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Gastro 7.5 Flashcards

1
Q

Causes of upper GI bleed?

A
  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
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2
Q

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

A

Tachycardia

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3
Q

Pro kinetic before endoscopy for upper GI bleed

A

Stat dose IV erythromycin 250mg

  • 30-120m pre-OGD
  • to promote gastric emptying & improve endoscopic visualisation
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4
Q

IV high-dose PPI before OGD for upper GI bleed

A
  • 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
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5
Q

Pre-OGD for suspected variceal bleed?

A

IV terlipressin/octreotide (splanchnic vasoconstrictor)

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

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6
Q

In upper GI bleed, when to offer:

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

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

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7
Q

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

A

transcatheter arterial embolisation

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8
Q

OGD failure in variceal bleed - next step?

A

transjugular intrahepatic porto-systemic shunt within 72h

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9
Q

Options for testing H. pylori?

A

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

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10
Q

H. pylori Rx ass with peptic ulcers

A

PPI + clarithromycin + amoxicillin/metronidazole for 1/52

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

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11
Q

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

A
  • long-term PPI

- higher risk of re-bleed

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12
Q

What is Forrest classification of upper GI bleeding?

A

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
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13
Q

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

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

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

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14
Q

Long-term adverse effects of PPI

A

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

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15
Q

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

A

HLA-DQ2

HLA-DQ8

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16
Q

Conditions ass with coeliac disease?

A 
dermatitis herpetiformis
T1DM
autoimmune liver disease
autoimmune thyroid disease
Turner's, William's, Down's syndrome
selective IgA deficiency
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17
Q

Sites of common genetic mutations causing pancreatitis?

A
  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
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18
Q

Recommended Rx of infected pancreatic necrosis

A

endoscopic drainage

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19
Q

What is type 3c diabetes?

A
  • 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
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20
Q

Long-term follow-up of chronic pancreatitis

A
  • 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
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21
Q

Causes of acute pancreatitis?

A 
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
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22
Q

Dx & Features of C diff?

A

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
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23
Q

Rx of C diff?

A

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

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24
Q

What is the trimodal death distribution following trauma?

A
  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
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25
Q

Trauma management - what thoracic injuries to suspect?

A 
simple pneumothorax
mediastinal traversing wounds
tracheobronchial tree injury
haemothorax
blunt cardiac injury
diaphragmatic injury
aortic disruption
pulmonary contusion
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26
Q

Rx of simple pneumothorax in thoracic trauma?

A

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

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27
Q

Causes of acute pancreatitis?

A 
Gallstones
Etoh
Trauma
Steroids
Mumps, Coxsackie B
Autoimmune e.g. PAN, Ascaris infection
Scorpion venom
Hypertriglyceridaemia, Hyperchylomicronaemia (e.g. hereditary lipoprotein lipase deificiency &amp; apolipoprotein CII deficiency), Hypercalcaemia, Hypothermia
ERCP
Drugs: azathioprine, mesalazine, bendroflumethiazide, furosemide, pentamidine, sodium valproate, steroids, didanosine (antiretroviral)
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28
Q

Anti-retroviral drug most characteristically ass with pancreatitis?

A

Didanosine

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29
Q

Commonest cause of biliary disease in pts with HIV?

A

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

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30
Q

What is ischaemic hepatitis?

A

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
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31
Q

NAFLD: what is the spectrum?

what does it represent?

A

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
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32
Q

What is NASH?

A

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

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33
Q

Factors ass with NAFLD?

A 
obesity
hyperlipidaemia
T2DM
jejunoilieal bypass
sudden weight loss/starvation
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34
Q

Features of NAFLD?

A

usually aSx
hepatomegaly
ALT ? AST
increased echogenecity on US

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35
Q

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

A

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)
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36
Q

Rx of NAFLD?

A

lifestyle changes esp weight loss & monitoring

- ongoing research into role of gastric banding & metformin etc

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37
Q

MoA of 5-ASA drugs?

A

5-ASA released in colon and not absorbed

  • acts as local anti-inflammatory
  • may inhibit prostaglandin synthesis
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38
Q

What is Sulfasalazine?

side-effects?

A

5-ASA + sulphapyridine (sulphonamide)

  • rashes
  • oligospermia
  • headache
  • heinz-body anaemia
  • megaloblastic anaemia
  • lung fibrosis
  • other SEs common to 5-ASAs
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39
Q

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

A
  • GI upset
  • headache
  • agranulocytosis
  • pancreatitis
  • interstitial nephritis
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40
Q

What is mesalazine?

A

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

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41
Q

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

A

NSAIDs, cOCP

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42
Q

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

A

Glucocorticoids (oral, topical, IV)

- Budesonide is an alternative in a subgroup

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43
Q

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

What can be used in addition?

