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Phase 2a diseases > Gatrointestinal > Flashcards

Gatrointestinal Flashcards

1
Q

What is Gastro-oesophageal reflux disorder (GORD)?

A
  • Prolonged or recurrent reflux of the gastric contents into the oesophagus.
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2
Q

What is the clinical presentation of gastro-oesophageal reflux disorder (GORD)?

A
  • Heartburn (often related to lying down, or following meals.)
  • Odynophagia (Pain when swallowing).
  • Regurgitation
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3
Q

What is the pathophysiology of GORD?

A

Potential pathologies of GORD are:

  • Atrophy and frequent transient relaxations of the lower oesophageal sphincter (LOS).
  • Increased mucosal sensitivity to gastric acid.
  • Hiatus hernia (Part of the stomach passes through the hiatus in the diaphragm).
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4
Q

What is the aetiology of GORD?

A
  • Smoking, alcohol.
  • Pregnancy
  • Obesity
  • Big meals
  • Complications, such as a hiatus hernia.
  • Inadequate LOS function (could be congenital or related to trauma).
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5
Q

What is the epidemiology of GORD?

A
  • 2-3x more common in men.

- 25% of adults will experience heartburn. Must be at least 2x per week to be considered GORD.

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6
Q

What are the diagnostic tests used to investigate GORD?

A
  • Endoscopy

- Barium swallow (rarely used, as isn’t too effective for diagnostic purposes).

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7
Q

What are the treatments for GORD?

A

1st line:

  • Usually conservative. This includes lifestyle management, such as weight loss, avoidance of alcohol where possible, stopping smoking.
  • PPI’s for 1 month.

2nd line:

  • H2 antagonist (such as ranitidine or famotidine - H2 antagonists usually end in “-idine”)

GOLD STANDARD:
- Anti-reflux surgery. Rarely carried out in practice.

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8
Q

What are the potential complications of GORD?

A
  • Oesophageal stricture formation (Tightening of the oesophagus), resulting in dysphagia.
  • Barret’s Oesophagus. Involves the replacement of the squamous epithelium at the distal end of the oesophagus with columnar epithelium. This can result in cancer developing.
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9
Q

What are the potential causes of upper GI bleeding (3 causes)? And what do these involve?

A
  • Mallory-weiss tear. This is mucosal lacerations in the upper GI tract.
  • Oesophageal-gastric varices. This is dilated veins at the portal-systemic venous system junctions, leading to variceal haemorrhage.
  • Peptic ulceration. Breakdown of the GI mucosa inside or adjacent to an acid-secreting area.
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10
Q

What is the clincal presentation of a Mallory-weiss tear?

A
  • Typically, a bout of retching or vomiting developing into haematemesis (vomiting of blood).
  • Can also present with syncope, light headedness and dizziness (typical signs of blood loss).
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11
Q

What is the clinical presentation of oesophageal-gastric varices?

A
  • Haematemesis
  • Liver disease
  • Pallor
    Shock (along with hypotension and high heart rate).
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12
Q

What is the clinical presentation of a peptic ulcer?

A
  • Burning epigastric pain.
  • Nausea.
  • Heartburn.
  • Flatulence (Gas buildup in abdomen).
  • Occasionally, a painless haemorrhage may be present.
  • If there is a duodenal peptic ulcer, the patient will experience more pain when they are hungry and more pain at night (both due to more duodenal movement).
  • If there is a stomach ulcer, patient will experience more pain while eating.
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13
Q

Which bacterium is associated with the overwhelming majority of peptic ulcers?

A
  • H. pylori (Helicobacter Pylori).
  • This is a gram negative, curved rod (resembling a spiral) shaped bacteria.
  • Responsible for >80% of peptic ulcers (both gastric and duodenal).
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14
Q

What is the pathophysiology of a Mallory-Weiss tear?

A
  • Sudden increase in pressure in the distal oesophagus.
  • Due to the distal oesophagus being nondistensible, the mucosa may tear.
  • Causes blood to enter the oesophagus and then be vomited out.
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15
Q

What is the pathophysiology of oesophageal-gastric varices?

