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Alimentary System > Upper GI Conditions > Flashcards

Upper GI Conditions Flashcards

1
Q

What type of muscle is the Oesophagus made of?

A
  • Upper 3-4cm = skeletal muscle

- The remainder = smooth muscle

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2
Q

What type of epithelium is present in the Oesophagus?

A

Non-keratinised stratified squamous epithelium

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3
Q

What should you enquire about when a pt. presents with Dysphagia?

A
  • Type of food (solid vs liquid)
  • Pattern (progressive, intermittent)
  • Associated features (weight loss, regurgitation, cough)

• Location:
o ?Oropharyngeal
o ?Oesophageal

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4
Q

What are the common causes of Oesophageal Dysphagia?

A
  • Benign stricture
  • Malignant stricture (ie. oesophageal cancer)
  • Motility disorders (ie. achalasia, presbyoesophagus)
  • Eosinophilic oesophagitis
  • Extrinsic compression (ie. Lung cancer)
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5
Q

When is Endoscopy used in Oesophageal Disease?

A
  • Investigation of Dysphagia

- Reflux symptoms with alarm features

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6
Q

When is Barium Swallow (Contrast Radiography) used in Oesophageal Disease?

A
  • Investigation of Dysphagia in certain cases (less-invasive than endoscopy)
  • Used in “high” dysphagia prior to endoscopy to exclude a pharyngeal pouch or post-cricoid web
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7
Q

When are pH studies used in Oesophageal Disease?

A
  • Investigation of Refractory Heartburn or Reflux (GORD)

refractory to meds -> to check if the meds are acc working!

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8
Q

When is Manometry used in Oesophageal Disease?

A
  • Investigation of Dysphagia / suspected motility disorder, refractory GORD

(to check if the LOS is opening and closing properly to prevent food/acid going back up)

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9
Q

What symptoms are associated with Reflux?

A
  • Heartburn = retrosternal pain/discomfort
  • Waterbrash = acidic taste in the back of the mouth
  • Cough
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10
Q

What are the common symptoms of Diffuse Oesophageal Spasm?

A

Severe, intermittent chest pain +/- dysphagia -> precipitated BY FOOD

(nb. confused with Angina/MI)

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11
Q

How is Diffuse Oesophageal Spasm diagnosed?

A
  • Barium swallow
  • > corkscrew appearance
  • Manometry
  • > abnormal contractions
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12
Q

What is the treatment for Diffuse Oesophageal Spasm?

A

Smooth muscle relaxants

ie. nitrates, CCBs

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13
Q

What are the Achalasia?

A
  • Progressive dysphagia for solids AND liquids (!!!) (from the beginning)
  • Dysphagia
  • Regurgitation + chest infection
  • Weight loss
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14
Q

How is Achalasia diagnosed?

A

Combo of…

  • Barium swallow
  • > Rat’s tail appearance!
  • Manometry
  • > high pressure in LOS at rest (>45mmHg), failure of LOS to relax after swallowing, absence of useful peristaltic contractions in the lower oesophagus
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15
Q

What causes Achalasia?

A

Degeneration of inhibitory neurones in the Myenteric Plexus of the distal oesophagus and LOS

  • > lack of peristaltic contractions and failure of LOS to relax
  • > high resting LOS pressure on Manometry, dysphagia, regurgitation of solids AND liquids, etc..
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16
Q

What is the Treatment of Achalasia?

A
  • Heller’s Myotomy = 1st line!!
  • Endoscopic balloon dilatation
  • Nitrates, CCBs
  • > (pts unfit for more invasive treatments)
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17
Q

What are the complications of GORD?

A
  • Oesophagitis + ulceration
  • Benign Oesophageal Stricture
    (-> nb. difficulty swallowing solids THEN liquids)
  • Barrett’s Oesophagus
  • Oesophageal Adenocarcinoma
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18
Q

What are the common symptoms of GORD?

A
  • Heartburn
  • > (retrosternal discomfort)
  • Waterbrash
  • > (acidic taste in the back of the mouth)
  • Cough
  • Sleep disturbance
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19
Q

What are the risk factors for GORD?

