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Intro and Development to GI > Physiology of Swallowing > Flashcards

Physiology of Swallowing Flashcards

1
Q

α-Amylase (Ptyalin) –

A

Hydrolyses starch
Inactivated at pH <4

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2
Q

Mucin

A

Lubricates food
Assists mastication
Facilitates deglutition
Aids speech (By facilitating movements of lip &tongue)
Protects oral mucosa by neutralising acid

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3
Q

Lactoferrin

A

binds iron & arrests bact. multiplication & dental caries (bacteriostatic) Keeps mouth moist Solvent for molecules that stimulate taste buds. Vehicle for excretion of heavy metals(lead),viruses (polio,rabies ) & drugs.

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4
Q

IgA

A

confers local immunity

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5
Q

Lingual lipase

A

digestion of fat (active in stomach)

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6
Q

Proline rich protein

A

binds toxic tannin & maintains oral pH

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7
Q

Nerve growth factor

A

growth of sympathetic ganglia
Regulation of water balance
Middle ear pressure adjustment
Regulation of temperature (mainly in animals)

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8
Q

Kallikrein

A

requires acidic pH activates bradykinin, potent vasodilator, Kallikrein is released when the metabolism of the salivary glands increases; it is responsible in part for increased blood flow to the secreting glands. Saliva also contains the blood group substances A, B, AB, and O.

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9
Q

Anions

A

Chloride, Bicarbonate, Phosphate,
Halides (Iodine& Fluorine)

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10
Q

Cations

A

Sodium, Potassium, Calcium, Magnesium

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11
Q

Unique properties of Salivary secretion

A

Large volume relative to mass
Low osmolality
High potassium concentration
Specific organic material

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12
Q

Primary secretion

A

Acinar cells
Isotonic to plasma
Secrete Ptyalin, mucus and ions

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13
Q

Secondary Secretion-Modification by duct cells

A

Duct system
Rate of flow
Hypotonic to plasma

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14
Q

Acinar-Primary secretion

A

Basolateral membrane
Na-K pump
Na-K-2Cl symporter
Apical membrane
Cl and HCO3- anion channel
Sodium and water paracellularly

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15
Q

Modification by duct cells- Secondary secretion

A

Na-K pump
Apical membrane
Na-H Na and Cl reabsorption
Cl- HCO3- K and HCO3- secretion
H-K
Aldosterone

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16
Q

rough objects cause

A

less salivation and occasionally even inhibit salivation

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17
Q

The salivatory nuclei are located approximately at the juncture of the medulla and pons and are

A

excited by both taste and tactile stimuli from the tongue and other areas of the mouth and pharynx.

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18
Q

sour taste (caused by acids), elicit

A

copious secretion of saliva—often 8 to 20 times the basal rate of secretion

19
Q

Theappetite areaof the brain

A

is located in proximity to the parasympathetic centers of the anterior hypothalamus, and it functions to a great extent in response to signals from the taste and smell areas of the cerebral cortex or amygdala.

20
Q

The parasympathetic preganglionic fibers are delivered by

A

the facial and glossopharyngeal nerves to autonomic ganglia

21
Q

The sympathetic preganglionic nerves originate

A

at the cervical ganglion

22
Q

Sympathetic saliva activity

A

is thicker compared to saliva produced during increased parasympathetic activity. The sympathetic nerves originate from the superior cervical ganglia and travel along the surfaces of the blood vessel walls to the salivary glands.

23
Q

Reflex secretion

A

Condition reflex
Cephalic phase
No gastric and intestinal phase

24
Q

Sympathetic

A

Norepinephrine
β-adrenergic
cAMP
Protein ≫ fluid secretion

25
Q

Deglutition reflex

A

Stimulus : food in mouth
Receptor : touch receptors
Afferents : V, IX and X cranial nerve
Centre : deglutition center, medulla & lower pons
Efferents : V, IX, X and XII
Effector organ : pharyngeal muscles
Response : involuntary stage of swallowing

26
Q

Swallowing center is located in the

A

Medulla

27
Q

Stage II- pharyngeal

A

Involuntary
Soft palate elevated – nasal cavity
Larynx rises
Vocal cords approximated
Breathing inhibited
Deglutition apnea
Epiglottis closes the laryngeal opening