A

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
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44
Q

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

A

5-ASA drugs, but not as effect as steroids

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45
Q

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

A

+ Azathioprine/Mercaptopurine/Methotrexate

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46
Q

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

A

Infliximab

- pts usually continue on azathioprine/methotrexate

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47
Q

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

A

Metronidazole

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48
Q

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

A

Azathioprine/Mercaptopurine

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49
Q

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

A

Methotrexate

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50
Q

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

A

5-ASA drugs e.g. mesalazine

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51
Q

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

A

small bowel cancer
colorectal cancer
osteoporosis

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52
Q

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

A

Stricturing terminal ill disease -> Ileocaecal resection

  • segmental small bowel resections
  • stricturoplasty
  • sub-total colectoy
  • panproctocolectomy
  • staged subtotal colectomy
  • protectomy
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53
Q

Fistulae in Crohn’s disease?

A
  • 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
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54
Q

When to consider IBS?

How to diagnose in terms of Sx?

A
  • 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
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55
Q

When considering IBS what are red flag Sx?

A

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

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56
Q

3 Drug causes of dyspepsia?

What 3 drugs may cause reflux by reducing lower oesophageal sphincter pressure?

A
  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
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57
Q

What is PBC: 1ry biliary cholangitis?

A
  • 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
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58
Q

Diseases ass with PBC?

A
  • Sjogrens 80%
  • RA
  • systemic sclerosis
  • thyroid disease
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59
Q

Dx of PBC - what Ab?

A
  • AMA M2 present in 98%, v specific
  • smooth muscle Ab in 30%
  • raised serum IgM
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60
Q

Rx of PBC:

  • what supplements?
  • what drug Rx?
  • what for pruritus?
  • what if e.g. bilirubin >100?
A
  • fat-soluble vitamins
  • ursodeoxycholic acid
  • cholestyramine for pruritus
  • liver Tx - recurrence may occur in gift but not usually a problem
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61
Q

What are the 3 types of colon cancer?

A

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

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62
Q

What gene mutations are involved in sporadic colon cancer?

A

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

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63
Q

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?

A

HNPCC

  • often proximal colon, usually poorly differentiated & highly aggressive
  • MSH2 60%
  • MLH1 30%
  • endometrial (they are in general at higher risk of other cancers)
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64
Q

Amsterdam criteria used to aid Dx of HNPCC?

A
  • at least 3 family members with colon cancer
  • across at least 2 generations
  • at least 1 Dx <50yrs
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65
Q

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?
A
  • 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
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66
Q

What is Gardner’s syndrome?

A

Variant of FAP

  • esteems of skull & mandible
  • retinal pigmentation
  • thyroid carcinoma
  • epidermoid cysts on skin
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67
Q

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

A
  • chronic inflammation
  • lesions may be multifocal
  • prognosis worse than if without UC
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68
Q

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

A
  • disease duration >10yrs
  • pts with pancolitis
  • onset before 15yrs old
  • unremitting disease
  • poor compliance to treatment
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69
Q

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

A

5 yr colonoscopy

  • extensive colitis with no active endoscopic/histological inflammation
  • or left-sided colitis
  • or Crohn’s colitis <50% of colon
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70
Q

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

A

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+
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71
Q

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

A

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
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72
Q

2 methods used to Dx coeliac disease?

A
  • immunology
  • jejunal biopsy
  • both normally reverse on a gluten-free diet
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73
Q

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

A 
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
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74
Q

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

A
  • subtotal villous atrophy
  • crypt hyperplasia
  • increase in intraepithelial lymphocytes
  • lamina propria infiltration with lymphocytes
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75
Q

Important causes of subtotal villous atrophy?

A
  • Coeliac disease
  • Tropical sprue
  • Dermatitis herpetiformis
  • Lymphoma
  • HIV-related enteropathy
  • Giardiasis
  • Hypogammaglobulinaemia
  • Radiation
  • Whipple’s disease
  • Zollinger–Ellison syndrome
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76
Q

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?

A

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

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77
Q

What is Budd-Chiara syndrome?
Features?
Causes?

A

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
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78
Q

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?

A

oesophageal cancer

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79
Q

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

A

Oesophagitis

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80
Q

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

A

oesophageal candidiasis

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81
Q

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?

A

Achalasia

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82
Q

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?

A

Pharyngeal pouch

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83
Q

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

A

systemic sclerosis

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84
Q

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

A

Myasthenia gravis

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85
Q

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?

A

Globus hystericus

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86
Q

Extrinsic causes of dysphagia?

A

Medistinal mass

Cervical spondylosis

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87
Q

Oesophageal wall causes of dysphagia?

A

Achalasia
Diffuse oesophageal spasm
Hypertensive lower oesophageal sphincter

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88
Q

Intrinsic causes of dysphagia?

A

Tumours
Strictures
Oesophageal web
Schatzki rings

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89
Q

Neurological causes of dysphagia?

A 
CVA
Parkinson's disease
MS
Brainstem pathology
Myasthenia gravis
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90
Q

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

A

Ambulatory oesophageal pH & manometry studies

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91
Q

GORD: what are the indications for OGD?

What can be considered if OGD negative i.e. what is the gold standard test for Dx?

A
  • 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
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92
Q

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?
A
  • 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
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93
Q

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

A
  • 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
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94
Q

Dx of PSC? what is shown?

Complications?

A
  • **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
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95
Q

When to consider bariatric surgery in severe obesity?

