Oesophagus Disorders Flashcards

1
Q

Anatomy of oesophagus?

A
  • Fibromuscular tube (25cm) of striated squamous epithelium
  • Posterior to trachea
  • Begins at end of laryngopharynx
  • Joins stomach a few cm from diaphragm (at cardiac orifice)
  • Extends from lower border of cricoid cartilage (C6) to cardiac orifice of stomach (T12)
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2
Q

Composition of oesophagus wall?

A

striated muscle in upper part
smooth muscle in lower part
mixture in middle
LOS both squamous + columnar epithelium coexist

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3
Q

Role of oesophagus?

A
  • Transports food to stomach
  • Secretes mucus
  • Swallowing (deglutition)
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4
Q

What promotes transport of ingested food into stomach?

A

Relaxation of sphincters (UOS + LOS) which involves contraction + relaxation of oesophagus which transports food via GIT

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5
Q

Describe how food reaches stomach

A
  • swallows food down throat
  • food approaches upper oesophageal sphincter
  • opens so food/bolus can enter oesophagus
  • rhythmic waves of muscular contractions + relaxations = peristalsis propel food downward
  • food passes via lower oesophageal sphincter
  • into stomach (reservoir)
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6
Q

Muscle structure of oesophagus?

A
  • Skeletal muscles surrounds oesophagus below pharynx (1/3)

- Smooth muscles surround lower (2/3)

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7
Q

Structure of upper oesophageal sphincter (UOS)?

A
  • Striated muscle
  • Musculo-cartilaginous structure
  • Composed of posterior surface of thyroid cartilage, cricoid cartilage, hyoid bone, cricopharyngeus, thyropharyngeus, cranial cervical oesophagus muscles
  • 3 muscles spread upwards, posteriorly, insert into oesophageal submucosa after crossing muscle bundles of opposite side
  • Thyrophrangeus = obliquely oriented
  • Cricophrayngeus = transversely oriented
  • Between 2 muscles = zone of sparse musculature – Killian Triangle forms, Zenker’s diverticulum might emerge
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8
Q

Role of UOS?

A
  • Area of high pressure zone between pharynx + cervical oesophagus
  • Constricted to avoid air entering oesophagus
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9
Q

Structure of lower oesophageal sphincter (LOS)?

A

smooth muscle

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10
Q

Role of LOS?

A

-Acts as flap valve
-Area of high pressure zone located where oesophagus merges with stomach
-Has intrinsic + extrinsic components :
intrinsic = oesophageal muscles under neurohormonal influence
extrinsic = diaphragm muscle (adjunctive external sphincter)

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11
Q

Effect of malfunction of intrinsic and extrinsic components of LOS?

A

GORD

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12
Q

Muscle arrangment of oesephagus?

A
  • Inner circular + outer longitudinal muscles
  • Upper part = striated
  • Middle third = gradual transition from striated to smooth
  • Lower end = smooth muscle

Killian’s triangle →Zenker’s diverticulum

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13
Q

Role of pharyngeal raphe?

A

raphe that’s origin + insertion for pharyngeal constrictors (thyropharyngeal part of inferior, middle, superior pharyngeal constrictor muscle)

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14
Q

Define raphe + eg?

A

a groove, ridge, or seam in an organ or tissue marking line where 2 halves fused in embryo
eg connecting ridge between 2 halves of medulla oblongata or tegmentum of midbrain

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15
Q

Control of function of UOS?

A

Afferent inputs to motor neurons

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16
Q

Reflexes lead to?

A

Contraction/relaxation

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17
Q

What’s Sellick manoeuvre?

A

=when anaesthetics press on cricoid cartilage during
endotracheal intubation to prevent gastric reflux

Intubate: put tube in, commonly used to refer to insertion of breathing tube into trachea for mechanical ventilation

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18
Q

Weak spot of thyropharyngeus + cricopharyngeus muscles?

A

Pharyngeal diverticulum

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19
Q

Role of cricoid cartilage?

