Gastro Flashcards
Brush border enzymes? And enzyme in saliva?
- Maltase: cleaves disaccharide maltose to glucose + glucose
- Sucrase: cleaves sucrose to fructose and glucose
- Lactase: cleaves disaccharide lactose to glucose + galactose
Amylase found in saliva and breaks starch down into sugar
GI Hormones?
GI Acid - mediators, factors increasing and decreasing?
Mediators
- Gastrin
- Vagal stimulation
- HIstamine
Increasing
- Gastrinoma
- Small bowel resection
- Systemic mastocytosis (increased histamine levels)
- Basophilia
Decreasing
- Drugs - H2 antagonists, PPIs
- Hormones - secretin, VIP, GIP, CCK
Where does a pharyngeal pouch arise?
Killian’s dehiscence (triangular area in wall of pharynx between thyropharyngeus and cricopharyngeus muscles)
Stereotypical histories for causes of gastroenteritis?
Incubation periods of causes of gastroenteritis?
- 1-6 hrs: Staphylococcus aureus, Bacillus cereus
- 12-48 hrs: Salmonella, Escherichia coli
- 48-72 hrs: Shigella, Campylobacter
- > 7 days: Giardiasis, Amoebiasis
Leading causes of C.diff?
Previously clindamycin
Now 2nd/3rd gen cephs (Ciprofloxacin)
Exotoxins?
Released by gram +ve bacteria
- Diphtheria - diphtheric membrane on tonsils caused by necrotic mucosal cells –> necrosis of myocardial, nerual and renal tissue
- S.aureus –> acute gastroenteritis, toxic shock syndrome, staphylococcal scalded skin syndrome
- Clostridium tetani - lockjay
- Choleras –> activation adenylate cyclase –> rasied cAMP, increased chloride secretion
Acute management of varices?
- Resuscitation
- Correct clotting - FFP, vitamin K, beriplex
- Terlipressin (constriction of splanchnic vessels, contraindicated in IHD –> Octreotide as alternative)
- Prophylactic abx
- Endoscopy –> band ligation
- Sengstaken-blakemore tube (if endoscopy not ready and uncontrolled haemorrhage)
- Transjugular intrahepatic portosytemic shunt (TIPSS) if above fails
Prophylaxis of variceal haemorrhage?
- Propranolol: Reduced rebleeding and mortality compared to placebo
- Endoscopic variceal band ligation (EVL) is superior to endoscopic sclerotherapy. Performed at two-weekly intervals until all varices have been eradicated. PPI cover is given to prevent EVL-induced ulceration
Management of Barrett’s oesophagus?
- Endoscopic surveillance with biopsies
- Low grade dysplasia: high-dose proton pump inhibitor for 8-12 weeks
- High grade dysplasia: surgery or cryotherapy.
Typical histories of causes of dysphagia?
What is achalasia? What is the gold standard test? What is seen on the test?
Failure of oesophageal peristalsis
LOS contracted, esophagus above dilated.
Test = oesophageal manometry
- In achalasia - loss of peristalsis of distal oesophagus, failure of LOS to relax during swallowing (increased residual relaxing pressure)
- In scleroderma - loss of peristalsis in distal oesophagus but lower resting LOS pressure
Management of achalasia?
- Intra-sphincteric injection of botulinum toxin
- Heller cardiomyotomy
- Balloon dilation
- Drug therapy has a role but is limited by side-effects
Boerhaave’s syndrome?
- Full thickness laceration/perforation of oesophagus
- Left side of lower oesophagus
- Odynophagia and surgical emphysema in the neck
- CXR - pneumomediastinum, gas effusion, pneumothorax
- Oesophagram to confirm leak - water soluble contrast then barium if no leak demonstrated
- Causes - vomiting (against closed glottis - bulimia), foreful coughing (obstruction by food)
- Early operation is management
H.pylori associations?
- Peptic ulcer disease (95% of duodenal ulcers, 75% of gastric ulcers)
- Gastric cancer
- B cell lymphoma of MALT tissue (eradication of H pylori 80% causes regression)
- Atrophic gastritis
Sensitivity/Specificity of H.pylori tests?
