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YEAR 3 & 5 CORE CONDITIONS > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

What can cause GORD?

A
  • Abnormalities of lower oesophageal sphincter e.g. transient relaxation
  • Hiatus hernia
  • Oesophageal dysmotility
  • Increased abdominal pressure e.g. pregnancy
  • Gastric acid hypersecretion e.g. Ellison Zollinger syndrome
  • Delayed gastric emptying
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2
Q

Which drugs can increase the risk of GORD and why?

A

Tricyclic antidepressants
Anticholingergics
Nitrates
Calcium channel blockers

They all relax the tone of gastrooesophageal sphincter

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3
Q

What are some symptoms of GORD?

A
  • Heartburn - retrosternal burning pain that worsen with lying down and after eating
  • Belching
  • Acid brash (regurgitation)
  • Increased salivation
  • Odynophagia
  • Chronic cough
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4
Q

What condition is GORD often associated with?

A

Asthma

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5
Q

What investigations should be done for GORD?

A
  • Empirical therapy - if GORD is clinically suspected and there are no indications for endoscopy, start a short trial of PPIs
  • Endoscopy - if signs of complicated disease (e.g. dysphagia, odynophagia, weight loss)
  • Oesophageal pH monitoring - measured over 24h via NG tube with pH probe; sudden drops to pH < 4 = acid reflux
  • Barium swallow - to rule out hiatus hernia
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6
Q

What is the endoscopic grading of oesophagitis?

A

Savary-Miller system
Grade 1: single/multiple erosions on a single fold
Grade 2: multiple erosions on multiple folds
Grade 3: multiple circumferential erosions
Grade 4: ulcer, stenosis or oesophageal shortening
Grade 5: Barrett’s (columnar metaplasia AKA intestinal metaplasia)

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7
Q

What are the conservative, medical and surgical management optoins for GORD?

A

Conservative
• Small portions and avoid eating < 3 hours before bedtime
• Lose weight
• Avoid nicotine, alcohol, coffee

Medical

  • Antacids
  • PPIs for 2 months - omeprazole, lansoprazole

Surgical

  • Fundoplication - the gastric fundus is wrapped around the lower oesophagus and secured to form a cuff, which narrows the distal oesophagus and GOJ to prevent reflux
  • Laparoscopic insertion of magnetic bead band
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8
Q

What are some side effects of PPIs?

A

Headache
GI upset
Increased risk of C. difficile
Low magnesium - tetany, ventricular tachycardia

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9
Q

What is a contra indication of PPIs?

A

Osteoporosis

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10
Q

What drugs do PPIs interact with?

A

They are CYP450 inhibitors so they increase concentration of drugs metabolised by CYP450 system

Drugs metabolised by CYP450 system:

  • Warfarin
  • COCP
  • Theophylline - methylxanthine for COPD
  • Corticosteroids
  • Tricyclic antidepressants
  • SSRIs
  • Pethidine - analgesia
  • Statins
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11
Q

When are H2 receptor antagonists used over PPIs?

A

Pregnancy

Pre-op - quicker onset than PPIs

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12
Q

What are some red flag symptoms for upper GI cancer?

A
  • Dysphagia
  • Dyspepsia with weight loss, anaemia or vomiting
  • Family history
  • Barrett’s oesophagus
  • Upper abdominal mass
  • Jaundice
  • Pernicious anaemia
  • Peptic ulcer surgery
  • > 55 years
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13
Q

How do antacids interact with other drugs?

A 
Decrease absorption of gastric protected drugs e.g. metformin
Increase excretion of aspirin + lithium
Decrease serum concentrations of:
- ACE inhibitors
- Cephalosporins
- Ciprofloxacin
- Tetracyclines
- Digoxin
- PPIs
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14
Q

What is the pathophysiology of the main cause of peptic ulcers?

A

H. Pylori infection
It produces ammonia in order to neutralise the acid of the stomach.
The ammonia is directly toxic to epithelial cells, leading to inflammation
The inflammation causes depletion of the alkaline mucus and atrophy of the lining, leading to ulcers

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15
Q

What is the 2nd most common cause of peptic ulcers and why?

