Gastroenterology Flashcards
List common differentials for dysphagia & their distinguishing features
Oesophageal Ca - WL, anorexia, vomiting during eating. PMHx of barrets/ GORD/ excessive smoking or alcohol use
Oesophagitis - Hx of heartburn. Odynophagia but no weight loss and systemically well
Oesophageal candidiasis - history of HIV or steroid use
Achalasia - dysphagia to both liquids and solids from the start. Heartburn and regurgitation of food. Regurgitation can lead to cough/ aspiration.
Pharyngeal pouch - more common in older men, usually not seen but if so it is a midline lump that gurgles on palpation. Typical sx of dysphagia, regurgitation, aspiration and cough with halitosis.
Systemic sclerosis - Other features of CREST syndrome - Calcinosis, Raynaud’s, Oesophageal dysmotility, sclerodactyly, telangiectasia. As well as oesophageal dysmotility the LES is relaxed - contrasting to achalasia where LES pressure is increased.
Myasthenia gravis - other sx including extraocular muscle weakness or ptosis, dysphagia to both liquids and solids.
Globus hystericus - Hx of anxiety, symptoms are intermitted and relieved by swallowing. Usually painless.
Key differences - Crohns vs UC - Presenting sx
Presenting symptoms:
Crohns - non bloody diarrhoae, WL, mouth ulcers, perianal disease.
UC - bloody diarrhoea more common and abdominal pain LLQ + tenesmus.
Key differences - Crohns vs UC - Extra intestinal manifestations
Crohns - Gallstones are more common in crohns due to reduced bile acid resoprtion.
UC - Primary sclerosing cholangitis more common.
What is primary sclerosing cholangitis
PSC - chronic liver disease characterised by inflammation and fibrosis of the bile ducts leading to cirrhosis and liver failure. Strongly associated with UC but not Crohns. Pathogenesis unclear but thought immune mediated damage to biliary epithelium which can be triggered by gut derived antigens in genetically susceptible individuals. 80% of those with PSC have concurrent UC only 3% associated with crohn’s.
Key differences - Crohns vs UC - complications
Crohns - Obstruction, fistulas and colorectal cancer
UC - Risk of colorectal cancer is higher in UC
Key differences - Crohns vs UC Pathology
Crohns - lesions seen anywhere from mouth to anus and skip lesions.
Histology:
Inflammation in ALL layers from mucosa to serosa.
Increased Goblet cells.
Granulomas Common
UC - Inflammation starts at rectum and never spreads beyond IC valve. Continuous disease.
Histology:
Inflammation from mucosa to lamina propria ( submucosa only).
Neutrophils migrate through the walls of glands to form Crypt Abscesses.
Depletion of Goblet cells and mucin from gland epithelium.
Granulomas rare.
Key differences - Crohns vs UC Endoscopy results
Crohns - transmural inflammation and presence of granulomas.
Discontinuous lesions, skip lesions, strictures, linear ulceration.
UC - Mucosal and submucosal inflammation, polymorphonuclear cells aggregate. Continuous lesions, Prescence of crypts, formation of residual mucosal tissue that has the appearance of polyps ( pseudopolyps).
Key differences - Crohns vs UC on radiology
Crohns - Small bowel enema has high sensitivity and specificity for terminal ileum. Strictures “ Kantors string sign”. Proximal bowel dilation. “ Rose thorn” ulcers, Fistula.
UC- Barium enema - Loss of haustrations, Superficial ulceration “ pseudopolyps” , colon narrow and short “ Drain pipe colon.”
Equation for units of Alcohol
Milliliters of drink (mls) x ABV ( percentage strength of drink) / 1000.
E.g. Half standard 175 ml glass of wine - 87.5 x 12/ 1000 = 1.05 units
Gastric cancer: RF
1) Older > 75 yrs
2) male
3) H pylori infection
4) Atrophic gastritis
5) Pernicious anaemia
6) Diet - salt and nitrates
7) Smoking
8) Blood group A
Symptoms Gastric cancer
Abdominal pain - vague, epigastric, dyspepsia
WL
Anorexia
N & V
Dysphagia - if cancer in proximal stomach
Upper GI bleed ( minority)
Lymphatic spread - L supraclavicular Node ( Virchows node), periumbilical node ( Sister mary joseph nodule).
Investigations and key histological finding in Gastric cancer
Endoscopy with biopsy - Signet ring cells ( large vacuole that pushes nucleus to the side). Higher number of signet cells associated with worse prognosis.
Staging CT
MX Gastric Ca
Surgical - depending on extent and side but include:
Endoscopic mucosal resection
Partial Gastrectomy
Total gastrectomy
Chemotherapy
SBP - define and pathology
SBP - is an infection of the ascitic fluid in patients with Cirrhosis.