A
  • Pregnancy
  • Obesity
  • Drugs lowering LOS pressure
  • Smoking
  • Alcoholism
  • Hypomotility (ie. systemic sclerosis)
  • Hiatus Hernias
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20
Q

Which drugs lower LOS pressure? (increase reflux symptoms and risk of GORD)

A
  • Nicotine (smoking)
  • Alcohol
  • Dietary Xanthines (ie. caffeine)
  • Anti-muscarinics
  • CCBs
  • Nitrates
  • Tricyclics
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21
Q

What is the difference in the LOS in Achalasia vs. GORD?

A
  • The LOS doesn’t open in Achalasia -> high resting pressure
  • The LOS doesn’t shut properly in GORD -> bc of low-resting pressure (ie. due to drugs, alcohol, smoking, etc…)
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22
Q

How is GORD diagnosed?

A
  • Clinical Diagnosis
  • (Endo only used in certain cases…)
  • (24hr oesophageal pH monitoring +/- manometry may help diagnosis when Endo is normal)
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23
Q

When should you refer a patient for UGIE/EGD?

A
  • Everyone with Dysphagia
  • ≥55 and ALARMs or persistent symptoms (ie. dyspepsia, heartburn, reflux, etc)
  • Acute GI bleed
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24
Q

What is the aetiology of GORD?

A
  • Increased transient relaxations of the LOS
  • > (most common!)
  • Hypotensive LOS
  • Delayed gastric emptying
  • Delayed Oesophageal emptying
  • Hiatus Hernia
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25
Q

What is the treatment of GORD?

A
  • Lifestyle measures: weight loss, smoking cessation, small regular meals, remove precipitating drugs/foods
  • Drugs: PPIs, Alginates (Gaviscon) -> empiric w/o investigation!
  • (Anti-reflux surgery (Fundoplicayion) in hella refractory cases)
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26
Q

Which drugs should you avoid in GORD?

A

Lower LOS pressure:

  • Nitrates
  • Anti-Muscarinics/Anti-Cholinergics
  • CCBs

Damage Mucosa:

  • NSAIDs
  • K+ salts
  • Bisphosphonates
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27
Q

What is the metaplastic change in Barrett’s Oesophagus?

A

Non-keratinising stratified squamous epithelium to columnar epithelium (found in stomach)

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28
Q

What causes Barrett’s Oesophagus?

A

Chronic GORD

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29
Q

What is the treatment of Barrett’s Oesophagus?

A
  • EMR (Endoscopic Mucosal Resection)

- RFA (Radio-Frequency Ablation)

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30
Q

What are the Clinical Features of Oesophageal Cancer?

A
  • Progressive Dysphagia (90%)
  • Anorexia and Weight loss (75%)
  • Odynophagia
  • Retrosternal chest pain
  • Cough
  • Pneumonia
  • Hoarse Voice (vocal cord paralysis)
  • Haematemesis
31
Q

What are the Risk Factors for Oesophageal Cancer?

A

Squamous cell carcinoma

  • Achalasia
  • Caustic strictures - nitrosamine exposure, hot drinks
  • Plummer-Vinson syndrome

Adenocarcinoma

  • Barrett’s Oesophagus
  • Obesity
  • Male sex
  • Middle age
  • Caucasian
32
Q

What is the Investigation of choice for diagnosis of Oesophageal cancer?

A
  • Flexible Endoscopy (oesophagoscopy) + Biopsy
33
Q

What is the Investigation of choice for staging of Oesophageal cancer?

A
  • EUS

- CT chest + abdomen

34
Q

What is the radical treatment of Oesophageal cancer?

A
  • Surgical oesophagectomy +/- adjuvant or neoadjuvant chemo

only for localised disease T1/T2

35
Q

What is the palliative treatment of Oesophageal cancer?

A

Palliation of Dysphagia -> top priority

  • Endoscopic stenting
  • Endoscopic laser
  • Palliative Chemo/RT

(most ppl at presentation have incurable disease)

36
Q

How is Eosinophilic Oesophagitis diagnosed?

A
  • via Endoscopy and Biopsy

- ≥15 eosinophils per high-power microscopy field on oesophageal biopsy

37
Q

What is the typical clinical presentation of Eosinophilic Oesophagitis?

A
  • Children and Young adults
  • Males
  • Dysphagia
  • Food stuck in throat (food bolus obstruction)

(due to strictures)

38
Q

What is the treatment of Eosinophilic Oesophagitis?

