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Digestive System Module > Lecture 7 > Flashcards

Lecture 7 Flashcards

1
Q

What part of the upper GI tract are involved in swallowing?

A
  1. Oral cavity (mouth)
  2. Pharynx (throat)
  3. UES Upper Esophageal Sphincter
  4. Esophagus
  5. LES Lower Esophageal Sphincter + gastroesophageal junction
  6. Stomach
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2
Q

What sort of action is swallowing?

A

Swallowing= highly complex reflex

mainly involuntary

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3
Q

What are 2x outcomes is Swallowing fails to be precise?

A
  1. Choking
  2. Aspiration: “things go down the wrong way”
    - risk of aspiration is pneumonia. can be severe in people who have recurrent or silent aspiration
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4
Q

Motor and sensory components of swallowing

A
  1. Oral phase- Voluntary. Striated muscle
  2. Pharyngeal Phase- Involuntary. Striated muscle
  3. Oesophageal Phase - Involuntary. Striated and smooth muscle
    - swallowing controlled by both Cortex + brainstem (if have stroke in either area can develop swallowing disorders)
    - swallowing centre in brainstem receives sensory input from receptors in Posterior mouth and Upper pharynx
    - innervates swallowing muscles via cranial nerves
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5
Q

Oral phase

A

Voluntary
Oral Cavity:
2x Superior Boundary: Hard palate + Soft palate
3x Anterior & Lateral Boundary: Labium/Lip + Cheek + Tongue Body
2x Inferior Boundary: Genlohyoid + Mylohohyoid muscles (support mouth floor)
4x Posterior Boundary: Ulva (from soft palate) + Palatine tonsil + Tongue Root + Lingual tonsil (under tongue)
Phases:
1. Preparatory Phase: Bolus formation
2. Transfer Phase: Bolus propelled into pharynx

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6
Q

Oral Preparatory Phase

A

Mastication (chewing)
-breaks down solids into size, shape and consistency suitable for transport
-Teet: grinding
Tongue + Cheeks: Co-rodinate movement needed. Positions solids over the grinding surfaces (evenly distributed over teeth)
Saliva for dissolving + lubrication

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7
Q

Oral Transfer Phase

A

Once bolus adequately prepared
Tip of tongue moves into contact with hard palate (so food doesnt fall out)
Closes off the anterior oral cavity
Bolus is pushed into the back of the mouth

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8
Q

Pharyngeal Phase

A
  1. Nasopharynx (in tough with nasal cavity)
  2. Oropharynx (behind mouth)
  3. Hypopharynx (leads into oesophagus. Close to Larynx–> Trachea)
    Slightly less than 1s (involuntary and fast)
    Bolus enters pharynx from back of mouth and exits the UES Upper Oesophageal Sphincter
    3x passages have to be closed:
  4. Mouth (food will go fowards)
  5. Upper Airway (food out nose)
  6. Lower Airway (protect trachea to avoid aspiration)
    Order:
    a) Tongue pushes against palate to seal the back of the mouth (Oropharynx)
    b) Soft palate elevates and proximal pharyngeal wall moves medially to seal off the upper airway i.e. nasopharynx
    c) Epiglottis swings down and vocal cords and arytenoids adduct to seal off the lower airway (i.e. laryngeal vestibule leading into trachea)
    -Bolus descends through pharynx by peristalsis at 30-40cm/s
    UES Upper Esophageal Sphincter opens (relax so bolus can enter)
    Bolus leaves pharynx
    Eritinoids have to come together when swallow
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9
Q

UOS Upper Oesophageal Sphincter

A

A sphincter is normally in a state of tonic contraction (closed at rest), relaxing intermittently as required by normal physiological functioning
Composed of group of muscles
acts as barrier between pharynx and oesophagus
1. Cricopharyngeus
2. Inferior Pharyngeal Constrictor
3. Cervical Oesophagus
Contracted/closed most of the time (normal pressure 30-200 mmHg)
UOS prevents:
1. air insufflating (distending) the stomach (air doesnt enter freely into oesophageal while talking)
2. reflux of contents into pharynx and larynx during oesophageal peristalsis
Relaxes/Opens when swallowing, belching or vomiting
-With swallowing, UOS opens (very brief ~0.5s) due to:
1. Cricopharyngeus relaxes (close to epiglottis)
2. Suprahyoid and thyrohoid muscles contract (under jaw)
3. Pressure of descending bolus distending the UOS

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10
Q

Oesophagus

A

Extends from UOS to LOS (upper to lower oesophageal sphincters)
~20-25cm long (depending how tall a person is)
Mucosa- stratified squamous epithelium
Upper1/3: striated muscle
Lower2/3: smooth muscle
Landmarks: some structures sit close to oesophagus. Top–> Bottom
1. Cricoid (of crico-pharyngeus muscle)
2. Aortic Arch (anterior to posterior over left main bronchus and sits behind oseophagus)
3. Left main Bronchus (sits anteriorly causing indendation)
4. Diaphragm (oesophagus often slightly narrowed here)

