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Phase 2A Tom > GI > Flashcards

GI Flashcards

1
Q

What is inflammatory bowel disease?

A

An umbrella term for the two main diseases causing inflammation of the GI tract.

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2
Q

What are the two main causes of IBD?

A

Ulcerative colitis and Crohn’s disease

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3
Q

What is Crohn’s diease?

A

Transmural inflammation of the GI tract (anywhere from mouth to anus).

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4
Q

Where is the most commonly affected area of Crohn’s?

A

Terminal ileum and Colon

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5
Q

Describe the epidemiology of Crohn’s?

A
  • Has a peak onset in early life (20-40 years).
  • More common in female than male
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6
Q

What genetic mutations can cause Crohn’s?

A

CARD15 and NOD2 mutation

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7
Q

What pathogens can cause Crohn’s?

A
  • Mycobacterium paratuberculosis,
  • Listeria
  • Pseudomonas
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8
Q

What is thought to cause Crohn’s disease?

A
  • Immune system is thought to be triggered by a pathogen. These pathogens get through the wall due to defect
  • This causes the immune system to target the foreign pathogen. The immune cells invade deep into the mucosa and organise themselves into granulomas eventually forming ulcer.
  • These ulcers go through all layers known as TRANSMURAL this occurs in patches known as skip lesions
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9
Q

What is the endoscopic appearance of Crohn’s?

A

Cobblestone appearance

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10
Q

What are the signs of Crohn’s?

A
  • Abdominal tenderness
  • Fever
  • Mouth ulcers
  • Rectal examination will show blood, skin tags, fissures and fistulas
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11
Q

What are the symptoms of Crohn’s?

A
  • Weight loss
  • Diarrhoea
  • Abdominal pain (most common in RLQ where the ileum is)
  • Lethargy and malaise also symptom
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12
Q

What are the investigations for Crohn’s?

A
  • Faecal calprotectin (released by intestines when inflamed)
  • C- reactive protein is a good indication of current inflammation
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13
Q

What is the diagnostic investigation for Crohn’s and what will it show?

A

Colonoscopy- will show mucosal inflammation (deep ulcers, skip lesions and cobblestone appearance)

Histology will show transmural inflammation with granulomas and goblet cells

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14
Q

What is the management for inducing remission in Crohn’s?

A
  • Elemental diet (nutrients in pre digested form)
  • First-line is glucocorticoids e.g., prednisolone and hydrocortisone)
  • Immunosuppressants- should not be used alone
  • Biological therapy
  • Adjunct use antibiotics
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15
Q

What are some immunosuppressants used to treat Crohn’s? Levels of what should be measured before using them?

A
  • Azathioprine
  • Methotrexate
  • Mercaptopurine

Levels of Thiopurine methyltransferase should be measured before using

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16
Q

What are the biological therapies used to treat Crohn’s?

A

Infliximab and Adalimumab

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17
Q

How would you maintain remission in Crohn’s?

A
  • First line= Azathioprine or mercaptopurine
  • Second line- Methotrexate with Infliximab
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18
Q

When and what surgery could be used to treat Crohn’s?

A
  • When distal ileum is inflamed can surgically resect the area to prevent flare ups
  • Also used to treat strictures and fistulas
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19
Q

What are the key things to remember for Crohn’s?

A

NESTS
N- No blood or mucus
E- entire GI tract
S- Skip lesions
T- Terminal ileum and transmural
S- Smoking is a big risk factor

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20
Q

What is Ulcerative colitis?

A

A type of IBD that typically involves the rectum and variable lengths of the colon. Will never spread beyond the ileocecal valve

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21
Q

Describe the epidemiology of UC?

A
  • Bimodal peak at 15-25 and 55-70
  • More common in non-smokers
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22
Q

What is the gene implicated in UC?

A

HLA-B27

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23
Q

What are some other risk factors for UC?

A
  • Non smoker
  • NSAIDs
  • Chronic stress/depression
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24
Q

Describe the pathophysiology of UC?

A
  • Ulcers tend to form along the inner surface or lumen of the large intestine and rectum
  • Thought to be autoimmune in nature cytotoxic T cells attack the lining of the colon
  • Also thought that patients have higher proportion of gut bacteria that release sulphides
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25
Q

Describe the pathophysiology of UC?

A
  • Ulcers tend to form along the inner surface or lumen of the large intestine and rectum
  • Thought to be autoimmune in nature cytotoxic T cells attack the lining of the colon
  • Also thought that patients have higher proportion of gut bacteria that release sulphides
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26
Q

What antibodies are found in patients with UC?

A

p-ANCAs -perinuclear antineutrophilic cytoplasmic antibodies) in their blood - antibodies that target antigens in the body’s own neutrophil

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27
Q

What are the signs of UC?

A
  • Abdominal tenderness
  • Fever - in acute UC
  • Tachycardia - in acute severe UC
  • Fresh blood on rectal examination
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28
Q

What are some cutaneous signs of UC?

A
  • Erythema nodosum - inflammatory disorder affecting subcutaneous fat.
  • Pyoderma gangrenosum - rapidly enlarging, very painful ulcer.
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29
Q

What are the symptoms of UC?

A
  • Diarrhoea
  • Blood and mucus in stool
  • LLQ pain
  • Weight loss
  • Cramping rectal pain
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30
Q

What investigations would you do for UC?

A
  • Faecal calprotectin
  • LFT to screen for PSC
  • Raised C-reactive protein
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31
Q

What is the gold standard for UC and what would it show?

A

Colonoscopy and biopsy

Would show:
-shallow ulceration
- No inflammation beyond submucosa
- Crypt abscesses
- Goblet cell depletion

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32
Q

What is the scoring system used to test the severity of UC?

A

Truelove and Witts’ severity index

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33
Q

What is the management for inducing remission in mild UC?

A
  • First line: Aminosalicylate (mesalazine)
  • Second line corticosteroid (prednisolone)
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34
Q

What is the management for inducing remission in severe UC?

A
  • First line: IV corticosteroid hydrocortisone
  • Second line IV ciclosporin
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35
Q

How would you maintain remission in UC?

A
  • Aminosalicylate, azathioprine, mercaptopurine
    -May use biological therapy e.g., Infliximab if nothing else is working
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36
Q

What are the surgical options for UC?

A
  • Removal of the colon and rectum (panproctocolectomy)
  • Left with ileostomy or or J-pouch this is where small intestine is used to make rectum

Surgery will be curative

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37
Q

What is a complication of UC?

A
  • STI of stoma
  • Toxic megacolon
  • Perforation
  • Colonic adenocarcinoma
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38
Q

What % of patients with UC will develop colonic adenocarcinoma?

A

3-5%

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39
Q

What are the key things to remember for UC?

