Gastrointestinal Flashcards
Treatment for Wilson’s disease (copper accumulation in the eye)
- Penicillamine, trentine- chelating agents. It works to treat Wilson’s disease by binding to the extra copper in the body and causing it to leave the body through the urine.
- Avoid high-copper foods
- Liver transplant- last resort
Metabolic abnormalities include increased copper absorption from the small intestine and decreased hepatic copper excretion.
Autosomal recessive- genetic
How should you administer vitamin B12?
NICE guidelines suggest that for people with neurological involvement, we initially administer hydroxocobalamin (a type of B12) 1mg IM on alternative days until there are no further improvements in symptoms.
This is called a ‘loading dose’ and it is given as it allows for rapid repletion of B12 levels. This helps reverse the anaemia and neurological symptoms quicker.
Once this loading dose has been given, you give maintenance therapy via 1mg of hydroxocobalamin every 2-3 months IM.
Common cause of hepatomegaly?
Right heart failure (cor pulmonale)- Common with COPD
Alcohol
Hepatitis A B C
Drug abuse
Medication to help PREVENT variceal bleeding?
Propranolol.
This is a non-selective beta-blocker which decreases portal venous pressure by reducing cardiac output and splanchnic blood flow.
First-line management for non-alcoholic liver disease? Non-alcoholic steatohepatitis (NASH).
Weight loss.
Non-alcoholic steatohepatitis (NASH) is a progressive form of non-alcoholic fatty liver disease (NAFLD), which can lead to cirrhosis, hepatocellular carcinoma and liver failure. Weight loss being the most effective intervention.
How do you work out alcohol units?
Alcohol units = volume (ml) x ABV / 1,000
Which drug increases the risk of bacterial infection in GI?
PPIs Omeprazole- risk factor for C. difficile infection
Which investigation is appropriate for pancreatic cancer?
High-resolution CT scanning.
CT scan of the abdomen, which can demonstrate a mass and show a double duct sign caused by dilation of the common bile duct and pancreatic duct in response to the tumour.
If pancreatic cancer is suspected, but CT scan is negative, endoscopic US with biopsy may be indicated.
Treatment for achalasia? A condition in which the muscles of the lower part of the oesophagus fail to relax, preventing food from passing into the stomach.
Pneumatic dilatation- air-filled cylinder-shaped balloon disrupts the muscle fibres of the lower oesophageal sphincter, which is too tight in patients with achalasia.
How often is the pneumococcal vaccine given and who will benefit most with a pre-existing GI condition?
Once every 5 years
Coeliac disease diagnosed patients
Investigations for variceal bleeding?
Bloods- FBC, U&E, LTF, G&S coagulation (platelet count/ transfusion, prothrombin)
Endoscopy
CT- liver, portal vein, spleen for signs of cirrhosis
Management for variceal bleeding?
Variceal bleeding acute-
A-E assessment
2 cannulas
1L 0.9 IV saline
- Endoscopy
- Terlipressin 2mg IV
- Prophylactic antibiotic therapy + blood transfusion
- Rubber band ligation- compressing varices with tight rubber band
- N-butyl-2cyanoscrylate- tissue adhesive solution to treat bleeding (gastric varices)
- Sengstaken- Blakemore tube
- Trans-jugular intrahepatic portosystemic shunts TIPS- if not controlled by band ligation (synthetic vessel that connects hepatic vein and portal vein)
Non-variceal bleeding
Clips
Thermal coagulation with adrenaline
Fibrin/ thrombin with adrenaline
PPIs
Investigations for GORD?
<55- start with treatment unless red flag symptoms (weight loss, dysphagia, haematemesis, melena, anorexia)
> 55- refer to endoscopy with biopsy and start pH monitoring
Management for GORD?
Complications of GORD?
Reduce weight
Stop smoking
Reduce alcohol, fatty meals, coffee
Small regular meals
Antacids
H2 antagonists
PPIs- lansoprazole/omeprazole
Laparoscopic fundoplication- if not responded to PPI
Complication: Barret’s oesophagus -> adenocarcinoma
Squamous -> columnar epithelium
Investigations for peptic ulcers?
Bloods- FBC, CRP, U&E, LFT, clotting factors (PT, platelets)
H. pylori detection- urea breath test, stool antigen test, endoscopy with biopsy
Rapid urease test- CLO (gastric biopsy in urea)
Biopsy- rule out IBD, cancer ect
Endoscopy
Management for peptic ulcers?