A
  • Topical/swallowed corticosteroids
  • Dietary elimination
  • Endoscopic dilatation (in severe strictures)
39
Q

What are the risk factors for Gastric Cancer?

A
  • H. Pylori infection (!!!)
  • Pernicious Anaemia
  • Atrophic Gastritis
  • Adenomatous Polyps
  • Smoking
  • Diet (high nitrate, high salt, pickling, low Vitamin C)
40
Q

What is the clinical presentation of Gastric cancer?

A
  • Often non-specific -> ALARMS symptoms should prompt investigation with UGIE! *
  • Dyspepsia (pain in the upper epigastrium, esp. after eating)
  • Weight loss
  • Vomiting
  • Dysphagia
  • Anaemia
41
Q

What is the investigation of choice for diagnosis of Gastric cancer?

A
  • UGIE/EGD + Biopsy
42
Q

What is the investigation of choice for staging of Gastric cancer?

A
  • CT Chest/Abdo

- Staging Laparoscopy (in pts w locally-advanced tumours)

43
Q

What is the radical treatment of Gastric cancer?

A

Proximal:
- Total Gastrectomy -> usually open surgery

Distal:
- Partial (Subtotal) Gastrectomy -> usually laparoscopic (“keyhole”) surgery

44
Q

What is the definition of Dyspepsia?

A
  • Pain or discomfort in the upper abdomen

- for 4 weeks

45
Q

How common is Dyspepsia?

A

Occurs in roughly 25-40% of ppl

Frequent GP consultations

46
Q

What are organic causes of Dyspepsia?

A

Upper GI

  • GORD
  • Peptic Ulcer
  • Gastritis
  • Gastric cancer

Other systemic disease

  • Gallstones
  • Pancreatic disease
47
Q

What are functional causes of Dyspepsia?

A
  • Non-Ulcer Dyspepsia -> H. Pylori (most common!!)
  • Smoking and Alcohol
  • IBS
  • Psychological (ie. anxiety, depression)
48
Q

Which drugs precipitate Dyspepsia?

A
  • NSAIDs
  • Corticosteroids
  • CCBs
  • Nitrates
  • Theophylline
49
Q

What are the symptoms of Dyspepsia?

A
  • Epigastric pain - often related to hunger, specific foods, time of day
  • Fullness after meals
  • Heartburn (retrosternal pain)
  • Tender Epigastrium
  • Beware: ALARMS symptoms!! (refer for Upper GI)
50
Q

Should you do any investigations for Dyspepsia?

A
  • Bloods: FBC, ferritin, LFTs, U+Es, Ca2+, glucose, coeliac serology (tTG-IgA)
  • UGIE: if ALARMS symptoms present
51
Q

What are the ALARMS symptoms?

A
  • Anorexia
  • Loss of Weight
  • Anaemia (iron-deficiency)
  • Recent onset or persistent despite treatment >55yrs
  • Malaena/Haematemesis (GI bleeding) or Mass
  • Swallowing problems (Dysphagia)
52
Q

What is the management of Dyspepsia? (summarised)

A
  • Dysphagia, >55 and ALARMs or persistent symptoms (ie. in this case dyspepsia) -> UGIE
  • If just Dyspepsia: Lifestyle measures, Gaviscon, antacids
  • If no improvement with meds: test for H. Pylori
  • If +ve: H. Pylori eradication treatment -> if no improvement then Urea breath test -> if shown to be eradicated then treat as H. Pylori -ve (and give PPIs)
  • If -ve: PPIs (Omeprazole) or H2-Receptor Antagonists (Ranitidine) -> if no improvement then refer for UGIE
53
Q

What type of bacterium is H. Pylori?

A
  • Gram-negative
  • Spiral-shaped
  • Micro-aerophilic
54
Q

What is the pathogenesis of H. Pylori infection?

A
  • H. Pylori releases urease

- Increases pH -> allows H. Pylori to attach itself to the epithelium and penetrate into the gastric mucosa

55
Q

What are the Clinical outcomes of H. Pylori infection?

A
  • Asymptomatic or Chronic Gastritis (>80%)
  • Chronic Atrophic Gastritis / Intestinal Metaplasia (15-20%)
  • GU or DU (15-20%)
  • Gastric Cancer / MALT Lymphoma (<1%)
56
Q

What are the characteristics of Antral-predominant H. Pylori infection?

