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Case 6 > Case 6 - Therapeutics of the Upper Gastrointestinal Tract > Flashcards

Case 6 - Therapeutics of the Upper Gastrointestinal Tract Flashcards

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1
Q

The gut wall consists of four layers which are:

A

mucosa - inner mucosa facing the inner hole
(lumen)
submucosa - a connective tissue containing nerves, blood vessels and lymphatic vessels
muscularis externa (or propria) - layers of smooth muscle are known collectively as this, and this also contains nerves
serosa or adventitia - a covering of connective tissue

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2
Q

Mucosa is divided into 3 different layers, which are:

A

epithelium then under this is lamina propria (connective tissue layer) then under this is muscularis mucosae

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3
Q

what is the mucosa?

A

a mucous membrane that lines the GI tract and secretes mucus that lubricates and protects the GI tract

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4
Q

what is the submucosa?

A

a layer of connective tissue that contains blood vessels, lymph vessels and nerves

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5
Q

what is the muscularis made up of?

A

muscularis is made up of two layers of smooth muscle - one circular and one longitudinal

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6
Q

what is the serosa/adventitia?

A

Serosa/adventitia is a connective tissue covering that secretes a fluid to lubricate the outside of the GI tract

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7
Q

what type of epithelium lines the oesophagus and anus

A

stratified squamous epithelium

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8
Q

what type of epithelium lines the stomach

A

simple columnar epithelium

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9
Q

what type of epithelium lines the small intestine

A

simple columnar epithelium

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10
Q

what type of epithelium lines the large intestine

A

simple columnar epithelium

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11
Q

what is dyspepsia?

A

Dyspepsia is an umbrella term to describe a range of symptoms associated
with the upper gastrointestinal tract and includes upper abdominal pain or
discomfort, heartburn, acid reflux , nausea and vomiting

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12
Q

The underlying causes of dyspepsia include what?

A

gastric and duodenal ulcers, gastro-oesophageal
reflux disease (GORD) and oesophageal or gastric cancers.

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13
Q

GORD is caused by what?

A

GORD is caused by reflux of acid or bile from the stomach into the oesophagus, or
beyond.

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14
Q

classical symptoms of GORD include?

A

heartburn, regurgitation, reflux,
odynophagis (painful swallowing) or dysphagia.

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15
Q

diagnosis of GORD is based on what?

A

Diagnosis is on the basis of
endoscopy.

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16
Q

The signs of GORD include what [2 things]

A

include chest pain and
oesophagitis which are not
the same condition

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17
Q

what is oesophagitis and what’s it caused by?

A

Oesophagitis
is inflammation of the
oesophageal mucosa. It is
caused by frequent reflux of
stomach contents causing
damage to the oesophageal
mucosa.

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18
Q

Complications of GORD

A

*Oesophageal ulcers.
*Oesophageal haemorrhage.
*Anaemia due to chronic blood loss (usually secondary to severe oesophagitis)
*Oesophageal stricture
*Aspiration pneumonia.
*Barrett’s oesophagus (columnar metaplasia of the distal oesophagus), which
has malignant potential and an increased risk of developing oesophageal
adenocarcinoma.
*Oral problems, such as dental erosions, gingivitis, and halitosis.

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19
Q

Important anatomical
features which prevent
reflux are :

A

Lower Oesophageal sphincter
The oesophagogastric junction

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20
Q

The Lower Oesophageal
Sphincter is
comprised of what

A

the external LOS (or diaphragmatic sphincter which exerts a ‘pinchcock‘ action at the
terminal oesophagus), smooth muscle and
anatomical angle of the oesophagus.

these all normally seal off the stomach from
the oesophagus. They relax upon swallowing.

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21
Q

A loose lower oesophageal
sphincter (lower muscular tone)
can be caused by?

A

smoking, alcohol
and too much caffeine
consumption.

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22
Q

The oesophagogastric junction is
an important anatomical region
because of its essential functions
in relation to being a site of?

A

structural defects, inflammation,
metaplasia (change in epithelial
cell type) and neoplasia (new or
abnormal cell growth) in disease,
but particularly reflux.

