Gastroenterology Flashcards

Question

Describe the following oesophageal disorders - Oesophageal spasm - Mallory Weiss Syndrome - Plummer Vinson Syndrome - Boerhaave Syndrome

Answer 1

**Oesophageal spasm** - rare. elderly women. - Diffuse (uncoordinated spasm -> dysphagia) or nutcracker oesophagsu (coordinated but excessive -> severe, crushing, central retrosternaal chest pain episodes) **Mallory Weiss Syndrome** - severe vomiting --> painful mucosal lacerations at gastroesophageal junction -> haematemsis - Common in alcoholics. Self-resolving. - Ix as per any cause of upper GI bleed **Plummer-Vinson Syndrome** (unknown cause) - Triad: Dysphagia (due to oesophageal webs); Glossitis, IDA - Treat w/ iron supplementation + dilation of webs **Boerhaave Syndrome** - Severe vomiting or iatrogenic-> oesophageal rupture/perforation - severe sudden onset retrosternal chest pain, resp distress, subcut emphysema following severe vomiting/retching (mackler's triad) - CXR- pneumomediastinum + intra-thoracic air-fluid levels - CT w contrast - air/fluid in mediastinum or pleural cavity w/ leak of contrast from oesophagus - Manage: Resus + surgery to control leak

Answer 2

All present in acute phase w/ jaundice, RUQ pain, hepatomegaly, fever, raised LFTs, flu-like prodrome **Hepatitis A** Route: faecal-oral Course: acute + self-limiting Chronic disease: No Cancer: No Vaccine: Yes (given to at risk e.g. travel, MSM, IVDU, chronic liver disease, some occupation) **Hepatitis B** Route: infected body fluid, vertical Chronic: Yes (but only 10%) Cancer: yes Vaccine: Yes (given as part of routine schedule and then again to at risk groups. Healthcare workers + CKD have Anti-HbS checked to check response (>100 adequate, 10-100 needs further dose, <10 = non-responder, needs to repeat course) Management: Pegylated interferon **Hepatitis C** Route: body fluid, vertical Chronic: Yes in >50% --> cirrhosis, sjogren's arthralgia, porphyria cutanea tarda Cancer: yes Vaccine: No Management: interferon based (95% clearance) **Hepatitis D** Route: same as B (so often co-infection); can also have superinfection (start w/ B then later D infection) Chronic: yes (higher risk in superinfection) Cancer: Yes Vaccine: No Treatment: interferon **Hepatitis E** Route: faecal-oral Chronic: No Cancer: No Vaccine: No Management: supportive

Answer 3

**Autoimmune Hepatitis** - Mostly in young women - Presentation: chronic liver disease or acute hepatitis; amenorrhoea (common) - Ix: ANA, SMA, LKM1 antibodies, IgG raised, inflammation + piecemeal/bridging necrosis on biopsy - Mx: steroids, immunosupressants, transplant **Drug-Induced Liver Disease** Hepatocellular picture: paracetamol, alcohol, statins, amiodrone, Anti-TB (except ethambutol), Antiepileptics Cholestatic picture: COCP, abx (fluclox, co-amox, erythromycin), steroids, sulphonylureas Cirrhosis: methotrexate, methyldopa, amiodarone **Fatty Liver** - Types: steatosis, steatohepatitis, cirrhosis/fibrosis - RF: obesity, T2DM, raised lipid - Present: normally asymptomatic, hepatomegaly - Ix ALT>AST (whereas alcoholic AST>ALT), increased echogenicity on USS, ELF (blood test to look for enhanced fibrosis or fibroscan if blood test not available) - Management: Life-style changes + monitoring

Answer 4

**Pathophysiology** Live failure = inability to perform normal function Can be: acute, acute-on-chronic or chronic Causes: drugs, autoimmune, infection, fatty liver or pregnancy **Presentation** - May be signs of chronic liver disease: clubbing, palmar erythema, duputrens, spider naevi, gynaecomastia - Acutely: - Jaundice - Hepatic encephalopthy - confusion, altered GCS, asterixis, constructional apraxia. Treat cause + give lactulose or rifaximin - Coagulopathy - Low Albumin - Hepatorenal syndrome - Hypoglycaemia - Ascites - Cerebral oedema - Increased infection risk (treat w/ IV ceftriaxone) **Investigations** - to determine cause + check liver/renal function/coag Coagulopathy : - Mostly low clotting factors --> increased bleeding risk --> increased PT, APTT + low fibrinogen - BUT factor VIII is high (as good hepatic function needed to clear it) SO at paradoxically increased VTE risk - Also in chronic liver disease there is less synthesis of protein C + S and anti-thrombin (these are all anticoags so --> increased thrombosis risk) **Management** - ITU supportive care +/- transplant