A

NSAID use - they inhibit prostaglandin synthesis which reduces the production of the protective alkaline mucus

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16
Q

What shape is H Pylori and what gram stain is it?

A

Spiral shaped bacteria

Gram-negative

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17
Q

What are the alarm symptoms of peptic ulcer?

A

ALARMS

Anaemia (iron deficiency)
Loss of weight
Anorexia
Recent onset
Melaena/haematemesis
Swallowing difficulty
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18
Q

How do stomach/duodenal ulcers present?

A

Stomach

  • Pain worse on eating
  • Haematemesis

Duodenal

  • Pain relieved by eating
  • Pain wakes patient up in the night
  • Melaena
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19
Q

Which type of peptic ulcer is more common?

A

Duodenal ulcers are 4x more common

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20
Q

What tests can you do for H Pylori?

A

Stool antigen test = diagnostic

Carbon-13 urea breath test = to check if eradication was successful

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21
Q

What is the treatment for H Pylori?

A

Triple therapy

Amoxicillin 1g + clarithromycin 500mg + PPI (all taken twice daily for 1 week)

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22
Q

What are the main complications of peptic ulcers?

A

Bleeding
Perforation
Malignancy
Decreased gastric outflow

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23
Q

Who must get an endoscopy?

A

Anyone with dysphagia

> 55 years and persistent symptoms or ALARM symptoms

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24
Q

If H. Pylori test is negative, how do you treat a peptic ulcer?

A

PPIs for 2 months

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25
Q

What are the most common causes of acute GI bleeds?

A
  1. Peptic ulcer = 50%
  2. Oesophago-gastric varices (due to portal hypertension e.g. liver cirrhosis) = 10-20%

Others:

  • Mallory-Weiss tear (due to severe vomiting e.g. alcoholism or bulimia)
  • Malignancy
  • Gastritis/oesophagitis
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26
Q

What are the risk factors for poor prognosis/re-bleeding?

A 
Age > 60
Cardiovascular disease
Respiratory disease
Hepatic impairment
Coagulopathy 
Malignancy
  1. Is the patient more susceptible to the effects of anaemia, such as coronary artery disease?
  2. Is the patient at risk of fluid overload with aggressive resuscitation (such as renal disease)?
  3. Will the bleeding be harder to control, owing to anticoagulation, liver disease or thrombocytopaenia?
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27
Q

What scores are used to assess risk of mortality in Upper GI bleeds

A

Rockall score

Glasgow-Blatchford score

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28
Q

What is Boerhaave’s syndrome? What sign can be found on examination

A

Oesophageal perforation

Sign - subcutaneous/surgical emphysema

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29
Q

What blood levels would indicate a GI bleed?

A

Low Hb

High urea out of proportion to creatinine indicates large blood meal

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30
Q

What is the acute management of an upper GI bleed?

A
  • 2 wide bore cannulae in antecubital fossae
  • Take bloods - U+Es, FBC, group + save, coagulation screen, LFTs, VBG
  • 500ml 0.9% sodium chloride in 15 min
  • Activate ‘Major Haemorrhage’ protocol - FFP + 4 units of RBCs
  • Prescribe terlipressin + prophylactic antibiotics
  • Call GI reg to organise endoscopy
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31
Q

What are some causes of portal hypertension?

A

Pre-hepatic - thrombosis (portal or splenic vein)

Hepatic

  • Cirrhosis (most common in UK)
  • Schistosomiasis (most common worldwide)
  • Sarcoidosis

Post-hepatic

  • Right heart failure
  • Constrictive pericarditis
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32
Q

What is the prevalence of IBS?

A

10-20% of UK population

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33
Q

What is the criteria used to diagnose IBS and what does it consist of?

A

Manning Criteria

Abdominal discomfort or pain that is relieved by defecation OR associated with altered bowel frequency or stool form
AND at least 2 of:
- Altered stool passage (e.g. straining or urgency)
- Abdominal bloating
- Symptoms made worse by eating
- Passage of mucus

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34
Q

What are some exacerbating factors of IBS?

A

Stress
Menstruation
Gastroenteritis = post-infectious IBS

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35
Q

What tests should be done in IBS?

