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2a Medicine > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

What is GORD?

A

Prolonged or recurrent reflux of the gastric contents into the oesophagus.

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2
Q

What is the cause of GORD?

A
  • Obesity
  • Hiatus hernia: LOS sphincter can’t close properly
  • LOS hypotension
  • Loss of oesophageal peristaltic function
  • Overeating
  • Systemic sclerosis.
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3
Q

What are the risk factors for GORD?

A
  • Obesity
  • Male
  • Increased abdominal pressure e.g. pregnancy or obesity
  • Smoking, alcohol
  • Hiatus hernia complication
  • Pregnancy.
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4
Q

What is the pathophysiology of GORD?

A

An increase in transient lower oesophageal sphincter relaxations due to reduced tone of the lower oesophageal sphincter. This results in reflux of gastric acid, pepsin, bile and duodenal contents back into the oesophagus. There is increased mucosal sensitivity to gastric acid. The lower oesophageal sphincter relaxes independently of a swallow, allowing gastric acid etc. to flow back into the oesophagus.

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5
Q

What are the symptoms of GORD?

A
  • Heart burn, related to lying down and meals
  • Odynophagia (painful swallowing)
  • Hoarse throat
  • Wheezing
  • Regurgitation
  • Acidic taste in mouth.
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6
Q

What are the signs of GORD?

A
  • Chest pain aggravated by bending, stooping and lying

* Nocturnal asthma due to aspiration of gastric contents into the lung.

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7
Q

What are the investigations for GORD?

A
  • Usually diagnosed on clinical finding as long as there are no alarm bells e.g. weight loss, haematemesis and dysphagia
  • Oesophago-gastro-duodenoscopy (endoscopy) may show oesophagitis and hiatus hernia
  • Barium swallow
  • 24 hour intraluminal pH monitoring.
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8
Q

What is the management for GORD?

A
  • Lifestyle changes: small regular meals, weight loss, stop smoking
  • Antacids e.g. Gaviscon (magnesium carbonate/magnesium hydroxide)
  • Proton pump inhibitor e.g. Iansoprazole, omeprazole, if severe
  • H2 receptor antagonists e.g. cimetidine, ranitidine
  • Surgery.
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9
Q

What are the complications of GORD?

A
  • Barret’s oesophagus: the epithelium of the oesophagus undergoes metaplasia and changes from squamous to columnar epithelium with goblet cells. This is irreversible. There is a risk of progressing to oesophageal cancer as this is premalignant for adenocarcinoma of oesophagus
  • Peptic stricture: inflammation of the oesophagus resulting from gastric acid exposure which causes narrowing and stricture of the oesophagus. Causes worsening dysphagia.
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10
Q

What is the histological change in Barret’s oesophagus?

A

Metaplasia and changes from squamous to columnar epithelium with goblet cells.

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11
Q

What are peptic ulcers?

A

A break in the epithelial cells which penetrate down to the muscularis mucosa of either the stomach or the duodenum.

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12
Q

What is the most common cause of a peptic ulcer?

A

H.Pylori. 90% of duodenal ulcers and 80% of gastric ulcer.

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13
Q

What type of bacteria is H.Pylori?

A

Gram negative.

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14
Q

What does H. Pylori cause?

A

Gram negative bacteria that lives in the gastric mucus and secretes urease which splits urea in stomach into CO2 + ammonia. Ammonia + H+ makes ammonium. Ammonium, proteases, phospholipases and vacuolating cytotoxic A damages gastric epithelium. This causes inflammatory response reducing mucosal defence and leading to mucosal damage. There is a reduced duodenal bicarbonate production. It also causes acid secretion:
1. Gastrin release from G cells
2. Triggers release of histamine so more acid secretion
3. Increases parietal cells mass so more acid secretion
Decreases somatostatin (released from D cells) so more acid secretion.

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15
Q

What are the causes of peptic ulcer?

A
  • H. Pylori: most common.
  • NSAIDs e.g. aspirin: reduced production of prostaglandins. Mucus secretion stimulated by prostaglandins. COX-1 is needed for prostaglandin synthesis and NSAIDs inhibit COX-1 so mucous isn’t secreted and there is reduced mucosal defense and so mucosal damage.
  • Mucosal ischaemia: stomach cells not supplied with sufficient blood and so cells die off and don’t produce mucin. Gastric acid attacks those cells and so cells die leading to formation of an ulcer. Treat with H2 blocker
  • Increased acid: overwhelms mucosal defence. Acid attacks mucosal cells and so cells die forming an ulcer. Stress and increase acid production. Treat with PPI and H2 blocker
  • Bile reflux: duodeno-gastric reflux. Regurgitated bile strips away mucus layer and so there is reduced mucosal defence.
  • Alcohol.
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16
Q

What are the risk factors for peptic ulcer?

A
  • Elderly

* Developing countries due to H. pylori.

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17
Q

Are duodenal or gastric ulcers more common?

A

Duodenal ulcers are 2-3x more common than gastric ulcers.

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18
Q

How are duodenal ulcers relieved?

A

By eating.

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19
Q

How are gastric ulcers worsened?

A

By eating. Also associated with NSAIDs/aspirin use.

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20
Q

What are peptic ulcers a risk factor for?

A

Gastric cancer due to chronic inflammation.

They account for 50% of all upper GI bleeds.

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21
Q

What is the pathophysiology of peptic ulcers?

A

Depending on the aetiology, a reduction in protective prostaglandins or an increase in gastric acid secretions causes the acidic contents of the stomach/duodenum to break down the mucosa. H Pylori can infect mucosa following this damage so further damage through inflammation and proteases.

Ulcer results in gastritis (inflammation of gastric cells). Usually gastric mucosa is protected by mucin produced by the gastric cells.

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22
Q

What are the symptoms of peptic ulcer?

A 
•	Acquisition usually asymptomatic but can cause nausea, vomiting and fever
•	Burning epigastric pain
•	Bloating
•	Vomiting
•	Haematemesis
•	Dyspepsia
•	Nausea
•	Heartburn
•	Flatulence
•	Occasionally painless haemorrhage.
Duodenal is more pain when the patient is hungry and at night.
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23
Q

What are the signs of peptic ulcer?

A
  • Duodenal ulcer pain often occurs when patient is hungry, eating and classically occurs at night, weight loss
  • Gastric ulcer pain often occurs several hours after meals, weight gain, relieved by eating
  • Anorexia.
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24
Q

What are the investigations for peptic ulcers?

A
  • Endoscopy with biopsy: biopsy urease test e.g. CLO test and histology
  • Stool antigen test for H. pylori
  • Urea breath test
  • Blood test for IgG antibodies, can be positive for a year after treatment.
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25
Q

What is the management for peptic ulcers?

A
  • Lifestyle: reduce smoking, stress and alcohol
  • Stop NSAIDs
  • Antibiotics for H.pylori (remember CAP): clarithromycin, amoxicillin and PPI e.g. omeprazole
  • PPI e.g. lansoprazole and omeprazole
  • H2 antagonists e.g. cimetidine to reduce acid release
  • Surgery for complications.
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26
Q

What medication reduces acid release?

A

H2 antagonists e.g cimetidine.

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27
Q

What are the antibiotics to treat H.Pylori?

A

Remember CAP: clarithromycin, amoxicillin and PPI e.g. omeprazole.

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28
Q

What are the red flags for cancer?

A
  • Unexplained weight los
  • Anaemia
  • Evidence of GI bleeding e.g. melaena or haematemesis
  • Dysphagia
  • Upper abdominal mass
  • Persistent vomiting.
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29
Q

What are the complications of peptic ulcers?

A
  • Upper GI bleed
  • Duodenal ulcers can grow deeper until it hits an artery (most commonly the gastrodueodenal artery) which causes massive haemorrhage and shock
  • Perforation requires immediate surgical consult
  • Obstruction
  • Peritonitis as acid enters the peritoneum
  • Acute pancreatitis if ulcer reaches pancreas.
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30
Q

What is Coeliac disease?