A

CLOSEUP
C- Continuous inflammation
L- Limited to colon and rectum
O- only superficial
S- Smoking protects
E- Excrete blood and mucus
U- Use Aminosalicylate
P- PSC

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40
Q

What are the extra intestinal signs of IBD?

A

A PIE SAC
- Ankylosing spondylitis (HLA B27!)
- Pyoderma gangrenosum
- Iritis (aka anterior uveitis)
- Erythema nodosum
- Sclerosing cholangitis
- Aphthous ulcers / amyloidosis
- Clubbing

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41
Q

What is irritable bowel syndrome/

A

A chronic condition characterised by abdominal pain associated with bowel dysfunction. It is a functional bowel disorder. Tom Coles suffers with it.

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42
Q

What are the 3 types of IBS?

A

IBS-C- with constipation
IBS-D with constipation and diarrhoea
IBS-M with both

(tom has the diarrhoea one)

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43
Q

What is the epidemiology of IBS?

A
  • It affects women more than men
  • More common in younger adults <40 years
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44
Q

What are the risk factors for worse symptoms of IBS?

A
  • Acute gastroenteritis
  • Stress
  • Menstruation
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45
Q

What causes the pain in IBS?

A
  • People with IBS often have visceral hypersensitivity which means the sensory nerve endings of the intestinal walls have a strong response to stimuli e.g., stretch after a meal
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46
Q

What causes the abnormal gut motility in IBS?

A
  • Eating foods such as short chain carbohydrates can act to draw water across the GI wall and into the lumen
  • The increased visceral sensitivity can also cause the smooth muscle to spasm creating diarrhoea if water is not absorbed properly
  • In addition, the unabsorbed short-chain carbohydrates are often metabolised by gastrointestinal bacterial flora which produce gas that could trigger more bloating, spasm, or pain.
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47
Q

What can alter the gut reactivity?

A

environmental (personal life stresses or abuse)

luminal (certain foods, bacterial overgrowth or toxins, or gut distension or inflammation)

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48
Q

What are the symptoms of IBS?

A
  • Fluctuating bowel habit
  • Diarrhoea
  • Constipation
  • Abdominal pain: worse after eating and better after opening of bowels
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49
Q

What are the diagnostic criteria for IBS?

A
  • Abdominal pain relieved on opening bowel
    And two of
  • Abnormal stool passage
  • Bloating
  • Worse after eating
  • PR mucus
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50
Q

What tests would you perform for IBS to rule out other causes?

A
  • FBC, CRP would be normal
  • Normal faecal calprotectin
  • Negative coeliac disease (anti-TTG antibodies)
  • Cancer is ruled out on colonoscopy
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51
Q

What is the management for IBS?

A
  • Loperamidefor diarrhoea
  • Laxatives for constipation.
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52
Q

What is coeliac disease?

A

A systemic autoimmune disorder that affects the small intestine that is triggered by the ingestion of gluten peptides

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53
Q

What are the genes that can cause coeliac disease?

A

HLA-DQ2
HLA-DQ8

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54
Q

What are the two auto-antibodies associated with coeliac disease?

A

Anti-TTG
Anti-EMA

These antibodies relate to disease activity and will rise with more active disease and may disappear with effective treatment.

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55
Q

What are some risk factors for coeliac disease?

A

T1DM
IgA deficiency

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56
Q

What happens in someone with coeliac disease?

A

Inflammation affects the small intestine particularly the jejunum. This causes atrophy of the intestinal villi and crypt hypertrophy

These villi are used to help absorb nutrients so coeliac will result in malabsorption.

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57
Q

What area of the intestine is most affected by coeliac disease?

A

Jejunum

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58
Q

What are the extra intestinal symptoms of coeliac disease?

A
  • Dermatitis herpetiformis
  • Angular stomatitis
  • Mouth ulcers
  • failure to thrive
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59
Q

What are the intestinal symptoms of coeliac disease?

A
  • Diarrhoea
  • Weight loss
  • Bloating
  • B12 deficiency
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60
Q

What are the investigations for coeliac disease?

A
  • 1st line raised anti-TTG antibodies
  • 2nd line raised anti-EMA
    Gold standard- duodenal biopsy villous atrophy, Crypt hyperplasia and intraepithelial lymphocytes

TTG and anti-EMA antibodies are IgA. Some patients have an IgA deficiency. When you test for these antibodies, it is important to test for total Immunoglobulin A levels because if total IgA is low because they have an IgA deficiency then the coeliac test will be negative even when they have coeliacs. In this circumstance, you can test for the IgG version of anti-TTG or anti-EMA antibodies or simply do an endoscopy with biopsies.

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61
Q

What are the complications of untreated coeliac diease?

A
  • Vitamin deficiency
  • Anaemia
  • Osteoporosis
  • Ulcerative jejunitis
  • Enteropathy-associated T-cell lymphoma (EATL) of the intestine
  • Non-Hodgkin lymphoma (NHL)
  • Small bowel adenocarcinoma (rare)
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62
Q

What is gastritis?

A

Gastritis refers to inflammation of the lining of the stomach associated with mucosal injury.

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63
Q

What are the different ways to classify gastritis?

A
  • Location: Antral or pangastritis
  • Time: Acute or chronic
  • Type: Erosive or non-erosive
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64
Q

What are the causes acute gastritis?

A
  • H.Pylori infection
  • Alcohol abuse
  • Stress (critically ill/post surgery)
  • NSAIDs
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65
Q

What are the causes of chronic gastritis?

A
  • H.Pylori infection
  • Autoimmune gastritis (parietal and intrinsic factor antibodies)
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66
Q

How does H.Pylori cause gastritis?

A
  • It produces urease which converts urea to ammonia and CO2 which is toxic since the ammonia will react with HCL to form ammonium.
  • The ammonium will damage the gastric mucosa resulting in less mucus production
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67
Q

What are the clinical manifestations of gastritis?

A
  • Nausea
  • Abdominal bloating
  • Vomiting
  • Epigastric pain
  • Indigestion
  • Haematemesis- “coffee ground” vomiting and melaena
  • Iron deficiency anaemia due to constant bleeding
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68
Q

What is the general investigation for gastritis?

A
  • Endoscopy will show gastric inflammation and atrophy
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69
Q

How would you test for autoimmune gastritis?

A

Testing for autoimmune gastritis

  • Look for anti-IF (intrinsic factor) antibody and anti-parietal cell antibodies
  • Raised gastrin levels, reduced pepsinogen
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70
Q

What are the tests for H.Pylori?

A
  • CLO test Urea breath test
  • Stool antigen test

Before testing, stop PPI for at least 2 weeks; antibiotics for 4 weeks

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71
Q

How would you treat gastritis not caused by H.Pylori?

A
  • Remove causative agents such as alcohol/NSAIDs
  • Reduce stress
  • H2 antagonists e.g. ranitidine or cimetidine - to reduce acid release
  • PPIs e.g. lansoprazole or omeprazole - to reduce acid release
  • Antacids - neutralise acid to relieve symptoms
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72
Q

How do you treat a H.Pylori infection?