A
  • FBC to check for anaemia
  • CRP
  • Coeliac screening
  • Faecal calprotectin for potential IBD
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36
Q

What advice can be given for constipation in IBS?

A
  • Increase water and fibre intake
  • Physical activity
  • Simple laxatives but avoid lactulose which can aggravate bloating when it ferments
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37
Q

What advice can be given for diarrhoea in IBS?

A

Avoid:

  • Sweeteners
  • Alcohol
  • Caffeine
  • Fibre

Loperamide after each loose stool

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38
Q

What are the main risk factors for Crohn’s disease?

A
  • Family history - NOD2 gene

- Smoking increases risk by 3-4x

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39
Q

What causes Crohn’s disease?

A

Autoimmune response against gut flora

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40
Q

What is the macroscopic and microscopic histopathology of Crohn’s?

A 
Macroscopic
• Cobblestone appearance
• Pinpoint lesions - small, aphthous haemorrhagic mucosal defects
• Thickened bowel wall 
• Fistulae and abscesses

Microscopic
• Skip lesions present
• Transmural inflammation -> fibrosis and stenosis -> fistulae and abscesses
• Creeping fat
• Non-caseating granulomas - lots of cells clumped together
• Lots of lymphocytes (lots of purple) = autoimmune

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41
Q

How does Crohn’s present?

A
  • Aphthous ulcers
  • Chronic diarrhoea
  • Colicky abdominal pain, worse after eating
  • Weight loss
  • Anal fistula/abscess
  • Malnourished due to decreased absorption
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42
Q

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

A
  • Pyoderma gangrenosum
  • Episcleritis (painless red eye)
  • Anterior uveitis
  • Erythema nodosum
  • Ankylosing spondylitis
  • Calcium oxalate kidney stones
  • Gallstones
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43
Q

What investigations are done for IBD?

A
  • Stool culture to exclude infection if first presentation
  • Faecal calprotectin tests for GI inflammation
  • Colonoscopy + biopsy
  • MRI to detect fistulae
  • FBC, CRP, ESR, B12, folate
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44
Q

How do you treat a flare of Crohn’s?

A

Prednisolone 40mg per day for 1 week then taper by 5mg each week for 7 weeks - first line

Mesalazine - second line

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45
Q

How do you induce or maintain remission for someone suffering frequent exacerbations of Crohn’s?

A

Azathioprine - first line (always check TPMT activity first
Mercaptopurine - second line
Methotrexate - possible add on therapy to either

Infliximab in refractory or fistulating disease

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46
Q

What is the histolopathology of ulcerative colitis?

What is the defining lesion?

A
  • Crypt abscesses = defining lesion
  • Micro ulcers
  • Inflammatory polyps
  • Inflammation is NOT transmural
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47
Q

What does ulcerative colitis most commonly affect?

A

The rectum (proctitis)

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48
Q

How does ulcerative colitis present?

A
  • Diarrhoea with blood + mucus
  • Cramping abdominal discomfort
  • Tenesmus (proctitis)
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49
Q

What is an acute complication of ulcerative colitis?

A

Toxic megacolon = fulminant colitis

  • Acute colonic dilatation so transverse colon is > 6cm diameter
  • Extension of inflammation beyond mucosa
  • Loss of contractility leads to accumulation of gas and fluid
  • Risk of perforation
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50
Q

What signs would be seen on examination in toxic megacolon?

A
  • Firm, distended abdomen
  • Rebound tenderness + guarding
  • Absent bowel sounds
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51
Q

In ulcerative colitis:

a) What is used to induce remission?
b) What is used to maintain remission?

A

Steroids to induce remission - prednisolone 40mg OD with tapering dose

Mesalazine = 5-aminosalicylate OD to maintain remission

Surgery if failing to respond to medical therapy

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52
Q

What are the main poultry-associated causes of gastroenteritis? How can you distinguish between them?

A

Salmonella
Campylobacter

Incubation period

  • Salmonella = 12-36 hours
  • Campylobacter = 1-10 days

Campylobacter is more likely to cause bloody stools

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53
Q

Which viruses commonly cause gastroenteritis?

