Gastro 7.5

Question 1

Causes of upper GI bleed?

Answer 1

1. peptic ulcer
2. gastritis/duodenitis
3. vatical bleed
4. erosive oesophagitis
5. Mallory-Weiss tear
6. tumours
7. aorto-enteric fistual, AV malformation, Dieulafoy lesion

Question 2

Most sensitive early objective measure/observation of haemodynamic status with upper GI bleed?

Answer 2

Tachycardia

Question 3

Pro kinetic before endoscopy for upper GI bleed

Answer 3

Stat dose IV erythromycin 250mg

• 30-120m pre-OGD
• to promote gastric emptying & improve endoscopic visualisation

Question 4

IV high-dose PPI before OGD for upper GI bleed

Answer 4

• bolus then infusion can be given
• if ongoing bleed/visible vessel, can continue infusion for 72h
• reduces bleeding stigmata and need for endoscopic haemostatic intervention
• doesn’t reduce re-bleeding rates or mortality

Question 5

Pre-OGD for suspected variceal bleed?

Answer 5

IV terlipressin/octreotide (splanchnic vasoconstrictor)

- usually with broad-spectrum Abx because of high risk severe bacterial infections in these high risk pts

Question 6

In upper GI bleed, when to offer:

• platelet transfusion?
• FFP?
• PCC?
• recombinant factor VIIa?

Answer 6

plts: active bleed, plts <50
FFP: fibrinogen<1 or PT/INR/APTT > 1.5xULN
PCC: active bleed + warfarinised
- do not use recombinant factor VIIa except when all other methods failed

Question 7

When OGD fails to achieve haemostasis in upper GI bleed, or re-bleed despite OGD, what is an alternative to re-look OGD/surgery?

Answer 7

transcatheter arterial embolisation

Question 8

OGD failure in variceal bleed - next step?

Answer 8

transjugular intrahepatic porto-systemic shunt within 72h

Question 9

Options for testing H. pylori?

Answer 9

Withhold PPI for 2/52

1. urea breath test
2. stool Ag test

If can’t withhold PPI for 2/52 as concern of bleed/re-bleed:
3. Serology test - but H. pylori Ab remain after Rx, lowering specificity

Question 10

H. pylori Rx ass with peptic ulcers

Answer 10

PPI + clarithromycin + amoxicillin/metronidazole for 1/52

If ass gastric ulcer (vs duodenal), continue PPI until control OGD performed 6-8wks later

Question 11

Long-term Rx for peptic ulcers NOT ass with H. pylori/NSAIDs?

Answer 11

• long-term PPI

- higher risk of re-bleed

Question 12

What is Forrest classification of upper GI bleeding?

Answer 12

To help describe peptic ulcers at OGD - prognostic info on risk of re-bleed, & mortality

1a - active spurting
1b active oozing
1c - non-bleeding visible vessel
2a - adherent clot
2b - flat pigmented spot
2c - clean ulcer base

Question 13

Restarting aspirin for 2ry prevention of CVD after OGD for upper GI bleed due to peptic ulcer?

Answer 13

• same day if adherent clot/flat haematin spot/clean base

- restart 3days after endoscopic haemostasis achieved if visible vessel/active bleed + lifelong pPI

Question 14

Long-term adverse effects of PPI

Answer 14

inc risk hip fracture
inc risk C diff infection
inc risk pneumonia
low Na, low Mg

Question 15

Prevalence of coeliac disease increases in those who are seropositive for which HLA subtypes?

Answer 15

HLA-DQ2

HLA-DQ8

Question 16

Conditions ass with coeliac disease?

Answer 16

dermatitis herpetiformis
T1DM
autoimmune liver disease
autoimmune thyroid disease
Turner's, William's, Down's syndrome
selective IgA deficiency

Question 17

Sites of common genetic mutations causing pancreatitis?

Answer 17

1. PRSS1 mutation (cationic trypsinogen) - unique to pancreatitis
2. SPINK1 mutation (pancreatic secretory trypsin inhibitor PSTI) - also unique
3. CFTR - ass with pancreatitis as a result of cystic fibrosis

Question 18

Recommended Rx of infected pancreatic necrosis

Answer 18

endoscopic drainage

Question 19

What is type 3c diabetes?

Answer 19

• 2ry to pancreatic (exocrine) disease, e.g. inflammation, neoplasia, resection, that disrupts pancreas & body’s ability to produce insulin
• total beta cell loss or dysfunction leads to reduced insulin production
• insufficient insulin secretion
• microvasc complications if not treated
• nearly 50% require insulin within 5yrs

Question 20

Long-term follow-up of chronic pancreatitis

Answer 20

• HbA1c/6months if not yet diabetic
• bone mineral density assessment every 2yrs (inc fracture risk & reduced BMD)
• if 3c diabetes, assess/6months for benefit of insulin therapy

Question 21

Causes of acute pancreatitis?

Answer 21

Gallstones
Ethanol
Trauma
Steroids
Mumps, coxsackie B
Autoimmune e.g. PAN, Ascaris infection
Scorpion venom
Hypertriglyceridaemia, Hyperchlymicronaemia, Hypercalcaemia, Hypothermia
ERCP
Drugs: Azathioprine, Mesalazine, Didanosine, Bendroflumethiazide, Furosemide, Pentamidine, Steroids, Sodium valproate

Question 22

Dx & Features of C diff?

Answer 22

Dx by C diff toxin in stool

• abdo pain, diarrhoea
• raised WCC
• severe toxic megacolon may develop
• Gram +ve rod, produces exotoxin that causes intestinal damage leading to pseudomembranous colitis. Can develop when gut flora suppressed by broad-spectrum Abx

Question 23

Rx of C diff?

Answer 23

1st line PO metronidazole 10-14days
PO Vancomycin if severe/not responding
PO Vanc + IV Metronidazole if life-threatening

Question 24

What is the trimodal death distribution following trauma?

Answer 24

1. Immediately - eg brain or high spinal injury, cardiac/great vessel damage; low salvage rate
2. Early hours post-injury - splenic rupture, subdural haematoma, haemopneumothoraces
3. Days post-injury - sepsis, multi-organ failure

Question 25

Trauma management - what thoracic injuries to suspect?

Answer 25

``` simple pneumothorax mediastinal traversing wounds tracheobronchial tree injury haemothorax blunt cardiac injury diaphragmatic injury aortic disruption pulmonary contusion ```

Question 26

Rx of simple pneumothorax in thoracic trauma?

Answer 26

Chest drain (aspiration risky as could be due to lung laceration & convert to tension)

Question 27

Causes of acute pancreatitis?

Answer 27

``` Gallstones Etoh Trauma Steroids Mumps, Coxsackie B Autoimmune e.g. PAN, Ascaris infection Scorpion venom Hypertriglyceridaemia, Hyperchylomicronaemia (e.g. hereditary lipoprotein lipase deificiency & apolipoprotein CII deficiency), Hypercalcaemia, Hypothermia ERCP Drugs: azathioprine, mesalazine, bendroflumethiazide, furosemide, pentamidine, sodium valproate, steroids, didanosine (antiretroviral) ```

Question 28

Anti-retroviral drug most characteristically ass with pancreatitis?

Answer 28

Didanosine

Question 29

Commonest cause of biliary disease in pts with HIV?

Answer 29

Sclerosing cholangitis due to e.g. CMV, cryptosporidium & microsporidia - pancreatitis may be 2ry to antiretroviral e.g. Didanosine, or by opportunistic infection e.g. CMV

Question 30

What is ischaemic hepatitis?

Answer 30

Diffuse hepatic injury resulting from acute hypo perfusion ('shock liver') - Dx in presence of an inciting event & massive rise in aminotransferase levels - often in conjunction with AKI tubular necrosis or other end organ dysfunction

Question 31

NAFLD: what is the spectrum? | what does it represent?

Answer 31

Hepatic manifestation of the metabolic syndrome, hence insulin resistance thought to e the key mechanism - steatosis - fat in the liver - NASH - fat with inflammation - progressive disease may cause fibrosis & cirrhosis

Question 32

What is NASH?

Answer 32

non-alcoholic steatohepatitis, liver changes similar to alcoholic hepatitis but in absence of etch abuse - progression of disease may be responsible for what was previously labelled as cryptogenic cirrhosis

Question 33

Factors ass with NAFLD?

