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Passmed Medicine > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

Explain the interpretation of Hep B serology?

A

Hepatitis B antigen: positive if there is ongoing infection (both acute or chronic).

Anti-Hep B core antibody: means the person has come in contact with the actual virus. IgM = acute, IgG = chronic.

Anti-Hep B surface antibody: means the person has immunity (either natural or vaccine).

Hepatitis E antigen: marker of infectivity.

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2
Q

What are the hallmark features of Crohn’s Disease?

A
  • Whole GI tract can be affected
  • Skip lesions
  • Transmural inflammation - all layers of the bowel are affected
  • Non-caseating granulomas
  • increased goblet cells
  • Sinus/fistula formation
  • “Cobblestone” mucosa appearance
  • Rose-thorn ulcers
  • “Kantor’s Sign” - narrowing of the terminal ileum due to stricturing in the context of Crohn’s
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3
Q

What are the hallmark features of Ulcerative colitis?

A
  • No inflammation beyond submucosa!
  • Widespread ulceration, only in the colon and no skip lesions
  • Inflammatory cell infiltrate in lamina propria
    • If neutrophils migrate through the bowel wall -> crypt abscess
  • Pseudopolyp formation
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4
Q

What are the clinical features of pancratic cancer?

A
  • Painless Jaundice (+ enlarged gallbladder = Courvoisier’s Sign)
  • Non-specific anorexia, weight loss, epigastric pain
  • Loss of exocrine function:
    • Steatorrhoea
  • Loss of endocrine function:
    • Diabetes
  • Atypical back pain
  • Migratory thrombophlebitis (Trousseau sign) - more common than with other cancers
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5
Q

What is Rovsing’s Sign?

A
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6
Q

What is Budd-Chiari Syndrome?

A

Budd-Chiari Syndrome is hepatic vein thrombosis.

This is usually seen on context of underlying haematological malignancy or another pro-coagulatn condition.

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7
Q

How does Budd-Chiari Syndrome present?

A

It presents with the triad:

  1. Sudden onset abdominal pain
  2. Ascites (exudate)
  3. Tender hepatomegaly
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8
Q

How is Coeliac’s Disease investigated?

A

Importantly, if patients are already on a gluten-free diet they need to start eating gluten again for 6 weeks before the investigations.

Serology:

  • Anti-TTG (an IgA antibody) - best
  • Anti-endomyseal antibody (IgA)
  • Check for IgA deficiency (can lead to false negative)
  • Anti-gliadin

Duodenal biopsy:

  • Villous atrophy
  • Crypt hyperplasia
  • Increase in intraepithelial lymphocytes
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9
Q

What is Plummer Vinson Syndrome?

A

Plummer Vinson syndrome is a rare disease characterised by:

  • Difficulty in swallowing (both dysphagia and odynophagia secondary to oesophageal webs)
  • Glossitis
  • Iron-deficiency anaemia
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10
Q

What do you know about Hep D?

A
  • Single stranded RNA virus
  • Requires Hep B to infect
  • Superinfection is associated with fulminant hepatitis
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11
Q

Which blood test can help to distinguish between an upper GI and lower GI bleed in a patient with malaena?

A

Urea - it is raised in upper GI bleed as the protein in the blood gets digested.

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12
Q

What is Pellagra?

A

Pellagra is Vitamin B3 deficiency.

Clinical features are:

  • Dermatitis
  • Diarrhoea
  • Dementia
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13
Q

How would you investigate someone with suspected haemochromatosis?

A

Bloods:

  • Transferrin saturation + ferritin
  • Consider checking for the HFE gene mutation if there is a family history

MRI:

  • May show decreased organ signal intensity

Liver biopsy:

  • Pearl’s stain

(Joint X-Rays typically show chondrocalcinosis)

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14
Q

What is the managment for someone with haemochromatosis?

A
  1. First line is venesection, keeping trasnferritin saturation below 50%
  2. Iron chelation therapy (e.g. desferrioxamine or deferasirox)
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15
Q

Describe the managment of Crohn’s.

