g a s t r o Flashcards
what are the key sx seen in patients with gastro/hepatology disease
abdominal pain jaundice haematemesis malaena diarrhoea nausea and vomiting
what are differentials for abdominal pain
https://litfl.com/abdominal-pain-ddx/
what are differentials for haematemesis
VINTAGE
- Varices
- Inflammation
Oesophago-gastro-duodenitis PUD: DU is commonest cause - Neoplasia
Oesophageal or gastric Ca - Trauma
Mallory-Weiss Tear = Mucosal tear due to vomiting
Boerhaave’s Syndrome Full-thickness tear, 2cm proximal to LOS - Angiodyspepsia and vascular abnormalities
Angiodysplasia
HHT
Dieulafoy lesion: rupture of large arteriole in stomach or
other bowel - Generalised bleeding diathesis
Warfarin, thrombolytics CRF - Epistaxis
what are the differentials for dysphagia
1. Inflammatory Tonsillitis, pharyngitis Oesophagitis: GORD, candida Oral candidiasis Aphthous ulcers 2. Mechanical Block Luminal FB Large food bolus Mural Benign stricture Web (e.g. Plummer-Vinson) Oesophagitis Trauma (e.g. OGD) Malignant stricture Pharynx, oesophagus, gastric Pharyngeal pouch Extra-mural Lung Ca Rolling hiatus hernia Mediastinal LNs (e.g. lymphoma) Retrosternal goitre Thoracic aortic aneurysm 3. Motility Disorders Local Achalasia Diffuse oesophageal spasm Nutcracker oesophagus Bulbar / pseudobulbar palsy (CVA, MND) 4. Systemic Systemic sclerosis / CREST MG
what are the differentials for diarrhoea
- Acute
Suspect gastroenteritis Travel, diet, contacts? - Chronic
Diarrhoea alternating ̄c constipation: IBS
Anorexia, ↓wt., nocturnal diarrhoea: organic cause - Bloody
Vascular: ischaemic colitis
Infective: campylobacter, shigella, salmonella, E. coli,
amoeba, pseudomembranous colitis
Inflammatory: UC, Crohn’s
Neoplastic: CRC, polyps - Mucus
IBS, CRC, polyps - Pus
IBD, diverticulitis, abscess
what are the ddx for jaundice
pre hepatic = excess BRR production = haemolytic anaemia, ineffective erythropoiesis (thalassaemia)
hepatic unconjugated = reduced BR uptake: drugs - contrast, RMP, CCF
hepatic unconjugated = reduced BR conjugation: hypothyroidism, Gilbert’s, Crigler-Najjar
hepatic uncojugated = neonatal jaundice = both increase production and reduced conjugation
what are the features to ask about in history of suspected upper GI bleed
Previous bleeds Dyspepsia, known ulcers Liver disease or oesophageal varices Dysphagia, wt. loss Drugs and EtOH Co-morbidities
what are signs to look out for O/E in upper GI bleed
signs of CLD PR:melaena Shock? Cool, clammy, CRT>2s ↓BP (<100) or postural hypotension (>20 drop) ↓ urine output (<30ml/h) Tachycardia ↓GCS
what are the common causes of upper GI bleeding
PUD: 40% (DU commonly) Acute erosions / gastritis:20% Mallory-Weiss tear: 10% Varices: 5% Oesophagitis: 5% Ca Stomach / oesophagus:<3%
what score is used to determine severity of bleed/ mortality
Rockall score
can be done pre and post endoscopy
Initial score pre-endoscopy
Age
Shock: BP, pulse
Comorbidities
Final score post-endoscopy
Final Dx + evidence of recent haemorrhage:
Active bleeding
Visible vessel
Adherent clot
Initial score ≥3 or final >6 are indications for surgery
what are oesophageal varices and what is the pathophysiology. which veins are affected
Portal HTN → dilated veins sites of porto-systemic anastomosis: L. gastric and inferior oesophageal veins
what are the causes of portal HTN
Pre-hepatic: portal vein thrombosis
Hepatic: cirrhosis (80% in UK), schisto (commonest
worldwide), sarcoidosis.
