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MRCP Revision > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

Acute Pancreatitis retinopathy

A

Puertscher retinopathy: cotton wool spots - temporary or permanent blindness.

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2
Q

Causes of acute pancreatitis

A

(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)

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3
Q

Amylase vs lipase for pancreatitis

A

amylase 75% raised, specificity 90%. Lipase better, longer half-life

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4
Q

Compl of acute pancreatitis

A

peripancreatic fluid collection 25%
psuedocysts
necrosis
abscess
haemorrhage
ARDS

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5
Q

peripancreatic fluid collection

A

lack granulation wall/fibrous tissue. Can become pseudocysts/abscesses. Self-resolving

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6
Q

pancreatic pseudocysts

A

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

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7
Q

Pancreatic necrosis

A

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.

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8
Q

Pancreatic abscess

A

often from infected pseudocysts. Rx: drainage

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9
Q

Pancreatic haemorrhage

A

necrosis involving vascular structures or iatrogenic. Grey Turner’s sign if retroperitoneal.

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10
Q

ARDS mortality rate

A

20%

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11
Q

Causes of chronic pancreatitis

A

80% ETOH excess, Genetic (CF, haemochromatosis), ductal obstruction (tumours, stones, structural abnormalities including pancreas divisum, annular pancreas).

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12
Q

Sx of chronic pancreatitis

A

pain worse 15-30mins post meal, steatorrhoea (pancreatic insufficiency, usually 5-25yrs post pain onset), DM (>20yrs post onset).

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13
Q

Ix for chronic pancreatitis

A

CT pancreas best (sensitivity 80%, specificity 85%)

AXR (calcification in 30%)

faecal elastase (assesses exocrine function if imaging inconclusive).

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14
Q

Rx for chronic pancreatitis

A

enzyme supplements, analgesia, antioxidants

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15
Q

Pancreatic Ca commonest type and location

A

80% adenocarcinoma
head of pancreas

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16
Q

Pancreatic ca assx

A

age, smoking, diabetes, chronic pancreatitis, HNPCC, MEN, BRCA2, KRAS.

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17
Q

Sx for pancreatic ca

A

painless jaundice, abdo mass, weight loss, exocrine + endocrine loss of function, atypical back pain, migratory thrombophlebitis (Trousseau sign).

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18
Q

Ix pancreatic ca

A

high-res CT pancreas (double duct sign - CBD + pancreatic duct dilatation), USS (sensitivity 60-90%).

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19
Q

Rx for pancreatic ca

A

<20% suitable for surgery at dx, Whipple’s resection (SE: dumping syndrome, peptic ulcers) + adjuvant chemo, ERCP stenting for palliation

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20
Q

Ascending cholangitis

A

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.

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21
Q

Primary biliary cholangitis

A

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)

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22
Q

Biopsy for PBC findings

A

dense lymphoid infiltrates of hepatic portal tracts with chronic inflammation and hepatocyte necrosis

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23
Q

Primary sclerosing cholangitis

A

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

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24
Q

Post-cholecystectomy syndrome

A

Sx: dyspepsia, vomiting, pain, flatulence, diarrhoea 40%.

Rx: low fat diet, cholestyramine, PPIs if dyspepsia.

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25
Q

Cholangiocarcionoma

A

RF: PSC

Sx: persistent biliary colic, jaundice, RUQ mass, periumbilical lymphadenopathy (Sister Mary Joseph node) + left supraclavicular (Virchow node), raised Ca19-9

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26
Q

Coeliac disease assx:

A

1% of pop
HLA DQ2 (95%), DQ8 (80%), dermatitis herpetiformis, autoimmune (T1DM, autoimmune hepatitis).

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27
Q

Ix for coeliac

A

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.

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28
Q

Rx for coeliac

A

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.