A
  • Increased Acid production
  • Low risk of Gastric cancer
  • DU disease
57
Q

What are the characteristics of Corpus-predominant H. Pylori infection?

A
  • Decreased Gastric acid (increased pH)
  • Gastric atrophy
  • Gastric cancer
58
Q

How is the diagnosis of H. Pylori infection made?

A
  • Urea (13C) Breath Test
  • Stool Helicobacter Antigen Test (SAT)
  • (Nb. Refer for UGIE if dysphagia, ≥55 with ALARMs or persistent symptoms, or acute GI bleed)
  • should NOT be performed within 2 weeks of treatment with a PPI or within 4 weeks of antibacterial treatment due to false-negatives*
59
Q

What is the Treatment for H. Pylori?

A
  • Remove precipitating drugs (NSAIDs!!)
  • Eradication treatment (triple therapy) for 7 days: PPI + Clarithromycin + Amoxycillin (or Metronidazole if Penicillin allergy) (CA(M)P)
60
Q

What causes Gastritis?

A
  • Autoimmune (parietal cells)
  • Bacterial (H. Pylori)
  • Chemical (bile/NSAIDs)
61
Q

What is more common, DU or PU?

A

DU!!

62
Q

What are the possible causes of PU/DU?

A
  • H. Pylori infection (= majority !!)
  • NSAIDs
  • Smoking
  • Rarely: Zollinger-Ellison syndrome (inc. gastrin production), Hyperparathyroidism, Crohn’s disease
63
Q

What are the symptoms of PU/DU?

A
  • Epigastric pain (relieved by antacids) -> may be the only sign!
  • Nocturnal/hunger pain
  • Back pain (posterior DU)
  • Nausea (+ occasionally vomiting)
  • Weight loss + anorexia
  • Haematemesis and/or Melaena, or Anaemia (Bleeding GU/DU)
64
Q

What is the treatment for Gastritis/PU/DU?

A
  • H.Pylori-causing ulcers = Eradication Therapy
  • Acid-reducing drugs: PPIs (omprazole), H2-Receptor Antagonists (ranitidine)
  • Removal of precipitating drugs (ie. NSAIDs, anti-platelets)
  • Surgery, if complicated disease
65
Q

What are the complications of Gastritis/PU/DU?

A
  • Acute bleeding -> malaena, haematemesis
  • Chronic bleeding -> iron-deficiency anaemia
  • Perforation
  • Fibrotic stricture (narrowing)
  • Gastric Outlet Obstruction - oedema or stricture
66
Q

What is the most common cause of Gastric Outlet Obstruction?

A

Peptic Ulcer Disease

90% of cases

67
Q

What are the clinical features of Gastric Outlet Obstruction?

A
  • Vomiting -> Metabolic Alkalosis
  • Early satiety, abdominal distension, weight loss
  • Gastric splash (abdominal auscultation)
  • Dehydration
  • Bloods: Low Cl, Na+ and K+, Renal impairment
68
Q

How is a diagnosis of Gastric Outlet Obstruction made?

A
  • UGIE (after prolonged fast/aspiration of stomach contents)

- Nature of the vomiting: infrequent, projectile and large volume

69
Q

What is the treatment of Gastric Outlet Obstruction?

A
  • Medical: H. Pylori eradication therapy, PPIs
  • Endoscopic balloon dilatation
  • Surgery
70
Q

What are the symptoms of Gastric cancer?

A
  • Presents late in Western countries *
  • Dyspepsia
  • Early satiety
  • Nausea & vomiting
  • Weight loss
  • GI bleeding
  • Iron-deficiency Anaemia
  • Gastric Outlet Obstruction
71
Q

What is the Aetiology of Gastric cancer?

A
  • Long-term H. Pylori infection (main cause!!)/Gastritis
  • Obesity
  • Environmental risk factors: Smoking, Diet (high salt, high nitrates, low fruit + veg)
  • FH of Stomach cancer
72
Q

What is the management of Gastric cancer?

A
  • Histological diagnosis: Endoscopy + biopsy

- Staging: CT Chest/Abdo

73
Q

What is the radical treatment of Gastric cancer?

A
  • Surgery + adjuvant or neoadjuvant chemo

Alimentary System (11 decks)

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