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3b specialties > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

What are the two main characteristic features of acute upper GI bleed?

A

Haematemesis and/or malaena

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2
Q

Give 2 groups of patients with higher prevalence of UGIB.

A

Men, low SES, elderly

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3
Q

What are the two most common causes of UGIB?

A

Ulcer bleeds and variceal bleeds.

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4
Q

Name 3 risk factors for an UGIB?

A

NSAIDs, aspirin, anticoagulants, H. pylori

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5
Q

What are the two assessment tools for risk stratification in UGIB advocated by NICE? At what point should each be used?

A

Glasgow-Blatchford score at first assessment, then the full Rockall score following endoscopy.

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6
Q

What does the Glasgow-Blatchford score predict more accurately than the Rockall score?

A

An individual’s need for intervention and transfusion. Both score similarly on predicting mortality.

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7
Q

In an UGIB, what management significantly reduces mortality

A

Early, intensive resuscitation

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8
Q

How should haemodynamic stability be acheived in UGIB?

A

Use of IV crystalloid/colloid, blood transfusion, O2 therapy, correction of coagulopathy

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9
Q

What strategy of blood transfusion is used in UGIB and why?

A

Restricted blood transfusion therapy (e.g. Hb of 70-90g/L), associated with better 6 week survival and reduced risk of rebleeding

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10
Q

If there is a high suspicion of variceal bleeding in an UGIB (e.g. liver cirrhosis, signs of liver disease, previous variceal bleeding) what two drugs should you give?

A

IV terlipressin.

Prophylactic broad spectrum Abx due to increased risk of bacterial infection.

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11
Q

What investigation is used to diagnose the cause of UGIB and give prognostic details?

A

Endoscopy

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12
Q

When should endoscopy occur following an UGIB in:

a) a haemodynamically stable patient
b) an unstable patient

A

a) Within 24 hours of admission

b) Immediately following resuscitation

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13
Q

What are 2 intervention options for non-variceal UGIB?

A

1) mechanical method (e.g. clips) with adrenaline
2) thermal coagulation with adrenaline
3) injection of thrombin with adrenaline

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14
Q

If interventional endoscopic techniques don’t stop bleeding in non-variceal UGIB, what should be considered?

A

Interventional radiology or surgery

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15
Q

What is the first line treatment for oesophageal varices?

A

Endoscopic band ligation

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16
Q

First line treatment for gastric varices?

A

Endoscopic intravariceal injection of cyanoacrylate tissue glue

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17
Q

What should be considered for oesophageal varices if band ligation doesn’t work?

A

TIPS- transjugular intrahepatic portosystemic shunt

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18
Q

What therapy should be used following haemostasis in high risk UGIB patients? Give length of treatment and route of administration.

A

72 hours IV PPI

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19
Q

What should you do if a patient is on aspirin with an UGIB?

A

Acutely- withhold until haemostasis acheived, then restart within 7 days (ideally 1-3 days after)

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20
Q

What should you do if a patient is on an NSAID with an UGIB?

A

Acutely= stop NSAID. Review need for NSAID. If still needed, restart COX-2 selective NSAID (e.g. celecoxib) at lowest dose with PPI.

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21
Q

What is the first step in diagnosis of coeliac disease?

A

Tissue transglutaminase antibodies + immunoglobulins (total IgA)

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22
Q

Why do you have to measure immunoglobulins alongside TTG antibodies for the diagnosis of coeliac disease?

A

Because 2-5% of patients are IgA deficient, and TTG antibodies are mostly IgA. So may get a false negative result if you just measure TTG Abs

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23
Q

What is second line serological testing option for coeliac disease?

A

IgA Anti-endomysial and IgG anti-gliadin antibodies.

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24
Q

What is the gold standard investigation for diagnosis of coeliac disease? What should patients be instructed to do prior to this investigation.

A

OGD and duodenal biopsy. Patients advised to continue gluten-rich diet for at least 6 weeks prior to testing.

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25
Q

What are the 3 classical histological findings of coeliac disease?

A

Subtotal villous atrophy
Crypt hyperplasia
Lymphocytic infiltration of lamina propria

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26
Q

Those with coeliac disease should avoid foods containing what three ingredients?

A

Wheat, rye, barley

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27
Q

What monitoring do patients with coeliac disease require?