A

State of heightened immunological responsiveness to ingested gluten in genetically susceptible individuals. Ingestion of gluten stimulates the immune system to attack the small intestine.

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31
Q

What is the most common age of presentation for Coeliac disease?

A

Most common age for presentation is 4th to 6th decade. For every paediatric case diagnosed there are 9 adult cases.

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32
Q

What is Coeliac disease associated with?

A

Other autoimmune conditions e.g. type 1 diabetes mellitus and thyrotoxicosis.

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33
Q

What is gluten found in?

A
  • Wheat
  • Barley
  • Rye.
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34
Q

What are the risk factors for Coeliac disease?

A
  • Other autoimmune diseases (type 1 diabetes mellitus, thyroid diseases, Sjogren’s)
  • IgA deficiency
  • Breast feeding
  • Age of introduction to diet
  • Rotavirus infection in infancy increases risk.
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35
Q

What is the pathophysiology of Coeliac disease?

A

A-gliadin is the toxic portion of gluten and is resistant to proteases in the small intestinal lumen. Gliadin binds to secretory IgA in the mucosal membrane. Gliadin IgA is transcytosed to the lamina propria via HLA DQ2 and DQ8. Gliadin binds to tissue transglutaminase (ttG) and is deaminated which increases its immunogenicity. Deaminated gliadin is taken up by macrophages and expressed on MHC II complex. T helper cells release inflammatory cytokines and stimulate B cells. This causes villous atrophy, crypt hyperplasia and intraepithelial lymphocyte infiltration which leads to reduced SA to absorb nutrients. This means B12, folate and iron can not be absorbed which causes anaemia.

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36
Q

What is the classification of Coeliac disease?

A 
Classification using Marsh Classification:
•	0: normal
•	1: raised intra epithelial lymphocytes
•	2: raised IEL + crypt hyperplasia
•	3a: partial villous atrophy
•	3b: subtotal villous atrophy
•	3c: total villous atrophy.
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37
Q

What are the symptoms of Coeliac disease?

A 
Classical:
•	Diarrhoea
•	Steatorrhea (fatty stools due to reduced fat absorption in intestines)
•	Abdominal pain
•	Abdominal distension
•	Weight loss
•	Failure to thrive
•	Nutritional deficiency.
Non-classical:
•	Dermatitis herpetiformis; red raised patches, often with blisters that burst on scratching, commonly seen on elbows, knees and buttocks caused by IgA deposition. Histology shows IgA deposits with accumulations of neutrophils, treated with dapsone
•	IBS symptoms
•	Iron deficiency anaemia
•	Osteoporosis
•	Chronic fatigue
•	Ataxia
•	Peripheral neuropathy
•	Hyposplenism
•	Amenorrhoea
•	Infertility.
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38
Q

What are the investigations in Coeliac disease?

A

Serology:
• Anti-tissue transglutaminase (tTG)
• Anti-endomysial antibody (EMA)
• Anti-gliadin.

Endoscopies with duodenal biopsies:
• Histology: villous atrophy, crypt hyperplasia and intraepithelial lymphocytes
• Reduced folds in duodenum and jejunum, increased folds in ileum
• Scalloping of mucosa
• Biopsies: evidence of villous atrophy.

FBC:
• Low haemoglobin
• Low B12
• Low ferritin.

Autoimmune conditions screening e.g. type 1 diabetes mellitus and autoimmune thyroiditis.

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39
Q

What is the management of Coeliac disease?

A
  • Gluten free diet must be strict and lifelong so no barley, wheat or rye
  • Dietitian review to correct vitamin deficiencies
  • DEXA scan for orthopaedic risk
  • Inform 10% risk in 1st degree relatives.
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40
Q

What are the complications of Coeliac disease?

A
  • T cell lymphoma
  • Osteoporosis
  • Anaemia
  • Infertility
  • Hyposplenism
  • Vitamin deficiency: steatorrhea, night blindness, bruising, osteoporosis.
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41
Q

What is malabsorption?

A

The failures to fully absorb nutrients in the small intestine either because of the destruction to the epithelium or due to a problem in the lumen meaning food cannot be digested.

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42
Q

What disorders of the small intestine resulting in malabsorption?

A
  • Coeliac
  • Tropical sprue
  • Crohn’s
  • Parasitic infection.
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43
Q

What are the causes of malabsorption?

A
  • Insufficient intake consider psychosocial causes
  • Defective intraluminal digestion: pancreatic insufficiency due to pancreatitis and cystic fibrosis, defective bile secretion (lack of fat solubilisation) due to biliary obstruction or ileal resection (decreased bile salt uptake), or bacterial overgrowth
  • Insufficient absorptive area: villi and microvilli produce massive surface area to absorb nutrients. Gluten sensitive enteropathy (Coeliac disease) due to villous atrophy and crypt hyperplasia. Crohn’s typically in the terminal ileum. Extensive surface parasitasion e.g. Giardia Lamblia where parasite eats food, need metronidazole for one week. Small intestinal resection or bypass, are procedures for morbid obesity. Crohn’s disease has coble stone mucosa so can’t absorb anything or may be due to infarcted small bowel
  • Lack of digestive enzymes: disaccharidase deficiency is lactose intolerance or bacterial overgrowth causes brush border damage
  • Defective epithelial transport: abetaliporoteinemia or primary bile acid malabsorption (mutations in bile acid transporter protein)
  • Lymphatic obstruction: lymphoma or TB.
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44
Q

What are the symptoms of malabsorption?

A
  • Weight loss
  • Steatorrhoea
  • Diarrhoea.
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45
Q

What are the signs of malabsorption?

A
  • Anaemia: decreased iron, B12, folate
  • Bleeding disorders: decreased vitamin K
  • Oedema: decreased protein
  • Metabolic bone disease: decreased vitamin D
  • Neurological features..
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46
Q

What are the investigations of malabsorption?

A
  • FBC: increased/decreased MCV, decreased calcium/iron/B12 and folate, and increased INR
  • Stool sample microscopy
  • Coeliac tests.
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47
Q

What is topical sprue?

A

Severe malabsorption of two or more substances accompanied by diarrhoea and malnutrition.

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48
Q

Who does tropical sprue affect?

A

Occurs in residents or visitors to tropical areas where the diseases in endemic, most of Asia, some Caribbean islands, Puerto Rico and parts of South Africa.

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49
Q

What is the pathophysiology of topical sprue?

A

Partial villous atrophy with malabsorption. Onset is acute and occurs either a few days or many years after being in the tropics.

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50
Q

What are the symptoms of topical sprue?

A
  • Diarrhoea

* Anorexia.

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51
Q

What are the signs of topical sprue?

A
  • Weight loss
  • Severe malabsorption
  • Abdominal distension.
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52
Q

What would bloods show in topical sprue?

A

Anaemia due to malabsorption of B12, folate and iron

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53
Q

What would the jejunal biopsy show in topical sprue?

A

Jejunal biopsy: abnormal showing partial villous atrophy.

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54
Q

What is the management for topical sprue?

A
  • Leave region

* Folic acid daily and tetracycline for up to 6 months.

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55
Q

What is inflammatory bowel disease?

A

Inflammation anywhere from the mouth to anus. Causes fibrous cobblestone scarring.

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56
Q

What are the 2 types of inflammatory bowel disease?

A
  • Crohn’s disease: affects any part of the GI tract (mouth to anus)
  • Ulcerative colitis: only affects the colon.
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57
Q

What type of scarring does IBD cause?

A

Cobblestone.

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58
Q

What is the pathophysiology of IBD?

A

Occurs when mucosal immune system exerts an inappropriate response to luminal antigens such as bacteria which may enter the mucosa via a leaky epithelium.

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59
Q

What is Crohn’s?

A

Transmural, granulomatous inflammation affecting any part of the GI tract.

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60
Q

Who does Crohn’s most commonly affect?

A
  • Highest incidence and prevalence in Northern Europe, UK and North America
  • F>M
  • Presents mostly at 20-40.
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61
Q

What are the risk factors for Crohn’s?

