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PHYSL214 > Gastrointestinal Physiology > Flashcards

Gastrointestinal Physiology Flashcards

1
Q

What are the four functions of the GI tract?

A
  1. Motility.
  2. Digestion.
  3. Absorption.
  4. Secretion.
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2
Q

What are the two purposes of motility in the GI tract?

A
  1. Movement of contents from mouth to anus.

2. Mixing of contents to facilitate digestion and absorption.

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3
Q

What is digestion?

A

Process of breaking down large particles of food and high-molecular-weight substances into smaller molecules.

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4
Q

What is absorption?

A

Movement of products of digestion across the intestinal epithelium into the body.

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5
Q

Where does absorption mostly occur?

A

In the proximal duodenum.

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6
Q

What is secretion?

A

Release of substances into the lumen of the GI tract, which facilitates digestion, absorption and motility.

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7
Q

What are the accessory organs?

A

The salivary glands, liver, pancreas, and gallbladder.

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8
Q

What is the epithelium?

A

The barrier of cells that nutrients must traverse to be absorbed into the body.

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9
Q

What are the functions of the capillaries and lymphatics in the submucosa layer?

A

Aiding in transport to and from the intestine.

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10
Q

What two layers make up the smooth muscle of the GI tract?

A

Circular and longitudinal layers.

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11
Q

What is the function of the myenteric plexus?

A

Control multiple (layer of nerves) aspects of motility and secretion

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12
Q

What is the function of the endocrine cells of the GI lumen?

A

Secrete hormones into blood that regulate digestion and appetite.

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13
Q

What is the function of exocrine cells in the GI lumen?

A

secrete substances into the lumen that aid digestion.

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14
Q

What are the six sphincters of the GI tract?

A

Upper esophageal, lower esophageal, pyloric, ileocecal, internal anal, external anal.

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15
Q

What are the three functions of the mouth?

A

Mastication (chewing), preparation for swallowing via saliva (moisten food bolus), onset of digestion (salivary amylase).

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16
Q

Describe the act of swallowing in 3 steps:

A

Oral phase: a voluntary collection of food bolus into the pharynx by the tongue to initiate involuntary reflex.

Pharyngeal phase: involuntary contraction of pharyngeal muscles to push food into esophagus, soft palate elevates to prevent backflow into nasal passage.

Esophageal phase: Bolus travels down the esophagus by peristaltic contraction, epiglottis covers the glottis to prevent flow of bolus into trachea.

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17
Q

What is the function of the stomach?

A

Storing ingested material, continuation of digestion, regulation of emptying into small intestine.

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18
Q

How does the stomach mechanically dissolve food bolus?

A

Folded surfaces (rugae) facilitate using peristaltic waves.

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19
Q

How does the stomach chemically digest food bolus?

A

HCl: denatures proteins and cleaves pepsinogen into pepsin.
Pepsin: enzyme that breaks down proteins.

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20
Q

What is chyme?

A

Ingested food that leaves the stomach.

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21
Q

What is the antrum?

A

Layer of stomach that contributes to digestion. Secretes pepsinogen, mucus, and gastrin.

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22
Q

What are the three sections of the small intestine?

A

Duodenum, jejenum, ileum.

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23
Q

How does the small intestine contribute to absorption?

A

Microvilli increase surface area to increase contact between intestinal contents and epithelium.

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24
Q

What is the function of the large intestine?

A

Functions to store and concentrate undigested material prior to its excretion.

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25
Q

What is the cecum?

A

The ‘pocket’ between the small intestine and the large intetsine. Responsible for digesting cellulose but is too small to do so in humans.

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26
Q

What is the appendix?

A

Branching appendage of the cecum, thought to be vestigial or haven for gut bacteria.

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27
Q

What are the 4 sections of the colon?

A

Ascending colon, transverse colon, descending colon, sigmoid colon.

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28
Q

What do the colon sections contribute to (functionality)

A

Absorption of ions, water, bacterial metabolism.