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11
Q

Oesophageal Phase

A

UOS relaxes, bolus enters oesophagus, oesophageal peristalsis initiated propelling food distally into stomach

  1. Primary Peristalsis
    - initiated by swallowing
    - continuation of pharygneal contraction wave (pharynx starts peristalsis)
    - slower that pharyngeal peristalsis 3-5cm/s
  2. Secondary Peristalsis:
    - Initiated by distension in oesophagus (e.g. food stuck or gastric acid coming up)
    - Stretch receptors are stimulated, initiates local reflex response triggering peristalsis
    - intent to clear oesophagus (of food + gastric acid)
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12
Q

Oesophageal Peristalsis

A
  1. Parasymphathetic and Sympathetic nerves (ANS Autonomic Nervous System)
  2. Enteric Nervous System
    - Plexus of nerves embedded in the wall of the GI tract:
    a) Submucosal plexus (Submucosa)
    b) Myenteric Plexus (between muscularis Externa’s circular + longitudinal muscles)
    - can operate autonomously/independantly -co-ordination of reflexes
    - also communicates with parasympathetic and sympathetic nervous systems
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13
Q

Serosa vs Adventitia. Related to Oesophagus

A

Serosa: Smooth membrane which secretes fluid for lubrication
Adventitia: CT layer that binds structures
-Oesophagus is mostly covered in adventitia
-In the abdomen, intra-peritoneal organs are surrounded by serosa. Retroperitoneal organs are surrounded by adventitia
Serosa surrounding abdominal organs= Visceral Peritoneum

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14
Q

Normal Motility Study

A

Swallow glass of water “wet swallow”. Peaks= oesophageal contraction. Propogation top-bottom
Normal primary peristalsis of 30-80mmHg
Circular muscle layer- contraction above and relaxation below bolus
Longitudinal muscle layer (oesophagus shortens during peristalsis)

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15
Q

Gastro-oesophageal junction

A

Squamo-columnar junction

  • junction between oesophagus and stomach
  • Z line - characterisitic appearance
  • Transition between stratified squamous (oesophagus) and columnar (gastric) epithelium
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16
Q

LOS Lower Oesophageal Sphincter

A

Close to squamo-columnar junction
specialised segment of smooth muscle
LOS is contracted i.e. closed most of the time (normal pressure 20-35mmHg)
Relaxation of LOS can be related or unrelated to swallowing
- LOS begins to relax 1-2s after swallowing, lasts 5-10 sec, followed by hyper-contraction
- LOS also (intermittently) relaxes transiently when not swallowing and can be physiological (different to UOS)
–Occurs at regular intervals and only in upright position (not sleeping, daytime, quite regularily)
– mediated by vagus nerve
– releases air from stomach (belching)

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17
Q

Gastroscopy

A

flexible telescope
inserted from mouth into oesophagus and into stomach
-better for structural conditions (can examine mucosa of oesophagus closely)
-can take biopsy
-cannot access function and motility/movement of oesophagus

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18
Q

Barium Swallow

A

X-ray test
allows for examination of oesophagus in motion as a person swallows
-cant take biopsy as is x-ray
-can access function and motility/movement of oesophagus

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19
Q

24-hr pH study

A

particularly useful with people who may have reflux, with unusual systems or cant 100% diagnose gastric reflux
Thin catheter inserted into oesophagus for 24Hrs
Catheter sits just above Gastro-oesophageal junction
-carry on with normal activities
-Reflux activity measured by drop in pH
(monitors pH of distal oesophagus over 24hr period)
-can se if there is excessive amounts of acid-reflux

20
Q

Manometry

A

Very similar to pH study, except not required for 24hours
Patient performs swallows with water
-sits between Upper and lower O Sphincters
-contraction measured as wave. With this can determine whether propogation is normal and if contraction is normal
Thin catheter with pressures sensors sits in oesophagus

21
Q

Structural Oesophageal Diseases

A

Diseases that cause visible changes in structure

  • Inflammation
  • Ischaemia/necrosis
  • Ulceration
  • Bleeding
  • Narrowing
  • Masses
  • Diverticulum
22
Q

Motility Oesophageal Diseases

A

Dysmotility
-abnormal contraction of oesophageal muscles
(no problem with structure)

23
Q

Functional Oesophageal Diseases

A

Disorder of motility, sensation and brain-gut dysfunction
(no known structural abnormality that can be seen, and no know motility issues)
-Hypersensitive
-Irritable Bowel Syndrome