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29
Q

Coeliac compl

A

anaemia (iron, folate, B12 def), hyposplenism, osteoporosis, osteomalacia, lactose intolerance, enteropathy-associated T-call lymphoma of small intestine, subfertility, rare - oesophageal ca

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30
Q

Bile acid malabsorption

A

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)

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31
Q

Small intestinal bacterial overgrowth syndrome

A

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

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32
Q

Inherited causes of unconjugated hyperbilirubinaemia

A

Gilbert’s
Crigler-Najjar

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33
Q

Gilbert’s

A

aut rec. Mild UDP-glucuronyl transferase deficiency. 1-2%. Benign. Jaundice only in illness, exercise, fasting. Ix: IV nicotinic acid shows rise

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34
Q

Crigler-Najjar

A

Type 1: Aut rec. Absolute UDP-glucuronosyl transferase def. No survival beyond adulthood
Type 2: More common than type 1, less severe. Rx: ?phenobarbital

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35
Q

Inherited causes of conjugated hyperbilirubinaemia

A

Dubin-Johnson syndrome
Rotor syndrome

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36
Q

Dubin-Johnson syndrome

A

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

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37
Q

Rotor syndrome

A

Aut rec. Defect in hepatic uptake and bilirubin storage. benign.

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38
Q

Oesophageal causes of UGIB

A

varices
oesophagitis
oesophageal ca
mallory weiss

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39
Q

Gastric causes of UGIB

A

ulcer
gastric ca
Dieulafoy lesion
diffuse erosive gastritis

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40
Q

Duodenal causes of UGIB

A

ulcer
aorto-enteric fistula

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41
Q

Oesophageal varices Rx

A

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

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42
Q

Prophylaxis of bleed for oesophageal varices

A

propanolol, endoscopic band ligation (two-weekly intervals until varices eradicated, with PPI cover to prevent ligation-associated ulcers)

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43
Q

Oesophagitis UGIB sx

A

small volume bleed, often streeks in vomit, rare malaena, usually with GORD-type hx

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44
Q

Oesophagela ca UGIB sx

A

small volume unless major vessels eroded (preterminal event)

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45
Q

Mallory weiss tear UGIB sx

A

brisk small to moderate volume, rare malaena

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46
Q

Gastric ulcer UGIB sx

A

small volume common unless erosion into significant vessels

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47
Q

Gastric Ca UGIB sx

A

frank haematemesis or blood mixed with vomit, prodromal dyspepsia, constitutional sx. Major vessel erosion causes large volume bleed

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48
Q

Diulafoy lesion

A

AV malformation, difficult to detect, large volume UGIB

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49
Q

Diffuse erosive gastritis

A

underlying cause eg NSAIDs, can be large volume bleed

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50
Q

Duodenal ulcer UGIB sx

A

posteriorly sited, can erode to gastroduodenal artery. Pain occurs several hrs post eating

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51
Q

Aorto-enteric fistula UGIB sx

A

past AAA surgery, high mortality

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52
Q

What score is used post-endoscopy in UGIBs

A

Rockall score post-endoscopy: risk of rebleeding/mortality. Includes age, shock features, co-morbidities, aetiology, endoscopic stigmata

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53
Q

Boerhaave’s

A

severe vomiting –> oesophageal rupture

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54
Q

Anal fissure RFs

A

constipation, IBD, STIs

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55
Q

Anal fissue sx

A

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).

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56
Q

Rx for anal fissure

A

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

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57
Q

Angiodysplasia

A

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

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58
Q

IBS dx

A

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.

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59
Q

IBS Rx

A

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

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60
Q

Gastrin

A

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

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61
Q

CCK

A

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

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62
Q

Secretin

A

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

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63
Q

Vasoactive intestinal peptide (VIP)

A

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

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64
Q

Somatostatin

A

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

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65
Q

Ascites causes

A

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)

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66
Q

Ascites Rx

A

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

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67
Q

SBP

A

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

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68
Q

Acute liver failure

A

Causes: Paracetamol, ETOH, viral hepatitis, acute fatty liver of pregnancy. Sx: jaundice, coagulopathy, hypoalbuminaemia, hepatic encephalopathy, renal failure

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69
Q

Alcoholic liver disease

A

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

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70
Q

Budd-Chiari

A

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

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71
Q

NAFLD

A

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

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72
Q

NAFLD biopsy

A

triglyceride accumulation with myofibroblast proliferation

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73
Q

Cirrhosis dx

A

transient elastography, Enhanced Liver fibrosis score for NAFLD, liver biopsy.