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29
Q

What is the general function of the accessory organs (GI)?

A

Secrete substances into the GI tract to aid in digestion.

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30
Q

What are the 3 salivary glans?

A

Parotid salivary gland, sublingual salivary gland, submandibular salivary gland.

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31
Q

What do the salivary glands secrete?

A

Water and mucus, and salivary amylase.

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32
Q

Where do the salivary gland secretions empty?

A

Into the oral cavity.

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33
Q

What does the liver secrete?

A

Bile salts (fat digestion), bicarbonate (neutralize chyme), organic waste product.

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34
Q

What does the gallbladder do?

A

Stores bile and concentrates it for release during feeding.

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35
Q

What do the liver and gallbladder have in common?

A

Both empty into the small intestine via the bile duct.

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36
Q

What is the exocrine function of the pancreas?

A

Acinar cells secrete into the small intestine via the pancreatic duct (bicarbonate, pancreatic amylase, trypsin, chymotrypsin, pancreatic lipase.)

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37
Q

What are the two general patterns of motility?

A

Peristalsis and segmentation.

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38
Q

How is peristalsis triggered?

A

Luminal contents stretching intestinal wall. Initiates circular contraction behind stimulant and relaxation in front of it.

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39
Q

Is peristalsis independent of extrinsic innervation?

A

Yes, but can be modulated.

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40
Q

Describe the activation and mechanism of peristalsis in 3 steps.

A
  1. Local stretch of receptors causes the release of serotinin. Increases 5HT activity activates sensory neurons that activate myenteric plexus.
  2. Neurons upsteam activate and cause smooth muscle contraction.
  3. Neurons downstream are activated (inhibited) to cause smooth muscle relaxation.
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41
Q

What factors in the myenteric plexus are responsible for smooth muscle contraction?

A

Substance P, Acetylcholine.

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42
Q

What factors in the myenteric plexus are responsible for smooth muscle relaxation?

A

Nitric oxide NO2, vasoactive intestinal polypeptide.

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43
Q

What is the function of segmentation?

A

Mixing of contents in situ without propelling luminal contents along the intestine.

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44
Q

What are the three steps of segmentation?

A
  1. Local contractions separate the intestine into pockets.
  2. Subsequent contractions divide pockets centrally (offset split contents).
  3. Rhythmic contractions continue to subdivide pockets and mix contents.
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45
Q

Where does segmentation primarily occur?

A

Small intestine.

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46
Q

Where does rhythmic contraction originate?

A

In pacemaker interstitial cells of Cajal; create underlying oscillations known as basic electrical rhythm BER.

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47
Q

What neurotransmitter increases BER activity?

A

Acetylcholine.

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48
Q

What neurotransmitter decreases BER activity?

A

Epinephrine.

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49
Q

What occurs after segmentation stops?

A

Sweeping wave contraction; myoelectric complex MMC.

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50
Q

What is the function of migrating myoelectric complex?

A

To move undigested material into the large intestine.

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51
Q

Where do MMC contractions start?

A

In the stomach.

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52
Q

What are the three phases of MMC?

A
  1. quiescent period.
  2. irregular electrical and mechanical activity.
  3. burst of regular electrical and mechanical activity.
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53
Q

How is MMC controlled?

A

Circulating levels of motilin, Increase triggers MMC.

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54
Q

When are motilin levels lowest?

A

During ingestion of a meal.

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55
Q

What are the three major components of the lower esophageal sphincter?

A
  1. Internal sphincter.
  2. External sphincter.
  3. Clasp and sling fibres.
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56
Q

What is the function of the lower esophageal sphincter?

A

Relaxes upon swallowing to allow food into the stomach, contracts in response to acetylcholine to prevent reflux of stomach contents into the esophagus.

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57
Q

Receptive relaxation

A

Stomach relaxes upon entrance of bolus in order to allow increase in stomach volume with marginal increase in pressure.

