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MSRA > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

What is dyspepsia and what causes it?

A

The presence of upper GI symptoms (incl nausea, vomiting, pain/discomfort, heartburn) for 4 weeks or more

DDs - functional, ulcer, duodenitis, oesophagitis/GORD, malignancy, gastritis

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2
Q

What are the red flag symptoms for dyspepsia?

A

Anaemia (iron deficiency)
Loss of weight
Anorexia
Recent onset/progressive symptoms
Meleana/haematemesis
Swallow difficulty
~~~

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3
Q

How should new dyspepsia (for over 4 weeks) be investigated?

A

Under 55 - stop drugs causing dyspepsia, lifestyle changes. antacids etc. If 4 weeks still symptoms, test for H. pylori and treat
Over 55 or ALARMS signs - refer for 2WW endoscopy as need to rule out cancer

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4
Q

How long before an H pylori test or OGD should you stop usual meds?

A

2 weeks - PPI, ranitidine

4 weeks - bismuth, antibiotics

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5
Q

Describe H pylori testing

A

Choice between:

  • Carbon 13 urea breath test
  • Stool antigen test
  • Lab-based serology
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6
Q

When should H pylori eradication therapy be offered?

A

Patients who have tested positive for H pylori and have PUD

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7
Q

What is peptic ulcer disease and what causes it?

A

A break in the superficial epithelial cells penetrating down to the mucosa - this can be gastric or duodenal.

Caused by H pylori, NSAID use, smoking, stress

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8
Q

How do you differentiate between duodenal and gastric ulcers?

A

DUODENAL - Gnawing epigastric pain BEFORE meals or at night, which is relieved by eating (these are 4x more common)

GASTRIC - Gnawing epigastric pain AFTER meals

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9
Q

Where do gastric ulcers usually occur?

A

On the lesser surface of the stomach (elsewhere are usually malignant)

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10
Q

How should those with PUD be managed?

A

H PYLORI POSITIVE:
Associated NSAID use - full dose PPI for 2 months then eradication therapy
No NSAID use - first line eradication therapy

H PYLORI NEGATIVE:
- Full dose PPI therapy for 4-8 weeks

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11
Q

Describe H pylori eradication therapy

A

7 day, twice daily course of:

  • Lansoprazole
  • Amoxicillin
  • Clarithromycin/metronidazole

If no response try whichever abx was not used first line
If pen allergic do bottom two abx

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12
Q

Describe H pylori eradication therapy (if previous exposure to clarithromycin and metronidazole)

A

7 day, twice daily course of:

  • Lansoprazole
  • Amoxicillin
  • Tetracycline
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13
Q

What follow up is offered for H pylori eradication therapy?

A

Urea breath test - if not effective try second line regime

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14
Q

What is functional dyspepsia?

A

Non ulcer dyspepsia this may be due to a hypersensitive oesophagus or functional heartburn (non acid stimulus) - treat with PPI, psychotherapy, bismuth

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15
Q

What is GORD?

A

Reflux of stomach contents causing symptoms (dyspepsia, hoarseness, cough). Often defined as 2 or more episodes of heartburn a week.

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16
Q

What causes GORD?

A
  • LOS hypotension
  • Hiatus hernia
  • Loss of oesophageal peristaltic function
  • Abdo obesity
  • Gastric acid hyper secretion
  • Slow gastric emptying
  • Overeating
  • Smoking/alcohol
  • Pregnancy
  • Drugs
  • Systemic sclerosis
  • H. pylori
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17
Q

Which drugs can cause GORD?

A
  • Tricyclics
  • Anticholinergics
  • Nitrates
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18
Q

How is GORD investigated?

A

BLOODS - FBC, U&E
IMAGING - endoscopy
OTHER - barium swallow, C13 urea breath test or stool antigen test

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19
Q

What are the criteria for endoscopy in GORD?

A

ALARM symptoms or over 55

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20
Q

What are the complications of GORD?

A
  • Oesophagitis
  • Benign oesophageal stricture
  • Barretts oesophagus
  • Iron deficiency
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21
Q

How should H pylori negative GORD be managed?

A

Lifestyle:
Pillows, diet, alcohol, stress management

Drugs:
Antacids, alginates

If oesophagitis present:
1st line - high dose PPI for 4 or 8 weeks (eg. lansoprazole)
2nd line - switch to another PPI or H2RA therapy (eg. ranitidine)

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22
Q

How should H pylori positive GORD be managed?

A

Triple eradication therapy

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23
Q

How is severe GORD managed?

A

Severe GORD must be confirmed by pH monitoring/manometry, if drugs are not working.

Management is surgical - Nissen fundoplication, HALO, stretta ablation.

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24
Q

What classification is used to assess severity of GORD?

A

Los Angeles classification - describes the extent of the mucosal break.

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25
Q

What is Nissen fundoplication?

A

Gastric fundus wrapped around the lower oesophageal sphincter to prevent reflux from happening.

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26
Q

When is surgery considered in peptic ulcer disease?

A
  • Haemorrhage
  • Perforation
  • Pyloric stenosis
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27
Q

Which elective surgeries can be offered for PUD?

A

Vagotomy - denervation of the the vagus supply where it supplies the LOS and stomach to reduce the rate of gastric secretion

Gastrectomy - rare! only potentially in Zollinger Ellison syndrome

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28
Q

Which emergency surgeries can be offered for PUD?

A

Haemorrhage - adrenaline, diathermy, surgery

Perforation - laparoscopic repair, commence H pylori eradication post op

Pyloric stenosis - endoscopic balloon dilatation, drainage procedure and vagotomy

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29
Q

What are the symptoms of pyloric stenosis in adults?

A

Vomiting large amounts of food hours after meals - this is due to scarring in duodenal ulcers

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30
Q

What is Zollinger-Ellison syndrome?

A

A rare condition in which one or more tumors form in your pancreas or the upper part of your small intestine (duodenum). These tumors, called gastrinomas, secrete large amounts of the hormone gastrin, which causes your stomach to produce too much acid.

The gastronome is usually found in the pancreas! 60% are malignant.

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31
Q

What are the symptoms of Zollinger-Ellison syndrome?

A
  • Abdo pain
  • Dyspepsia
  • Chronic diarrhoea and steatorrhea
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32
Q

How is Zollinger-Ellison syndrome diagnosed?

A

Measure 3 fasting serum gastrin levels on different days. Positive test is >1000pg/mL, with gastric pH <2.

Use CT/endoscopic US to stage and OGD to evaluate ulceration.

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33
Q

How is Zollinger-Ellison syndrome managed?

A

High dose PPI

Chemo/surgery if malignancy.

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34
Q

Which familial cancer is Zollinger-Ellison syndrome associated with?

A

MEN1

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35
Q

What is Barretts oesophagus?

A

Replacement of normal squamous epithelium with metaplastic columnar epithelium, due to GORD.

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36
Q

How is Barretts oesophagus diagnosed?

A

Biopsy of endoscopically visible columnar cells

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37
Q

Which criteria is used in Barretts?

A

Prague criteria (looks at C - circumferential extent and M - maximum extent)

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38
Q

How is Barretts oesophagus managed?

A

No premalignant changes - biopsy and endoscopy every 1-3 years

Low grade dysplasia - endoscopy every year

High grade dysplasia - endoscopic therapy, oesophageal resection, eradicative mucosectomy, mucosal ablation

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39
Q

What is gastritis?

A

Inflammation of the lining of the stomach, presenting with epigastric pain, vomiting, haematemesis

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40
Q

How can gastritis be prevented?

A

Give PPI gastroprotection when prescribing long term NSAIDS

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41
Q

How can gastritis be treated?

A

Ranitidine/PPI. H pylori eradication if indicated (may need quadruple therapy with bismuth). Endscopic quarterly.

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42
Q

What are the different types of endoscopy?