A
  • Liver disease causes hypertension in the portal veins.
  • Hypertension in the systemic-hepatic venous junction leads to venous system distension (varices).
  • This distension causes damage to the oesophageal vasculature, leading to bleeding into the oesophagus.
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16
Q

What is the pathophysiology of Peptic ulceration?

A
  • Occurs either due to reduction in protective prostaglandins in the GI tract, or an increase in gastric acid secretion.
  • As a result, acid secreted by the GI tract breaks down either the stomach (gastric) or duodenal mucosa, resulting in ulcer formation.
  • The pain felt will depend on the acidity of the area with the ulcer.
  • H. pylori may then also infect the mucosa itself, leading to further inflammatory damage.
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17
Q

What is the aetiology of Mallory-Weiss tears?

A
  • Trauma caused to the oesophagus by frequent/chronic coughing, retching, vomiting and even hiccuping.
  • Can also be damaged as a result of excessive alcohol intake.
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18
Q

What is the aetiology of oesophageal-gastric varices?

A
  • Portal hypertension. This is why the vast majority of patients who have oesophageal-gastric varices will also have chronic liver disease.
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19
Q

What is the aetiology of peptic ulceration?

A
  • H. Pylori presence. This results in increased gastric acid secretion, and subsequent disruption of the mucosal protective layer. In the duodenum, there is reduced bicarbonate production, which is used to raise the pH.
  • NSAIDs taken frequently/over a long period of time. NSAIDs reduce prostaglandin production (interfere with the COX pathway), and these prostaglandins provide mucosal protection in the upper GI.
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20
Q

What is the epidemiology of the three causes of upper-GI bleeding?

A

Mallory-weiss tears:

  • 4-8% of all upper gastrointestinal.
  • More common in alcoholics and bulimics (excessive vomiting damages the distal oesophagus).

Oesophageal-gastric varices:
- Causes 10-20% of all upper GI bleeding.

Peptic ulcers:

  • Cause 50% of all upper GI bleeding (most common cause).
  • Approx. 75% of peptic ulcers will be duodenal rather than gastric.
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21
Q

What are the diagnostic tests for upper GI bleeding?

A
  • Endoscopy (Usually used when Mallory-Weiss tear or oesophageal-gastric varices are suspected.)
  • H. Pylori is tested for when peptic ulcer is suspected cause of bleeding. This requires a urea breath test or a stool antigen test. Sometimes, endoscopy may be used but this is much more invasive so not common.
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22
Q

What are the treatment options for Mallory-Weiss tears?

A
  • Tear tends to rapidly (within 24 hours) heal on its own.

IF LARGER TEAR:

  • ABC + resuscitate (provide oxygen, open airways, correct fluid losses).
  • Blood transfusion if required. (hypovolemic shock)
  • Give PPI or anti-emetic depending on symptoms (nausea/vomiting. Use PPI to reduce acidity of fluids reaching the tear).
  • Identify and plan modification to any co-morbidities.
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23
Q

What are the potential treatment options for oesophageal-gastric varices?

A

IF SMALL WAIT AND MONITOR WITH ANNUAL ENDOCSCOPY.

IF MEDIUM:

  • Diagnostic endoscopy
  • Non-selective B-blocker (eg. propanolol).

IF AN ACUTE VARICEAL BLEED:
1st - ABC + resuscitate (Provide oxygen, open airways, treat potential shock).

2nd - Urgent endoscopy

3rd - Calculate Rockall score. Assesses how severe an upper GI bleed is.

  • Provide terlipressin (1st line drug). This will reduce the dilation of the splanchnic blood vessels, reducing blood flow to the hepatic system and subsequently reducing bleeding.

MANAGEMENT AFTER BLEED:
- Non-selective B blocker (propanolol).

  • Consider endoscopic band ligation (Insertion of a constrictive band around the varices, to mechanically constrict them).
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24
Q

What are the potential treatment options for peptic ulcers?

A

1st line:

  • STOP NSAIDS
  • Stop smoking
  • PPI for 4 weeks (omeprazole).

IF H. PYLORI IS CAUSE:
- Triple therapy is used (PPI + 2 antibiotics is 1st line - usually clarithromycin, amoxicilin, and omeprazole (the PPI))

ANOTHER ENDOSCOPY IN 6 WEEKS. If not healed, biopsy to check for malignancy.

