Brs Gastro Physiology Set

Front 1

What is the function of the epithelial cells in the gastrointestinal (GI) tract?

Back 1

Epithelial cells are specialized in different parts of the GI tract for secretion or absorption.

Front 2

contraction of circular smooth muscle in GI tract?

Back 2

decrease in diameter

Front 3

actions of gastrin?

Back 3

(G cells of antrum) inc'd gastric H+; stim growth of gastric mucosa

Front 4

What are the structural components of the GI tract?

Back 4

Epithelial cells
Muscularis mucosa
Circular muscle
Longitudinal muscle
Submucosal plexus (Meissner's plexus) and myenteric plexus

Front 5

What are the different types of muscle in the GI tract? What are their functions?

Back 5

Muscularis mucosa: contraction causes a change in the surface area for secretion or absorption.
Circular muscle: contraction causes a decrease in diameter of the lumen of the GI tract.
Longitudinal muscle: contraction causes shortening of a segment of the GI tract.

Front 6

contraction of longitudinal smooth muscle in GI tract?

Back 6

shortening

Front 7

what stimulates release of gastrin?

Back 7

sm peptides, amino acids in stomach lumen; stomach distention; vagus (via GRP)

Front 8

How is the epithelium of the GI tract specialized?

Back 8

Different regions are specialized for secretion or absorption

Front 9

What consists of the enteric nervous system of the GI tract? Where are they located?

Back 9

Submucosal plexus (Meissner's): between submucosa and circular muscle
Myenteric plexus (Auerbach's): between circular and longitudinal muscle

Front 10

Extrinsic Innervation of GI tract?

Back 10

PNS and SNS

Front 11

where is CCK from?

Back 11

I cells of duodenum

Front 12

What does the muscularis mucosa do?

Back 12

Contraction causes a change in the surface area for secretion or absorption

Front 13

What innervates the GI tract?

Back 13

Extrinsic innervation: para and sympathetic nervous systems
Intrinsic innervation: enteric nervous system

Front 14

Intrinsic Innervation of GI tract?

Back 14

Myenteric Plexus and Meissner's Plexus

Front 15

5 actions of CCK

Back 15

1. stim gallbladder contraction and Oddi relaxation; 2) stim pancreatic enzyme secretion; 3) potentiates secretin-induced stim of pancreatic bicarb secretion; 4) stim growth of exocrine pancrease; 5) inhibits gastric empyting

Front 16

What does the circular muscle of the GI tract do?

Back 16

Causes the lumen to decrease in diameter

Front 17

What makes up the parasympathetic nervous system of the GI tract? What structures do they innervate?

Back 17

Vagus nerve innervates the esophagus, stomach, pancreas, and upper large intestine.
Pelvic nerve innervates the lower large intestine, rectum, and anus.

Front 18

PNS is usually (1) on GI tract.

PNS innervation of GI tract is via (2) and (3) nerves.

Back 18

1 = excitatory
2 = vagus
3 = pelvic

Front 19

what stimulates release of CCK from duodenum?

Back 19

small peptides, amino acids; fatty acids and monoglycerides (not TGs b/c can't cross intestinal membrane)

Front 20

What does the longitudinal muscle of the GI tract do?

Back 20

Shortens a segment of the GI tract

Front 21

What does the intrinsic innervation control?

Back 21

Myenteric plexus: primarily controls the motility of the GI smooth muscle.
Submucosal plexus: primarily controls secretion and blood flow.

Front 22

PRE PNS fibers synapse in (1); POST PNS fibers leave (2) and innervate (3), (4) and (5).

Back 22

1 = myenteric and meissners plexus
2 = myenteric and meissners plexus
3 = smooth muscle
4 = secretory cells
5 = endocrine cells

Front 23

actions of secretin?

Back 23

1. stim pancreatic bicarb (potentiated by CCK) and inc'd growth of exocrine pancrease; 2) stim bicarb and H2O secretion by liver and inc'd bile production; 3) inhibits H+ by gastric parietal cells

Hint 23

None

Front 24

What are the functions of the submucosal plexus and the myenteric plexus?

Back 24

These make up the enteric nervous system of the gut
They integrate the motility, secretory, and endocrine functions of the GI tract

Front 25

What are the four "official" GI hormones?

Back 25

Gastrin
Cholecystokinin (CCK)
Secretin
Glucose-dependent insulinotropic peptide (GIP)

Front 26

PNS vagus nerve innervates what part of the GI tract? (4)

Back 26

1 - esophagus
2- stomach
3 - pancreas
4 - upper large intestine

Front 27

what stimulates release of secretin from S cells of duodenum?

Back 27

H+ and fatty acids in duodenum

Front 28

What is another name for the submucosal plexus?

Back 28

Meissner's plexus

Front 29

What are the actions of gastrin?

Back 29

1) Increases H+ secretion by the gastric parietal cells
2) Stimulates growth of gastric mucosa by stimulating the synthesis of RNA and new protein.

Front 30

PNS pelvic nerve innervates what part of the GI tract? (3)

Back 30

1 - lower large intestine
2 - rectum
3 - anus

Front 31

actions of GIP (gastric inhibitory peptide)

Back 31

1. stimulates insulin release (this is why oral glucose better!) 2. inhibits H+ secretion

Front 32

What is another name for the myenteric plexus?

Back 32

Auerbach's plexus

Front 33

What changes are seen in patients with gastrin-secreting tumors?

Back 33

Patients with gastrin-secreting tumors have hypertrophy and hyperplasia of the gastric mucosa, due to the stimulation of RNA and protein synthesis by gastrin.

Front 34

SNS is usually (1) on GI tract.

SNS originate from (2).

PRE SNS synapse on (3).
POST SNS synapse on (4).

Back 34

1 = inhibitory
2 = T8-L2 in spinal cord
3 = prevertebral ganglion (Ach)
4 = myenteric and meissners plexus (NE)

Front 35

what stimulates release of GIP from K cells?

Back 35

fatty acids, amino acids, oral glucose (only GI hormone that responds to fat, protein, and carbs!)

Front 36

Is the parasympathetic nervous system generally inhibitory or excitatory in the GI tract?

Back 36

Excitatory

Front 37

Where is gastrin secreted from? What is the stimuli for the secretion of gastrin?

Back 37

Gastrin is secreted from G cells of the gastric antrum.
Gastrin is secreted in response to:
a) small peptides and amino acids in the lumen of stomach
b) Distention of the stomach
c) Vagal stimulation, mediated by gastrin-releasing peptide (GRP)

Front 38

Intrinsic Innveration of GI tract?

Consists of (1) reflexes that relay information within (2)

Back 38

enteric nervous system:
- myenteric plexus
- meissner's plexus
1 = local
2 = GI tract

Front 39

what inhibits release of somatostatin?

Back 39

vagal stimulation

Front 40

What nerves convey parasympathetic fibers to the gut?

Back 40

The vagus and pelvic nerves

Front 41

What inhibits gastrin secretion?

Back 41

H+ in the lumen of the stomach inhibits gastrin release (negative feedback).
Somatostatin inhibits gastrin release.

Front 42

Myenteric Plexus aka. (1), is located between (2) and primarily controls (3)

Back 42

1 - Auerbach plexus
2 - outer long. and inner circular smooth mm.
3 - GI motility

Front 43

effect of His on GI

Back 43

increased H+ secretion directly and indirectly by potentiating effects of gastrin and vagal stim

Front 44

Where do parasympathetic fibers synapse in the gut?

Back 44

Both the submucosal and myenteric plexuses

Front 45

What is CCK homologous to? Where does the biologic activity of CCK arise from?

Back 45

CCK is homologous to gastrin (the five C-terminal amino acids are the same).
The biologic activity of CCK resides in the C-terminal heptapeptide.

Front 46

Meissner's Plexus aka (1), is located between (2) and primarily controls (3)

Back 46

1 - submucosal plexus
2 - inner circular mm and submucosa
3 = GI secretion and blood flow

Front 47

actions of VIP?

Back 47

relaxation of GI smooth mm (LES!); stimulate pancreatic bicarb; inhibits H+

Front 48

What specific structures are innervated by the vagus nerve?

Back 48

Esophagus
Stomach
Pancreas
Upper large intestine

Front 49

What are the actions of CCK?

Back 49

1) stimulates contraction of the gallbladder and simultaneously causes relaxation of the sphincter of Oddi for secretion of bile.
2) stimulates pancreatic enzyme secretion.
3) Potentiates secretin-induced stimulation of pancreatic HCO3- secretion.
4) Stimulates growth of the exocrine pancreas.
5) Inhibits gastric emptying

Front 50

What are the 4 "official" GI hormones?

Back 50

gastrin
CCK
secretin
glucose-dependent insulinotropic peptide (GIP)

Front 51

basal electric rhythm of a) stomach b) duodenum c) ileum

Back 51

a) 3 Hz; b) 12 Hz; c) 8-9 Hz

Front 52

What are vagovagal reflexes?

Back 52

Reflexes where both the afferent and efferent pathways are contained in the vagus nerve

Front 53

Where is CCK released from?
What are the stimuli for release of CCK? Why do TGs not stimulate CCK release?

Back 53

CCK is released from the I cells of the duodenal and jejunal mucosa by:
1) small peptides and amino acids
2) Fatty acids and monoglycerides.

Triglycerides do not stimulate the release of CCK because they cannot cross intestinal cell membranes.

Front 54

All of the biological activity of Gastrin resides in (1).

Back 54

1 - last 4 CT amino acids

Front 55

gastroileal reflex?

Back 55

food in stomach--> increased peristalsis in ileum and relaxation of ileocecal sphincter

Front 56

What specific structures are innervated by the pelvic nerve?

Back 56

Lower larger intestine
Rectum
Anus

Front 57

What are the actions of secretin?

Back 57

Secretin reduces the amount of H+ in the lumen of the small intestine.
1) Stimulates pancreatic HCO3- secretion and increases growth of the exocrine pancreas. Pancreatic HCO3- neutralizes H+ in the intestinal lumen.
2) Stimulates HCO3- and H2O secretion by the liver, and increases bile production.
3) Inhibits H+ secretion by gastric parietal cells.

Front 58

Gastrin is produced in (1) as little gastrin with (2) amino acids

Back 58

1 = G cells of stomach (antro-duodenal cells)
2 = 17 aa

Front 59

gastrocolic reflex?

Back 59

food in stomach--> increased colon motility and frequency of mass movements

Front 60

Is the sympathetic nervous system generally inhibitory or excitatory in the GI system?

Back 60

Inhibitory

Front 61

Where is secretin released from?
What are the stimuli for secretin release?

Back 61

Secretin is released by the S cells of the duodenum in response to:
1) H+ in the lumen of the duodenum
2) Fatty acids in the lumen of the duodenum

Front 62

ACTIONS OF GASTRIN

increases (1)
stimulates growth of (2)

Back 62

1 = gastric acid secretion
2 = growth of gastric mucosa

Front 63

composition of saliva

Back 63

high K+, HCO3-; low NaCl (hypotonic, unless made rapidly); alpha amylase, lingual lipase, kallikrein

Front 64

What is the pathway of sympathetic innervation?

