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Gastrointestinal > Disorders of the Upper GI tract > Flashcards

Disorders of the Upper GI tract Flashcards

1
Q

What is the normal function of the oesophagus?

A
  • Deglutition - striated muscle
  • UOS (upper oesophageal sphincter) relaxes
  • Food enters oesophagus
  • Primary peristaltic wave triggered
  • LOS relaxes as soon as swallow initiated
  • Food into stomach
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2
Q

What are the common oesophageal disorders?

A

-GORD ( gastro-oesophageal reflux disease)
=Oesophagitis (inflammation)
=Barrett’s oesophagus
=Benign oesophageal stricture
-Oesophageal Motility disorders ( e.g. Achalasia)
-Eosinophilic oesophagitis
-Oesophageal cancer

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3
Q

What are the common symptoms of oesophageal disease?

A
  • Dysphagia (difficulty swallowing, late-stage cancer)
  • Odynophagia (painful swallowing)
  • Heartburn (acid refluxing often retro sternally)
  • Acid regurgitation (in mouth)
  • Waterbrash (increased salivation due to discomfort)
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4
Q

What are the less common symptoms of oesophageal disease?

A
  • Chest pain
  • Food regurgitation
  • Food bolus obstruction
  • Globus (sensation that something at back of throat)
  • Cough (acid in respiratory system)
  • Dysphonia ( altered voice, irritated vocal chords)
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5
Q

What is dysphagia?

A
  • Difficulty in swallowing solids or liquids
  • Alarm symptom for immediate evaluation to define the exact cause and initiate appropriate therapy
  • Classified as either Oropharyngeal or Oesophageal
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6
Q

Describe Oropharyngeal causes of dysphagia

A

-Neuromuscular
-Skeletal Muscular Disorders
-Mechanical obstruction (narrowing/ blockage)
-Miscellaneous
=Decreased saliva (medications, radiation, Sjogren syndrome= reduced salivation)
=Alzheimer Disease
=Depression

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7
Q

Describe Oesophageal causes of dysphagia

A

-Mechanical obstruction
-Motility Disorders
-Miscellaneous
=Diabetes
=Alcoholism
=Gastro-oesophageal reflux

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8
Q

What are the clinical signs of oesophageal disease?

A
  • Dental erosion in GORD
  • Weight loss
  • Anaemia
  • Lymphadenopathy
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9
Q

Describe reflux with transient lower oesophageal relaxations

A
  • More common
  • Daytime reflux
  • Small or no HH (hiatus hernia, where upper part of stomach slides through diaphragm in chest)
  • Often no oesophagitis
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10
Q

Describe reflux with low lower oesophageal sphincter pressures

A
  • Less common (20%) but most severe
  • Nocturnal reflux
  • Often large hiatus hernia (inflammation)
  • More severe oesophagitis
  • Barrett’s
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11
Q

What are the typical symptoms of GORD?

A
  • Heartburn (burning discomfort behind the breast bone spreading upwards/ pyrosis)
  • Acid regurgitation (effortless, often meal related, postural)
  • Waterbrash (hypersalivation secondary to gastro-oesophageal reflux)
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12
Q

How do we investigate oesophageal disease?

A

-Endoscopy and biopsy
-Barium swallow
-Oesophageal function tests (Manometry, pH and Impedence monitoring= detect material refluxing into oesophagus that isn’t acidic)
=for motility pattern
=measure exposure of acid over 24hrs

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13
Q

What investigations are used if suspicion of cancer?

A
  • Urgent upper GI endoscopy
  • CT
  • CT-PET (spread)
  • Endoscopic ultrasound (staging)
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14
Q

What is reflux oesophagitis?

A
  • Result of gastro oesophageal reflux
  • If acid stays in oesophagus for long enough= linear erosions
  • Grade A to D (depending on circumference and severity)
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15
Q

Describe Barrett’s Oesophagus

A

-Specialised Intestinal metaplasia in the lower oesophagus
-Commonest in obese men >50
-Often asymptomatic
-Premalignant
=low grade dysplasia
=high grade dysplasia
=adenocarcinoma
-Approx. 0.3% p.a (ie 1/300pt years)
-Surveillance vs. Ablation
-Long term Tx with proton pump inhibitors (omeprazole)

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16
Q

What are the complications of GORD?

A
  • (Oesophagitis)
  • Peptic stricture (benign narrowing of oesophagus)
  • Barrett’s oesophagus
  • Adenocarcinoma
17
Q

What is the treatment for GORD?