Answer 33

``` obesity hyperlipidaemia T2DM jejunoilieal bypass sudden weight loss/starvation ```

Question 34

Features of NAFLD?

Answer 34

usually aSx hepatomegaly ALT ? AST increased echogenecity on US

Question 35

What does NICE recommend in aSx incidental fatty changes on liver ultrasound? What is suggested if this isn't available?

Answer 35

ELF: enhanced liver fibrosis blood test to check for advanced fibrosis - combo of hyaluronic acid + pro collagen III + tissue inhibitor of metalloproteinase 1 - algorithm of values results in a blood test score If not available: - non-invasive tests to assess severity - FIB4 score of NAFLD fibrosis score - can be used in combo with a FibroScan (liver stiffness measurement assessed with transient elastography)

Question 36

Rx of NAFLD?

Answer 36

lifestyle changes esp weight loss & monitoring | - ongoing research into role of gastric banding & metformin etc

Question 37

MoA of 5-ASA drugs?

Answer 37

5-ASA released in colon and not absorbed - acts as local anti-inflammatory - may inhibit prostaglandin synthesis

Question 38

What is Sulfasalazine? | side-effects?

Answer 38

5-ASA + sulphapyridine (sulphonamide) - rashes - oligospermia - headache - heinz-body anaemia - megaloblastic anaemia - lung fibrosis - other SEs common to 5-ASAs

Question 39

5-ASA drug side-effects (common to mesalazine & sulfasalazine etc)

Answer 39

- GI upset - headache - agranulocytosis - pancreatitis - interstitial nephritis

Question 40

What is mesalazine?

Answer 40

Delayed release form of 5-ASA, avoiding sulphapyridine side-effects seen with sulfasalazine

Question 41

Some studies suggest an increased risk of Crohn's relapse 2ry to what?

Answer 41

NSAIDs, cOCP

Question 42

1st line to induce remission in Crohn's disease?

Answer 42

Glucocorticoids (oral, topical, IV) | - Budesonide is an alternative in a subgroup

Question 43

1st line to induce remission in Crohn's disease? | What can be used in addition?

Answer 43

Glucocorticoids (oral, topical, IV) - Budesonide is an alternative in a subgroup - Enteral feeding with an elemental diet may be used in in addition or instead if a concern with steroid side-effects e.g. in young children

Question 44

2nd line drugs to induce remission in Crohn's disease?

Answer 44

5-ASA drugs, but not as effect as steroids

Question 45

What can be used to induce remission in Crohn's as add-on medication? (but not mono therapy)

Answer 45

+ Azathioprine/Mercaptopurine/Methotrexate

Question 46

What is used to induce remission in refractory or fistulating Crohn's disease?

Answer 46

Infliximab | - pts usually continue on azathioprine/methotrexate

Question 47

How to induce remission in isolated peri-anal Crohn's disease?

Answer 47

Metronidazole

Question 48

1st line drugs to maintain remission in Crohn's disease?

Answer 48

Azathioprine/Mercaptopurine

Question 49

2nd line drug to maintain remission in Crohn's disease?

Answer 49

Methotrexate

Question 50

What drug should be considered to maintain remission in Crohn's disease if a pt has had previous surgery?

Answer 50

5-ASA drugs e.g. mesalazine

Question 51

What are people with Crohn's disease at increased risk of?

Answer 51

small bowel cancer colorectal cancer osteoporosis

Question 52

What is the commonest disease pattern in Crohn's? What does it usually lead to? What are other surgical procedures involved?

Answer 52

Stricturing terminal ill disease -> Ileocaecal resection - segmental small bowel resections - stricturoplasty - sub-total colectoy - panproctocolectomy - staged subtotal colectomy - protectomy

Question 53

Fistulae in Crohn's disease?

Answer 53

- may form between rectum & skin (perianal) or small bowel & skin - between loops of bowel can occur ->bacterial overgrowth & malabsorption - Rx of enterocutaneous fistulae involves controlling sepsis, optimising nutrition, imaging the disease & planning definitive surgical Rx

Question 54

When to consider IBS? | How to diagnose in terms of Sx?

Answer 54

- abdo pain &/or bloating &/or change in bowel habit - abdo pain relieved by defecation/ass with altered bowel frequency stool form, with 2/4 of: - altered stool passage - abdo bloating, distension, tension, hardness - Sx worse by eating - passage of mucus - may also have features such as lethargy, nausea, backache, bladder Sx

Question 55

When considering IBS what are red flag Sx?

Answer 55

rectal bleeding unexplained/unintentional weight loss FX of bowel/ovarial cancer onset after 60yrs age

Question 56

3 Drug causes of dyspepsia? What 3 drugs may cause reflux by reducing lower oesophageal sphincter pressure?

Answer 56

1. NSAIDs 2. bisphosphonates 3. steroids - calcium channel blockers - nitrates - theophyllines - although calcium channel blockers & nitrates occasionally used in achalasia because of their effect on the LOS

Question 57

What is PBC: 1ry biliary cholangitis?

Answer 57

- chronic liver disorder typically in middle-aged females 9:1 - thought to be autoimmune, where interlobular bile ducts become damaged by a chronic inflammatory process causing progressive cholestasis, which may eventually progress to cirrhosis - classic presentation: itching in a middle-aged woman

Question 58

Diseases ass with PBC?

Answer 58

- Sjogrens 80% - RA - systemic sclerosis - thyroid disease

Question 59

Dx of PBC - what Ab?

Answer 59

- AMA M2 present in 98%, v specific - smooth muscle Ab in 30% - raised serum IgM

Question 60

Rx of PBC: - what supplements? - what drug Rx? - what for pruritus? - what if e.g. bilirubin >100?

Answer 60

- fat-soluble vitamins - ursodeoxycholic acid - cholestyramine for pruritus - liver Tx - recurrence may occur in gift but not usually a problem

Question 61

What are the 3 types of colon cancer?

Answer 61

sporadic 95% hereditary non-polyposis colorectal carcinoma 5% familial adenomatous polyposis <1%

Question 62

What gene mutations are involved in sporadic colon cancer?

Answer 62

More than half show alleic loss of the APC gene Further series of gene abnormalities lead to invasive carcinoma e.g.: - activation of K-ras oncogene - p53 deletion - DCC tumour suppressor gene deletion

Question 63

Commonest form of inherited colon cancer? where does it usually develop? 7 mutations have been identified - which affect genes involved in DNA mismatch repair leading to micro satellite instability - what are the commonest genes involved? - what is the commonest associated cancer?

Answer 63

HNPCC - often proximal colon, usually poorly differentiated & highly aggressive - MSH2 60% - MLH1 30% - endometrial (they are in general at higher risk of other cancers)

Question 64

Amsterdam criteria used to aid Dx of HNPCC?

Answer 64

- at least 3 family members with colon cancer - across at least 2 generations - at least 1 Dx <50yrs

Question 65

FAP: familial adenomatous polyposis = hundreds of polyps form by age 30-40, inevitably develop carcinoma - genetics? - how can genetic testing be done? - usual Rx? - what other tumours are they at risk from?

Answer 65

- autosomal dominant - mutation in APC (adenomatous polyposis coli) tumour suppressor gene on chr 5 - analyse DNA from WBCs - total colectomy with ileo-anal pouch formation in their twenties - duodenal tumours

Question 66

What is Gardner's syndrome?

Answer 66

Variant of FAP - esteems of skull & mandible - retinal pigmentation - thyroid carcinoma - epidermoid cysts on skin

Question 67

Why is there increased risk of colon cancer in UC? lesions? prognosis?

Answer 67

- chronic inflammation - lesions may be multifocal - prognosis worse than if without UC

Question 68

Factors that increase risk of colon cancer in pts with UC?

Answer 68

- disease duration >10yrs - pts with pancolitis - onset before 15yrs old - unremitting disease - poor compliance to treatment

Question 69

Risk stratification for colonoscopy surveillance in IBD (?colon cancer) - Lower risk?

Answer 69

5 yr colonoscopy - extensive colitis with no active endoscopic/histological inflammation - or left-sided colitis - or Crohn's colitis <50% of colon

Question 70

Risk stratification for colonoscopy surveillance in IBD (?colon cancer) - Intermediate risk?

Answer 70

3 yr colonoscopy - extensive colitis with midl active endoscopy/histological inflammation - or post-inflammatory polyps - or FHx of bowel ca in a 1st degree relative aged 50+

Question 71

Risk stratification for colonoscopy surveillance in IBD (?colon cancer) - Higher risk?

Answer 71

1 yr followup colonoscopy - extensive colitis with mod/severe active endoscopic/histological inflammation - or stricture in past 5yrs - or dysplasia in past 5yrs declining surgery - or PSC/Tx for 1ry sclerosing cholangitis - or FHx bowel ca in 1st degree relative aged <50yrs

Question 72

2 methods used to Dx coeliac disease?

Answer 72

- immunology - jejunal biopsy - both normally reverse on a gluten-free diet

Question 73

Immunology in coeliac disease: - 1st choice most specific Ab? others?

Answer 73

``` Anti-TTG Ab IgA most specific Also: - endomyseal Ab IgA - anti-gliadin Ab IgA/IgG NOT recommended by NICE - anti-casein Abs found in some ```

Question 74

Jejunal biopsy in coeliac disease - what 4 things may be found?

Answer 74

- subtotal villous atrophy - crypt hyperplasia - increase in intraepithelial lymphocytes - lamina propria infiltration with lymphocytes

Question 75

Important causes of subtotal villous atrophy?

Answer 75

* Coeliac disease * Tropical sprue * Dermatitis herpetiformis * Lymphoma * HIV-related enteropathy * Giardiasis * Hypogammaglobulinaemia * Radiation * Whipple’s disease * Zollinger–Ellison syndrome

Question 76

Crohn's disease pt has an ileocaecal resection. C/o diarrhoea at clinic, with normal CRP and no focal changes on small bowel enteroclysis What is the cause? What should benefit?

Answer 76

Bile salt malabsorption common cause of diarrhoea after ill resection - oral Cholestyramine

Question 77

What is Budd-Chiara syndrome? Features? Causes?

Answer 77

Hepatic vein thrombosis - usually seen in a procoagulant condition 1. abdo pain, sudden-onset, severe 2. ascites 3. tender hepatomegaly - polycythaemia rubra vera - thrombophilia: activated protein C resistance, antithrombin III deficiency, protein C&S deficiencies, antiphospholipid syndrome - pregnancy, OCP

Question 78

Dysphagia may be associated with weight loss, anorexia or vomiting during eating Past history may include Barrett's oesophagus, GORD, XS smoking or alcohol use Dx?

Answer 78

oesophageal cancer

Question 79

May be history of heartburn Odynophagia but no weight loss and systemically well Dx?

Answer 79

Oesophagitis

Question 80

Dysphagia, odynophagia with e.g. Hx of HIV or other RFs such as steroid inhaler use Dx?

Answer 80

oesophageal candidiasis

Question 81

Dysphagia of both liquids and solids from the start Heartburn Regurgitation of food - may lead to cough, aspiration pneumonia etc INCREASE in LOS pressure Dx?

Answer 81

Achalasia

Question 82

More common in older men Represents a posteromedial herniation between thyropharyngeus and cricopharyngeus muscles Usually not seen but if large then a midline lump in the neck that gurgles on palpation Typical symptoms are dysphagia, regurgitation, aspiration and chronic cough. Halitosis may occasionally be seen Dx?

Answer 82

Pharyngeal pouch

Question 83

Dysphagia As well as oesophageal dysmotility the lower oesophageal sphincter (LES) pressure is DECREASED other features e.g. calcinosis, Raynauds Dx?

Answer 83

systemic sclerosis

Question 84

Dysphagia with liquids as well as solids Other Sx may include extraocular muscle weakness or ptosis Dx?

Answer 84

Myasthenia gravis

Question 85

Dysphagia, May be Hx of anxiety Sx are often intermittent and relieved by swallowing Usually painless - the presence of pain should warrant further Ix for organic causes Dx?

Answer 85

Globus hystericus

Question 86

Extrinsic causes of dysphagia?

Answer 86

Medistinal mass | Cervical spondylosis

Question 87

Oesophageal wall causes of dysphagia?

Answer 87

Achalasia Diffuse oesophageal spasm Hypertensive lower oesophageal sphincter

Question 88

Intrinsic causes of dysphagia?

Answer 88

Tumours Strictures Oesophageal web Schatzki rings

Question 89

Neurological causes of dysphagia?

