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Phase 2a > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

What is inflammatory bowel disease?

A

The umbrella term for two main diseases that causes inflammation of the GI tract - Crohn’s and ulcerative colitis.

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2
Q

Is IBD always continuously inflamed?

A

No, associated with periods of remission and exacerbation.

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3
Q

What is the acronym for remembering the features of Crohn’s disease?

A

NESTS:
-No blood or mucous.
-Entire GI tract affected.
-Skip lesions on endoscopy.
-Terminal ileum most affected and Transmural inflammation.
-Smoking is a RF.

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4
Q

What is the acronym for remembering features of ulcerative colitis?

A

CLOSEUP:

-Continuous inflammation.
-Limited to colon and rectum.
-Only superficial mucosa affected.
-Smoking is protective.
-Excrete blood/mucous.
-Use aminosalicyclates.
-Primary sclerosing cholangitis association.

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5
Q

Who is affected most by IBD?

A

Jewish people.

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6
Q

What causes IBD?

A

Unclear - autoimmune condition.

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7
Q

What is IBD a big risk factor for?

A

Colorectal cancer and other autoimmune diseases.

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8
Q

What is the gold standard investigation for IBD?

A

Colonoscopy and biopsy.

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9
Q

Which investigation may be positive in UC but not Crohn’s?

A

May be pANCA positive in UC.

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10
Q

Compare and contrast UC and Crohn’s.

A
  1. UC affects the bowel and rectum.
    -Crohn’s affects the entire GI tract.
  2. UC affects only the mucosa layer.
    -Crohn’s is transmural inflammation.
  3. UC has continuous inflammation.
    -Crohn’s has ‘skip lesions’.
  4. In UC, smoking is protective.
    -In Crohn’s smoking is a RF.
  5. In UC, there is blood and mucous.
    -In Crohn’s there is rarely blood and mucous.
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11
Q

What is the main risk factor for IBD?

A

Family history.

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12
Q

Has Crohn’s or UC more genetic association?

A

Crohn’s has a stronger genetic link.

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13
Q

Explain the epidemiology of Crohn’s.

A

Presents ages 20-40. Northern European.
-Affects females more than male.
-More Jewish people affected.

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14
Q

Explain the epidemiology of UC.

A

Presents ages 20-40y.
-Affects females and males equally.
-More common in Jewish people.
-Incidence 3x higher in non-smokers.

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15
Q

Is UC or Crohn’s more common?

A

Ulcerative colitis is more common.

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16
Q

How does ulcerative colitis usually present?

A

LLQ pain, cramps and discomfort.
-Episodic diarrhoea with blood and mucous.
-Fever, anorexia, malaise and weight loss.

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17
Q

Which condition is commonly associated with ulcerative colitis?

A

Primary sclerosing cholangitis (90%).

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18
Q

What are the blood and stool results in someone with IBD?

A

Raised WCC, platelets, CRP and ESR in blood.
Raised foecal calprotectin in stool.

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19
Q

What is used to rule out infections in IBD?

A

Stool samples to test for bacteria.

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20
Q

What is the aim of treatment for IBD?

A

To induce remission of the disease.

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21
Q

What are the 1st and 2nd line treatments for UC?

A

1st - Aminosalicyclate (mesalazine).
2nd - Steroids (prednisolone).

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22
Q

How is remission maintained in ulcerative colitis?

A

With immunosuppressants:
-Azathioprine and methotrexate.

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23
Q

What is a curative option for UC?

A

Surgery - to remove the inflamed bowel portion and making a stoma.

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24
Q

What are colonic complications of IBD?

A

Colorectal cancer, blood loss and perforation.

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25
Q

Which two autoimmune conditions are associated with IBD?

A

Ankylosing spondylitis and arthritis.

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26
Q

What exacerbates and triggers flare ups in IBD?

A

NSAIDs, certain foods, chronic stress and depression.

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27
Q

Why are symptoms of Crohn’s more broad than UC?

A

The whole GI tract is affected and symptoms will arise from where the inflammation is.

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28
Q

What are small bowel symptoms of Crohn’s?

A

Abdominal pain, weight loss.
-Terminal ileum = RLQ pain.

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29
Q

What are colonic symptoms of Crohn’s?

A

Bloody diarrhoea (not as common), shitting pain.

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30
Q

What are systemic symptoms in IBD attacks?

A

Fever, fatigue, malaise, anorexia/weight loss.