Back 64

Fibers originate between T8 and L2
Synapse in the prevertebral ganglia
Synapse in the myenteric and submucosal plexuses, as well as directly upon blood vessels and smooth muscle
Cell bodies in the plexuses send information to smooth muscle, secretory, and endocrine cells

Front 65

What are the actions of glucose-dependent insulinotropic peptide (GIP)?

Back 65

1) Stimulates insulin release from the pancreas in the presence of an ORAL glucose load (oral glucose is more effective than IV in causing insulin release).
2) Inhibits H+ secretion by gastric parietal cells.

Front 66

Main Stimuli for Secretion of Gastrin?
- small peptides/amino acids esp. (1)
- stomach (2)
- vagal stimulation via (3)

Back 66

1 = Phe, Trp
2 = distension of stomach
3 = GRP (gastrin-releasing peptide) --> not blocked by atropine

Front 67

parasympathetic regulation of saliva production?

Back 67

CN VII, IX (via muscarinic R IP3 or Ca); inc'd production

Front 68

What does the enteric nervous system do?

Back 68

Coordinates and relays information from the parasympathetic and sympathetic systems to the GI tract
Uses local reflexes to relay information within the GI tract
Controls most GI activity, especially motility and secretion, even if there is no extrinsic innervation?

Front 69

Where is GIP released from? What are the stimuli for GIP release?

Back 69

GIP is secreted by the duodenum and jejunum.
GIP is the only GI hormone released in response to fat, protein, and carbohydrate.

Front 70

INHIBITION OF GASTRIN

negative feedback from (1)
hormone (2)

Back 70

1 = H+ in lumen of stomach
2 = somatostatin

Front 71

sympathetic regulation of saliva production

Back 71

increased production, via beta adrenergic stim (cAMP)

Front 72

What is the extrinsic innervation of the gut?

Back 72

Sympathetic and parasympathetic nervous system

Front 73

What are the GI paracrine enzymes? What are their functions?

Back 73

Somatostatin: inhibits the release of all GI hormones
Histamine: increases gastric H+ secretion

Front 74

Zollinger-Ellison Syndrome

Back 74

tumors of pancreas or duodenum that release gastrin
- excessive gastric acid secretion

Front 75

composition of aq part of pancreatic secretions?

Back 75

always ISOTONIC, more bicarb than in plasma; if low flow rate--high Na Cl; if high flow rate--high Na HCO3-

Front 76

What is the intrinsic innervation of the gut?

Back 76

Enteric nervous system

Front 77

What are the GI neurocrines? What are their functions?

Back 77

VIP: produces relaxation of the GI smooth muscle (including the lower esophageal sphincter); stimulates pancreatic HCO3- secretion and inhibits gastric H+ secretion.
GRP (bombesin): stimulates gastrin release from G cells.
Enkephalins: stimulate contraction of GI smooth muscle; inhibit intestinal secretion of fluid and electrolytes.

Front 78

CCK is homologous to (1) with the same (2) but the biological activity of CCK depends on the (3)

Back 78

1 = gastrin
2 = 5 terminal CT amino acid residues
3 = CT heptapeptide

Front 79

what does sucrase do?

Back 79

degrades sucrose to glucose and fructose

Front 80

What does the myenteric plexus do?

Back 80

Controls motility of GI smooth muscle

Front 81

What are slow waves?
Where do they originate from?

Back 81

Oscillating membrane potentials that occur spontaneously in the GI tract.
They originate from the interstitial cells of Cajal, the pacemaker of the GI smooth muscle.

Front 82

CCK is produced by (1) in the (2).

Back 82

1 = I cells
2 = duodenal and jejunal mucosa

Front 83

what does SLGT 1 in intestine do?

Back 83

transports glucose and galactose into cells, Na+-dependent

Front 84

What does the submucosal plexus do?

Back 84

Controls secretion and blood flow
Receives sensory information from chemoreceptors and mechanoreceptors

Front 85

What is the lowest frequency of slow waves/contractions? Highest frequency?

Back 85

Stomach: 3 slow waves/min
Duodenum: 12 slow waves/min

Front 86

What stimulates secretion of CCK? (2)

Back 86

1 - small peptides and amino acids
2 - fatty acids and monoglycerides

Front 87

how is fructose transported into intestinal cells?

Back 87

facilitated diffusion

Front 88

What are GI hormones?

Back 88

Substances that are released from endocrine cells in the GI mucosa that travel via the portal circulation to systemic circulation, and then exert a physiologic action upon target cells

Front 89

Where does the swallowing reflex originate?

Back 89

The swallowing reflex is coordinated in the medulla. Fibers in the vagus and glossopharyngeal nerves carry information between the GI tract and the medulla.

Front 90

ACTIONS of CCK
- stimulates contraction of (1) and relaxation of (2)
- increases pancreatic (3) and (4) secretion
- stimulates growth of (5)
- inhibits (6)

Back 90

1 = gallbladder
2 = Sphincter of Oddi
3 = pancreatic enzyme
4 = HCO3-
5 = exocrine pancreas
6 = gastric emptying

Front 91

optimum pH for pepsin activity?

Back 91

1-3 (in pH>5, denatures)

Front 92

What are the GI hormones?

Back 92

Gastrin
Cholecystokinin (CCK)
Secretin
Glucose-dependent insulinotropic peptide (GIP)

Front 93

What is "receptive relaxation"? What GI hormone participates in this?

Back 93

"Receptive relaxation" is a vagovagal reflex that is initiated by distention of the stomach and is abolished by vagotomy.
The orad region of the stomach relaxes to accomodate the ingested meal.
CCK participates by increasing the distensibility of the orad (top) stomach.

Front 94

Secretin is homologous to (1).

Which aa are necessary for biologic action of secretin? (2)

Back 94

1 = glucagon
2 = ALL aa are necessary

Front 95

(hypothetical) deficiency of enterokinase--> ?

Back 95

no activation of pancreatic proteases b/c it converts tyrpsinogen into trypsin and tryspin then cleaves all the others

Hint 95

None

Front 96

What are the types of gastrin, and what is the difference?

Back 96

Little gastrin -- 17 amino acids, secreted in response to a meal
Big gastrin -- 34 amino acids, not a dimer of little gastrin

Front 97

What is the gastrocolic reflex?

Back 97

The presence of food in the stomach increases the motility of the colon and increases the frequency of mass movements.

Front 98

Secretin is produced in (1).

Back 98

S cells of duodenal-jejunal mucosa

Front 99

why might hypersecretion of gastrin cause steatorrhea?

Back 99

low duodenal pH inactivates pancreatic lipase

Front 100

Where is the biologic activity of gastrin located?

Back 100

The 4 C' amino acids

Front 101

What are the functions of saliva?

Back 101

1) Initial starch digestion by α-amylase (ptyalin) and initial triglyceride digestion by lingual lipase
2) Lubrication of the ingested food by mucus
3) Protection of the mouth and esophagus by dilution and buffering of ingested foods.

Front 102

What are the stimuli for secretion of secretin? (2)

Back 102

1 = H+ in lumen of duodenum
2 = fatty acids in lumen of duodenum

Front 103

what would a lack of apoprotein B do in intestine?

Back 103

cause steatorrhea b/c apo B necessary for transporting chylomicrons out of intestinal cells

Front 104

What does gastrin do?

Back 104

Stimulates HCl secretion by parietal cells
Stimulates growth of the gastric mucosa by stimulating the synthesis of RNA and new protein

Front 105

What is the composition/characteristics of saliva?

Back 105

1) High volume
2) High K+ and HCO3- concentrations
3) Low Na+ and Cl- concentrations
4) Hypotonicity
5) Presence of α-amylase, lingual lipase, and kallikrein.

Front 106

ACTIONS of Secretin

- stimulates pancreatic and hepatic (1) secretion
- (2) bile production
- increases growth of (3)
- inhibits (4)

Back 106

1 - HCO3-
2 - stimulates bile production
3 - exocrine pancreas
4 - gastric H+ secretion

Front 107

what happens to K+ in GI?

Back 107

dietary K+ absorbed paracellularly; activly secreted in colon (similar to in kidney)

Hint 107

None

Front 108

What is observed in patients with gastrin-secreting tumors?

Back 108

Hypertrophy and hyperplasia of the gastric mucosa

Front 109

What determines the composition of saliva?

Back 109

The salivary flow rate. The higher the flow rate, the more saliva resembles plasma.

Front 110

GIP is homologous to (1) and (2).

GIP is secreted by (3)

Back 110

1 = glucagon
2 = secretin
3 = duodenum and jejunum

Front 111

how does Vibrio Cholerae cause diarrhea?

Back 111

toxin binds R in luminal membrane, activates AC which causes increase cAMP--> lumenal Cl- channels open. Na and H2O follow Cl--> secretory diarrhea!!

Front 112

Where is gastrin produced?

Back 112

G cells in the antrum of the stomach

Front 113

What are the three glands that produce saliva?

Back 113

Parotid
Submandibular
Sublingual

Front 114

What stimulates release of GIP? (what's so special about this hormone)

Back 114

FAT, PROTEIN and CARB

- the only hormone to respond to all 3

Front 115

What causes gastrin to be produced?

Back 115

Small peptides and amino acids in the lumen of the stomach
Stomach distention
Vagal stimulation mediated by gastrin-releasing peptide (GRP)

Front 116

How is saliva formed? What effect does aldosterone have?

Back 116

The acinus produces an initial saliva with a composition similar to plasma (same concentrations of Na, K, Cl, HCO3).
The ducts modify the initial process by:
reabsorbing Na and Cl, and secreting K and HCO3.

Aldosterone acts on the ductal cells to increase the reabsorption of Na and secretion of K (like in the renal distal tubule).

Front 117

ACTION of GIP
- stimulates (1)
- inhibits (2)

Back 117

1 - insulin secretion (oral glucose load is more effective)
2 - gastric H+ secretion

Front 118

What amino acids are the most important gastrin secretagogues?

Back 118

Phenylalanine
Tryptophan

Front 119

What regulates saliva production?

Back 119

Saliva production is increased by both sympathetic and parasympathetic activity. Parasympathetic stimulation (CN VII and IX) is more important though.

Front 120

What is the stimulus for somatostatin secretion?

Back 120

- H+ in lumen of GI tract

Front 121

Why doesn't atropine block vagally mediated gastrin secretion?

Back 121

The mediator of the vagal effect (the neurotransmitter, if you will) is GRP, not ACh

Front 122

What is the sympathetic innervation of salivary glands?

Back 122

Sympathetic receptors on acinar and ductal cells are β-adrenergic.

Front 123

What inhibits somatostatin release?

Back 123

somatostatin release is inhibited by VAGAL stimulation (PNS)

Front 124

What inhibits gastrin secretion?

Back 124

H in the stomach lumen
Somatostatin

Front 125

What are the gastric cell types, and what do they secrete?