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23
Q

what is the main mechanism that
leads to pathological reflux into the oesophagus, and name other factors involved too

A

Increased frequency of transient LOS relaxation is the main mechanism that
leads to pathological reflux into the oesophagus. Other factors include increased
intra-abdominal pressure, poor oesophageal peristalsis, delayed gastric emptying.

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24
Q

what is a hiatus hernia

A

occurs when a region of the proximal stomach moves through the diaphragm into the thorax
[When the fundus of stomach starts to move up from the diaphragm. The top of the stomach has slid up through the diaphragm]

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25
what can worsen symptoms of hiatus hernia
Obesity and pregnancy will raise intra-abdominal pressure on lying down and can exacerbate reflux remember hiatus hernia is linked to GORD
26
Barrett’s oesophagus is characterised by what?
characterised by metaplasia (abnormal growth) of the lining of the lower oesophagus, which changes from stratified squamous to simple columnar together with the presence of goblet cells that are not normally present in this region of the GI tract [increased goblet cells].
27
name Histamine H2 Antagonists used for upper GI tract
Famotidine and Cimetidine
28
Histamine H2 receptor antagonists include Famotidine and Cimetidine - how do they work?
they block stimulatory actions of histamine on the parietal cell. Although gastrin also promotes gastric acid secretion (and GI motility) the effect is indirect through histamine release. Pepsinogen requires acid for conversion to pepsin, so when acid secretion is reduced so too is pepsin production.
29
the changes that occur in Barrett's oesophagus are considered to be what?
metaplasia and increased goblet cells consider Barrett's oesophagus to be a premalignant condition because it is associated with a high incidence of further transition to oesophageal adenocarcinoma
30
Side effects of Histamine H2 receptor antagonists like Famotidine and Cimetidine
diarrhoea, headache and dizziness
31
a) what is histamine released from? b) what stimulates ECL cells? c) what stimulates gastrin release?
a) ECL cells (enterochromaffin cells) b) gastrin (released from G cells) stimulate ECL cells c) Distension of antrum of stomach stimulate gastrin release
32
what happens when you give histamine H2 anatagonist to a patient? [think of what they become susceptible to]
If you give H2 antagonist to pateint→ you lower the acid of the stomach and the acid is also an antibacterium so they have become more susceptible to H.pylori and other bacteria
33
what is cimetidine?
Cimetidine is a cytochrome p450 inhibitor, which is involved in phase 1 metabolism of liver
34
what are the proton pump inhibitors (PPIs) used for upper GI tract
omeprazole lansoprazole esomeprazole
35
how the proton pump inhibitors (PPIs) omeprazole, lansoprazole and esomeprazole work?
irreversibly inhibits the Hydrogen-Potassium ATPase (proton pump), supressing hydrochloric acid secretion
36
These drugs are __1__bases and therefore have a high affinity for __2__environments. The drug is converted into its active form in low pH environments.
1 - weak 2 - acidic
37
side effects of PPI's
diarrhoea, nausea & headaches.
38
recommendations with using PPI's
Proton Pump Inhibtors have a long duration of action that allows once daily treatment although twice daily doses are recommended in cases of severe oesophagitis or to eradicate the bacteria H.pylori. They are most effective taken about 30 minutes before a meal. New recommendations suggest weaning off PPIs - bc: If you block PPI on parietal cells you will really reduce HCl secretion. PPI only give if serious Dr are recommended to not use PPI as it renders susceptibility having less antibacterium and less pepsin.
39
name antacids used for upper GI tract
Aluminium Hydroxyde or Magnesium carbonate
40
how do the antacids (Aluminium Hydroxyde or Magnesium carbonate) work
neutralise the gastric hydrochloric acid. Reduced acidity will decrease the pain of heartburn.
41
alginates include?
Gaviscon
42
how do alginates (gaviscon) work
forms a ‘raft‘ that floats on the surface of stomach contents. Alginates are believed to increase the viscosity and adherence of mucous to the oesophageal mucosa, forming a protective agent.
