heartburn Flashcards

1
Q

what is dyspepsia?

A

recurrent epigastric pain, heartburn or symptoms of acid with or without bloating, nausea or vomiting

aka: reflux, indigestion, tummy ache, bloating, heartburn

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2
Q

what are the causes of dyspepsia?

A

gastroenteritis: symptoms include fevers, vomiting or diarrhoea

coeliac disease

inflammatory bowel disease

upper GI malignancy

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3
Q

what are the symptoms of GORD?

A
  • heartburn
  • chest pain
  • difficulty swallowing
  • regurgitation of food or sour liquid
  • sensation of lump in throat

patients may also experience belching or excess salivation in the mouth known as water brash

discomfort worsens after eating or lying down and can feel like a burning pain behind the sternum

leads to oesophagitis where the reflux irritates the oesophagus

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4
Q

what is gastritis?

A

inflammation of gastric mucosa and often resolves itself

can be symptomatic and problematic when caused by infections, medications such as NSAIDs or alcohol excess

severe cases lead to ulceration

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5
Q

what is pancreatitis?

A

can be associated with pancreatic insufficiences such as steatorrhoea or diabetes

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6
Q

what is functional dyspepsia

A

individuals suffers symptoms of dyspepsia but routine investigations do not reveal causative dyspepsia. Endoscopy can sometimes reveal elements of gastritis

The term functional dyspepsia exists because the findings do not correlate with the degree of symptoms for gastritis

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7
Q

what kind of pain does gallbladder disease have?

A

pain would be more colicky in nature (type of intermittent, spasmodic pain that occurs when a hollow tube contracts to try and relieve an obstruction, e.g gallstones)

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8
Q

how does peptic ulcer disease occur?

A

Due to gastric or duodenal ulceration

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9
Q

how is coronary heart disease related to dyspepsia?

A

in some patients, cardiac ischaemia, which would normally present as an angina type pain would present as dyspepsia or atypical pain (not gastric cause)

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10
Q

what investigations are done for dyspepsia?

A
  • testing for H.Pylori
  • FBC
  • LFT
  • alcohol history
  • medication history
  • weight
  • ECG
  • stool sample
  • abdominal radiograph
  • echocardiogram
  • digital rectal examination
  • upper GI endoscopy
  • CT scan
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11
Q

Where does H.Pylori infect?

A

H.Pylori’s site of infection is the stomach even though it has HCl in it

Foveolar cells create an alkaline mucus to coat and give a gel of protection to the lining of the stomach from the HCl

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12
Q

How does H.Pylori move?

A

For locomotion it uses the flagella to propel it and is guided by a chemotactic gradient towards the stomach lining

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13
Q

How is H.Pylori not affected by HCl?

A

H.Pylori synthesises Urease to convert urea and water into NH3 and CO2

The NH3 is basic and neutralises the acid forming a very thin buffering layer to protect H.Pylori

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14
Q

Describe the mechanism of H.Pylori

A

For adhesion to the host epithelial cells it uses Lipopolysaccharides and BabA

cagA disrupts the tight junctions between cells in the stomach lining leading to an inflammation - cagA strains of H.Pylori are more associated with gastric diseases

vacA causes the cells in the stomach lining to undergo apoptosis and die

The underlining is more exposed to the corrosive effects of gastric HCl acid leading to ulcers

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15
Q

what are tests for H.Pylori?

A
  • Carbon-13 urea breath test: probes for urease
  • Stool antigen test: probes for H.Pylori Catalase
  • Serum serology test: probes for human proteins (human antibodies in response to exposure to H.Pylori)
  • CLO test: probes for urease
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16
Q

what are the benefits of Carbon-13 urea breath test and stool antigen test?

A
  • non-invasive, simple, safe
  • high sensitivity and specificity
  • can be used for diagnosis and as a test of cure
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17
Q

what are the disadvantages of the carbon-13 breath test?

A
  • Requires specialist analysing equipment, smaples may need sending away
  • If the patient is on antibiotics or PPIs the results might be falsely negative
  • Requires fasting conditions
18
Q

what are the disadvantages of a stool antigen test?