Back 125

Parietal cells, located in the body: secrete HCl and intrinsic factor.
Chief cells, located in the body: secrete pepsinogen.
G cells, located in the antrum: secrete gastrin

Front 126

Main action of somatostatin is? (2)

Back 126

1 = inhibits release of ALL GI hormones
2 = inhibits gastric H+ secretion

Front 127

What is Zollinger-Ellison syndrome?

Back 127

Gastrinoma
Gastrin is secreted by non-B cell tumors of the pancreas

Front 128

What is the mechanism of gastric H+ secretion?

Back 128

In parietal cells, CO2 and H2O are converted to H+ and HCO3- via carbonic anhydrase.
H+ is secreted into lumen of stomach by H-K ATPase. Cl is secreted along with H; thus the secreted product is HCl. HCO3- in the cells is absorbed into bloodstream in exchange for Cl- (Cl-HCO3 exchange)

Front 129

Where is histamine secreted in the GI tract? (1)

Histamines increases (2)

Back 129

1 = mast cells of gastric mucosa
2 = gastric H+ secretion (direct, and potentiates effects of gastrin and vagal stimulation)

Front 130

How does the structure of CCK compare to that of gastrin?

Back 130

33 amino acids
Homologous to gastrin
Shares the same C' 5 amino acids with gastrin

Front 131

What stimulates gastric H+ secretion?

Back 131

a) Vagal stimulation (via ACh at M3 receptors; via GRP at G cells)
b) Gastrin
c) Histamine
d) Potentiating effects of ACh, histamine, and gastrin

Front 132

VIP is homologous to (1) and is considered a (2) hormone.

Back 132

1 = secretin
2 = neurocrine hormone (released from neurons)

Front 133

Where is the biologic activity of CCK located?

Back 133

The C' 5 amino acids

Front 134

Where is histamine released from? What is its effect?

Back 134

Histamine is released from enterochromaffin-like (ECL) cells in the gastric mucosa and diffuses to the nearby parietal cells.
Histamine stimulates H+ secretion by activating H2 receptors on parietal cells.

Front 135

VIP produces (1), stimulates (2) and inhibits (3).

These actions resemble (4) hormone.

Back 135

1 = relaxation of GI smooth muscle
2 = HCO3- secretion from pancreas
3 = gastric H+ secretion

Front 136

Why does CCK have some of gastrin's activity in addition to its own function?

Back 136

It contains the biologically active gastrin motif

Front 137

What inhibits gastric H+ secretion?

Back 137

a) Low pH (<3.0) in stomach
b) Somatostatin
c) Prostaglandins

Front 138

What hormone mediates pancreatic cholera?

Back 138

VIP (vasoactive intestinal peptide)

Front 139

What does CCK do?

Back 139

Stimulates contraction of the gallbladder to release bile
Relaxes the sphincter of Oddi
Stimulates growth of the exocrine pancreas
Inhibits gastric emptying

Front 140

What are the protective factors (against acid) in the gastric mucosa?

Back 140

Mucus, HCO3-, prostaglandins, mucosal blood flow, and growth factors.

Front 141

GRP aka (1) is released from (2) that innervate G cells.

GRP stimulates (3)

Back 141

1 = bombesin
2 = vagal nerve endings
3 = gastrin release (from G cells)

Front 142

What causes CCK to be released?

Back 142

Small peptides and amino acids in the intestinal lumen
Fatty acids and monoglycerides

Front 143

What is the difference between gastric and duodenal ulcers, besides the location?

Back 143

Gastric H+ secretion is increased in duodenal ulcers, as opposed to gastric ulcers in which H+ secretion is decreased (secreted H+ leaks back through the damaged gastric mucosa).

Front 144

Enkephalins stimulate contraction of (1) particularly the (2); and inhibit (3).

Back 144

1 = contraction of GI smooth mm.
2 = pyloric, ileocecal and LES sphincters
3 = intestinal secretion of fluid and electrolytes

Front 145

Where is CCK produced?

Back 145

I cells of the duodenal and jejunal mucosa

Front 146

What is the composition/characterization of pancreatic secretion?

Back 146

1) High volume
2) Same Na and K concentrations as plasma
3) Much higher HCO3- concentration than plasma
4) Much lower Cl- concentration than plasma
5) Isotonicity
6) Pancreatic lipase, amylase, and proteases

Front 147

The action of opiates to treat diarrhea is mediated by ?

Back 147

enkephalins

Front 148

Why don't triglycerides stimulate CCK release?

Back 148

They cannot cross intestinal cell membranes

Front 149

What determines the composition of the aqueous component of pancreatic secretions?

Back 149

Flow rate.
At low flow rates, pancreatic secretions is mainly Na and Cl.
At high flow rates, it is mainly Na and HCO3-.
Regardless of rate, pancreatic secretions are isotonic.

Front 150

Striated muscle in the GI tract is located in ... (3) areas?

Back 150

1. upper 1/3 of esophagus
2. pharynx
3. external anal sphincter

Front 151

What are the important structural features of secretin?

Back 151

27 amino acids
Homologous to glucagon
All amino acids are required for activity

Front 152

What stimulates the pancreatic secretions? Where do these stimulations arise from?

Back 152

Secretin: secreted by S cells of duodenum in response to H+.
CCK: secreted by I cells of the duodenum in response to small peptides, amino acids, and fatty acids.
ACh (via vagovagal reflexes): released in response to H+, small peptides, amino acids, and fatty acids.

Front 153

Phasic contractions of GI smooth mm. occur in ... (3) areas?

Back 153

1. esophagus
2. stomach
3. small intestine

Front 154

What does secretin do?

Back 154

Stimulates pancreatic bicarbonate secretion
Promotes growth of the exocrine pancreas
Stimulates bicarbonate and water secretion by the liver
Increases bile production
Inhibits acid secretion by parietal cells

Front 155

What is the composition of bile?

Back 155

Bile contains bile salts, phospholipids, cholesterol, and bile pigments (bilirubin).

Front 156

Tonic contractions occur in .... (4) areas?

Back 156

1. lower esophageal sphincter
2. orad stomach
3. ileocecal sphincter
4. internal anal sphincter

Front 157

What stimulates secretin release?

Back 157

H in the duodenal lumen
Fatty acids in the duodenal lumen

Front 158

What substances cause the contraction of the gallbladder?

Back 158

CCK
ACh

Front 159

Pacemaker cells for GI smooth muscle?

Back 159

Interstitial Cajal cells

Front 160

What hormones is GIP homologous to?

Back 160

Secretin
Glucagon

Front 161

Where and how is bile recycled?

Back 161

The terminal ileum contains a Na-bile cotransporter, which is a secondary active transporter that recirculates bile acids to the liver.

Front 162

What is a "slow wave" ?

Back 162

oscillating membrane potential that occurs spontaneously

Front 163

What does GIP do?

Back 163

Stimulates insulin release in response to oral glucose (NOT intravenous glucose)
Inhibits acid secretion by parietal cells

Front 164

In what form are carbohydrates absorbed?

Back 164

Only monosaccharides are absorbed. Carbohydrates must be digested to glucose, galactose, and fructose for absorption to proceed.

Front 165

Slow waves determine the pattern of (1) but are not themselves (1).

Back 165

1 = action potentials

Front 166

What causes GIP to be released?

Back 166

Fatty acids in the duodenal lumen
Amino acids
Oral glucose loads

Front 167

What enzymes break down carbohydrates?

Back 167

α-Amylases: hydrolyze 1,4-glycosidic bonds in starch
Maltase, α-dextrinase, and sucrase: hydrolyze oligosaccharides to glucose
Lactase, trehalase, and sucrase: degrade disaccharides to monosaccharides.

Front 168

Slow waves are due to opening of what kind of channels?

Back 168

Ca2+ channels for depolarization
K+ channels for hyperpolarization

Front 169

What are paracrine factors?

Back 169

Released from endocrine cells
Instead of going into systemic circulation, they diffuse over short distances to act upon target cells

Front 170

How is glucose absorbed?

Back 170

Glucose is transported from the intestinal lumen into the cells by Na-dependent cotransport (SGLT1).
Glucose is transported from cell to blood by facilitated diffusion (GLUT2).

Front 171

frequency of slow waves is not influenced by (1)
frequency of slow waves sets the maximum (2)

Back 171

1 = neuronal or hormonal inputs
2 = frequency of contraction of smooth muscle

Front 172

What are the GI paracrine factors?

Back 172

Somatostatin
Histamine

Front 173

How is galactose absorbed? Fructose?

Back 173

Galactose is absorbed in the same way as glucose: through SGLT1 cotransporter (with Na), and GLUT2.

Fructose is transported exclusively by facilitated diffusion. First it is absorbed from the lumen with GLUT5, and sent to the blood with GLUT2. It cannot be absorbed against a concentration gradient.

Front 174

frequency of slow waves in stomach = (1)

frequency of slow waves in duodenum = (2)

Back 174

1 = 3 waves/min

2 = 12 waves/ min

** characteristic for each part of the GI tract

Front 175

What does somatostatin do?

Back 175

Inhibits the release of all GI hormones
Inhibits gastric acid secretion?

Front 176

What are the enzymes responsible for protein digestion?

Back 176

Endopeptidases
Exopeptidases
Pepsin
Pancreatic proteases (trypsin, chymotrypsin, elastase, carboxypeptidase A and B)

Front 177

where is the swallowing centre located?

what nerves mediate the swallowing reflex?

Back 177

medulla

vagus N. and glossopharyngeal N.

Front 178

Where is somatostatin produced?

Back 178

Cells throughout the GI tract

Front 179

How does pepsin function?

Back 179

Pepsin is secreted as pepsinogen by the chief cells of the stomach. Pepsinogen is activated to pepsin by gastric H+. The optimum pH for pepsin is 1-3. When pH >5 (as in duodenum, pepsin is denatured.

Front 180

intraesophageal pressure equals (1) which is lower than (2).

Back 180

1 = intrathoracic pressure
2 = atmospheric pressure

Front 181

Where is histamine produced?

Back 181

Mast cells of the gastric mucosa

Front 182

How does trypsin function?

Back 182

Trypsinogen is activated to trypsin by a brush border enzyme, enterokinase.
Trypsin converts chymotrypsinogen, proelastase, and procarboxypeptidase A and B (and trypsinogen) to their active forms.

Front 183

What is a primary peristaltic contraction in esophagus?

Back 183

area of high pressure behind food bolus, with distension in front of bolus, moves down esophagus and propels food down --> accelerated by gravity

Front 184

What causes GIP to be released?

Back 184

Fatty acids in the duodenal lumen
Amino acids
Oral glucose loads

Front 185

How are proteins absorbed?

Back 185

Proteins can be absorbed as amino acids, dipeptides, and tripeptides.
Na-dependent amino acid cotransport occurs in the luminal membrane. AAs are then transported from cell to blood by facilitated diffusion.
Dipeptides and tripeptides are absorbed through H+-dependent cotransport. In intestinal cells, cytoplasmic peptidases hydrolyze them to amino acids.