- Urea breath test - sensitivity 95-98%, specificity 97-98%
- Rapid urease (CLO) test - sensitivity 90-95%, specificity 95-98%
- Serum antibody - sensitivity 85%, specificity 80%
- Culture gastric biopsy - sensitivity 70%, specificity 100%
- Gastric biospy (histology) - sensitivity 95-99%, specificity 95-99%
- Stool antigen test - sensitivity 90%, specificity 95%
Peutz-Jegers sydnrome?
- Autosomal dominant
- Numerous harmatomatous polyps in the GI tract
- Pigmented freckles on lips, face, palms and soles
- 50% die by age 60 from GI cancer
- Histological appearance = arborisation
Most common oesophageal cancer? RIsk factors for both? Most common location?
- Adenocarcinoma is most common
- Squamous cell carcinoma is the other
- Middle 1/3 is most common
Gastric cancer associations?
- H. pylori infection (although it is protective against esophageal cancer)
- Blood group A: gAstric cAncer
- Gastric adenomatous polyps
- Pernicious anemia
- Smoking
- Diet: salty, spicy, nitrates
- May be negatively associated with duodenal ulcer
Dukes Staging?
- Duke A (Stage I) - tumour confined to the bowel wall (i.e. mucosa and submucosa).
- Duke B (Stage II) - invades through the muscle wall.
- Duke C (Stage III) - involves lymph nodes
- Stage IV - distant metastases
Prognostic indicators post-complete bowel ca resection?
- Poorly differentiated histological type.
- Tumour adherence to adjacent organs.
- Bowel perforation.
- Colonic obstruction at the time of diagnosis.
- Venous invasion by the tumour
Bowel ca - adjuvant chemo and radio?
- Adjuvant chemotherapy in high risk stage II and all stage III
- Adjuvant radiotherapy in rectal carcinomas - combined with chemo in stage II/III to reduce risk of local/metastatic relapse
Three types of colon cancer?
- Sporadic (95%)
- Hereditary non-polyposis colorectal carcinoma (HNPCC, 5%)
- Familial adenomatous polyposis (FAP, <1%)
Common mutation in sporadic bowel ca?
- >50% colon cancers show allelic loss of the adenomatous polyposis coli (APC) gene
- activation of the K-ras oncogene, deletion of p53 and DCC tumour suppressor genes lead to invasive carcinoma
HNPCC - what is it? Criteria? Screening?
- Autosomal dominant condition - most common inherited colon cancer
- 90% develop cancers - poorly differentiated and highly aggressive
Amsterdam Criteria
- At least 3 family members with colon cancer
- Span at least two generations
- At least one case diagnosed before 50 years
Screening
- Colonoscopy every 2 years from 20 to 40 years age then annually
- Check mutation in DNA or mismatched repair gene.
FAP?
- Rare autosomal dominant condition
- Leads to formation of hundreds of polyps by age 30-40
- Inevitably develop cancer
- Due to mutation in APC (ch 5)
- Management - total colectomy with ileo-anal pouch formation in 20s
- FAP families also at risk from duodenal tumours
Zollinger-Ellison syndrome?
Excessive levels of gastrin, usually from a gastrin secreting tumour usually of the duodenum or pancreas. Leads to multiple gastroduodenal ulcers.
- Presentation = abdominal pain, diarrhea and malabsorption.
- Diagnosis = Fasting gastrin levels OR secretin stimulation test (secretin normally suppresses gastrin - in ZE it is not suppressesd as gastrin source is not the stomach)
Gastric MALT Lymphoma? VIPoma?
(VIP = vasoactive intestinal peptide - in SI, pancreas; stimulates secretion by pancreas and intenstines; inhibites acid and pepsinogen secretion)
Gastric MALT Lymphoma
- Associated with H.pylori (95%)
- Good prognosis - if low grade 80% respond to H.pylori eradatication
- Paraproteinaemia may be present
VIPoma
- 90% arise from pancreas
- Large volume diarrhoea, weight loss, dehydration, hypokalaemia, hypochloraemia (gastric acid production low)
What is angiodysplasia associated with?