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31
Q

What are the colonoscopy and biopsy findings in IBD?

A

UC - Continuous and mucosal inflammation.
Crohn’s - Skip lesions and transmural inflammation.

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32
Q

Why does Crohn’s disease lead to anaemia and vitamin deficienies?

A

Inflammation affects the small intestine so vitamin absorption, leading to anaemia.

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33
Q

What is the first line treatment for Crohn’s?

A

Steroids (prednisolone).

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34
Q

How is remission maintained in Crohn’s?

A

Immunosuppressants:
-Azathioprine.
-Methotrexate.

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35
Q

What surgery option is available for Crohn’s?

A

If the terminal ileum is affected, it can be removed and and an ileostomy (stoma) is done.

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36
Q

What is coeliac disease?

A

Autoimmune condition causing inflammation of the mucosa of the small intestine in response to gluten. Causes villous atrophy, crypt hyperplasia and malabsorption.

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37
Q

Where does coeliac disease affect?

A

Mostly the jejunum.

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38
Q

Describe the epidemiology of coeliac disease.

A

Equal in men and women and can start at any age.

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39
Q

When does coeliac disease usually present?

A

Infancy, and in middle age.

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40
Q

What type of disease is coeliacs?

A

Autoimmune - T4 hypersensitivity.

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41
Q

What are the two main risk factors for coeliac disease?

A

-Autoimmune disease (thyroid, Addison’s, T1DM, auto hep, PSC, PBC).
-Family history (HLADQ2 and HLADQ8).

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42
Q

Describe the genetic associations of coeliac disease.

A

HLA-DQ2 (90%).HLA-DQ8.

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43
Q

Describe the pathophysiology of coeliac disease.

A

T4 hypersensitivity - Autoantibodies are created in response to exposure to gluten to the small intestine.
-Villous atrophy and crypt hyperplasia.

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44
Q

Which autoantibodies are present in coeliac disease?

A

Anti-TTG and anti-EMA autoantibodies (IgA).

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45
Q

How does coeliac disease present in infants?

A

Failure to thrive.

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46
Q

How does coeliac disease present?

A

Diarrhoea, steatorrhoea, fatigue, weight loss, pain.
-Mouth ulcers, anaemia, dermatitis herpetiformis.

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47
Q

What are three rare symptoms of coeliac disease?

A

Neuro Sx:
-Peripheral neuropathy, ataxia, epilepsy.

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48
Q

Why does coeliac disease cause anaemia?

A

Villous atrophy causes malabsorption causing iron, folate and B12 deficiencies.

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49
Q

What is the first line investigation used in coeliac disease?

A

Serum antibodies:
-Total IgA.-Anti-TTG.-Anti-EMA.

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50
Q

What is the gold standard investigation in coeliac disease?

A

Duodenal biopsy.
-Crypt hypertrophy and villous atrophy.

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51
Q

What are three other investigations for coeliac disease and why?

A

Genetic testing (confirm gene), FBC (investigate anaemia) and DEXA scan (investigate osteoporosis).

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52
Q

How is coeliac disease managed?

A

Lifelong gluten free diet.
-Monitor complications and coeliac antibodies.

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53
Q

What are four complications of coeliac disease?

A

Vitamin deficiency, anaemia, osteoporosis, cancer (lymphoma, oesophageal, gastric, small/large bowel).

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54
Q

What is irritable bowel syndrome?

A

A group of functional chronic bowel disorders without an organic cause.

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55
Q

Describe the epidemiology of IBS.

A

Onset usually below 40y.
-More common in females.
-Affects 20% of Western world.

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56
Q

What causes IBS?

A

Unknown, there are theories of causes but thought to be related to psychology (stress, anxiety, drugs and a poor diet).

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57
Q

What are the types of IBS?

A

IBS-C - Mostly constipation.
IBS-D - Mostly diarrhoea.
IBS-M - Mixed and alternating.

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58
Q

What are the six risk factors for IBS?

A

GI infections, previous severe long-term diarrhoea, anxiety/depression, stress, trauma/abuse, eating disorders.

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59
Q

How does IBS usually present?

A

Diarrhoea, constipation, ado pain/cramps, bloating.
-Altered stool form and frequency.
-Change in bowel habit.
-Worse after eating.
-Relieved by defaecating.

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60
Q

When should IBS be considered?

A

ABC:
-Abdominal pain.
-Bloating.
-Change in bowel habit.

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61
Q

What type of diagnosis is IBS?

