BIOL 0800 Reading- Chapter 15 Flashcards

1
Q

What acid is in the stomach?

A

HCl

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2
Q

What is pepsin?

A

Protein-digesting enzymes in the stomach

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3
Q

What two molecule types are typically not digested well by acid in the stomach?

A

Polysaccharides and fats

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4
Q

How much absorption of organic nutrients occurs in the stomach?

A

Virtually none

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5
Q

Where does most absorption of nutrients occur?

A

In the small intestine

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6
Q

What is the duodenum?

A

The initial segment of the small intestine

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7
Q

What is the jejunum?

A

The second segment of the small intestine

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8
Q

What is the ileum?

A

The third, longest segment of the small intestine

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9
Q

What are the three segments of the small intestine?

A

Duodenum, jejunum, ileum

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10
Q

What two organs secrete substances into the duodenum?

A

Pancreas and liver

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11
Q

How does the pancreas contribute to digestion?

A

Secretes digestive enzymes and a fluid rich in HCO3- to neutralize the acidic chyme

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12
Q

What does the liver do?

A

Secretion of bile to break down fast

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13
Q

What does the gallbladder do?

A

Stores secreted bile

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14
Q

What are the four layers of the GI wall?

A

Mucosa, submucosa, muscularis externa, serosa

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15
Q

What are the three layers of the mucosa?

A

Epithelium, lamina propria, muscularis mucosa

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16
Q

What is the submucosa?

A

Major blood and lymphatic vessels, submucosal plexus

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17
Q

What is the submucosal plexus?

A

Network of neyrons

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18
Q

What is the muscularis externa?

A

Circular muscle and myenteric plexus

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19
Q

How do circular muscles work?

A

Fibers oriented in circulate pattern around the tube so that contraction produces a narrowing of the lumen

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20
Q

What is the myenteric plexus?

A

Second network of neurons: innervated by nerves from the autonomic NS and has neurons that project to the submucosal plexus

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21
Q

What kinds of nerves innverate the myenteric plexus?

A

Autonomic nervous system

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22
Q

What is the serosa?

A

Thin layer of connective tissue to connect outer surface of tube to abdominal wall

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23
Q

What is a lacteal?

A

Single, bind-ended lymphatic vessel that is at the center of each villi

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24
Q

Most of the fat absorbed in the small intestine goes where?

A

Through the lacteals, to be emptied through the lymphatic systme into the thoracic duct

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25
Q

What is the hepatic portal vein?

A

The vein through which absorbed nutrients drain from the small intestine to the vena cava

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26
Q

What does the hepatic portal vein allow?

A

Material absorbed into the intestinal capillaries to be processed by the liver before entering general circulation: detox

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27
Q

What biological accounts for the liver’s function as detox?

A

Hepatic portal vein: carries intestinally absorbed material through liver before returning it to capillary circulation

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28
Q

What are Peyer’s patches?

A

Patches in the SI to secrete inflammatory mediators (cytokines) to alter motility of harmful substances not destroyed by acidity

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29
Q

What happens to amylase in the stomach?

A

It gets inactivated! Oh no!

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30
Q

What are the products of salivary and pancreatic amylase?

A

Maltose and short, branched glucose

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31
Q

What happens to carbs after salivary and pancreatic amylase converts them into maltose/short glucose?

A

Broken down, along with sucrose and lactose, into the three monosaccharides (glucose, fructose, galactose) in the brush border

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32
Q

Where are carbs completely broken into monosaccharides?

A

In the brush border of the small intestine

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33
Q

How does fructose get reabsorbed from the brush border?

A

Facilitated diffusion visual glucose transporter GLUT

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34
Q

How do glucose and galactose get reabsorbed from the brush border?

A

Secondary active transport coupled to Na via sodium-glucose cotransporter SGLT

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35
Q

How do all three monsaccharides get transported from the epithelium to the interstitial fluid?

A

GLUT transporters’ facilitated diffusion

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36
Q

Where does protein digestion begin?

A

Stomach with pepsin

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37
Q

What substances digest protein in stomach vs SI?

A

Pepsin in stomach, trypsin and chymotrypsin in SI

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38
Q

What organ secretes trypsin and chymotrypsin into the SI for protein digestion?

A

Pancreas

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39
Q

What happens after pepsin/trypsin/chymotrypsin partially fragment proteins in the stomach/SI?

