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Phase 2- GI > Week 1 > Flashcards

Week 1 Flashcards

1
Q

At what vertebral level does the oesophagus begin?

A

C6

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2
Q

At what vertebral level does the oesophagus enter the stomach?

A

T7

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3
Q

Describe the muscular composition of the oesophagus.

A

The superior third is composed of skeletal muscle, the middle third a combination of skeletal and smooth, and the inferior third is composed of smooth muscle.

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4
Q

What is the term used to describe a sphincter which is functional, but not anatomically visible?

A

Physiological

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5
Q

How many sphincters are there in the oesophagus, and what are they called?

A
  1. Lower oesophageal sphincter, and upper oesophageal sphincter
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6
Q

What are the three regions of the oesophagus?

A

Cervical, thoracic and abdominal.

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7
Q

What are the four histological layers of the oesophagus?

A

Mucosa, sub-mucosa, muscularis externa and adventitia

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8
Q

What type of epithelium is present in the oesophagus?

A

Stratified squamous (non keratinised) epithelium

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9
Q

What two muscle types are present in the muscularis externa?

A

Inner circular layer, and outer longitudinal

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10
Q

What are the 5 mechanisms that normally protect the oesophagus from gastro-oesophageal reflux disease?

A

Intrinsic sphincter, extrinsic sphincter, intra-abdominal oesophagus, flap valve and secondary peristalsis

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11
Q

What is the term used to describe a rapidly diminishing response to a drug, especially after long term use?

A

Tachyphylaxis

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12
Q

Where is the major site of bile salt reabsorption?

A

Ileum

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13
Q

What is the primary role of secretin?

A

Stimulates the secretion of bicarbonate in the duodenum (promotion of alkanisation of small intestinal contents)

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14
Q

What is the major cause of peptic ulcer disease in the duodenum and distal stomach?

A

Helicobacter pylori infection

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15
Q

What can the suppression of gastric acid secretion increase susceptibility to?

A

Enteric infection

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16
Q

How much acid production is reduced by PPIs?

A

90%

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17
Q

What its the condition in which oesophageal epithelium changes from stratified squamous to columnar known as?

A

Barrett’s oesophagus

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18
Q

In Barrett’s oesophagus, what type of epithelium does the stratified squamous epithelium change to?

A

Columnar

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19
Q

What can Barrett’s oesophagus develop into?

A

Oesophageal cancer

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20
Q

How is the gastrointestinal tract organised?

A

Mucosa (split into epithelium, lamina propria, muscular mucosa), submucosa (messier’s (submucosal) plexus), muscular propria (circular muscle, myenteric plexus, longitudinal muscle) and serosa or adventitia

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21
Q

What does circular smooth muscle cause?

A

Constriction of the gut

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22
Q

What does longitudinal smooth muscle cause?

A

Shortening of gut

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23
Q

What does the mouth contain?

A

3 salivary glands (parotid, submandibular and sublingual glands), producing 0.5L of saliva per day, controlled by cranial nerves VII and IX

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24
Q

What does the mouth secrete?

A

Mucus, amylase, bicarbonate, thiocyanate and lysosyme

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25
Q

What is the function of mouth secretions?

A

Mucus for lubrication, amylase to digest starch, bicarbonate to neutralise acid and thiocyanate and lysosyme to act as bactericidal agents

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26
Q

What are dental caries and what can they lead to?

A

Tooth decay which can lead to root infection

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27
Q

What is the purpose of swallowing?

A

Reduces particle size within the food bolus, mixes food with saliva (lubrication + enzymes) and increases surface area

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28
Q

Is swallowing voluntary or involuntary?

A

Once started it becomes involuntary. Swallowing centre is within reticular formation of brainstem

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29
Q

How many sphincters does the oesophagus have?

A

Two: upper and lower oesophageal sphincter

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30
Q

What are the two muscular layers of the oesophagus?

A

Circular and longitudinal

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31
Q

What is the function of the lower oesophageal sphincter?

A

Prevents contents of the stomach refluxing into the the oesophagus

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32
Q

What is the innervation of the oesophagus?

A

Innervation by both sympathetic and parasympathetic nerves (myenteric plexus)

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33
Q

What does parasympathetic innervation of the oesophagus regulate?