A

provides attachment points for cricothyroid muscle, posterior + lateral cricoarytenoid muscles, ligaments vital for opening/closing airways + speech

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20
Q

What are efferent nerves?

A

motor nerves that communicate need for action on part of organs or muscles to maintain efficiency of body

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21
Q

How cervical oesophagus runs?

A
  • Begins at lower end of pharynx (C6 or lower border of cricoid cartilage)
  • Extends to thoracic inlet (suprasternal notch); 18 cm from upper incisors
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22
Q

Features of thyroid cartilage?

A
  • Largest of 9 cartilages of laryngeal skeleton

- Doesn’t encircle larynx in full (cricoid cartilage encircles larynx)

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23
Q

How does trachea run?

A
  • Anterior to oesophagus
  • Connected to oesophagus by loose connective tissue
  • Connects pharynx to stomach
  • Begins in neck at pharyngo-oesophageal junction (C5-C6 vertebral interspace at inferior border of cricoid cartilage)
  • Descends anteriorly to vertebral column via superior + inferior mediasternum
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24
Q

Define dehiscence

A

splitting at maturity along a built-in line of weakness in a plant structure to release its contents
involve complete detachment of a part, structures that open like this are dehiscent

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25
Q

Intrinsic components of LOS?

A

-Thick circular smooth muscle layers
-Clasp-like semicircular smooth muscle fibres (encircle gastroesophageal junction medially) on right side : myogenic activity (some resting tone), but less ACh-responsive
-Oblique gastric muscle fibres on left lateral side :
prevent regurgitation (responsive to cholinergic innervation)

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26
Q

Why’s reflux common in infants?

A

oblique angle underdeveloped in infants, oesophagus makes a vertical junction with stomach

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27
Q

What’s myogenic?

A

contractions initiated by cells within (myocytes) so no nerve innervation required for contraction

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28
Q

What’s angle of his (oblique angle)?

A

-Acute angle created between entrance to stomach (cardia), oesophagus

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29
Q

Role of angle of his (oblique angle)?

A

Forms a valve = preventing reflux of duodenal bile, enzymes, gastric acid from entering oesophagus so no irritation of oesophageal lining, inflammation, Barrett’s oesophagus

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30
Q

Extrinsic components of LOS?

A

-Crural diaphragm encircles LOS:
forms channel so oesophagus enters abdomen
-Fibres of crural diaphragm has a “pinchcock-like” (clamp regulates flow of fluid via tube) action (extrinsic sphincter; diaphragmatic sphincter)- myogenic tone

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31
Q

Antireflux barriers?

A
  • Sphincters : LOS diaphragmatic sphincter

- Anatomic configuration at gastroesophageal junction (mucosal folds)

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32
Q

Role of diaphragm in LOS?

A

=extrinsic component LOS has diaphragm muscle

-Adjunctive external sphincter raises pressure in terminal oesophagus related to movements of respiration

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33
Q

Role of crural diaphragm?

A
  • Form oesophageal hiatus
  • Encircles proximal 2-4cm of LOS
  • Determines inspiratory-spike-like increase in LOS pressure as measured by oesophageal manometry
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34
Q

What’s oesophageal opening created by?

A

loop of right crux of diaphragm

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35
Q

Innervation of oesophagus?

A

Cholinergic (via ACh)

Non-cholinergic, NANC in control of tone of LOS

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36
Q

What causes contraction of intrinsic sphincters?

A

Ach, SP

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37
Q

What causes relaxation of intrinsic sphincters?

A

NO + VIP

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38
Q

Describe how NO causes relaxation of smooth muscle cells

A
  • NO interacts with AC
  • converts GTP -> cGMP
  • cGMP activates PKG
  • PKG acts on myosin phosphatase on smooth muscle cells
  • causes smooth muscle relaxationis an enzyme which. The
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39
Q

Role of myosin phosphatase?

