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Phase 2 1. Gastroenterology > FRS 1. Oesophageal anatomy, physiology, and pharmacology. Acid secretion > Flashcards

FRS 1. Oesophageal anatomy, physiology, and pharmacology. Acid secretion Flashcards

1
Q

Describe the structure of the oesophagus

A

Muscular tube
~ 25cm long (depends on height of person)

3 regions along its length:
o cervical
o thoracic – suprasternal notch to diaphragm
o abdominal – last few cm

Bordered by upper and lower oesophageal sphincters

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2
Q

What are the layers of the oesophagus?

A
  • mucosa
  • submucosa
  • muscularis - inner circular/outer longitudinal
  • adventitia - loosely packed connective tissue
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3
Q

Describe the mucosa of the oesophagus

A
  • nonketatinised stratified squamous epithelium
  • pH 7
  • adapted for shear stress (stratified), not for acidic environments
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4
Q

Describe the lower oesophageal sphincter

A

 LES is a physiological sphincter  internal sphincter, not a visible narrowing but maintains tone to make
sure pressure is 10-15 mmHg higher than surrounding
 External sphincter of diagram
 LES (intrinsic and diaphragm) prevents acid from refluxing into the oesophagus
 The angle of the entry of the oesophagus into the stomach also plays a role in preventing reflux

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5
Q

What are the factors that prevent reflux?

A

 Intrinsic sphincter tone
 Extrinsic sphincter (pinch of crural diaphragm)
 Intra-abdominal length of oesophagus
 Angle of His/Flap Valve
 Secondary pesistalsis/swallowed bicarbonate

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6
Q

What is the angle of his/ flap valve?

A

o acuteanglecreated between the cardia at the entrance to the
stomach, and the oesophagus.
o Forms a valve, preventing reflux

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7
Q

What is secondary pesistalsis/swallowed bicarbonate

A

If acid comes up into the oesophagus, secondary peristalsis clears it from the oesophagus

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8
Q

What is reflux a consequence of?

A

o Increased stress on the barrier

o Malfunction of the barrier

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9
Q

What are the causes of barrier malfunction in reflux?

A

Impaired Defences
o Hiatus hernia
o Transient lower oesophageal relaxations (TLOSRs) -
burping
o Low sphincter pressure – caused by e.g. smoking
o Impaired oesophageal clearance – oesophageal
dysmotility

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10
Q

What are the causes of stress on barrier in reflux?

A

o Increased intra-abdominal pressure - Hiatus hernia,
obesity (chronic pressure weakens barrier)
o Reduced gastric emptying

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11
Q

What is a hiatus hernia

A

Protrusion of part of the stomach through the diaphragmatic hiatus and into the chest
Affects about 20% of population

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12
Q

What are the two types of hiatus hernia?

A

 Sliding (80%): gastro-oesophageal junction slides through hiatus
 Rolling: fundus of stomach protrudes through hiatus alongside GOJ
o Does not predispose to reflux

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13
Q

What is reflux?

A

retrograde passage of acidic gastric contents into oesophagus

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14
Q

What is GORD?

A

symptoms due to reflux sufficient to impair quality of life or cause complications
o Heartburn
o Regurgitation
o Epigastric pain (dyspepsia)
o Nausea
o (Extra-oesophageal symptoms: non-cardiac chest pain, pharyngeal symptoms, wheeze)

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15
Q

What is the mechanism of swallowing?

A

 Complex reflex
 Food bolus pushed up against soft palate and into pharynx
 UES relaxes, respiration pauses, glottis closed
 Primary peristaltic wave propels bolus towards stomach.
 LOS opens at initiation of swallow
 Secondary peristalsis occurs locally in response to distension

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16
Q

What is dysphagia?

A

Symptom of difficulty in swallowing

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17
Q

What are the structural causes of dysphagia

A

Intrinsic lesion:
 Foreign body
 Stricture – Benign/Malignant
 Rings/webs

Extrinsic causes
 Lymph nodes
 Goitre
 Enlarged LA

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18
Q

What are the functional causes of dysphagia?

A

Motility Disorders:
 Achalasia
 Oesophageal spasm

Neuromuscular Disorders:
 Cerebrovascular Disease
 Bulbar palsy

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19
Q

What are the complications of chronic acid reflux

A
  • oesophagitis
  • peptic stricture
  • barret’s oesophagus
  • oesophageal cancer
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20
Q

What is oesophagitis?

