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Year 5 Core Conditions > Gastrointestinal System > Flashcards

Gastrointestinal System Flashcards

1
Q

In which part of the GI system is iron, folate and calcium absorbed?

A

Proximal small intestine

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2
Q

At which point of the GI system is B12 absorbed?

A

Terminal ileum

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3
Q

What are the two types of contrast studies performed during GI investigations?

A
  1. Barium enema

2. Gastrografin studies

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4
Q

When is doing a gastrografin better than a barium enema?

A

When there is a risk of perforation - so acute abdomen situations - where you don’t want barium in the peritoneal cavity

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5
Q

What is a lactose-hydrogen breath test commonly used for?

A

To determine lactose intolerance

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6
Q

What are the causes of malabsorption? (9)

A
  1. Coeliac disease
  2. Protein-losing enteropathy
  3. Whipple’s disease
  4. Bacterial overgrowth
  5. Short bowel syndrome
  6. Tropical sprue
  7. Crohn’s disease
  8. Lactose intolerance
  9. Chronic pancreatitis
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7
Q

What are the symptoms of malabsorption? (3)

A
  1. Diarrhoea
  2. Steatorrhoea
  3. Weight loss
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8
Q

What are the signs of malabsorption? (3)

A
  1. Anaemia
  2. Oedema
  3. Hypovitaminosis
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9
Q

What investigations should be carried out in suspected cases of malabsorption? (2)

A
  1. Bloods - FBC, U&Es, LFT, albumin, calcium, folate, B12, vitamin D, coagulation, coeliac serology, TFTs
  2. Imaging: OGD, sigmoidoscopy
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10
Q

What are the most common causes of acute pancreatitis? (2)

A
  1. Alcohol

2. Gallstones

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11
Q

What are the other causes of pancreatitis?

A 
Gall stones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion bite
Hypercalcaemia 
ERCP
Drugs (e.g. thiazide diuretics)
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12
Q

How does acute pancreatitis present? (3)

A
  1. Severe epigastric pain (often radiates to the back)
  2. Nausea
  3. Vomiting
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13
Q

What are the signs of acute pancreatitis?

A
  1. Tachycardia
  2. Pyrexia
  3. Hypotension
  4. Abdominal tenderness
  5. Reduced bowel sounds (secondary to ileus)
  6. Grey-turners sign or Cullen’s sign
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14
Q

What investigations should be carried out when suspecting pancreatitis? (5)

A
  1. Bloods - FBC, U&Es, LFTs, serum amylase (>1000IU/ml)
  2. ABG
  3. USS
  4. CT
  5. MRCP (magnetic resonance cholangiopancreatography)
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15
Q

What is the treatment for acute pancreatitis? (6)

A
  1. Analgesia
  2. IV fluids
  3. O2
  4. Urinary catheter
  5. NJ feeding (to avoid pancreatic stimulation)
  6. ERCP if gallstone obstructing bile duct
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16
Q

What are the complications of acute pancreatitis? (5)

A
  1. Pseudocyst
  2. Abscess
  3. Adult respiratory distress syndrome
  4. Renal failure
  5. Chronic pancreatitis
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17
Q

What is the Ranson criteria for acute pancreatitis? (aka modified glasgow criteria)

A 
PANCREAS
P - P02 <60mmHg/7.9kPa
A - age >55years
N - neutrophils WBC>15
C - calcium >2mmol/L
R - renal function urea >16mmol/L
E - enzymes LDH >600iu/L, AST>200iu/L
A - albumin <32g/L
S - sugar: glucose>10mmol/L

three or more positive factors detected within 48 hours of onset suggest severe pancreatitis (refer to HDU/ITU)

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18
Q

What causes jaundice?

A

An excess of bilirubin

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19
Q

What are the different ways jaundice can be classified?

A
  1. Unconjugated or conjugated

2. Pre-hepatic/hepatic/post-hepatic

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20
Q

What are the causes of pre-hepatic unconjugated bilirubin jaundice? (5)

A

These are mainly due to haemolysis:

  1. Immune mediated haemolysis - blood transfusions, SLE
  2. DIC
  3. HELLP
  4. Sepsis
  5. Malaria
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21
Q

What is the hepatic cause of unconjugated bilirubin jaundice?

A

Gilbert’s syndrome - impaired conjugation

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22
Q

What are the hepatocellular dysfunction causes of conjugated bilirubin jaundice? (5)

A

Hepatocellular dysfunction:

  1. Infection - viral Hep B, C, EBV, CMV
  2. Toxins - alcohol, drugs - paracetamol overdose, antibiotics, TB medication, statins
  3. Neoplastic - HCC
  4. Metabolic - Wilson’s, haemochromatosis
  5. Autoimmune hepatitis
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23
Q

What are the common causes of cirrhosis? (3)

A
  1. Alcohol liver disease
  2. NAFLD
  3. Hep B and C
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24
Q

The causes of conjugated bilirubin jaundice can be categorised into what?

A
  1. Hepatocelular dysfunction

2. Impaired hepatic excretion

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25
Q

What are the impaired hepatic excretion causes of conjugated bilirubin jaundice? (7)

A
  1. Gallstones/biliary system stones
  2. Primary biliary cirrhosis
  3. Primary sclerosis cholangitis
  4. Pancreatic carcnoma
  5. Cholagiocarcinoma
  6. Heart failure
  7. Budd Chiari (occlusion of the hepatic vein)
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26
Q

What medications cause jaundice?

A
  1. Dapsone (anti-malarial) - causes haemolysis
  2. Paracetamol, TB drugs - isoniazid, pyrazinamine - cause hepatitis
  3. Flucloxacillin, co-amoxiclav, erythromycin, chlorpromazine, prochlorperazine - cholestasis
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27
Q

What is the normal level of bilirubin in the blood? (range)

A

3-17 umol/L

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28
Q

In someone with jaundice, with dark urine and pale stools, what type of jaundice dose this indicate?

A

Post-hepatic (obstructive) jaundice

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29
Q

What are the stigmata of chronic liver disease found on the hands? (5)

A
  1. Clubbing
  2. Liver flap
  3. Leuchonychia (hypoalbuminaemia)
  4. Dupytren’s contracture
  5. Palmar erythema (increase in oestrogen)
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30
Q

What are the stigmata of chronic liver disease found on the skin? (4)

A
  1. Jaundice
  2. Spider naevi (>5)
  3. Caput medusae
  4. Bruising
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31
Q

What is caput medusae?

A

Enlarged superficial epigastric veins due to portal hypertension

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32
Q

What are the abdominal stigmata seen in chronic liver disease? (3)

A
  1. Ascites
  2. Hepatomegaly
  3. Splenomegaly
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33
Q

What are the facial stigmata synonymous with chronic liver disease? (2)

A
  1. Jaundiced sclera

2. Bleeding gums (coagulopathy, decreased production of clotting factors)

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34
Q

Why in liver disease are levels of vitamin K low?

A

The liver synthesises bile aids and secretes them into the small intestine where they play a critical role in the absorption of vitamin K …so no bile acids = no vitamin K

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35
Q

The liver produces all clotting factors except what?

