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BRS Phys > Ch 6 > Flashcards

Ch 6 Flashcards

1
Q

Contraction of circular muscle has what effect on the GI lumen?

A

Decrease in diameter

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2
Q

Contraction of longitudinal muscle has what effect on the GI lumen?

A

Shortening of the segment

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3
Q

What two plexi make up the enteric nervous system?

A

Meissner’s (submucosal) and Auerbach’s (myenteric)

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4
Q

What two layers is Auerbach’s (myenteric) plexus located between?

A

Circular and longitudinal muscle

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5
Q

What does Auerbach’s (myenteric) plexus control?

A

Motility of GI smooth muscle

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6
Q

What does Meissner’s (submucosal) plexus control?

A

GI secretions

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7
Q

What are the two functions (main and minor) of gastrin?

A

Main - increase H+ secretion Minor - Stimulation of growth of gastric mucosa

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8
Q

Name 3 stimuli for gastrin releaseetin

A

Small peptides/amino acids (phenylalanine/tryptophan are the most potent) Stomach distension Vagal stimulation (through GRP, NOT ACH!)

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9
Q

What cells release gastrin and where are they located?

A

G cells - antrum of stomach

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10
Q

Name 2 things that inhibit gastrin release

A

Decreased stomach pH Somatostatin

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11
Q

What are the two most potent stimulators of gastrin release?

A

Phenylalanine and tryptophan

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12
Q

Atropine will have what effect on gastrin production?

A

NO EFFECT! Gastrin release is stimulated by parasympathetics (CN X) increasing GRP (gastrin releasing peptide), NOT ACH!

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13
Q

Patient with pancreatic mass has elevated stomach acid. Dx?

A

Zollinger-Ellison syndrome (gastrinoma)

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14
Q

Jejunal ulcers are pretty much pathognomonic for…

A

Zollinger-Ellison syndrome (pancreatic gastrinoma)

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15
Q

What cells release CCK and where are they located?

A

I cells of the duodenum and jejunum

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16
Q

What are two stimuli for CCK secretion?

A

Small peptides/amino acids and fatty acids

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17
Q

Name 5 effects of CCK.

A

Stimulates gallbladder contraction Relaxes the sphincter of Oddi

Increases pancreatic HCO3- secretion

Inhibits gastric emptying Stimulates pancreas/GB growth

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18
Q

What effect does CCK have on gastric emptying?

A

Slows it

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19
Q

What cells secrete secretin and where are they located?

A

S cells in the duodenum

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20
Q

Name two stimuli for secretin secretion.

A

H+ ions in duodenum Fatty acids in duodenum

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21
Q

Name 3 effects of secretin

A

Stimulates pancreatic HCO3- release Inhibits H+ secretion by gastric parietal cells

Increases bile production

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22
Q

What is the main role of GIP?

A

Stimulate insulin release

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23
Q

Is oral or IV glucose more potent in causing insulin release?

A

Oral, because it induces release of GIP

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24
Q

What is the only GI hormone that is released in response to fat, protein AND carbohydrate?

A

GIP

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25
Q

What is the function of somatostatin?

A

Inhibits release of ALL GI hormones

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26
Q

What is the function of GI histamine?

A

Increases H+ secretion directly and by potentiating effects of gastrin and CN X

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27
Q

What are the functions of VIP?

A

Produces relaxation of GI smooth muscle (especially LES) Stimulates pancreatic HCO3-, inhibits H+ secretion

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28
Q

What are the SSX of a VIPoma?

A

WDHA syndrome - Watery Diarrhea, Hypokalemia, Achlorhydria (pancreatic cholera)

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29
Q

What are slow waves?

A

Oscillating membrane potentials inherent to some GI smooth muscle

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30
Q

What cells are the “pacemaker” of the GI tract?

A

Interstitial cells of Cajal - generate slow waves

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31
Q

What is the mechanism for slow wave production?

A

Cyclic opening of calcium channels (depolarization) followed by opening of potassium channels (repolarization)

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32
Q

Where along the GI system is slow wave frequency lowest? Highest?

A

Lowest - stomach (3 slow waves/minute) Highest - duodenum (12 slow waves/minute)

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33
Q

Where in the brainstem is the swallowing center?

A

Medulla

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34
Q

What hormone causes the lower esophageal sphincter to relax while swallowing?

A

VIP

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35
Q

What is receptive relaxation?