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74
Q

Causes of decompensation in cirrhosis

A

constipation (toxic product accumulation), infection, electrolyte imbalance, UGIB, increased ETOH intake

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75
Q

Liver biopsy contraindication

A

INR>1.4, Pltlt<60, anaemia, extrahepatic biliary obstruction, hydatid cyst, haemangioma, uncooperative pt, ascites

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76
Q

Cirrhosis biopsy features

A

excess collagen and extracellular matrix deposition in periportal and pericentral zones leading to formation of regenerative nodules

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77
Q

Child Pugh score.

A

Grading cirrhosis

<7 A, 7-9 B, >9 C. BAPEA bilirubin, albumin, PT, encephalopathy, ascites

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78
Q

MELD

A

grading cirrhosis

uses bilirubin, creatinine, INR

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79
Q

Ischaemic hepatitis

A

usually exceeds 50x upper limit of normal/1000u/L, with other end-organ dysfunction and AKI (ATN)

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80
Q

HCC epidemiology

A

3rd most common Ca worldwide.

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81
Q

HCC RFs

A

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)

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82
Q

HCC ix

A

USS +/- AFP in high risk groups (cirrhotic patients 2ndary to HBV/HCV/Haemochromatosis/ETOH men)

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83
Q

HCC Rx

A

surgery (early), transplant, radiofrequency ablation, transarterial chemoembolisation, sorafenib (multikinase inhibitor)

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84
Q

Drug causes of hepatocellular damage

A

Paracetamol, valproate, phenytoin, MAOIs, halothane, anti-TB (RIP), statins, ETOH, amiodarone, methyldopa, nitrofurantoin

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85
Q

Drug causes of cholestatic liver damage

A

COCP, penicillins, erythromycin, testosterone, phenothiazines (chlorpromazine, prochlorperazine), sulphonylureas, fibrates,

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86
Q

Drug causes of cirrhosis

A

methotrexate
methyldopa
amiodarone

87
Q

Autoimmune hepatitis assx

A

Young to middle-aged females, autoimmune, hypergammaglobulinaemia, HLA B8, DR3.

88
Q

Autoimmune hepatitis sx

A

T-cell mediated progressive necro-inflammatory process

acute hepatitis 25%, CLD, amenorrhoea (common). Raised IgG (hypergammaglobulinaemia).

89
Q

Autoimmune hepatitis biopsy

A

piecemeal necrosis - inflammation extending beyond limiting plate, bridging necrosis.

90
Q

Rx autoimmune hepatitis

A

steroids, immunosuppressants,
transplant

91
Q

Types of autoimmune hepatitis

A

Type I: ANA +/- anti SMA. Adults + children
Type II: anti LKM1. children only
Type III: soluble liver-kidney antigen. Middle aged adults

92
Q

liver abscesses

A

Most common: S aureus in children, E Coli adults. Rx: drainage + Abx (amox + cipro + metro or cipro + clindamycin)

93
Q

Coagulaopathy of liver disease

A

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.

94
Q

Hepatosplenomegaly causes

A

CLD with portal HTN, glandular fever, malaria, hepatitis, lymphoproliferative disorders, myeloproliferative disorders (e.g. CML), amyloidosis

95
Q

Hepatorenal syndrome

A

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

96
Q

Hepatic encephalopathy Sx

A

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.

97
Q

Hepatic encephalopathy grading

A

I: irritability. II: confusion, inappropriate behaviour. III: incoherent, restless. IV: coma.

