GI medicine 2 Flashcards

1
Q

Budd-Chiari Syndrome

  1. What is it?
  2. What can cause it?
  3. What clinical features are seen?
  4. What investigation should be done?
A
  1. thrombosis of the hepatic portal vein
    • polycythaemia
    • thrombophilia: activated protein c resistance, protein C and S deficiency, antithrombin III deficiency
    • pregnancy
    • COCP
    • severe, sudden abdominal pain
    • ascites
    • tender hepatomegaly
  2. US with doppler
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2
Q

Carcinoid Tumours

  1. What are they?
  2. What clinical features are seen?
  3. What investigations can be done?
  4. How is it treated?
A
  1. liver mets (sometimes lung tumour) causing release of serotonin

NOTE: because can be lung tumour could also appear with Cushing’s as tumour secretes ACTH too

    • flushing
    • diarrhoea
    • bronchospasm (therefore hear a wheeze)
    • hypotension

mnemonic: pretty girl tumour

    • urine 5-HIAA
    • plasma chromogranin A y
  1. somatostatin analogues - octreotide
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3
Q

Clostridium difficile

  1. What antibiotics can cause it?
  2. How is it diagnosed?
  3. How is it treated if
    a) first episode
    b) recurrent episode
    c) life-threatening (+ when would this be?)
A
    • clindamycin
    • cephalosporins (start cef/ceph)
    • co-amoxiclav
    • ciprofloxacin (and other fluoroquinolones)
  1. c. diff stool TOXIN
    (antigen only confirms the presence of the bacteria)
  2. a)
    1st line: oral vancomycin
    2nd line: oral fidaxomicin
    3rd line: oral vancomycin + IV metronidazole

b) oral fidaxomicin (alternatively can give oral vancomycin if after 12 weeks)

c)
if hypotensive, ileus or toxic megacolon
oral vancomycin and IV metronidazole

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4
Q

Coeliac disease

  1. What is it associated with:
    a) conditions?
    b) HLA class
  2. What clinical features are seen?
  3. What complications can be seen?
A
  1. a)
    - dermatitis herpetiformis
    - autoimmune: autoimmune hepatitis, type 1 diabetes

b) HLA-DQ2 (95%) and HLA-DQ8

    • diarrhoea
    • abdominal pain + bloating
    • weight loss
    • fatigue
    • unexplained anaemia
    • children: failure to thrive / altering growth
    • lactose intolerance
    • enteropathy-associated T cell lymphoma of the small intestine
    • subfertility, hypoSplenism

mnemonic: LES (Claire’s dad) has coeliac

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5
Q

Coeliac Disease Investigations

  1. What investigations are done?
  2. What must you ensure prior to testing?
A
    • serology: transglutaminase antibodies (IgA)
    • endoscopy + biopsy: villous atrophy, crypt hyperplasia, increased intraepithelial lymphocytes, infiltration of lymphocytes into lamina propria

NOTE: therefore if IgA is low TTG test is null and void

  1. patient has continued gluten free diet (if possible) for at least 6 weeks prior to testing
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6
Q

How is coeliac disease managed?

A
gluten-free diet 
avoid: 
wheat: bread, pasta, pastries 
barley: beer 
rye 
oats (however some can tolerate) 

NOTE: whiskey is made with barley but this is removed during distillation so is therefore safe to drink

+ pneumococcal vaccine with booster every 5 years due to hyposplenism

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7
Q
  1. Which GI cancer is Lynch syndrome (HNPCC) highly associated with?
  2. Which cancer is this most mutation next most likely to cause in
    a) females
    b) males
A
  1. colorectal cancer

2.

a) endometrial cancer
b) pancreatic cancer

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8
Q

Cancer referral

  1. When should you make
    a) urgent referral
    b) non-urgent referral
  2. What should be done if a patient has reflux symptoms but does not meet the referral criteria?
A

1.

