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2a > GI > Flashcards

GI Flashcards

1
Q

What is GORD?

A
  • Oesophagitis secondary to refluxed gastric contents
  • Reflux of gastric contents into the oesophagus is normal. Clinical symptoms only occur when there is prolonged contact of gastric contents with the oesophageal muscosa.
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2
Q

What are the causes of GORD?

A
  • Anything that increases intra-abdo pressure/weakness of lower oesophageal sphincter
  • Pregnancy
  • Obesity
  • Smoking, alcohol, fatty meals, coffee
  • Large meals
  • Achalasia
  • Hiatus hernia
  • Drugs: TCAs, anticholinergics, nitrates, CCBs, bisphosphonates, NSAIDs
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3
Q

Normal defence mechanisms of oesophageal muscosa against reflux?

A

Surface – mucus and water layer trap bicarbonate, acts as as weak buffering system

Epithelium – apical cell membranes in the junctional complexes between cells act to limit diffusion of H+ into cells (this mechanism is impaired in oesophagitis)

Post-epithelium - bicarbonate normally buffers acid in the cells and intracellular spaces

Sensory mechanisms – acid stimulates the primary sensory neurones in the oesophagus by activating the canniloid-1 receptor

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4
Q

Presentation of gord?

A
  • Heartburn: aggravated by bending/lying
  • Regurgitation of food and acid, particularly when bending or laying
  • Odynophagia (painful swallowing)
  • Cough/nocturnal asthma - from aspiration
  • Chest pain
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5
Q

How is GORD diagnoseD?

A
  • Clinical diagnosis
  • Trials of PPI: If sx persist, ambulatory pH and imedance monitoring
  • OGD
  • GOld standard for diagnosis is 24hour oesophageal pH monitoring
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6
Q

Indications for performing OGD in someone with reflux

A
  • Age >55
  • Symptoms > 4weeks or tx resistant
  • Dysphagia
  • Relapsing sx
  • Weight loss
  • Haematamesis
  • Anaemia
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7
Q

Conservative treatment for GORD?

A
  • Lifestyle changes: weight loss, avoid excess alcohol, caffeine and aggravating foods, smok cessation
  • Antacids
  • ## Raising bedhead
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8
Q

What medications can be used for GORD?

A
  • Alginate containing antacids: first line, forms foam raft on contents
  • PPIs: block luminal secretion of gastric acid
  • H2 receptor antagonists
  • Dopamine antagonist pro-kinetic agents
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9
Q

What mnemonic can be used to help remember GORD meds? x

A 
GORD
Gaviscon (antacid)
Omeprazole (PPIs)
Ranitidie (h2 resceptor antagonist)
Domperidone (prokinetic)
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10
Q

What are the surgical management options for GORD?

A
  • Nissen fundoplication

w/ Laparoscopic approach

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11
Q

Complications of GORD?

A
  • Oesophagitis
  • Ulcers
  • Anaemia
  • Benign strictures
  • Barrett’s oesophagus
  • Oesophageal carcinoma
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12
Q

What is a Mallory-Weiss tear?

A
  • A linear muscosal tear occuring at the oesophageal-gastric junction
  • Produced by sudden increase in intra-abdominal pressure
  • Often occurs after a bout of coughing or retching and is classically seen after alcohol dry heaves
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13
Q

Risk factors for Mallory-Weiss tear?

A
  • Excessive alcohol ingestion
  • Hiatus hernia
  • Gallstones/Cholecystitis
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14
Q

How do mallory-weiss tears present?

A
  • Acute upper GI bleeding

- Presents with haematemesis

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15
Q

Management of mallory-weiss tears?

A
  • Most bleeds are minor and pt discharged within 24hrs
  • Early endoscopy confrims diagnosis and allows therapy if needed
  • Surgery with sewing the tear is rarely needed
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16
Q

What is a peptic ulcer?

A
  • A breach in a membrane of the mucosa in or adjacent to an acid bearing area
  • Consists of a break in the superficial epithelial cells penetrating down to the muscular mucosa of either the stomach or the duodenum
  • Caused by a reduction of gastric mucosal resistance to acid
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17
Q

Most common sites for peptic ulcer?

A

Dueodenum: more common. Particularly in the duodenal cap

Stomach: Most commonly on lesser curvature

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18
Q

How does the stomach normally present itself agaisnt gastric acid?

A

1) Mucus production by goblet cells (alkaline mucus)
2) High turnover of cells
3) Feedback loops
4) Tight junctions between cells

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19
Q

What are some causes of peptic ulcers?

A
  • Helicobacter pylori and NSAIDs/Aspirin
  • Corticosteroids alongside NSAIDs further increases risk
  • Hyperparathyroidism
  • Zollinger-Ellison syndrome
  • Vascular insuffiency
  • Sarcoidosis
  • Crohns disease
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20
Q

Risk factors for peptic ulcers?

A
  • Smoking
  • Alcohol
  • Steroids
  • NSAIDs
  • Stress
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21
Q

What is Zollinger-Ellison syndrome?

A

A condition in which a gastrin-secreting tumour or hyperplasia of the islet cells in the pancreas causes overproduction of gastric acid, resulting in recurrent peptic ulcers

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22
Q

Presentation of peptic ulcers?

A
  • Recurrent, burning epigastric pain
  • Duodenal ulcer: Pain relieved by eating
  • Gastric ulcer: Pain worsened by eating
  • Pain relieved by antacids
  • Nausa
  • Vomiting
  • Anorexia and weight loss
  • back pain
  • Heartburn
  • Flatulence
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23
Q

Investigations of PUD?

A
  • Patients <55 with ulcer-type symptoms should undergo non-invasive testing for H Pylori infection: C13 Urea breath test, Stool antigen test , sreology, culture, histology
  • Endoscopy can be used
  • Barium meal if ?obstruction
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24
Q

Management of PUD

A
  • Treat underlying cause + lifestyle measure: Stop NSAIDS, stop smoking, reduce alcohol intake
  • Treat H.Pylori - omeprazole, clarithromycin, and metranidazole for 7-14days
  • Surgery - if recurrent haemorrahge
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25
Q

What is Helicobacter Pylori?

A
  • Gram negative spiral bacteria
  • Associated with a range of gastrointestinal problems
  • Has a flagellum
  • Produces urease
  • Adheres to gastric epithelial cells in gastric pits
  • Protected from gastric acid by the juxta-mucosal mucus layer which traps bicarbonate
  • Most patients with the infection are asymptomatic
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26
Q

Diseases associated with H Pylori?

A
  • PUD (95% of duodenal ulcers, 75% of gastric ulcers)
  • Gastric cancer
  • B Cell lymphoma of MALT tissue
  • Atrophic gastritis
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27
Q

Presentation of H. Pylori?

A
  • As PUD: Epigastric pain, nausea, anorexia
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28
Q

Investigations for H. Pylori infection?

A
  • C-13 urea breath test: Gold standard
  • Serology: for serum antibody detection
  • Stool antigen test: immunoassage using monoclonal antibodies
  • Culture
  • Histology
  • Biopsy urease test
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29
Q

Treatment of H. Pylori?

A

7 day course of:

1) A PPI + Amoxicillin + Clarithromycin
or
2) A PPI + Metronidazole + Clarithromycin

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30
Q

If H.Pylori treatment fails?

A

If triple therapy eradication fails give: bismuth + metronidazole + tetracycline + PPI for 14 days (but bear in mind bismuth tablets are extremely unpleasant so be aware of issues with compliance)

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31
Q

What are gastro-oesophageal varices?

A
  • Abnormally dilated veins with a torturous course

- Around oesophagus and stomach

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32
Q

What are the causes of oesophageal varices?

A
  • Portal hypertension due to liver cirrhosis (either from alcohol or viral)
  • Acute hepatitis
  • Schistosomiasis
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33
Q

What are risk factors for variceal bleeding?

A
  • Decompensation of liver disease
  • Malnourishment
  • Excess alcohol intake
  • Physical exercise
  • Circadian rhythms
  • Increased intra abdo pressure
  • Aspirin
  • NSAIDs
  • Bacterial infection
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34
Q

How do varices present?

A
  • Haematemesis
  • Abdo pain
  • Dysphagia/odynophagia
  • Confusion 2ndary to encephalopathy
  • Pallor
  • Hypotension and tachycardia
  • Reduced urine output
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35
Q

What investigation for varices?

A

Endoscopy - to exclude bleeding from other sites/confirm site

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36
Q

Management of acute variceal haemorrhage?

A
  • ABCDE
  • Correct clotting: FFP, Vit K
  • Vasoactive agents: Terlipressin
  • Prophylactic antibiotics in pt with liver cirrhosis
  • Endoscopy: Variceal band ligation
  • Sengstaken-blakemore tube if uncontrolled haemorrhage
  • Transjugular intrahepatuc portosystemic shunt (TIPSS) - if above measures fail
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37
Q

How to prevent re-bleed of varices?

A
  • Propanolol

- Endoscopic variceal band ligation

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38
Q

What is achalasia?

A
  • Failure of oesophageal peristalsis and relaxation of lower oesophageal sphincter (LOS)
  • Due to degenerative loss of ganglia from Auerbach’s plexus
  • Leading to impaired oesophageal emptying
  • LOS contracted, oesophagus above dilated
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39
Q

Clinical features of achalasia?

