Functions of the Mouth and Oesophagus and Associated Diseases Flashcards

1
Q

define the process of digestion

A

conversion of dietary nutrients into a form that the small intestine can absorb

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2
Q

the mouth contains three very important structures:

A

the teeth
tongue
salivary glands

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3
Q

what are the functions of the tongue?

A

Receptors on the tongue allow you to detect what is in your mouth (taste)
Facilitates the movement of food during mastication
Assisting in swallowing

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4
Q

what are the functions of the mouth?

A

Mastication (teeth): allows for increased SA of the food which allows for more efficient digestion by enzymes when the food enters the small bowel (small intestine).
Initiation of carbohydrate + fat metabolism: Salivary amylase + lingual lipase is released - not for actually gaining nutritional value from food but for beginning breakdown.
Lubrication: Bolus is lubricated by saliva - important in swallowing process

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5
Q

what is one way of describing the oesophagus?

A

Conduit - tube that provides a way of passing something

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6
Q

what three glands are the salivary glands made up of?

A

parotid gland
sublingual gland
submandibular gland

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7
Q

what do the salivary glands act as?

A

They act as exocrine glands and secretory organs

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8
Q

what enzymes do exocrine salivary glands produce?

A

Exocrine glands → produce amylase + lipase

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9
Q

what do secretory salivary glands produce?

A

Secretory organs → produce:
Mucous
Lubrication – helps slip food down
Hydration → keeps oral mucosa moist + prevents dehydration/cell death
Cytoprotection → protects oral + oesophageal mucosa from damage
Fluid
Antibacterial function:
IgA - antibodies bind to pathogenic antigen
Lysosomes - attacks bacteria’s cell wall leading to cell lysis
Lactoferrin - protein which binds iron + is bactericidal (limits bacteria getting iron which is important for their viability)

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10
Q

watch lecture for this question
(just checked lecture and he doesn’t go through it??)

A

Bind and neutralise protein toxin
Block attachment of viruses to cells
Opsonise bacteria
Activate complement
Activate NK cells
Taken up by M cells in the
bowel to stimulate
lymphoblasts and subsequent
secretion of more IgA

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11
Q

what is the structure of salivary glands?

A
  • Similar to pancreas
  • Collection of ducts lined by ductal cells which end at acini (made of acinar cells)

Acinar cells:
- Produce enzymes, which ultimately move through the ducts and enter the mouth.
- Also release NaCl and water into the ducts

Ductal cells (+Goblet cells)
- Goblet cells produce mucous
- Ductal cells secrete water and electrolytes –> modifies the secretions of the acinar cells inside the duct.
- They extract Na+ and Cl- ions from the secretions and secrete K+ and HCO3- –> this means saliva is hypotonic (lower osmotic pressure than a particular fluid) and alkaline.
- Alkaline saliva protects teeth from bacterial acid.
- It also neutralises gastric acid that refluxes into the oesophagus from the stomach.

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12
Q

how many litres is secreted a day (from salivary glands)?

A

Total volume secreted is 1.5 L a day
If someone has oesophageal obstruction, you have to give them this + extra 1.5 L of water
Each salivary gland has its own unique secretion:
Sublingual gland produces very mucous rich saliva.
Parotid gland produces watery secretion
Submandibular produced mixed (water and mucous) secretion

NB. serous = low glycoprotein content ∴ very watery, mucous = very viscous

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13
Q

name 2 salivary gland diseases

A

Sjögren’s Syndrome
Mumps virus (parotitis)

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14
Q

what is Sjögren’s Syndrome?

A

Autoimmune attack of salivary + tear glands
This results in Dry mouth (xerostomia) + dry eyes
Commonly affects women + associated with rheumatoid arthritis (as also autoimmune)

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15
Q

what is Mumps virus (parotitis)?

A

Parotitis: Swollen parotid glands
Prodrome (early symptom) of fever + headache
Associated with orchitis (inflamed testicles)
Prevention: MMR vaccine

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16
Q

what part of the nervous system controls secretion?