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25
Q

What are the potential complications of Mallory-Weiss tears?

A
  • Hypovolaemic shock (severe fluid loss that can lead to death - rare).
  • Rebleeding (wound re-opens).
  • MI (often related to the hypovolaemic shock).
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26
Q

What are the potential complications of oesophageal-gastric varices?

A
  • Significant risk of death

- High chance of rebleeding after initial occurrence.

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27
Q

What are the potential complications of peptic ulcers?

A
  • Can cause an upper GI bleed.

- Cancer risk increased.

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28
Q

What is gastritis?

A

Inflammation of the gastric mucosa (generally the stomach).

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29
Q

What are the two different types of gastritis?

A
  • Acute or chronic
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30
Q

What is the clinical presentation of gastritis?

A

Usually asymptomatic.

Sometimes:

  • Functional dyspepsia (indigestion).
  • Upper abdominal pain (epigastric).
  • Nausea and vomiting.
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31
Q

What types of white blood cells are associated with chronic gastritis? Which are associated with acute gastritis?

A

Chronic:
- Mononuclear cell infiltration (lymphocytes, plasma cells, macrophages).

Acute:
- Neutrophilic infiltration.

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32
Q

What is the pathophysiology of gastritis?

A
  • Local inflammatory response to infection by H. pylori.

- The presence of H. pylori can increase the amount of gastric acid secretion, causing further inflammation.

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33
Q

What is the aetiology of gastritis?

A

Most commonly caused by a H. Pylori infection.

However, could also be:

  • autoimmune gastritis
  • viral gastritis
  • duodeno-gastric reflux (alkaline substances secreted by the duodenum pass backwards into the stomach).
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34
Q

What are the investigations used for gastritis?

A
  • 1st line: Helicobacter Pylori breath test and FBC.
  • Endoscopy. The gastric mucosa may appear reddened, but will sometimes appear normal.
  • Biopsy. This can detect histological changes.
  • Blood and stool tests. Can detect inflammation or erosions in the stomach.
  • Faecal occult blood test (used to find sub-visual blood in faeces).
  • Faecal calprotectin. High calprotectin indicates inflammation in the body, such as that associated with gastritis.
  • Stool culture.
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35
Q

What treatment is given for gastritis?

A

IF MILD:

  • Encourage fluid intake
  • Small, light, non-fatty meals.
  • Anti-motility agents (CONTRAINDICATED IF INFECTIVE CAUSE).

IF MODERATE - SEVERE:

  • Stop NSAIDS and aspirin.
  • Give PPI (omeprazole 1st line) or H2 antagonist (famotidine 2nd line).

IF H. PYLORI SUSPECTED CAUSE:
- Triple therapy (PPI + 2 antibiotics - omeprazole, amoxicillin and clarithromycin).

IF CAMPYLOBACTER CAUSE:

  • May cause neurological symptoms.
  • Neuro symptoms + gastritis = campylobacter (usually).
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36
Q

What are the potential complications of gastritis?

A

Peptic ulceration.

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37
Q

What are the potential sequelae to gastritis?

A
  • Peptic ulceration
  • Pernicious anaemia (Occurs due to B12 deficiency, which is associated with gastritis and the associated autoimmune attack.)
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38
Q

What is gastropathy?

A
  • Injury to the gastric mucosa with epithelial cell damage and regeneration.
  • Different to gastritis as there is little-to-no inflammation.
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39
Q

What is the clinical presentation of gatropathy?

A
  • Indigestion

- Vomiting

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40
Q

What is the pathophysiology of gastropathy?

A

Reduction in protective prostaglandins (usually as a result of NSAID use) results in the acidic contents of the stomach/ duodenum breaking down the mucosa.

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41
Q

What is the aetiology of gastropathy?

A
  • Most commonly, over/long-term use of NSAIDs.

Could also be:

  • Severe stress
  • High alcohol intake
  • CMV (cytomegalovirus)
  • Herpes simplex infection
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42
Q

What are the investigations used to diagnose gastropathy?

A
  • Endoscopy. This allows erosions of the stomach/duodenum to be seen, along with any sub-epithelial haemorrhages.
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43
Q

What treatment is offered to patients with gastropathy?