A

General Points:

  • Smoking cessation is key

Remission induction:

  • Steroids (oral, topical or IV)
  • Enteral feeding with elementary diet
  • 5-ASA drugs (e.g. mesalazine) used but evidence is less good
  • AZA/MTX or mercaptopurine as add on
  • Infliximab

Matinenance:

  • Azathioprine or mercaptopurine
  • MTX second line

Surgery:

  • 80% of Crohn’s will eventually have surgery
  • Most commonly ileocaecal resection
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16
Q

What is small bowel bacterial overgrowth syndrome?

A

This is characterised by excessive amounts of bacteria in the small bowel resulting in GI symptoms.

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17
Q

What are risk factors for Small bowel bacterial overgrowth syndrome?

A
  • Diabetes
  • Scleroderma (dysmotility)
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18
Q

What are the symptoms of Small bowel bacterial overgrowth syndrome?

How is it diagnosed?

A
  • Chronic diarrhoea
  • bloating and flatulence
  • Abdominal pain

Diagnosed by:

  • Hydrogen breath test
  • Small bowel aspiration and culture (but quite invasive so not often done)
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19
Q

What infection is commonly associated with diarrhoea, steatorrhoea?

A

Giardia lamblia - causes malabsorption and therefore greasy stools can occur.

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20
Q

What is carcinoid syndrome?

A
  • Carcinoid syndrome usually occurs when metastases are present in the liver and release serotonin into the sytemic circulation.
  • Can also occur with lung metastases, because they can release serotonin directly into the systemic circulation before it gets cleared by the liver.

Clinical features:

  • Flushing
  • Diarrhoea
  • Bronchospasm
  • hypotension
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21
Q

What are the investigations and management for carcinoid syndrome?

A

Investigations:

  • Urinary 5-HIAA
  • Plamsa chromogranin

Management:

  • Treat the underlying cause
  • Somatostatin analogues (e.g. ocreotide)
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22
Q

What is the mode of inheritance of Peutz-Jeghers Syndrome?

A

Autosomal Dominant

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23
Q

What ithe features of Peutz-Jeghers Syndrome?

A
  • Hamartomatous polyps in GI tract (mainly small bowel)
  • Pigmented lesions on lips, oral mucosa, face, palms and soles
  • Intestinal obstruction (e.g. intussusception)
  • GI bleeding
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24
Q

What is the treatment for C. Diff infection?

A
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25
Q

What is the mode of inheritance for haemochromatosis?

A

Autosomal recessive.

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26
Q

What are the components of the Child-Pugh Score?

What is this score used for?

A

The Child-Pugh score is used in the assessment of severity of liver cirrhosis.

A - Albumin

B - Billirubin

C - Clotting

D - Distension (Ascited)

E - Encepalopathy

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27
Q

What is the mainstay of treatment of alcoholic fatty liver disease?

A

Lifetyle changes, in particular weight loss, are key.

Insulin sensitising medication may play a role - ongoing research.

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28
Q

Which hepatobiliary condition is Crohn’s associated with?

A

Crohn’s is associated with the formation of gallstones.

This is as terminal ileitus leads to problems with bile salt absorption.

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29
Q

What criteria can be used for the grading of clinical severity of UC?

A

Truelove and Witts’ criteria.

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30
Q

What is the first line treatment for acute autoimmune hepatitis?

A

Steroids.

(Nb: acute autoimmune hepatitis can present with amenorrhoea in women)

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31
Q

What is the medical term for having a lump in the throat that isn’t there?

A

Globus Pharyngus.

This is the persistent sensation of having a lump in the throat when there is none.

Symptoms are often intermittent and relieved by swallowing food/drink.

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32
Q

What is the treatment for pharyngeal pouch?

A

SURGICAL REPAIR

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33
Q

What is xerostomia?

In which 2 conditions can this occur?

A

Xerostomia is dry mouth.

This is seen in Sjögren’s syndrome and in PBC: (the two are associated)

  • 70% of PBC have this
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34
Q

Why do patients with coeliac disease require regular immunisations?

A

Patients with coeliacs have functional hyposplenism.

For this reason, coeliac patients are offered the pneumococcal vaccine every 5 years.

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35
Q

Describe the iron studies you would expect a patient with haemochromatosis to have.