Answer 89

``` CVA Parkinson's disease MS Brainstem pathology Myasthenia gravis ```

Question 90

What studies are required to evaluate conditions e.g. achalasia & pts with GORD being considered for fundoplication surgery?

Answer 90

Ambulatory oesophageal pH & manometry studies

Question 91

GORD: what are the indications for OGD? | What can be considered if OGD negative i.e. what is the gold standard test for Dx?

Answer 91

- age >55 - Sx >4wks or persistent Sx despite Rx - dysphagia - relapsing Sx - weight loss Generally there is poor correlation between Sx & endoscopy appearance *Consider 24h oesophageal pH monitoring*

Question 92

Colorectal cancer in the UK is 3rd commonest - what does is usually develop from? - what is lifetime risk? - what is the screening programme? - what happens at colonoscopy?

Answer 92

- adenomatous polyps - lifetime risk 5% - FOB test every 2 yrs to those aged 60-74 in Eng, 50-74 in Scot - if abnormal, offered colonoscopy - reduces mortality by 16% - 5/10 normal - 4/10 polyps, amy be removed - 1/10 cancer

Question 93

What is PSC: 1ry sclerosing cholangitis? Features? Associations?

Answer 93

- biliary disease characterised by inflammation & fibrosis of intra & extra hepatic bile ducts, unknown aetiology - RUQ pain, fatigue, cholestais: jaundice & pruritus - UC 4% have PSC, 80% PSC have UC - Crohn's - HIV

Question 94

Dx of PSC? what is shown? | Complications?

Answer 94

* **ERCP: multiple biliary strictures giving a beaded appearance - ANCA may be +ve - liver Bx may show fibrous obliterative cholangitis 'onion skin' - cholangiocarcinoma 10% - inc risk colorectal ca

Question 95

When to consider bariatric surgery in severe obesity? | When to consider it as a 1st line option?

Answer 95

- BMI>40 or 35-40 with significant comorbidity that would improve with weight loss - all non-surg measures failed to achieve/maintain clinical beneficial weight loss at least 6m - if will/do receive intensive specialist management - generally fit for anaesthesia & surgery - commit to need for long-term followup Consider 1st line if BMI>50 & surgery appropriate - consider Orlistat before surgery if waiting time is long

Question 96

3 main types of Bariatric surgery?

Answer 96

1. 1rily restrictive: laparoscopic-adjustable gastric banding LAGB, or sleeve gastrectomy 2. 1rily malabsorptive: classic BPD biliopancreatic diversion has now been largely replaces by biliopancreatic diversion with duodenal switch 3. mixed: Roux-en-Y gastric bypass surgery

Question 97

Bariatric surgery: what produces less weight loss than malabsorptive or mixed procedures but as it has fewer complications it is normally the 1st-line intervention in patients with a BMI of 30-39?

Answer 97

LAGB: mainly restrictive, laparoscopic-adjustable gastric banding

Question 98

Bariatric surgery: what is generally considered if BMI >40?

Answer 98

``` Gastric bypass (mixed) or sleeve gastrectomy (restrictive) - sleeve may be done as a sole procedure or an initial procedure prior to bypass ```

Question 99

Bariatric surgery: when are 1rily malabsorptive procedures done?

Answer 99

Reserve for the v obese e.g. BMI >60

Question 100

Features of acute appendicitis?

Answer 100

Abdo pain: - peri-umbilical (visceral stretching of appendix lumen which is a midgut structure) - radiating to RIF pain (localised parietal peritoneal inflammation) - migratory, worse on coughing/speed bumps. Children can't hop on right LL. - anorexia, nausea/vomit 1-2x, mild fever - pelvic appendicitis may cause localised rectal irritation leading to some loos stools (pelvic abscess can also cause diarrhoea)

Question 101

Examination in acute appendicitis

Answer 101

- tender, guarding, rebound, local/generalised peritonitis if perforation - retrocaecal appendicitis may have relatively few signs - DRE may reveal boggy sensation if pelvic abscess, or even tenderness with a pelvic appendix

Question 102

Dx of acute appendicitis? | What score can be used to suggest the likelihood of it?

Answer 102

- Hx, Ex, raised inflame markers - urine to exclude pregnancy, renal colic, UTI - US useful in females. May show free fluid - CT but not usually Alvarado score: 8 criteria

Question 103

Rx in appendicitis?

Answer 103

- lap appendicectomy - metronidazole reduces wound infection rates - copious abdominal lavage if perforated appendix - broad-spectrum Abx if no peritonitis, can consider interval appendicectomy - be aware of underlying caecal malignancy or perf'd sigmoid diverticular disease in older pts - solely IV Abx ass with longer hospital stay and unto 20% go on to have an appendicectomy within 12m

Question 104

RFs for hepatocellular carcinoma?

Answer 104

Main RFs: - cirrhosis e.g. 2ry to HBV (worldwide), HCV (UK) - etoh - haemochromatosis - PBC Others: alpha-1 AT deficiency, hereditary tyrosinosis, glycogen storage disease, aflatoxin, porphyria cutanea tarda, male sex, diabetes mellitus, metabolic syndrome, OCP, anabolic steroids

Question 105

Features of hepatocellular carcinoma? How should screening be considered?

Answer 105

- tends to present late - may have features of cirrhosis e.g. jaundice, ascites, RUQ pain, hepato/splenomegaly, pruritus - may present as decompensation in a pt with chronic liver disease - can be 2ry e.g. multiple blood transfusions Screening: US +/- AFP for high-risk groups e.g. - cirrhosis 2ry to HBV/HCV/haemochromatosis - men with cirrhosis 2ry to etch

Question 106

Rx options in hepatocellular carcinoma?

Answer 106

- early: surgical resection - liver Tx - radio frequency ablation (usually palliative) - transarterial chemoembolisation (usually palliative) - SORAFENIB: multikinase inhibitor

Question 107

What is the H. pylori test where pt consumes drink containing 13C isotope enriched urea, then exhales with mass spectrometry analysis? How long do you need to wait if pt has had Abx/antisecretory e.g. PPI?

Answer 107

Urea breath test - urea is broken down by H pylori urease - mass spec calculated amount of 13C CO2 - shouldn't be performed within 4 WEEKS - sens 95-98%, spec 97-98%

Question 108

What is the H pylori test where a biopsy sample is mixed with urea & pH indicator, and a colour change occurs if there's H pylori urease activity?

Answer 108

Rapid urease test e.g. CLO test | - sens 90-95% spec 95-98%

Question 109

What is the limitation of the serum Ab H pylori test?

Answer 109

Remains positive after eradication | - sens 85% spec 80%

Question 110

What is the benefit of culture of gastric biopsy as an H pylori test?

Answer 110

- provides Abx sensitivities info - sens 70% spec 100% - Can also do gastric biopsy alone without culture, with sens 95-99% spec 95-99%

Question 111

What is Wilson's disease? | What is the genetic defects?

Answer 111

Autosomal recessive disorder characterised by XS copper deposition in the tissues Metabolic abnormalities inc: increased copper absorption from small bowel, decreased hepatic copper excretion ***Defect in the ATP7B gene on chr 13***

Question 112

Features of Wilson's disease?

Answer 112

- onset usually 10-25yrs, children present with liver disease whereas adults it is often neuro Liver: - hepatitis, cirrhosis Brain: - basal ganglia degeneration, speech, behavioural & psych problems, asterixis, chorea, dementia Cornea: - Kayser-Fleischer rings Also: - renal tubule acidosis eso Fanconi syndrome, haemolysis, blue nails

Question 113

Dx by serum & urine in Wilson's disease?

Answer 113

- Reduced serum caeruloplasmin (also reduced serum copper as 95% is carried by caeruloplasmin) - Increased 24h urinary copper excretion

Question 114

1st line Rx for Wilson's disease? Alternative ? Newer one under Ix?

Answer 114

PENICILLAMINE chelates copper Trientine Hydrochloride also a copper chelator Tetrathiomolybdate under Ix

Question 115

What is Gilberts syndrome? What are the features? Ix?

Answer 115

Autosomal recessive condition of defective bilirubin conjugation due to deficiency of UDP glucuronyl transferase - unconjugated hyperbilinaemia (so not in urine) - jaundice may only be seen during intercurrent illness - Bilirubin rise after prolonged fasting or IV nicotinic acid, no Rx required

Question 116

Recognised associations of autoimmune hepatitis? | What is the ass raised Ig subtype?

Answer 116

- other autoimmune disorders - hypergammaglobulinaemia - HLA B8, DR3 - IgG

Question 117

Type I autoimmune hepatitis - what Ab? - who does it affect?

Answer 117

ANA &/or anti-smooth muscle Ab SMA | - adults & children

Question 118

Type II autoimmune hepatitis - what Ab? - who does it affect?

Answer 118

- anti-liver/kidney microsomal type 1 Ab LKM1 | - children only

Question 119

Type III autoimmune hepatitis - what Ab? - who does it affect?

Answer 119

- soluble liver-kidney Ag | - middle-aged adults

Question 120

Features of autoimmune hepatitis? | What is on liver biopsy?

Answer 120

- usually insidious onset - may present with signs of chronic liver disease - acute hepatitis: fever, jaundice etc in 25% - amenorrhoea is common - ANA/SMA/LKM1 Abs, raised IgG levels - extrahepatic clinical features common Liver Bx: inflammation extending beyond limiting plate ('piecemeal necrosis'), bridging necrosis

Question 121

Rx of autoimmune hepatitis?

Answer 121

- steroids, other immunosuppressants e.g. Azathioprine | - liver Tx

Question 122

Which laxative is shown to have carcinogenic potential?

Answer 122

Co-Danthramer & Co-Danthrusate= genotoxic, carcinogenic | - only be prescribed in palliative pts with refractory constipation

Question 123

Examples of osmotic laxatives?

Answer 123

lactulose macrogols rectal phosphates

Question 124

Examples of stimulant laxatives?

Answer 124

``` senna docusate bisacodyl glycerol (co-danthramer) ```

Question 125

Examples of bulk-forming laxatives?

Answer 125

ispaghula husk | methylcellulose

Question 126

Examples of faecal softener laxatives?

Answer 126

arachis oil enemas, not commonly prescribed

Question 127

Bile-acid malabsorption 1ry cause? 2ry causes?

Answer 127

Chronic diarrhoea due to XS production of bile acid - underlying GI disorder causing reduced bile acid absorption e.g. ileal disease in Crohn's - cholecystectomy - coeliac disease - small bowel bacterial overgrowth

Question 128

Ix of choice for bile acid malabsorption? | Rx?

Answer 128

SeHCAT: uclear test using gamma-emitting selenium molecule in selenium homocholic acid taurine or tauroselcholic acid - scans done 7 days apart to assess retention/loss of radio labelled SeHCAT Rx Bile acid sequestrate e.g. cholestyramine

Question 129

What is haemochromatosis?

Answer 129

Autosomal recessive disorder of iron absorption & metabolism resulting in iron accumulation - inheritance of mutations in HFE gene on both copies of chr 6 - carrier rate of 1 in 10 (!)

Question 130

Screening for haemochromatosis in family members?

Answer 130

HFE mutation genetic testing

Question 131

Diagnostic test for haemochromatosis?

Answer 131

Molecular genetic testing for C282Y & H63D mutations | Liver Bx: Perl's stain

Question 132

Typical iron study profile in patient with haemochromatosis? | What is characteristically shown on joint X-rays?

Answer 132

Tranferrin sat >55% men >50% women Raised ferritin >500 & Iron LOW total iron binding capacity Chondrocalcinosis

Question 133

Monitoring adequacy of venesection in haemochromatosis?

Answer 133

Transferrin sat should be kept <50% | Serum ferritin conc <50

Question 134

Screening for haemochromatosis in general population?

Answer 134

**Transferrin saturation most useful**; ferritin should also be measured but not usually abnormal in early stages of iron accumulation

Question 135

What is angiodysplasia? Association? Dx?

Answer 135

Vascular deformity of GI tract which predisposes to bleeding & iron-deficiency anaemia - seen in elderly - ass with aortic stenosis = reduction in vWF as blood passes through narrow aortic valve; Rx is of aortic stenosis Dx with colonoscopy - mesenteric angiography if acutely bleeding

Question 136

Rx of angiodysplasia?

Answer 136

Endoscopic cautery or Argon plasma coagulation - antifibrinolytics e.g. Transexamic acid - oestrogen may also be used?

Question 137

Drug causes of mainly hepatocellular liver disease?

Answer 137

- paracetamol - valproate, phenytoin - MAO-Is - statins - etoh - amiodarone - methyldopa - nitrofurantoin - halothane - anti-TB: RIP

Question 138

Drug causes of mainly cholestatic (+/- hepatitis) liver disease?

Answer 138

- OCP - ABx: co-amoxiclav, flucloxacillin, erythromycin - sulphonylureas - fibrates - phenothiazines e.g. chlorpromaxine, prochlorperazine - nifedipine rarely

Question 139

Drug causes of mainly cirrhotic liver disease?

Answer 139

Methotrexate Methyldopa aMiodarone

Question 140

Blatchford score at 1st assessment of acute upper GI bleed: | what are the components?

Answer 140

Urea Hb systolic BP Others: tachycardia, melaena presentation, syncope presentation, hepatic disease, cardiac failure

Question 141

Resuscitation in acute upper GI bleed? | After?

Answer 141

ABC, access platelet transfusion if actively bleeding, plts<50 FFP if fibrinogen <1 or PT/INR/APTT >1.5X normal PCC if on warfarin & actively bleeding OGD immediately if severe, otherwise within 24h

Question 142

Management of non-variceal acute upper GI bleeding?

Answer 142

PPI not recommended pre-OGD if suspected non-variceal - should be given if non-variceal upper GI bleed & stigmata or recent haemorrhage shown at endoscopy If further bleeding: - repeat OGD, interventional radiology, surgery

Question 143