A

Fragments broken down by carboxypeptidase from pancreas and aminopeptidase from SI epithelium

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40
Q

Where are carboxypeptidase and aminopeptidase produced?

A

In the pancreas and the epithelium of the SI

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41
Q

What do carboxypeptidase and aminopeptidase do?

A

Break down protein fragments in the SI into AAs

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42
Q

How do free aas enter the epithelial cells of the SI?

A

Secondary active transport coupled to Na+ cotransporters: different transporters for different aas

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43
Q

Can short chains of aas be absorbed to the SI epithelium?

A

Yes: couples to hydrogen ion gradient

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44
Q

What happens to di and tripeptides that were transported into the epithelial cells of the SI coupled to hydrogen ion gradient?

A

Broken down into single amino acids and leave through facilitated diffusion

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45
Q

What enzyme is responsible for fat digestion?

A

Lipase

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46
Q

Where is lipase produced?

A

In the pancreas

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47
Q

What does lipase do?

A

Breaks a triglyceride into a monoglyceride and two fatty acids

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48
Q

What are the main emulsifying agents in digestion?

A

Phospholipids ingested or secreted in bile, and bile salts

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49
Q

What is colipase?

A

Protein secreted by pancreas to lodge on lipid droplets to bind the lipase enzyme

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50
Q

What are micelles?

A

Very small emulsion droplets: bile salts, monoglycerides and fatty acids: with polar side out and nonpolar side in

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51
Q

How do micelles increase absorption?

A

Continuously break down and reform, keep the lipids emulsified, while also allowing small amounts of broken-down lipids into the fluid to cross the membrane into the epithelial cells

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52
Q

What happens to monoglycerides and fatty acids in the epithelial cells?

A

Resynthesized into triglycerides for passage through to the interstitial fluids

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53
Q

Why is it advantageous that lipids leave the epithelial cells for the interstitium as triglycerides rather than fatty acids and monoglycerides?

A

Maintains the concentration gradient so that monoglycerides and fatty acids keep diffusing into the epithelium

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54
Q

What are chylomicrons?

A

Small extracellular fat droplets released by the smooth ER when the triglycerides were reformed

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55
Q

Where do chylomicrons go after formation?

A

To the lacteals! Because those have big pores and let the chylomicrons out easily

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56
Q

How are fat soluble vitamins absorbed? (ADEK?)

A

Same way as fats: broken into micelles

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57
Q

How are water soluble vitamins absorbed?

A

Through diffusion or mediated transport, EXCEPT for B12

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58
Q

Why is B12 tricky for absorption?

A

It’s a large charged molecule

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59
Q

How is B12 absorbed?

A

Binds to an intrinsic factor protein, which binds to sites on epithelial ileum for endocytosis

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60
Q

Where is intrinsic factor for B12 produced?

A

Acid-secreting cells of the stomach

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61
Q

What is the most abundant solute in chyme?

A

Na+

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62
Q

How does water absorption occur in the small intestine?

A

Wherever there’s a water concentration gradient created by actively transported solutes (Na+)

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63
Q

What solutes are absorbed with Na+ to cause water diffusion?

A

Cl- and HCO3-

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64
Q

What happens to iron in the small intestine?

A

Acitvely transported into epithelial cells, mostly bound into ferritin (intracellular iron storage) to be released to the blood side onto transferrin

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65
Q

How does the body control storage of iron?

A

Increased transcription of gene for ferritin: increased binding of iron in SI epithelial cells, so increased iron storage and reduced release into the bloodstream

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66
Q

What are four luminal stimuli to initiate GI reflexes?

A

Wall distension, chyme osmolarity, chyme acidity, and chyme concentration of specific digestion products: monosac, Fas, peptides, aas, etc.

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67
Q

What is the enteric NS?

A

GI’s own nervous system: submucosal plexus and myenteric plexus

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68
Q

How does activity in one half of the enteric NS affect the other?

A

Interrelated because the axons of one synapse with the neurons of the other

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69
Q

In which direction can impulses conduct along plexuses of the enteric NS?

A

Both directions: stimulation at one plexus point can affect other areas, like SI to stomach and lower intestinal tract muscle

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70
Q

What is the difference in influence of myenteric vs submucosal plexus?

A

Submucosal is mostly for secretory activity, and myenteric is mostly for smooth muscle activity

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71
Q

What kinds of neurons are in the enteric NS?