A

Annual BMI monitoring

Annual review to assess diet adherence, symptom control, need for further investigations (e.g. DXA scan)

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28
Q

What is the first line treatment of prevention of variceal bleeding?

A

Non-cardioselective beta-blockers e.g. propranolol, carvedilol, labetalol.

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29
Q

What is the most common reason for iron deficiency anaemia in post-menopausal women and adult men?

A

Blood loss from the GI tract

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30
Q

What is the cell morphology in iron deficient anaemia?

A

Hypochromic, microcytic

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31
Q

Name 2 other types of anaemia that are microcytic hypochromic other than IDA.

A

Thalassaemia, sideroblastic anaemia, some anaemias of chronic disease

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32
Q

What is the most powerful test for iron deficiency?

A

Serum ferritin

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33
Q

Say whether the following markers would be high or low in IDA;

  • ferritin
  • transferrin saturation
  • TIBC
  • red cell zinc protoporphyrin
  • serum transferrin receptor
A
  • low
  • low
  • high
  • high
  • high
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34
Q

When taking a history for IDA, what counts as a significant family history of colorectal cancer?

A

One affected first degree relative <50, or two affected first degree relatives

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35
Q

All patients with IDA should be screened for?

A

Coeliac disease (with serology)

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36
Q

In postmenopausal women and adult men with confirmed IDA, what further investigations would you do?
When would you not investigate further in these groups?

A

Upper and lower GI imaging e.g. OGD and colonoscopy.

You wouldn’t investigate further if there is a history of significant overt non-GI blood loss.

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37
Q

What is the treatment to correct iron deficiency? Give drug, dose, route, and length of treatment.

A

Ferrous sulfate 200mg 2-3 times daily PO, continued for 3 months after the iron deficiency is corrected.

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38
Q

What is second line treatment for iron deficiency if a patient can’t tolerate PO ferrous sulfate?

A

IV infusions e.g. iron sucrose or ferric carboxymaltose.

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39
Q

When are blood transfusions indicated in the treatment of IDA?

A

If a patient has symptomatic anaemia even following iron therapy, or if they are at risk of cardiovascular instability as a result of their anaemia

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40
Q

Iron deficiency occurs in 5-12% of otherwise healthy premenopausal women. Give 3 causes.

A

Menstruation, increased demands in pregnancy and breastfeeding, dietary insufficiency.

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41
Q

Give 3 situations where a premenopausal woman should be further investigated for IDA.
What investigation should they all receive?

A
  • All should have coeliac screen
  • OGD for women with IDA and upper GI symptoms
  • Colonoscopy if colonic symptoms, strong FH of colon cancer, persistent IDA after iron therapy and treatment of causes
  • Premenopausal women with IDA but without menstruation (hysterectomy, contraceptives)
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42
Q

How is GI bleeding investigated if colonoscopy is contraindicated?

A

CT colonography

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43
Q

What prep is needed for a CT colonography

A

Bowel prep 2 days before= laxatives and drinking clear fluids (including water, black tea and coffee, clear soup)

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44
Q

Is H. pylori gram negative or gram positive?

A

Gram negative

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45
Q

What does H pylori produce that allows it to survive in low pH conditions?

A

Urease

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46
Q

How does H pylori increase risk of gastric and duodenal ulceration?

A

Stimulates gastrin production and inhibits somatostatin production, resulting in increase in acid secretion

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47
Q

Give 2 ways of testing for H pylori.

A

Carbon-13 urea breath test
Stool antigen testing
Lab-based serological testing

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48
Q

What medication must be stopped prior to breath testing for H pylori and why?

A

PPIs stopped 2 weeks prior, as may result in false positive breath tests.

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49
Q

How is H pylori eradicated?

A

7 day course of triple therapy:

High dose PPI with 2 twice-daily antibiotics

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50
Q

What is the typical triple therapy regime for H pylori eradication?

A

High-dose PPI (e.g. lansoprazole 30mg) + amoxicillin + clarithromycin/metronidazole

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51
Q

How long following triple therapy is retesting to check for eradication of H pylori and what is the method?

A

6-8 weeks with carbon-13 urea breath test

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52
Q

Which of the forms of IBD is more common?

A

UC

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53
Q

Ulcerative colitis frequently presents with what clinical feature? Give 2 other abdominal clinical features.

