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Medicine year 1 semester 2 > Case 11- Pathology 2 > Flashcards

Case 11- Pathology 2 Flashcards

1
Q

Helicobacter pylori (H. pylori)

A

A Gram-negative, spiral-shaped bacterium, is the most common cause of non-NSAID-associated peptic ulcer disease.

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2
Q

H pylori urease activity

A

1) Enzymes that cause release of bicarbonate which protects the bacteria from the acidic environment. It also produces ammonia which damages the surrounding epithelia.
2) H.pylori can also damage the surrounding tissue by producing factors such as proteases, phospholipases and vacuolating cytotoxin A.
3) It also inhibits antral D-cell somatostatin release leading to decreased inhibition of gastrin release. This causes more gastric acid secretion.

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3
Q

H.pylori gastrin

A

H.pylori releases inflammatory mediators which inhibit the Somatostatin secretions by D cells. Decreased somatostatin secretion causes the release of Gastrin from G cells. Through urease activity H.Pylori also release ammonia increasing the pH which stimulates gastrin secretion. Activation of Gastrin from both these mechanisms leads to Parietal cell proliferation causing the gastric mucosa to secrete more H+ ions. This predisposes the development of duodenal ulcer disease.

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4
Q

How is H.pylori transmitted

A

Via the oral route

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5
Q

Symptoms of a gastric ulcer

A 
Main symptom= Abdominal pain
• Heartburn
• Weight loss
• Loss of appetite
• Bloating
• Burping
• Nausea
• Vomiting (vomit may be bloody or look like coffee grounds)
• Black, tarry stools
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6
Q

H.pylori virulence factors (1-3)

A
  1. Urease- weakens and liquifies the protective mucin lining of the gastric epithelial cells. This exposes the epithelial cells to the surrounding acidic environment leading to increased cell damage and necrosis. Mucin liquification facilitates H.pylori attachment and engagement directly with the epithelial cells.
  2. It uses its four to six flagellae to move in corkscrew fashion through the gastric mucus layer
  3. lipopolysaccharides (LPS) (endotoxins), which are components of the bacteria’s outer membrane degrade and damage the gastric mucosa. Initiate inflammatory response
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7
Q

H.pylori vrulence factors (4-7)

A
  1. lipases and proteases are secreted by the bacteria and degrade the gastric mucosa.
  2. Cytotoxin-associated protein A (Cag A) - Cag A is inserted into the cytoplasm. Within the host cell, Cag A influences host signalling pathways and host cellular functions, including acid secretion, cytokine release, cellular proliferation and apoptosis, cell polarity, and cell motility. Disrupts tight junctions
  3. Vacuolating cytotoxin protein (VacA)- within the lamina propria VacA interferes with the activation and proliferation of T lymphocytes. VacA also leads to alterations in mitochondrial membrane permeability and induces apoptosis. Disrupts epithelial junctions.
  4. Adhesins- allow attachment to epithelial cells,
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8
Q

Deglutition (swallowing)

A

The complex process that transfers a food bolus from the mouth through the pharynx and oesophagus into the stomach. Solid food is masticated (chewed) and mixed with saliva to form a soft bolus (mass) that is easier to swallow.

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9
Q

Stages of Deglutition

A
  • Stage 1- voluntary; the bolus is compressed against the palate and pushed from the mouth into the oropharynx, mainly by movements of the tongue and soft palate.
  • Stage 2- involuntary and rapid: the soft palate is elevated sealing off the nasopharynx and the oropharynx and laryngopharynx.
  • Stage 3- involuntary: sequential contraction of all three pharyngeal constrictor muscles creating a peristaltic ridge that forces the food bolus inferiorly into the oesophagus.
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10
Q

Dysphagia

A

A persons ability to eat and drink is disrupted

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11
Q

Causes of Dysphagia- Diverticulae

A

Can occur in the pharynx or oesophagus. A Zenker diverticulum is a pulsion diverticulum of the hypopharynx that occurs at a weak spot in the muscular wall. The diverticulum forms a pouch that enters just above the cricopharynx muscle with the body of the pouch extending lower. The pouch can enter through the diverticulum resulting in coughing or aspiration.