A

Proctoscopy - examines the rectum in pts with history of bright red PR bleed

Sigmoidoscopy - examines 20-25cm of distal colon , give phosphate enema before

Flexi sigmoidoscopy - reaches up to the splenic flexure, requires evacuation of distal colon

OGD - can be diagnostic and therapeutic, looks at oesophagus, stomach and duodenum, no PPI for 2 weeks before and NBM for 4 hours

Colonoscopy - can be diagnostc and therapeutic, looks at colon and terminal ileum, no iron for 1 week post op and no solid food for 12-24hr, give sodium picosulfate before, do PR first

Ballooon enteroscopy - examines small bowel from duodenum to ileum using specialized enterescope

Capsule endoscopy - for evaluation of obscure GI bleeding after negative gastroscopy and colonoscopy

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43
Q

What are some relative CIs for OGD?

A

COPD, recent MI

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44
Q

What is the first line investigation for abdo distension?

A

Ultrasound

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45
Q

What is the first line investigation for acute abdomen?

A

CT (although x-ray often used first)

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46
Q

What is the first line investigation for evaluation of rectal cancers and abscesses/fistulae in anal region?

A

MRI

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47
Q

What is the first line investigation for staging most GI cancers?

A

Ct/MRI/PT

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48
Q

What is barium swallow used for?

A

Investigation of dysphagia, hiatus hernia

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49
Q

What is a hiatus hernia?

A

Sliding (80%) - gastro-oesophageal junction slides up into the chest so that it lies above the diaphragm. Often asymptomatic but may cause reflux

Rolling (20%) - gastro-oesophageal junction remains in abdomen but a bulge of stomach herniates up into the chest. Acid reflux uncommon but may cause severe pain due to strangulation

Risk factors include increased abdominal pressure (ascites, multiparty) and obesity

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50
Q

How is hiatus hernia managed?

A
  • Weight loss
  • Antacids
  • Surgery if rolling HH (due to risk of strangulation), only in sliding HH if no improvement despite medical therapy
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51
Q

What is a hernia?

A

The protrusion of a viscus or part of a viscus through a defcet of the walls of its containing cavity into an abnormal position

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52
Q

Which is the most common type of hernia?

A

Inguinal - presents as a lump in the groin

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53
Q

What do the following terms mean in reference to hernias:

a) reducible?
b) incarcerated/irreducible?
c) obstructed?
d) strangulated?

A

a) Reducible – when the contents of the hernia can be manipulated back into its original position through the defect from which it emerges
b) Incarcerated hernia (irreducible) – the hernia is compressed by the defect causing it to be irreducible (i.e. unable to be pushed back into its original position)
c) Obstructed hernia – refers mainly to hernias containing bowel, where the contents of the hernia are compressed to the extent the the bowel lumen is no longer patent and causes bowel obstruction
d) Strangulated hernia – the compression around the hernia prevents blood flow into the hernial contents causing ischaemia to the tissues and pain

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54
Q

Where is the deep inguinal ring located?

A

Just above the mid-point of the inguinal ligament

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55
Q

Where is the superficial inguinal ring located?

A

Above and medial to the pubic tubercle

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56
Q

What is a direct inguinal hernia?

A

A direct inguinal hernia is caused by a weakness in the posterior wall of the inguinal canal. The abdominal contents (usually just fatty tissues, sometimes with bowel) are forced through this defect and enter the inguinal canal. This means that the contents emerge in the canal medial to the deep ring.

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57
Q

What is an indirect inguinal hernia?

A

The abdominal contents pass through the deep inguinal ring, passing through the inguinal canal and can exit via superficial ring.

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58
Q

How can you distinguish between direct and indirect inguinal hernias on examination?

A
  • Reduce the hernia
  • Occlude the deep internal ring with two fingers
  • Ask the patient to cough or stand
  • If hernia is restrained it is indirect, if not it is direct.
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59
Q

When and how should an inguinal hernia be repaired?

A

WHEN
Pain, alterered bowel habits, strangulation

HOW
Open - Reduces contents back into abdominal cavity and places a mesh (eg. lichenstein) to strengthen the posterior wall and prevent reherniation.

Laparoscopic - as name suggests, can be transabdominal pre peritoneal (through the peritoneal cavity) or totally extraperitoneal. Benefits of less post-op pain and quicker recovery.

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60
Q

What are the features of:
a) congenital inguinal hernia?
b) congenital umbilical hernia?

A

Congenital inguinal hernia:
- Indirect hernia resulting from failure in closure of processus vaginalus
- More likely to be right sided
- Should be surgically repaired ASAP

Congenital umbilical hernia:
- More common in premature/afro-caribbean babies
- Vast majority self-resolve before 4-5yrs old

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61
Q

What is a femoral hernia?

A

When bowel enters the femoral canal, presenting as a mass in the upper medial thigh, pointing down to the leg. More likely to be irreducible and strangulate. More common in women.

These are found INFERIOR and LATERAL to the puibic tubercle.

High risk of obstruction and strangulation - must be repaired

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62
Q

What is NAVY VAN?

A

Passing beneath the inguinal ligament are some important structures travelling to the upper leg. Most notably this includes the femoral artery, the femoral vein and the femoral nerve. The order in which these structures lie is easily remembered by the ‘NAVY VAN’ mnemonic. With the ‘Y’ signifying the creases of the groin, it illustrates how from lateral to medial the structures lie nerve, artery and then the vein.

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63
Q

How are femoral hernias managed?

A

Same way as inguinal hernias! Surgical repair recommended due to high change of strangulation.

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64
Q

Name 3 other hernias

A

Incisional - follow breakdown of muscle closure after surgery
Epigastric - pass through linea alba above umbilicus
Paraumbilical - just above or below umbilicus, RF include obesity and ascites

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65
Q

What is achalasia?

A

Aperistalsis of the oesophague and impaired relaxation of the LOS - presents as intermittent dysphagia, regurgitation of food from dilated oesophagus, spontaneous chest pain and aspiration pneumonia.

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66
Q

What causes achalasia?

A
  • Autoimmune
  • Neurodegenerative
  • Viral

Mechanism unknown, potentially inflammation and degeneration of myenteric plexus of oesophagus

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67
Q

What does CXR/barium swallow of achalasia show, and how is it managed??

A

CXR: Fluid level in dilated oesophagus
Swallow: Dilated tapering oesophagus

Treat with endoscopic balloon dilatation or laparoscopic Hellers cardiomyotomy, then PPIs. If not suitable for surgery, give botulinum toxin injection/CCBs/nitrates.

Slight risk of squamous carcinoma of oesophagus.

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68
Q

What can cause dysphagia?

A

MECHANICAL - malignant or benign stricture, lung cancer, lymph nodes, restrosternal goitre, aortic aneurosym, pharyngeal pouch

MOTILITY - achalasia, diffuse oesophageal spasm, systemic sclerosis, neurological bulbar palsy

OTHER - oesophagitis, globus (functional)

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69
Q

What causes benign oesophageal stricutres?

A

GORD, corrosvies, surgery, radiotherapy, prolonged NG intubation

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70
Q

How are benign oesophageal strictures managed?

A

Endoscopic balloon dilatation

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71
Q

What is diffuse oesophageal spasm?

A

Swallowing accompanied by marked contraction of the oesophagus, causing chest pain and dysphagia. This is due to high amplitude peristalitic contractions.

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72
Q

What does barium swallow show with diffuse oesophageal spasm?

A

Corkscrew oesophagus

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73
Q

How is oesophageal spasm treated?

A

PPI for reflux.

Antispasmodics, nitrates, CCBS, GABA receptor agonists (baclofen) for spasm.

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74
Q

What are lower oesophageal rings?

A
  1. Mucosal (Schatzkis ring, B ring) - a ring located at squamocolumnar mucosal junction, associated with characteristic history of intermittent bolus obstruction
  2. Muscular (A ring) - located proximal to mucosal ring, causes dysphagia

Rings may require dilatation but usually just conservative management.

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75
Q

What is Plummer-Vinson syndrome?

A
  • A rare disease characterised by difficulty swallowing, IDA, glossitis, cheilosis and oesophageal webs
  • Treat with iron supplementation and mechanical widening of the oesophagus
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76
Q

What is eosinophilic oesophagitis?