A

A diagnosis of exlcusion.

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62
Q

How is IBS diagnosed?

A

-Once all organic causes are rules out (IBD, coeliacs, cancer).
-Normal bloods (FBC, ESR, CRP, coeliac screen).
-Normal foecal calprotectin.
-Normal colonoscopy and biopsy.

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63
Q

How is IBS managed?

A

Eat a healthy diet and exercise.
-Regular small meals.
-Adequate fluids.
-Reduce processed foods.
-Limit caffeine and alcohol.

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64
Q

What are the medications used for IBS?

A

1st - loperamide (diarrhoea), laxatives (constipation).
2nd - Tricyclic antidepressants.
3rd - SSRIs.

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65
Q

What else can be used to help people with IBS who are stressed?

A

CBT.

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66
Q

What is GORD?

A

Gastro-oesophageal reflux disease.-When stomach acid refluxes back into the oesophagus due to decreased LOS pressure and irritates the lining of the oesophagus.

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67
Q

Why is the oesophagus more sensitive to stomach acid?

A

The oesophagus has squamous epithelia which is more sensitive to stomach acid whereas the stomach has columnar epithelia.

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68
Q

What are the five causes of GORD?

A

Hiatal hernia, alcohol, obesity, pregnancy, smoking.

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69
Q

What are the symptoms of GORD?

A

Dyspepsia (indigestion):
-Heartburn, acid regurgitation, bloating, nocturnal cough, hoarse voice.
-Retrosternal or epigastric pain.

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70
Q

When are symptoms of GORD worse and why?

A

When laying down as acid refluxes easier.

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71
Q

When is endoscopy done in GORD?

A

When there are red flags that suggest malignancy or serious conditions.

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72
Q

What are seven red flags when investigating GORD?

A

Weight loss, N+V, haematemesis, dysphagia, low haemoglobin, raised platelets, resistant to treatment.

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73
Q

What is the treatment for GORD?

A

Lifestyle, medications (omeprazole) and surgery.

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74
Q

How is lifestyle changed in GORD?

A

Losing weight, avoid smoking, reduce tea/coffee and alcohol, smaller meals and avoid heavy meals before bed.

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75
Q

Which medications are used to treat GORD?

A

-Heartburn medication when required.
-PPIs (omeprazole/lansoprazole) to reduce acid secretion.

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76
Q

How is surgery used to treat GORD?

A

Laparoscopic fundoplication to tighten the LOS and decrease the amount of acid refluxing into the oesophagus.

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77
Q

What is a complication of GORD?

A

Barrett’s oesophagous.

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78
Q

What is Barrett’s oesophagus?

A

Metaplasia from squamous to columnar epithelium in the lower oesophagus.

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79
Q

Do symptoms of GORD get worse in Barrett’s oesophagus?

A

No, they typically improve.

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80
Q

Who is Barrett’s oesophagus more common in?

A

Middle aged males.

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81
Q

What is the typical presentation of Barrett’s oesophagus?

A

Middle aged man with a long history of GORD and dysphagia.

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82
Q

How is Barrett’s oesophagus diagnosed?

A

OGD and biopsy.

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83
Q

What is Barrett’s oesophagus a risk factor for?

A

Adenocarcinoma of the oesophagus as Barrett’s oesophagus is premalignant.

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84
Q

What is the progression of Barrett’s oesophagus?

A

No dysplasia - Low grade dysplasia - High grade dysplasia - Adneocarcinoma.

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85
Q

How is Barrett’s oesophagus treated?

A

With strong PPIs to reduce acid secretion and RF ablation surgery (destroys cells so they’re replaced with normal).

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86
Q

Why is Barrett’s oesophagus monitored?

A

It is a big risk factor for oesophageal cancer (adenocarcinoma).

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87
Q

What is a peptic ulcer?

A

Ulceration of the mucosa of the stomach (gastric) or the duodenum (duodenal).

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88
Q

Which peptic ulcers are most common?

A

Duodenal ulcers are more common.

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89
Q

What are the five risk factors for peptic ulcers?

A

Smoking, H. pylori, stress, drugs (NSAIDs) and alcohol.

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90
Q

Describe the pathophysiology of peptic ulcers.

A

Mucosa is prone to ulceration from:
-Breakdown of protective layer.
-Increase in stomach acid.

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91
Q

What increases the breakdown of protective layer of the stomach/duodenum?

A

NSAIDs or H. pylori.

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92
Q

What increases the secretion of stomach acid?