A

Relaxation of the orad region of the stomach in preparation for a food bolus

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36
Q

In what disorder does the LES fail to relax?

A

Achalasia (bird’s beak sign on barium swallow)

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37
Q

What GI organ has a 3rd muscle layer and what is the layer called?

A

Stomach - has oblique layer in addition to circular and longitudinal

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38
Q

What GI hormone participates in receptive relaxation?

A

CCK

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39
Q

Explain stomach retropulsion.

A

Food in the stomach is moved towards a firmly shut pylorus, and is shot back into more orad regions of the stomach, causing mixing

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40
Q

What hormone produces migrating myoelectric complexes?

A

Motilin

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41
Q

What is the function of migrating myoelectric complexes?

A

To clear the a GI organ of any remaining material

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42
Q

What drug can be used as a motilin analog to increase MMC’s?

A

Erythromycin

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43
Q

Gastric emptying is fastest when stomach contents are of what tonicity?

A

Isotonic

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44
Q

How does fat slow gastric emptying?

A

Through release of CCK

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45
Q

Explain the gastroileal reflex.

A

Food in the stomach triggers increased peristalsis in the ileum and relaxation of the ileocecal valve - this delivers contents to the LI

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46
Q

How often per day do colonic mass movements occur?

A

1-3 times per day

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47
Q

Explain the rectosphincteric reflex.

A

As the rectum fills with feces, it contracts and the internal anal sphincter relaxes

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48
Q

Explain defecation

A

When it is convenient (lol), the external anal sphincter relaxes. Rectal smooth muscle contracts, expelling feces

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49
Q

Explain the gastrocolic reflex

A

Presence of food in the stomach increases the motility of the colon and increases the frequency of mass movements

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50
Q

Where does carbohydrate digestion start?

A

In the mouth with salivary amylase (ptyalin)

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51
Q

Explain the ionic characteristics of saliva relative to plasma.

A

Saliva has higher K+ and HCO3- and less Na+ and Cl- than plasma It is always HYPOTONIC to plasma (even in high flow rates)

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52
Q

How do salivary ductal glands handle Na, Cl, HCO3, and K?

A

Reabsorb Na and Cl back into the blood Secrete K and HCO3 into the saliva

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53
Q

What happens to salivary concentrations of Na, Cl, HCO3 and K in high flow rates (parasympathetic stimulation) RELATIVE TO NORMAL?

A

Na/Cl concentrations will be higher than in normal saliva (not reabsorbed as much) K/HCO3 concentrations will be lower than in normal saliva (not secreted as much)

However: the fluid will STILL BE HYPOTONIC TO PLASMA!

54
Q

What happens to salivary concentrations of Na, Cl, HCO3 and K in low flow rates (sympathetic stimulation) RELATIVE TO NORMAL?

A

Na/Cl concentrations will be lower than in normal saliva (reabsorbed more) K/HCO3 concentrations will be higher than in normal saliva (secreted more) However: the fluid will STILL BE HYPOTONIC TO PLASMA!

55
Q

What effect does aldosterone have on saliva production?

A

Causes more Na reabsorption and K secretion (just like in the kidney!)

56
Q

Why is saliva always hypotonic to plasma?

A

Because the ductal cells are impermeable to water, so there is always a net reabsorption of solute with respect to water.

57
Q

What does excess parasympathetic stimulation do to saliva production? Sympathetic?

A

Both INCREASE, but parasympathetic stimulation is more powerful

58
Q

What cells secrete pepsinogen?

A

Chief cells

59
Q

What cells secrete intrinsic factor?

A

Parietal

60
Q

What stomach cells secrete H+ ions?

A

Parietal

61
Q

What 2 things are secreted by parietal cells?

A

H+ and intrinsic factor

62
Q

What do chief cells secrete?

A

Pepsinogen

63
Q

Where are chief cells primarily located in the stomach?

A

Body

64
Q

Where are parietal cells primarily located in the stomach?

A

Body

65
Q

Explain the pump that pumps H+ ions into the gastric lumen.

A

It is a H/K ATPase which antiports hydrogen into the lumen in exchange for potassium

66
Q

What is the prototypical proton pump inhibitor?

A

Omeprazole

67
Q

Explain “alkaline tide”

A

HCO3- produced by carbonic anhydrase in gastric parietal cells is reabsorbed into the blood in exchange for chloride which is secreted to make HCl. Thus, the pH of the blood leaving the stomach is relatively high.