A
  • Dysphagia of BOTH liquids and solids
  • Variation in severity of sx
  • Heartburn
  • Regurg of food, particularly at night - may lead to cough, aspiration pneumonia
  • Spontaneous chest pain due to oesophageal spasm
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40
Q

Investigating achalasia?

A
  • Manometry: excessive LOS tone which doesnt relax on swallowing, most important diagnostic test
  • Barium swallow: shows expanded oesophagus, fluid level, birds beak
  • CXR: wide mediastinum, fluid level
  • OGD
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41
Q

Management of achalasia?

A
  • No cure – goals of treatment are symptom relief and improvement of oesophageal emptying
  • Intra-sphincteric injection of BoTox
  • Heller cardiomyotomy – surgical division of the LOS
  • Endoscopic balloon dilatation
  • Drug therapy - has a role but is limited by side-effects
    • Oral nitrates
    • Nifedipine (CCB)
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42
Q

Main side effect of treatment for achalasia?

A

GORD

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43
Q

Relationship between oesophageal motility and scleroderma?

A
  • The oesophagus is involved in almost all patients with this disease
  • Diminished peristalsis and oesophageal clearance due to replacement of the smooth muscle by fibrous tissue
  • Detected manometrically or by barium swallow
  • LOS pressure is decreased, allowing reflux with consequent mucosal damage
  • Initially no symptoms, then dysphagia and heartburn
  • Similar motility abnormalities may be found in other autoimmune disorders, particularly if Reynaud’s phenomenon is present
  • Treatment is the same for reflux and benign stricture
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44
Q

What is gastritis?

A

Inflammation of the gastric mucosa

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45
Q

What is gastropathy?

A

Injury to the gastric mucosa associated with epithelial cell damage and regeneration. Little or no accompanying inflammation (eg damage due to NSAID use)

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46
Q

What are the causes of gastritis?

A
  • Most common is H Pylori
  • NSAIDs and Aspirin
  • Alcohol excess
  • Autoimmune: eg pernicious anaemia
  • CMV
  • HSV
  • Duodeno-gastric reflux
  • Crohns disease
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47
Q

Symptoms of gastritis?

A
  • Indigestion (dyspepsia)
  • Epigastric pain
  • Loss of appetite
  • Bloating
  • Retching
  • Nausea
  • Vomiting
  • Early satiety/feeling particularly full after a meal
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48
Q

Investigations for gastritis?

A
  • Clinical diagnosis in most cases
  • Gastroscopy is gold standard
  • Biopsy
  • H. Pylori testing (urea breath + stool antigen)
  • Barium swallow
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49
Q

Management of gastritis?

A 
Conservative:
  - Smaller meals + avoiding spicy/acidic foods
  - No alcohol
  - No smoking
  - Reducing stress
  - Stop NSAID use
Medication:
  - Antacids
  - H2 blocker - ranitidine
  - PPI
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50
Q

What is coeliac disease?

A
  • Autoimmune condtion caused by sensitivity to gluten

- Leads to villous atrophy, causing malabsorption

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51
Q

Causes of coeliac?

A
  • Gluten sensitivity
  • Genetic factors
  • Environmental factors: Breastfeeding, age of introduction of gluten, rotavirus infection in pregnancy
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52
Q

Risk factors/associations for coeliac disease?

A
  • T1DM
  • Atopy
  • Thyroid disease
  • Sjorgens syndrome
  • IBS
  • Autoimmune hepatitis
  • ## IgA deficiency
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53
Q

Presentation of coeliac disease?

A
  • Chronic or intermittent diarrhoea
  • Steatorrhoea
  • Failure to thrive
  • Persistent or unexplained gi sx inc. N+V
  • Prolonged fatigue and malaise
  • Recurrent abdo pain, cramping or distension
  • W loss
  • Unexplained anemia
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54
Q

Non Gi sx of coeliac?

A
  • Mouth ulcers and angular stomatitis
  • Infertility
  • Neuropsychiatric symptoms (anxiety and depression)
  • Rare: Tetany, osteomalacia, weakness, neuropathy
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55
Q

Skin consequence of coeliac disease?

A

Dermatitis Herpetiformis

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56
Q

How to investigate coeliac disease?

A
  • Immunology and jejunal biopsy

- Must be on a gluten diet at time

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57
Q

What will be seen on immunology for coeliac disease?

A
  • Tissue transglutaminase antibodies (IgA)
  • Endomysial antibodies
  • Anti-casein antibodies in some
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58
Q

What is seen on jejunal biopsy for coeliac?

A
  • Villous atrophy

- Crypt hyperplasia

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59
Q

Management of coeliac disease?

A
  • Education
  • Lifelong gluten free diet
  • Correct any vitamin deficiencies
  • Pneumococcal vaccine
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60
Q

Complications of coeliac disease?

A
  • Anaemia: Iron, folate and B12
  • Hyposplenism
  • Osteoporosis, osteomalacia
  • Lactose intolerance
  • Enteropathy-associated T-cell lymphoma of small intestine
  • Subfertility, unfavourable preg outcomes
  • RARE: Oesophageal cancer, other malignancies
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61
Q

What is dermatitis herpetiformis?

A
  • An itchy, symmetrical eruption of vesicles and crusts over the extensor surfaces of the body with deposition of granular IgA
  • Associated with a gluten-sensitive enteropathy – usually asymptomatic as the jejunal abnormalities are not as severe in coeliac disease
  • Same inheritance and immunological abnormalities as coeliac disease
  • The skin condition responds to dapsone (used to treat leprosy)
  • Both skin and gut will improve on gluten free diet
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62
Q

What is tropical sprue?

A
  • A progressive small intestinal disorder presenting with diarrhoea, steatorrhea and megaloblastic anaemia
  • Occurs in residents or visitors to endemic areas in the tropics (Asia, some Caribbean islands, Puerto Rico and parts of South America)
  • The term ”tropical sprue” is reserved for severe malabsorption (of 2 or more substances - particularly fat and b12) accompanied by diarrhoea and malnutrition
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63
Q

Presentation of tropical sprue?

A
  • Can be acute or chronic
  • DIarrhoea
  • Steatorrhoea
  • Anorexia
  • Abdominal distension
  • Weight loss
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64
Q

Investigating tropical sprue?

A
  • Acute infective causes of diarrhoea must be excluded (especially Giardia which can produce a syndrome very similar to tropical sprue)
  • Malabsorption should be demonstrated, particularly fat and B12
  • Small bowel mucosal biopsy – partial villous atrophy, less severe but similar to in coeliac
  • Coeliac screening
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65
Q

Management of tropical sprue>

A
  • Many pt improve when leave area
  • Folic acid
  • Abx: eg tetracycline for 6 months
  • Replace fluid nd electrolytes
  • Correct any nutritional deficiencies
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66
Q

What is Crohns disease?

A
  • IBD affecting anywhere from mouth to anus, but often terminal ileum and colon
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67
Q

Cause of crohns?

A
  • Unknown
  • Genetic susceptibility
  • Environmental factors: Hygeine, NSAIDs, Smoking, stress
  • Intestinal microbiota - increased E Coli
  • Host immune response
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68
Q

Microscopic changes associated with Crohns?

A
  • transmural inflammation
  • Increase in chronic inflammatory cells
  • Lymphoid hyperplasia
  • Granulomas (non-caseating epithelioid cell aggregates with Langerhans giant cells)
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69
Q

Macroscopic changes associated with Crohns?

A
  • Mouth to anus with skip lesions
  • Involved bowel has a thickened wall an a narrow lumen
  • Cobblestone appearance (ulcers and fissures)
  • ## Fistulae and abcess
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70
Q

Symptoms of crohns disease?

A
  • Triad: Diarrhoea, abdo pain, weight loss
  • Non-specific sx: weight loss, lethargy, low grade fever, malaise
  • Loss of appetite, N+V
  • Steatorrhoea
  • Perianal disease - skin tags or ulcers
  • Anal disease - fistulae to bladder/vagina/abdo wall
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71
Q

Extra-intestinal features of crohns?

A
  • Erythema nodosum
  • Pyoderma gangernosum
  • Arthritis
  • Uveitis, epislceritis, conjucntivitis
  • Osteoporosis
  • Clubbin
  • PSC
  • Fatty liver
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72
Q

Investigations for crohns?

A

Bloods: CRP, anaemia, low vit D and B12
Stool: Faecal calprotectin
Colonoscopy w/ biopsy is diagnostic
Small bowel enema

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73
Q

Specific crohns features seen on small bowel enema?

A
  • Strictures - kantors string sign
  • Proximal bowel dilatation
  • Rose thorn ulcers
  • Fistulae
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74
Q

How to induce remission in crohns disease?

A
  • Glucocorticoids eg. Prednisolone
  • Enteral feeding with an elemental diet
  • 5-ASA drugs eg. mesalazine
  • Azathioprine or mercaptopurine
  • Infliximab
  • Metronidazole for isolated peri-anal disease
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75
Q

How to maintain remission in crohns?

A
  • Stop smoking
  • Azathioprine or mercaptopurine
  • Methotrexate
  • 5-ASA;s
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76
Q

Surgical options for Crohns?