A

Stress, alcohol, caffeine, smoking and spicy food.

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93
Q

How do peptic ulcers usually present?

A

Epigastric pain, N+V, dyspepsia, iron deficiency anaemia, haematemesis and melaena.

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94
Q

What are the red flags in peptic ulcers?

A

Haematemesis, coffee ground vomit, anaemia and dysphagia.

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95
Q

If no red flags are present, how are peptic ulcers investigated?

A

Stool antigen test and urease breath test (H. pylori).

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96
Q

If red flags are present, how are peptic ulcers diagnosed?

A

Endoscopy and biopsy.

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97
Q

How are peptic ulcers managed?

A

-If on NSAIDs, stop.
-If H. pylori - triple therapy CAP (clarythromycin, amoxicillin, PPI).
-High dose PPIs to reduce acid secretion.

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98
Q

Where are most gastric ulcers located?

A

The lesser curve of the stomach.

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99
Q

Where are most duodenal ulcers located?

A

First part of duodenum at the posterior wall.

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100
Q

Which type of peptic ulcer is worse on eating and which is better in eating?

A

Worse on eating - gastric.
Better in eating - duodenal.

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101
Q

Which peptic ulcer is worse between meals?

A

Duodenal ulcers.

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102
Q

Which peptic ulcer is relieved by anti-acids?

A

Gastric ulcers.

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103
Q

What is a common complication of a duodenal ulcer?

A

Ruptured gastroduodenal artery and bleeding.

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104
Q

What are three complications of peptic ulcers?

A

Bleeding, perforation and peritonitis, pyloric stenosis.

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105
Q

What is gastritis?

A

Inflammation of the stomach’s mucosal lining.

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106
Q

What are the four main causes of gastritis?

A

NSAIDs, H. pylori, bile reflux and stress.

107
Q

How does gastritis usually present?

A

Epigastric pain with diarrhoea, N+V and dyspepsia.
-Bloating, burping and lost appetite.

108
Q

What is the gold standard investigation for gastritis?

A

Endoscopy and biopsy.

109
Q

If H. pylori is suspected for causing gastritis, what investigation is done?

A

Stool antigen test and urease breath test.

110
Q

How is gastritis treated?

A

Treat the cause.
-If H. pylori, triple therapy CAP (clarythromycin, amoxicillin and PPI).

111
Q

What is the most common surgical emergency?

A

Appendectomy for appendicitis.

112
Q

What is the appendix?

A

A vestigial organ with a disputed functionality - attached to the large intestine.

113
Q

What is appendicitis?

A

Sudden inflammation of the appendix.

114
Q

What mostly causes appendicitis?

A

Obstruction within the appendix.

115
Q

What is the peak age of appendicitis?

A

10-20.

116
Q

What are the most common causes of appendicitis?

A

Faecolith (hard solid faeces).
-Lymphoid hyperplasia, trauma and worms.

117
Q

What is the presentation of appendicitis?

A

Umbilical pain which localises to McBurney’s point.
-Guarding, pyrexia, N+V.
-Rosving’s sign (RUQ pressure causes LLQ pain).

118
Q

In appendicitis, what does rebound and percussion tenderness signify?

A

Peritonitis.

119
Q

Where is McBurney’s point?

A

2/3rds the way from the umbilicus to the anterior superior iliac spine (ASIS).

120
Q

What is the gold standard investigation for appendicitis?

A

CT scan.

121
Q

Why would USS be used in diagnosing appendicitis?

A

In women to rule out pregnancy.In children, as CT is too much harmful radiation.

122
Q

What are the blood results in appendicitis?

A

Raised WCC, ESR and CRP.

123
Q

Which other test is done in appendicitis and what does it rule out?

A

Urinalysis:
-Rule out UTI.
-Rule out pregnancy (HCG).

124
Q

What is the gold standard treatment for appendicitis?

A

Appendectomy with IV antibiotics pre and post operatively.

125
Q

What are two complications of appendictis?

A

Peritonitis and abscesses.

126
Q

What is a diverticulum?

A

An outpouching of colonic mucosa.

127
Q

What is diverticulosis?

A

Multiple diverticulum without inflammation or infection.

128
Q

Is diverticulosis common? What is it associated with?

A

Very common above aged 50.
-Associated with higher age, low fibre diets, obesity and NSAIDs.

129
Q

What is diverticular disease?

A

When diverticula cause symptoms.

130
Q

What is diverticulitis?

