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Bloc E - GI & Metabolism > Feb15 M1-Physiology - Esophagus > Flashcards

Feb15 M1-Physiology - Esophagus Flashcards

1
Q

3 phases of deglutition

A

oral, pharyngeal, esophageal

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2
Q

2 types of dysphagia

A
  • dysphagia can be coughing, chocking if oropharyngeal

- or regurg and food stuck if esophageal

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3
Q

2 causes of dysphagia

A

mechanical obstruction (or structural abnormality) or neuromotor defect

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4
Q

muscles in esophagus

A

proximal = SKM, then SKM and SM transition then SM (LES is SM)

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5
Q

oral phase charact and 4 steps

A

only voluntary one

  1. moistening
  2. mastication
  3. through formation (tongue moves food and holds liquid)
  4. tongue mvmt posteriorly to move bolus to the back and trigger swallowing
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6
Q

site of the voluntary center for swallowing

A

precentral gyrus (initiates swallow)

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7
Q

precentral gyrus linked closely to what

A

deglutition centre in the medulla, responsible for involuntary coordination

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8
Q

4 causes of anomalies in the oral phase of swallowing

A
  1. neurom defect
  2. congenital (cleft palate)
  3. obstruction (ex. neoplasm)
  4. trauma or inflammation
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9
Q

3 prerequisites to the oral phase of swallowing

A
  1. make pressure
  2. prevent dissipation of that pressure
  3. decrease resistance (for bolus passage)
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10
Q

when swallowing becomes automatic

A

when bolus touches tonsils

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11
Q

4 steps of pharyngeal phase to protect airways (nasal reflux)

A
  1. raise soft palate.
  2. raise base of the tongue
  3. vocal cords come together (are below glottis)
  4. tilting forward of epiglottis
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12
Q

3 steps of pharyngeal phase to move from pharynx to esophagus

A
  1. forward AND upward movement of the larynx + relaxation of esophagus
  2. propagated contraction of pharyngeal constrictors
  3. relaxation of UES
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13
Q

what is needed for OPENING of UES

A
  1. forward AND upward movement of the larynx + relaxation of esophagus
  2. relaxation of UES (relaxation doesn’t mean opening)
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14
Q

pharyngeal phase 7 steps: sensory afferents to the medulla (medullary swallowing center) travel in what cranialnerves

A

5, 9, 10 (10 is vagus)

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15
Q

pharyngeal phase 7 steps: motor efferents from the medulla (medullary swallowing center) travel in what cranial nerves

A

5, 7, 9, 10 (vagus), 12

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16
Q

other mechanism to protect airways by medullary deglutition center (or central pattern generator)

A

deglutition apnea (last a us): the deglutition centre inhibits the respiratory centre in the medulla

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17
Q

3 types of things causing oropharyngeal dysphagia

A
  1. obstruction or increased resistance (intra + extra luminal obstructions + xerostomia)
  2. myogenic
  3. nervous system
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18
Q

other name for UES

A

cricopharyngeus muscle

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19
Q

innervation of UES and consequence

A

vagus (PSS) impulse via a PRIMARY ORDER neuron. UES has nicotinic Ach receptor: MAKES THE MUSCLE CONTRACT

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20
Q

how to make pharyngeal constrictors (muscles) (UES) relax

A

stop vagus Ach (N) input to the UES

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21
Q

what are the ICCs (interstitial cells of Cajal)

A

cells of the myenteric plexus (Auerbach’s) located between inner circular and outer longitudinal

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22
Q

2 plexuses of ENS

A 
submucosal plexus (Meissner's) : PSS
myenteric plexus (Auerbach's): SS and PSS to muscles
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23
Q

dual innervation of smooth muscle in the gut

A

vagus to Auerbach’s plexus: Ach (Nicotinir R)

neuron in Auerbach’s plexus to SM: Ach (muscarinic R on muscle (+) or inhibitory ntr like NO on muscle (-))

24
Q

vago-vagal reflex present where

A

between deglutition centre and SKM upper esoph OR deglutition centre and SM and back to deglutition centre via vagus afferent

25
Q

entero-enteric reflex is where

A

between Auerbach’s plexus neurons and SM (distal esophagus and LOS)

