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MRCP > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

Which drugs can cause pancreatitis?

A

Steroids And Alcohol are Very Demanding For My Pancreas

Steroids

Azathioprine

Alcohol

Valproate (Na)

Didanosine

Furosemide, also bendroflumethiazide

Mesalazine

Pentamidine

*pancreatitis is 7 times more common in patients taking mesalazine than sulfasalazine

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2
Q

Symptoms of pancreatitis?

A

Gradual/sudden severe epigastric or central abdo pain
o Radiates to the back, relieved on sitting forward
Vomiting

Signs:

  • Tachycardia, fever, jaundice, shock
  • Periumbilical bruising (Cullen’s sign)
  • Flank bruising (Grey Turner’s sign)
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3
Q

What AXR finding might you see in pancreatitis?

A

Sentinel loop

A sentinel loop is a short segment of adynamic ileus close to an intra-abdominal inflammatory process.

The sentinel loop sign may aid in localising the source of inflammation. For example, a sentinel loop in the upper abdomen may indicate pancreatitis, whilst one in the right lower quadrant may be due to appendicitis.

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4
Q

Complications of acute pancreatitis?

A

Early – shock, renal failure (give lots of fluid), DIC, sepsis
Late – Pancreatic necrosis + pseudocyst (fluid in lesser sac), abscess, bleeding (from elastase enzyme – produced in the pancreas – eroding a major vessel), thrombosis

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5
Q

What scoring systems do we use in acute pancreatitis and when?

A

48hrs after onset
Glasogw-Imrie Pancreatitis Criteria
3+ indicates severe pancreatitis

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6
Q

What is HELLP syndrome?

A

Haemolysis, elevated LFTs, low platelets
Unclear cause, more common in preeclampsia/eclampsia

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7
Q

Tumour markers and related Ca?
Alpha-fetoprotein (FP)
Calcitonin
CA 125
CA 19-9
CA15-3
CEA
-hCG
Paraproteins
Thyroglobulin

A

Alpha-fetoprotein (FP) - Germ cell/testicular or Hepatocellular
Calcitonin - Medullary thyroid
CA 125 - Ovarian
CA 19-9 - Pancreatic
CA15-3 - Breast
CEA - Colorectal
-hCG - Germ cell/testicular or Gestational trophoblastic
Paraproteins - Myeloma
Thyroglobulin - Thyroid

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8
Q

Bowel Ca screening?

A

UK screening:
NHS Bowel Cancer Screening Programme
• Offers screening every 2 years to all men/women aged 60-75 (increased to 56 year olds also)
• Uses faecal occult blood home testing kits (FIT test)
• Test 1 bowel motions
• Approx. 2% of tests are positive  then offered a specialist nurse appt + colonoscopy
• Reduces RR of death by 16%

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9
Q

What proportion of people with a positive FIT test will have Ca?

A

At colonoscopy, approximately:
5 out of 10 patients will have a normal exam
4 out of 10 patients will be found to have polyps which may be removed due to their premalignant potential
1 out of 10 patients will be found to have cancer

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10
Q

Complications of liver failure?

A

o Liver failure –
Coagulopathy ( F2, 7, 9, 10 causes INR)
Encephalopathy (liver flap, confusion)
Hypoalbuminaemia (oedema, leukonychia)
Sepsis (pneumonia, septicaemia)
Spontaneous bacterial peritonitis (SBP)
Hypoglycaemia

o Portal hypertension –
Ascites
Splenomegaly
Portosystemic shunt including oesophageal varices

o Increased risk of HCC

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11
Q

What is the gender divide for PBC?

A

F>M 9:1

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12
Q

What is the pathophysiology of PBC?

A

Interlobular bile ducts become damaged by a chronic inflammatory process causing progressive cholestasis which may eventually progress to cirrhosis. The classic presentation is itching in a middle-aged woman

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13
Q

Associated conditions with PBC?

A

Sjogren’s syndrome (seen in up to 80% of patients)
rheumatoid arthritis
systemic sclerosis
thyroid disease

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14
Q

Which Abs are positive in PBC?

A

AMA 98%
Smooth muscle Abs in 30%

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15
Q

Management of PBC?

A

first-line: ursodeoxycholic acid
slows disease progression and improves symptoms
pruritus: cholestyramine
fat-soluble vitamin supplementation
liver transplantation
e.g. if bilirubin > 100 (PBC is a major indication)
recurrence in graft can occur but is not usually a problem

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16
Q

Complications of PBC?

A

cirrhosis → portal hypertension → ascites, variceal haemorrhage
osteomalacia and osteoporosis
significantly increased risk of hepatocellular carcinoma (20-fold increased risk)

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17
Q

What is the blood test picture for PBC?

A

Bloods – raised: alk phos, gamma-GT and mildly raised AST + ALT
In later disease = raised bilirubin, low albumin, raised PTT

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18
Q

Which drugs can cause hepatocellular damage?