A

Von willibrand factor

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36
Q

In terms of LFTs, where is the problem if ALT is raised, and what about for ALPs?

A

ALT usually indicates hepatic cellular dysfunction whereas ALP is gall bladder - an obstructive picture

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37
Q

If there is a raised in ALP alongside a raised gamma-glutamyl transferase (GGT) what does this indicate?

A

That the problem is suggestive of biliary epithelial damage and bile flow obstruction. - it is highly suggestive of cholestasis

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38
Q

What are the causes of an isolated ALP raise without raised GGT? (4)

A
  1. Bony metastases/primary bone tumour
  2. Vitamin D deficiency
  3. Recent bone fractures
  4. Renal osteodystrophy
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39
Q

If LFTs are normal but a patient is jaundiced, what does this commonly indicate?

A

A pre-hepatic cause

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40
Q

What are the two most common causes of isolated jaundice?

A
  1. Gilberts syndrome

2. Haemolysis - check FBC

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41
Q

Where is albumin produced and what is its role?

A

Produced by the liver and helps to bind water, cations, fatty acids and bilirubin. It also plays a key role in maintaining oncotic pressure of blood

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42
Q

In LFT derangement of ALT and AST, which one is most raised in chronic liver disease?

A

ALT>AST in chronic liver disease

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43
Q

What are the causes of AST being more raised than ALT?

A

Cirrhosis and acute alcoholic hepatitis

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44
Q

What are all the things screened for in a non invasive liver screen (NILS)? (7)

A
  1. FBC, U&Es, INR, glucose, lipid profile, albumin
    2 Viral screen (Hep B, C, CMV, EBV)
  2. Autoimmune liver screen + immunoglobulins (e.g. ANA, anti DS-DNA, ANCA, IgG)
  3. Tumour markers - AFP - alpha fetoprotein
  4. Metabolic - haemochromatosis (iron studies, ferritin+iron), Wilsons (copper, serum ceruloplasmin), alpha-1-antitrypsin
  5. Toxins - paracetamol
  6. Imaging - USS
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45
Q

What is important to ask a patient who presents with jaundice or abnormal LFTs? (8)

A
  1. Blood transfusion history
  2. IVDU?
  3. Tattoos
  4. Sexual activity (Fitz-Hugh-Curtis)
  5. Travel history
  6. Alcohol use
  7. Family history
  8. Drug history
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46
Q

What is hereditary haemochromatosis? (7)

A
  1. Autosomal recessive
  2. Disorder of iron metabolism and absorption
  3. Deposits in joints, liver, heart, pancreas, skin, testicles
  4. Middle aged men (40-60)
  5. Signs and symptoms -
    early: fatigue, arthralgia, erectile dysfunction
    later: bronze/grey skin, decompensated liver disease, cardiomyopathy, diabetes
  6. Tests, biopsy, genetic screening
  7. Management - venesection
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47
Q

What are the features of Wilson’s disease?

A
  1. Autosomal recessive
  2. Increased Cu absorption and decreased secretion
  3. Onset usually between 10-25 years
  4. Children: liver disease, young adults: neurological dysfunction
  5. Presents with: liver dysfunction - hepatitis and cirrhosis, neurological (basal ganglia degeneration, dysarthria, ataxia and chorea), eyes (Kayser Fleischer rings)
  6. Management: Penicillamine (copper chelator)
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48
Q

What causes autoimmune hepatitis?

A

Unknown aetiology - autoantibodies against hepatocytes surface antigens

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49
Q

Who is most affected by autoimmune hepatitis?

A

Young or middle aged women

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50
Q

What tests should be performed when investigating autoimmune hepatitis?

A
  1. IgG
  2. Type 1: ANA, ASMA
  3. Type 2: anti-liver kidney microsomal type 1 antibodies
  4. Type 3: SLA
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51
Q

What is the management of autoimmune hepatitis?

A
  1. Steroids
  2. Immunosuppressants - Azathioprine
  3. Transplant
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52
Q

What is primary biliary cholangitis?

A

A progressive autoimmune disease of the biliary system causing intrahepatic cholestasis, scarring, fibrosis and cirrhosis. It is caused by unknown environmental triggers and is thought to have a genetic predisposition.

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53
Q

What are the signs/symptoms of primary biliary cholangitis?

A
  1. Cholestatic jaundice
  2. Liver disease
  3. Liver failure
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54
Q

What is the M rule associated with PBC? (3)

A
  1. Middle aged women
  2. IgM
  3. AMA
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55
Q

What is primary sclerosing cholangitis?

A

Inflammation and fibrosis of intra- and extra- hepatic bile ducts - a biliary system disease of unknown cause

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56
Q

What are the signs/symptoms of PSC?

A
  1. Liver disease/failure

2. Ascending cholangitis

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57
Q

What are the risk factors or association with PSC? (2)

A

Male gender

IBD

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58
Q

What are you at increased risk of if you have PSC?

A

Colon + liver + gall bladder cancers - yearly colonoscopies are required

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59
Q

What investigations/tests are done in suspected PSC? (3)

A
  1. Autoantibodies - ANA, ANCA
  2. MRCP
  3. Biopsy
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60
Q

What are the indications for haemodialysis?

A 
AEIOU
Acid-base problems
Electrolyte problems
Intoxications
Overload, fluid
Uraemic symptoms
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61
Q

What are the differentials for rectal bleeding? (5)

A
  1. Anal fissures
  2. Haemorrhoids
  3. Crohns
  4. UC
  5. Rectal cancer
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62
Q

What are the features of anal fissures - how can it present? (3)

A
  1. Bright red blood which occurs post-defecation
  2. Constipation
  3. Painful
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63
Q

What are the features of haemorrhoids - how may the person present? (2)

A
  1. Bright red blood on toilet paper and in toilet bowel

2. Post defecation on toilet paper, not mixed in.

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64
Q

What are the features of Crohn’s? (7)

A
  1. Diarrhoea usually non-bloody
  2. If there is blood - can be mixed in
  3. Altered bowel habits
  4. Fissures can occur
  5. Weight loss
  6. Abdominal pain
  7. Mouth ulcers
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65
Q

What are the features of ulcerative colitis? (3)

A
  1. Blood mixed in with stool
  2. Diarrhoea
  3. Proctitis
    - NO perianal disease
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66
Q

What are the features of someone presenting with rectal cancer? (2)

A
  1. Bright red blood

2. Weight loss

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67
Q

What investigations should be done for someone with rectal bleeding? (5)

A
  • Bedside
    1. Stool MC&S - need to exclude campylobacter, c.diff, salmonella, e.coli
    2. Faecal calprotectin
  • Bloods
    3. FBC, ESR, CRP, U&Es, LFTs, pANCA
    -Imaging
    4- AXR
    5. Colonoscopy
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68
Q

What is faecal calprotectin?

A

Faecal calprotectin (or fecal calprotectin) is a biochemical measurement of the protein calprotectin in the stool. Elevated faecal calprotectin indicates the migration of neutrophils to the intestinal mucosa, which occurs during intestinal inflammation, including inflammation caused by inflammatory bowel disease (but not IBS).

