Gastroenterology Flashcards
Describe the pathology of ulcerative colitis:
- red raw mucus that bleeds easily
- from rectum up to ileocaecal valve, continuous
- can present with toxic megacolon or lead drain pipe colon
- loss of haustrations and pseudo polyps on barium enema
- inflammatory cells infiltrate lamina propriety
- neutrophils migrate to gland walls and create crypt abscesses
- depletion of goblet cells and mucin from epithelium
- no inflammation beyond submucosa (unless fulminant disease)
What are the extra-intestinal manifestations for UC and Crohn’s:
related to disease activity: -episcleritis (more common in Crohn's) -pauciarticular, asymmetrical arthritis -osteoporosis -erythema nodosum not related to disease activity: -uveitis (more common UC) -primary sclerosis cholangitis (more common UC) -polyarticular, symmetrical arthritis -clubbing -pyoderma gangrenosum
What classifies are mild, moderate and severe UC flares?
- mild: <4 stools/day, no systemic disturbance
- moderate: 4-6 stools/day, minimal systemic disturbance
- severe: >6 stools/day, systemic disturbance
How do you treat mild-moderate flare ups and severe flare ups of UC?
mild-moderate:
- proctitis: topical ASA
- procto-sigmoiditis: topical ASA or oral ASA or oral ASA with topical corticosteroid or oral ASA with oral corticosteroid
- extensive disease: hospital, IV ciclosporin, IV corticosteroids
Maintaining remission following mild to moderate UC flare-up and following severe lapse or >=2 exacerbations/year:
mild to moderate:
-proctitis and proctosigmoiditis: topical ASA or oral ASA with rectal ASA or oral ASA
-left sided and extensive: low maintenance dose oral ASA
after severe lapse:
-oral azathioprine
-oral mercaptopurine
Explain the pathology of Crohn’s including histology and what is seen on a small bowel enema:
- anywhere from mouth to anus
- inflammation to serosa - prone to strictures, fistulas, adhesions
- deep ulcers and skip lesions
- goblet cells and granulomas
- Kantor’s string sign
- proximal bowel dilation
- rose-thorn ulcers
- fistulae
Inducing remission in Crohn’s:
- glucocorticoids for 5 days followed by infliximab
- azathioprine or mercaptopurine as add ons with TMPT check
- metronidazole for peri-anal disease
Maintaining remission in Crohn’s:
- azathioprine or mercaptopurine
- methotrexate
What is coeliac disease and what are the typical signs and symptoms:
- autoimune sensitivity to gluten
- villous atrophy leads to malabsorpiton
- HLA DQ8 and DQ2
- diarrhoea
- failure to thrive
- persistent GI symptoms
- fatigue
- weight loss
- anaemia
What are the conditions associated with Coeliac?
- autoimmune thyroid
- dermatitis herpetiformis
- IBS
- type I diabetes
What are the complications of Coeliac?
- anaemia
- hyposplenism
- osteoporosis
- lactose intolerance
- enteropathy associated T cell lymphoma of small intestine
- subfertility
- rarely oesophageal cancer
How do you investigate Coeliac?
- re-introduce gluten 6 weeks before testing
- tissue transglutaminase antibodies
- endomyseal IgA antibodies
- anti-casein
- duodenal biospy: villous atrophy, crypt hyperplasia, increased intraepithelial lymphocytes, lamina propria infiltration with lymphocytes
What is peutz-jeghers and what does it cause?
- autosomal dominant
- LKB1, STK11
- polyps not malignant but manny die from GI cancer
- GI bleeding
- obstruction e.g. intussusception
- hamarmatous polyps
- pigmented lesion on lips, palms, soles and face
What is a pharyngeal pouch and how does it present?
- posteromedial diverticulum through Kilian’s dehiscence
- more common in males and elderly
- causes halitosis, neck swelling which gurgles, dysphagia, regurgitation, aspiration
- manage surgically
What is the main risk factor for oesophageal candidiasis?
steroid inhaler use
How does systemic sclerosis present?
dysphagia CREST -calcinosis -Raynaud's -oeophageal dysmotility -sclerodactlyly -telangiectasia LES pressure is decreased instead of increase (e.g. in achalasia)
How does myasthenia gravis present?
- dysphagia with liquids and solids
- intraocular muscle weakness, ptosis
How does globus hystericus present?
- may have history of anxiety
- symptoms intermittent and relieved by swallowing
- usually painless
What is carcinoid syndrome and how does it present?
