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Finals > Gastro > Flashcards

Gastro Flashcards

1
Q

Younger women with deranged LFTs and signs of liver disease. Differential?

A

Autoimmune hepatitis

Viral hepatitis

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2
Q

Is azathioprine safe to use in pregnancy?

A

Yes

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3
Q

Conditions associated with autoimmune hepatitis?

A

Hashimoto’s thyroiditis, RA, Grave’s, IBD, pleurisy, AIHA

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4
Q

Stepwise plan of autoimmune hepatitis

A
  1. Autoimmune profile –> ANA and SMA
  2. Protein electrophoresis –> high titres IgG suggestive
  3. Arrange other bloods –> FBC, LFTs
  4. Consider liver biopsy –> interface hepatitis + plasma cells +++
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5
Q

Approach for autoimmune hepatitis

A
  1. Watchful waiting –> asymptomatic, pre-cirrhotic
  2. Immunosuppression –> pred 40mg PO, taper and add azathioprine for long term
  3. Liver transplant in severe disease
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6
Q

How is remission of autoimmune hepatitis monitored?

A

Measuring AST/ALT and IgG levels post-therapy

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7
Q

What is primary biliary cirrhosis?

A

Chronic autoimmune disease characterised by progressive destruction of small intrahepatic bile ducts, resulting in cirrhosis

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8
Q

Clinical features of PBC?

A

Fatigue + pruritus = earliest

Jaundice = late

Other –> hepatosplenomegaly, facial hyperpigmentation, xanthelasma

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9
Q

How does PBC cause xanthelasma?

A

Dietary cholesterol metabolised in liver and excreted in bile. In PBC there is fibrosis of the biliary tracts causing cholestasis. Cholesterol accumulates and deposits around the eyes and tendons.

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10
Q

Stepwise plan for PBC?

A
  1. LFTs –> primary cholestatic picture
  2. Autoimmune profile + Ig electrophoresis
  3. Imaging –> exclude extrahepatic obstruction (US / MRI)
  4. Consider biopsy –> if unclear = lymphocytic infiltration with granulomatous changes
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11
Q

Management of PBC?

A
  1. Ursodeoxycholic acid
  2. Symptomatic treatment –> pruritus (cholestyramine), malabsorption (replace fat-soluble vitamins)
  3. Consider liver transplant
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12
Q

What is hereditary haemochromatosis?

A

An autosomal recessive genetic disorder characterised by excess iron deposition throughout the body

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13
Q

Early features of haemochromatosis

A

Non-specific = fatigue, abdo pain, arthralgia, ED

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14
Q

Late complications of haemochromatosis

A

Endocrine –> diabetes, hypogonadism

Cardiac –> arrhythmias, cardiomyopathy

Hepatic –> hepatomegaly, cirrhosis

MSK –> bronze skin, arthralgia

Neuro –> mood disturbances, memory impairment

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15
Q

What causes bronzing of skin in hereditary haemochromatosis?

A

Excess haemosiderin deposition + haemosiderin-induced melanocyte activation

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16
Q

What mutation causes haemochromatosis?

A

HFE gene on chromosome 6 –> regulates hepcidin

Hepcidin inhibits ferroportins in gut –> increased iron absorption

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17
Q

How do you manage haemochromatosis?

A
  1. Dietary advice –> low iron, avoid alcohol
  2. Regular venesection –> stimulate bone marrow to produce new RBCs and use up iron
  3. Chelation therapy –> IV desferrioxamine (if CI)
  4. Genetic counselling –> first degree
  5. Liver transplant –> end stage
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18
Q

What is hepatocellular carcinoma?

A

The commonest primary cancer arising from liver hepatocytes

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19
Q

Causes of HCC?

A

Chronic HBV and HCV

Cirrhosis –> ALD, HHC, PBC

Fungal infection –> Aspergillus

Misc –> PSC, androgenic steroids, COCP use

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20
Q

How would you investigate HCC?

A
  1. Imaging –> US for screening, otherwise CT / MRI
  2. Consider liver biopsy
  3. Tumour markers –> alpha-fetoprotein (6 month follow up)
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21
Q

How would you manage HCC?

A

Non-cirrhotic –> hepatic resection

Single nodule <5cm or <3 nodules <3 cm –> liver transplant

Consider RFA

Multinodular, intermediate –> trans-arterial chemoembolisation

Advanced –> chemotherapy (e.g. SORAFENIB)

Palliative care

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22
Q

What is the differential for a RIF mass?

A

Crohn’s disease, appendix mass / abscess, caecal carcinoma, ovarian/renal mass, TB

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23
Q

Clinical features of Crohn’s?

A

Diarrhoea, often not bloody

Abdo discomfort +/- weight loss

Aphthous ulcers, glossitis, fistulae

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24
Q

What are some extra-abdominal manifestations of Crohn’s?

A

Derm –> erythema nodosum, pyoderma gangrenosum

Eyes –> anterior uveitis, episcleritis

MSK –> arthritis, AnkSpond

Liver –> gallstones

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25
Q

How would you investigate Crohn’s?

A
  1. Bloods –> FBCs, LFTs, haematinics
  2. Stool testing –> MC&S (exclude infection), faecal calprotectin
  3. Imaging –> AXR +/- erect CXR, MRI pelvis, capsule endoscopy
  4. Endoscopy –> ileocolonoscopy + biopsy
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26
Q

Describe the management of Crohn’s in terms of inducing remission.

A
  1. First line = oral/IV corticosteroids
  2. Consider budesonide or 5-ASA therapy in some situations
  3. Add-on in resistive (2+ exacerbations/year) cases –> azathioprine or 6-MP (or methotrexate if CI)
  4. Consider biologics –> e.g. infliximab, adalimumab
  5. Consider surgery
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27
Q

Describe the management of Crohn’s in terms of maintaining remission.

