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GI- Week 1 > Prunuske: Oral and Esophageal Physiology > Flashcards

Prunuske: Oral and Esophageal Physiology Flashcards

1
Q

Achalasia

A

failure of lower esophageal sphincter to relax

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2
Q

Aspiration

A

inhalation of oropharnygeal or gastric contents into the respiratory track

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3
Q

GERD

A

heartburn due to inappropriate closure of lower esophageal sphincter allowing stomach contents to reflux into the esophagus

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4
Q

Deglutition

A

swallowing

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5
Q

Dysgeusia

A

distorted ability to taste

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6
Q

Dysphagia

A

difficulty swallowing

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7
Q

Halitosis

A

bad breath

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8
Q

Manometry

A

test to measure pressure in GI tract

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9
Q

Xerostomia

A

dry mouth

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10
Q

What secretes salivary secretions and what are they modified by? What is ultimately produced?

A

Secreted by ACINUS and ionic content modified by DUCT CELLS produces ALKALINE HYPOTONIC solution.

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11
Q

What is in slavary secretions?

A
  1. Water
  2. Digestive Enzymes: salivary α-amylase (ptyalin), lingual lipase, RNAase, DNAase
  3. Mucins lubricate and protect oral mucosa
    4. Defense molecules: Lysozyme, IgA, lactoferrin, peroxidase, defensins
    5. Epidermal and nerve growth factors
    .6. Bicarbonate
  4. Sex steroids
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12
Q

What is secreted by most salivary glands?

A 
SEROUS cells (water, amylase) and 
MUCOUS (mucin) cells

1.5 L/day

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13
Q

What controls the flow of saliva form salivary glands?

A

myoepithelial cells

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14
Q

How does the composition of saliva differ between parotid, submandibular and sublingual glands?

A

Parotid – entirely serous (25% volume)

Submandibular- mixed (70% volume)

Sublingual – mainly mucous (5% volume)

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15
Q

What does the ionic concentration of saliva depend on?

A

flow rate

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16
Q

What happens to saliva at fast flow rates?

A

saliva resembles PLASMA with higher HCO3- (more alkaline)

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17
Q

What happens to saliva at slow flow rates?

A

the duct have time to make significant changes in ionic concentration but do not alter volume as ducts are impermeable to water. Leads to a hypotonic solution

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18
Q

PNS affect on saliva secretion?

A

Getting ready to eat food!

VIP/Ach>
muscarinic receptors>
increases secretion of WATERY saliva

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19
Q

SNS affect on saliva?

A

NE>
B1 and A1>
increase secretion of VISCOUS saliva

*constricts blood vessels and decreases blood flow resulting in viscous saliva

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20
Q

What enzymes are secreted in the oral cavity?

A

Salivary amylase

Lingual lipase

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21
Q

What stimulates salivary amylase and what does it do?

A

Activated by Cl in saliva>
hydrolyzes alpha-1,4 glycosidic linkages in starch.

*Active until acid penetrates the bolus in the stomach

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22
Q

What does lingual lipase do?

A

breaks down triglycerides

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23
Q

What are the two occasions that salivary enzymes are increased?

A

pancreatic insufficiency

Neonates

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24
Q

What causes dysguesia?

A

infection
aging
nutritional deficiencies

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25
Q

How do we know what we taste? What does this lead to?

A

Taste ligands bind to receptors>
activates G proteins and secondary messengers> release neurotransmitters onto primary sensory neurons>
Taste signals to nucleus tractus solitarius>
leading to gastric acid secretion.

26
Q

Why is buccal and sublingual absorption of drugs important?

A

avoid first-pass metabolism

27
Q

What causes xerostomia?

A
  • SjÖgren syndrome- autoimmune disorder that destroys exocrine glands
  • Many medications: muscarinic antagonists, decongestants, and antihistamines
  • Secondary to head and neck radiation
  • Dehydration due to diarrhea, vomiting, fever, diuretics
  • Sialolithiasis (submandibular)
  • Nerve damage related to injury or diabetes
  • Postmenopausal hyposalivation
28
Q

What are the consequences of too little saliva production?

A

Increased likelihood of opportunistic infections

Halitosis due to production of hydrogen sulfide by bacteria and accumulation of dead cells

Decrease in oral pH leads to tooth decay

Decrease in taste

Problems with speech

Dysphagia> Poor nutrition

29
Q

How do you treat and manage dry mouth?

A

Gum, artificial saliva, switch medicines

Parasympathomimetics like pilocarpine
stimulate flow but also cause hypotension,
respiratory distress, and gastrointestinal disorder

30
Q

What causes swallowing?

A

when bolus is small enough an involuntary reflex is initiated by mucosal mechanoreceptors

*Can be overridden voluntarily (swallow pill) but UES and LES events are involuntary.

31
Q

What happens to the UES and LES between swallows?