A
  • Family history: mutation of NOD2 gene of chromosome 6
  • Smoking
  • Female
  • Chronic stress
  • NSAIDs.
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62
Q

What is the pathophysiology of Crohn’s?

A

Originates in mucosa and works through layers of bowel. Affects any part of the gut from the mouth to the anus (commonly ileum and colon).

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63
Q

What is seen macroscopically in Crohn’s?

A
  • Skip lesions
  • Cobblestone appearance due to ulcers and fissures in mucosa
  • Thickened and narrow.
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64
Q

What is seen microscopically in Crohn’s?

A
  • Transmural: affects all layers of bowel
  • Non-caseating granulomas (aggregations of epithelioid histiocytes)
  • Goblet cells.
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65
Q

What is the immune response in Crohn’s?

A

Effector T cells predominating over regulatory T cells causes pro-inflammatory cytokines IL12, IL5, IL17 and interferon gamma which stimulates macrophages to produce Tumour Necrosis Factor Alpha, IL1 and IL6. Neutrophils, mast cells and eosinophils are also activated. All of this causes a wide variety of inflammatory mediators which causes cell damage.

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66
Q

What are the symptoms of Crohn’s?

A

• Diarrhoea
• Right lower quadrant abdominal pain (ileum)
• Fatigue, fever, nausea, vomiting
• Tenderness
Small bowel:
• Weight loss
• Abdominal pain.
Terminal ileum:
• Right iliac fossa pain mimicking appendicitis.
Colonic:
• Blood and mucus with diarrhoea and pain.

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67
Q

What are the signs of Crohn’s?

A
  • Blood in stool
  • Malabsorption
  • Mouth ulcers
  • Extra-intestinal feature: erythema nodosum, anal fissures, episcleritis.
Remember CHRISTMAS:
C obblestones
H igh temperatures
R educed lumen
I ntestinal fistulae
S kip lesions
T ransmural
M alabsorption
A bdominal pain
S ubmucosal fibrosis.
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68
Q

What is the diagnostic investigation in Crohn’s?

A

Diagnostic.

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69
Q

What are the investigations in Crohn’s?

A
  • Biopsy
  • Barium enema
  • Stool sample to rule out infectious diseases
  • FBC: raised ESR/CRP, often low haemoglobin due to anaemia
  • Faecal calprotectin: indicates IBD but not specific.
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70
Q

How do you distinguish between Crohn’s and UC?

A

Sigmoidoscopy/rectal biopsy.

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71
Q

What is the management of Crohn’s?

A
  • Oral corticosteroids e.g. budesonide and prednisolone, induce remission but don’t prevent relapse
  • IV hydrocortisone in severe flare ups
  • Add anti-TNF antibodies e.g. Infliximab if no improvement. Has a predisposition for TB (night sweats, haemoptysis and weight loss)
  • Consider adding thiopurines (azathioprine, has side effects) or methotrexate to remain in remission if there are frequent exacerbations
  • Surgery: doesn’t cure disease.
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72
Q

What are the complications of Crohn’s?

A

Bowel:
• Malabsorption: disease extent, surgical resection
• Obstruction from strictures: abscesses, acute swelling, chronic fibrosis
• Perforation: acute abdomen
• Fistula formation
• Anal: skin tags, fissure, fistula
• Neoplasia: colorectal cancer.
Systemic: amyloidosis (rare).
May cause short stature in children and osteoporosis.

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73
Q

What is ulcerative colitis?

A

Continuous chronic inflammation of only the colon. Inflammatory condition of the colon mucosa up to the ileocaecal valve (never affects proximally from the IVC). Ulcers form along the lumen of the intestine.

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74
Q

Who does ulcerative colitis most commonly affect?

A
  • Affects males and females equally

* Presents mostly at 15-30.

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75
Q

What are the risk factors for ulcerative colitis?

A
  • Family history
  • NSAIDs: associated with onset of IBD and flares of disease
  • Chronic stress and depression triggers flares
  • Smoking relieves UC.
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76
Q

What relieves ulcerative colitis?

A

Smoking.

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77
Q

What is the pathophysiology of ulcerative colitis?

A

Mucosal inflammation originating in the anus and continuously progressing proximally. No granulomata. Goblet cell depletion and crypt abcesses.
Remains in mucosa and does not go through the full wall of the bowel. Only affects the colon.

Paneth cells are involved in innate immunity and suggest an inflammatory condition when found in the descending colon.

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78
Q

What is seen macroscopically in ulcerative colitis?

A
  • Continuous inflammation (no skip lesions)
  • Ulcers
  • Pseudo-polyps.
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79
Q

What is seen microscopically in ulcerative colitis?

A
  • Mucosal inflammation
  • No granulomata
  • Depleted goblet cells
  • Increased crypt abscesses.
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80
Q

What are the symptoms of ulcerative colitis?

A 
•	Left lower quadrant abdominal pain
•	Fever
•	Diarrhoea with blood and mucus
•	Cramps. 
Extragastrointestinal:
•	Arthralgia
•	Fatty liver
•	Gall stones.
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81
Q

What are the signs of ulcerative colitis?

A
  • Rectal tenesmus: incontinence, urgency, bleeding
  • Tender distended abdomen
  • Clubbing
  • Erythema nodusum.
Remember ULCERATIONS
U lcers
L arge intestine
C arcinoma risk ok
E xtra-intestinal manifestations: uveitis, erythema nodosum, sclerosing cholagnitis
R emnants of older ulcers (psudo polyps)
A bscesses in cryots
T oxic megacolon risk ok
I nflamed, red, granular mucosa
O riginates at rectum
N eutrophil invasion
S tool is bloody and has mucous.
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82
Q

What is the diagnostic investigation for ulcerative colitis?

A

Colonoscopy.

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83
Q

What are the investigations in ulcerative colitis?

A 
Colonoscopy is diagnostic.
Other:
•	Biopsy: crypt abscesses
•	Barium enema
•	Bloods: FBC shows raised ESR and CRP with low haemoglobin, test for pANCA which is negative in Crohn’s, iron deficiency anaemia
•	Faecal calprotectin
•	Stool sample: rule out infectious causes
•	CT/MRI
•	Abdominal X-ray.
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84
Q

What is the management for ulcerative colitis?

A
  • Anti-inflammatory e.g. sulfasalazine or mesalamine (5-aminosalicylic acid) absorbed in small intestine. Gives choice of remission and relapse prevention.
  • Immunosuppressors: corticosteroids, azathioprine
  • Anti-TNF drugs: infliximab
  • Colectomy with ileo-anal anastomosis indicated in patients with severe UC not responding to treatment
  • Surgery indicated for severe colitis that fails to respond to treatment.
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85
Q

What are the complications of ulcerative colitis?

A 
Liver:
•	Fatty change
•	Chronic pericholangitis
•	Sclerosing cholangitis.
Colon:
•	Blood loss
•	Toxic dilation
•	Colorectal cancer.
Skin:
•	Erythema nodosum
•	Pyoderma gangrenosum.
Joints: 
•	Ankylosing spondylitis
•	Arthritis.
Eyes:
•	Iritis
•	Uveitis
•	Episcleritis.
Psychosocial and sexual problems.
Frequent relapse.
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86
Q

What is irritable bowel syndrome?

A

A group of mixed abdominal symptoms for which no organic cause can be found. Relapsing functional bowel disorder associated with a change in bowel habit.

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87
Q

What are the types of irritable bowel syndrome?

A

IBS-C: with constipation
IBS-D: with diarrhoea
IBS-M: with constipation and diarrhoea.

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88
Q

What is the epidemiology of IBS?

A

• Age of onset <40
• F>M
Common in Western world, affects 1 in 5.

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89
Q

What exacerbates the symptoms of IBS?

A

Stress, food, gastroenteritis or menstruation.

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90
Q

What are the causes of IBS?