68
Q

Name 3 stimuli for H+ release

A

Gastrin, Ach (CN X), Histamine

69
Q

What is the prototypical histamine blocker used for GERD?

A

Cimetidine (potent CYP450 inhibitor)

70
Q

Where are mucous cells most prevalent in the stomach?

A

Antrum

71
Q

Atropine will have what effect on acid secretion?

A

Decrease it (blocks the direct pathway, does not decrease acid secretion mediated by gastrin)

72
Q

Which subset of receptors does histamine bind in the stomach and what is its second messenger?

A

H2, cAMP (Gs)

73
Q

What role do prostaglandins play in the stomach?

A

Inhibit H+ secretion by activating Gi (this is why NSAIDs, which block prostaglandin synthesis, cause ulcers)

74
Q

What is produced by H. pylori that allows it to survive in the acidic environment of the stomach?

A

Urease

75
Q

Exocrine pancreatic secretions contain high levels of which ion?

A

HCO3-

76
Q

Explain how pancreatic duct cells handle the Cl- and HCO3-

A

Secrete HCO3- in exchange for Cl-

77
Q

As the flow rate of exocrine pancreatic juice increases, what happens to the concentration of HCO3- and Cl- in the fluid?

A

HCO3- increases Cl- decreases

78
Q

What receptor and second messenger does secretin work through?

A

Gs, cAMP

79
Q

What receptor and second messenger does CCK work through?

A

Gq, Ca/IP3

80
Q

What is the main function of bile salts?

A

Form micelles for emulsification of fats

81
Q

How does the gallbladder concentrate bile salts?

A

Removes solutes and water (isoosmotically)

82
Q

Which cells produce bile?

A

Hepatocytes

83
Q

Bile salts are formed after conjugation of bile acids with one of which two things?

A

Glycine or taurine

84
Q

How are bile acids reabsorbed in the small intestine?

A

Sodium/bile acid cotransporter (symport)- located in the terminal ileum

85
Q

Where are bile salts reabsorpbed in the small intestine?

A

Terminal ileum

86
Q

Patient with severe Crohn’s disease has steatorrhea. What is going on?

A

Crohn’s disease commonly affects the terminal ileum, which is the site of reabsorption of bile acids. Lack of bile can lead to steatorrhea.

87
Q

What bonds are broken by salivary and pancreatic amylases?

A

Alpha 1, 4

88
Q

Lactase degrades glucose into which two monosaccharides?

A

Galactose and glucose

89
Q

Trehalase degrades trehalose into…

A

Two glucose molecules

90
Q

Sucrase degrades sucrose into…

A

Glucose and fructose

91
Q

Explain how glucose and galactose are absorbed in into epithelial cells in the small intestine.

A

Secondary active transport by a sodium/glucose transporter (SGLT-1)

92
Q

Explain how glucose, galactose, and fructose are absorbed into the blood from small intestine epithelial cells.

A

Facilitated diffusion through GLUT-2 transporters

93
Q

Explain how fructose is reabsorbed in the small intestine

A

Absorbed into the small intestine cells by GLUT 5 transporters (facilitated diffusion), and into the blood via GLUT 2 transporters

94
Q

What is the function of enteropeptidases?

A

Degradation of proteins by hydrolysis of interior peptide bonds

95
Q

What is the unction of exopeptidases?

A

Degradation of proteins by cleaving one amino acid at a time from the C terminus

96
Q

How, and into what is pepsinogen activated?

A

Pepsinogen is activated into pepsin by a low pH (between 1 and 3)

97
Q

What is the function of pepsin?

A

Protein degradation

98
Q

What enzyme activates trypsinogen into trypsin?

A

Enterokinase

99
Q

What is the function of trypsin?

A

Conversion of the pancreatic proenzymes chymotrypsinogen, proelastase, proelastase, and procarboxypeptidase into their active forms

100
Q

What is the function of enterokinase?

A

Activates trypsinogen into trypsin

101
Q

What 3 sizes of proteins can be absorbed in the small instestine?

A

Amino acids, dipeptides, tripeptides

102
Q

How are amino acids absorbed in the small intestine?

A

Secondary active transport (symport) with sodium

103
Q

How are di- and tripeptides absorbed in the small intestine?

A

Secondary active transport (symport) with hydrogen ions

104
Q

Where does lipid digestion begin?

