Investigations of GI Disorders Flashcards
General Hx and PE
Hx
- abdominal pain, change in bowel habit, vomiting/ nausea
- constitutional symptoms
- travel history/ food intake
- family history
PE
- general: pallor, jaundice, stigmata of CLD
- abdominal: tenderness, organomegaly, mass, ascites, bowel sounds
Rationale
Always start from least invasive!
Blood tests -> imaging -> endoscopy
–> diagnosis, severity and monitor
General Investigations
Blood: CBC, LRFT, Amylase, Blood gas, CRP, CEA
Stool: microscopy, culture, occult blood
Imaging: USG biliary system, liver, kidney, appendix; CT for malignant diseases
Endoscopy: OGD, sigmoidoscopy/ colonoscopy
Differential Dx of RUQ pain
Ulcer disease
Pancreatitis, Pancreatic CA
Gallbladder/ liver/ biliary tract pathology
Intestines
Interpretation of Amylase Levels
Sensitivity and Specificity depends on cutoff level used
300 IU/L: 95% sensitivity but only 70-90% specificity
1000 IU/L: 60% sensitivity, 100% specificity
==> >1000 IU/L is DIAGNOSTIC of acute pancreatitis but doesn’t suggest severity and prognosis
RR in PWH = 28-100 IU/L - LOW SPECIFICITY! usually take 3x upper limit of normal as cutoff for pancreatitis
Conditions associated with increased amylase
Pancreatic
- pancreatitis
- cancer
- trauma
- pseudocyst (persistent elevation)
Inflammation of the retroperitoneum
- perforated peptic ulcer
- peritonitis
Non-abdominal
- salivary gland disease
- ketoacidosis (ketones compete with amylase for urinal secretion)
Reduced clearance
- macroamylasaemia
Drugs (compete for excretion)
- azathioprine
- sulphonamides
- tetracycline
- salicylate
- valproic acid
Further tests for acute pancreatitis, tests for equivocal amylase levels
After confirming Dx: Aetiology - gallstone vs metabolic cause - Hx! - USG abdomen
Severity
- Ranson’s criteria
Management:
- monitoring electrolytes and blood gas for complications
- pain relief
If amylase is equivocal or present late after onset of pain:
- urine amylase
- plasma lipase
(both elevated for longer than plasma amylase)
Ranson’s Score
Predicts mortality
Initial presentation
- Age >55 yrs
- WBC > 16x10^9/L
- Glucose >10 mmol/L
- LDH >350 IU/L
- AST >250 IU/L
At 48 hrs
- Hct drop >10%
- Urea >16 mmol/L
- Ca <2 mmol/L
- PO2 <8 kPa
- Base deficit >4 mEq/L
- Fluid sequestration >6 L
0-2 = 0% 3-4 = 15% 5-6 = 40% >7 = 100%
Persistent amylase elevation DDx
Normally have rapid renal clearance with return to normal value within 1 week
DDx of persistent elevation:
- pancreatic pseudocyst (no cell lining; common sequelae of acute and chronic pancreatitis)
- macroamylasaemia
- chronic pancreatitis (though usually normal levels)
(+ renal failure)
Macroamylasaemia
AutoAb against amylase forms big immune complexes that aren’t filtered into the urine –> reduced renal clearance
2.5% of cases with amylase elevation (degree of elevation much lower than pseudocyst)
Amylase clearance <1% (vs >2% in pancreatitis)
Amylase clearance calculation
[Amylase]Ur/ [Amylase]Bld // [Cr}Ur/ [Cr]Bld
Peptic ulcers characteristics: response to food, malignant potential, a/w H. Pylori, biopsy areas, rescope needed?
Gastric ulcer
- food worsens pain
- 65-95% H. pylori
- has malignant potential
- biopsy at antrum for HP and ulcer edge
- rescope needed to check healing of ulcer
Duodenal ulcer
- food relieves pain
- 80-95% H. pylori
- no malignant potential
- biopsy at antrum
- no need rescope
H. Pylori
Produces urease to convert urea into NH3 for alkaline conditions to counter acid
–> likes acidic env –> Antrum
Treatment: triple therapy (amoxicillin, clarithromycin, PPI)
Malignancy of lower GI tract prevalence
Small bowel CA is rare
Colon CA is leading cause of cancer deaths worldwide
Effects of colon CA (3)
Ulceration and invasion – bleeding
== ascending and transverse colon: anaemia (bacteria metabolises Hb so can’t see blood)
== descending colon: per rectal bleeding
Obstruction – late stage, advanced disease
Secretion – e.g. mucus into bowel lumen, tumour markers (specific substances)
Lab detection of colon CA
Bleeding from tumour
- anaemia
- occult blood in stools
Secretion from tumour
- CEA
Limitations of existing tumour markers
Low sensitivity and specificity
Different markers for different types of cancers
Most cancers don’t secrete specific markers
Faecal Occult Blood Test
Only 30-40% sensitivity for screening (one-off)
Yearly screening in average-risk group
- detect up to 92% of CRCs
NOT for symptomatic patients with bowel habit change/ per rectal bleed/ unexplained iron deficiency anaemia –> go straight to endoscopy!!!
Guaiac-based FOBT vs Faecal immunochemical test (FIT): target of detection, limitations
gFOBT
- detect pseudoperoxidase activity from haem –> catalyses the oxidation of colourless chromogen with H2O2 to form blue colour
- false positives: plants e.g. turnips, cucumber containing peroxidase; meat with haem from myoglobin; NSAIDS causing upper GI bleed releasing Haem
- false negatives: vitamin C >250 mg/day has antioxidant effect that reverses the oxidation reaction
- 3 samples needed (bleeding is intermittent)
FIT
- detect globin portion of undegraded Hb –> polyclonal anti-Hb Ab forms conjugate IC with Hb which is captured on test strip
- limitations: nil, no dietary requirements, not sensitive to upper GI bleed (globin degraded)
- 1-2 samples
Interpretation of FOBT and advantages
- 67% sensitivity and 10% PPV = one positive test unreliable and need further tests before proceeding to CLN
- 91% specificity and 99.5 NPV = one negative test can exclude CA colon
Advantages:
- fast bedside test, non-invasive, no special skill/ equipment, FIT can improving sensitivity and specificity to almost 100%, low running cost
(endoscopy expensive, long operation time and invasive)
Screening guidelines for FOBT in HK
> 50 low risk group
- FOBT every 1-2 years or
- Flexible sigmoidoscopy every 5 years or
- Colonoscopy every 10 years
High risk group (e.g. Fam Hx, overweight, low exercise, low veg/fibre diet)
- Colonoscopy every 3-5 years after 40
