Peptic ulcers and GORD Flashcards

1
Q

What us dyspepsia?

A

A Group of symptoms that suggest UGI disease:

• Persistent or recurrent Pain or discomfort in epigastrium (‘ulcer-like’)
may include
• Heartburn/ regurgitation (‘GORD-like’)
• Bloating, nausea, vomiting, excess wind (‘dysmotility-like’)
• Early satiety and post-prandial fullness

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2
Q

What are the red flag symptoms in upper GI conditions?

A
• Dysphagia
• Weight loss (unintentional)
• Persistent vomiting
• Epigastric mass
• GI bleeding
• Iron deficiency
• New onset dyspepsia/ persistent unexplained symptoms > 55y
- Blood in stool (melena)
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3
Q

What are 4 most common causes if dyspepsia, list in order

A

50-75 % Non-ulcer dyspepsia
• 15-25% Peptic ulcer disease
• 5-15% Oesophagitis
• <2% Cancer

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4
Q

What is Non- ulcer dyspepsia (functional dyspepsia)?

A
When someone suffers from upper GI pain and discomfort with but when an endoscopy is conducted no lesions are found. 
H. pylori may be responsible for some cases 
Disturbances include issues in: 
• GI motility
• Visceral sensation
• Gastric accommodation
• Intestino-gastric reflexes
• Gastric acid sensitivity
• Psycho-social factors
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5
Q

How is Non- ulcer dyspepsia (functional dyspepsia) treated?

A
Improves with time and
symptomatic treatment (PPI)
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6
Q

Which drugs can cause dyspepsia?

A
NSAIDS
Steroids
Bisphosphonates 
Metformin
Theophylline 
Calcium antagonists
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7
Q

What happens when a patient has red flag GI symptoms?

A

2 week referral for gastroscopy

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8
Q

What are the different causes of epigastric pain?

A

GERD
Peptic ulcers
Dyspepsia
Gastritis
Pancreatitis
Cancers (gastric, oesophageal, pancreatic)
Referred or misappropriate pain (pelvic pain)- always consider pregnancy and give a pregnancy test

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9
Q

What are the risk factors for GORD?

A

Obesity (increased pressure in the abdomen)

Smoking

Increased age

Family history - genetic association

Hiatal hernia - part of the upper stomach pushes up through the diaphragm

NSAIDS, caffeine, alcohol

Pregnancy

Certain drugs are known to relax the lower oesophageal sphincter ( calcium channel blockers)

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10
Q

What is GORD?

A

The symptoms and mucosal damage found in GERD is caused by the reflux of gastric contents into distal oesophagus’.

Can be caused by excessive relaxation of the lower oesophageal sphincter which causes the back flow of stomach content into the oesophagus

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11
Q

How is the pain in heart burn often described?

A

Burning pain/ heart burning pain
It can radiate along the oesophagus so the pain can be described as epigastric but also substernal pain (below or behind the sternum)

Typically presents after meals and is made worse by lying down or bending over

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12
Q

Outside of pain which other symptoms may patients mention when describing GORD?

A
Sore throat- erosion due to the acid
Hoarseness of the voice- if larynx is affected
Cough or wheeze 
bad taste in their mouth (metallic)
Vomiting/ Nausea 
Regurgitation 
Dyspepsia 
Dysphagia (difficulty swallowing)
Odynophagia (painful swallowing)
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13
Q

What are the differential diagnosis for someone with heart burn/ chest pain?

A

Angina (more of a crushing pain)

Achalasia (failed relaxation of LOS after swallowing)- typically presents as dysphagia, pain with eating. Less of a burning sensation

Eosinophilic oesophagitis

Pericarditis

Ischaemic heart disease

Peptic ulcer disease- Comes on at night and is limited to epigastrium. Does not radiate up the oesophagus

Malignancy

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14
Q

How is GORD diagnosed?

A

2 week Therapeutic trial with proton pump inhibitor for patients with clear GORD symptoms without alarm symptoms

pH-
- 24-hour pH testing/ monitoring (Gold standard)
- Prolonged wireless pH capsule testing
(Usually combined with gastroscopy)- used when questioning GORD or when PPI trial therapy fails

Gastroscopy-
Used for those with red flag symptoms, suspected complications, not responding to treatment, considered for surgery
(50% have no lesions on endoscopy)

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15
Q

What is the classification criteria for GORD?

