GI presenting symptoms Flashcards

1
Q

The mouth - leukoplakia

A

An oral mucosa white patch that will not rub off and is not attributable to any other known disease. It is a pre-malignant lesion with a transformation rate that ranges from 0.6% to 18%.

Oral hair leukoplakia is a shaggy white patch on the side of the tongue seen in HIV and caused by EBV.

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2
Q

The mouth - apthous ulcers

A

20% will get these shallow painful ulcers in the mouth that will heal without scarring.

  • Causes – Crohns or coeliac disease, Behcet’s disease, trauma, erythema multiforme, lichen planus, pemphigus, pemphigoid or infections e.g. herpes simplex, syphilis or Vincent’s angina.
  • Management of minor ulcers – avoid oral trauma e.g. hard toothbrushes or foods such as toast and acidic food and drinks. Hydrocortisone lozenges or antimicrobial mouthwashes may help.
  • Management of severe ulcers – give systemic steroids e.g. 30-60mg oral Prednisolone for a week. Perform a biopsy on any ulcer that fails to heal within 3 weeks to exclude malignancy.
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3
Q

The mouth - candidiasis

A
  • Causes white patches or erythema of the buccal mucosa. Patches may be hard to remove and bleed when scraped.
  • Risk factors – extremes of age, diabetes mellitus, antibiotics or immunosuppression e.g. long term corticosteroids (including inhalers), cytotoxics, malignancy or HIV.
  • Management – give 100,000U Nystatin suspension (swill and swallow) or amphotericin lozenges.
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4
Q

The mouth - chelitis

A

Angular stomatitis – fissuring of the corners of the mouth can have many causes including problems with dentures, candidiasis or a deficiency of either iron or riboflavin (aka vitamin B2).

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5
Q

The mouth - gingivitis

A

Gum inflammation ± hypertrophy occurs with poor oral hygiene, drugs (phenytoin, ciclosporin, nifedipine), pregnancy, vitamin C deficiency, acute myeloid leukaemia or Vincent’s angina.

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6
Q

The mouth - microstomia

A

The mouth is too small - from thickening and tightening of the perioral skin (after burns or in epidermolysis bullosa – destructive skin and mucous membrane blisters) or systemic sclerosis.

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7
Q

The mouth - oral pigmentation

A
  • Brown – perioral brown spots characterise Peutz-Jegher’s and pigmentation anywhere in the mouth suggests Addison’s disease, drugs e.g. anti-malarials and consider malignant melanoma.
  • Telangiectasia – capillary dilation occurs in systemic sclerosis or Osler-Weber-Rendu syndrome.
  • Fordyce glands – creamy yellow spots at the border of the oral mucosa and the lip vermilion (the upper border of the lips). These are sebaceous cysts which are common and benign.
  • Black tongue – colonisation of Aspergillus niger may cause a black tongue.
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8
Q

The teeth

A

A blue line at the border of the teeth and the gums may suggest lead poisoning and yellow brown discolouration of the teeth may be caused by childhood tetracycline (antibiotic) exposure.

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9
Q

The tongue

A
  • Xerostomia – a dry, furred tongue can occur in dehydration, after tetracycline or radiotherapy, in Crohn’s disease, Sjogren’s syndrome or Mikulicz’s syndrome (parotid gland enlargement).
  • Glossitis – a smooth, red, sore tongue can be caused by iron, folate or vitamin B12 deficiency.
  • Macroglossia – the tongue is too big – caused by myxoedema, acromegaly or amyloidosis.
  • A Ranula is a bluish salivary retention cyst on one side of the frenulum (named after frog throat).
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10
Q

Tongue malignancy

A
  • Typically appears on the edge of the tongue as a raised ulcer with firm edges and environs. The main risk factors for development are smoking and alcohol.
  • Spread – anterior third to the submental nodes, middle third to the submandibular nodes and posterior third to the deep cervical nodes.
  • Management – radiotherapy or surgery – 5 year survival is 80%.
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11
Q

Dysphagia - causes

A

Can be divided into mechanical and motility causes:

  • Mechanical block – malignant stricture (oesophageal, gastric or pharyngeal), benign stricture (oesophageal web or peptic stricture), extrinsic pressure (lung malignancy, mediastinal lymph nodes, retrosternal goitre, aortic aneurysm or left atrial enlargement) or a pharyngeal pouch.
  • Motility – achalasia, diffuse oesophageal spasm, systemic sclerosis, myasthenia gravis, bulbar palsy, pseudobulbar palsy, syringobulbia, bulbar poliomyelitis or Chagas’ disease.
  • Other – oesophagitis (infection – candida or HSV of reflux oesophagitis) or globus hystericus.
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12
Q

Dysphagia - questions to ask

A
  • Was there difficulty swallowing solids and liquids from the start? – if yes then suspect a motility disorder or a pharyngeal cause. If no suspect a stricture either benign or malignant.
  • Is it difficult to make the swallowing movement? – if yes then suspect a bulbar palsy.
  • Is swallowing painful (odynophagia)? – if yes suspect malignancy, oesophageal ulcer or spasm.
  • Is the dysphagia intermittent or constant and getting worse? – if it is intermittent suspect an oesophageal spasm but if constant and worsening suspect a malignant stricture.
  • Does the neck bulge or gurgle on drinking? – if yes suspect a pharyngeal pouch.
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13
Q

Dysphagia - signs

A

Is the patient cachectic or anaemic? Examine the mouth and feel the supra-clavicular nodes (Virchow’s node enlargement suggests intra-abdominal malignancy) and signs of systemic disease e.g. systemic sclerosis or central nervous system disease.