A
  • PPI (reduce acidity in GI tract).

- Removal of causative agent (often reduce NSAID use).

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44
Q

What are the potential complications of gastropathy?

A
  • Peptic ulceration.
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45
Q

What are the two main oesophageal motility disorders?

A
  • Achalasia

- Systemic sclerosis (Scleroderma).

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46
Q

What is achalasia?

A
  • Peristalsis of the oesophagus, along with failure of the lower oesophageal sphincter to relax.
  • Leads to impaired oesophageal emptying.
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47
Q

What is systemic sclerosis (Scleroderma)?

A
  • A multi-system autoimmune disease.

- Increased fibroblastic activity leads to the abnormal growth of connective tissue.

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48
Q

What are the two types of systemic sclerosis?

A
  • Limited cutaneous systemic sclerosis (Otherwise known as CREST syndrome).
  • Diffuse cutaneous systemic sclerosis.
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49
Q

What is the clinical presentation of achalasia?

A
  • A long history of dysphagia for both solids AND liquids.
  • Retrosternal chest pain, that isn’t cardiac related.
  • Weight loss.
  • Regurgitation.
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50
Q

What is the clinical presentation of limited cutaneous systemic sclerosis compared to that of diffuse cutaneous systemic syndrome?

A

LIMITED cutaneous systemic syndrome:

  • Raynaud’s phenomenon (Skin hardening in hands or face)
  • Joint pain and swelling (MSK).
  • CREST: Calcinosis, Raynaud’s, Esophageal dysmotility, Sclerodactyly and Telangiectasia. (This is where the name CREST syndrome comes from).

DIFFUSE cutaneous systemic syndrome:

  • The same symptoms as seen in limited SSc, but with a more rapid and widespread onset.

E.g. Heartburn, reflux oesophagitis, delayed gastric emptying, pulmonary fibrosis, pulmonary arterial hypertension.

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51
Q

What are the percentages of systemic sclerosis that can be attributed to both limited and diffuse disease?

A
  • 70% is limited.

- 30% is diffuse.

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52
Q

Which parts of the body does limited cutaneous systemic sclerosis affect?

A
  • Face
  • Forearms
  • Lower leg (up to the knee).
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53
Q

Which parts of the body does diffuse cutaneous systemic sclerosis affect?

A
  • All of those affected by limited cutaneous systemic sclerosis (Face, forearms, lower legs)
  • Arms
  • Thighs
  • Trunk
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54
Q

What is the pathophysiology of systemic sclerosis (SSc)?

A
  • Excessive collagen production and deposition.

- Vascular damage and inflammation.

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55
Q

What is the aetiology of systemic sclerosis?

A
  • Unknown

- Probably a genetic component.

56
Q

What is the epideiology of systemic sclerosis (SSc)?

A
  • Very rare
  • More common in women
  • Rare in children
57
Q

What are the diagnostic tests for systemic sclerosis?

A

1st line:

  • Serum autoantibody testing.
  • Standard inflammatory measurements/ investigations such as CRP and ESR, CXR and creatinine measurements.

NEW DIAGNOSTIC OPTIONS:

  • Scl 70 testing. This is an antibody test with 0.85 sensitivity and 0.99 specificity, making it a very powerful diagnostic tool for scleroderma.
58
Q

What are the treatment options for scleroderma (systemic sclerosis)?

A
  • NO DEFINITIVE CURE. TREAT SYMPTOMS (E.g tamponade treated with prednisolone - a corticosteroid).
59
Q

What is the pathophysiology of achalasia?

A
  • Decrease in the ganglionic cells in the nerve plexus of the oesophageal wall and degeneration in the vagus nerve.
  • The smooth muscle in the oesophagus and the LOS fails to relax, resulting in dysphagia.
60
Q

What are the potential treatments for achalasia?

A

AIM IS TO RELAX THE MUSCLES OF THE OESOPHAGUS, ESPECIALLY THE LOS.

1st line:

  • Nitrates (isosorbide dinitrate orally) where surgery is not an option, to open up the blood vessels and promote blood flow.
  • POTENTIALLY USE A CCB (verapamil)

2nd line:
- Botox may be an option for patients too, to try and reduce unwanted contraction of the smooth muscle cells in the oesophagus.