When to consider it as a 1st line option?

A
  • 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

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96
Q

3 main types of Bariatric surgery?

A
  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
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97
Q

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?

A

LAGB: mainly restrictive, laparoscopic-adjustable gastric banding

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98
Q

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

A 
Gastric bypass (mixed) or sleeve gastrectomy (restrictive)
- sleeve may be done as a sole procedure or an initial procedure prior to bypass
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99
Q

Bariatric surgery: when are 1rily malabsorptive procedures done?

A

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

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100
Q

Features of acute appendicitis?

A

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)
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101
Q

Examination in acute appendicitis

A
  • 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
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102
Q

Dx of acute appendicitis?

What score can be used to suggest the likelihood of it?

A
  • 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

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103
Q

Rx in appendicitis?

A
  • 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
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104
Q

RFs for hepatocellular carcinoma?

A

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

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105
Q

Features of hepatocellular carcinoma?

How should screening be considered?

A
  • 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
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106
Q

Rx options in hepatocellular carcinoma?

A
  • early: surgical resection
  • liver Tx
  • radio frequency ablation (usually palliative)
  • transarterial chemoembolisation (usually palliative)
  • SORAFENIB: multikinase inhibitor
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107
Q

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?

A

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%
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108
Q

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?

A

Rapid urease test e.g. CLO test

- sens 90-95% spec 95-98%

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109
Q

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

A

Remains positive after eradication

- sens 85% spec 80%

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110
Q

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

A
  • provides Abx sensitivities info
  • sens 70% spec 100%
  • Can also do gastric biopsy alone without culture, with sens 95-99% spec 95-99%
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111
Q

What is Wilson’s disease?

What is the genetic defects?

A

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

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112
Q

Features of Wilson’s disease?

A
  • 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
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113
Q

Dx by serum & urine in Wilson’s disease?

A
  • Reduced serum caeruloplasmin
    (also reduced serum copper as 95% is carried by caeruloplasmin)
  • Increased 24h urinary copper excretion
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114
Q

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

A

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

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115
Q

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

A

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
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116
Q

Recognised associations of autoimmune hepatitis?

What is the ass raised Ig subtype?

A
  • other autoimmune disorders
  • hypergammaglobulinaemia
  • HLA B8, DR3
  • IgG
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117
Q

Type I autoimmune hepatitis

  • what Ab?
  • who does it affect?
A

ANA &/or anti-smooth muscle Ab SMA

- adults & children

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118
Q

Type II autoimmune hepatitis

  • what Ab?
  • who does it affect?
A
  • anti-liver/kidney microsomal type 1 Ab LKM1

- children only

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119
Q

Type III autoimmune hepatitis

  • what Ab?
  • who does it affect?
A
  • soluble liver-kidney Ag

- middle-aged adults

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120
Q

Features of autoimmune hepatitis?

What is on liver biopsy?

A
  • 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

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121
Q

Rx of autoimmune hepatitis?

A
  • steroids, other immunosuppressants e.g. Azathioprine

- liver Tx

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122
Q

Which laxative is shown to have carcinogenic potential?

A

Co-Danthramer & Co-Danthrusate= genotoxic, carcinogenic

- only be prescribed in palliative pts with refractory constipation

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123
Q

Examples of osmotic laxatives?

A

lactulose
macrogols
rectal phosphates

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124
Q

Examples of stimulant laxatives?

A 
senna
docusate
bisacodyl
glycerol
(co-danthramer)
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125
Q

Examples of bulk-forming laxatives?

A

ispaghula husk

methylcellulose

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126
Q

Examples of faecal softener laxatives?

A

arachis oil enemas, not commonly prescribed

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127
Q

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

A

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
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128
Q

Ix of choice for bile acid malabsorption?

Rx?

A

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

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129
Q

What is haemochromatosis?

A

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 (!)
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130
Q

Screening for haemochromatosis in family members?

A

HFE mutation genetic testing

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131
Q

Diagnostic test for haemochromatosis?

A

Molecular genetic testing for C282Y & H63D mutations

Liver Bx: Perl’s stain

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132
Q

Typical iron study profile in patient with haemochromatosis?

What is characteristically shown on joint X-rays?

A

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

Chondrocalcinosis

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133
Q

Monitoring adequacy of venesection in haemochromatosis?

A

Transferrin sat should be kept <50%

Serum ferritin conc <50

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134
Q

Screening for haemochromatosis in general population?

A

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

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135
Q

What is angiodysplasia?
Association?
Dx?

A

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

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136
Q

Rx of angiodysplasia?

A

Endoscopic cautery or Argon plasma coagulation

  • antifibrinolytics e.g. Transexamic acid
  • oestrogen may also be used?
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137
Q

Drug causes of mainly hepatocellular liver disease?

A
  • paracetamol
  • valproate, phenytoin
  • MAO-Is
  • statins
  • etoh
  • amiodarone
  • methyldopa
  • nitrofurantoin
  • halothane
  • anti-TB: RIP
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138
Q

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

A
  • OCP
  • ABx: co-amoxiclav, flucloxacillin, erythromycin
  • sulphonylureas
  • fibrates
  • phenothiazines e.g. chlorpromaxine, prochlorperazine
  • nifedipine rarely
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139
Q

Drug causes of mainly cirrhotic liver disease?