A
  • Ileocaecal resection
  • Segmental small bowel resections
  • Stricturoplasty
  • Colonic surgery: Sub-total colectomy, panproctocolectomy
  • Surgical management of fistulae
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77
Q

Complications that can arise from Crohns?

A
  • Fistulae
  • Small bowel cancer
  • Colorectal cancer
  • OP
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78
Q

What is Ulcerative Colitis?

A
  • Form of IBD
  • Inflammation restricted to colon
  • Continuous
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79
Q

Causes of ulcerative colitis?

A
  • Unknown
  • Genetic
  • Environment: Smok and breastfeeding protetctive
  • Psycho: chronic stress, deprivation
  • Intestinal microbiota
  • Host immune response
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80
Q

Macrosopic changes in UC?

A
  • Colon only
  • Reddended mucosa, inflamed and bleeds easily
  • Extensive ulceration
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81
Q

Microscopic changes in UC?

A
  • Mucosa shows chronic inflammatory cell infiltrate in the lamina propria
  • Crypt abcesses
  • Goblet cell depletion
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82
Q

Presentation of UC?

A
  • Intermittent sx
  • Bloody diarrhoea
  • Mucus in stool
  • Urgency
  • Tenesmus
  • Abdo pain
  • Malaise, lethargy, anorexia, w loss
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83
Q

Extraintestinal manifestations of UC?

A
  • Mouth ulcers
  • Arthritis
  • Erythema nodosum
  • Pyoderma gangrenosum
  • Uveitis
  • PsC
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84
Q

Investiagtions for US?

A

Bloods: ID anaemia, WCC and platelets raised, ESR and CRP raised, pANCA+Ve

Colonoscopy with biopsy gold standard

Barium enema

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85
Q

Signs of UC on barium enema?

A
  • Loss of haustrations
  • Superficial ulcerations - psuedopolyps
  • Narrow and short colon
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86
Q

What is toxic megacolon?

A
  • Serious complication with UC
  • Plain AXR sows dilated, thin-walled colon with diameter >6cm, gas filled and contains mucosal islands
  • Risk of perforation…needs surgery
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87
Q

How to induce remission in UC?

A
  • Rectal aminosalicylates
  • Oral aminosalicylates
  • Oral prednisolone
  • Severe colitis needs IV steroids
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88
Q

How to maintain remission in UC?

A
  • Oral aminosalicylates - mesalazine
  • Azathioprine and mercaptopurine
  • Surgery: colectomy
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89
Q

What is intestinal obstruction?

A

Blockage to the transit of intestinal contents through the gut

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90
Q

What is volvulus?

A

Twist/rotation of bowel segment

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91
Q

What are adhesions?

A

Sticking together of bowel contents.

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92
Q

What is intussusception?

A

Telescoping of one part of the bowel into a more distal part.

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93
Q

What is atresia?

A

Absence of opening or failure of development of a hollow structure.

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94
Q

Complications of untreated bowel obstruction?

A
  • Ischaemia
  • Necrosis
  • Perforation
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95
Q

Clinical features of bowel obstruction?

A
  • Vomiting: Projectile, faeculant
  • Pain: Colicky
  • Constipation and obstipation
  • Abdo distension
  • Tenderness
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96
Q

Management principles of bowel obstruction?

A
  • ABCDE
  • Fluid resus
  • Pain relief
  • Decompress - NG tube
  • Accurate diagnosis
  • Surgery
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97
Q

Causes of SBO in adults?

A
  • Adhesions - commonest in developed world, usually due to prev abdo surgery
  • Hernia
  • Crohns
  • Malignancy
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98
Q

Causes of SBO in children?

A
  • Appendicitis
  • Intussusception
  • Atresia
  • Hypertrophic pyloric stenosis
  • Volvulus
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99
Q

Rare causes of SBO?

A
  • Radiation
  • Gallstones
  • Diverticulitis, appendicitis
  • Abcess
  • Foreign bodies - ie hair balls in ill
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100
Q

Symptoms of SBO?

A
  • Pain: Colicky to start, precedes pain
  • Vomiting: follows pain. Projectile. Bilous/faecal. If coffee>necrosis
  • Nausea/Anorexia
  • Distension
  • Constipation
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101
Q

Signs of SBO?

A
  • Tachycardia, hypotension, pyrexia
  • Tenderness
  • Abdo distension
  • Resonance: tympanic sounds (gas filled)
  • Bowel sounds: increased in early stages,, absent later
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102
Q

Investigating SBO?

A
  • Bloods: FBC, U&E, lactate
  • Radiology: Plain erect Xray - SB loops with fluid levels
  • CT: investigation of choice. w/contrast
  • Ultrasound
  • MRI
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103
Q

Management of SBO?

A
  • Aggressive fluid resus
  • Nasogastric decompression
  • Analgesia and antiemetic
  • Early surgical consultation
  • IV abx
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104
Q

Causes of LBO in adults?

A
  • Malignancy (90% in the west)
  • Volvulus (50% of africa cases)
  • Paralytic ileus
  • Strictures
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105
Q

Causes of LBO in children?

A
  • Imperforate anus
  • Hirchsprungs disease
  • Cystic Fibrosis - meconium ileus
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106
Q

Pathophysiology of LBO?

A
  • The colon proximal to the obstruction dilates
  • Increased colonic pressure causing decreased mesenteric bloodflow
  • Mucosal oedema – transudation of fluid and electrolytes from the lumen in the bowel wall
  • The arterial supply is compromised causing mucosal ulceration – leading to full thickness necrosis and perforation
  • Bacterial translocation (from inside the bowel leaking out due to perforation) = sepsis (so patient may even present with signs of septic shock)

If ileocaecal wall is competent the caecum is likely to perforate
If ileocaecal valve is incompetent then faeculent vomiting can occur

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107
Q

Where do colorectal tumours cause obstruction?

A
  • 70% on left side - distal to transverse colon
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108
Q

Symptoms of LBO due to malignancy or strictures?

A
  • Average of 5 day sx
  • Abdo discomfort
  • Fullness/bloating/nausea
  • Altered bowel habit: Tenesmus, difficulty opening bowels, blood in stool, constipation
  • Abdo pain - colicky, tender
  • Vomiting
  • W loss
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109
Q

Symptoms of LBO due to volvulus?

A
  • Sudden onset
  • Pain
  • Localised tenderness and distension
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110
Q

Clinical signs of LBO?

A
  • Abdo distension: Resonance on percussion, sounds tinkling then absent, tender
  • Palpable mass
  • Rigidity and peritonitis
  • DRE: empty rectum, hard stools, blood
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111
Q

Investigations for LBO?

A
  • Proctoscopy/Sigmoidoscopy
  • Bloods: FBC, U&E, lactate
  • Ct+/- contrast is best
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112
Q

Management of LBO?

A
  • NBM
  • O2
  • IV Fluid resus
  • Monitor urine
  • NG decompression
  • Antibiotics
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113
Q

How to treat suspected perforation?

A
  • Laparotomy
  • Resect perforated segment
  • Irrigate
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114
Q

How to manage LBO due to colorectal cancer?

A
  • Initial resus as normal
  • Relieve obstruction - stent decompression
  • CT staging
  • Neoadjuvant therapy - shrink before surgery
  • Surgery
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115
Q

Normal max diameter of large bowel?

A

55mm

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116
Q

Normal max diamter of small bowel?

A

35mm

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117
Q

What is non-mechanical bowel obstruction?

A
  • Adynamic obstruction, paralytic ileus

- Failure of peristalsis

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118
Q

Causes of non-mechanical bowel obstruction?

A
  • Post op: Laparotomy, thoracotomy
  • Ileus associated with systemic illness: MI, pancreatitis, sepsis
  • Narcotic ileus: Intestinal movements stop when on morphine
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119
Q

Symptoms of non-mechanical bowel obstruction?

A
  • Painless distension
  • Vomiting
  • Absent or minimal bowel sounds - tinkling
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120
Q

Investigations for non-mechanical bowel obstruction?

A
  • Bloods: FBC, U&E, magnesium

- Radiology: XR, CT

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121
Q

How to manage non-mechanical bowel obstruction?

A
  • NBM
  • IV fluids
  • NG aspiration
  • Tx of underlying cause
  • Avoid opiates
  • Support nutrition
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122
Q

What is blood supply to colon?

A
  • Superior and inferior mesenteric arteries
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123
Q

Common predisposing factors for bowel ischaemia?

A
  • Increasing age
  • AF
  • Endocarditis, malignancy (as they cause emboli)
  • CVD rf: Smoking, htn, hyperlipidaemia, diabetes
  • Cocaine
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124
Q

Common features of bowel ischaemia?

A
  • Abdo pain
  • Rectal bleeding
  • Diarrhoea
  • Fever
  • Bloods: Raised WBC
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125
Q

What causes acute mesenteric ischaemia?

A
  • Embolism resulting in occulusion of an artery which supplies the small bowel
  • Eg the SMA
  • Classically they have hx of AF
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126
Q

Management of acute mesenteric ischaemia?

A
  • Urgent surgery req

- Poor prog :/

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127
Q

What is chronic mesenteric ischaemia?

A
  • Relatively rare clinical diagnosis
  • May be thought of as ‘intestinal angina’
  • Colicky, intermittent abdo pain occurs
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128
Q

What is ischaemic colitis?