A

Autonomic NS controls secretion predominantly via the paraNS

17
Q

what are the 4 phases of swallowing?

A
  1. Oral Preparatory Phase: food is manipulated in mouth + masticated to reduce it to a consistency that can be swallowed
  2. Oral Phase: tongue propels food posteriorly until the pharyngeal swallow is triggered
  3. Pharyngeal Phase: once pharyngeal swallow is triggered, bolus is transported through the pharynx
    With Coordinated closure of the glottis via movement of the epiglottis (falls)
    With Cessation (ceasing) of breathing
    With Relaxation of upper oesophageal sphincter (UOS)
  4. Oesophageal Phase: oesophageal peristalsis carries the bolus from the Upper Oesophageal sphincter (UOS) through to the oesophagus to the lower oesophageal sphincter (LOS)
18
Q

what is the anatomy of the oesophagus?

A

The Oesophagus is not gravity fed tube –> food/drink moves down due to peristalsis.
Anatomy:
The top 1/3 of the oesophagus is composed of striated muscles, the bottom 1/3 is composed of smooth muscle and finally the middle 1/3 contains a mixture.
It starts in the thorax and ends up in the abdomen
Oesophageal hiatus: hole in diaphragm through which oesophagus and vagus nerve pass
The oesophagus has a normal GI tract structure:
- Mucosa (stratified squamous epithelium)
- Inner circular muscle
- Outer longitudinal muscle
- BUT, no serosa (easier for cancer to grow) or mesentery

19
Q

what is the histology of the oesophagus?

A

Stratified squamous epithelium to Gastroesophageal (GO) junction (where oesophagus meets the GO sphincter -> to enter the stomach) = Z line

20
Q

what is Gastro-oesophageal reflux disease (GORD)?

A

The main function of the GO sphincter (LOS) is to prevent reflux - stop stomach juice being refluxed up into oesophagus and causing damage.
GORD: chronic acid reflux from the stomach, across the GO sphincter, into the oesophagus.
Very common

21
Q

what are the 5 causes of GORD?

A
  1. Obesity: Greater intraabdominal pressure therefore acid is forced up (reflux)
  2. Pregnancy: increased intra-abdominal pressure
  3. Hiatus hernia
    Sliding (common): the GOJ, the abdominal part of the oesophagus, and frequently the cardia of the stomach slides upwards through the diaphragmatic hiatus into the thorax.
    Rolling: an upward movement of the gastric fundus occurs to lie alongside a normally positioned GOJ, which creates a ‘bubble’ of stomach in the thorax.
  4. Iatrogenic: caused by drugs that lower tone at the LOS –> leads to enhanced reflux e.g.:
    Beta agonist
    Anticholinergic
    Benzodiazepines
  5. Zollinger-Ellison syndrome (Z-E syndrome)
    Gastrin secreting tumour –> hypersecretion of gastrin. Therefore, the stomach makes more acid –> more full stomach => increased likelihood of reflux
22
Q

list some symptoms of GORD

A

Heartburn: This is characterised by retrosternal discomfort and a burning sensation. These occur following eating and are exacerbated by exercise and lying down
Dysphagia: Hard to swallow, due to inflammation or stricture and affects 30%
Regurgitation: of food or sour liquid
Laryngopharyngeal reflux: characterised by chronic cough, hoarse voice secondary to reflux into pharynx and chronic ear ache.
BUT symptoms of GORD correlate poorly with actual oesophagitis → 40% of people with oesophageal adenocarcinoma have never had reflux and some patients with reflux don’t develop oesophagitis.

23
Q

what is the outcome of GORD?

A

Oesophagitis: This is because the oesophagus has not evolved to be bathed by stomach juice –> causes damage to mucosal lining
Oesophageal stricture: narrowing of the oesophageal lumen
Barrett’s metaplasia: Pink = normal stratified squamous mucosa of oesophagus. Red = BM - becomes simple intestinal columnar epithelia (oesophagitis is precursor to BM)
Individuals with BM are predisposed to developing oesophageal adenocarcinoma

24
Q

how to diagnose GORD?