A

An allergic inflammatory condition of the oesophagus, causing dysphagia, food impaction, heartburn, pain. Male, white, middle aged.

Mucosal furrowing, loss of vascular pattern seen on endoscopy, due to a thickened mucosa.

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77
Q

How is eosinophilic oesophagitis managed?

A

Swallowed inhaled steroids preparations eg. fluticasone, budesonide, systemic steroids, monoclonal antibodies.

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78
Q

What causes oesophageal perforation/rupture and how is it managed?

A

Endoscopic dilatation, NG tube insertion. More likely if malignant strictures.
Rupture occurs from violent vomiting, alcohol ingestion.

Place stent over the hole and perform water soluble contrast x-ray after 2-3 days to check.

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79
Q

What are the RF for oesophageal cancer?

A

Alcohol, diet, smoking, achalasia, Plummer-Vinson syndrome, obesity, Vit A/C deficiency, nitrosamine exposure, reflux/barrets oesophagus

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80
Q

What is the histopathology of oesophageal cancer?

A

Squamous carcinoma in upper and middle third (55%) - related to alcohol, achalasia
Adenocarcinoma in lower third (45%) - related to GORD, barretts (THIS IS NOW MORE COMMON IN UK/US)

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81
Q

How does oesophageal cancer present?

A

Dysphagia, weight loss, retrosternal chest pain, hoarseness, cough. Usually around age 60-70.

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82
Q

How is oesophageal cancer diagnosed?

A

Oesophagoscopy with biopsy

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83
Q

How is oesophageal cancer staged?

A

TNM staging system
T - tumour invasion (Tis, T1-4)
N - lymph node invasion (Nx unable to be assesed, N0, N1)
M - metastases (M0, M1)

Do F-18 FDG PET CT, EUS to determines this.

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84
Q

What is the prognosis for oesophageal cancer?

A

Since over 70% preesnt after stage 3, 5 year survival rates are LOW (10%)

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85
Q

How is oesophageal cancer managed?

A

Surgery - only if tumour has not infiltrated outside of oesophageal wall (T1/T2)

Chemoradiation - stage 2b/3

Palliative - endoscopic dilatation, laser and brachytherapy, insertion of metal stent to aid feeding.

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86
Q

Describe the mucosal structure of the stomach

A

Smooth muscle has 3 layers - outer longitudinal, inner circular and inner oblique.

Mucosa of upper 2/3 of stomach contains parietal cells that secrete hydrochloric acid and chief cells that secrete pepsinogen. Antrum mucosa contains mucus secreting cells and G cells that secrete gastrin, and D cells that secrete somatostatin.

Mucosal barrier protects gastric epithelium; prostaglandins stimulate mucus secretion (these are inhibited by NSAIDS - cause ulcers!)

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87
Q

How does stomach acid secretion work?

A
  1. Histamine stimulates Gs via H2 receptors to ACTIVATE secretion
  2. Prostaglandin E2 activates the Gi protein to INHIBIT secretion
  3. Somatostatin inhibits histamine and gastrin release and therefore acid secretion
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88
Q

Which factors affect gastric emptying?

A

Osmoreceptors in duodenal mucosa control gastric emptying by local reflexes and release of gut hormones

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89
Q

What is the difference between gastritis and gastropathy?

A

Gastritis - inflammation associated with mucosal injury

Gastropathy - epithelial cell damage without inflammation

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90
Q

What causes gastritis?

A

H. pylori (80%)
Autoimmune (5%)
Viruses (5%)

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91
Q

What causes gastropathy?

A 
Irritants - NSAIDS, alcohol
Bile reflux
Severe stress
Trauma/shock
Renal failure
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92
Q

What is the incidence and RF for gastric cancer?

A

Geography (Japan, eastern europe), male, H. pylori, EBV, diet high in nitrosamines, smoking, genetic, pernicious anaemia (due to atrophic gastritis)

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93
Q

Describe the histopathology of gastric cancer

A

Adenocarcinoma, two types:

  1. Intestinal - differentiated, ulcerating/polypoid - strong environmental association and with atrophic gastritis
  2. diffuse - undifferentiated, worse prognosis, loss of E-cadherin
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94
Q

What are the symptoms of gastric cancer?

A

Non-specific - EARLY SATIETY, dyspepsia, weight loss, vomiting, dysphagia, anaemia, mass, Virchows node

Due to this most patients present with advanced disease with mets

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95
Q

What is a krukenberg tumour?

A

A Krukenberg tumor refers to a malignancy in the OVARY that metastasized from a primary site, classically the GI TRACT, although it can arise in other tissues such as the breast. Gastric adenocarcinoma, especially at the pylorus, is the most common source.

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96
Q

How is gastric cancer diagnosed?

A

Gastroscopy and multiple ulcer edge biopsies

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97
Q

How is gastric cancer staged?

A

EUS for depth of invasion, CT/MRI for staging, laparoscopic staging if advanced

TNM classification (as oesophageal) 
Stage 1 - T1N0M0, T1N1M0, T2N0,M0
Stage 2 - T1N2M0, T2N1M0, T3N0M0
Stage 3 - T2N2M0, T3N1M0, T4N0M0, T3N2M0
Stage 4 - everything else

ie - as soon as there are mets, it is stage 4

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98
Q

What is the prognosis for gastric cancer?

A

Poor, <10% overall for 5 year survival.

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99
Q

How is gastric cancer treated?

A

Surgery - most effective if suitable
Chemoradiation (cisplatin)
Palliative
Targeted therapy if HER2 positive (trastuzumab)

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100
Q

What is dumping syndrome?

A

Fainting and sweating after eating due to food of high osmotic potential being dumped in the jejunum - this is a side effet of gastrectomy.

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101
Q

What other lumps may be found on gastrocopy?

A

GIST - GI stromal tumours, sometimes malignant and may ulcerate and bleed

Polyps - usually asymptomatic, may be cystic, adenomatous, fibroid

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102
Q

How can you distinguish between UGI bleed and LGI bleed?

A

UGI - haematemesis ‘coffee ground’, meleana,

LGI - passage of dark blood and clots without shock

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103
Q

What causes GI bleed?

A
  • Peptic ulceration (most comm0on)
  • Varices
  • NSAIDS
  • Mallory Weiss tear
  • Viral infections (developing countries)
  • Malignancy
  • Bleeding after PCI
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104
Q

How should patients with upper GI bleed be managed initially?

A
  1. ABCDE, high flow 02
  2. Insert two large bore cannulae and take FBC, U&E, LFT, group and save, cross match
  3. Give IV fluids whilst waiting for crossmatch
  4. Insert catheter, monitor urine output
  5. Organise ABG, CXR, ECG, stop NSAIDS/aspirin/clopidogrel/warfarin
  6. Consider central line for inotropes (but not for fluid resus)
  7. Transfuse until haemodynamically stable (consider platelets and FFP)
  8. Monitor obs until stable
  9. Give PPI (omeprazole) if bleeding ulcer
  10. Arrange urgent endoscopy - may need banding/angiography/embolization

IF ON WARFARIN GIVE PCC TO REVERSE

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105
Q

When should platelets and FFP be given in an UGI bleed?

A

Platelets - actively bleeding and have a platelet count of less than 50 x 109/litre.

Prothrombin complex - actively bleeding and on warfarin

FFP - actively bleeding and have a prothrombin time (or international normalised ratio) or activated partial thromboplastin time greater than 1.5 times normal. Also needed if over 4 units transfused in one go?

Cryoprecipitate - If a patient’s fibrinogen level remains less than 1.5 g/litre despite fresh frozen plasma use

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106
Q

Why should calcium be given to patients receiving multiple blood transfusions?

A

Transfusions associated with hypocalcemia - risk of fatal neurological and cardiovascular dysfunction

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107
Q

Which risk assessment scores can be used in UGI bleed?