A
  • Psychosocial: stress, depression, anxiety
  • Psychological stress and trauma
  • GI infection gastroenteritis
  • Sexual, physical or verbal abuse
  • Eating disorders.
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91
Q

What is the pathophysiology of IBS?

A

Dysfunction in the brain-gut axis results in disorder of intestinal mobility and/or enhances visceral sensitivity. Recurrent abdominal pain with no inflammation.

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92
Q

What are the symptoms of IBS?

A
  • Abdominal pain relieved by defecating or passing of wind
  • Bloating
  • Alternating bowel habits
  • Constipation
  • Diarrhoea
  • Sensation of incomplete evacuation (tenesmus).
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93
Q

What are the signs of IBS?

A
  • Mucus in stools
  • Change in stool frequency
  • Change in stool consistency
  • Sensation of incomplete emptying
  • Urgency
  • Worsening symptoms after food.
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94
Q

How is a diagnosis of IBS made?

A

Since there is nothing physical to be found, diagnosis is made by ruling out differentials:
• FBC: anaemia
• ESR and CRP: inflammation
• Coeliac serology for EMA and tTG: if either positive then high chance of coeliac
• Faecal calprotecting: raised in IBD
• Colonoscopy: to rule out IBD or colorectal cancer.

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95
Q

What is the management for IBS?

A

• Lifestyle modification: fluids, avoid caffeinated drinks, alcohol and fizzy drinks, fibre (in wind and bloating not diarrhoea and bloating)
• Treat symptoms:
Pain and bloating: buscopan
Constipation: laxative e.g. senna, less fibre
Diarrhoea: anti-motility e.g. loperamide, more fibre
• If none of the above work, amitriptyline.

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96
Q

What is colorectal cancer?

A

Cancer in the bowel.

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97
Q

What is the most common type of colorectal cancer?

A

Adenocarcinoma.

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98
Q

Where do the majority of colorectal cancers occur?

A
  • Majority occur in distal colon. The more distal the cancer, the more visible the blood and mucus will be
  • Most are left side.
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99
Q

What are the risk factors for colorectal cancer?

A
  • Increasing age
  • Family history
  • Genetic predisposition:
  • Familial adenomatous polyposis: apc bound to GSK. Beta catenin binds apc complex in high levels of apc. In mutations, apc protein misfolded so can’t bind to beta catenin. Beta catenin able to move into nucleus so endothelial proliferation and adenoma
  • Hereditary non-polyposis colorectal cancer: normally two DNA protein repair genes. Some individuals born with just one which leaves them susceptible
  • Colorectal
  • Ulcerative.
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100
Q

What is the Duke staging of colorectal cancer?

A

A. 95% 5 year survival, limited to muscularis mucosae
B. 75% 5 year survival, traverses bowel lining and into submucosa (not lymph)
C. 35% 5 year survival, involvement of regional lymph nodes
D. 25% 5 year survival, metastases.

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101
Q

What has a 100% lifetime risk of colorectal cancer?

A

Familial adenomatous polyposis: APC gene causes >100 polyps to develop in teenage years.

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102
Q

What is the staging and prognosis of colorectal cancer?

A

Staging and prognosis:
• R0: tumour completely excised locally
• R1: microscopic involvement of margin by tumour
• R2: macroscopic involvement of margin by tumour.

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103
Q

What is the pathophysiology of colorectal cancer?

A

Progression from normal epithelium (prevention) to adenoma (endoscopic resection) to colorectal adenocarcinoma (surgical resection) to metastatic colorectal adenocarcinoma (chemotherapy, palliative care).

Adenomatous polyps develop over time, and can become malignant through activation of oncogenes and inactivation of tumour suppressor genes. The greater the number of polyps, the greater the chance of malignancy.
Polypoid mass with ulceration. Spreads by direct infiltration through the bowel wall then spread to lymphatic and blood vessels and metastasise to liver and lung.

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104
Q

What are the symptoms of colorectal cancer?

A

Right-sided carcinoma:
• Usually asymptomatic until they present with iron deficiency anaemia due to bleeding
• May present with a mass in right iliac fossa
• Weight loss
• Abdominal pain.

Left sided and sigmoid carcinoma:
• Change in bowel habit with blood and mucus in stools
• Diarrhoea
• Alternation constipation and diarrhoea.

Rectal carcinoma:
• Rectal bleeding and mucus
• When cancer grows, it will have thinner stools and tenesmus (cramping rectal pain).

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105
Q

What are the emergency signs of obstruction in colorectal cancer?

A
  • Absolute constipation
  • Colicky abdominal pain
  • Abdominal distension
  • Vomiting (faeculent).
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106
Q

What is the gold standard investigation for colorectal cancer?

A

Colonoscopy.

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107
Q

Other than colonoscopy, what are the investigations for colorectal cancer?

A
  • Digital rectal exam: 38% of colorectal cancers are detected
  • Double contrast barium enema.
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108
Q

What are the differential diagnoses for colorectal cancer?

A 
Anorectal pathology:
•	Haemorrhoids
•	Anal fissure
•	Anal prolapse.
Colonic pathology:
•	Diverticular disease
•	IBD
•	Ischaemic colitis.
Small intestine and stomach pathology:
•	Massive upper GI bleed (haematochezia)
•	Meckel’s diverticulum.
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109
Q

What is the management of colorectal cancer?

A
  • Surgery ideally with end to end anastomosis
  • Endoscopic stenting
  • Radiotherapy
  • Adjuvant chemotherapy.
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110
Q

Where does colorectal cancer often metastasise too?

A

Liver and lungs.

111
Q

What cancer is in the middle and upper third of the oesophagus?

A

Squamous cell carcinoma occurs in middle third (40%) and upper third (15%) of the oesophagus.

112
Q

What cancer is in the lower third of the oesophagus?

A

Adenocarcinomas occur in the lower third of oesophagus and cardia of stomach and account for the majority of oesophageal tumours (45%).

113
Q

What are the causes of oesophageal squamous cell carcinomas?

A
  • High levels of alcohol consumption
  • Achalasia: disorder where oesophagus has reduced/no ability to do peristalsis and transport food down
  • Tobacco use
  • Obesity: since this increases reflux
  • Smoking
  • Low fruit and veg consumption.
114
Q

What are the causes of adenocarcinoma of the oesophagus?

A
  • Barret’s oesophagus
  • GORD
  • Smoking
  • Obesity.
115
Q

What are the risk factors for oesophageal cancer?

A

Oesophageal squamous cancer: smoking, alcohol.
Oseophageal adenocarcinoma: obesity.
Achalasia.
Barrett’s oesophagus.

116
Q

What is the pathophysiology of oesophagus cancer?

A

Oesophagus is lined by squamous epithelium. Stomach is lined by columnar glandular epithelium. Oesophageal epithelium undergoes metaplasia to stomach epithelium.

117
Q

What are the symptoms of oesophageal cancer?

A
  • Early has no symptoms
  • Pain due to impaction of food or infiltration of cancer into adjacent structures
  • Dysphagia: difficulty swallowing solids at first then fluids. If there is dysphagia to solids and liquids from the start then this indicated benign disease.
118
Q

What are the signs of oesophageal cancer?

A
  • Majority have no physical signs (detectable when advanced)
  • Lymphadenopathy
  • Anorexia
  • Weight loss.
119
Q

What are the investigations in oesophageal cancer?

A
  • Oesophagoscopy with biopsy
  • Barium swallow to see strictures
  • CT/MRI/PET for tumour staging.
120
Q

What is the management for oesophageal cancer?

A
  • Surgical resection. Considerations include: is the patient medically fit, severity of cancer, is it resectable?
  • Chemotherapy +/- radiotherapy
  • Palliative care.
121
Q

What are the types of benign oesophageal tumours?

A
  • Leiomyomas most common
  • Papillomas
  • Fibrovasular polyps
  • Haemangiomas
  • Lipomas.
122
Q

What is the pathophysiology of benign oesophageal tumours?

A

Leiomyomas are smooth muscle tumours arising from oesophageal wall. They are intact, well encapsulated and are within overlying mucosa. They are slow growing.