A

Los Angeles classification-

Grade A: ≥1 mucosal break, each ≤ 5mm (limited to mucosal fold)

Grade B: ≥1 mucosal break > 5mm. Not continuous between top of mucosal folds (limited to mucosal fold)

Grade C: ≥1 mucosal break, continuous between top of mucosal folds (goes over the mucosal fold, not circumferential

Grade D: mucosal breaks involving more than three quarters of luminal circumference

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16
Q

What are the Extra-oesophageal manifestations of GORD?

A
  • Middle ear problems
  • Chronic sinusitis
  • Dental erosions and (bad breath) halitosis
  • Sore throat/ pharyngitis/ laryngitis
  • Cough
  • Asthma
  • Aspiration pneumonia
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17
Q

How is the conservative treatment for GORD?

A

Education and life style modification:

  • Weight loss
  • Smoking cessation
  • Dietary modification (do not eat 2 hours before sleeping)
  • Eliminate foods which trigger symptoms if possible
  • Try sleep with the head of the bed elevated
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18
Q

What is the medical treatment options for GORD?

A

PPI’s - PPIs prevent acid production within the stomach through inhibition of H+/K+ ATPases in parietal cells.

alternatives - Ranitidine (histamine receptor antagonist) and over the counter antacids

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19
Q

What is the surgical treatment options for GORD?

A

Nissen fundoplication - involves wrapping the fundus of the stomach around the lower oesophagus

20
Q

What are the complications of GORD?

A

Erosive oesophagitis: Inflammation of the oesophagus, which can lead to ulcers, bleeding and peptic stricture formation.

Stricture: scarring and narrowing of the oesophagus due to repeated damage. Can cause dysphagia

Barrett’s oesophagus: a premalignant condition due to columnar metaplasia. Predisposes to the development of oesophageal adenocarcinoma.

21
Q

Peptic ulcer disease is an umbrella term for which ulcers?

A

Gastric ulcers and Duodenal ulcers

22
Q

What are the 2 most common causes of peptic ulcers?

A

H.pylori infection (main cause of duodenal ulcers but also a main cause of gastric) and NSAID (main cause of gastric ulcers)

23
Q

Which drugs are associated with peptic ulcers

A

NSAIDS
Corticosteroids
Bisphosphonates
SSRI’s

24
Q

Which conditions are associated with peptic ulcer development?

A

Zollinger- Ellison syndrome

Acute stress

Malignancy

Inflammatory- Crohn’s

Delayed gastric emptying

25
Q

What is Zollinger- Ellison syndrome?

A

This syndrome occurs due to a gastrinoma within the pancreas ( Islet Langerhans non beta cell tumour) which causes the hyper secretion of gastrin hormone.

This causes hypergastrinemia. Excess gastrin causes more acid to be secreted in the stomach. It also causes the gastric mucosa to hypertrophy which causes an increase in the number of parietal cells. Parietal cells produce hydrochloric acid, so more hydrochloric acid will be produced resulting in peptic ulcers.

26
Q

What are the signs and symptoms of Zollinger- Ellison syndrome?

A
Diarrhoea
Epigastric pain
Heart burn 
Weight loss
GI bleeding
 Pallor 
Jaundice 
Hepatomegaly 
malabsorbtion
27
Q

What is the clinical triad associated with Zollinger Ellison syndrome?

A
  1. Peptic ulcers disease
  2. Islet of Langerhans non beta cell tumour
  3. Gastric acid hyper secretion

(thing PIG)

28
Q

Which investigations are conducted and why to diagnose Zollinger Ellison syndrome?

A

Fasting gastrin levels
FBC (patient will be anaemic)
Amylase (to rule pancreatitis)
Measure level of calcium, phosphate and Parathyroid hormone to check for multiple endocrine neoplasia type 1
Secretin stimulation test (gastrin will go up significantly in response to this test)
Upper GI endoscopy and biopsy to assess for malignancy (especially in the context of GI bleeding and weight loss)

29
Q

Which other condition can be associated with Zollinger Ellison syndrome?

A

multiple endocrine neoplasia type 1

30
Q

What are the 2 phenotypic responses to H pylori infection- DU pathway and GU pathyway

A

DU pathway- - antral gastritis

  • increased acid secretion
  • gastric metaplasia
  • duodenal ulcer

GU pathway-

  • corpus gastritis
  • decreased acid secretion
  • gastric atrophy
  • dysplasia & neoplasia
31
Q

Which type of peptic ulcer is most associated with malignancy?

A

Gastric ulcers

32
Q

Which type of peptic ulcer is most common and by how much?

A

Duodenal ulcers (4X)

33
Q

Which test are used in the investigation of peptic ulcers?