A

Triple threat (PPI and 2 antibiotics) twice a day for 7 days
- 1st line PPI, 1g amoxicillin and clarithromycin 500mg

  • If penicillin allergy then give metronidazole 400mg as well as instead
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73
Q

What are the complications of gastritis?

A
  • Peptic ulcers
  • Bleeding and anaemia
  • MALT lymphoma (mucosa-associated lymphoid tissue)
  • Gastric cancer
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74
Q

What is Peptic ulcers disease?

A

A break in the mucosal lining of the stomach or duodenum more than 5 mm in diameter.

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75
Q

What are more common gastric or duodenal ulcers?

A

Duodenal ulcers are more common than gastric ulcers.

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76
Q

What is the main cause of PUD?

A

H.Pylori is responsible for 95% of duodenal ulcers and 75% of gastric ulcers

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77
Q

What drugs can cause PUD?

A
  • NSAIDs inhibit COX enzyme which is needed for prostaglandin synthesis
  • SSRIs, steroids and bisphosphonates can also cause as they break down the protective layer
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78
Q

What lifestyle factors can cause PUD?

A
  • Smoking and alcohol: may lead to increased acid.
  • Caffeine: may lead to increased acid.
  • Stress: may lead to increased acid.
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79
Q

What other health conditions can cause PUD?

A
  • Zollinger-Ellison syndrome:a gastrinoma (tumour) that results in numerous peptic ulcers due to elevated gastrin levels
  • Blood type O
  • Raised intracranial pressure:causes vagal stimulation which increases acid production (Cushing’s ulcer).
  • Severe burn:hypovolaemia secondary to a burn causes reduced perfusion of the stomach leading to necrosis (Curling ulcer)
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80
Q

What are the signs of PUD?

A
  • Hypotension and tachycardia
  • Epigastric tenderness
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81
Q

What are the symptoms of PUD?

A
  • Burning epigastric pain
  • Nausea
  • Hematemesis or melaena- caused by the perforation of an artery
  • Indigestion (Dyspepsia)
  • Reduced appetite
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82
Q

What is the gold standard test for PUD?

A

Endoscopy and biopsy. It excludes malignancy. Will not be performed for non-bleeding ulcers

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83
Q

What is used to stratify the risk for a GI bleed?

A

Glasgow Blatchford score

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84
Q

What factors are considered in the GBS?

A
  • HB
  • Urea
  • BP
  • Gender
  • Tachycardia
  • Melaena
  • Syncope
  • Hepatic disease history
  • Cardiac failure present
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85
Q

What is the difference in pain onset between a gastric and duodenal ulcer?

A

Gastric ulcer is worse after eating and duodenal is better 1-2 hours after eating but then worsens 2 hours after

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86
Q

Which artery is perforated in gastric vs duodenal ulcers?

A

Gastric= Left gastric
Duodenal= Gastroduodenal

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87
Q

What are the signs of perforation in gastric vs duodenal ulcers?

A
  • Gastric= haematemesis and melena
  • Duodena= Melaena and haematochezia
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88
Q

How would you treat an active peptic ulcer bleed?

A

First line:
- IV crystalloid
- Blood transfusion
- Endoscopy
- High dose IV PPI

  • Second line
    Surgery or embolization (blocking abnormal vessels) by interventional radiology: reserved for cases where adequate haemostasis is not achieved at endoscopy
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89
Q

What are the complications of PUD?

A
  • Perforation: life-threatening as ulcer penetrates the duodenum or stomach into the peritoneal cavity causing peritonitis. May also allow air to collect under the diaphragm and irritate the phrenic nerve causing referred shoulder pain. Requires surgical intervention!
  • Gastric outlet obstruction/ pyloric stenosis: caused by obstruction of the pylorus due to an ulcer and subsequent scarring. Presents with abdominal pain, distension, vomiting and nausea after eating
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90
Q

What is GORD?

A

Reflux of stomach contents into the oesophagus.

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91
Q

How common is GORD?

A

Has a prevalence as high as 10-20%

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92
Q

What are the lifestyle risk factors for developing GORD?

A
  • Obesity
  • Pregnancy
  • Smoking
  • NSAIDs, caffeine and alcohol
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93
Q

What are the biological risk factors for GORD?

A
  • Hiatus hernia- pushes the stomach up into the diaphragm
  • Male sex
  • Scleroderma: muscle of the lower oesophageal sphincter is replaced by connective tissue, so it can’t contract properly.
  • Zollinger-Ellison syndrome: increased gastrin causes increased HCl secretion
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94
Q

Describe how food normally moves from the oesophagus to the stomach

A
  • Normally food is moved into the stomach via peristalsis. At the gastro-oesophageal junction the sphincter relaxes to allow food to enter the stomach and after entry the sphincter relaxes to prevent reflux.
  • If the LOS relaxes inappropriately (due to drop in pressure) then the stomach contents will wash back into the oesophagus and cause acid reflux
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95
Q

Describe the pathophysiology of GORD?

A
  • When there is very low pressure in the oesophagus reflux will persist for longer becoming pathological.
  • Persistent acid reflux damages the mucosa causing inflammation. This will eventually lead to oedema and erosion of the mucosa.
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96
Q

What happens to the oesophageal mucosa as GORD progresses?

A
  • The epithelium will become damaged and replaced by scar, making the walls thicker and the lumen narrower
  • As there is damage there will be metaplasia of the cells going from stratified squamous to simple columnar (Barret’s oesophagus). This can eventually lead to adenocarcinoma (3-5%)
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97
Q

What are the key symptoms of GORD?

A
  • Heart burn
  • Regurgitation which is worse when lying down
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98
Q

What are someo other symptoms of GORD?

A
  • Epigastric pain
  • Dysphagia (difficulty swallowing)
  • Dyspepsia (indigestion)
  • Extra-oesophageal: cough, asthma, dental erosion
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99
Q

What are the initial investigations for GORD in people without red flag symptoms?

A
  • Can be diagnosed based on clinical presentation and based on whether PPI trial would resolve the symptoms
  • PH monitoring
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100
Q

What are the the red flag symptoms for GORD?

A

ALARMS
A- Anaemia
L- Loss of weight
A- Anorexia
R- Recent onset
M- Melaena
S- Swallowing difficulties

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101
Q

When would you refer for 2 week endoscopy? (gord)

A

Dysphagia or
Age ≥ 55yo with weight loss and 1 of the following:
- Upper Abdo pain
- Reflux
- Dyspepsia (indigestion)

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102
Q

What investigations would you perform for a clinical diagnosis of GORD?

A
  • FBC (anaemia)
  • 24-hour pH monitoring (pH <4 for more than 4% of the time is abnormal)
  • Upper GI endoscopy
  • Manometry (rule out motility disorders)
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103
Q

What are lifestyle changes for managing GORD?