A
  • An acute but transient compromise in blood flow to the large bowel
  • More likely to occur in the ‘watershed’ areas such as splenic flexure that are located at the borders of the aterrial territories
  • May lead to: inflammation, ulceration and haemorrhage
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129
Q

Classical investigation for ischaemic colitis?

A
  • ‘thumbprinting’ on AXR

- Due to mucosal oedema/haemorrhage

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130
Q

Management of ischaemic colitis?

A
  • Usually supportive
  • Surgery may be needed in minority
  • Indcations for surgery: Generalised peritonitis, perforation, ongoing haemorrgage
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131
Q

What are haemorrhoids?

A
  • A swollen vein or group of veins in region of anus
  • Most common cause of rectal bleeding
  • It is the enlargement/congestion of normal mucosal vascular cushions which contribute to anal continence
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132
Q

Different types of haemorrhoids?

A

External:

  • Originate below the dentate line
  • Prone to thrombosis, may be painful

Internal:

  • Originate above the dentate line
  • Do not generally cause pain
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133
Q

How can internal haemorrhoids be graded?

A

Grade 1 - do not prolapse out of anal canal
Grade 2 - prolapse on defecation but reduce spontaneously
Grade 3 - can be manually reduced
Grade 4 - Cannot be reduced

134
Q

Causes/rf for haemorrhoids?

A
  • Low fibre diet causing patient to overly strain when having a bowel movement
  • Pregnancy
  • Prolonged sitting on the toilet
  • Obesity
  • Diarrhoea (both acute and chronic)
  • Colon cancer
  • Previous rectal surgery
  • Spinal cord injury and lack of erect
    posture
135
Q

Symptoms of haemorrhoids?

A
  • Painless rectal bleeding
  • Pruritus ani
  • Pain
  • Soiling may occur with 3rd or 4th degree
136
Q

Diagnosis of haemorrhoids?

A
  • Inspection
  • Rectal exam
  • Proctoscopy
137
Q

Management of haemorrhoids?

A
  • Soften stools: Increase dietary fibre and fluids
  • Topical local anaesthetics and steroids eg anusol
  • Outpatient tx: Rubber band ligation, injection scleropathy
  • Surgery: If large and symptomatic
  • New treatments: Doppler guided haemorrhoidal artery ligation and stapled haemorrhoidopexy
138
Q

How do acutely thrombosed external haemorrhoids present?

A
  • Typically present with significant pain
  • On examination
    • Purple, oedematous, tender subcutaneous perianal mass
  • If patient presents within 72 hours, referral should be considered for excision
  • Otherwise, patients can usually be managed with:
    • Stool softeners, ice packs and analgesia
  • Symptoms usually settle within 10 days
139
Q

What are anal fissures?

A
  • A tear in the lower anal canal distal to the dentate line which produces pain on defecation
  • Location: midline 6 and 12 o’clock postios
140
Q

Causes of anal fissures?

A
  • Most cases: constipation/hard stool tears lining of anal canal
  • Can occur in IBD - perianal abcesses and anal fistulae may complicate
  • Other causes: persistent diarrhoea, pregnancy, childbirth, unusally tight anal sphincter muscles
141
Q

Symptoms of anal fissures?

A
  • Pain on defecation (sharp pain)
  • Often followed by deep burning pain that may last several hours
  • Bleeding when passing stool - small amount of bright red blood in stools or on toilet paper
142
Q

Features of chronic anal fissures?

A
  • Symptoms of >6weeks

- Triad of: Ulcer, sentinel pile, enlarged anal papillae

143
Q

How is anal fissure diagnosed?

A
  • Clinical diagnosis: Hx and exam
  • Peri-anal inspection
  • Rectal exam often not possible due to pain
  • Proctoscopy can be done under anaesthesia to exclude other disease
144
Q

How are anal fissures treated?

A
  • Local anaesthetic gel
  • Stool softeners
  • Botox on chronic fissures
  • Reduce risk by: High fibre diet, well hydrated pt, not ignoring urge to pass stools, exercising regularly
145
Q

What is an anal fistula?

A
  • Abnormal communication between anus and the perianal skin
  • Usually due to previous ano-rectal abcess
  • Can be : intersphincteric, transsphincteric, suprasphincteric, extrasphincteric
146
Q

What rule is used to determind location of the anal fistula?

A
  • Goodsalls rule
147
Q

Causes of anal fistulae?

A
  • Previous abcess (common cause)
  • Crohns disease
  • Anorectal cancer
  • TB
  • HIV/AIDS
  • Chlamydia
  • Syphilis
  • Previous ulcer
  • Complication of surgery
  • Complication of a congenital problem
148
Q

Risk factor for anal fistulae?

A
  • Smoking - as it impairs healing
149
Q

How to investigate anal fistula?

A
  • Endo-anal ultrasound

- MRI and or exam under anaesthetic

150
Q

Management of anal fistula?

A
  • Surgical incision and drainage

- Antibiotics

151
Q

What is a pilonidal sinus/abcess?

A
  • Small hole or tunnel under the skin that usually develops in the cleft of the buttocks where the buttocks seperate
  • More than one hole may develop that are often linked by tunnels under the skin
  • Dont normally cause sx unless infected.
152
Q

Main infecting organisms of ano-rectal abcess?

A
  • E.Coli

- Staph aureus

153
Q

Possible positions of rectal abcess?

A
  • Perianal
  • Ischiorectal
  • Pelvirectal
  • Intersphincteric
154
Q

Risk factors for pilnonidal sinuses?

A
  • Obesity
  • Large amount of body hair
  • Having a job that involves a lot of sitting/driving
155
Q

How are pilonidal sinuses/abcesses treated?

A
  • Keep area clean and dry
  • Remove hair near sinus
  • Antibiotics
  • Pus drainage and surgical incision
156
Q

What is irritable bowel syndrome?

A
  • A functional bowel disease causing an alteration in bowel habit and other GI symptoms
  • Can be classified according to pattern:
    • IBS w/ constipation
    • IBS w/ diarrhoea
    • Mixed IBS
157
Q

When should a diagnosis of IBS be considered?

A

If the patient has had the following for at least 6 months:

  • Abdo pain and/or
  • Bloating and/or
  • Change in bowel habit
158
Q

Diagnostic criteria for IBS?

A
  • Abdominal pain relieved by defecation or associated with altered bowel habit
  • Plus 2 of the following:
    • Altered stool passage (straining, urgency, incomplete evac)
    • Abdo bloating, distension or hardness
    • Symptoms made worse by eating
    • Passage of mucus
  • Features such as lethargy, nausea, backache and bladder symptoms may also support dx
159
Q

red flag features in IBS hx?

A
  • Rectal bleed
  • Weight loss
  • FHx of bowel or ovarian cancer
  • Onset after 60yrs
160
Q

Cause of IBS?

A
  • Thought to be of biospychsocial origin - brain gut axis
  • Depression and anxiety
  • GI infection
  • Stress and trauma
  • Abx therapy
  • Sexual, physical, verbal abuse
  • Pelvic surgeryu
  • Eating disorders
161
Q

Risk factors for IBS?

A
  • Female gender
  • Traumatic life event
  • High hypo-chondrial anxiety scores
  • Prev episodes of infectious diarrhoea
162
Q

Symptoms of IBS?

A
  • Crampy abdominal pain relieved by defecation or the passage of wind
  • Altered bowel habit
  • Sensation of incomplete evacuation
  • Abdominal bloating and distention
  • Diarrhoea without pain (formed stools followed by loose mushy stools, mainly in the morning)
  • Systemic symptoms, can co-exist with:
    • Chronic fatigue syndrome
    • Fibromyalgia
    • TMJ syndrome
163
Q

Investigating IBS?

A
  • Exam usually normal
  • Initial ix by GP - FBC/ESR/CRP +coeliac
  • Sigmoidoscopy with air sufflation may reproduce pain
  • Rectal biopsy to exclude IBD
  • Colonoscopy, esp in >50 to r/o sinister pathology
  • It is a diagnosis of exclusion.
164
Q

First line pharmacological remedies for symptomatic relief in IBS?

A

Remedy according to predominant symptom?

  • Pain: antispasmodic agents (mebevrine, peppermint oil)
  • Constipation: laxatives (soluble fibre supplements)
  • Diarrhoea: loperamide
165
Q

Second line pharma treatment for IBS?

A
  • Low dose TCAs eg. amitriptyline 5-10mg

- SSRI can be used too

166
Q

Psychological interventions for IBS?

A
  • CBT
  • Hypnotherapy
  • Psychological therapy
167
Q

General dietary advice for IBS?

this has loads on it

A
  • Explore dietary triggers and refer to a dietician
  • Have regular meals and take time to eat
  • Avoid missing meals or leaving long gaps between eating
  • Drink at least 8 cups of fluid per day (water or herbal tea)
  • Restrict tea and coffee to 3 cups per day
  • Reduce intake of alcohol and fizzy drinks
  • Consider limiting intake of high fibre food (wholemeal and whole grains)
  • Reduce intake of ‘resistant starch’ often found in processed foods
  • Limit fresh fruit to 3 portions per day
  • For diarrhoea – avoid sorbitol (found in some fruits)
  • For wind and bloating – consider increasing intake of oats and linseeds
168
Q

What is diverticular disease?

