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Physio II > Exam 4- Intro to GI and Swallowing > Flashcards

Exam 4- Intro to GI and Swallowing Flashcards

1
Q

What are the 4 functions of the GI tract?

A

Boundary (between external and internal environments), musculature, digestion, and absorption

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2
Q

Absorption in the GI tract occurs via what 3 processes?

A

Diffusion, carrier transport, endocytosis

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3
Q

Oral and anal events are regulated by what portion of the nervous system?

A

Somatic nerves via skeletal muscle

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4
Q

The mid-esophagus to internal anal sphincter are controlled by what portion of the NS?

A

ANS via visceral smooth muscle (enteric nervous system)

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5
Q

In addition to absorption of nutrients, what must also be reabsorpted to prevent imbalances?

A

7-8 L of GI secretions

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6
Q

What 6 processes move food through the GI tract (start to finish)?

A

Ingestion, mechanical digestion, propulsion, chemical digestion, absorption, defecation

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7
Q

What are the layers of the GI tract from serosal to luminal side?

A

Serosa, longitudinal muscle, myenteric plexus, circular muscle, submucosa, submucosal plexus, mucosa

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8
Q

What are the 3 layers of the mucosa from outside to inside?

A

Muscularis mucosae, lamina propria, epithelium

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9
Q

What is the outer most layer of the GI tract that continues to the mesentery?

A

Serosa

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10
Q

What 2 layers of the GI tract are part of the enteric nervous system (ENS)?

A

Submucosal plexus and myenteric plexus

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11
Q

What layer of the GI tract is composed of collagen, elastin, glands, and blood vessels?

A

Submucosa

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12
Q

Auerbach’s is aka?

Meissner’s is aka?

A

Auerbach’s = Myenteric plexus

Meissner’s = Submucosal plexus

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13
Q

What layer of the mucosa changes the shape of the epithelial layer?

A

Muscularis mucosae

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14
Q

Which layer of the mucosa is mostly connective tissue but also contains some blood and lymph vessels?

A

Lamina propria

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15
Q

Which layer of the mucosa is responsible for absorptive and secretory functions?

A

Epithelial cells

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16
Q

What effect does venous drainage from the GI tract into the portal vein have on the liver?

A

Perfuses the liver

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17
Q

Venous drainage from the pancreas stomach, sm & lg. intestine empties into where?

A

Portal vein

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18
Q

What does parallel organization of splanchnic circulation allow for?

A

Regulation of flow to individual organs

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19
Q

What does series organization of splanchnic circulation allow for?

A

Liver is exposed to all absorbed substances

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20
Q

What is the pathway of nerve transmission in the GI tract? (4 steps)

A

Chemo/ mechanoreceptors → afferent nerves → submucosal/ myenteric plexuses → CNS (via ANS)

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21
Q

The ENS does NOT require what in order to carry out most functions?

A

ANS input (it is self-contained)

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22
Q

What does the myenteric (Auerbach’s) plexus innervate?

A

Longitudinal and circular smooth muscle layers

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23
Q

Which plexus if primarily concerned with control of gut movements?

A

Myenteric (Auerbach’s) plexus

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24
Q

What does the submucosal (Meissner’s) plexus intervate? (3)

A

Glandular epithelium, intestinal endocrine cells, and submucosal blood vessel

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25
Q

What plexus is primarily concerned w/ control of intestinal secretion?

A

Submucosal plexus

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26
Q

SNS stimulation via what nerves innervates from the esophagus to the proximal colon?

A

Celiac ganglia

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27
Q

SNS stimulation via what nerves innervates the distal colon and rectum?

A

Superior and inferior mesenteric ganglia

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28
Q

PNS stimualtion via what nerve innervates from the esophagus to the proximal colon?

A

Vagus nerve

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29
Q

PNS stimulation via what nerves innervates the distal colon and rectum?

A

Sacral → pelvic nerve

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30
Q

What effect does SNS release of NE on intramural plexuses, vascular smooth muscle, and secretory cells have?

A

Inhibitory effect

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31
Q

What are the differences between SNS and PNS innervation of the gut?

A

SNS ouput synapse @ ganglia → POSTsynaptic → GI plexuses vs PNS output (pre-synaptic) → GI plexuses

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32
Q

What is the largest endocrine organ in the body?

A

GI tract (15+ hormone secreting cells)

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33
Q

What do GI peptides regulate? (3)

A

Smooth muscle, secretion of fluid/enzymes, growth of GI cells

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34
Q

GI peptides fall into what 3 categories?

A

Hormones, paracrines, neurocrines

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35
Q

Where are GI hormones released from?

A

Endocrine cells (disperesed throughout GI tract)

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36
Q

What are the 4 known GI hormones?

A

Gastrin, Cholecystokinin (CCK), Secretin, Gastric inhibitory peptide

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37
Q

What cells release gastrin?

A

Gastric G cells

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38
Q

What cells release CCK?

A

Duodenal and jejunal I cells

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39
Q

What cells release secretin?