GOLD STANDARD:
- Surgical division of lower oesophageal sphincter, or endoscopic balloon dilatation of the oesophagus.

61
Q

What is the aetiology of achalasisa?

A

Unknown.

62
Q

What are the investigations for achalasia?

A
  • Barium swallow

- Upper GI endoscopy

63
Q

What are the potential complications of achalasia?

A
  • If left untreated, person may inhale material that becomes trapped in the oesophagus and choke.
  • achalasia also increases the chance of a person developing oesophageal cancer.
64
Q

What are the potential complications of systemic sclerosis (both diffuse cutaneous and limited cutaneous)?

A
  • Malnutrition due to swallowing problems.

- Obstructions of the GI tract due to reduced gastric motility.

65
Q

What is coeliac disease?

A

Immune mediated inflammatory response to gluten intake.

66
Q

What is the clinical presentation of a patient with coeliac disease?

A

Range of possible symptoms, with onset at any age (however, incidence peaks in infancy and the 5th decade):

  • Persistent GI symptoms
  • Faltering growth
  • Prolonged fatigue
  • Unexplained weight loss
  • Severe mouth ulcers
  • Iron, B12 and/or folate deficiency (anaemia).
  • IBS
  • Family history of coeliac disease.
67
Q

What is the key thing to ask if suspecting someone has coeliac?

A
  • Ask about their diet.

- Will potentially require a detailed history to come to a diagnosis.

68
Q

What is the pathophysiology of coeliac disease?

A
  • a-Gliadin is the toxic portion of gluten.
  • It leaks through the enterocytes, and triggers an immune response in the bowel.
  • This inflammatory response results in the release of mediators, which cause cell damage (villous atrophy and crypt hyperplasia).
  • The inflammatory process occurs via HLA-DQ2 or HLA-DQ8 (Human Leukocyte Antigens).
69
Q

What is the aetiology of coeliac disease?

A
  • Strong genetic association between coeliac disease and presence of the HLA DQ2/8 gene.
  • Attacks are stimulated in response to gluten in the diet.
70
Q

What is the epidemiology of coeliac disease?

A

1/100 in the UK. Therefore, prevalence is very high.

71
Q

What investigations are used to diagnose coeliac disease?

A

SEROLOGY: IgA tissue transglutaminase antibodies.

  • This test has a very high sensitivity and specificity for coeliac disease.
  • Endomysial antibodies (EMA) are also useful when diagnosing coeliac disease, as they have high sensitivity and specificity.
72
Q

What is the treatment for coeliac disease?

A
  • Gluten-free diet

- Nutritional supplementation as required (ergocalciferol for Vit. D2, and calcium carbonate for Ca2+)

73
Q

What are the potential complications of coeliac disease?

A
  • Increased incidence of malignancy.

- This can be combatted by adopting a gluten free diet.

74
Q

What are the two types of IBD?

A
  • Ulcerative colitis.

- Crohn’s disease.

75
Q

What is the difference between IBS and IBD?

A
  • IBD can cause inflammation and permanent harm to the bowel, whereas IBS causes no inflammation and will rarely require hospitalisation or surgery.
  • IBD can be seen during diagnostic imaging (e.g. colonoscopy) due to the inflammation, whereas IBS will usually shown no sign of disease or inflammation during the investigational imaging.
76
Q

What is ulcerative colitis?

What is Crohn’s disease?

A

UC - Continuous chronic inflammation of ONLY THE COLON (usually the descending colon/sigmoid colon). It is primarily mucosal (only affects the innermost layers of the bowel).

CD - Intermittent chronic inflammation of THE ENTIRE GI TRACT. It is transmural (affects every layer in the bowel).

77
Q

What is the clinical presentation of ulcerative colitis?

A
  • Recurrent diarrhoea (often containing blood and mucus).

- Some extra GI manifestations, such as arthralgia (joint pain), fatty liver and gall stones.

78
Q

What is the clinical presentation of Crohn’s disease?

A

Symptoms depend on the region of the bowel affected:

  • Small bowel IBD will cause weight loss and abdominal pain.
  • Terminal ileum IBD will cause right iliac fossa pain - this can sometimes mimic the pain seen in appendicitis.
  • Colonic IBD causes diarrhoea containing blood and mucus , along with pain in the location of the inflammation.