A

Adrenergic and cholinergic neurons; and neurotransmitter-releasing neurons

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72
Q

What are the main effectors of enteric NS neurons?

A

Muscle cells and exocrine glands

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73
Q

What kinds of neurons, sympathetic or parasympathetic, innervate the plexuses of the enteric NS?

A

Both! Allow CNs to influence motility and secretory activity of GI tract

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74
Q

What are the two types of neural0reflex arcs?

A

Short reflexes and long reflexes

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75
Q

What is a short reflex?

A

From receptors through nerve plexuses to effector cells

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76
Q

What is a long reflex?

A

From receptors to CNS by afferent nerves, then back to nerve plexus and effector cells through autonomic neurons

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77
Q

Where do hormones for regulating GI activity come from?

A

Cells scattered in the stomach and SI

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78
Q

What stimulates endocrine cells to secrete regulatory hormones to the GI tract?

A

Chyme: if it touches the endocrine cell on the luminal side, the endocrine cell will secrete hormones to the basolateral side into the blood to reach target cells by circulation

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79
Q

What are the four GI hormones?

A

Secretin, cholecystokinin (CCK), gastrin, and glucose-dependent insulinotropic peptide (GIP)

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80
Q

What are the two generalizations of GI hormones?

A

They participate in feedback control to regulate one aspect of the GI environment, and they affect multiple kinds of target cells

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81
Q

What triggers CCK secretion into the blood from the SI?

A

Fatty acids and amino acids in the SI

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82
Q

What happens when CCK is released into the blood after being triggered by fatty acids and amino acids?

A

Stimulates the pancreas to increase digestive enzyme secretion; causes gallbladder to contract and deliver bile salts

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83
Q

What is potentiation?

A

How secretin (stimulates pancreatic bicarb secretion) and CCK (weak stimulus for pancreatic bicarb secretion) TOGETHER cause major secretion of bicarb: whole is greater than sum of parts

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84
Q

Why does potentiation for secretin and CCK exist?

A

Because even though CCK is a weak stimulus for bicarb secretion from the pancreas, it amplifies the stimulation of secretin

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85
Q

What is the point of potentiation?

A

Small changes in plasma concentration of one GI hormone can have large effects on the actions of other GI hormones

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86
Q

What is leptin?

A

Peptide hormone: released from adipose cells, influences good intake and metabolic rate; induces satiety

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87
Q

What is ghrelin?

A

Peptide hormone: released from stomach during fasting; induces hunger

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88
Q

What are incretins?

A

GI hormones that alter insulin secretion from pancreatic islet cells

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89
Q

Which of the four main GI hormones is an incretin?

A

GIP: glucose-dependent insulinotropic peptide

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90
Q

What are the three phases of neural and hormonal control of the GI system?

A

Cephalic, gastric, and intestinal

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91
Q

Gastrin: what kind of hormone, where produced, stimuli for release?

A

Peptide; stomach; AAs, peptides in stomach, parasympathetic nervous

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92
Q

CCK: what kind of hormone, where produced, stimuli for release?

A

Peptide; SI; AAs , FAs in SI

93
Q

Secretin: what kind of hormone, where produced, stimuli for release?

A

Peptide, SI; acid in small intestine

94
Q

GIP: what kind of hormone, where produced, stimuli for release?

A

Peptide; SI; glucose, fat in SI

95
Q

What factors inhibit gastrin release?

A

Acid in stomach; somatostatin

96
Q

Gastrin: how does it affect stomach acidity and motility?

A

Stimulates

97
Q

CCK: how does it affect stomach acidity and motility?

A

Inhibits

98
Q

Secretin: how does it affect stomach acidity and motility?

A

Inhibits

99
Q

How does CCK affect the pancreas activity?

A

Stimulates enzyme secretion; potentiates secretin’s effect on bicarb release

100
Q

How does secretin affect pancreas activity?

A

Stimulates bicarb release; potentiates CCK’s effect on enzyme secretion

101
Q

How does GIP affect pancreas activity?

A

Stimulates insulin secretion

102
Q

How do secretin and CCK affect liver activity?

A

Secretin stimulates bicarb secretion, and CCK potentiates it

103
Q

How does CCK affect gallbladder activity?

A

Stimulates gallbladder contraction

104
Q

How does CCK affect the sphincter of Oddi?

A

Relaxes it

105
Q

How does gastrin affect the SI and LI?

