8. Heartburn Flashcards

1
Q

Dyspepsia

A

Dyspepsia, also known as indigestion, refers to discomfort or pain that occurs in the upper abdomen, often after eating or drinking. It includes symptoms such as heartburn.

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2
Q

Functional Dyspepsia

A

Functional dyspepsia: signs and symptoms of dyspepsia but with no causative abnormalities found under routine examination.

About 75% of patients with functional dyspepsia have gastritis (inflammation of the gastric mucosa). May be present on endoscopy findings in patients with functional dyspepsia.

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3
Q

GORD

A

Gastro-Oesophagal Reflux Disease

Features oesophagitis (inflammation of the oesophageal lining) resulting from the acid reflux into the oesophagus irritating the oseophageal lining.

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4
Q

Peptic ulcer disease

A

Ulcer: an open sore on an external or internal surface of the body, caused by a break in the skin or mucous membrane which fails to heal.

Peptic ulcers could include duodenal and gastric ulcers.

Duodenal ulcers are more common than gastric ulcers.

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5
Q

Effects of Stress

A

Stress changes physiology and so can irritate gastric lining and lead to ulcer formation.

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6
Q

Coeliac Disease

A

Coeliac disease is a condition where your immune system attacks your own tissues when you eat gluten.

Coeliac disease will manifest systemic symptoms (eg: fever, nausea and weight loss) , so it does not line up with Mr Mueller’s presentation. It may also result in nutritional deficiencies.

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7
Q

Inflammatory Bowel Disease

A

Inflammatory Bowel Disease is an umbrella term used to describe disorders that involve chronic inflammation of your digestive tract.

IBD manifests symptoms (some systemic) that do not line up with Mr Mueller’s presentation (eg: fever, nausea, weight loss, bloody diarhhoea). It may also result in nutritional deficiencies.

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8
Q

Pancreatitis

A

Acute pancreatitis pain is mainly epigastric (below your ribs in the area of your upper abdomen) and radiates towards the back. Patients are typically much more unwell than Mr Mueller.

There will also be systemic symptoms of fever, nausea, vomiting.

The symptoms of acute pancreatitis do not line up with Mr Mueller’s presentation.

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9
Q

Medication side effects

A

Some medications may affect the gastric lining. Eg: NSAIDs (Non-steroidal anti-inflammatory drugs), such as ibuprofen.

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10
Q

Gall bladder disease

A

Gallbladder disease presents with colic type pain: an intermittent, spasmodic type pain, caused by trying to expel contents against an obstruction (eg: gallstones).

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11
Q

Gastroenteritis

A

Inflammation of the stomach and intestines, typically resulting from bacterial toxins or viral infection and causing vomiting and diarrhoea.
Would present with vomiting, diarrhoea, fever, etc.

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12
Q

Coronary Heart Disease

A

Some CHD patients may present with epigastric or abdominal pain, an atypical presentation for CHD.

Mr Mueller has risk factors for CHD.

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13
Q

Upper GI Malignancy

A

Symptoms include fever, weight loss, night sweats.

Additional symptoms (eg: difficulty swallowing) are important to consider.

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14
Q

Alcohol history:

A
  • Alcohol is part of any routine history taking.
  • Alcohol is a risk factor for dyspepsia and gastric ulceration.
  • Mr Mueller was not very specific about how much he is drinking.
  • Recommended weekly intake: 14 units.
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15
Q

Medication history:

A
  • Part of any routine history taking.
  • Electronic systems can be used to see what prescribed medications the patient is taking, but it is still important to inquire to see if there are any over-the-counter medications being taken.
  • In Mr Mueller’s case, it is important to ask about the herbal remedies he is taking.
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16
Q

Digital rectal examination:

A
  • Not every patient needs one: there are specific criteria to do one for a patient.
  • Main reason to do this examination: if there is blood loss through the rectum and in stools, particularly if there is concern over GI malignancy.
  • Always have a chaperone present.
  • Externally inspect for fissures, tears, haemorrhoids, masses and abnormalities.
  • Insert the finger and feel for masses or abnormalities.
  • If the patient is male, we can feel the prostate and identify any nodularities that may indicate an enlarged prostate or prostate cancer.
  • Once the finger is removed, can observe if there is any blood present, its colour, stool colour, presence of mucus or other materials.
  • Melena is digested blood due to bleeding in the upper GI tract. If there is an upper GI malignancy or an ulcer that bleeds, the blood gets digested in the intestine, darkening and forming more offensive-smelling stool.
17
Q

Investigations: Bedside Tests

A

Weight:

  • Can be used to calculate BMI.
  • Can assess weight loss if patient returns, which may indicate malignancy or other underlying conditions.