A

inflammation of squamous mucosa secondary to acid damage. Can cause strictures

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21
Q

What is a peptic stricture

A

narrowing or tightening of the oesophagus that causes swallowing difficulties.
o Complication of untreated chronic oesophagitis, causes dysphagia

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22
Q

What is Barret’s oesophagus

A

metaplasia in the cells of the lower portion of theoesophagus
o Characterised by replacement of the normalstratified squamous epitheliumlining of the
oesophagus by simple columnar epithelium withgoblet cells(which are usually found lower in
thegastrointestinal tract).
o Columnar transformation of squamous mucosa (squamous  columnar) is caused by chronic
acid damage
o Pre-cancerous condition. Patients should be monitored regularly for dysplasia

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23
Q

Describe oesophageal cancer

A

accumulating cellular genetic changes causing dysplasia and ultimately cancer

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24
Q

What are the treatment options for GORD?

A
  • lifestyle changes
  • pharmacotherapy
  • surgical management
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25
Q

Describe the lifestyle changes adopted in the management of GORD

A

 Weight loss
 Elevate head of bed at night
 Avoid precipitants, e.g. coffee, chocolate, tomatoes, alcohol,and fatty
or spicy food

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26
Q

What are the pharmacotherapy options in the treatment of GORD

A
  • PPIs
  • H2 receptor antagonsists
  • antacids
  • alginates
  • mucosal agents
  • prokinetics
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27
Q

What are PPIs?

A

Proton-pump inhibitors (mainstay oftherapy)

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28
Q

What is the mechanism of action of PPIs?

A

 Accumulate selectively in the canaliculi of the parietal cells
 Undergo an acid-catalysed rearrangement to the active drug
 This cationic sulfenamide binds irreversibly with sulphydryl groups on the proton pump causing inhibition
 Irreversible inhibition leads to longer duration of action compared to H2RAs

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29
Q

What are the side effects of PPIs?

A 
o Diarrhoea (esp. Lansoprazole)
o Rash
o Headache
o Infections – C. diff
o Interact with cytochrome P450 - Clopidogrel (?Pantoprazole)
o Long-term use - ?GNETs
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30
Q

What is the mechanism of action of H2 receptor antagonists?

A

Competitively block histamine receptors on the

parietal cell

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31
Q

What are the side effects of H2 receptor antagonists?

A 
o Diarrhoea
o Deranged LFTs
o Headache
o Dizziness
o Fatigue
o Rash

Tachyphylaxis

32
Q

Tachyphylaxis:

A

a rapid decrease in the response to a drug due to previous (long term) exposure to that
drug

33
Q

List examples of H2 receptor antagonists

A

o Cimetidine
o Ranitidine
o Famotidine
o Nizatidine

34
Q

What is the mechanism of action of antacids

A

o Raise the pH of gastric secretions
o Decrease pepsin activity
o Some bind bile acids
o Duration of action depends on rate of gastric emptying

35
Q

What are antacids?

A

predominantly aluminium and magnesium salts => neutralise the effects of stomach acid

36
Q

What are the side effects of antacids?

A

o Al salts – constipation
o Mg salts – diarrhoea
o Some formulations have high Na levels – avoid in cardiac/renal disease
o Interact with tetracyclines, digoxin, iron, prednisilone.

37
Q

What are alginates?

A

 Giant Pacific Kelp - Macrocystis pyrifera
o Algin extracted
 Sodium alginate used in treatment of GORD
 Mixture of polyurionic acids
 Added to antacid preparations as foaming agents
 Layer of foam on stomach contents – mechanical barrier to reflux.

38
Q

Name examples of prokinetics and how they work

A

 Metoclopramide/domperidone
 Both increase gastric emptying and increase LOS pressure
 Metoclopramide also acts on cholinergic systems in GI tract to increase ACh release
 Useful GORD and functional dyspepsia
o Early satiety, belching, nausea +/or bloating

39
Q

What are the side effects of domperidone?

A

drowsiness, diarrhoea, hyperprolactinaemia

40
Q

Give an example of a mucosal agent and how it works

A

 Complex sucrose polymer, cytoprotective agent
o sucrose sulfate-aluminium complex
o Binds to the ulcer, creating a physical barrier that protects the gastrointestinal tract from
stomach acid and prevents the degradation of mucus
o Anionic sulphate binds to positively charged glycoproteins in ulcer
 Forms a ‘paste’, impeding diffusion of acid and acting as buffer for 6-8 hours

41
Q

Describe the surgical management of GORD

A

 Repair of hiatal hernia, if one is present.
o Involves tightening the opening in the diaphragm with stitches
 Laparoscopic Nissen fundoplication
o Wrapping the fundus of the stomach around the end of the
oesophagus with stitches.
o The stitches create pressure at the end of the oesophagus,
reinforcing the lower oesophageal sphincter
o This helps prevent stomach acid and food from flowing up from
the stomach into the oesophagus.