``` Management of variceal acute upper GI bleeding: pre-OGD? if oesophageal? if gastric? if not controlled? ```

Answer 143

- Pre-OGD: Terlipressin & prophylactic Abx - Band ligation for oesophageal varices - Injection of N-butyl-2-cyanoacrylate for gastric varies - TIPS: Transjugular intrahepatic portosystemic shunts if otherwise not controlled

Question 144

Vessel responsible with a posteriorly-sited duodenal ulcer which can present with major bleeding?

Answer 144

Gastroduodenal artery

Question 145

What is Zollinger-Ellison syndrome? | 30% occur as part of what?

Answer 145

XS levels of GASTRIN, usually from a gastrin-secreting tumour of duodenum/pancreas - MEN type I

Question 146

Features of Zollinger-Ellison syndrome?

Answer 146

- severe multiple gastroduodenal ulcers - gastric acid hyper secretion - diarrhoea, malabsorption (gastrin activates pancreatic lipase, precipitating bile acids) - non-beta cell islet tumour of pancreas may be present i.e. gastrinoma

Question 147

Dx of Zollinger-Ellison syndrome?

Answer 147

Fasting gastrin levels = single best screen test Secretin stimulation test: paradoxical dramatic increase in gastrin (normally little/no effect)

Question 148

3 main conditions of ischaemia to the lower GI tract?

Answer 148

acute mesenteric ischaemia chronic mesenteric ischaemia ischaemic colitis

Question 149

Common features in bowel ischaemia?

Answer 149

- abdo pain, sudden-onset severe & out-of-keeping with physical exam findings when Acute mesenteric ischaemia - rectal bleeding - fever - diarrhoea - elevated WCC ass with lactic acidosis

Question 150

Common predisposing factors in bowel ischaemia? | Dx?

Answer 150

- inc age - AF esp for mesenteric ischaemia - other causes of emboli: endocarditis, malignancy - CVD RFs: smoking, htn, diabetes - cocaine: ischaemic colitis sometimes seen in young pts after cocaine use Dx by CT

Question 151

How does acute mesenteric ischaemia usually occur?

Answer 151

ambolism resulting in artery occlusion which supplies small bowel e.g. SMA - classically Hx of AF - severe, sudden-onset abdo pain out of keeping with physical exam findings - urgent surgery, poor prognosis

Question 152

How does chronic mesenteric ischaemia usually occur?

Answer 152

- non-specific features, may be thought of as 'intestinal angina' - colicky, intermittent abdo pain

Question 153

How does ischaemic colitis usually occur? What may be seen on AXR? Rx?

Answer 153

Acute but transient compromise in blood flow to large bowel, which may lead to inflammation, ulceration & haemorrhage - more likely in 'watershed' areas e.g. splenic flexure, that are located at borders of territory supplied by superior & inferior mesenteric arteries AXR: 'thumbprinting' due to mucosal oedema/haemorrhage supportive Rx - surgery may be required in a minority if cons measures fail - indication inc: generalised peritonitis, perforation or ongoing haemorrhage

Question 154

What is melanosis coli? what is shown on histology? association?

Answer 154

Disorder of pigmentation of bowel wall - Pigment-laden macrophages - ass with laxative abuse esp anthraquinone compounds e.g. senna

Question 155

What is achalasia?

Answer 155

Failure of oesophageal peristalsis & of relaxation of LOS due to degenerative loss of ganglia from Auerbach's plexus i.e. LOS contracted, oesophagus above dilated - typically presents middle-aged

Question 156

Clinical features of achalasia?

Answer 156

- dysphagia of both liquids& solids - typically variation in severity of Sx - heartburn - regurgitation of food - may lead to cough, aspiration pneumonia etc - malignant change in small number of pts

Question 157

Gold standard test for achalasia? | What does CXR & barium swallow show?

Answer 157

Manometry: XS LOS tone which doesn't relax on swallowing CXR: wide mediastinum, fluid level Barium swallow: grossly expanded oesophagus, fluid level, 'birds beak' appearance

Question 158

Rx in Achalasia?

Answer 158

- intra-sphincteric injection of botulinum toxin - Heller cardiomyotomy - balloon dilatation - drug Rx has a role but limited by side-effects

Question 159

What is the most accurate method of re-testing for H. pylori?

Answer 159

Carbon-13 urea breath test | - do 4wks after eradication Rx

Question 160

What enzyme is mainly responsible for breaking down starch into sugars?

Answer 160

Amylase - in saliva & pancreatic secretions

Question 161

What brush-border enzyme involved in carb breakdown cleaves maltose -> glucose+glucose? sucrose -> fructose + glucose? lactose -> glucose + galactose

Answer 161

maltase sucrase lactase

Question 162

Dx of liver cirrhosis? What further Ix may be recommended if cirrhosis is diagnosed?

Answer 162

- Traditionally liver biopsy but ass with adverse effects e.g. bleeding, pain - Other techniques e.g. transient elastography & acoustic radiation force impulse imaging increasingly used, recommended in NICE guidelines - Pts with NAFLD, enhanced liver fibrosis score to screen for pts is recommended by NICE OGD - check for varies - in people with a new Dx of cirrhosis Liver US every 6months +/- AFP to check for HCC

Question 163

What is transient elastography/Fibroscan? | When to offer it as part of cirrhosis screening?

Answer 163

- uses a 50 MHz wave passed into the liver from a small transducer on the end of an US probe - measures the 'stiffness' of the liver which is a proxy for fibrosis - HCV infection - men who drink >50units & women who drink >35units/wk and have done for several months - people Dx with eton-related liver disease

Question 164

Common causes of decompensation in pt with cirrhotic liver disease?

Answer 164

``` infection electrolyte imbalances constipation dehydration upper GI bleeds increased etoh intake ```

Question 165

HBV serology: | what does HBsAg imply?

Answer 165

acute disease if present for 1-6months | chronic infective disease if present >6months

Question 166

HBV serology: | what does Anti-HBs imply?

Answer 166

Immunity - either exposure or immunisation | - negative in chronic disease

Question 167

HBV serology: | what does Anti-HBc imply? IgM? IgG?

Answer 167

Previous/Current infection IgM - acute/recent present for approx 6months IgG anti-HBc persists

Question 168

HBV serology: | what does HbeAg imply?

Answer 168

Results from breakdown of core Ag from infected liver cells | - therefore = marker of infectivity

Question 169

Histology in gastric cancer?

Answer 169

Signet ring cells - contain a large vacuole of mucin which displaces the nucleus to one side - higher numbers ass with a worse prognosis

Question 170

Associations with gastric cancer?

Answer 170

``` H pylori blood group A gastric adenomatous polyps pernicious anaemia smoking salty, spicy, nitrates in food may be negatively ass with duodenal ulcer ```

Question 171

Features of gastric cancer? Dx? Staging?

Answer 171

- dyspepsia, nausea & vomit, anorexia & weight loss, dysphagia Dx = OGD + biopsy Staging = CT CAP (or endoscopic US recently shown to be superior) Laparoscopy to identify occult peritoneal disease PET CT for junctional tumours

Question 172

Gastric cancer - there can be a stepwise progression through intestinal metaplasia -> atrophic gastritis & subsequent dysplasia -> cancer. Staging system = TNM What is the risk of LN involvement related to?

Answer 172

Size & depth of invasion | - early cancers confined to submucosa have a 20% incidence of LN metastasis

Question 173

How are tumours of the gastro-oesophageal junction classified?

Answer 173

Type 1 = true oesophageal cancers, may be ass with Barretts Type 2 = Carcinoma of the cardia (incidence rising), from cardiac-type epithelium or short segments with intestinal metaplasia at the oesophagogastric junction Type 3 = sub-cardial cancers that spread across the junction, involving similar nodal stations to gastric cancer

Question 174

Surgical Rx in gastric cancer: - proximal disease >5-10cm from OG junction? - <5cm from OG junction? - type 2 junctional tumours extending into oesophagus? What may play a role in early gastric cancer confined to the mucosa and perhaps submucosa? What else?

Answer 174

Subtotal gastrectomy Total gastrectomy Oesophagogastrectomy Endoscopic submucosal resection Lymphadenectomy should be performed e.g. D2 nodal dissection Most pts will receive chemo either pre/post-op

Question 175

Coeliac disease is strongly ass with which HLAs?

Answer 175

HLA-DQ2 95% | HLA-DQ8 80%

Question 176

Which conditions should be screened for coeliac disease? | Which signs & Sx?

Answer 176

- autoimmune thyroid - dermatitis herpetiformis - IBS - T1DM - 1st degree relatives with coeliac - chronic/intermittent diarrhoea - failure to thrive or faltering growth in children - persistent/unexplained GI Sx inc nausea & vomiting - prolonged fatigue/TATT - rec abdo pain, cramping or distension - sudden/unexpected weight loss - unexplained iron-deficiency anaemia or other unspecified anaemia

Question 177

Consequences/complications of coeliac disease?

Answer 177

- Enteropathy-ass T cell lymphoma of small bowel - Hyposplenism - anaemia:, iron, folate>B12 - osteoporosis osteomalacia, lactose intolerance - subfertility, unfavourable pregnancy outcomes - rarely oesophageal cancer, other malignancies

Question 178

5 causes of hepatosplenomegaly?

Answer 178

- chronic liver disease with portal hypertension (before liver becomes small) - infections: EBV, malaria, hepatitis - lymphoproliferative disorders - myeloproliferative disorders e.g. CML - amyloidosis

Question 179

What sort of bacteria is H pylori? Rx? What are the associations?

Answer 179

Gram negative 7 days of: - PPI + Amoxicillin/Metronidazole + Clarithromycin or - peptic ulcer disease 95% duodenal, 75% gastric - gastric cancer - B cell lymphoma of MALT tissue (eradication of h pylori causes regression in 80%) - atrophic gastritis

Question 180

What part of small bowel do all gastric bypass operations bypass? What is it the 1ry site of absorption for?