A

Methotrexate
Methyldopa
aMiodarone

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140
Q

Blatchford score at 1st assessment of acute upper GI bleed:

what are the components?

A

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

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141
Q

Resuscitation in acute upper GI bleed?

After?

A

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

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142
Q

Management of non-variceal acute upper GI bleeding?

A

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

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143
Q 
Management of variceal acute upper GI bleeding:
pre-OGD?
if oesophageal?
if gastric?
if not controlled?
A
  • 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
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144
Q

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

A

Gastroduodenal artery

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145
Q

What is Zollinger-Ellison syndrome?

30% occur as part of what?

A

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

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146
Q

Features of Zollinger-Ellison syndrome?

A
  • 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
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147
Q

Dx of Zollinger-Ellison syndrome?

A

Fasting gastrin levels = single best screen test

Secretin stimulation test: paradoxical dramatic increase in gastrin (normally little/no effect)

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148
Q

3 main conditions of ischaemia to the lower GI tract?

A

acute mesenteric ischaemia
chronic mesenteric ischaemia
ischaemic colitis

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149
Q

Common features in bowel ischaemia?

A
  • 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
150
Q

Common predisposing factors in bowel ischaemia?

Dx?

A
  • 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

151
Q

How does acute mesenteric ischaemia usually occur?

A

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
152
Q

How does chronic mesenteric ischaemia usually occur?

A
  • non-specific features, may be thought of as ‘intestinal angina’
  • colicky, intermittent abdo pain
153
Q

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

A

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
154
Q

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

A

Disorder of pigmentation of bowel wall

  • Pigment-laden macrophages
  • ass with laxative abuse esp anthraquinone compounds e.g. senna
155
Q

What is achalasia?

A

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

156
Q

Clinical features of achalasia?

A
  • 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
157
Q

Gold standard test for achalasia?

What does CXR & barium swallow show?

A

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

158
Q

Rx in Achalasia?

A
  • intra-sphincteric injection of botulinum toxin
  • Heller cardiomyotomy
  • balloon dilatation
  • drug Rx has a role but limited by side-effects
159
Q

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

A

Carbon-13 urea breath test

- do 4wks after eradication Rx

160
Q

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

A

Amylase - in saliva & pancreatic secretions

161
Q

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

A

maltase
sucrase
lactase

162
Q

Dx of liver cirrhosis?

What further Ix may be recommended if cirrhosis is diagnosed?

A
  • 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

163
Q

What is transient elastography/Fibroscan?

When to offer it as part of cirrhosis screening?

A
  • 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
164
Q

Common causes of decompensation in pt with cirrhotic liver disease?

A 
infection
electrolyte imbalances
constipation
dehydration
upper GI bleeds
increased etoh intake
165
Q

HBV serology:

what does HBsAg imply?

A

acute disease if present for 1-6months

chronic infective disease if present >6months

166
Q

HBV serology:

what does Anti-HBs imply?

A

Immunity - either exposure or immunisation

- negative in chronic disease

167
Q

HBV serology:

what does Anti-HBc imply? IgM? IgG?

A

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

168
Q

HBV serology:

what does HbeAg imply?

A

Results from breakdown of core Ag from infected liver cells

- therefore = marker of infectivity

169
Q

Histology in gastric cancer?

A

Signet ring cells

  • contain a large vacuole of mucin which displaces the nucleus to one side
  • higher numbers ass with a worse prognosis
170
Q

Associations with gastric cancer?

A 
H pylori
blood group A
gastric adenomatous polyps
pernicious anaemia
smoking
salty, spicy, nitrates in food
may be negatively ass with duodenal ulcer
171
Q

Features of gastric cancer?
Dx?
Staging?

A
  • 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

172
Q

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?

A

Size & depth of invasion

- early cancers confined to submucosa have a 20% incidence of LN metastasis

173
Q

How are tumours of the gastro-oesophageal junction classified?

A

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

174
Q

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?

A

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

175
Q

Coeliac disease is strongly ass with which HLAs?

A

HLA-DQ2 95%

HLA-DQ8 80%

176
Q

Which conditions should be screened for coeliac disease?

Which signs & Sx?

A
  • 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
177
Q

Consequences/complications of coeliac disease?

A
  • 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
178
Q

5 causes of hepatosplenomegaly?

A
  • chronic liver disease with portal hypertension (before liver becomes small)
  • infections: EBV, malaria, hepatitis
  • lymphoproliferative disorders
  • myeloproliferative disorders e.g. CML
  • amyloidosis
179
Q

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

A

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
180
Q

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

A

Duodenum

Iron & Calcium

181
Q

Commonest complication of ERCP?

A

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

182
Q

1st line pharm Rx for IBS?

A

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

183
Q

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

A
  • if optimal.maximal tolerated doses of pre laxatives from different classes haven’t helped
  • & they’ve had constipation for at least 12months
184
Q

2nd line pharm Rx for IBS?