A

Peristalsis via the vagus nerve

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34
Q

What is the arterial supply of the upper oesophagus?

A

Superior and inferior thyroid arteries

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35
Q

What is the arterial supply of the middle oesophagus?

A

Branches of the bronchial, intercostal and descending aorta arteries

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36
Q

What is the arterial supply of the lower oesophagus?

A

Branches of the left gastric, left inferior phrenic and splenic arteries

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37
Q

What reduces the chance of infarction of the oesophagus?

A

Dense anastomoses within the submucosa

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38
Q

What is the venous drainage of the oesophagus?

A

IVC, azygous vein, hemiazygous vein, left gastric vein (to portal vein), and short gastric vein (to spleen to splenic vein to portal vein)

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39
Q

What are the functions of the stomach?

A

Primarily as a reservoir to store large quantities of ingested food, initiates digestive process, acid secretion, releases contents in controlled fashion into the duodenum

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40
Q

What are the main anatomical regions of the stomach?

A

Cardia, body, fundus, pyloric antrum, canal and sphincter

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41
Q

What is the function of gastric acid?

A

Converts inactive pepsinogen to the active enzyme pepsin, also kills a large number of bacteria that enter the stomach

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42
Q

What are the secretions of the stomach?

A

Hydrogen ions (by parietal cells), pepsin (precursor pepsinogen produced by chief cells), intrinsic factor (parietal), mucus and water

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43
Q

What stimulates acid secretion in the stomach?

A

Histamine (produced by ECL cells near parietal cells), gastrin (acts on the cholecystokinin-2 receptor), acetylcholine (neurotransmitter of vagus nerve (parasympathetic) at muscarinic receptor)

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44
Q

What stops acid secretion?

A

1 hour post-ingestion secretion is at its peak, then food starts moving through the duodenum. There is less volume in the stomach, and pH is at its lowest. Gastrin is inhibited at lower pH (<3), and low pH also stimulates somatostatin, a broadly inhibitory hormone. Duodenal enterogastrones, are also released (GIP, secretin, CCK).

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45
Q

What are the phases of gastric secretion?

A
  1. Cephalic (sight/smell/taste food)
  2. Gastric Phase (food in stomach-duodenum)
  3. Intestinal
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46
Q

Describe the cephalic phase:

A

Sight/smell/taste of food —> vagus nerve activates parietal and gastrin cells —> moderate stimulation of HCl/pepsinogen

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47
Q

Describe the gastric phase:

A

Distension of stomach and proteins in the antrum —> vago-vagal reflex + gastrin (+histamine) —> strong stimulation of HCl/Pepsinogen

(some foods directly stimulate gastrin release (protein/peptides, coffee, calcium rich)

Food products, particularly peptides, impinging on and distension of the antrum cause the release of gastrin by local (intramural ) neural and by local chemical reflexes

48
Q

Describe the intestinal phase:

A
  • Proteins in duodenum stimulate gastrin (an excitatory secretion), HCl in duodenum stimulates secretin (an inhibitory secretion), and lipids in the duodenum stimulate peptide YY (an inhibitory secretion)
  • Amino acids directly impinging on the duodenal mucosa may trigger the release of a small amount of gastrin
49
Q

What are the main anatomical components of the duodenum?

A

Superior duodenal flexture, descending part, horizontal part, ascending part, duodenojujenal flexure and minor and major duodenal papillae

50
Q

What do Brunner’s glands secrete?

A

Bicarbonate

51
Q

What are the functions of the jejunum and ileum?

A

To mix foodstuffs and digestive secretions/enzymes, circulation of all intestinal contents to facilitate contact with mucosa, propulsion of intestinal content towards terminal ileum

52
Q

What are the major anatomical structures in the small intestine?

A

Brunner’s glands, crypt of Lieberkuhn gland, tubular gland, lumen, villi, mucosa, muscularis mucosa, submucosa, circular muscle, longitudinal muscle, serosa, peritoneum

53
Q

Describe motility in the small intestine:

A

Controlled by a migrating motility complex

  1. Segmentation contractions (non-synchronised contractions) of circular smooth muscle to mix chyme
  2. Pendular contractions of longitudinal muscle to propel chyme
  3. Villus movements brought about by muscularis mucosa
  4. Peristaltic waves arising from duodenal bulb propelling food towards terminal ileum
54
Q

What are the secretions from the crypts in the small intestine?