A

Infection and inflammation of diverticula.

131
Q

What is the most common site for diverticular diseases and why?

A

Sigmoid colon:
-Smallest lumen diameter, highest pressure of the colon.

132
Q

What is Meckel’s diverticulum?

A

Common congenital abnormality of GI tract leading to diverticula.
Affects 2% of population, normally asymptomatic.

133
Q

Describe the pathophysiology of diverticula.

A

Increased pressure over time causes gaps to form in areas of circular muscles and the mucosa herniates through, forming diverticula.

134
Q

Why don’t diverticula form in the rectum?

A

It has an outer longitudinal muscle that surrounds the rectum.

135
Q

Which areas of the colon are vulnerable to the development of diverticula?

A

Areas that aren’t covered by tenia coli.

136
Q

What are the five risk factors for diverticula?

A

Ageing, increased colon pressure, chronic cough and connective tissue disorders (ED, M), bad diet (no fibre, fat).

137
Q

How does diverticulitis present?

A

Triad - LLQ pain, constipation and fresh rectal bleeding.
-Fever, diarrhoea, N+V.

138
Q

What is the gold standard investigation of diverticular diseases?

A

CT scan.

139
Q

What are the bloods findings in diverticulitis?

A

Raised ESR, CRP and WCC.

140
Q

What is the management for diverticulosis?

A

Asymptomatic, watch and wait.

141
Q

How is diverticular disease managed?

A

Bulk forming laxatives, high fibre diet.
Surgery considered to remove affected area.

142
Q

How is diverticulitis treated?

A

Co-amoxiclav (Abx), analgesia, IV fluids and liquid food.

143
Q

What are six complications of diverticular diseases?

A

Perforation, bleeding, peritonitis, fistula, obstruction, abscesses.

144
Q

What is helicobacter pylori?

A

A gram negative bacteria that lives in the stomach.

145
Q

Why is helicobacter pylori harmful?

A

Can cause damage to stomach lining, causing gastritis, ulcers and increasing the risk of stomach cancer.

146
Q

How does helicobacter pylori live in the stomach?

A

Lives in the gastric mucosa and avoids the acid by secreting ammonia, which neutralises the acid.

147
Q

Which tests are used to detect helicobacter pylori?

A

-Urea breath test.
-Stool antigen test.
-Endoscopy - rapid urease test.

148
Q

How is helicobacter pylori treated?

A

Triple therapy (CAP) for 7 days:-Clarythromycin, amoxicillin and PPI.

149
Q

What are the two types of oesophageal cancer? Where are they found and what are they associated with?

A

-Adenocarcinoma (lower 1/3rd) , associated with Barrett’s oesophagus
-Squamous cell carcinoma (upper 2/3rd), associated with smoking and alcohol.

150
Q

How does oesophageal cancer present?

A

Presents when advanced - ALARMS:
-Anaemia, loss of weight, anorexia, recent sudden symptom worsening, melaena/haematemesis, swallowing progressively difficult.

151
Q

What is the gold standard investigation for oesophageal cancer?

A

OGD and biopsy.

152
Q

What is used in oesophageal cancer for staging?

A

CT/PET scan.

153
Q

How is oesophageal cancer treated?

A

If fit - chemo, radio and surgery.
If unfit and old - palliative.

154
Q

What type of tumours is gastric cancer?

A

Mostly adenocarcinomas.

155
Q

What are the two types of gastric cancer? How common are they? What is the prognosis of them?

A

T1 - Well differentiated. 80%, better prognosis.
T2 - Undifferentiated. 20%, worse prognosis.

156
Q

What are RFs/causes for gastric cancer?

A

H. pylori, smoking, gastritis, FHx.

157
Q

How does gastric cancer usually present?

A

Epigastric pain, N+V, anorexia, weight loss, anaemia, TATT, dysphagia.

158
Q

What are other signs of gastric cancer?

A

Signs of metastases - liver (jaundice).

159
Q

How is gastric cancer investigated?

A

OGD and biopsy.
-CT/MRI/PET for staging.

160
Q

What is the management for gastric cancer?

A

Nutritional support, chemo, radio, surgery.

161
Q

What is the 5y survival for gastric cancer?

A

60% of people live for 5y.

162
Q

Are small intestine cancers common?

A

No, rare.
-1% of all GI cancers.

163
Q

What type of tumours are SI cancer mostly?

A

Mostly adenocarcinomas.

