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Block D - Digestion and Metabolism > Physiology -- Deglutition and Dysphagia > Flashcards

Physiology -- Deglutition and Dysphagia Flashcards

1
Q

3 functional activities of the GIT

A
  1. Propulsion
  2. Secretion & digestion
  3. Absorption
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2
Q

What do the pressure gradients of the GIT result from?

A

Coordinated contraction of muscular elements in the GI wall

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3
Q

Magnitude of the pressure gradient in the GIT

A

5 - 30 mm Hg

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4
Q

Stimulus to generate contractions in the GIT

A

Physiological distension

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5
Q

What does physiological distension cause?

A
  • Stimulation of stress muscle fibres
  • Neurotransmitter release (ENS)
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6
Q

What is the ENS modulated by?

A

ANS and hormones

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7
Q

2 types of contraction

A

Segmentation and Peristalsis

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8
Q

Define segmentation

A

Standing rings of contraction

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9
Q

Define peristalsis

A

Propagated contraction

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10
Q

5 sphincters in the GIT from top to bottom

A
  1. Upper esophageal
  2. Lower esophageal
  3. Pyloric
  4. Ileocecal
  5. Internal and external anal
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11
Q

3 requirements for flow

A
  • Generate pressure
  • Prevent dissipation of pressure
  • Decrease resistance
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12
Q

3 phases of swallowing

A
  1. Oral
  2. Pharyngeal
  3. Esophageal
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13
Q

Alteration in the phases of swallowing can result in what?

A

Dysphagia

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14
Q

Define dysphagia

A

Difficulty or delay in passage of solid or liquid food bolus that is sensed by the patient within seconds of initiaiton of a swallow attempt

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15
Q

Prevalence of dysphagia in people over 65

A

15%

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16
Q

2 types of dysphagia

A
  • Oropharyngeal
  • Esophageal
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17
Q

Define esophageal dysphagia

A

Food stuck in the center of the chest

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18
Q

Define oropharyngeal dysphagia

A

Coughing or choking

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19
Q

2 mechanisms that can result in dysphagia

A
  • Mechanical obstruction and/or structural abnormality
  • Neuromotor
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20
Q

Type of control exhibited in the oral phase

A

Voluntary control

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21
Q

2 neural components of the oral phase

A
  1. Ability to initiate (voluntary –> cortex)
  2. Coordinated movements (reflex; involuntary –> medulla)
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22
Q

4 abnormalities in the oral phase

A
  1. Neuromuscular defect
  2. Congenital abnormalities
  3. Bucco-pharyngeal obstruction
  4. Trauma and inflammation
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23
Q

How do neuromuscular defects cause abnormalities in the oral phase

A

Prevent generation of pressure

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24
Q

How do congenital abnormalities cause abnormalities in the oral phase?

A

Promote dissipation of pressure

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25
Q

How can bucco-pharygneal obstruction cause abnormalities in the oral phase?

A

Increase resistance to flow

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26
Q

DIfferential diagnosis of dysphagia in the event of trauma and inflammation causing abnormalitites in the oral phase

A

Odynophagia

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27
Q

3 prerequisites for propulsion

A
  • Generation of pressure
  • Prevention of the dissipation of pressure
  • Decrease resistance
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28
Q

Pharyngeal receptors bring afferent neurons to which part of the brain?

A

Deglutition center

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29
Q

Deglutition reflexes sent out from the deglutition center resulting from the information received from the pharyngeal receptors

A
  • Protective reactions
  • Deglutition apnea
  • Relax UES
  • Contract pharyngeal constrictors
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30
Q

Trigger areas for deglutition reflexes

A
  • Soft palate
  • Uvula
  • Palatine tonsil
  • Root of tongue
  • Epiglottis
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31
Q

What does the deglutition center have a direct inhibitor influence on? What does this lead to?

A

Respiratory center –> deglutition apnea

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32
Q

6 steps in the pharyngeal phase

A
  1. Raise soft palate
  2. Raise base of tongue
  3. Vocal cords come together
  4. Forward and upward movement of larynx
  5. Propagated contraction of pharyngeal constrictors
  6. Relaxation of UES
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33
Q

Where do the impulses for the closure of the cricopharyngeus originate?

