia = failure of oseophageal peristalsis + failure of relaxation of lower oesophageal sphincter (LOS) i.e. LOS contracted + dilated oesophagus
  • Aetiology: degenerative loss of ganglia from Auerbach’s plexus
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14
Q

Patient presents with a long history of dysphagia which has been remained the same (non-progressive), burning chest pain, coughing, not systemtically unwell.

What are they likely to have?

A

Peptic Stricture (also called Oesophageal Stricture)

  • Account for the majority of benign oesophageal strictures
  • Caused by exposure to stomach acid
  • Endstage results of chronic GORD oesophagitis
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15
Q

Progressive dysphagia of solids but not liquids is suggestive of what kind of oesophageal issue?

A

Mechanical obstruction or stricture

  • Dysphagia of liquids is suggestive of neurological, muscular or achalasia
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16
Q

What is an OGD?

A

Oesophago-gastro-duodenoscopy

17
Q

What are the guidelines on referring patients suspected of Oesophageal cancer?

A

Offer URGENT direct access upper gastrointestinal endoscopy (to be performed within 2 weeks) to assess for oesophageal cancer in people:

  1. With dysphagia OR
  2. aged ≥ 55 with weight loss + any of the following:
    • Upper abdominal pain
    • Reflux
    • Dyspepsia (indigestion)

Other situations to consider non-urgent direct access upper gastrointestinal endoscopy:

  • Haematemesis
  • ≥ 55 with:
    • Treatment‑resistant dyspepsia
    • Upper abdo pain + ↓ Hb levels
    • ↑ platelet count with any of the following:
      • nausea
      • vomiting
      • weight loss
      • reflux
      • dyspepsia
      • upper abdo pain
    • nausea or vomiting with any of the following:
      • weight loss
      • reflux
      • dyspepsia
      • upper abdo pain
18
Q

When gaining consent from a patient for a procedure, what points need to be covered?

A
  1. Explain purpose of the procedure:
    • What does /might it involve?
    • E.g. endoscopy - involves putting a tube with a camera on it down your throat so we can have a look at the tube (oesophagus) leading to your stomach for any abnormalities. If we find something abnormal, a biopsy (that’s a small sample) might be taken for the lab to examine.
  2. Advise on risks of the procedure:
    • E.g. endoscopy - it does involve some risks, some of which are common, such as some post-op pain or bleeding, and some are rarer and can be more serious, such a perforation. Generally, the benefits largely outweigh the risks associated and this will help provide both us and you with a better idea of what’s going on.
  3. Advise on alternatives if pt is not happy
  4. Advise about pre-procedure things to do and not to do:
    • What to bring? - might want a friend/family due to anaesthesia
    • Medication - take most of your medication as normal, but any anti-coagulants need to stop beforehand
  5. Assess capacity
  6. Direct to NHS choices website for more info + offer for a superior to come have a more detailed chat about the procedure
19
Q

The majority of Oesophageal cancers are what 2 types?

A

Squamous cell carcinoma (SCC) or adenocarcinoma (ACA)

20
Q

What are the 3 most common features of un-perforated peptic ulcers?

Which is more common duodenal or gastric ulcers?

How does pain often differentiate duodenal vs gastric ulcers?

A

Features:

  1. Epigastric pain - made better (duodenal) or worse (gastric) by eating, relieved by antacids, can occur at night
  2. Nausea
  3. Hx of NSAID or alcohol use

Commonality: duodenal > gastric

Pain:

  • Duodenal = relieved by eating, pain on empty stomach
  • Gastric = worse when eating

Other symptoms of peptic ulcers:

  • Dyspepsia (indigestion)
  • Heartburn
  • Vomiting
  • Loss of appetite
  • Weight loss

NB Peptic ulcer = just class of ulcer, gastric and duodenal are more specific

21
Q

Which organism is associated with peptic ulcer disease?

A

Helicobacter pylori

22
Q

What does ‘triple therapy’ for H.pylori eradication in peptic ulcers?

A

7-day course of:

  1. PPI (e.g. omeprazole, lansoprazole or esomeprazole)
    • H2-receptor antagonist if PPI not tolerated
  2. Clarithryomycin
  3. Amoxicillin or metronidazole
23
Q

What are the 3 methods for testing for H.pylori infection?

A
  1. Urea breath test
  2. Stool antigen test
  3. Blood test for antibodies (less commonly used)
24
Q

What are some risk factors for developing peptic ulcer disease? (6)

A
  1. NSAIDs
  2. Smoking
  3. Alcohol excess
  4. FHx of peptic ulcers
  5. Physical stress e.g. major trauma or surgery or ICU admission ‘stress ulcer’
  6. Hypersecretory syndromes e.g. Zollinger-Ellison syndrome
25
Q

What is Zollinger-Ellison Syndrome?