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58
Q

Describe gastric peristalsis

A

Wave initiates at upper part of stomach and increases in size as it moves down the stomach, mixing contents and forcing pyloric sphincter closed. Small volume of liquid chyme is forced through sphincter.

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59
Q

What are the 4 extrinsic factors of gastric emptying?

A
  1. Stomach and intestinal contents.
  2. Acidity.
  3. Distension.
  4. Hypertonicity.
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60
Q

How does stomach content affect gastric emptying?

A

Meals rich in protein or fat will delay gastric emptying.

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61
Q

How does acidity affect gastric emptying?

A

Exposure of duodenum to acidity inhibits gastric emptying via feedback loop.

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62
Q

How does distension affect gastric emptying?

A

Distension of stomach increases peristatic contracts and emptying. Distension of the duodenum inhibits emptying.

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63
Q

How does hypertonicity affect gastric emptying?

A

Emptying is fastest when duodenal contents are isotonic. Hypertonic solutions in the duodenum inhibit gastric emptying.

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64
Q

What is Belching?

A

Air is unavoidably swallowed during eating and drinking and is regurgitated by belching because air in the stomach increases gastric volume. The LES will relax and allow air to escape.

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65
Q

Vomiting

A

Involuntary expulsion of stomach contents caused by reverse peristalsis. Preceded by salivation to protect esophageal and mouth tissue. Glottis closes to prevent aspiration. Abdominal wall muscles contract to increase abdominal pressure.

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66
Q

What are vomitting triggers?

A

Digestive, sensory, emetics (induces vomiting), social cues, or miscellaneous (anxiety).

67
Q

Ileocecal valve

A

separates illeum and colon, is squeezed closed when colon pressure is high .

68
Q

Gastroileal reflex

A

Opens when food is released from stomach to make room in small intestine.

69
Q

Mass Action Contraction

A

Unique to the colon; 10/day, move feces forward. Simultaneous contractions of segments.

70
Q

Defecation

A

Increases in rectal pressure caused by MAC initiates reflex;

  1. Internal sphincter is under involuntary control via smooth muscles; relaxes under pressure.
  2. External sphincter in under voluntary control by skeletal muscles, contracts under pressure.
71
Q

What occurs at a certain high rectal pressure?

A

Reflex that triggers the involuntary relaxation on external anal sphincter, allows feces to be passed.

72
Q

How can defecation by delayed?

A

Voluntary contraction of external anal sphincter.

73
Q

What does prolonged distension of rectum initate?

A

Reverse movement that drives rectal contents into sigmoid colon.

74
Q

How can defecation be initiated?

A

Voluntary straining, contraction of abdominal muscles and relaxation of puborectalis to low the pelvic floor.

75
Q

How long does it take for a meal to pass through a healthy adult?

A

appx. 50 hours.

76
Q

What four general factors trigger gastrointestinal response?

A
  1. Volume.
  2. Osmolarity.
  3. Acidity.
  4. Nutrient composition.
77
Q

What is the receptor type and effector of each stimuli affecting gastrointestinal response?

A
  1. Volume = mechanoreceptors = smooth muscle.
  2. Osmolarity = osmoreceptors = exocrine glands.
  3. Acidity = chemoreceptors = exocrine glands.
  4. Nutrients = chemoreceptors = exocrine glands.
78
Q

What two neural reflex loops exist in the GI?

A
  1. Short reflex (within the wall of intestine myenteric plexus)
  2. Long reflex (travels to CNS)
79
Q

What is the short loop?

A

Stimulus is received by receptor, signal passed on to nerve plexus which activates a smooth muscle or gland to trigger a response.

80
Q

What is the long loop?

A

Stimulus in lumen is received by receptors and trigger a signals that travels through afferent neurons into the CNS.
Signal is modified by emotional state and/or hunger, before being conducted down efferent autonomic neurons to to nerve plexus. The nerve plexus then stimulates an effector cell to create a response.

