Gastroenterology Flashcards
Acute Pancreatitis retinopathy
Puertscher retinopathy: cotton wool spots - temporary or permanent blindness.
Causes of acute pancreatitis
(GET SMASHED) Gallst, ETOH, Trauma, Steroids, Mumps, autoimmune (PAN), ascaris, scorpion ven, Hypertriglyceridaemia, hyperchylomicronaemia, hyperCa, hyperthermia, ERCP, Drugs
(DID steroids, diuretics BEcome VAMP DIDanosine, steroids, diuretics, Bendro, Valproate, Azathioprine, Mesalazine, Pentamidine)
Amylase vs lipase for pancreatitis
amylase 75% raised, specificity 90%. Lipase better, longer half-life
Compl of acute pancreatitis
peripancreatic fluid collection 25%
psuedocysts
necrosis
abscess
haemorrhage
ARDS
peripancreatic fluid collection
lack granulation wall/fibrous tissue. Can become pseudocysts/abscesses. Self-resolving
pancreatic pseudocysts
from peripancreatic fluid collection, may or may not communicate with ductal system. Walled off by fibrous/granulation tissue, occurs 4wks or more post-attack. Mostly retrogastric. 75% with persistently elevated amylase. Ix: CT, ERCP, MRI, endoscopic USS.
Rx: 50% self-resolve in 12 wks, endoscopic/surgical cystogastrostomy or aspiration
Pancreatic necrosis
Either of parenchyma or surrounding fat. Rx: Sterile necrosis should be managed conservatively (early necrosectomy assx with high mortality). Some centres do fine-needle aspiration sampling of necrotic tissue if infection suspected.
Pancreatic abscess
often from infected pseudocysts. Rx: drainage
Pancreatic haemorrhage
necrosis involving vascular structures or iatrogenic. Grey Turner’s sign if retroperitoneal.
ARDS mortality rate
20%
Causes of chronic pancreatitis
80% ETOH excess, Genetic (CF, haemochromatosis), ductal obstruction (tumours, stones, structural abnormalities including pancreas divisum, annular pancreas).
Sx of chronic pancreatitis
pain worse 15-30mins post meal, steatorrhoea (pancreatic insufficiency, usually 5-25yrs post pain onset), DM (>20yrs post onset).
Ix for chronic pancreatitis
CT pancreas best (sensitivity 80%, specificity 85%)
AXR (calcification in 30%)
faecal elastase (assesses exocrine function if imaging inconclusive).
Rx for chronic pancreatitis
enzyme supplements, analgesia, antioxidants
Pancreatic Ca commonest type and location
80% adenocarcinoma
head of pancreas
Pancreatic ca assx
age, smoking, diabetes, chronic pancreatitis, HNPCC, MEN, BRCA2, KRAS.
Sx for pancreatic ca
painless jaundice, abdo mass, weight loss, exocrine + endocrine loss of function, atypical back pain, migratory thrombophlebitis (Trousseau sign).
Ix pancreatic ca
high-res CT pancreas (double duct sign - CBD + pancreatic duct dilatation), USS (sensitivity 60-90%).
Rx for pancreatic ca
<20% suitable for surgery at dx, Whipple’s resection (SE: dumping syndrome, peptic ulcers) + adjuvant chemo, ERCP stenting for palliation
Ascending cholangitis
E coli common. Charcot’s triad 20-50%: fever 90%, RUQ pain 70%, jaundice 60%. Reynold’s pentad: hypotension + confusion. Ix: USS for bile duct dilation + CBD stones. Rx: IV abx, ERCP after 24-48hrs to relieve obstruction.
Primary biliary cholangitis
middle aged females (9:1). Interlobular bile ducts damaged by chronic inflammatory process, causing progressive cholestasis, may progress to cirrhosis.
Assx: Sjogren’s (80%), RhA, systemic sclerosis, thyroid disease.
Sx: asymptomatic/itching/fatigue (early), cholestatic jaundice, hyperpigmentation (esp over pressure points), RUQ pain (10%), xanthelasma, xanthomata, clubbing, hepatosplenomegaly, liver failure (late).
Dx: AMA M2 subtype (98%), smooth muscle abs (30%), raised IgM, USS/MRCP (exclude extrahepatic obstruction).
Rx: ursodeoxycholic acid, colestyramine for pruritis, fat-soluble vitamin supplementation, liver transplantation if bilirubin>100.
Compl: cirrhosis, osteomalacia/porosis, HCC (20x risk)
Biopsy for PBC findings
dense lymphoid infiltrates of hepatic portal tracts with chronic inflammation and hepatocyte necrosis
Primary sclerosing cholangitis
inflammation + fibrosis of intra + extra-hepatic bile ducts.
Assx: UC (80%, 4% of UC have PSC), Crohn’s (less than UC, HIV (due to CMV, Cryptosporidium, Microsporidia).
Sx: cholestasis, jaundice, RUQ pain, fatigue.
Ix: ERCP/MRCP show multiple ‘beaded’ biliary strictures, p-ANCA +ve, liver biopsy (fibrous, obliterative cholangitis- ‘onion skin’).
Compl: CCA (10%), colorectal Ca
Post-cholecystectomy syndrome
Sx: dyspepsia, vomiting, pain, flatulence, diarrhoea 40%.
Rx: low fat diet, cholestyramine, PPIs if dyspepsia.
Cholangiocarcionoma
RF: PSC
Sx: persistent biliary colic, jaundice, RUQ mass, periumbilical lymphadenopathy (Sister Mary Joseph node) + left supraclavicular (Virchow node), raised Ca19-9
Coeliac disease assx:
1% of pop
HLA DQ2 (95%), DQ8 (80%), dermatitis herpetiformis, autoimmune (T1DM, autoimmune hepatitis).