ECG (Electrocardiogram):

  • Can test for coronary heart disease.
18
Q

Investigations: Blood Tests

A

FBC (Full blood count):

  • A blood test.
  • Checking for anaemia and raised platelets.
  • If there is a bleeding ulcer or GI malignancy, there may be anaemia.
  • In certain conditions, including cancer, there is cytokine release, increasing platelet production, leading to thrombocytosis (raised platelets).

LFT (Liver function test):

  • A blood test.
  • Can assess liver function and biliary system.
  • Can assess for liver damage due to alcohol intake.
  • Can look at enzymes being released from biliary system.
19
Q

Investigations: Imaging

A

Abdominal radiograph (abdominal X-rays):

  • Imaging
  • Not very good at looking at soft tissues, so does not give a lot of information.
  • Used only for intestinal obstruction or abdominal perforations.

CT Scan:

  • Imaging
  • Good view of soft tissues, better diagnostic capabilities than abdominal radiograph
  • Radiation exposure
  • Patient will need to go into a hospital
  • Not appropriate for Mr Mueller at this stage, as we have not investigated diagnoses much.
20
Q

Investigations: Special Tests

A

Testing for H.pylori:

  • Bacterium that is implicated in dyspepsia, gastritis, ulcer disease and some types of cancer.

Stool sample:

  • Can be either for parasites, cysts and ova, or for MC&S (microscopy, culture and sensitivity).
  • These are used to test for an infection.
  • Mr Mueller is not reporting fever, change in stools, etc. so we are not worried about an infection.

Echocardiogram:

  • Scan of the heart.
  • Requires visit to a hospital.
  • Could consider if there are abnormalities on ECG.

Upper GI Endoscopy:

  • Very invasive, with some risks.
  • Patient has to visit hospital, may require sedation.
  • Not the most appropriate investigation at this stage.
  • Could visualize the oesophagus, stomach, upper duodenum, look for gastritis and signs of ulceration.
21
Q

H pylori Test Result

A

All histories, exams and investigations done on Mr Mueller were normal except for H.pylori test (stool antigen test).

Mr Mueller tested positive for H pylori.

22
Q

H pylori: Acid neutralisation

A

Most pathogens will die inside the stomach due to hydrochloric acid, but H pylori is able to survive this environment.

NB: Mucus helps the epithelia survive the acidic pH. The mucus is released by foviola cells, which line the gastric mucosa.

Acid neutralisation:

  • H pylori produces urease, which hydrolyses urea to produces ammonia, which neutralises the acid around the bacterium. This neutralisation happens in a very localised space around the bacterium. The impact on the overall pH in the stomach will be minimal.
  • Carbon dioxide produced in the hydrolysis of urea could be used when diagnosing H pylori infection.
23
Q

H pylori: Locomotion

A

Locomotion:

  • Flagella are used to swim.
  • H pylori needs to migrate closer to epithelial cells, where the pH is closer to neutral.
24
Q

H pylori: Adhesion

A

Adhesion:

  • H pylori uses many different molecules to bind to the surface of epithelial cells.
  • Two examples are: LPS and BabA.
25
Q

H pylori: Toxins

A
  • 50% of the human population has H pylori in their stomachs, but in most cases it does no harm as the strain involved does not produce toxins.
  • Toxin production is dependent on the strain of bacteria.
  • Examples of toxins: cagA and vacA. There are many variants (subtypes) of these toxins, some subtypes more dangerous than others).
  • cagA disrupts tight junctions between epithelial cells, causing mucus and then gastric acid to enter the mucosa. This leads to ulceration and inflammation of the gastric mucosa (gastritis).
  • vacA apoptoses epithelial cells by creating pores on them. This leads to a gap in the epithelium, so mucus and then gastric acid enters the mucosa, causing ulceration and inflammation of the gastric mucosa (gastritis).
26
Q

Testing for H pylori

A

Tests can identify different strains of H pylori (eg: by detecting toxins). These will be positive or negative depending on strain.

One of the tests performed is for urease, which will be positive in anyone with H pylori.

For some tests, a threshold number of H pylori is required for the test to be positive.

27
Q

HCl Secretion

A

Histamine can bind to H2 receptors to increase acid secretion. The histamine is produced by enterochromaffin cells in the stomach.