24
Q

Gastro-Oesophageal Reflux Disease GORD

A

Most common condition of oesophagus
Movement of gastric contents into the oesophagus
Gastric contents contain acid- erosive to oesophagus
(Oesophagus not sturctured deal with acid (not columnar epithelium w their goblet cells))
Reflux occurs during transient relaxation of LOS
-often get reflux after eating. More eaten= More stomach will distend. more pressure placed on sphincter
-above diaphagm. Diaphagm is support for sphincter helping it to stay shut.
Transient LOS relaxation is physiological
-Lets air out of stomach
–only becomes pathological when too much gastric juice also refluxes into oesophagus causing symptoms/disease
-disease is debilitating symptoms that affect the quality of life

25
Q

Contributing Mechanisms to GORD

A
  1. Hypotensive LOS
    - not contracting tight enough (too lax/excessive relaxation)
    - can be born with
    - Caffeine, alcohol, chocolate, fats (can get reflux after alcohol)
    - certain medications e.g. beta-blockers, nitrates, calcium channel blockers
  2. Hiatus Hernia
    - Note: not all people with hiatus hernia have reflux
    - common contributor
    - relevant, but not main part of the pathophysiology
  3. Impaired Oesophageal Peristalsis
    - reduced clearance (of acid via secondary peristalsis of oesophagus)
26
Q

Hiatus Hernia

A

The hiatus is an opening in the diaphragm, where oesophagus passes through to joint the stomach
The diaphragm acts as additional support, like a sphincter, constricting around the GO junction
A hernia is when part of an organ protrudes through an opening in the muscle/tissue that is meant to hold it in place
Hatius hernia: top stomach passes through hiatus, into the chest (herniates through weak part of diaphragm and sits above).
1. now have section acting as chamber for food to sit in. Gastric Acid Can now reflux freely into distal oesophagus.
2. LOS Lower Oesophageal SPhincter/The GO junction has lost support from diaphragm. Weakens sphincter, precipitating to reflux

27
Q

GORD Symptoms

A

Symptoms occur due to:
Gastric acid coming in contact with oesophagus
-Oesophageal mucosa sensitive to acidic pH
-Normal pH in oesophagus 6-7
-pH of gastric contents 1-2 (unless buffered by food)
-Nerve fibres in oesophagus are sensitive to acidic pH, give sensation of “burning”
Eventual complications of chronic acid exposure
-Heartburn/chest discomfort: burning sensation or discomfort over the (bottom) chest
-Regurgitation: Food or liquid coming back up into mouth
-Sour or bitter taste in mouth
-May be worse soon after eating or lying down (e.g. bed time)

28
Q

Complications of GORD

A

GORD can be viewed as a disease due to abnormal motility of oesophagus (and stomach)
But it can also cause structural complications:
1. Reflux Oesophagitis
-damage to oesophagus mucosa by reflux leading to inflammation, ulceration and bleeding
2. Peptic Stricture
-Prolonged inflammation of oesophageal mucosa by reflux can lead to fibrosis and scarring (tightening)
-Barrett’s Oesophagus
-Cancer

29
Q

Reflux Oesophagitis

A

damage to oesophagus mucosa by reflux leading to inflammation, ulceration and bleeding
Pain/discomfort in chest
1. Bleeding- haematemesis (vommiting blood)
2. Dysphagia- difficulty swallowing
-Linear ares of ulceration- red and inflamed- due to chronic exposure
-over time, if inflammation untreated, can cause Narrowing=Peptic Stricture (significant tightening of lower Oesophagus)

30
Q

Barret’s Oesophagus

A

Damage to oesophageal epithelium by chronic acid exposure from GORD can lead to Barrett’s oesophagus
Intestinal Metaplasia= Oesophageal epithelium (squamous epithelium) transforms –> to become like Gastric epithelium (columnar epithelium w. goblet cells) - trying to adapt for protection -but increased risk of dyspalsia and cancer
Males, over 50, increased BMI, smoker with chronic GORD
Increased risk of Oesophageal Adenocarcinoma
-no regular circular line around transformation zone
- squamous=lighter
columnar=darker

31
Q

Evolution from Barrett’s Oesophagus to Cancer

A

Squamous oesophagus –>(injury:acid and bile reflux nitrous oxide)
Chronic Inflammation –> (genetics:, gender, race , 7x other factors (cox-2))
—Accumulate genetic changes continue to increase over remaining development—
Barrets Metaplasia –>
Low-grade Dysplasia (if not treated, increases risk of abnormal cells forming) –>
High-grade Dysplasia (low grade abdormal cells become high grade abnormal cells) –>
Invasive Adenocarcenoma
-main driver of this transformation is ongoing acid reflux