164
Q

What are risk factors for SI cancer?

A

Chronic SI disease (coeliacs, Crohn’s).

165
Q

What is the diagnosis and treatment for SI cancer?

A

The same for gastric cancer.

166
Q

How common is bowel cancer?

A

Very common, 4th most common in the UK.

167
Q

Where does bowel cancer most commonly metastasise to?

A

Mostly the liver.
-Lung and bone.

168
Q

What is the most common type of bowel cancer?

A

Adenocarcinoma.

169
Q

What are common precursors to bowel cancer?

A

Adenomas (polyps). They are spontaneous and benign growths that are normal with age but have the ability to progress to bowel cancer.

170
Q

What are seven risk factors for developing bowel cancer?

A

-Inherited genetic predisposition/family history.
-Adenomas/polyps, age.
-Alcohol and smoking.
-IBD and diet (red meat, low fibre).

171
Q

Which two inherited conditions increase the risk of bowel cancer?

A

-Familial adenomatous polyposis (FAP).
-Lynch syndrome.

172
Q

What is familial adenomatous polyposis?

A

An autosomal dominant mutation of the tumour suppressor gene APC which leads to 1000s of polyps developing in the bowel.
-This leads to inevitable bowel cancer usually before age 40.

173
Q

How is FAP treated?

A

Prophylactic removal of the entire colon to prevent bowel cancer.

174
Q

What is Lynch syndrome?

A

Hereditary non polyposis colorectal cancer.
-Autosomal dominant mutation of DNA mismatch repair gene.
-Increases risk of all cancers, but especially colorectal cancer.
-Doesn’t cause polyps, but tumours in isolation.

175
Q

What are the five red flags for bowel cancer?

A

-Change in bowel habit.
-Unexplained weight loss.
-Rectal bleeding.
-Unexplained abdominal pain.
-Iron deficiency anaemia.

176
Q

Where are the most common locations for colorectal cancer?

A

Rectum and sigmoid colon.

177
Q

What is a sign of colorectal cancer?

A

Tenesmus (needing to poo when empty).

178
Q

What does fresh rectal bleeding mean in colorectal cancer?

A

Closer to the anus.

179
Q

How is bowel cancer screened for?

A

FIT test - detects micro blood particles in the poo.

180
Q

Who is bowel cancer screened in?

A

Everyone aged above 60y.

181
Q

When is a FIT test used?

A

To screen for bowel cancer.
-In those who don’t qualify for an urgent cancer referral.

182
Q

What is the gold standard investigation for bowel cancer?

A

Colonoscopy/sigmoidoscopy and biopsy.

183
Q

Who is offered colonoscopies at regular intervals?

A

Those at risk of developing colorectal cancer:
-FAP, Lynch syndrome, IBD.

184
Q

When is a sigmoidoscopy used over colonoscopy?

A

When there is fresh rectal bleeding.

185
Q

Which two classifications are used in staging bowel cancer?

A

Duke’s criteria and TNM staging.

186
Q

Describe duke’s criteria for staging in bowel cancer.

A

A - Confined to submucosa.
B - Extends through to muscle of bowel.
C - Lymph node involvement.
D - Metastatic disease.

187
Q

Describe TNM staging in bowel cancer.

A

T (tumour):
T1 - Submucosa. T2 - Muscle layer.T3 - Outer layer (serosa). T4 - Through serosa and reaches other organs.
N (nodes): N0 - No spread. N1 - 1-3 nodes. N2 - 3+ nodes.
M (metastases): M0 - No metastases. M1 - Metasatses.

188
Q

How is colorectal cancer managed?

A

Surgical resection.
-Chemo, radio.
-Palliative care.

189
Q

What is a complication of bowel cancer?

A

Obstruction of the large intestine (may present as this).

190
Q

What is a Mallory-Weiss tear?

A

A lower oesophageal mucosal tear due to sudden increased intra-abdominal pressure.

191
Q

How does a Mallory-Weiss tear usually present?

A

Young male with acute history of retching and eventually haematemesis.

192
Q

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

A

Alcohol, chronic cough, bulimia and hyperemesis gravidarum (severe N+V in pregnancy).

193
Q

What is important in distinguishing Mallory-Weiss tear and oesophageal varices?

A

For Mallory-Weiss tear there is no history of liver disease and portal hypertension.

194
Q

How does a Mallory-Weiss tear usually present?

A

Haematemesis.
-Wretching and vomiting.
-If severe - hypotension.