A

nitrofurantoin

V: Valproate
A: Amiodarone
M: Methyldopa
P: Pyrazinamide
I: Isoniazid
R: Rifampicin
E: PhenYtoin (sounds like “E”)
S: Simvastatin

Largely TB and neuro drugs ^

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19
Q

Which drugs can cause cholestasis?

A

combined oral contraceptive pill
antibiotics: flucloxacillin, co-amoxiclav, erythromycin*
anabolic steroids, testosterones
phenothiazines: chlorpromazine, prochlorperazine
sulphonylureas
fibrates
rare reported causes: nifedipine

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20
Q

Which drugs can cause liver cirrhosis mam?

A

methotrexate
methyldopa
amiodarone

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21
Q

Tumour markers

A

Alpha-fetoprotein (FP) -> Germ cell/testicular or Hepatocellular
Calcitonin -> Medullary thyroid
CA 125 -> Ovarian
CA 19-9 -> Pancreatic
CA15-3 -> Breast
CEA -> Colorectal
-hCG -> Germ cell/testicular or gestational trophoblastic
Paraproteins -> Myeloma
Thyroglobulin -> Papillary + follicular Thyroid

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22
Q

Which type of mets can be treated with curative intent?

A

Colorectal Ca mets, usually to liver

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23
Q

What are the most common histological type of colorectal Ca?

A

adenocarcinomas

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24
Q

What age does bowel cancer screening start and how often?

A

60-75, every two years

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25
Q

What does the gas look like in excessive alcohol use?

A

Metabolic ketoacidosis
Elevated anion gap
Normal or low glucose

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26
Q

What is the anion gap?

A

The anion gap is a measurement of the difference-or gap-between the negatively charged and positively charged electrolytes
Na+ – (Cl- + HCO3-)
Causes of high anion gap: lactate, toxins, ketones, renal

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27
Q

What causes Wernicke’s encephalopathy?

A

Lack of B1

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28
Q

What are the symptoms of Korsakoff’s?

A

Confabulation

Lack of insight

Apathy

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29
Q

What are the symptoms of ALD?

A
  • Malaise
  • Anorexia
  • D&V
  • Tender hepatomegaly +/- jaundice
  • Bleeding
  • Ascites
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30
Q

How to treat ALD?

A

Stop alcohol (e.g. with chlordiazepoxide)
Vit K 3/7 + thiamine
Prednisolone 5/7

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31
Q

How do you determine the need for steroids in ALD?

A

Maddrey score (looks at prothrombin time and bilirubin)
If score <32, pt has mild-mod alc liver disease
If >32, patient has severe alc hepatitis and may need steroids

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32
Q

What is Budd-Chiari syndrome?

A

Hepatic vein thrombosis

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33
Q

What causes Budd-Chiari syndrome?

A

polycythaemia rubra vera
thrombophilia
combined oCP: accounts for around 20% of cases
pregnancy

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34
Q

What is the triad of symptoms in Budd-Chiari syndrome?

A

abdominal pain: sudden onset, severe
ascites → abdominal distension
tender hepatomegaly

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35
Q

How do you investigate for Budd-Chiari syndrome?

A

USS with doppler flow studies - first line
Hepatic venogram

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36
Q

What are the side effects of Omeprazole?

A

Diarrhoea (risk of C. diff)
Abdo pain
Vomiting

Microscopic colitis

Hyponatraemia, hypomagnesaemia

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37
Q

What is the most common histological type of pancreatic cancer?

A

Adenocarcinoma

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38
Q

What are the RFs for pancreatic cancer?

A

age, smoking, DM, chronic pancreatitis, HNPCC, BRCA2 gene

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39
Q

Presentation of pancreatic cancer?

A
  • PAINLESS jaundice
  • Courvoisier’s law – painless obstructive jaundice + a palpable GB is unlikely to be gallstones
  • Anorexia, WL, epigastric pain
  • Loss of exocrine function – steatorrhoea
  • Loss of endocrine function – DM
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40
Q

Management of pancreatic Ca?

A

<20% suitable for surgery
Whipple’s resection (pancreaticoduodenectomy) is performed for resectable lesions in the head of the pancreas
Adjuvant chemo following surgery
Palliation – ERCP + stenting

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41
Q

What might you see on USS in pancreatic cancer?

A

the ‘double duct’ sign - the presence of simultaneous dilatation of the common bile and pancreatic ducts

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42
Q

What is the role of D-cells?

A

Produce somatostatin (inhibits HCl)

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43
Q

What is the role of G-cells?

A

Produce gastrin (stimulates HCl)

Important in Zollinger-Ellison syndrome

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44
Q

What is the role of gastric parietal cells?

A

Produce acid (HCl) + intrinsic factor

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45
Q

What is the role of enterochromaffin cells?

A

Produce histamine (stimulates HCl)

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46
Q

What is the role of chief cells?

A

Produce pepsinogen (converted to pepsin which helps to break down proteins)

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47
Q

What is the most common form of inherited colon cancer?

A

HNPCC

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48
Q

What is Peutz-Jeghers syndrome?

A

Condition where you can develop hamartomatous polyps (benign growth)

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49
Q

What is Dubin-Johnson Syndrome?