A

NaCl/NaHCO3- (neutralises gastric acid), Amylase (starch digestion), enteropeptidase (activates trypsinogen)

55
Q

What are the secretions from the villus tips in the small intestine?

A

Brush border enzymes (digestion): enteropeptidase, chymotrypsin, carboxypeptidase and elastase

56
Q

What does the pancreatic duct merge with to form the hepatopancreatic ampulla?

A

Common bile duct

57
Q

Where does the ampulla of vater enter the duodenum?

A

Duodenal papilla, 2/3rds down the length of the duodenum

58
Q

What are the two functional divisions of the pancreas?

A
  1. Endocrine pancreas
    - throughout parenchymal tissue islands of endocrine tissue (islets of Langerhans)
    - beta cells producing insulin
    - alpha cells producing glucagon
  2. Exocrine pancreas
59
Q

What are the two parts of the exocrine pancreas?

A
  1. Aqueous/bicarbonate component

2. Enzymatic

60
Q

What is secreted by the acinar cells of the pancreas?

A

Acinar cells secrete pro-enzymes (trypsinogen, chymotrypsinogen, pro-carboxypeptidase, pro-elastae) and NaCl

61
Q

What is secreted by the duct cells of the pancreas?

A

Bicarbonate (stimulated by secretin, which is secreted in response to HCl in the duodenum)

62
Q

How are duodenal ulcers treated?

A

Surgical:
Vagotomy, subtotal gastrectomy, antrectomy
Medical:
H2 antagonists, PPIs

63
Q

How does H. pylori survive in the acidic environment of the stomach?

A

H. pylori has an enzyme (urease) which converts urea (in the gastric juice and blood) to ammonium bicarbonate. This is an alkali and neutralises the environment around H. pylori

64
Q

What is the relationship between H. pylori infection and age?

A

As age increase, the percentage of the population infected with H. pylori increases

65
Q

What does the relationship between H. pylori infection and age reflect?

A

Living conditions and socio-economic status when born

66
Q

How does H. pylori infection cause duodenal ulcers?

A
  • H. pylori deregulates D cells (which are stimulated by the presence of H+ ions), causing more acid to be secreted, in the absence of negative feedback
  • Increased gastrin release due to H. pylori infection leads to increased acid secretion, which leads to increased duodenal acid load, and ulceration
67
Q

How does acetylcholine stimulate and regulate acid secretions?

A

Acetylcholine released from local cholinergic fibres stimulates H+ secretion directly or through stimulation of G cells to release gastrin. Also acts via enterochromaffin-like cells (ECL) cells by releasing histamine

68
Q

How is H. pylori infection treated?

A

PPI plus H. pylori eradication therapy

69
Q

What is the outcome of H. pylori infection?

A

50% of general population have H. pylori; 80% have no associated disease, 5-15% develop peptic ulcer disease, 1-3% develop gastric cancer

70
Q

What are the different outcomes of H. pylori infection?

A

No atrophy -> duodenal ulcer

Chronic atrophic gastritis -> gastric cancer

71
Q

What determines progression to atrophic gastritis and gastric cancer?

A

H. pylori infection leads to superficial gastritis, which develops to atrophic gastritis and hypochlorhydria (under the influence of host genetics, and bacterial strain) which develops to dyplasia and cancer (more common in males, smoking and diet thought to have an influence too)

72
Q

What was the summary of the study aimed to study gastric secretory status of general population volunteers with and without H. pylori?

A

In adult general population:

  1. H. pylori infection is associated with reduced intragastric acidity
  2. H. pylori positives have reduced parietal and Chief cell densities

This likely represents the H. pylori gastritis producing atrophy of gastric mucosa (may explain the negative association between H. pylori and reflux disease

73
Q

How many lobes does the liver have?

A

4 lobes and 8 segment

74
Q

What is the blood supply of the liver?

A

Supplied than the right and left hepatic arteries (oxygenated blood) and the portal vein (absorbed nutrients)

75
Q

How is the portal vein formed?