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12
Q

Causes of Dysphagia- Webs or strictures (narrowing)

A

May occur in the pharynx, oesophagus or sphincters. These can obstruct bolus passage and are usually more symptomatic with solid food than liquids.

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13
Q

Dysphagia= Motor/Neuronal impairment- pharynx

A
  • A delay in triggering the pharyngeal swallow can result in food falling into the airway during the delay where the airway is open.
  • Reduced peristalsis in the pharynx (unilateral/bilateral) will leave food residue in the pharynx after swallowing that can fall or be inhaled into the airways.
  • Cricopharyngeal dysfunction can result in material remaining in the pyriform sinus, after a swallow. Aspiration can cause this material to enter the airway.
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14
Q

Dysphagia= Motor/Neuronal impairment- Larynx

A
  • Reduced laryngeal elevation causes food to catch at the top of the airway. This residual food is then aspirated during the inhalation after a swallow.
  • Reduced laryngeal closure may result in food penetrating the larynx during the pharyngeal swallow.
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15
Q

Two main types of Dysphagia

A

Caused by problems with the:
• Mouth or throat- known as oropharyngeal dysphagia.
• Oesophagus (the tube that carries food from the mouth to the stomach)- known as oesophageal dysphagia.

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16
Q

Neurological causes of Dysphagia

A

Damage to the nervous system can interfere with the nerves responsible for starting and controlling swallowing

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17
Q

Examples of Neurological causes of Dysphagia

A
  • A stroke.
  • Neurological conditions that cause damage to the brain and nervous system over time, including Parkinson’s disease, multiple sclerosis, dementia and motor neurone disease.
  • Brain tumours.
  • Myasthenia gravis- a rare condition that causes your muscles to become weak.
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18
Q

Congenital and developmental conditions which cause Dysphagia

A

‘Congenital’ refers to something you are born with. Developmental conditions affect the way you develop.
• Learning disabilities.
• Cerebral palsy- affects movement and co-ordination.
• A cleft lip and palate- a birth defect that causes a gap or split in the upper lip or roof of the mouth.

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19
Q

Causes of Dysphagia- Obstruction

A

Conditions that cause an obstruction in the mouth or a narrowing of the oesophagus can make swallowing difficult.

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20
Q

Examples of obstructive causes of Dysphagia

A
  • A laryngeal or oesophageal cancer.
  • Pharyngeal (throat) pouches
  • Eosinophilic oesophagitis
  • Radiotherapy treatment
  • Gastro-oesophageal reflux disease (GORD)
  • Infections like tuberculosis or thrush can lead to inflammation of the oesophagus.
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21
Q

Causes of Dysphagia- Pharyngeal (throat) pouches

A

Pharyngeal (throat) pouches- large sacks that develop in the upper part of the oesophagus, they reduce the ability to swallow both liquids and solids. It’s a rare condition that mainly affects older people.

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22
Q

Causes of Dysphagia- Eosinophilic oesophagitis

A

Eosinophilic oesophagitis- a type of white blood cell (eosinophil) builds up in the lining of the oesophagus due to a reaction to foods, allergens or acid reflux; the build-up damages the lining of the oesophagus and causes swallowing difficulties.

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23
Q

Causes of Dysphagia- Radiotherapy treatment

A

Radiotherapy treatment- can cause scar tissue which narrows the passageway in your throat and oesophagus.

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24
Q

Causes of Dysphagia- GORD

A

Gastro-oesophageal reflux disease (GORD)- stomach acid can cause scar tissue to develop, narrowing your oesophagus.

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25
Q

Causes of Dysphagia- Muscular condition

A

Any condition which affects the muscles used to push food down the oesophagus and into the stomach can cause Dysphagia
• Scleroderma- where the immune system attacks healthy tissue, leading to a stiffening of the throat and oesophagus muscles.
• Achalasia- where muscles in the oesophagus lose their ability to relax and open to allow food or liquid to enter the stomach.