A
  • dephosphorylates regulatory chain of myosin II
  • occurs in smooth muscles
  • initiates relaxation
  • so myosin phosphatase undoes muscle contraction process initiated by initiated by myosin light-chain kinase
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40
Q

What’s upper part of oesophagus innervated by?

A

striated muscle
somatic motor neurons of vagus w/o interruption
-Vagus nerve
-Splanchnic nerves (thoracic sympathetic trunks)

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41
Q

What’s lower part of oesophagus innervated by?

A

smooth muscles
visceral motor neurons of vagus with interruptions (synapse with postganglionic neurons; cell bodies in oesophagus, splanchnic plexus)

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42
Q

What’s oesophageal plexus?

A

encircles oesophagus

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43
Q

What are somatic motor neurons?

A

alpha, beta, gamma efferent neurons (muscle contraction)

alpha motor neurons = innervate skeletal muscle + cause muscle contractions that generate movement

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44
Q

Define viscera

A

internal organs in main cavities of body eg intestines.

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45
Q

What are splanchnic nerves?

A
  • Paired visceral nerves (contribute to innervation of internal organs)
  • Carry sensory fibres from organs (visceral afferent fibres) + ANS fibres (visceral efferent fibres)
  • Carry sympathetic fibres except pelvic splanchnic nerves which carry para fibres
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46
Q

Where do integration of impulses occur?

A

nucleus of tractus solitarius (NTS), nucleus ambiguus (NA), dorsal vagal nucleus

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47
Q

Features of dorsal vagal nucleus?

A
  • Of vagus nerve or posterior motor nucleus of vagus
  • Cranial nerve nucleus for vagus nerve in medulla
  • Lies under floor of 4th ventricle
  • Serves para vagal functions in GIT, lungs, other thoracic + abdominal vagal innervations.
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48
Q

Role of nucleus ambiguus?

A

contain cell bodies for preganglionic para vagal neurons that innervate the heart reside

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49
Q

How phrenic nerve passes?

A
  • originates from the 4th cervical nerve, but also receives contributions from 5th + 3rd cervical nerves (C3-C5) so receives innervation from parts of both cervical plexus + brachial plexus of nerves
  • passes down between lung + heart
  • reaches diaphragm
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50
Q

Role of phrenic nerve?

A
  • Breathing
  • Innervates external, internal intercostal muscles, diaphragm
  • Passes motor info to diaphragm
  • Receives sensory info fro diaphragm
  • Contain motor, sensory, sympathetic nerve fibres
  • Provide only motor supply to diaphragm
  • Provide sensation to central tendon
  • Supplies mediastinal pleura + pericardium
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51
Q

Describe swallow reflex

A
  • excitation of receptors in pharynx (oesophageal peristalsis + relaxation)
  • afferent stimulus travels to nucleus solitarius
  • set of events from dorsal vagal nucleus, nucleus ambiguus mediates oesophageal peristalsis + sphincter relaxation
  • efferent impulses pass to pharyngeal musculature + tongue
  • vagal efferent fibres communicate with myenteric neurons
  • mediates relaxation of LOS
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52
Q

eg of postganglionic transmitters

A

NO, VIP

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53
Q

What’s contraction of crural diaphragm controlled by?

A

inspiratory centre in brainstem + nucleus of phrenic nerve

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54
Q

What’s crural diaphragm innervated by

A

right + left phrenic nerves via ACh

55
Q

Describe reflux reflex

A
  • transient lower oesophageal sphincter relaxation, the principal mechanism of reflux uses same efferent neural pathway as swallow reflex.
  • origin of afferent signals for transient lower oesophageal sphincter relaxation in pharynx, larynx, or stomach
  • efferent pathway is in vagus nerve
  • NO = postganglionic neurotransmitter relaxes LOS
56
Q

Afferent impulses that triggers swallowing?

A

in trigeminal, glossopharyngeal, vagus nerves

57
Q

Efferent impulses from swallowing?

A

pass to pharyngeal musculature + tongue

58
Q

Features of trigeminal nerve?