A

Bloody diarrhoea

Colicky abdominal pain, tenesmus, may have constipation and/or fresh PR bleeding if localised rectal disease

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54
Q

Give 5 investigations for suspected UC in primary care and the likely results.
What result is an important marker of severity?

A

FBC- low Hb, raised WCC, raised platelets
CRP/ESR- raised
LFTs- low albumin (important marker of severity)
U&Es- electrolyte disturbance, signs of dehydration?
TFTs- rule out hyperthyroidism
Serum ferritin, vit B12/folate, vit D- may be low with malabsorption
Faecal calprotectin- raised with inflammation, normal in IBS
Coeliac serology- rule out coeliac disease
Stool MC&S (including Clostridium dificile)- to rule out infective cause

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55
Q

What radiological imaging is indicated to assess presence of complications of UC?

A

AXR +/- erect CXR

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56
Q

What is regarded as the best modality to diagnose UC and assess disease severity and extent?

A

Full ileocolonoscopy with 2 biopsies at a minimum of 5 sites.

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57
Q

When is colonoscopy contraindicated in IBD and what is used instead to confirm the diagnosis?

A

Contraindicated in acute colitis due to association with a high risk of perforation. Flexible sigmoidoscopy performed instead to confirm the diagnosis.

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58
Q

Macroscopic features of UC, true or false:

  • Continuous
  • Only ever affects up to the ascending colon
  • Strictures
A
  • True
  • False, may occasionally affect the terminal ileum = backwash ileitis
  • False, strictures very rare in UC (although do occur)
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59
Q

Give 3 microscopic features of UC

A

Confined to the mucosa
Crypt abscesses common
Goblet cell dysplasia common
Rarely granuloma formation

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60
Q

True/false: fistula formation occurs in UC.

A

False- the inflammation is confined to the mucosa so fistula formation doesn’t occur (unlike in Crohn’s)

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61
Q

Outline the management of inducing remission in severe UC.

A
  1. Urgent hospital admission
  2. IV corticosteroids (or cyclosporin if steroids CI)
  3. VTE prophylaxis (pts are prothrombotic)
  4. Add IV cyclosporin if unresponsive to steroids after 72 hours
  5. Consider urgent surgery- if acute complications of failure to respond to medical therapy.
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62
Q

What are first line agents for inducing remission of UC in mild/moderate disease?

A

Aminosalicylates e.g. mesalazine

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63
Q

In patients with distal disease, what form of aminosalicylates might be useful to use?

A

Topical e.g. suppositories or enemas

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64
Q

What is used to induce remission of mild/mod UC if aminosalicylates are CI (or as an add-on if no improvement after 4 weeks)?

A

PO corticosteroids

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65
Q

If there is no adequate response to Aminosalicylates or corticosteroids, what may be added to induce remission in mild/mod UC?

A

Tacrolimus

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66
Q

What type of drug is tacrolimus?

A

Calcineurin inhibitor

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67
Q

What class of drugs may be used to induce remission in UC if conventional therapies haven’t worked?

A

Biologic agents e.g. infliximab

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68
Q

What criteria are useful in evaluating the severity of an acute exacerbation of UC?

A

Truelove and Witts

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69
Q

What are first line agents for maintaining remission in UC?

A

Aminosalicylates e.g. mesalazine, sulfasalazine

70
Q

If a patient with UC has had >2 severe exacerbations in a year requiring corticosteroid therapy, or unresponsive to oral aminosalicylates, what drugs should be considered?

A

Immunosuppressive drugs e.g. mercaptopurine or azathioprine

71
Q

If a patient is chronically symptomatic with UC and fails to respond to medical theapy, what may be considered?

A

Elective surgery

72
Q

Aside from medical/surgical therapy, give 3 important aspects of management of UC.

A
  • Colorectal cancer surveillance
  • Monitor for osteoporosis
  • Monitor for vit B12/folate, iron, vit D, calcium deficiency
  • Psychological impact
  • Extra-intestinal manifestations
  • Vaccinations e.g. influenza, pneumococcal
73
Q

Give 3 GI clinical features of Crohn’s disease.

A

Diarrhoea (often not bloody), abdominal discomfort, weight loss, aphthous ulcers, glossitis, fistulae

74
Q

The investigations for Crohn’s are very similar to those of UC. What 3 extra imaging investigations may be done and why?