A

Duodenal S cells

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40
Q

What cells release gastric inhibitory peptide (GIP)?

A

Duodenal and jejunal K cells

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41
Q

What stimulate secretion of gastin? (3)

A

Small peptides/ AAs, stomach distension, vagal stimulation

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42
Q

What stimulate secretion of CCK? (2)

A

Small peptides and AA, fatty acids

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43
Q

What stimulate secretion of secretin? (2)

A

H+ in the duodenum, fatty acids in duodenum

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44
Q

What stimulate secretion of GIP? (3)

A

Fatty acids, AAs, oral glucose

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45
Q

What hormone ↑ gastric H+ secretion and stimulates growth of gastric mucosa?

A

Gastrin

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46
Q

What 2 hormones ↑ pancreatic HCO3- secretion?

A

CCK and Secretin

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47
Q

What 2 hormones ↓ gastic H+ secretion?

A

Secretin and GIP

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48
Q

What hormone stimulates contraction of the gallbladder and relaxation of the sphincter of Oddi?

49
Q

What hormones increases insulin secretion from pancreatice B cells?

A

GIP (why we are able to reactive so quickly to oral glucose)

50
Q

What hormones inhibits trophic effects of gastrin on gastric mucosa?

51
Q

What hormone ↑ biliary HCO3- secretion?

52
Q

What hormones inhibit gastric emptying?

A

CCK, secretin, GIP

53
Q

What hormone stimulates growth of the exocrine pancreas and gallbladder?

54
Q

Paracrine are carried via what to target cells? (2)

A

Capillaries or diffusion

55
Q

What are the 2 GI paracrines?

A

Somatostatin and histamine

56
Q

What hormone is released from D cells and inhibits release of all gut hormones?

A

Somatostatin

57
Q

What hormone is a non-peptide paracrine?

58
Q

Neurocrines are synthesized in neurons and released in response to what?

A

Action potential

59
Q

What are the main GI neurocrines? (4)

A

Acetylcholine, norepinephrine, vasoactive intestinal peptide (VIP), gastrin-releasing peptide (GRP) (others: enkephalins, neuropeptide Y, substance P)

60
Q

What neurocrine increases salivary, gastric and pancreatic secretions, relaxes sphincters, and increases contraction of wall smooth muscle?

A

Acetylcholine (PNS - cholinergic neurons)

61
Q

What neurocrine causes increased salivary secretion, sphincter contraction and relaxation of wall smooth muscle?

A

Norepinephrine (SNS - adrenergic neurons)

62
Q

What neurocrine caues relaxation of smooth muscle and increases GI secretions (intestinal and pancreatic)?

A

Vasoactive intestinal peptide (VIP) (PNS, ENS - neurons of enteric NS)

63
Q

What neurocrine increases gastrin secretion?

A

Gastrin-releasing peptide (GRP) (PNS)

64
Q

Does NO released from the neurons of the enteric NS result in relaxation or contraction of smooth muscle?

A

Relaxation

65
Q

GRP is released from what neurons?

A

Vagal neurons of the gastric mucosa

66
Q

What is the structure of visceral smooth muscle cells w/in the GI tract? How are the organized?

A

Long and slender. Organized in packed bundles (functional unit) separated by connective tissue

67
Q

How are visceral smooth muscle cells connected and what does this allow for?

A

Connected by low resistance gap junctions, allows for electrical propagation between adjacent fibers

68
Q

What do VSMC exhibit of the resting membrane potential due to variations in Ca2+ and K+ conductances?

A

Spontaneous oscillations (slow waves/ basic electrical rhythm)

69
Q

What happens if slow waves of VSMC reach depolarization threshold?

A

Action potential will superimpose on slow wave resulting in strong contraction of smooth muscle

70
Q

What cells initiate BER via long branched processes into the VSMC?

A

Interstitial cells of Cajal/ stellate pacemaker cells

71
Q

Do ACh or NE affect BER frequency?

72
Q

What effect does ACh have on the activity of VSMC? (3)

A

Increases: BER amplitude, number of spike potentials, VSMC tension

73
Q

What effect does NE have on the activity of VSMC? (3)

A

Decreases: BER amplitude, number of spike potentials, VSMC tension

74
Q

What are the 2 patterns of GI motility?

A

Segmentation and peristalsis

75
Q

Contraction and relaxation of adjacent segments (agitation/mixing type movement) is what GI motility pattern?

A

Segmentation

76
Q

Peristalsis requires contraction behind the bolus of food and relaxation ahead of the bolus of food. This results in what kind of movement?

A

Directed propulsive

77
Q

What are the 3 phases of digestion?

A

Cephalic, gastric, early and late intestinal

78
Q

During what phase are there low levels of motor, secretory and digestive activity?

A

Interdigestive

79
Q

Towards the end of what phase will you have a sense of hunger?

A

Interdigestive

80
Q

What is decribed by cycles of motor activity from the stomach to the ileum during the interdigestive phase?