A

CN 5
Sensation in face
1 on each side of pons with 3 major bundles:
-ophthalmic nerve (V1)
-maxillary nerve (V2)
-mandibullary nerve (V3) for motor functions - chewing, biting

59
Q

Role of glossopharyngeal nerve?

A
  • Branch to tongue
  • Taste + general sensation
  • Serve carotid body, carotid sinus, parotid gland (major salivary gland), palatine tonsils (tonsils on left and right side of back of throat)
60
Q

Features of nucleus of tractus solitarius?

A

=brainstem nucleus on each side of upper medulla

  • Lies lateral to dorsal nucleus of vagus
  • Has many connecting neurons
  • Medial to spinal tract + nucleus of trigeminal nerve
  • Has afferent fibres extending inferiorly within upper medulla as the tract of solitarius
61
Q

What initiates swallowing?

A
  • Voluntary – collect material on tongue + push backwards into pharynx (skeletal muscle, mucus membrane)
  • Waves of involuntary contractions push material into oesophagus

mouth→oropharynx→laryngopharynx→oesophagus

62
Q

Reflex responses when swallowing?

A
  • Inhibition of respiration (breathing)- nasopharynx closed off
  • Closure of glottis (around vocal cords) by epiglottis (prevents food from entering trachea)
  • Ring of peristaltic waves (4cm/s) behind food move it towards stomach (primary peristalsis)
  • 2nd wave of peristalsis moves food remnants along (secondary peristalsis)
  • Coordinated opening + closing of upper, lower sphincters
63
Q

What’s primary peristalsis?

A

Ring of peristaltic waves (4cm/s) behind food move it towards stomach

64
Q

What’s secondary peristalsis?

A

2nd wave of peristalsis moves food remnants along

65
Q

Where’s swallowing centre?

A

brain stem; sensory + cortical input with respect to swallowing integrated in NTS + NA

66
Q

What moves food towards stomach + along GIT?

A

Progressive muscular contractions + relaxations

67
Q

Cause of oropharyngeal dysphagia?

A

Swallowing difficulty by inability of UOS to open or discoordination of timing between opening of UOS + pharyngeal push of ingested bolus

68
Q

Describe secondary peristalsis

A
  • relaxation of UOS so food passes
  • UOS closes as soon as food passes
  • glottis opens
  • breathing resumes
  • LOS opens + stays open throughout swallowing
  • LOS closes after material passed
  • large food material doesn’t reach stomach after 1st peristaltic wave
  • food distenses oesophagus lumen stimulating receptors
  • repeated waves of peristalsis (secondary peristalsis)
69
Q

What prevents reflux of gastric contents?

A
  • LOS closes after material passed
  • “Pinchcock” effect of diaphragmatic sphincter on lower oesophagus
  • Plug-like action of mucosal folds in cardia which occludes lumen of gastro-oesophageal junction:
  • abdominal pressure acting on intra-abdominal parts of oesophagus
  • valve-like effect of oblique entry of oesophagus into stomach in adults
70
Q

Where’s anti-reflux barrier?

A

region of gastro-oesophageal junction where transition from smooth muscles that line oesophagus to rugal folds (wrinkles or gastric folds)

71
Q

When does gastro-oesophageal junction must maintain competence?

A
  • At rest

- Raised intra abdominal pressure

72
Q

What happens if gastro-oesophageal sphincter becomes incompetent?

A

GORD

73
Q

Describe transition from smooth oesophageal lining to rugal folds

A
  • empty state = mucosa + submucosa thrown into folds

- distended = folds “ironed out” + flat

74
Q

What’s Collar of Helvitius (or loop of Willus)?

A

where circular muscular fibres of the oesophagus join oblique fibres of stomach

75
Q

What’s zigzag line (Z-line)?

A

squamocolumnar mucosal junction between oesophagus + stomach – invisible radiologically

76
Q

Role of mucous cells?

A

secrete an alkaline mucus that protects epithelium against shear stress + acid

77
Q

Role of parietal cells?

A

secrete HCl aicd

78
Q

Role of chief cells?