43
what do antacids and alginates contain that mean they can be used in combination?
Gaviscon contains sodium alginate, sodium bicarbonate (sodium hydrogencarbonate) and calcium carbonate (antacids) to maximise the relief of heartburn
44
Surgical Options for stage 3 upper GI conditions
Fundoplication: standard surgical treatment for GORD. 2 types: * Laparoscopic Nissen fundoplication * LINX® magnetic anti-reflux device
45
how does fundoplication work?
Tightens and reinforces the Lower Oesophageal Sphincter. The upper part of the stomach is wrapped around the outside of the lower oesophagus to strengthen the sphincter.
46
what is functional dyspepsia
Functional dyspepsia (FD) is a common (perhaps the most) gastrointestinal disorder characterised by chronic or recurrent upper abdominal symptoms without any identifiable structural cause on endoscopy.
47
Functional dyspepsia is defined by the Rome IV criteria as the presence of one or more of the following:
Symptoms for at least 3 months, with symptom onset at least 6 months before diagnosis Postprandial fullness– immediately after eating Early satiety Epigastric pain or burning in the absence of structural disease (e.g., ulcers, cancer) Bloating/belching, nausea and reflux
48
Causes or contributing factors of functional dyspepsia
Gastric motility dysfunction Visceral hypersensitivity Helicobacter pylori infection (in some cases) NNT (number needed to treat) = 14 Psychosocial factors (e.g., stress, anxiety) Altered gut-brain axis
49
management of functional dyspepsia
Lifestyle and dietary advice: Smaller, low-fat meals, avoid caffeine, alcohol, smoking
50
Pharmacological management of functional dyspepsia
H. pylori eradication (if positive) Proton pump inhibitors (PPIs) – reduce acid Prokinetics – for motility symptoms (e.g., domperidone) Tricyclic antidepressants (low dose e.g., amitriptyline) – for visceral hypersensitivity Psychological therapies – e.g., CBT for stress-related symptoms
51
Stomach ulcers form in response to what?
form in response to increased hydrochloric acid release or an impaired barrier (mucous layer damage).
52
Ulcers can occur in the __1__but are more common in the __2__.
1 - stomach 2 - duodenum
53
Most common cause of stomach ulcer is __1__, followed by ___2___ then ___3___
1 - H.Pylori infection, 2 - NSAIDs 3 - cancer
54
rarer causes of stomach ulcers?
Rarer causes include gastric tumour (Gastrinoma of pancreas - Zollinger Ellison syndrome), Crohn’s disease and Stress
55
Mucosal damage results in __1__secretion and consequently MORE ___2___ release.
1 - histamine 2 - HCl
56
Who needs endoscopy?
* GI bleeding * Iron deficiency anaemia * Unintentional weight loss & dyspepsia * Dysphagia * Persistent vomiting * Epigastric mass (endoscopy = treatment) * >55 & persistent / recent onset dyspepsia
57
A Mallory-Weiss tear produces what?
bright red blood after numerous vomiting episodes, normally after drinking large quantity of alcohol or hiatus hernia.
58
mallory-weiss tear diagnosis is confirmed with what?
Diagnosis is confirmed with endoscopy
59
treatment of mallory-weiss tear
Treatment (Endoscopic): Active bleeding can be supressed with Band ligation and Haemaclips Adrenaline injection causing constriction of blood vessels at the site of the tear. And promotes clot formation.
60
Most common cause of pyloric stenosis is?
infantile hypertrophic pyloric stenosis [pyloric stenosis - a narrowing of the opening between the stomach and the small intestine.]
61
what happens in pyloric stenosis?
A reflux of a child who is vomiting profusely → child is losing lots of volume, vomiting up lots and lots of HCl so losing acid and chloride. Metabolic alkalosis (alkalosis – losing lots of acid) Gastric secretions are rich in H⁺ and Cl⁻ Loss of H⁺ = metabolic alkalosis (due to reduced acid) Loss of Cl⁻ = hypochloraemia Volume depletion (dehydration), so the Na+ in body is lowered and this is detected, and it Stimulates RAAS (renin–angiotensin–aldosterone system) the trigger for aldosterone release is low Na+ in body and so aldosterone inserts Na+ channels in the nephron (the distal convoluted tubule part), but this is in exchange for K+ and H+ excretion in the nephron, so you worsen hypokalaemia and sustain alkalosis

Case 6 (13 decks)

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