Ix for coeliac
anti-TTG abs (IgA), endomyseal abs (IgA),
endoscopic biopsy is gold standard dx (duodenal usually) - villous atrophy (reverses on gluten-free diet), crypt hyperplasia, increase in intraepithelial lymphocytes, lamina propria infiltration with lymphocytes.
Rx for coeliac
gluten free diet (avoid wheat, barley, rye, oats), monitor anti-TTB abs for compliance.
Immunisation (due to functional hyposplenism), pneumococcal vaccine with booster every 5 years.
Coeliac compl
anaemia (iron, folate, B12 def), hyposplenism, osteoporosis, osteomalacia, lactose intolerance, enteropathy-associated T-call lymphoma of small intestine, subfertility, rare - oesophageal ca
Bile acid malabsorption
Sx: chronic diarrhoea/steatorrhoea, vitamin ADEK malabsorption.
Primary - excess bile acid production.
Secondary - reduced bile acid absorption.
Often with ileal disease: Crohn’s. Other causes: cholecystectomy, coeliac, small intestinal bacterial overgrowth.
Ix: SeHCAT scans. Rx: bile acid sequestrants (e.g. cholestyramine)
Small intestinal bacterial overgrowth syndrome
excessive bacteria in small bowel.
RF: neonatal congenital GI abnormalities, scleroderma, DM.
Sx: chronic diarrhoea, bloating, flatulence, abdo pain.
Dx: hydrogen breath test, small bowel aspiration, culture, abx trial.
Rx: correct underlying, rifaximin
Inherited causes of unconjugated hyperbilirubinaemia
Gilbert’s
Crigler-Najjar
Gilbert’s
aut rec. Mild UDP-glucuronyl transferase deficiency. 1-2%. Benign. Jaundice only in illness, exercise, fasting. Ix: IV nicotinic acid shows rise
Crigler-Najjar
Type 1: Aut rec. Absolute UDP-glucuronosyl transferase def. No survival beyond adulthood
Type 2: More common than type 1, less severe. Rx: ?phenobarbital
Inherited causes of conjugated hyperbilirubinaemia
Dubin-Johnson syndrome
Rotor syndrome
Dubin-Johnson syndrome
aut rec. Iranian Jews. Conjugated hyperbilirubinaemia. Defect in canillicular multispecific organ anion transporter (cMOAT) protein. Defective hepatic bilirubin excretion due to multidrug resistance protein 2 (MRP2). Grossly black liver
Rotor syndrome
Aut rec. Defect in hepatic uptake and bilirubin storage. benign.
Oesophageal causes of UGIB
varices
oesophagitis
oesophageal ca
mallory weiss
Gastric causes of UGIB
ulcer
gastric ca
Dieulafoy lesion
diffuse erosive gastritis
Duodenal causes of UGIB
ulcer
aorto-enteric fistula
Oesophageal varices Rx
large volume, malaena, re-bleeds common.
Rx: resus +/- Sengstaken-Blakemore tube + terlipressin (splanchnic vasoconstrictor), octreotide, IV abx (prophylactic, quinolones), endoscopy (band ligation), TIPSS if all fails
Prophylaxis of bleed for oesophageal varices
propanolol, endoscopic band ligation (two-weekly intervals until varices eradicated, with PPI cover to prevent ligation-associated ulcers)
Oesophagitis UGIB sx
small volume bleed, often streeks in vomit, rare malaena, usually with GORD-type hx
Oesophagela ca UGIB sx
small volume unless major vessels eroded (preterminal event)
Mallory weiss tear UGIB sx
brisk small to moderate volume, rare malaena
Gastric ulcer UGIB sx
small volume common unless erosion into significant vessels
Gastric Ca UGIB sx
frank haematemesis or blood mixed with vomit, prodromal dyspepsia, constitutional sx. Major vessel erosion causes large volume bleed
Diulafoy lesion
AV malformation, difficult to detect, large volume UGIB
Diffuse erosive gastritis
underlying cause eg NSAIDs, can be large volume bleed
Duodenal ulcer UGIB sx
posteriorly sited, can erode to gastroduodenal artery. Pain occurs several hrs post eating
Aorto-enteric fistula UGIB sx
past AAA surgery, high mortality
What score is used post-endoscopy in UGIBs
Rockall score post-endoscopy: risk of rebleeding/mortality. Includes age, shock features, co-morbidities, aetiology, endoscopic stigmata
Boerhaave’s
severe vomiting –> oesophageal rupture
Anal fissure RFs
constipation, IBD, STIs
Anal fissue sx
longitudinal/elliptical tears of squamous lining of distal anal canal. Acute<6wks, chronic >6wks.
bright red, painful rectal bleed, 90% on posterior midline (consider underlying cause eg IBD if alternative locations found).
Rx for anal fissure
acute: stool softening with high-fibre/fluid diet, bulk-forming laxatives (or lactulose), lubricants (eg petroleum jelly), topical anaesthetics, analgesia
Chronic: topical GTN. If ineffective 8wks → sphincterotomy/botulinum toxin
Angiodysplasia
Heyde’s syndrome (AS assx), elderly. Sx: anaemia, GI bleed.
Dx: colonoscopy, mesenteric angiography if acute.
Rx: endoscopic cautery/argon plasma coagulation, antifibrinolytics (TXA), oestrogens
IBS dx
ABC for >6months (abdo pain, bloating, change in bowel habit). Abdo pain relieved by defecation or altered bowel frequency stool form + 2/4 of : altered stool passage (straining/urgency/incomplete evacuation), boating/distension/abdo tension/hardness, worsened by eating, mucus passage.