A

Typical iron study profile in patient with haemochromatosis:

  • transferrin saturation > 55% in men or > 50% in women
  • raised ferritin (e.g. > 500 ug/l) and iron
  • low TIBC
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36
Q

How is ulcerative colitis severity determined?

A
  • Mild: < 4 stools a day, with only a small amount of blood.
  • Moderate: 4-6 stools/day, varying amounts of blood but no systemic upset.
  • Severe: > 6 bloody stools/day. Features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers).
37
Q

Summarise the remission induction of mild-moderate ulcerative colitis.

A
  • Topical ± oral (depending on disease extent) aminosalicylate
  • Add topical or oral steroid if remission not achieved within 4 weeks
38
Q

Summarise the remission induction of severe ulcerative colitis.

A

These patients should be admitted to hospital.

  • IV steroids (or IC ciclosporin if steroids contraindicated)
  • Consider surgery, or dual therapy ciclosporin + steroids
39
Q

Describe the maintenance management for ulcerative colitis.

A
  • Topical ± oral aminosalicylate (depending on site affected)
  • Add oral azathioprine or mercaptopurine if ≥ 2 disease flares in the past year.
40
Q

What is the drug used to treat Wilson’s disease?

A

Penicillamine is first-line.

Trientine hydrochloride is an alternative chelating agent.

41
Q

What do you know about Wilson’s disease?

A
  • Autosomal recessive disorder, ATP7B gene on chromosome 13
  • Excessive copper deposition in tissues, eps:
    • Brain: basal ganglia degeneration, psychiatric problems
    • Liver: hepatitis, cirrhosis
    • Eyes: Kayser-Fleischer Rings
    • Kidneys: Renal tubular acidosis
  • Diagnosis:
    • Reduced serum caeruloplasmin
    • Reduced serum copper
    • Increased 24 hour urinary copper
42
Q

What is the most common causative organism in traveller’s diarrhoea?

A

Enterotoxogenic E. coli.

43
Q

Which two vessels are connected in a TIPS?

A

The portal vein to the hepatic vein.

44
Q

In which conditions would you see air in the biliary tree on AXR?

A

Gallstone ileus.

You would also see small bowel obstruction.

45
Q

How often should patients with coeliacs disease have blood tests?

A

Coeliacs disease patietns should have annual blood tests for:

  • FBC
  • Ferritin
  • TFTs
  • LFTs
  • B12 and folate
46
Q

What is Barrett’s oesophagus?

A

This is the metaplasia of the lower oesophageal mucosa, with the usualy squamous epithelium being replaced by columnar epithelium.

This incraeses the risk of oesophagela adenocarcinoma by 50-100 times.

47
Q

What is the management for someone who has Barrett’s oesophagus?

A
  • Endoscopic surveillance with biopsies every 3-5 years. Continue if metaplasia is shown.
  • High-dose PPIs

-> If dysplasia is identified, endoscopic intervention is offered:

  • Endoscopic mucosal resection
  • Readiofrequency ablation
48
Q

What are the risk factors for Barrett’s oesophagus?

A
  • GORD is the single strongest risk factor
  • Male (7x more than women)
  • Smoking
  • Central obesity

(not that EtOH is NOT an independent risk factor for Barrett’s - it is a risk factor for GORD though)

49
Q

How long before urea breath test should anitsecretory medications or antibiotics be stopped?

A

Antisecretory medications (PPIs, H2-antagonists) for 2 weeks.

ABx for 4 weeks.

50
Q

What is current advice regarding alcohol consumption for men and women?

A

Both sexes should:

  • Drink no more than 14 units per week
  • Spread this over 3 days or more

Best not to drink at all during pregnancy.

51
Q

Which score can be used to assess malnutrition?

A

The MUST (malnutrition universal screening tool). score

52
Q

What are the adverse effects of PPIs?

A
  • Osteoporosis -> increased risk of fractures
  • Hyponatraemia and hypomagnesaemia
  • Increased risk of C. diff infections
  • Microscopic colitis
53
Q

Which vessel clasically bleeds as a complication of PUD?

A

The Gastroduodenal artery. This is typically associated with a posterior duodenal ulcer.