A

Benign AR liver condition
Defective excretion of bilirubin into the bile
Caused by a defective transporter protein (MRP2)

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50
Q

What can be used to reverse the effect of dabigatran (anticoagulant)?

A

Idarucizumab (Praxbind)

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51
Q

When should you give a platelet transfusion in GI bleed?

A

If platelets <30 in normal people

Consider if plts <100 in patients with severe bleeding or bleeding at a critical site

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52
Q

What should you give to a patient actively bleeding on warfarin?

A

Prothrombin Complex Concentrate

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53
Q

Which three class of drugs commonly cause dyspepsia?

A

NSAIDs
bisphosphonates
steroids

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54
Q

What is Crohn’s Disease and which area is most commonly affected?

A

a chronic inflammatory disease characterised by transmural granulomatous inflammation affecting the mouth to the anus (esp terminal ileum/proximal colon – ileocaecal valve)

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55
Q

Management of Crohn’s Disease?

A

Smoking cessation + optimise nutrition

To induce remission:
First line - prednisolone PO, hydrocortisone IV
Second line - mesalazine (5-ASA)

If not working, can add-on immunosuppression – azathioprine, mercaptopurine or methotrexate

Maintaining remission:
If 2+ flares in 12m/steroids cannot be reduced without flares:
Usually continue on mercaptopurine or azathioprine

Severe Crohn’s – TNF-alpha: Infliximab/Adalimumab (adults only)

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56
Q

Extraintestinal signs of IBD?

A

Joints – arthritis (more © in Crohn’s)
Skin – erythema nodosum, pyoderma gangrenosum
Eyes – Uveitis (© UC), scleritis, episcleritis (© Crohns)
Kidneys – oxalate renal stones (© Crohns)
Liver – PSC (© UC), gallstones (© Crohns)
Haemotological – DVTs

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57
Q

What can you see on endoscopy of Crohn’s vs UC?

A

Crohn’s - cobblestone appearance
UC - pseudopolyps

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58
Q

What are the radiological signs for Crohn’s and UC?

A

Crohn’s:
strictures: ‘Kantor’s string sign’
proximal bowel dilation
‘rose thorn’ ulcers
fistulae

UC:
loss of haustrations
superficial ulceration, ‘pseudopolyps’
long standing disease: colon is narrow and short -‘drainpipe colon’

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59
Q

Treatment of UC?

A

Inducing remission:

Distal disease: TOPICAL Aminosalicylates (5-ASA) – sulfasalazine/mesalazine (decrease relapse rates)

Wait 4 weeks, then add in: PO aminosalicylates or PO steroids

Widespread disease: TOPICAL and PO high-dose aminosalicylates

Wait 4 weeks, then add in: PO steroids

Severe colitis: treat in hospital with IV steroids +/- ciclosporin if required

Maintaining remission:

Topical and/or PO aminosalicylate

Following a severe relapse 2+ exacerbations in the past year: PO azathioprine or PO mercaptopurine

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60
Q

Is colon Ca more common in Crohn’s or UC?

A

UC

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61
Q

What is hepatorenal syndrome?

A

= cirrhosis + ascites + renal failure
Cirrhosis leads to increased portal venous system => ascites develop => loss of fluid from the blood vessels causes activation of the RAAS and fluid to be retained. If this is not adequate to maintain perfusion to the kidneys then renal dysfunction may develop

To do with SPLANCHNIC VESSEL DILATATION following loss of fluid to ascites (which then activates the RAS system)

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62
Q

What are some symptoms of hypophosphataemia?

A

Muscle weakness
Fatigue
Bone pain

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63
Q

What does somatostatin do?

A

Essentially inhibits the release of other types of hormones. Inhibits CCK (enzyme that improves digestion) and HCl

DSi

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64
Q

What is the role of I cells?

A

Located in the upper small intestine, produce CCK (responsible for the secretion of enzyme-rich fluid from the pancreas, and contraction of the gallbladder and relaxation of the sphincter of Oddi - without which gallstones may form)

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65
Q

What are red flag symptoms to inquire about before making a diagnosis of IBS?

A

rectal bleeding
unexplained/unintentional weight loss
family history of bowel or ovarian cancer
onset after 60 years of age

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66
Q

Other than CC, what other Ca is HNPCC most associated with? What is it also known as?

A

Endometrial Ca

Lynch syndrome

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67
Q

In obese patients, what is the cut-off BMI for referral to bariatric surgery?

A

NICE bariatric referral cut-offs
with risk factors (T2DM, BP etc): > 35 kg/m^2
no risk factors: > 40 kg/m^2

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68
Q

What are the grades of hepatic encephalopathy?

A

Grade I: Irritability
Grade II: Confusion, inappropriate behaviour
Grade III: Incoherent, restless
Grade IV: Coma

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69
Q

Treatment of hepatic encephalopathy?