Stop NSAIDS
NSAIDS + H. pylori = 8-week PPI + eradication therapy (clarithromycin, amoxicillin, metronidazole, levofloxacin)
No NSAIDS + no H. pylori = 4-6 weeks PPI
Endoscopy
Stop smoking
Lifestyle change
Pathophysiology of oesophageal varices?
Oesophageal varices- dilated sub-mucosal veins in lower oesophagus due to portal vein hypertension causing blood to flow into smaller vessels and capillaries causing bleeding/dilation.
Other
Mallory Weiss Tears
Peptic ulcer disease = Gastric cancer Duodenal ulcer
High urea but normal creatinine = upper GI bleed
Pathophysiology of GORD?
Complications?
Abnormality of lower oesophageal sphincter causing reflux of gastric contents into oesophagus.
Can lead to a change in cell structure of the oesophagus
Squamous cells -> columnar cells = Barrett’s oesophagus (metaplastic= not cancerous)
Epithelial cell change can cause Barrett’s oesophagus due to chronic GORD
GORD -> Barrett’s oesophagus -> invasive adenocarcinoma
Pathophsiology of peptic ulcers?
Most common- H. pylori- causes excessive gastrin production and inhibits somatostatin production leading to increased acid production leading to erosion formation
Causes:
NSAIDS- inhibit COX-1 enzyme production that function to protect the gastric mucosa
Alcohol- irritate and weaken stomach lining -> inflammation
Smoking- inhibits prostaglandin secretion in gastric mucosa -> inflammation -> weakened stomach walls -> acid erosions
Gastric ulcers- pain exacerbated by eating
Duodenal ulcers- pain alleviated by eating and worse 2-3 hours after stomach is empty or at night
What is IBS?
Investigations for IBS?
GI sensitivity towards stimuli leading to a group of symptoms to occur and persist for a long time and require long-term self-management
Exclude red flag symptoms- weight loss, blood in stool, rectal bleed, >60, FHx of bowel cancer
Rome criteria
Medical history
Blood- rule out coeliac
Faecal-calprotectin
Stool sample- rule out IBD
Management for IBS?
Lifestyle- physical activity
Regular small meals
Avoid high fibre, carbonated drinks, caffeine
Probiotics
Healthy eating
Psychological support
Laxatives- constipation
Anti-diarrheal- diarrhoea
Adequate sleep
Plenty fluids
What is malabsorption?
Conditions that cause malabsorption- These Definitely Cause Absorption Problems (TDCAB)
Difficulty of digestion and absorption of nutrients
T- tropical sprue
D- disaccharide deficiency (lactose)
C- coeliac + Crohn’s
A- A-beta lipoproteinemia
P- Pancreatic insufficiency (pancreatitis)
Other:
Short bowel syndrome- small intestine is surgically shortened or damaged and cannot absorb enough nutrients.
Cystic fibrosis- excess mucus plugging lead to malfunction of pancreas enzymes
Pathophysiology of coeliac disese?
Commonly autoimmune
Associated with HLA-DQ2 haplotype which is present on antigen-presenting cells that initiate an inflammatory cascade
Gliadin peptides in gluten are resistant to digestive enzymes and remain in sub-endothelium of small intestine
Loss of immune tolerance leading to immune response
Investigations for coeliac disease?
Blood- FBC, U&E, LFT, ESR
Serology- anti-TTG and total IgA
Endoscopy- duodenal biopsy for histology findings
HLA genetic testing- HLA-DQ2
Management for coeliac disease?
Gluten free diet
Supplements- Fe, Ca
B12 injections
Pneumococcal vaccines- once every 5 years
Psychological help
Yearly GP reviews
Prednisolone- if inflammation continues
Underlaying conditions- SIBO
Pathophysiology of Crohn’s?
type of chronic IBD causing granulomatous inflammation affecting any part of the GI tract.
Chronic inflammation from T-cell activation leading to tissue injury
Crypt inflammation and abscesses, which progress to tiny focal aphthoid ulcers.
Mucosal lesions may develop into deep ulcers with mucosal oedema, creating a cobblestoned appearance to the bowel.
Investigations for Crohn’s?