98
Q

Precipitants of hepatic encephalopathy

A

infection, GI bleed, TIPS, constipation, sedatives, diuretics, hypoK, renal failure, increased dietary protein

99
Q

Rx for hepatic encephalopathy

A

treat underlying + lactulose + rifaximin. Embolisation of portosystemic shunts, liver transplant in select few

100
Q

Crohn’s sx

A

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

101
Q

Crohn’s compl

A

obstruction, fistula colorectal Ca

102
Q

Crohn’s endoscopy features

A

cobblestone appearance, skip lesions, deep ulcers, inflammation of all layers from mucosa to serosa, with granulomas, increased goblet cells

103
Q

Crohn’s small bowel enema

A

Kantor’s string sign for strictures, proximal bowel dilatation, rose thorn ulcers, fistulae

104
Q

Inducing remission in Crohn’s

A

steroids. 5-ASA 2nd line. Azathioprine/mercaptopurine as add-on. Infliximab in refractory disease

105
Q

Maintaining remission in Crohn’s

A

stop smoking, azathioprine/mercaptopurine (assess for TPMT activity). Methotrexate 2nd line.

106
Q

Perianal fistulae in Crohn’s management

A

Ix: MRI (determines if abscess, if fistula is simple/complex). Rx: oral metronidazole, infliximab, drainage seton for complex fistulae, incision + drainage for abscess + abx.

107
Q

Compl in Crohn’s

A

small bowel Ca (x40), colorectal Ca (x2), osteoporosis

108
Q

Ulcerative colitis features

A

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.

109
Q

Triggers for UC

A

stress, NSAIDs, abx, smoking cessation

110
Q

Compl for UC

A

Colorectal Ca (more than CD)

111
Q

Factors increasing risk for colorectal ca in UC

A

disease duration >10 yrs, pancolitis, onset<15yrs, unremitting disease, poor compliance to Rx

112
Q

Colonoscopy surveillance in UC by risk

A

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

113
Q

Contraix for colonoscopy in UC

A

severe colitis due to perf risk - do flexi sig instead

114
Q

Endscopy features in UC

A

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

115
Q

Barium enema in UC

A

loss of haustra, pseudopolyps, superficial ulceration, drainpipe colon (long-standing disease)

116
Q

Severity in UC

A

(Truelove and Witts): mild<4stools/day, moderate 4-6, severe>6 stools + systemic upset

117
Q

Inducing remission in UC

A

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

118
Q

Maintaining remission in UC

A

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

119
Q

Extra-intestinal IBD features related to disease activity

A

pauciarticular, asymmetric arthritis (most common extra-intestinal feature), erythema nodosum, episcleritis (more in CD), osteoporosis

120
Q

Extra-intestinal IBD features unrelated to disease activity

A

polyarticular, symmetric arthritis, uveitis (UC more common), pyoderma gangrenosum, clubbing, PSC (UC more common)

121
Q

Acute mesenteric ischaemia

A

embolism, AF hx. Sx: sudden, severe pain out-of-keeping with physical exam. Rx: urgent surgery. Poor prognosis

122
Q

Chronic mesenteric ischaemia

A

relatively rare, intestinal angina, colicky, intermittent abdo pain

123
Q

Ischaemic colitis

A

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)

124
Q

aminosalicylate action

A

5-ASA released in colon, inhibits prostaglandin synthesis.

125
Q

Sulphasalazine features and SE:

A

sulphapyridine (sulphonamide) + 5-ASA. SE (mostly sulph-related): rashes, oligospermia, headache, Heinz body anaemia, megaloblastic anaemia, fibrosis + other 5-ASA SEs:

126
Q

Mesalazine features and SE

A

delayed release form of 5-ASA. SE: GI upset, headache, agranulocytosis, pancreatitis (7x more in mesalazine than sulfalazine), interstitial nephritis

127
Q

Olsalazine

A

2x 5-ASA linked by diazo bond, broken by colonic bacteria

128
Q

H Pylori

A

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)

129
Q

Urea breath tests for H Pylori

A

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

130
Q

Rapid urease test for H pylori

A

biopsy sample with urea + pH indicator. Sensitivity 90-95%, specificity 95-98%.