A
  • Weight loss
  • Reduce alcohol intake
  • Eat smaller meals
  • Avoid eating before going to bed (no food 2 hours before bed)
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104
Q

What are the medical managements for GORD

A
  • PPI- this will lower acid production within the stomach
  • H2 receptor antagonist e.g., ranitidine reduces stomach acid
  • Antacids e.g., Gaviscon
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105
Q

What is the surgical management for GORD?

A
  • Nissen fundoplication: wrapping the fundus of the stomach around the lower oesophagus to tighten the sphincter
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106
Q

What is Barret’s oesophagus defined as?

A

Barrett’s oesophagus describes metaplasia (transformation of one differentiated cell type to another differentiated cell type) of the lower oesophageal lining from stratified squamous epithelium to mucous secreting columnar epithelium with goblet cells.

Barrett’s is classified as short segment (< 3 cm) and long segment (> 3 cm).

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107
Q

What is appendicitis?

A

Acute appendicitis is an acute inflammation of the vermiform appendix, most likely due to obstruction of the lumen of the appendix.

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108
Q

What are the different positions of the appendix?

A
  • Most commonly thedescending intraperitoneal or retrocaecal position
  • Retrocaecal and pelvic appendicitis are often more difficult to distinguish clinically
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109
Q

What is the epidemiology of appendicitis?

A
  • Appendicitis is the most common acute abdominal condition in the UK requiring surgery
  • The highest incidence is between 10-20 years of age
  • M>F
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110
Q

What causes appendicitis?

A
  • Normally occurs due to luminal obstruction
  • As the appendix continues to secrete mucus the fluid and mucus build up and increase the pressure this causes it to get bigger and push on the visceral nerve fibres causing pain
  • This will lead to bacterial overgrowth
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111
Q

What can cause the luminal obstruction in appendicitis?

A
  • Faecolith (hard mass of stool),
  • Undigested seeds,
  • Foreign body,
  • Pinworm infection,
  • Lymphoid hyperplasia of Peyer’s patches,
  • Fibrous strictures.
112
Q

What are the mechanisms of pain in appendicitis?

A
  • Peri-umbilical pain: inflammation of the appendix and visceral peritoneum irritates autonomic nerves of the embryological midgut → referred pain to the umbilical region
  • Right iliac fossa pain: due to localised inflammation of the parietal peritoneum
113
Q

What are the key presentations of appendicitis?

A

Central abdominal pain which migrates to the right iliac fossa, low-grade pyrexia and anorexia. 50% of patients present with this characteristic history

114
Q

What are the signs of appendicitis ?

A
  • RIF pain on palpation worse when hand is released (rebound tenderness)
  • Rovsing’s sign- pain in right iliac fossa is worsened by pressing on the left iliac fossa
  • Psoas sign pain is worse on hip extension
  • Obturator sign pain is worse by flexing and inwardly rotating the hip
115
Q

What are the symptoms of appendicitis?

A
  • Periumbilical pain (referred pain) which migrates to the right iliac fossa (McBurney’s point)
  • Reduced appetite and anorexia
  • Nausea and vomiting
  • Diarrhoea
  • Low grade fever
116
Q

What are the investigations for appendicitis?

A
  • Blood test (WCC, ESR, CRP)
  • Abdominal US (in children and pregnant women)
  • Abdominal CT with contrast
  • Urinalysis (exclude UTI)
  • Pregnancy test
117
Q

What is guarding and rebound tenderness?

A

Guarding - when abdominal muscles tense up
Rebound tenderness - pain when releasing pressure on palpation

118
Q

What is the management for appendicitis?

A
  • Fluids
  • Analgesia
  • Antiemetics (ondansetron)
  • IV antibiotics pre surgery (ceftriaxone and metronidazole)
119
Q

What is the management for appendicitis?

A
  • Prompt appendicectomy:laparoscopicappendicectomy is the treatment of choice, using a three-port approach. Occasionally, anopenapproach is required, with a 2-3 inch incision just below McBurney’s point.
  • Significantabdominal lavageis required for perforated appendicitis
120
Q

What is diverticular disease?

A

Diverticular disease may be defined as any clinical state caused by symptoms pertaining to colonic diverticula and includes a wide-ranging spectrum from asymptomatic to severe and complicated disease

121
Q

What is diverticulosis?

A

The presence of diverticula (out-pouching) in an asymptomatic patient

122
Q

What is diverticulitis?

A

Diverticulitis refers to inflammation and infection of diverticula.

123
Q

Describe how diverticula form?

A
  • Large intestine contains areas of smooth muscle. Where this muscle is penetrated with blood vessels are areas of weakness. Increased pressure in the lumen causes a gap to form in this muscle allowing the mucosa to herniate through. It happens in areas that are not covered by teniae coli
124
Q

Why do diverticula not form in the rectum?

A

As the rectum has an extra layer of longitudinal muscle that surrounds it this adds extra support.

125
Q

Where is the most common area for the formation of diverticula?

A

Mainly form in sigmoid colon but can also affect right colon

126
Q

What are the risk factors for developing diverticular disease?

A
  • Increasing age
  • Low fibre diets
  • Obesity
  • NSAIDs
  • Smoking
127
Q

What can cause diverticulitis?

A
  • When faecal matter becomes lodged in the diverticula or more often due to the erosion of the diverticular wall from high luminal pressure
  • This can cause inflammation and the rupture of vessels leading to bleeding
128
Q

What are the symptoms of diverticular disease?

A
  • Bowel habits changed
  • Bloating a flatulence
  • Left lower quadrant pain
  • Nausea and vomiting
129
Q

What are the signs and symptoms of diverticulitis?

A
  • Pyrexia
    • Left lower quadrant or iliac fossa tenderness and guarding: in diverticulitis
    • Left iliac fossa tender mass: suggests an abscess (20%)
    • Rigidity, guarding, rebound or percussion tenderness: suggests perforation
    • Digital rectal examination: fresh blood and pelvic tenderness
    • Tachycardia and hypotension: if septic
130
Q

What are the investigations for diverticular disease?

A
  • Examinations: tenderness and guarding, distended and tympanic to percussion, no bowel sounds
  • FBC will show inflammation
  • GOLD STANDARD Contrast CT scan
131
Q

When should colonoscopy be used for diverticular disease?

A

Colonoscopy:should generally be avoided in acute diverticulitis due to the risk of perforation, and is used if the diagnosis is unclear or alternative pathology is suspected

132
Q

What is the management for mild diverticulitis?

A
  • Oral co-amoxiclav (at least 5 days)
  • Analgesia (avoiding NSAIDs and opiates, if possible)
  • Only taking clear liquids (avoiding solid food) until symptoms improve (usually 2-3 days)
  • Follow-up within 2 days to review symptoms
133
Q

How would you manage severe diverticulitis?