A
  • low-dose tricyclic antidepressants e.g. amitriptyline 5-10mg used in preference to SSRIs
185
Q

Non-pharm options for IBS?

A

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

186
Q

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

A

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

187
Q

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

A
  • 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
188
Q

What is HELLP syndrome?

A

haemolysis
elevated liver enzymes
low platelets in pregnancy

189
Q

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

A

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

190
Q

How can malabsorption be broadly divided?

A
  • Diarrhoea, steatorrhoea, weight loss
    Intestinal e.g. villpus atrophy
    Pancreatic eg enzyme deficiency of production/secretion
    Biliary ege bile salts
191
Q

Intestinal causes of malabsorption?

A

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

192
Q

Pancreatic causes of malabsorption?

A

chronic pancreatitis, CF, pancreatic cancer

193
Q

Biliary causes of malabsorption?

A

biliary obstruction, PBC

194
Q

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

A
  • bacterial overgrowth ege systemic sclerosis, diverticulae, blind loop
  • short bowel syndrome
  • lymphoma
195
Q

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

A

Adenocarcinoma

196
Q

Where are the majority of tumours?

What are RFs for oesophageal cancer?

A
  • 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
197
Q

Features of oesophageal cancer?

A

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

198
Q

Dx of oesophageal cancer?

A

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

199
Q

Rx of oesophageal cancer?

What is the biggest surgical challenge?

A
  • 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

200
Q

Extra-Intestinal features of IBD related to disease activity?

A

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

201
Q

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

A 
Arthritis: polyarticular, symmetric
Uveitis (commoner in UC)
Pyoderma gangrenosum
Clubbing
PSC (much commoner in UC)
202
Q

Pathology of Crohn’s disease?

Ix?

A

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
203
Q

Features of Crohn’s disease?

A
  • 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
204
Q

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

A

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
205
Q

Ix of choice for Crohn’s disease?

What is seen?

A

Colonoscopy

  • deep ulcers
  • skip lesions
  • leading to cobblestone appearance
206
Q

Histology in Crohn’s disease?

A
  • goblet cells
  • granulomas
  • inflammation in all layers from mucosa to serosa
207
Q

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

A
  • high sens & spec for examination of terminal ileum
  • strictures: Kantors string sign
  • proximal bowel dilation
  • rose thorn ulcers
  • fistulae
208
Q

What is an anal fissure?
Features?
RFs?

A

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
209
Q

Rx of acute anal fissure <6wks ?

A
  • 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)
210
Q

Rx of chronic anal fissure >6wks?

A

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

211
Q

Acute Rx of variceal haemorrhage?

A
  • 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
212
Q

Prophylaxis of vatical haemorrhage?

A

Propranolol - reduces rebleeding & mortality vs placebo

endoscopic variceal band ligation at 2wkly intervals until all varies eradicated with PPI cover

213
Q

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

A 
Bilirubin
Albumin
Prolonged PT
Encephalopathy
Ascites
Score of 5-15
Severity graded as:
<7 = A
7-9 = B
>9 = C
214
Q

What is MELD scoring?

A

Model for End-Stage Liver Disease
- Formula that uses combo of bilirubin, creatinine & INR to predict survival

3month mortality based on the score

215
Q

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?

A

Complete course of vaccination + hepatitis immunoglobulin

- HBV not transmitted via breastfeeding

216
Q

DDx of hyperamylasaemia?

A 
acute pancreatitis
pancreatic pseudocyst
mesenteric infarct
perforated viscus
acute cholecystitis
DKA
217
Q

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

A

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

218
Q

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

A 
clinical impression
APACHE II>8
Glasgow score 3+
persisting multiple organ failure
CRP>150
219
Q

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

A

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

220
Q

Modified Glasgow score for acute pancreatitis?

A 
PaO2 low
Age >55
Neutrophilia
Calcium low
Renal urea high
Enzymes LDH high
Albumin low
Sugar high
221
Q

How to assess severity of acute pancreatitis?

A

Glasgow, Ranson scoring systems & APACHE II

Biochemical i.e. CRP

222
Q

Rx of acute pancreatitis?

A

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

223
Q

What is Peutz-Jeghers syndrome?

What is the genetics?

A

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
224
Q

Features of Peutz-Jeghers syndrome?

A
  • 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

225
Q

Acanthosis nigricans is ass with which malignancy?

A

gastric cancer

226
Q

Acquired ichthyosis is ass with which malignancy?

A

lymphoma

227
Q

Acquired hypertrichosifs lanuginosa is ass with which malignancy?

A

GI & lung cancer

228
Q

Dermatomyositis is ass with which malignancy?

A

ovarian & lung cancer

229
Q

Erythema gyratum repens is ass with which malignancy?

A

lung cancer, breast

230
Q

Erythroderma is ass with which malignancy?

A

lymphoma

231
Q

Migratory thrombophlebitis is ass with which malignancy?

A

pancreatic cancer

232
Q

Necrolytic migratory erythema is ass with which malignancy?

A

glucagonoma

233
Q

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

A

myeloproliferative disorders

234
Q

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

A

haematological malignancy eg myelodysplasia

235
Q

Tylosis is ass with which malignancy?

