Physiology of Swallowing Flashcards

(44 cards)

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
Deglutition reflex
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
Swallowing center is located in the
Medulla
27
Stage II- pharyngeal
Involuntary Soft palate elevated – nasal cavity Larynx rises Vocal cords approximated Breathing inhibited Deglutition apnea Epiglottis closes the laryngeal opening
28
Stage III- Esophageal stage
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
The function of the UES
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
The function of the LES
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
Relaxation of the LES is mediated by
he vagus nerve mediated by VIP and by NO.
32
Propulsive segment mechanism
Part behind the bolus (stimulus) Circular contract Longitudinal muscle relax
33
Receiving segment mechanism
In front of bolus Receives bolus Circular muscles relax Longitudinal muscles contract
34
Retrograde direction of neurotransmitters deynin
Release substance P and Ach Contraction of circular smooth muscle Propulsion of food
35
Sympathetic stimulation
Inhibits peristalsis
36
Anterograde direction of neurotransmitters kinesin
VIP and NO Relaxation of circular smooth muscle
37
Parasympathetic stimulation
Stimulates peristalsis
38
PRIMARY Esophageal peristalsis
Initiated by deglutition reflex When bolus enters esophagus, contraction is initiated Acts of swallowing initiates Vagal fibers
39
SECONDARY Esophageal peristalsis
When food remains after primary peristalisis Mechanoreceptors activated by food Intrinsic nerves
40
Hormones that increase LES Pressure
Gastrin, Motilin, Substance P, Histamine and Antacids protein meals α-adrenergic agonists β-adrenergic antagonists Cholinergic agonists
41
What modulators decrease LES pressure
Secretin Cholecystokinin Somatostatin Vasoactive intestinal peptide (VIP) Progesterone β-adrenergic agonists α-adrenergic antagonists Anticholinergic agents Fat Chocolate Peppermint Theophylline Prostaglandins E2, I2
42
Esophageal achalasia
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
Reflux esophagitis
Inappropriate lower esophageal sphincter relaxation results (decreased/loss of tone) .
44
Gastroesophageal reflux disorder (GERD)
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