Week 7 Upper GI Disorders Flashcards

1
Q

Symptoms of oesophageal disease?

A
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2
Q

Fill in these blanks with regard to dianosing dysphagia

A
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3
Q

What is Esophageal achalasia?

A

This is a type of dysphagia where the smooth muscles in the oesophagus fails to relax, which can cause the lower oesophageal sphincter to remain closed

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4
Q

What is Eosinophilic esophagitis

A

A type of dysphagia caused by allergic inflamation of the oesophagus

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5
Q

What is an pharyngeal pouch?

A

A herniation of the upper oesophagus causing dysphagia and regurgitation of old food

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6
Q

What investigations are there into oesophageal disease?

A
  • Endoscopy and biopsy
  • Barium swallow
  • Oesophageal function tests (Manometry, pH and Impedence monitoring)
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7
Q
  • 35 y old male is referred to GI clinic because of
    persistent worsening heartburn in the last 6 months
  • Regurgitation of food and fluid after eating
  • Acid taste at back of throat
  • Recently visited his dentist who has found dental erosions
  • Has put on 2 stones of weight in the last 2
  • Denies difficulty swallowing
  • He has been using rennies bought over the counter with only temporary effect.

Diagnosis?

A

Diagnosis?
* GORD
* Probable Hiatus hernia as rather severe

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8
Q

What is a hiatus hernia?

A

This is where part of the stomach pertrudes through the diaphragm and puts pressure on the lower oesophageal sphincter often leading to acid ruflux and GORD

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9
Q

What are the differences between reflux caused by intermittant lower oesophageal relaxations and refluxs caused by lower oesophageal sphincter pressure?

A
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10
Q

What would reflux with a nocternal pattern indicate?

A
  • Hiatus hernia
  • More likely to lead to Barrat’s oesophagus
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11
Q

What is more common? Oesophageal reflux with hiatus hernia or oesophageal reflux with a hiatus hernia?

A

Oesophageal reflux with hiatus hernia

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12
Q

Fill in the blanks for these mechanism that can cause GORD

A
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13
Q

What actually is the external oesophageal sphincter?

A

The diaphragmatic crural fibres

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14
Q

What is the clinical name for hypersalivation secondary to acid reflux mixing with stomach acid and leading to an acidic taste in the mouth?

A

Waterbrash

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15
Q

Stages of treatment for GORD

A
  1. Lifestyle measures (smoking, alcohol, diet, weight reduction)
  2. Mechanical (posture, clothing, elevate bed-head)
  3. Antacids
  4. Acid suppression (PPIs-omeprazole , H2RA-ranitidine)
  5. Surgical- fundoplication
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16
Q

What is an oesophageal stricture?

A

Narrowing of oesophagus

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17
Q

What are the causes of oesophageal stricture?

A

Benign:

GORD (up to 10%)
Barrett’s
Extrinsic compression
Post-radiotherapy
Anastomotic ( following surgery / oesophagectomy)
Rings and webs
Corrosive ( accidental or suicidal ingestion)

Malignant:

Oesophageal cancer

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18
Q

What are the treatment options of oesophageal stricture?

A

Proton pump inhibitors (e.g. omeprazole)

Dilatation:

CRE balloon
Push dilators

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19
Q

What is Barrat’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

Surveillance vs. Ablation

20
Q

This patient presented with progressive dysphagia initially for solids then in both liquids and solids.

He is 65 y old and he has lost 3 stones of weight in the last 2 months. He has a history of GORD for 30 years, his BMI is 34 despite weight loss. Diagnosis?

A

Oesophageal cancer

21
Q

Main differences between oesophageal adenocarcinoma and squamous cell carcinoma?

A

Adenocarcinoma:

Lower third oesophagus
Younger People
Reflux (Barrett’s)
Obesity
More common
Increasing

Squamous cell carcinoma:

Mid/upper oesophagus
Older People
Smoking
Alcohol
Less common
Declining

22
Q

General definition of Adenocarcinoma vs Squamous cell carcinoma

A

Both are epithelial cell cancers (adenocarcinoma can be in any gland).

Adenocarcinomas originate in glandular cells, which produce fluids like mucus, while squamous cell carcinomas arise from squamous cells, which are flat, scale-like cells.

23
Q

In oesophageal cancer what is the difference in site of the cancer in adenocarcinma vs squamous cell carcinoma?

A

Adenocarcinoma:
Lower third

Squamous cell carcinoma:
Middle and Upper third

24
Q

In oesophageal cancer what is the difference in cause of the cancer in adenocarcinma vs squamous cell carcinoma?