A

oesophageal cancer

236
Q

What are villous adenomas?

Possible features?

A

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
237
Q

Presenting features of haemochromatosis?

A
  • 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
238
Q

Which complications of haemochromatosis are reversible?

A
  • cardiomyopathy
  • skin pigmentation
  • elevated LFTs & hepatomegaly may be
239
Q

Which complications of haemochromatosis are irreversible?

A
  • cirrhosis
  • diabetes mellitus
  • hypogonadotrophic hypogonadism
  • arthropathy
240
Q

Clinical features of Crohns disease?

A

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

241
Q

Clinical features of UC?

A

Bloody diarrhoea more common
LIF abdo pain
Tenesmus

242
Q

Why do Crohn’s disease pts get gallstones?

A

2ry to reduced bile acid reabsorption

- they are also more likely to get oxalate renal stones

243
Q

Histology in UC?

A
  • 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
244
Q

What is seen on colonoscopy in UC?

A
  • widespread ulceration with preservation of adjacent mucosa, which has the appearance of polyps - pseudo polyps
  • continuous disease
245
Q

What is seen on barium enema in UC?

A
  • loss of haustrations
  • superficial ulceration, pseudopolyps
  • longstanding disease: colon is narrow & short - drainpipe colon
246
Q

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

A

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
247
Q

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

A

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

248
Q

When should acetylcysteine be given in a paracetamol OD?

How is it infused?

A
  • 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

249
Q

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

A 
Arterial pH <7.3, 24h after ingestion
or all of the following:
1. PT >100
2. creatinine >300
3. grave III/IV encephalopathy
250
Q

Features of acute pancreatitis?

A
  • 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
251
Q

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

A

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

252
Q

What is alcoholic ketoacidosis?

How does it typically present?

What is most appropriate Rx?

A
  • 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

253
Q 
What is ascending cholangitis?
What is the commonest predisposing factor?
Charcot's triad?
Other features?
Rx?
A 
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
254
Q

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

A

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
255
Q

How to Ix pernicious anaemia?

A
  • 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
256
Q

What is the Schilling test (pernicious anaemia)?

A
  • radiolabelled B12 given 2x
  • 1st on its own
  • 2nd with oral intrinsic factor
  • urine B12 levels measured
257
Q

Pathophysiology of hepatorenal syndrome?

A
  • 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
258
Q

Type 1 hepatorenal syndrome?

A
  • rapidly progressive
  • doubling of serum Cr >221 or halving of CrCl to <20 over a period of <2wks
  • v poor prognosis
259
Q

Type 2 hepatorenal syndrome?

A
  • slowly progressive

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

260
Q

Rx options for hepatorenal syndrome?

A
  • Vasopressin analogues (e.g. Terlipressin) - cause vasoconstriction of splanchnic circulation
  • volume expansion with 20% albumin
  • TIPS
261
Q

necrolytic migratory erythema is ass with which cancer?

A

glucagonoma

262
Q

What is carcinoid syndrome?

A
  • 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
263
Q

Features of carcinoid syndrome:

  • what is often the earliest Sx?
  • others?
A
  • 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
264
Q

Ix of carcinoid syndrome?

A
  • urinary 5-HIAA

- plasma chromogranin A y

265
Q

Rx of carcinoid syndrome?

A
  • somatostatin analogues e.g. OCTREOTIDE

- diarrhoea: cyproheptadine may help

266
Q

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

A

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
267
Q

RFs for Barretts?

A
  • GORD is strongest RF
  • male 7:1
  • smoking
  • central obesity
268
Q

Rx of Barrett’s?

If dysplasia is identified?

A
  • 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
269
Q

Features of cholangiocarcinoma?

A
  • persistent biliary colic Sx
  • ass with anorexia, jaundice, weight loss
  • palpable mass in RUQ (Courvoisiers sign)
  • periumbilical lymhadenopathy & left supraclavicular adenopathy may be seen
270
Q

Commonest organisms found in pyogenic liver abscesses?

A

staph aureus - children

E coli - adults

271
Q

Rx of pyogenic liver abscess?

A
  • amoxicillin + ciprofloxacin + metronidazole

- if pen allergic: clindamycin + ciprofloxacin

272
Q

What happens to clotting factors in liver failure?

A

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

273
Q

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

A
  • 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
274
Q

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

A
  • 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
275
Q 
Ix in chronic pancreatitis:
AXR?
CT?
functional test?
Rx?
A

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)
276
Q

Commonest organism found on ascitic fluid culture in SBP?

A

E coli

277
Q

Clinical features of PBC?

A

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
278
Q

Complications of PBC?

A
  • malabsorption: osteomalacia, coagulopathy
  • sicca syndrome occurs in 70%
  • portal hypertension: ascites, variceal haemorrhage
  • hepatocellular cancer 20X increased risk
279
Q

Causes of jejunal villous atrophy?

A 
coeliac disease
tropical sprue
hypogammaglobulinaemia
GI lymphoma
Whiles disease
cows milk intolerance
280
Q

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

A

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

281
Q

What is a pharyngeal pouch?