IBS Rx
antispasmodic agents for pain, laxatives (avoid lactulose) for constipation (linaclotide 2nd line), loperamide for diarrhoea. Low-dose TCAs 2nd line. Others: psych interventions (CBT, hypnotherapy), alternative medicines (but not acupuncture or reflexology). Diet advice: regular meals, don’t miss meals, drink 8 cups of fluid or more per day, restrict caffeine, reduce ETOH, limit high-fibre foods, reduce resistant starch, limit fresh fruit, avoid sorbitol for diarrhoea, increase oats, linseeds for wind/bloating
Gastrin
from G cells in gastric antrum
Stimulus: Gastric distension, vagal (mediated by gastrin-releasing peptide), luminal peptides/amino acids.
Inhibited by: low antral pH, somatostatin
Actions: increases acid secretion by gastric parietal cells
CCK
from small intestinal I cells
Stimulus: partially digested proteins, triglycerides
Actions: increases enzyme-rich pancreatic fluid secretion, GB contraction, relaxation of sphincter of Oddi, reduces gastric emptying, trophic effect on pancreatic acinar cells, induces satiety
Secretin
from upper small intestinal S cells
Stimulus: acidic chyme, fatty acids
Action: increases HCO3 rich fluid from pancreas and hepatic duct cells, reduces gastric acid secretion, trophic effect on pancreatic acinar cells
Vasoactive intestinal peptide (VIP)
from small intestine, pancreas
Stimulus: neural
Action: stimulates pancreatic and intestinal secretion, inhibits acid and pepsinogen secretion
VIPomas: 90% from pancreas Sx: large volume diarrhoea, weight loss, dehydration, hypoK, hypochlorhydia
Somatostatin
pancreatic D cells and stomach
Stimulus: fat, bile salts and glucose in intestinal lumen
Action: reduces acid, pepsin, gastrin pancreatic enzyme, insulin, glucagon secretion, inhibits gastrin’s trophic effects, stimulates gastric mucous production
Ascites causes
SAAG>11g/L (portal HTN): liver (cirrhosis/ALD, acute liver failure, mets), cardiac (RHF, constrictive pericarditis), Budd-Chiari, Portal vein thrombosis, veno-occlusive disease, myxoedema
SAAG<11g/L: hypoalbuminaemia (nephrotic syndrome, severe malnutrition eg Kwashiorkor), malignancy (peritoneal carcinomatosis), infections (peritonitic TB), others (pancreatitis, bowel obstruction, biliary ascites, postop lymphatic leak, serositis in connective tissue diseases)
Ascites Rx
restrict sodium. Fluid restrict if Na<125. Spironolactone +/- furosemide.
Drainage if tense ascites + albumin cover (Compl: ascites recurrence, hepatorenal syndrome delusional hypoNa, mortality).
Proph abx - oral ciprofloxacin or norfloxacin with protein levels <15g/l (prevents SBP). Consider TIPS
SBP
Sx: ascites, abdo pain, fever. Dx: ascitic tap neutrophil count >250cells/ul (E Coli most common).
Rx: IV cefotaxime. Abx prophylaxis if past SBP, if fluid protein<15g/l or Child-Pugh at least 9 or hepatorenal (oral cipro/norfloxacin). ALD is poor prognosis in SBP
Acute liver failure
Causes: Paracetamol, ETOH, viral hepatitis, acute fatty liver of pregnancy. Sx: jaundice, coagulopathy, hypoalbuminaemia, hepatic encephalopathy, renal failure
Alcoholic liver disease
Ix: GGT. AST:ALT >2. Rx: prednisolone for acute attack if Maddrey’s discriminant function>32(assess who would benefit from steroids, includes PT, bilirubin), pentoxyphylline (STOPAH showed prednisolone better)
Biopsy: steatohepatitis: macrovesicular fatty change with giant mitochondria, spotty necrosis, fibrosis
Budd-Chiari
hepatic vein thrombosis. Causes: PRV, thrombophilias, pregnancy, COCP (20%). Sx: Triad - sudden, severe abdo pain, ascites (with distension), tender hepatomegaly. Ix: USS with Doppler flow studies
NAFLD
Assx: obesity, T2DM, hyperlipidaemia, jejunoileal bypass, sudden weight loss/starvation. Related to insulin resistance. Ix: enhanced liver fibrosis blood test to assess for advanced fibrosis (hyaluronic acid + procollagen III + tissue inhibitor of metalloproteinase I). Non-invasive tests: FIB4, NAFLD fibrosis scores + fibroscan
NAFLD biopsy
triglyceride accumulation with myofibroblast proliferation
Cirrhosis dx
transient elastography, Enhanced Liver fibrosis score for NAFLD, liver biopsy.
Causes of decompensation in cirrhosis
constipation (toxic product accumulation), infection, electrolyte imbalance, UGIB, increased ETOH intake
Liver biopsy contraindication
INR>1.4, Pltlt<60, anaemia, extrahepatic biliary obstruction, hydatid cyst, haemangioma, uncooperative pt, ascites
Cirrhosis biopsy features
excess collagen and extracellular matrix deposition in periportal and pericentral zones leading to formation of regenerative nodules
Child Pugh score.
Grading cirrhosis
<7 A, 7-9 B, >9 C. BAPEA bilirubin, albumin, PT, encephalopathy, ascites
MELD
grading cirrhosis
uses bilirubin, creatinine, INR
Ischaemic hepatitis
usually exceeds 50x upper limit of normal/1000u/L, with other end-organ dysfunction and AKI (ATN)
HCC epidemiology
3rd most common Ca worldwide.