A

Centraly

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34
Q

What mediates the closure of the cricopharyngeus

A

Vagus releasing ACh at neuromuscular junction –> muscle contraction

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35
Q

How does the cricopharyngeus relax?

A

Cessation of impulses from vagus releasing ACh

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36
Q

4 characteristics of the pharyngeal phase

A
  • Involuntary
  • Rapid
  • “Stereotyped”
  • Temporospatial coordination
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37
Q

3 defects in the pharyngeal phase

A
  • Failure of propulsion
  • Obstruction to flow
  • Psychological factors
38
Q

2 effects caused by failure of propulsion in pharyngeal phase

A
  • Generates less pressure
  • Increases dissipation of pressure
39
Q

4 parts that can be involved in the failure of propulsion in the pharyngeal phase

A
  • Brain
  • Cranial nerves
  • Myoneural junction
  • Muscle
40
Q

Effect of obstruction to flow causing pharyngeal phase defects

A

Increased resistance

41
Q

2 causes of obstruction to flow in pharyngeal phase

A
  • Mass effect
  • Incomplete sphincter relaxation
42
Q

Psychological factor that can cause defective pharyngeal phase

A

Globus hystericus

43
Q

3 esophageal forces

A
  1. Pharyngeal momentum
  2. Gravity
  3. Peristalsis
44
Q

What force is generated each time that we swallow

A

A single primary peristaltic wave (part of the deglutition reflexes)

45
Q

Time of propagation of one wave of primary peristalsis along the length of the esophagus

A

8 - 10 seconds

46
Q

Describe the vagal innervation from the deglutition center to generate primary peristalsis (diagram)

A
47
Q

Consequence of cutting the vagal fibres high up in the neck on primary peristalsis

A
48
Q

Consequence of cutting vagal fibres transthoracically on primary peristalsis

A

Primary peristalsis continues because the distal esophagus has the enteric circuitry necessary for the propagation of the peristaltic wave (orange fibres in diagram)

49
Q

Define “vago-vagal reflex”

A

Reflex produced due to the vagal afferent nerves sending information to the brain centers, which send out efferent vagal nerves

50
Q

What is essential for initiating peristalsis in the proximal esophagus

A

Vagus

51
Q

What is required for the continuation and propagation of peristalsis in the distal esophagus

A

Intactness of ENS

52
Q

Stimulus for secondary peristalsis

A

Local distension (i.e. food lodged in esophagus)

53
Q

Similarities between primary and secondary peristalsis

A
  • Upper esophagus requires vagus
  • Lower esophagus requires ENS
  • Pressure generated is 30 - 60 mmHg
54
Q

Differences between primary and secondary peristalsis

A
  • Different stimuli
    • Primary = pharyngeal receptors
    • Secondary = local distension
  • Different frequency
    • Primary = only 1 contraction per swallow
    • Secondary = many contractions until bolus is displaced
55
Q

Define deglutitive inhibition

A

Central inhibition of primary peristaltic wave resulting from rapid, repeated stimulation of pharyngeal receptors (i.e. sipping fluid through a straw)

56
Q

How are liquids brought through the esophagus?

A

Deglutitive inhibition –> cessation of stimulation of pharyngeal receptors –> single peristaltic wave sweeps over esophagus –> empty contents

57
Q

3 facotrs influencing esophageal transport

A
  • Viscosity of bolus
  • Temperature of bolus
  • Posture of subject
58
Q

What type of control is exhibited in the closure of the LES

A

Myogenic

59
Q

What type of control is exhibited in the relaxation of the LES?

A

Neurogenic –> local release of NANC

60
Q

Compare the characteristics of the upper esophageal sphincter vs. the lower esophageal sphincter

A
61
Q

When closed, what is the magnitude of the resistance to flow provided by the lower esophageal sphincter?

A

10 - 30 mm Hg

62
Q

6 characteristics of the LES musculature (in vitro)

A
  1. More collagen fibres
  2. Lower RMP; partially contracted at RMP
  3. More resistant to stretch
  4. Sensitive to hypoxia
  5. Ca++ dependent
  6. More sensitive to transmitters and hormones
63
Q

Does gastrin provide modulation of the LES?