Answer 5

Causes of ascites can be split into two groups: - Serum-ascites albumin gradient (SAAG) >11 = due to portal HTN Pre-hepatic: portal vein thrombosis Hepatic: cirrhosis, alcholic liver disease, liver mets, fibrosis (wilsons, haemochromatosis) Post-hepatic: hepatic vein thrombosis, budd chiari - SAAG <11 e.g. hypoalbuminaemia; malignancy, infection (Tuberculous peritonitis), pancreatitis, bowel obstruction, serositic in connective tissue disease **Management** - Reduce dietary Na, fluid restirction - Spironolactone +/- loop diuretics - ?drainage in tense ascites - Prophylactic abx (protects from SBP) if ascities protein <15 until the ascites has resolved

Answer 6

**Pathophysiology** - Infection of ascites - Mostly E.Coli **Presentation** - Ascites, abdo pain, fever **Diagnosis** - Neutrophils >250 cells/ul in ascitic fluid **Management** - IV cefotaxime Prophylactic ciprofloxacin or norfloaxcin in patients w/ ascites protein <15 OR previous SBP

Answer 7

**Pathophysiology** - Risk Factors: - Chronic Hepatitis B (main worldwide) + C (main in Europe) - Liver cirrhosis - secondary to alcohol, haemaochromatosis, primary biliary cirrhosis - Other: Alpha 1 antitrypsin deficiency, aflatoxin, COCP, steroids, male, DM, metabolic syndrome BUT Wilson's doesnt cause it **Presentation** - Tends to present late w/ features of liver cirrhosis or failure: jaundice, ascites, RUQ pain, hepatomegaly, pruritis, splenomegaly - Can present as decompensation in someone w/ chronic liver disease - Raised AFP **Investigation** - Screening w/ USS +/- AFP in high risk patients: liver cirrhosis secondary to Hep B, C or haemochromatosis, men w/ liver cirrhosis secondary to alcohol **Management** - Early: surgical - Liver tranplsnt, ablation, transarterial chemoembolisation, chemo

Answer 8

**Pathophysiology** - RF: age, H.pylori, atrophic gastritis, diet (salt + nitrates), smoking, Blood group A **Presentation** - Abdo pain (vague, epigastric, dyspepsia) - Weight loss + anorexia - Nausea + vomiting - Dysphagia: esp if in prox stomach - Overt upper GI bleeding in minority - Virchow's node - Periumbilical node (sister mary joseph nodule) **Investigation** - OGD + biopsy (can see signet ring cells) - CT for staging **Management** - Surgical: endoscopic mucosal resection, partial/total gastrectomy - Chemo

Answer 9

**Pathophysiology** - Carcinoid syndrome due to tumour release of serontonin into systemic circulation **Presentation** - Flushing (often earliest sign) - Diarrhoea - Bronchospasm - Hypotension - Right heart valvular stenosis - Pellagra - ACTH/GNRH may also be release -> cushing **Investigations** - Urinary 5-HIAA - Plasma chromogranin Ay **Management** Somatostatin analogues eg. ocreotide

Answer 10

**Pathophysiology** Ischaemia to lower GI tract falls into: - Acute or chronic mesenteric ischaemia *mesenteric ischaemia - typically small bowel, due to emboli, sudden onset severe sx needing urgent surgery* - Ischaemic colitis - *colitis typically large bowel, multifactorial, transient compromise of blood flow more likley in watershed areas e.g. splenic flexure. less severe sx. Bloody diarrhoea. Thumbprinting on imaging. Conservatively managed.* Common risk factors: age, AF, CVS disease, cocaine, sources of emboli e.g. endocarditis **Presentation** - Abdo pain - in acute MI tends to be sudden + severe + out of keeping w/ examination - PR bleeding - Diarrhoea - Fever - Bloods - raised WCC w/ lactic acidosis - Chronic MI - rare, vague sx, 'intestinal angina' **Investigation** - CT - AXR shows thumbprinting in ischaemic colitis due to mucosal oedema/haemorrhage **Management** - Acute mesenteric ischaemia -> urgent surgery - Ischaemic colitis - supportive +/- surgery if peritonitis, perforation or ongoing haemorrhage