A

secrete pepsin, a proteolytic enzyme

79
Q

Role of G cells?

A

secrete gastrin hormone

80
Q

Types of secretory epithelial cells that cover stomach surface + extend down into gastric pits + glands?

A

mucous, parietal, chief, G cells

81
Q

SUMMARY

A
  • Anti-reflux barriers stop reflux of gastric contents into the oesophagus
  • Anti-reflux barriers: LOS, diaphragmatic sphincter, gastro-oesophageal junction
  • Both sphincters maintain tonic closure of sphincter + relax upon swallowing, but can also relax w/o swallow, because transient spontaneous relaxation reflex (TSR) of LOS
  • LOS: smooth muscles; myogenic (tonic contraction), neurogenic properties; vagal innervation (NO, VIP)
  • Diaphragmatic sphincter: striated muscles that exhibit tone + contract due to excitatory nerves
  • Swallowing + TSR of LOS relax diaphragm
  • Loss of inhibitory mechanisms of sphincters –> achalasia
  • Dysfunctional anti-reflux barriers →GORD or dysphagia
  • Increased frequency of TSR of LOS → GORD
82
Q

Types of oesophageal disorders?

A
  • Achalasia : Disorders of motility or peristalsis of oesophagus (assess the motor function of UOS, LOS, oesophageal body)
  • GORD: Reflux of stomach acids into oesophagus; regurgitation (weak LOS)
  • Aphagia: Swallowing difficulty must determine the cause
  • Oesophageal spasm: Abnormal oesophageal contractions + food is ineffectively reaching stomach
  • Diffuse oesophageal spasm: Chest pain coming from oesophagus (~angina)
83
Q

What’s achalasia?

A
  • Failure to relax (disease of muscle of oesophagus; causes swallowing difficulties)
  • Oesophageal motor disorder characterised by increased LOS pressure, diminished to absent peristalsis in distal oesophagus composed of smooth muscle, lack of a coordinated LOS relaxation in response to swallowing
84
Q

Pathophysiology of achalasia?

A
  • 1/100,000 presents at any age
  • Impaired LOS relaxation;
  • Accompanied by impaired peristalsis;
  • Food + liquids fail to reach stomach –> dilation of lower oesophagus;
  • Long period of sporadic dysphagia
  • Regurgitation of food
85
Q

Aetiology of achalasia?

A
  • Disorders of motility or peristalsis of oesophagus (assess motor function of UOS, LOS, oesophageal body)
  • Damage to innervation of oesophagus
  • Degenerative lesions to vagus + loss of myenteric plexus ganglionic cells in oesophagus
  • Initiating factor unknown - autoimmune or triggered by infection
86
Q

Effect of loss of ganglionic cells in oesophagus mesenteric plexus?

A

-Vital inhibitory neurons induce LOS relaxation + coordinate proximal-to-distal peristaltic contraction of oesophagus
In Achalasia lack of coordination of contraction + relaxation of LOS

87
Q

Role ofmyenteric plexus?

A

major nerve supply to GIT + controls motility

88
Q

Development of achalasia?

A
  • genetic predisposition
  • eg HLA (human leukocyte antigen) class II susceptibility, gene mutations, certain SNPs (single nucleotide polymorphism) have a viral trigger (herpes simplex virus 1, varicella zoster, measles)
  • aggressive inflammatory response
  • interactions between T-cell–mediated inflammatory infiltrate, extracellular matrix turnover proteins, development of humoral response (myenteric antibodies)
  • apoptosis of ganglionic neurons
  • myenteric plexitis + fibrosis
  • impaired relaxation of LOS + no oesophageal peristalsis
89
Q

Symptoms of achalasia?

A
  • Dysphagia = difficult or painful swallowing (solids + liquids) since LOS fails to relax enough to allow food to be emptied into stomach; poor peristalsis
  • Vomiting/regurgitation
  • Weight loss = failure to thrive
  • Heartburn =
  • retrosternal burning sensation due to oesophageal dysmotility
  • retention of ingested (acidic) food
  • generation of lactic acid from decomposition of retained food
  • retention of acid reflux in oesophagus due to poor emptying + incomplete relaxation of LOS
90
Q

Diagnosis of achalasia?

