So, i attended a conference yesterday at G-Hotel, Penang. It was called The TARGET Program (Treatment And Relief of GastrointEsTinal disorders) and is one of the programs of the Malaysian Society of Gastroenterology and Hepatology. The best part of the whole experience is the fact that i was called “Doctor” for a few times and to be honest, that 1 second feeling of satisfaction before i correct them saying I’m still a medical student was awesome. I met a doctor who used to be an IMU student (now working for the army) and apparently Dr Hla Yee Yee (my lecturer now) used to be her lecturer too. She mentioned a few names I don’t know, probably they left the uni before i joined. The talks were more like normal lectures except for the fact that it was in a beautiful high class restaurant where people don’t drink water directly from the water bottle and most of my “classmates” are 20-40 years older than me. AND, each lasts for a maximum of 40 minutes (mostly 30 minutes).
It was a good experience and a lot of revision and new knowledge, and here are some points from my scribbled notes.
*If there are any wrong information (PLEASE alert me), they must be due to my own carelessness while taking down the notes :)
Talk 1: Per rectal bleeding (PRB); who and when to refer – Dr Akhtar Qureshi (Sunway Medical Centre)
- Acute lower GI bleed –> bleeding distal to ligament of Treitz
- Massive upper GI bleeding can present as PR bleed (PRB)
- If it’s black tarry–> malena, red/maroon–> hematochezia. There is no such thing as ‘fresh’ malena.
- Source of bleed if a patient presents with PRB – 85% is from colon
- Clinical features (identify source of bleeding from Hx and PE and do Ix to confirm):
1) Hx: Based on age, with pain/painless and significant past medical history. Bleeding: amount? color (maroon – it’s been long since it bled, red – fresh blood)? Blood is mixed or separate from the stool (if it lines the outside of the stool = most commonly [MC] from rectum. If it’s mixed with the stool = usually it’s bleeding from left colon)? When (after passing stool only it starts to bleed?)? Is bleeding the main complaint or pain?
2) PE: IPAD (Inspection, PAlpation, Digitation)- Inspection (skin tags/hemorrhoids), PAlpation (if there’s pain especially, palpate at at the 12 and 6 o’clock position around the anus. Digitation – DRE (avoid if patient comes with pain).
3) Investigations/Ix: Proctoscopy/ Mesentericangiography/ Meckel scan (esp if PRB in child/babies)/ Barium enema (not good to identify bleeding)/ capsule endoscopy.
- Common conditions:
1) Anal fissures: Most common in stressed young adults. Pain (is the main symptom, so avoid DRE) + bleeding. Treatment (Rx): Analgesia, stool softener, topical oinment, Ca antagonist.
2) Hemorrhoids: Bright red painless bleeding. NOT painful unless complicated with thrombosis or gangrene. Main cause is straining too hard esp in constipated patients. Rx: Non-operative (avoid constipation/straining/take stool softener), Medication (only for the bleeding-Flavinoids), Surgery for severe bleeding, Rubber banding (is completely painless but must be place the band above the dentate line).
3) Chronic diverticular disease – (arterial bleeding) most commonly on the right side. 85% cases will resolve/stop spontaneously. 25% cases will have episodes of re-bleed.
- Most common cause of painFUL rectal bleed is : Anal fissure (may also be severe thrombosed piles but this is not common).
- Most common cause of painLESS rectal bleed is : Hemorrhoid
- Hx of altered bowel habits with PRB for more than 2 weeks, suspect: Colorectal cancer
- Definition of tenesmus in Malaysia’s context: incomplete emptying of the rectum
Talk 2: AntiPlatelet Therapy (APT), NSAIDs and PUD bleeding – Datuk Dr Tan Huck Joo (Sunway Medical Centre)
- Most common causes of Upper GastroIntestinal (UGI) bleeding : H. pylori, NSAIDs and Aspirin.
- Clopidogrel + Aspirin is better in reducing cardiovascular (CVS) events in patients with acute coronary syndrome (ACS) but increases significantly (2-3 folds) the risk of GI bleed. Dual APT with Prasugrel/Ticagrelor (+ aspirin) is more effective than Clopidogrel + Aspirin but of course, brings a higher risk of GI bleed and more expensive.