A
  • Supportive management:NBM, IV fluids and analgesia
  • IV antibiotics:co-amoxiclav is typical but depends on local guidelines
  • Acute PR bleeding: transfuse blood products and arrange angiographic embolization (blocks blood vessels) if available, otherwise, surgery is required
  • Surgery:
134
Q

What surgical procedure would be performed for diverticulitis?

A
  • Hartmann’s procedure- removing the affected section of the bowel and creating an alternative path for faeces to be passed
135
Q

What are the complications of diverticulitis?

A
  • Perforation
  • Peritonitis
  • Peridiverticular abscess
  • Large haemorrhage requiring blood transfusions
  • Fistula (e.g., between the colon and the bladder or vagina)
  • Ileus / obstruction
136
Q

What is a Mallory-Weiss tear (MWT)?

A

Mallory-Weiss tear (MWT) refers to longitudinal lacerations limited to the mucosa and submucosa, at the border of the gastro-oesophageal junction.

137
Q

Describe the epidemiology of MWT

A
  • MWT accounts for up to 15% of cases of upper GI bleeding
  • MWT is more common in men than in women
  • The age of presentation may vary but is most common in people aged between 30 and 50 years
138
Q

What are the risk factors for MWT?

A
  • Persistent vomiting
  • Alcoholism
  • Chronic cough
  • Hiatus hernia
  • Heavy lifting or straining
139
Q

What causes a MWT?

A

A sudden rise in intra-abdominal and transmural pressure across the gastro-oesophageal junction secondary to wrenching or vomiting in the presence of a pre-existing damaged gastric mucous membrane, which is often related to alcoholism.

140
Q

What are the symptoms of MWT?

A
  • Fresh blood following period of vomiting particularly after drinking alcohol.
  • Melaena
  • Epigastric pain
141
Q

What is the gold standard investigation for a MWT?

A
  • Upper GI endoscopy: gold-standard required for all patients as an inpatient or outpatient depending on the Glasgow Blatchford score
    • Usually shows a single longitudinal tear (there can be multiple tears) in the mucosa at the gastro-oesophageal junction
142
Q

What is Boerhaave’s syndrome?

A

Spontaneous perforation of the oesophagus, usually due to vomiting, which ruptures all the layers of the oesophageal wall

143
Q

What is the first line treatment for MWT?

A

Mild bleeding doesn’t require treatment

Upper GI endoscopy- mechanical clipping using adrenaline, then thermal coagulation then Sclerotherapy with adrenaline (delivers medication to the tear to stop bleeding)

144
Q

What are the complications of MWT?

A
  • Rebleeding: usually occurs within the first 24 hours, but is rare after endoscopy
  • Hypovolaemic shock: only occurs with life-threatening, persistent bleeds, which are very rare following MWT
  • Oesophageal perforation: a rare complication
145
Q

What is diarrhoea?

A

The abnormal passage of three or more loose or liquid stools per day. By having 6 of these every day, Tom Coles has a rare condition known as double diarrhoea.

146
Q

What is the epidemiology of diarrhoea?

A

2nd leading cause of death in children < 5 globally

This makes my joke about Toms double diarrhoea less entertaining.

147
Q

What is the most common cause of diarrhoea?

148
Q

What is the most common viral diarrhoea in children?

149
Q

What is the most common cause of viral diarrhoea in adults and where can you catch it?

A

Norovirus- caught on cruise ships, hospitals and restaurants

150
Q

What is the most common cause of diarrhoea in Tom Coles?

151
Q

What is another cause of viral diarrhoea?

A

Traveller’s diarrhoea- symptoms are fever, nausea, vomiting, cramps or bloody stools during trip abroad

152
Q

What is the most common cause of bacterial diarrhoea?

A

Campylobacter jejuni

Investigate: Charcoal Cefazolin Sodium Deoxycholate Agar (CCDA) or PCR
Cause: Undercooked chicken (after BBQs!)
Usually self limiting = no treatment

153
Q

What is clostridium difficile infection?

A
  • Some antibiotics interfere with the balance of the bacteria in the bowel which can cause the C. diff bacteria to multiply and produce toxins
  • Antibiotics all start with C
  • Investigate with stool antigen or PCR
154
Q

How do you treat a C. diff infection?

A
  • Metronidazole, vancomycin, stop antibiotics
155
Q

What are the two types of parasitic diarrhoea?

A

Giardia lamblia – most common
Treat: metronidazole
Cryptosporidium (helminth parasite)

156
Q

What bacteria cause watery diarrhoea?

A

Vibrio cholerae
E. coli (ETEC)
Clostridium perfringens
Bacillus cereus
S. Aureus

157
Q

What bacteria cause bloody mucoid diarrhoea?

A

Shigella
E. coli (EIEC, EHEC)
Salmonella enteridis
V. parahaemolyticus
C. diff
C. jejuni

158
Q

What is a bowel obstruction and what are the 3 types?

A

The interruption of passage through the bowel. Can be a surgical emergency
Small bowel obstruction (most common)
Large bowel obstruction
Pseudo-obstruction

159
Q

What % of cases do small bowel obstructions account for?

160
Q

What are the causes of a small bowel obstruction?

A
  • Bowel adhesions post surgery they are the most common cause (75%)
  • Hernia (most likely femoral or inguinal)
  • Stricture formation from crohn’s
  • Gallstone ileus - gallstone within lumen of small bowel
161
Q

Describe the pathophysiology of SBO?

A
  • When peristalsis occurs against a obstruction it results in pain, distension and constipation
  • Dilation of the proximal bowel leads to compression of the mesenteric vessels and mucosal oedema.
  • This results in transudation of large volumes of electrolyte-rich fluid into the bowel (‘third-spacing’). Eventually, as arterial supply is compromised, bowel ischaemia occurs with risk of perforation and subsequent faecal peritonitis and sepsis
162
Q

What are the signs of SBO?

A
  • Abdo tenderness and distension (less severe than LBO)
  • Tinkling bowel sounds in mechanical and absent in functional
  • Rectal exam will be empty
  • Tachycardia and hypotension due to third spacing of fluid
163
Q

What are the symptoms of SBO?

A
  • colicky, central or generalised Abdo pain
  • Nausea and vomiting early sign in SBO
  • Abdominal bloating
164
Q

What is the first line investigation for SBO?

A

Abdominal x-ray will show small bowel dilation of greater than 3 cm (coiled-spring appearance)

165
Q

What is the gold standard investigation for SBO?

A

CT abdomen and pelvis with contrast

166
Q

What is the first-line treatment for SBO?

A

‘drip’ (IV fluids) and ‘suck’ (NG tube)
and also IV antibiotics (cefotaxime and metronidazole)
Analgesia and anti-emetics

167
Q

What are the surgical treatments for SBO?