Front 186

What is the purpose of secondary peristaltic contraction in esophagus?

Back 186

clears the esophagus of any remaining food

Front 187

Where is GIP produced?

Back 187

Duodenum and jejunum

Front 188

What do the lipases do?

Back 188

Lingual lipases digest some of the ingested triglycerides to monoglycerides and fatty acids.
Pancreatic lipases hydolyze lipids to fatty acids, monoglycerides, cholesterol, and lysolecithin.

Front 189

Relaxation of the LES is mediated by (1) nerve and (2) neurotransmitter

Back 189

1 = vagus nerve
2 = VIP

Front 190

What are the GI paracrine factors?

Back 190

Somatostatin
Histamine

Front 191

What are the pancreatic lipases?

Back 191

Pancreatic lipase
Cholesterol ester hydrolase
Phospholipase A2

Front 192

Gastroesophageal reflux aka. (1) occurs when the tone of the (2) is (3)

Back 192

1 = heart burn
2 = LES
3 = decreased

Front 193

What causes somatostatin to be produced?

Back 193

Acid in the lumen

Front 194

How do micelles function?

Back 194

Micelles bring the products of lipid digestion into contact with the absorptive surface of the intestinal cells. Fatty acids, monoglycerides, and cholesterol diffuse across the luminal membrane into the cells. Glycerol is hydrophilic and is not contained in the micelles.

Front 195

Achalasia

Back 195

LES does not relax and food accumulates in esophagus

Front 196

What does histamine do?

Back 196

Increases gastric acid secretion

Front 197

After transport into the cells, where do the products of lipid digestion go?

Back 197

In the intestinal cells, they are re-esterified to triglycerides, cholesterol ester, and phospholipids, and with apoproteins form chylomicrons. These are transported out by exocytosis, and transferred to lymph vessels.

Front 198

Oxyntic glands are located in what region of the stomach?

Back 198

orad region

Front 199

What are neurocrine factors?

Back 199

Molecules that are synthesized in the neurons of the GI tract
Move by axonal transport down the axon
Released by action potentials in the nerves
Diffuse across the synaptic cleft to act upon target cells

Front 200

What are some causes of malabsorption of lipids (steatorrhea)?

Back 200

a) Pancreatic disease: pancreas cannot synthesize adequate amounts of enzymes (pancreatitis, cystic fibrosis)
b) Hypersecretion of gastrin
c) Ileal resection: leads to a depletion of bile acid
d) Bacterial overgrowth: may lead to deconjugation of bile acids and early absorption in small intestine.
e) Decreased number of intestinal cells (tropical sprue)
f) Failure to synthesize apoprotein B: inability to form chylomicrons (abetalipoproteinemia)

Front 201

The stomach has an additional layer of smooth muscle.. the (1) layer.

Back 201

oblique smooth muscle layer

Front 202

What are the GI neurocrine factors?

Back 202

Vasoactive intestinal peptide (VIP)
GRP (bombesin)
Enkephalins

Front 203

How is K absorbed or secreted?

Back 203

Dietary K is absorbed in the small intestine by passive diffusion via a paracellular route.
K is actively secreted in the colon, stimulated by aldosterone.

Front 204

Receptive Relaxation is a (1) reflex that is initiated by (2). It is characterized by (3) and is potentiated by (4) hormone.

Back 204

1 = vagovagal reflex
2 = distension of stomach
3 = orad region of stomach relaxes to accomodate incoming food
4 = CCK

Front 205

What hormone is VIP homologous to?

Back 205

Secretin

Front 206

What is retropulsion?

Back 206

when distal antrum is closed, and caudad region contracts food is propelled back into stomach to be mixed

Front 207

Where is VIP produced?

Back 207

Neurons in the mucosa and smooth muscle of the GI tract

Front 208

Gastric contractions are increased by (1) and decreased by (2)

Back 208

1 = vagal stimulation
2 = sympathetic stimulation

Front 209

What does VIP do?

Back 209

Relaxes the GI smooth muscle, including the lower esophageal sphincter
Stimulates pancreatic bicarbonate secretion
Inhibits gastric acid secretion

Front 210

Migrating Myoelectric Complex
- frequency? (1)
- when? (2)
- mediated by? (3)
- function? (4)

Back 210

1 = every 90 minutes
2 = during fasting
3 = motilin
4 = to clear the stomach of residual food

Front 211

What factor mediates pancreatic cholera?

Back 211

VIP

Front 212

Gastric Emptying is slowed by (3).

Back 212

1 = hypertonic/hypotonic chyme
2 = fat (via CCK)
3 = H+ in duodenum

Front 213

Under what conditions might VIP be abnormally secreted?

Back 213

Pancreatic islet cell tumors

Front 214

Role of segmentation contractions?

Back 214

mix the intestinal contents with no net forward movement

Front 215

Where is GRP produced?

Back 215

The vagus nerve branches innervating the G cells

Front 216

Role of Peristaltic contractions?

Back 216

propel the chyme through small intestine

Front 217

What does GRP do?

Back 217

Stimulates gastrin release from G cells

Front 218

Peristaltic reflex is coordinated by (1).

Back 218

enteric nervous system

Front 219

What are the two enkephalins?

Back 219

Met-enkephalin
Leu-enkephalin

Front 220

Gastroileal reflex is mediated by (1). Presence of food in the (2) triggers relaxation of (3) and delivery of intestinal contents to (4).

Back 220

1 = ANS
2 = stomach
3 = relaxation of ileocecal sphincter
4 = large intestine

Front 221

Where are the enkephalins produced?

Back 221

Nerves in the mucosa and smooth muscle of the GI tract

Front 222

In the large instestine, segmentation contractions produce (1)

Back 222

haustra

Front 223

What do enkephalins do?

Back 223

Stimulate contraction of GI smooth muscle, especially sphincters
Inhibits intestinal secretion of fluid and electrolytes

Front 224

mass movements in the large intestine occur (1)

Back 224

1-3 times/day

Front 225

What sphincters are targeted by enkephalins?

Back 225

Lower esophageal
Pyloric
Ileocecal

Front 226

Most colonic water absorption occurs in the (1).

Back 226

proximal colon

Front 227

Why are opiates useful for treating diarrhea?

Back 227

They inhibit the intestinal secretion of fluid and electrolytes

Front 228

rectosphincteric reflex

Back 228

presence of feces in rectum relaxes the internal anal sphincter

Front 229

Where in the GI tract would you find skeletal muscle?

Back 229

Pharynx
Upper 1/3 of the esophagus
External anal sphincter

Front 230

Valsalva Maneuvre

Back 230

intra-abdominal pressure is increased by expiring against a closed glottis --> necessary for defecation

Front 231

What happens when you depolarize a ring of smooth muscle?

Back 231

It contracts, decreasing the diameter of that segment of GI tract
This is the basis for peristalsis

Front 232

Gastrocolic reflex
- presence of food in the (1) increases (2) and frequency of (3)

Back 232

1 = stomach
2 = motility of colon
3 = mass movements

Front 233

What is the difference between tonic and phasic contractions?

Back 233

Tonic -- sustained over long periods of time (minutes to hours)
Phasic -- occur over brief periods of time

Front 234

Gastrocolic reflex has a rapid (1) component and a slower (2) component, mediated by (3)

Back 234

1 = PNS (stomach distension)
2 = hormonal
3 = CCK and gastrin

Front 235

What parts of the GI tract exhibit phasic contractions?

Back 235

Esophagus
Gastric antrum
Small intestine

Front 236

Megacolon (Hirschsprung's Disease)

- results in (1) of involved segment
- dilation and accumulation (2) to constriction
- (3)

Back 236

absence of colonic enteric nervous system

1 = constriction
2 = proximal
3 = severe constipation

Front 237

What parts of the GI tract exhibit tonic contractions?

Back 237

Lower esophageal sphincter
Orad stomach
Ileocecal sphincter
Internal anal sphincter

Front 238

Functions of Saliva (3)

Back 238

- digestion of starch and triglycerides
- lubrication
- protection

Front 239

What are slow waves?

Back 239

Oscillating membrane potentials inherent to the GI smooth muscle
Occur spontaneously

Front 240

Composition of Saliva:
- high (1)
- low (2)
- tonicity? (3)
- enzymes? (4)

Back 240

1 = K+ and HCO3-
2 = Na+ and Cl-
3 = hypotonicity
4 = a-amylase, lingual lipase, kallikrein

Front 241

Where do slow waves originate?

Back 241

The interstitial cells of Cajal
Serve as the pacemaker for the GI smooth muscle

Front 242

low flow rate saliva?

Back 242

lowest osmolarity with highest K+ conc.

Front 243

Are slow waves and action potentials the same thing?

Back 243

No
However, slow waves determine the pattern of action potentials, and therefore modulate the pattern of contraction
Basically, the periodicity of the slow waves determines when action potentials can occur

Front 244

high flow rate saliva?

Back 244

composition is closest to the of plasma --> does not have as much time for reabsorption of NaCl

Front 245

How are slow waves produced?

Back 245

There is cyclic opening of Ca channels (which causes depolarization) followed by opening of K channels (which causes repolarization)
Depolarization brings the membrane potential close to threshold, increasing the probability that an action potential will occur
Action potentials are produced on top of the background of slow waves, and initiate the contraction of smooth muscle cells

Front 246

Function of Salivary Acinus?

Back 246

produces initial saliva with composition isotonic and almost identical to plasma

Front 247

What is the frequency of slow waves throughout the GI tract?

Back 247

Varies, but for a given region it is constant and characteristic

Front 248

Function of Salivary Ducts?

Back 248

- reabsorb Na+ and Cl-

- secrete K+ and HCO3-
- saliva becomes hypotonic in ducts bc it is reabsorbing ions yet impermeable to water

Front 249

How do slow waves and action potentials differ in terms of their regulation?

Back 249

Action potentials are influenced by neural and hormonal input; slow waves are not

Front 250

Why is HCO3- low with low flow rate and increased with high flow rate? (even though it is secreted?)

Back 250

HCO3- is selectively stimulated when saliva secretion is stimulated

Front 251

What sets the maximum frequency of contractions for a given region of the GI tract?

Back 251

Slow wave frequency

Front 252

Production of saliva is stimulated by both (1) but (2) is more important

Back 252

1 = PNS and SNS
2 = PNS

Front 253

Where is slow wave frequency the lowest? Highest?

Back 253

Lowest: stomach (3/min)
Highest: duodenum (12/min)

Front 254

PNS stimulation of saliva is enhanced by (4)

Back 254

1 - conditioning
2 - smell
3 - food
4 - nausea

Front 255

What does chewing do to food?

Back 255

Mixes it with saliva to lubricate
Decreases the size of food particles to facilitate swallowing and digestion

Front 256

PNS stimulation of saliva is inhibited by (4)

Back 256

1 - dehydration
2 - sleep
3 - anticholinergic drugs
4 - fear

Front 257

How does the swallowing reflex work?