A

MRI pelvis- useful in perianal disease to evaluate extent of disease and look for fistulae
MRI enterography or capsule endoscopy- to assess small bowel disease
Upper GI endoscopy- in patients with upper GI symptoms

75
Q

Macroscopic features of Crohn’s, true or false:

  • Continuous inflammation
  • Commonly affects terminal ileum and ascending colon
  • Stricture formation
A
  • False, skip lesions/cobblestone pattern
  • True, but can be anywhere from mouth to anus
  • True
76
Q

Give 3 microscopic features of Crohn’s disease.

A

Transmural inflammation, extensive fibrosis with fissuring, non-caseating granuloma formation common, fistula formation.

77
Q

What drug class is used first line for inducing remission in Crohn’s?

A

PO or IV corticosteroids

78
Q

What drugs could be used in distal ileal or right-sided colonic Crohn’s disease as an alternative to steroids? When should they not be used?

A

Budesonide or 5-ASA (aminosalicylates e.g. mesalazine). Not to be used in severe episodes

79
Q

What is used as add-on therapy in severe Crohn’s?

A

Azathioprine/methotrexate or 6-MP

80
Q

Levels of what enzyme need to be checked before starting azathioprine or 6-MP and why?

A

Thiopurine methyltransferase. Up to 10% have lowered TPMT activity and so are more susceptible to thiopurine toxicity.

81
Q

What drugs are considered in Crohn’s to induce remission if conventional therapy has be unsuccessful?

A

Biologics eg. infliximab and adalimumab

82
Q

When might surgery be considered as an alternative to medical therapy to induce remission in Crohn’s

A

If it’s localised distal ileal disease

83
Q

First line agents for maintaining remission of Crohn’s?

What is an alternative second line agent?

A

Azathioprine or 6-MP

Methotrexate

84
Q

What is the management for strictures in Crohn’s disease?

A

Balloon dilatation, or surgery

85
Q

Monitoring requirements for Crohn’s?

A

Assessment for osteopenia/porosis

Colonoscopic surveillance for colorectal cancer offered to patients whose symptoms started 10 years ago

86
Q

Name 5 extra-intestinal manifestations of IBD.

A

Skin - Erythema nodosum, Pyoderma gangrenosum
Eyes - Anterior uveitis, Episcleritis
MSK- Arthritis, Ankylosing spondylitis
Biliary- Gallstones (more common in Crohn’s), PSC, cholangiocarcinoma (more common in UC)
Renal stone
Amyloidosis

87
Q

In patients with simple perianal Crohn’s disease, what may be used first line?

A

PO antibiotics e.g. metronidazole or ciprofloxacin

88
Q

What blood marker classically rises with an upper GI bleed and why?

A

Urea. Blood is digested into protein in the stomach, absorbed into the portal system and then metabolised into urea.

89
Q

True/false: ileostomies are generally spouted whereas colostomies are flush with the skin?

A

True- to prevent corrosive effluent from coming into contact with skin

90
Q

What are two emergency complications of UC?

A

Toxic megacolon and perforation

91
Q

What is the pathophysiology of achalasia?

A

Aperistalsis of the oesophagus and inadequate relaxation of the LOS due to degenerative loss of ganglia from Auerbach’s plexus resulting in reduced parasympathetic tone.

92
Q

How does achalasia present?

A

Progressive dysphasia affecting both solids and liquids. Regurgitation, retrosternal chest pain.

93
Q

Achalasia has a small associated risk of developing which cancer?

A

Squamous cell carcinoma of the oesophagus

94
Q

What is the first line investigation for achalasia, and what is the classic sign?

A

Barium swallow- bird’s beak appearance

95
Q

What is the gold standard investigation for diagnosis of achalasia? What result is diagnostic?

A

Oesophageal manometry. High resting pressure of the LOS.

96
Q

Other than barium swallow and manometry, what two investigations may you perform for achalasia?

A

CXR- widened mediastinum due to dilated oesophagus behind heart
Upper GI endoscopy- to rule out malignancy

97
Q

If the patient is fit, what is the first line treatment option for achalasia?

A

Surgical myotomy (Heller procedure)

98
Q

What management option is used in older patients with comorbidities for treating achalasia?

A

Endoscopic pneumatic dilatation of the lower sphincter

99
Q

Patients unfit or unwilling to have invasive treatment for achalasia should receive? Why is this not first line?