HCC RFs
chronic HBV (commonest worldwide), chronic HCV (commonest Europe), cirrhosis, ETOH, haemochromatosis, PBC, A1AT, hereditary tyrosinosis, glycogen storage disease, aflatoxin, contraceptives, anabolic steroids, PCT, males, DM, metabolic syndrome. (Note - Wilson’s is not cause)
HCC ix
USS +/- AFP in high risk groups (cirrhotic patients 2ndary to HBV/HCV/Haemochromatosis/ETOH men)
HCC Rx
surgery (early), transplant, radiofrequency ablation, transarterial chemoembolisation, sorafenib (multikinase inhibitor)
Drug causes of hepatocellular damage
Paracetamol, valproate, phenytoin, MAOIs, halothane, anti-TB (RIP), statins, ETOH, amiodarone, methyldopa, nitrofurantoin
Drug causes of cholestatic liver damage
COCP, penicillins, erythromycin, testosterone, phenothiazines (chlorpromazine, prochlorperazine), sulphonylureas, fibrates,
Drug causes of cirrhosis
methotrexate
methyldopa
amiodarone
Autoimmune hepatitis assx
Young to middle-aged females, autoimmune, hypergammaglobulinaemia, HLA B8, DR3.
Autoimmune hepatitis sx
T-cell mediated progressive necro-inflammatory process
acute hepatitis 25%, CLD, amenorrhoea (common). Raised IgG (hypergammaglobulinaemia).
Autoimmune hepatitis biopsy
piecemeal necrosis - inflammation extending beyond limiting plate, bridging necrosis.
Rx autoimmune hepatitis
steroids, immunosuppressants,
transplant
Types of autoimmune hepatitis
Type I: ANA +/- anti SMA. Adults + children
Type II: anti LKM1. children only
Type III: soluble liver-kidney antigen. Middle aged adults
liver abscesses
Most common: S aureus in children, E Coli adults. Rx: drainage + Abx (amox + cipro + metro or cipro + clindamycin)
Coagulaopathy of liver disease
Factor 9 paradoxically supra-normal (synthesised in endothelial cells around body, hepatic clearance), but all other factors low (synthesised in hepatic endothelial cells), meaning paradoxical pro-thrombotic risk.
Reduced protein C, protein S (vit K dependent), anti-thrombin (non-vit K dependent) synthesis.
Hepatosplenomegaly causes
CLD with portal HTN, glandular fever, malaria, hepatitis, lymphoproliferative disorders, myeloproliferative disorders (e.g. CML), amyloidosis
Hepatorenal syndrome
due to splanchnic vasodilation resulting in RAAS activation, causing renal vasoconstriction.
Type 1: rapidly progressive, doubling of creatinine within 2 wks, very poor prognosis
Type 2: slowly progressive, poor prognosis, but patients may live for longer
Rx: terlipressin, 20% albumin (volume expansion), TIPS
Hepatic encephalopathy Sx
due to excess ammonia + glutamine from bacterial breakdown of proteins. Sx: confusion, altered GCS, asterixis, constructional apraxia (inability to draw 5-pointed star), triphasic slow waves on EEG, raised ammonia.
Hepatic encephalopathy grading
I: irritability. II: confusion, inappropriate behaviour. III: incoherent, restless. IV: coma.
Precipitants of hepatic encephalopathy
infection, GI bleed, TIPS, constipation, sedatives, diuretics, hypoK, renal failure, increased dietary protein
Rx for hepatic encephalopathy
treat underlying + lactulose + rifaximin. Embolisation of portosystemic shunts, liver transplant in select few
Crohn’s sx
commonly terminal ileum + colon, anywhere from mouth to anus with skip lesions. Advise to stop smoking.
Sx: non-bloody diarrhoea, weight loss, upper GI sx, mouth ulcers, perianal disease, RIF mass, gallstones (2ndary to reduced bile acid reabsorption), oxalate renal stones
Crohn’s compl
obstruction, fistula colorectal Ca
Crohn’s endoscopy features
cobblestone appearance, skip lesions, deep ulcers, inflammation of all layers from mucosa to serosa, with granulomas, increased goblet cells
Crohn’s small bowel enema
Kantor’s string sign for strictures, proximal bowel dilatation, rose thorn ulcers, fistulae
Inducing remission in Crohn’s
steroids. 5-ASA 2nd line. Azathioprine/mercaptopurine as add-on. Infliximab in refractory disease
Maintaining remission in Crohn’s
stop smoking, azathioprine/mercaptopurine (assess for TPMT activity). Methotrexate 2nd line.
Perianal fistulae in Crohn’s management
Ix: MRI (determines if abscess, if fistula is simple/complex). Rx: oral metronidazole, infliximab, drainage seton for complex fistulae, incision + drainage for abscess + abx.
Compl in Crohn’s
small bowel Ca (x40), colorectal Ca (x2), osteoporosis
Ulcerative colitis features
Peak incidence 15-25yrs + 55-65yrs.
bloody diarrhoea, urgency, tenesmus, abdo pain (LLQ), extraintestinal features. always starts at rectum, never spreads beyond IC valve, continuous.