A

Lactulose first-line, with the addition of rifaximin for the secondary prophylaxis
lactulose - works by promoting the excretion of ammonia + increasing the metabolism of ammonia by gut bacteria
rifaximin - modulates the gut flora resulting in decreased ammonia production

other options include embolisation of portosystemic shunts and liver transplantation in selected patients

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70
Q

Why do you get confused in hepatic encephalopathy?

A

Ammonia travels to brain, broken down by astrocytes which also convert glutamate to glutamine, this causes influx of water and subsequent development of cerebral oedema

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71
Q

Which procedure can cause hepatic encephalopathy?

A

Transjugular Intrahepatic Portosystemic Shunt - produce when variceal bleeding cannot be controlled. Blood bypasses the liver to reduce pressure on portal system. Means that that blood does not pass through the liver and ammonia is not extracted.

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72
Q

How do you treat ongoing diarrhoea in Crohn’s patient post-resection with normal CRP?

A

Cholestyramine

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73
Q

What is the most common age/gender for AI hepatitis?

A

Young/middle-aged women

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74
Q

Presentation of AI hepatitis?

A

Jaundice, acne, no period
Also fever, malaise, polyarthralgia

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75
Q

Types of AI hepatitis?

A

Diagnosis of exclusion
Classification is based on IgG levels, auto-Abs and histology
Type 1: ASMA and ANA +ve, raised IgG
Type 2: Anti-liver/kidney microsomal type 1 (LKM1) Abs +ve, ASMA + ANA -ve
Type 3: Abs against soluble liver antigen (SLA) or liver-pancreas antigen

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76
Q

Management of AI hepatitis?

A

steroids
other immunosuppressants e.g. azathioprine
liver transplantation

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77
Q

Which 4 conditions is H. Pylori infection associated with?

A

peptic ulcer disease (95% of duodenal ulcers, 75% of gastric ulcers)
gastric cancer
B cell lymphoma of MALT tissue (eradication of H pylori results causes regression in 80% of patients)
atrophic gastritis

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78
Q

What is haemochromatosis?

A

inherited disorder of iron metabolism, increased intestinal iron absorption leads to iron deposits in the joints, liver, heart, pancreas, pituitary, adrenals and skin

79
Q

Who normally gets haemochromatosis?

A

Middle-aged men

80
Q

Which gene is responsible for haemochromatosis and what is the inheritance pattern?

A

HFE gene mutation on Chr 6, AR

81
Q

Symptoms of haemochromatosis?

A

Early –
• No symptoms
• Tiredness
• Arthralgia (2nd+3rd MCP joints + knee pseudogout)
• Loss of erections
Later –
• Slate-grey/bronzed skin pigmentation
• Signs of CLD – hepatomegaly/cirrhosis
• Dilated cardiomyopathy
• Osteoporosis
Endocrinopathies – DM, hypogonadism for dysfunction in pituitary

82
Q

Investigations for haemochromatosis?

A

Blood – raised LFTs and serum ferritin, RAISED TRANSFERRIN SATURATION, low TIBC
Radiology – X-ray shows chondrocalcinosis in joints (stressed joints show more signs of damage that rested joints), liver MRI may show Fe overload
Liver biopsy – Perl’s stain quantifies iron loading and assesses severity
ECG/Echo – if cardiomyopathy suspected

Genetic testing - molecular genetic testing for the C282Y and H63D mutations

83
Q

Treatment of haemochromatosis?

A

Venesection required for life
Iron chelating agents (desferoximine)

84
Q

Pathophysiology of Wilson’s Disease?

A

The absorption of copper and transportation to the liver is intact. The incorporation into caeruloplasmin in hepatocytes and its excretion into bile are impaired. Therefore copper accumulates in the liver and later in other organs e.g. basal ganglia and cornea

85
Q

Treatment of Wilson’s Disease?

A

Chelating agents – lifelong penicillamine

86
Q

What does ischaemic colitis look like on XR?

A

thumb-printing - mucosal oedema/haemorrhage

87
Q

Where is ischaemic colitis most commonly found?

A

Splenic flexure

88
Q

What are the different types of Hep B antigen?

A

HBeAg is present 1-3 months after acute illness – implies high infectivity (this Ag is released during replication)
HBsAg (first marker to appear) is present 1-6 months after exposure
If HBsAg is still present >6 months, means patient is now a carrier

89
Q

What is Charcots triad?

A

Fever, RUQ pain, jaundice

90
Q

What is Reynold’s pentad?

A

Charcots triad + hypotension + confusion

91
Q

What is the 1st line and what is the best method of Dx for ascending cholangitis?

A

1st - USS
Best - CT

92
Q

Treatment for ascending cholangitis?

A

Fluid resuscitation + abx (cefuroxime + metronidazole)
ERCP after 24-48hrs to relieve obstruction

93
Q

Do the polyps in Peutz-Jeghers syndrome turn malignant?

A

No, but if you have the syndrome you are more likely to develop CC from other sites in the bowel

94
Q

Treatment for IBS

A

first line - antispasmodics + lactulose/loperamide
Can use linaclotide (laxative if constipated for >12m and other methods don’t work)
second line - TCAs (low dose)
After 12 months: CBT

95
Q

How can you investigate for bile acid malabsorption and how does this present?