A 
Norovirus = most common 
Adenovirus
Rotavirus
Sapovirus 
CMV
54
Q

What usually causes Listeria gastroenteritis?

A

Cold meats
Soft cheeses
Pâté

Avoid these foods in pregnancy due to risk of miscarriage

55
Q

What causes E. Coli gastroenteritis?

A

Under-cooked beef

Unpasteurised milk

56
Q

How does E. Coli gastroenteritis present?

A 
Bloody diarrhoea (E Coli 0157 is haemolytic) 
Risk of developing haemolytic uraemic syndrome
57
Q

Name some intestinal parasites that can cause gastroenteritis

A

Giardia
Cryptosporidium
Entamoeba histolytica

58
Q

What is the incubation period for viruses, bacteria and parasites?

A 
Viruses = 1-3 days
Bacteria = < 1 week (can be hours) 
Parasites = weeks
59
Q

What are the main causes of dysentery?

A
  • E. Coli
  • Shigella
  • Campylobacter (25%)
  • Salmonella
  • C. Difficile
  • CMV
  • Entamoebic histolytica
  • Trichuriasis = whipworm
60
Q

What is the definition of diarrhoea?

A

> 3 episodes of loose stools per day

61
Q

What investigation should be done in gastroenteritis?

A

Stool MC&S

  • Toxins
  • Culture of bacteria
  • PCR
  • Oocytes in cyclospora and cryptosporidium
62
Q

How do you treat gastroenteritis?

A

Hydration - oral rehydration solution

Antimotility agents e.g. loperamide (do not give in dysentery because need to get rid of the infection)

63
Q

Why should you not give antibiotics in food poisoning?

A

If it is E. Coli, there is risk of haemolytic uraemic syndrome

64
Q

How do you treat C. Difficile?

A

Metronidazole

Vancomycin if metronidazole didn’t work

65
Q

What is the mechanism of loperamide?

A

Opioid receptor agonist and non-selective calcium channel blocker
This reduces peristalsis
This increases the time substances stay in the intestine so more water can be absorbed

66
Q

What are the contraindications of loperamide?

A

Acute IBD - risk of perforation

C. difficile + other dysentery

67
Q

What is the mechanism of laxatives?

A

They increase water and electrolyte secretion from the mucosa to increase peristalsis

68
Q

What are the side effects of laxatives?

A

Diarrhoea
Melanosis coli
Tolerance (often abused in anorexia)

69
Q

What are the contraindications of laxatives?

A

Bowel obstruction - risk of perforation
Diabetes - senna is high in sugar
Haemorrhoids

70
Q

What does mesalazine interact with?

A

PPIs - they increase the pH so the gastric protection is broken down in the stomach

Lactulose - decreases the pH of stools so it prevents release in the colon

71
Q

When is mesalazine contraindicated?

A

Aspirin hypersensitivity

72
Q

What are some important side effects of mesalazine?

A

Oligospermia

Leucopenia

73
Q

What are the 2 types of oesophageal carcinoma? Where is each more common?

A

Adenocarcinoma - developed world

Squamous cell carcinoma - developing world

74
Q

What are the risk factors for adenocarcinoma of the oesophagus?

A 
Barrett's oesophagus 
Cured meats, low fruit and veg
High fat intake 
GORD
Obesity
75
Q

What are the risk factors for squamous cell carcinoma of oesophagus?

A 
Thermal injury - hot drinks
Smoking
Excessive alcohol
HPV virus 
Achalasia
76
Q

Which parts of the oesophagus is affected in each type of oesophageal carcinoma?

A

Adenocarcinoma - lower third

Squamous cell carcinoma - upper and middle thirds

77
Q

What is the treatment for oesophageal carcinoma?

A

Adenocarcinoma - neoadjuvant chemotherapy then oesophagectomy

Squamous cell - definitive chemo-radiotherapy (SCCs are difficult to operate on)

78
Q

Where are rates of gastric carcinoma particularly high?

A

Japan
China
South America

79
Q

What are some risk factors for gastric carcinoma?

A
  • H. Pylori infection
  • Smoking
  • Atrophic gastritis
  • Pernicious anaemia
  • Nitrosamines - cured meats
  • High salt, pickling
  • High alcohol intake
80
Q

What signs might be found on examination of gastric cancer?