A

pouches of mucosa extrude through the colonic muscular wall via weakened areas near blood vessels to form diverticula

169
Q

What is diverticulosis?

A

the presence of diverticula (multiple outpouchings of the bowel wall)

170
Q

What is diverticulitis?

A

implies inflammation, which occurs when faeces obstruct the neck of the diverticulum

171
Q

Most common site for diverticular disease?

A
  • Between taenia coli where vessels pierce the muscle to supply the mucosa
  • For this reason the rectum (no taenia coli) is often spared
172
Q

Symptoms of diverticular disease?

A
  • Altered bowel habit
  • PR bleeding
  • Abdominal pain
173
Q

Complications of diverticular disease?

A
  • Diverticulits
  • Haemorrhage
  • Fistula development
  • Perforation and faecal peritonitis
  • Perforation and abcess development
  • Development of diverticular phelgmon
174
Q

How to diagnose diverticular disease?

A

Pt will undergo either:

  • Colonoscopy
  • CT cologram
  • Barium enema
175
Q

What is the Hinchey classification of severity for diveritcular disease?

A

I – Para-colinic abscess
II – pelvic abscess
III - purulent peritonitis
IV - faecal peritonitis

176
Q

How is diverticular disease treated?

A
  • Increase dietary fibre intake
  • Mild attacks of diverticulitis may be managed with Abx
  • Peri-colonic abscesses – drained surgically or radiologically
  • Recurrent episodes of acute diverticulitis requiring hospitalisation are a relative indication for a segmental resection
  • Hinchey IV perforations will require resection and usually stoma
177
Q

Most common site for diverticulosis?

A
  • Sigmoid colon

- Multiple outpouchings of the bowel wall

178
Q

Presentation of diverticulosis?

A
  • Painful diverticular disease:
    • Altered bowel habit
    • Colicky left sided abdo pain
    • High fibre diet recommended
  • Diverticulitis
179
Q

How does acute diverticulitis present?

A
  • Severe left iliac fossa pain and tenderness
  • Anorexia, nausea and vomiting
  • Change in bowel habit – constipation or diarrhoea
  • Urinary frequency, urgency or pain (bladder irritated by inflamed bowel)
  • Features of infection – pyrexia, raised WBC and CRP
  • PR bleeding in some cases

Usually affects 50-70 year olds
80% of patients are >50

180
Q

How does chronic diverticulits present?

A
  • Intermittent abdominal pain - particularly in LLQ
  • Bloating
  • Change in bowel habit - constipation or diarrhoea
181
Q

Physical signs of diverticulitis?

A
  • Low grade fever
  • Tachycardia
  • Tender LIF
  • Possible reduced bowel sounds
  • Guarding, rigidity and rebound tenderness
  • Lack of improvement with tx suggests abcess
182
Q

Risk factors for diverticulitis?

A
  • Age
  • Lack of dietary fibre
  • Obesity
  • Sedentary lifestyle
  • Smoking
  • NSAID use
183
Q

Investigating diverticulits?-

A

FBC - raised WCC
CRP - raised
Erect CXR - may show pneumoperitoneum if perforation
AXR - may show dilated bowel loops, obstruction of abcesses
CT - best imaging modality

Avoid colonoscopy initially due to increased risk of perforation in diverticulitis

184
Q

How is diverticulits managed?

A

Mild attacks: Oral antibiotics

More significant req admission:

  • NBM
  • IV fluids
  • IV ABx - typically a cephalosporin + metronidazole
185
Q

What are the possible complications of diverticulits?

A
  • Abscess formation
  • Peritonitis
  • Obstruction
  • Perforation
186
Q

What is Meckels diverticulum?

A
  • A congenital diverticulum of the small intestine
  • Remnant of the vitelline duct (aka omphalomesenteric duct)
  • Contains ectopic ileal, gastric or pancreatic mucosa
  • Rules of 2s: 2% of population, 2 feet from ileocaecal valve, 2inches
187
Q

How does meckels diverticulum present?

A
  • Usually aymptomatic
  • Abdo pain mimicking appendicitis
  • Rectal bleeding
  • Intestinal obstruction secondary to:
    • Omphalomesenteric band, volvulus, intussuception.`
188
Q

How is meckels diverticulum managed?

A
  • Removal if narrow neck or symptomatic
  • Options are between:
    • wedge excision
    • formal small bowel resection and anastamosis
189
Q

What is acute appendicitis?

A
  • The most common acute abdominal condition requiring surgery
  • Can occur any age, commonly 10-20
  • Occurs when the luemn of the appendix becomes obstructed by a faecolith
  • The bacteria inside the faecolith stagnate inside the appenix
  • Causes inflammation
190
Q

Presentation of appendicitis?

A

Abdominal pain:

  • Peri-umbilical initially
  • Migrates to RIF - McBurneys point
  • Pain often worse on coughing, going over speed bumps
  • Children cant hop on their right leg due to pain

Other features: N+V, Diarrhoea, Low grade fever, anorexia

191
Q

Signs of appendicitis on abdo exam?

A
  • Localised peritonism (tenderness and guarding)
  • Rebound tenderness in RIF
  • May be a tender mass present if there is an appendiceal abcess
192
Q

What investigations should be done for appendicitis?

A
  • Blood tests: Raised WBC, CRP and ESR
  • Urinalysis: Exclude preg, exclude UTI and renal colic. May show leucocytes but no nitrates
  • USS: Inflamed appendix and/or mass
  • CT scans: Highly sensitive and specific. gold standard.
193
Q

Management of appendicitis?

A
  • Appendicectomy
  • Metronidazole to reduce wound infection rates
  • If perforated appendicitis - abdominal lavage
194
Q

Complications of appendicitis?

A
  • Gangrene or perforation

- Leading to localised abcess formation or generalised peritonitis

195
Q

2 histological types of oesophageal cancer?

A
  • Squamous cell carcinoma: usually middle 1/3 of oesophagus

- Adenocarcinoma: lower 1/3rd

196
Q

What are the causes/rf of squamous cell carcinoma of the oesophagus?

A
  • Smoking
  • Excess alcohol consumption
  • Pre-existing oesophageal disease (achalasia and strictures)
  • Coeliac disease
  • Reflux
  • Scleroderma
  • Diets rich in nitrosamines (bacon, cured meats, beer)
197
Q

What are causes/rf of adenocarcinoma of the oesophagus?

A
  • GORD
  • Barretts oesophagus
  • Smoking
  • Obesity
198
Q

Symptoms of oesophageal cancer?

A
  • Dysphagia (increases as tumour grows, solids then liquids)
  • Vomiting
  • Weight loss and anorexia
  • Odynophagia
  • Hoarse voice
  • Cough
  • GI bleeding - haematemesis, melena
  • Dyspepsia and reflux sx
  • Symptoms of anaemia
199
Q

Signs of oesophageal cancer?

A
  • Anaemia
  • Malnutrition
  • Supraclavicular lymphadenopathy (virchows node)
  • Pleural effusion
  • Hepatomegaly
  • Ascites
  • Vocal cord paralysis/voice change
200
Q

Investigations for oesophageal cancer?

A
  • Upper GI endoscopy: First line investigation
  • Contrast swallow
  • Staging: Ct chest, abdo, pelvis
201
Q

Management of oesophageal cancer?

A
  • Operable disease managed by surgical resection
  • Neoadjuvant chemotherapy
  • Stenting is option for palliation, however sx relief only
202
Q

Main complications of oesophageal cancer resection?

A
  • Anastomotic leak: Intrathoracic anastomosis will result in mediastinitis. high mortality.
203
Q

What type of cancer is gastric cancer?

A

Adenocarcinoma - because stomach cells are secretory

204
Q

When does gastric cancer often present?

A

70-80yrs.

205
Q

Risk factors/associations of gastric cancer?

A
  • H.Pylori infection
  • Blood group A
  • Gastric adenomatous polyps
  • Pernicious anaemia
  • Smoking
  • Aspirin
  • Diet: salt, spicy, nitrates
  • Low socioeconomic groups
206
Q

How does gastric cancer present?

A
  • Dyspepsia
  • N+V
  • Anorexia and W loss
  • Dysphagia
  • Outflow obstruction
  • If metastasis: ascites and hepatomegaly
207
Q

How is gastric cancer investigated?

A
  • Diagnosis: Endoscopy and biopsy
  • Staging: CT or endoscopic ultrasound
  • Laparoscopy to identify occult peritoneal disease
  • PET CT
208
Q

How is gastric cancer treated?

A
  • Proximal disease greater than 5-1-cm from the OG junction – sub-total gastrectomy
  • Total gastrectomy if tumour is <5cm from OG junction
  • Surgical options – gastric resection, lymphadenectomy, reconstruction
  • Pre-op chemo improves survival
  • Adjuvant chemotherapy after surgery if operable
  • Palliative chemotherapy if inoperable
209
Q

What are the types of cancers that can affect small intestines?

A

These are RARE

  • Adenocarcinoma – 50% increased incidence in Coeliac and Crohn’s
  • Non-Hogkin’s lymphoma – may be B or T cell in origin, increased frequency in coeliac disease
  • Benign small intestinal tumours
    - Peutz-Jeghers syndrome (autosomal dominant)
    - Familial adenomatous polyposis (FAP)
  • Carcinoid tumours
210
Q

How do small bowel tumours present?