A

Botulinum injections into the sphincter. Disease frequently recurs

100
Q

A patient presents to the GP complaining of intermittent dysphagia (both solids and liquids), and transient retrosternal chest pain. What is the most likely diagnosis?

A

Oesophageal spasm

101
Q

What is the characteristic sign on barium swallow of oesophageal spasm?

A

Corkscrew oesophagus

102
Q

What is the first and second line options for oesophageal spasm?

A

1st line= trial of PPIs

2nd line= nitrates and CCBs

103
Q

A pharyngeal pouch is a/an (1) outpouching of the oesophagus through the Killian dehiscence, the weak area of the (2).

1) posterolateral/posteromedial/anterolateral/anteromedial
2) circular oesophageal muscle/longitudinal oesophageal muscle/cricopharyngeus muscle/cricoarytenoid muscle

A

1) Posteromedial

2) Cricopharyngeus muscle

104
Q

A patient presents to their GP complaining of progressive dysphagia, regurgitation and halitosis. The GP suspects a pharyngeal pouch. What is the investigation of choice? What investigation is discouraged and why? What is the management?

A

Barium swallow
Endoscopy strongly discouraged as perforation of pouch may occur.
Management is surgical, if patient is symptomatic.

105
Q

Hiatus hernias are classified as sliding, rolling or mixed. Which is the most common form?
Patients with which type should be considered for repair and why?

A

a) Sliding (80%)

b) Rolling, as there’s an increased risk of strangulation

106
Q

What are the red flag symptoms requiring urgent referral for OGD for suspected oesophageal malignancy according to NICE guidance?

A
  • Dysphagia

- Over 55 with weight loss and dyspepsia

107
Q

Management of GORD

A
  1. Lifestyle modification (stop smoking, dietary advice, weight loss, antacids)
  2. PPI therapy for 4-8 weeks
  3. Low-dose PPI/switch to H2 antagonist if symptoms persist or recur
  4. Surgery
108
Q

What is the surgical management for GORD? When is it indicated?

A

Laparoscopic Nissen fundoplication. Indicated in confirmed GORD, have responded to PPI therapy but don’t wish to take long-term PPIs/can’t tolerate long term/have severe disease.

109
Q

What are 3 complications of a Nissen fundoplication?

A

Dysphagia, abdominal bloating, recurrence of GORD.

110
Q

If surgical intervention for GORD is being considered, what investigation must be done? What is diagnostic for GORD?

A

Ambulatory intraluminal pH monitoring.

A pH of <4, at more than 4% of the time is diagnostic.

111
Q

Give 3 complications of GORD.

A

Oesophagitis, Barret oesophagus, oesophageal carcinoma, benign oesophageal stricture.

112
Q

What is the histological transformation that occurs in Barrett oesophagus?

A

From normal oesophageal squamous epithelium to columnar gastric epithelium.

113
Q

What is the management of Barrett oesophagus in the case of:

a) Low-grade dysplasia
b) High-grade dysplasia

A

a) Conservatively, with continuous surveillance

b) Surgical oesophagectomy

114
Q

More associated with SCC or AC of the oesophagus:

a) Smoking and drinking
b) Obesity
c) Barrett oesophagus

A

a) SCC
b) AC
c) AC

115
Q

Investigation for patient with suspected oesophageal malignancy?

A

Urgent OGD within 2 weeks. Biopsies for histology

116
Q

What % of patients with oesophageal malignancy present with metastatic disease?

A

70%- treatment is therefore mostly palliative (chemo/radiotherapy and stenting)

117
Q

Which are more common, duodenal or gastric ulcers? How can you tell the difference from the history?

A

Duodenal significantly more common. Epigastric pain of duodenal ulcers tends to improve on eating, whereas with gastric it gets worse.

118
Q

Complications of peptic ulcers include perforation or bleeding. Which complication are the following types of ulcers more likely to cause:

a) Anterior duodenal ulcers
b) Posterior duodenal ulcers

A

a) perforation

b) bleeding

119
Q

Posterior duodenal ulcers are more likely to cause bleeding because of their proximity to which vessel?

A

Gastroduodenal artery

120
Q

Gastric cancer is typically of what histology?

A

Adenocarcinoma

121
Q

Give 4 risk factors associated with gastric cancer.