A

SeHCAT test
Diarrhoea, steatorrhoea

96
Q

What is the D-xylose absorption test?

A

D-xylose is a type of sugar that is absorbed in the proximal small intestine

Measures the level of the sugar in the blood/urine to indicate if the small intestine is effectively absorbing nutrients

97
Q

Treatment of hepatorenal syndrome?

A

Management: Terlipressin, volume expansion with 20% albumin
Transjugular intrahepatic portosystemic shunt
Ultimate treatment may require liver-kidney transplant

98
Q

Management of ascites?

A

Bed rest, fluid restriction, low-salt diet
Spironolactone first, if poor response – add furosemide
Chart daily weight
Therapeutic paracentesis with albumin infusion may be tried

99
Q

Most common organism seen in spontaneous bacterial peritonitis?

A

E. coli

100
Q

Treatment of SBP?

A

Cefotaxime

101
Q

Antibodies tested in coeliac disease?

A 
tissue transglutaminase (TTG) antibodies (IgA) are first-choice according to NICE 
endomyseal antibody (IgA) 
needed to look for selective IgA deficiency, which would give a false negative coeliac result 
anti-gliadin antibody (IgA or IgG) tests are not recommended by NICE
102
Q

Which test can be used to confirm Gilbert Syndrome?

A

IV nicotinic acid test

103
Q

How long after taking a PPI and abx can you do the C13 reactive breath test?

A

PPI - 2 weeks
Abx - 4 weeks

104
Q

If H. pylori eradication unsuccessful, what should you do?

A

Retest with C13 breath test, then re-treat with PPI, amox + metro/clarithromycin

105
Q

Name three brush board enzymes and what they break carbohydrates down into?

A

maltase: cleaves maltose -> glucose + glucose
sucrase: cleaves sucrose -> fructose and glucose
lactase: cleaves lactose -> glucose + galactose

106
Q

In patients with a gastric bypass, what supplement will they need?

A

All gastric bypass ops pass the duodenum where iron is absorbed, therefore nearly all menstruating women need iron supplements

107
Q

What is the worrying complication from C. diff?

A

Toxic megacolon

108
Q

What laxative should be avoided in IBS?

A

Lactulose

SE: increases gas and bloating in the stomach

109
Q

What are VIPomas and where are they found?

A

rare cancer caused by a type of pancreatic neuroendocrine tumor, which is tumor that arises from cells that produce hormones - allowing the tumor itself to produce hormones
Most commonly found in the pancreas

110
Q

What test should be done before commencing azathioprine/mercaptopurine in Crohn’s disease?

A

TPMT activity test - testing for the presence of the enzyme that metabolises these drugs

111
Q

What is the most common cause of HCC in the UK and worldwide?

A

UK - hep C
Worldwide - hep B

112
Q

Which HLA is most strongly associated with Coeliac?

A

HLA DQ2

113
Q

What is the most likely Dx with the following symptoms - dysphagia, aspiration pneumonia, halitosis?

A

Pharyngeal pouch

114
Q

What cell change occurs in Barretts and what is the M:F ratio?

A

Squamous to Columnar to (poss) Adenocarcinoma
S -> C -> A

M:F 7:1

115
Q

What markers can be used to indicate severe pancreatitis?

A

CRP and elements of the Glasgow Pancreatitis Score

116
Q

What is the presentation of gastric Ca?

A
  • Often non-specific
  • Dyspepsia (pain, for >1m and >50yrs demands Ix)
  • WL
  • Vomiting
  • Dysphagia (difficulty swallowing)
  • Anaemia
117
Q

What cells may be seen on histology of gastric Ca?

A

Signet ring cells

118
Q

What are the RFs for gastric Ca?

A

Elderly

H. pylori infection
blood group A: gAstric cAncer
gastric adenomatous polyps
pernicious anaemia
smoking
diet: salty, spicy, nitrates
may be negatively associated with duodenal ulcer

119
Q

With respect to coagulation in liver disease, which clotting factor is raised?

A

Factor 8

120
Q

Why are clotting factors 2, 7, 9 and 10 grouped together?

A

All need vitamin K for synthesis

121
Q

Which monoclonal Ab is used to prevent recurrent C. diff?

A

Bezlotoxumab

122
Q

What is the ECG abnormality that can occur with hypomagnesaemia?

A

Torsades-des-pointes

123
Q

What is Angiodysplasia?

A

a vascular deformity of the gastrointestinal tract which predisposes to bleeding and iron deficiency anaemia. There is thought to be an association with aortic stenosis.

Looks like a telangiectasia

124
Q

What is Heyde syndrome?

A

a triad of aortic stenosis, an acquired coagulopathy and anaemia due to bleeding from intestinal angiodysplasia

125
Q

What does the H stand for in the GETSMASHED mnemonic for the causes of pancreasitis?

A

Hypertriglyceridaemia, Hyperchylomicronaemia (ultra low density lipoproteins), Hypercalcaemia, Hypothermia

126
Q

How do you treat chronic anal fissures?

