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Gastroenterology > Gastro > Flashcards

Gastro Flashcards

1
Q

What are the diagnostic indications for upper GI endoscopy? (6)

A 
Haematemesis
Persistent vomiting
New dyspepsia (if ≥55 years)
Gastric biopsy (? cancer)
Duodenal biopsy
Iron deficiency (cancer; hiatus hernia)
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2
Q

What are the therapeutic indications for upper GI endoscopy? (4)

A

Treatment of a bleeding lesion
Variceal banding and sclerotherapy
Stricture dilatation
Stent insertion (e.g. for palliation of oesophagel malignancy)

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3
Q

What instuctions should be give pre-procedure in upper GI endoscopy? (4)

A
  • Stop PPIs 2 wks pre-op if possible
  • Stop warfarn 5 days pre-op (restart 5 days post-op- can give LMWH 2 days post-op)
  • Nil by mouth 4 hours before
  • Don’t drive for 24 hours after if sedation is used
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4
Q

Why should PPIs be stopped 2 weeks before an upper GI endoscopy?

A

They mask pathology

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5
Q

What sedation/anaesthesia is used for an upper GI endoscopy? (3)

A
  1. Midazolam IV (for minimal sedation)
  2. Propofol for deeper sedation (should be administered by an anesthetist)
  3. Pharynx is sprayed with a local anaesthetic before the endoscope is passed
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6
Q

What conditions can be confirmed or ruled out on an upper GI endoscopy? (4)

A
  1. Oesophagitis
  2. Duodenal/stomach ulcer
  3. Duodenitis and gastritis
  4. Cancer of the stomach or duodenum
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7
Q

How thick is an upper GI endoscope?

A

Width of the little finger

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8
Q

What are the complications of upper GI endoscopy? (6)

A
  1. Sore throat
  2. Amnesia from the sedation
  3. Perforation (
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9
Q

What is the gold standard for diagnosisng coeliac disease?

A

Duodenal biopsy

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10
Q

How should a patient be prep’d for sigmoidoscopy? (3)

A
  • On the day before the procedure take 2 Picolax sachets (one at 8am and one at 6pm)
  • Fluids only for 12 hours before the procedure
  • Sometimes an enema is given upon the patient arriving into hospital
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11
Q

What parts of the bowel are seen on colonoscopy?

A

The whole colon and the terminal ileum

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12
Q

What parts of the bowel are seen on gastroscopy?

A

Oesophagus, stomach, duodenum

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13
Q

What are the diagnostic indications for colonoscopy? (6)

A
  • Rectal bleeding
  • Iron deficiency anaemia
  • Persistant diarrhoea/otherwise altered bowel habit
  • Biopsy of lesion seen on barium enema
  • Assessment or suspicion of IBD
  • Colon cancer- surveillance (screening usually done by flexible sigmoidoscopy)
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14
Q

What are the therapeutic indications for colonoscopy? (5)

A
  • Stent insertion
  • Haemostasis (e.g. by clipping vessel)
  • Volvulus untwisting
  • Pseudo-obstruction
  • Removal of polyps (polypectomy)
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15
Q

How is a patient prep’d for colonoscopy?

A
  • Low residue diet 1-2 days pre-op
  • Clear fluid but no solid food after lunch on the day befor
  • Bowel clensing solution- sodium picosulfate (Picolax)- is given for the morning and afternoon on the day before
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16
Q

What are the complications of a colonoscopy?

A

Abdominal discomfort
Incomplete examination
Haemorrhage after biopsy or polypectomy
Perforation (0.1%)

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17
Q

What are the absolute contraindications for colonscopy?

A
  • Failure to obtain consent
  • Toxic megalcolon
  • Fulminant colitis
  • Known colonic perforation
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18
Q

What advice should be given post-operatively following any form of endoscopy when a sedative is used?

A

No driving, operating heavy machinery or drinking alcohol for 24 hours

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19
Q

What are the relative contra-indications for colonoscopy?

A
  • Acute diverticulitis
  • Large AAA
  • Immediately post-op
  • Recent MI/PE
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20
Q

What medications should be stopped 1 wk prior to colonoscopy?

A
  • Iron supplements (hardens stool therefore harder to evacuate the bowel)
  • Aspirin and NSAIDS
  • Anticoagulants- warfarn
  • No insulin during fasting period
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21
Q

What are the indications for liver biopsy? (5)

A
  • Raised LFTs
  • Chronic viral, alcohol or autoimmune hepatitis
  • Suspected cirrhosis
  • Suspected liver cancer
  • Biopsy of hepatic lesion
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22
Q

What are the contra-indications for liver biopsy? (4)

A

Uncooperative patient
Prolonged PTT
Low platelet count
Extra-hepatic cholestasis

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23
Q

What pre-op guidelines should be followed prior to a liver biopsy? (3)

A
  • Nil by mouth for 8 hours
  • Ensure INR 100x10^9
  • Give analgesia
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24
Q

How is local anaesthetic administered for a liver biopsy?

A

Liver borders and percused out and where there is dullness in the mid-axillary line in expiration, lidocaine 2% is infiltrated down to the liver capsule

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25
Q

Describe how a liver biopsy is taken

A

Under sedation with US/CT guidance. Breathing is rehearsed and biopsy taken with the breath held in expiration. Afterwards lie on right side for 2 hours then in bed for 4 hours

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26
Q

What are the complications of liver biopsy? (4)

A
  • Local pain
  • Pneumothorax
  • Bleeding (
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27
Q

What are the causes of apthous ulcers?

A
  • CD
  • Coeliac
  • Bechet’s
  • Infections: HSV/syphyllis/Vincent’s angina
  • Reiter’s
  • SLE
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28
Q

What is Vincent’s angina?

A

Also known as necrotising ulcerative gingivitis or trench mouth. A common non-contagious infection of the gums with grate like ulcers and bleeding, painful gums and ulceration of inter-dental papillae

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29
Q

What are the common causes of infective ulcers?

A

Herpes simplex 1
Coxsackie A
Herpes Zoster

(mouth infections are most commonly viral)

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30
Q

What is the cause of an oral, hairy leukoplakia?

A

EBV- almost pathognomonic of HIV infection

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31
Q

How does oral squamous cell carcinoma present?

A

An indolent (causing little or no pain) ulcer on the lateral borders of the tongue or floor of the mouth

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32
Q

What are the risk factors for candidiasis?

A

Extremes of age
DM
Antibiotics
Immunosuppression (long term steroids, HIV)

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33
Q

How is oral candidiasis treated?

A

Nystatin suspension or amphotericin lozenges

Fluconazole for oropharyngeal thrush

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34
Q

What is the main cause of angular chelitis?

A

Iron/riboflavin (B2) deficiency

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35
Q

How is Vincent’s angina treated?

A

Oral metronidazole and good oral hygiene

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36
Q

In what condition is microstomia seen?

A

Scleroderma

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37
Q

What condition is characterized by peri-oral brown spots?

A

Peutz-Jegher’s syndrome

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38
Q

Describe the genetics of Peutz-Jegher’s syndrome

A

It is an autosomal dominant condition with germline mutations of tumour supressor gene STK11

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39
Q

What are the symptoms of Peutz-Jegher’s syndrome?

A

Muco-cutaneous dark freckles on the lips, oral mucosa, palms and soles + multiple GI polyps causing obstruction or bleeds. 15x increased risk of GI cancer

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40
Q

In what conditions might telangiectasia be seen around the mouth?

A

Systemic sclerosis

Osler-Weber-Rendu syndrome

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41
Q

What is Osler-Weber-Rendu syndrome?

A

An autosomal dominant condition of hereditary telangiectasia on the skin and mucous membranes causing epitaxis and GI bleeds

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42
Q

What might be suggested by a blue line at the gum margin?

A

Led poisoning

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43
Q

What might cause a yellow brown discolouration of the teeth?

A

Prenatal or childhood tetracycline exposure

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44
Q

What drugs can cause xerostermia? (7)

A 
ACEi
Antidepressants
Antihistamines
Antipsychotics
Diuretics
Anti-cholinergics
Opiates
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45
Q

What are the causes of white intra-oral lesions? (6)

A 
Leukoplakia
Candidiasis
Carcinoma
Hairy oral leucoplakia
Smoking
Lupus
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46
Q

What is leukoplakia?

A

An oral mucosal white patch that will not rub off and is not attributable to any other known disease
It is premalignant with a transformation rate of 0.6-18%

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47
Q

What is glossitis?