81
Q

Enteroendocrine cells

A

Hormonal enteric cells (in stomach lining and pancreas)

82
Q

Gastrin: (site of prod, trigger, response in stomach, pancreas, liver, gallbladder)

A

Prod: stomach.
Trigger: amino acids/peptides.
Stomach: stimulates acid secretion and motility.
No response in liver, pancraes, or gallbladder.

83
Q

CCK: (site of prod, trigger, response in stomach, pancreas, liver, gallbladder)

A 
Prod: small intestine
Trigger: amino acids, fats.
Stomach: inhibits acid secretion and motility.
Pancreas: stimulates enzyme secretion.
Gall bladder: stimulates contraction.
No response in liver.
84
Q

Secretin (site of prod, trigger, response in stomach, pancreas, liver, gallbladder)

A

Prod: small intestine
Trigger: high acid
Stomach: inhibits acid secretion and motility.
Pancreas/Liver: stimulates bicarbonate secretion
No response in gall bladder

85
Q

GIP (site of prod, trigger, response in stomach, pancreas, liver, gallbladder)

A

Prod: small intestine
Stomach: no response
Pancreas: stimulates insulin secretion.
No response in gall bladder or liver.

86
Q

What are the three phases of GI regulation?

A
  1. Cepahlic
  2. Gastric
  3. Intestinal
87
Q

Where do majority of GI secretions come from?

A

Accessory glands

88
Q

What are the salivary secretions? Function?

A

Water, electrolytes, mucus, enzymes, immune modulators.

FXN: lubrication, digestion, immune response.

89
Q

How is salivary secretion primarily regulated?

A

In the cephalic phase by the parasympathetic system.

90
Q

What are the gastric secretion? FXN?

A

Mucus, HCl, enzymes, hormones.

FXN: lubrication, digestion, pepsin production, secretion of hormones into blood stream.

91
Q

Regulation of HCl production

A

Gastrin released from G-cells activates HCl production in parietal cells (in response to high fat/protein foods.)
Somatostatin released by D-cells in response to increase in stomach acidity inhibits the production of HCl.
HCl production is also stimulated by histamine at the H2 receptor, acetylcholine at the muscarinic receptor.

92
Q

Where is histamine secreted in the stomach?

A

From the ECL cell.

93
Q

Pancreatic secretions and functions.

A

Bicarbonate (neutralize acidity)

Enzymes (digestion)

94
Q

What are the two pancreatic cell types?

A
  1. Exocrine cells (secrete enzymes)

2. Duct cells (secrete bicarbonate)

95
Q

How is bicarbonate regulated?

A

Acid in stomach increases and triggers chemoreceptors that cause an increase in secretin secretion from the duodenum.
Plasma secretin increases as a result, which triggers a release of bicarbonate secretion from the pancreas.
Bicarbonate flows into small intestine and neutralizes intestinal acid.

96
Q

How are pancreatic enzymes regulated?

A
  1. Intestinal fatty acid and amino acids content increases.
  2. Small intestine secrets CCK.
  3. Plasma CCK increases.
  4. Pancreas secreted enzymes via common bile ducts.
  5. Enzymes flow into small intestine.
  6. Digestion of fats and protein in small intestine increases.
97
Q

Liver secretions and functions

A

Water
Bile salts (solubilize water-insoluble fats)
Bilirubin (hemoglobin breakdown product)
Fats (cholesterol)

98
Q

Where is dilute bile continuously produced?

A

The liver.

99
Q

Intestinal secretions and functions

A

Water/electrolytes (maintain fluidity)
Mucus (Lubrication)
Enzymes (aid digestion)

100
Q

What is water secretion into small intestine driven by?

101
Q

Crypts of Lieberkuhn

A

Invaginations that surround base of intestinal villi. Secretory cells that excrete ions that drive the flow of water into lumen.