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69
Q

What are the key features of ulcerative colitis - the course and areas of IBD and symptoms? (7)

A
  1. Relapsing and remitting
  2. Inflammation always starts at rectum and never spreads beyond ileocecal valve
  3. No inflammation beyond submucosa (doesn’t affect all three layers)
  4. Episodic or chronic blood diarrhoea
  5. Cramp abdominal pain LLQ
  6. Tenesmus
  7. Proctitis
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70
Q

What is backwash ileitis?

A

A reflux of colonic contents into the distal few centimetres of the ileum through the ileocaecal valve. …this can make the distinction between UC and CD more difficult

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71
Q

What are the extra-intestinal manifestations of UC? (4)

A
  1. MSK - arthritis (typically affecting sacroiliac and other large joints)
  2. Skin - erythema nodosum
  3. Eyes - episcleritis, anterior uveitis, or iritis
  4. Hepatobiliary - primary sclerosing cholangitis
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72
Q

What is the TRUELOVE and WITTS criteria?

A

It classifies UC into mild, moderate and severe episodes, dependent on the number of bowel motions, rectal bleeding and systemic features.

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73
Q

What is classed as mild UC?

A

<4 bowel motions per day with a small amount of blood and no systemic features

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74
Q

What is classed as moderate UC?

A

4-6 bowel motions, varying amounts of bleeding but no systemic features

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75
Q

What is classed as severe UC?

A

More than 6 bowel motions, bloody diarrhoea and systemic features e.g. tachycardia and/or pyrexia

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76
Q

What is the first line treatment for people with mild-moderate UC?

A

Topical aminosalicylates e.g. rectal mesalazine (if not response within 4 weeks, add an oral aminosalicylate, and no response again then steroid - topical or oral)

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77
Q

What is the treatment for moderate UC? (2)

A
  1. Rectal or oral aminosalicylates (increased dose compared to mild)
    …if needed;
  2. Oral prednisolone (then taper down)
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78
Q

What is the treatment for extensive UC? (2)

A
  1. Rectal and high dose oral aminosalicylates
    …If needed;
  2. No remission - oral aminosalicylates and oral steroids
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79
Q

What is the treatment for severe UC?

A
  1. IV steroids
  2. IV ciclosporin (if steroids aren’t effective after 72 hours OR if worsening despite steroid treatment)
    3.
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80
Q

What is the recommendation with regards to oral aminosalicylates compared to topical?

A

If someone doesn’t want to use topical aminosalicylates they can have oral has first-line, however they must be informed it is not as effective

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81
Q

Which drugs will sometimes be given by a specialist in moderate-severely active UC?

A

Biologics and Janus kinase inhibitors

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82
Q

What is the top differential for a person with known UC presenting with severe abdominal pain, distention and pyrexia. With HR 120 and BP 90/60?

A

Toxic megacolon - where the deeper layer of the bowel becomes affected, with >6cm thumbprinting. Caused by anti-diarrhoeal agents and codeine. Decompression should be attempted.

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83
Q

In terms of distribution, how are UC and Crohn’s different?

A

Crohns affects anywhere mouth to anus whereas UC is the rectum and colon

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84
Q

In terms of depth, whats the difference between UC and Crohns?

A

Crohn’s is transmural whereas UC is superficial

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85
Q

What are the signs of Crohn’s disease? (3)

A
  1. RIF mass
  2. Perianal disease
  3. Extraintestinal same as UC
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86
Q

What are the recommended investigations for Crohn’s?

A 
Same as for UC
\+
Barium swallow
\+ 
Additional bloods - B12 and albumin
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87
Q

Why is a barium swallow indicated for Crohns?

A

It will show strictures, gross mucosal changes and the presence of fistulas. It is also useful for showing the length of the bowel.

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88
Q

What are the complications of Crohn’s?

A
  1. Fistula
  2. Abscess
  3. Colorectal cancer
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89
Q

What is the treatment for mild Crohns?

A
  1. Corticosteroid

2. Add on = azathioprine or mercaptpurine

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90
Q

When is an add on indicated?

A

When the patient experiences two or more inflammatory exacerbations within a 12 month period

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91
Q

What needs to be checked before azathioprine or mercaptpurine are started and why?

A

TPMT - thiopurine methyltransferase - this is one of the enzymes involved in the metabolism of these drugs, and patients with low levels of this enzyme are at a risk of life-threatening bone marrow suppression

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92
Q

What is the treatment for severe Crohns disease?

A

IVI
IV hydration
IV steroids

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93
Q

Which drugs are used when a patient is in remission with Crohn’s?

A
  1. Azathioprine or mercaptpurine

2. Methotrexate (second line)

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94
Q

What are the signs/symptoms associated with a pharyngeal pouch?

A

Patients often complain of regurgitation of foul smelling liquid, halitosis is noted, episodic dysphagia.

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95
Q

Why is upper GI endoscopy potentially hazardous for people with a pharyngeal pouch?

A

Because there is a risk of perforation

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96
Q

What is Killians dehiscence?

A

It is a triangular area of weakness in the wall of the pharynx. It is where pharyngeal pouches are known to develop.

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97
Q

What is achalasia?

A

It is primarily a disorder of motility of the lower oesophageal sphincter. The smooth muscle layer of the oesophagus has impaired peristalsis and failure of the sphincter to relax causes fictional stenosis or functional oesophageal stricture. Most causes have no known underlying cause, but a small proportion occurs secondary to other conditions e.g. oesophageal cancer.

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98
Q

What controls the tone and activity of the muscles in the oesophagus?

A

The muscles are controlled by a balance of excitatory transmitters such as acetylcholine and substance P, and inhibitory transmitters such as nitric oxide and vasoactive intestinal peptide (VIP).

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99
Q

In addition to oesophageal cancer, what else is thought to contribute to the development of achalasia?

A

It is thought that it could be an autoimmune reaction to viral infections and additionally genetic factors.

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100
Q

What is the mean age of diagnosis of achalasia?

A

53

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101
Q

What is the most common presenting feature of achalasia?

A

Dysphagia

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102
Q

In addition to dysphagia, how else can achalasia present? (5)

A
  1. Regurgitation (occurs in 80-90%)
  2. Chest pain (often described as retrosternal and occurs after eating)
  3. Heartburn
  4. Weight loss (can suggest malignancy)
  5. Nocturnal cough (feature of later disease)
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103
Q

What can sometimes be seen on CXR for someone with achalasia?

A

Vastly dilated oesophagus behind the heart - however this is rarely seen in practice

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104
Q

Due to the risk of perforation of a malignancy, what tends to be done to investigate potential achalasia?

A

Barium swallow - this show the characteristic birds beak - the oesophagus is dilated and the contrast material slowly passes into the stomach as the sphincter opens intermittently. The image resembles a birds beak. This is in contrast to the rats tail appearance of carcinoma of the oesophagus.

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105
Q

In patients who are fit enough for surgery, what is the first-line treatment for achalasia?

A

Heller myotomy

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106
Q

A patient presents with multiple non-healing leg ulcers, feels generally unwell, and has pale conjunctivae, poor dentition and bleeding gums. What is the most likely cause?