A

Stimulates ileum motility, and mass movement of LI

106
Q

What is the cephalic phase on GI regulation?

A

Initiated when receptors in head stimulated by sight/smell/taste/chewing

107
Q

What kinds of neurons are involved in the cephalic phase?

A

Parasympathetic fibers in vagus nerves: activate neurons in GI plexus to affect secretory/contractile activity

108
Q

What is the gastric phase of GI regulation?

A

Initiated by four stimuli: gastric distension, acidity, AAs, and peptides formed during digestion

109
Q

What kind of neurons are involved in the gastric phase?

A

Short and long neural reflexes; also affected by gastrin release

110
Q

What is the intestinal phase of GI regulation?

A

Initiated by stimuli in intestinal tract: distension, acidity, osmolarity, digestive products

111
Q

What kinds of neurons are involved in the intestinal phase?

A

Short and long neural reflexes; also affected by the four gastric hormones (secretin, gastrin, CCK, GIP)

112
Q

What four stimuli initiate the gastric phase?

A

Gastric distension, acidity, AAs, and peptides

113
Q

What four stimuli initiate the intestinal phase?

A

Gastric distension, chyme acidity, chyme osmolarity, and chyme concentration of digestive products

114
Q

How is chewing initiated?

A

Somatic nerves to skeletal muscles; mechanoreceptors in gums/hard palate/tongue –> reflexive inhibition of jaw muscles to cycle between contraction/relaxation

115
Q

What are the three pairs of salivary glands?

A

Parotid, sublingual, and submandibular

116
Q

How do sympathetic and parasympathetic nerves affect salivation?

A

Both stimulate salivary secretion, but parasympathetic has a great response

117
Q

What nerve stimulation causes swallowing?

A

Mediated by pressure receptors in pharynx: afferent impulses to swallowing center in medulla oblongata of brainstem; elicits swallowing by efferent fibers to muscles in pharynx/esophagus/respiratory muscles

118
Q

Why does pressure want to push contents into the esophagus down from the pharynx and up from the stomach?

A

Because there’s higher pressure in the pharynx (Patm)and in the stomach-end of the esophagus (supra Patm) than in the esophagus (sub Patm)

119
Q

Why isn’t contents pushed into the esophagus because of pressure differences?

A

Because of esophageal sphincters

120
Q

How does the composition of the two esophageal sphincters differ?

A

Upper is skeletal muscle, lower is smooth muscle

121
Q

Why can we swallow when upside down or without gravity?

A

Because peristaltic waves constitute the esophageal phase of swallowing

122
Q

What kind of nervous input allows the esophageal phase of swallowing?

A

Somatic nerves for upper sphincter, and autonomic nerves for lower sphincter; afferent fibers from esophagus to the swallowing center

123
Q

Where is the swallowing center?

A

Medulla oblongata of brainstem

124
Q

How does the lower esophageal sphincter stay closed even without swallowing?

A

Underneath the diaphragm: the abdominal pressure is the same on the esophagus and stomach

125
Q

Why is there sometimes heartburn in late pregnancy?

A

The fetus pushes the esophagus up above the diaphragm: no pressure maintenance for esophagus and stomach, so higher pressure on the stomach forces the sphincter open and allows gastric contents into the esophagus

126
Q

What is the fundus vs antrum of the stomach?

A

Upper and lower parts

127
Q

What substances are secreted by the body of the stomach?

A

Pepsinogen, mucus, and HCl

128
Q

Which half of the stomach has a thicker layer of smooth muscle?

A

The antrum: secrete less acid, but more gastrin

129
Q

What half of the stomach secretes less acid, but more gastrin?

A

The antrum

130
Q

What are parietal cells?

A

On gland wall: secrete acid and intrinsic factor (for B12)

131
Q

What are chief cells?

A

On gland wall: secrete pepsinogen

132
Q

Which cells secrete acid/intrinsic factor vs pepsinogen?

A

Parietal for acid/IF and chief for pepsinogen

133
Q

What are canaliculi?

A

Invaginations of the luminal membrane of parietal cells: increase surface area to maximize secretion

134
Q

What are enteroendocrine cells?

A

In the antrum: secrete gastrin

135
Q

What are enterochromaffin-like cells?

A

Release paracrine agent histamine

136
Q

What are D cells?

A

Secret somatostatin

137
Q

How is HCl produced in the stomach?