A

Epigastric mass
Virchow’s node
Acanthosis nigricans
Hepatomegaly, jaundice, ascites if metastatic disease

81
Q

Explain an endoscopy procedure to a patient

A
  1. Check the patient’s understanding
  2. Endoscopy = a tube that is only the size of your middle finger with a camera at the end will go down your gullet to look at your stomach and the first bit of your bowel
  3. Why they need it
  4. Pre-procedure - fast for at least 6 hours before and have no fluids 3 hours before. If you are being sedated, make sure you have someone to take you home.
  5. How it’s performed - lie on the bed on your side; some anaesthetic spray will be sprayed in your mouth; the tube is inserted and gas is used to inflate the bowel
  6. Risks - you may get some bloating and pain. Rare risks include perforation, infection, bleeding
82
Q

How might gastric cancer present?

A

Dyspepsia - not responsive to PPIs and worse when eating
Early satiety
Vomiting
Melaena
Non-specific cancer sx: weight loss, anaemia

83
Q

What are some risk factors for colorectal cancer?

A
  • IBD
  • Family history - FAP, HNPCC
  • Diet low in fibre, high is processed meat
  • Smoking
  • Alcohol
84
Q

What drug can be used to prevent colorectal cancer?

A

Apirin 75mg daily

85
Q

How does left sided colorectal cancer present?

A
  • Rectal bleeding with mucus
  • Early change in bowel habit
  • Tenesmus
  • Mass in LIF
  • Obstruction (left colon is narrower and doesn’t expand as easily)
86
Q

How does right sided colorectal cancer present?

A
  • Weight loss
  • Anaemia
  • Abdominal pain
  • Mass in RIF
  • More advanced at presentation
87
Q

What investigations are done for colorectal cancer?

A

Colonoscopy + biopsy - diagnostic
FBC - microcytic anaemia
Faecal occult blood
CEA tumour marker - used to monitor disease progression

88
Q

What is the screening programme for colorectal cancer?

A
  1. All 55+ years are invited for a one off flexible sigmoidoscopy
  2. All 60-74 year olds are invited to do a home test every 2 years
  3. Over 75s can ask for a home test kit every 2 years
89
Q

What is the classification of colorectal cancer?

A 
Duke's criteria 
A - limited to muscularis mucosae
B - extension through muscularis mucosae
C - involvement of regional lymph nodes 
D - distant metastasis
90
Q

What genes are linked to coeliac disease?

A

HLA-DQ2 (95%)

HLA-DQ8

91
Q

When should coeliac disease be suspected?

A

Anaemia (iron or B12 deficiency)
Weight loss
Diarrhoea (steatorrhoea)

92
Q

What is seen on histology of coeliac disease?

A

Villous atrophy
Crypt hyperplasia

Stages
• Stage 1 - increased intraepithelial lymphocytes
• Stage 2 - increased inflammatory cells and crypt hyperplasia
• Stage 3 - all the above + villous atrophy

93
Q

What are some extra-intestinal manifestations of coeliac disease?

A

B12 deficiency - peripheral neuropathy, ataxia
Iron deficiency - angular stomatitis, anaemia
Aphthous ulcers
Osteoporosis
Dermatitis herpetiformis

94
Q

What is the first line investigation for coeliac disease?

What investigation is the gold-standard for diagnosis of coeliac disease?

A

All tests must be done whilst eating a gluten-containing diet

  1. Total IgA and IgA tissue transglutaminase = 1st choice
  2. If the first test was only weakly positive, test IgA EMA (endomysial antibodies)
  3. If IgA is deficient, test IgG

Duodenal/jejunal biopsy = gold-standard diagnostic

95
Q

What causes appendicitis?

A

Lumen of appendix becomes obstructed with:
- Faecolith = hard mass of faecal matter
- Lymphoid hyperplasia
- Filarial worms
Then gut organisms invade the appendix wall

96
Q

What are some complications of acute appendicitis?