A
  • Patients might prefer other tests
  • Samples need refrigeration
  • If the patient is on antibiotics or PPIs, the results might be falsely negative
  • Sufficient evidence lacking for use as a test of cure
19
Q

what are the advantages of serum serology test?

A
  • Cheap and widely available
  • Maybe useful for diagnosing a patient that is newly infected
20
Q

what are the disadvantages of serum serology test?

A
  • IgM poorly sensitive for new infection
  • IgG does not tell you if infection is current (as will remain positive after infection cleared)
  • Cannot test for cure
21
Q

what are the advantages of CLO test?

A
  • High sensitivity and specificity
  • Instantaneous result
22
Q

what are the disadvantages of CLO test?

A
  • If the patient is on antibiotic or PPIs, the result might be falsely negative
  • Invasive
23
Q

Describe the secretion of HCl

A
  • Blood from CO2 diffuses into the parietal cells and combines with water by carbonic anydrase to form carbonic acid which dissociates into H+ and bicarbonate
  • Bicarbonate is transported into basolateral side by bicarbonate chloride antiporter (AE1 Transporter) so Cl- from blood enters the parietal cell
  • H+ transported from parietal cell to apical side by H+/K+ ATPase which is a proton pump
  • Chloride channel on apical membrane tarnsports Cl- from parietal cell onto the apical side to combine with H+ to form HCl
24
Q

what stimulates production of HCl?

A

ACh, H2 and Gastrin receptors stimulate this production of HCl

H2 receptors initiates signalling cascade that results in getting the proton pump from the cytoplasm to the apical cell membrane

25
Q

what are the treatments for dyspepsia?

A
  • PPIs
  • H2 antagonists
  • Antacids
26
Q

how do PPIs work?

A

Reduce HCl production as well as weak inhibiting antibacterial, anti-urease and anti-ATPase activity

PPIs cause the antibiotics to concentrate which enhances the effect of the antibiotic

Only 80% of acid production is blocked by PPIs

27
Q

List two examples of PPIs

A

Lansoprazole and Omeprazole

28
Q

List two examples of H2 antagonists

A

Cimetidine and Ranitidine

29
Q

How do antacids work?

A

inhibit HCl by neutralisation

30
Q

List two examples of antacids

A

aluminium hydroxide and magnesium carbonate

31
Q

what is hiatus hernia?

A

Hiatus hernia occur when part of the abdominal viscera herniate through the oesophageal opening in the diaphragm

32
Q

Describe the mechanism of hiatus hernia and how it can lead to GORD

A

They can occur due to a widening of the diaphragmatic hiatus, pulling up of the stomach (e.g due to oesophageal shortening) or pushing up of the stomach (e.g due to increased intra-abdominal pressure)

Whatever the mechanism, the function of the lower oesophageal sphincter is compromised and the anti-reflux barrier is lost, allowing stomach contents to reflux into the oesophagus

33
Q

What are risk factors of hiatus hernia?

A

male gender, obesity, age, pregnancy and a genetic predisposition

34
Q

what are the two variants of hiatus hernia?

A

sliding and rolling

35
Q

what is sliding hiatus hernia?

A
  • 85-95% of cases
  • GOJ moves upwards
  • predominantly causes symptoms of GORD
36
Q

rolling hiatus hernia

A
  • 5-15% of cases
  • GOJ remains in place
  • a portion of the stomach, bowel, pancreas or spleen herniates into the chest next to the GOJ
37
Q

what lines the oesophagus?

A

stratified squamous epithelium

38
Q

what lines the stomach?

A

columnar epithelium and specialised cells such as parietal cells, G cells, foviola cells, chief cells

39
Q

what is barrett’s oesophagus?

A

Stratified squamous epithelium of the lower oesophagus is replaced by columnar epithelium and goblet cells typical of the small intestine (metaplasia) as well as columnar epithelium of the stomach.

Cardiac mucosa refers to mucosa of the cardia region of the stomach.

The oesophagus will first feature stomach-type epithelium, then small intestine type epithelium

40
Q

when are dysplastic cells considered to be adenocarcinoma?

A

When dysplastic cells breach the basement membrane and invade the underlying tissue, the mass is considered adenocarcinoma.