A

Emergency laparotomy would be performed in cases where there is:
- Evidence of bowel ischaemia
- A non-adhesional cause e.g., hernia
- Failure of conservative management

Adhesiolysis- performed for a adhesional obstruction and recurrent adhesional obstructions

168
Q

What are the complications of SBO?

A
  • Bowel ischaemia
  • Sepsis
  • Aspiration pneumonia
  • Short gut syndrome
169
Q

What are the causes of LBO?

A
  • Colorectal cancer is the most common (90% of cases)
  • Volvulus- torsion of the colon around itself and the mesentery
  • Stricture
  • Intussusception (more common in children) is when the bowel fold within itself
  • Hirschprung’s disease: where neonates are born without innervation to the colon or rectum
170
Q

What are the symptoms of LBO?

A
  • Continuous abdominal pain
  • Severe abdominal distension
  • Constipation first followed by vomiting, bilious and then faecal
  • Absent bowel sounds
171
Q

What would you see on an abdominal x-ray for LBO?

A

Dilation of large bowel greater than 6cm
Dilation of caecum greater than 9cm

172
Q

What is pseudo-obstruction?

A

Clinical picture mimicking colonic obstruction but with no mechanical cause dilation without obstruction

Also known as Ogilvie syndrome.

173
Q

What can cause a pseudo-bowel obstruction?

A
  • Puerperium: the period after child birth
  • Post operative states
  • Trauma/sepsis
  • Drugs
  • cardiorespiratory and neurological disorders
174
Q

What is the pathophysiology of pseudo-obstruction

A

Parasympathetic nerve dysfunction → absent smooth muscle

Complication: bowel ischaemia and perforation

175
Q

What are the symptoms of pseudo-obstruction?

A
  • Rapid progressive abdominal distension
176
Q

What is the first line investigation for pseudo-bowel obstruction and what would it show?

A
  • A large gas filled bowel greater than 10cm dilated
177
Q

How would you treat a pseudo-bowel obstruction?

A

Drip and suck
IV neostigmine- can encourage motility

  • Endoscopic colonic decompression can be used in those failing to respond.
  • Those at increasing risk of or who have developed complications (e.g. necrosis, perforation) will typically need surgical management, if appropriate.
178
Q

What is achalasia?

A

Degeneration of ganglions in Auerbach’s/myenteric plexus (in muscularis externa)

179
Q

What is the pathophysiology of achalasia?

A

The nerves in the LOS don’t work properly. This means the LOS can’t relax leading to an obstruction

180
Q

What are the symptoms of achalasia?

A

Dysphagia: unable to swallow both solids and liquids (Oesophageal cancer: Solids first, then unable to swallow liquids over time)
Heartburn
Food regurgitation

181
Q

What are the first line investigations for achalasia?

A

Endoscopy
Barium swallow (Bird beak sign)

182
Q

What is the gold standard test for achalasia?

183
Q

What is the treatment for achalasia?

A
  1. Lifestyle
  2. Nitrates/CCB to relax LOS
  3. Botox to relax LOS
  4. Surgery: cardiomyotomy
184
Q

What is ischaemic colitis?

A

Bowel ischaemia that affects the large bowel. Due to pathology in the inferior mesenteric artery.

185
Q

What are the non-occlusive causes of ischaemic colitis?

A
  • Heart failure
  • Septic shock
  • Vasopressors
  • Recent CABG
  • Renal impairment
  • PVD
  • Cocaine use
186
Q

What are the occlusive causes of IC?

A
  • Arterial/venous thrombus
  • Embolism
  • Hernia/Volvulus/tumours
187
Q

What are the risk factors for IC?

A
  • Atrial fibrillation major risk factor
  • IE- can cause in younger patient’s
  • Vasculitis- can cause in younger patient’s
188
Q

What are the signs of IC?

A
  • Abdominal tenderness and distension
  • Haemodynamic instability (Shock)
  • Abdominal bruit (turbulent blood flow)
189
Q

What are the symptoms of IC?

A
  • Colicky lower left side abdominal pain- wore after eating
  • Diarrhoea
  • Haematochezia- passage of fresh blood
  • Fever
  • Abdominal bruit
190
Q

What area is most likely to be affected in IC?

A

The splenic flexure as it is the most distal despite duel supply. The rectum is resistant to ischaemia due to duel supply from IMA and internal iliac

191
Q

What are the investigations for IC?

A
  • ABG will show metabolic acidosis (raised lactate)
  • 1st line would be CT contrast/angiography
  • GOLD STANDARD colonoscopy
192
Q

What is the supportive management for IC?

A
  • Nil by mouth (NG tube potentially)
  • IV fluids
  • Broad spectrum antibiotics
  • Unfractionated heparin
193
Q

What are the surgical treatments of IC?

A
  • Embolectomy
  • Thrombolysis
  • Mesenteric angioplasty and stenting
  • Laparotomy and resection of ischaemic/ necrotic segments
  • Stoma formation
194
Q

What are the complications of IC?

A
  • Bowel infarction and perforation: ischaemia can result in necrosis and subsequent perforation. This can lead to peritonitis and profound sepsis
  • Systemic inflammatory response syndrome (SIRS) progressing into a multi-organ dysfunction syndrome, mediated by bacteria translocation across the dying gut wall
  • Strictures: patients with ischaemic bowel managed conservatively have a risk of developing strictures
195
Q

What is mesenteric ischaemia?

A

Bowel ischaemia which affects the small bowel. It refers to pathology affecting the superior mesenteric artery.

196
Q

What are the differences between IC and mesenteric ischaemia?

A

The area that is affected and mesenteric tends to be more serious

197
Q

What is chronic mesenteric ischaemia?

A

The result of narrowing of the mesenteric blood vessels by atherosclerosis. This results in intermittent abdominal pain, when the blood supply cannot keep up with the demand.

198
Q

What are the symptoms CMI?

A
  • Central colicky abdominal pain after eating
  • Weight loss
  • Abdominal bruit
199
Q

What is the management for CMI?

A
  • Reducing modifiable risk factors
  • Secondary prevention (statins and antiplatelet)
  • Revascularisation to improve blood flow
200
Q

What are the two types of oesophageal cancer?

A

Adenocarcinoma and squamous cell carcinoma

201
Q

Where are adenocarcinomas more common?

A

In the developed world

202
Q

Where are squamous cell carcinomas more common?

A

Developing world

203
Q

What are the risk factors for an adenocarcinoma of the oesophagis?

A
  • Barret’s oesophagus
  • Obesity
  • Male sex
  • Smoking
  • Coeliac disease
204
Q

What are the risk factors for SSC?

A
  • Smoking- more associated than with adenocarcinoma
  • Alcohol
  • Achalasia
  • Plummer-Vinson syndrome: rare disease characterised by difficulty swallowing, iron-deficiency anaemia, glossitis,
  • Hot drinks
  • Nitrosamines(dietary)
205
Q

What causes SSC and what part of the oesophagus is affected?