28
Q

Stage III- Esophageal stage

A

Pressure is lower than in the pharynx and stomach
Esophagus withstand the entry of air and gastric contents
The barrier functions by the presence of sphincters
Muscle an inner layer circular and outer longitudinal
UES thickened circular muscle (cricopharyngeal) is striated
The distal third is smooth muscle lower esophageal sphincter (LES)
The middle third is composed of a mixture of muscle types
Transport by peristalisis- primary and secondary

29
Q

The function of the UES

A

Separates the pharynx and the upper part of the esophagus is the UES
Striated muscle and high resting tone
Constricts and prevents entry of air into the stomach
During swallowing- UES relaxes and glottis is closed
Reflexly relaxes- neutrally mediated

30
Q

The function of the LES

A

To prevent reflux of gastric contents into the esophagus. Remains tonically contracted. The LES maintains a resting tone that is the result of both intrinsic myogenic properties of the sphincteric muscle and cholinergic regulation.
Basal tone- vagal Ach fibers
Gastrin increases tone
Secretin decreases- relaxation
To permit coordinated movement of ingested food into the stomach from the esophagus after swallowing
Deglutition or distention of esophagus- causes relaxation

31
Q

Relaxation of the LES is mediated by

A

he vagus nerve mediated by VIP and by NO.

32
Q

Propulsive segment mechanism

A

Part behind the bolus (stimulus)
Circular contract
Longitudinal muscle relax

33
Q

Receiving segment mechanism

A

In front of bolus
Receives bolus
Circular muscles relax
Longitudinal muscles contract

34
Q

Retrograde direction of neurotransmitters deynin

A

Release substance P and Ach
Contraction of circular smooth muscle
Propulsion of food

35
Q

Sympathetic stimulation

A

Inhibits peristalsis

36
Q

Anterograde direction of neurotransmitters kinesin

A

VIP and NO
Relaxation of circular smooth muscle

37
Q

Parasympathetic stimulation

A

Stimulates peristalsis

38
Q

PRIMARY Esophageal peristalsis

A

Initiated by deglutition reflex
When bolus enters esophagus, contraction is initiated
Acts of swallowing initiates
Vagal fibers

39
Q

SECONDARY Esophageal peristalsis

A

When food remains after primary peristalisis
Mechanoreceptors activated by food
Intrinsic nerves

40
Q

Hormones that increase LES Pressure

A

Gastrin, Motilin, Substance P, Histamine and Antacids
protein meals
α-adrenergic agonists
β-adrenergic antagonists
Cholinergic agonists

41
Q

What modulators decrease LES pressure

A

Secretin
Cholecystokinin
Somatostatin
Vasoactive intestinal peptide (VIP)
Progesterone
β-adrenergic agonists
α-adrenergic antagonists
Anticholinergic agents
Fat
Chocolate
Peppermint
Theophylline
Prostaglandins E2, I2

42
Q

Esophageal achalasia

A

achalasia-Disordered peristalsis and increased lower esophageal sphincter tone. Result of defective innervation of smooth muscle in the esophageal body and LES esophageal sphincter.
LES is tightly contracted and does not relax in response to swallowing due to partial loss of neurons in the wall of the esophagus.
Disorder caused by defective inhibitory pathways of the esophageal enteric nervous system.
Injecting botulinum toxin into the LES diminishes the activity of the excitatory pathways
Loss of normal peristalsis in the esophageal body is often seen in achalasia,

43
Q

Reflux esophagitis

A

Inappropriate lower esophageal sphincter relaxation results (decreased/loss of tone) .

44
Q

Gastroesophageal reflux disorder (GERD)

A

Normally LES is tonically contracted.
Occurs when the LES allows the acidic contents of the stomach to reflux back into the distal part of the esophagus.
Reflux of acid content
Loss of LES tone (ie, the opposite of achalasia)
Increased frequency of transient relaxations
Loss of secondary peristalsis after a transient relaxation
Increased stomach volume or pressure, or increased acid production.
Recurrent reflux can damage the mucosa, resulting in inflammation.
Commonly referred to as heartburn or indigestion

Intro and Development to GI (4 decks)

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