Back 257

Coordinated in the medulla
Mediated by the vagus and glossopharyngeal nerves

Front 258

Salivary Stimulation - Mechanism
PNS acts via (1) receptor and (2) 2nd messenger
SNS acts via (3) receptor and (4) 2nd messenger

Back 258

1 = muscarinic Ach receptor
2 = PLC -> IP3 and Ca2+
3 = b-adrenergic
4 = cAMP

Front 259

What is the sequence of events in swallowing?

Back 259

The nasopharynx closes and breathing is inhibited
The laryngeal muscles close the glottis and elevate the larynx
Peristalsis begins in the pharynx to propel food toward the esophagus
As this happens, the upper esophageal sphincter relaxes so the bolus can pass

Front 260

What do parietal cells secrete?

Back 260

HCl
intrinsic factor

Front 261

How does the esophagus maintain a closed environment?

Back 261

Sphincters at both ends prevent air from entering (and the lower sphincter prevents gastric reflux)

Front 262

What do chief cells secrete?

Back 262

pepsinogen

Front 263

What is the intraesophageal pressure?

Back 263

Since the esophagus is in the thoracic cavity, intraesophageal pressure = thoracic pressure
Note that this pressure is lower than atmospheric pressure

Front 264

What do G cells secrete?

Back 264

gastrin

Front 265

What is the sequence of events in the esophagus after swallowing has been initiated?

Back 265

The upper esophageal sphincter relaxes to allow food to pass; it then contracts again to prevent reflux
A primary peristaltic contraction moves the bolus down, and gravity facilitates this
A secondary persistaltic contraction occurs
The lower esophageal sphincter relaxes to allow food to pass
The stomach undergoes receptive relaxation

Front 266

Proton pump inhibitors inhibit (1)

ex. (2)

Back 266

H+/K+ ATPase on apical membrane of parietal cells --> blocks H+ secretion

Front 267

What is a primary peristaltic contraction?

Back 267

The creation of high pressure behind a bolus and low pressure in front of it

Front 268

alkaline tide

Back 268

HCO3- produced in parietal cells in absorbed into blood stream in exchange for Cl-; pH of venous blood increases

Front 269

What is a secondary peristaltic contraction?

Back 269

Clears the esophagus of any remaining food

Front 270

PNS increases H+ secretion by acting directly on (1) and indirectly by stimulating (2)

Back 270

1 = muscarinic receptors (parietal cells) - Ach
2 = G cells (via GRP)

Front 271

What causes the lower esophageal sphincter to relax?

Back 271

Parasympathetic stimulation
Mediated by the neurotransmitter VIP

Front 272

What receptor does gastrin act on? what 2nd messenger?

Back 272

1. CCKb on parietal cells
2. IP3/Ca2_

Front 273

What is gastroesophageal reflux and what causes it?

Back 273

Heartburn
Can occur if the tone of the lower esophageal sphincter is decreased
This allows gastric contents to reflux into the esophagus

Front 274

Histamine is released by (1). and stimulates H+ secretion by (2).

Ex. of an H2 receptor blocker (3)

Back 274

1 = enterochromaffin cells (ECL)
2 = activating H2 receptors
3 = cimetidine

Front 275

What causes achalasia?

Back 275

Food accumulates in the esophagus
The lower esophageal sphincter does not relax during swallowing to allow food passage

Front 276

Potentiation

Back 276

response to simultaneous admin. of 2 stimulants is greater than the sum of either alone

Front 277

How many muscular layers does the stomach have?

Back 277

Three:
Inner circular
Middle longitudinal
Outer circular/oblique

Front 278

low pH (< 3.0) (1) gastrin secretion and thus (2)

Back 278

1 = inhibits
2 = inhibits H+ secretion

Front 279

What are the three anatomic divisions of the stomach?

Back 279

Fundus
Body
Antrum

Front 280

Direct pathway of somatostatin inhibition of gastric H+ secretion

Back 280

binds Gi coupled receptor, decreases cAMP (antagonizes histamines effects)

--> same mechanism seen with prostaglandins

Front 281

What is the orad stomach?

Back 281

The fundus and proximal body
This is the region that receives the ingested meal

Front 282

indirect pathway of somatostatin inhibition of gastric H+ secretion

Back 282

inhibits release of histamine and gastrin

Front 283

What is the caudad stomach?

Back 283

The antrum and distal body
This is the region that contracts to mix food and propel it into the duodenum

Front 284

Peptic Ulcer Disease

Back 284

loss of the protective mucous barrier and/or excessive secretion of H+ and pepsin

Front 285

What type of reflex is receptive relaxation of the stomach?

Back 285

Vasovagal

Front 286

damaging factors leading to peptic ulcer disease (7)

Back 286

alcohol
NSAIDs
smoking
stress
H.pylori infection
H+
pepsin

Front 287

What is receptive relaxation of the stomach?

Back 287

The orad region of the stomach relaxes to accommodate the ingested meal
CCK increases the distensibility of the stomach

Front 288

protective factors against peptic ulcer disease (5)

Back 288

mucous
HCO3-
prostaglandins
mucosal blood flow
GFs

Front 289

What is retropulsion?

Back 289

A wave of contraction closes the distal antrum
This propels food back into the stomach to be mixed

Front 290

Gastric ulcers have decreased (1) and increased (2); they are caused by (3)

Back 290

1 = H+ secretion
2 = increased gastrin (bc decreased negative feedback)

Front 291

How does the autonomic nervous system modulate the frequency of gastric contractions?

Back 291

Parasympathetic -- increases frequency
Sympathetic -- decreases frequency

Front 292

How does H.Pylori survive in acidic stomach environment?

Back 292

contains urease --> alkalinizes local environment

Front 293

What is the migrating myoelectric complex?

Back 293

Even during the fasting state, the stomach contracts every 90 minutes or so to clear the stomach of residual food
This is mediated by motilin

Front 294

diagnostic test for H.pylori?

Back 294

drinking a solution of 13C urea, which is converted to 13CO2 urease and measured in expired air

Front 295

How does the stomach empty?

Back 295

The caudad region of the stomach contracts, which propels food into the duodenum

Front 296

duodenal ulcers are characterized by (1) and (2); it can be caused by (3)

Back 296

1 = increased H+ secretion
2 = increased gastrin secretion in response to a meal
3 = h.pylori

Front 297

How does the tonicity of stomach contents affect gastric emptying?

Back 297

Gastric emptying is fastest when stomach contents are isotonic

Front 298

three drugs that block gastric H+ secretion

Back 298

atropine - inhibits Ach muscarinic R. on parietal cells
cimetidine - blocks H2 histamine R.
omeprazole - inhibits H+K+ ATPase

Front 299

How does fat affect gastric emptying?

Back 299

It inhibits it by stimulating the release of CCK

Front 300

Composition of Pancreatic Juice:
- high (1)
- same (2) as plasma
- higher (3) than plasma
- lower (4) than plasma
- tonicity? (5)
- enzymes? (6)

Back 300

1 = volume
2 = Na+, K+
3 = HCO3-
4 = Cl-
5 = isotonicity
6 = pancreatic amylase, lipase and proteases

Front 301

How does acid in the duodenum affect gastric emptying?

Back 301

Inhibits it
H+ receptors in the duodenum signal to the gastric smooth muscle

Front 302

at low flow rates, pancreatic secretion is composed mainly of (1) and (2)

Back 302

1 = Na+
2 = Cl-

Front 303

What is the primary function of the small intestine?

Back 303

Digestion and absorption of nutrients

Front 304

at high flow rates, pancreatic secretion is composed mainly of (1) and (2)

Back 304

1 = Na+
2 = HCO3-

Front 305

What are the type of contractions observed in the small intestine?

Back 305

Segmentation contractions
Peristaltic contractions
Gastroileal reflex

Front 306

Secretin acts on pancreatic (1) cells to increase (2) via (3) 2nd messenger

Back 306

1 = ductal cells
2 = HCO3- secretion
3 = cAMP

Front 307

What are small intestinal segmentation contractions?

Back 307

These are contractions that mix the intestinal contents
A section contracts and chyme is propelled forward AND backward
This segment then relaxes and the food moves back into that region
This causes mixing without any net forward motion of chyme

Front 308

What are small intestinal peristaltic contractions?

Back 308

Highly coordinated contractions that propel chyme through the small intestine toward the colon
There is simultaneous contraction behind the bolus and relaxation in front of it, resulting in caudal propulsion

Front 309

CCk acts on the pancreatic (1) cells to increase (2) and potentiates the effect of (3) via (4) 2nd messenger.

Back 309

1 = acinar cells
2 = pancreatic enzyme secretion
3 = secretin
4 = IP3/Ca2+ system

Front 310

What does bile contain? (4)

Back 310

bile salts
phospholipids
cholesterol
bile pigments (bilirubin)

Front 311

What stimulates peristaltic contractions of the small intestine?

Back 311

The enteric nervous system

Front 312

What do choleretic agents do?

Back 312

increase bile formation

Front 313

What is the gastroileal reflex?

Back 313

The presence of food in the stomach triggers peristalsis in the ileum, as well as relaxation of the ileocecal sphincter
This allows intestinal contents to be delivered to the colon

Front 314

What are the primary bile acids?

Back 314

cholic acid
chenodeoxycholic acid

Front 315

What factors mediate the gastroileal reflex?

Back 315

The extrinsic ANS
Possibly gastrin

Front 316

What are the secondary bile acids?

Back 316

deoxycholic acid
lithocolic acid

Front 317

What is the path of food within the large intestine?

Back 317

Cecum
Ascending colon
Transverse colon
Descending colon
Sigmoid colon
Rectum
Anal canal

Front 318

What amino acids do bile acids get conjugated with?

Back 318

glycine and taurine

Front 319

What are haustra?

Back 319

Sac-like segmentation within the large intestine
They are formed by segmentation contractions of the colon

Front 320

Contraction of the gallbladder is caused by (1) and (2)?

Back 320

1 = CCK
2 = Ach

Front 321

How is colonic reflux into the ileum prevented?

Back 321

When the proximal colon is filled with fecal material, the ileocecal sphincter contracts

Front 322

Where is the Na+-bile acid cotransporter located? What is its role?

Back 322

terminal ileum

impt. for recirculation of bile acids

Front 323

Where does most colonic water absorption occur?

Back 323

The proximal colon

Front 324

which form of carbohydrates can be absorbed?

Back 324

monosaccharides

Front 325

How does the consistency of poop change as you go along the colon?

Back 325

Water is absorbed in the proximal colon
Feces become more solid as they move distally

Front 326

alpha amylase
- function?
- location?

Back 326

- degrades a-1,4 glycosidic bonds in starch yielding maltose, maltotriose and a-limit dextrins

Front 327

What is responsible for the movement of feces?

Back 327

Mass movements of the colon
These movements cause colonic contents to move distally over long distances

Front 328

main monosaccharides used for energy? (3)

Back 328

glucose
fructose
galactose

Front 329

How many mass movements do we typically experience?

Back 329

1-3 per day

Front 330

Absorption of Glucose/Galactose in small intestine?
- transporters?