32
Q

Oesophageal Cancer

A

2x types: Adenocarcinoma (adenoCa) (GORD, Barrett’s), squamous cell carinoma (SqCC)
GORD- risk of Barrett’s - risk of oesophageal adenoCa
Smoking, alcohol, diet - risk of SqCC “lifetsyle cancer”
In Western countries, oesophageal adenoCa more common. seeing less as reflux is better treated
Presents similarily except:
-adenCa more likely to be in distal oesophagus/GO junction
-SqCC more likely higher up in oesophagus

33
Q

Ring/Web

A

The terms oeosphageal web and ring are often used interchangeably
Thin mucosal membrane
-can sometimes obstruct passage of food (therefore some people complain of dysphagia (difficulting swallowing))
Schatzki ring- found distally, typically associated with hiatus hernia, aetiology/cause uncertain

34
Q

Senker’s diverticulum

A

Pharyngeal pouch (at back)
Excessive pressure causes the weakest portion of the pharynx to balloon out
Conditions such as poor swallowing(dysphacia), impair relaxation of cricopharyngeus(prior to swallowing) -presure in pharynx becomes excessive, and weakest part of pharynx (At back where diverticulum occurs) will balloon out and form a pocket
More common in elderly

35
Q

Stricture

A

Peptic: i.e. Reflux relates
Caustic i.e. Caustic injury (swallow acid/bleach)
Post-radiotherapy
Post-surgical i.e. anastomotic (joining together where surgery has occured)
Malignant (cancer)
Present/Results in: Dysphagia

36
Q

Reflux Oesophagitis

A

GORD can result in severe oesophagitis or stricture

37
Q

Oesophageal Candidiasis

A

White plaque coating oesophagus

  • candida/thrush
  • usually occurs in people who are immuno supressed
38
Q

Ulceration

A 
Herpes simplex virus
Cytomegalovirus
Pill-induced:
-Doxycycline- sit up + large galss of water. otherwise can get stuck in oesophagus and result in erosion and ulcer formation
-Bisphosphonates
39
Q

Eosinophilic OEsophagitis

A

Eosinphils infiltrate the epithelium of oesophagus
Allergy-mediated
Patient may have history of atopy: asthma, hayfever, eczema
-circular lines up and down oeosphagus + fissures running up and down

40
Q

Motility disorders of the Oesophagus

A

Structure, mucosa of oesophagus is normal- appears to be visibly normal
Present with difficulty swallowing-dysphagia
More likely to be intermittent/variable symptoms
May affect liquids as much as solids - in contrast to structural narrowing (e.g. cancer or stricture), which tend to affect solids only
Problem with
1. innervation to smooth muscle (loss of function or co-ordination)
2. or direct muscle damage
Achalasia most common moltility disorder

41
Q

Achalasia

A

Most common Motility disorder of oesophagus
Degeneration of nerves in oesophagus (Neurodegenerative condition)
-Myenteric plexus
-LOS inhibitory nerves
-cause uncertain
1. Loss of peristalsis in distal oesophagus
2. failure of LOS to relax with swallow(contracted all of the time/wont relax when swallow)
Symptoms:
-oeosphagus dilate: pressure increase + retains food (as sphincter too tight and wont relax)
- characteristic Barrium swallow/ xray appearance of “birds beak”

42
Q

Diffuse Oesophageal Spasm

A

“Corkscrew Oesophagus”
Non-peristaltic or simultaneous onset of contraction in oesophagus
-Peristalsis is occuring but not in right order/ randomly occuring at different segements (spasming)
In addition to dysphagia, can cause chest pain (intermittent spasms)

43
Q

Nutcracker Oesophagus

A

Normal peristalsis, but contractions very high amplitude

-i.e. wave of contractions propagate down oesophagus normally, but just too strong

44
Q

Scleroderma

A

systemic condition (Manifestation of a more general disease)
CT connective Tissue Disease (effects organs including oesophagus)
Hardening (fibrosis) of skin and CT connective tissue
(Rubbery hose-pipehollow tube)
When oesophagus is affect, damage occurs to submucosa, muscle layers, nerves -oesophagus turns into rubbery hose-pipe
Peristalsis is absent, contractions weak, LOS is no tone
1. Dysphagia- as food cannot be propelled
2. Severe reflux - acid comes up and not shifted down into stomach

45
Q

Manometry

A

Can be useful to differentiate between conditions

  • Normal: good amplitude of propagations from left to right in co-ordinated fashion. LOS pressurenormally dips down
  • Achalasia : Weak peristalsis at bottom=small peaks. LOS consistently high pressure
  • Diffuse Oesophageal Spasm-degree of peristalsis. 2x contractions instead of one

Digestive System Module (38 decks)

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