123
Q

What are the symptoms of benign oesophageal tumours?

A
  • Usually asymptomatic: usually found incidentally on barium swallowing
  • Dysphagia
  • Retrosternal pain
  • Food regurgitations
  • Recurrent chest infections.
124
Q

What are the investigations for benign oesophageal tumours?

A
  • Endoscopy
  • Barium swallowing
  • Biopsy.
125
Q

What is the management for benign oesophageal tumours?

A
  • Endoscopic removal

* Surgical of larger tumours.

126
Q

What is the most common type of small intestine cancer?

A

Adenocarcinoma.

127
Q

What are the risk factors for small intestine cancer?

A
  • Family history
  • Coeliac disease
  • Crohn’s disease.
128
Q

What are the symptoms of small intestine cancer?

A

Abdominal pain, diarrhoea and weight loss.

129
Q

What are the signs of small intestine cancer?

A
  • Anorexia
  • Anaemia
  • Palpable mass.
130
Q

What are the investigations for small intestine cancer?

A
  • Ultrasound
  • Endoscopic biopsy
  • CT/MRI scan.
131
Q

What is the management for small intestine cancer?

A
  • Surgical resection

* Radiotherapy.

132
Q

What are the causes of gastric cancer?

A
  • Smoking

* H. Pylori increases risk at population level. Increases risk of peptic ulcers which leads to gastric cancer.

133
Q

What are the symptoms of gastric cancer?

A
  • Epigastric pain: constant and severe
  • Vomiting, nausea and anorexia
  • Weight loss
  • Dysphagia if tumour is found in fundus
  • Anaemia from occult blood loss
  • Liver metastasis leads to jaundice.
134
Q

What are the signs of gastric cancer?

A
  • Hepatomegaly
  • Epigastric mass
  • Jaundice
  • Troisier’s sign (enlarged left supraclavicular node (Virchow’s node)).
135
Q

What are the investigations for gastric cancer?

A
  • Gastroscopy with biopsy
  • Endoscopic ultrasound
  • CT/MRI to stage
  • PET scan.
136
Q

What is the management for gastric cancer?

A
  • Nutritional support

* Gastroectomy partial or total and combination chemotherapy.

137
Q

What is appendicitis?

A

Inflammation of the appendix. Should be considered for all right sided pain if appendix has not already been removed.

138
Q

Where are the appendix?

A

Located at McBurney’s point which lies 2/3 of the way from the umbilicus to the anterior superior iliac spine.

139
Q

What are the causes of appendicitis?

A

Obstruction:
• Faecolith: stones made of faeces which obstructs the lumen of the appendix
• Filarial warms
• Undigested seeds
• Lymphoid hyperplasia: can obstruct tube and lymphoid follicles can grow during viral infection
• Bacteria: campylobacter jejuni, Yersinia, salmonella, bacillus cereus.

140
Q

What is the pathophysyiology of appendicitis?

A

Occurs when the lumen of the appendix becomes obstructed. Intestinal lumen (including appendix) is always producing mucus and fluids to prevent pathogens from entering the blood stream and keep the tissue moist. When the appendix is obstructed, fluid and mucus build up increasing the pressure in the appendix causing it to expand and press on the afferent visceral nerve fibres nearby which causes the abdominal pain. Bacteria is now trapped and able to multiple resulting in invasion of gut organisms into the appendix wall which becomes inflamed and infected. This is liable to rupture, letting infected and faecal matter into the peritoneal cavity which can cause life threatening peritonitis. Alternatively can form an appendix abscess where the omentum localises the infection which presents as a tender mass. This leads to oedema, ischaemia, necrosis, perforation and inflammation.

141
Q

What are the symptoms of appendicitis?

A
  • Acute pain in umbilicus/RIF: may originate in umbilical region then progress to RIF
  • Nausea
  • Vomiting
  • Fever.
142
Q

What are the signs of appendicitis?

A
  • Tender mass in RIF with guarding
  • Guarding
  • Rebound tenderness with palpation
  • Pyrexia.
143
Q

What is the gold standard investigation for appendicitis.

A

CT abdomen.

144
Q

What are the investigations in appendicitis?

A

CT abdomen is gold standard.
• Bloods: FBC raised white blood cell count, elevated CRP and ESR
• Ultrasound: especially in women and children
• Pregnancy test
• Urinalysis.

145
Q

What is the management for appendicitis?

A
  • Laparoscopic appendectomy
  • Appendix mass can be treated with IV fluids ans antibiotics.
  • Drainage of appendix abscesses.
146
Q

What are the complications of appendicitis?

A
  • If the appendix ruptures, infected and faecal matter will enter the peritoneum resulting in life threatening peritonitis with rebound tenderness
  • Appendix abscesses: can be on appendix or subphrenic (under diaphragm).
147
Q

What is gastritis?

A

Inflammation of the stomach lining that is associated with mucosal injury.

148
Q

What causes pernicious (B12 deficiency) anaemia?

A

Autoimmune atrophic gastritis.

149
Q

What are the causes of gastritis?

A
  • H. Pylori infection: most common
  • Autoimmune gastritis: the cause of pernicious anaemia associated with antibodies to gastric parietal cells and IF
  • Viruses e.g. CMV and HSV
  • Duodenogastric reflux: whereby bile salts enter stomach and damage mucin protection resulting in gastritis
  • Crohn’s disease
  • Mucosal ischaemia
  • Increased acid
  • Aspirin and NSAIDs e.g. naproxen
  • Alcohol.
150
Q

What is the pathophysiology of H.Pylori gastritis?

A
  • Lives in gastric mucus
  • Secretes urease which splits urea in stomach into CO2 + ammonia
  • Ammonia + H makes ammonium
  • Ammonium, proteases, phospholipases and vacuolating cytotoxin A damages gastric epithelium
  • Causes inflammatory response reducing mucosal defense
  • Also causes increased acid secretion: Gastrin release (from G cells) so more acid secretion. Triggers release of histamine so more acid secretion. Increases parietal cells mass so more acid secretion. Decreases somatostatin (released from D cells) so more acid secretion.
151
Q

What is the pathophysiology of autoimmune gastritis?

A

ffects the fundus and body of the stomach so atrophic gastritis and loss of parietal cells with IF deficiency resulting in pernicious anaemia (low RBCs due to low B12).

152
Q

What is the pathophysiology of aspirin and NSAID gastritis?

A

Aspirin and NSAIDs e.g. naproxen: inhibits prostaglandins (which stimulate mucus production) via the inhibition of cyclo-oxygenase resulting in less mucus production and therefore gastritis.

153
Q

What are the symptoms of gastritis?

A
  • Epigastric pain
  • Nausea or recurrent upset stomach
  • Vomiting
  • Indigestion.
154
Q

What are the signs of gastritis?

A
  • Loss of appetite
  • Abdominal bloating
  • Haematemesis.
155
Q

What are the investigations for gastritis?

A
  • Endoscopy
  • Biopsy and histology
  • H. Pylori urea breath test
  • H. Pylori stool antigen test.
156
Q

What is the management for gastritis?

A 
CAP:
•	Clarithromycin
•	Amoxicillin
•	PPI e.g. omeprazole.
H2 antagonists e.g. ranitidine or cimetidine reduce acid release.
157
Q

What is the prevention of gastritis?

A

Prevention: give PPIs alongside NSAIDs as this also prevents bleeding from acute stress ulcers and gastritis often seen with ill patients (especially burn patients).

158
Q

What is diarrhoea?

A

Abnormal passage of loose or liquid stool more than 3 times daily.

159
Q

What are the types of diarrhoea?

A

Acute: lasts less than 2 weeks.
Persistent: lasts 2-4 weeks.
Chronic: lasts longer than 4 weeks.

Water: non-inflammatory (enterotoxin or superficial adherence/invasion). Location is in the proximal small bowel.
Bloody, mucoid: inflammatory (invasion/cytotoxin). Location is in the colon.

160
Q

What are the causes of diarrhoea?