A

1) Barium radiography (barium swallow): dilatation of oesophagus with beak deformity at lower end + evaluate entire swallowing channel (mouth, pharynx, oesophagus)
2) Oesophageal manometry: absent peristalsis

91
Q

Why do a oesophageal manometry?

A
  • Determine cause of non-cardiac chest pain
  • Evaluate cause of reflux (regurgitation) of stomach acid (GORD?)
  • Determine cause of dysphagia (does UOS/LOS contract + relax properly?)
  • Allows evaluation of strength of coordination of muscle contractions
  • Relaxation function of LOS enable food to enter stomach

Overall if oesophagus contracting + relaxing properly

92
Q

Define aphagia

A

inability or refusal to swallow

93
Q

Normal results of oesophageal manometry?

A
  • Normal LOS pressure = 15mmHg but when swallowing, less than 10 mm Hg – as it relaxes to let food pass into stomach
  • LOS pressure <26 mmHg + normal muscle contractions upon swallowing
  • Pressure of muscle contractions moving food down oesophagus is normal
  • Muscle contractions follow normal pattern down oesophagus
94
Q

GORD results of oesophageal manometry?

A

Low LOS pressure suggests GORD, but note that GORD can occur in individuals with normal LOS pressure

95
Q

High results of oesophageal manometry?

A

> 100 mm Hg is achalasia

> 200 mm Hg is nut cracker achalasia

96
Q

What type of disease is achalasia + diff types?

A
  • Heterogeneous disease
  • 3 distinct types based on manometric patterns
  • Type I (classic) = minimal contractility in oesophageal body
  • Type II = intermittent periods of panesophageal pressurisation
  • Type III (spastic) = premature or spastic distal oesophageal contractions
97
Q

Abnormal results of oesophageal manometry show/are characterised by?

A
  • Presence of muscle spasms in oesophageal body so increased tone
  • Achalasia = high LOS pressure which fails to relax after swallowing
  • Weak contractions along length of oesophagus
98
Q

Effect of loss of inhibitory neurons secreting VIP + NO?

A

unopposed excitatory activity + failure of LOS relaxation.

99
Q

Procedure of oesophageal manometry?

A
  • spray local anaesthetic/apply a numbing gel (no sedation)
  • lubricated pressure-sensitive tube (catheter) inserted into nostril→ throat → oesophagus→ stomach
  • take deep breath + swallow water
  • measure strength + coordination of muscle contractions
  • evaluates strength + relaxation function of LOS
  • slowly remove catheter
  • data helps determine where in oesophagus to place pH probe
100
Q

Characteristic manometric findings?

A

-LOS fails to relax upon wet swallow (<75% relaxation)
-Pressure of LOS :
<26mm Hg is normal
>100 is achalasia
> 200 is nut cracker achalasia.
-Aperistalsis in oesophageal body
-Relative increase in intra-oesophageal pressure as compared with intra-gastric pressure

101
Q

Role of calcium channel blockers used in achalasia + eg?

A

relax the oesophageal sphincter

nifedipine, verapamil

102
Q

Why surgical myotomy?

A

provides best long term control of symptoms

103
Q

Why laparoscopic myotomy used in achalasia?

A

initial treatment for most individuals with achalasia

104
Q

Why is old age a favourable predictor for pneumatic dilation?

A
  • LOS has 2 components:
  • clasp fibres encircling gastroesophageal junction medially
  • gastric sling fibres on left lateral side
  • in PD, only clasp fibres targeted so gastric sling fibres remain unaffected so contribute to residual LOS tone
  • tone higher in younger patients
  • Patients with long-standing symptoms have mild improvement in oesophageal emptying as dramatic relief from dysphagia
  • Perceive less pain compared to younger when balloon distended in oesophagus
  • Expected to have weaker LOS muscles that might be easily torn during PD
105
Q

Why Is pneumatic dilation less effective in younger men?