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14
Q

Dysphagia - investigations

A

FBC for anaemia, U+Es for dehydration and CXR for mediastinal fluid level, absent gastric bubble or aspiration.

Upper GI endoscopy ± biopsy is usually first line investigation but a barium follow through ± video fluoroscopy is useful to diagnose high dysphagia or dysmotility e.g. achalasia.

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15
Q

Diffuse oesophageal spasm

A

Causes intermittent dysphagia and chest pain.

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16
Q

Achalasia

A

The lower oesophageal sphincter fails to relax (due to degeneration of the myenteric plexus) and causes dysphagia, regurgitation, substernal cramps and weight loss.

  • Investigations - the barium swallow will show a dilated, tapering oesophagus.
  • Management – endoscopic balloon dilation then proton pump inhibitors. Botulinum toxin injection can be used for patients unsuitable for an invasive procedure.
  • Prognosis – long term achalasia is a risk factor for developing oesophageal malignancy.
17
Q

Benign oesophageal stricture

A

Can be caused by gastro-oesophageal reflux disease, corrosives, surgery or radiotherapy.

Treatment is also with endoscopic balloon dilation.

18
Q

Oesophageal malignancy

A

Associated with men, gastro-oesophageal reflux, tobacco, Barrett’s oesophagus, achalasia or Paterson-Brown-Kelly (aka Plummer-Vinson) syndrome (a triad of post-cricoid dysphagia, an upper oesophageal web and iron deficiency).

19
Q

Dyspepsia - Definition and Symptoms

A
  • Definition – a non-specific group of symptoms related to the upper gastrointestinal tract.
  • Non-specific symptoms – epigastric pain e.g. related to hunger, eating specific foods or time of day and may be associated with bloating and fullness after meals or heartburn.
  • Alarm symptoms – anaemia, weight loss, anorexia, recent onset, progressive symptoms, malaena or haematemesis or dysphagia.
20
Q

Dyspepsia - Causes

A

Duodenal or gastric ulceration, oesophagitis or gastro-oesophageal reflux disease, gastritis, duodenitis, non-ulcer dyspepsia or gastric malignancy.

21
Q

Dyspepsia - Management

A
  • If patient is >55 years or has alarm features listed above – perform an upper GI endoscopy.
  • If not advise the patient on lifestyle changes and try over the counter antacids e.g. magnesium trisilicate for 4 weeks. If there is no improvement test the patient for H. pylori:
  • If positive – eradicate with e.g. PAC500 regime (PPI, amoxicillin and clarithromycin 500mg BD) or PMC 250 (PPI, metronidazole and clarithromycin 250mg BD) for 7 days.
  • If negative – 20mg Omeprozole OD or 150mg Ranitidine BD (H2 blocker) for 4 weeks.
  • Consider upper GI endoscopy if H. pylori is not eradicated or symptoms persist with treatment.
22
Q

Duodenal Ulcers - Risk Factors

A

These are 4 times more common than gastric ulcers.

  • Major risk factors include H. pylori and drugs e.g. aspirin, NSAIDs and steroids.
  • Minor risk factors include increased gastric acid secretion, increased gastric emptying, blood group O and smoking (the role of stress is controversial).
23
Q

Duodenal Ulcer - Features and Diagnosis

A
  • Clinical features – epigastric pain typically before meals or at night and relieved by eating or drinking milk. 50% are asymptomatic but others experience recurrent episodes of pain.
  • Diagnosis – upper GI endoscopy (stop PPI 2 weeks before procedure), test for H. pylori infection and measure gastrin when not taking PPIs if you suspect Zollinger-Ellison syndrome.
24
Q

Gastric Ulcers

A

Occur mainly in the elderly and risk factors include H. pylori infection, smoking, NSAIDs, reflux of duodenal contents, delayed gastric emptying, stress e.g. neurosurgery or burns.

  • Symptoms – can be asymptomatic or cause epigastric pain related to meals ± weight loss.
  • Investigations – upper GI endoscopy to exclude malignancy (stop PPI 2 weeks before procedure) and take multiple biopsies from the rim and base and brushings for cytology.
25
Q

Ulcers - Management

A
  • Lifestyle advice – avoid food that worsens symptoms and stop smoking (as it delays healing).
  • H. Pylori eradication – triple therapy regimes are 80-85% effective at eradication.
  • Drugs to reduce acidPPIs are the most effective e.g. 30mg Lansoprazole OD PO for 4 weeks for duodenal ulcers and 8 weeks for gastric ulcers. H2 receptor antagonists may have a place for individual responders – 300mg Ranitidine PO each night for 8 weeks.
  • NSAID associated ulcers – stop NSAIDs if possible and give PPIs for treatment and prevention.
26
Q

Ulcers - Complications

A

Bleeding, perforation, transformation into malignancy and decreased gastric outflow.