A

Viral: most cases caused by viruses e.g. rota/norovirus.

Bacterial:
•	Campylobacter
•	Shigella
•	Salmonella
•	C.perfringens
•	S.aureus
•	B.cereus
•	E.coli
•	C.diff
•	Parasites (e.g. giardia, crypto).

Children: rotavirus.

Adults: norovirus, campylobacter.

Antibiotics: these can give rises to antibiotic induced C. Diff diarrhoea. Rule of C’s:
• Clindamycin
• Ciprofloxacin (quinolones)
• Co-amoxiclav (penicillins)
• Cephalosporins (particularly 2nd and 3rd generation).

Infective:
• Intraluminal infection
• Systemic infections e.g. sepsis, malaria.

Non-infective:
•	Cancer
•	Chemical e.g. poisoning, sweeteners, side effects
•	IBS/malabsorption
•	Endocrine e.g. T4
•	Radiation.
Causes of watery: 
Bacterial:
•	Vibrio cholerae
•	E. coli (ETEC)
•	Clostridium perfringens
•	Bacillus cereus
•	S. Aureus.
Viral:
•	Rotavirus
•	Norovirus.
Parasitic:
•	Giardia
•	Cryptosporidium. 
Causes of bloody, mucoid diarrhoea:
Bacterial:
•	Shigella
•	E.coli (EIEC, EHEC)
•	Salmonella enteridis
•	V. parahaemolyticus
•	C. diff
•	C. jejuni.
Parasitic:
•	Entamoeba histolytica.
161
Q

What are the risk factors for diarrhoea?

A

Immunosuppressed: particularly to cryptosporidium, mycobacteria, microsporidia, CMV, HSV.

162
Q

What is the history for diarrhoea?

A
  • Onset/duration: acute (viral/bacterial), chronic (parasites and non-infectious)
  • Family History
  • Characteristics of stool: floating (fat content, malabsorption/coeliac), blood or mucus (inflammatory, invasive infection, cancer), watery small bowel infection
  • Food/drink: dodgy takeaways (food poisoning), meat/BBQs (campylobacter), poultry (salmonella)
  • Travel: no cholera in UK, foreign travel, very common and self-limiting
  • Immunocompromised e.g. HIV, diabetes, chemo, transplant, steroids (crypto, CMV etc.)
  • Unwell contacts: more likely to be infective
  • Fresh water/swimming: cryptosporidian, giardia
  • Animals: reptiles (salmonella), puppies (campylobacter)
  • Medications: recent antibiotics, C diff. or side effects
  • Any neuro signs: Clostridium botunilum (descending weakness), C. jejuni causes GBS 1-3 weeks after diarrhoeal episode (ascending weakness).
163
Q

What are the stool tests done in diarrhoea?

A
  • Stool culture
  • Faecal calprotectin
  • Faecal occult blood
  • Microscopy
  • Ova, cysts and parasites
  • Toxin detection.
164
Q

What are the blood tests in diarrhoea?

A
  • FBC
  • Inflammatory markers (FBC/CRP)
  • Blood culture.
165
Q

What are the causes of infective diarrhoea?

A
  • Enterotoxigenic e.coli (30-70%)
  • Campylobacter (5-20%)
  • Shigella (5-20%)
  • Non-typhoidal Salmonella (5%)
  • V.parahaemolyticus (shellfish)
  • Viral (10-20%)
  • Cholera
  • Vibrio cholerae
  • Contaminated food/water
  • Cholera toxin
  • Profuse watery “rice water” diarrhoea 🡪 up to 20L a day
  • Vomiting
  • Rapid dehydration
  • Doxycycline and fluids
  • Parasites
  • Protozoal (5-10% more chronic)
  • Cyrpto
  • Giardia
  • Entamoeba
  • Worms
  • Schistosomiasis
  • Strongyloides
  • C Diff.
  • Many are asymptomatic but can become a problem if the normal gut flora is altered, most notably is due to broad spectrum antibiotics
  • Altered gut flora can also occur due to acid reducing drugs such as PPIs, NG feeding and immunocompromise.
166
Q

What are the risk factors for infective diarrhoea?

A
  • Foreign travel
  • PPI or H2 antagonist use
  • Crowded area
  • Poor hygiene.
167
Q

What are the symptoms for diarrhoea?

A
  • Recurrent diarrhoea
  • Vomiting and nausea
  • Fever
  • Fatigue
  • Muscle pain
  • Steatorrhea.
168
Q

What are the diarrhoea red flags?

A
  • Dehydration
  • Electrolyte imbalance
  • Renal failure
  • Immunocompromise
  • Severe abdominal pain.
169
Q

What are cancer risk factors?

A
  • Over 50
  • Chronic diarrhoea
  • Weight loss
  • Blood in stool
  • FH cancer.
170
Q

What is needed for a diagnosis of infective diarrhoea?

A 
3 or more unformed stools per day plus one of the following:
•	Abdominal pain
•	Cramps
•	Nausea
•	Vomiting
•	Dysentery.
171
Q

What does blood in diarrhoea suggest?

A

Bacteria: E. Coli and Shigella ALL cause bloody stools.

172
Q

What are the investigations in infective diarrhoea?

A
  • Stool sample

* If chronic, sigmoidoscopy and bloods.

173
Q

What is the management for infective diarrhoea?

A
  • Rehydration
  • Antibiotics: metronidazole or oral vancomycin
  • Barrier nursing: side room, gloves and apron
  • Fluids + electrolytes monitoring and replacement
  • E.g. oral rehydration sachets
  • IV replacement
  • Antiemetics: treat vomiting e.g. metoclopramide
  • Antimotility agents (not in inflammatory diarrhoea).
174
Q

What is an intestinal obstruction?

A

Arrest/blockage of onward propulsion of intestinal contents.

175
Q

How are intestinal obstructions classified?

A

Classification:
According to site: large bowel/small bowel/gastric.
Extent of luminal obstruction: partial/complete.
According to mechanism:
• Mechanical/true (intraluminal/extraluminal)
• Paralytic (pseudo obstruction): failure of peristalsis but no mechanical obstruction. Caused by drugs, post op, trauma, intra-abdominal abscess. Unknown mechanism but thought to be neural increased SNS discharge, toxins and metabolic distension. A sign is usually painless distension
According to pathology: simple, closed loop, strangulation, intussusception.

176
Q

What is a pseudo obstruction?

A

Failure of peristalsis but no mechanical obstruction.
Caused by drugs, post op, trauma, intra-abdominal abscess.
Unknown mechanism but thought to be neural increased SNS discharge, toxins and metabolic distension.
A sign is usually painless distension.

177
Q

What are the mortality rates for pseudo obstruction?

A
  • Untreated strangulated obstruction: 100%
  • Strangulated small bowel treated >36 hours: 25%
  • Strangulated small bowel treated <36 hours: 8%
  • Mechanical large bowel obstruction 20% and if perforated 40%
  • Non-mechanical (pseudo) obstruction: 15-30%.
178
Q

What are the causes for intestinal obstruction?

A
  • Crohn’s
  • Adhesions
  • Malignancy
  • Diverticulitis
  • Volvulus
  • Hernias
  • Hirschsprung’s disease.
179
Q

How does diverticulitis cause intestinal obstruction?

A

Outpouchings in the sigmoid. Usually occurs in sigmoid colon. Diverticular pouchings form at gaps in the wall of the gut where blood vessels penetrate. In a low fibre diet, the colon must push harder to move things along (fibre helps gut motility) so pressure increases. This can get inflamed or burst resulting in acute peritonitis and death

180
Q

How do NSAIDs cause intestinal obstruction?

A

Repeated ulceration then fibrosis.

181
Q

How does Hirschsprung’s disease cause intestinal obstruction?

A

Developmental abnormality where neonates born without complete innervation of colon to rectum. Dilated upper bowel. Ganglionic segment at sigmoid responsible for contraction of bowel. Aganglionic segments can’t contract so bowel obstruction.

182
Q

How does volvulus cause intestinal obstruction?