131
Q

Serum antibody for H pylori

A

+ve after eradication. Sensitivity 85%, specificity 80%

132
Q

gastric biopsy culture for H pylori

A

sensitivity 70%, specificity 100%

133
Q

Gastric biopsy for H pylori

A

Sensitivity 95-99%, specificity 95-99%

134
Q

Stool antigen test for H Pylori

A

sensitivity 90%, specificity 95%

135
Q

Gastric MALT lymphoma

A

95% H pylori assx, good prognosis. Sx: paraproteinaemia. Rx: H pylori eradication if low grade (80% respond).

136
Q

C Diff features and toxins

A

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).

137
Q

RF for C Diff

A

2nd/3rd gen cephalosporins (leading cause), clindamycin, PPIs.

138
Q

Severity classification for C Diff

A

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

139
Q

Dx for C diff

A

C diff toxin

140
Q

Rx for C Diff

A

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)

141
Q

Preventing spread for C diff

A

isolation in SR until no more diarrhoea for 48hrs + disposable gloves and apron + hand washing

142
Q

Hep B serology

A

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

143
Q

HBV in pregnancy

A

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

144
Q

HBV biopsy

A

mononuclear infiltration of liver lobules with hepatocyte necrosis and Kupffer cells hyperplasia

145
Q

Whipple’s disease

A

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

146
Q

Pernicious anaemia

A

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

147
Q

Wilson’s genetics

A

Aut rec. ATP7B gene defect, Chr 13.

148
Q

Wilson’s sx

A

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.

149
Q

Wilson’s ix

A

slit lamp examination, reduced serum caeruloplasmin, reduced total serum Cu, increased 24hr urinary Cu excretion, genetic analysis of ATP7B gene.

150
Q

Wilson’s Rx

A

penicillamine (Cu chelator), trientine hydrochloride, tetrathiomolybdate

151
Q

Haemochromatosis genetics

A

Aut rec, HFE gene, Chr 6. 1/200 Europeans.

152
Q

HH sx

A

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

153
Q

HH Ix

A

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.

154
Q

Rx for HH

A

venesection (monitor transferrin sats (<50%) + ferritin (<50)), desferrioxamine 2nd line

155
Q

High ferritin causes

A

Without iron overload: inflammation, ETOH excess, liver disease, CKD, malignancy. Ix: transferrin sats low (<45% females, <50% males)

With iron overload: HH, repeated transfusions

156
Q

reduced ferritin cause

A

IDA

157
Q

Zollinger-Ellison

A

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)

158
Q

Carcinoid tumours - when do you get carcinoid syndrome

A

when liver mets present due to serotonin release, as well as when lung carcinoid, with mediators not being cleared by liver.

159
Q

Carcinoid tumours sx

A

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).

160
Q

Ix for Carcinoid

A

urinary 5-HIAA, plasma chromogranin A y

161
Q

Rx carcinoid

A

somatostatin analogues (octreotide)
Cyproheptadine for diarrhoea

162
Q

Oesohpageal Ca sx

A

dysphagia + constitutinal, small volume bleed unless major vessels eroded (preterminal event). May be recurrent.

163
Q

Oesoph ca ix

A

upper GI scope for dx. Endoscopic ultrasound for locoregional staging. CTCAP, PET CT for staging and mets.

164
Q

Oesoph ca rx

A

surgery (Ivor-Lewis oesophagectomy, risk of anastomotic leak) + adjuvant chemo

165
Q

Oesoph ca types and RFs

A

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

166
Q

oeophagitis sx

A

heartburn hx, odynophagia

167
Q

oesophageal candidiasis rf

A

HIV, steroid inhalers

168
Q

Pharyngeal pouch

A

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

169
Q

Achalasia sx

A

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.

170
Q

Achalasia ix

A

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)

171
Q

Achalasia rx

A

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

172
Q

Systemic sclerosis - how it causes dysphagia

A

other sx of CREST seen, lower oesophageal sphincter pressure reduced

173
Q

Myasthenia gravis dysphagia to what

A

liquids + solids

174
Q

Globus hystericus sx

A

hx of anxiety, intermittent, relieved by swallowing, painless, dysphagia

175
Q

Plummer-Vinson syndrome

A

dysphagia + glossitis + IDA. Rx: iron + web dilation

176
Q

Barrett’s

A

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

177
Q

Hydatid cysts

A

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).