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26
Q

Complications of Dysphagia

A

Dysphagia can lead to cough or choking, when food goes down the ‘wrong way’ and blocks your airway. This can lead to chest infection, such as aspiration pneumonia which requires urgent medical treatment. Aspiration pneumonia can develop after accidentally inhaling something such as a small piece of food. Dysphagia can affect your quality of life, you may avoid eating and drinking due to fear of choking leading to malnutrition and dehydration

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27
Q

Symptoms of aspiration pneumonia

A
  • A wet, gurgly voice while eating or drinking.
  • Coughing while eating or drinking.
  • Difficulty breathing- breathing may be rapid and shallow.
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28
Q

Gastroscopy

A

A gastroscopy is a procedure where an endoscope is used to look inside the oesophagus (gullet), stomach and first part of the small intestine (duodenum). This is often referred to as an upper gastrointestinal endoscopy or Oesophagogastroduodenoscopy (OGD). Used to check symptoms, confirm a diagnosis or treat a condition

29
Q

What is attached to the Gatroscopy

A

They have a video chip and lens at the tip of the instrument to relay colour images to a television monitor. It can also contain forceps for biopsies, snares for polypectomy and needles for injections.

30
Q

Symptoms that are investigated using a gastroscopy

A

Abdominal pain, heartburn or indigestion, persistently feeling sick, Dysphagia, anaemia (could be internal bleeding). As well as severe bleeding which may cause a sharp, sudden pain in your abdomen, vomiting blood or passing stools (faeces) that are very dark.

31
Q

Conditions a Gastroscopy can diagnose

A
  • Stomach ulcers- open sores in the lining of the stomach and small intestine.
  • Gastro-oesophageal reflux disease (GORD).
  • Coeliac disease.
  • Barrett’s oesophagus- abnormal cells lining the oesophagus.
  • Portal hypertension- causes varices to develop in the lining of the stomach and oesophagus.
  • Stomach cancer and oesophageal cancer
32
Q

Biopsy

A

When you remove a small sample of tissue for testing

33
Q

Gastroscopy- Treatment

A
  • To stop bleeding inside the stomach or oesophagus, i.e caused by varices.
  • Widen a narrowed oesophagus that causes pain or swallowing difficulties- this is caused by GORD, oesophageal cancer or radiotherapy to the oesophagus.
  • Remove cancerous tumours, non-cancerous growths (polyps) or foreign objects
  • Provide nutrition through a feeding tube
34
Q

Contraindications of Gastroscopy

A

Severe chronic obstructive pulmonary disease, recent myocardial infarction, severe instability of the atlanto-axial joints, utilisation in an emergency procedure.

35
Q

GI- plain x-ray

A

Are used in investigations of an acute abdomen. They are used when obstruction or perforation is suspected, though CT is more sensitive. CT scans take longer to arrange and are more costly. When a patient has a perforated duodenal ulcer there will be air underneath the diaphragm. Interpretation depends on the analysis of gas shadows inside and outside the bowel.

36
Q

GI- ultrasound

A

Involves no radiation and is the first line investigation for abdominal distension i.e. ascites, mass or suspected inflammatory conditions. It can be used to guide biopsies or percutaneous drainage. The ultrasound does not image the lumen of the stomach or oesophagus wall as these are hollow organs. An US is not used when diagnosing dyspepsia disorders such as GORD, Barrett’s oesophagus and peptic ulcer disease.

37
Q

GI- CT

A

Is the first choice in the diagnosis of dyspepsia disorders. CT is used as first line treatment for the acute abdomen. It is sensitive to small volumes of gas from perforated viscus as well as leakage or contract from the gut lumen. The CT is widely used in cancer staging and guidance for biopsies of tumours and lymph nodes. CT scans are not used for the diagnosis of dyspepsia disorders such as GORD, Barrett’s oesophagus and peptic ulcer disease. A CT scan is not used for mucosal lesions

38
Q

GI- Barium swallow

A

Examines the oesophagus and proximal stomach, its main use is for dysphagia. Anatomical lesions and motility disorders can be investigated. You observe the passage of bread covered in barium. You use a CT scan

39
Q

GI= Double-contrast barium meal

A

Examines the oesophagus, stomach and duodenum. Barium is given to produce mucosal coating. Granules producing carbon dioxide in the stomach create a double contrast between gas and barium. Is useful in the detection of Ulcers and Cancer. You use a CT scan. OGD gastroscopy is a more sensitive test for small superficial mucosal lesions and bleeding.