A
  • LOS muscles stronger among men

- Higher LOS tone in younger men

106
Q

Why endoscopic balloon dilation of LOS or surgery for achalasia?

A

weaken sphincter

107
Q

Why heller’s myotomy used for achalasia?

A

laparoscopic (minimally invasive) surgical procedure used to treat achalasia

108
Q

Why botulinum toxin used in achalasia?

A
  • neurotoxic protein from Clostridium botulinum
  • blocks cholinergic nerve endings (stops ACh release) in ANS
  • Well tolerated, safe, efficacious
  • But PD superior to botulinum toxin
109
Q

What’s reflux?

A

Retro-grade movement of gastric content into oesophagus due to relaxation of LOS - brief, relatively infrequent occuring after meals in normal individuals (transient spontaneous LOS relaxation)

110
Q

Why does salivia come from reflux?

A
  • stimulates salivia
  • saliva is an effective natural antacid
  • dilutes + neutralises refluxed gastric contents
111
Q

Effet of low rate of salivation?

A
  • lack of ability to swallow own saliva
  • prolongation of contact of refluxed material with oesophagus
  • oesophageal irritation + oesophageal damage
  • gastro-oesophageal reflux disease (GORD)
112
Q

What’s gastro-oesophageal reflux disease (GORD)?

A
  • Retro-grade movement of gastric content into oesophagus due to relaxation of the LOS –> burning sensation in chest after meals – angina-like pain
  • When reflux more frequent + troublesome
113
Q

Causes of reflux in those with GORD?

A

-Transient spontaneous LOS relaxation (TSR)
98% of reflux events associated with TSR LOS
60% in patients (40% from malfunction of extrinsic + intrinsic of LOS)
-Resting LOS pressure too weak to resist pressure within stomach
-Sudden relaxation of LOS that’s not induced by swallowing

114
Q

What’s intrinsic component

A

Thick circular muscle layers of oesophagus :

  • clasp-like semicircular smooth muscles (↑myogenic activity, less ACh responsive)
  • sling-like oblique fibres (little resting tone, ACh-responsive)
115
Q

Features of pneumatic dilation?

A
  • Effective alternative to surgery
  • Response to PD depends on age, gender, size of the balloon
  • Long-term response predicted with help of post-PD manometry + timed barium oesophagogram
  • Balloon size chosen according to gender
  • Performed with diff dilators of variable balloon compliances eg low compliance polyethylene pneumatic dilator (Rigiflex dilator)
116
Q

Features of transient spontaneous relaxation reflex (TSR) of LOS?

A
  • pathway for TSR of LOS is vagal reflex pathway
  • triggered by gastric distention or pharyngeal stimulus + integration that occurs in brainstem
  • threshold for triggering TSR lowered by concurrent stimulation of pharynx (+ larynx)
  • threshold increased by supine posture
117
Q

Factors that contribute to severity of GORD?

A
  • Weak or uncoordinated oesophageal contractions
  • Time oesophagus exposed to gastric acid
  • ↑Gastric acid secretion + bile in gastric contents
  • Pressure placed on anti-reflux barrier
  • Impaired gastric emptying alone –> severe GORD
118
Q

When does reflux occur?

A

after eating, lying down (supine), delayed gastric emptying

119
Q

Overall, GORD is caused by?

A

Reflux of gastric contents through the LOS (acid or bile)
Chronic oesophagitis (erosive or non-erosive)
Prevalence: 30%

120
Q

Factors associated with GORD?

A

Pregnancy
Obesity
Fat, chocolate, coffee, alcohol ingestion
Large meals, tomatoes, orange juice, onions,
Cigarette
Drugs (eg anticholinergic agents, calcium channel blockers, nitrate drugs)

121
Q

Describe complications of GORD?