Acetylcholine can bind to ACh receptors to increase acid secretion. The ACh is secreted by the vagus nerve as part of the parasympathetic nervous system.

Gastrin can bind to gastrin receptors to increase acid secretion. Gastrin is an endocrine hormone.

Potassium enters lumen through potassium pumps.

28
Q

Drug interventions for HCl Secretion

A

Helicobacter pylori treatment involves suppressing acid secretion in order to concentrate the amount of antibiotic.

Suppressing acid secretion is also useful in the treatment of many other diseases (eg: gastritis, GORD).

Antacids neutralise stomach acid to a certain degree. Eg: Gaviscon.

H2 antagonists block the histamine receptor. Eg: Ranitidine.

Proton pump inhibitors (PPI) inhibit the H+-K+ ATPase. Eg: Omeprazole.
They are better medications than H2 antagonists because:

  1. H2 receptors are present in other tissues, so there are side effects in other tissues. Proton pump inhibitors will only inhibit proton pumps in the stomach. So PPIs are much more specific.
  2. PPIs have some antibacterial and anti-urease activity.

PPIs are tried before H2 antagonists. A combination of the two can be used if the PPIs don’t work, or the H2 antagonists can be used alone.

29
Q

Carbon-13 Breath Test

A

This is the best test available to determine whether H pylori infection has been cured.

The patient ingests urea with C13 instead of C12. The urea should pass straight through if there is no H pylori.

If H pylori is present, it hydrolyses the urea to produce carbon dioxide containing the C13. So the C13 is breathed out.

If there is no C13 detected by the breath test, the patient is negative for H pylori.

30
Q

H pylori treatment

A

Amoxicillin and Clarithromycin are antibiotics, which target the H pylori. Use of Omeprazole to reduce acid secretion concentrates these antibiotics.

Mr Mueller’s C13 breath test was negative, so he is now negative for H pylori. But he still has dyspepsia, so the H pylori must not have been causing it.

31
Q

Treatment-resistant dyspepsia

A

If omeprazole, then ranitidine or a combination of the two have been used but dyspepsia remains, it is treatment-resistant dyspepsia.

32
Q

OGD report

A

OGD is oesophago-gastro-duodenoscopy, or a GI endoscopy. It is conducted when dyspepsia proves to be treatment-resistant.
According to the OGD, there is a sliding hiatus hernia.

CLO test (Campylobacter-like organism test) is used to test for H pylori. (Checks for urease)

Omeprazole is used to reduce symptoms by decreasing acid reflux.

33
Q

Sliding Hiatus Hernia

A

Oesophagus enters abdomen through the diaphragm. Lower oesophagal sphincter is diaphragm surrounding the oesophagus.

Hiatus: hole that the oesophagus passes through.

The hiatus can be loosened by drugs such as calcium channel blockers, beta blockers and nitrates.

Usually, it is a physical element increasing the size of the hiatus, such as obesity and physical trauma such as excess coughing, vomiting and straining against constipation.

If the size of the hiatus increases, part of the stomach moves up through the hiatus when the thorax is at negative pressure during breathing.

When the negative pressure drops, that part of the stomach moves down.

When the stomach moves up through the hiatus hernia, the pressure draws up acid, to which the lower oesophagus is exposed.

There is no mucus lining the oesophagus to protect it from the acid.

NB: 85-95% of hiatus hernia cases are sliding.

Sliding hiatus hernia causes classical GORD presenting with acid reflux.

34
Q

Rolling Hiatus Hernia

A

The hiatus gets bigger, but something else passes through the hole.

This re-establishes the sphincter. So the stomach will not move into and out of the thorax.

If another part of the stomach has been wedged into the space, there will no major symptoms.

If there is small intestine, pancreas or spleen wedged into the space, there will be obstruction to flow of the contents of those organs.

If there are symptoms, an operation may have to be conducted to push the contents out of the hole and close the enlarged hiatus.

It does not cause acid reflux.

35
Q

Lining of the GI tract

A

The oesophagus is lined by stratified squamous epithelium.

The stomach is lined by columnar epithelium. There are also specialized cells embedded, such as parietal cells, G cells, foviola cells (produce mucus), chief cells, etc.

The small intestine contains columnar epithelium (enterocytes) as well as goblet cells (produce mucus).

36
Q

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

37
Q

Metaplasia, Dysplasia and Adenocarcinoma

A

Barrett’s oesophagus features metaplasia.

Dysplasia (carcinoma-in-situ) refers to cells that show features of cancer cells but the cells have not breached the basement membrane to invade underlying tissue.

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