A

Adenocarcinoma:
Obesity and GORD

Squamous cell carcinoma:
Smoking and alcohol

25
What is the order of investigations for oesophageal cancer?
If suspicion of cancer * Urgent upper GI endoscopy + biopsy for diagnosis * CT * CT-PET to look for metastases * Endoscopic ultrasound to stage cancer
26
Staging of oesophageal cancer?
Same as for colon cancer. TNM
27
What are the causes of achalasia?
Degenerative lesion of oesophageal innervation
28
What is the presentation of achalasia?
Presents with dysphagia to liquids and solids, weight loss, chest pain Endoscopic appearances usually normal
29
Treatment for achalasia?
* Endoscopic pneumatic dilatation * Surgical myotomy (cut into muscle to relive spasm of constriction * Botox injection to LOS
30
37 y old female with 6 months history of intermittent dysphagia for liquids and solids. Now things are really bad and she unable to drink a glass of water without taking her time. Lost confidence in swallowing and her weight gone down by 2 stones since symptoms started. Investigations: had a normal UGE. What is this?
Achalasia Hint is normal UGE
31
28 year old man with history of asthma presented to ENT with 3 weeks hx of dysphagia and bolus obstruction. He has a history of allergies to nuts and shellfish An endoscopy was performed and little was reported apart from some red lines and some subtle nodularity What is the differential diagnosis?
Eosinophilic oesophagitis * Children and young adults * Recurrent dysphagia or food bolus obstruction, regurgitation * Association with atopy * Food allergies in children > adults * M > F 3:1 * Furrows, rings, crepe paper fragility, strictures (or ‘normal’) at endoscopy
32
What is the treament for eosinophilic oesophagitis?
* PPI therapy – may help some patients * 6-food elimination diets – children > adults (dairy, eggs, nuts, soya, shellfish, wheat) * Swallowed topical steroid - orodispersible budesonide (Jorvesa) -fluticasone dry powder inhaler * Dilation - for strictures if present
33
What is the pharmacology of a PPI? How long till they wear off?
Irriversibly bind to proton pumps They are unstable in acid so need coating New pumps take 24h for synthesis Rebound hypersecretion on cessation
34
What is the connection between PPIs and NSAIDs?
PPIs can prevent against stomach ulcers caused by NSAIDs Should be co-prescribed with any long term NSAID use
35
What are osme adverse effects of PPIs?
Plus Iron deficiency and enteric infections
36
What cell type produces pepsinogen?
Chief cells Hint: the chief needs their protein
37
Why can PPIs lead to B12 deficiency? Why doesn't this lead to a protein defecit?
* Dietry B12 is protein bound * Chief cells release pepsinogen * Acidic environment is then required to convert pepsinogen into pepsin which breaksdown proteins * With the raised pH by PPIs there isn't enough pepsin to break proteins down and release B12 formt he proteins so that it can be absorbed in the duodenum * The reason it doesn't cause a protein defecit is because the other protein enzyms released by the pancreas (trypsin, chymotrypsin) pick up the slack for protein digestion. However by this point it's too late for poor B12
38
Why do PPIs lead to iron deficiency?
Non-Heme Iron (from plants, grains): Must be converted from ferric (Fe³⁺) → ferrous (Fe²⁺) form for absorption. This reduction process requires stomach acid. Ferrous iron is absorbed mainly in the duodenum.
39
67 y old man Abdominal pains increasing for 3/12 Vomiting 1-2 h after eating Epigastric pains Loss of appetite 4 kg weight loss On aspirin for ischaemic heart disease. No fresh blood in stool but intermittently tarry stool On examination * epigastric tenderness * Bloods: Hb 110g/dl (n>130) * Deficient in iron ( ferritin 5, n>15)
* Probably upper GI pathology with chronic blood loss! * Peptic ulcer ( gastric or duodenal) * In view of age gastric cancer needs excluding.
40
Investigations for of H. Pylori?
Testing: urea breath testing best studied stool antigen testing also recommended first line serology only accurate pre-treatment testing > 2 weeks off PPI therapy testing > 4 weeks after antibiotics
41
Absorption problems from H. Pylori?
Similar to PPIs as acidic environment reduced Iron deficiency B12 deficiency
42
H. Pylori treatment?
PPIs + Antibiotics
43
If H. pylori raises pH to survive, why do we treat it with a PPI?
PPIs raise stomach pH further to enhance antibiotic effectiveness, reduce acid damage, and promote healing.
44
How do PPIs improve antibiotic effectiveness in H. pylori treatment?
Higher pH increases the stability and activity of acid-sensitive antibiotics like amoxicillin and clarithromycin.
45
What are the components of standard triple therapy for H. pylori?
PPI + clarithromycin + metronidazole (or amoxicillin as second line)
46
What are the definitions of obesity as defined by BMI?