A

Vitamin C deficiency -scurvy - leads to defective synthesis of collagen, resulting in capillary fragility (bleeding tendency) and poor wound healing

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107
Q

What are people with primary sclerosing cholangitis at risk ok?

A

Cholangiocarcinoma (10%)

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108
Q

Which IBD is more associated with primary sclerosing cholangitis?

A

Ulcerative colitis - 80% of patients with PSC have UC

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109
Q

What investigation is gold standard for PSC and what will it show?

A

MRCP - showing multiple biliary strictures giving a ‘beaded’ appearance

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110
Q

Which blood test may be positive for PSC?

A

ANCA

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111
Q

Which blood test may be positive for PBC?

A

Anti-mitochondrial antibody

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112
Q

What is the single stronger risk factor for developing Barrett’s oesophagus?

A

GORD

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113
Q

What is given to patients long-term if they have an episode of spontaneous bacterial peritonitis?

A

Ciprofloxacin

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114
Q

What is the most common cause of spontaneous bacterial peritonitis? - which organism if found of ascitic fluid culture?

A

E.coli

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115
Q

What is spontaneous bacterial peritonitis?

A

It is a form of peritonitis usually seen in patients with ascites secondary to liver cirrhosis - features include ascites, abdominal pain and fever.

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116
Q

What is the management for spontaneous bacterial peritonitis?

A

IV cefotaxime

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117
Q

What is hepatorenal syndrome?

A

It is a complication of end-stage liver disease, which occurs in patients who have chronic liver dysfunction with cirrhosis and ascites, and also in acute liver failure. In hepatorenal syndrome, there is impaired renal function which is often precipitated by events lowering blood pressure. The end result is intra-renal arteriolar vasoconstriction.

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118
Q

What is the criteria for the diagnosis of hepato-renal syndrome in cirrhosis?

A
  1. Cirrhosis with ascites
  2. Serum creatinine >1.5mg/dL
  3. Absence of shock
  4. Absence of hypovolaemia
  5. No current or recent treatment with nephrotoxic drugs
  6. Absence of parenchymal renal disease as defined by proteinuria <0.5g/day and normal renal USS
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119
Q

What is transient elastography?

A

It can be known by its brand name ‘Fibroscan’ and it used a 50-MHz wave passed into the liver from a small transducer on the end of an US probe. It measures the stiffness of the liver which is a proxy for fibrosis/cirrhosis.

120
Q

What is first-line prophylaxis for variceal bleeding?

A

Propanolol

121
Q

What is chronic pancreatitis?

A

It is an inflammatory condition which can ultimately affect both the exocrine and endocrine functions of the pancreas.

122
Q

What is the main cause of chronic pancreatitis, in 80% of cases?

A

Alcohol excess

123
Q

In addition to alcohol, what are the other causes of chronic pancreatitis? (3)

A
  1. Cystic fibrosis
  2. Haemochromatosis
  3. Duct obstruction e.g. tumours, stones, structural abnormalities including annular pancreas
124
Q

What are the features of chronic pancreatitis, how can is present? (4)

A
  1. Pain is typically worse 15-30 minutes following a meal
  2. Steatorrhoea (pancreatic insufficiency)
  3. Severe abdominal pain
  4. Diabetes develops in the majority of patients - typically more than 20 years after symptoms began
125
Q

What investigations are performed for chronic pancreatitis? (3)

A
  1. AXR - shows pancreatic calcification in 30% of cases
  2. CT - pancreatic calcification specificity 85%, sensitivity 80%
  3. Faecal elastase may be used to assess exocrine function
126
Q

What is the management for chronic pancreatitis? (3)

A
  1. Pancreatic enzyme supplements
  2. Analgesia
  3. Antioxidants (limited evidence base - one study suggests benefit in early disease)
127
Q

What type of staging is used in colon cancer?

A

Dukes classification

128
Q

What is Dukes A?

A

The tumour is confined to the muscosa

129
Q

What is Dukes B?

A

The tumour is invading the bowel wall

130
Q

What is Dukes C?

A

The tumour has lymph node metastases

131
Q

What is Dukes D?

A

Distant metastases

132
Q

What are solitary rectal ulcers associated with? (clinical presentation)

A

Chronic constipation and straining with occasional blood being passed

133
Q

What is the first line treatment for fissures in ano? (3)

A
  1. GTN ointment 0.2% or diltiazem cream applied topically is the usual first line treatment.
  2. Botulinum toxin for those who fail to respond.
  3. Spincterotomy for those who fail to respond
134
Q

What are the complications of acute pancreatitis? (6)

A
  1. Peripancreatic fluid collections
  2. Pseudocysts
  3. Pancreatic necrosis
  4. Pancreatic abscess
  5. Haemorrhage
  6. Acute respiratory distress syndrome
135
Q

How often does a peripancreatic fluid collection occur after acute pancreatitis and what happens with it?

A

Occurs in 25% of cases, may resolve to develop into pseudocysts or abscesses. They are managed conservatively as aspiration and drainage may precipitate infection

136
Q

How long after acute pancreatitis do pseudocysts tend to occur?

A

4 weeks or more

137
Q

What is associated with pseudocysts when doing blood tests?

A

A persistent mildly elevated amylase

138
Q

When do pancreatic abscesses occur?

A

Typically as a result of an infected pseudocyst

139
Q

What is the strongest risk factor for anal cancer?

A

HPV infection

140
Q

80% of anal cancers are what? e.g. adenocarcinoma

A

Squamous cell carcinomas

141
Q

Which type of laxative should be prescribed for someone with an anal tissue?

A

Bulk-forming laxatives

142
Q

If someone is being treated correctly for ascending cholangitis and sepsis, yet they remain febrile with rigors, what is the most likely explanation?

A

Abscess or deep-seated infection

143
Q

What is the severe complication B12 deficiency can cause?

A

Subacute combined degeneration of the spinal cord.

144
Q

What are the features of subacute combined degeneration of the spinal cord? (3)

A
  1. Loss of vibration sense
  2. Ataxia
  3. Absent ankle reflexes
145
Q

If someone has a gallstone in the biliary tree but it is not causing jaundice, where is it most likely to be found?

A

Cystic duct (or gallbladder)- the stone cannot be lodged anywhere that would cause a back-up of bile towards the liver

146
Q

What is hepatic encephalopathy?

A

It is defined as a spectrum of neuropsychiatric abnormalities in patients with liver failure, after exclusion of other known brain disease. It can be subdivided ito covert and overt. It develops in up to 50% of people with cirrhosis.

147
Q

What is covert hepatic encephalopathy?

A

It is subclinical - a less severe manifestation of hepatic encephalopathy and requires psychometric testing for diagnosis. It is associated with increased admissions to hospital, and can also affect a persons employment and driving ability.

148
Q

What are the features of hepatic encephalopathy? (7)

A
  1. Personality changes
  2. Intellectual impairment
  3. Reduced levels of consciousness
  4. Confusion
  5. Mood impairment - depression, irritability, euphoria
  6. Amnesia
  7. Coma
149
Q

What are the common precipitants for hepatic encephalopathy? (8)

A
  1. AKI
  2. Electrolyte imbalance
  3. GI bleeding
  4. Infection
  5. Constipation
  6. Sedative drugs e.g. benzodiazepines, opiates, antidepressants, antipsychotic drugs
  7. Diuretics
  8. High protein intake
150
Q

What is the grading for hepatic encephalopathy?