NOTE: Crohn’s can affect multiple patches of the bowel at once, which will lead to a combination of these symptoms.

79
Q

How does smoking affect ulcerative colitis and Crohn’s disease?

A
  • Smoking decreases severity of UC

- Smoking increases the severity of Crohn’s disease.

80
Q

What is the pathophysiology of Ulcerative colitis?

A
  • Mucosal inflammation that originates in the anus, and continuously progresses proximally.
  • Results in the depletion of goblet cells, and the reduction in secretion of protective prostaglandins causes crypt abscesses.
  • There is no granulomata in ulcerative colitis.
81
Q

What is the pathophysiology of Crohn’s disease?

A
  • Transmural inflammation that occurs anywhere in the GI tract in patches.
  • Causes deep ulcers and fissures, leading to the bowel having a cobblestone appearance.
  • 50% of Crohn’s disease will have granulomata.
82
Q

What is the aetiology of irritable bowel disease (Crohn’s and UC)?

A
  • There is a genetic link in both, but a very strong genetic link in Crohn’s.
  • Stress and depression increase the likelihood of an IBD attack occurring.
  • If effector T-cells are overpowering the regulatory T-cells, this leads to over-secretion of pro-inflammatory cytokines (IL12, 5, 7 etc.)
  • These cytokines stimulate the production of TNF-a, IL-1 and IL-6 by the macrophages.
  • Neutrophils, mast cells and eosinophils are also activated.
  • The wide variety of inflammation mediators being activated results in cell damage.
83
Q

What is the epidemiology of IBD?

A
  • Usually presents in teens and 20’s.

- 4 per 1000 in the UK

84
Q

What are the investigations for IBD?

A
  • Investigations generally aim to differentiate between Crohn’s and UC.
  • Sigmoidoscopy
  • Rectal biopsy
  • Look for location, spread, and nature of the inflammation to differentiate between the two.
85
Q

What is the treatment for ulcerative colitis?

A

MILD CASES:
1st line - 5-Aminosalicyclic acid (most commonly mesalazine) to be applied topically.

MODERATE-SEVERE cases:
1st line: biological agents (e.g. infliximab)

2nd line: oral corticosteroids (prednisolone) may be used.

SEVERE/UNTREATED:
- Potential to perform surgical resection (colectomy).

86
Q

What is the treatment for Crohn’s disease?

A
  • Stop smoking (Exacerbates the disease).

Inducing remission:

  • Steroids (prednisolone) 1st line
  • Mesalazine if contraindicated.
  • 2 or more exacerbations in one year, consider adding azathioprine (2nd line).
  • If severe, consider a TNF-a inhibitor (infliximab).

Maintaining remission:

  • Azathioprine.
87
Q

What are the potential complications of IBD?

A
  • Psychosocial problems.
  • Sexual problems (especially for UC).
  • Frequent relapse/ attacks.
  • Bowel obstruction due to stricture.
  • If occurring in children, may result in short stature (especially for Crohn’s disease).
  • The risk of developing colorectal cancer or osteoporosis is raised for those with IBD (Crohn’s or UC).
88
Q

What is IBS?

A
  • Irritable bowel syndrome
  • Relapsing functional bowel disorder associated with a change in bowel habit.
  • No organic cause established.
89
Q

What is the clinical presentation of IBS?

A
  • Crampy abdominal pain that is RELIEVED BY DEFECATION/WIND.
  • Altered bowel habits.
  • Abdominal bloating.
90
Q

What is the aetiology of IBS?

A
  • Generally unknown

- No organic cause can be established.

91
Q

What is the epidemiology of IBS?

A
  • Associated with psychological stress

- More common in women.

92
Q

How is IBS diagnosed?

A
  • NOT a diagnosis of exclusion
  • Diagnosed clinically, usually from the history.
  • Sometimes a coeliac screen will be used to exclude coeliac disease.
93
Q

What is the treatment for IBS?

A

Lifestyle modification:

  • Lots of fluids
  • More fibre with diarrhoea, less with constipation.

Pharmaceutical:

  • Laxatives for constipation.
  • Antidiarrhoeals for diarrhoea (e.g. loperamide).
94
Q

What are the three main types of GI tract cancer?