Back 330

SGLT Na+-dependent cotransport on luminal membrane
GLUT2 on basolateral membrane via facilitated diffusion

Front 331

What are the types of contractions observed in the colon?

Back 331

Segmentation contractions -- mixing
Mass movements -- forward propulsion

Front 332

method of fructose absorption?

Back 332

facilitated diffusion, down conc. gradient

Front 333

What is the sequence of events for defecation?

Back 333

As the rectum fills with feces, it contracts and the internal anal sphincter relaxes
When the rectum is about 25% full, you feel the urge, but you can control the tone of the external anal sphincter
When it is convenient to defect, you voluntarily relax the external anal sphincter
The smooth muscle of the rectum contracts and poop is pushed out
Intra-abdominal pressure is increased by expiring against a closed glottis (Valsalva maneuver)

Front 334

optimum pH for pepsin activity?

Back 334

pH 1 - 3

Front 335

What is the rectosphincteric reflex?

Back 335

Opening of the internal anal sphincter due to rectal distention

Front 336

in what form are proteins absorbed?

Back 336

amino acids
di and tri peptides

Front 337

What is the gastrocolic reflex?

Back 337

The presence of food in the stomach increases colonic motility and the frequency of mass movements
Food stretching the stomach produces a rapid parasympathetic component
A slower hormonal component is mediated by CCK and gastrin

Front 338

method of amino acid absorption?
- luminal mb? (1)
- basolateral mb? (2)

Back 338

1 - Na+dep. aa co-transport
2 - facilitated diffusion via specific aa. carrier (neutral, acidic, basic and imino acids)

Front 339

What are some disorders of the frequency of colonic segmentation contractions?

Back 339

Irritable bowel syndrome -- increased segmentation contractions; may occur after periods of stress and result in constipation
Diarrhea -- decreased segmentation contractions

Front 340

how are di and tri peptides absorbed?

Back 340

H+ dependent co-transport across luminal membrane; hydrolyzed by proteases in the cytoplasm

Front 341

What is Hirschprung's Disease?

Back 341

Also known as megacolon
There is no colonic enteric nervous system in one region
This results in constriction of the involved segment
There is huge dilation and accumulation of intestinal contents proximal to the constriction
Produces severe constipation

Front 342

Colon has a (1) epithelium.

Small intestine and gallbladder have a (2) epithelium.

Back 342

1 = tight
2 = leaky

Front 343

What is the sequence of events for vomiting?

Back 343

A wave of peristalsis begins in the small intestine and moves the GI contents toward the stomach
Gastric contents are pushed into the esophagus
Before the upper esophageal sphincter opens, retching occurs
When/if you generate enough pressure to open the upper esophageal sphincter, vomiting occurs

Front 344

Absorption of Na+ in intestinal cells? (4)

Back 344

1. passive diffusion
2. Na+glucose/ Na+ aa cotransport
3. NaCl transport
4. Na+/H+ exchange

Front 345

What are the neurological regions involved in vomiting, and what triggers them?

Back 345

Vomiting center of the medulla: tickling the back of the throat, gastric distention, vestibular stimulation (motion sickness)
Chemoreceptor trigger zone in the fourth ventricle: stimulated by emetics, radiation, and vestibular stimulation

Front 346

Absorption of Cl- in intestinal cells? (3)

Back 346

1. passive diffusion - paracellular (follows Na+)
2. Na+/Cl- cotransport
3. Cl- / HCO3- exchange

Front 347

What are the functions of saliva?

Back 347

Initial starch digestion by amylase
Initial triglyceride digestion by lingual lipase
Lubrication of food with mucous
Protection of the mouth and esophagus by diluting and buffering ingested food

Front 348

dietary K+ is (1) in the small intestine via (2) and secreted in the (3)

Back 348

1 = absorbed
2 = paracellular route
3 = colon (stimulated by aldosterone)

Front 349

What is the chemical composition of saliva?

Back 349

Water
High K and HCO3
Low Na and Cl
Overall hypotonic
Amylase, lingual lipase, kallikrein

Front 350

H20 absorption is (1) in the small intestine/gallbladder; whereas, in the colon, H20 permeability is (2).

Back 350

1 = isoosmotic
2 = decreased

Front 351

How does the chemical composition of saliva change with flow rate?

Back 351

As flow rate increases
Na, HCO3, Cl concentration increase
Osmolarity increases
K concentration decreases

Front 352

what is the primary ion secreted into the intestinal lumen?

Back 352

Cl-

Front 353

When is saliva similar to the composition of plasma?

Back 353

At high salivary flow rates (up to 4 ml/min)

Front 354

Cholera Toxin
- mechanism?
- causes?

Back 354

1 - permanently activates Gs by ADP ribosylation, increases cAMP and Cl- are open; Na+ and H20 follow Cl- out
2 - secretory diarrhea

Front 355

What are the salivary glands?

Back 355

Parotid
Submandibular
Sublingual

Front 356

water-soluble vitamins are absorbed via (1)

Back 356

Na+ dependent co-transport

Front 357

What is the structure of a salivary gland?

Back 357

There is an acinus (blind end) that is lined with acinar cells, which secrete the initial saliva
A branching duct system of columnar epithelium modifies the secretion

Front 358

fat soluble vitamins ex. (1) are absorbed via (2)

Back 358

1 = vitamins A, D, E ,K
2 = incorporation into fat micelles

Front 359

How is saliva ejected into the mouth?

Back 359

Myoepithelial cells lining the acini and ducts contract to expel the glandular contents

Front 360

How is vitamin B12 absorbed?

Back 360

intrinsic factor must be present to complex vit. B12 and bind receptor on ileal cells

Front 361

What is the function of the salivary acinus?

Back 361

Produces an initial saliva that has a composition similar to plasma
This initial saliva is isotonic and has the same electrolyte concentrations as plasma

Front 362

Absorption of Ca2+ depends on...

Back 362

1,25 dihydoxycholecalciferol and calbindin D-28K

Front 363

What is the function of the salivary duct?

Back 363

Modification of the initial saliva
Na and Cl are reabsorbed
K and HCO3 are secreted
Saliva becomes hypotonic because the ducts are relatively impermeable to water

Front 364

In what form is iron absorbed?

Back 364

heme iron
free Fe2+

Front 365

How does aldosterone affect salivary composition?

Back 365

It acts upon the ductal cells to increase Na reabsorption and K secretion, just like in the distal tubule of the nephron

Front 366

Why is saliva most like plasma at high flow rates?

Back 366

There is less time for absorption and secretion to occur, so Na, K, and Cl concentrations will be the same as in plasma
This is not true for HCO3, which is selectively stimulated when salivation is stimulated

Front 367

Peptides that INCREASE FOOD intake (9)

Back 367

G O B G G M N A E

Hint 367

ghrelin
orexin a and b
beta-endorphin
galanin
GHRH
MCH
neuropeptide Y
agouti-related peptide
endocannabinoids

Front 368

What controls saliva production?

Back 368

Parasympathetic and sympathetic stimulation
GI hormones do NOT affect salivation

Front 369

peptides that DECREASE FOOD intake (14)

Back 369

L P P P C M G G I V C I I T

Hint 369

leptin CK
PYY
PP
POMC
CRH
MSH
glucagon
GLP-1
insulin
vasopressin
CART
IL1
IL6
TNFa

Front 370

What is the effect of parasympathetic stimulation upon salivation flow rate? Sympathetic stimulation?

Back 370

They BOTH increase flow rate, but parasympathetic stimulation is more important

Front 371

Motilin
- where is it produced? (1)
- when is it produced? (2)
- function?

Back 371

1 = enterochromaffin cells
2 = released periodically during fasting
3 = initiates migrating motor complex

Front 372

What is the parasympathetic innervation to the salivary glands?

Back 372

CN VII and IX

Front 373

Obestatin
- function? (1)

Back 373

counteracts effect of motilin

Front 374

How does parasympathetic stimulation facilitate salivation?

Back 374

Transport processes in the acinar and ductal cells are increased
Vasodilation is induced

Front 375

pancreatic polypeptide
- where is it made?
- what stimulates its release?
- function?

Back 375

1 = F cells in pancreatic islets
2 = protein digests (Phe, Trp) AND vagal cholinergic activity
3 = inhibits pancreatic secretion, induces satiety

Front 376

What is the parasympathetic signaling pathway for the induction of salivation?

Back 376

Activation of muscarinic receptors on acinar and ductal cells
IP3 is produced
Intracellular [Ca] increases

Front 377

PYY
- where is it made? (1)
- what stimulates its release? (2)
- functions? (3)

Back 377

1 = L cells of ileum/colon
2 = fatty meal and cholinergic stimulation
3 = inhibits secretin-CCK effects and inhibits food intake

Front 378

Why does atropine cause dry mouth?

Back 378

It is an anticholinergic drug, and cholinergic signaling stimulates salivation

Front 379

NPY
- where? (1)
- main functions? (2)

Back 379

1 = neurons of CNS esp. hypothalamus
2 = controls food intake and appetite AND blocks transmission of pain signals in brain

Front 380

How does sympathetic stimulation facilitate salivation?

Back 380

Increases the production of saliva
Promotes the growth of salivary glands

Front 381

Constrictors of GI Smooth MM?

Back 381

Ach
Substance P

Front 382

What is the sympathetic signaling pathway for the induction of salivation?

Back 382

Activation of B-adrenergic receptors on acinar and ductal cells
cAMP concentration increases

Front 383

Relaxants of GI Smooth MM?

Back 383

VIP
PACAP
ATP
GABA
NO

Front 384

What environmental factors increase saliva production?

Back 384

Food in the mouth
Smell
Conditioned reflexes
Nausea
These things all act through activation of the parasympathetic nervous system

Front 385

Mechanism of Peristalsis?

Back 385

stretching of gut --> release of 5HT from EC-cell --> stimulates cGRP neurons to release Ach/SP behind stretch AND release relaxants ahead of stretch

Front 386

What environmental factors decrease saliva production?

Back 386

Sleep
Dehydration
Fear
Anticholinergic drugs
These things all act through the inhibition of the parasympathetic nervous system

Front 387

LES tone is increased by? (5)

Back 387

Ach
gastrin
H.pylori
motilin
ghrelin

Front 388

What are the secretory cells of the stomach?

Back 388

Parietal cells: located in the body, secrete HCl and intrinsic factor
Chief cells: located in the body, produce pepsinogen
G cells: located in the antrum, produce gastrin

Front 389

LES tone is decreased by? (5)

Back 389

secretin
CCK
GIP
VIP/NO
P4 (pregnancy)

Front 390

What is the mechanism of gastric acid secretion?

Back 390

In the parietal cells, carbonic anhydrase catalyzes the conversion of CO2 and water to H and HCO3
H is secreted into the stomach lumen through the H-K ATPase
Cl is also secreted along with H, so the final secretion product is HCl
The HCO3 is absorbed into the bloodstream in exchange for Cl via the Cl-HCO3 exchanger

Front 391

swallowing center (1) the respiratory centre

Back 391

inhibits

Front 392

How does omeprazole work?