A

A smooth, atrophic tongue

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48
Q

What causes glossitis?

A

Iron, folate or B12 deficiency

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49
Q

What are the main oesophageal symptoms?

A
  • Dysphagia
  • Heartburn
  • Regurgitation
  • Odynophagia (painful swallowing)
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50
Q

What dysphagia history would be typical of a mechanical stricture?

A

Short history of progressive dysphagia initially for solids then for liquids

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51
Q

What investigation should be done if a mechanical stricture is the suspected cause of dysphagia? What is being looked for?

A

Emergency OGD to look for a malignant oesophageal stricutre

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52
Q

What dysphagia history would be typical of a motility disorder?

A

Slow onset dysphagia for both solids and liquids

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53
Q

What investigation should be done if a motility disorder is the suspected cause of dysphagia?

A

Barium swallow

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54
Q

What may aggravate the pain of heart burn?

A

Bending or lying down

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55
Q

What may relieve the pain of heart burn?

A

antacids

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56
Q

What are the causes of mechanical dysphagia?

A
  • Malignant stricutre
  • Benign stricture
  • Extrinsic pressure e.g. lung cancer; retrosternal goitre; aortic aneurysm
  • Pharyngeal pouch
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57
Q

What motility disroders can cause dysphagia?

A

Achalasia
Diffuse oesophageal spasm
Systemic sclerosis
Neurological bulbar palsy (Parkinson’s disease; Wilson’s disease; Myasthenia gravis)

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58
Q

What is suggested if the patient has difficulty making the swallowing movement and coughs on attempting to do so?

A

Bulbar palsy

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59
Q

What is acalasia?

A

Achalasia is primarily a disorder of motility of the lower oesophageal or cardiac sphincter. The smooth muscle layer of the oesophagus has impaired peristalsis and failure of the sphincter to relax causes a functional stenosis or functional oesophageal stricture.

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60
Q

What is conditions might you suspect if there is painful swallowing and dysphagia?

A

Cancer
Oesophageal ulcer
Candida
Spasm

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61
Q

What might predispose a non-immunosuppressed patient to candida infection?

A

Asthmatic/COPD patient with poor steroid inhaler technique

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62
Q

What might make you suspect a pharyngeal pounch in a patienth with dysphagia?

A

There is gurgling and the neck bulges on drinking

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63
Q

Where in the oesophagus are squamous cell tumours usually found?

A

Middle third

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64
Q

Where in the oesophagus are adenocarcinomas usually found?

A

Lower third

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65
Q

What is the most common aeitiological cause of adenocarcinoma of the oesophagus?

A

Barrett’s metaplasia

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66
Q

What is the management of a malignant oesophageal tumour?

A

Surgical resection combined with peri-operative chemotherapy

N.B. over half of patients have unresectable locally advanced disease. Overally prognosis is poor- 10% 5 year survival

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67
Q

What is the first line Ix for suspected oesophageal malignancy?

A

OGD with biopsy of tumour

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68
Q

What is indicated by coffee ground vomiting?

A

GI bleeding

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69
Q

What may be indicated by vomiting occurring in the morning?

A

Pregnancy

Raised ICP

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70
Q

What may be indicated by vomiting preceded by loud gurgling?

A

GI obstruction

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71
Q

What may be indicated by vomiting that relieves pain?

A

Peptic ulcer

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72
Q

What ABG result indicates severe vomiting?

A

Metabolic, hypochloraemic alkalosis

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73
Q

What are the causes of GORD?

A 
LOS hypotension
Hiatus hernia
Loss of oesophageal peristaltic function
Abdominal obesity
Gastric acid hypersecretion
Slow gastric emptying
Systemic sclerosis
Pregnancy
Alcohol
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74
Q

What is more common, a sliding or a rolling hiatus hernia?

A

Sliding (80%)

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75
Q

What is the typical patient with a hiatus hernia?

A

Obese woman >55 years

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76
Q

What is the best diagnostic test for a hiatus hernia?

A

Barium swallow

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77
Q

What are the indications for surgery in a hiatus hernia?

A
  • Intractable symptoms despite aggressive medical treatment
  • Complications- oesophagitis; benign stricture; ulcer
  • Rolling hernia- should be repared prophylactically even in asymptomatic patients due to risk of strangulation
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78
Q

What are the symptoms of GORD?

A

Heart burn is the main symptom
Also:
- Belching
- Acid brash (acid regurgitation)
- Water brash (greatly increased salivation”my mouth fills with saliva”)
- Odynophagia
- Cough and nocturnal asthma due to aspiration of gastric contents into the lungs

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79
Q

In which patients with clinical features of GORD is an OGD performed?

A
  • New onset heart burn >55
  • Patients with symptoms suspicious of upper GI malignancy
  • To document any complications of reflux
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80
Q

What is step 1 of the WHO pain ladder?

A

Non-opioid e.g. aspirin, paracetamol or NSAID

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81
Q

What is step 2 of the WHO pain ladder?

A

Weak opioid for mild to moderate pain e.g. codeine+/- non-opioid

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82
Q

What is step 3 of the WHO pain ladder?

A

Strong opioid for moderate to severe pain e.g. morphine or fentanyl +/-

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83
Q

What is the MOA of paracetamol?

A

Peripheral: COX2/COX3 inhibitor (thereby inhibiting prostaglandin production)

Central: activates descending serotonergic pathways

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84
Q

What is the maximum daily dose of paracetamol?

A

4g (1g per 4-6 hours)

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85
Q

What is the mechanism of action of NSAIDS?

A

Inhibitors of COX1/2

COX catalyses the formation of prostaglandins and thromboxane from arachidonic acid. Prostaglandins act as messenger molecules in the process of inflammation

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86
Q

What is the role of COX-1

A

It is an enzyme expressed in almost all mammalian cells which has a “housekeeping” regulating many physiological processes. e.g. in the stomach it up-regulates prostaglandin production.

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87
Q

What is the role of prostaglandins in the gut?

A

Prostaglandins serve a protective role in the gut, preventing the gut mucosa from being eroded by its own acid (so COX inhibition hear can cause GI problems e.g. ulceration) (PGI2)

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88
Q

What is the role of COX-2

A

It is an isoenzyme which is specific to inflamed tissue- causes release of prostaglandins at sites of inflammation only

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89
Q

What are the risk factors for NSAID use?

A
  • Age >65
  • Previous ulcer disease
  • Major organ impairment
  • Concomitant antiplatelet, anticoagulant, corticosteroid or SSRI
  • Alcohol and tobacco use
  • H. pylori infeciton
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90
Q

What is the mechanism of action of NSAIDS?

A

REVERSIBLE inhibitors of COX1/2

COX catalyses the formation of prostaglandins and thromboxane from arachidonic acid. Prostaglandins act as messenger molecules in the process of inflammation

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91
Q

What are the risk factors for NSAID use? (6)

A
  • Age >65
  • Previous ulcer disease
  • Major organ impairment
  • Concomitant antiplatelet, anticoagulant, corticosteroid or SSRI
  • Alcohol and tobacco use
  • H. pylori infection
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92
Q

What is the MOA of aspirin?

A

Irreversible inactivation (by acetylation) of COX–> reduced production of thromboxane and prostaglandins.

Thromboxane is a prothrombotic agent (hence use of aspirin as an anti-platelet agent)

Prostaglandin is a pro-inflammatory agent (hence use of aspirin as an anti-inflammatory)

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93
Q

Why is aspirin not prescribed in children (

A

It is linked to Reyes syndrome, a potentially fatal syndrome which has detrimental effects on the brain and liver, as well as causing hypoglycaemia. Reye’s syndrome is associated with aspirin consumption by children with viral illness

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94
Q

What are the non-anti-inflammatory uses of aspirin?

A

-Anti-platelet action in cardiovascular disease
- Rheumatic fever
Possible reduction in risk and onset of Alzheimer’s disease

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95
Q

What are the non-anti-inflammatory uses of aspirin?

A

-Anti-platelet action in cardiovascular disease
- Rheumatic fever
Possible reduction in risk and onset of Alzheimer’s disease

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96
Q

What is the mechanism of action of opioids?

A

Act as agonists at three different receptors: µ, ∂ and k. (µ is principally involved in the analgesic effect.) Have there mode of action in the peri-aqueductal greay matter and in the dorsal horn (substantia gelatinosa)

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97
Q

Why does codeine exhibit different potency in different individuals?