A
  • Abdominal pain
  • Diarrhoea
  • Anorexia
  • Anaemia
211
Q

What are carcinoid tumours?

A

Originate from enterochromaffin cells of the intestine (produce histamine and serotonin)

212
Q

What is carcinoid syndrome?

A
  • The term applied to the symptoms that arise as a result of serotonin (5-HT), kinins, histamine and prostaglandins being released into the circulation by the tumour
  • Usually occurs when metastases are present in the liver and release serotonin into the systemic circulation
  • May also occur with lung carcinoid as mediators are not ‘cleared’ by the liver
213
Q

What are the features of carcinoid syndrome?

A
  • Flushing
  • Diarrhoea
  • Bronchospasm + wheezing
  • Hypotension
  • Right heart valvular stenosis
  • Other molecules such as ACTH and GHRH may also be secreted resulting in, for example, Cushing’s syndrome
214
Q

How to diagnoise carcinoid tumour/syndrome?

A
  • Urinary 5-HIAA levels raised (breakdown product of serotonin)
  • Plasma chromogranin A
  • Liver USS scan
215
Q

Treatment of carcinoid syndrome/tumours?

A
  • Somatostatin analogues eg. octreotide
  • Diarrhoea give cyproheptadine
  • Tumour reduced via surgery or chemo
216
Q

3 different types of colon cancer?

A

1) sporadic (95%)
2) hereditary non-polyposis colerectal carcinoma
3) familial adenomatous polyposis

217
Q

What is the histology of colorectal cancer?

A

Adenocarcinoma

218
Q

Inheritance pattern of HNPCC?

A
  • Autosomal dominant
  • Most common inherited cancer
  • aka Lynch Syndrome
219
Q

If you have HNPCC, what are you also at risk of?

A
  • Endometrial cancer (commonly)
  • Gastric cancer
  • Pancreatic cancer
220
Q

Criteria for HNPCC diagnosis?

A

Amsterdam criteria

1) At least 3 family members with colon cancer
2) The cases span at least 2 generations
3) At least once case diagnosed before age 50

221
Q

Inheritance pattern of FAP?

A

AD

Mutation in the tumour suppression gene called adenomatous polyposis coli gene (APC) on chromosome 5

222
Q

What are the features of FAP?

A
  • Formation of hundreds of polyps by age 30-40yrs
  • Inevitable they will develop carcinoma of large bowel
  • Gardners syndrome is an FAP variant, you also get: osteoma of skull/mandible, retinal pigmentation, thyroid carcinoma and epidermoid cysts
223
Q

How to manage FAP?

A
  • Genetic testing: analyse DNA from WBC

- Total colectomy with ileo-anal pouch formation in their 20s

224
Q

Risk factors for colorectal cancer?

A
  • Fhx
  • Diet: lack of fibre, red meat, alcohol
  • Smoking
  • Past history of bowel conditions - adenoma, ulcerative colitis
225
Q

Where are large bowel cancers often found?

A
  • Rectal 40%
  • Sigmoid 30%
  • Asc colon and caecum 15%
  • Transverse colon 10%
  • Descending colon 5%
226
Q

Generic features of bowel cancer?

A
  • Bleeding
  • Mucous
  • Change in bowel habit
  • Difficulty defecating of bowel obstruction
  • Weight loss
  • Night sweats/fevers
  • Hepatomegaly
227
Q

How does rectal cancer present?

A

Early: PR bleeding, mucus
Late: Thin stools, tenesmus

228
Q

How does left sided and sigmoid cancer present?

A

Change in bowel habit: Diarrhoea, constipation, thin/altered stools
PR bleeding

229
Q

How does right sided bowel cancer present?

A
  • Later than left sided
  • Anaemia
  • Mass
230
Q

How may bowel cancer present acutely?

A

Bowel obstruction with four cardinal signs

1) Absolute constipation
2) Colicky abdo pain
3) Abdominal distension
4) Vomiting

231
Q

When to refer URGENT to colorectal?

A
  • Patients ≥ 40 with unexplained weight loss AND abdominal pain
  • Patients ≥ 50 with unexplained rectal bleeding
  • Patients ≥ 60 years with iron deficiency anaemia OR change in bowel habit
  • Occult blood found in faeces
232
Q

When to refer 2WEEKWAIT to colorectal?

A
  • Rectal or abdominal mass
  • Unexplained anal mass or anal ulceration
  • Patients < 50 years with rectal bleeding AND any of the following explained symptoms/findings:
    • Abdominal pain
    • Change in bowel habit
    • Weight loss
    • Iron deficiency anaemia
233
Q

Investigations for colorectal cancer?

A
  • Tumor markers: CEA can be useful
  • Colonoscopy is gold standard with biopsy and polyp removal.
  • Double contrast barium enema
  • CT colonoscopy
234
Q

Risks of colonoscopy?

A
  • Bleeding
  • Infection
  • Perforation
  • Missed dx
  • Anaesthetic risks
235
Q

How is colorectal cancer staged?

A

TNM

Dukes

236
Q

TNM staging for colorectal?

A 
T0 = tumour confined to mucosa
T1 = tumour invades submucosa
T2 = tumour invades muscularis propria
T3 = tumour invades serosa
T4 = tumour invades other organs
N0 = no nodal involvement, N1 = 1-3 nodes involved, N2 = ≥ 4 nodes
M0 = no distant mets, M1 = distant mets present
237
Q

Dukes classification of colorectal?

A

A: Tumour confined to mucosa
B: Tumour invading bowel wall
C: LN metastases
D: Distant mets

238
Q

Management of colorectal cancer?

A
  • MDT meeting essential – decides on surgical/non-surgical/both
  • Surgery - only chance of cure
  • Resection – tailored to the patient and tumour location
  • Post-operative (adjuvant) chemotherapy – increases survival
  • Radiotherapy – either pre-operative or palliative to improve symptoms
  • If liver mets – hepatic resection offered
  • Palliative chemotherapy – for those with unresectable metastatic disease, improves QoL and median survival
  • Palliative surgery – stents, bypass, diversion stomas
239
Q

What is peritonitis?

A

Inflammation of the peritoneum

240
Q

Difference between localised and generalised peritonitis?

A

Localised:

  • Occurs with all acute inflammatory GI conditions
  • Management depends on the underlying condition e.g. appendicitis, cholecystitis

Generalised

  • Occurs as a result of rupture of an abdominal viscus (e.g. perforated DU or appendix)
  • Sudden onset of abdominal pain which becomes rapidly generalised
  • Patient is shocked and lies still as movement exacerbates the pain
241
Q

Causes of primary peritonitis?

A
  • Extremely rare
  • Haematogenous - originates/carried in the blood or from LN
  • Risk groups:
    • Liver disease (Spontaneous bacterial peritonitis)
    • Females
    • Immune compromised
    • Post-splenectomy
    • Peritoneal dialysis pts
    • Patients with ascites
242
Q

Causes of secondary peritonitis?

A
  • Perforation of hollow viscus (generalised peritonitis)
    • Peptic ulcer, colonic diverticulum, appendix
  • Inflammation of abdo organs (localised peritonitis)
  • Peritoneal dialysis
  • TB
  • Ischaemia of hollow viscus
  • Chemical contamination eg glove left in after surgery
243
Q

Symptoms of peritonitis?

A
  • Acute presentation
  • Pain
  • Tenderness
  • Systemic sx: Nausea, chills, rigors, dizziness, weakness, immobile due to pain
244
Q

Clinical exam findings for peritonitis?

A 
General exam:
 - Pyrexia, tachycardic, signs of shock
 - Confusion
 - Pt lie still
Abdo exam:
 - Guarding
 - Hard, rigid abdomen
 - Rebound tendernes
 - Silent abdomen (ominous sign)
245
Q

Investigating ?peritonitis?

A
  • Blood tests: FBC,U&E,amylase, LFTs, CRP
  • ABG - look for sepsis
  • Plaiin XR
  • CT abdo
  • Culture: Blood and ascitic fluid
246
Q

How to manage peritonitits?

A
  • ABCDE approach to resuscitation
  • Sepsis 6
  • Broad spectrum IV antibiotics
  • Treat underlying cause
    • Medical Mx of primary peritonitis – IV Abx (SPB, PID, PD related)
    • Surgical Mx of secondary peritonitis – repair or removal of perforated viscus
247
Q

What is a hernia?

A

Protrusion of a viscus or part of a viscus through a natural orifice or weakness into another compartment.

All abdo wall hernias present as a lump

248
Q

Common types of hernia?

A 
Inguinal (direct or indirect)
Femoral
Umbilical
Paraumbilical
Epigastric
Incisional 
Parastomal
Hiatus
249
Q

How to classify hernias?

A 
Reducible
Irreducible 
Incarcerated
Obstructed
Strangulated
250
Q

What is a reducible hernia?

A
  • Can be pushed back in
  • Can be spontaneous or manual
  • Most are reducible when they first appear
251
Q

What is an irreducible hernia?

A
  • Impossible to return contents of hernia to abdo cavity
  • Usually involve bowel
  • Can be partial or complete
252
Q

What is hernial incarceration?

A
  • Contents of hernia sac are stuck inside by adhesions
253
Q

What is an obstructed hernia?