40
Q

Acute abdomen

A

Sudden, severe abdominal pain

41
Q

GI- Manometry

A

Used in the assessment and diagnosis of oesophageal disease. It is performed by passing a catheter through the nose and into the oesophagus and measure the pressure generated within the region of the lower oesophageal sphincter (LOS) and the body of the oesophagus. Used when the diagnosis has not been achieved by history, barium radiology or endoscopy

42
Q

GI- pH monitory

A

A 24 hour ambulatory monitor which uses a pH sensitive probe positioned in the lower oesophagus. It is used to identify acid reflux episodes. 24-hour pH monitoring (combined with manometry) should be used to confirm reflux before surgery. Excessive reflux is defined as a pH below 4 for more than 4% of the time. There should be a good correlation between reflux and symptoms.

43
Q

Biochemical markers for gastric disease

A

Used less often due to the effectiveness of endoscopy

44
Q

Biochemical tests- Gastric pepsinogen levels

A

Used for gastric cancer screening. A low serum pepsinogen 1 concentration and a low serum pepsinogen 1:2 ratio are suggestive of the presence of atrophic gastritis, a risk factor for gastric cancer. Samples are collected by a nasogastro tube. This test is used to identify who would benefit from a gastric cancer screening with an upper endoscopy.

45
Q

Biochemical tests- Pentagastrin stimulation tests

A

Used to detect hypo/hyper gastric acid secretion. Pentagastrin is a synthetic peptide which stimulates gastric secretion in a manner similar to natural gastrin. A Pentagastrin stimulation challenge can help establish if a patient is prone to hyper / deficient acid secretion. Samples are collected by a nasogastro tube.

46
Q

Biochemical tests- Augment histamine test meal

A

Used to detect hypo/hyper gastric acid secretion. Histamine is an important stimulant of gastric acid secretion. An augment histamine test meal challenge can show if a patient is prone to hyper / deficient acid secretion. Samples are collected by a nasogastro tube.

47
Q

Biochemical tests- tubeless gastric analysis

A

Used to detect gastric acid pH levels. A tube is passed into the stomach to collect gastric juice. You administer a cation exchange resin which gets quantitatively exchanged with the H+ ions of gastric juice. The resin is then excreted in the urine and can be used to estimate gastric acidity.

48
Q

Non-invasive Biochemical tests for the H.pylori infection

A

1) H.pylori (faecal) antigen test
2) H.pylori serology tests
3) Carbon 13 urea breath test (UBT)

49
Q

H.pylori stool (faecal) antigen test

A

H.pylori within the stomach is excreted in stool, enzyme immunoassay commercial kits can then assess this. The limitations are that the recent use of:
1) Proton pump inhibitors (PPI) (within 2 weeks)
2) Antimicrobials (within 4 weeks)
3) Bismuth (within 4 weeks)
4) Histamine 2 (H2) blockers (within 2 weeks)
May cause false-negative results.

50
Q

H.pylori serology tests

A

The presence of serum IgG antibodies against H.pylori provides a reliable assessment of current or previous infection. Most common serologic tests are based on enzyme linked immunosorbent assay (ELISA) technology. The limitations are that the presence of antibodies can remain for a long time after infection, so a positive result does not necessarily mean that there is an active infection. Serologic tests can not detect eradication after treatment. Blood test

51
Q

Carbon 13 urea breath test (UBT)

A

Carbon 13 labelled urea is given orally which breaks down into CO2 and ammonia, after 15 to 20 minutes labelled CO2 is detected in breath samples. The concentration of the labelled carbon is measured using a mass or infrared spectrometer. The limitations are similar to those observed in a stool antigen test. False negative results may be observed in patients who are taking antisecretory therapy, bismuth, or antibiotics and patients with upper gastrointestinal bleeding. To reduce false negative results, the patient should be off antibiotics for at least four weeks and off PPIs for at least two weeks.

52
Q

Invasive biochemical tests for H.pylori which require an OGD biopsy

A

1) Rapid urease tests
2) Molecular tests
3) Culture

53
Q

Rapid urease tests

A

Also known as CLO (Campylobacter-like organism test). The test is performed at the time of gastroscopy. A biopsy of mucosa is taken from the antrum of the stomach and is placed in a medium containing urea and an indicator like phenol red. The urease produced by H. pylori hydrolyses urea to ammonia, which raises the pH of the medium, and changes the colour of the specimen from yellow (NEGATIVE) to red (POSITIVE).