102
Q

Lactose

A

Glucose and galactose

103
Q

Maltose

A

Glucose and Glucose

104
Q

What is the major energy source for humans?

A

Fat (triglycerides)

105
Q

Protein primary structure

A

Linear sequence of amino acids

106
Q

Secondary structure of protein

A

Alpha helices or beta sheet

107
Q

Tertiary structure of protein

A

3D structure formed by folding of polypeptide

108
Q

Quaternary structure of protein

A

Assembly of multiple polypeptides to form a complex

109
Q

Supramolecular protein assemblies

A

Protein complexes, myofilaments, etc.

110
Q

Amylase

A

Cleaves glycosidic bond between subunits of polysaccharides.

111
Q

Brush Border Ezymes

A

bound to brush border of the intestinal epithelium, hydrolyze multiple disaccharides

112
Q

How is glucose/galactose absorbed?

A

Secondary active transport via SLGT-1 transporter

1 molecule of glucose/galactose for every 2 sodium ions.

113
Q

GLUT2

A

Facilitated diffusion of glucose and galactose into interstitial space.

114
Q

How is fructose absorbed?

A

Facilitated diffusion by the GLUT5 and GLUT2 transporter.

115
Q

What are the three nondigestible polysaccharides

A

Cellulose, lignin, chitin.

116
Q

What is the fate of nondigestible polysaccharides?

A
  1. Delay of gastric emptying.
  2. Impaired absorbtion
  3. Fiber fermentation in colon.
  4. Fecal bulking.
117
Q

Emulsification

A

Breakdown of fat globules into droplets that are easier to digest into free fatty acids. Requires mechanical digestion and emulsifying agents in bile (phospholipids and bile salts).

118
Q

Lipolysis

A

Fat breakdown: emulsion droplets are acted upon by lipase enzymes from the pancreas, collapse of triglycerides into fatty acids.

119
Q

How is dietary fat absorbed?

A

Fatty acids and monoglycerides are taken up into epithelial cells and repackaged into triglycerides for secretion into circulation by chylomicrons.

120
Q

How is dietary protein digested?

A

Digestion mediated by proteolytic enzymes (proteases). Begins in stomach; highly acidic environment denatures proteins, The secretion of pepsin also cleaves large polypetides.
Digestion continues in the duodenum where pancreatic enzymes and the intestinal brush border enzymes cleave the proteins further into individual amino acids.

121
Q

How are pancreatic enzymes activated?

A

Activity of enterokinase and trypsin

122
Q

Enterokinase

A

Tethered to the intestinal epithelium, cleaves trypsinogen into trypsin.

123
Q

Trypsin

A

Cleaves other pancreatic proenzymes into activated forms.

124
Q

Where can protein digestion occur?

A
  1. Intestinal lumen
  2. Intestinal brush border
  3. Inside intestinal epithelial cells.
125
Q

How are dipeptides and tripeptides absorbed?

A

Secondary active transport by the transporter PepT1. Takes in one hydrogen per peptide.

126
Q

How do amino acids exit the epithelium?

A

Facilitated diffusion through amino acid transporters

127
Q

How is the proton gradient maintained in the intestinal epithelium during dipeptide/tripeptide absorbtion?

A

NHE transporter (sodium/hydrogen exchanger) exchanges an intracellular hydrogen for an extracellular sodium.

128
Q

How is the sodium gradient maintained in the intestinal epithelium during dipeptide/tripeptide absorbtion?

A

Sodium potassium ATPase pump.

129
Q

How are amino acids absorbed into the intestinal epithelium?

A

Relies on a sodium gradient (secondary active transport); amino acid is pulled into cell by accompanying a sodium ion moving with its gradient.

130
Q

Water soluble vitamins

A

Vitamin C

B complex vitamins

131
Q

Where are water soluble vitamins primarily absorbed?

A

First part of the small intestine. Mostly coupled to sodium co-transporters.

132
Q

Fat soluble vitamins

A

Vitamin A, D, E, and K

133
Q

How is iron absorbed?