42
Q

What are the red flag symptoms of dyspepsia

A

 Iron deficiency anaemia (may indicate bleeding)
 Unintentional weight loss
 Dysphagia
 Persistent vomiting
 Epigastric mass
 >55 with unexplained and persistent dyspepsia

43
Q

Describe atrophic gastritis

A
  1. chronic inflammation of fundic glands
  2. parietal cell atrophy
  3. resulting in reduced acid secretion (hypochlorhydria or achlorhydria)
  4. => increased gastrin production
44
Q

Describe endoscopy as an investigation of oesophageal disorders

A

 Can be performed with topical anaesthesia or conscious sedation
 Direct visualisation of upper GI tract to d2
 Diagnosis of structural and mucosal abnormalities, e.g. Hiatus hernia, tumours, Barrett’s oesophagus
 Allows mucosal biopsy
 Therapeutic intervention
 Complications

45
Q

What is Radio frequency ablation?

A

 Used to remove tissue affected by Barrett’s oesophagus

 Endoscopic technique in which diseased tissue is exposed to heat energy and destroyed

46
Q

What is the gold standardfor diagnosis ofgastroesophageal reflux disease?

A

Oesophageal pH monitoring

47
Q

What is Oesophageal pH monitoring

A

 Provides direct physiologic measurement of acid in theoesophagus and is the most objective method to
o document reflux disease
o assess the severity of the disease
o monitor the response of the disease to medical or surgical treatment

48
Q

How is an oesophageal pH monitoring test performed?

A

 the sensor is placed 5cm above upper border of thelower oesophageal sphincter (LOS) determined byoesophageal manometry.
 To measure proximal oesophageal acid exposure the second sensor is placed 1-5 below the lower border of theupper oesophageal sphincter(UOS).
 Oesophageal pH monitoring is performed for 24 or 48 hours and at the end of recording, a patients tracing is analysed and the results are expressed using six standard components.
 Of these 6 parameters, a pH score calleda DeMeester Scoreis been calculated
o This is a global measure of oesophageal acid exposure.
o A Demeester score > 14.72 indicates reflux.

49
Q

How is a reflux episode defined in oesophageal pH monitoring?

A

A reflux episode is defined as oesophageal pH drop below 4

o pH below 4 is damaging because pepsin is active at pH 4

50
Q

What constitutes a normal and abnormal result on oesophageal pH monitoring

A

Normal pH trace would show relatively constant pH around 7 with a few short dips in the day

Abnormal:
o Episodes of change in pH are more frequent and more prolonged

51
Q

What is the benefit of high resolution manometry?

A

 Allows recording of pressures within the oesophagus and proximal
stomach.
 Oesophageal manometry measures the rhythmic muscle contractions
that occur in your oesophagus when you swallow  assesses motility
 Oesophageal manometry also measures the coordination and force
exerted by the muscles of your oesophagus

52
Q

How is high resolution manometry performed?

A

 Catheter inserted through nose with local anaesthetic spray.
 Display showing pressures as colour plot or lines
 Diagnosis of motility disorders eg oesophageal spasm,

53
Q

How is Radio frequency ablation performed?

A

 An electrode mounted on a balloon catheter or an endoscope is used to deliver heat energy directly to
the diseased lining of the oesophagus
 Tissue sloughs off over 48 to72 hours following the procedure.
 Over a period of six to eight weeks, this tissue is replaced by normal (squamous) lining

54
Q

What is Melena

A

(Black blood) = partially digested, therefore it must originate from the upper GI tract and have
been mixed with acid

55
Q

How does the functional anatomy differ in different regions of the stomach

A

o Gastric body contains oxyntic glands
 Contains parietal cells that secrete HCl and INTRINSIC FACTOR
o Gastric antrum contains pyloric glands
 Contain G cells that secrete GASTRIN

56
Q

What are the key actors of gastric secretion?

A

 Acetylcholine (neuronal – parasympathetic)
 Gastrin (G cell – endocrine)
 Histamine (ECL cell – paracrine)
 Somatostatin (D cell – endocrine)

57
Q

Describe the processes during the cephalic phase

A

 ACh acts on parietal cells
 ACh acts on G cells to increase gastrin secretion  this increases acid production by stimulating parietal
cell via CCK2
o Stimulates ECL cells to secrete histamine  these act on H2 receptors on parietal cells,
increasing acid secretion

 ACh inhibits D cells, inhibiting somatostatin production (inhibits the inhibitor)

58
Q

Describe the processes during the gastric phase

A

 When food is ingested, proteins in food buffer acid, increasing the pH in the stomach
 Gastrin is produced in response to elevated pH, stimulating increased acid production
 More acid is produced in response

59
Q

Describe the processes during the intestinal phase

A

 When food leaves the stomach, gastric pH drops
 D cells secrete somatostatin in response, which inhibits acid production
 Acid secretion falls

60
Q

What are the functions of gastric acid?