A

Both are closed to prevent entry of air and gastric contents since the esophagus is present in low pressure environment of the thorax

32
Q

What coordinates swallowing w/ respiration and speech?

A
  1. MUCOSAL MECHANORECEPTORS>
    CN 9 and 10>
    Medullary swallowing center (brain stem)
  2. SOMATIC NERVES>
    Ach- nicotinic>
    contraction of STRIATED msucles of UES and top 1/3 of esophagus
  3. AUTONOMIC NERVES>
    ACh- nicotinic>
    smooth muscle in BOTTOM 2/3 of esophagus
33
Q

What happens when swallowing is unsuccessful?

A

choke
aspiration
goes through nose
cough

34
Q

What does the nasopharynx do?

A

Prevents bolus from entering the nasal cavity

35
Q

What does hte oropharynx do?

A

contraction propels bolus into esophagus

36
Q

What does the hypopharynx/laryngopharynx do?

A

Relax/segregate food and air

37
Q

What triggers the swallowing reflex?

A

Tongue contacting the hard palate pushes bolus against SOFT PALATE and triggers reflex

38
Q

What happens to breathing as a bolus passes the closed airway?

A

It’s inhibited!

  1. Longitudinal muscles of posterior pharynx contract
  2. Epiglottis folds down to prevent material from enteirng trachea
  3. Relaxation of cricopharyngeal muscle leads to opening of distal pharynx and upper esophageal sphincter
39
Q

What moves food downward into the esophagus?

A

Peristaltic waves aided by gravity

40
Q

What can dysphagia/odynophagia lead to?

A

can lead to aspiration and malnutrition

41
Q

What causes dysphagia/odynophagia?

A

structural abnormalities (esophageal cancer or diverticula)

functional abnormalities (stroke leading to neural disorder)

42
Q

What is the esophageal phase of swallowing/primary peristalsis?

A
  1. Sphincter pressures are higher than atmospheric and fall during a swallow
  2. Esophageal pressure increases as the peristaltic wave sweeps down the esophagus
  3. The esophageal phase may last 10 seconds or more and is aided by gravity.
43
Q

How does the activation of mechanoreceptors lead to peristalsis?

A

Mechanoreceptors sense distension or changes in pH :

contraction (ACh) ABOVE

relaxation (NO/VIP) BELOW

44
Q

What happens to larger/colder boluses?

A

Propelled w/ greater force but more SLOWLY

45
Q

Neural control of esophageal peristalsis comes from…

A

parasympathetic nerves and enteric neurons

46
Q

What is the difference between circular muscles and longitudinal muscles in esophageal peristalsis?

A

Circular muscles CONTRACT upstream of the bolus and relax downstream

Longitudinal muscles RELAX upstream and contract downstream

47
Q

What happens if a bolus becomes stuck?

A

Distension/acid in the esophagus causes just SMOOTH MUSCLE to be contracted.

ENTERIC NEURONS produce a strong peristaltic wave ABOVE the obstruction.

48
Q

What are retrograde movements?

A

eructation
vomiting
regurgitation

49
Q

What do retrograde movements require?

A

relaxation of the upper and lower sphincters (don’t require additional esophageal movements)

50
Q

What are diffuse esophageal spasms?

A

uncoordinated contractions can cause the regurgitation of food or liquids

51
Q

What is nutcracker esophagus?

A

painful contractions

52
Q

What physiological features contribute to sword swallowing?

A

Need to HYPEREXTEND neck

INHIBIT pharyngeal reflex

FLIP epiglottis

RELAX upper and lower
esophageal sphincters

Don’t try this at home
Risk of perforating esophagus

53
Q

What controls the lower esophageal sphincter?

A

ENTERIC PLEXUS of neurons

54
Q

What is the state of hte lower esophgaeal sphincter between swallows and during swallows?

A

CLOSED BETWEEN swallows due to cholinergic neurotransmission

RELAXED DURING swallows due to NO and VIP neurotransmission

55
Q

What is GERD?

A

Reflux of acidic gastric contents into the esophagus d/t relaxation of the lower esophageal sphincter

56
Q

Reflux

A

normal physiologic process cleared by peristalsis

57
Q

What’s the difference between mild and severe reflux?

A

Mild- heart burn

Severe- epithelial erosion and barrett’s esophagus

58
Q

How do you treat GERD?

A

elevation of bed, change diet, *PPI, antacids

59
Q

What can contribute to GERD?

A

obesity
pregnancy (increased progesterone)
eructation
hiatal hernia

60
Q

What is Achalasia?

A

failure of LES to RELAX d/t LOSS of myenteric ganglion cells

Leads to:
regurgitation, dysphagia of solids

61
Q

What leads to a “bird beak”

A

achalasia leads to bird beak as well as dilation of esophagus

62
Q

How can you cause contraction in a pt w/ achalasia?

A

Requires ACh—> tx w/ botulinum toxin

GI- Week 1 (12 decks)

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