195
Q

How is Mallory-Weiss tear diagnosed?

A

OGD (endoscopy).

196
Q

What is the Rockall score?

A

Used for patients that have had endoscopy to calculate their risk of rebleeding and mortality in upper GI bleeds.

197
Q

What is the Glasgow-Blatchford score?

A

Scoring system in suspected upper GI bleeding on initial presentation.

198
Q

How is a Mallory-Weiss tear managed?

A

Most spontaneously heal within 24h.
-Most require no further treatment.

199
Q

How is a severe Mallory-Weiss tear managed?

A

OGD and banding/clipping.

200
Q

What are the four most common causes of upper GI bleeding?

A

Peptic ulcers (stomach/duodenum), oesophageal varices, Mallory-Weiss tear, stomach/duodenum cancers.

201
Q

How do upper GI bleeds usually present?

A

-Haematemesis, coffee-ground vomit, melaena, hypotension/tachycardia (if large).
-Signs of underlying pathology.

202
Q

How often are upper GI bleeds fatal?

A

10% of the time.

203
Q

What is intestine obstruction?

A

When there is a blockage in the bowel which prevents the passage of food, water and gas.

204
Q

How common are SI and LI obstructions?

A

SI are more common than LI obstruction.SI makes up 70% and LI makes up 30%.

205
Q

Describe the pathophysiology of intestinal obstruction.

A

Obstruction results in the build up of gas and foecal matter which results in vomiting and dilation of intestines proximal to the obstruction.

206
Q

What is the gold standard investigation for intestinal obstruction?

A

Non-contract CT of abdomen.

207
Q

What is the first line investigation for intestinal obstruction and what does it show?

A

XRAY - dilated bowel loops and transluminal fluid gas shadows.

208
Q

What are the blood results of intestinal obstruction?

A

Electrolyte imbalances, metabolic alkalosis (due to vomiting) and raised lactate (bowel ischaemia).

209
Q

What is the initial management of intestinal obstruction?

A

Drip and suck:
-Nil by mouth.
-IV fluids.
-NG tube.

210
Q

How is intestinal obstruction treated?

A

Surgery to correct the underlying cause.

211
Q

What causes small intestine obstruction?

A

-Adhesions (mc) - scar tissue that binds contents together.
-Hernias, Crohn’s and malignancy.

212
Q

What causes large intestine obstruction?

A

-Malignancy (mc, 90%).
-Volvulus (twisting).
-Intussusception (mc in children) - intestine slides into itself.
-Crohn’s, diverticulitis.

213
Q

What are four serious complications of intestinal obstruction?

A

Hypovolaemic shock, bowel ischaemia and bowel perforation and sepsis.

214
Q

What are the five features of intestine obstruction?

A

-Vomiting (bile).
-Abdominal distension.
-Diffuse abdominal pain.
-Absolute constipation.
-Tinkling sounds.

215
Q

What are the three main causes of intestinal obstruction?

A

Adhesions (SI), hernias (SI) and malignancy (LI).

216
Q

What are the four main causes of adhesions?

A

Abdominal or pelvic surgery/infections.
Endometriosis.
Peritonitis.

217
Q

Compare the symptoms of SI and LI obstructions.

A

SI - Vomiting then constipation.
LI - Constipation then vomiting.

218
Q

What is a pseudo-obstruction?

A

When there are symptoms of intestinal obstruction but no mechanical obstruction.

219
Q

What is the definition of diarrhoea?

A

3 or more watery stools per day.

220
Q

What is the difference between acute and chronic diarrhoea?

A

Acute - <14 days.
Chronic - >28 days.

221
Q

What are five types of diarrhoea?

A

Watery, secretory, functional, steatorrhoea, inflammatory.

222
Q

What is the most common cause of diarrhoea in adults?

A

Norovirus.

223
Q

What are the six main causes of diarrhoea?

A

IBD, coeliac, malignancy, inflammation, hyperthyroidism and infective.

224
Q

What is the most common cause of diarrhoea?

A

Viral.

225
Q

What are the main viral causes of diarrhoea in children and adults?

A

Children - rotavirus.
Aduts - norovirus.

226
Q

What are the six main bacterial causes of diarrhoea?

A

Campylobacter (mc), E. coli, shigella, salmonella, C. diff and cholera.

227
Q

What three other things can cause diarrhoea?

A

Worms, parasites and antibiotics.

228
Q

How does diarrhoea present?