178
Q

Gastric Ca most common ca type

A

2% of cancers. Adenocarcinoma most common

179
Q

Gastric Ca RF

A

H pylori, pernicious anaemia, atrophic gastritis, diet (salt, salt-preserved foods, nitrates), East Asian ethnicity, smoking, blood group A

180
Q

Gastric Ca Sx

A

abdo pain (epigastric, dyspepsia), weight loss, anorexia, N&V, dysphagia, UGIB, lymphatic spread (Virchow’s node - left supraclavicular, Sister Mary Joseph’s node - periumbilical).

181
Q

Gastric Ca Ix

A

OGD + biopsy (signet ring cells - large mucin vacuole displacing nucleus to one side, higher number = worse prognosis), CTCAP +/- PET for staging

182
Q

Gastric Ca Rx

A

surgical (endoscopic mucosal resection, partial/total gastrectomy) + chemo

183
Q

Colorectal Ca genetics

A

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)

184
Q

Screening for colorectal Ca

A

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.

185
Q

Anal ca

A

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

186
Q

Maltase

A

maltose→ 2x glucose

187
Q

Sucrase

A

sucrose → fructose + glucose.

188
Q

Lactase

A

lactose → glucose + galactose

189
Q

Threadworms

A

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

190
Q

oesinophilic oesophagitis RF

A

allergies/asthma/atopy, males (3:1), FHx allergies, Caucasian, age 30-50yrs, autoimmune disease.

191
Q

Oesinophilic oesophagitis sx

A

failure to thrive in children, dysphagia, strictures/fibrosis (56%), food impaction (55%), regurgitation/vomiting, anorexia, weight loss.

192
Q

Ix eosinophilic oesophagitis

A

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).

193
Q

Rx for eosinophilic oesophagitis

A

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)

194
Q

Compl of eosoniphilic oesophagitis

A

strictures 56%, impaction 55%, Mallory-Weiss tears

195
Q

eosinophilic oesophagitis prognosis

A

chronic, likely to come back

196
Q

Refeeding syndrome effect on electrolytes

A

low PO4, K, MG

197
Q

Refeeding syndrome Sx

A

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)

198
Q

How does refeeding syndrome affect PO4

A

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)

199
Q

What predisposes one to refeeding syndrome

A

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

200
Q

How to prevent refeeding syndrome

A

if not eaten for >5 days, refeed at no more than 50% of requirements for 1st 2 days

201
Q

Intrahepatic cholestasis of pregnancy

A

1%, 3rd trimester, most common. Sx: pruritis (palms+soles), no rash, high bilirubin. Rx: ursodeoxycholic acid, weekly LFTs, induction at 37wks. Compl: stillbirth

202
Q

Acute fatty liver of pregnancy

A

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)

203
Q

HELLP

A

haemolysis, elevated LFTs, Low platelets

204
Q

Jejunal villous atrophy causes

A

coeliac, tropical sprue, hypogammaglobulinaemia, GI lymphoma, Whipple’s disease, cow’s milk intolerance

205
Q

PPI SE

A

hypoNa, hypoMg, osteoporosis, microscopic colitis, C Diff risk

206
Q

Bariatric surgery referrals

A

BMI>35 with RF (HTN, T2DM etc), >40 without RF

207
Q

Forms of bariatric surgery

A

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

208
Q

Peutz-Jeghers

A

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

209
Q

Villous adenoma

A

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

210
Q

Melanosis coli

A

laxative abuse (esp senna), histology: pigment laden macrophages

211
Q

Malnutrition definition

A

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)

212
Q

Alcoholic ketoacidosis

A

non-diabetic, euglycaemic. Due to episodes of starvation resulting in lipolysis. Rx: saline + thiamine

213
Q

Drugs causing dyspepsia

A

NSAIDs, bisphosphonates, steroids. Drugs can cause reflux by reducing lower oesophageal sphincter pressure: CCBs, nitrates, theophyllines

214
Q

Laxative forms

A

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)

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