A

Requires conversion to morphine by P450 enzymes in the liver- different conversion ability of different individuals affects potency

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98
Q

What is the mechanism of action of tramadol?

A
  1. Opioid agonist

2. Weak noradrenaline/5HT re-uptake inhibitor

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99
Q

In what types of pain are strong opioids not particularly effective?

A

Neuropathic pain

Chronic, non-cancer pain

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100
Q

What are the side effects of pethidine?

A

tends to cause restlessness (rather than sedation like morphine)
Has anti-muscarinic effect –> dry mouth and blurred vision

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101
Q

In what situation is pethidine used?

A

Labour

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102
Q

What drug is used to reverse opiate overdose? What is it’s mechanism?

A

Naloxone

µ receptor competitive antagonist

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103
Q

What drugs may be used to treat neuropathic pain?

A

Gabapentin
Tricylclic antidepressent
Anti-convulsants e.g. carbamazapine

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104
Q

What drugs are used for pain relief in MI?

A

GTN

Morphine

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105
Q

What non-opioid drug class may be used for pain relief in migraine sufferers?

A

5-HT1D agonists- triptans

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106
Q

What non-opioid drug may be used for pain relief in malignancy?

A

Dexamethasone

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107
Q

What non-opioid drug may be used for pain relief in intestinal colic?

A

Hyoscine butylbromide

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108
Q

What non-opioid drug may be used for pain relief in muscle spasm?

A

Benzodiazepines

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109
Q

What non-opioid drug may be used for pain relief in muscle spasm?

A

Benzodiazepines

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110
Q

How many moles of sodium are in 1L of normal saline (0.9% NaCl)?

A

155mmols

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111
Q

What changes in ion balance may be caused by malnutrition?

A

Retention of sodium and water and repletion of potassium, phosphate, calcium and magnesium

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112
Q

What might occur if you give a malnourished patient IV glucose?

A

Pulmonary oedema and cardiac arrhythmia (re-feeding syndrome)

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113
Q

What electrolyte disturbances are caused by loop diuretics?

A

Hypovolaemia

Hypokalaemia

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114
Q

Describe the rule of thirds in a 70kg man

A

70kg man:

  • 2/3 of body weight is water (42L)
  • 2/3 of water is intra-cellular, (25L); 1/3 is extracellular (14L)
  • Of extra-cellular water, 1/3 is intra-vascular
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115
Q

What are the two groups of colloids?

A

Semi-synthetics (hydroxyethyl starches, gelatins)

Plasma derivatives (albumin)

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116
Q

What is the major advantage of colloids in resuscitation?

A

They do not cross the capillary membrane (in theory) so remain in the intra-vascular compartment (i.e. for ever 1L of fluid given, 1L remains in the plasma)

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117
Q

What are the disadvantages of colloids? (5)

A
  • Cost
  • Potential allergen
  • Often some leakage out of the capillaries anyway
  • Effect coagulation and can increase bleeding risk
  • Can precipitate renal failure
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118
Q

What are the disadvantages of crystalloids?

A
  • Remain in the intravascular space for less time, thus larger volume is needed to achieve effect (3-4 L of crystalloid per 1L of blood)
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119
Q

What are the advantages of crystalloids?

A
  • Safe
  • Cheap
  • Constituents determine distribution (dextrose gets everywhere, Na is confined to the ECF so NaCl remains extra-cellular)
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120
Q

What is the standard formula to work out how many L of fluid to give someone in a day?

A

4ml/kg/hr for the 1st 10 kg
2ml/kg/hr for the 2nd 10 kg
1ml/kg/hr for every kg after that

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121
Q

What is the standard fluid regimen?

A

1L 0.9% saline
2L 5% dextrose
+20-40mmol KCl

“two sweet one salty”

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122
Q

What are the 5 r’s of fluid prescribing?

A 
Resuscitate
Routine maintenance
Redistribution
Replacement
Reassessment
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123
Q

What is the standard fluid regimen for routine maintenance?

A

1L 0.9% saline
2L 5% dextrose
+20-40mmol KCl

“two sweet one salty”

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124
Q

What are the 5 r’s of fluid prescribing?

A 
Resuscitate
Routine maintenance
Redistribution
Replacement
Reassessment
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125
Q

What is a fluid challenge?

A

Used in resuscitation: 2 wide bore cannulas, one in each ante-cubital fossa

500mL of NaCl 0.9% or Hartmann’s over 5-15 minutes

Then re-evaluate using ABCDE approach

Further fluid boluses up to 2000mL can be givem

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126
Q

How might the fluid challenge be altered in a patient with severe sepsis?

A

Albumin 4-5%

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127
Q

How should obese people be managed in terms of routine fluid maintenance?

A

Adjust maintenance volume to fit their ideal body weight

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128
Q

What do NICE guidelines recommend as the initial fluid prescription for routine maintenance?

A
  • 25-30ml/kg/day of water
  • approx 1mmol/kg/day of sodium, potassium and chloride
  • 50-100g/day of glucose to limit starvation ketoacidosis
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129
Q

In which patients do NICE suggest you might prescribe less fluid?

A
  • Older/frail
  • Renal impairment or cardiac failure
  • Malnourished and at risk of refeeding syndrome
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130
Q

When prescribing for routine maintenance alone, what regimen might you use other then 2 sweet 1 salty?

A

NaCl 0.18% in 4% glucose with 27 mmol/L potassium

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131
Q

What are the clinical features of hypovolaemia?

A

In order of increasing severity:

  1. Thirst
  2. Cool extremities
  3. Increased CRT
  4. Increased RR
  5. Tachycardia
  6. Hypotension
  7. Reduced UO
  8. Reduced GCS
Also:
loss of skin turgour
dry mucous membranes
sunken eyes
absence of JVP
postural BP drop
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132
Q

What are the biochemical signs of hypovolaemia?

A 
Raised Hb/haematocrit
Raised urea/creatinine
Hyperkalaemia/hypernatraemia
Raised BM
Raised Calcium
Hyperlactaemia/metabolic acidosis (if very hypovolaemic)
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133
Q

What are the clinical features of hypovolaemia? (8)

A

In order of increasing severity:

  1. Thirst
  2. Cool extremities
  3. Increased CRT
  4. Increased RR
  5. Tachycardia
  6. Hypotension
  7. Reduced UO
  8. Reduced GCS
Also:
loss of skin turgour
dry mucous membranes
sunken eyes
absence of JVP
postural BP drop
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134
Q

What are the biochemical signs of hypovolaemia?

A 
Raised Hb/haematocrit
Raised urea/creatinine
Hyperkalaemia/hypernatraemia
Raised BM
Raised Calcium
Hyperlactaemia/metabolic acidosis (if very hypovolaemic)
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135
Q

What signs of hypovolaemia might be seen on an echocardiogram?

A

Collapse of the LV

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136
Q

What are the clinical features of hypervolaemia? (3)

A
  • Raised JVP
  • Generalised oedema (weight gain, ascites)
  • Pulmonary oedema (increased RR; crackles; orthopnoea)
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137
Q

What are the biochemical signs of hypervolaemia?

A
  • Raised urea/creatinine
  • Raised LFTs
  • Hyponatraemia
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138
Q

What signs of hypervolaemia might be seen on an echocardiogram?

A

Reduced LVEF

Distended RV

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139
Q

What are the five key principles of the mental capacity act?

A
  1. Presumption of capacity unless proven otherwise
  2. Individuals should be supported as much as possible to make their own decisions
  3. Unwise decisions do not necessarily indicate lack of capacity
  4. Acts/decisions made on behalf of a person who lacks capacity must be done in their best interests
  5. Anything done for or on behalf of a person who lacks capacity should be the least restrictive of their basic rights and freedoms
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140
Q

What are the 7 key changes/provisions of the mental capacity act?

A
  1. Definition and assessment of capacity
  2. Best interests checklist
  3. Advanced decisions/statments
  4. Lasting power of attorney
  5. Court of protection and Deputies of Court
  6. Independent mental capacity advocate
  7. Willful neglect as a new criminal offence
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141
Q

What are the requirements for demonstrating capacity under the MCA?

A
  1. Understand information
  2. Retain information
  3. Weigh up information and reach a decision
  4. Communicate the decision
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142
Q

How is capacity assessed?

A
  1. Does the patient have an impairment/disturbance of the mind/brain?
  2. If yes, does this impairment hinder the patient’s ability to understand/retain/weigh-up/communicate
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143
Q

What is meant by enhancing capacity?