A

Glasgow Blatchford score - used at first assessment, if=0 may not need admission

Rockall score - can be used pre and post endoscopy to predict chance of bleed in non-variceal upper GI haemorrhage. Looks at age, shock, comorbodity (pre) and diagnosis/signs of recent haemorrhage (post)

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108
Q

When should endoscopy be performed in UGI bleed?

A

Haemodynamicaly unstable - immediately after resus

Haemodynamically stable - within 24h

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109
Q

Which endoscopic signs are associated with rebleeding?

A
  • Active arterial bleeding
  • Visible vessel
  • Adherent clot/black dot
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110
Q

What are the best ways of monitoring blood transfusion for adverse effets?

A

Pulse rate and venous pressure - a CVP line may be needed if organ failure/risk of heart failure

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111
Q

How should bleeding ulcers be treated at endoscopy?

A

2 or 3 haemostatic methods:

  • Adrenaline injection
  • Thermal coagulation with heat probe
  • Endoscopic clipping

Also start PPI and eradication therapy if indicated AFTER endoscopy

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112
Q

What are the indications for surgery in UGI bleed?

A
  • Severe bleeding despite transfusion 6U if >60yo
  • Active or uncontrollable bleeding at endoscopy
  • Initial rockall >3 or final >6
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113
Q

What are oesophageal varices?

A

Enlarged veins in the oesophagus. Form from portal hypertension and formation of collateral veins between the portal and systemic systems, secondary to liver fibrosis.

They develop when portal pressure is >10mmHg.

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114
Q

What are the RF for variceal bleeds?

A
  • Increased portal pressure
  • Variceal size
  • Endoscopic features of variceal wall eg. haematocystic spots
  • Child pugh score >8
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115
Q

How are varices managed prophylactically?

A

Propranolol
Endoscopic variceal band ligation - 2 weekly until all varices eradicated

Secondary - as above + transjugular intrahepatic porto-systemic shunt (TIPS)

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116
Q

How is acute variceal bleeding managed?

A
  1. Resuscuitate until haemodynamically stable but avoid saline
  2. Correct clotting abnormalities + prophylactic IV antibiotics
  3. IV TERLIPRESSIN!!!!!!!
  4. Endoscopic banding
  5. Balloon tamponade with Minnesota tube/Sengstaken-Blakemore tube if uncontrollable bleeding
  6. TIPSS (shunt) if all measures fail
117
Q

What causes lower GI bleed?

A

Massive bleeds
- Ischaemic colitis
- Diverticular disease

Small bleeds
- Haemorrhoids
- Anal fissures
- Solitary rectal ulcer
-

118
Q

How is LGI bleed managed acutely?

A

Usually stop by themselves - if not or haemodynamically unstable follow the protocl for UGI bleed.

119
Q

What causes chronic GI bleed?

A

Cancer (particularly ascending colon)

Coeliac disease

120
Q

How should chronic GI bleed be investigated?

A

Usual bloods, endoscopy, colonoscopy, CT

If no cause found, capsule endoscopy

121
Q

Describe the structure of the small intestine

A

Duodenum - jejunum - ileum

Mucosal folds called villi and microvili found on enterocytes - these greatly increase the surface area.

Each villus has a core containing blood vessels, lymphatics, plasma cells and lymphocytes. The lamina propria is a thin layer of connective tissue that lies underneath the epithelial layer, containing plasma cells, lymphocytes, macrophages, eosinophils and mast cells.

Enterocytes are found at the bottom of the crypts of Lieberkuhn.

122
Q

What artery supplies that small intestine?

A

Branches of the superior mesenteric artery

123
Q

What is the enteric nervous system?

A

The nervous system that controls bowel functioning, involving two plexuses - the myenteric plexus and submucosal plexus.

This controls gut motility!

124
Q

What is the physiology of the small bowel?

A
  • Digestion and absorption of nutrients and ions
  • Regulation of fluid absorption and secretion

It has physical and innate defence systems to prevent colonization and invasion by pathogens.

125
Q

What is the role of the duodenum?

A
  1. Takes in secretions from the pancreas and gallbladder, by producing CCK and secretin
  2. Slows gastric emptying
  3. Increases pancreatic activity
126
Q

What is the role of the jejunum?

A

Lots of villi to increase surface area, involved in nutritional absorption and regular peristalsis

127
Q

What is the role of the ileum?

A

Absorption of vitamin B12 and bile salts and whatever products of digestion were not absorbed by the jejunum

128
Q

What are taenia coli?

A

Three separate longitudinal ribbons of smooth muscle on the outside of the ascending, transverse, descending and sigmoid colons. They contract lengthways to produce haustra

129
Q

What is the role of the large intestine?

A
  1. Absorption of water and minerals
  2. Mass movement (peristalsis twice an hour)
  3. Defaecation
130
Q

What are the symptoms of intestinal obstruction?

A
  • Vomiting
  • Colicky pain (may be faeculent = severe)
  • Constipation (may not be absolute) or diarrhoea
  • Distension (due to increased production of gas - can compress surrounding veins and cause ischaemia)
  • Tinkling bowel sounds
  • Fever and tachycardia (sepsis may occur as anaerobic bacteria produce toxins which get into the bloodstream)
  • Hypotensive or septic shock
131
Q

What are the main causes of small bowel obstruction?

A
  • Post op adhesions (75%)
  • Hernias

(intussusception rare but if so will be at the ileocaecal valve)

132
Q

What are the main causes of large bowel obstruction?

A
  • Colon cancer
  • Constipation
  • Diverticular stricture
  • Volvulus (sigmoid or caecal)
133
Q

What is an ileus?

A

A functional obstruction of the bowel from reduced motility - painless, bowel sounds will be absent.

This is due to absence of normal peristaltic contractions - may be due to surgery, peritonitis, electrolyte imbalances, spinal injury.

134
Q

How can you differentiate between small and large bowel obstruction on AXR?

A

Small bowel - AXR shows central gas shadows with VALVULAE CONNIVENTES the completely cross the lumen and no gas in the large bowel. Considered dilated if small bowel >3cm in diameter

Large bowel - AXR shows peripheral gas shadows proximal to the blockage but not in the rectum. You can also see HAUSTRA which do not cross the lumens width.

135
Q

What is Riglers sign?

A

A sign of pneumoperitoneum from bowel perforation - when gas is outlining both sides of the bowel wall - ‘double wall sign’

If perforation suspected should do an erect CXR to look for air under the diaphragm

136
Q

What do simple/closed/strangulated mean in reference to bowel obstruction?

A

Simple - one obstructing point with no vascular compromise

Closed - obstruction at two points forming a loop of grossly distended bowel at risk of perforation (usually at caecum where bowel is thinnest

Strangulated - compromised blood supply, PERITONITIS

137
Q

What is a sigmoid volvulus?

A

Occurs when the bowel twists on its mesentery to produce rapid, severe strangulated obstruction

AXR: coffee bean!!

138
Q

How is sigmoid volvulus managed?

A
  • Sigmoidoscopy

- Insertion of flatus tube

139
Q

What investigations should be done for bowel obstruction?

A

BLOODS: FBC, U&E, amylase, LFTs
IMAGING: AXR, erect CXR (CT if unclear)
OTHER: gastrografin contrast XR, consider colonoscopy but risk of perforation

140
Q

How is bowel obstruction managed?

A

Drip and suck - NGT and IV fluids to rehydrate and correct electrolyte imbalance

If strangulated or closed loop, emergency surgery needed (usually only large bowel!)

141
Q

How is abdominal wound dehiscence managed?

A
  • Cover wound with saline soaked gauze
  • Broad spectrum IV abx
  • Analgesia and IV fluids
  • Return to theatre
142
Q

What is acute mesenteric ischaemia and what causes it?

A 
Acute reduced blood supply to the intestine. Small bowel requires a lot of blood and nutrients! 
Due to :
- Arterial thromobosis/embolus
- Non-occlusive disease (related to cardiac output, hypovolaemia)
- Venal thrombosis 
- Trauma
- Vasculitis
- Radiotherapy
- Strangulation
143
Q

How does acute mesenteric ischaemia present?

A

Clinical triad!!!