Post-hepatic: Budd-Chiari, RHF, constrict pericarditi
what is the first line and second line bleed prevention for oesophageal varices
1O: β-B, repeat endoscopic banding
2O: β-B, repeat banding, TIPSS
how does TIPPS work
interventional radiology creates articifical channel between hepatic vein and portal vein = reduce portal pressure
describe the acute management of upper GI bleed
100% O2, protect airway
2 x 14G cannulae + IV crystalloid infusion up to 1L.
Bloods: FBC, U+E (↑ urea), LFTs, clotting, x-match
6u, ABG, glucose
Blood if remains shocked
Group specific or O- until X-matched
Variceal Bleed
Terlipressin IV (splanchnic vasopressor)
Prophylactic Abx: e.g. ciprofloxacin 1g/24h
Maintenance
Crystalloid IVI, transfuse if necessary (keep Hb≥10)
Catheter + consider CVP (aim for >5cm H2O)
Correct coagulopathy: vit K, FFP , platelets
Thiamine if EtOH
Notify surgeons of severe bleeds
Urgent Endoscopy Haemostasis of vessel or ulcer:
Adrenaline injection
Thermal / laser coagulation
Fibrin glue
Endoclips
Variceal bleeding:
2 of: banding, sclerotherapy, adrenaline,
coagulation
Balloon tamponade ̄c Sengstaken-Blakemore tube
Only used if exsanguinating haemorrhage or failure of endoscopic therapy
TIPSS if bleeding can’t be stopped endoscopically
After endoscopy
Omeprazole IV + continuation PO (↓s re-bleeding)
Keep NBM for 24h → clear fluids → light diet @ 48h
Daily bloods: FBC, U+E, LFT, clotting
H. pylori testing and eradication
Stop NSAIDs, steroids et.c.
Indications for Surgery
Re-bleeding
Bleeding despite transfusing 6u
Uncontrollable bleeding at endoscopy
Initial Rockall score ≥3, or final >6.
Open stomach, find bleeder and underrun vessel.
describe the macroscopic similarities and differences between UC and Crohn’s
UC = rectum and colon + backwash ileus. continuous distribution, no strictures.
Crohn’s = mouth to anus esp terminal ileum. skip lesions. strictures.
describe the microscopic similarities and differences between UC and Crohn’s
UC = mucosal, crypt abscesses, shallow borad ulceration, pseudopolyps, drainpipe colon due to loss of haustral markings, string sign of Kantour - narrowing of lumen
Crohn’s = transmural, cobblestone mucosa, fibrosis, non caseous granuloma, fistulae, rose thorn ulcers
describe the aetiology of UC and Crohn’s
UC = smoking protective, TH-2 mediated `Crohn's = smoking increases risk, TH1/TH17 mediated
describe the presentation, sx in IBD and differences in UC vs Crohn’s
systemic = fever, malaise, anorexia, wt loss in active disease
abdominal = diarrhoea (bloody in UC), abdominal discomfort, tenesmus, faecal urgency
what are the clinical signs seen in IBD
tender, distended abdomen
aphthous ulcers, glossitis
abdominal tenderness
Crohn’s;
RIF mass
perianal abscess, fistulae
tags
anal/ rectal strictures
what are extra abdominal manifestations of IBD
1. Joints Arthritis (non-deforming, asymm) Sacroiliitis Ank spond 2. HB PSC + cholangiocarcinoma (esp. UC) Gallstones (esp. Crohn’s) Fatty liver 3. Other Amyloidosis Oxalate renal stones (esp. Crohns) 4. Skin Clubbing Erythema nodosum Pyoderma gang (esp. UC) 5. Eyes Iritis Episcleritis Conjunctivitis
what are the complications seen in IBD
- toxic megacolon = diameter greater than 6cm, risk of perforation
- malignancy = CRC, cholangiocarcinoma
- strictures = obstruction
- venous thrombosis
Crohns
- fistulae