- Observations (temp, RR, BP, SpO2, HR)
- Bloods- FBC, CRP, LFT, U&E, ESR vitamins and electrolytes (B12, folate, K+, Ca+, Na+)
- Stool- cultures, faecal calprotectin
- Imaging- Ileocolonoscopy, biopsy, capsule endoscopy, CT, pelvic MRI (perianal disease- fistulae/ abscess)
- Colonoscopy- cobblestone appearance of GI tract
Management for Crohn’s?
Step-up apporach
Tier 1: Steroids (e.g. prednisolone, budesonide)
Tier 2: Immunomodulators (e.g. azathioprine, mercaptopurine, methotrexate)- CHECK TPMT
Tier 3: Biologics (e.g. adalimumab, stelara, infliximab)
Maintaining remission
Smoking cessation + lifestyle
Azathioprine + mercaptopurine- post surgery (check TPMT)
Alternative- methotrexate
Surgery
50- 80% require surgery at least once in their lives
Indications for surgery: Drug failure, obstruction, perforation, fistulae, abscesses.
Colectomy, proctocolectomy, ileostomy, fistula removal
Monitoring- for osteoporosis due to vit D deficiency due to small bowel resection
Colorectal cancer surveillance
Perianal disease- oral antibiotics, immunosuppression (azathioprine), surgery (abscess drainage)
What is Ulcerative colitis?
Investigations for UC?
Type of IBD- UC causes abnormal reactions of the immune system cause inflammation and ulcers on the inner lining of the large intestine.
Crypt formation- Affects mucosa/ submucosa
Investigations:
* Observations (temp, RR, BP, SpO2, HR)
* Bloods- FBC, CRP, LFT, U&E, ESR vitamins and electrolytes (B12, folate, K+, Ca+, Na+)
* Stool- cultures, faecal calprotectin
* AXR
* Acute- sigmoidoscopy
* Colonoscopy- once controlled with biopsy due to risk of perforation
Management for UC?
Follow Truelove and Witts criteria
Acute + bleeding: First line
1. IV corticosteroids
2. Pro-coagulation therapy for bleeding
3. Cyclosporin/ anti-TNFa (immunosuppressant) if unresponsive to steroids
4. Urgent surgery (perforation/ mega colon)
Mild: First line
1. Rectal 5-ASA (aminoacylates- mesalazine)
2. Oral 5-ASA (mesalazine)- if no remission
3. Oral corticosteroids- if no oral-ASA remission
4. Tacrolimus- immunosuppressive agent
Moderate- First line
1. Rectal and oral 5-ASA
2. Oral prednisolone- if no response to 5-ASA
Maintenance- oral/topical 5-ASA, 6-MP (severe exacerbations)
Surgery- Required at some stage by 20%
Subtotal colectomy- removal of most colon but sigmoid left
Completion proctectomy (permanent stoma)- removal of all colon
Ileo-anal pouch
What is proctitis?
Inflammation starting at the rectum and not spreading beyond the ileocaecal valve.
Proctitis is the most common disease pattern in UC and is seen in 40-50% of the cases.
Bloody diarrhoea, tenesmus, and mucoid discharge are the presenting features of proctitis.
Inflammation in UC starts as proctitis and does not usually spread beyond the ileocaecal valve.
Colorectal cancer investigations?
FIT + CEA tumour marker
Colonoscopy with biopsy
Flexible sigmoidoscopy- if patient is severely unwell
Contrast CT (chest, Abdo, pelvis)- evaluate tumour size/ spread
MRI- pelvic/ liver
Ovarian cancer investigation?
History
Bloods- raised CA125 tumour marker
Pelvic exam
Pelvic ultrasound
Pelvic CT
Genetic testing- BRCA1/2 mutation
Haemorrhoid treatment?
Increase fluid, fibre
Laxatives
Topical- anusol, anusol
Non-surgical- RBL
Surgical- haemorrhoidal artery ligation or haemorrhoidectomy
What is Cholelothiasis?
Gallstone development in gallbladder due to excess bile products (cholesterol).
Liver makes bile -> bile stored in the gallbladder-> excess cholesterol in bile leads to accumulation of cholesterol or bilirubin in the bottom on the gallbladder -> stones grow and harden -> stones travel and get stuck in cystic duct -> biliary colic
Cholesterol gallstones- unpigmented
Calcium-billirubinate gallstones (pigmented and visible on X-RAY)
Cholelothiasis management?