a)
- dysphagia
- abdominal mass consistent with stomach cancer

=/> 55 with weight loss AND one of:

  • upper abdominal pain
  • dyspepsia
  • reflux

b)
haematemesis

=/> 55 with:

  • treatment resistant dyspepsia
  • anaemia + upper abdominal pain
  • low platelets with an upper GI symptom
  • N+V with another upper GI symptom

NOTE: upper GI symptoms: N+V, reflux, dyspepsia, abdo pain, weight loss

  1. Review medications for possible causes of dyspepsia
  2. Lifestyle advice
  3. Try PPI for one month OR a ‘test and treat’ approach for H. pylori
    if symptoms persist after either of the above approaches then the alternative approach should be tried
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9
Q

What features are associated with oesophageal candidiasis?

A
  • HIV

- steroid inhaler use

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10
Q

Ferritin

  1. a) How often is increased ferritin due to iron overload?
    b) What can you use to determine if the increased ferritin is due to iron overload?
  2. What can cause iron overload?
  3. What can cause increased ferritin but not iron overload?
  4. What can cause decreased ferritin?
A
  1. a) 10%

b) transferrin saturation

  1. primary: hereditary haemochromatosis

secondary: repeated blood transfusions

    • inflammation (as ferritin acute phase reactant)
    • alcohol
    • liver disease
    • chronic kidney disease
    • malignancy
  1. iron deficiency anaemia
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11
Q

Gastric Cancer

  1. What are the risk factors?
  2. What clinical features are seen?
  3. What investigations are done?
A
    • h. pylori
    • atrophic gastritis
    • diet: nitrates and salt
    • smoking
    • blood type
    • abdominal pain +/- dyspepsia
    • nausea and vomiting
    • dysphagia
    • weight loss and anorexia

mnemonic: think of one leading to the other
3. endoscopy + biopsy: signet ring cells (more indicates worse prognosis)

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12
Q

GORD

  1. What are the indications for endoscopy?
  2. What should you consider if endoscopy is negative?
  3. How should it be managed if
    a) endoscopically proven oesophagitis?
    b) endoscopically negative
A
    • > 55 years old
    • symptoms > 4 weeks or persisting despite treatment
    • relapsing of symptoms
    • weight loss
    • dysphagia
  1. 24hr oesophageal pH monitoring which is gold standard test
  2. a) PPI for 1 month, double dose if no response

b) PPI for 1-2 months, offer H2RA or pro kinetic (e.g. cisapride, domperidone, metoclopramide) if no response

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13
Q

Gilbert’s Syndrome

  1. What is it?
  2. What clinical feature is seen?
  3. What is seen on investigation?
A
  1. deficiency of glucoronosyltransferase
    (used to conjugate bilirubin)
  2. jaundice on illness, exercise, fasting
  3. unconjugated hyperbilirubinaemia following prolonged fasting or IV nicotinic acid

(no need to recheck blood results in future can simply reassure)

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14
Q

Haemochromatosis

  1. What is it?
  2. What clinical features are seen?
  3. Which complications are reversible?
A
  1. disorder of iron absorption and metabolism resulting in iron accumulation
  2. early: fatigue, impotence, arthralgia (often hands)
  • bronze skin pigmentation
  • liver cirrhosis
  • diabetes
  • heart failure (dilated cardiomyopathy)
  • hypogonadism (2nd to cirrhosis + pituitary dysfunction)
    • skin pigmentation
    • cardiomyopathy
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15
Q

Haemochromatosis Investigation and Management

  1. Investigation
    a) What will be seen on iron studies?
    b) What tests are diagnostic?
    c) What is seen on XR?
  2. How is it managed?
A
  1. a)
    - raised ferritin
    - transferrin saturation >55% males >50% females

b) Liver biopsy: Perl’s stain
c) chondrocalcinosis

  1. 1st line: venesection
    2nd line: desferrioxamine
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