- strictures = obstruction
- abscesses = abdominal, anorectal
- malabsorption = fat = gallstones, steatorrhoea, b12 megaloblastic anaemia, vit d osteomalacia, protein oedema
what investigations are required in ulcerative IBD
Bloods:
FBC: ↓Hb, ↑WCC LFT: ↓albumin
↑CRP/ESR
Blood cultures
Stool
MCS: exclude Campy, Shigella, Salmonella… CDT: C. diff may complicate or mimic
Imaging
AXR: megacolon (>6cm), wall thickening CXR: perforation
CT
Ba / gastrograffin enema
Lead-pipe: no haustra
Thumbprinting: mucosal thickening
Pseudopolyps: regenerating mucosal island
Ileocolonoscopy + regional biopsy: Baron Score
how is the severity of UC determined
Truelove and Witts criteria
motions, PR bleed, temp, HR, Hb, ESR
mild, moderate and severe
How is acute severe UC managed
Resus: Admit, IV hydration, NBM Hydrocortisone: IV 100mg QDS + PR Transfuse if required Thromboprophylaxis: LMWH Monitoring Bloods: FBC, ESR, CRP, U+E Vitals + stool chart Twice daily examination ± AXR
describe the acute complications of severe UC
- Perforation
Bleeding
Toxic megacolon (>6cm)
VTE
in severe acute UC if no improvement vs improvement
Improvement → oral therapy
Switch to oral pred + a 5-ASA
Taper pred after full remission
No Improvement → rescue therapy
On day 3: stool freq >8 or CRP >45
Predicts 85% chance of needing a colectomy during
the admission
Discussion between pt, physician and surgeon
Medical: ciclosporin, infliximab or visilizumab (anti-T cell)
Surgical
what drugs are used to induce UC remission
Oral Therapy
1st line: 5-ASAs
2nd line: prednisolone
Topical Therapy: mainly left-sided disease
Proctitis: suppositories
More proximal disease: enemas or foams
5-ASAs ± steroids (prednisolone or budesonide)
what drugs are used to maintain remission in UC
1st line: 5-ASAs PO – sulfasalazine or mesalazine
Topical Rx may be used in proctitis
2nd line: Azathioprine or 6-mercaptopurine
Relapsed on ASA or are steroid-dependent
Use 6-mercaptopurine if azathioprine intolerant
3rd line: Infliximab / adalimumab
what are the indications for surgery in UC
Toxic megacolon
Perforation
Massive haemorrhage
Failure to respond to medical Rx
what investigations are required for IBD Crohn’s, what results are expected
Bloods: (top 3 are severity markers) FBC: ↓Hb, ↑WCC
LFT: ↓albumin
↑CRP/ESR
Haematinics: Fe, B12, Folate
Blood cultures Stool
MCS: exclude Campy, Shigella, Salmonella…
CDT: C. diff may complicate or mimic Imaging
AXR: obstruction, sacroileitis CXR: perforation
MRI
Assess pelvic disease and fistula
Assess disease severity
Small bowel follow-through or enteroclysis
Skip lesions
Rose-thorn ulcers
Cobblestoning: ulceration + mural oedema
String sign of Kantor: narrow terminal ileum
Endoscopy
Ileocolonoscopy + regional biopsy: Ix of choice Wireless capsule endoscopy
Small bowel enteroscopy
how is severity of Crohn’s determined
temp, albumin reduces, ESR, CRP, WCC, HR increases
describe how acute severe Crohn’s is managed
Resus: Admit, NBM, IV hydration Hydrocortisone: IV + PR if rectal disease Abx: metronidazole PO or IV Thromboprophylaxis: LMWH Dietician Review Elemental diet Liquid prep of amino acids, glucose and fatty acids Consider parenteral nutrition Monitoring Vitals + stool chart Daily examination
what action is taken when no improvement or improvement in acute sever crohn’s
