Physiology Of The Mouth, Pharynx And Oesophagus Flashcards

1
Q

What are the functions of saliva?

A
  1. Lubricates/wets food for swallowing
  2. Helps with taste
  3. Begins digestion of starch + lipids
  4. Protects oral environment
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2
Q

How does saliva protect the oral environment?

A
  • Washes away bacteria + food particles
  • Keeps mucosa moist
  • Cools hot foods
  • Contents destroy bacteria
  • Maintains alkaline environment -> neutralizes acid produced by bacteria preventing teeth damage
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3
Q

How much saliva is produced each day? What is its pH?

A

800-1500ml

6.2-8.0 pH (depends on whether its resting or stimulated)

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4
Q

What type of solution is saliva relative to plasma?

A

Hypotonic

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5
Q

What does saliva contain?

A

H2O

High [K+], [HCO3-] + [Ca2+] but low [Na+] + [Cl-] relative to plasma

Mucous

Digestive enzymes (e.g. salivary α-amylase + lingual lipase)

Antibacterial agents like thiocynate ions, proteolytic enzymes (e.g. lysozyme) + Abs

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6
Q

Why is calcium high in saliva?

A

To stop Ca2+ moving out of teeth by decreasing the concentration gradient

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7
Q

What do antibacterial agents do in the saliva?

A

Proteolytic enzymes attack bacteria + aid thiocynate ions in entering bacteria having a bactericide effect

Digest food particles that would provide metabolic support for bacteria

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8
Q

Where are the 3 pairs of salivary glands? What type of saliva do they produce?

A
  1. Parotid (on side of cheek): serous saliva, watery + rich in enzymes
  2. Sublingual (under tongue): mucous saliva with no enzymes
  3. Submandibular (under mandibular bone): mixed serous + mucous saliva
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9
Q

What type of glands are salivary glands?

A

Exocrine

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10
Q

What are the other salivary glands present?

A

Many tiny buccal glands inside of cheek + mouth

Von Ebner’s glands of tongue

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11
Q

Where are the 2 main digestive enzymes of saliva produced?

A

α-amylase - mostly in parotid salivary glands

Lingual lipase - Von Ebner’s glands of tongue

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12
Q

What is the structure of salivary glands? What does each part do?

A

‘Bunch of grapes’ appearance including:

  • Acini lined by acinar cells; initially secrete saliva
  • Ducts lined by ducts cells; modify secretion
  • Myoepithelial cells; contract to eject saliva responding to NS signals
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13
Q

Does mucous stain a lighter or darker pink than serous acinus?

A

Lighter/paler

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14
Q

Explain the 1st step of saliva production.

A
  1. Isotonic ultrafiltrate diffuses from plasma through the acinar cells
  2. Mixes with enzymes e.g. α-amylase (serous cells) or mucins (mucous cells)
  3. Primary secretion drains into duct from acinar cells
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15
Q

Explain the 2nd step of saliva production.

A

Ductal modification in where there is absorption of Na+/Cl & secretion of K+/HCO3- via transporters (+ ATPase on basolateral membrane) = net absorption of solute

Ductal cells impermeable to H2O so H2O cannot follow the solute making the solution hypotonic + alkaline

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16
Q

What is resting saliva?

A

The lower flow rate of saliva due to it not being needed so there is more time for ductal modification making the solution more hypertonic relative to plasma as solutes have time to move more

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17
Q

What is stimulated saliva?

A

The higher flow rate of saliva when there is maximal salivation meaning there is less time for ductal modification so solution is more isotonic relative to plasma due to less solute movement

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18
Q

What is the exception to the resting vs stimulated saliva rule?

A

HCO3- because it is selectively stimulated when saliva production is stimulated so [HCO3-] increases with increases flow rate

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19
Q

What are the characteristic features of resting saliva?

A
Low volume
Highly modified
Very hypotonic
Neutral pH/slightly acidic
Few enzymes
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20
Q

What are the characteristic features of stimulated saliva?

A
High volume
Less modification
Less hypotonic
More alkaline (lots of bicarb)
Lots of enzymes
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21
Q

What are the hormonal factors involved in saliva secretion?

A

ADH + aldosterone: during dehydration/low vascular volume, Na+ & H2O reabsorption increases decreasing saliva volume

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22
Q

What does parasympathetic stimulation do to saliva secretion?

A

Increases it in response to:

  • Stimulation of taste via taste receptors + mechanoreceptors in mouth
  • Sight/smell of food
  • Nausea
  • Conditioned reflexes

Decreases it in response to:

  • Sleep
  • Fear
  • Dehydration
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23
Q

What does sympathetic stimulation do to saliva secretion?

A

Initially stimulates release of preformed mucous saliva but after that, decreases saliva flow e.g. when you get xerostomia through stress

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24
Q

What neural control is there over saliva secretion?