A

The process of taking all practical steps to help a patient reach capacity. A patient should not be treated as lacking capacity unless all practical steps have been taken without success

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144
Q

What measures might be taken to help a patient reach capacity?

A
  • Avoidance of jargon
  • Use of pictures
  • Use of translators
  • Treatment of concurrent pain
  • Allowing time for the patient to process the information
  • Ensuring a quiet, comfortable setting
  • Having a friend or relative present
  • Asking questions at the best time of day for that patient
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145
Q

Who is responsible for making best interest decisions in the absence of an LPA or Deputy of Court?

A

The doctor with responsibility for the patient’s care

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146
Q

What should doctors take into account when making a best interests checklist?

A
  1. Patient’s present wishes and feelings
  2. Patient’s past wishes and feelings
  3. Any beliefs and values that would be likely to influence the deicison
  4. Other factors the patient would be likely to consider if able to do so
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147
Q

Who should be consulted by the decision maker when coming up with a best interests checklist, according to the mental capacity act?

A

When practical and appropriate, the following must be consulted about the best interests of a patient who lacks capacity:

  • Anyone named by the person
  • Anyone engaged in caring for the person or interested in his welfare
  • Any donee of lasting power of attorney
  • Any deputy appointed by the court
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148
Q

Are advanced decisions legally binding?

A

Yes- all valid and applicable advanced decisions must be followed

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149
Q

What factors are required to make any advanced decision legally valid? What additional factors are required to make an advanced decision related to life-sustaining treatment?

A

Factors to make any advanced decision:

  1. Capacity
  2. Non-coercion
  3. Adequate inforamtion

Additional factors for decisions related to life-sustaining treatment:

  1. Witnessed
  2. Signed and dated
150
Q

What factors are necessary to ensure an advanced decision is applicable

A
  1. The patient has capacity at the time it is made
  2. The circumstances are the ones specified and have not changed in any way that would have resulted in a change of mind
  3. The advanced decision is not overridden by a more recent advanced decision
  4. The advanced decision is not overridden by someone with LPA which covers the decision in question who was appointed after the advanced decision
151
Q

What differentiates an advanced statement from an advanced decision?

A

Advanced statements are not legally binding, however, they must be considered when assessing best interests

152
Q

What is a lasting power of attornee?

A

A person (or donee) who a person with capacity has given the legal power to make decisions if/when that person no longer has capacity. The range of powers can be specified! Power to give consent to withdrawal of life-sustaining treatment must be explicitly stated

153
Q

How is an LPA appointed?

A
  • Both donor and donee must be over 18
  • Written document, signed by the donor
  • Donee must sign a statement saying they understand their duties, in particular the requirement to act in the donor’s best interests
  • Document must be certificated by independent 3rd party
154
Q

What is the Court of Protection?

A

A court appointed to resolve complex or disputed cases relating to mental capacity e.g. when it is unclear what the best interests of a patient who lacks mental capacity are

155
Q

What does the Court of Protection have the power to decide? What do they have the power to do?

A

Power to decide:

  • Whether or not a patient lacks capacity
  • Whether or not an intervention is in the best interests of a person who lacks capacity

Power to appoint Deputy of Court to make decisions

156
Q

What is a deputy of the court

A

A person appointed by the court to make a one off decision e.g. a parent caring for an over 18 yeard old with learning difficulties can apply to be made a deputy of the court

157
Q

What can a deputy of the court not do?

A

Make the decision to refuse life sustaining treatment

158
Q

What is an independent mental capacity advocate?

A

A person appointed to represent and support vulnerable people who lack capacity and who have no one else to consult (e.g. no family). Their role is to find out what is in the patient’s best interests and ensure this is being carried out. However, the doctor still makes the final decision about a patient’s best interests

159
Q

What is the GMC checklist of considerations to make when treating a patient, as set out by the Mental Capacity Act. (6)

A

The GMC say doctors must consider the following before treating a patient who lacks capacity:

  1. Whether the patient permanently or temporarily lacks capacity
  2. Which treatment option provides overall clinical benefit
  3. Evidence of the patient’s previously expressed preferences (advance decisions/statements)
  4. The healthcare team’s knowledge of the patient’s wishes, values and beliefs
  5. The family and friend’s knowledge about the patient’s preferences
  6. Which option least restricts the patient’s future choices
160
Q

What is advanced care planning?

A

A plan made between a patient and their care team while the patient still has capacity. This is a patient led process. Should be carried out sooner rather than later. Includes discussion of advanced decisions and statements

161
Q

What two questions should you ask before treating a patient who lacks capacity?

A
  1. Is there an LPA or Deputy of Court?

2. Is there an effective Advanced Decision?

162
Q

What symptoms are suspicious of GI malignancy in a patient with GORD (i.e. would prompt you to do an OGD)? (8)

A
  • Symptoms for >4w
  • Persistent vomiting
  • GI bleeding/iron deficiency anaemia
  • Palpable mass
  • Dysphagia
  • Symptoms persisting despite treatment
  • Weight loss
  • Relapsing symptoms
163
Q

What is the drug treatment for GORD?

A
  • First line= alginate containing antacid (e.g. gaviscon) + PPI e.g. omeprazole
  • If there is an incomplete response to PPI, add an H2 antagonist e.g. ranitidine
164
Q

How is GORD classified?

A

The Los Angeles Classification, 4 grades. Grade 1 is the lowest (1 or more mucosal breaks

165
Q

What are the complications of GORD? (5)

A 
Oesophagitis
Ulcers
Benign stricture
Iron deficiency
Barrett's oesophagys
166
Q

What is a Schatzki ring?

A

Localised mucosal stricture at the gastro-oesophgeal junction which can cause dysphagia. Development may be due to chronic GORD

167
Q

What is Barrett’s oesophagus?

A

An abnormal columnar epithelium replaces the squamous epithelium that normally lines the distal oesophagus. Occurs due to prolonged exposure of the oesophagus squamous epithelium to the acid reflux of GORD

168
Q

What is the major complication of Barrett’s oesophagus?

A

Oesophageal carcinoma (N.B. conversion is low 0.6-1.6% per year)

169
Q

What is the role of intrinsic factor?

A

Needed for absorption of vitamin B12

170
Q

What increases gastric acid secretion?

A

Vagal nerve stimulation
Histamine
Gastrin

171
Q

What reduces gastric acid secretion?

A

Somatostatin

172
Q

Which cells secrete somatostatin?

A

Antral D cells

173
Q

What are the roles of gastric acid?

A

Protective- destroys bacteria

Converts pepsinogen to pepsin- needed for protein digestion

174
Q

What cells secrete pepsinogen?

A

Chief cell in the fundus of the stomach

175
Q

What conditions are associated with H. Pylori infection?

A

Chronic active gastritis- mainly in the antrum of the stomach
Peptic ulcer disease
Gastric cancer
Gastric B cell lymphoma

176
Q

What conditions are associated with H. Pylori infection?

A

Chronic active gastritis- mainly in the antrum of the stomach
Peptic ulcer disease
Gastric cancer
Gastric B cell lymphoma

177
Q

What is the most accurate non-invasive test for H. pylori infection?

A

13C-urea breath test
Highly sensitive and specific
Hydrolysis of ingested 13C-urea by H. pylori produces 12C-urea in expired air

178
Q

What is a common cause of false negatives when using the urea-breath test to test for H. Pylori infection?

A

Recent use of PPIs, bismuth or antibiotics. Stop for >2w before testing

179
Q

What other non-invasive tests are there to test for H. Pylori infection (other than the breath test)

A

H. Pylori faecal antigen test:

180
Q

What invasive test may be done to look for H. Pylori infection?

A 
Rapid urease (CLO) test:
Performed on biopsy tissue obtained during endoscopy (only performed on patients already undergoing endoscopy)
The tissue is placed in an agar gel containing urea and a pH-sensitive indicator. In the presence of H pylori urease, the urea is metabolised to ammonia and bicarbonate and detected as a colour change
181
Q

What is the favoured treatment for H. pylori infection?

A

PPI based triple therapy regimens for 7 days e.g.

- Omeprazole + metronidazole + clarithromycin

182
Q

In what patients with dyspepsia should an urgent upper GI endoscopy be carried out?

A

Patients over 55 with any ALARMS symptoms:

  • Anaemia
  • Loss of weight
  • Anorexia
  • Recent onset/progressive symptoms
  • Malaena/haematemisis
  • Swallowing difficult
183
Q

What is the initial management of dyspepsia in a patient without alarm symptoms?