A

H/K ATPases pump H+ into lumen (K+ pumped out, but diffuses back in), and Cl- pumped in through Cl-/HCO3- countertransport, and then diffuses into lumen

138
Q

Where are the H+/K+ pumps in the stomach located?

A

In the parietal cells

139
Q

How does increased acid production occur?

A

By increased H+/K+ pump proteins being added to the parietal cell (fused from intracellular vesicles) to increase the number of pumps: like aquaporins for water permeability in the nephron!

140
Q

What four chemical messengers regulate H+/K+ pump increases?

A

Gastrin, ACh, histamine, and somatostatin

141
Q

What three kinds of cells are responsible for producing three of the four chemical messengers that increase acid production?

A

Enteroendocrine (gastrin), ECL (histamine), and D cells (somatostatin)

142
Q

Which of the four chemical messengers that affect acid production is inhibitory?

A

Somatostatin booooooooo

143
Q

Why is histamine really important for increasing acid production?

A

Potentiates the effect of gastrin and ACh

144
Q

What nervous system action mediates ACh release in parietal cells to stimulate H+/K+ pump addition to increase acid production?

A

Parasympathetic stimulation to stomach’s enteric system

145
Q

How does H+ affect gastrin and somatostatin secretion?

A

Inhibits, because already acidic enough; Stimulates, to reduce acid production

146
Q

Why does protein stimulate acid secretion?

A

Peptides stimulate acid secretion; protein is a buffer for H+, so protein decreases the H+ concentration, which decreases secretion inhibition

147
Q

How does duodenum acidity affect acid secretion? Why?

A

High duodenum acidity inhibits acid secretion by the stomach; because the activity of bile salts and enzymes is negatively impacted by acidity

148
Q

What are enterogastrones?

A

Hormones released by the intestinal tract that reflexively inhibit gastric activity: secretin and CCK

149
Q

When is pepsinogen converted to pepsin?

A

During exposure to low pH in the stomach; faster when pH is lower

150
Q

Why is it important for digestive enzymes to be zymogens?

A

Produced in inactive form: protects substrates from digestion, prevents damage to cells

151
Q

Why is pepsinogen neutralized in the SI?

A

The bicarb neutralizes the H+

152
Q

Why does pepsinogen secretion parallel acid secretion?

A

Because most of the factors that stimulate/inhibit acid secretion do the same for pepsinogen

153
Q

Why can the stomach “expand?”

A

Because the smooth muscles relax when food is about to enter: receptive relaxation

154
Q

How is receptive relaxation mediated?

A

Parasympathetic nervous input to enteric nerve plexuses; coordination provided by afferent input from stomach via vagus nerve and swallowing center in medulla oblongata; mediated by NO and serotonin from enteric neurons

155
Q

What two substances from the enteric neurons mediate receptive relaxation?

A

NO and serotonin

156
Q

What happens when the weak peristaltic wave reaches the thick antrum?

A

Gets stronger and produces powerful contraction to mix luminal contents and close the pyloric sphincter

157
Q

What is the pyloric sphincter for?

A

Closing the gap between the antrum and duodenum: only allows a small amount of chyme to enter the SI per peristaltic wave and contributes to mixing through backsplash

158
Q

What generates peristaltic waves in the stomach?

A

Pacemaker cells in longitudinal smooth muscle: spontaneous depo-repo cycles

159
Q

What is basic electrical rhythm of the stomach?

A

The spontaneous depo-repo cycles of the stomach’s smooth muscle that create peristalsis

160
Q

How are the slow waves of peristalsis conducted throughout the stomach?

A

Through gap junctions in the stomach’s longitudinal muscular layer, as well as through the stomach’s circular muscular layer

161
Q

What determines the frequency and strength of stomach contractile peristalsis?

A

Frequency determined by basic electric rhythm; Strength determined by number of action potentials generated at the peak of the slow-wave cycle , which is determined by neural and hormonal input to antral smooth muscle

162
Q

What factors inhibit gastric emptying?

A

Duodenum distension, presence of fat/acid/hypertonic solutions in the duodenum (also inhibit acid and pepsin secretion in the stomach) = prevents OVERFILLING of duodenum

163
Q

How does autonomic nerve fiber input affect gastric motility?

A

Input to stomach activated by CNS: increased in parasympathetic activity increases gastric motility

164
Q

How do parasympathetic and sympathetic input influence gastric motility?