Improvement → oral therapy Switch to oral pred (40mg/d) No Improvement → rescue therapy Discussion between pt, physician and surgeon Medical: methotrexate ± infliximab Surgical
what drugs are used to induce remission in Crohn’s
Supportive High fibre diet Vitamin supplements Oral Therapy 1st line Ileocaecal: budesonide Colitis: sulfasalazine 2nd line: prednisolone (tapering) 3rd line: methotrexate 4th line: infliximab or adalimumab
what investigations and management is given in Crohns peri anal disease
MRI + EUA Rx
Oral Abx: metronidazole
Immunosuppression ± infliximab Local surgery ± seton insertion
what drugs are used to maintain remission in Crohn’s
1st line: azathioprine or mercaptopurine 2nd line: methotrexate
3rd line: Infliximab / adalimumab
before using azathioprine what levels should be checked
+TPMT activity should be assessed before starting
what are the indications for surgery in crohns
Emergency
Failure to respond to medical Rx
Intestinal obstruction or perforation Massive haemorrhage
Elective
Abscess or fistula
Perianal disease Chronic ill health Carcinoma
what is the pathophysiology behind coeliac disease
HLA-DQ2 (95%) and DQ8
CD8+ mediated response to gliadin in gluten
how does coeliac present
GLIAD
gi malabsoption = carbs, fat, protein, vitamins
lymphoma and carcinoma = enteropathy associated T cell lymphoma, adenocarcinoma of small bowel
immune associations = PBC, T1DM, IgA deficiency
anaemia = MCV increased or decreased
dermatological = dermatitis herpetiformis, aphthous ulcers
what investigations are required in coeliac disease
Bloods: FBC, LFTs (↓alb), INR, Vit D and bone, red cell
folate, serum B12
Abs
Anti-endomysial IgA (95% specificity)
Anti-TTG IgA
Both above ↓ ̄c exclusion diet
Anti-gliadin IgG persist ̄c exclusion diet)
IgA ↑ in most but may have IgA deficiency
Stools
Stool cysts and antibody: exclude Giardia
OGD and duodenal biopsy
Subtotal villous atrophy
Crypt hyperplasia
Intra-epithelial lymphocytes
how is coeliac managed
Lifelong gluten-free diet Avoid: barley, rye, oats, wheat OK: Maize, soya, rice Verify diet by endomysial Ab tests Pneumovax as hyposplenic Dermatitis herpetiformis: dapsone
what is refeeding syndrome
emtabolic abnormalities which occur on feeding a person following a period of starvation.
It occurs when an extended period of catabolism ends abruptly with switching to carbohydrate metabolism
what are the metabolic consequences of referring syndrome
hypophosphataemia
hypokalaemia
hypomagnesaemia: may predispose to torsades de pointes
abnormal fluid balance
these abnormalities can lead to organ failure
which patients are at high risk of re feeding syndrome
low BMI
unintentional weight loss of 1-=15 percent over a few months
little nutritional intake
hx pf alcohol abuse, drug therapy inc insulin chemo
if a patient hasn’t eaten for > 5 days, aim to re-feed at
no more than 50% of requirements for the first 2 days
histology in crohns vs UC
CROHNS = inflammation in all layers from mucosa to serosa
increase goblet cells, granulomas
UC = no inflammation beyond submucosa, inflammatory cell infiltrate in lamina propria, crypt abscess, depletion of goblet cells, no granulomas
radiology in crohns vs UC
Crohns = small bowel enema = kantor string sign - structuring
proximal bowel dilation
rose thorn ulcers
fistulae
UC = loss of haustrations, pseudopolys, drainpipe colon
pain on swallowing is known as
odynophagia
