Gastroenterology Flashcards
How do you make a diagnosis of C diff infection and how do you determine severity?
Diagnose by detecting CDT (toxin) in stool
WCC to determine severity
Risk factors for C diff?
abx and PPIs
esp cephalosporins
What is the tx stepladder for C diff infections?
first-line therapy is oral vancomycin for 10 days
second-line therapy: oral fidaxomicin
third-line therapy/ in life- threatening cases: oral vancomycin +/- IV metronidazole
What drugs must be stopped before a urea breath test?
no antibiotics in past 4 weeks, no antisecretory drugs (e.g. PPI) in past 2 weeks
What is achalasia?
Most important diagnostic test?
What cancer does it increase the risk of?
How is it treated?
Definition: Failure of oesophageal peristalsis and of relaxation of the lower oesophageal sphincter (LOS) due to degenerative loss of ganglia from Auerbach’s plexus i.e. LOS contracted, oesophagus above dilated.
Presents with dysphagia of both solids and liquids from onset
Key test: Oesophageal manometry
- also shows grossly expanded oesophagus, fluid level and ‘bird’s beak’ appearance on barium swallow
increases the risk of squamous cell carcinoma of the oesophagus
First line: pneumatic (balloon) dilation
Surgical management when comorbidites/recurrence : Heller cardiomyotomy
How is appendicitis diagnosed?
Thin young male patients with a high likelihood of appendicitis (classic central abdominal pain that localises to the right iliac fossa) can be diagnosed clinically w/o a scan
Often do an USS in women for pelvic pathology
Raised inflammatory markers (e.g. CRP) and neutrophil predominant leucocytosis can aid in diagnosis
May be psoas sign positive- unable to stand on one leg comfortably and pain on hip extension
Best way to measure liver function in people with established disease?
Liver enzymes are a poor way to look at liver function - they are usually low in end-stage cirrhosis whereas coagulation e.g. prothrombin time and albumin are better measures
What is fetor hepaticus?
sweet and fecal breath, it is a sign of liver failure
Causes of acute liver failure?
paracetamol overdose
alcohol
viral hepatitis (usually A or B)
acute fatty liver of pregnancy
Features of acute liver failure?
jaundice
coagulopathy: raised prothrombin time
hypoalbuminaemia
hepatic encephalopathy
renal failure is common (‘hepatorenal syndrome’)
Raised urea + normocytic anaemia= ?
How much does urea need to be raised to be a significant case?
Upper GI bleed!
- a haemorrhage with an origin proximal to the ligament of Treitz
Urea is from protein meal (digestion of RBCs)
Urea of 15.4 mmol/l on a background of normal renal function is a significant bleed
Management of Upper GI bleed?
All patients with suspected upper GI bleed require an endoscopy within 24 hours of admission
IV PPIs given AFTER endoscopy (never before) if evidence of recent variceal haemorrhage
Repeated endoscopic intervention with no success (more acute bleeds) = surgical intervention
How is risk stratified in Upper GI bleeding?
the Glasgow-Blatchford score used at first assessment
helps clinicians decide whether patient patients can be managed as outpatients or not
the Rockall score is used after endoscopy
provides a percentage risk of rebleeding and mortality
Eq for alcohol units?
Alcohol units = volume (ml) * ABV / 1,000
Cause of metabolic acidosis in non-diabetic alcoholics? Tx?
Alcoholic ketoacidosis
- Often alcoholics will not eat regularly and may vomit food that they do eat, leading to episodes of starvation and ketone production
Will likely have normal or low blood glucose
treatment is an infusion of saline & thiamine
AST/ALT ratio in alcoholic hepatitis?
2:1
Management of alcoholic hepatitis?
glucocorticoids (e.g. prednisolone) are often used during acute episodes of alcoholic hepatitis
Maddrey’s discriminant function (DF) is often used to determine who would benefit from glucocorticoid therapy
- its calculated using prothrombin time and bilirubin concentration
pentoxyphylline is also sometimes used
Key investigation in unwell patient taking aminosalicylates?
A patient who is taking aminosalicylates and becomes unwell with a sore throat, fever, fatigue or bleeding gums needs an urgent full blood count to rule out agranulocytosis.
What do Anti-nuclear antibodies (ANA) and/or anti-smooth muscle antibodies (SMA) with raised IgG suggest?
Type 1 autoimmune hepatitis- common in young women, often also see secondary amenorrhea, tx with steroids
When is endoscopic intervention ( endoscopic mucosal resection or radiofrequency ablation) offered with Barrett’s oesophagus?
When dysplasia is seen
If not pts can be managed with endoscopic surveillance every 3-5 years and a high dose PPI
how does Budd-Chiari present and how is it investigated?
Budd-Chiari syndrome (hepatic vein thrombosis):
Presents with the triad of sudden onset abdominal pain, ascites, and tender hepatomegaly
Can do a Serum - Ascites Albumin Gradient (a raised SAAG (>11g/L) indicates that it is portal hypertension that has caused the ascites and makes Budd-Chiari more likely)
Investigate with doppler USS
For carcinoid syndrome (release of serotonin into systemic circulation), outline the presentation, test and tx
carcinoid syndrome-
Sx: flushing, diarrhoea, bronchospasm, hypotension, and weight loss
Caused by lung carcinoid or more commonly mets in the liver
Test urinary 5-HIAA
Give somatostatin analogues e.g. octreotide
Features of coeliac?
Coeliac disease:
- non specific symptoms like fatigue, anaemia and weight loss
- low ferritin/folate
- raised white cells/CRP due to inflammation
- raised tissue transglutaminase (TTG) antibody
- grey frothy stool
Coeliac disease increases the risk of developing enteropathy-associated T cell lymphoma
How long before testing should coeliac patients eat gluten? What is being tested for in serology?
6 weeks
tissue transglutaminase (TTG) antibodies (IgA)