Oesophageal diseases and Vomiting Flashcards
What are the categories of differentials for regurgitation?
Anatomic
Obstruction
Oesophagitis
Motility Disorders
Which are the 3 most common DDx for regurgitation?
Oesophagitis
Foreign Body
Megaoesophagus
What are the clinical signs of regurgitation?
Hypersalivation Odynophagia Anorexia - uncommon Dysphagia Nasal dischage Coughing (aspiration pneumonia)
How can regurgitation be distinguished from vomiting?
Vomiting:
- abdominal effort
- prodromal nausea
- digested food
- no swallowing pain
What is the relationship to eating? i.e. regurgitation is usually within 30 mins of eating
What other elements of history/examination can aid with diagnosis of regurgitation?
Oesophageal palpation
Lung ausculation - aspiration pneumonia
Concurrent disease?
BCS?
What is the next step after regurgitation has been defined as the problem?
Diagnostic Imaging - survey then possibly contrast radiographs
Endoscope if the above don’t help
What are the common causes of mega oesophagus?
Idiopathic megaoesophagus - management
Myasthenia gravis
Thymoma
Hypoadrenocorticism
Why is aspiration pneumonia likely with regurgitation?
Unlike vomiting, regurgitation is not associated with reflex closure of the larynx. Aspiration pneumonia is very serious and can be life threatening.
What are the things that can cause oesophagitis?
Chemical injury (including medication)
Gastrooesophageal reflux - GA, hiatal hernia, persistent vomiting, poorly positioned feeding tubes
Oesophageal FBs
How can oesophagitis be treated?
PPIs
Protectant e.g. sucralfate
Dietary changes - high protein - low fat food.
What is a serious complication of oesophagitis?
Strictures - narrowing/tightening of the oesophagus
Outline procedures for dealing with an oesophageal FB.
Endoscopic removal of push back to stomach.
Consider referral as this is an emergency and if not dealt with within 24hrs then it could lead to stricture of the oesophagus.
Describe the physiology of vomiting.
The chemoreceptor trigger zone in the brainstem can be affected by drugs, toxins, ureamia, infections etc. The vomiting centre in the brainstem can also be affected by the cortex, vagal and sympathetic afferent (e.g. with gastritis).
How can the problem of vomiting be refined?
Is it acute or chronic (chronic = >2-3 weeks)
Is the lesion primary (GI) or secondary (extra-GI)
What are the different primary causes of vomiting.
Dietary - indiscreation, intolerance, hypersensitivity
Infections - parasites, parvovirus
Inflammatory disease - gastritis, IBD, ulceration
Neoplasia
Obstruction - neoplasia, FB, gastric hypertrophy
Motility disorders/gastric volvulus
Which are the most common primary causes of vomiting?
Dietary indiscretion Infection Inflammatory disease Neoplasia FBs
Which of the primary causes of vomiting are most likely when the vomiting is chronic?
Inflammatory disease
Neoplasia
n.b. the others mentioned in the other questions are more likely to be acute.
What are the secondary causes of vomiting?
Uraemia - may see PU/PD Hypoadrenocorticism Hepatic disease Pancreatitis Toxin ingestion (acute vomiting) Drugs
What is the diagnostic approach with vomiting?
Bloodwork and urinanalysis if not clear whether primary or secondary as this will indicate a metabolic problem.
Diagnostic imaging if, after testing, a primary GI problem is suspected.
Endoscopy/biopsies if nothing else suspected
What is the course of treatment for acute vomiting usually?
What if this doesn’t work?
Fasting and symptomatic treatment
If the vomiting becomes chronic then an underlying cause needs to be elicited
What types of drug can be used to treat vomiting (when excess acid production? Briefly say why these can be used.
Anti-histamines and anticholinergics - H2 and M2 receptors on parietal cells. Histamine is produced by mast cells and Acetylcholine is from the vagus.
PPIs - these are the most potent. They prevent H+ secretion from the parietal cells
What is sucralfate?
It is a drug that forms a protective barrier in the stomach and oesophagus. It is formed from aluminium hydroxide and sucrose octasulphate. The latter reacts with HCl to form a sticky substance that binds to proteinaceous exudate often found at ulcer sites.
It also stimulates production of HCO3-, mucus and prostaglandin. Indicated for ulceration
What anti histamine drugs are there?
Cimetidine, Ranitidine, Famotidine (CRF)
Are the anti-histamines used for vomiting?
Yes frequently, however, there is no proven efficacy!
When is anti-emitic therapy indicated?
If the vomiting is debilitating and there is no obstruction
If there is marked fluid/electrolyte loss.
What is metaclopromide? Is it licenced?
PABA derivative. It antagonises D2 and 5-HT3 receptors centrally and cholinergic receptors peripherally. It has moderate efficacy and is licenced for veterinary use.
What is ondasteron and its efficacy?
It is a 5-HT3 antagonist and is very good for chemotherapy induced vomiting as it affects the chemoreceptor trigger zone.
Why is maropitant so potent?
It is a neurokin-1 receptor antagonist, which is the last step before vomiting. Have to be careful as it may mask underlying disease and is useful in any kind of vomiting unless obstructive.