Answer 180

Duodenum | Iron & Calcium

Question 181

Commonest complication of ERCP?

Answer 181

Acute pancreatitis - irritation of the pancreatic duct ny the Xray constrast material/cannula

Question 182

1st line pharm Rx for IBS?

Answer 182

pain - antispasmodic agents constipation - laxatives (but avoid lactulose) diarrhoea - loperamide 1st line

Question 183

For IBS patients with constipation who are not responding to conventional laxatives, when can LINACLOTIDE be considered?

Answer 183

- if optimal.maximal tolerated doses of pre laxatives from different classes haven't helped - & they've had constipation for at least 12months

Question 184

2nd line pharm Rx for IBS?

Answer 184

- low-dose tricyclic antidepressants e.g. amitriptyline 5-10mg used in preference to SSRIs

Question 185

Non-pharm options for IBS?

Answer 185

Psych - consider referral for CBT, hypnotherapy or psych therapy if Sx don't respond to pharm Rx after 12months and who develop a continuing Sx profile i.e. refractory IBS

Question 186

Intrahepatic cholestasis of pregnancy - when is it seen? Features ? Complications? Rx?

Answer 186

3rd trimester, in 1% - itch often palms & soles, raised bilirubin, no rash Rx: ursodeoxycholic acid for Sx relief, weekly LFTs, women typically induced at 37wks - inc rate of stillbirth but not gen ass with inc maternal morbidity

Question 187

Acute fatty liver of pregnancy - when does it occur? Features? Ix? Rx?

Answer 187

- rare, 3rd trimester or immediately after delivery - abdo pain, nausea & vomit, headache, jaundice, hypoglycaemia, severe disease may result in pre-eclampsia - ALT usually >500 - supportive - definitive Rx = delivery once stable

Question 188

What is HELLP syndrome?

Answer 188

haemolysis elevated liver enzymes low platelets in pregnancy

Question 189

What is small bowel bacterial overgrowth syndrome? RFs? Features? Dx?

Answer 189

SBBOS = disorder characterised by XS amounts of bacteria in small bowel leading to GI Sx - neonates with congenital GI abnormalities - scleroderma - diabetes mellitus - chronic diarrhoea, bloating, flatulence, abdo pain (IBS overlap) Dx = hydrogen breath test

Question 190

How can malabsorption be broadly divided?

Answer 190

- Diarrhoea, steatorrhoea, weight loss Intestinal e.g. villpus atrophy Pancreatic eg enzyme deficiency of production/secretion Biliary ege bile salts

Question 191

Intestinal causes of malabsorption?

Answer 191

coeliac disease, Crohn's, tropical sprue, Whipple's, Giardia, brush border enzyme deficiency e.g. lactase

Question 192

Pancreatic causes of malabsorption?

Answer 192

chronic pancreatitis, CF, pancreatic cancer

Question 193

Biliary causes of malabsorption?

Answer 193

biliary obstruction, PBC

Question 194

Causes of malabsorption that aren't pancreatic/biliary/intestinal?

Answer 194

- bacterial overgrowth ege systemic sclerosis, diverticulae, blind loop - short bowel syndrome - lymphoma

Question 195

What is now the most common type of oesophageal cancer and is more likely to develop in patients with a history of gastro-oesophageal reflux disease (GORD) or Barrett's

Answer 195

Adenocarcinoma

Question 196

Where are the majority of tumours? | What are RFs for oesophageal cancer?

Answer 196

- middle 1/3 of oesophagus - smoking, etoh - GORD, Barrett's - achalasia - Plummer-Vinson syndrome - squamous cell carcinoma linked to diet rich in nitrosamines - rarely coeliac disease, scleroderma

Question 197

Features of oesophageal cancer?

Answer 197

Dysphagia commonest presenting Sx Anorexia, weight loss, vomiting Others inc: odynophagia, hoarseness, malaena, cough

Question 198

Dx of oesophageal cancer?

Answer 198

OGD 1st line (Contrast swallow may help classify benign motility disorders) CT CAP for staging If CT doesn't show metastatic disease, local stage may be more accurately assessed by use of endoscopic US Staging laparoscopy to detect occult peritoneal disease - PET CT if this is negative

Question 199

Rx of oesophageal cancer? What is the biggest surgical challenge?

Answer 199

- Surgical resection if operable +/- Adjuvant chemo Ivor-Lewis type oesophagectomy is the most standard: mobilisation of stomach & division of oesophageal hiatus - right-sided thoracotomy, stomach brought into chest, oesophagus mobilised further - intrathoracic oesophagogastric anastomosis constructed Alternative surgical strategies inc: transhiatal resection for distal lesions, left thoraco-abdominal resection (difficult access due to thoracic aorta), total oesophagectomy (McKeown) with a cervical oesophagogastric anastomosis Anastomotic leak, with an intrathoracic anastomosis this will result in mediastinitis with high mortality - McKeown technique has an intrinsically lower systemic insult in the event of anastomotic leakage

Question 200

Extra-Intestinal features of IBD related to disease activity?

Answer 200

Arthritis commonest: pauciarticular, asymmetric Episcleritis (commoner in CD) Erythema nudism Osteoporosis

Question 201

Extra-Intestinal features of IBD not related to disease activity?

Answer 201

``` Arthritis: polyarticular, symmetric Uveitis (commoner in UC) Pyoderma gangrenosum Clubbing PSC (much commoner in UC) ```

Question 202

Pathology of Crohn's disease? | Ix?

Answer 202

Strong genetic susceptibility - inflammation in all layers down to series - which is why they're prone to strictures, fistulas & adhesions - commonly affects terminal ileum & colon but can occur anywhere from mouth to anus - raised inflammatory markers (CRP correlates with disease activity) - anaemia - low vit B12 & vitamin D - increased faecal calprotectin

Question 203

Features of Crohn's disease?

Answer 203

- non-specific e.g. weight loss, lethargy - diarrhoea most prominent in adults, may cause bloody diarrhoea - abdo pain most prominent Sx in children - perianal disease e.g. skin tags, ulcers - extra intestinal features more common in pts with colitis or perianal disease

Question 204

Dx of spontaneous bacterial peritonitis? Rx? Prophylaxis should be given to which pts with ascites? What Abx is given as prophylaxis?

Answer 204

Paracentesis: neutrophil count ?250 IV Cefotaxime - who've had an episode of SBP - fluid protein <15 + hepatorenal syndrome or Child-Pugh score 9+ Ciprofloxacin/Norfloxacin

Question 205

Ix of choice for Crohn's disease? | What is seen?

Answer 205

Colonoscopy - deep ulcers - skip lesions - leading to cobblestone appearance

Question 206

Histology in Crohn's disease?

Answer 206

- goblet cells - granulomas - inflammation in all layers from mucosa to serosa

Question 207

What is seen on small bowel enema in Crohn's disease?

Answer 207

- high sens & spec for examination of terminal ileum - strictures: Kantors string sign - proximal bowel dilation - rose thorn ulcers - fistulae

Question 208

What is an anal fissure? Features? RFs?

Answer 208

Longitudinal/elliptical tears of the squamous lining of the distal anal canal <6wks = acute >6wks = chronic 90% occur on the posterior midline - painful bright red rectal bleeding - constipation - IBD - STIs eg HIV, syphilis, herpes

Question 209

Rx of acute anal fissure <6wks ?

Answer 209

- diet advice - bulk-forming laxative 1st line, laxative if not tolerated - lubricants eg petroleum jelly can be tried before defecation - topical anaesthetics (topical steroids don't provide significant relief)

Question 210

Rx of chronic anal fissure >6wks?

Answer 210

cont acute Rx topical GTN 1st line if not effective after 8wks then consider 2ry referral for surgery/botulinum toxin

Question 211

Acute Rx of variceal haemorrhage?

Answer 211

- ABC, resuscitation, correct clotting with FFP, vitamin K - Vasoactive agent = TERLIPRESSIN, Octreotide - Abx prophylaxis - Quinolone - OGD: endoscopic variceal band ligation (superior to sclerotherapy) - Sengstaken-Blakemore tube if uncontrolled haemorrhage - TIPS: transjugular intrahepatic portosystemic shunt if above measures fail

Question 212

Prophylaxis of vatical haemorrhage?

Answer 212

Propranolol - reduces rebleeding & mortality vs placebo | endoscopic variceal band ligation at 2wkly intervals until all varies eradicated with PPI cover

Question 213

What are the features of Child-Pugh classification used to classify severity of cirrhosis?

Answer 213

``` Bilirubin Albumin Prolonged PT Encephalopathy Ascites Score of 5-15 Severity graded as: <7 = A 7-9 = B >9 = C ```

Question 214

What is MELD scoring?

Answer 214

Model for End-Stage Liver Disease - Formula that uses combo of bilirubin, creatinine & INR to predict survival 3month mortality based on the score

Question 215

What do you give to babies born to mothers who are chronically infected with hepatitis B or to mothers who've had acute hepatitis B during pregnancy? Breastfeeding?

Answer 215

Complete course of vaccination + hepatitis immunoglobulin | - HBV not transmitted via breastfeeding

Question 216

DDx of hyperamylasaemia?

Answer 216

``` acute pancreatitis pancreatic pseudocyst mesenteric infarct perforated viscus acute cholecystitis DKA ```

Question 217

What are features that may predict a severe attack of acute pancreatitis within 48h of admission to hospital, on initial assessment?

Answer 217

clinical impression of severity BMI >30 pleural effusion APACHE score>8

Question 218

What are features that may predict a severe attack of acute pancreatitis within 48h of admission to hospital, 24h after admission?

Answer 218

``` clinical impression APACHE II>8 Glasgow score 3+ persisting multiple organ failure CRP>150 ```

Question 219

What are features that may be evident of a severe attack of acute pancreatitis 48h after admission?

Answer 219

Glasgow score >3 CRP>150 Persisting or progressive organ failure

Question 220

Modified Glasgow score for acute pancreatitis?