- metastases in liver release serotonin
- may also be with lung
- causes flushing, diarrhoea, bronchospasm, hypotension, right heart valve stenosis
- other mol e.g. ECTH and GnRH
- pellagra rare as dietary tryptophan diverted to serotonin by tumour
Presentation of gallstones/cholelithiasis:
- colicky RUQ pain postprandially
- worse after fatty meal - increased CCK contracts bladder
- abnormal LFTs
- n&v
How can you distinguish biliary colic, acute cholecystitis, gallbladder abscess and cholangitis?
- biliary colic: colicky abdominal pain, no jaundice or fever
- acute cholecystitis: Murphy’s sign, sometimes deranged LFTs, vomiting, no jaundice
- gallbladder abscess: swinging pyrexia
- cholangitis: bile duct inflammation secondary to stones, Charcot’s triad, jaundice, severely septic and unwell
What size gallstones can be safely left?
<5mm
Where is diverticulosis most common?
sigmoid colon
Presentation of diverticulitis:
- change in bowel habit
- intermittent LLQ abdo pain
- n&v, bloating
- urinary frequency, urgency, dysuria,
- PR bleeding
- pneumaturia, faecaluria (fistula)
- low grade pyrexia
- reduced bowel sounds
- guarding, rigidity - perforation
- lack of improvement with Tx - abscess
Signs seen in pancreatitis:
- Cullen’s - periumbilical discolouration
- Grey-Turner’s - flank discolouration
- ischaemic Purtscher retinopathy
Factors seen in pancreatitis:
- > 55yo
- hypocalcaemia
- hyperglycaemia
- hypoxia
- neurtophilia
- increased LDH and AST
What are some causes of hyperamylasaemia other than pancreatitis?
- pancreatic pseudocyst
- mesenteric infarct
- perforated viscus
- acute cholecystitis
- DKA
Causes of pancreatitis:
- Gallstones
- Ethanol
- Trauma
- Steroids
- Mumps
- Autoimmune + ascaris infection
- Scorpion venom
- Hypertriglyceridaemia, hyperchylomicronaemia, hypercalcaemia, hypothermia
- ERCP
- Drugs
Complications of pancreatitis:
- peripancreatic fluid collections which may resolve or develop into pseudocysts or abscesses
- pseudocysts - 4 or more weeks after
- pancreatic necrosis
- pancreatic abscess - infected psuedocyst
- haemorrhage
- ARDS
Common features of GI ischaemia:
- abdominal pain
- rectal bleeding
- diarrhoea
- fever
- blood: increased WCC, lactic acidosis
Predisposing factors of GI ischaemia:
- age
- AF
- emboli causes: endocarditis, malignancy
- CVD risk factors: smoking, HTN, diabetes
- cocaine
Most common place for ischaemic colitis and signs on x-ray:
- watershed area e.g. splenic flexure - territory supplied by superior and inferior mesenteric
- thumbprinting on x-ray - mucosal oedema/haemorrhage
Causes of AAA:
- standard arterial disease: HTN, diabetes, smokers
- connected tissue disease
What is the protocol for managing AAA:
<3cm - no further action
3-4.4cm - small, rescan every year
4.5-5.4cm - medium, rescan every 3 months
>=5.5cm - large, refer within 2 weeks for vascular surgery
Mallory Weiss tear:
- history of antecedent vomiting
- painful mucosal lacerations at GO junction
- small amount of blood
- common in alcoholics
- resolves spontaneously
Hiatus hernia of gastric cardia:
- longstanding history of dyspepsia
- overweight
- no dysphagia or haematemesis
Oesophageal rupture investigation:
CXR: infiltrate or effusion
Peptic stricture:
- longer history dysphagia (not progressive)
- GORD symptoms
- no systematic features
Dysmotility disorders:
- episodic, non progressive dysphagia
- retrosternal pain
Plummer-Vinson syndrome:
- dysphagia (oesophageal web)
- glossitis
- iron deficiency anaemia
Boerhaave syndrome:
severe vomiting leads to rupture
Oesophageal adenocarcinoma vs squamous cell:
Adenocarcinoma:
-lower third near junction
-GORD, Barrett’s, smoking, achalasia, obesity
Squamous cell:
-upper two thirds
-smoking, alcohol, achalasia, Plummer Vinson, diet rich in nitrosamines
Causes of peptic ulcers:
- H Pylori: 95% duodenal ulcers, 75% gastric ulcers
- drugs: NSAIDs, SSRIs, corticosteroids, bisphosphonates
- Zollinger Ellison
Duodenal vs gastric ulcers:
- duodenal pain relived by eating, more common
- gastric worse after eating
What scoring system is used for acute GI bleeding?