A

In the mouth. A very minor amount of lipids are digested by lingual lipases.

105
Q

What enzymes carry out most of lipid digestion?

A

Pancreatic lipases

106
Q

What is the function of micelles?

A

To bring the products of lipid digestion into contact with the absorptive surface of the small intestine. Fatty acids, monoglycerides, and cholesterole diffuse across the luminal membrane into cells.

107
Q

What happens to the products of lipid digestion after they are absorbed into intestinal cells?

A

They are re-esterified and form chylomicrons

108
Q

Where are chylomicrons transferred to after being formed in small intestine cells?

A

Lymphatic system, then to the blood via the thoracic duct

109
Q

Why does cystic fibrosis cause steatorrhea?

A

Reduced secretion of pancreatic lipases = can’t digest fats

110
Q

Why does chronic diarrhea cause hypokalemia?

A

Potassium secretion in the large intestine is controlled by a flow-rate dependent mechanism. Excess flow = excess loss of potassium.

111
Q

What is the primary ion secreted along the length of the intestinal lumen?

A

Chloride (regulated through Gs, cAMP)

112
Q

How does V. cholerae cause diarrhea?

A

Increase cAMP (Gs), which causes excess chloride ion secretion. Water follows chloride, leading to diarrhea.

113
Q

How are most water soluble vitamins absorbed?

A

Through sodium dependent co-transport mechanisms

114
Q

Where is B12 absorbed?

A

Terminal lieum

115
Q

What is the function of intrinsic factor?

A

Required for absorption of B12. Lack of intrinsic factor (autoimmune gastritis, gastrectomy, etc.) results in pernicious anemia.

116
Q

Patient post total gastrectomy shows hypersegmented neutrophils on smear. What’s going on?

A

B12 deficiency (pernicious anemia). Loss of parietal cells and intrinsic factor leads to a B12 deficiency.

117
Q

What vitamin causes increased absorption of calcium from the gut?

A

Vitamin D (1,25 dihydroxycholecalciferol)

118
Q

What two diseases (one in adults, one in kids) are caused by vitamin D deficiency?

A

Adults - osteomalacia Kids- rickets

119
Q

Production of what intestinal calcium binding protein is increased by vitamin D?

A

Calbindin D-28K

120
Q

What enzyme conjugates bilirubin to glucuronic acid in the liver?

A

UDP glucuronyl transferase

121
Q

Explain the metabolism of hemoglobin.

A

Hemoglobin is degraded into bilirubin by the reticuloendothelial system (phagocytes in connective tissue). Bilirubin is carried to the liver, where it is conjugated by UDP glucuronyl transferase into conjugated bilirubin. Some conjugated bilirubin is excreted in the urine, the rest goes into the bile. Conjugated bilirubin is converted into urobilinogen in the gut. Most urobilinogen is returned to liver by enterohepatic circulation. The urobilinogen that isn’t returned to the liver is metabolized in the colon to urocobilin and stercobilin, which are excreted in feces.

122
Q

What metabolite of bilirubin is returned to the liver via enterohepatic circulation?

A

Urobilinogen

123
Q

What two metabolites of bilirubin are excreted in the feces?

A

Urobilin, stercobilin

124
Q

Name 3 functions of the liver with respect to carbohydrate metabolism.

A

Carries out gluconeogenesis, stores glucose as glycogen, and breaks down glycogen to release glucose into the blood

125
Q

What enzymes carry out phase I reactions of xenobiotic detoxification?

A

Cytochrome P450s

126
Q

What is the function of phase II detoxification reactions?

A

Conjugation of xenobiotics to make them more water soluble

127
Q

In what form and where is iron absorbed in the gut?

A

As Fe 2+ (ferrous) in the duodenum

128
Q

Where is folate absorbed in the gut?

A

Jejunum

129
Q

What are Peyer’s patches, where are they found, and what do they do?

A

Lymphoid tissue in the lamina propria and submucosa of ileum. They contain M cells that take up antigen and B cells that are activated to secrete IgA.

130
Q

What is the histological hallmark of ileal tissue?

A

Peyer’s patches

131
Q

What is the histological hallmark of duodenal tissue?

A

Brunner’s glands

132
Q

What is the main function of Brunner’s glands and where are they located?

A

They secrete a mucous-rich alkaline fluid in the duodenum to help protect it from acid coming from the stomach

BRS Phys (6 decks)

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