26
Q

forces involved in esophageal phase of deglutition

A
  1. pharyngeal momentum
  2. gravity
  3. peristalsis
27
Q

primary peristaltic wave def

A

wave of peristalsis when we swallow. 8-10 sec to propagate. part of deglutition reflex

28
Q

2 high pressure zones in the esophagus

A

UES and LES

29
Q

pressure changes in esophagus in response to primary peristalsis

A

causes propagation of a pressure complex (30-80 mmHg) that takes 10s

30
Q

2 nuclei of the medulla giving the vagus

A

nucleus ambiguus and dorsal motor nucleus of the vagus

31
Q

what generates peristalsis

A

central pattern generator (deglutition centre) of medulla relaxes downstream of bolus and contracts upstream of bolus

32
Q

cutting vagus high in neck vs transthoracically consequence

A

high in neck: pharyngeal phase problem + no primary peristalsis
transthoracically: if some fibers reach ENS, ENS can continue to propagate a normal peristalsis in SM

33
Q

primary peristalsis: role of vagus and ENS

A

vagus: initiating in proximal esophagus
ENS: continuation and propagation of primary peristalsis in distal esophagus

34
Q

stimulus for primary peristalsis

A

pharyngeal receptors sense bolus: vago-vagal reflex

35
Q

secondary peristalsis when and what

A

when local distension (bolus stuck or reflux) in esophagus: many waves until resolved

36
Q

secondary peristalsis: innervation needed

A

vagus needed in upper esophagus but lower esophagus is fine with ENS

37
Q

factors influencing esophageal transport (3)

A
  1. viscosity of bolus
  2. temperature of bolus
  3. posture of the subject
38
Q

why temp influences transport in esophagus

A

vago-vagal reflex where temperature sensing fibers cause inhibition of esophageal contractions if cold

39
Q

LES what forms it

A

phrenoesophageal ligament, diaphragm, SM of the esophagus

40
Q

UES vs LES closure

A

UES: neurogenic (vagus)
LES: myogenic tone

41
Q

UES vs LES relaxation

A

UES: central inhibition (Ach impulse STOPS)
LES: local neurogenic (NANC (NO))

42
Q

why LES differs from rest of GI tract + characteristics (6)

A

is hyperfunctioning and hypersensitive 1) more collagen 2) partially contracted at its RMP (resting membrane potention) : lower RMP 3) more resistant to stretch 4) sensitive to hypoxia 5) Ca dependent 6) more sensitive to hormones and ntrs

43
Q

stuff that increases LES activity and important note

A

gastrin (IN PHARMA DOSES)

44
Q

stuff that decreases LES activity and important note

A

secretin, CCK (IN PHARMA DOSES) + smoking, alcohol, morphine, fat, chocolate, carminatives (mechanisms with cAMP)

45
Q

one thing that lowers LES pressure at endogenous dose

A

progesterone

46
Q

pyrosis def

A

heartburn

47
Q

GERD leads to what changes in esophagus

A

metaplastic changes in mucosa (Barrett’s esophagus)

48
Q

3 diseases related to GERD

A
  1. esophagitis
  2. Barrett’s esophagus
  3. hiatal hernia (as cause)
49
Q

patients with GERD have what

A

defective secondary peristalsis + defective epithelial resistance in esophagus (damage)

50
Q

3 esophageal studies

A

radiology, endoscopy, intraluminal pressure recording (manometry)

51
Q

intraluminal pressure recording (manometry) explanation

A

use for dx + check dynamics of deglutition

52
Q

causes of esophageal dysphagia + one to remember

A

achalasia**, stricture, cancer, eosinophilic esophagitis, spasm, …

53
Q

achalasia def

A

absent esophageal peristalsis (SM) and failure of LES to relax with swallowing

54
Q

achalasia pathophgy + cause + consequence

A

kills inhibitory NO neurons. can’t relax LES. dysphagia. cause is unkown

55
Q

achalasia treatments

A
  • SM relaxants
  • botox (blocks Ach and excitation locally)
  • peumatic balloon dilatation (break muscle)
  • surgical myotomy (break muscle)

Bloc E - GI & Metabolism (58 decks)

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