A
  • Endoscopy – shows you if there is damage (does not 100% attribute to GORD though)
    So, you can then do:
  • 24hr pH monitoring
    Probe sat in oesophagus and records pH (acid levels) → defines reflux
    Especially useful if endoscopy is normal (but patient still feeling symptoms of GORD)
  • Contrast swallow
    Surpassed by endoscopy
    Demonstrates reflux
25
Q

what are the 3 ways you can treat GORD?

A
  1. Conservative
    Weight loss (as GORD is associated with obesity)
    Avoid alcohol/food close to bedtime (as GORD is more likely to happen after you have eaten and when you are in the supine position)
    Raise head off bed 20-30 cm (as reflux is more likely if lying down)
    Reduce alcohol intake
  2. Medical
    Decrease acid: proton pump inhibitors + H2 blockers
    Antacids increase pH
    Alginates (Gaviscon) coat mucosa
  3. Surgical
    Anti-reflux surgery → fundoplication (wrap stomach round itself + tighten angle)
    Repair hiatus hernia (if this is associated with reflux)
    A Vagotomy was historically done. It decreases acid production. But this also impacted functioning of sphincter so we do not do this anymore.
26
Q

what is Barrett’s metaplasia (BM)?

A

Metaplasia: ‘change of epithelial type in response to environmental stress’
Environmental stress is repeat exposure to stomach acid + bile
Barrett’s metaplasia: in the oesophagus the stratified squamous epithelial cells are replaced by simple columnar epithelium with goblet cells (normally only present in intestine)

27
Q

how does BM relate to GORD?

A

10% of GORD patients develop BM
BM is the pre-malignant condition for oesophageal adenocarcinoma (cancer of oesophagus)
0.5% convert to OAC per year from BM
There has been rising rates of OAC. This is thought to be primarily due to increased obesity

28
Q

how to manage BM?

A

Management of symptoms of reflux → conservative, medical + surgical
For monitoring the risk of malignant progression → surveillance endoscopy
This is controversial as it is expensive and labour intensive, and only 0.5% progress to adenocarcinoma (10% 5-year survival)
It also has no effect on overall survival from ADC
Majority of OAC arises in patients with undiagnosed Barrett’s metaplasia
However it is only current mechanism of identification

29
Q

what research has been done to predict if you have BM, dysplasia or ADC?

A

There are some biomarkers which can be used to tell us which patients with BM are most likely to develop OAC.
This will allow us to perform surveillance on only these individuals saving lots of money.
One method:
1. Patient with BM is given a capsule with an abrasive sponge inside.
2. Piece of sting is attached.
3. Patients swallow capsule holding string.
4. When capsule in stomach the acid degrades shell of capsule and sponge opens up and this abrasive sponge can be pulled up the oesophagus with string this means cells lining the oesophagus will be captured.
5. We can then see what proteins and DNA and RNA are in the cell and begin to identify which are predictive if you have BM, dysplasia or ADC. We can then develop signatures to see if individual with Bm will develop ADC.
6. You can also use non-invasive breath test which detect biomarkers in the breath to see if you have a disease.

29
Q

what are the types of oesophageal cancers?

A

Types: Squamous cell carcinoma (come from native squamous cells) + adenocarcinoma (ADC)
ADC is the type associated with BM
Survival for both is particularly low, as often involves elderly who are unfit for major surgery

Lower oesophagus – where you get most reflux
Increasing – due to obesity

30
Q

what is Achalasia?
(inc. symptoms, cause and treatment)

A

‘Failure of GO sphincter to relax’→ loss of myenteric plexus at lower oesophageal sphincter (LOS)
Symptoms:
Dysphagia → LOS remains contracted so food and drink can’t pass through
(contrast: in cancer only dysphagia with solids)
Regurgitation
Halitosis (bad breath)
Chest discomfort
Cause: unknown
Treatment: all given for relaxation of LOS
Botox injection at LOS to relax muscle
Oesophageal dilation – using a balloon to open up sphincter
Surgery → Heller’s myotomy (muscles of LOS cut therefore food + liquid can pass to stomach)