- Risk factors for UGI bleed:
1) Past Hx of UGIB
2) Concomitant use of NSAIDs/COX2i/antiplatelet or anticoagulant (eg. Warfarin)/corticosteroids.
3) Just started taking NSAIDs
4) H. pylori infection
- Primary prevention: To reduce risk of peptic ulcer disease (PUD) when taking Dual APT, PPI (eg. Esomeprazole) is better than H2RA (eg. Famotidine). BUT both are good.
- Primary prevention: Esomeprazole VS Famotidine in preventing GI bleed in ACS/STEMI patients (as they take dual APT + enoxaparin or thrombolytics) –> PPI is better.
- Secondary prevention: Screening and eradication of H. pylori and then adding PPI is better in preventing aspirin-induced recurrent PUD.
- (PPI + clopidogrel) < (PPI + clopidogrel) in reducing incidence of aspirin-induced PUD
- Most of causes of abnormal LFTs:
1) alcohol abuse
2) Medicines (Herbs/supplements/antibiotics/antiepileptics/HMG-CoA reductase inhibitor/NSAIDs/Sulfanylureas like Glipizid/anabolic steroids/ecstasy/glues or solvent)
3)Chronic hepatitis B and C
4) Steatosis and NASH (Non-alcoholic steatohepatitis)
5) Autoimmune hepatitis
- Repeat the test if the results were from a test done few weeks ago.
- If the level (of ALP/ALT) is <2x the upper limit of normal, most probably there are no clinical importance.
- ALP can be high in pregnant women in their 3rd trimester.
- Even if the abnormal LFT is with positive Hep B surface antigen – both can be totally unrelated.
- Other Ix: ceruloplasmin levels, Hepatitis serology, autoantibodies/immunoglobulins, ultrasound of the abdomen, PT and albumin(to see how ‘sick’ the liver is), iron studies.
- Can diagnose fatty liver (Non-alcoholic fatty liver disease/NAFLD) using ultrasound/CT. Spleen darker than liver (lighter) in ultrasound suggests fatty liver.
- NASH is getting more common in Malaysia and 10% of the cases progress to cirrhosis. To diagnose NASH you must do a biopsy.
- If abnormal LFT is due to statin, stop usage for a while or use ones with less effect like Rosuvastatin.
Talk 6: Practical issues in Colorectal Cancer (CRC) Screening in Primary Care – Datuk Dr Jayaram Menon (Queen Elizabeth Hospital)
- Target group to screen for colorectal cancer: 45-74 years old.
- Of those asymptomatic people that are diagnosed upon screening, around 90% will have localised cancer.
- Symptoms of colorectal cancer include abdominal pain, altered bowel habit, malena, lethargy, anemia w/o any other GI symptom, weight loss (only 6%).
- Risk of developing colorectal cancer:
1) History (Hx) of CRC or adenomatous polyp
2) Hx of inflammatory bowel disease
3) Family history (F/H) of CRC or adenomatous polyp
4) F/H of other cancers
- Adenomas is the one that most commonly predisposes patients to CRC.
- Screening – patient is asymptomatic. Surveillance – follow-up patients
- Stool-based tests to detect adenomatous polyps and cancer:
1) Fecal Immunochemical Test (FIT) has a high sensitivity for cancer.
2) Guaiac fecal occult blood test (gFOBT) done using feces from DRE (digital rectal examination) is NOT recommended.
- If a person has:
1) <10 hyperplastic polyps -repeat colonoscopy every 10 years
2) <3 adenomatous polyps -repeat colonoscopy every (..not sure..) years
3) >3 adenomatous polyps -repeat colonoscopy every 3 years
- CA level (tumor marker screening) – NOT reliable to detect cancers. It’s role is only significant to monitor patients after removing the tumor (follow-ups).
- CT colonoscopy -good for big polyps but NOT for those <1cm in size (can be missed). Plus, if feces is present (not enough preparation before colonoscopy), it can cover the polyps. And there’re also risks of radiation and the high cost.
Hope you gained something having read this. There are two more talks actually, but lets keep that for the next post. :)