A
  • Pressure from edges of hernia means bowel contents cannot pass through - causes feature of intestinal obstruction
254
Q

What is a strangulated hernia?

A
  • Ischaemia occurs –> gangrene and perforation of hernia contents
255
Q

What is an inguinal hernia?

A
  • Most common type of hernia
  • Accounts for 75% of abdo wall hernieas
  • 95% male
256
Q

Predisposing factos for inguinal hernia?-

A
  • Male gender
  • Chronic cough
  • Constipation
  • Urinary obstruction
  • heavy lift
  • Ascites
  • past abdo surgery
257
Q

Features of inguinal hernias?

A
  • Groin lump: disappears on pressure or where pt lies down
  • Discomfort and ache
  • Strangulation is rare
258
Q

Direct vs indirect inguinal hernia?

A
  • Direct: Through posterior wall of inguinal canal

- Indirect: Hernia through inguinal canal

259
Q

Management of inguinal hernia?

A

Treat medically fit patients even if they are asymptomatic
Surgical repair with polyproylene mesh

If patient not fit for surgery – hernia truss may be an option, no role in other patients

260
Q

When can pt return to work after hernia repair?

A

Open repair – 2-3 weeks (non manual work only)

Laparoscopic repair – 1-2 weeks

261
Q

Complications of hernia repair?

A

Early: Bruising and wound infection
Late: Chronic pain and recurrence

262
Q

Main risk of femoral hernia?

A

HIGH risk of strangulation

263
Q

How do femoral hernias present?

A

Mass on medial thigh.

More often women

264
Q

Treatment of femoral hernia?

A

Either:
Herniotomy: ligation and excision of sac
Herniorrhaphy: Repair of hernia defect (ie with mesh)

265
Q

What is an incisional hernia?

A
  • Occur through sites of surgical access into the abdominal cavity.
  • Most common following surgical wound infection

To minimise following midline laparotomyJenkins Ruleshould be followed:

 - This necessitates a suture length 4x length of incision
 - With bites taken at 1cm intervals, 1 cm from the wound edge.
  • Repair may be performed either at open surgery or laparoscopically and a wide variety of techniques are described
266
Q

Risk factors for incisional hernia?

A
  • Obesity
  • Emergency surgery
  • Wound infection post op
  • Persistent coughing
  • Poor nutrition
  • Heavy lifting
  • Other pre-existing health condition that slows healing eg HIV or diabetes
267
Q

What is an umbilical hernia?

A
  • Hernia through weak umbilicus
  • Usually presents in childhood
  • Often asymptomatic
  • Equal sex incidence
  • 95% will resolve by age 2
  • Thereafter try surgical repair
268
Q

Rf for umbilical hernia?

A
  • Black kids
  • Obesity
  • Ascites
  • Heavy lifting
  • Persistent coughing
  • Multiple pregnancies
269
Q

Management of umbilical hernia?

A

< 2 years – leave alone

> 2 years – surgical repair of the rectus sheath (Mayo repair)

270
Q

What is a hiatus hernia?

A

Herniation of part of the stomach above the diaphragm through the oesophageal hiatus

2 types:
Sliding
Rolling (Para-oesophageal)

271
Q

What are Sliding hiatus hernia?

A
  • Account for 95% of hiatus hernias
  • The gastroesophageal junction moves above the diaphragm
  • Asymptomatic unless there’s associated reflux
272
Q

What is a rolling hiatus hernia?

A
  • Uncommon
  • Gastric fundus rolls up through the hiatus alongside the oesophagus
  • Gastro-oesophageal junction remains below the diaphragm
  • Poses a serious risk of complications – gastric volvulus (rotation and strangulation of the stomach), bleeding and respiratory complications
  • Should be treated surgically
273
Q

What is a volvulus?

A
  • Complete twisting of a loop of intestine around its mesenteric attachment site
  • Resulting in compromised blood flow and closed-loop obstruction
  • Can occur at various locations e.g. stomach, small intestine, caecum, transverse and sigmoid colon
274
Q

Most common site for volvulus?

A
  • Sigmoid is 80% (LBO caused by sigmoid colon twisting on its mesentery)
  • Caecum is 20%
275
Q

Associations with sigmoid volvulus?

A
  • Older patients
  • Chronic constipation
  • Chagas disease (American trypanosomiasis)
  • Neurological conditions e.g. Parkinson’s disease, Duchenne muscular dystrophy
  • Psychiatric conditions e.g. schizophrenia
276
Q

Associations with caecal volvulus?

A
  • All ages
  • Adhesions
  • Pregnancy
277
Q

Features of volvulus?

A

Sx of BO:

  • Constipation
  • Abdo bloating
  • Abdo pain
  • N+V
278
Q

Diagnosis of volvulus?

A
  • Usually diagnosed on abdo film (XR)
  • Sigmoid: LBO (large dilated loop of colon) and Coffee Bean sign
  • Caecal: SBO seen
279
Q

Management of volvulus?

A

Sigmoid volvulus - rigid sigmoidoscopy with rectal tube insertion

Caecal volvulus - management is usually operative. Right hemicolectomy is often needed

280
Q

What is diarrhoea?

A
  • Liquid form loose stools

- Often frequent/urgent passing

281
Q

DIfference between chronic and acute diarrhoea?

A
  • Acute: Usually due to infection or food poisoning

- Chronic: defined as diarrhoea persisting for >14 days.

282
Q

List some infectious causes of diarrhoea?

A
  • Infectious = gastroenteritis. May occur at home or whilst travelling abroad
  • Viral – rotavirus, norovirus
  • Foodborne – often bacterial
  • Antibiotic associated diarrhoea (wipes out normal gut flora)
  • Travel related – E.coli, Giardiasis etc
  • Diarrhoea in the immunocompromised
  • Can be a feature of systemic infection (e.g. sepsis, malaria)
283
Q

Non infectious causes of diarrhoea?

A
  • IBD
  • Malabsoprtion eg Coeliac disease
  • Malignancy
  • Overflow w/ constipation
  • Endocrine eg thyrotoxicosis
  • Medicines eg. laxative abuse, metforin
284
Q

Clues about cause of infective diarrhoea?

A
  • History of contact with other cases - Norovirus
  • Small children – rotavirus
  • Fresh water – Aeromonas
  • Puppies, chicken restaurant – Campylobacter
  • Reptiles – Salmonella
  • Well water – Giardia
  • Flooding/water problems – Cryptosporidiosis
  • Raspberries – Cycospora
285
Q

Management of diarrhoea?

A
  • Oral rehydration salts (dioralyte)

- Loperamide: acts on opioid receptors to slow gut down. Doesnt cross BBB so no neuro sx

286
Q

Side effects and C/I for loperamide?

A

Side effects

  • Constipation
  • Abdominal cramps
  • Dizziness

Contraindications
- Ulcerative colitis
- Infective diarrhoea associated with bloody stools – as you actually want to
clear this kind of diarrhoea, not stop it

287
Q

Define travellers diarrhoea?

A

At least 3 loose watery stools in 24 hours

With or without one or more of:

  • Abdominal cramps
  • Fever
  • Nausea
  • Vomiting
  • Blood in the stool
288
Q

Most common cause of travellers diarrhoea?

A

E. Coli

289
Q

What is acute food poisoning?

A

Sudden onset of nausea, vomiting and diarrhoea after the ingestion of a toxin.

290
Q

Most common causes of acute food poisoning?

A
  • Staphylococcus aureus
  • Bacillus cereus
  • Clostridium perfringens
291
Q

Describe history of E.Coli diarrhoea?

A
  • Common amongst travellers
  • Watery stools
  • Abdominal cramps and nausea
  • Incubation period 12-48 hours
292
Q

Describe history of Giardasis diarrhoea?

A
  • Prolonged
  • Non-bloody diarrhoea
  • Incubation period > 7 days
  • Parasitic infection rather than bacterial
293
Q

Describe history of cholera diarrhoea?

A
  • Profuse, watery diarrhoea
  • Severe dehydration resulting in weight loss
  • Not common amongst travellers
294
Q

Describe hx of shigella diarrhoea?

A
  • Bloody diarrhoea
  • Vomiting and abdominal pain
  • Incubation period - 48-72 hours
295
Q

Describe hx of staph aureus infection?

A
  • Severe vomiting

- Short incubation period (1-6hrs)

296
Q

Describe hx of campylobacter diarrhoea?

A
  • Flu-like prodrome
  • Crampy abdominal pains
  • Fever
  • Diarrhoea which may be bloody
  • Complications include GBS
  • Incubation period 48-72 hours
297
Q

Describe hx of bacillus cereus?

A

Two types of illness seen:

  • vomiting within 6 hrs, stereotypically due to rice
  • Diarrhoeal illness occuring after 6hrs
298
Q

Describe hx of amoebiaisis diarrhoea?-

A
  • gradual onset bloody diarrhoea
  • abdo pain and tenderness
  • may last several weels
299
Q

What is Clostridium difficile?

A
  • A gram positive rod bacteria (purple in gram stain)
  • Often encountered in hospital setting
  • Develops when the normal gut flora are suppressed by broad spectrum antibiotics
300
Q

Main complication of C Diff?

A

Pseudomembranous colitis.

Occurs due to C.Diff exotoxin causing intestinal damage

301
Q

Risk facotrs for C Diff infection?