27
Q

Functional (non-ulcer) dyspepsia

A

Treatment is difficult and often unsatisfactory. H. pylori eradication may be beneficial but long term effects are unknown. There is limited supporting evidence for the use of PPIs or psychological therapy

28
Q

GORD - Definition

A

A condition which develops when the reflux of stomach contents causes troublesome symptoms – >2 episodes of heartburn per week and/or complications.

Dysfunction of the lower oesophageal sphincter predisposes to the gastro-oesophageal reflux of acid. If reflux is prolonged or excessive it may cause oesophagitis, benign oesophageal stricture or Barrett’s oesophagus.

29
Q

GORD - Predisposing Factors

A

Smoking, alcohol, obesity, pregnancy or drugs (TCAs, anticholinergics or nitrates).

Hiatus hernia, lower oesophageal sphincter hypotension, loss of oesophageal peristaltic function, gastric acid hypersecretion, delayed gastric emptying, surgery in achalasia, systemic sclerosis or Helicobacter pylori.

30
Q

GORD - Los Angeles Classification

A
  • Grade 1 – more than 1 mucosal break <5mm long not extending beyond 2 mucosal fold tops.
  • Grade 2 – a mucosal break >5mm long but limited to the space between 2 mucosal fold tops.
  • Grade 3 – a long mucosal break which involves <75% of the oesophageal circumference.
  • Grade 4 – a long mucosal break that involves >75% of the oesophageal circumference.
31
Q

GORD - Symptoms

A
  • Oesophageal – heartburn (burning, retrosternal discomfort related to meals, lying down, stooping or straining and relived by antiacids), belching, acid brash (acid or bile regurgitation), waterbrash (excessive salivation) and odynophagia (painful swallowing from oesophagitis).
  • Extra-oesophageal – nocturnal asthma, chronic cough, laryngitis (throat clearing) and sinusitis.
32
Q

GORD - Complications

A

Oesophagitis, ulcers, benign strictures, Barrett’s oesophagus (transformation of the distal oesophagus from squamous to columnar epithelium) and oesophageal adenocarcinoma.

33
Q

GORD - Investigations

A

Isolated symptoms do not require investigation but perform upper GI endoscopy if patient >55 years, symptoms >4 weeks, dysphagia, persistent symptoms despite treatment, relapsing symptoms or weight loss.

A barium swallow may show a hiatus hernia and 24 hour oesophageal pH monitoring ± manometry can help to diagnose GORD when endoscopy is normal.

34
Q

GORD - Conservative Management

A

Encourage weight loss, smoking cessation, raise the bed head and have small, regular meals.

Avoid hot drinks, alcohol, citrus fruits, tomatoes, onions, carbonated drinks, spicy food, coffee, tea, chocolate and eating <3 hours before going to bed.

Avoid drugs affecting oesophageal motility (nitrates, anticholinergics, tricyclic antidepressants or calcium channel blockers) or that damage the mucosa (NSAIDs, K+ salts or bisphosphonates).

35
Q

GORD - Medical and Surgical Management

A
  • Medical – give antacids e.g. 10mL Magnesium trisilicate mixture TDS or alginates e.g. 10-20mL Gaviscon advance TDS to relieve symptoms. For oesophagitis give 30mg Lansoprazole OD/BD.
  • Surgical – a Nissen’s fundoplication is indicated if symptoms are severe, refractory to medical therapy and there is severe reflux confirmed by pH monitoring. Atypical symptoms e.g. cough or laryngitis are less likely to improve following surgery than typical symptoms.
36
Q

Hiatus Hernia - Types

A

Are common affecting 30% of patients over 30 years and 50% have symptomatic GORD.

80% are sliding where the gastro-oesophageal junction slides into the chest (through diaphragm) causing lower oesophageal sphincter to become less competent.

20% are rolling where the junction remains in the abdomen but a section of the stomach herniates into the chest next to the oesophagus.

37
Q

Hiatus Hernia - Imaging

A

Barium swallow is the best diagnostic test.

Upper GI endoscopy can visualise the mucosa and diagnose oesophagitis but cannot reliably exclude a hiatus hernia.

38
Q

Hiatus Hernia - Management

A

Lose weight, stop smoking, eat smaller meals earlier in the evening, raise the head of the bed and treat the symptoms of reflux – with antacids, H2 receptor antagonists, proton pump inhibitors or alginate preparations (form a raft on top of the stomach).

Indications for surgery are intractable symptoms despite aggressive medical therapy or complications e.g. ulceration, bleeding or stricture formation. However it is also advised to electively repair a rolling hiatus hernia prophylactically as it may strangulate which would be an emergency.