A

Parasympathetic increases, sympathetic decreases

165
Q

Why does hypertonic duodenum lumen inhibit gastric emptying?

A

Too hypertonic lumen means too much water into the intestine: lowers blood volume and causes circulatory complications; intestinal distension can cause vomiting

166
Q

What is the difference in secretion of bicarb and digestive enzyme from the pancreas?

A

Bicarb is secreted from epithelial cells lining the pancreatic duct, and digestive enzymes are secreted from the pancreatic end of the duct system

167
Q

How is bicarb secreted by the pancreas?

A

Like H+ is secreted by the stomach except in reverse: H+ transported out of the cells by H+/K+ pump into blood, and bicarb secreted into the lumen

168
Q

What is enterokinase?

A

Enzyme in the luminal plasma of intestinal epithelial: proteolytic enzyme that splits peptide from pancreatic trypsinogen to form trypsin

169
Q

What is trypsin?

A

Proteolytic enzyme; activates pancreatic zymogens by splitting off a peptide; also digests ingested protein

170
Q

Why does pancreatic secretion increase during a meal?

A

Stimulation by secretin (for bicarb) and CCK (enzymes)

171
Q

Which four pancreatic enzymes digest proteins?

A

Trypsin, chemotrypsin, elastase (break peptide bonds) and carboxypeptidase (split terminal AA from carboxyl end of protein)

172
Q

What pancreatic enzyme digests fast?

A

Lipase: splits triglyceride into monoglyceride and two FAs

173
Q

What pancreatic enzyme digests carbs?

A

Amylase (splits polysaccharides into glucose and maltose)

174
Q

What pancreatic enzymes digest nucleic acids?

A

Ribonculease and deoxyribonuclease

175
Q

What is the major stimulus for bicarb release from the pancreas?

A

Acidity in the duodenum: BECAUSE its function is to neutralize the acid

176
Q

What is the major stimulus for digestive enzyme release from the pancreas?

A

Presence of FAs and AAs in the duodenum

177
Q

How do luminal acid and FAs activate their own digestion?

A

Act of afferent nerve endings in the intestinal wall to initiate reflexes to the pancreas to secrete enzyme and bicarb

178
Q

What kind of nerve input leads to increased pancreatic secretion during the cephalic and gastric stimuli?

A

Parasympathetic

179
Q

What are hepatic lobules?

A

Functional units of the liver

180
Q

What is a portal triad?

A

Branches of the hepatic artery/portal vein/bile duct at the periphery of each hepatic lobule

181
Q

From which two sources does the liver receive blood supply?

A

Hepatic portal vein (blood from SI to process absorbed nutrients), and hepatic arteries (bring oxygenated blood from aorta)

182
Q

How does blood leave lobules?

A

Blood drains into central veins that merge for form hepatic veins to empty into vena cava

183
Q

What are hepatic sinusoids?

A

Capillaries surrounding hepatocytes

184
Q

What are bile caniculi?

A

Small hepatocyte ducts that converge to form the common hepatic duct for bile transport

185
Q

What are the six main ingredients of bile?

A

Bile salts, lecithin, bicarb, cholesterol, pigments, and trace metals

186
Q

What is lecithin?

A

A phospholipid in bile: synthesized by liver: solubilize fat in the SI

187
Q

What happens to most of the bile salts in the intestine?

A

Absorbed by specific Na+ coupled transporters in the ileum, then transported through the portal vein to the liver

188
Q

In what portion of the SI are bile salts absorbed?

A

Ileum, through Na+ coupled transporters

189
Q

What drives the uptake of bile salts from portal blood into the hepatocyte, after it’s been absorbed from the ileum by Na+ coupled transporters into the portal vein?

A

Secondary active transport coupled to Na+

190
Q

What is enterohepatic circulation?

A

The recycling pathway of bile salts from the liver to SI to liver

191
Q

What is the predominant bile pigment?

A

Bilirubin: extracted from blood from damaged erythrocytes; yellowish color to bile and urine

192
Q

What are the two types of cells that product bile components, and which do they produce?

A

Hepatocytes (bile salts, cholesterol, lecithin, and pigments) and epithelail cells of bile ducts (bicarb)

193
Q

How does the liver produce cholesterol?

A

By extracting it from the blood or making it itself; when bile salts need to be replenished, reduces blood concentration of cholesterol

194
Q

When is bile secretion greatest?