  1. Acute severe abdo pain
  2. No abdo signs (soft)
  3. Rapid hypovolaemia and shock

Infarction usually happens about 12 hours later causing vomiting and bloody diarrhoea

144
Q

What do investigations show in acute mesenteric ischaemia?

A

Bloods - raised Hb, raised WCC, raised amylase, metabolic acidosis, lactate

Imaging - AXR shows gasless abdomen, CT/MRI angiography may show occlusion

Other - MR oximetry is reduced

145
Q

What are the complications of acute mesenteric ischaemia?

A
  1. Ileus
  2. Septic peritonitis (ischaemia causes ROS production and cell death. Reperfusion injury then causes damage/inflammation to epithelial lining of the small intestine)
  3. SIRS and multi organ dysfunction
146
Q

How is acute mesenteric ischaemia managed?

A
  1. Resuscitation with fluids
  2. Gentamicin and metronidazole
  3. Heparin
  4. Infusion of thrombolytics through angiography catheter
  5. Surgical removal of ischaemic bowel
147
Q

AF with abdo pain?

A

INVESTIGATE FOR MESENTERIC ISCHAEMIA

148
Q

What is chronic mesenteric ischaemia and what causes it?

A

aka ‘intestinal angina’

Chronic hypoperfusion of the intestine due to vascular disease.

149
Q

What are the symptoms of chronic mesenteric ischaemia?

A

Clinical triad!!

  1. Severe, colicky post-prandial abdo pain (gut claudication)
  2. Weight loss as eating hurts!
  3. Upper abdo bruit

May have PR bleed, malabsorption, nausea and vomiting

150
Q

How is chronic mesenteric ischaemia diagnosed?

A

CT angiography and contrast enhanced MR angiography

151
Q

How is chronic mesenteric ischaemia managed?

A

SURGERY - percutaneous transluminal angioplasty and stent insertion

152
Q

What is chronic colonic ischaemia?

A

aka ‘ischaemic colitis’

Hypoperfusion of the colon due to low flow in the IMA territory. Commonly affects the splenic flexure due to anatomy of vascular supply.

153
Q

How does chronic colonic ischaemia present?

A

Lower left abdo pain, bloody diarrhoea

154
Q

How is chronic colonic ischaemia diagnosed?

A

Flexi sigmoidoscopy and biopsy (shows epithelial cell apoptosis and lamina propria fibrosis) - barium swallow shows thumb printing at splenic flexure

155
Q

How is chronic colonic ischaemia managed?

A

Fluids and antibiotics!!!

If gangrenous (peritonitic/shock) need rests and surgical resection of affected bowel with stoma formation.

156
Q

What causes bloody diarrhoea?

A

Campylobacter (should stay off work!!), UC/Crohns, colorectal cancer

157
Q

What causes mucus in stools?

A

IBS, colorectal cancer, polyps

158
Q

What causes pus in stools?

A

IBD, diverticulitis, fistula

159
Q

What causes explosive diarrhoea?

A

Cholera, giardia, rotavirus

160
Q

What bloods should be done for diarrhoea?

A

FBC (look for iron deficiency anaemia, corresponding with IBD)

ESR/CRP (if raised, implies inflammatory or infective process, or cancer)

U&E (low potassium may be caused by severe D&V)

TSH (hyperthyroid can cause bowel symptoms)

Coeliac serology

161
Q

What other tests may be necessary in diarrhoea?

A
  • PR
  • Stool sample
  • C13 breath test
  • Sigmoidoscopy
  • Colonscopy
162
Q

How should diarrhoea be managed?

A

Lifestyle factors - drink fluids, stay off work
Primary care - codeine/loperamide to stop, treat cause (avoid antibiotics!!)
Secondary care - referral to specialist clinic (eg IBD)

163
Q

What bloods should be done for constipation?

A

Often none necessary, especially in the young.
If over 40, change in bowel habit, associate symptoms you should investigate.

FBC, ESR, U&E, Calcium, TFT

164
Q

What other tests may be necessary in diarrhoea?

A
  • Sigmoidoscopy
  • Colonoscopy
  • Barium enema
165
Q

How should constipation be managed?

A

Lifestyle factors - eat more fibre, drink fluids, exercise
Primary care - Bulking agents (eg bran/ispaghula husk), stimulant laxatives (eg. docusate, senna), stool softeners (eg. liquid paraffin), osmotic laxatives (eg. macrogol, lactulose)
Secondary care - if laxatives dont work, refer to secondary care for further invesitgations.

166
Q

What are the indications and contraindications for bulk forming laxatives?

A

eg. isphagula husk

I: colostomy, IBS, chronic constipation (affect takes days)
CI: faecal impaction, colonic atony

167
Q

What are the indications and contraindications for stool softeners?

A

eg. docusate

I: angina, stroke, hernia, post surgery, faecal impaction (any time you want to avoid straining)
CI: peanut allergy

168
Q

What are the indications and contraindications for stimulants?

A

eg. senna, bisacodyl

I: diet, bed rest, bowel prep
CI: crampy abdo pain, obstruction

169
Q

What are the indications and contraindications for osmotic laxatives?

A

eg. lactulose, phosphate, macrogol

I: hepatic encephalopathy
CI: bloating

170
Q

Which laxatives should be used for opiate induced constipation?

A

Stool softeners or osmotic

171
Q

Which laxatives should be used for faecal impaction?

A

Docusate or macrogol (?)

172
Q

Describe the structure of the colon and rectum

A
  • Made up of caecum, ascending, transverse, descending, sigmoid, rectum.
  • Muscle wall has inner circular layer and outer longitudinal layer.
  • The outer layer comes together to form the taenia coli which produces the haustral pattern seen.
173
Q

Describe the mucosa of the colon and rectum

A

Colon - columnar epithelial

Rectum - squamour epithelial

174
Q

Describe the blood supply to the colon

A

Caecum to splenic flexure - SMA

Splenic flexure to rectum - IMA

175
Q

How does defecation occur?

A
  1. Stool propelled into the rectum by colonic contractions
  2. After 100ml of stool filled, the rectum contracts and the internal anal sphincter relaxes
  3. This pushes the stool down into the proximal anal canal
  4. This increases the defecatory urge which can only be suppressed by contraction of the external sphincter and puborectalis muschles
  5. Once these relax, stool is expelled
176
Q

What are the common causes of incontinence?

A
  • Anal sphincter dysfunction (surgery, obstetric injury, trauma, crohns, radiation)
  • Rectal prolapse
  • Faecal impaction with overflow diarrhoea
  • Severe diarrhoea (infective, IBS, UC)
  • Neurological (spinal trauma, stroke, MS, diabetes, dementia)
177
Q

How can anal sphincter damaged by assessed?

A

Endoanal USS or pelvic MRI

178
Q

What is the difference between a diverticulum, diverticulosis, diverticulitis and diverticular disease

A

DIVERTICULUM - outpouching of gut wall, usually at site of entry of perforating arteries (occur in over 50% of patients over 50)

DIVERTICULOSIS - presence of diverticulum

DIVERTICULAR DISEASE - symptomatic presence of diverticulum (often inflamed)

DIVERTICULITIS - inflammation of a diverticulum (often when faeces obstruct the neck of the diverticulum, allowing bacteria to multiply and produce inflammation?

179
Q

What are the symptoms of diverticular disease and diverticulitis?

A

95% asymptomatic with disease. Often incidental finding on colonoscopy. May have intermittent LIF pain and rectal bleed.

Diverticulitis presents as severe LIF pain pyrexia, PR bleed, constipation, peritonoism. O/E tenderness, guarding, rigidity (similar to appendicits but opposite side!)

180
Q

What are the complications of diverticular disease?

A
  • Bowel perforation
  • Abscess formation
  • Fistulae
  • Peritonitis
181
Q

Where does diverticular disease usually occur?

A

Sigmoid colon

182
Q

How should diverticular disease be investigated and treated?

A

INVESTIGATION: Colonoscopy, barium enema, flexi sig.