A
  • Stop drugs causing dyspepsia e.g. NSAIDs
  • Lifestyle changes e.g. smoking cessation
  • OTC antacids

If no improvement after 4w test for H. Pylori infection

184
Q

What is the management of dyspepsia in a patient without alarm symptoms who does not improve after 4 weeks and tests negative for H. Pylori infection?

A

PPI

H2 receptor blocker e.g. ranitidine

185
Q

What is the management of dyspepsia in a patient without alarm symptoms who does not improve after 4 weeks and tests positive for H. Pylori infection?

A

Treatment to eradicate H. pylori

e.g. omeprazole + metronidazole + clarithromycin

186
Q

What are more common, duodenal or gastric ulcers?

A

Duodenal ulcers are 4x more common

187
Q

What are the major causes of duodenal ulcers?

A

H. pylori infection

Drugs (NSAIDs, seroids, SSRIs)

188
Q

What is the typical presenting history of a patient with a duodenal ulcer?

A

Epigastric pain typically before meals or at night relieved by eating or drinking milk

189
Q

What is Zollinger-Ellison syndrome?

A

An islet cell, gastrin-secreting tumor of the pancreas that stimulates the gastric parietal cells to maximal activity, with consequent gastrointestinal mucosal ulceration

190
Q

Where are gastric ulcers most commonly seen? What might be suggested by ulcers seen elsewhere?

A

The lesser curve of the stomach

Malignancy

191
Q

What are the risk factors for gastric ulceration?

A
  • H pylori infection
  • Smoking
  • NSAIDs
  • Reflux of duodenal contents
  • Delayed gastric emptying
192
Q

How does a gastric ulcer present?

A

Epigastric pain worse on eating

May be relieved by antacids

May also present with weight loss

193
Q

What are the major causes of duodenal ulcers?

A

H. pylori infection

Drugs (NSAIDs-(co-administration of aspirin further increases risk), steroids, SSRIs)

194
Q

What are the risk factors for gastric ulceration?

A
  • H pylori infection
  • Smoking
  • NSAIDs (co-administration of aspirin further increases risk)
  • Reflux of duodenal contents
  • Delayed gastric emptying
195
Q

How does a gastric ulcer present?

A

Epigastric pain worse on eating

May be relieved by antacids

May also present with weight loss

196
Q

How is an H. pylori negative peptic ulcer treated?

A

Usually associated with aspirin/NSAIDS so stop the offending drug and treat with PPIs

After ulcer healing, NSAIDs can usually be continued with PPI prophylaxis or COXIB used

197
Q

What is the main side effect of bismuth?

A

Turns stool black

198
Q

Describe the histopathology of gastric cancer?

A

Most commonly in the antrum and almost always adenocarcinoma

199
Q

What is the most common presenting symptom of gastric cancer?

A

Peptic ulcer pain/dyspepsia (hence testing of all patients >55 with dyspepsia for >4w)

200
Q

What is a common and worrisome extra-abdominal sign of gastric cancer?

A

Virchow’s node: large supraclavicular lymph node on the LEFT side (Trosier’s sign)

201
Q

What signs of gastric cancer suggest incurable disease?

A
  • Palpable epigastric mass (almost 50% have this on presentation)
  • Virchow’s node
  • Skin manifestations (dermatomyositis, ancanthosis nigricans)
  • Signs of periteoneal metastases (ascites)
  • Signs of liver metastases (hepatomegaly, jaundice)
202
Q

What is the first line investigation in suspected gastric cancer?

A

OGD + biopsy of any ulcers seen

203
Q

What are the common causes of upper GI bleeding?

A 
Peptic ulcers (50%)
Mallory-Weiss tear
Oesophageal varicies
Gastritis
Drugs (NSAIDS, aspirin, steroids)
Oesophagitis
Duodenitis
204
Q

What is a Mallory-Weiss tear?

A

Linear mucosal tear at the oesophagogastric junction causing peristant comitting/wretching and haematemisis

205
Q

What comorbidities suggest a bad prognosis for GI bleeds?

A

Cardiovascular disease
Respiratory disease
Hepatic or renal impairment
Malignancy

206
Q

What risk assessment tools are used in GI bleeding? What are they assessing?

A

Rockall score
Glasgow-Blatchford score

Help to identify patients at high risk of recurrant or life threatening haemorrhage

207
Q

What factors are taken into account in the Rockall scoring system?

A

Pre-endoscopy factors:

  • Age
  • Shock (BP and HR)
  • Presence of comorbidity

Post-endoscopy factors:

  • Diagnostic stigmata e.g. is there visible blood or clots?
  • Diagnosis (cause of bleed)
208
Q

What factors are taken into account to calculate the Glasgow-Blatchford score? What is the advantage of this score over Rockall?

A

Urea
Hb
Systolic BP
Other markers (HR; presentation with malaena; presentation with syncope; hepatic disease; cardiac failure)

Advantage= does not require endoscopy

209
Q

What is the acute management of a patient who has had a GI bleed and requires hospital admission?

A
  • Protect airway and give high flow oxygen
  • NBM
  • Insert 2 large bore cannulae and take blood for FBC; Us and Es; LFT; clotting screen; group and save; cross match
  • Start fluids
  • Insert urinary catheter
  • Transfuse with crossmatched blood until haemodynamically stable
  • Correct clotting abnormalitys (Vit K; platelets)
  • Arrange urgent endoscopy
  • Inform surgeons of bleed on admission
210
Q

Why is a FBC done on admission of a patient who has had a GI bleed?

A

To check for anaemia (N.B. early Hb may be normal as haemodilution has not taken place)

211
Q

Why are U&Es done on admission of a patient who has had a GI bleed?

A

Check urea- increased urea in proportion to creatinine indicates a recent blood meal

212
Q

Why are LFTs and a clotting screen done on admission of a patient who has had a GI bleed?

A

Check for evidence of liver failure (may suggest varicies)

213
Q

What ulcers are at highest risk of rebleed? Why?

A

Posterior duodenal ulcers due to proximity to the gastroduodenal artery

214
Q

What is suggested by a history of vomiting preceding a GI bleed?

A

Mallory-Weiss tear

215
Q

What endoscopy signs are associated with a high risk of rebleeding?

A 
Active arterial bleeding (80% risk of rebleed)
Visible vessel (50% risk)
Adherent clots/black dots (30% risk)
216
Q

What are the indications for surgery following a PU bleed?

A
  • Severe bleeding or bleeding despite transfusion of significant amount of blood (6U if >60; 8U if
217
Q

What are the causes of a lower GI colonic bleed? (5)

A 
Haemorroids
Anal fissure
Neoplasms
Colitis: UC/Crohn's/infective/ischaemic
Diverticular disease
Angiodysplasia
218
Q

What are the causes of a lower GI small intestine bleed? (5)

A

Neoplasms
Crohn’s
Meckel’s diverticulum
Angiodysplasia

219
Q

What combination of symptoms should lead to investigation of coeliac disease?

A

Diarrhoea + weight loss + anaemia (esp. if iron or B12 deficient)

220
Q

What genetic factors predispose patients towards coeliac disease?

A
  • Association between coeliac disease and HLADQ2- 95% of coeliac population are HLADQ2 positive
  • The rest are HLADQ8 positive
221
Q

What are the characteristic histological signs of coeliac disease?

A
  • Subtotal villous atrophy (also seen in tropical Sprue and Whipple’s)
  • Increased number of intra-epithelial lymphocytes
  • Crypt hyperplasia
222
Q

What are the characteristic histological signs of coeliac disease? (3)

A
  • Subtotal villous atrophy (also seen in tropical Sprue and Whipple’s)
  • Increased number of intra-epithelial lymphocytes
  • Crypt hyperplasia
223
Q

What serum antibodies are indicative of coeliac disease? In what coeliac patients might these antibodies be negative?

A

IgA tissue transglutaminase (tTG)
IgA endomesial antibody (EMA)

Both may be negative in IgA deficient patients (2% of the population)

224
Q

What investigation should be performed upon diagnosis of coeliac disease? Why?

A

DEXA scan- increased risk of osteoporosis in coeliac

225
Q

What is the management of coeliac disease? (5)

A
  • Life long gluten free diet
  • Correction of any vitamin deficiencies
  • Pneumococcal vaccine given as coeliac disease is associated with hyposplenism
  • Repeat serologic testing used to monitor recovery and adherence to diet (if gluten free, antibodies should be undetectable)
  • Re-biopsy in patients who do not respond to gluten free diet
226
Q

What are the complications of coeliac disease?