- Aortic stenosis
- vWF proteolysed in turbulent blood flow around aortic valve. vWF is most active in vascular beds with high shear stress (such as angiodysplasia) - deficiency increases bleeding risk from such lesions
Drug causes of pancreatitis?
Azathioprine, mesalazine, didanosine, bendroflumethiazide, furosemide, pentamidine, steroids, sodium valproate
Features of acute pancreatitis?
- Pain is typically worse 15 to 30 minutes following a meal
- Steatorrhoea: symptoms of pancreatic insufficiency usually develop between 5 and 25 years after the onset of pain
- Diabetes mellitus develops in the majority of patients.
Pancreatic pseudocyst?
- Complication of acute pancreatitis and are localised collections of pancreatic fluid and debris in the lesser sac
- Contained within a fragile wall of granulation tissue which eventually forms a fibrous capsule
Cannot be diagnosed until more than 6 weeks after acute attack
- Abdominal pain/mass
- Fever
- Persistently raised lipase/LFTs
Small pseudocysts resolve spontaneously - >6cm (can cause haemorrhage/infection) need endoscopic/percutaneous drainage or surgical management
Pancreatic cysts?
- Serous cystadenoma - benign
- Mucinous cystadenoma - benign but potentially malignant
Malabsorption?
UC vs Crohn’s?
Management of UC?
Inducing Remission
- Oral/rectal aminosalicylates or steroids
Maintaining Remission
- Oral aminosalicylates
- Cancer screening
Acute Flare
- IV steroids
- LMWH
- Elemental diet
- Monitoring - daily examination, bloods, AXR, stool chart
Factors increasing risk of cancer in UC?
- Disease duration > 10 years
- Patients with pancolitis
- Onset before 15 years old
- Unremitting disease
- Poor compliance to treatment
Mangement of Crohn’s?
General
- Stop smoking
- Some evidence suggests avoid NSAIDs/COCP
Inducing Remission
- Steroid/Budesonide - elemental diet can be used if concerned RE steroid side effects
- 5-ASA (Mesalazine) second line
- Azathioprine/Methotrexate/Mercaptopurine can be used as add on to steroid (not monotheraphy)
- Infliximab in refractory/fistulating disease
Maintaining Remission
- Azathioprine/Mercaptopurine
- Methotrexate
- 5-ASA (Mesalazine) should be considered if previous surgery
Surgery
- 80% eventually have surgery
Whipple’s disease?
- Rare multi-system disorder caused by Tropheryma whippelii infection
- HLA-B27 association - middle aged men
- Malabsorption: diarrhea, weight loss
- Large-joint arthralgia (seronegative arthropathy)
- Lymphadenopathy
- Skin: hyperpigmentation and photosensitivity
- Pleurisy, pericarditis
- Neurological symptoms (rare): ophthalmoplegia, dementia, seizures, ataxia, myoclonus
Whipple’s disease Ix and Mx?
Ix
- Jejunal biopsy shows deposition of macrophages containing Periodic acid-Schiff (PAS)
granules - CRP and ESR
- Hypoalbuminemia
Mx
- IV penicillin then oral co-trimoxazole for a year
Microscopic colitis triad?
- Watery diarrhoea
- Normal colonoscopy
- Increased inflammation of lamina propria of the colon
Associated with NSAIDs, PPIs, Ticlopidine, Cimetidine
Treatment is stopping the offending medication
Coeliac HLA associations? Associated conditions?
- HLA-DQ2, HLA-B8, HLA-DR3, HLA-DR7
- Dermatitis herpetiformis, T1DM, Autoimmune hepatitis
Complications of coeliac?