Answer 220

``` PaO2 low Age >55 Neutrophilia Calcium low Renal urea high Enzymes LDH high Albumin low Sugar high ```

Question 221

How to assess severity of acute pancreatitis?

Answer 221

Glasgow, Ranson scoring systems & APACHE II | Biochemical i.e. CRP

Question 222

Rx of acute pancreatitis?

Answer 222

IV fluids, analgesia Nutrition: enteral feeding may help prevent bacterial translocation from gut, thereby contributing to development of infected pancreatic necrosis Surgery: - early cholecystectomy if due to gallstones - early ERCP if stones obstructing biliary system - debridement/fine needle aspiration may help in pts who fail to settle with necrosis & worsening organ dysfunction - radiological drainage/surgical necrosectomy in pts with infected necrosis

Question 223

What is Peutz-Jeghers syndrome? | What is the genetics?

Answer 223

Autosomal dominant condition of numerous hamartomatous polyps in GI tract - ass with pigmented freckles on lips, face, palms, soles - 50% die from GI tract cancer by age 60 - autosomal dominant - responsible gene encodes serine threonine kinase LKB1 or STK11

Question 224

Features of Peutz-Jeghers syndrome?

Answer 224

- hamartomatous polyps in GI tract mainly small bowel - pigmented lesions on lips, oral mucosa, face, palms, soles - intestinal obstruction eg intussusception - GI bleeding - e.g. features of GI cancer Rx is conservative unless complications develop

Question 225

Acanthosis nigricans is ass with which malignancy?

Answer 225

gastric cancer

Question 226

Acquired ichthyosis is ass with which malignancy?

Answer 226

lymphoma

Question 227

Acquired hypertrichosifs lanuginosa is ass with which malignancy?

Answer 227

GI & lung cancer

Question 228

Dermatomyositis is ass with which malignancy?

Answer 228

ovarian & lung cancer

Question 229

Erythema gyratum repens is ass with which malignancy?

Answer 229

lung cancer, breast

Question 230

Erythroderma is ass with which malignancy?

Answer 230

lymphoma

Question 231

Migratory thrombophlebitis is ass with which malignancy?

Answer 231

pancreatic cancer

Question 232

Necrolytic migratory erythema is ass with which malignancy?

Answer 232

glucagonoma

Question 233

Pyoderma gangrenous (bullous & non-bullous) is ass with which malignancy?

Answer 233

myeloproliferative disorders

Question 234

Sweet's syndrome (tender purple plaques) is ass with which malignancy?

Answer 234

haematological malignancy eg myelodysplasia

Question 235

Tylosis is ass with which malignancy?

Answer 235

oesophageal cancer

Question 236

What are villous adenomas? | Possible features?

Answer 236

colonic polyps with the potential for malignant transformation - characteristically secrete large amounts of mucous, potentially resulting in electrolyte disturbances Majority are aSx, otherwise - non-specific lower GI Sx - secretory diarrhoea may occur - microcytic anaemia - hypokalaemia

Question 237

Presenting features of haemochromatosis?

Answer 237

- early Sx inc fatigue, ED, arthralgia often of hands - bronze skin pigmentation - liver stigmata of chronic disease, hepatiomegaly, cirrhosis, hepatocellular deposition - cardiac failure 2ry to dilated cardiomyopathy - hypogonadism 2ry to cirrhosis & pituitary dysfunction - hypogonadotrophic hypogonadism - arthritis esp hands

Question 238

Which complications of haemochromatosis are reversible?

Answer 238

- cardiomyopathy - skin pigmentation - elevated LFTs & hepatomegaly may be

Question 239

Which complications of haemochromatosis are irreversible?

Answer 239

- cirrhosis - diabetes mellitus - hypogonadotrophic hypogonadism - arthropathy

Question 240

Clinical features of Crohns disease?

Answer 240

Diarrhoea usually non-bloody Weight loss more prominent than in UC Upper GI Sx, mouth ulcers, perianal disease Abdo mass in RIF

Question 241

Clinical features of UC?

Answer 241

Bloody diarrhoea more common LIF abdo pain Tenesmus

Question 242

Why do Crohn's disease pts get gallstones?

Answer 242

2ry to reduced bile acid reabsorption | - they are also more likely to get oxalate renal stones

Question 243

Histology in UC?

Answer 243

- neutrophils migrate through walls of glands to form crypt abscesses - goblet cell & mucin depletion from gland epithelium - granulomas infrequent - no inflammation beyond submucosa - inflammatory cell infiltrate in lamina propria

Question 244

What is seen on colonoscopy in UC?

Answer 244

- widespread ulceration with preservation of adjacent mucosa, which has the appearance of polyps - pseudo polyps - continuous disease

Question 245

What is seen on barium enema in UC?

Answer 245

- loss of haustrations - superficial ulceration, pseudopolyps - longstanding disease: colon is narrow & short - drainpipe colon

Question 246

What is acute liver failure? What are the causes? Features?

Answer 246

Rapid onset of hepatocellular dysfunction leading to a variety of systemic complications - paracetamol OD, etoh, viral hepatitis usuall A/B, acute fatty liver of pregnancy - jaundice - coagulopathy: raised PT - hypoalbuminaemia - hepatic encephalopathy - renal failure common

Question 247

What is the main pathological process seen in the hepatocytes of patients with fulminant hepatitis e.g. massive paracetamol OD?

Answer 247

NECROSIS - affects entire acinus (panacinar necrosis) (apoptosis in mild cases of viral hepatitis)

Question 248

When should acetylcysteine be given in a paracetamol OD? | How is it infused?

Answer 248

- if staggered OD or doubt over time of ingestion, regardless of paracetamol concentration - if plasma conc on or above a single treatment line joining points of 100 at 4h & 15 at a5h, regardless of RFs of hepatotoxicity Acetylcysteine over 1h (instead of 15mins) to reduce number of adverse effects

Question 249

What are the King's College Hospital criteria for liver Tx (paracetamol liver failure)?

Answer 249

``` Arterial pH <7.3, 24h after ingestion or all of the following: 1. PT >100 2. creatinine >300 3. grave III/IV encephalopathy ```

Question 250

Features of acute pancreatitis?

Answer 250

- severe epigastric pain that may radiate through to the back - vomiting common - examination may reveal tenderness, ileum, & low-grade fever - periumbilical discolouration (Cullens). & flank discolouration (Grey-Turner's sign) rare - ischaemic retinopathy (Purtscher) rare - may cause temporary/permanent blindness

Question 251

What are the 2 common treatment for alcoholic hepatitis? Which is superior?

Answer 251

PREDNISOLONE is better than Pentoxyphylline, which was shown not to improve outcomes/survival at 28days

Question 252

What is alcoholic ketoacidosis? How does it typically present? What is most appropriate Rx?

Answer 252

- non-diabetic euglycaemic form of ketoacidosis, occurs in people who regularly drink large amounts of etoh - episodes of starvation -> malnourished -> etoh binge -> ketosis -> ketoacidosis - metabolic acidosis - raised anion gap - elevated serum ketone levels - normal/low glucose conc IV saline & thiamine

Question 253

``` What is ascending cholangitis? What is the commonest predisposing factor? Charcot's triad? Other features? Rx? ```

Answer 253

``` Bacterial infection of the biliary tree Gallstones 1. RUQ pain 70% 2. fever 90% 3. jaundice 60% - hypotension, confusion ``` - IV Abx - ERCP after 24-48h to relieve any obstruction

Question 254

What is the gold standard investigation of bacterial overgrowth? Other possible Ix?

Answer 254

Small bowel aspiration & culture - hydrogen breath test - 14C-xylose breath test - 14C-glycocholate breath test (low specificity) - in practice many give an empirical course of Abx as a trial

Question 255

How to Ix pernicious anaemia?

Answer 255

- anti gastric parietal cell Abs 90% sens - anti intrinsic factor Ab in 50% ***but specific - macrocytic anaemia - low WCC & plts - LDH may be raised due to ineffective erythropoiesis - low B12, hyperhsegmented polymorphs on film, megaloblasts in marrow - Schilling test

Question 256

What is the Schilling test (pernicious anaemia)?

Answer 256

- radiolabelled B12 given 2x - 1st on its own - 2nd with oral intrinsic factor - urine B12 levels measured

Question 257

Pathophysiology of hepatorenal syndrome?

Answer 257

- vasoactive mediators cause splanchnic vasodilation, which reduces systemic vascular resistance -> underfilling of the kidneys -> senses by juxtaglomerular apparatus -> activates RAAS -> renal vasoconstriction -> not enough to counterbalance the effects of the splanchnic vasodilation

Question 258

Type 1 hepatorenal syndrome?

Answer 258

- rapidly progressive - doubling of serum Cr >221 or halving of CrCl to <20 over a period of <2wks - v poor prognosis

Question 259

Type 2 hepatorenal syndrome?

Answer 259

- slowly progressive | - poor prognosis, but pts may live for longer than type 1

Question 260

Rx options for hepatorenal syndrome?

Answer 260

- Vasopressin analogues (e.g. Terlipressin) - cause vasoconstriction of splanchnic circulation - volume expansion with 20% albumin - TIPS

Question 261

necrolytic migratory erythema is ass with which cancer?

Answer 261

glucagonoma

Question 262

What is carcinoid syndrome?

Answer 262

- usually occurs when metastases are present in the liver & release SEROTONIN into the systemic circulation - may also occur with lung carcinoid as mediators aren't 'cleared' by the liver

Question 263

Features of carcinoid syndrome: - what is often the earliest Sx? - others?

Answer 263

* Flushing is often the earliest Sx - diarrhoea - bronchospasm - hypotension - right heart valvular stenosis (left heart can be affected in bronchial carcinoid) - other molecules e.g. ACTH & GHRH may also be secreted leading to e.g. Cushing's - pellagra can rarely develop s dietary tryptophan is diverted to serotonin by the tumour

Question 264

Ix of carcinoid syndrome?

Answer 264

- urinary 5-HIAA | - plasma chromogranin A y

Question 265

Rx of carcinoid syndrome?

Answer 265

- somatostatin analogues e.g. OCTREOTIDE | - diarrhoea: cyproheptadine may help

Question 266

What is Barrett's oesophagus? What is short & long? Histological features?

Answer 266

Metaplasia of the lower oesophageal mucosa from squamous epithelium -> COLUMNAR epithelium - increased risk oesophageal Adenocarcinoma 50-100X - short <3cm - long >3cm - length of affected segment correlates strongly with chances of identifying metaplasia - columnar epithelium may resemble that of either the cardiac region of stomach, or small bowel e.g. with goblet cells, brush border

Question 267

RFs for Barretts?

Answer 267

- GORD is strongest RF - male 7:1 - smoking - central obesity

Question 268

Rx of Barrett's? | If dysplasia is identified?

Answer 268

- endoscopic surveillance with biopsies: every 3-5yrs for those with Metaplasia - high-dose PPI (limited evidence base for if this reduces the change of progression to dysplasia or induces regression) - if dysplasia of any grade is identified, endoscopic intervention is offered e.g.: - endoscopic mucosal resection - radiofrequency ablation

Question 269

Features of cholangiocarcinoma?

Answer 269

- persistent biliary colic Sx - ass with anorexia, jaundice, weight loss - palpable mass in RUQ (Courvoisiers sign) - periumbilical lymhadenopathy & left supraclavicular adenopathy may be seen

Question 270

Commonest organisms found in pyogenic liver abscesses?

Answer 270

staph aureus - children | E coli - adults

Question 271

Rx of pyogenic liver abscess?

Answer 271

- amoxicillin + ciprofloxacin + metronidazole | - if pen allergic: clindamycin + ciprofloxacin

Question 272

What happens to clotting factors in liver failure?

Answer 272

All clotting factors low except for factor VIII which is paradoxically supra-normal

Question 273

Why is factor VIII paradoxically supra-normal in liver failure? What else predisposes chronic liver disease pts to thrombosis formation?