A

Increased intraluminal pressure -> ischaemia -> necrosis -> perforation -> peritonitis

Electrolyte imbalance from vomiting

Pelvic abscess

97
Q

What signs might be found on examination of appendicitis?

A
  • Tachycardia, tachypnoea, pyrexia
  • Tenderness at McBurney’s point (2/3rds umbilicus to ASIS)
  • Guarding due to peritonitis
  • Rovsing’s sign - pain in RIF on pressing over LIF
  • Psoas sign - pain on extending thigh
  • Cope sign - pain on flexion and internal rotation of R thigh
98
Q

How is appendicitis diagnosed? What tests must be done?

A

Clinical diagnosis

Bloods - raised WCC, CRP, ESR
Urinalysis to rule out UTI
Pregnancy test to rule out ectopic

99
Q

What is the management of appendicitis?

A

Nil by mouth
IV fluids
IV analgesia + anti-emetics
IV Abx (cefuroxime 1.5g/8hr plus metronidazole 500mg/8hr)
Laparoscopic appendectomy = curative gold-standard treatment (usually booked electively a few weeks after IV abx and fluids unless acute peritonitis)

100
Q

What are the causes of small bowel mechanical obstruction?

A

Adhesions (most common) e.g. prior abdo surgery, abdominal TB
Incarcerated hernias
Crohn’s disease

101
Q

How does small bowel obstruction present?

A
  • Early bilious vomiting
  • Less abdominal distention
  • Colicky pain high up in abdomen
102
Q

What are the causes of large bowel obstruction?

A

Tumours e.g. colon carcinoma - most common cause especially in elderly (typically sigmoid carcinoma)
Constipation
Volvulus
Diverticular stricture

103
Q

How does large bowel obstruction present?

A
  • More constant pain
  • Absolute constipation (no faeces or flatus)
  • Distention
  • Feculent vomiting - but this is a late sign
104
Q

What are the 2 categories of intestinal obstruction? How can you distinguish between them clinically?

A

Mechanical

  • High-pitched tinkling bowel sounds
  • Colicky abdominal pain
  • Vomiting

Functional

  • Bowel sounds absent
  • Less pain - but it is more diffuse and continuous
  • Marked abdominal distention
  • Absolute constipation
105
Q

What can cause paralytic ileus?

A
  • Recent abdominal surgery
  • Abdominal infections or inflammatory conditions
  • Medications - opioids, anticholinergics, antiparkinsonian drugs
  • Electrolyte disturbances

classic is someone on IV morphine post-operatively

106
Q

What would an abdominal X-ray of bowel obstruction look like depending on which bowel is affected?

A

Dilated bowel

  • Small bowel dilatation if >3cm
  • Large bowel dilatation if >6cm
  • Cecal dilatation if > 9cm

Small bowel obstruction - valvulae conniventes are visible (lines completely cross the bowel)

Large bowel obstruction - haustral lines visible

Rigler’s sign = pneumoperitoneum due to perforated bowel (both sides of bowel wall can be seen)

107
Q

What is the pathophysiology of Barrett’s oesophagus?

A
  • Intestinal metaplasia - Stomach acid damages the squamous epithelium, then it becomes replaced by columnar epithelium and goblet cells
  • The physiological transformation zone (Z-line) between squamous and columnar epithium is shifted upwards
  • If there is >3cm of columnar epithelium between Z-line and GOJ, there is a higher cancer risk
108
Q

What is the management of low-grade dysplasia in Barrett’s oesophagus?

A

High dose PPI and followed up with endoscopic surveillance at six monthly intervals

109
Q

What is the management of high-grade dysplasia in Barrett’s oesophagus?

A

Endoscopic resection of the abnormal areas (radiofrequency ablation, photodynamic ablation, or laser)

110
Q

What is the most common presenting symptom in oesophageal cancer?

A

Dysphagia
○ Progressive in nature - starts with solids only, before affecting liquids
○ Any patient with dysphagia should be assumed to have oesophageal cancer until proven otherwise

111
Q

What is the initial investigation in suspected oesophageal carcinoma?

A

Endoscopy (OGD) within 2 weeks +/- biopsy if there is any malignancy to send to histology

112
Q

What are the options for palliative management of oesophageal cancer?