Spread of bacteria can be haematogenous from intestines to ascitic fluid. Due to depression of immune function of the liver with cirrhosis, intestinal bacterial overgrowth and venous stasis ( portal HTN) that increases intestinal permeability to enteric bacteria.
Can be non intestinal from RTI/UTI.
Presentation of SBP
Patient with known end stage liver disease ( often decompensated).
Abdominal pain & tender
Ascites - shifting dullness, Flank dullness, fluid wave
Fever
N& V & Diarrhoea ( secondary to intestinal hypomotility and bacterial overgrowth)
Confusion/ hepatic encephalopathy
GI bleed.
Diagnosis of SBP
MX SBP
Paracentesis - neutrophil count > 250 cells/ ul
Most common organism is E Coli
IV cefotaxime
When do we give prophylactic abx in SBP?
Pts with prev ep SBP
Patients with fluid protein < 15 g/ l or Child pugh score of at least 9 or hepatorenal syndrome
NICE recommend: ‘Offer prophylactic oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less until the ascites has resolved’
DDx of Upper Gi bleed
Oesophageal causes:
Oesophagal varices - Large volume of fresh blood. Malaena from swallowed blood. HaemoD compromise. May stop spontaneously but rebleed is common.
Oesophagitis - small volume of fresh blood often streaking vomit, malaena rare. Often stops spont. Hx of GORD.
Cancer - small volume except as preterminal event with erosion of major vessels. Ax sx of dysphagia and WL.
Mallor weiss tear - small to mod volume bright red blood following repeated vomiting. Malaena rare and stops spontaneously.
Gastric causes:
Gastric ulcer - small volume bleed + ida. Erosion into significant vessel may produce considerable haemorrhage / haematemesis.
Gastric Ca - Frank haem or blood mixed w vomit. Usually prodromal sx of dyspepsia and constitutional sx.
Dielaufoy lesion - Often no prodromal features and AVM can produc considerable haemorrhage.
Erosive gastritis - haematemesis & epigastric discomfort. Usually NSAID usage.
Duodenal
Duodenal ulcer - posterior sited and may erode gastroduodenal artery. Pain usually several hours after eating.
Score used for assessment of upper Gi bleed
Glasgow Blatchford score - Estimates the risk of Upper GI bleed. Score of 0 suggests consideration of Early D/C.
Takes into account:
Hb count
Urea
SBP
HR
Syncope
Malena
Liver disease
Hf
Scoring used for endoscopy in Upper GI bleed
Rockall score = risk of rebleeding and mortality. Takes into account the endoscopy findings plus:
Age
Shock features
Comorbidities
Cause of bleeding
General management tips of Upper GI bleed
ABATED:
A-E approach
Bloods &
Access ( two wide bore cannula, FBC, Clotting, G&S , u&Es , LFTs)
Transfusions - Platelets if count < 50, Prothrombin complex concentrate to pts with warfarin. FFP to those with fibrinogen level < 1g/ L or PTT/INR/APTT > 1.5 x normal.
Endoscopy within 24 hours. Should be offered immediately after rescucitation to patients with a severe bleed.
Drugs - stops anticoagulants and NSAIDS
Management tips for non variceal bleeding
NICE do not recommend PPi before endoscopy to pts with suspected non variceal upper GI bleding although PPI should be given to pts with non variceal upper GI bleed & stigmata of recent haemorrhage shown at endoscopy.
Endoscopic mx - thermal cautery, mechanical clips, injection of saline/ adrenaline to induce tamponade with sclerosant.
C Diff infection - pathology
Gram +ve rod, produces exotoxin which causes intestinal damage leading to syndrome called pseudomembranous colitis.
C diff develops when normal gut flora are suppressed by broad spectrum abx. 3rd/4th gen cephalosporins - Ceftriaxone/ ceftazadime/ clindamycin.
Risk factors for C difficile
Broad spectrum abx
increasing age / prolonged hospital stay / nursing home resident
Exposure to infected family member
Hx of prev c diff
IBD
Immunosuppression
Mx of variceal bleeding
Terlipressin and prophylactic abx given to pts at presentation ( prior to endoscopy).
Band ligation and injections of sclerosing agents.
TIPS ( transjugular intrahepatic portosystemic shunt) if bleeding not controlled with above measures).
Features of C diff infection
Presence of RFs
Diarrhoea
Abdominal pain
Fever
N&V
Abdominal distention / tenderness
*A Raised WCC is characteristic & be aware severe toxic megacolon may develop.
Severity scale in C diff infection
Mild - normal wcc
Moderate - raised WCC but under 15, 3-5 loose stools/ day
Severe - WCC > 15 or acute creatinine rise > 50% above baseline. T > 38.5 or evidence of severe colitis ( abdominal or radiological signs).