Answer 273

- synthesised in endothelial cells throughout the body (the rest are purely made in hepatic endothelial cells) - activated factor VIII is usually rapidly cleared from bloodstream but this requires good hepatic function, so it leads to increases in circulating factor VIII - therefore pts with chronic liver disease aren't protected from venous thrombosis formation and are at an increased risk (in addition to increased bleeding risk with conventional coag studies) - reduced synthesis of protein c & s & anti-thrombin

Question 274

What is chronic pancreatitis? What is the cause 80% of the time? Features?

Answer 274

- inflammatory condition which ultimately affects both exocrine & endocrine functions of pancreas - etoh xs 80% - pain typically worse 15-30mins after a meal - steatorrhoea: 5-25yrs after onset of pain the Sx of pancreatic insufficiency develop - diabetes mellitus develops in majority, usually >20yrs after Sx begin

Question 275

``` Ix in chronic pancreatitis: AXR? CT? functional test? Rx? ```

Answer 275

AXR: pancreatic calcification 30% CT more sensitive for pancreatic calcification, send 80% spec 85% - faecal elastase may be used assess exocrine function if imaging inconclusive - pancreatic enzyme supplements, analgesia, antioxidants (limited evidence)

Question 276

Commonest organism found on ascitic fluid culture in SBP?

Answer 276

E coli

Question 277

Clinical features of PBC?

Answer 277

Early: may be aSx with just raised ALP, or fatigue, pruritus - cholestatic jaundice - hyperpigmentation, esp over pressure points - 10% have RUQ pain - xanthelasmas, xanthomata - clubbing, hepatosplenomegaly - late: may progress to liver failure

Question 278

Complications of PBC?

Answer 278

- malabsorption: osteomalacia, coagulopathy - sicca syndrome occurs in 70% - portal hypertension: ascites, variceal haemorrhage - hepatocellular cancer 20X increased risk

Question 279

Causes of jejunal villous atrophy?

Answer 279

``` coeliac disease tropical sprue hypogammaglobulinaemia GI lymphoma Whiles disease cows milk intolerance ```

Question 280

What drug has a well established association with severe sprue-like enteropathy with duodenal villous atrophy?

Answer 280

Olmesartan = A2RB - can develop months-years after the medication is started Also azathioprine, mycophenolate mofetil

Question 281

What is a pharyngeal pouch?

Answer 281

Posteromedial diverticulum through Killian's dehiscence (which is a triangle area in the wall of the pharynx between the thyropharyngeus & cricopharynxgeus muscles) - more common i older pts, 5X more in med

Question 282

Features of pharyngeal pouch? | Imaging?

Answer 282

- dysphagia - regurgitation - aspiration - neck swelling which gurgles on palpatin - halitosis Barium swallow with fluoroscopy

Question 283

Why is gallstone RUQ pain worse after a fatty meal?

Answer 283

When cholecystokinin levels are highest and gallbladder contraction is maximal

Question 284

Risks of ERCP?

Answer 284

Pancreatitis 1.5% Cholangitis 1.1% Bleeding 0.9% (rises to 1.5% if sphincterotomy performed) Duodenal perforation 0.4%

Question 285

Renal Tx: what are technical complications usually related to?

Answer 285

the ureteric anastomosis

Question 286

Renal Tx: what is the graft survival directly related to?

Answer 286

warm ischaemic time - longer warm ischaemic times increase the risk of acute tubular necrosis, which may occur in all types of renal Tx, and will usually recover provided other insults are minimised

Question 287

Technical renal Tx complication: sudden complete loss of urine output Dx? Rx?

Answer 287

Renal artery thrombosis | - immediate surgery may salvage the graft, delayed beyond 30mins are ass with a high rate of graft loss

Question 288

Technical renal Tx complication: uncontrolled hypertension, allograft dysfunction & oedema Dx? Rx?

Answer 288

Renal artery stenosis | - angioplasty

Question 289

Technical renal Tx complication: pain & swelling over the graft site, haematuria & oliguria Dx? Rx?

Answer 289

Renal vein thrombosis | - graft is usually lost

Question 290

Technical renal Tx complication: diminished urine output, rising creatinine, fever & abdo pain Dx? Rx?

Answer 290

Urine leaks | - USS shows perigraft collection, necrosis of ureter tip is commonest cause & the anastomosis may need revision

Question 291

Technical renal Tx complication: common complication in 15% that may present as a mass, if large may compress the ureter Dx? Rx?

Answer 291

Lymphocele | - may be drained with percutaneous technique & sclerotherapy, or intraperitoneal drainage

Question 292

3 main types or organ rejection (immunological reaction) after kidney Tx?

Answer 292

Hyperacute Acute Chronic

Question 293

Hyperacute Tx organ rejection: - when does it occur? - what are the RFs? - when do the macroscopic features manifest? - Rx?

Answer 293

- immediately through presence of pre-formed Ab - major HLA mismatch & ABO incompatibility; renal Tx are particularly susceptible - after completion of the vascular anastomosis & removal of clamps - kidney becomes mottled, dusky & vessels will thromboses - only Rx is graft removal - left in situ will result in abscess formation

Question 294

Acute Tx organ rejection: - when does it occur? - why does it usually occur?

Answer 294

- during first 6months, all organs are susceptible - usually T cell mediated, mononuclear cell infiltrates predominate, or vascular lesions - mostly managed medically

Question 295

Chronic Tx organ rejection: - when does it occur? - why does it usually happen? - RFs? - what organ specific changes may be seen?

Answer 295

- after the first months - Vascular lesions predominate with myointimal proliferation leading to organ ischaemia - all Tx with HLA mismatch are at risk, previous acute rejections and other immunosensitising events increase the risk - eg loss of acinar cells in pancreas Tx, & rapidly progressive coronary artery disease in cardiac Tx

Question 296

Opportunistic infection between 1-6months after Tx with clinical features of: fever, deranged transaminases, leukopenia & thrombocytopenia? Dx? Rx?

Answer 296

CMV infection - PCR Dx - Rx with GANCICLOVIR

Question 297

What is malnutrition?

Answer 297

BMI<18.5 Unintentional weight loss >10% within last 3-6months BMI <20 + unintentional weight loss >5% within last 3-6months

Question 298

How is malnutrition screened for? | when should it be done?

Answer 298

MUST: malnutrition universal screen tool is a 5step process to identify those malnourished/at risk/obese - on admission to care/nursing homes/hospital or if there is a concern - takes into account BMI, recent weight change & presence of acute disease - categorises into low, medium & high risk

Question 299

Gen management of malnutrition?

Answer 299

- dietician support if high risk - food-first approach with clear instructions rather than just prescribing oral NS/Ensure - if they are used they should be taken between meals instead of

Question 300

Which pts are at risk of malnutrition?

Answer 300

- eating nothing/little for >5days, who are likely to eat little for a further 5days - poor absorptive capacity - high nutrient losses - high metabolism

Question 301

When to consider pre-op enteral feeding in surgical pts due to have major abdo surgery?

Answer 301

- if malnourished, unsafe swallow/inadequate oral intake & functional GI tract

Question 302

Enteral feeding - when to comment duodenal/jejunal tube feed instead of gastric feed?

Answer 302

If there is upper GI dysfunction

Question 303

When to consider long-term gastrostomy?

Answer 303

If gastric feeding >4wks

Question 304

How should ITU pts have enteral feeding?

Answer 304

Continuous feeding for 16-24h (24h if on insulin)

Question 305

When can PEG tube be used after insertion?

Answer 305

4hours after insertion | - don't remove until >2wks after insertion

Question 306

Dyspepsia urgent referral for 2WW OGD guidelines?

Answer 306

- all with dysphagia - all with upper abdo mass - >55yrs with weight loss + upper abdo pain/reflux/dyspepsia

Question 307

Dyspepsia non-urgent referral for OGD guidelines?

Answer 307

- all with haematemesis >55yrs with: - Rx-resistant dyspepsia or - upper abdo pain with anaemia or - high platelets with nausea/vomit/weight loss/reflux/dyspepsia/upper abdo pain - nausea/vomit + weight loss/reflux/dyspepsia/upper abdo pain

Question 308

Dyspepsia: Managing patients who do not meet referral criteria ('undiagnosed dyspepsia')?

Answer 308

1. review meds for possible causes 2. lifestyle advice 3. trial full-dose PPI for 1month Or a test & treat approach for H pylori

Question 309

What should be tested before adding azathioprine/mercaptopurine therapy in Crohn's?

Answer 309

TPMT activity - some have a deficiency (involved in metabolism) therefore at higher risk of severe side effects from normal doses - if v low/absent, do not start - if below normal but not deficient, ca be started at a lower dose

Question 310

What is Plummer-Vinson syndrome? | Rx?

Answer 310

1. dysphagia 2ry to oesophageal webs 2. glossitis 3. iron-deficiency anaemia Rx with iron supplementation & webs dilatation

Question 311

What is Mallory-Weiss syndrome?

Answer 311

Severe vomiting -> painful mucosal lacerations at the GO junction -> haematemesis - common in alcoholics

Question 312

What is Boerhaave syndrome?

Answer 312

Severe vomiting -> oesophageal rupture

Question 313

Rx of Small bowel bacterial overgrowth syndrome?

Answer 313

- Correct underlying disorder - Abx: Rifaximin (low resistance) - Co-amoxiclav/Metronidazole may be effective in majority

Question 314

What is WHipple's disease?

Answer 314

Rare multisystem disorder caused by Tropheryma whipped infection - more common in HLA-B27+ & middle-aged men

Question 315

Features of Whipple's disease?

Answer 315

- malabsorption: diarrhoea & weight loss - large-joint arthralgia - lymphadenopathy - skin: hyperpigmentation & photosensitivity - pleurisy, pericarditis - neuro sx are rare but inc ophthalmoplegia, dementia, seizures, ataxia, myoclonus

Question 316

Ix of Whipple's disease?

Answer 316

Jejunal biopsy shows deposition of macrophages containing PAS: periodic acid-Schiff granules

Question 317

Rx of Whipples disease?

Answer 317

E.g. Oral Co-Trimoxazole for a year may have lowest relapse rate, sometimes preceded by a course of IV penicillin, but guidelines vary

Question 318

What is post-cholecystectomy syndrome?

Answer 318

- dyspepsia, vomiting, pain, flatulence, diarrhoea in upto40% posr-op - some ass with remnant stones & biliary injury - pain often due to sphincter of Oddi dysfunction, & development of surgical adhesions - Rx difficult, involves low fat diet & bile acid sequestrants e.g. cholestyramine, to bind XS bile acids, preventing lower GI signs - PPI can help if dyspeptic-like Sx

Question 319

What is a Dieulafoy lesion?

Answer 319

Gastric bleeding - AV malformation - often no prodrome before haematemesis & malaena

Question 320

What type of virus is hepatitis D? | Transmission?

Answer 320

Single-stranded RNA virus - incomplete RNA virus that requires hepatitis B sAg to complete its replication & transmission cycle - transmitted parenterally, similar to HBV, pts may be infected with both at the same time

Question 321

What is hepatitis D co-infection?

Answer 321

hepatitis B & D infection at the same time

Question 322

What is hepatitis D super-infection? | What is it ass with?

Answer 322

hepatitis B sAg positive pt subsequently develops a hepatitis D infection - ass with high risk of fulminant hepatitis, chronic hepatitis status & cirrhosis

Question 323

How to Dx hepatitis D? | Rx?