A

Topical GTN

127
Q

Gold standard investigation for pancreatic Ca?

A

High-resolution CT

128
Q

Most common organism for liver abscess?

A

Staphylococcus aureus in children and Escherichia coli in adults

129
Q

Treatment of liver abscess?

A
  • drainage (typically percutaneous) and antibiotics
  • amoxicillin + ciprofloxacin + metronidazole
130
Q

What is the biggest RF for anal cancer?

A

HPV infection causes 80-85% of SSCs of the anus

131
Q

What are the side effects for mesalazine?

A

GI upset, headache, agranulocytosis, pancreatitis, interstitial nephritis

132
Q

What should you give newborn babies whose mothers are hep B positive?

A

a complete course of vaccination + hepatitis B immunoglobulin

133
Q

What is the role of secretin?

A

Secretin increases secretion of bicarbonate-rich fluid from pancreas and hepatic duct cells

134
Q

What would you see on imaging in achalasia?

A

Dilated tapering oesophagus

135
Q

What would you see on imaging in oesophagitis?

A

Corkscrew oesophagus

136
Q

What would you see on imaging in oesophageal Ca?

A

Oesophageal stricture with apple core effect

137
Q

What is the main mechanism of action of terlipressin?

A

Acts on V1 receptors to increase systemic vascular resistance

Causes constriction of splenic vessels

138
Q

What is Whipple’s disease, how does it present and what test would you do?

A

More common in middle aged men + HLA B27
Rare multi-system disorder caused by Tropheryma whippelii infection
symptoms of abdominal pain, diarrhoea, steatorrhoea, migrating polyarthralgia, photosensitivity, skin hyperpigmentation, petechiae and peripheral oedema
Jejunal biopsy – shows deposits of macrophages containing Periodic acid-Schiff (PAS) granules

139
Q

What prophylaxis can be given for SBP?

A

Oral ciprofloxacin

140
Q

What is the role of faecal elastase?

A

To assess exocrine function in chronic pancreatitis

141
Q

What is the gene responsible for Wilson’s disease?

A

caused by a defect in the ATP7B gene located on chromosome 13

142
Q

What is the age of onset of Wilson’s and what are the symptoms?

A

10-25yrs

Liver – jaundice, pruritis, vomiting, ascites, oedema

Brain – CHOREA, dementia, parkinsonism, dysphagia, dysarthria

Mood – personality changes, anxiety, psychosis

Eyes - KF rings - due to copper accumulation in Descemet membrane

Blue nails, renal tubular acidosis, haemolysis

143
Q

Investigations in Wilson’s disease?

A

slit lamp examination for Kayser-Fleischer rings

reduced serum caeruloplasmin

reduced total serum copper (counter-intuitive, but 95% of plasma copper is carried by ceruloplasmin)

free (non-ceruloplasmin-bound) serum copper is increased

increased 24hr urinary copper excretion

144
Q

What is the name of the bacterial toxin released by H. pylori which disrupts the gastric mucosa?

A

CagA toxin

145
Q

Duodenal vs gastric ulcer:

Which is more common?
How commonly related to H. pylori?

How to treat?

A

Duodenal more common

Related to H. pylori: DU (90%), GU (80%)

PPI DU (4wks), GU (8wks)

146
Q

Scoring systems to use in acute variceal bleed and management?

A

Blatchford score at first assessment -> full Rockall score after endoscopy

Mx:

Plt transfusion if actively bleeding and plt <50

Give FFP if fibringen <1/PT or APTT >1.5x normal

Prothrombin complex if on warfarin

147
Q

Peaks of coeliac onset and peri-oral symptoms? Type of cell mediated disease? Biopsy results? Complications?

A

Onset infancy + 50-60yrs

Aphthous ulcers, angular stomatitis

T cell mediated

Biopsy: shortened villi, crypt hyperplasia, inflammatory infiltration

Complications: folate, B12, iron deficiency, risk T cell lymphomas

148
Q

What do Coeliac patients often suffer with meaning they benefit from pneumococcal vaccine + booster every 5 yrs?

What might be seen on blood film in this condition?

A

Functional hyposplenism

target cells

Howell-Jolly bodies

Pappenheimer bodies

siderotic granules

acanthocytes

149
Q

Histological differences with IBDs?

A

Crohns: affects from mucosa -> serosa, increased goblet cells, granulomas

UC: neutrophils migrate through the walls of glands to form crypt abscesses, depletion of goblet cells, granulomas are infrequent

150
Q

What eye changes can occur with acute pancreatitis (rare)? Glasgow scale?

A

ischaemic (Purtscher) retinopathy

PaO2 <8kPa

Age >55yrs

Neutrophilia (raised)

Calcium (low)

Renal function (raised urea)

Enzymes

Albumin (low)

Sugar (raised)

151
Q

How to manage diverticulitis?