Triggers for UC
stress, NSAIDs, abx, smoking cessation
Compl for UC
Colorectal Ca (more than CD)
Factors increasing risk for colorectal ca in UC
disease duration >10 yrs, pancolitis, onset<15yrs, unremitting disease, poor compliance to Rx
Colonoscopy surveillance in UC by risk
lower risk: extensive colitis, with no active inflammation, left sided or crohn’s colitis of <50% colon → 5yr f/u colonoscopy
Intermediate risk: extensive colitis with mild active inflammation or post-inflammatory polyps or FHx of colorectal Ca in 1st deg relative >50yrs → 3yr f/u colonoscopy
Higher risk: extensive colitis with inflammation or stricture or dysplasia or PSC or FHx of colorectal ca in 1st deg relative aged <50yrs → 1yr f/u colonoscpy
Contraix for colonoscopy in UC
severe colitis due to perf risk - do flexi sig instead
Endscopy features in UC
red, raw mucosa, bleeds easily, no inflammation beyond submucosa, widespread ulceration with preservation of adjacent mucosa with pseudopolyps, inflammatory cell infiltrate in lamina propria, neutrophils migrate through walls to form crypt abscesses, goblet cell depletion, infrequent granulomas
Barium enema in UC
loss of haustra, pseudopolyps, superficial ulceration, drainpipe colon (long-standing disease)
Severity in UC
(Truelove and Witts): mild<4stools/day, moderate 4-6, severe>6 stools + systemic upset
Inducing remission in UC
Proctitis: 1. Topical aminosalicylate. 2. (4 wks no remission) add oral aminosalicylate. 3. Add topical/oral steroids
Proctosigmoiditis/left-sided colitis: 1. Topical aminosalicylate. 2. (4wks no remission) add high-dose oral aminosalicylate +/- topical steroids. 3. Switch to oral aminosalicylates + oral steroids
Extensive disease: 1. Topical + high-dose oral aminosalicylate. 2. (4wks no remission) switch to high-dose oral aminosalicylate + oral steroids
Severe: admit + IV steroids (IV ciclosporin if steroids contraix). Add IV ciclosporin or consider surgery if no improvement after 72 hrs
Maintaining remission in UC
proctitis/proctosigmoiditis: topical/oral + topical/oral aminosalicylate
Left-sided/extensive: low dose oral
Severe or 2 or more exacerbations in last year: oral azathioprine/mercaptopurine
Extra-intestinal IBD features related to disease activity
pauciarticular, asymmetric arthritis (most common extra-intestinal feature), erythema nodosum, episcleritis (more in CD), osteoporosis
Extra-intestinal IBD features unrelated to disease activity
polyarticular, symmetric arthritis, uveitis (UC more common), pyoderma gangrenosum, clubbing, PSC (UC more common)
Acute mesenteric ischaemia
embolism, AF hx. Sx: sudden, severe pain out-of-keeping with physical exam. Rx: urgent surgery. Poor prognosis
Chronic mesenteric ischaemia
relatively rare, intestinal angina, colicky, intermittent abdo pain
Ischaemic colitis
acute, transient blood flow compromise to large bowel → inflammation, ulceration, haemorrhage. Splenic flexure most likely (dual supply from superior + inferior mesenteric arteries). Ix: AXR thumbprinting. Rx: supportive, surgery (if peritonitic, perf, ongoing haemorrhage)
aminosalicylate action
5-ASA released in colon, inhibits prostaglandin synthesis.
Sulphasalazine features and SE:
sulphapyridine (sulphonamide) + 5-ASA. SE (mostly sulph-related): rashes, oligospermia, headache, Heinz body anaemia, megaloblastic anaemia, fibrosis + other 5-ASA SEs:
Mesalazine features and SE
delayed release form of 5-ASA. SE: GI upset, headache, agranulocytosis, pancreatitis (7x more in mesalazine than sulfalazine), interstitial nephritis
Olsalazine
2x 5-ASA linked by diazo bond, broken by colonic bacteria
H Pylori
G-ve. Uses flagella to burrow into mucosal lining to reach epithelial cells, allows chemotaxis. Secretes urease, converted to NH3, alkalises gastric acidic environment. Releases bacterial cytotoxins eg CagA to disrupt gastric mucosa.
Assx: peptic ulcers (95% duodenal, 75% gastric), gastric Ca, B cell lymphoma of MALT tissue, atrophic gastritis. Rx: 7 days of PPI + amoxicillin + clarithromycin/metronidazole (or PPI + metron + clarith)
Urea breath tests for H Pylori
13C urea ingested, broken down by H pylori urease, exhale onto glass tube after 30 mins, mass spectrometry to calculate 13C CO2. Not to perform within 4 wks of abx or within 2wks of PPIs. Sensitivity 95-98%, specificity 97-98%. Can be used to assess for eradication
Rapid urease test for H pylori
biopsy sample with urea + pH indicator. Sensitivity 90-95%, specificity 95-98%.
Serum antibody for H pylori
+ve after eradication. Sensitivity 85%, specificity 80%
gastric biopsy culture for H pylori
sensitivity 70%, specificity 100%
Gastric biopsy for H pylori
Sensitivity 95-99%, specificity 95-99%
Stool antigen test for H Pylori
sensitivity 90%, specificity 95%
Gastric MALT lymphoma
95% H pylori assx, good prognosis. Sx: paraproteinaemia. Rx: H pylori eradication if low grade (80% respond).
C Diff features and toxins
anaerobic G+ve, spore-forming, toxin-producing bacillus (rod), transmitted faeco-orally via spore ingestions.
Exotoxins (Toxin A and B) acts on epithelial and inflammatory cells, leads to pseudomembranous colitis (multiple white plaques on GI mucosa on endoscopy).
RF for C Diff
2nd/3rd gen cephalosporins (leading cause), clindamycin, PPIs.
Severity classification for C Diff
mild - normal WCC.
Moderate - raised WCC<15, 3-5 loose stools/day.