54
Q

H.pylori molecular tests

A

You can use PCR, in situ hybridisation and real time PCR to detect H.pylori, assess antibiotic susceptibility and evaluate the presence of virulence factors. PCR is not routinely used for diagnosis because specificity has remained an issue and false positives are common, this may be related to uncultured mouth flora.

55
Q

H.pylori culture

A

Not routinely used as requires an invasive method (OGD) to obtain gastric samples

56
Q

How NSAIDS cause peptic ulcer disease

A

NSAID’s block the synthesis of protective PGE2 by blocking the cyclooxygenase pathway leading to increased acid secretion and mucosal damage, leading to ulcer formation.

57
Q

Functional Dyspepsia

A

Symptoms of dyspepsia are present but no underlying cause is found on the endoscope. You can test for the presence of H.pylori in a Carbon-13 breath test, stool antigen test or a laboratory based serology test. If re-testing to confirm the presence of H.pylori then a carbon-13 urea breath test should be used.

58
Q

Treatment for H.pylori eradication

A
  • First line treatment- a 7 day, twice daily course of a PPI (Proton Pump Inhibitor) and amoxicillin combined with either clarithromycin or metronidazole.
  • Second line treatment- same as first line treatment but for clarithromycin or metronidazole use whatever was not used for first line treatment.
59
Q

Treatment for functional dysphagia without H.pyloria

A

A 4 week course of a proton pump inhibitor (PPI) or a H2 blocker

60
Q

Treatment for GORD

A

Stop any NSAID’s and eradicate H.pylori
Full dose of PPI for 4 or 8 weeks. If symptoms recur after initial treatment, offer a PPI at the lowest does possible to control symptoms. Offer H2 receptor antagonist therapy if inadequate response to PPI. If an oesophageal stricture is present the patient should remain on long term full-dose PPI treatment.

61
Q

Treatment for severe oesophagitis

A

Full dose PPI for 8 weeks, maintenance treatment should also be offered. Endoscopy is not routinely used to diagnose Barrett’s oesophagus but maybe considered if the patient has GORD.

62
Q

Examples of PPI’s

A

Omeprazole and lansoprazole

63
Q

PPI’s

A

PPI’s are a weak base which require an acidic environment in order to activate the drug. Omeprazole protects the drug from early degradation following oral administration. In the intestine the pro-drug enters the parietal cells and is concentrated in the parietal cell canaliculi. The high concentration ensures that when the drug is activated to its sulfenamide form it is close to the H+/K+ ATPase pump. This reduces acid secretion by up to 95%

64
Q

When are PPI’s given

A

Short term treatment of gastric and duodenal ulcers, hypersecretory states such as Zollinger-Ellison syndrome, GORD, NSAID associated ulcer and Dyspepsia

65
Q

Drugs used to treat gastritis, peptic ulcer and reflux disease

A

H2 receptor antagonists, Antacids, Bismuth salts, Sucralfate

66
Q

H2 receptor antagonists

A

Examples include Ranitidine, Famotidine and Cimetidine. These drugs act as competitive antagonists of histamine H2 receptors leading to the reduced action of histamine in acid production. Cimetidine has problems with drugs interactions as it uses the cytochrome P450 enzyme with other drugs.May be used for treatment of gastric and duodenal ulcers, GORD, Dyspepsia and NSAID ulcers when PPI is not appropriate.

67
Q

Antacids

A

Weak bases which quickly neutralise in the short term the hyperacidity of the stomach in dyspepsia. Examples include salts of sodium bicarbonate (avoid in patients with a high salt diet), Magnesium hydroxide, Magnesium carbonate and Aluminium hydroxide gel.

68
Q

Bismuth salts

A

Bismuth salts are toxic to H.pylori and interfere with their ability to adhere to gastric mucosa. They are administered orally and can be considered for treatment for mild dyspepsia.

69
Q

Sucralfate

A

A complex of aluminium hydroxide and sulphated sucrose which forms a protective coating on the mucus, lasts up to 3 hours. However, the coating may reduce antacid and other drug efficacy as it forms a paste reducing absorption of drugs. It may be used as an alternative when treating peptic ulcer disease.

Medicine year 1 semester 2 (61 decks)

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