A
  • Anaemia
  • 2ndry lactose incolerance (low lactase on brush border causing bloating, colic, wind and diarrhoea after milk products)
  • Increased incidence of malignancy
  • Osteoporosis
  • Hyposplenism
227
Q

What is dermatitis herpetiformis?

A

Unbearably itchy blisters found in groups on the elbows, knees and scalp associated with coeliac disease

228
Q

How is dermatitis herpetiformis treated?

A

The itch caused by the inital attack with respond to dapsone (antibiotic) within 48 hours. Subsequent attacks are usually preventable with a gluten free diet although low doses of dapsone may be required as prophylaxis in ~30%

229
Q

What is the main side effect of dapsone?

A

Haemolytic anaemia

230
Q

What is tropical sprue?

A

Villous atrophy with malabsorption occuring in the middle East and Carribean.

231
Q

What is tropical sprue?

A

Villous atrophy with malabsorption occuring in the middle East and Carribean.

232
Q

What are the symptoms of tropical sprue?

A

Diarrhoea
Steatorrheoa
Megaloblastic anaemia

233
Q

How is tropical sprue treated?

A

Folic acid and tetracycline

234
Q

What is short bowel syndrome?

A

Extensive resection of the small bowel leaving ≤1m of bowel. Majority of cases occur after bowel resection due to Crohn’s disease, mesenteric ischaemia or volvulus

235
Q

What is Meckel’s diverticulum?

A

Most common malformation of the GI tract, present in ~2% of the population. A diverticulum projects from the wall of the ileum ~60cm from the ileocaecal valve.

236
Q

What is Meckel’s diverticulitis?

A

~50% of Meckel’s diverticulae contain gastric mucosa which secretes acid, and peptic ulceration may occur

237
Q

How does Meckel’s diverticulitis present?

A

Lower GI bleeding, perforation, inflammation (presentation similar to appendicitis) or with obstruction due to associated band

238
Q

What are carcinoid tumours?

A

A diverse group of tumours which arise from enterochromaffin cells, by definition capable of secreting 5HT.

239
Q

What differentiates carcinoid syndrome from carcinoid tumours?

A

Patients with carcinoid tumours have carcinoid syndrome only if they have liver metastases

240
Q

What differentiates carcinoid syndrome from carcinoid tumours?

A

Patients with carcinoid tumours have carcinoid syndrome only if they have liver metastases

241
Q

What is a carcinoid crisis?

A

Occurs when a carcinoid tumour outgrows its blood supply or is handled too much during surgery so that mediators flood out. There is life threatening vasodilation, tachycardia, hypotension and hyperglycaemia.

242
Q

How is a carcinoid crisis treated?

A

High dose octerotide- somatostatin analogue

243
Q

What non-invasive test is used to diagnosis carcinoid syndrome?

A

Detection of 5-hydroxyindoleatic acid (5-HIAA), the breakdown product of serotonin, in the urine

244
Q

What non-invasive test is used to diagnosis carcinoid syndrome?

A

Detection of 5-hydroxyindoleatic acid (5-HIAA), the breakdown product of serotonin, in the urine

245
Q

Describe the relationship between cigarette smoking and different types of inflammatory bowel diseases

A

Smoking reduces risk of ulcerative colitis but increases risk of Crohn’s disease

246
Q

What are differences between Crohn’s disease and ulcerative colitis in terms of the regions of the GI tract affected?

A

Crohn’s: affects any part of the GI tract; discontinuous involvement (skip lesions)

UC: affects only the colon- begins distally in the rectum and extends proximally to varying degrees. Continuous involvement

247
Q

What are the macroscopic differences between CD and UC?

A
  • Crohns: Deep ulcers and fissures in mucosa- cobblestone appearance

UC: red mucosa which bleeds easily; ulcers and pseudopolyps in severe disease

248
Q

What are the macroscopic differences between CD and UC?

A
  • Crohns: Deep ulcers and fissures in mucosa- cobblestone appearance

UC: red mucosa which bleeds easily; ulcers and pseudopolyps in severe disease

249
Q

What are the microscopic differences between CD and UC?

A

CD: Transmural inflammation; Granulomas in 50%

UC: Not transmural; no granulomata; goblet cell depletion; cell abscesses

250
Q

What extra-abdominal organs may be affected by UC?

A
  • Eyes
  • Joints
  • Skin
  • Hepatobiliary system
251
Q

What are the ocular manifestations of UC?

A

Conjunctivitis
Episcleritis
Iritis

252
Q

What are the joint manifestations of UC?

A

Large joint arthritis
Sacroilitis
Ankylosing spondylitis

253
Q

What are the skin manifestations of UC?

A

Clubbing
Apthous oral ulcers
Erythema nodosum
Pyoderma gangrenosum

254
Q

What are the hepatobiliary manifestations of UC?

A

Fatty liver
Sclerosing cholangitis
Cholangiocarcinoma
Gallstones

255
Q

What investigations should be done in suspected UC?

A
  • FBC
  • ESR and CRP
  • Stoole MC&S
  • AXR
  • Barium enema
  • Colonoscopy
256
Q

Why is an FBC done in suspected UC?

A

Check for anaemia- either normocytic normochromic anaemia of chronic disease or due to deficiency of iron, B12 or folate

257
Q

Why is stool culture done in suspected UC?

A

To exclude infective causes of symptoms (e.g. Campylobacter, C. diff, salmonella, and E. coli )

258
Q

What are the complications of UC? (4)

A

Perforation and bleeding
Toxic megacolon
Venous thrombosis
Colonic cancer

259
Q

How is mild UC treated?

A
  • 5-ASA (e.g. sulfasalazine or mesalazine) are the first line treatment for remission induction/maintainance
  • Steroids e.g. prednisolone 20mg/d PO +/- steroid foams PR to induce remission. If improvement within 2 weeks reduce steroids slowly, if not treat as moderate UC
260
Q

How is mild UC treated?

A
  • 5-ASA (e.g. sulfasalazine or mesalazine) are the first line treatment for remission induction/maintainance
  • Steroids e.g. prednisolone 20mg/d PO +/- steroid foams PR to induce remission. If improvement within 2 weeks reduce steroids slowly, if not treat as moderate UC
261
Q

How is moderate UC defined?

A

4-6 motions per day but otherwise well

262
Q

How is moderate UC treated?

A

Oral prednisolone (gradually reducing dose from 40mg/d to 20mg/d over 6w) + 5-ASA + twice daily steroid enemas. Reduce steroids gradually if improving. If no improvement over 2 w treat as severe UC

263
Q

How is severe UC defined?

A

≥6 motions a day and unwell

264
Q

How is severe UC treated?

A
  • Admit for NBM and IV fluids e.g. 2 sweet 1 salty maintenance fluids
  • Give IV hydrocortison (100mg/6hr) + rectal steroids
  • If Hb
265
Q

What is suggestive of very severe UC requiring more intense therapy following hospital admission?

A

Day 3: CRP>45 and/or >8 stools/day. 85% chance colectomy will be needed on this admission in these patients

266
Q

What is the major complication of ileo pouch-anal anastamosis (IPAA) surgery for UC? How is this treated?

A

Pouchitis. Treated with metronidazole or ciprofloxacin for 2w

267
Q

What is the treatment of toxic megacolon?

A

Steroids, antibiotics, fluids and IV ciclosporin form the mainstay of treatment

If decompression of the bowel is not achieved, or the patient does not improve within 24 hours, total colectomy is indicated

268
Q

What investigations should be done in suspected UC?

A
  • FBC
  • ESR and CRP
  • Stoole MC&S
  • AXR
  • Barium enema (rarely due to risk of peritonitis)
  • Colonoscopy
269
Q

What is the treatment of toxic megacolon?

A

Steroids, antibiotics, fluids and IV ciclosporin form the mainstay of treatment

If decompression of the bowel is not achieved, or the patient does not improve within 24 hours, total colectomy is indicated

270
Q

What part of the gut is most commonly affected by Crohn’s disease?

A

Terminal ileum (in ~70%)

271
Q

What genetic mutations increase risk of Crohn’s?

A

NOD2/CARD15 gene mutations

272
Q

How is Crohn’s classifed?

A

Vienna classification. Complex. Divides Crohn’s into 24 groups depending on age (> or

273
Q

How are mild attacks of Crohn’s treated?