Severe - WCC>15, creatinine>50% baseline, temp>38.5, or abdo/radiological sx of severe colitis.
Life-threatening - low bp, partial/complete ileus, toxic megacolon or CT evidence of severe disease
Dx for C diff
C diff toxin
Rx for C Diff
1st episode: 1. oral vanc 10 days. 2. Oral fidaxomycin. 3. Oral vanc +/- IV metronidazole
Recurrence (20% post 1st episode, 50% after 2nd episode): within 12wks oral fidaxomicin. After 12 wks oral vanc or fidaxomycin
Life-threatening: oral vanc + IV metronidazole + ?surgery
Others: bezlotoxumab (mAb vs toxin B), faecal microbiota transplant (if 2 or more past episodes)
Preventing spread for C diff
isolation in SR until no more diarrhoea for 48hrs + disposable gloves and apron + hand washing
Hep B serology
HBsAg 1st marker, present for 1-6 months, >6 months is chronic disease.
Anti-HBs = immunity/exposure.
Anti-HBc = exposure (IgM in acute/recent, for 6 months, IgG persists).
HbeAg from breakdown of core antigen from liver cells, marker of replication, infectivity
HBV in pregnancy
all pregnant women get screened.
Babies of chronic HBV mothers or past acute HBV mothers get complete vaccination course + HBIG.
C section does not reduce vertical transmission.
Breastfeeding safe
HBV biopsy
mononuclear infiltration of liver lobules with hepatocyte necrosis and Kupffer cells hyperplasia
Whipple’s disease
Tropheryme whippelii.
Assx: HLA-B27, middle-aged men.
Sx: malabsorption (diarrhoea, weight loss), large-joint arthralgia, lymphadenopathy, hyperpigmentation, photosensitivity, pleurisy, pericarditis, neuro sx (rare, ophthalmoplegia, dementia, seizures, ataxia, myoclonus).
Ix: jejunal biopsy shows deposition of macrophages containing Periodic acid-Schiff granules.
Rx: oral co-trimoxazole for a year, sometimes preceded by IV penicillin
Pernicious anaemia
most common cause of B12 def. Anti-Intrinsic factor (50%) +/- anti-parietal cell abs (90%). RF: Females (1.6:1, middle-old age), autoimmune assx, blood group A. Rx: IM B12 3 injections/wk for 2 wks then 3 monthly if no neuro sx, more frequent if sx. Compl: gastric ca risk
Wilson’s genetics
Aut rec. ATP7B gene defect, Chr 13.
Wilson’s sx
Onset 10-25yrs. Sx: liver (hepatitis, cirrhosis), neuro (Cu deposition in basal ganglia, esp putamen, globus pallidus → degeneration. Speech, behavioural, psychiatric problems 1st. Also: asterixis, chorea, dementia, parkinsonism), Kayser-Fleischer rings (green-brown rings, due to Cu deposition in Descemet membrane), RTA (esp Fanconi’s syndrome), haemolysis, blue nails.
Wilson’s ix
slit lamp examination, reduced serum caeruloplasmin, reduced total serum Cu, increased 24hr urinary Cu excretion, genetic analysis of ATP7B gene.
Wilson’s Rx
penicillamine (Cu chelator), trientine hydrochloride, tetrathiomolybdate
Haemochromatosis genetics
Aut rec, HFE gene, Chr 6. 1/200 Europeans.
HH sx
early - fatigue, erectile dysfunction, arthralgia, bronze skin, DM, liver disease, cardiac failure (dilated CDM), hypogonadotrophic hypogonadism (2ndary to cirrhosis, pituitary dysfunction), arthritis (esp hands)
Skin pigmentation and CDM reversible with treatment
HH Ix
Transferrin sats best screening for general population, HFE mutation testing for family members.
Iron studies: transferrin sats>55% in men, >50% in women, raised ferritin (>500), raised iron, low TIBC. LFTs.
Genetic testing for C282Y, H63D mutations. MRI (quantify liver +/- cardiac iron).
Liver biopsy if hepatic cirrhosis suspected.
Rx for HH
venesection (monitor transferrin sats (<50%) + ferritin (<50)), desferrioxamine 2nd line
High ferritin causes
Without iron overload: inflammation, ETOH excess, liver disease, CKD, malignancy. Ix: transferrin sats low (<45% females, <50% males)
With iron overload: HH, repeated transfusions
reduced ferritin cause
IDA
Zollinger-Ellison
Gastrin-secreting tumour, majority in 1st part of duodenum, 2nd most common in pancreas. Assx: Men I (30%). Sx: mutliple gastroduodenal ulcers, diarrhoea, malabsorption. Dx: fasting gastrin levels (best screening test), secretin stimulation test (marked increase in gastrin)
Carcinoid tumours - when do you get carcinoid syndrome
when liver mets present due to serotonin release, as well as when lung carcinoid, with mediators not being cleared by liver.
Carcinoid tumours sx
flushing (1st sx), diarrhoea, bronchospasm, low bp, right heart valvular stenosis (Tricuspid insufficiency, pulmonary stenosis - TIPS- most common. Left heart affected in bronchial carcinoid), Cushing’s syndrome (ACTH secretion), Acromegaly (GHRH secretion), pellagra (dietary tryptophan diverted to serotonin by tumour).
Ix for Carcinoid
urinary 5-HIAA, plasma chromogranin A y
Rx carcinoid
somatostatin analogues (octreotide)
Cyproheptadine for diarrhoea
Oesohpageal Ca sx
dysphagia + constitutinal, small volume bleed unless major vessels eroded (preterminal event). May be recurrent.