A

The superior and inferior mesenteric veins join with the splenic veins to form the portal vein. It carries venous blood from the small intestine

76
Q

What is the venous drainage of the liver?

A

There are 3 hepatic veins (draining from left, middle and right lobes) which all drain into the IVC

77
Q

What vitamins and minerals are stored in the liver?

A

Vitamin A, D, K, B12 and iron and copper

78
Q

What is the function the gallbladder?

A

Concentrates and stores bile

79
Q

What is the histology of the gallbladder?

A

Single layer of epithelial cells, lamina propria, single muscle layer and serosal layer. The gallbladder secretes prostaglandin which protects the surface from bile

80
Q

What is the innervation of the gallbladder?

A

The vagus and splanchnic nerves regulate motility

81
Q

What are the types of jaundice?

A

Pre-haptic (haemolytic anaemia, resorption of haematoma), hepatic (viral, alcohol, autoimmune, drugs) and post-hepatic (obstruction, mechanical)

82
Q

What are the functions of the large intestine?

A

Motility, absorption of water, absorption of vitamins (K),

83
Q

What can cause bowel obstruction?

A

Malignancy, hernias, inflammatory bowel disease, impacted faeces, adhesions, volvulus (twisting of the bowel), pseudo-obstruction (disrupted muscle/nerve coordination, or surgery, infection, medication (opiates))

84
Q

What is the normal anatomy of the large intestine?

A

Completes absorption of water and sodium, and secretes mucous (no digestive enzymes). Normal LI has crypts, columnar and goblet cells, and has a lamina propria and submucosa similar to the small bowel

85
Q

What are the main features of ulcerative colitis?

A

Inflammation and continuous ulceration throughout the colonic mucosa
Idiopathic, relapsing, caecum-rectum, pain, bloody diarrhoea, increased risk of cancer- colonoscopy every 5 years

86
Q

What are the main features of Crohn’s disease?

A

Idiopathic, chronic transmural inflammation. Anywhere from mouth to anus, but most common at small bowel and right sided. Skip lesions, abdominal pain, diarrhoea, weight loss, obstructive symptoms (iron deficiency)

87
Q

What is gastro-oesophageal reflux disease?

A

Retrograde passage of acidic gastric contents into oesophagus

88
Q

What are the complications of GORD?

A

Heartburn, regurgitation, epigastric pain (dyspepsia), nausea, maybe some extra-oesophageal symptoms (non-cardiac chest pain, wheeze)

89
Q

What is the normal structure of the oesophagus?

A

Muscular structure, 25 cm in length connecting the pharynx and the stomach. Divided into three regions: cervical, thoracic and abdominal. Bordered by upper and lower oesophageal sphincters

90
Q

What are the layers of the oesophageal wall?

A

Muscosa: stratified squamous epithelium, lamina propria and muscularis mucosa (smooth muscle)
Submucosa
Muscularis externa: circular muscle layer (skeletal muscle), connective tissue, longitudinal muscle (skeletal)
Adventitia

91
Q

What mechanisms protect against GORD?

A

Intrinsic and extrinsic sphincters, intra-abdominal oesophagus, angle of His/flap valve and secondary peristalsis

92
Q

What impaired defences can cause GORD?

A

Hiatus hernia, transient lower oesophageal relaxations, low sphincter pressure, impaired oesophageal clearance.

93
Q

How else can GORD be caused?

A

Increased offences- increased intra-abdominal pressure and reduced gastric emptying

94
Q

What is a hiatus hernia?

A

Protrusion of part of the stomach through the diaphragmatic hiatus and into the chest.

95
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

96
Q

What are “red flag” GI symptoms (indicative of cancer)?

A

Unexplained weight loss, dysphagia, persistent vomiting, evidence of GI blood loss or upper abdominal mass

97
Q

What are the mechanisms of swallowing?

A

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

98
Q

What are the structural causes of dysphagia?

A 
Intrinsic lesion:
- foreign body
- stricture
   - benign
   - malignant
- rings/webs
Extrinsic causes:
- lymph nodes
- goitre
- enlarged left atrium
99
Q

What are the functional causes of dysphagia?