A
  • Arises from squamous epithelium. It occurs in the upper 2/3rds of the oesophagus.
  • Occurs when tissue is exposed to risk factors like cigarette smoke, alcohol or hot fluids meaning there are more cell divisions increasing the risk of a malignant tumour
206
Q

What causes adenocarcinomas and what part of the oesophagus is affected?

A
  • Arises form columnar glandular epithelium in the lower 1/3rd of the oesophagus.
  • It most frequently occurs as a result of GORD.
207
Q

What are the symptoms of oesophageal cancer?

A
  • Lymphadenopathy
  • Vocal cord paralysis
  • Melaena

arent these signs?

208
Q

What are the symptoms of oesophageal cancer?

A
  • Progressive dysphagia
  • Regurgitation
  • Vomiting
  • Hoarseness
  • Weight loss
209
Q

What is the first-line investigation for SSC/adenocarcinoma?

A

Upper GI endoscopy (OGD) and biopsy: first-line investigation and allows for visualisation of masses and biopsy

210
Q

What would be used to determine the severity of the cancer (oesophageal)?

A

CT/MRI of the chest and abdomen (staging and metastases)

211
Q

What is the treatment for an localised adenocarcinoma/SSC?

A

Surgical resection and chemoradiotherapy

212
Q

What treatment is used for HER2 positive metastatic cancer/

A

Trastuzumab (Herceptin)

213
Q

What is the prognosis for oesophageal cancer?

A

5 year survival rate is 15% as diagnosis is often made late. 55% if caught early

214
Q

What are the 4 types of gastric cancer?

A
  • Adenocarcinoma
  • Lymphoma-chronic H.Pyloriinfection, can cause excessive B-cellproliferation, which makes these cells more prone to have mutations and develop lymphoma.
  • Carcinoid- - Originates in the neuroendocrine cell e.g. G-cells of the stomach.
  • Leiomyosarcoma- smooth muscle cells from the gastric wall.
215
Q

What are the two types of adenocarcinoma?

A

Intestinal (type 1), or well-differentiated adenocarcinoma; and diffuse(type 2), or undifferentiated adenocarcinoma. Intestinal is the most common!

216
Q

What are the risk factors for developing a gastric intestinal adenocarcinoma?

A
  • Male
  • Older age
  • H.Pylori- accounts for 60%
  • Chronic/atrophic gastritis
217
Q

What are the risk factors for developing a gastric diffuse adenocarcinoma?

A
  • Female
  • Younger age
  • Blood type A
  • H.Pylori
218
Q

Describe the pathophysiology of intestinal gastric adenocarcinoma?

A
  • H.Pylori releases virulence factors e.g., cagA. This causes damage and leads to an inflammatory response (gastritis)
  • The normal epithelium of the stomach gets continuously damaged and repaired. Over time, the stomach cells in the epithelium undergo metaplasia and eventually dysplasia

occurs in the antrum adn lesser curvature

219
Q

What is the histology of intestinal gastric adenocarcinoma

A

Well-differentiated tubular

220
Q

What gene is mutated in diffuse gastric adenocarcinoma?

221
Q

Describe the pathophysiology of a diffuse gastric adenocarcinoma?

A
  • CDH1 gene codes for tumour suppressor protein E-cadherin. Helps cells stick to each other and controls cell cycle
  • When it isn’t working cells detach and divide uncontrollably. Can spread very easily
222
Q

What can diffuse gastric adenocarcinoma cause?

A
  • Gastric linitis plastica- where the stomach wall grows thick and hard and looks like a leather bottle
223
Q

What is the histology of diffuse gastric adenocarcinoma?

A
  • Poorly differentiated signet ring cells
224
Q

What are the symptoms of gastric cancer?

A
  • Weight loss
  • Haematemesis and melaena
  • Dysphagia
  • Anorexia
  • Epigastric pain
225
Q

What are the signs of gastric cancer/

A
  • Acanthosis nigricans: darkening of the skin at the axilla and other skin folds
  • Troisier’s sign: an enlarged, hard Virchow’s node (left supraclavicular node)
  • Iron deficiency anaemia
226
Q

What are investigations for gastric cancer?

A
  • Upper GI endoscopy (gastroscopy) + biopsy
  • Endoscopic ultrasound
  • CT/MRI of the chest and abdomen (staging and metastases)
227
Q

How common is bowel cancer?

A

The 4th most common cancer in the UK

228
Q

What are the risk factors for developing bowel cancer?

A
  • Familial adenomatous polyposis (FAP)
  • Hereditary nonpolyposis colorectal cancer (HNPCC)
  • IBD
  • Diet high in red and processed meat and low in fibre
229
Q

What is FAP?

A

Familial adenomatous polyposis

  • Is an autosomal dominant condition involving the tumour suppressor gene APC
  • It results in many polyps forming along the large intestine.
  • Patients will have whole intestine removed to prevent the development
230
Q

What is HNPCC?

A

Hereditary nonpolyposis colorectal cancer

It is also known as Lynch syndrome. It is an autosomal dominant condition that results from mutations in mismatch repair genes (MMR).
- Patients are at higher risk of number of cancers and doesn’t develop adenomas

231
Q

What are the signs and symptoms of bowel cancer?

A
  • Change in bowel habit
  • Unexplained weight loss
  • Rectal bleeding
  • Unexplained abdominal pain
  • Iron deficiency
  • Abdominal/rectal mass

Right side tumours are often asymptomatic and will only present with iron deficiency

232
Q

When would you be referred for suspected bowel cancer?

A
  • Over 40 with abdominal pain and unexplained weight loss
  • Over 50 with unexplained rectal bleeding
  • Over 60 with iron deficiency anaemia or change in bowel habit
233
Q

What is the blood test used for testing bowel cancer?

A

CEA tumour marker used not in screening but testing relapse

234
Q

What is the gold standard test for bowel cancer?

A

Colonoscopy and biopsy.

235
Q

What are some other tests for bowel cancer?

A

Sigmoidoscopy involves an endoscopy of the rectum and sigmoid colon only. This may be used in cases where the only feature is rectal bleeding. There is the obvious risk of missing cancers in other parts of the colon.

CT colonography is a CT scan with bowel prep and contrast to visualise the colon in more detail. This may be considered in patients less fit for a colonoscopy but it is less detailed and does not allow for a biopsy.

236
Q

What is the at home screening test for bowel cancer?

A
  • Faecal immunochemical test looks for the amount of human haemoglobin in the stool
  • Test used to be faecal occult blood test which detected blood in stools but used to detect meat blood
237
Q

Who are FIT tests sent to?

A

Sent every 2 years for people from 60-74

238
Q

What is the dukes classification?

A

Used to asses bowel cancer previously been replaced by TMN.