Life threatening - Hypotension, partial or complete ileus, Toxic megacolon or CT evidence of severe disease/
Diagnosis of C diff infection
Detection of C Diff Toxin in stool CDT
C diff antigen positivity only shows exposure to bacteria rather than a current infection.
Management of C diff infection
Management of recurrent C diff
1st line - oral vancomycin 10 d
2nd line - oral fidaxomicin
3rd line - oral vanc +/- IV metronidazole
Life threatening - Oral vancomycin AND IV metronidazole.
Other therapy:
Monoclonal antibody Bezlotoxumab ( NICE not currently supporting).
Faecal microbiota transplant - in those who have had two or more episodes.
Recurrent episode - occurs in 20% of pts, increasing to 50% if 2nd infection. If reccurence before 12 weeks - oral fidaxomicin. After 12 weeks - oral vanc or fidaxomicin.
SE’s of PPi
Low Na/ mg
Osteoporosis - increased risk fractures ( malabsorption of mg and Ca)
Microscopic colitis
Increased risk of C diff infection
Can mask symptoms of gastric cancer.
Hepatocellular vs cholestatic vs mixed disease - pattern of ALT/ALP and ALT/ALP ratio
Metoclopramide SE/Cautions
Metoclopramide is a DR receptor antagonist. Has prokinetic actions and is useful in the mx of nausea, diabetic gastroparesis, and in mx of nausea from migraine.
SE:
Exyrapyramidal effects - acute dystonia and oculogyric crisis. Tardive dyskinesis, parkinsonism, hyperprolactinaemia.
Avoid in bowel obstruction
Coeliac disease - 1st line ix
First-line investigations for coeliac disease should include a serum immunoglobulin IgA tissue transglutaminase antibody (tTGA) and total IgA. Testing for specific IgA antibodies must be done alongside a total IgA level, as if the patient has an IgA deficiency, the results may be falsely negative. Selective IgA deficiencies are also more common in people with coeliac disease.
Mx of UC - inducing remission
Treating mild - moderate UC :
Proctitis - Rectal aminosalicylate ( mesalazine). If remission not achieved in 4 weeks add oral aminosalicyate. If still not achieved add topical or oral steroid.
Proctosigmoiditis / L sided UC - Topical aminosalicylate. If remission not achieved in 4 weeks switch to high dose oral aminosalicylate and topical steroid. If still not achieved offer oral steroid.
Extensive disease - topical rectal aminosalicylate PLUS oral. IF remission not achieved in 4 weeks stop topical and offer high dose oral + steroid.
Severe UC - Hospital admission, IV steroid 1st line. IV ciclosporin if steroid CI. If after 72 hours unsuccessful then consider adding IV ciclosporin to IV steroid or consider surgery.
UC mx - maintaining remission
Following mild- mod flare of UC:
Proctitis & proctosigmoiditis - Topical rectal aminosalicylate alone OR oral aminosalicylate plus topoical OR oral aminosalicylate alone.
Left sided and extensive UC - Low dose oral aminosalicylate.
Following severe relapse or >= 2 exacerbations / yr then oral azathioprine or oral mercaptopurine.
Severities of UC
The severity of UC is usually classified as being mild, moderate or severe:
mild: < 4 stools/day, only a small amount of blood
moderate: 4-6 stools/day, varying amounts of blood, no systemic upset
severe: >6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers)
Mx of variceal haemorrhage
A-E - rescucitation, correct clotting and tranfusions ( FFP/Vit K/ platelets)
Terlipressin ( causes vasoconstriction of the splanchnic circulation reducing bleeding)
Prophylactic IV abx - Quinolones
Endoscopy - bang ligation, sclerotherapy, TIPSS if above fails.
Prophylaxis of variceal haemorrhage
Propanolol - reduced rebleeding and mortality
Endoscopic band ligation ( superior to sclerotherapy). Performed at two weekly intervals until all varices have been eradicated. PPI cover given to prevent EVL induced ulceration.
Guidance on re-testing with H Pylori?
NICE guidance advises that we should not routinely offer H. pylori re-testing, however we can consider re-testing if:
There has been poor compliance to eradication therapy
Aspirin or NSAID is indicated
There is a family history of gastric malignancy
The person requests re-testing
They advise that re-testing should ideally be done 8 weeks after initial eradication therapy and the carbon-13 urea breath test should be used first-line.
What is Primary biliary cirrhosis?
Autoimmune condition with progressive inflammation & damage to the cholangiocytes lining the intrahepatic ducts. Leads to obstruction of bile flow and cholestasis. Ultimately leads to liver fibrosis , cirrhosis and liver failure.