A
  1. Stop smoking + lifestyle advice
  2. First-line = azathioprine or 6-MP (never use long-term steroids)
  3. Alternative = MTX
  4. Stricture management –> balloon dilatation via colonoscopy, otherwise surgery
  5. Monitoring –> assess osteopenia/-porosis, colonoscopy surveillance for colorectal Ca if >10 years since symptom onset
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28
Q

Describe the management of Crohn’s in terms of managing perianal disease.

A
  1. Consider oral ABx –> e.g. metro / cipro
  2. Consider immunosuppression –> azathioprine +/- infliximab
  3. Consider surgery
29
Q

What are some major features of oesophageal disorders?

A

Dysphagia –> slow progressive + heartburn = peptic stricture; rapid = malignancy; to both liquid and solid progressive = achalasia

Odynophagia –> oesophagitis, e.g. reflux/infection

Substernal discomfort –> reflux of gastric contents into oesophagus, worse when lying

Regurgitation

30
Q

What is the main sign of oesophageal disease?

A

Weight loss due to decreased intake of food

31
Q

Which test is used to assess H. pylori post-eradication therapy?

A

Urea breath test

32
Q

Most common organisms in pyogenic liver abscesses?

A

Children = S. aureus

Adults = E. Coli

33
Q

Management of pyogenic liver abscess?

A

Image-guided drainage + IV antibiotics

Amoxicillin + ciprofloxacin + metronidazole

Allergic –> ciprofloxacin + clindamycin

34
Q

Diagnostic marker of choice for carcinoid syndrome?

35
Q

What is the name of the stain used in biopsy for HHC?

36
Q

Typical iron study in patient with HHC

A

Transferrin sat >55% or >50%

Raised ferritin and iron

Low TIBC

37
Q

What markers of iron study are aimed for in venesection for HHC?

A

Transferrin <50%

Ferritin <50

38
Q

Which gastro drug can cause hypomagnesaemia?

A

Omeprazole

39
Q

List some adverse effects of PPIs

A

Hyponatraemia, hypomagnesaemia

Osteoporosis

Microscopic colitis

Inc. risk C. Diff

40
Q

Single most important investigation for patient with severe flare of UC?

A

AXR –> exclude toxic megacolon

41
Q

What is coeliac disease?

A

An autoimmune disorder triggered by gluten consumption, resulting in small bowel inflammation and subsequent malabsorption.

42
Q

Which HLA is coeliac disease associated with?

43
Q

What should be assessed before starting therapy with azathioprine or mercaptopurine?

A

Thiopurine methyltransferase (TPMT) activity

44
Q

What constitutes a MILD flare of UC?

A

< 4 stools daily +/- blood

No systemic disturbance

Normal ESR and CRP

45
Q

What constitutes a MODERATE flare of UC?

A

4 - 6 stools a day

Minimal systemic disturbance

46
Q

What constitutes a SEVERE flare of UC?

A

> 6 stools a day

Evidence of systemic disturbance

47
Q

What are some systemic disturbances that can be caused by a severe UC flare?

A

Fever, tachycardia

Acute abdomen

Anaemia

Hypoalbuminaemia

48
Q

Causes of pancreatitis

A

GET SMASHED

Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion venom
Hypercalcaemia, hypothermia
ERCP
Drugs
49
Q

What drugs can cause pancreatitis?

A 
Azathioprine
Mesalazine
Bendroflumethiazide
Furosemide
Steroids
Sodium Valproate
50
Q

Antibodies for autoimmune hepatitis type I?

A

ANA and SMA

51
Q

Antibodies for autoimmune hepatitis type II?

52
Q

Antibodies for autoimmune hepatitis type III?

A

soluble liver-kidney antigen

53
Q

Melanosis coli

A

Laxative abuse

54
Q

Treatment for Wilson’s disease

A

Penicillamine

55
Q

Wilson’s disease mutation

A

ATP7B gene on Chr 13

56
Q

Clinical presentation of coeliac disease.

A

GI –> malabsorption, unexplained weight loss

Metabolic –> IDA, B12/folate deficiency, hypocalcaemia, faltering growth

Derm –> dermatitis herpetiformis, severe aphthous oral ulcers

Misc –> autoimmune conditions, lymphoma

57
Q

Most common inherited colorectal cancer

58
Q

What is SAAG used for?

A

SAAG usually < 11

SAAG > 11 implies portal hypertension

59
Q

What is the most specific and sensitive marker of cirrhosis in chronic liver disease?

A

Thrombocytopenia (< 150)

60
Q

What neutrophil count in ascitic tap is diagnostic of SBP?

61
Q

Management of SBP?

A

IV cefotaxime

62
Q

MoA of loperamide?

A

Loperamide is a μ-opioid receptor agonist which does not have systemic effects as it is not absorbed through the gut

63
Q

Epigastric pain + diarrhoea

A

Zollinger-Ellison syndrome

64
Q

Triad of intestinal angina?

A

Colicky post-prandial abdo pain
Weight loss
Abdominal bruits

65
Q

Most common site of diverticula?

A

Sigmoid colon

66
Q

Unruptured sigmoid volvulus —> Rx?

A

rigid sigmoidoscopy + flatus tube insertion

67
Q

The hepatic portal vein is formed by the union of _ + _ ?

A

Superior mesenteric and splenic veins

68
Q

Tumour marker for cholangiocarcinoma?

69
Q

dyspepsia and over 55?

Finals (19 decks)

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