A

Define:

  • High levels of gastrin - often from gastrin secreting tumour of duodenum or pancreas
  • ~30% occur as part of MEN type 1 (multiple endocrine neoplasia)

Features:

  • Multiple gastroduodenal ulcers
  • Diarrhoea
  • Malabsorption

Diagnosis:

  • Fasting gastrin levels (single best screen test) - will be high despite fasting
  • Secretin stimulation test
    • Secretin normally inhibits gastrin release from G-cells - but gastrinoma cell secrete gastrin in response to secretin
26
Q

What are the 3 main complications of peptic ulcers?

A
  1. Internal bleeding
    • ​​Most commonly low volume bleeds - thus presents as iron-deficient anaemia
    • Erosion of a significant vessel can cause: haematemesis ‘coffee-grounds’ or malaena - either of which can present with or without hypovolemic shock
  2. Perforation
    • ​​More common in the duodenum
    • Causes peritonitis and pneumoperitoneum
  3. Gastric outlet obstruction
    • ​​Epigastric pain
    • Postprandial vomiting (after meals)
    • Normally due to pancreatic cancer or primary gastric cancer
27
Q

Which 2 scoring systems can be used in cases of upper GI bleeding?

A
  1. Glasgow-Blatchford Bleeding Score (GBS)
    • Risk stratification of patients with upper GI bleeding
    • Doesn’t require OGD to calculate risk - thus can be used prior to sending for endoscopy
    • GBS score > 0 suggests ‘High-risk’ –> likely to require medical intervention and thus can’t be managed as outpatient
  2. Rockall score (RS)
    • Risk stratification of patients with upper GI bleed + completed endoscopy
    • Requires OGD to calculate risk - use after endoscopy
    • Rockall score < 3 carries good prognosis
28
Q

Which of the following medications are linked with the formation of peptic ulcers or GI bleeds?

  • Potassium channel activators e.g. Nicorandil
  • Corticosteroids
  • Antiplatelets
  • NSAIDs
  • Anticoagulants
  • SSRIs
A

ALL of them

  • Nicorandil (K+ channel activator) = associated with risk of GI ulceration, including perianal ulceration
  • Ulcers that result from nicorandil are refractory to treatment, including surgery (they respond only to withdrawal of nicorandil)
29
Q

A proton-pump inhibitor should be given to prevent peptic ulcers in someone taking long-term aspirin or clopidogrel?

  • No
  • Yes
  • Yes - only if high risk for developing peptic ulcer
A

Yes - only if high risk for developing peptic ulcer

Those patients at high risk are those:

  • On high dose aspirin
  • Older patients
  • Hx of peptic ulcer or GI bleed
  • With serious co-morbid conditions e.g CVD, hepatic or renal impairment, diabetes or hypertension)
  • With H. Pylori infection + taking concomitant medications which also increase risk of ulcers or GI bleed (e.g. NSAIDs)
30
Q

Who should be screened for Barrett’s Oesophagus?

A
  1. Pts with chronic / severe GORD (duration >5yrs or at least twice weekly symptoms or symptoms interfering with QoL)
  2. AND at least 3 of:
    1. Age > 50yrs
    2. Male
    3. Caucasian
    4. Obese
    5. Smoking
  3. OR - FHx of Barrett’s oesophagus or oesophageal adenocarcinoma
31
Q

Define Peptic Ulcer

A
  • A break in stomach/duodenum mucosa down to submucosa that is > 5cm in diameter
    • Ulcers smaller < 5cm = erosions
  • Occur due to inbalance of:
    • Factors promoting mucosal damage: gastric acid, pepsin, H.pylori and NSAIDs)
    • Factors promoting gastroduodenal defense (prostaglandins, mucus, bicarbonate, mucosal blood flow)
32
Q

How do you treat a peptic ulcer?

A

Active bleeding ulcer:

  1. 1st line = Endoscopy +/- blood transfusion + PPI
  2. 2nd line = surgery / interventional radiology

H.Pylori positive:

  1. 1st line = H.pylori eradication ‘triple therapy’
  2. 2nd line = Alternative eradication regimen

H.Pylori negative

  1. 1st line = Full dose PPI for 4-8 weeks (if not on NSAIDs)
  2. 2nd line = H2-receptor antagonist
  3. Repeat endoscopy in 6-8 weeks to monitor ulcer