Answer 11

**Angiodysplasia** - Vascular deformity of GI tract - predisposes to bleeding + IDA. Typically in elderly or in hereditary haemorrhagic telangiectasia. - Presentation: asymptomatic, painless occult PR bleeding (most), acute haemorrhage (10% - depends on location of malformation can -> haematemesis, melaena, PR blood) - Diagnosis: colonscopy or mesenteric angiography if acutely bleeding - Mx: endoscopic cautery, tranexamic acid, ?oestrogens **Ferritin** - Raised ferritin WITHOUT iron overload Inflammation (acute phase reactant) Alcohol Liver disease CKD Malignancy - Raised WITH iron overload Hereditary haemochromatosis Secondary to repeat transfusions Transferring saturation helps determine if iron overload is present. If <45% in females or <50% in males then no overload present. - Low ferritin - Iron deficiency anaemia

Answer 12

**Pathophysiology** - Lymphoid hyperplasia or faecolith obstructs appendiceal lumen -> oedema, ischaemia +/- perforation **Presentation** - Periumbilical abdo pain, migrates to RIF - N+V, occassioanlly diarrhoea, mild pyrexia, anorexia - worse on coughing. can't hop. Examination - localised or generalised peritonitis - Rosving's (palpation of LIF causes pain in RIF) - Psoas sign (pain on extending hip if retrocaecal appendix) **Investigation** - Raised inflammatory markers (mostly neutrophils) - ?USS - eg. in females where differential is pelvic organ pathology - ?CT **Management** - Appendicectomy + prophylactic IV abx - If peritonitis/perforation/appendix mass - broad spectrum abx N.B. in older patients need to consider underlying caecal malignancy or perforated sigmoid diverticular diseas

Answer 13

**Diverticulosis** - Multiple outpouchings of bowel wall, mostly in sigmoid colon *- Asymptomatic * - RFs: age, low fibre fiet **Diverticular Disease** - Symptomatic diverticulosis - Altered bowel habit, colicky left sided abdo pain - Managed w/ high fibre diet **Diverticular bleed** - Diverticulum erodes into vessel --> large volume painless bleed - most self-limiting + conservatively managed. May need embolisation or surgical resection if not. **Diverticulitis** - Infected diverticular --> LIF pain/tenderness, anorexia, N+V, diarrhoea, fever, raised inflammatory markers - Complications: abscess, peritonitis, obstruction (stricture), perforation, fistula - Management: - Mild - PO abx - Other: hospital - NBM IVI + IV abx (cephalosporin + metronidazole) - If performation --> hartmann's procedure (+ abx etc)

Answer 14

**Causes** Oesophageal - *Varices* - often haemodynamic compromise. May stop spontaneously but re-bleeds common. - *Oesophagitis* - hx of GORD, low vol fresh blood - *Cancer* - small vol, unless preterminal erosion of large vessels. - *Mallory Weiss Tear* - small-mod vol following vomiting Gastric: - *Ulcer* - small vol bleed + IDA. OR can erode vessel -> haemorrhage + haematemesis - *Cancer*- frank haematemesis w/ altered blood - *Diuelafoy lesion* - AV malformation -> no prodrome -> haematemsis + melaena - *Diffuse erosive gastritis* - triggered by NSAID use -> haematemesis + epigastric discomfort -> large vol bleed w/ haemodynamic compromise Duodenal - Ulcer - pain several hours after eating, haematemesis, melaena, epigastric discomfort - Aorto-enteric fistula - rare but high mortality **Presentation** - Melaena, Haematemesis, Raised urea - Plus signs of underlying cause - Dysphagia/weight loss - cancer - Dyspepsia - ulcer - Stigmata of chronic liver disease - varices

Answer 15

**Both** Risk assess w/: 1. Glasgow -Blatchford (pre-endoscopy) - Takes into account: urea, Hb, BP, pulse, co-morbidities, syncope, melaena - score = 0 - early discharge 2. Rockall Score (after endoscopy) - gives % rebleeding + mortality Resuscitate - ABC - Platelets transfusion (if active bleed + plt <50) - FFP (fibrinogen <1 or PT/APTT >1.5x normal) - Prothrombin complex if on warfarin + actively bleeding Endoscopy (within 24h for any major bleed) **Non-variceal** - No PPI pre-endoscopy - BUT if endoscopy shows recent haemorrhage then give PPI **Variceal** - Terlipressin and prophylactic abx (IV quinolone) pre-endoscopy - Band ligation for oesophageal varices OR injection of N-butyl-2-cyanoacrylate for gastric (if not successful - TIPS or sengstaken blakemore tube) - Prophylaxis of variceal haemorrhage: - Propanolol - Band ligation every 2/52 until all varices eradicated w/ PPI cover

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Gastroenterology Flashcards

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