A
  • Prednisolone PO (30mg/d for 1w then 20mg/d for 4w)
  • See as outpatient in clinic every 3w
  • If symptoms resolve, reduce prednisolone by 5mg every 2-4 weeks
  • Stop steroids when parameters are normal
274
Q

How are severe attacks of Crohn’s treated?

A
  • Admit for IV steroids, NBM and IV fluids
  • Rectal steroids for anal disease
  • Metronidazole helps in anal disease
  • If improving after 5d transfer to oral prednisolone
  • If no improvement, can try infliximab/adalimumab
275
Q

What drug is added to management of Crohn’s disease in patients requiring ≥2 courses of antibiotics in a year?

A

Azathioprine

276
Q

What are the side effects of azathioprine? (3)

A

Bone marrow suppression
Acute pancreatits
Allergic reactions

277
Q

What investigation should be carried out before azathioprine is prescribed?

A

Measure of TPMT levels

Thiopurine methyltransferase (TPMT) is needed for metabolism of AZA. ~1 in 300 people have low TPMT activity so AZA is CI in these patients due to risk of pancytopaenia

278
Q

What are the side effects of sulfasalazine?

A

Bloody diarrhoea
Steven-Johnson’s syndrome
Acute pancreatitis
Renal impairment

279
Q

What are the side effects of sulfasalazine?

A

Bloody diarrhoea
Steven-Johnson’s syndrome
Acute pancreatitis
Renal impairment

280
Q

What are the main drugs used in treatment of CD?

A
  • Steroids
  • AZA
  • TNF-alpha inhibitors
  • (sulfasalazine- used less in CD than in UC)
281
Q

What are the contra-indications for treatment with TNF-alpha inhibitors?

A

Sepsis
Increased LFTs (>3x above the top end of normal)
Concurrent ciclosporin or tacrolimus

282
Q

What are the side effects TNF-alpha inhibitors

A

Rash

Reactivation of TB- screen for TB before starting treatment

283
Q

What are the side effects TNF-alpha inhibitors

A

Rash

Reactivation of TB- screen for TB before starting treatment

284
Q

What features are poor prognostic indicators in Crohn’s?

A

Age

285
Q

What features are poor prognostic indicators in Crohn’s?

A

Age

286
Q

What are the Roma criteria for constipation?

A

Presence of ≥2 of the following:
- Straining for ≥25% of BMs
- Lumpy or hard stools in ≥25% of BMs
- Sensation of incomplete evacuation for ≥25% of BMs
- Manual manoeuers to facilitate at least 25% if BMs e.g. digital evacuation, support of the pelvic floor
-

287
Q

What may be indicated by constipation with rectal bleeding?

A

Colorectal cancer

288
Q

What may be indicated by constipation with abdominal distension and active bowel sounds?

A

Stricture/GI obstruction

289
Q

What may be indicated by constipation with menorrhagia?

A

Hypothyroidism

290
Q

What are the common causes of constipation? (7)

A
  • Low fibre diet
  • Inadequate fluid intake/dehydration
  • Immobility or lack of exercise
  • Old age
  • Post-operative
  • Irritable bowel syndrome
  • Hospital environment (lack of privacy; having to use a bed pan)
291
Q

What are the metabolic/endocrine causes of constipation? (4)

A
  • Hypothyroidism
  • Hypercalacaemia
  • Hypokalaemia
  • Porphyria
292
Q

What drugs can cause constipation? (6)

A
  • Opioids
  • Anticholinergics e.g. tricyclics
  • Iron
  • Calcium channel blockers
  • Lithium
  • Diuretics
293
Q

What drugs can cause constipation? (6)

A
  • Opioids
  • Anticholinergics e.g. tricyclics
  • Iron
  • Calcium channel blockers
  • Lithium
  • Diuretics
294
Q

What are the neuromuscular causes of constipation?

A
  • Hirschsprung’s disease
  • Systemic sclerosis
  • Diabetic neuropathy
295
Q

What is Hirschsprung’s disease?

A

Absence of parasympathetic ganglion cells in the myenteric and submucosal plexus in the rectum leading to an aganglionic segment of the rectum which is unable to relax, causing a functional obstruction and constipation

296
Q

What are the indications for further investigation in a constipated patient?

A
  • Age >40
  • Recent change in bowel habit
  • Associated symptoms of weight loss, PR mucus/blood or tenesmus
297
Q

What are the 4 classes of drug used to treat constipation?

A
  • Bulk forming laxatives (e.g. bran; isphaghula husk- fybogel)
  • Osmotic laxatives e.g. magnesium salts, lactulose
  • Stimulants e.g. senna
  • Stool softeners e.g. arachis oil
298
Q

How long to bulk forming laxatives take to work?

A

1-3 days

299
Q

What is the MOA of bulk forming laxatives?

A

Increase foecal mass which stimulates peristalsis

300
Q

What are the contraindications for taking bulk forming laxatives?

A

Difficulty in swallowing
Intestinal obstruction
Colonic atony
Faecal impaction

301
Q

In what conditions should stimulant laxatives not be used?

A

Intestinal obstruction

Acute colitis

302
Q

What are the pure stimulant laxatives?

A
  • Bisacodyl (ducolax)

- Senna

303
Q

What laxative has a dual stimulant and softening action?

A

Docusate sodium

304
Q

What is the MOA of osmotic laxatives?

A

Retain fluid in the bowel- stimulate bowel movement by causing the intestine to hold more water

305
Q

What is the MOA of osmotic laxatives?

A

Retain fluid in the bowel- stimulate bowel movement by causing the intestine to hold more water

306
Q

What is osmotic diarrhoea?

A

Large quantities of non-absorbed hypertonic substances in the bowel lumen draw fluid into the intestine.

307
Q

What are the causes of osmotic diarrhoea?

A
  • Ingestion of non-absorbable substances e.g. a laxative such as magnesium sulfate
  • Generalised malabsorption so that high concentrations of a solute e.g. glucose remain in the lumen
  • Specific malabsorptive defect e.g. dissaccharidase deficiency
308
Q

What is secretory diarrhoea?

A

Active intestinal secretion of fluid and electrolytes as well as decreased absorption.

309
Q

How do you differentiate between osmotic and secretory diarrhoea?

A

Osmotic diarrhoea stops when the patient stops eating or the malabsorbative substance is discontinued. Secretory diarrhoea continues when the patient fasts

310
Q

What are the causes of secretory diarrhoea?

A
  • Enterotoxins e.g. from E. coli, cholera toxin
  • Hormone secreting tumours
  • Bile salts in the colon following ileal disease, resetion or idiopathic bile acid malabsorption
  • Fatty acids in the colon following ileal resection
311
Q

What are the causes of inflammatory diarrhoea?

A

Damage to intestinal mucosal cells leads to loss of fluid and blood and defective absorption of fluid and electrolytes e.g. in IBD, or following salmonella/shingella infection

312
Q

What are the causes of motility related diarrhoea?

A

Thyrotoxicosis

313
Q

What are the most common causes of diarrhoea? (6)

A
  • IBS
  • Gastroenteritis
  • Parasites/protozoa
  • Colorectal cancer
  • Crohns/UC
  • Coeliac
314
Q

What drugs cause diarrhoea?

A
  • Antibiotics (erythromycin is prokinetic; others cause overgrowth of bowel organisms or alter bile salts)
  • Propanolol
  • PPIs
  • NSAIDs
  • Digoxin
  • Laxatives
  • Alcohol
315
Q

What is microscopic colitis?

A

Condition in which colonic mucosa looks normal on endoscopy but histological examination reveals mucosal inflammation. N.B. does not progress to overt bowel disease

316
Q

How does microscopic colitis present?

A

Chronic, watery diarrhoea in a middle ages or elderly person

317
Q

How is microscopic colitis treated?

A

1st line= budesonid

ASAs, bismuth and loperomide in resistant cases

318
Q

How are organic causes and functional causes of chronic diarrhoea (>2w) distinguished?

A

Organic e.g. IBD: stool weight >250g

Functional e.g. IBS: stool weight

319
Q

What are the classic causes of steatorrhoea?

A

Coeliac

Giardia

320
Q

What are the classic causes of steatorrhoea?

A

Coeliac

Giardia

321
Q

What is suggested by a low MCV or iron deficiency in a patient with chronic diarrhoea?

A

Coeliac or CRC

322
Q

What is suggested by a high MCV in a patient with chronic diarrhoea?