Oesoph ca ix
upper GI scope for dx. Endoscopic ultrasound for locoregional staging. CTCAP, PET CT for staging and mets.
Oesoph ca rx
surgery (Ivor-Lewis oesophagectomy, risk of anastomotic leak) + adjuvant chemo
Oesoph ca types and RFs
Adenocarcinoma: most common in west. Lower third. RF: GORD, Barrett’s, smoking, obesity
Squamous cell cancer: most common in developing world. Upper two-thirds. RF: smoking, ETOH, achalasia, Plummer-Vinson, nitrosamine-rich diet
oeophagitis sx
heartburn hx, odynophagia
oesophageal candidiasis rf
HIV, steroid inhalers
Pharyngeal pouch
Zenker’s diverticulum. Posteromedial diverticulum through Killian’s dehiscence (triangular area in wall of pharynx between thyropharyngeus and cricopharyngeus muscles). Older, men (5x). Sx: dysphagia, regurgitation, aspiration, neck swelling which gurgles on palpation, halitosis. Ix: barium swallow + dynamic video fluoroscopy. Rx: surgery
Achalasia sx
failure of oesophageal peristalsis/relaxation of lower oesophageal sphincter due to degenerative loss of ganglia from Auerbach’s plexus. Middle-aged, equally common in men + women.
Sx: dysphagia of both solids+liquids, heartburn, regurgitation, malignant change in some.
Achalasia ix
oesophageal manometry (excessive lower oesophageal sphincter tone, doesn’t relax on swallowing), barium swallow (bird’s beak appearance, expanded oesophagus, fluid level), CXR (widened mediastinum, fluid level)
Achalasia rx
pneumatic (ballooon) dilation 1st line. Heller cardiomyotomy if recurrent or persistent symptoms. Intra-sphincteric botulinum toxin use if high risk. Nitrates, Ca channel blockers limited in use
Systemic sclerosis - how it causes dysphagia
other sx of CREST seen, lower oesophageal sphincter pressure reduced
Myasthenia gravis dysphagia to what
liquids + solids
Globus hystericus sx
hx of anxiety, intermittent, relieved by swallowing, painless, dysphagia
Plummer-Vinson syndrome
dysphagia + glossitis + IDA. Rx: iron + web dilation
Barrett’s
metaplasia of lower oesophageal mucosa (squamous → columnar), risk of adenocarcinoma 50-100x. Short (<3cm) or long (>3cm). Histology: columnar epithelium, goblet cells, brush border, resembles gastric cardiac region. RF: GORD, males (7:1), smoking, central obesity. Rx: high dose PPIs, endoscopy every 3-5yrs for metaplasia, radiofrequency ablation for low-grade dysplasia, endoscopic resection if higher grade
Hydatid cysts
endemic in Mediterranean/Middle East. Echinococcus granulosus. Outer capsule: multiple small daughter cysts, precipitate type 1 hypersensitivity reaction. Sx: 90% of cysts in liver + lungs, Symptomatic if cysts>5cm diameter, morbidity from cysts bursting, infection, organ dysfunction (biliary, bronchial, renal, cerebrospinal fluid outflow obstruction), biliary rupture has triad of colic, jaundice, urticaria. Ix: USS 1st line, CT (best to differentiate between hydatid, amoebic, pyogenic cysts), serology (primary diagnosis, for follow-up post treatment). Rx: surgery (ensure cyst walls not ruptured, contents sterilised).
Gastric Ca most common ca type
2% of cancers. Adenocarcinoma most common
Gastric Ca RF
H pylori, pernicious anaemia, atrophic gastritis, diet (salt, salt-preserved foods, nitrates), East Asian ethnicity, smoking, blood group A
Gastric Ca Sx
abdo pain (epigastric, dyspepsia), weight loss, anorexia, N&V, dysphagia, UGIB, lymphatic spread (Virchow’s node - left supraclavicular, Sister Mary Joseph’s node - periumbilical).
Gastric Ca Ix
OGD + biopsy (signet ring cells - large mucin vacuole displacing nucleus to one side, higher number = worse prognosis), CTCAP +/- PET for staging
Gastric Ca Rx
surgical (endoscopic mucosal resection, partial/total gastrectomy) + chemo
Colorectal Ca genetics
Sporadic (95%), HNPCC (5%, Aut Dom, proximal colon, DNA mismatch repair gene mutations leading to microsatellite instability, MSH2 60%, MLH1 30%, Amsterdam criteria), FAP (<1%, APC, Chr 5, also duodenal tumour risk. Rx: total proctocolectomy with ileal pouch anal anastomosis in 20s)
Screening for colorectal Ca
FIT screening, every 2yrs, aged 60-74 in England, 40-74 Scotland. >74 may request screening. Abs vs human Hb in faeces (better than faecal occult blood test as it is specific for human Hb, from animal Hb). colonoscopy if abnormal → 50% have normal exam, 40% have polyps (removed due to premalignant potential), 10% have cancer.
Anal ca
80% Squamous cell. Others: melanomas, lymphomas, adenocarcinomas. Lymphatic drainage to inguinal LN from anal margin tumours, proximal tumours to pelvic LNs. RF: HPV16, 18 (80-85%), anal intercourse, high lifetime sexual partner numbers, MSM, HIV, immunosuppression, cervical Ca, smoking. Sx: perianal pain/bleeding, palpable lesion, faecal incontinence, rectovaginal fistula. T staging (Tx cannot assess, T0 no evidence, Tis in situ, T1 2cm or less, T2 2-5cm, T3 >5cm, T4 invades adjacent organs
Maltase
maltose→ 2x glucose
Sucrase
sucrose → fructose + glucose.