A
  • Broad spectrum abx: 3rd gen cephalosporins are leading cause (cefotaxime and ceftriaxone etc)
  • Use of PPI and H2 receptor antagonists
  • Being hospitalised
  • Contact with infected persons
302
Q

Clinical features of C Diff?

A
  • Diarrhoea
  • Abdo pain
  • Raised WBC count
  • If severe: Toxic megacolon
303
Q

Diagnosis of C Diff how?

A
  • Stool sample: Detection of clostridium difficile toxin in the stool
304
Q

How is C Diff treated?

A
  • Isolate
  • First line therapy – oral metronidazole for 10 - 14 days
  • If severe or not responding to metronidazole – oral vancomycin may be used
  • Patients who don’t respond to vancomycin may respond to oral fidaxomicin
  • For life-threatening infections – combination of oral vancomycin and IV metronidazole should be used
  • Patients with severe and unremitting colitis should be considered for colectomy
305
Q

Why is diarrhoea common in pt with HIV?

A
  • May be due to opportunistic infections

- Or due to effects of virus itself

306
Q

Causes of diarrhoea in HIV patients?

A
  • Most common = cryptosporidium
    - Detected with modified Ziehl-Neelsen stain for acid fast bacilli
  • Other protozoa too
  • Cytomegalovirus
  • Mycobacterium avium intracellulare
  • Giardia
307
Q

What causes amoebiasis?

A
  • Entamoeba histiolytica
  • Spread by faecal oral route
  • 10% of worlds pop are chronically infected
308
Q

Features of amoebiasis?

A
  • Can be asymptomatic
  • Can cause mild diarrhoea or severe amoebic dysentery
  • Can also cause liver and colon abscesses
  • Amoebic dysentery:
    - Profuse, bloody diarrhoea
    - Stool microscopy – trophozoites
    - Treat w/ metronidazole
  • Amoebic liver abscess:
    - Usually a single mass in the right lobe (may be multiple)
    - Features - fever, RUQ pain
    - Serology positive in >90%
309
Q

How is malnutrition diagnosed?

A

Unintentional weight loss greater than 10% within the last 3-6 months

Or A body mass index of less than 18.5kg/m²

Or A body mass index of less than 20kg/m² and unintentional weight loss greater than 5% within the last 3-6 months

310
Q

How can pancreatitis be classified?

A

Acute pancreatitis = inflammation of a previously normal pancreas. The inflammation that occurs is reversible

Chronic pancreatitis = continuing inflammation with irreversible structural changes

311
Q

Exocrine functions of pancreas?

A
  • The exocrine glands of the pancreas produce enzymes used for digestion
  • These enzymes include
    • Trypsin and chymotrypsin – protein digestion
    • Amylase – carbohydrate digestion
    • Lipase – breakdown of fats
  • These are released into the pancreatic duct when food enters the stomach
  • Ampulla of Vater releases these into the duodenum
312
Q

Endocrine functions of pancreas?

A
  • Endocrine component of the pancreas consists of islet cells (islets of Langerhans) which release hormones directly into the bloodstream
  • The 2 main hormones are
    • Insulin – acts to lower blood sugar
    • Glucagon – acts to raise blood sugar
313
Q

Causes of acute pancreatitis?

A 
Most commonly = gallstones and alcohol
IGETSMASHED
Idiopathy
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion stings
Hypothermia/hypercalcaemia
ERCP (endoscopic retrograde cholangiopancreatography)
Drugs - azathioprine, oestrogens, steroids, didanosine
314
Q

Sx of acute pancreatitis?

A
  • Severe epigastric pain - may radiate through to back
  • Vomiting
  • Anorexia/Nausea
  • Hx of gallstones or alcohol abuse
315
Q

Signs of acute pancreatitis?

A
  • Abdominal examination – widespread tenderness and guarding
  • Ileus – may have absent bowel sounds
  • Low-grade fever
  • In severe cases – signs of septic shock: tachycardia, hypotension, dehydration, oliguria
  • Described but rare
    - >Periumbilical discolouration - Cullen’s sign
    - >Flank discolouration – Grey-Turner’s sign
316
Q

How can acute pancreatitis be classified?

A

Oedematous – 70%
Severe/necrotising – 25%, necrosis
Haemorrhage – 5% (this is when you will see Cullen’s/Grey Turner’s sign)

317
Q

Blood tests for suspected acute pancreatitis?

A

Serum amylase – 3x higher than normal level (but there are other reasons for hyperamylasaemia). Serum amylase levels do not correlate with disease severity

Serum lipase – raised, more sensitive and specific than serum amylase. It also has a longer half life

Urinary amylase – will still be raised if the patient present late and the serum amylase levels have dropped again

FBC, CRP, U&E, LFT, plasma Ca2+ and ABGs – measured on admission and at 24-48 hours to assess the severity of the pancreatitis

318
Q

What else can cause raised amylase?

A
  • Acute pancreatitis
  • Pancreatic pseduocyst
  • Mesenteric infarct
  • Perforated viscus/peptic ulcer
  • Acute cholecystitis
  • Diabetic ketoacidosis
319
Q

Imaging for ?acute pancreatitis?

A
  • Erect CXR to r/o perforated peptic ulcer
  • Abdominal USS for gallstones
  • Contrast CT
  • ERCP
320
Q

Scoring systems for pancreatitis severity?

A
  • Abbreviated Glasgow scoring system
  • Ranson criteria
  • Balthazar Score
  • APACHE score – may also be used but usually only done in intensive care

CRP can also be used to assess severity

321
Q

Components of abbreviated glasgow system?

A

Composed of 8 clinical indicators (PANCREAS), score of >3 indicates the for supportive ITU treatment or anaesthetic review

  • PaO2 < 8 kPa – low
  • Age > 55 years
  • Neutrophils > 15x10^9 – raised
  • Calcium < 2 mmol/l – low
  • Raised urea > 15 mmol/l
  • Elevated enzymes (LDH or AST)
  • Albumin < 32 g/l - low
  • Sugar – serum glucose >15 mmol/l - raised
322
Q

management of pancreatitis?

A
  • Analgesia very important
  • ABCDE approach to resuscitation/shock
  • Surgery:
    • Patients with acute pancreatitis due to gallstones should undergo early cholecystectomy
    • Patients with obstructed biliary system due to stones – ERCP
    • Patients who fail to settle with necrosis and have worsening organ dysfunction may require debridement
    • Patients with infected necrosis - either radiological drainage or surgical necrosectomy
323
Q

How is mild pancreatitis managed?

A

Medical therapy consisting of

  • Pain control – tramadol or other opiates, fentanyl
  • NBM
  • IV fluids
  • NG tube

Monitor for complications

324
Q

Management of severe pancreatitis?

A
  • The same medical therapy for mild disease (IV fluids, analgesia)
  • Consider ITU
  • Prophylactic Abx – usually cephalexin/metronidazole
  • Nasogastric or nasojejunal feeding
  • ERCP within 48 hours if gallstones – extraction can be performed
  • Anticoagulation with LMWH for DVT prophylaxis
325
Q

Complications of acute pancreatitis?

A

Systemic inflammatory response syndrome

Multiple organ dysfunction syndrome (MODS) – pancreatitis causing loss of body homeostatic mechanisms

326
Q

What is chronic pancreatitis?

A
  • Inflammation of pancreas lasting >12 weeks
  • Damage is irreversible
  • Can lead to dysfunction of both exocrine and endocrine functions of pancreas. Leading to malabsoption and diabetes respectively.
  • Difficult to dx and manage
327
Q

Causes of chronic pancreatitis?

A
  • 80% of cases due to alcohol
  • Autoimmune
  • Idiopathic
  • Cystic fibrosis
  • Trauma
  • Hypercalcaemia
328
Q

Features of chronic pancreatitis?

A
  • Epigastric pain – typically worse 15-30 minutes after a meal
  • Exocrine dysfunction - causing steatorrhea and other symptoms of pancreatic insufficiency (usually develops 5-25 years after the onset of pain)
  • Endocrine dysfunction – DM occurs in majority of patients, usually 20 years after symptoms begin
  • Severe weight loss and anorexia
  • Nausea and vomiting
  • Can occasionally present with jaundice – due to obstruction of CBD during its course through the fibrosed head of pancreas
329
Q

How is chronic pancreatitis investigated?

A 
Imaging:
 - Abdo XR - can show calcification
 - USS
 - CT - more sensitive
 - MRCP and endoscopic USS
 - ERCP
Functional/biochemical
 - Faecal elastase - reduced
 - Blood glucose - raised, indicated DM
 - Serum amylase
330
Q

Management of chronic pancreatitis?

A
  • Advise patient to stop drinking alcohol
  • Analgesia
  • Surgical resection combined with drainage of the pancreatic duct into the small bowel
  • ERCP – to amend pancreatic strictures or stones
  • Pancreatic enzyme supplements – useful for those with steatorrhoa, may reduce frequency of attacks of pain in those with recurrent symptoms
  • If diabetes has occurred – dietary control, oral hypoglycaemics or insulin
331
Q

Complications of chronic pancreatitis?

A
  • Pseudo-cyst (fluid collection surrounded by granulation tissue)
  • Ascites and pleural effusion
  • Pancreatic cancer

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