A
  • Oesophageal - cancer of the oesophagus.
  • Gastric - cancer of the stomach.
  • Colorectal - cancer in the bowel.
95
Q

What are the symptoms of oesophageal cancer?

A

No early symptoms.

Late symptoms:

  • Dysphagia
  • Weight loss
  • Heart burn
  • Haematemesis
  • Hoarse voice

Some of these symptoms can be caused by the cancer putting pressure on the laryngeal nerve.

96
Q

What are the two main types of oesophageal cancer and where are they typically found?

A
  • Squamous oesophageal cancer. Typically found in the proximal 2/3 of the oesophagus.
  • Adenocarcinoma. Typically found in the distal 1/3 of the oesophagus.
97
Q

What is the aetiology of squamous oesophageal cancer?

A
  • Smoking
  • Alcohol
  • Nitrous amines (e.g. barbecue food, tobacco)
98
Q

What is the aetiology of oesophageal adenocarcinoma?

A
  • Barrett’s oesophagus

- Obesity

99
Q

What investigations are used for suspected oesophageal cancer?

A

Gold standard and 1st line:

  • Oesophagoscopy with biopsy.
  • CT/MRI to stage the cancer.
100
Q

What are the potential treatments for oesophageal cacner?

A
  • Oesophagectomy with chemotherapy.
101
Q

What are the symptoms of gastric cancer?

A

Often very non-specific symptoms:

  • Dyspepsia
  • Weight loss
  • Vomiting
  • Dysphagia
  • Anaemia

Signs:

  • Epigastric mass
  • Hepatomegaly
  • Jaundice
  • Troisler’s sign (enlarged left supraclavicular/Virchow’s node)
102
Q

What is the most common type of gastric cancer?

A
  • 90% are adenocarcinomas.

- Most also involve the pylorus.

103
Q

What are the risk factors associated with gastric cancer?

A
  • H. Pylori infection.
  • Smoking
  • Gastritis
  • Pernicious anaemia
104
Q

What are the investigations used for gastric cancer?

A
  • Gastroscopy with biopsy.

- Then a CT/MRI to stage the cancer.

105
Q

What is the treatment for gastric cancer?

A
  • Gastrectomy (partial or total) + chemotherapy.
106
Q

What are the symptoms of colorectal cancer?

A

Most are found in the descending colon. Symptoms are:

  • Rectal bleeding
  • Intestinal obstruction (colicky pain, bowel habit)

For colorectal cancer in the ascending colon/caecum, symptoms are:

  • Iron deficiency anaemia
  • Mass in right iliac fossa
  • Other non-specific symptoms
107
Q

What is the pathophysiology of colorectal cancer?

A
  • Adenomatous benign polyps develop in the bowel over time.
  • These may eventually become malignant as a result of oncogene activation/ tumour suppressor gene deactivation.
  • The number of adenomatous polyps directly correlates to a persons risk of developing colorectal cancer.
108
Q

What are the risk factors associated with colorectal cancer?

A
  • Age
  • Family history
  • Western diet
109
Q

What investigations are used for colorectal cancer?

A
  • DRE
  • Colonoscopy + biopsy
  • Faecal occult blood test may be used for screening purposes
110
Q

What is the treatment for colorectal cancer?

A
  • Surgery, ideally with end to end anastomosis. Can fit a stoma bag if this is not possible.
  • Chemotherapy alongside this.
111
Q

Where does colorectal cancer commonly metastasise to?

A
  • Liver

- Lung

112
Q

What is appendicitis?

A

Inflammation of the appendix.

113
Q

What are the symptoms of appendicitis?

A
  • Pain spreading from the umbilicus to the right iliac fossa. (Tender with guarding).

More generalised symptoms are:

  • Nausea
  • Localised tenderness
  • Diarrhoea/constipation
  • Pyrexia
114
Q

What is the pathophysiology of appendicitis?

A
  • The appendiceal lumen becomes obstructed.

- Gut flora invade the appendix wall, which proceeds to become inflamed and infected.

115
Q

What are the potential complications of appendicitis?

A
  • Rupture of the appendix wall, leading to faecal matter entering the peritoneal cavity - this can cause serious peritonitis.
116
Q

What is the aetiology of appendicitis?

