Dyspepsia Flashcards

1
Q

Red flag symptoms in context of dyspepsia

- ALARMS 55

A
Anaemia (Fe2+)
Loss of weight
Anorexia
Recent onset, progressive
Melaena/haematemesis
Swalllow difficulty 
55 years +

Also…

  • Epigastric mass
  • Persistent vomiting
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2
Q

Causes of dyspepsia.

a) most common
b) other causes

A

a) Functional (non-ulcer) dyspepsia, GORD

b) PUD, oesophagitis, oesopageal/stomach Ca

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3
Q

Common associated symptoms

A
Epigastric discomfort
Fullness or bloating
Excessive flatus
Nausea
Fatty food intolerance
Reflux/heartburn (note: this is NOT dyspepsia)
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4
Q

Investigations for dyspepsia

A
  • Bloods: FBC, CRP/ESR
  • H. Pylori test (carbon-13 urea breath test, stool antigen test or PPI trial for 1 month)
  • OGD if red flags/resistant to treatment
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5
Q

Peptic ulcer disease.

a) Risk factors (big 2 and some others)
b) Clinical features - gastric vs duodenal
c) Investigations
d) Complications

A

a) H. pylori, NSAIDs/aspirin;
- Smoking, alcohol, stress, steroids (if on NSAIDs also)
- Zollinger-Ellison syndrome: causes gastrin-secreting tumours (gastrinomas) that result in PUD

b) Epigastric pain, usually 1 to 3 hours postprandial (though duodenal ulcers may improve on eating), pain may radiate to the back if posterior, often relieved by antacids;
nausea, bloating, oral flatulence, intolerance of fatty foods (also occurs in gallstones),

c) - Bloods: FBC
- H. pylori testing: C-13 urea breath test or trial PPI for 1 month - if either test is positive, commence Rx.
- if warning signs - upper GI endoscopy

d) - Erosions may cause haemorrhage/ acute UGIB (classically erode into gastroduodenal artery)
- Perforation and acute abdomen

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6
Q

Management of PUD

a) General measures
b) H. Pylori -positive
c) NSAID-positive
d) H. pylori and NSAID-negative

A

a) Smoking cessation, limit alcohol, take NSAIDs/aspirin and other medications with food or avoid if possible

b) Triple eradication therapy (once H. pylori confirmed by breath test or one-month trial PPI):
- PPI + amoxicillin + clarithromycin/metronidazole (7 - 14 days)
- If they had an ulcer, repeat endoscopy at 6-8 weeks to see if resolution (if just dyspepsia, no need for review unless symptomatic)

c) - Stop NSAID
- 2 months of PPI
- Gastroscopy at 2 months to see resolution of ulcer

d) - Take detailed history and examine for other causes (e.g. Zollinger-Ellison syndrome)

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7
Q

GORD.

a) Risk factors (via 3 main mechanisms)
b) Clinical features (main 1 and others, including atypical)
c) vs. PUD
d) Investigations
e) Management

A

a) - Increased intra-abdominal pressure: Pregnancy.
Obesity. Tight clothes. Big meals. Hiatus hernia.
- Relaxed lower oesophageal sphincter: surgery in achalasia, systemic sclerosis, smoking, drugs (TCAs, anticholinergics, nitrates and CCBs).
- Direct mucosal damage: NSAIDs, potassium salts, bisphosphonates, alcohol

b) - Heartburn: burning feeling, rising from the stomach towards the neck, related to meals, lying down, stooping and straining. It is relieved by antacids
- Retrosternal discomfort, acid brash - regurgitation of acid or bile.
- Water brash - this is excessive salivation.
- Odynophagia/dysphagia - related to stricture secondary to reflux-associated inflammation
- Atypical: non-cardiac chest pain, cough, hoarseness, wheeze

c) Heartburn (burning retrosternal pain) vs. dyspepsia (epigastric pain or discomfort)

d) Bloods: FBC
- Imaging: CXR (hiatus hernia), barium swallow
- Upper GI endoscopy
- Special tests: oesophageal pH monitoring

e) - Conservative: weight loss, smoking cessation, reduce alcohol, raise head of bed, smaller and more frequent meals, avoid drugs that relax LOS/damage mucosa
- Medical: PPI
-

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8
Q

Acute upper GI bleed (UGIB): causes

- main 2 + others

A

Main 2: PUD, oesophageal varices;

Others:

  • Gastritis, oesophagitis,
  • Mallory-Weiss tear, Boerhaave syndrome,
  • malignancy,
  • vascular malformation
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9
Q

Presentation of acute UGIB:

- five ways in which bleeding may present

A
  • Asymptomatic: found incidentally (low Hb)
  • Haematemesis: bright-red, implies active haemorrhage.
  • Coffee-ground vomit: bleeding that has ceased or has been relatively modest.
  • Melaena: black tarry stools, usually due to acute UGIB but occasionally bleeding from the small bowel or right side of the colon.
  • Haemodynamic collapse: shock, syncope, coma
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10
Q

Acute UGIB: management

a) Assessment
b) Investigations
c) Who to admit?
d) Do what assessment of mortality?
e) Initial management
f) Variceal bleeding
g) Non-variceal bleeding

A

a) - A-E: signs of blood loss (anaemia, pallor), dehydration and shock (low BP, raised HR, low urine output, prolonged CRT, confusion, reduced GCS),
- Stigmata of disease (e.g. liver disease, malignancy)

b) - Bloods: FBC (anaemia, platelets), LFTs, UEs (urea raised in UGIB), creatinine, clotting, group/save and cross-match units
- CXR (perforation)
- UGI endoscopy (gold standard)

c) Anyone >60, witnessed haematemesis, haemodynamic instability or known liver disease/varices

d) - Rockall score (eg. age, shock, comorbidities, diagnosis)
- Glasgow-Blatchford Score (eg. Hb, urea, HR, SBP, syncope, melaena, heart failure, liver disease)

f) - Terlipressin
- Band ligation

g) - OGD + mechanical clips +/- adrenaline
- PPI
- If unresponsive to medical/surgical management, insert a Sengstaken–Blakemore tube for tamponade of bleed

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11
Q

Oesophageal spasm.

a) Clinical features
b) Investigations
c) Management

A

a) Spasms of cardiac-like chest/epigastric pain (can be misdiagnosed as angina), dysphagia, reflux

b) - UGI endoscopy
- ECG / angiography to rule out cardiac cause
- Oesophageal manometry (gold-standard)
- Barium swallow - corkscrew appearance

c) Lack of evidence: can try medications to relax oesophageal tone (e.g. CCBs, nitrates), botulinum toxin, surgery (e.g. myotomy - used for achalasia)

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