No intervention required for asymptomatic
Cholecystectomy: Surgical removal of gallbladder
Carried out if pt is symptomatic and/or gallstones have potential to lead to complications
1. ERCP can be used to remove gallstones before or during surgery
2. Laparascopic cholecystectomy (keyhole surgery) is keyhole surgery with less complications and faster recovery
Cholelithiasis investigations?
Bedside: GI exam
Lab:
1. Urinalysis to exclude differentials
2. LFTs to see for raised bilirubin
3. Alkaline Phosphatase (ALP) non-specific marker enzyme originating in liver
4. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) enzymes p
Imaging:
1. Ultrasound is 1st line for symptoms of gallstones (more sensitive than CT scans)
2. MRCP- an MRI scan w/ specific protocol to produce detailed image of biliary system
3. ERCP which involves inserting endoscope down oesophagus, past stomach to duodenum and opening of bile duct
-> helps to see stones, clear them, insert stents to improve bile duct drainage
What is cholecystitis?
Causes?
Types?
Inflammation of the gallbladder due to blockage of cystic duct preventing gallbladder from draining
Causes:
Infection
Bile duct obstruction
Tumours
Types:
Calculous cholecystitis: Common in 95% of cases
Gallstones stuck in cycstic duct -> Bile builds up in gallbladder -> distention and gallbladder becomes inflamed
Acute cholecystitis:
Gangrenous cholecystitis: necrosis and perforation of the gallbladder wall as a result of ischemia following progressive vascular insufficiency.
Perforated gallbladder: The gallbladder splits open and can spread infection and lead to peritonitis or abscess
Emergency surgery required for latter two
Investigations for cholecytisis?
Labs:
Bloods- CRP and WBC
Bedside: GI exam
Murphy’s sign: placing hand in RUQ and applying pressure. Patient asked to take deep breath in. Gallbladder moves down, comes into contact with hand and results in acute pain and stopping of inspiration
Imaging:
Abdominal ultrasound to see for thickening of gallbladder wall, presence of stones, fluid around gallbladder
MRCP if bile duct stone suspected but not seen on ultrasound scan
Management for cholecystis?
- Pain relief
- IV fluids
- Abx initially IV, then oral (as per local guidelines)
- NG tube if necessary for vomiting
- Cholecystectomy which can either be carried out during acute admission within 72 hours of symptoms, or delayed 6-8 weeks after acute episode to allow inflammation to settle
- ERCP to remove stones
If there is gallbladder empyema- gangrenous cholecystitis.
- IV abx
- Cholecystectomy or cholecystostomy if patient is not well enough for surgery
->latter refers to inserting drain into gallbladder to drain infected contents
What is MRCP and ERCP?
MRCP- Magnetic resonance cholangiopancreatography type of MRI used to visualise the biliary system, blockages, and tumours. SCAN
ERCP- Endoscopic retrograde cholangiopancreatography used to diagnose and treat problems in the liver, gallbladder, bile ducts, and pancreas. It combines X-ray and an endoscope. PROCEDURE
ERCP bile duct treatment-bile- balloons and baskets attached to the catheters can be passed into the ducts allowing stone removal.
What does Courvoisiers Law state about cholangiocarcinoma?
Patients with jaundice and a palpable gallbladder often have a malignant obstruction of the common bile duct and is unlikely to be a gallstone- 70% of time
Cholangiocarcinoma investigations?
GI exam
Bloods- LFT, albumin, bilirubin, ALT, CA19-1 tumour marker
Imaging- CT, MRCP, ERCP, ultrasound
Cholangiocarcinoma management?
Poor prognosis- 12-18 months
Involves MDT
Resectable surgery- if early diagnosis
Chemo/radio therapy
Palliative and end of life treatment
How is coeliac disease diagnosed?
Coeliac serology- TTG/ IgA
Must eat gluten diet for 6-weeks before test to prevent false negative
Endoscopic biopsy- confirm/ exclude
First-line treatment for C. difficile infection?
Oral vancomycin is the first-line antibiotic for use in patients with C. difficile infection
What drug can increase risk of cholestasis?
Oral contraceptive pill
Explain microcytic anaemia
MCV <80 fL/cell (femtolitres)- reduced average size of RBC
Presents as- Low Fe+/ ferritin
Types- iron deficiency, thalassemia, sideroblastic anaemias
High Fe+= thalassemia + sideroblastic
Low Fe+= iron-deficiency