A
  • Formation of a faecolith (hard mass of impacted faeces) that obstructs the lumen of the appendix.
117
Q

What are the investigations used for appendicitis?

A
  • CRP/ESR is first line to assess the need for imaging.

- If risk is high enough, CT should be requested (Gold standard).

118
Q

What are the potential treatment options for appendicitis?

A
  • Gold standard is appendectomy.

- In patients not suitable for surgery, paracetamol + antibiotics.

119
Q

What are the two categories of intestinal obstruction? What are they?

A
  • Mechanical. A physical factor is preventing the movement of contents through the intestinal tract. Causes backing up of the GI tract and inability to empty (vomiting + constipation).
  • Functional (or “ileus”). Bowel ceases to function and there is no peristalsis. This results in impaction of faecal matter, as it can no longer move along the intestine.
120
Q

What are the symptoms of mechanical intestinal obstruction?

A
  • Colicky abdominal pain, associated with vomiting. (earlier in small bowel blockage).
  • Absolute constipation meaning no stool or gas passage at all. (earlier with large bowel blockage).
  • Distension of bowel.
121
Q

What is the aetiology of mechanical intestinal obstruction?

A

Small bowel obstruction:
- Adhesions (sticking together) especially following surgery - very common.

  • Intussusception (telescoping) very common also.
  • Strangulated hernia
  • Volvulus (twisting)
  • Possibly malignancy

Large bowel obstructions:

  • Most often colorectal cancer.
122
Q

Which is most common - small or large bowel mechanical intestinal obstruction?

A
  • Small bowel more common.
123
Q

What investigation is used to diagnose mechanical obstruction?

A
  • Abdominal X-ray.
124
Q

What is the treatment for mechanical intestinal obstruction?

A
  • Fluid replacement
  • Analgesia
  • Nasogastric decompression
  • Consider surgery to correct the blockage.
125
Q

What is the clinical presentation of a patient with functional intestinal obstruction?

A
  • Often no pain.
  • Reduced bowel sounds.
  • Constipation and vomiting.
126
Q

What is the pathophysiology of functional intestinal obstruction?

A
  • Bowel ceases to function, resulting in the absence of peristalsis.
127
Q

What is the aetiology of functional intestinal blockage?

A
  • Most often a post operative effect of major abdominal surgery.
  • Possibly due to the nerves or muscles associated with the intestine becoming damaged.
128
Q

What investigation is used for functional intestinal blockage?

A
  • Abdominal X-ray.

- Gas will be seen throughout the bowel.

129
Q

What treatment is usually given for functional intestinal obstruction?

A

Usually treatment is conservative:

  • Fluid replacement
  • Analgesia (PRN)
  • Intestinal decompression with a nasogastric tube
130
Q

What is diverticular disease?

A

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

131
Q

What are the symptoms of diverticular disease?

A

95% of cases asymptomatic. Can cause (due to luminal narrowing):

  • Pain
  • Constipation
  • Bleeding
  • Diverticulitis

In severe cases:

  • Left iliac fossa pain
  • Fever
  • Nausea
132
Q

What is the pathophysiology of diverticular disease?

A
  • The mucosa of the bowel herniates through weakened muscular walls near blood vessels.
  • These herniations can lead to perforation, fistula formation with nearby structures or intestinal obstruction.
133
Q

What is the difference between diverticulosis and diverticulitis?

A

Diverticulosis - presence of diverticula.

Diverticulitis - Inflammation that occurs when faeces obstruct the neck of the diverticulum.

134
Q

What are the risk factors associated with diverticular disease?

A
  • Low fibre diet
135
Q

What are the investigations used for diverticular disease?

A
  • ESR/CRP raised suggests potential diverticulitis.

- Then perform contrast CT of abdomen to look for diverticular disease/ potential acute diverticulitis signs.

136
Q

What is the treatment of diverticular disease?

A
  • For asymptomatic diverticular disease, increase fibre.
  • For diverticulitis, antibiotics (amoxicillin 1st line).
  • Analgesics (paracetamol).
  • Consider surgical resection for patients with frequent attacks of diverticulitis.

Phase 2a diseases (18 decks)

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