A

Parasympathetic (most important)

Sympathetic

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25
Q

What are the signs and symptoms of dry mouth (xerostomia)?

A
Burning/scalding sensation in mouth
Dry/painful throat
Dry/rough tongue
Dry/cracked lips
Problems swallowing/speaking
Altered taste
Halitosis
Dental caries + periodontal disease 
Oral infections e.g. candidiasis
Difficulty keeping dentures in place
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26
Q

What are the potential causes of xerostomia?

A
Side effect of medication (e.g. TCA, antimuscarinic or β-blockers)
Dehydration
Anxiety
Lifestyle (e.g. smoking)
Radiation therapy for head + neck cancer
Damage to salivary glands or innervation
Sjogrens syndrome
Medical conditions (e.g. poorly controlled diabetes, AD)
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27
Q

What is Sjogrens syndrome?

A

Autoimmune destruction of salivary + lacrimal glands causing xerostomia + dry eyes

Other glands can be involved causing dyspareunia, dry skin, dysphagia, otitis media + pulmonary infection

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28
Q

Where are receptors for taste found?

A

Tongue
Palate
Larynx
Pharynx

29
Q

What are the 5 classifications of taste?

A
Sweet 
Sour
Bitter
Salty 
Umami
30
Q

Where are the taste buds found?

A

Papillae:

  1. Fungiform (medial + anterior of tongue x 2)
  2. Foliate (more posterior + lateral of tongue x 2)
  3. Circumvallate (completely posterior + lateral to midline of tongue x 2)`
31
Q

What do taste buds contain?

A

Taste receptor cells
Supporting cells
Basal cells

32
Q

What does the umami receptor bind?

A

Glutamate (in protein-rich food + MSG)

33
Q

What do basal cells in taste buds do?

A

Precursors to taste receptor cells + replace cells sloughed off the tongue

34
Q

What are taste receptor cells?

A

Chemoreceptors (specialised epithelial cells) that transduce a chemical stimuli into an electrical signal

They respond to all taste types but may respond best to one type

35
Q

How does the taste sensation work?

A
  1. CNs carry afferent info on taste
  2. Saliva needed as solvent
  3. Also requires olfaction (i.e. taste tells you jam is sweet, but smell tells you its strawberry jam)
  4. Signal carried to medulla + then to other regions of brain e.g. sensory cortex
36
Q

What does chewing (mastication) involve?

A

Physical digestion i.e. breaking up food to increase SA for enzyme action

Teeth: cut (incisors) + crush (molars) food

37
Q

What are the muscles of chewing (mastication)?

A

Masseter
Temporalis
Medial + lateral pterygoid
Suprahyoid of neck

38
Q

What other facial features are involved in chewing (mastication)? What do they do?

A

Movement of mandible, tongue, lips + cheek help mix food with saliva creating a bolus for swallowing

39
Q

What is the pharynx?

A

A muscular tube with 2 layers that interconnects the nasal cavity, oral cavity, larynx + oesophagus

It is the extension/top of the alimentary canal

40
Q

What are the 3 parts of the pharynx and their boundaries?

A

Nasopharynx (behind nasal cavity): extends from skull base to soft palate

Oropharynx (posterior to oral cavity): from soft palate to epiglottis

Laryngopharynx (posterior to larynx): from epiglottis to cricoid cartilage

41
Q

What are the 2 main muscular layers of the pharynx?

A

Inner longitudinal

External circular (made up of 3 pharyngeal constrictors; superior, middle + inferior)

42
Q

What happens when the pharynx contracts?

A

Shortens + widens pharynx when swallowing

Elevates larynx when swallowing

Focuses bolus of food into oesophagus by peristalsis

43
Q

What is special about the lower part of the inferior pharyngeal constrictor muscle?

A

Forms the UOS

44
Q

What is the oesophagus?

A

Muscular tube that transports food by peristalsis, passing through the oesophageal hiatus in the diaphragm + ending at the cardiac opening of the stomach

45
Q

What type of muscle is the oesophagus made up of?

A

Internal circular + external longitudinal muscle layers:

  • Superior 1/3 = voluntary striated muscle
  • Middle 1/3 - voluntary striated muscle + SM
  • Inferior 1/3 = SM under autonomic control
46
Q

What are the 4 points of compression/narrowing of the oesophagus?

A
  1. Junction between pharynx + oesophagus (UOS)
  2. Crossed by aortic arch in superior mediastinum
  3. Where it is posterior to L main bronchus in posterior mediastinum
  4. Where it passes through diaphragm at oesophageal hiatus
47
Q

What is the lower oesophageal sphincter (LOS)? What does it do?

A

Physiological (NOT anatomical) sphincter at the gastro-oesophageal junction which allows food through + prevents reflux of gastric contents into the oesophagus

48
Q

What oesophageal sphincter has the higher resting basal tone?

A

LOS

49
Q

What are the additional components of the lower oesophageal sphincter (LOS) that help shut it?