A
  • Oesophageal stent
  • Radiotherapy + chemotherapy to reduce tumour size
  • Nutritional support - thickened fluid, nutritional supplements
  • Radiologically-Inserted Gastrostomy (RIG) - can be inserted to bypass the obstruction if dysphagia becomes too severe
113
Q

How are gastric cancers treated?

A
  • Peri-operative chemotherapy - 3 cycles of neoadjuvant + 3 cycles of adjuvant
  • Proximal gastric cancers - total gastrectomy
  • Distal gastric cancers - subtotal gastrectomy
114
Q

What are the NICE guidelines for referral for urgent investigation for colorectal cancer?

A
  • ≥40yrs with unexplained weight loss and abdominal pain
  • ≥50yrs with unexplained rectal bleeding
  • ≥60yrs with iron‑deficiency anaemia or change in bowel habit
  • Positive occult blood screening test
115
Q

What signs can be seen on imaging of sigmoid volvulus?

A

CT abdo-pelvis with IV contrast - dilated sigmoid colon with ‘whirl sign’

AXR - coffee-bean sign arising from LIF

116
Q

What are the management options for bowel obstruction?

A

Remove the cause e.g. medications, do enema for impaction, correct electrolytes

Conservative - for patients that are haemodynamically stable

  • Bowel rest
  • NG tube insertion
  • IV fluids and electrolytes

Surgical (exploratory laparotomy) - for patients that are haemodynamically unstable or have signs of ischaemia/necrosis

117
Q

What signs are seen on AXR in Crohn’s and UC?

A

Thumb-printing = Crohn’s

Lead-piping = Ulcerative colitis

118
Q

What side of the abdomen would an ileostomy and a colostomy be on?

A

Ileostomy = right

Colostomy = left

119
Q

What is the hallmark electrolyte abnormality in refeeding syndrome?

A

Low phosphate

120
Q

What is the pathophysiology behind achalasia?

A

Idiopathic degeneration of the myenteric plexus causes failure of relaxation of oesophageal sphincter

121
Q

How does achalasia present?

A
  • Difficulty swallowing both liquids and solids
  • Regurgitation of food
  • Retrosternal chest pain
122
Q

What investigation is done to diagnose achalasia and what is seen?

A

Barium swallow - bird’s beak appearance of distal oesophagus

123
Q

What are the different management options for achalasia depending on the patient?

A

Heller’s cardiomyotomy - for patients that are fit and can undergo surgery
- Fibres of the lower oesophagus are cut longitudinally to relieve pressure

Endoscopic balloon dilatation - for older, less fit patients

Injection of botox

Calcium channel blockers (e.g. nifedipine) and nitrates

  • Often ineffective
  • Reserved for unfit patients who are unable to tolerate other therapies
124
Q

What are the indications for surgery in ulcerative colitis?

A

Acute fulminant UC
Toxic megacolon with little improvement after 48-72 h of IV steroids
Symptoms worsening despite IV steroids

125
Q

What is a severe side effect of mesalazine?

A

Agranulocytosis

126
Q

What classification is used for severity of UC?

A

Truelove and Witts

127
Q

What sign is seen on AXR of UC?

A

Lead pipe appearance

128
Q

What is the conservative management of intestinal obstruction?

A

Bowel rest
NG tube (Ryles tube) insertion - aspirate stomach contents with syringe then attach a bag for free drainage
IV fluids and electrolytes

Depending on cause:

  • Enema for faecal impaction
  • Sigmoidoscopic detorsion for sigmoid volvulus
129
Q

Which patients is conservative management of intestinal obstruction appropriate for?

A

For patients with partial bowel obstruction or complete bowel obstruction but no signs of ischaemia/necrosis/clinical deterioration

130
Q

When is surgical management of intestinal obstruction indicated?

A

Haemodynamic instability
Signs of ischaemia/necrosis
Persistent partial obstruction >3-5 days
Closed-loop obstruction

131
Q

What medications should be stopped in bowel obstruction?

A

Pro-kinetic medications

  • Metoclopramide
  • Erythromycin
  • Domperidone

YEAR 3 & 5 CORE CONDITIONS (30 decks)

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