TREATMENT: conservative eg. high fibre diet, smooth muscle relaxants eg. mebevarine

183
Q

How should diverticulitis be investigated?

A

BLOODS: FBC, ESR, U&E
IMAGING: CT colonography, erect CXR, US (these are also to look for complications)

184
Q

How do you treat uncomplicated acute diverticulits?

A
  • Analgesia
  • Oral co-amoxiclav if systemically unwell
  • Safety netting
185
Q

How do you treat complicated acute diverticulitis and the complications?

A

a) No complications- NBM, IV fluids, IV co-amoxiclav
b) Abscess - CT guided percutaneous abscess drainage
c) Perforation - surgical - primary anastamoses or Hartmann procedure at laparotomy (temporary colostomy and partial colectomy)
d) Haemorrhage - ABCDE (see LGI bleed)
e) Fistulae - surgical

186
Q

What is Hartmanns procedure?

A

Resection of the bowel with stoma formation

187
Q

What is a primary anastamosis?

A

Join in the bowel, with ot without stoma formation

188
Q

What is a sporadic adenoma?

A

A benign colorectal polyp which has the potential to become malignant. There are 3 types:

  1. Tubular
  2. Tubulovillous
  3. Villous
189
Q

How are sporadic adenomas managed, incl surveillance?

A

Endoscopic removal is usually advised due to the malignant potential.

Colonic surveillance is advised for people who have had adenomas removed and are at high risk of developing colorectal cancer (multiple large polyps)

Low risk - 5 year colonoscopy
Medium risk - 3 year colonoscopy
High risk - 1 year colonoscopy

190
Q

What are the 2WW criteria for colorectal cancer?

A
  • Age >40 with unexplained weight loss
  • Age >50 with unexplained rectal bleeding
  • Age>60 with iron deficiency anaemia or change in bowel habit
  • Positve FIT test (faecal immunochemical test - looks at occult blood)
191
Q

What is the most common type of colorectal cancer?

A

Adenocarcinoma, usually located in the sigmoid colon

192
Q

How do patients with bowel cancer present?

A

Acute - bowel obstruction, perforation, peritonitis

Chronic - iron deficiency anaemia, change in bowel habit, tenesmus, palpable mass

193
Q

What are the typical features of a cancer in the ascending colon?

A

Iron deficiency anaemia, weight loss, abdo pain

194
Q

What are the typical features of a cancer in the descending colon?

A

Change in bowel habit, PR bleed (as lumen is narrower and stool is hard), obstruction more likely, tenesmus

195
Q

What are the RF for colorectal cancer?

A
  • Neoplastic polyps
  • Genetic predisposition (FAP, HNPCC)
  • IBD
  • Diet/alcohol/smoking
196
Q

What is the pathology of FAP?

A

Mutation in the APC gene, involved in the tumour suppressor pathway.

Can be classical or attenuated (presents later)

197
Q

How are Lynch syndrome and FAP transmitted?

A

Dominant inheritance

198
Q

What are the colonic and extracolonic features of FAP?

A

Colonic - abdo pain and >6wk change in bowel habit at age 16

Extracolonic - retinal pigmentation, childhood hepatoblastoma, thyroid cancer

199
Q

How is FAP managed?

A

Affected individuals should be offered a total colectomy as malignancy is inevitable

200
Q

A patient with known FAP presents with an osteoma and a soft tissue tumour. What are you worried about?

A

Gardners syndrome

201
Q

A patient with known FAP presents with confusion and CT scan shows brain tumour. What are you worried about?

A

Turcot syndrome

202
Q

What is the pathology of Lynch Syndrome/Hereditary non polyposis colorectal cancer?

A

Mutation in MLH1 mismatch repair gene, leading to a cascade of mutations that cannot be repaired.
This will occur at areas of repeated DNA sequences known as microsatellites.
This leads to a frameshift mutation and a new truncated peptide.

This has two actions:

  1. Generation of adenomas
  2. The body mounts an inflammatory response against this foreign peptide
203
Q

What is microsatellite instability?

A

Failure to repair repetitive sequences of DNA, due to faulty mismatch repair genes. This is characteristic of lynch syndrome and is rarely seen in sporadic colorectal cancer

204
Q

What are the symptoms and complications of Lynch syndrome?

A

Usually asymptomatic

Can progress to COLORECTAL and ENDOMETRIAL cancer (aged 40)

205
Q

How is Lynch Syndrome diagnosed?

A

Amsterdam Criteria

206
Q

How is Lynch Syndrome managed?

A
  1. Surveillance
  2. Chemoprophylaxis with low dose aspirin
  3. Surgical prophylaxis
207
Q

How can biopsy differentiate between Lynch syndrome and sporadic colon cancer?

A

Do a biopsy of tumour tissue and do MSI and BRAF test.

MSI high - lynch syndrome
BRAF high - sporadic cancer

208
Q

A person with known lynch syndrome presents with sebaceous skin tumours. What are you worried about?

A

Miur Torre Syndrome

209
Q

What tests should be done to diagnose colorectal cancer?

A

Colonoscopy with biopsy

CT colonography with air inflation

210
Q

What tests should be done to stage colorectal cancer?

A

CT thorax and abdomen

Do MRI if rectal cancer

211
Q

What tests should be done to monitor disease and effectiveness of treatment in colorectal cancer?

A

CEA

212
Q

Describe the staging of colorectal cancer

A

TNM staging - if any nodal spread should have chemo

Dukes Criteria

213
Q

How is colorectal cancer managed surgically?

A

Right hemicolectomy - caecal, ascending or proximal transverse tumour

Left hemicolectomy - distal transverse, descending tumour

High anterior resection- sigmoid tumour

Anterior resection (TME) - upper or low rectal tumour

Abdomino-perineal excision of rectum - anal verge tumour

Hartmanns (resection of sigmoid colon and end colostomy) - emergency surgery due to perforation (don’t form anastamosis due to risk of leak)

CONSIDER LAPAROSCOPIC AND ENDOSCOPIC SURGERY

214
Q

Which types of bowel surgery will result in a permanent colostomy?

A

Abdomino-perineal resection for rectal cancer

215
Q

What is the use of radio/chemo in colorectal cancer?

A

Radiotherapy usually just palliative (this is due to risk of toxicity) but used preop in rectal cancer

Chemotherapy used as an adjuvant in advanced disease or if squamous cancer (commonly FOLFOX and FOLFIRI)

Targeted theraies (bevacizumab and cetuximab) for metastatic disease

216
Q

What is the prognosis of colorectal cancer?

A

5 year survival is 50%

217
Q

Describe the screening programme for colorectal cancer

A

People age 60-75 have 2 yearly FIT tests (50-74 in Scotland)

People aged 55 have one-off flexi sig (not available nationally)

218
Q

What are haemorrhoids?

A

Dilated anal cushions, causing bleeding, itch and potential discharge.

219
Q

How should haemorrhoids be investigated?

A
  • Abdo exam
  • PR exam
  • Proctoscopy - internal haemorrhoids
  • Rigid segmoidoscopy
220
Q

How are haemorrhoids classified?

A

1st degree - remain in rectum
2nd degree - prolapse through anus on defecation but spontaenously reduce
3rd degree - prolapse but require digital reduction
4th degree - persistently prolapsed

221
Q

How are haemorrhoids managed?

A

Conservative - increase fluids and fibre
Medical - topical analgesics, stool softener
Non-operative - rubber band ligation, sclerosants (phenol injected into pile), cryotherapy, infra-red coagulation
Surgical - excisional haemorrhoidectomy or stapled haemorrhoidopexy

222
Q

What are the symptoms of an anal fissure?

A

Severe pain, minimal blood
Visible tear (usually posterior midline due to pressure - if unusual location/size, think CROHNS/syphilis/herpes/trauma)

Acute <6 weeks
Chronic > 6 weeks

223
Q

How is an anal fissure managed?