54
Q

What are predisposing factors for bowel ischaemia?

A
  • Age
  • AF and other causes of emboli (endocarditis, malignancy)
  • Cardiovascular disease risk factors
  • Cocaine (in young people this can be a cause)
55
Q

What are common clinical features of mesenteric ischaemia?

A
  • Abdominal pain - often sudden onset and out of keeping with physical exam findings
  • Rectal bleeding
  • Diarrhoea
  • Fever
  • Elevated lactate
56
Q

How would you investigate mesenteric ischaemia?

A

CT is the investigation of choise

57
Q

What is the most common organism responsible for spontaneous bacterial peritonitis?

A

E. coli

58
Q

Which MEN is associated with gastrinomas?

A

MEN-I

The other endocrine neoplasias are:

  • Parathyroid
  • pituitary
  • Insulinoma
59
Q

Why do patietns with intestinal angina suffer from weight loss?

A

Mainly because they notice that eating brings on the pain.

Also because there is reduced blood flow to the gut, and therefore less absorption of food.

60
Q

How does oesophagitis present?

A

Oesophagitis often presents with a history of:

  • heart burn
  • Odynophagia
  • Absence of weight loss or systemic symptoms (which would point towards more sinister diagnosis)
61
Q

What type of cancer is more common with GORD?

A

Adenocarcinoma of the oesophagus.

Typically in the lower 1/3rd of the oesophagus.

62
Q

What type of cancer is more common in smokers/EtOH consumers?

A

Squamous cell cancer is more common in people who use tobacco of the drug EtOH.

SCC more commonly affects the middle/upper part of the oesophagus.

63
Q

How is oesophageal cancer investigated?

A

First-line test:

  • Upper GI endoscopy

Others:

  • Contrast swallow in classifying motility disorders - doesn’t help assess tumour
  • CT - staging. If metastatic disease is identified, then more complex imaging is requried, e.g. PET-CT
    • If no metastasis is identified, then endoscopic USS is performed. This is also the best one to perform to assess mural invasion
64
Q

Summarise the managment of oesophagel cancer.

A

If operable, surgical resection is done:

  • Ivor-Lewis 2 stage oesophagectomy.
  • McKeown 3 stage
  • Transhiatal
  • Laparoscopic

Adjuvant chemotherapy is usually given.

65
Q

What are the complications of oesophagectomies?

A
  • Anastomotic leak, with an intrathoracic anastomosis this will result in mediastinitis.
  • Damage to surroudnign structure:
    • Laryngeal nerve -> hoarseness
  • Reflux disease
  • Respiratory illness (either post surgical or due to apsiration)
66
Q

Why can an oesophageal cancer present with hoarse voice?

A

It can compress the phrenic nerve and therefore lead to hoarse voice.

67
Q

What is Garnders Syndrome?

A

Autosomal dominant form of familial adenomatous polyposis.

There are multiple colonic polyps due to a mutation in APC gene on chromosome 5. Also associated with skull osteomas, thyroid cancer, epidermoid cyst.

Risk of cancer is high, and thus colectomy recommended.

(If just colon: FAP, if extra features: Gardner’s syndrome)

68
Q

What is hereditary nonpolyposis colorectal cancer?

A

Aka. Lynch Syndrome this is an autosomal dominant condition with mutations in a DNA mismatch repair gene.

It leads to colorectal and endometrial cancer at young age.

Also associated with pancreatic cancers.

69
Q

What are the potential side effects of PPIs?

A
  • Electorlyte disturbances:
    • Hyponatraemia (cause unclear)
    • Hypomagnasaemia
  • Osteoporosis: increased risk of fractures
  • Microscopic colitis
  • Increased risk of C. diff infections
70
Q

What is the investigation of choice for suspected PSC?

A

MRCP. This is preferred to ERCP as it is less invasive.

71
Q

How can the COCP lead to jaundice?

A

The COCP is associated with drug-induced cholestasis.

This would still lead to an obstructive LFT picture.

72
Q

What medications can be used for the treatment of IBS, treating diarrhoeal and constipation symptoms?

A

Loperamide for the management of diarrhoeal symptoms, linaclotide for the managment of contipation symptoms.

