GI presenting symptoms Flashcards
(38 cards)
The mouth - leukoplakia
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.
The mouth - apthous ulcers
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.
The mouth - candidiasis
- 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.
The mouth - chelitis
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).
The mouth - gingivitis
Gum inflammation ± hypertrophy occurs with poor oral hygiene, drugs (phenytoin, ciclosporin, nifedipine), pregnancy, vitamin C deficiency, acute myeloid leukaemia or Vincent’s angina.
The mouth - microstomia
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.
The mouth - oral pigmentation
- 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.
The teeth
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.
The tongue
- 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).
Tongue malignancy
- 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%.
Dysphagia - causes
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.
Dysphagia - questions to ask
- 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.
Dysphagia - signs
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.
Dysphagia - investigations
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.
Diffuse oesophageal spasm
Causes intermittent dysphagia and chest pain.
Achalasia
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.
Benign oesophageal stricture
Can be caused by gastro-oesophageal reflux disease, corrosives, surgery or radiotherapy.
Treatment is also with endoscopic balloon dilation.
Oesophageal malignancy
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).
Dyspepsia - Definition and Symptoms
- 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.
Dyspepsia - Causes
Duodenal or gastric ulceration, oesophagitis or gastro-oesophageal reflux disease, gastritis, duodenitis, non-ulcer dyspepsia or gastric malignancy.
Dyspepsia - Management
- 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.
Duodenal Ulcers - Risk Factors
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).
Duodenal Ulcer - Features and Diagnosis
- 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.
Gastric Ulcers
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.