A

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

282
Q

Features of pharyngeal pouch?

Imaging?

A
  • dysphagia
  • regurgitation
  • aspiration
  • neck swelling which gurgles on palpatin
  • halitosis
    Barium swallow with fluoroscopy
283
Q

Why is gallstone RUQ pain worse after a fatty meal?

A

When cholecystokinin levels are highest and gallbladder contraction is maximal

284
Q

Risks of ERCP?

A

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

285
Q

Renal Tx: what are technical complications usually related to?

A

the ureteric anastomosis

286
Q

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

A

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

287
Q

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

A

Renal artery thrombosis

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

288
Q

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

A

Renal artery stenosis

- angioplasty

289
Q

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

A

Renal vein thrombosis

- graft is usually lost

290
Q

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

A

Urine leaks

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

291
Q

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

A

Lymphocele

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

292
Q

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

A

Hyperacute
Acute
Chronic

293
Q

Hyperacute Tx organ rejection:

  • when does it occur?
  • what are the RFs?
  • when do the macroscopic features manifest?
  • Rx?
A
  • 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
294
Q

Acute Tx organ rejection:

  • when does it occur?
  • why does it usually occur?
A
  • during first 6months, all organs are susceptible
  • usually T cell mediated, mononuclear cell infiltrates predominate, or vascular lesions
  • mostly managed medically
295
Q

Chronic Tx organ rejection:

  • when does it occur?
  • why does it usually happen?
  • RFs?
  • what organ specific changes may be seen?
A
  • 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
296
Q

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

A

CMV infection

  • PCR Dx
  • Rx with GANCICLOVIR
297
Q

What is malnutrition?

A

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

298
Q

How is malnutrition screened for?

when should it be done?

A

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
299
Q

Gen management of malnutrition?

A
  • 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
300
Q

Which pts are at risk of malnutrition?

A
  • eating nothing/little for >5days, who are likely to eat little for a further 5days
  • poor absorptive capacity
  • high nutrient losses
  • high metabolism
301
Q

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

A
  • if malnourished, unsafe swallow/inadequate oral intake & functional GI tract
302
Q

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

A

If there is upper GI dysfunction

303
Q

When to consider long-term gastrostomy?

A

If gastric feeding >4wks

304
Q

How should ITU pts have enteral feeding?

A

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

305
Q

When can PEG tube be used after insertion?

A

4hours after insertion

- don’t remove until >2wks after insertion

306
Q

Dyspepsia urgent referral for 2WW OGD guidelines?

A
  • all with dysphagia
  • all with upper abdo mass
  • > 55yrs with weight loss + upper abdo pain/reflux/dyspepsia
307
Q

Dyspepsia non-urgent referral for OGD guidelines?

A
  • 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
308
Q

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

A
  1. review meds for possible causes
  2. lifestyle advice
  3. trial full-dose PPI for 1month Or a test & treat approach for H pylori
309
Q

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

A

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
310
Q

What is Plummer-Vinson syndrome?

Rx?

A
  1. dysphagia 2ry to oesophageal webs
  2. glossitis
  3. iron-deficiency anaemia

Rx with iron supplementation & webs dilatation

311
Q

What is Mallory-Weiss syndrome?

A

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

312
Q

What is Boerhaave syndrome?

A

Severe vomiting -> oesophageal rupture

313
Q

Rx of Small bowel bacterial overgrowth syndrome?

A
  • Correct underlying disorder
  • Abx: Rifaximin (low resistance)
  • Co-amoxiclav/Metronidazole may be effective in majority
314
Q

What is WHipple’s disease?

A

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

315
Q

Features of Whipple’s disease?

A
  • malabsorption: diarrhoea & weight loss
  • large-joint arthralgia
  • lymphadenopathy
  • skin: hyperpigmentation & photosensitivity
  • pleurisy, pericarditis
  • neuro sx are rare but inc ophthalmoplegia, dementia, seizures, ataxia, myoclonus
316
Q

Ix of Whipple’s disease?

A

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

317
Q

Rx of Whipples disease?

A

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

318
Q

What is post-cholecystectomy syndrome?

A
  • 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
319
Q

What is a Dieulafoy lesion?

A

Gastric bleeding

  • AV malformation
  • often no prodrome before haematemesis & malaena
320
Q

What type of virus is hepatitis D?

Transmission?

A

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
321
Q

What is hepatitis D co-infection?

A

hepatitis B & D infection at the same time

322
Q

What is hepatitis D super-infection?

What is it ass with?

A

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

323
Q

How to Dx hepatitis D?

Rx?

A

PCR of hepatitis D RNA

- Interferon currently used but poor evidence base

324
Q

Necrolytic migratory erythema is ass with which malignancy?

A

GLUCAGONOMA

325
Q

What is referring syndrome and what are the metabolic consequences?

A

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
326
Q

When are pts considered at high risk of referring syndrome?

A

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
327
Q

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

A

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

328
Q

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

A
  • 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
329
Q

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

A

IDARUCIZUMAB (PRAXBIND)

- nb resuscitation is main Rx, and improves outcomes

330
Q

Commonest location of colorectal cancer?