A
  • Lifestyle measures (smoking, alcohol, diet, weight reduction)
  • Mechanical (posture, clothing, elevate bed-head)
  • Antacids
  • Acid suppression (PPIs-omeprazole , H2RA-ranitidine)
  • Surgical- fundoplication
18
Q

Describe Achalasia

A
  • Failure of the LOS relaxation
  • Absence of peristalsis
  • Hypertonic LOS
  • Rat-tailed effect
  • Incidence 1/100,000
  • Degenerative lesion of oesophageal innervation
  • Presents with dysphagia to liquids and solids, weight loss, chest pain
  • Endoscopic appearances usually normal (sometimes dilation, absent peristalsis and pooling of fluid)
  • Can progress to oesophageal dilatation and respiratory complications
  • BoTox (paralyse), Endoscopic Dilatation (risk of perforation), Surgical myotomy (cut sphincter), POEM (knife through layers, clips in incision)
19
Q

Describe Eosinophilic oesophagitis

A

-Common presentation with Food bolus obstruction, dysphagia
-Younger age, M>F, prevalence 50/100,000
-History of atopy (asthma, hay fever, food allergies)
-Endoscopy - furrows, rings, exudates, strictures
-Biopsy for diagnosis ( >15 eosinophils /pof)
-Treatment
=Diet – elimination (egg, wheat, milk, nuts, soya, fish)
=Drugs – PPI, topical steroids ( budesonide fluticazone)
=Dilatation – for strictures
-Natural history/course uncertain
=first described1993, 15X rise in prevalence since

20
Q

What is an oesophageal stricture and what are the causes?

A

-Narrowing of the gullet
-Benign
=GORD up to 10%
=Barrett’s
=Extrinsic compression (mediastinum/ lung)
=Post-radiotherapy
=Anastomotic ( following surgery / oesophagectomy)
=Rings and webs
=Corrosive ( accidental or suicidal ingestion)
-Malignant
=Oesophageal cancer

21
Q

How do we treat benign strictures?

A

-Proton pump inhibitors (e.g. omeprazole) if not severe and due to inflammation
-Dilatation
–Push dilators
=Celestin gradual dilators up to 18mm
=Savary-Gillard polyvinyl dilators

22
Q

Describe oesophageal adenocarcinoma

A
  • Lower third oesophagus
  • Younger
  • Reflux (Barrett’s)
  • Obesity
  • More common
  • Increasing
23
Q

Describe oesophageal squamous cell carcinoma

A
  • Mid/upper oesophagus
  • Older
  • Smoking
  • Alcohol
  • Less common
  • Declining
24
Q

Describe staging and treatment of oesophageal cancer

A
  • TNM system of staging ( T=tumour N=Nodes M= metastases)
  • Patient deemed fit for surgery and had preoperative chemotherapy followed by surgery.
  • Confirmed T3N1 on excised specimen.
  • 5-y survival 5-10% increased to 20-30% after chemotherapy /surgery
25
Q

What are the palliation aims for malignant strictures?

A
  • 2/3rds of tumours
  • To relieve the symptoms without necessarily altering the course of the disease or prolonging life if curative treatment not possible.
  • The emphasis is to improve quality of life.
  • Stents
26
Q

How may a motility problem present?

A
  • Intermittent dysphagia but progressive

- Normal endoscopy

27
Q

How do you treat eosinophilic oesophagitis?

A

Topical steroids= orodispersible Budesonide (Jorvesa)

28
Q

What are the main hints in the diagnosis of dysphagia?

A
  • In the elderly think of neurological causes particularly if intermittent / long standing or sinister causes (oesophageal Ca) if new, progressive with regurgitation and weight loss.
  • Oesophageal Ca presents with progressive dysphagia for solids first then liquids.
  • In the younger think of dysmotility (achalasia, or 2ndary to acid reflux,).
  • In dysmotility syndromes dysphagia for liquids is as bad as for solids.
  • Young patients with food bolus obstruction: think of eosinophilic oesophagitis.
  • If hoarse voice think of ENT causes, advanced tumour
  • If regurgitation of food or previous days think of pharyngeal pouch (fills up with food= compression, empties pouch)
29
Q

What bacteria causes gastric ulcers?

A
  • Helicobacter pylori
  • Gastric pits, interferes with acid secretion, inflammatory cell recruitment
  • Alters balance between hyper acidity and mucosal defence
30
Q

Describe diagnosis of H.pylori

A 
-Non-invasive
=Breath test (C-13 labelled urea, bicarbonate formed and breathed out)
=Antibody measurement (serology)
=Stool antigen test
-Invasive
=Culture
=Histology
=CLO test (petri dish with pH indicator with urea, split to ammonia so yellow to red)
31
Q

What is the first line therapy for H.pylori?

A

90% efficacy
Lansoprazole 30mg twice daily (or omeprazole 20 mg BD)
Clarithromycin 500mg twice dailyMetronidazole 400mg twice daily all three for 1 week only

32
Q

What is the second line therapy for H.pylori?

A

85-90%
Lansoprazole 30mg twice daily(or omeprazole 20 mg BD)
Clarithromycin 500mg twice dailyAmoxycillin 1g twice daily all three for 1 week only
Note: For patients allergic to penicillin, repeat 1st line regimen as 2nd line Eradication is confirmed by a C13 breath test 6-12 weeks later

Gastrointestinal (48 decks)

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