A

Sigmoid colon has a “floppy” mesentery. Sigmoid colon can twist. Causes obstruction of the sigmoid. If there is ischaemia and infarction, sigmoid colon is resected.

183
Q

How do adhesions cause intestinal obstruction?

A

Fibrosis after surgery. Fibrous connections between loops of small bowel so bowel becomes kinked. Corrected surgically

184
Q

What are the symptoms of intestinal obstruction?

A
  • Anorexia
  • Nausea
  • Vomiting: forceful, regurgitation, containing bile, faeculant (can occur in small bowl, brewing for a long time) and coffee ground/altered blood
  • Abdominal pain (mechanical)
  • Distension/swelling: more proximal means less distension, smaller the loop, the lesser the swelling initially and swelling could be a hernia which could lead to obstruction
  • Altered bowel habits: constipation (not moving bowels, can pass wind) or obstipation (can’t pass faeces or wind).
185
Q

What are the signs of intestinal obstruction?

A
  • Tinkling bowel sounds

* Tympanic percussion.

186
Q

Is large or small bowel obstruction more common?

A

Small bowel accounts for 60-75% of intestinal obstruction.

Large bowel accounts for 25% of all intestinal obstruction.

187
Q

What are the causes of small bowel obstruction?

A

Adhesions:
• Usually secondary to abdominal surgery
• Increased incidence in pelvic surgery, gynae surgery and colorectal surgery
• Can occur as early as 3-4 weeks but usually takes a few years.
Hernia: abnormal protrusion of an organ or tissue out of the body cavity in which it normally lies. Untreated it can result in strangulation.
Malignancy.
Crohn’s.

188
Q

What can untreated obstruction lead to?

A
  • Ischaemia
  • Necrosis
  • Perforation.
189
Q

What is the most common type of small bowel obstruction?

A

• Mechanical obstruction is most common e.g. adhesions, hernia and Crohn’s.

190
Q

What is the pathophysiology of small bowel obstruction?

A

Obstruction of the bowel leads to bowel distension above the block with increased secretion of fluid into the distended bowel. Also leads to proximal dilatation resulting in:
• Increased secretions and swallowed air in small bowel
• More dilatation leads to decreased absorption and mucosal wall oedema
• Increased pressure with intramural vessels becoming compressed so ischaemia and/or perforation.

191
Q

What are the symptoms of small bowel obstruction?

A
  • Pain: initially colicky (starts and stops then diffuse). Is higher in the abdomen than in large bowel obstruction
  • Vomiting following pain: occurs earlier in small bowel obstruction compared to large bowel obstruction
  • Nausea
  • Anorexia.
192
Q

What are the signs of small bowel obstruction?

A
  • Obstipation: constipation with no passage of wind
  • Increased bowel sounds
  • Tympanic percussion
  • Tenderness: suggests strangulation
  • Less distension as compared to large bowel (since more distal the obstruction, the greater the distension).
193
Q

What are the investigations for small bowel obstruction?

A
  • Abdominal X-ray: shows central gas shadow that completely cross the lumen and no gas in large bowel
  • Abdominal CT
  • FBC.
194
Q

What is the management for small bowel obstruction?

A
  • Aggressive fluid resuscitation
  • Bowel decompression
  • Analgesia and anti-emetic
  • Antibiotics
  • Surgery.
195
Q

What are the causes of large bowel obstruction?

A
  • Colorectal malignancy is the most common

* Volvulus (loop of the intestine twists around itself).

196
Q

What is the pathophysiology of colonic volvulus?

A
  • Axis rotation based off mesentery and a 360˚ twist so closed loop obstruction
  • Fluid and electrolytes shift into closed loops so increased pressure and tension in the loop causing impaired colonic blood flow
  • Leads to ischaemia, necrosis and perforation of loop of bowel if untreated.
197
Q

What is the pathophysiology of large bowel obstruction?

A
  • Colon proximal to obstruction dilates
  • Increased colonic pressure and decreased mesenteric blood flow so mucosal oedema (transudation of fluid and electrolytes from lumen)
  • This can compromise the arterial blood supply and also cause mucosal ulceration so full thickness necrosis and perforation.
198
Q

What are the symptoms of large bowel obstruction?

A

Large bowel has a larger lumen as well as circular and longitudinal muscles so the ability of the large bowel to distend is much greater. The symptoms present slower and later than in small bowel obstruction. Presentation is on average 5 days of symptoms.

  • Abdominal pain: more constant than in SBO
  • Vomiting: more faecal like.
199
Q

What are the signs of large bowel obstruction?

A
  • Abdominal distension
  • Palpable mass: hernia, distended bowel loop or caecum
  • Constipation
  • Fullness/bloating.
200
Q

What are the investigations for large bowel obstruction?

A
  • Abdominal X-ray: peripheral gas shadows proximal to the blockage
  • DRE: empty rectum, hard stools and blood
  • FBC: low Hb (sign of chronic occult blood loss)
  • CT/MRI.
201
Q

What is the management of large bowel obstruction?

A
  • Aggressive fluid resuscitation
  • Bowel decompression
  • Analgesia and anti-emetic
  • Antibiotics
  • Surgery.
202
Q

What are diverticular?

A

Pouches of mucosa extrude through the colonic muscular wall to form diverticular.

203
Q

What percentage of people above the age of 50 have diverticulitis?

A

50%.

204
Q

What is the cause of diverticulitis?

A

Related to a low fibre diet causes increased intracolonic pressure and herniation at sites of weakness.

205
Q

What is the pathophysiology of diverticulitis?

A

Herniation of mucosa through weakened muscular walls near blood vessels. Can lead to perforation, fistula formation with bladder or vagina or intestinal obstruction.

206
Q

What is diverticulosis?

A

The presence of diverticula.

207
Q

What is diverticulitis?

A

Inflammation, which occurs when faeces obstruct the neck of the diverticulum.

208
Q

What are the symptoms of diverticulitis?

A

Asymptomatic in 95% of cases.
Symptoms that do occur relate to luminal narrowing:
• Pain
• Constipation
• Bleeding
• Diverticulitis.
In severe cases: left iliac fossa pain, fever and nausea.

209
Q

What are the investigations for diverticulitis?

A

CT scan. Possible ultrasound.

210
Q

What is the management for diverticulitis?

A

Antibiotics.

Rarely surgery for frequent attacks or complications.

211
Q

What are the complications of diverticulitis?

A

Perforation, fistula, formation with bladder or vagina, intestinal obstruction.
Bleeding can be massive.

212
Q

What are the causes of ischaemic colitis?

A
  • Atherosclerosis
  • Thrombosis
  • Emboli
  • Decreased CO and arrhythmias
  • Vasculitis.
213
Q

What are the risk factors for ischaemic colitis?

A
  • Contraceptive pill
  • Vasculitis
  • Thrombophilia.
214
Q

What artery is occluded in ischaemic colitis?

A

Occlusion of a branch of the superior mesenteric artery or inferior mesenteric artery.
Results in a watershed area of the colon, most commonly at the splenic flexure.

215
Q

Where is pain felt in ischaemic colitis?

A

Left lower quadrant.

216
Q

Where does ischaemic colitis most commonly occur?

A

At the splenic flexure.

217
Q

What is the sign for ischaemic colitis?

A

Bloody diarrhoea.

218
Q

What are the investigations for ischaemic colitis?

A
  • CT/MRI angiography
  • Stool analysis
  • Ultrasound and abdominal CT
  • Colonoscopy and biopsy are gold standard, done after attack.
219
Q

What is the gold standard investigation for ischaemic colitis?

A

Colonoscopy and biopsy.

220
Q

What is the management for ischaemic colitis?

A
  • Symptomatic management
  • Fluid replacement
  • Antibiotics to reduce infection risks due to translocation of bacteria across possible dying gut wall
  • Surgery for gangrene, perforation or stricture.
221
Q

Where does acute mesenteric ischameic almost always involve?

A

Small bowel.