- Anemia: iron, folate and vitamin B12 deficiency (folate deficiency is more common than vitamin B12 deficiency in coeliac disease)
- Hyposplenism
- Osteoporosis
- Lactose intolerance
- Enteropathy-associated T-cell lymphoma of small intestine
- Subfertility, unfavourable pregnancy outcomes
- Rare: esophageal cancer, other malignancies
Coeliac investigations?
Immunology
- Tissue transglutaminase (TTG) antibodies (IgA) first line
- Endomyseal antibody (IgA)
Jejunal Biopsy
- Reintroduce gluten for at least 6 weeks prior to testing
- Villous atrophy, crypt hyperplasia, increase in intraepithelial lymphocytes, lamina propria infiltration with lymphocytes
Causes of jejunal villous atrophy other than Coeliac?
- Tropical sprue
- Hypogammaglobulinemia
- Gastrointestinal lymphoma
- Whipple’s disease
- Cow’s milk intolerance
What is Tropical Sprue? Diagnosis? Treatment?
Most common in Cairbbean/Far East. SI malabsorption, thought to be infectious in origin.
Diagnosis
- Jejunal biopsy
- Villous atropgy, villous crypts, mononuclear cellular infiltrates, enlarged epithelial cells, large nuclei secondary to folate and/or B12 deficiency
Treatment
- Tetracyclines up to 6 months
- Folate and B12 correction
Short bowel syndrome management?
- >100cm jejunum - can have oral intake
- <100cm then TPN
Diagnosis and management of SBP?
- Ascitic tap - neutrophils >250 cells/ul
- Management = IV cefotaxime
- Prophylactic abx
- patients who have had an episode of SBP
- patients with fluid protein <15 g/l and either Child-Pugh score of at least 9 or hepatorenal syndrome
- Give ciprofloxacin or norfloxacin
Ascities Classification?
- Serum-ascites albumin gradient (SAAG)
- Classifies ascites into portal hypertensive (<1.1 g/dL) and non-portal hypertensive (>1.1 g/dL)
LFTs?
- Bilirubin
- Breakdown of heme –> binds albumin and taken up by liver –> conjugated which makes it water soluble –> excreted in urine
- If mentions no bili in urine then it is unconjugated
- Albumin
- Sensitive marker of hepatic function (not in acute phase, long half life - 20 days)
- Transferases (ALT/AST)
- Rise indicates hepatocellular damage - >1000 suggests drug induced hepatitis, acute viral hepatitis, ischaemic/autoimmune hepatitis
- GGT
- Related to bile ducts. Raised in cholestasis (raised ALP), but if ALP normal suggests induction of hepatic metabolic enzymes (alcohol or enzyme inducing drugs)
- ALP
- Bile ducts and bone
- Physiologiclaly increased in bone turnover (adolesence) and 3rd trimester (produced by placenta)
AST/ALT ratio?
- Chronic Liver disease - ALT > AST
- Established cirrhosis - AST > ALT
Ratio > 2 suggests alcoholic liver disease, <1.0 suggests non-alcoholic liver disease
Causes of hepatomegaly?
Common
- Cirrhosis - in early, later decreases in size. Non-tender, firm.
- Malignancy - metastatic or primary. Hard, irregular liver edge.
- RHF - firm, smooth tender liver edge. May be pulsatile.
Other
- Abscess: pyogenic, amoebic
- Glandular fever
- Hematological malignancies
- Hemochromatosis
- Hydatid disease
- Malaria
- Primary biliary cirrhosis
- Sarcoidosis, amyloidosis
- Viral hepatitis
Hep B antibody/antigen summary?
HBsAg => + Infected
HBeAg => + Infectivity marker high
AntiHBs => + Cured / Vaccinated
AntiHBc =>if IgM + => acute infection if IgG + => chronic infection
In window period everything is negative but AntiHBc (IgM) => +
Mnemonic for drugs causing hepatocellular picture?
- • Statins
- • Paracetamol
- • Anti-tuberculosis: isoniazid, rifampicin, pyrazinamide
- • Nitrofurantoin
- • Sodium valproate
- • Halothane
- • MAOIs/Methyldopa
- • Alcohol/Amiodarone
- • Phenytoin