A

 Kills bacteria
 Denatures proteins
 Aids in absorption of iron, vitamin B12 and calcium
o Calcium is oxidised from Ca 2+ to Ca 3+ to assist in absorption

61
Q

What does gastric mucous production depend on?

A

prostaglandins

62
Q

How are prostaglandins produced?

A

Arachidonic acid pathway
o AA is broken down into prostaglandins by COX-1 (constitutive)
o COX-2 (inducible) is responsible for inflammatory effects
 PGI 2 and PGE

63
Q

Why do NSAIDs causes peptic ulceration?

A

NSAIDs cause peptic ulceration because they are non-selective COX inhibitors

However, selective COX-2 inhibitors have been unsuccessful and were withdrawn from the market
because of cardiovascular toxicity

64
Q

How does peptic ulcer disease occur?

A

imbalance between attack (acid) and defence

65
Q

What are the hypersecretory causes of peptic ulcer disease?

A

o Zollinger Ellison Syndrome (gastrin producing tumour)
 Can be controlled with antisecretory drugs
o Helicobacter pylori antral gastritis

66
Q

What are the defence-reducing causes of peptic ulcer disease

A

o NSAIDs
o “Stress” ulceration (e.g. following major trauma or burns)
 less COX-1 action because of excessvie COX-2 action
 reduced by nasogastric feeding and antisecretory drugs
o H pylori infection corpus/pan gastritis

67
Q

What are the complications of peptic ulcer disease?

A

 Erosion into blood vessel
 Perforated peptic ulcer  erosion through outside wall of stomach or duodenum causes acute leak of
gastric contents or air into peritonitis
o Acute pan-abdominal pain
 Anaemia – tired and breathless, pale conjunctiva

68
Q

What is the link between h. pylori and peptic ulcer disease

A

High urease activity => catalyses the reaction between urea and water to form ammonia

69
Q

What are the reasons of decline in h. pylori causing peptic ulcer disease?

A

o Now mostly colonises the antrum and not the body
o This decreases somatostatin production, increases gastrin production  increased overall acid
secretion (hypersecretion)
o Mucous protection layer is less effective
o Prone to duodenal ulcers and ulcers in the pre-pyloric region
o Slight protective effect against gastric and duodenal cancers
o Treat, usually no need for repeat endoscopies

70
Q

What causes and what is the consequences of Acid hyposecretion?

A

dominates in the East (Japan etc.)
o Pan gastritis
o Parietal cells and oxyntic glands are inflamed =>decreased acid production
o Inflammation wears away the gastric defence, leaving people at risk of ulcers and gastric cancer
o Stomach becomes colonised by other bacteria (due to hyposecretion of acid)
o Repeat endoscopies

71
Q

How is H. pylori tested for?

A
  1. blood test
  2. stool test
  3. breath test
  4. endoscopy
72
Q

What is the use of blood test in H. pylori testing

A

serology for h pylori antibodies
NB: will always be positive even after infection has cleared. Therefore useful for primary investigation
only, not follow-up after treatment

73
Q

How are stool tests used in H. pylori testing

A

test for bacteria antigen

74
Q

How is breath tested for H. pylori

A

– urea breath test

  • patient given urea that is labelled with C 13 /C 14
  • then asked to breathe out into bag to determine how much of the exhaled carbon is labelled
  • no helicobacter, urea will be absorbed and urinated out, only C 12 in breath test
  • positive test will show heavier carbon isotope in exhaled air
75
Q

How is H. pylori identified on endoscopy

A

test urease activity on gastric biopsy, or microscopic analysis (histological biopsy)
- rapid urease test (contains pH indicator). Production of ammonia changes colour from yellow to red

76
Q

How are PPIs uptaken in the body?

A

The low pH in the stomach converts all of the PPI to the ionised form, which cannot be absorbed. It
therefore has to be packaged in enteric coating
 It is absorbed in the small intestine and is transported to parietal cells
o Here is becomes ionised and is trapped within the parietal cells
o PPI forms an unbreakable disulphide bond with the proton pump, blocking it

77
Q

What is the reason behin reducing pH in ulcer treatment

A

 Can’t heal an ulcer/eradicate H pylori without reducing acid secretion
 The pH need to be > 4 for extended period of time to allow for the stomach/duodenum to heal

Phase 2 1. Gastroenterology (20 decks)

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