A

Grade 0 = sub-clinical, normal mental status but minimal changes to memory, concentration and intellectual function and co-ordination.
Grade I = mild confusion, euphoria, depression, decreased attention slow ability to perform mental tasks, irritability, disordered sleep cycle
Grade 2 = drowsiness, lethargy, gross deficits in ability to perform mental tasks, personality changes, inappropriate behaviour, intermittent disorientation
Grade 3 = somnolent but rousable, unable to perform mental tasks, disorientation to time and place, marked confusion, amnesia, speech present but incomprehensible
Grade 4 = coma, with or without response to painful stimuli

151
Q

What are the signs for people with mild-moderate hepatic encephalopathy? (4)

A
  1. Flapping tremor (asterixis)
  2. Fetor hepaticus (a sweet musty aroma of the breath)
  3. Hyperventilation
  4. Hypothermia
152
Q

What investigations are performed in suspected hepatic encephalopathy? (4)

A
  1. Psychometric tests - this is very useful in the diagnosis of sub-clinical hepatic encephalopathy
  2. Arterial or serum ammonia levels (will be raised)
  3. ECG (apparently useful prognostically)
  4. MRI/CT scan - exclude other causes of altered mental state e.g. intracranial lesions
153
Q

What are the differential diagnoses for hepatic encephalopathy? (7)

A
  1. Intracranial lesions - haemorrhage, tumour
  2. Infection - meningitis, intracranial abscess
  3. Metabolic - hypoglycaemia, AKI
  4. Other causes of hyperammonaemia e.g. ureterosigmoidostomy, inherited urea cycle disorders
  5. Toxic - substance abuse
  6. Drugs - sedative hypnotics, antidepressants
  7. Post-seizure
154
Q

What is the management of hepatic encephalopathy? (5)

A
  1. Early diagnosis and aggressive identification and management of precipitating factors
  2. Avoidance of sedative drugs
  3. Lactulose - this reduces the absorption of gut-derived neurotoxins, particularly ammonia
  4. Neomycin or other ABX to reduce the amino acid production by decreasing the conc. of ammonia-forming colonic bacteria
  5. Flumazenil
155
Q

What drug can be given to reduce the recurrence of episodes of overt hepatic encephalopathy in adults?

156
Q

What is a hiatus hernia?

A

It refers to the herniation of a part of the abdominal viscera through the oesophageal aperture of the diaphragm. The vast majority involve only the herniation of a part of the gastric cardia through the muscular hiatal aperture of the diaphragm, however, rarely, larger ones can allow other organs to enter the thoracic cavity such as the spleen and pancreas

157
Q

What are the risk factors for developing a hiatus hernia? (9)

A
  1. Obesity
  2. Pregnancy
  3. Ascites
  4. Increasing age
  5. Genetic predisposition
  6. Shortening of the oesophagus - thought to occur by virtue of reflex contraction of oesophageal longitudinal muscles, evoked by intraluminal acid
  7. Previous GI surgery
  8. Trauma to the chest and abdomen
  9. Skeletal deformities e.g. scoliosis, kyphosis, and pectus excavatum
158
Q

What is Budd-Chiari syndrome?

A

A condition which occurs when there is obstruction of the hepatic veins. It includes any condition in which where is obstruction to venous flow from the small hepatic veins to the interior vena cava.

159
Q

What are the haematological causes of Budd-Chiara syndrome?

A
  1. Polycythaemia vera
  2. Thrombophilic conditions e.g. deficiency protein C, S, factor V Leiden
  3. Anti-phospholipid syndrome
  4. Post bone marrow transplant
160
Q

Where is the cut off for an upper GI bleed compared to a lower GI bleed?

A

Ligament of treitz (duodenum - jejunum border)

161
Q

Name 4 common causes of frank haematemasis?

A
  1. Oesophageal varices
  2. Mallory-Weiss tears
  3. Gastric/duodenal ulcers
  4. Oesphagitis
162
Q

What are the criteria in the Glasgow-Blatchford score used to calculate the risk of an upper GI bleed and need for urgent endoscopy? (8)

A
  1. Blood pressure
  2. Heart rate
  3. Urea
  4. Haemoglobin
  5. Melaena
  6. History of liver disease
  7. History of heart and renal failure
  8. Syncope
163
Q

List some alarming features associated with dyspepsia that would indicate investigation for malignancy? (6)

A
  1. Weight loss
  2. Iron-deficiency anaemia
  3. Age >50
  4. Not responding to PPI treatment for GORD
  5. Dysphagia
  6. Epigastric mass
164
Q

What is the blood test used to detect coeliac disease?

A

Anti-TTG

IgA Anti-tissue Transglutaminase Antibody

165
Q

Which types of laxatives should be used first line in adults with chronic constipation with no sinister features? (2)

A
  1. Bulk forming laxatives e.g. ispaghula husk
  2. Stool softeners e.g. lactulose
    A mixed preparation like Movicol can also be useful
166
Q

What is the first-line treatment for hepatic encephalopathy?

A

Lactulose –> removal of ammonia/acids/neurotoxins from the GI tract, stops absorption
Neomycin (ABX) can also be used

167
Q

How much weight loss as a % warrants further investigation for unintentional weight loss?

168
Q

Which drug is used first line in acute alcohol withdrawal for treatment of symptoms?

A

Chlordiazepoxide

169
Q

Which blood tests should be monitored in a patient with refeeding syndrome? (4)

A
  1. U&Es
  2. Phosphate
  3. Magnesium
  4. Calcium
    - initially monitored every 24 hours for the first 4 days
170
Q

Name some causes of portal hypertension? (5)

A
  1. Cirrhosis
  2. Budd-Chiari syndrome
  3. Congenital biliary atrasia
  4. Compression tumour
  5. Portal vein thrombosis
171
Q

On examination of the hands, what features may be found in someone with liver cirrhosis? (6)

A
  1. Flapping tremor
  2. Clubbing
  3. Leukonychia (caused by low albumin)
  4. Palmar erythema
  5. Dupuytren’s contract
  6. Bruising
172
Q

How is non-alcoholic fatty liver disease (NAFLD) managed?

A
  1. Lifestyle - weight loss, vitamins, cholesterol lowering, sometimes urosdeoxycholic acid (helps the flow of bile if fat is obstructing this)
  2. TIPS procedure
173
Q

Name some causes of ascites? (5)

A
  1. Cirrhosis
  2. Nephrotic syndrome
  3. Heart failure
  4. Meigs syndrome
  5. Malignancy
174
Q

What is the definition of acute severe UC?

A 
1. >6 bloody stools per day 
AND
2. Systemic toxicity (one of the following):
-Temperature >37.8
-Heart rate >90
-Hb <105g/l
-CRP >30mg/l
175
Q

What are the baseline investigations when someone presents with an acute severe flare of UC? (4)

A
  1. FBC, U&E, LFTs, magnesium
  2. Stool microbiology and C.diff
  3. Radiology (AXR or CT)
    Second line screening for:
  4. Hep B and C, HIV and VZV, TB
176
Q

If someone with an acute severe flare of UC is found to be C.diff positive, what is the treatment?