A

H. pylori infection, alcohol consumption and smoking, consumption of salted and smoked foods, AI atrophic gastritis, familial adenomatous polyposis, male>female 2:1, more common in Asia

122
Q

Name 3 possible causative organisms of dysentery

A

Campylobacter jejuni, salmonella, shigella, E. coli (EHEC 0157:H7), Entamoeba histolytica

123
Q

Name 5 causes of diarrhoea.

A

Acute- acute flare of IBD, diverticulitis, ischaemic colitis, drug-induced, infective
Chronic- laxative overuse, hyperthyroidism, hypercalcaemia, colorectal cancer, IBS, IBD

124
Q

Is Clostridium difficile gram-positive or gram-negative?

A

Gram positive

125
Q

What drugs are associated with C. diff colitis?

When do symptoms typically manifest following therapy?

A

‘C’ antibiotics e.g. co-amoxiclav, cephalosporins, ciprofloxacin, clindamycin.
5-10 days after antibiotic therapy

126
Q

Investigations for C diff?

A

Bloods- FBC, U&E, albumin, CRP
Stool MC&S including C. diff cytotoxin analysis
Imaging- AXR may show colonic dilatation

127
Q

Outline the 3 main components of managing C. diff.

A
  1. Infection control- side room, barrier nursing
  2. Medication review- stop causative agents (PPIs, Abx)
  3. Antibiotic therapy- 10-14 days PO 400mg metronidazole
128
Q

What is the treatment for severe C. diff disease?

A

IV metronidazole + ORAL vancomycin

129
Q

What 2 haplotypes is coeliac diseases highly associated with?

A

HLA-DQ2 - 95% pts

HLA-DQ8 - 80% pts

130
Q

What is the name of the associated cutaneous manifestation of coeliac disease?
What is the distribution of this rash, typically?

A

Dermatitis herpetiformis

Typicaly affects the extensor surfaces (elbows, knees, buttocks)

131
Q

Name 3 associated conditions with coeliac disease.

A

Autoimmune- T1DM, thyroid disease, PBC

Cancer- lymphoma, breast, small bowel

132
Q

What test can confirm a diagnosis of SIBO?

A

Hydrogen breath test

133
Q

How is SIBO treated?

A

Underlying cause treated if possible, otherwise cyclical antibiotic regime.

134
Q

Over 50% of small bowel malignant tumours are of which type?

A

Adenocarcinoma

135
Q

What 2 investigations can be used to identify small bowel tumours?

A

Capsule endoscopy or CT

136
Q

What cells do neuroendocrine tumours/carcinoid tumours arise from?
Where do they commonly occur?

A

Enterochromaffin cells of the intestine

Terminal ileum and appendix

137
Q

Patients with neuroendocrine tumours typically present with obstructive symptoms. In fewer than 10%, ectopic hormone production produces systemic symptoms.

a) what is this called?
b) what hormone is released?
c) what symptoms would you expect?
d) what investigation helps diagnosis?

A

a) Carcinoid syndrome
b) Serotonin (5-HT). Other vasoactive substances released include prostaglandins, kinins, substance P
c) Facial flushing, chronic diarrhoea, wheezing, palpitations, abdominal pain
d) urinary 5-HIAA

138
Q

The mainstay treatment for carcinoid tumours of the intestine is surgical resection. What drug class may be used for symptomatic control of carcinoid syndrome? Give 2 examples of drugs.

A

Somatostatin analogues

Octreotide and lanreotide

139
Q

Give 2 clinical features of IBS

A

Abdominal pain or discomfort
Bloating
Change in bowel habit

140
Q

Give 2 possible triggers of altered GI sensitivity towards stimuli that occurs in IBS.

A

Physiological/psychological stress, certain foods, bacterial overgrowth

141
Q

True/false: IBS is a diagnosis of exclusion.

A

False- the diagnosis should be made positively on symptom-based criteria

142
Q

What criteria can be used to aid diagnosis of IBS?

A

Rome criteria

143
Q

What are the 4 main components of managing IBS.

A

1) Lifestyle changes- physical activity, leisure time
2) Dietary changes- regular meals, hydration, avoid high fibre/caffeinated and carbonated foo/drinks
3) Pharmacological therapy- based on predominant symptom e.g. anti-spasmodics, laxatives, antimotility
4) Psychological therapy- CBT, psychotherapy, hypnotherapy if refractory to medical therapy

144
Q

What diet does NICE advocate for IBS?

A

Low FODMAP diet

145
Q

What is second-line pharmacological therapy for IBS?