A

Conservative - increase fibre, fluids, hygeine advice
Medical - bulk-forming laxatives/stool softeners, lubricants, topical GTN/lidocaine
Other - botox injection/sphinceterotomy (if not effective after 8 weeks for GTN)

Acute 1st line - bulk-forming laxatives
Chronic 1st line - topical GTN,

224
Q

What are the symptoms of a perianal abscess?

A

Pain, discharge, itch. May be systemically unwell. Usually caused by gut organisms but associated with DM, Crohns, malignancy, fistulae

225
Q

How is a perianal abscess managed?

A

Surgery - incise and drain under GA

226
Q

What are the symptoms of a fistulae?

A

This is an abnormal communication between the skin and the anal canal - due to blockage of deep IM gland ducts causing an abscess and bursting to form a fistulae.

Causes pain, discharge, itch

227
Q

How is an anal fistula managed?

A

Fistulotomy and excision (depends on depth of fistula)
High - seton suture
Low - laid open to heal by secondary intention

228
Q

What can cause abdominal distension?

A

Flatus, fat, fluid, faeces, fetus

229
Q

What can cause ascites (with/without portal hypertension)?

A

WITH - Cirrhosis, portal nodes, Budd-Chiari syndrome

WITHOUT - Malignancy, infections eg. TB, CCF, pancreatitis, nephrosis, myxoedema

230
Q

What is the first line investigation for abdominal lumps?

A

Ultrasound

231
Q

What is peritonitis?

A

Inflammation of the peritoneum, typically caused by perforation of a peptic/duodenal ulcer, diverticulum, appendix, bowel or gallbladder. Generalised peritonitis is a surgical emergency, often involves E coli infection.

Signs: prostration, shock, lying still, positive cough test, tenderness, rebound, guarding, rigidity

232
Q

How is peritonitis managed?

A

Tests - FBC, CRP, U&E, amylase, LFT, ABG, urinalysis, erect CXR (gas), AXR, USS/CT

Treatment - Laparotomy (after resuscitation) but quickly to prevent abscess formation

233
Q

What is colic?

A

Regularly waxing and waining pain, caused by muscular spasm in a hollow viscus. Pt will be walking around the room.

234
Q

What does sudden onset acute abdo pain suggest?

A
  • Perforation
  • Rupture (eg. ectopic pregnancy, aorta, spleen)
  • Torsion
  • Acute pancreatitis
  • Mesenteric infarction
235
Q

How does acute appendicitis occur?

A

Obstruction of the lumen of the appendix with a faecolith (stone made of faeces), causing colonisation by E coli and Bacteroids, oedema, ischaemia, necrosis and perforation

236
Q

What are the symptoms of acute appendicitis?

A

Periumbilical pain that moves to the RIF
Anorexia
Vomiting (often from the pain)
Constipation/diarrhoea

237
Q

What are the specific signs in appendicitis?

A

Rosving’s sign - pain > in RIF when you press on LIF
Psoas sign - pain on extending hip if retrocaecal appendix
Cope sign - pain on flexion and internal rotation of right hip

238
Q

What is the gold standard imaging in acute appendicitis?

A

CT however may be too slow! (always do FBC, CRP and urinary pregnancy test to rule out ectopic)

239
Q

How is acute appendicitis managed?

A

Appendicectomy (can be open or laparoscopic) then IV fluids and ?IV antibiotics

240
Q

What are some DDs for acute appendicitis?

A
  • Non specific mesenteric lymphadenitis
  • Acute terminal ileitis due to Crohns
  • Gynae eg. ruptured ectopic
  • Inflamed Meckels diverticulum
  • Functional bowel disease
  • Pyelonephritis
  • Ovarian torsion
241
Q

What is Rovings sign?

A

Palpation of the left lower quadrant produces pain in the right lower quadrant - this is indicative of appendicitis

242
Q

What is Murphys sign?

A

Pain on taking a deep breath, when the examiner is pressing down on the right upper quadrant - this is indicative of cholecystitis

243
Q

What is McBurneys point?

A

A point that lies one-third of distance laterally on a line drawn from the umbilicus to the right anterior superior iliac spine - this is where the appendix lies

244
Q

How is IBD investigated, diagnosed and monitored?

A

Investigations:

  • FBC - anaemia, malabsorption
  • Low albumin
  • Raised CRP/ESR
  • Faecal calprotectin

Diagnosis:
- Colonoscopy with biopsy (UC) or radiology (Crohns)

*avoid colonoscopy if severe colitis due to risk of rupture > flexsig

Monitoring:
TPMT - used often for monitoring treatment

245
Q

Where does UC affect?

A

Anywhere distal to the ileocaecal valve (often anal sparing)
Most common site is rectum

Spreads proximally from rectal sigmoid area to splenic flexure - left sided colitis

If reaches transverse colon - extensive colitis

246
Q

Describe the inflammation in UC

A

Uniform and continuous
Confined to the sunmucosa (superficial)
Crypt abscesses
Pseudopolyps
Drainpipe colon

247
Q

What are the symptoms of UC?

A

Crampy abdo pain, bloody diarrhoea, tenesmus, fatigue, systemically unwell during attacks

Extra-intestinal:
- Arthritis
- Erythema nodosum
- Osteoporosis
- Uveitis
- PSC
- Clubbing

Mild <4 stools daily
Moderate 4-6 stools, some blood
Severe >6 bloody stool, systemic upset

248
Q

What are the complications of UC?

A
  • Perforation
  • Toxic megacolon
  • Venous thrombosis
  • Colon cancer (should have colonoscopy everey 1-5 years with multiple biopsies at regular intervals

These may necessitate a stoma (about 20% of patients)

249
Q

How is UC treated?

A

Mild to moderate:
- Topical aminosalicylate eg. mesalazine/sulfasalazine suppositories/enema

If no remission in 4 weeks or extensive colitis:
- Add oral aminosalicylate or oral/topical steroids

Moderate to severe:
- Topical aminosalicylate and high dose oral salicylate (+/- steroids after 4 weeks)
- Tofacitinib, Vedolizumab, Infliximab (should have tried other options first unless contraindicated)

Acute severe:
- IV hydrocortisone
- IV cyclosporin
- Infliximab

Maintaining remission:
- Topical aminosalicylate or oral salicylate if extensive
- Oral azathioprine/mercaptopurine if multiple relapses or severe disease

250
Q

Where does Crohns disease affect?

A

Mainly terminal ileum and proximal colon, but can affect anywhere in the gut (often rectal sparing)

251
Q

Describe the inflammation in Crohns disease

A

Transmural, skip lesions (unaffected bowel between areas of active disease)

Granulomas, cobblestone appearance, pseudopolyps

252
Q

What are the symptoms for Crohns disease?

A

Abdo pain, diarrhoea, fatigue, mouth ulcers (primary), systemically unwell

More common in females

Extra-intestinal:
- Arthritis
- Erythema nodosum
- Episcleritis
- Pyoderma gangrenosum
- Clubbing

253
Q

What are the complications of Crohns?

A
  • Small bowel obstruction (due to narrowing and thickening)
  • Abscess formation
  • Fistulae
  • Perforation and rectal haemorrhage
  • Anal strictures
  • Granulomas
  • Colon cancer

COMPLICATIONS MORE SERIOUS DUE TO TRANSMURAL PATHOLOGY

254
Q

How is Crohns treated?

A

First presentation/single episode:

  • Prednisolone PO
  • Hydrocortisone IV
  • Budenoside (if steroids CI)

INDUCING REMISSION (if >2 exacerbations in a year and TPMT positive):

  • Azathioprine PO
  • Mercaptopurine PO
  • Methotrexate (if cant tolerate above two)
  • Add in infliximab (if refractory or fistulating)
255
Q

How can you tell if a stoma bag is an ileostomy or colostomy?

A

Ileostomy - protect skin due to enzymes, right sided

Colostomy - ok to touch skin, left sided

256
Q

What drug should be used in fistulating Crohns?

A

Metronidazole/ciprofloxacin (if isolated peri-anal disease)

Infliximab

257
Q

What are the extracolonic features of IBD?