A

Dietary iron is typically in the ferric form, but is reduced by reductase in the brush border its into ferrous form. DMT1 transporter facilitates diffusion into cell, where ferrous iron is bound to ferritin and transported into the circulation. Once in circulation, iron reverts to its ferric form.

134
Q

The liver receives blood supply from the _____, and venous drainage via the ____.

A
  1. Aorta.

2. Vena Cava.

135
Q

Hepatic Portal

A

The vein in which absorptive segments of the GI tract drain into. Leads to the liver.

136
Q

Hepatic lobules

A

Functional anatomy of the liver; contain the portal triad (portal vein, hepatic artery, bile duct) which nourishes hepatocytes, carries bile, and transports nutrients from GI.

137
Q

How does blood come in contact with hepatocytes?

A

Blood travelling through sinusoids can flow through gaps in the endothelial cells (fenestrations) entering the space of Disse.

138
Q

Liver’s role in carbohydrate metabolism

A

Glycogenesis, glycogenolysis, and gluconeogenesis.

139
Q

Liver’s role in lipid metabolism

A

Storage of triglycerides, energy production, lipoprotein secretion, lipogenesis.

140
Q

Function of CYP family

A

to detoxify xenobiotics and toxins through oxidation.

141
Q

How is ammonia generated?

A

Amino acid metabolism.

142
Q

How is ammonia metabolized?

A

Into urea and excreted through urine.

143
Q

How is bile secreted?

A

By hepatocyte into bile canaliculi, which drains it into bile ducts.

144
Q

Enterohepatic circulation

A

Circulation system between GI and liver, circulation of nutrients and bile.

145
Q

Bilirubin and biliverdin

A

Bile pigments produced when RBC are broken down in the liver. Bilirubin is bound to albumin which is metabolized into bilirubin glucuronide, easily transported for excretion.

146
Q

What is jaundice caused by?

A

Free or conjugated bilirubin in circulation is deposited into tissue casuing a yellow-ish appearance.

147
Q

Pre-hepatic jaundice

A

Increased breakdown of RBC

148
Q

Hepatic jaundice

A

Liver disease

149
Q

Post-hepatic jaundice

A

Obstruction of bile secretion

150
Q

How does the stomach not digest itself?

A

Mucosa layer contains bicarbonate, protects epithelial cells.

151
Q

What bacteria caused ulcers?

152
Q

How to diagnose ulcers

A

Medical history and physical exm
Laboratory test for H. Pylori
Endoscopy
Barium mean (x-ray)

153
Q

Treatment of ulcers

A

Antibiotics (if H.pylori positive)
Antacids
Proton pump inhibitor
Histamine blockers (H2)

154
Q

What are the two forms of gallstones?

A

Cholesterol, calcium bilirubinate

155
Q

How are cholesterol stones formed?

A

The concentration of cholesterol in bile increases to point of precipitation. Becomes “super-saturated”

156
Q

Where do larger gallstones get stuck?

A

Inside gallbladder. May cause pain but no consequence of digestion; bile from liver will move directly to duodenum.

May get stuck in common bile duct, meaning bile secretion is impaired.

May get trapped in ampulla of vater, block all secretions.

157
Q

How to diagnose gallstones

A

Medical history and physical exam
Ultrasound
CT scan

158
Q

How to treat gallstones

A

Medication that dissolves gallstones (bile salt)

Surgical removal of gallbladder

159
Q

Causes of colitis

A

Infection, IBD, allergic reaction, ischemia.

160
Q

Colitis

A

Inflammation of inner lining of colon

161
Q

What bacteria is found in colitis infections?

A

C. difficile.

162
Q

What can colitis lead to?

A

Failure to trigger an immune response; multiple organ dysfunction.

163
Q

Colitis treatment

A

Antibiotic therapy.

**Fecal microbiota transplant

PHYSL214 (5 decks)

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