A

FBC (may show iron deficiency anaemia)
LFT (for differential of biliary or gall stones pathology)
ECG (epigastric pain = suspect cardiac)
Non- invasive H-pylori testing =
- 13 C breath test- 13C urea ingested and converted to 13CO in presence of urease (very specific and sensitive, can not use PPI’s while testing)
Serological test- blood test for IgG antibodies against H pylori (not good to test for eradication as antibodies can stay in blood serum)

Stool antigen test- H pylori antigen in faeces. Good for diagnosis and eradication. Must be off PPI’s before using

Invasive tests=

Urease test using a biopsy from the mucosa during endoscopy

Histology examination on a biopsy

Culture using biopsy sample- useful for assessment of antibiotic sensitivities

34
Q

How are peptic ulcers treated?

A

Life style modifications=

Avoid triggers e.g. coffee, spicy food

Stop NSAIDS

Obesity - aim to loose weight

Stop smoking, reduce alcohol

Mental health- Assess patient for anxiety and depression that may effect symptoms

Negative for H pylori = 4-8 weeks of PPI full dose

H Pylori and No NSAID association = first line treatment

  • 7 day course of PPI

Non-penicillin allergy

  • Proton pump inhibitor
  • Amoxicillin
  • Clarithromycin/metronidazole

Penicillin allergy

  • Proton pump inhibitor
  • Clarithromycin
  • Metronidazole

Association with NSAIDs: Patients are given two months of full-dose PPI, after this is complete they are given first-line eradication therapy.

35
Q

What is the second line treatment for peptic ulcers and when is it used?

A

Used if first line therapy fails

Non-penicillin allergy

  • Proton pump inhibitor
  • Amoxicillin
  • Clarithromycin/metronidazole
  • Quinolone/tetracycline
Penicillin allergy
- PPI
- Metronidazole
- Levofloxacin/tetracycline
Bismuth
36
Q

When should a patient with peptic ulcers be referred to a specialist?

A

patients with disease that has not responded to second-line therapy or with unexplained symptoms.

37
Q

What are the potential complications of a peptic ulcer?

A

perforation, haemorrhage and gastric outlet obstruction.

Gastric outlet obstruction: May occur secondary to inflammation, ulceration and scarring leading to narrowing and stricturing of the gastric outlet. Patients tend to present with nausea and vomiting, abdominal pain and distention.

38
Q

If a patient is suffering from a Haemorrhage due to a peptic ulcer, which artery is likely effected?

A

posterior duodenal ulcer eroding through into the gastroduodenal artery

However many occur secondary to erosions through smaller-sized blood vessels within the submucosa.

39
Q

How would a patient present if suffering from the complications of peptic ulcer disease?

A

Perforation- Sever abdominal pain + signs of infection

Haemorrhage - Can cause massive upper GI bleeding = life threatening. Can also be mild and chronic resulting in iron deficiency anaemia.

Gastric outlet obstruction - May occur secondary to inflammation, ulceration and scarring leading to narrowing and stricturing of the gastric outlet. Patients tend to present with nausea and vomiting, abdominal pain and distention.

40
Q

If a patient is suffering from a Haemorrhage due to a peptic ulcer, which artery is likely effected?

A

posterior duodenal ulcer eroding through into the gastroduodenal artery

However many occur secondary to erosions through smaller-sized blood vessels within the submucosa.

41
Q

What is the ultimate effect of CYP 17 inhibition drug is used?
What happens when dexamethasone is combined with the drug?

A

CYP 17 inhibition alone -
Androgen precursors reduce preventing the synthesis of oestrogens and androgens and pregnenolone rises

Plus dexamethasone -
ACTH is suppressed and
therefore pregnenolone
will fall

42
Q

What are the main differences between Enzalutamide and Bicalutamide?

A

Enzalutamide- Has a 5 times greater affinity for androgen receptors

Also prevents androgen receptor binding DNA and co-activator proteins

It is able to overcome bicalutamide resistance

43
Q

Which chemotherapy agent is often used in prostate cancer? What is its mode of action and what are its side effects?

A

Docetaxel and Cabazetaxel - microtubule acting cytotoxic (inhibition of microtubular depolymerization)

Side effects- Infection, fatigue, hair loss

shown to improve
survival by an average of 3 months in patients who are castrate
resistant

44
Q

What is the difference between Cabazetaxel and Docetaxel?

A

Cabazetaxel is a modified taxane to overcome docetaxel resistance

45
Q

By how much has Abiraterone and Enzalutamide been shown to prolong life?

A

Abiraterone- 3.9 months

Enzalutamide- 5-2 months