A

mild attacks can be treated with oral antibiotics

more significant episodes are managed in hospital. Patients are made nil by mouth, intravenous fluids and intravenous antibiotics (typical a cephalosporin + metronidazole) are given

152
Q

What is the rule of 2 in Meckel’s diverticulum?

A

occurs in 2% of the population, is 2ft from the ileocaecal valve, is 2 inches long, 2x as likely in men, occurs around 2yrs age

153
Q

RFs for bowel ischaemia?

A

Atrial fibrillation

Increasing age, cocaine use, emboli risk (Ca, endocarditis)

154
Q

Acute mesentic ichaemia: common site? cause? presentation? Ix and Tx?

A

Almost always in small bowel

superior mesenteric artery thrombosis/embolism, mesenteric vein thrombosis, non-occlusive

TRIAD: severe acute abdo pain, NO signs, shock

Ix: Raised Hb (due to plasma loss), raised WCC, raised LDH

Tx: IV fluids, abx, heparin/surgery

155
Q

Chronic mesenteric ischaemia: cause?

A

95% are d/t atherosclerosis in all 3 mesenteric arteries

Colickly, intermittent abdominal pain occurs: ‘intestinal angina’

156
Q

Management of ischaemic colitis?

A

usually supportive
- surgery may be required in a minority of cases if conservative measures fail

157
Q

Inheritence of FAP, genetic cause and result?

A

AD

formation of hundreds of polyps by the age of 30-40 years

Defect in APC gene on Chr 5

158
Q

Amsterdam criteria for Dx HNPCC?

A

3+ family members with a confirmed Dx of CC, one of whom is a first degree (parent, child, sibling) relative of the other two.
Two successive affected generations.
1+ CC Dx <50 yrs
FAP has been excluded.

159
Q

What is Gardner’s syndrome?

A

A form of AD FAP

Extra colonic diseases include: skull osteoma, thyroid cancer and epidermoid cysts

Due to colonic polyps most patients will undergo colectomy to reduce risk of colorectal cancer

160
Q

Who qualifies for a 2ww in CC?

A

patients >= 40 years with unexplained weight loss AND abdominal pain

patients >= 50 years with unexplained rectal bleeding

patients >= 60 years with iron deficiency anaemia OR change in bowel habit

tests show occult blood in their faeces

161
Q

What might you see around the mouth in Peutz-Jegher’s syndrome?

A

buccal pigmentation is an important sign

162
Q

How to assess mural invasion in oesophageal cancer?

A

Endoscopic USS

163
Q

What are Boerhaave syndrome and Plummer-Vinson syndrome?

A

Boerhaave syndrome = severe vomiting → oesophageal rupture

PV syndrome = Triad of: dysphagia (secondary to oesophageal webs), glossitis, iron-deficiency anaemia
Treatment includes iron supplementation and dilation of the webs

164
Q

What is constructional apraxia?

A

inability to draw a 5-pointed star

Seen in hepatic encephalopathy

165
Q

Prophylaxis of UGIB in patients with known varicies?

A

Propranolol

Prophylactic banding if med-large varicies

166
Q

What is Transient elastography and who to offer it to? If this diagnoses liver cirrhosis, what else should you do?

A

(FibroScan) – passes waves through the liver to measure the ‘stiffness’

Offer to:

people with hepatitis C virus infection

men who drink >50 units/week + women who drink >35 units/week and have done so for several months

people diagnosed with alcohol-related liver disease

With new Dx of cirrhosis:

NICE recommend doing an upper endoscopy to check for varices + liver USS every 6 months (+/- alpha-feto protein) to check for HCC

167
Q

Two main RF for NAFLD? What is NASH? Ix and Mx?

A

Obese and DM

NASH = most severe form

Usually asymptomatic, hepatomegaly

​ALT > AST

Enhanced liver fibrosis (ELF) blood test is a combination of hyaluronic acid + procollagen III + tissue inhibitor of metalloproteinase 1

Mx: lifestyle + WL

168
Q

PSC associations? Ix? Tx? Complications?

A

UC and HIV

Ix: MRCP or ERCP - ‘beaded’ appearance

p-ANCA may be positive

ANA/SMA may be +ve

Tx: Ursodeoxycholic acid, cholestyramine, liver transplant

Complications: Cholangiocarcinoma, CC

169
Q

Composition of gallstones?

A

Pigment stones – small, friable

Cholesterol stones – large, often only one, © female, obesity

Mixed stones – faceted (majority - 50%)

170
Q

Do you get jaundice in acite cholecystitis?

A

No

171
Q

What is Post-cholecystectomy syndrome and how to Mx?

A

Up to 40% of patients develop it

Typically symptoms of dyspepsia, vomiting, pain, flatulence and diarrhoea

Difficult to manage: try low-fat diet, cholestyramine, PPI

172
Q

What is Mirizzi’s syndrome?

A

extrinsic compression from impacted stone on common hepatic duct

173
Q

Treatment of HCC?

A

early disease: surgical resection

liver transplantation

radiofrequency ablation

transarterial chemoembolisation

sorafenib: a multikinase inhibitor

174
Q

Features of cholangiocarcinoma? Causes? Mx?