A

Vancomycin PO 500mg 6-hourly for 10 days

177
Q

What is the standard management for acute severe UC? (3)

A
  1. IV hydrocortisone 100mg 6-hourly OR IV methylprednisolone 60-80mg daily
  2. LMWH prophylaxis
    (considered withholding 5-ASA)
  3. Sigmoidoscopy within 24 hours including CMV screen
178
Q

If in the treatment of acute severe UC, there is no resolve after 3 days with IV steroids, what treatment can be added second line - and what happens if the second line therapy doesn’t help?

A

IV infliximab 5mg/kg OR IV ciclosporin 2mg/kg

If these treatments don’t work then colectomy/emergency colectomy is required

179
Q

If the IV steroids helps in the treatment of acute severe UC, what can then happen after 3 days?

A
  1. Switch to oral prednisolone 40mg daily
  2. Commence thiopurine if not already receiving
  3. Recommence 5-ASA if had been withheld
180
Q

What is the first line treatment for mild-moderate acute proctitis/UC?

A

Step 1. Start 1g 5-ASA suppository once daily (usually at night)

181
Q

If the 5-ASA suppository for mild/moderate UC does not work, what treatment can be added?
If this treatment doesn’t work, what is next in the treatment ladder?

A

Step 2. Oral 5-ASA 2-3grams
-no resolve
Step 3. Corticosteroid suppository e.g. 5mg prednisolone and continue oral 5-ASA with dose increased to 4-4.8g daily

182
Q

What is first line treatment for severe/extensive proctitis/UC and also step 4 for mild/moderate?

A

Oral prednisolone 40mg OD, weaning over 6-8 weeks to induce remission

If this doesn’t work, biologic therapy will be considered for induction and/or maintenance of remission

183
Q

In UC, where does it start and finish (pathology location)?

A

Begins in the rectum and extends proximally, stopping at the ileocaecal junction

184
Q

Macroscopically and microscopically what are the features of UC? (10)

A 
Macroscopic: 
1. Continuous
2. Reddened mucousa
3. Shallow ulcers
4. Inflammation that bleeds easily 
5. Loss of mucosal folds and haustra
6. Strictures
7. Pseudopolyps 
Microscopic:
8. Only affects the lamina propria - mucosal/submucosal 
9. Goblet cell depletion 
10. Crypt abscesses
185
Q

What are the macroscopic and microscopic features of Crohn’s disease? (12)

A 
Macroscopic:
1. Skip lesions
2. Thickened bowel
3. Narrowed lumen
4. Deep ulcers
5. Mucosal fissures
6. Cobblestone appearance 
7. Fistulae (30%)
8. Abscesses (50%)
9. Aphthoid ulcers 
Microscopic:
10. Transmural
11. Lymphoid hyperplasia
12. Non-caseating granulomas (Langhan's cells)
186
Q

What are the presenting complaints for both Crohn’s and UC? (3 for Crohn’s and 4 for UC)

A 
Crohns:
1. Diarrhoea
2. Abdominal pain - RLQ +/- mass
3. Weight loss
Ulcerative colitis
1. Bloody diarrhoea
2. Abdominal pain - most before/during defecation 
3. Mucus PR
4. Tenesmus/faecal urgency
187
Q

What are the extra-intestinal eye manifestations in both UC and Crohn’s? (3)

A
  1. Uveitis
  2. Episcleritis
  3. Conjunctivitis
188
Q

What are the extra intestinal manifestations for joints in both UC and Crohn’s? (1)

A

Ank sponk (HLA-B27)

189
Q

What joint manifestations are reported just in people with Crohn’s? (2)

A
  1. Arthralgia

2. Inflammatory back pain

190
Q

What joint manifestations can occur in people with UC? (2)

A
  1. OA

2. Sacrolitis

191
Q

What are the extra intestinal skin manifestations for both Crohn’s and UC?

A
  1. Erythema nodosum

2. Pyoderma gangrenosum

192
Q

What is the hepatobiliary extra intestinal manifestation that can occur in both Crohn’s and UC, and which one does it far more commonly occur in?

A

Primary sclerosing cholangitis - more common in UC

193
Q

In addition to faecal calprotectin, what else is tested in a stool sample which will be raised in bowel inflammation?

A

Lactoferrin

194
Q

What can be seen on AXR in UC? (2)

A
  1. Lead pipe colon due to loss of haustra

2. Distention - toxic megacolon

195
Q

What can be seen on AXR in Crohn’s? (1)

A

Bowel distention - toxic megacolon

196
Q

What can be seen on USS for both UC and Crohn’s?

A

Bowel wall thickening

197
Q

In terms of treatment, what is first line for someone with Crohn’s?

A

Azathioprine and mercaptopurine

198
Q

How is hepatitis A spread?

A

Faeco-oral route

199
Q

What blood test can be performed for UC but not Crohn’s?

200
Q

In the management of an upper GI bleed, what should be done?

A
  1. An A-E assessment
  2. New set of obs
  3. Calculate Glasgow-Blatchford score
  4. BLOOD TRANSFUSION if Hb <70
  5. Vitamin K if PT>13.5
  6. FFP if PT >20
  7. Platelets if <50
201
Q

Why is a CXR performed in someone with an upper GI bleed?

A

They may have aspirated or had an oesophageal perforation

202
Q

In addition to the A-E assessment and transfusions, what else is given to patients with oesophageal varices?

A
  1. Terlipressin 2mg IV stat

2. Ciprofloxacin 200mg IV BD

203
Q

In someone who presented with upper GI bleed who has since had an endoscopy what is the management if it is non-variceal?

A
  1. 72-hour PPI infusion

2. Stop NSAIDs

204
Q

If someone had a GI bleed due to duodenal ulcer, what is the treatment? (3)

A

Most common cause of duodenal ulcers is H.pylori. Triple eradication therapy:

  1. PPI
  2. Clarithromycin
  3. Amoxicillin OR metronidazole
205
Q

What is the treatment for gastric ulcers?

A

After PPI and stopping any NSAID use, re-scope for biopsy prior to discharge as there is a high risk of malignancy. If H.pylori infection then treat using triple eradication therapy.

206
Q

What is the treatment for post-endoscopy variceal bleeds?

A
  1. Terlipressin 2mg QDS for 5 days
  2. Ciprofloxacin 72 hours
  3. Propanolol - causes a decrease in portal vein pressure so reduces the risk of bleeding
207
Q

What does terlipressin do for post-endoscopy variceal bleeding?

A

Terlipressin reduces the portal vein pressure and decreases the pressure in oesophageal varices

208
Q

Why are antibiotics prescribed post-variceal bleed?

A

They reduce the risk of spontaneous bacterial peritonitis

209
Q

During endoscopy for upper GI bleeds, what is done to treat ulcers and varices respectively?

A 
Ulcers = Adrenaline and haemospray
Varices = band ligation
210
Q

In terms of the Glasgow-Blatchford scale, what score would mean same day endoscopy?