A

Migrating motor complex (MMC)

81
Q

What regulated the migrating motor complex (MMC)

A

The “candidate” hormone motilin from the upper duodenum

82
Q

What is the “housekeeping” function of the MMC?

A

Removes undigested material from stomach (begins 2 hrs post prandial & stop when meal is taken)

83
Q

What type of contractions are produced by the MMC?

A

Intense and slow, 90 minute intervals

84
Q

What phase of digestion triggers autonomic and endocrine reflexes (prepares the GI tracts) via the anticipation of eating and 1st sensory contact w/ food?

85
Q

The cephalic phase of digestion is due to activation of what neural response?

A

PNS efferents (sight, smell, gustatory afferents enhance PNS)

86
Q

During the cephalic phase, PNS activity increases secretion of what things? (4)

A

Saliva, gastric acid, gastrin, pancreatic enzymes

87
Q

What is the daily salivary output?

A

0.5-1/5 L/day (flow rate varies w/ chewing)

88
Q

What is the site of formation of saliva?

A

Acinar cells in salivary glands

89
Q

What are the 5 components of saliva?

A
  1. Mucus (lubricant) 2. a-amylase (starts starch digestion) 3. lingual lipase (starts fat digestion) 4. slightly alkaline solution (moistens food) 5. IgA & kallikrein
90
Q

What is the role of IgA and kallikrein in saliva?

A

Increase bradykinin = increased BF to salivary glands

91
Q

Saliva is hypo or hypertonic to plasma?

92
Q

What ions are present at a lower concentrations in saliva, compared to plasma?

A

Na+ and Cl-

93
Q

What ions are present at a higher concentrations in saliva, compared to plasma?

A

K+ and HCO3-

94
Q

What 2 things change as saliva secretion rates increases?

A

Saliva becomes isotonic compared to plasma and pH increases (increased HCO3-)

95
Q

How does saliva change from isotonic to hypotonic after being release from acinar cells?

A

Salivary ducts are impermable to water, Na, Cl out > K, HCO3

96
Q

Nervous regulation of salivary secretion is mostly via what?

A

PNS (SNS contributes slight/ short-lived, mostly mucus secretion)

97
Q

What stimulates the salivary gland (in medulla)?

A

Taste and tactile stimulation in mouth (also smell)

98
Q

ACh and VIP from PNS nerve endings stimulate what with regards to the salivary response? (4)

A
  1. saliva secretion 2. vasodilation 3. salivary duct dilation 4. secretion of amylase, lipase and mucus
99
Q

What is the PNS pathway for saliva regulation?

A

PNS → CN VII, X → release ACh on M receptors → IP3, Ca → Saliva

100
Q

What stimulates the PNS to increase saliva production? (3)

A

Operant conditioning, food/smell, nausea

101
Q

Will there be increased or decreased salivary secretion during dehydration, fear and sleep?

102
Q

What area of the brain coordinates swallowing?

A

Medullary swallowing center (first voluntary then reflexive)

103
Q

What are the 3 phases of swallowing?

A

Oral (buccal), pharyngeal, esophageal

104
Q

During the oral phase of swallowing, what is stimulated after a bolus is formed during mastication and pushed voluntarily by the tongue toward the pharynx?

A

Stimulation of somatosensory receptors → involuntary swallowing reflex

105
Q

How is the pharyngeal phase of swalloing controlled?

A

Reflexively

106
Q

What process is inhibited during the entire pharyngeal phase of swallowing?

107
Q

What prevents reflux into nasopharynx during pharyngeal phase of swallowing?

A

Upward movement of soft palate

108
Q

During the pharyngeal phase of swallowing, the epiglottis moves to cover the opening to the larynx and the larynx moves upwards against the epiglottis. What does this prevent?

A

Food from entering the trachea

109
Q

What is reflexivley inhibited and relaxes briefly during the pharynageal phase of swallowing?

A

UES (perstaltic waves propels food through the open sphincter)

110
Q

What causes the LES to relax during the esophageal phase of swallowing?

111
Q

At what point during the esophageal phase of swallowing does the LES contract?

A

As bolus passes into stomach

112
Q

An incomplete swallow or gastric regurgitation results in a second peristaltic wave/ secondary swallow. What is this controlled by?

113
Q

What is used to measure the esophageal pressure changes during swallowing?

A

Esophageal manometry (used if there is dysfunction)

114
Q

What disorder is caused by failure of the LES fails to relax during swallowing resulting in food accumulation/ dilation of esophagus?

115
Q

What are the 2 potential causes of achalasia?

A

Degeneration of myenteric plexus, defective release of NO and VIP

116
Q

During achalasia, when will food enter the stomach?

A

When esophageal pressure > LES pressure

117
Q

What is the cause of reflux esophagitis?

A

Loss of LES tone (or overindulgence)

118
Q

What does reflux esophagitis result in?

A

Acid reflux from stomach to esophagus = heartburn/ ulceration

Physio II (14 decks)

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