A
  • persistent biliary colic symptoms
  • associated with anorexia, jaundice and weight loss
  • a palpable mass in the right upper quadrant (Courvoisier sign)
  • periumbilical lymphadenopathy (Sister Mary Joseph nodes) and left supraclavicular adenopathy (Virchow node) may be seen

70% unsuitable for surgery, 5yr survival 30%

Causes: Flukes, PSC, Biliary cysts, HBV/HCV, DM

175
Q

Management of C. diff?

A

Vancomycin 10-14 days

Second line, give oral fidaxomicin

Life-threatening: PO vancomycin + IV metronidazole

Stop opioids (which are antimotility + anti-peristaltic)

176
Q

What is Melanosis coli and what might you see on biopsy?

A

a disorder of pigmentation of the bowel wall, associated with laxative abuse

Pigment laden macrophages

177
Q

Causes and features of carcinoid syndrome?

A

Serotonin secreting tumour

flushing (often earliest symptom)

diarrhoea, bronchospasm, hypotension

right heart valvular defects (tricuspid regurg, pulm stenosis)

ACTH and GHRH may also be secreted resulting in, for example, Cushing’s syndrome

pellagra can rarely develop

Ix: urinary 5-HIAA, plasma chromogranin A y

Mx: octreotide, for diarrhoea: cyproheptadine may help

178
Q

Causes of hepatosplenomegaly?

A

HSM Mneomnic
H: Haematological diseases as Myeloproliferative disease/
Hepatitis
E: EBV
P: Portal hypertension
A: Amyloidosis
TO: TOxoplasmosis
S: Sarcoidosis
P: Pernicious anemia
LE: LEishmania, malaria
N: Neiman pick (Lipid storage disease)
Omegaly: Acromegaly

179
Q

RFs, features, Ix and Mx of small bowel bacterial overgrowth syndrome?

A

RFs: scleroderma, DM

Many features overlap with IBS

Dx: hydrogen breath test (the patient is fasted and then given a glucose drink. Bacteria will metabolise the glucose and produce hydrogen compounds which are then measured in the breath) , small bowel aspiration + culture

Mx: Rifaximin, co-amox/metro also effective

180
Q

Igs associated with:

Alcoholic liver disease

Primary biliary cirrhosis

Autoimmune hepatitis

A

Alcoholic liver disease: IgA

PriMary biliary cirrhosis: IgM

Autoimmune hepatitis: IgG

181
Q

What is Zollinger-Ellison syndrome?

A

= excessive levels of gastrin, usually from a gastrin secreting tumour usually of the duodenum or pancreas

30% occur as part of MEN type 1

Features: multiple gastroduodenal ulcers, diarrhoea, malabsorption

Ix: fasting gastrin levels - the single best screen test

Also can do secretin stimulation test

182
Q

What are villous adenomas?

A

Villous adenomas are colonic polyps with the potential for malignant transformation. They characteristically secrete large amounts of mucous, potentially resulting in electrolyte disturbances.

Majority are asymptomatic, possible features:

non-specific lower gastrointestinal symptoms

secretory diarrhoea may occur

microcytic anaemia

hypokalaemia

183
Q

What is the most common complication of ERCP?

A

Pancreatitis

184
Q

Which is more common, haematochromatosis or CF?

A

haematochromatosis

185
Q

What does a high vs low serum-albumin gradient suggest?

A

High = non-peritonitic e.g. liver disorders

Low = peritonitis e.g. peritoneal carcinomatosis (malignancy) and tuberculosis peritonitis

186
Q

Complication of cholestasis during pregnancy?

A

Stillbirth

187
Q

Three common causes of hepatomegaly?

A

Cirrhosis: if early disease, later liver decreases in size. Associated with a non-tender, firm liver

Malignancy: metastatic spread or primary hepatoma. Associated with a hard, irregular. liver edge

Right heart failure: firm, smooth, tender liver edge. May be pulsatile

188
Q

Outside of iron overload (e.g. haemochromatosis/transfusions), what can cause a raised ferritin?

A

Inflammation (due to ferritin being an acute phase reactant)
Alcohol excess
Liver disease
Chronic kidney disease
Malignancy

189
Q

What breaks starch into sugars and where is this enzyme found?

A

Amylase, found in saliva and pancreatic secretions

190
Q

Gold standard test for achalasia and first-line Mx?

A

oesophageal manometry

Mx: pneumatic (balloon) dilation

191
Q

What is eosinophilic oesophagitis, what causes it, M:F ratio + age of onset, symptoms, Ix and Mx?

A

Caused by allergy to food (we think)

3:1 M:F, onset 30-50s

Symptoms: dysphagia, strictures, food impaction etc

Ix: no improvement with PPI, endoscopy shows eosinophils

Mx: diet modification, topical steroids (e.g. inhaled), oesophageal dilatation

192
Q

What are caput medusae?

A

A cluster of swollen veins in your abdomen - related to liver disease

193
Q

What is H. pylori not associated with?

A

GORD

MRCP (14 decks)

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