A

A score >5

211
Q

What are the functions of the liver? (5)

A
  1. Excretion of bilirubin
  2. Excretion of oestrogen
  3. Production of clotting factors
  4. Production of albumin
  5. Filter blood from GI tract back to the heart in portal venous system
212
Q

What are the two types of cirrhosis?

A

Compensated and decompensated

213
Q

Dieulafoy’s lesion …

A

Upper GI bleed - lesion found in stomach

A Dieulafoy lesion is a tortuous arteriole, typically located in the upper stomach, which cause an upper GI bleed

214
Q

What is Boerhaave syndrome?

A

The Mackler triad for Boerhaave syndrome: vomiting, thoracic pain, subcutaneous emphysema. It typically presents in middle aged men with a background of alcohol abuse.

215
Q

Which test is recommended for H.pylori post-eradication therapy?

A

Urea breath test

216
Q

What is the urea breath test?

A

Urea breath test
- Patients consume a drink containing carbon isotope 13 (13C) enriched urea
- Urea is broken down by H. pylori urease
- After 30 mins patient exhale into a glass tube
- Mass spectrometry analysis calculates the amount of 13C CO2
-Should not be performed within 4 weeks of treatment with an antibacterial or within 2 weeks of an antisecretory drug (e.g. a proton pump inhibitor)
sensitivity 95-98%, specificity 97-98%
- May be used to check for H. pylori eradication

217
Q

A gastric volvulus presents with a triad of what features?

A
  1. Vomiting
  2. Pain
  3. Failed attempts at inserting an NG tube
218
Q

How does Budd-Chiari present? (3)

A

Triad of:

  1. Acute abdominal pain - sudden onset and severe
  2. Ascites
  3. Tender hepatomegaly
219
Q

What are the causes of Budd-Chiari syndrome? (4)

A
  1. Polycythaemia ruba vera
  2. Thrombophilia
  3. Pregnancy
  4. Oral contraceptive pill
220
Q

What is the recommended investigation for someone with suspected Budd-Chiari syndrome?

A

USS dopper flow studies

221
Q

What are the common precipitants for decompensation in people with liver failure/cirrhosis/chronic hep B etc? (6)

A
  1. Constipation
  2. Infection
  3. Electrolyte imbalances
  4. Dehydration
  5. Upper GI bleeds
  6. Increased alcohol intake
222
Q

What is the most likely cause of an isolated rise in bilirubin in a young patient?

A

Gilberts syndrome

223
Q

What is carcinoid syndrome?

A

It usually occurs when metastases are present in the liver and release serotonin into the systemic circulation. It may also occur with lung carcinoid as mediators are not cleared by the liver

224
Q

What are the features of carcinoid syndrome?

A
  1. Flushing (often earliest symptom)
  2. Diarrhoea
  3. Bronchospasm
  4. Hypotension
  5. Right heart valvular stenosis
  6. Cushing’s syndrome
  7. Pellagra
225
Q

What is the diagnostic marker for carcinoid syndrome?

A

A 24 hour urine collection which shows 5-HIAA (5-hydroxyindoleacetic acid)

226
Q

What is the treatment for carcinoid syndrome?

A
  1. Somatostatin analogues - octreotide

2. Cyproheptadine

227
Q

When should PPIs be stopped before upper GI endoscopy?

A

2 weeks prior to the procedure - so that pathology can be seen

228
Q

In IBD, which one has an increase in goblet cells and which one a decrease?

A 
Crohns = increase in goblet cells
UC = decrease
229
Q

In IBD, which one is colorectal cancer more common?

230
Q

For an oesophageal cancer, which mode of investigation is best to assess mural invasion?

A

Endoscopic ultrasound

231
Q

How can you differentiate between type 1 and 2 hepatorenal syndrome?

A

Type 1 develops acutely (<2 weeks) whereas type 2 develops more chronically and is associated with a gradual decline in renal function

232
Q

What is hepatorenal syndrome and when does it occur?

A

It is a complication of end-stage liver disease - people with CKD with ascites and cirrhosis, and also acute liver failure. There is impaired renal function which is often precipitated by events lowering blood pressure.

233
Q

What can precipitate/risk factors for hepatorenal syndrome? (4)

A
  1. Spontaneous bacterial peritonitis - 30% will develop HRS
  2. GI bleed
  3. Superimposed infection e.g. pneumonia
  4. Alcoholic hepatitis
234
Q

What is the criteria in order for diagnosis of hepatorenal syndrome? (6)

A
  1. Cirrhosis with ascites
  2. Serum creatinine >1.5mg/dL
  3. Absence of shock
  4. Absence of hypovolaemia
  5. No current or recent treatment with nephrotoxic drugs
  6. Absence of parenchymal renal disease (<0.5g/day of proteinuria), normal renal USS
235
Q

How is type 1 hepatorenal syndrome defined?

A

Doubling of serum creatinine in less than 2 weeks and a very low eGFR (<20). Associated with a very poor prognosis, and precipitated by events such as variceal bleed, spontaneous bacterial peritonitis

236
Q

How is type 2 hepatorenal syndrome defined?

A

A more gradual decline in renal function, associated with serum retention and refractory ascites

237
Q

Which electrolyte abnormalities are common in HRS? (2)

A
  1. Hyperkalaemia - should be treated aggressively

2. Hyponatraemia - dilutional

238
Q

What is the management of type 1 HRS? (4)

A
  1. Admit to hospital, monitor fluid status closely, restrict fluids in necessary, treat any infections and avoid nephrotoxic drugs
  2. Splanchnic vasoconstrictors - terlipressin + albumin replacement
  3. TIPS - transjugular intrahepatic portosystemic shuunt
  4. Liver transplantation
239
Q

How does terlipressin help in HRS?

A

It leads to an increased blood pressure and GFR, through constriction of splanchnic blood vessels (alternatives include noradrenaline or midodrine)

240
Q

What does TIPS do?

A

It reduces ascites in patients with portal hypertension

241
Q

What is the treatment for type 2 HRS?

A
  1. Diuretics and sodium restriction
  2. Paracentesis to control gross ascites
  3. TIPS sometimes indicated
    (Type 2 may need to be treated the same as type 1)
242
Q

Is there anything that can be given to prevent HRS?

A

Albumin administration, especially in patients with bacterial peritonitis

243
Q

Why is albumin given when treating large volume ascites through paracentesis?

A

It reduces post-paracentesis circulatory dysfunction

244
Q

What are signet ring cells associated with?

A

Gastric adenocarcinoma

245
Q

How many units of alcohol are in a bottle of wine 12%?

246
Q

What are the most common organisms to cause pyogenic liver abscesses in adults and children?

A 
Adults = E.coli
Children = Staph.aureus
247
Q

What is the first line treatment for pyogenic liver abscesses?

A

IV ABX + image-guided percutaneous drainage

248
Q

Whats is the last resort option for treatment of anal fissures after all medical options have been tried?

A

Sphincterotomy - it releases the painful spasms of the torn sphincter with a clean incision and accelerates healing

249
Q

What condition can cause pain on swallowing (odynophagia) and is a complication of inhaled steroid therapy?

A

Oesophageal candidiasis

250
Q

Kantor’s string sign is seen in which condition?