A

R crus of diaphragm (contracts acting like a pinchcork)

Acute angle at which oesophagus enters stomach

Mucosal folds at gastro-oesophageal junction (acts like ‘cork in the bottle’)

+ve intra-abdominal pressure collapses oesophagus preventing reflux

50
Q

What is gastro-oesophageal reflux disease (GORD)?

A

Reflux of acidic contents through LOS occurring when normal anti-reflux mechanisms are impaired

51
Q

What is reflux oesophagitis?

A

Mucosa of oesophagus becomes damaged due to acidic irritation

52
Q

How can normal anti-reflux mechanisms become impaired?

A

Increased frequency of transient lower oesophageal sphincter relaxations (TLESRs)

Increased intra-abdominal pressure e.g. pregnancy

Low LOS pressure

Hiatus hernia prevents normal functioning of LOS + disrupts diaphragmatic action on LOS

53
Q

What are the signs and symptoms of gastro-oesophageal reflux disease (GORD)?

A

Heartburn: burning lower chest pain radiating upwards (related to meals, worse on bending/lying down + relieved by antacids)

Acid brash: acid in back of throat

Regurgitation of stomach contents

Water brash: increased salivation in response to acid presence

54
Q

What is the correlation between symptoms and pathological severity in gastro-oesophageal reflux disease (GORD)?

A

Poor because a patient may not have many symptoms but severe oesophagitis in endoscopy or vice versa

55
Q

What are the risk factors associated with gastro-oesophageal reflux disease (GORD)?

A
Pregnancy
Obesity
Fat
Coffee
Chocolate
Alcohol
Large meals
Smoking
Certain drugs e.g. antimuscarinics
Systemic sclerosis
Achalasia treatment
Hiatus hernia
56
Q

What is Barrett’s oesophagus?

A

Metaplasia of stratified squamous epithelium of oesophagus to columnar mucosa so there is proximal displacement of squamocolumnar junction between 2 cell types seen high up in the oesophagus

57
Q

What are the causes of Barrett’s oesophagus?

A

Complication of GORD

Hiatus hernia

58
Q

What do patients with Barrett’s oesophagus have an increased risk of?

A

Oesophageal adenocarcinoma

59
Q

Explain the oral (voluntary) phase of swallowing.

A
  1. Tongue moves bolus from oral cavity back towards oropharynx
  2. Sensory receptors in soft palate + anterior pharynx detect bolus + send info via CNs to swallowing centre in medulla
  3. Swallowing reflex initiated

Duration = up to 1 second

60
Q

Explain the pharyngeal (involuntary) phase of swallowing.

A
  1. Soft palate elevates blocking off nasopharynx
  2. Respiration inhibited, glottis closes, larynx elevates + epiglottis tilts to cover opening of larynx to protect respiratory tract
  3. UOS opens
  4. Peristaltic wave of contraction of pharyngeal constrictor muscles propels food through sphincter into oesophagus

Duration = 1 second

61
Q

Explain the oesophageal phase of swallowing.

A
  1. UOS closes preventing reflux into pharynx
  2. Larynx falls, glottis opens + respiration commences
  3. Primary peristaltic wave (coordinated by swallowing reflex) propels food down oesophagus + stretch receptors detect bolus presence
  4. LOS relaxes to allow bolus into stomach
  5. Secondary peristaltic wave may occur (mediated by ENS - brain not needed as it is a localised system)
62
Q

What are the stages of swallowing?

A
  1. Oral (voluntary)
  2. Pharyngeal (involuntary)
  3. Oesophageal
63
Q

Why is it important to assess swallowing?

A

It is an important brainstem function that must be checked in head injury, post-surgery or stroke for e.g. because dysfunctional swallowing is associated with a high risk of aspiration which can cause pneumonia

64
Q

How do you assess swallowing?

A
  1. History + examination
  2. Speech + language therapy (SLT):
    - Clinical assessment
    - Bedside swallow test
    - Instrumental assessment
  3. Barium swallow
  4. Manometry
65
Q

What is achalasia?

A

Loss of coordination of peristalsis of lower oesophagus + spasm of LOS preventing food from moving easily through oesophagus into stomach -> dilation + hypertrophy of oesophagus superior to area of functional obstruction+ damage to Auerbach’s plexus

66
Q

What are the symptoms of achalasia?

A

Intermittent dysphagia for solids/liquids

Regurgitation of food

Retrosternal chest pain

67
Q

How would you be able to determine the difference between dysphagia associated with oesophageal carcinoma or achalasia?

A

Dysphagia tends to be more rapid with cancer but cannot rule it out on history so must do:

  • CXR
  • Barium swallow
  • Endoscopy
  • Manometry
68
Q

What instrumental assessments can be done on swallowing?

A

Videofluoroscopic swallowing study

Fibreoptic endoscopic evaluation of swallowing