A

Amitriptyline

146
Q

What is the investigation modality of choice for ischaemic bowel disease?

A

CT angiogram

147
Q

If bowel ischaemia is suspected, what investigation should be done urgently?

A

Urgent ABG with lactate analysis. High lactate is consistent with cell hypoxia/ischaemia

148
Q

Give 3 causes of ischaemic bowel disease.

A

Primary atherosclerosis, distal embolism (associated with atrial fibrillation), vasculitis, septic shock, hypoperfusion

149
Q

True/false: diverticulitis typically presents with RIF pain and pyrexia.

A

False, typically it’s LIF pain and pyrexia

150
Q

What imaging is the best to establish a diagnosis of diverticulitis?

A

Contrast-enhanced CT

151
Q

Management of asymptomatic diverticular disease?

A

High-fibre diet, laxatives for constipation

152
Q

Management of mild diverticulitis?

A

Oral hydration and bowel rest.

7 day course of PO co-amoxiclav and metronidazole

153
Q

Management of severe diverticulitis?

A

Admitted, NBM
IV fluids, analgesia, supportive therapy
IV antibiotics based on local guidelines
Surgery if indicated

154
Q

Name 3 complications of diverticulitis.

A

Perforation, major haemorrhage, abscess, strictures

155
Q

Give 3 features associated with a higher risk of malignant transformation of adenomatous polyps.

A

Size >1.5cm
Multiple polyps (>=5)
Sessile nature (not pedunculated)
Villous nature

156
Q

Most polyps are detected incidentally on colonsocopy/ Should they be removed and why?

A

Yes- to reduce the risk of colorectal cancer development

157
Q

Frequency of colonoscopic surveillance following polypectomy depends on what two factors?

A

Size and number of polyps

158
Q

The inherited polyposis syndromes FAP and HNPCC are both AR inherited, true or false?

A

False- they’re both AD

159
Q

Familial adenomatous polyposis presents with hundreds to thousands of adenomas, which develop predominantly where?

A

In the colon and rectum.

160
Q

What is the best treatment option to prevent cancer development with FAP?

A

Early prophylactic colectomy and lifelong follow up

Genetic testing for first degree relatives

161
Q

Give 5 risk factors for colorectal cancer

A

FH, inherited polyposis syndrome, diet high in red meat and saturated fat and low in fibre, sedentery lifestyles (smoking, obesity, alcohol excess), IBD, radiation exposure

162
Q

Occult bleeding, anaemia, constipation, late obstruction, colicky abdo pain and weight loss are more typical presentations for a left or right-sided CRC?

A

Right-sided lesion.

163
Q

What is the first line investigation for CRC?

What are alternatives if this is CI?

A

Colonoscopy

Flexible sigmoidoscopy or CT colonogram (e.g. if patient can’t have colonoscopy due to comorbidities

164
Q

Fresh PR bleeding, loose stools, early obstruction are more typical in left or right sided lesions of CRC?

A

Left-sided lesions

165
Q

Imaging for staging of CRC should be:

a) contrast enhanced CT C/A/P
b) non-contrast CT C/A/P
c) MRI C/A/P
d) AXR

A

a) contrast enhanced CT CAP

166
Q

What marker is used to monitor treatment response and follow up in CRC?

A

Serum carcinoembryonic antigen

167
Q

What are the two staging classifications that can be used for CRC?

A

TNM and Duke classification

168
Q

Classification of haemorrhoids is based on what two factors?

A 
Prolapse and reducability.
1= no prolapse
2= prolapse on straining but reduces spontaneously
3= prolapse but manually reducible
4= permanently prolapsed
169
Q

What is the main difference in presentation of haemorrhoids and anal fissure?

A

Patients with anal fissures present with very severe anal pain.

170
Q

Acute management of anal fissure?

Chronic management?

A

Soften stool- high fibre diet, high fluid intake, laxatives
Lubricants before defecation, topical anaesthesia, analgesia

Continue above techniques, topical GTN first line, CCBs second line. May need surgical sphincterotomy

171
Q

Presentation of anorectal abscess?

A

Extreme pain (may be unable to sit), anal/perianal discharge, occasionally systemic upset (pyrexia)

172
Q

What are the 3 main sites of anorectal abscesses?

A

Perianal, intersphincteric, ischiorectal.

3b specialties (15 decks)

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