A
  • Conjunctivitis
  • Iritis
  • Mouth ulcers
  • Fatty liver
  • Liver abscess
  • Venous thrombosis
  • Large joint arthritis
  • Erythema nodosum
  • Pyoderma gangrenosum

These are due to release of cytokines eg. TNFa

258
Q

When do you diagnose IBS?

A

Abdo pain and discomfort, bloating or a change in bowel habit for at least 6 months.

This pain should be relieved by defection or associated with altered bowel frequency or stool form.

This should be accompanied by at least 2 of:

  • Altered stool passage
  • Abdominal bloating
  • Symptoms exacerbating by eating
  • Passage of mucus
259
Q

What test is performed to diagnose IBS?

A

Diagnosis of exclusion.

Do FBC, ESR, CRP and faecal calprotectin, coeliac test to distinguish from IBD

260
Q

How is IBS managed?

A

CONSERVATIVE:
High fibre diet (FODMAP), fluids, encourage physical activity

MEDICAL:
1st line: antispasmodics eg mebevarine, hyoscyamine or laxatives, loperamide if needed
2nd line: linaclotide, TCA, SSRI

OTHER:
CBT, psychological therapy (often associated with ME, fibromyalgia, affective disorders)

261
Q

What is the cause of Coeliac disease?

A

Autoimmune - associated with HLADQ2 and DQ8 genetics

262
Q

How does coeliac disease present?

A
  • Foul smelling stools and steatorrhoea
  • Abdo pain/bloating
  • Nausea and vomiting
  • Mouth ulcers
  • Angular stomatitis
  • Weight loss, failure to thrive
  • Fatigue
  • Osteomalacia
  • Unexplained iron deficiency and folate anaemia

Peak presentation in infancy and aged 50-60

263
Q

How does coeliac present biochemically?

A

Macrocytic anaemia (low B12/ferritin)

Positive IgA and tTG - if weakly positive, do EMA or DGP

HLA typing - HLA-DG2/8 in most individuals (this is not used in initial diagnosis, only in specialist setting or refractory coeliac)

264
Q

What does small bowel biopsy show in coeliac?

A
  • SUBTOTAL VILLOUS ATROPHY
  • Biopsy should be of duodenal or jejunum

- Increased intra epithelial WBCS and crypt hyperplasia

265
Q

How is coeliac managed?

A

Lifelong gluten free diet - this can be monitored by serial tests for EMA and TTG

Patient should have pneumococcal vaccinations every 5 years (due to splenic atrophy)

266
Q

What are the complications of coeliac?

A
  • Anaemia
  • Secondary lactose intolerance
  • GI T-cell lymphoma
  • Risk of malignancy
  • Myopathies
  • Neuropathies
  • Hyposplenism
  • Ulcerative jejunitis
267
Q

What is dermatitis herpetiformies?

A

Blistering, sub epidermal eruption of skin associated with gluten-sensitive enteropathy - improves from gluten free diet

268
Q

What conditions can cause malabsorption in the small bowel?

A
  • Coeliac disease
  • Whipples disease
  • Parasite
  • Thyrotoxicosis
  • Zollinger-Ellison syndrome
  • Lymphoma
  • Diabetes mellitus
269
Q

Which tumours can arise in the small intestine?

A

Relatively resistant to neoplasia!

  • Adenocarcinoma of small intestine (duodenum)
  • Lymphoma (ileum)
  • IPSID
  • Carcinoid tumours
270
Q

What are 3 different types of colostomy?

A
  1. Loop - entire loop of bowel is exteriorised and partially divided, forming 2 stomas that are joined together. These are usually temporary
  2. End - bowel divided and proximal end brought out as a stoma. Distal end may be resected (AP resection), closed and left (Hartmanns procedure) or exteriorised forming a mucus fitstulae
  3. Paul-Mikulicaz - double barrelled colostomy in which colon is divided completely and each end is exteriorised as two separate stomas.
271
Q

What is a low anterior resection?

A

When all or part of the rectum is excised and the proximal colon anastomosed to the top of the anal canal

272
Q

How is parenteral nutrition administered?

A

Nutrition given through central venous line or PICC (peripherally inserted central catheter). Insertion is sterile and requires x-ray to check.

Check weight, fluid balance, urine glucose daily through PEG nutrition.

273
Q

What is refeeding syndrome?

A

After a period of starvation, insulin and phosphate levels drop. When refeeding begins, insulin rises and this increases cellular uptake of phosphate

Causes hypophosphatemia within 4 days, leading to rhabdomyolysis, red and white cell dysfunction, respiratory insufficiency, arrhythmias, cariogenic shock, seizures and sudden death.

Treat with parenteral phosphate and oral supplementation.

274
Q

What is Boerhaaves syndrome?

A

Transmural tear of distal oesophagus, induced by a sudden increase in pressure

Classical triad:

  1. Vomiting (often with alcohol excess)
  2. Abdo/chest pain
  3. Subcutaneous emphysema
275
Q

What is a paralytic ileus?

A

Complication of bowel surgrey - no peristalsis causing pseudo-obstruction

May be caused by deranged electrolytes, replace IV

276
Q

What does it mean if a stoma is spouted?

A

That it is an ileostomy - protects skin from acidic bowel contents

277
Q

What is an end ileostomy?

A

An end ileostomy is usually done following complete excision of the colon or where the ileocolic anastomosis is not planned. It may be used to defunction the colon, but a reversal is difficult.

278
Q

What is a loop ileostomy?

A

A loop ileostomy involves taking a loop of the ileum, performing a horizontal incision and bringing it up to the skin. It is indicated to defunction the colon, for example, after rectal cancer surgery. Eventually, it can be reversed.

279
Q

What is a loop jejunostomy?

A

A loop jejunostomy is rarely used as a very high output stoma. It may be used following emergency laparotomy with planned early closure.

280
Q

What is a percutaneous jejunostomy?

A

A percutaneous jejunostomy involves the insertion of a feeding tube directly into the jejunum. You would notice a tube on the abdomen of the patient rather than a stoma bag.

281
Q

What is the grading system for internal haemorrhoids?

A

Grade I Do not prolapse out of the anal canal
Grade II Prolapse on defecation but reduce spontaneously
Grade III Can be manually reduced
Grade IV Cannot be reduced

282
Q

What is the location of a femoral hernia?

A

Inferolateral to pubic tubercle

283
Q

What is the location of an inguinal hernia?

A

Supermedial to the pubic tubercle

284
Q

What is a pharyngeal pouch?

A

Posteromedial diverticulum through Killians dehisecnce (area in pharynx)

Presents with dysphagia, regurgitation, aspiration, neck swelling which gurgles on palpitation, halitosis

Investigate with barium swallow

Surgical management

285
Q

What is Peutz-Jeghers syndrome? How is it managed?

A
  • AD condition for gene encoding LKB1 or STK11
  • Numerous hamartomatous polyps in GI tract
  • Pigmented freckles on lips, face, palms and soles
  • Pts will die from GI tract cancer

Management:
- Conservative unless complications develop

286
Q

How is c.difficile infection classified?

A

Mild
- Normal WCC

Moderate
- High WCC
- 3-5 loose stools daily

Severe:
- high WCC/creatinine/temp 38.5/severe colitis

Life threatening:
- Hypotension
- Partial or complete ileus
- Toxic megacolon or severe disease on CT

287
Q

How is c.difficle managed?

A

First episode:
- 1st line oral vancomycin 10d
- 2nd line oral fidaxomicin
- 3rd line oral vancomycin +/- IV metronidazole

Recurrent episodes:
- Oral fidaxomicin if within 12 weeks
- Oral vanc/fidax if after 12 weeks
- Consider faecal transplant

Life threatening:
- ADMIT
- Oral vanc + IV metro
- May require surgery

288
Q

What is melanosis coli?

A
  • Disorder of pigmentation of the bowel wall
  • Histology shows pigment-laden macrophages
  • Associated with laxative abuse esp senna f
289
Q
A

MSRA (24 decks)

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