222
Q

Which artery is most commonly occluded in acute mesenteric ischaemia?

A
  • Superior mesenteric artery thrombosis is most common
  • Superior mesenteric artery embolism (e.g. due to AF)
  • Mesenteric vein thrombosis is common in younger patients with hypercoagulable states.
223
Q

What is the triad of symptoms in mesenteric ischaemia?

A
  • Acute severe abdominal pain
  • No abdominal signs
  • Rapid hypovolaemia resulting in shock: pale skin, weak rapid pulse, reduce urine output, confusion.
224
Q

What is the diagnostic investigation for acute mesenteric ischaemia?

A

Laparotomy.

225
Q

What do bloods show in acute mesenteric ischaemia?

A

Metabolic acidosis and high lactate.

226
Q

What is the management of acute mesenteric ischaemia?

A
  • Surgery to remove dead bowel
  • Fluid resuscitation
  • Antibiotics: IV gentamicin and IV metronidazole
  • IV heparin to reduce clotting.
227
Q

What is a Mallory-Weiss tear?

A

Linear mucosal tear occurring at the oesophagogastric junction and produced by a sudden increase in intra-abdominal pressure.

228
Q

What are the risk factors for a Mallory-Weiss tear?

A
  • Alcoholism
  • Forceful vomiting
  • Eating disorders
  • Male
  • NSAID abuse.
229
Q

What is the pathophysiology of a Mallory-Weiss tear?

A

Vomiting, coughing, retching etc. increases intra-abdominal pressure which forces stomach contents into the oesophagus, dilating it and causing a tear.

230
Q

What are the symptoms of a Mallory-Weiss tear?

A
  • Vomiting
  • Abdominal pain
  • Haematemesis
  • Retching
  • Postural hypotension
  • Dizziness
  • Melena.
231
Q

What is the investigation for a Mallory-Weiss tear?

A

Endoscopy.

232
Q

What is the management of a Mallory-Weiss tear?

A
  • Most bleeds are minor and heal in 24 hours

* Surgery for repair of tear.

233
Q

What is dyspepsia?

A

One of the following:
• Postprandial (after eating) fullness
• Early satiation
• Epigastric pain or burning for more than 4 weeks.

Inexact term to describe a number of upper abdominal symptoms e.g. heart burn, acidity, epigastric pain, fullness. Indigestion may be used to describe symptoms.

234
Q

How common is dyspepsia?

A

Common, affecting up to 25% of population a year.

235
Q

What are the causes of dyspepsia?

A
  • GI tract disorders

* Peptic ulcers.

236
Q

What are the symptoms of dyspepsia?

A
  • Reflux when lying flat
  • Heartburn
  • Acid taste due to reflux
  • Bloating
  • Indigestion.
237
Q

What is the management for dyspepsia?

A
  • Reassurance

* Dietary review.

238
Q

What are haemorrhoids (piles)?

A

Enlarged vascular mucosal cushions in the anal canal.

239
Q

What are the 2 types of piles?

A

Internal: above dentate line.
External: below dentate line.

240
Q

What are the risk factors for haemorrhoids (piles)?

A
  • Constipation
  • Prolonged straining
  • Increases abdominal pressure (ascites)
  • Heavy lifting.
241
Q

What are the symptoms of internal haemorrhoids (piles)?

A
  • Painless unless strangulated (upper anal canal has no nerve fibres). Strangulated means the blood supply to the haemorrhoid has been cut off
  • 1st degree: does not prolapse
  • 2nd degree: prolapse on straining, spontaneous reduction
  • 3rd degree: prolapse on straining, manual reduction
  • 4th degree: permanently prolapse, no reduction.
242
Q

What are the symptoms of external haemorrhoids (piles)?

A
  • Painful and itchy
  • Visible on external examination
  • Can coexist with the above.
243
Q

What is the pathophysiology of haemorrhoids (piles)?

A

Vascular mucosal cushions function to maintain anal continence. When they enlarge, the vessels are brought closer to abrasion and can bleed into the anus.

244
Q

What are the investigations for haemorrhoids (piles)?

A

DRE: internal won’t be palpable

Proctoscopy.

245
Q

What is the management for haemorrhoids (piles)?

A

Increase fluid and fibre.
Pain relief.
Intervention: rubber band ligation (tie a band around it and necrotise it).
Surgical haemorrhoidectomy.

246
Q

What is a complication of haemorrhoids (piles)?

A

Skin tags.

If internal strangulated can cause ischaemia and then gangrene.

247
Q

What is an anorectal abscess?

A

Collection of pus in the anal or rectal region.

248
Q

What are the causes of an anorectal abscess?

A

Infection of an anal fissure.

249
Q

What are the risk factors for an anorectal abscess?

A
  • Diabetes
  • STI
  • Immunocompromised
  • IBD
  • Twice as common in men.
250
Q

What is the pathophysiology of an anorectal abscess?

A

Infection of one of the anal sinuses which leads to inflammation and the formation of an abscess.

251
Q

What are the symptoms of an anorectal abscess?

A
  • Painful, hardened tissue in the perianal area
  • Discharge of pus from the rectum
  • A lump or nodule
  • Tenderness
  • Fever
  • Constipation.
252
Q

What is the investigation for an anorectal abscess?

A

DRE.

253
Q

What is the management for an anorectal abscess?

A

Surgical drainage.

Pain relief.

254
Q

What is the main complication of an anorectal abscess?

A

Approximately 40% lead to a fistula in ano.

255
Q

What is a fistula in ano?

A

This is a chronic abnormal communication between the epithelialised surface of the anal canal and the perianal skin.

256
Q

What is a fissure-in-ano?

A

Tear in the mucosa of the anal canal.

257
Q

What are the 2 types of fissure-in-ano?

A

Primary: no apparent cause.
Secondary: due to underlying condition.

258
Q

What are the causes of fissure-in-ano?

A

Constipation: a hard stool tears the anal mucosa.
IBD: ulceration as part of inflammation.
Rectal malignancy.

259
Q

What is the pathophysiology of a fissure-in-ano?

A

Blood vessels of the anal mucosa are very close to the surface. Lesions can cause bleeding under the pressure of defecation.

260
Q

What are the symptoms of a fissure-in-ano?

A

Pain on defecation.

Bright red blood on defecation.

261
Q

What is the management for a fissure-in-ano?

A

Simple pain relief.

Warm baths.

262
Q

What is a pilonidal sinus?

A

Obstruction of natural hair follicles above the anus.

263
Q

Who is a pilonidal sinus most common in?

A

10:1 male to female ratio.

More common in obese Caucasians.

264
Q

What is the cause of a pilonidal sinus?

A

Congenital.

265
Q

What is the pathophysiology of a pilonidal sinus?

A

Ingrowth of hair excited a foreign body reaction and causes abscess with foul smelling discharge.

266
Q

What are the symptoms of a pilonidal sinus?

A

Small hole about 6cm above the anus.
Usually no symptoms until infected then a pus filled abscess.
Infection can cause pain, swelling and redness.

267
Q

What is the management of a a pilonidal sinus?

A

Asymptomatic: keep clean through hygiene and shave hair around the area.
Infection: consider excision of the sinus tract and closure. Skin flaps can be used to cover the defect.

268
Q

What is the gut?

A

Mouth to anus.

269
Q

What are adhesions?

A

Abdominal structures sticking to one other:
• Bowel loops or omentum
• Other solid organs
• Abdominal wall.

270
Q

What is intussusception?

A

Part of the intestine slides into an adjacent part of the intestines (telescoping). One hollow structure into its distal hollow structure.

271
Q

How do proton pump inhibitors work?

A

Inhibit gastric hydrogen release, preventing production of gastric acid.

272
Q

How do H2 receptor antagonists work?

A

Blocks histamine receptors on parietal cells reducing acid release.

273
Q

What are examples of proton pump inhibitors?

A

Lansoprazole, omeprazole.

274
Q

What are examples of H2 receptor antagonists?

A

Cimetidine.

2a Medicine (11 decks)

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