Blatchford score
Resuscitation for acute GI bleeding:
- ABC, wide bore venous access
- platelet transfusion if needed
- FFP if decreased fibrinogen , PTT
- prothrombin complex concentrate if on warfarin and active bleeding
Management of Varices:
- ABCDE and correct clotting
- vasoactive agents: terlipressin, octreotide
- band ligation
- sclerotherapy
- Sengstaken-Blakemore tube
- TIPSS (connects hepatic to portal vein)
Varices prophylaxis:
- propranolol
- endoscopic vatical band ligation
H. Pylori, management and investigations:
- gram negative
- associated with peptic ulcers, gastric cancer, B cell lymphoma of MALT tissue, atrophic gastritis
- no association with GORD
- PPI + amoxicillin + clarithromycin
- PPI + metronidazole + clarithromycin
- urea breath test (good post eradication)
- serum antibody (positive after eradication)
- gastric biopsy
- stool antigen
- rapid urease
C diff
- gram positive rod
- pseudomembranous colitis - loss of bowel architecture and thumb-printing
- caused by clindamycin, ceftriaxone, cefaclor, PPI
- diagnosis by CDT in stool, antigen shows exposure not current infection
- can develop severe toxic megacolon
- first line metronidazole 10-14 days
- oral vancomycin
- fidaxomicin
- life threatening: oral vancomycin and IV metronidazole
- also bezlotoxumab
- stop opioid medications
How do you treat GORD?
- endoscopically proven: full dose PPI 1-2mo, no response double dose 1 mo
- not proven: full dose PPI 1 mo, no response H2RA or pro kinetic 1 mo
Complications of GORD:
- oesophagitis
- ulcers
- anaemia
- benign strictures
- Barret’s
- oesophageal carcinoma
Angiodysplasia, diagnosis and management:
- vascular deformity of GI tract predisposing to iron def anaemia and bleeding
- assoc with aortic stenosis
- diagnose with colonoscopy and mesenteric angiography if acute bleeding
- use endoscopic cautery or argon plasma coat
- antifibrinolytics e.g. tranexamic acid
Achalasia, features, investigations and treatment:
- degenerative loss of ganglia from Averbach’s plexus
- contracted sphincter and dilated oesophagus
- dysphagia of both liquid and solids, regurgitation of food, heartburn
- oesphageal manometry, bird’s beak on barium swallow, (tertiary contractions give rise to corkscrew appearance), wide mediastinum on CXR
- treat with intra-sphincteric injection of botulinum toxin
- Heller cardiomyotomy
- pneumatic balloon dilation
Alcohol Ketotacidosis:
- malnourishment breaks down fat - ketones
- metabolic acidosis
- elevated anion gap
- elevated serum ketone gap
- normal or low glucose
- treat with saline and thiamine
Diagnosis and management of SBP: (+most common bacteria)
- paracentesis: neutrophil count >250cells/uL
- most commonly e-coli
- IV cefotaxime
When would you give someone antibiotic prophylaxis for SBP?
- previous episode
- fluid protein <15g/L and either Child Pugh score of 9 or hepatorenal syndrome
- oral ciprofloxacin or norfloxacin if cirrhosis and ascites
SAAG >11g/L
indicates portal hypertension
-cirrhosis, alcoholic hepatitis, cardiac ascites, mixed ascites, massive liver metastases, fulminant hepatic failure, Budd-Chiari, portal vein thrombosis, veno-occlusive disease, myxoedema, fatty liver of pregnancy
SAAG <11g/L
- peritoneal carcinomatosis
- tuberculous peritonitis
- pancreatic ascites
- bowel obstruction
- biliary ascites
- postoperative lymphatic leak
- serositis in CTD
Management of ascites:
- reduce dietary sodium
- fluid restriction if sodium <125mmol/L
- aldosterone antagonist e.g. spironolactone
- drainage if tense ascites (albumin cover to reduce paracentesis induced circulatory dysfunction)
- prophylactic Abx to reduce risk SBP (ciprofloxacin or norfloxacin)
- TIPS
Features of refeeding syndrome:
- metabolic abnormalities after starvation
- catabolism switches abruptly to carb metabolism
- hypophosphataemia, hypokalaemia, hypomagnasaemia (Torsades), abnormal fluid balance, organ failure
Risk factors of refeeding syndrome:
- BMI <16kg/m2
- unintentional weight loss >15% in 3-6 months
- little nutritional intake >10 days
- reduced ions prior to feeding
- history of alcohol abuse, drug therapy, chemo, diuretics, antacids
What is Whipple’ disease and what are the features?