Lactase
lactose → glucose + galactose
Threadworms
Enterobius vermicularis. Common in children, spread with swallowing eggs. Asymptomatic 90%. Sx: perianal itching esp at night, vulval in girls. Dx: apply sellotape perinaally → microsocpy for eggs. Rx: anthelmintic hygiene, mebendazole for children >6months age single dose
oesinophilic oesophagitis RF
allergies/asthma/atopy, males (3:1), FHx allergies, Caucasian, age 30-50yrs, autoimmune disease.
Oesinophilic oesophagitis sx
failure to thrive in children, dysphagia, strictures/fibrosis (56%), food impaction (55%), regurgitation/vomiting, anorexia, weight loss.
Ix eosinophilic oesophagitis
endoscopy (Reduced vasculature, thick mucosa, mucosal furrows, strictures, laryngeal oedema) + Biopsy: dense eosinophil epithelial infiltration, >15 eosinophils on high power microscopy for diagnosis, epithelial desquamation, eosinophilic microabscesses, abnormally long papillae. Can trial PPIs (no improvement).
Rx for eosinophilic oesophagitis
modify diet (elemental diet, exclusion of 6 food groups assx with allergies, targeted elimination diet), topical steroids (fluticasone 8 wks), oesophageal dilatation (56% require this at some point due to strictures)
Compl of eosoniphilic oesophagitis
strictures 56%, impaction 55%, Mallory-Weiss tears
eosinophilic oesophagitis prognosis
chronic, likely to come back
Refeeding syndrome effect on electrolytes
low PO4, K, MG
Refeeding syndrome Sx
hypoPO4 results in muscle weakness + myocardial (HF) + diaphragm (Resp failure).neuro (confusion, seizures, coma, due to disturbed ATP metabolism), haem (tissue hypoxia, haemolysis, due to reduced 2,3-diphosphoglycerate levels in RBCs), rhabdomyolysis (low PO4 → impaired ATP production → muscle breakdown)
How does refeeding syndrome affect PO4
Shift from fat to carb metabolism causes insulin secretion + increased cellular glucose uptake → intracellular shift of PO4 (used in ATP synthesis + 2,3-diphosphoglycerate in RBCs)
What predisposes one to refeeding syndrome
At risk if:
One of: BMI<16, unintentional weight loss >15% over 3-6 months, little nutritional intake >10 days, hypoK/PO4/Mg before feeding
Two or more of: BMI<18.5, unintentional weight loss >10% over 3-6 months, little nutritional intake >5 days, Hx of ETOH/insulin use/chemo/diuretics/antacids
How to prevent refeeding syndrome
if not eaten for >5 days, refeed at no more than 50% of requirements for 1st 2 days
Intrahepatic cholestasis of pregnancy
1%, 3rd trimester, most common. Sx: pruritis (palms+soles), no rash, high bilirubin. Rx: ursodeoxycholic acid, weekly LFTs, induction at 37wks. Compl: stillbirth
Acute fatty liver of pregnancy
rare, 3rd trimester/immediately post-delivery. Sx: abdo pain, N&V, headache, jaundice, hypoglycaemia, pre-eclampsia in severe. Ix: ALT elevated. Rx: supportive, delivery. (Gilbert’s, Dubin-Johnson may be exacerbated during pregnancy)
HELLP
haemolysis, elevated LFTs, Low platelets
Jejunal villous atrophy causes
coeliac, tropical sprue, hypogammaglobulinaemia, GI lymphoma, Whipple’s disease, cow’s milk intolerance
PPI SE
hypoNa, hypoMg, osteoporosis, microscopic colitis, C Diff risk
Bariatric surgery referrals
BMI>35 with RF (HTN, T2DM etc), >40 without RF
Forms of bariatric surgery
Restrictive:
Laparoscopic adjustable gastric banding: 1st line, BMI 30-39, less weight loss than malabsorptive or mixed, fewer compl
Sleeve gastrectomy: stomach reduced to 15% of original size
Intragastric balloon: can be left in for max 6 months
Malabsorptive: Biliopancreatic diversion with duodenal switch: for very obese
Mixed restrictive + malabsorptive: Roux-en-Y gastric bypass
Peutz-Jeghers
aut dom, LKB1 or STK11, genes encoding serine threonine kinase. Sx: hamartomatous polyps, SBO, GI bleed, pigments on lips, oral mucosa, face, palms, soles. 50% die from GI cancer by 60yrs age
Villous adenoma
colonic polyps with malignant potential, large mucous secretion, potential electrolyte disturbances. Sx: majority asymptomatic, may have non-specific lower GI sx, secretory diarrhoea, microcytic anaemia, hypoK
Melanosis coli
laxative abuse (esp senna), histology: pigment laden macrophages
Malnutrition definition
BMI<18.5, unintentional weight loss >10% over last 3-6 months, BMI <20 + unintentional weight loss >5% over last 3-6 months. 10% of over 65. MUST assessment (Malnutrition Universal Screen Tool)
Alcoholic ketoacidosis
non-diabetic, euglycaemic. Due to episodes of starvation resulting in lipolysis. Rx: saline + thiamine
Drugs causing dyspepsia
NSAIDs, bisphosphonates, steroids. Drugs can cause reflux by reducing lower oesophageal sphincter pressure: CCBs, nitrates, theophyllines
Laxative forms
bulk-forming laxatives: ispaghula husk, methylcellulose. Stool softeners: arachis oil enemas. Stimulants: senna, docusate, bisacodyl, glycerol, co-danthramer (carcinogenic potential so rx for palliative only)