Back 392

It inhibits the H-K ATPase and blocks H secretion by the parietal cells

Front 393

Afferent limb of swallowing reflex

Back 393

trigeminal, glossopharyngeal, vagal

Front 394

What is the alkaline tide?

Back 394

As acid is secreted into the stomach, base is absorbed into the bloodstream, which causes plasma pH to increase
This HCO3 will eventually be secreted by the pancreas

Front 395

Efferent limb of swallowing reflex

Back 395

trigeminal, facial, hypoglossal, vagal

Front 396

How does vomiting contribute to metabolic alkalosis?

Back 396

Gastric acid never reaches the small intestine
Therefore, there is no stimulus for pancreatic HCO3 secretion
The arterial blood becomes alkaline

Front 397

Innervation of Colon
- proximal SNS ? (1)
- distal SNS? (2)
- rectum/internal anal sphincter? (3)
- external anal sphincter? (4)

Back 397

1 = superior mesenteric ganglion
2 = infereior mesenteric ganglion
3 = hypogastric plexus
4 = pudendal N.

Front 398

What is the DIRECT pathway for vagal stimulation of gastric acid secretion?

Back 398

The vagus nerve innervates the parietal cells and stimulates them
ACh binds to M3 muscarinic receptors
IP3 is generated and intracellular [Ca] increases

Front 399

Tenia coli are formed from (1).

Which plexus is concentrated in tenia? (2)

Back 399

1 = longitudinal smooth mm.
2 = myenteric plexus

Front 400

What is the INDIRECT pathway for vagal stimulation of gastric acid secretion?

Back 400

The vagus nerve innervates G cells
Gastric secretion is stimulated
The neurotransmitter is GRP

Front 401

haustral contractions

Back 401

local circular mm. contractions

Front 402

How does atropine inhibit gastric acid secretion?

Back 402

It is a cholinergic muscarinic antagonist, so it blocks the direct vagal pathway
However, it has no effect upon the direct pathways

Front 403

adynamic paralytic ileus

Back 403

- inhibition of smooth mm. of gut and disappearance of motor activity
- following trauma or surgery
- may be due to activation of opiod receptors or excessive NE discharge

Front 404

What effect would a vagotomy have upon parasympathetic stimulation of gastric acid secretion?

Back 404

It would eliminate both the direct and the indirect pathways

Front 405

blind loop syndrome

Back 405

- normal passage of intestinal contents is disturbed due to blind loop
--> massive overgrowth of bacteria with malabsorption and steatorhea

Front 406

What is the pathway for gastrin stimulation of acid secretion?

Back 406

Gastrin interacts with the CCK8 receptor on parietal cells
Generates IP3/Ca

Front 407

Saliva Composition at Low rates of secretion?

Back 407

low Na+ and Cl - (lots reabsorbed)
high K+ and HCO3- (lots secreted)

Front 408

What is the pathway for histamine stimulation of acid secretion?

Back 408

Histamine binds H2 receptors on the parietal cell membranes
Adenylyl cyclase is activated via a Gs protein
cAMP is produced

Front 409

xerostomia

Back 409

deficient salivation

Front 410

How does cimetidine work?

Back 410

Blocks the H2 receptor so histamine cannot stimulate acid secretion

Front 411

EGF and saliva

Back 411

saliva is rich in EGF which helps stimulate GI mucosal cell proliferation, repair and healing

Front 412

What is potentiation?

Back 412

When the response to two simultaneous stimulants is greater than the sum of responses to the stimulants given alone
This means that low concentrations of stimulants given together can produce maximal effects

Front 413

"gastric barrier"

Back 413

surface mucosa cells in the pyloric region secrete a thick, HCO3- rich mucous AND epithelial cells are connected by TJ that contribute to resistance of mucosal damaga

Front 414

What factors inhibit gastric acid secretion?

Back 414

Low pH (less than 3.0)
Somatostatin
Prostaglandins

Front 415

How does acidic pH inhibit gastric acid secretion?

Back 415

As acid is produced, the pH of the stomach decreases
When it goes below 3.0, a negative feedback loop inhibits further acid production

Front 416

How does somatostatin inhibit gastric acid secretion?

Back 416

Direct pathway -- binds to receptors on the parietal cells that are coupled to adenylyl cyclase by a Gi protein, which decreases cAMP levels (opposes the histamine pathway)
Indirect pathway -- inhibits release of histamine and gastrin

Front 417

How do prostaglandins inhibit gastric acid secretion?

Back 417

They activate a Gi protein, which inhibits adenylyl cyclase and decreases cAMP levels

Front 418

What is peptic ulcer disease?

Back 418

Ulcerative lesions of the gastric or duodenal mucosa
Can occur when the mucous barrier is breached or when there is excessive production of H and pepsin
Protective factors: mucous, HCO3, prostaglandins, mucosal blood flow, growth factors
Damaging factors: H, pepsin, H pylori, NSAIDs, stress, smoking, alcohol

Front 419

How do gastric ulcers impact gastric acid secretion?

Back 419

Acid secretion is decreased because the secreted H leaks back through the damaged mucosa and inhibits its own production via a negative feedback loop

Front 420

How do gastric ulcers impact gastrin production?

Back 420

Gastrin secretion is increased because low acid concentrations stimulates the G cells

Front 421

What bacteria is a major cause of gastric ulcers?

Back 421

Helicobacter pylori

Front 422

How does H pylori survive in the acidic environment of the stomach?

Back 422

It produces urease, which converts urea to NH3
This establishes a zone of neutrality in the otherwise-acidic stomach

Front 423

How does H pylori cause gastric ulcers?

Back 423

Colonizes the gastric mucosa
Releases damaging cytotoxins

Front 424

What is the diagnostic test for H pylori infection?

Back 424

You drink a solution of 13C-urea
If you have H pylori, it will be converted to 13CO2 by bacterial urease, and this can be measured in the expired air

Front 425

How do duodenal ulcers impact gastric acid secretion?

Back 425

Acid secretion is increased

Front 426

How do duodenal ulcers impact gastrin production?

Back 426

Gastrin production in response to a meal is increased, but the baseline level may be normal

Front 427

How does H pylori infection in the duodenum alter GI hormonal signaling?

Back 427

Somatostatin secretion is inhibited, so gastric acid secretion is stimulated
Intestinal absorption of bicarbonate is inhibited

Front 428

What is Zollinger-Ellison syndrome?

Back 428

A gastrin-secreting tumor of the pancreas causes increased acid secretion
Acid secretion continues unchecked because the gastrin secreted by the tumor is not subject to acid-mediated negative feedback

Front 429

Why is cimetidine such a good acid inhibitor?

Back 429

It blocks histamine stimulation
It also blocks histamine's potentiation of ACh

Front 430

What kinds of things are found in pancreatic secretion? (in general)

Back 430

HCO3 to neutralize the acidic chyme that is delivered to the duodenum
Digestive enzymes

Front 431

How does the composition of pancreatic secretion compare to plasma?

Back 431

Same Na and K concentrations as plasma
Much higher HCO3
Much lower Cl
Isotonic
Contains lipase, amylase, and proteases

Front 432

How does the composition of pancreatic secretion change with flow rate?

Back 432

At low flow rates, the pancreatic juice is made mostly of Na and Cl
At high flow rates, the secretion is mostly Na and HCO3
Pancreatic secretions are isotonic, regardless of flow rate

Front 433

What do the acinar cells of the pancreatic glands do?

Back 433

They produce the initial pancreatic secretion, which is mostly Na and Cl

Front 434

What do the ductal cells of the pancreatic glands do?

Back 434

Secrete HCO3 and absorb Cl via Cl-HCO3 antiport in the luminal membrane
The ducts are permeable to water, so water flows in to increase the volume and make the secretion isosmotic

Front 435

What does secretin do?

Back 435

Acts upon the pancreatic ductal cells to increase HCO3 secretion
Thus, when acid enters the duodenum, HCO3 is released into the lumen to neutralize it

Front 436

What second messenger does secretin use?

Back 436

cAMP

Front 437

How does CCK act upon the pancreas?

Back 437

Causes the acinar cells to increase production of amylase, lipase, and proteases
Potentiates the effect of secretin on the ductal cells

Front 438

What second messenger does CCK use?

Back 438

IP3 and increased intracellular Ca

Front 439

How does ACh affect pancreatic secretion?

Back 439

ACh is released in response to acid and partly digested food in the duodenal lumen
Stimulates enzyme secretion by the acinar cells
Potentiates the effect of secretin on HCO3 secretion

Front 440

What is cystic fibrosis?

Back 440

A disorder of pancreatic secretion
A mutation in the CFTR gene causes a defect in Cl channels
Associated with pancreatic enzyme insufficiency, which results in malabsorption and steatorrhea

Front 441

What are the main components of bile?

Back 441

Bile salts
Phospholipids
Cholesterol
Bile pigments (bilirubin)

Front 442

How do bile salts aid in absorption?

Back 442

They are amphipathic molecules, so they orient themselves around lipid molecules and keep them dispersed in micelles
This is known as emulsification

Front 443

What are micelles?

Back 443

Above a critical micellar concentration, bile salts form micelles
The bile salts are positioned on the outside of the micelle with their hydrophilic portions dissolved in the aqueous luminal fluid
Free fatty acids and monoglycerides are present inside the micelle, and have been essentially solubilized for intestinal absorption

Front 444

Where is bile produced?

Back 444

The liver

Front 445

Where is bile stored?

Back 445

It drains to the gallbladder via the hepatic ducts, and is stored/concentrated there until release

Front 446

What are choleretic agents?

Back 446

Things that stimulate the formation of bile

Front 447

How is bile formed?

Back 447

Hepatocytes synthesize primary bile acids (cholic acid and chenodeoxycholic acid) from cholesterol
In the intestine, the bacteria convert some primary bile acid to secondary bile acids (deoxycholic acid and lithocholic acid)
Bile acids are conjugated with glycine or taurine to form bile salts (taurocholic acid, etc)
Electrolytes and water are added to the bile
During the interdigestive period, the gallbladder is relaxed and fills with bile. The sphincter of Oddi is closed

Front 448

When is new bile made?

Back 448

Some bile is reabsorbed, and some is lost in the feces
New bile is made to compensate for fecal loss

Front 449

How does the gallbladder concentrate bile?

Back 449

Isosmotic absorption of solutes and water

Front 450

What hormones mediate contraction of the gallbladder?

Back 450

CCK
ACh

Front 451

How do secreted bile acids circulate back to the liver?

Back 451

The terminal ileum has an Na-bile cotransporter, which is secondary active
Since bile acids aren't recirculated until the terminal ileum, they are present for maximal lipid absorption throughout the upper small intestine

Front 452

How does ileal resection affect bile recirculation?

Back 452

Bile acids are no longer recirculated to the liver and are secreted in the feces
This depletes the bile acid pool and impairs fat absorption, which causes steatorrhea

Front 453

What is the intestinal brush border?