A 
Rectal 40%
sigmoid 30%
ascending colon &amp; caecum 15%
transverse colon 10%
descending 5%
331
Q

bronze diabetes with hepatomegaly - what is the gene defect?

A

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)

332
Q

Dysfunctional protein ass with Wilson’s disease?

A

ATP7B

333
Q

Enzyme deficiency ass with Gilbert’s disease?

A

glucuronyl transferase

334
Q

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

A

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

335
Q

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

A

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

336
Q

Liver biopsy Dx: Triglyceride accumulation with proliferation of myofibroblasts?

A

NAFLD

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

337
Q

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

A

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

338
Q

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

A

Primary biliary cirrhosis

- usually affects small-medium sized bile ducts

339
Q

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

A

ascending cholangitis

340
Q

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

A

Selective IgA deficiency

  • more common in pts with coeliac
  • therefore should check IgA levels
  • if they have it, should measure anti-TTG IgG instead
341
Q

Ix of choice to Dx primary sclerosing cholangitis?

A

ERCP: multiple biliary structures giving a ‘beaded’ appearance

342
Q

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

A

Pseudomembranous colitis - C diff

343
Q

Contra-indications to percutaneous liver biopsy?

A
  • anaemia
  • low platelets <60
  • deranged clotting e.g. INR >1.4
  • extrahepatic biliary obstruction
  • ascites
  • hydatid cyst
  • haemangioma
  • uncooperative pt
344
Q

Classification of severity of UC?

A

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

345
Q

Inducing remission in UC:

- for distal colitis what is 1st line & 2nd line?

A

Rectal Mesalazine is best

- others inc rectal steroids then oral aminosalicylates

346
Q

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

A

Oral Aminosalicylates

347
Q

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

A

Oral prednisolone

348
Q

Rx of severe colitis in UC?

A

IV steroids etc in hospital

349
Q

Maintaining remission in UC?

A

Oral aminosalicylates

  • can also then consider azathioprine & mercaptopurine
  • probiotics may help prevent relapse in pts with mild-mod disease
350
Q

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

A

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
351
Q

Common causes of hepatomegaly?

A

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

352
Q

Causes of hepatomegaly (except CCC)?

A 
viral hepatitis, EBV
malaria
progenic, amoebic abscess
hydatid disease
haemaological malignancies
haemochromatosis
PBC
sarcoid, amyloid
353
Q

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

A
  • from small bowel & pancreas
  • neural stimulation
    1. stimulates secretion by pancreas & intestines
    2. inhibits acid & pepsinogen secretion
354
Q

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

A
  • Pancreas 90%
  • dehydration, weight loss, large volume diarrhoea
  • hypokalaemia, hypochlorhydia
355
Q

What are the RFs for oesophageal ca - adenocarcinoma?

A
  • etoh, smoking

- Barretts, GORD

356
Q

What are the RFs for oesophageal ca - squamous carcinoma?

A
  • etoh , smoking
  • Achalasia
  • Plummer-vinson
357
Q

What is the probable aetiology of hepatic encephalopathy?

A
  • 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
358
Q

Features of hepatic encephalopathy?

A
  • 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
359
Q

Precipitating factors of hepatic encephalopathy?

A
  • infection eg SBP
  • GI bleed
  • constipation
  • post-TIPS
  • drugs: sedatives, diuretics
  • hypokalaemia
  • renal failure
  • increased dietary protein (uncommon)
360
Q

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

A
  • treat any underlying precipitating cause
  • LACTULOSE: promotes excretion of ammonia & increases metabolism of ammonia by gut bacteria

(embolisation of portosystemic shunts, liver Tx)

361
Q

2ry prophylaxis of hepatic encephalopathy?

A

RIFAXIMIN: modulates gut flora resulting in decreased ammonia production

362
Q

Abx most likely to cause pseudomembranous colitis?

A

clindamycin RR 31.8
3rd gen cephalosporins 14.9
ciprofloxacin 5.0

363
Q

2ry causes of hypertriglyceridaemia?

A
  • high etch intake
  • T2DM
  • renal disease
  • pregnancy
  • bulimia nervosa
  • drugs: ciclosporin, oestrogens, corticosteroids
364
Q

Management of high triglycerides >20?

A

if not due to xs etoh or poor glycemic control then:

-> refer for urgent specialist review e.g. regional lipid clinic

365
Q

Management of high triglycerides 10-20?

A
  • 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
366
Q

What is the Ix of choice to detect liver cirrhosis?

A

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

367
Q

what is the main cause of hepatorenal syndrome?

A

splanchnic vasodilation

368
Q

How are pts with hepatocellular carcinoma managed?

A

Barcelona Classification for Liver Cancer Treatment System

369
Q

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?

A

Sorafenib = multiple tyrosine kinase inhibitor

370
Q

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?

A

Consider liver Tx

- RFA (radiofrequency ablation) or TACE (transarterial chemoembolisation)

371
Q

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

A

Surgical resection

372
Q

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

A

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

exam (21 decks)

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