Linaclotide for a CLOT, loperamide for the sLOP.

73
Q

How does chronic Hep B present on licht microscopy?

A

Ground glass hepatocytes

74
Q

What is hepatorenal syndrome?

A

Hepatorenal syndrome is renal failure 2° to liver failure.

The splanchinic vasodilation triggered by portal hypertension; there is systemic release of vasodilators, leading to inadequate renal perfusion and thus a fall in GFR.

There are 2 types:

  • 1: Rapidly progressive (< 2 weeks; doubling of serum creatinine or halving of creatining clearance). This is associataed with poor prognosis
  • 2: Slowly progressive (>2 weeks). Better prognosis but still poor.
75
Q

Decribe the prophylaxis of variceal haemorrhage.

A

Propanolol is first-line.

Endoscopic variceal band ligation can be performed in several sessions until all have been eradicated.

76
Q

What is gastroparesis?

A

Gastroparesis is delayed gastric emptying 2° to decreased peristaltic waves. This is commonly due to diabetic neuropathy.

  • symptoms include erratic blood glucose control, bloating and vomiting
  • management options include metoclopramide, domperidone or erythromycin (prokinetic agents)
77
Q

What are medications licensed for the treatmnet of hepatic encepalopathy?

A

Management of hepatic encephalopathy is designed to treat associated hyperammonemia.

  • Lactulose: decreases gut transit time and thereofore makes absorption of ammonia less
  • Rifamixin: non-absorbable derivative of rifampicin. Affects intestinal flora
  • Neomycin: kills intestinal bacteria that produce ammonia
78
Q

How do you classiviy the severits of UC?

A

Mild:

  • < 4 stools a day
  • Only small amount of blood

Moderate:

  • 4-6 stools a day
  • Varying amounts of blood
  • No systemic upste

Severe:

  • > 6 bloody stools a day
  • Features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers)
79
Q

Other than early-onset COPD, what could be a consequence of A1AT-deficiency?

A

A1AT deficiency is also associated with an increased risk of HCC.

80
Q

Summarise the management of NAFLD.

A
  • Mainstay of treatment is lifestyle changes (particularly weight loss) and monitoring
  • Gastric banding, insulin-snesitising drugs (metformin, pioglitazone)
81
Q

Summarise the invetigations for NAFLD.

A

NAFLD shouldn’t be screened for - usually picked up incidentally e.g. on liver USS.

If suspected, confirm with fibroscan. Also do test for “enhanced liver fibrosis”.

82
Q

What is the most specfic lab finding in a patient wtih liver cirrhosis in the setting of CLD?

A

Thrombocytopenia.

The normally liver makes and releases TPO (Thrombopoetin) which stimulates platelet production. If the liver isn’t working properly it doesn’t release TPO as usual which means that less platelets are made.

83
Q
A
84
Q

What test is done to assess for liver cirrhosis?

A

Tramsoemt elastography, aka. Fibroscan®

85
Q

What can lead liver dysfunction post MI?

A

Ischaemic hepatitis

This can result froma cute hypoperfusion of the liver, e.g. in cardiac arrest. ALT levels are elevated.

86
Q

For which patients should you consider antibiotic prophylaxis if they have ascites?

A

ABx prophylaxis should be given to patients with ascites if:

  • They have had a previous episode of SBP
  • Protein in ascitic fluid is <15 g/L and either hepatorenal syndrome or Child-Pugh ≥9

In these patients, offer ciprofloxacin

87
Q

What is the treatment of ascites 2° to liver disease?

A
  • Restricting dietary sodium ± fluid restriction
  • Spironolactone (or another aldosterone antagonist).
    • Loop diuretics are often added
  • Drainage if tense ascites
    • Large-volume paracentesis for the treatment of ascites requires albumin cover
    • Paracentesis induced circulatory dysfunction can occur due to large volume parancentesis. Associated with high rates of recurrence + hepatorenal syndrome
  • Prophylactic antibiotics are offered to patients with an ascitic protein of 15g/L or less
  • TIPS considered in some patients
88
Q

What do pigment loaden macrophages in the bowel wall indicate?

A

Laxative abuse

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