Dukes A- confined to mucosa and part of the muscle wall

Dukes B- extending through the muscle of the bowel wall

Dukes C- Lymph node involvement

Dukes D- Metastatic disease

239
Q

What is the TMN

A

Tumour, Node, Metastasis

240
Q

What is assessed in the tumour part of TMN?

A

Tx- unable to asses size
T1- submucosa involvement
T2- Involvement of the muscle
T3- involvement of the subserosa and serosa (outer layer), but not through the serosa
T4- Spread through the serosa and reaching other tissues and organs

241
Q

What is assessed in the node part of TMN?

A

NX- unable to asses
N0- No nodal spread
N1- spread 1-3
N2- spread to more than 3 nodes

242
Q

What is assessed in the metastasis part of TMN?

A

M0- no metastasis
M1- Metastasis

243
Q

What is the prognosis for bowel cancer?

A

Early localised disease has a 5-year survival between 95% and 100%, whilst metastatic disease has a survival between 5% and 10%

244
Q

What is the management for bowel cancer?

A
  • Surgical resection
  • Radiotherapy
  • Chemotherapy
245
Q

What is Zenker’s diverticulum?

A

The outpouching into the pharynx causing food to become stuck

246
Q

What are the symptoms of Zenker’s diverticulum?

A

pseudo-choking + bad breath + infection

247
Q

What is pseudomembranous colitis? (PMC)

A

Inflammation of the colon due to a overgrowth of C.diff and a recent history of antibiotic use.

248
Q

What are the risk factors for developing PMC?

A
  • Recent antibiotic use
  • Staying in a hospital/nursing home
  • older age
  • IBD
  • Use of PPI
  • Immunocompromised
249
Q

What are the investigations for PMC?

A
  • FBC will show raised WCC
  • Stool sample (presence of C.diff)
  • Colonoscopy (raised yellow plaques)
250
Q

What will the histology of PMC look like?

A

Owl eye inclusion body for CMV

251
Q

How do you treat PMC?

A

Stop causative agent
Start another antibiotic that is effective against C.difficile
Oral fidaxomicin, vancomycin, metronidazole

252
Q

What are hammorrhoids?

A
  • A normal spongy vascular structure that acts as a cushion for stools as they pass through
  • Haemorrhoidal disease is when they get disrupted swollen and inflamed
253
Q

What are internal and external haemorrhoids?

A

Internal are above the dentate line and external are below the dentate line

254
Q

What is the dentate line?

A

a line which divides the upper two-thirds and lower third of the anal canal.

255
Q

What are the four grades of internal haemorrhoids?

A

Grade I: no protrusion outside the anal canal.

Grade II: protrusion outside the anus during bowel movement, but they retract spontaneously.

Grade III: prolapsed haemorrhoids that don’t retract spontaneously, but they can be pushed back in manually.

Grade IV: prolapsed haemorrhoids that cannot be manually pushed back in.

256
Q

What can cause haemorrhoids?

A
  • Straining during bowel movements
  • Chronic diarrhoea
  • Anal sex
  • Congestion from a pelvic tumour, pregnancy, congestive heart failure and portal hypertension
257
Q

What are the symptoms haemorrhoids?

A
  • Usually asymptomatic
  • Can cause itching, burning and vague discomfort
  • Painless passage of bright red blood not mixed in with the stools
  • Straining
  • Constipation
  • Lump around or inside the anus
258
Q

What are the investigations for haemorrhoids?

A
  • External haemorrhoids are visible on inspection
  • Internal haemorrhoids can sometimes be felt on a digital rectal exam
  • GOLD STANDARD proctoscopy is required for proper visualisation and inspection
259
Q

What do internal haemorrhoids look like with proctoscopy?

A
  • Internal haemorrhoids look like bulging purplish-blue veins
  • Prolapsed internal haemorrhoids appear dark pink, glistening, and are sometimes tender masses at the anal margin
260
Q

What are the differentials for haemorrhoids?

A

Anal fissures
Diverticulosis
Inflammatory bowel disease
Colorectal cancer

261
Q

What is the conservative management for haemorrhoids?

A
  • Topical treatments e.g., Anusol
  • Give treatment for constipation of present
262
Q

What are the treatments for the first and second degree haemorrhoids?

A
  • Rubber band ligation
  • Infrared coagulation
  • Injection scleropathy
  • Bipolar diathermy
263
Q

What are the surgical treatments for 3rd and 4th degree haemorrhoids?

A
  • Haemorrhoidectomy
  • Stapled haemorrhoidectomy
  • Haemorrhoidal artery ligation
264
Q

What is an anal fistula?

A

An abnormal connection between the epithelial surface of the anal canal and skin - it is essentially a track that communicates between the skin and anal canal/rectum

265
Q

What are the causes of an anal fistula?

A
  • Perianal sepsis
  • Abscesses
  • Crohn’s
  • TB
  • Diverticular disease
266
Q

What are the signs and symptoms of an anal fistula?

A
  • Throbbing pain worse when sitting, defecation or activity
  • Malodorous discharge
  • Pruritis ani
  • Perianal skin may become inflamed
267
Q

What are the investigations for an anal fistula?

A
  • MRI
  • Endoanal ultrasound
268
Q

What is the management for a anal fistula?

A

Surgical - Fistulotomy (cutting along the whole length of the fistula to open it up so it heals as a flat scar) and excision

269
Q

What is an anal fissure?

A

A tear in the lower anal canal distal to the dentate line usually due to trauma

270
Q

What are the causes of an anal fissure?

A
  • Hard faeces
  • Anal trauma
  • Rarely Crohn’s/TB
271
Q

What are the symptoms of an anal fissure?

A
  • Extreme pain on passing motion
  • Blood in stool on wiping
272
Q

What are the conservative treatments of an anal fissure?

A
  • Increase dietary fibre and fluids
  • Use of stool softener
273
Q

What are the medical treatments of an anal fissure?

A
  • Lidocaine ointment + GTN ointment or topical diltiazem
  • 2nd line: Botulinum toxin injection (botox) and topical diltiazem
  • Surgery if medication fails: lateral partial internal sphincterotomy (the internal sphincter is divided to lower its resting pressure, which helps improve blood supply to the fissure and allows faster healing).
274
Q

What is an anal absecess?

A

Superficial infection that appears as a tender red lump under the skin near the anus.

275
Q

Risk factors for anal abscess?

A
  • Perianal abscesses make up 45% of anorectal abscesses (most common type)
  • F>M
  • 2-3 times more common in those who have anal sex
276
Q

How does an abscess form?

A

An abscess forms when normal tissue is split apart and that new space is invaded by nearby pathogens like bacteria. This leads to an immune response.

277
Q

What is the treatment for an abscess

A
  • Surgical excision and drainage
  • Treatment with antibiotics

Phase 2A Tom (15 decks)

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