A

Alcohol Abuse

Vit B12 malabsor[tion

323
Q

What is suggested by a eiosinophilia or iron deficiency in a patient with chronic diarrhoea?

A

Parasitic cause

324
Q

How is giardia treated?

A

Metronidazole

325
Q

How is infective diarrhoea treated?

A

Do not use antibiotics unless there are features of systemic illness

If there are symptoms of systemic illness give ciprofloxacin PO (+ metronidazole if giardia is suspected)

326
Q

What causes pseudomembranous colitis?

A

C. diff

327
Q

How should symptomatic C. diff infection be treated?

A

Metronidazole for ≤10 days (N.B. in recurrent disease repeate metronidazole only once as overuse causes irreversible neuropathy)
(vancomycin is better in severe disease)

328
Q

How should symptomatic C. diff infection be treated?

A

Metronidazole for ≤10 days (N.B. in recurrent disease repeate metronidazole only once as overuse causes irreversible neuropathy)
(vancomycin is better in severe disease)

329
Q

What diagnostic finding is pathagnomonic of primary biliar cirrhosis?

A

Presence of auto-antibodies against components of the pyruvate dehrdogenase complex

N.B. the pyruvate dehydrogenase complex is located in the mitochondria and the antibody to it is typically found in primary biliary cirrhosis (in clinical practice and anti-mitochondrial antibody is sent)

330
Q

What drug is given in alcoholic liver disease to help prevent Wernicke’s encephalopathy and Korsakoff’s psychosis?

A

Vitamin B1 (thiamine)

331
Q

A 47 year old woman has generalised pruritis, jaundice, dry eyes and mouth. She is otherwise well and drinks no alcohol. She has a markedly raised alkaline phosphatase. Which is the single most useful investigation?

A

Anti-mitochondrial antibodies (likely diagnosis is PBC)

332
Q

Which single combination of hepatitis viruses are routinely tested for in blood for transfusion?

A

B and C

333
Q

Which single combination of hepatitis viruses are routinely tested for in blood for transfusion?

A

B and C

334
Q

What findings on FBC would be consistent with alcoholic hepatitis?

A

High MCV

Anaemia

335
Q

A 42 year old man felt a sharp pain at the back of his ankle while playing badminton. He thought that somebody may have kicked him from behind. He is now unable to walk normally. Which is the single most likely diagnosis?

A

Achilles tendon rupture

336
Q

Which is the single most appropriate initial therapy in a 60 year old man with bilateral knee pain due to osteoarthritis?

A

Paracetamol

337
Q

A 22 year asthmatic woman has a painful right hip and inability to weight bear. She is otherwise well. She has had a number of recent admissions during which she needed high dose steroids. Her x-ray shows some destruction of her right femoral head. What is the single most likely diagnosis?

A

Avascular necrosis (side effect of steroid therapy)

338
Q

A 22 year asthmatic woman has a painful right hip and inability to weight bear. She is otherwise well. She has had a number of recent admissions during which she needed high dose steroids. Her x-ray shows some destruction of her right femoral head. What is the single most likely diagnosis?

A

Avascular necrosis (side effect of steroid therapy)

339
Q

When taking a focused history, what is the single most effective way to encourage the patient to provide the maximum amount of clinically relevant information during your consultation?

A

Start with an open question

340
Q

What is the single most likely indication for transplantation in a patient with PBC?

A

low serum albumin

341
Q

A 74 year old woman has carcinoma of the colon. Which is the single most likely associated condition?

A

Sporadic adenomatous polyps

342
Q

A 72 year old woman has dysphagia, regurgitation of food and severe halitosis. She has a small mass on the left side of her neck. Which is the single most appropriate investigation?

A

She has a pharyngeal pouch. The best way to delineate this would be by barium swallow

343
Q

A 43 year old man has pancreatic adenocarcinoma. Which single factor conveys risk in the development of this disease?

A

Chronic recurrent pancratitis

344
Q

A 72 year old woman has breathlessness one day after a dynamic hip screw. Her respiratory rate is 25 breaths per minute; pulse rate 90bpm, BP 110/70 mmHg and oxygen saturation 90% on room air. Her heart sounds are normal and her chest is clear. Which is the single most appropriate treatment?

A

LMWH

345
Q

A 22 year old man has bloody diarrhoea and abdominal cramps. He ate chicken the previous night. Which is the single most likely infective agent?

A

Campylobacter enteritis

346
Q

A 22 year old man has bloody diarrhoea and abdominal cramps. He ate chicken the previous night. Which is the single most likely infective agent?

A

Campylobacter enteritis

347
Q

A 42 year old man with active Crohn’s colitis, treated with high dose steroids presents with severe upper abdominal pain and vomiting. Which is the single most likely diagnosis?

A

Perforated peptic ulcer

348
Q

What is the commonest cause of unconjugated hyperbilirubinaemia?

A

Gilbert’s disease

349
Q

How is Gilbert’s disease inherited?

A

Autosomal dominant

350
Q

How does Gilbert’s disease present?

A

Jaundice with no other symptoms

351
Q

How does Gilbert’s disease present?

A

Jaundice with no other symptoms

352
Q

A 58 year old man with mild mitral valve disease is about to undergo cholecystectomy. Which single intervention is required at anaesthetic induction?

A

DVT prophylaxis with TED stockings

N.B. for uncomplicated cardiac valve lesions, prophylactic IV antibiotics are not recommended by NICE guidelines

353
Q

What is the most likely colorectal cancer?

A

Adenocarcinoma

354
Q

Which patients require annual influenza vaccination?

A

Patients with:

  • Immunosupression
  • Chronic heart disease
  • Chronic renal disease
  • Chronic hepatic disease
355
Q

In clinical trials, treatment groups of subjects are often similar with respect to their characteristics at baseline. Which single statement best describes the method which accounts for this?

A

Randomisation

356
Q

Which of the modified Glasgow criteria for predicting severity of pancreatitis is associated with poorest prognosis?

A

Low calcium

357
Q

What features are likely to be seen on the Us and Es of a patient taking spironolactone?

A

Low sodium
High potassium
Raised Urea
Raised creatinine

358
Q

What features are likely to be seen on the Us and Es of a patient taking spironolactone?

A

Low sodium
High potassium
Raised Urea
Raised creatinine

359
Q

Which single symptom best describes peritonitis?

A

abdominal rigidity

360
Q

What type of fracture around the proximal femur is most likely to result in AVN of the femoral head?

A

Intracapsular fracture

361
Q

A 46 year old man has recent 2 stone weight loss one year after a total gastrectomy and Roux-en-Y reconstruction for gastric cancer. He has been eating solids and fluids throughout. Which is the single likeliest cause for his weight loss?

A

Recurrence

362
Q

A 70 year old man has a 4 hour history of an acutely painful right lower leg. The leg is pale and he is in atrial fibrillation. What is the single most appropriate immediate investigation?

A

Femoral artery angiography (as the history is suggestive of an arterial embolus, diagnosed by arteriography)

363
Q

A 70 year old man has a 4 hour history of an acutely painful right lower leg. The leg is pale and he is in atrial fibrillation. What is the single most appropriate immediate investigation?

A

Femoral artery angiography (as the history is suggestive of an arterial embolus, diagnosed by arteriography)

364
Q

A 71 year old man develops bloody diarrhoea three days after abdominal aortic aneurysm repair. He has a distended, tender abdomen with no active bowel sounds. Which is the single most likely diagnosis?

A

Mesenteric ischaemia

365
Q

What is the single best treatment for intra-abdominal perforation, as identified by air under the diaphragm on erect CXR?

A

Laparotomy and omental patch

366
Q

What is the likely diagnosis in a 59 year patient presenting with signs of infection and a cylindrical, hard, tender mass in the left iliac fossa?

A

Diverticulitis

367
Q

A 29 year old man has a high temperature, with perianal tenderness, erythema and a fluctuant swelling. Whichis the single most likely diagnosis?

A

Perianal abscess

368
Q

A 72 year old man with chronic obstructive pulmonary disease is undergoing elective cholecystectomy. Which single preoperative measure is most appropriate in his work-up?

A

Respiratory function tests

369
Q

What is the single most appropriate medication to control the blood glucose of a type 2 diabetic perioperatively?

A

IV sliding scale insulin

370
Q

A 72 year old man with chronic obstructive pulmonary disease is undergoing elective cholecystectomy. Which single preoperative measure is most appropriate in his work-up?

A

Respiratory function tests

Gastroenterology (1 decks)

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