A
  • Oesophagus has squamous mucosa
  • acid reflux
  • desquamation of oesophageal cells (injury of squamous mucosa)
  • ↑cell loss
  • basal cell hyperplasia
  • excessive desquamation → ulceration
  • ulcers haemorrhage, perforate, heal by fibrosis with strictures
  • Barrett’s oesophagus + oesophageal cancer
122
Q

Pathophysiology of GORD?

A
  • Resting LOS tone is low or absent
  • LOS tone fails to increase when lying flat or during pregnancy
  • Poor oesophageal peristalsis so ↓ clearance of acid
  • Hiatus hernia impairs LOS + diaphragm closing mechanisms
  • Delayed gastric emptying
123
Q

Symptoms of GORD?

A

Heartburn and acid regurgitation
Wake up at night – reflux irritates the larynx
Dysphagia

124
Q

Investigating GORD?

A
  • Low dose proton pump inhibitor (PPI) challenge is 1st line
  • Upper GI endoscopy
  • Manometry
  • 24hr ambulatory pH monitoring
125
Q

Findings from continuous pH monitoring?

A

Normal reflux on a daily basis so GORD implies presence of excess reflux + heartburn doesn’t improve when lying down

126
Q

Pregnancy + GORD?

A
  • Foetus increases pressure on abdominal contents + pushes terminal segments of oesophagus into thoracic cavity
  • Last trimester of pregnancy associated with increased abdominal pressure + forces gastric contents into oesophagus
  • Heartburn subsides in last months of pregnancy as uterus descends into pelvis
127
Q

Describe heartburn after a large meal

A
  • eating large meals
  • less efficient LOS
  • gastric contents episodically refluxed into oesophagus
  • heartburn
  • ulcer, scarring, obstruction, perforation of lower oesophagus
128
Q

Potential long term effects of GORD?

A
  • Oesophagitis, oesophageal strictures
  • Squamous cell carcinoma
  • Barrett’s syndrome-predispose someone to oesophageal adenocarcinoma
  • Oesophageal ulcer
129
Q

When’s manometry ordered?

A

Symptoms of:

  • heartburn or nausea after eating (GORD)
  • problems swallowing (feeling that food is stuck behind breast bone - achalasia)
130
Q

Management + drug treatment of GORD?

A
  • Life-style changes - raise head of bed at night, weight loss, modify food
  • ↓Foods + drink which cause symptoms
  • Laparoscopic anti-reflux surgery (Nissen fundoplication – wrap fundus around LOS strengthening it + creates valve mechanism)
  • Take antacids
  • Take H2 receptor antagonists + proton pump inhibitors
  • Take metoclopramide/domperidone enhancing peristalsis + help gastric acid clearance
  • Fundoplication causes dysphagia as it reduces distensibility of LOS
131
Q

Lifestyle changes that alleviate symptoms of GORD?

A
  • Avoid large meals : increase likelihood of increased gastric (stomach) pressure + reflux
  • Lose weight
  • Avoid foods that increase gastric acidity
  • Avoid foods that slow gastric emptying
  • Avoid lying down after meals - elevate head of bed
  • Avoid some drugs + smoking
  • Decease fat intake : decrease LES pressure + delay stomach emptying –> increasing risk of reflux
  • Avoid chocolate : contains methylxanthine, which reduces LES pressure by causing relaxation of smooth muscle
  • Avoid coffee : promote gastroesophageal reflux
132
Q

Role of antacids in GORD?

A
  • Neutralise gastric acid; ↑ pH of gastric lumen

- Inhibit peptic activity + stop acid secretion

133
Q

Features of anatcids?

A
  • Magnesium salts→ diarrhoea
  • Aluminium salts→ constipation
  • Use mixture of 2 to ensure bowel function
  • Combine alginates eg gaviscon with antacids for oesophageal reflux
  • Alginic acid + saliva form a raft which floats on content of gastric lumen + protects oesophageal mucosa from reflux
  • ↓acid secretion + heal ulcer, but removal of H. pylori is vital to stop ulcer returning.