- multi system disorder by infection of Tropheryma Whippelii
- more common in HLA B27 and middle aged men
- malabsorption: diarrhoea and weight loss
- large joint arthralgia
- lymphadenopathy
- hyperpigmentation and photosensitivity
- pleurisy and pericarditis
- neuro symptoms
Investigation and management of Whipple’s disease:
- jejunal biopsy - macrophages containing periodic acid Shiff granules (PAS)
- oral co-trimoxazole and IV penicillin
What is the most common inheritable CRC?
HNPCC
Symptoms with villous adenoma:
- non-specific lower GI
- secretory diarrhoea
- microcytic anaemia
- hypokalaemia
Zollinger Ellison syndrome (features and diagnosis)
- excessive gastrin, usually duodenum or pancreas
- 30% as part of MEN I
- multiple gastroduodenal ulcers, diarrhoea, malabsorption
- diagnose with fasting gastrin level, secretin simulation test
What happens in Barret’s oesophagus, risk factors and management:
- metaplasia of lower oesophageal mucosa
- squamous becomes columnar
- increased risk of adenocarcinoma
- short: <3cm
- RF: GORD, male, smoking, central obesity
- Manage: endoscopic surveillance biopsy every 3-5 years, high dose PPI, endoscopic mucosal resection, radio frequency ablation
Histology of gastric cancer:
- signet ring cells
- contain mucin vacuoles which displace nucleus to side
- increased number = poorer prognosis
Associations of gastric cancer:
- H Pylori
- blood group A
- gastric adenomatous polyps
- pernicious anaemia
- smoking
- diet: salty, spicy, nitrates
- negatively associated with duodenal ulcers
Tumour types of GO junction:
- Type I: true oesophageal cancers associated with Barrett’s
- Type II: carcinoma of cardia, arising from cardiac type epithelium or short segments intestinal metaplasia at OG junction
- Type III: sub cardial, spread across junction
Treatment of gastric cancer:
- > 5-10cm from OG junction - sub-total gastrectomy
- total if <5cm
- type II - oesophagogastrectomy
- confined to muscosa (early) - endoscopic sub-mucosal resection
- lymphadenectomy
- chemotherapy
Most common location for CRC:
- rectal
- sigmoid
Types of CRC:
- 95% sporadic
- 5% HNPCC
- <1% FAP
FAP
- more than 100 adenomatous polyps in colon and rectum
- APC gene (over 80% of CRC)
- autosomal dominant
- 100% incidence if untreated
What is Gardner’s syndrome in FAP:
- osteomas of skull and mandible
- retinal pigmentation
- thyroid cancer
- epidermoid cysts on skin
Turcots syndrome:
- polyposis
- colonic tumours
- CNS tumours
- APC, MLH1 and PMS2
HNPCC
- most common inheritable (Lynch syndrome)
- CRC without extensive polyposis
- more right sided, histologically more mutinous and dense lymphocytic infiltrates
- associated with endometrial cancer, pancreatic, renal and CNS
- MSH2, MLH1 and PMS2
- Amsterdam criteria
What is the Amsterdam criteria?
- must have 3 in 2 successive generations showing HNPCC tumours with 1 >50yo
- exclude FAP
Cowden disease
- multiple hamartomas
- many mucocutaneous lesions, trichilemmomas, oral papillomas and aural keratosis
- breast cancer and thyroid disease
- PTEN
MYH associated polyposis
- autosomal recessive, multiple adenomatous polyps in GI tract
- in colon - KRAS mutations (oncogenes)
CRC screening:
Faecal Immunochemical Test -screening every 2 years men and women 60-70yo -type of faecal occult blood test -abnormal results - colonoscopy Flexible sigmoidoscopy
Referral in CRC:
Urgent (within 2 weeks)
->=40yo with unexplained weight loss AND abdominal pain
->=50 yo with unexplained rectal bleeding
->=60 yo with iron deficiency anaemia or change in bowel habit
-occult blood in faeces
Consider
-rectal/abdominal mass
-unexplained anal mass or ulceration
-<50yo with rectal bleeding and pain, change in weight or anaemia