A

Depends on the cause:
-Infective tends to be acute.
-Non-infective has a longer history.

229
Q

How is diarrhoea treated?

A

Depends on the underlying cause:
-Viral is self limiting.
-Bacterial - antibiotics.

230
Q

What are the two main complications of diarrhoea?

A

Dehydration and electrolyte loss.

231
Q

What is achalasia?

A

Rare disorder where there is impaired oesophageal peristalsis and the LOS doesn’t open.

232
Q

What is the cause of achalasia?

A

Idiopathic.

233
Q

How does achalasia present?

A

Non-progressive dysphagia, substernal pain, food regurgitation, coughing.

234
Q

How is achalasia diagnosed?

A

-Manometry - measures oesophagus pressure at different points.
-X-RAY and barium swallow.
-Endoscopy.

235
Q

How is achalasia treated?

A

-Nitrates - relax oesophagus.
-Balloon stenting.
-Removal of LOS.

236
Q

What is ischaemic colitis?

A

Ischaemia of the arterial supply to the colon, which then gets inflamed due to hypoperfusion.

237
Q

What are the three most commonly affected sites of ischaemic colitis?

A

Splenic flexure (mc), sigmoid colon and caecum.

238
Q

What causes ischaemic colitis?

A

Affects IMA:
-Thrombosis (mc), emboli, decreased CO and arrhythmias.

239
Q

What are the features of ischaemic colitis?

A

Sudden onset LLQ pain and bright bloody stools.
-Signs of hypovolaemic shock.

240
Q

How is ischaemic colitis diagnosed?

A

GS - colonoscopy and biopsy.
-Rule out other causes.

241
Q

How is ischaemic colitis treated?

A

IV fluid, antibiotics.
-Treat underlying cause (remove clot).
-Surgery if infarct and gangrenous.

242
Q

What are the complications of ischaemic colitis?

A

Perforation, peritonitis and infarct bowel.
-Strictures and obstruction.

243
Q

What is mesenteric ischaemia?

A

Ischaemia of the small intestine.

244
Q

When should mesenteric ischaemia be suspected?

A

AF with severe abdominal pain.

245
Q

What are the two types of mesenteric ischaemia?

A

Acute and chronic.

246
Q

What causes mesenteric ischaemia?

A

Affects SMA:
-Thrombosis (mc) and emboli (due to AF).

247
Q

What are the symptoms of mesenteric ischaemia?

A

Triad:
-Central acute severe abdominal pain.
-No abdominal signs of examination.
-Rapid hypovolaemic shock.

248
Q

What are the risk factors for mesenteric ischaemia?

A

Same as cardiovascular disease and AF.

249
Q

How is mesenteric ischaemia diagnosed?

A

CT angiogram.

250
Q

What is the mortality of acute mesenteric ischaemia?

A

50%.

251
Q

How is mesenteric ischaemia treated?

A

Revascularisation and surgery if bowel is infarct.

252
Q

What are five perianal disorders?

A

Hemorrhoids, perianal abscess, anal fistula, anal fissure and pilonidal abscess.

253
Q

What is the most severe complications of ulcerative colitis?

A

Toxic megacolon.

254
Q

What is toxic megacolon? What are its features?

A

Extreme inflammation and distention of the bowel.
-Acute colonic distention with severe bloody diarrhoea 6+ times daily.

255
Q

How does toxic megacolon appear on AXR?

A

Very distended colon.

256
Q

How does toxic megacolon appear on AXR?

A

Very distended colon.

257
Q

What is the treatment of toxic megacolon?

A

Supportive therapy, antibiotics and aminosalicyclates, if no improvement in 36h - surgery.

258
Q

What is Cullen’s sign?

A

Superficial bruising in the subcutaneous fat around the umbilicus.

259
Q

What is Grey Turner’s sign?

A

Bruising of the flanks - between bottom rib and hip.

260
Q

What do Cullen’s and Grey Turner’s signs signify?

A

Acute pancreatitis and intra-abodminal bleeding.

261
Q

What does Rosving’s sign signify?

A

Appendicitis.

262
Q

What is Rosving’s sign?

A

When you press the left iliac fossa, it results in pain of the right iliac fossa.

263
Q

Describe the CMV infection.

A

Affects 50% of adults asymptomatically.
-Presents in HIV/AIDS as the latent infection gets reactivated and causes problems such as colitis.
-Characteristic ‘owl eye’ inclusions on pathology.

Phase 2a (15 decks)

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