A

ONLY in large (pharmacologic) doses!!

64
Q

3 gut hormones that have an effect on LES

A
  • Gastrin (increase tone)
  • Secretin (decrease tone)
  • CCK (decrease tone)
65
Q

Special hormone that decreases LES tone and the specific period when it has an effect

A

Progesterone decreases sphincter tone during the last trimester of pregnancy (reason for reflux during this period)

66
Q

6 external influences on the LES and their effects

A
  • Cigarette smoking
  • Alcohol (high doses)
  • Morphine, valium
  • Fat
  • Chocolate
  • Carminatives

All decrease LES tone

67
Q

Factors that affect the LES (Venn diagram)

A
68
Q

Define pyrosis

A

Heartburn: retrosternal burning sensation, radiating upwards from the xiphoid towards the neck

69
Q

Rate of occurrence of reflux in healthy individuals + duration

A

1 - 4 instances per hour (usually <30 sec)

70
Q

Define transient LES relaxation (TLESr)

A

Reflux occurring in healthy individuals

71
Q

3 disordered functions associated with GERD

A
  • Ineffective esophageal clearance of refluxate
  • Less effective secondary peristalsis
  • Defective epithelial resistance to damage by refluxate
72
Q

Why does an increase in intraabdominal pressure cause a greater than expected increasei in LES pressure?

A

Reflex tightening of the LES (vago-vagal reflex)

73
Q

3 ways to examine the esophagus

A
  • Radiology
  • Endoscope
  • Intraluminal pressure recording (manometry)
74
Q

Esophageal resting pressure

A

-5 mm Hg

75
Q

UES resting pressure

A

+80 mm Hg

76
Q

LES resting pressure

A

+20 mm Hg

77
Q

Pharyngeal resting pressure

A

0 mm Hg

78
Q

Stomach resting pressure

A

+5 mm Hg

79
Q

Describe the normal manometric recordings in response to swallowing

A
  • 8 - 10 sec for wave to reach distal esophagus
  • Pressure complex = 30 - 80 mm Hg
  • LES relaxes early
80
Q

Describe the manometric findings of a patient with achalasia

A
  • LES does not relax with wet swallows
  • Wet swallows do not produce peristaltic pressure waves in the esophagus
  • Instead, there are low-amplitude, simultaneous P waves with a nearly identical configuration (not sequential)
81
Q

Define achalasia

A

Failure to relax:

  • Aperistalsis
  • Incomplete relaxation of LES with swallowing
  • Increased resting tone of LES
82
Q

Potential cause for achalasia

A

Dysfunction of inhibitory neurons in distal esophagus:

  • NO
  • VIP
83
Q

3 categories of oropharyngeal dysphagia

A
  • Structural
  • Myogenic
  • Nervous system
84
Q

3 types of structural oropharyngeal dysphagia

A
  • Poor dentition, xerostomia
  • Intraluminal
  • Extraluminal
85
Q

3 intraluminal causes of oropharyngeal dysphagia

A
  • Diverticulae
  • Webs
  • Oropharyngeal tumors
86
Q

3 extraluminal causes for structural oropharyngeal dysphagia

A
  • Osteophytes
  • Thyromegaly
  • Lymphadenopathy
87
Q

5 causes for nervous system-related oropharyngeal dysphagia

A
  • Head injury
  • Brainstem tumors
  • Stroke
  • MS
  • Parkinson’s
88
Q

2 types of esophageal dysphagia

A
  • Structural
  • Motility abnormalities
89
Q

4 intraluminal causes for esophageal dysphagia

A
  • Stricture
  • Schatzki’s ring
  • Cancer
  • Eosinophilic esophagitis
90
Q

Extraluminal cause for esophageal dysphagia

A

Mediastinal tumors (lymphoma, lung cancer)

91
Q

5 motility abnormalities that may cause esophageal dysphagia

A
  • Achalasia
  • Esophageal spasm
  • Secondary achalasia from tumor infiltration
  • Diabetes
  • Collagen vascular disorders

Block D - Digestion and Metabolism (29 decks)

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