A

Crohn’s - it is a string like configuration in keeping with a stricture seen on barium study

251
Q

What is the first line treatment for autoimmune hepatitis?

252
Q

What is the first-line treatment for primary biliary sclerosis?

A

Ursodeoxycholic acid

253
Q

What is Zollinger-Ellison syndrome, and what is it associated with?

A

It is the presentation of epigastric pain and diarrhoea due to multiple peptic ulcers. High-dose PPIs are given.
1/3 of these patients have MEN type 1.

254
Q

What is MEN-1 commonly associated with?

A

Hyperparathyroidism

255
Q

What is central pontine myelinolysis?

256
Q

Which artery supplies the foregut?

257
Q

Which artery supplies the midgut?

A

Superior mesenteric artery

258
Q

Which artery supplies the hindgut?

A

Inferior mesenteric artery

259
Q

Where is the pain most commonly in Crohn’s disease, and where is it commonly in ulcerative colitis?

A 
Crohn's = RIF
UC = LIF
260
Q

Intestinal angina, is also known as what?

A

Chronic mesenteric ischaemia

261
Q

What is intestinal angina classically characterised by? - a triad

A
  1. Severe, colicky post-prandial abdominal pain
  2. Weight loss
  3. Abdominal bruit
262
Q

What are the features of mesenteric ischaemia? (5)

A
  1. Typically affects the small bowel
  2. Due to embolism
  3. Sudden onset, severe symptoms
  4. Requires urgent surgery
  5. High mortality rates
263
Q

What are the features of ischaemic colitis? (5)

A
  1. Affects the large bowel typically
  2. Mulifactorial
  3. Transient, less severe symptoms, including blood diarrhoea
  4. ‘Thumbprinting’
  5. Conservative management
264
Q

What are the common features of bowel ischaemia? (5)

A
  1. Abdominal pain - in acute mesenteric ischaemia this is often sudden severe and out of keeping with physical exam findings
  2. Rectal bleeding
  3. Diarrhoea
  4. Fever
  5. Bloods typically show an elevated WCC with a lactic acidosis
265
Q

What is involved in an emergency Hartmann’s procedure?

A

It is the resection of the rectosigmoid colon - an end colostomy is formed and rectal stump sewn. It is indicated by perforation of the rectosigmoid bowel and subsequent peritonitis.

266
Q

If a colorectal cancer site is: caecal, ascending or proximal transverse colon, what type of resection will be performed and what type of anastomosis?

A

Right hemicolectomy, forming an ileo-colic anastmosis

267
Q

If the sigmoid colon is found to be cancerous, what type of resection will be performed?

A

High anterior resection

268
Q

If the distal transverse or descending colon is found to be cancerous, what type of resection will be performed?

A

A left hemicolectomy

269
Q

Autoimmune hepatitis is associated with positive blood results for which antibodies? (2)

A

Anti-nuclear antibody and anti-smooth muscle antibodies

270
Q

What is Sister Mary Josephs node?

A

A palpable nodule in the umbilicus due to a metastasis of malignant cancer within the pelvis or abdomen

271
Q

Which cancer is the second most commonly associated with HPNCC?

A

Endometrial

272
Q

Coeliac disesae increases the risk of developing which type of cancer?

A

Enteropathy-associated T cell lymphoma

273
Q

Which blood tests should be performed in someone with suspected coeliac disease? (2)

A

Total IgA and IgA TTG

274
Q

Which gene is associated with HPNCC?

275
Q

What is the triad for acute liver failure?

A
  1. Encephalopathy
  2. Jaundice
  3. Coagulopathy
276
Q

What is the most common cause of hepatocellular carcinoma in the UK?

A

Hepatitis C

277
Q

Which investigation is the standard procedure of choice to diagnose primary sclerosing cholangitis?

278
Q

What are the features of carcinoid syndrome? (7)

A
  1. Flushing
  2. Diarrhoea
  3. Bronchospasm
  4. Hypotension
  5. Right heart valvular stenosis
  6. Pellagra
  7. Cushing’s syndrome
279
Q

When does carcinoid syndrome occur?

A

Usually as a result of carcinoid tumour - when metastases are present in the liver and release serotonin into the systemic circulation. May also occur in lung carcinoid as mediators are not cleared by the liver.

280
Q

What are the investigations of choice in suspected carcinoid syndrome? (2)

A
  1. Urinary 5-HIAA

2. Plasma chromogranin A y

281
Q

What is the treatment for carcinoid syndrome?

A

Somatostatin analogues e.g. octreotide

282
Q

Why is epidural analgesia indicated instead of other routes for patients post-operatively on GI wards?

A

Epidural analgesia helps to accelerate the return of normal bowel function after abdo surgery

283
Q

Achalasia increases the risk of which type of oesophageal cancer?

A

Squamous cell carcinoma

284
Q

Pigmented gallstones are associated with which condition?

A

Sickle cell anaemia

285
Q

What is given first line to treat acute severe alcoholic hepatitis?

A

Corticosteroids

286
Q

Which scoring system is used to determine severity of alcoholic hepatitis?

287
Q

What is the management for acute cholecystitis?

A

IV antibiotics + laparoscopic cholecystectomy within 1 week

288
Q

What is acute cholecystitis?

A

It describes inflammation of the gallbladder.

289
Q

What are the features of acute cholecystitis? (4)

A
  1. RUQ pain
  2. Fever and signs of systemic upset
  3. Mildly deranged LFTs (especially if Mirizzi syndrome)
  4. Murphys sign (inspiratory arrest upon palpation of the RUQ)
290
Q

What is the difference between acute cholecystitis and ascending cholangitis?

A

Acute cholecystitis is inflammation of the gallbladder wall, with RUQ pain and fever (raised WBC and CRP) whereas ascending cholangitis is obstruction and stasis within the biliary tract leading to a bacterial infection. Presenting with charcot’s triad or Reynolds pentad (RUQ pain, fever, jaundice, confusion, hypotension), with raised WBC, CRP, ALP, AST, ALT and bilirubin.

291
Q

If a colorectal tumour is found to involve the anal sphincter, what type of resection is required?

A

Abdominoperineal (AP) resection

292
Q

Chagas disease can cause what type of bowel obstruction?

A

Sigmoid volvulus

293
Q

If someone is found to has a gastric MALT lymphoma, what is the treatment?

A

H.pylori eradication

294
Q

What diagnosis should be considered in young female patients presenting with AKI after initiation of an ACE inhibitor?

A

Fibromuscular dysplasia

295
Q

What is fibromuscular dysplasia?

A

It describes the proliferation of cells in the walls of the arteries, causing the vessels to bulge or narrow. It is an idiopathic, segmentary, non-inflammatory and non-atherosclerotic disease that can affect all layers of both small and medium sized vessels. It most commonly affects the renal arteries. Radiologists play an important role in its diagnosis as the string of beads signs is commonly seen.

296
Q

Passmed Q - A 22 year old female with a history of diarrhoea and weight loss has a colonoscopy which shows on biopsy: pigment laden macrophages suggestive of melanosis coli. What is this associated with?

A

Laxative abuse

Year 5 Core Conditions (25 decks)

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