Presentation of PBC
Typically affects females
40- 60 yrs
often asymptomatic on initial presentation then picked up with abnormal LFTs. Bile acids , bilirubin and cholesterol normally excreted via bile ducts build up in the blood. Bile acids cause itching, bilirubin causes jaundice. Lack of bile acids leads to malabsorption of fats and greasy stools, lack of bilirubin excretion leads to pale stools and dark urine. Raised cholesterol leads to deposits in the skin called xanthelasma & xanthomas in skin or tendons ( large cholesterol deposits in tendons). Increased risk CV disease.
Symptoms:
Fatigue
Itching
Abdo pain / RUQ pain
Jaundice
Pale greasy stools
Dark urine
Examination:
Xanthoma and xanthelasma
Excoriation
Hepatomegaly
Signs of liver cirrhosis ( splenomegaly and ascites)
Clubbing
haemochromatosis
1) inheritance pattern
2) Genetic problem
3) presentation
Haemochromatosis is an Autosomal Recessive disorder. ( require 2x copies to inherit disorder).
Mutations in human haemochromatosis protein ( HFE) gene on chromosome 6, gene important in regulating iron metabolism. ( Encodes for a gene that regulates the expression of iron regulating hormone hepcidin, get low expression of hepcidin therefore uncontrolled duodenal absorption of iron).
Iron accumulates in multiple organs including liver, heart, anterior pituitary, pancreas & joints.
Presentation: * often later presentation in women due to iron loss with menses, typical age > 40 yrs men, later for W *
Chronic tiredness
Joint pain
Pigmentation ( bronze skin)
Anterior pit signs:
Testicular atrophy and erectile dysfunction
Amenorrhoea
Cognitive symptoms - memory and mood disturbance
Hepatomegaly
Complications of haemochromatosis ?
Iron accumulation in multiple organs:
Pituitary - hypogonadism, testicular atrophy, ED, amenorrhoea
Thyroid - hypothyroid
Cardiac - arrythmias and cardiomyopathy
Liver - cirrhosis & hepatocellular carcinoma
Pancreas - T1 DBM
Chondrocalcinosis
Oesophageal Cancer:
Most common type
Two types , where are they most common, location in oesophagus and Rf’s?
Adenocarcinoma is now the most common type of oesophageal cancer and is more likely to develop in patients with a history of gastro-oesophageal reflux disease (GORD) or Barrett’s.
Key RFs - male, increasing age, smoking & alcohol, barretts , GORD, hiatus hernia , FHX, Low SE status
Non white race - higher risk SCC
Presentation of primary sclerosing cholangitis?
Investigation
Risks
Often pts asymptomatic at diagnosis with problem picked up on abnormal LFTs.
Male
BG UC
Abdominal pain ruq
Fatigue
Jaundice
Itching
hepatomegaly
Splenomegaly
Investigation:
Deranged LFT - ALP & obstructive picture
Autoantibodies LESS helpful , pANCA +Ve (ANA, Anti SMA )
imaging - MRCP diagnostic - showing bile duct strictures “ beaded appearance”.
Limited role for liver biopsy - fibrous, obliterative changes
Colonoscopy for ? UC
Risks –> increased risk cholangiocarcinoma and colorectal cancer
Presentation of Wilsons disease?
Presenting symptoms result from excessive copper in tissues including the liver, brain and cornea.
Uusally presents in teenager or young adult ( 10-25 yrs) , rarely > 40 yrs. Liver problems usually arise first in children, whereas neurological disease in adults.
Liver –> hepatitis and later cirrhosis
Neurological –>
Tremor & parkinsonism ( rigidity, bradykinesia) due to deposition in basal ganglia.
Dystonia
Speech difficulties
Psychiatric –> abnormal behaviour, depression, cognitive impairment and psychosis.
Kayser Fleischer rings - deposition in cornea.
Haemolytic anaemia
Renal tubular damage
Ascites causes
Grouped into transudative causes or exudative causes based on the serum albumin to ascitic gradient ( SAAG)
SAAG = Serum Albumin - Ascitic fluid albumin
> 11g - transudative
< 11g - exudative
Transudative causes of ascites: ( SAAG > 11g/L)
1) Cirrhosis ( NAFLD/ Alcoholic cirrhosis/ Hep b/c)
2) Acute liver failur
3) liver mets
4) R Heart failure
5) Portal vein thrombosis / Budd chiari ( triad of occlusion of hepatic veins, abdo pain and ascites)
Exudative causes: SAAG < 11g/L
Hypoalbuminaemia - nephrotic syndrome or severe malnutrition
Malignancy - peritoneal mets
Infection - TB peritonitis
Pancreatitis
Biliary ascites
Bowel obstruction
Post op lymph leak