Back 453

The intestinal mucosa has villi, and the villi have microvilli; these microvilli are the brush border
This increases the absorptive surface area

Front 454

What types of sugars are absorbed

Back 454

Monosaccharides
Therefore, carbohydrates must be digested to monosaccharides before absorption can occur

Front 455

What are the three monosaccharides that can be absorbed?

Back 455

Glucose
Galactose
Fructose

Front 456

What does amylase do?

Back 456

Hydrolyzes the 1,4-glycosidic bonds in starch
This gives maltose, maltotriose, and branched structures known as alpha-limit dextrins

Front 457

Where is amylase found?

Back 457

Saliva and pancreatic secretion

Front 458

Where are maltase, a-dextrinase, and sucrase found?

Back 458

In the intestinal brush border

Front 459

What do maltase, a-dextrinase, and sucrase do?

Back 459

They digest the oligosaccharide amylase digestion products to glucose monomers

Front 460

What does lactase do?

Back 460

Cleaves lactose to glucose and galactose

Front 461

What does trehalase do?

Back 461

Cleaves trehalose to glucose

Front 462

What does sucrase do?

Back 462

Cleaves sucrase to glucose and fructose

Front 463

How are glucose and galactose absorbed?

Back 463

They are transported into the cells by Na-dependent transport via SGLT1
The sugar is transported uphill and Na is transported downhill
The sugar is then transported into the blood by facilitated diffusion using GLUT2
The Na-K ATPase maintains the Na gradient

Front 464

What would happen to glucose and galactose absorption if you poisoned the Na-K ATPase?

Back 464

It would be abolished because it requires the Na gradient established by the ATPase

Front 465

How is fructose absorbed?

Back 465

Transported by facilitated diffusion (GLUT5)
Therefore, it cannot be absorbed against a concentration gradient

Front 466

What is lactose intolerance?

Back 466

Brush border lactase doesn't work
You cannot hydrolyze lactose to glucose and galactose
Nonabsorbed lactose and water remain in the lumen of the GI tract and cause osmotic diarrhea

Front 467

What do endopeptidases do?

Back 467

Degrade proteins by hydrolyzing interior peptide bonds

Front 468

What do exopeptidases do?

Back 468

Hydrolyze one amino acid at a time from the C' of proteins and peptides

Front 469

What is the zymogen precursor of pepsin?

Back 469

Pepsinogen

Front 470

What activates pepsinogen to pepsin?

Back 470

Gastric acid

Front 471

What is the optimum pH for pepsin's function?

Back 471

1-3

Front 472

What happens to pepsin when pH exceeds 5?

Back 472

It becomes denatured
Therefore, as bicarbonate is secreted into the intestine, the pH increases and pepsin is inactivated

Front 473

What are the proteases produced by the pancreas?

Back 473

Trypsin
Chymotrypsin
Elastase
Carboxypeptidase A
Carboxypeptidase B

Front 474

What catalyzes the conversion of trypsinogen to trypsin?

Back 474

Enterokinase, a brush border enzyme

Front 475

How are the pancreatic proteases activated?

Back 475

Trypsinogen is activated to trypsin
Trypsin activates the rest of the zymogens (including trypsinogen)

Front 476

How are the pancreatic proteases inactivated?

Back 476

They will eventually degrade each other, and are absorbed along with dietary proteins

Front 477

What sorts of protein digestive products can be absorbed?

Back 477

Single amino acids
Dipeptides
Tripeptides

Front 478

How are free amino acids absorbed?

Back 478

Na-dependent amino acid cotransport occurs across the luminal membrane
The amino acids are then delivered to the blood by facilitated diffusion
This diffusion utilizes four separate carriers for neutral, acidic, basic, and imino amino acids

Front 479

How are dipeptides and tripeptides absorbed?

Back 479

H-dependent cotransport of peptides occurs across the luminal membrane
The peptides are hydrolyzed to amino acids by cytoplasmic peptidases
Amino acids are delivered to the blood by facilitated diffusion

Front 480

Is the absorption of free amino acids faster or slower than the absorption of di and tripeptides?

Back 480

Slower

Front 481

Where does lipid digestion take place?

Back 481

Stomach
Small intestine

Front 482

How are lipids digested in the stomach?

Back 482

Mixing breaks lipids into droplets, which increases the surface area for digestion by pancreatic enzymes
Lingual lipase digests some TAGs to monoglycerides and fatty acids
CCK slows gastric emptying, so there is plenty of time for digestion to proceed to completion

Front 483

How are lipids digested in the small intestine?

Back 483

Bile acids emulsify lipids to increase the surface area for digestion
Pancreatic lipases hydrolyze lipids to fatty acids, monoglycerides, cholesterol, and lysolecithin
The hydrophobic digestion produces are solubilized by bile acids in micelles

Front 484

What are the pancreatic lipases?

Back 484

Pancreatic lipase
Cholesterol ester hydrolase
Phospholipase A2

Front 485

How are lipids absorbed?

Back 485

Micelles bring the products of lipid digestion to the absorptive surface of the small intestine
Fatty acids, monoglycerides, and cholesterol diffuse across the luminal membrane into the cells
These digestion products are then re-esterified to glycerol, cholesterol, and phospholipids
Packaged with apoproteins into chylomicrons
Chylomicrons are transported out by exocytosis
They go into the lymph vessels and are added to the bloodstream via the thoracic duct

Front 486

What is abetalipoproteinemia?

Back 486

Lack of apoprotein B
You can no longer transport chylomicrons out of the intestinal cells

Front 487

What is pancreatic disease?

Back 487

Pancreatitis, cystic fibrosis
The pancreas can't produce enough digestive enzymes for lipid digestion

Front 488

What is the primary symptom of lipid malabsorption?

Back 488

Steatorrhea

Front 489

How does gastrin hypersecretion contribute to lipid malabsorption?

Back 489

Acid secretion increases
Duodenal pH decreases
This inactivates pancreatic lipase

Front 490

How does ileal resection contribute to lipid malabsorption?

Back 490

Bile acids do not recirculate to the liver
This depletes the bile acid pool

Front 491

How does bacterial overgrowth contribute to lipid malabsorption?

Back 491

This can lead to deconjugation of bile acids
The bile acids are absorbed too early in the upper small intestine
Now bile acids are not present throughout the small intestine to aid in lipid absorption

Front 492

How do the number of intestinal cells affect lipid absorption?

Back 492

If you don't have enough cells, obviously you won't have enough absorption
Somehow this is relevant in the case of tropical sprue

Front 493

How does abetalipoproteinemia contribute to lipid abnormality?

Back 493

You can no longer form chylomicrons

Front 494

How do electrolytes and water cross the intestinal epithelium?

Back 494

Cellular route -- crosses the cell membrane
Paracellular route -- moves between cells, across tight junctions

Front 495

How are epithelial cells attached to each other at the luminal membrane?

Back 495

Tight junctions

Front 496

How does the permeability of epithelial tight junctions vary throughout the GI tract?

Back 496

They can be tight/impermeable, such as in the colon
They can also be leaky/permeable, such as in the small intestine and gallbladder

Front 497

How is Na absorbed across the apical membrane of the small and large intestine?

Back 497

It always moves down its electrochemical gradient via:
Passive diffusion through Na channels
Na-glucose cotransport
Na-amino acid cotransport
Na-Cl cotransport
Na-H exchange

Front 498

What Na transport mechanisms are the most important in the small intestine?

Back 498

Na-glucose cotransport
Na-amino acid cotransport
Na-H exchange

Front 499

What Na transport mechanisms are most important in the colon?

Back 499

Passive diffusion via Na channels

Front 500

Where in the GI tract does aldosterone stimulate Na reabsorption?

Back 500

In the colon, via Na channels

Front 501

How is Na transported out of the intestinal enterocytes?

Back 501

Na-K ATPase

Front 502

How does Cl absorption accompany Na absorption throughout the GI tract?

Back 502

Passive paracellular diffusion
Na-Cl cotransport
Cl-HCO3 exchange

Front 503

How is dietary K absorbed?

Back 503

It is absorbed in the small intestine via passive paracellular diffusion

Front 504

How is K secreted in the colon?

Back 504

Stimulated by aldosterone

Front 505

How does diarrhea contribute to hypokalemia?

Back 505

The increased flow rate increases K secretion
Excessive K is lost in the feces

Front 506

How is water absorbed in the GI tract?

Back 506

Water absorption is secondary to solute absorption
It is isosmotic in the small intestine and gallbladder
In the colon, water permeability is low, so the feces may be hypertonic

Front 507

How are electrolytes secreted into the GI lumen?

Back 507

Electrolytes are transported from the blood to the lumen
The secretory mechanisms are found in the crypts

Front 508

Where in the intestinal architecture are the electrolyte absorptive mechanisms found?

Back 508

In the villi

Front 509

What electrolytes are secreted in the intestine?

Back 509

Cl is the primary secreted ion
Na passively follows Na
Water follows NaCl

Front 510

How is Cl secreted into the intestine?

Back 510

Transported through Cl channels that are regulated by cAMP

Front 511

How does Vibrio cholerae cause diarrhea?

Back 511

Produces cholera toxin
This toxin catalyzes ADP-ribosylation of the alpha subunit of the Gs protein coupled to adenylyl cyclase
This permanently activates AC
Intracellular cAMP increases and the Cl channels in the luminal membrane open
Na and water follow Cl into the lumen, leading to secretory diarrhea

Front 512

Besides Vibrio cholerae, what bacterium can also commonly cause diarrhea (and via a similar mechanism)?

Back 512

E coli

Front 513

How are the fat-soluble vitamins absorbed?

Back 513

They are incorporated into micelles and are absorbed with other lipids

Front 514

What are the fat-soluble vitamins?

Back 514

A, D, E, and K

Front 515

How are the water-soluble vitamins (except vitamin B12) absorbed?

Back 515

Na-dependent cotransport (usually)

Front 516

How is vitamin B12 absorbed?

Back 516

Forms a complex with intrinsic factor
This complex binds a receptor on the ileal cells and is reabsorbed there

Front 517

How does gastrectomy cause pernicious anemia?

Back 517

You are removing the parietal cells, which produce intrinsic factor
B12 injections are required to prevent anemia

Front 518

How is Ca absorbed?

Back 518

Depends upon the presence of adequate amounts of the active form of vitamin D (1,25-dihydroxycholecalciferol)
Vitamin D is made in the kidney
Vitamin D induces the synthesis of the intestinal Ca-binding protein calbindin D-28K

Front 519

What causes rickets and osteomalacia?

Back 519

Vitamin D deficiency
Chronic renal failure

Front 520

How is iron absorbed?

Back 520

Absorbed as heme iron (bound to Hb or myoglobin) or as free Fe2+
In the intestine, heme iron is degraded and Fe2+ is released
Free Fe2+ binds apoferritin and is transported into the blood
In the blood, Fe2+ circulates bound to transferrin, which delivers it to the liver
Iron is then transported from the liver to the bone marrow for hemoglobin synthesis

Front 521

What is the most common cause of anemia?

Back 521

Iron deficiency