A 
Motility disorders:
- achalasia
- oesophageal spasm
Neuromuscular disorders:
- cerebrovascular disease
- bulbar palsy
100
Q

What test would be done to investigate dysphagia?

A

Upper GI endoscopy: can be performed with topical anaesthesia or conscious sedation. Direct visualisation of upper GI tract, and allows mucosal biopsy. Diagnosis of structural and mucosal abnormalities (hiatus hernia, tumours, Barrett’s oesophagus). Therapeutic intervention possible

101
Q

What are the complications of GORD?

A

Oesophagitis (inflammation of squamous mucosa secondary to acid damage, can cause strictures), can lead to Barrett’s oesophagus (columnar transformation of squamous mucosa caused by chronic acid damage), can lead to adenocarcinoma (accumulating cellular genetic changes causing dysplasia and ultimately cancer)

102
Q

What tests can be done to examine oesophageal function?

A

High resolution manometry: allows recording of pressures within the oesophagus and proximal stomach. Catheter inserted through nose with local anaesthetic spray. Display showing pressures as colour plot or lines. Diagnosis of motility disorders (e.g. oesophageal spasm)

103
Q

How can GORD be managed?

A

Lifestyle measures: weight loss, stopping smoking and reducing alcohol, as well as avoiding precipitants
Pharmacotherapy: antacids and alginates, mucosal agents, H2 receptor antagonists, PPI and pro-kinetics

104
Q

How do antacids work?

A

They are mostly aluminium and magnesium salts, and they raise the pH of gastric secretions and decrease pepsin activity. Some bind bile acids. Duration of action depends of rate of gastric emptying

105
Q

What are some problems with antacids?

A

Aluminium salts can cause constipation
Magnesium salts can cause diarrhoea
Some formulations have high Na levels- unsuitable in cardiac or renal disease
They interact with tetracyclines, digoxin, iron or prednisilone

106
Q

How do alginates work?

A

Mixture of polyurionic acids. Added to antacid preparations as foaming agents- layer of foam on stomach contents- mechanical barrier to reflux

107
Q

How do pro-kinetics work?

A

Metoclopramide/domperidone- not increase gastric emptying and increase LOS pressure. Metoclopramide also acts on cholinergic systems in GI tract to increase ACh release.
Can cause drowsiness, diarrhoea and hyperprolactinaemia

108
Q

How does sucralfate work?

A

Sucralfate is a complex sucrose polymer. Anionic sulphate binds to positively charged glycoproteins in ulcer, which forms a paste impeding diffusion of acid and acts as a buffer for 6-8 hours

109
Q

What are some H2 receptor antagonists?

A

Cimetidine, ranitidine, famotidine and nizatidine

110
Q

How do H2 receptor antagonists work?

A

Competitively block histamine receptors on the parietal cell, reducing acid secretion

111
Q

What are some side effects of H2 receptor antagonists?

A

Diarrhoea, deranged LFTs, headache, dizziness, fatigue and rash. Tachyphylaxis (decreased response due to long term exposure) also occurs

112
Q

How do PPIs act?

A

Accumulate selectively in the acid space 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

113
Q

How does gastrin stimulate and regulate acid secretions?

A

Gastrin acts on G receptors of parietal cells to stimulate expression of the gene for proton pump and to stimulate the incorporation of the proton pump into the canalicular membrane. Gastrin also stimulates release of histamine from ECL cells which then acts on H2 receptors of parietal cells

114
Q

How does histamine stimulate and regulate acid secretions?

A

Histamine is released from the gastric mucosa and acts on H2 receptors to release H+ through a cyclic AMP-mediated process

115
Q

What normally prevents gastric juice from refluxing into the oesophagus?

A
  • Portion of the oesophagus in muscle of diaphragm
  • Smooth muscle tone at the lower oesophageal sphincter
  • Angle between oesophagus and stomach
116
Q

What protects gastric epithelium from damage by gastric juice?

A
  • Surface epithelial cell secretion of bicarbonate/alkaline
  • Mucus neutralising the acid neck cell secretion of mucus restricting the diffusion of acid
  • Combination of the two above carpets the gastric surface

Phase 2- GI (5 decks)

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