A

During and just after a meal

195
Q

What stimulates secretion of salt solution from bile ducts?

A

Secretin in response to acid in the duodenum

196
Q

What happens when the sphincter of Oddi is closed?

A

Bile is shunted into the gallbladder for storage

197
Q

What is the signal for gallbladder contraction and sphincter relaxation?

A

CCK: because duodenum fat is a trigger for CCK release

198
Q

What is the primary ion for determining the magnitude of fluid secretion in the SI?

A

Cl-, controlled by hormonal and paracrine signals

199
Q

What amount of fluid secreted by the SI is absorbed back into the blood?

A

Basically all of it, following the absorption of ions from the lumen to the blood

200
Q

What is peristaltic segmentation?

A

In the SI: rhythmic contraction and relaxation of the intestine every few centimeters: for mixing and surface area contact

201
Q

What initiates segmentation peristalsis?

A

Pacemaker cells in circular smooth muscle layer: basic electrical rhythm produces membrane potential oscillations

202
Q

How does the basic electrical rhythm of the SI and stomach differ?

A

Stomach is constant (3/min), but for SI, the frequency varies along the intestine (as you go along, slower frequency)

203
Q

How does parasympathetic/sympathetic activity affect segmentation force?

A

Parasympathetic increases, sympathetic decreases

204
Q

What happens when segmentation peristalsis ends?

A

Peristaltic migrating myoelectrical complex activity (MMC) beings

205
Q

What is MMC activity?

A

Peristalsis continues for several feet and dies out, then starts again a little further down: moves all material to LI

206
Q

What hormone most likely initiates MMC?

A

Motilin by enteric and autonomic nervous systems

207
Q

What is the gastroileal reflex?

A

When segmentation intensity in the ileum increases during gastric emptying

208
Q

What is intestino-intestinal reflex?

A

When large distension of the intestine, injury, or infection leads to complete motility cessation

209
Q

What are the three parts of the LI?

A

Cecum, colon, rectum

210
Q

What is the ileocecal valve?

A

Sphincter between ileum and cecum: circular muscle innervated by sympathetic nerves

211
Q

What kind of nerves innervate the ileocecal valve?

A

Sympathetic

212
Q

What is the appendix?

A

Projection from the cecum, nonessential

213
Q

What is the colon?

A

Three segments: ascending, transverse, descending, sigmoid

214
Q

What is the difference in surfaces of the SI and LI?

A

Less surface area in LI because shorter, nonconvoluted, lacks villi

215
Q

What are the secretions of the LI?

A

Mucus, bicarb, and potassium

216
Q

What is the primary function of the LI?

A

Store and concentrate fecal material before defecation

217
Q

What is the primary absorptive process in the LI?

A

Reabsorption of water following active transport of Na+ out of the lumen

218
Q

Which way does K+ travel between blood and LI lumen?

A

Transported from blood to lumen, most likely through cAMP mediated process

219
Q

How does bicarb get secreted into the LI lumen?

A

By coupling with Cl- absorption form the lumen

220
Q

What happens to fiber in the LI?

A

Converted into short-chain fatty acids by bacteria, absorbed by passive diffusion (acidity neutralized be presence of bicarb); produces gas

221
Q

How does parasympathetic/sympathetic input affect colonic contractions?

A

Parasympathetic increases, sympathetic decreases

222
Q

What is a mass movement?

A

A wave of intense contraction of the LI, usually coinciding with gastroileal reflex (gastric emptying)

223
Q

What is the difference between internal and external anal sphincter?

A

Internal is smooth muscle, and external is skeletal and under voluntary control

224
Q

What is the defecation reflex?

A

Neurally mediated: initiated by mass movement of fecal material into the rectum; triggered by rectum distension

225
Q

What happens during the defecation reflex?

A

Initial contraction of external sphincter with relaxation of internal sphincter, increased sigmoid colon peristalsis

226
Q

Why doesn’t the high stomach acidity break down the stomach walls?

A

Musocal lining is alkalinic, and contains proteins that neutralize the H+ near the membrane; tight junctions prevent leakage to underlying structures; damaged cells are replaced quickly

227
Q

Where is the vomiting center located?

A

Medulla oblongata of brainstem

228
Q

What is the area postrema?

A

Outside blood-brain barrier; sensitive to toxins and initiates vomiting