Answer 323

PCR of hepatitis D RNA | - Interferon currently used but poor evidence base

Question 324

Necrolytic migratory erythema is ass with which malignancy?

Answer 324

GLUCAGONOMA

Question 325

What is referring syndrome and what are the metabolic consequences?

Answer 325

Abnormalities which occur on feeding a person following a period of starvation - low phosphate (reactive hyperinsulinaemia) -> heart failure, skeletal muscle weakness - low potassium - low magnesium - abnormal fluid balance - above can lead to organ failure

Question 326

When are pts considered at high risk of referring syndrome?

Answer 326

1+ of: - BMI<16 - unintentional weight loss >15% over 3-6months - little nutritional intake >10days - low potassium/phosphate/magnesium prior to feeding Or 2+ of: - BMI <18.5 - unintentional weight loss >10% over 3-6monts - little nutritional intake >5days - Hx of e.g. etoh abuse, drug Rx inc insulin, chemo, diuretics & antacids

Question 327

How to re-feed if a pt hasn't eaten for >5days?

Answer 327

no more than 50% of requirements for the first 2 days

Question 328

What do bags of TPN usually contain? What is the risk of peripheral infusion? complications of TPN?

Answer 328

- Combo of glucose, lips & essential electrolytes - exact composition determined by pts nutritional requirements - thrombophlebitis - longer term should be via central e.g. PICC - sepsis, re-feeding syndromes, hepatic dysfunction

Question 329

What is a recently developed mAb fragment that binds both free & thrombin-bound Dabigatran with a v high affinity to rapidly neutralise activity? And therefore Dabigatran is the only NOAC with a commercially available antidote atm

Answer 329

IDARUCIZUMAB (PRAXBIND) | - nb resuscitation is main Rx, and improves outcomes

Question 330

Commonest location of colorectal cancer?

Answer 330

``` Rectal 40% sigmoid 30% ascending colon & caecum 15% transverse colon 10% descending 5% ```

Question 331

bronze diabetes with hepatomegaly - what is the gene defect?

Answer 331

HFE = protein that regulates iron absorption -> complex at basolateral membrane -> if bound to transferrin + iron as the membrane of duodenal crypt cells, it prevents maturation & therefore absorption of iron in the bowel = when mutated -> failure of complex formation -> constant maturation of duodenal crypt cells -> unregulated uptake or iron (auto recessive hereditary haemochromatosis)

Question 332

Dysfunctional protein ass with Wilson's disease?

Answer 332

ATP7B

Question 333

Enzyme deficiency ass with Gilbert's disease?

Answer 333

glucuronyl transferase

Question 334

Liver biopsy Dx: XS collagen & extracellular matrix deposition in periportal & pericentral zones, leading to formation of regernative nodules?

Answer 334

CIRRHOSIS (XS etoh damages hepatocytes throung reactive oxygen species. Kupffer cells are activated, XS profibrotic cytokines produced, leading to XS fibrous tissue formation)

Question 335

Liver biopsy Dx: macrovesicular fatty change with giant mitochondria, spotty necrosis & fibrosis?

Answer 335

ETOH consumption i.e. ETOH Steatohepatitis - may reverse if person stops drinking (but doesn't indicate cirrhosis)

Question 336

Liver biopsy Dx: Triglyceride accumulation with proliferation of myofibroblasts?

Answer 336

NAFLD | - e.g. fatty diet, insulin resistance, dyslipidaemia

Question 337

Liver biopsy Dx: Mononuclear infiltration of liver lobules with hepatic necrosis & Kupffer cells hyperplasia?

Answer 337

VIRAL hepatitis infection e.g. hep A & E in acute hepatitis, B & C in chronic

Question 338

Liver biopsy Dx: Dense lymphoid infiltrates of hepatic portal tracts with chronic inflammation & hepatocyte necrosis?

Answer 338

Primary biliary cirrhosis | - usually affects small-medium sized bile ducts

Question 339

Charcots triad: RUQ pain, fever, jaundice. Dx?

Answer 339

ascending cholangitis

Question 340

What is most likely to increase the likelihood of a false negative serology test for coeliac disease?

Answer 340

Selective IgA deficiency - more common in pts with coeliac - therefore should check IgA levels - if they have it, should measure anti-TTG IgG instead

Question 341

Ix of choice to Dx primary sclerosing cholangitis?

Answer 341

ERCP: multiple biliary structures giving a 'beaded' appearance

Question 342

Diarrhoea + Sigmoidoscopy: multiple white plaques adhered to the gastrointestinal mucosa?

Answer 342

Pseudomembranous colitis - C diff

Question 343

Contra-indications to percutaneous liver biopsy?

Answer 343

- anaemia - low platelets <60 - deranged clotting e.g. INR >1.4 - extrahepatic biliary obstruction - ascites - hydatid cyst - haemangioma - uncooperative pt

Question 344

Classification of severity of UC?

Answer 344

Mild <4stools/day, only small amount of blood Moderate 4-6stools/day, varying amount of blood, no systemic upset Severe >6bloody stools + features of systemic upset: fever, tachycardia, anaemia, raised inflammatory markers

Question 345

Inducing remission in UC: | - for distal colitis what is 1st line & 2nd line?

Answer 345

Rectal Mesalazine is best | - others inc rectal steroids then oral aminosalicylates

Question 346

1st line inducing remission in UC (not distal disease)?

Answer 346

Oral Aminosalicylates

Question 347

2nd line inducing remission in UC (not distal disease) when failed to respond after 4wks?

Answer 347

Oral prednisolone

Question 348

Rx of severe colitis in UC?

Answer 348

IV steroids etc in hospital

Question 349

Maintaining remission in UC?

Answer 349

Oral aminosalicylates - can also then consider azathioprine & mercaptopurine - probiotics may help prevent relapse in pts with mild-mod disease

Question 350

What is Dubin-Johnson syndrome? What is in the urine? What is the defect?

Answer 350

benign autosomal recessive disorder in hyperbilirubinaemia - Conjugated, in the urine - defect in the canalicular multi specific organic anion transporter (cMOAT) protein - causes defective hepatic bilirubin excretion

Question 351

Common causes of hepatomegaly?

Answer 351

Cirrhosis - non-tender, firm liver - if early (later leads to smaller) Cancer - hard, irregular liver edge - metastatic spread or 1ry lymphoma CCF - firm, smooth, Tender liver edge - right heart failure, may be pulsatile

Question 352

Causes of hepatomegaly (except CCC)?

Answer 352

``` viral hepatitis, EBV malaria progenic, amoebic abscess hydatid disease haemaological malignancies haemochromatosis PBC sarcoid, amyloid ```

Question 353

VIP: vasoactive intestinal peptide what is the source? how is it stimulated? what are its actions?

Answer 353

- from small bowel & pancreas - neural stimulation 1. stimulates secretion by pancreas & intestines 2. inhibits acid & pepsinogen secretion

Question 354

VIPoma: where do most arise from? what Sx does it cause? what metabolic derangements?

Answer 354

- Pancreas 90% - dehydration, weight loss, large volume diarrhoea - hypokalaemia, hypochlorhydia

Question 355

What are the RFs for oesophageal ca - adenocarcinoma?

Answer 355

- etoh, smoking | - Barretts, GORD

Question 356

What are the RFs for oesophageal ca - squamous carcinoma?

Answer 356

- etoh , smoking - Achalasia - Plummer-vinson

Question 357

What is the probable aetiology of hepatic encephalopathy?

Answer 357

- XS absorption of ammonia & glutamine from bacterial breakdown of proteins in the gut - seen in acute & chronic liver failure - in cirrhosis, some pts develop features e.g. midlc cognitive impairment (minimal/covert) before the features become more recognisable

Question 358

Features of hepatic encephalopathy?

Answer 358

- confusion, altered GCS - asterix: liver flap, arrhythmic negative myoclonus with a frequency of 3-5Hz - consturctional apraxia: inability to draw a 5 pointed star - triphasic slow waves on EEG - raised ammonia level

Question 359

Precipitating factors of hepatic encephalopathy?

Answer 359

- infection eg SBP - GI bleed - constipation - post-TIPS - drugs: sedatives, diuretics - hypokalaemia - renal failure - increased dietary protein (uncommon)

Question 360

Rx of hepatic encephalopathy: general? 1st line? (other options?)

Answer 360

- treat any underlying precipitating cause - LACTULOSE: promotes excretion of ammonia & increases metabolism of ammonia by gut bacteria (embolisation of portosystemic shunts, liver Tx)

Question 361

2ry prophylaxis of hepatic encephalopathy?

Answer 361

RIFAXIMIN: modulates gut flora resulting in decreased ammonia production

Question 362

Abx most likely to cause pseudomembranous colitis?

Answer 362

clindamycin RR 31.8 3rd gen cephalosporins 14.9 ciprofloxacin 5.0

Question 363

2ry causes of hypertriglyceridaemia?

Answer 363

- high etch intake - T2DM - renal disease - pregnancy - bulimia nervosa - drugs: ciclosporin, oestrogens, corticosteroids

Question 364

Management of high triglycerides >20?

Answer 364

if not due to xs etoh or poor glycemic control then: | -> refer for urgent specialist review e.g. regional lipid clinic

Question 365

Management of high triglycerides 10-20?

Answer 365

- repeat with a feasting level - r/v for potential 2ry causes - address lifestyle factors - start high-potency statin e.g. atorvastatin, rosuvastatin, monitor LFTs & CK - can use vibrates but they lower triglycerides through increasing activity of lipoprotein lipase - other pharm options inc omega-3-acid ethyl esters & nicotinic acid

Question 366

What is the Ix of choice to detect liver cirrhosis?

Answer 366

Transient elastography = Fibroscan - measures stiffness of liver as proxy for fibrosis

Question 367

what is the main cause of hepatorenal syndrome?

Answer 367

splanchnic vasodilation

Question 368

How are pts with hepatocellular carcinoma managed?

Answer 368

Barcelona Classification for Liver Cancer Treatment System

Question 369

What drug has been shown to prolong survival in those with hepatocellular carcinoma with a Child-Pugh A/B cirrhosis, good performance status and evidence of vascular, lymphatic or extra hepatic spread?

Answer 369

Sorafenib = multiple tyrosine kinase inhibitor

Question 370

Rx if hepatocellular carcinoma with child-pugh A & B and 2-3tumours <3cm or 1 tumour<5cm without vascular invasion or extra hepatic spread ? What can you use as a bridge Rx beforehand?

Answer 370

Consider liver Tx | - RFA (radiofrequency ablation) or TACE (transarterial chemoembolisation)

Question 371

Rx if hepatocellular carcinoma with child-pugh A cirrhosis without signs of portal HTN with single lesions <2cm?

Answer 371

Surgical resection

Question 372

Rx if hepatocellular carcinoma with Child-Pugh C cirrhosis and end-stage liver disease?

Answer 372

Best supportive care - symptomatically, palliative care input etc - poor candidates for therapy as they lack any hepatic functional reserve to tolerate either resection, TACE or RFA