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GI > PHYS: Metabolism > Flashcards

PHYS: Metabolism Flashcards

1
Q

What is the major site for both absorption and digestion in the GI tract?

A

small intestine

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2
Q

True or False: almost all digestion and absorption of carbs and protein is completed by the duodenum

A

FALSE: almost all digestion and absorption of carbs and protein is completed by the MID JEJUNUM

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3
Q

In which division are the vili the longest?

A

duodenum (where most absorption occurs)

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4
Q

What characteristic of the small intestine epithelium gives the greatest increase in surface area/absorption?

A

brush border (microvilli)

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5
Q

What are the two types of digestive enzymes?

A

1) luminal enzymes (secreted in salivary, gastric, and pancreatic juices)
2) Membrane bound enzymes (on apical membrane of intestinal epithelial cells)

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6
Q

What enzymes break down carbs and where are they made?

A
  • Saliva/pancreas: amylase

- Intestinal mucosa: sucrase, maltase, lactase, alpha-dextrinase

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7
Q

What enzymes break down protein and where are they made?

A
  • Stomach: pepsin
  • Pancreas: trypsin, chymotrypsin, carboxypeptidase, elastase
  • Intestinal mucosa: amino-oligopeptidase, dipeptidase, enterokinase
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8
Q

What enzymes break down lipids and where are they made?

A
  • Saliva: lingual lipase

- Pancreas: lipase colipase, phospholipase A2, cholesterol ester hydrolase

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9
Q

List the endopeptidases.

A

Pepsin
Trypsin
Chymotrypsin
Elastase

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10
Q

List the exopeptidases.

A

carboxypeptidase A and B

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11
Q

How do endopeptidases and exopeptidases differ?

A

Endopeptidases hydrolyze the interior peptide bonds of proteins while exopeptidases hydrolyze 1 AA at a time from the C-terminal ends of proteins and peptides

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12
Q

What are the two major paths of absorption?

A

Cellular path

Paracellular path

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13
Q

What is the first barrier that must be crossed in the cellular path?

A

glycocalyx (unstirred water layer that is a barrier to fat-soluble molecules)

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14
Q

What is the paracellular path?

A
  • substances move across the tight junctions between intestinal epithelial cells, through the lateral intercellular spaces, and into the blood.
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15
Q

Which part of the small intestine has the loosest epithelium/tight junctions?

A

duodenum (and it gets tighter as you move along

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16
Q

True or false: In order to be absorbed, all ingested carbohydrates must be in the form of monosaccharides

A

TRUE

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17
Q

List the three monosaccharides.

A

glucose
galactose
fructose

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18
Q

Does any starch metabolism occur in the stomach?

A

no (salivary amylase is broken down by the acid)

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19
Q

What is the MOA of alpha-amylase (pancreatic)?

A

Has the ability to cleave interior 1,4-glycosidic bonds of starches (but is unable to cleave beta-linkages of cellulose and other indigestible carbs) into disaccharides

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20
Q

List the disaccharides generated by pancreatic amylase?

A

alpha-limit dextrins, maltose and maltotriose

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21
Q

True or false: amylase can produce glucose.

A

FALSE

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22
Q

Where are the enzymes located that break disaccharides down into monosaccharides?

A

intestinal brush-border enzymes (alpha-dextrinase, maltase, sucrase)

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23
Q

What is trehalose broken down into?

A

2 glucose

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24
Q

What is lactose broken down into?

A

glucose + galactose

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25
Q

What is sucrose broken down into?

A

glucose and fructose

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26
Q

What two types of sugar does sucrase break down?

A

maltitriose and sucrose

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27
Q

What are the 3 disaccharides found in the diet?

A

trehalose
lactose
sucrose

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28
Q

True or false: trehalose, lactose and sucrose are NOT acted upon by amylase.

A

TRUE (they are already disaccharides)

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29
Q

Transport of monosaccharides across the lumen is dependent on what?

A

the concentration gradient set up by the sodium/postassium ATPase

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30
Q

What are the two apical membrane transporters that bring monosaccharides into intestinal epithelial cells?

A

SGLT-1

GLUT-5

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31
Q

What does SGLT-1 transport?

A

transports 1 glucose or galactose with 2 sodium ions into the cell (along the concentration gradient set up by the Na+/K+ ATPase)

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32
Q

What happens to the SGLT-1 transporter after bringing in sugar?

A

Na+ actively transported out allowing for the release of sugar and the transporter gets recycled back to the apical membrane

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33
Q

What does GLUT-5 do?

A

allows for facilitated diffusion of fructose along its concentration gradient

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34
Q

What is present on the basolateral membrane to allow monosaccharides to flow down their concentration gradients into the blood?

A

GLUT-2 transporters

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35
Q

What is released from chief cells in the stomach?

A

pepsinogen

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36
Q

How does pepsinogen get activated to pepsin?

A

low pH of stomach

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37
Q

What does pepsinogen do?

A

breaks down proteins into amino acids and oligopeptides

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38
Q

Where does pepsinogen function?

A

in the DUODENUM (HCO3- from pancreas)

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39
Q

True or false: pepsin is required for normal protein breakdown.

A

FALSE (not essential)

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40
Q

True or false: all proteases secreted by the pancreas are in “precursor” form.

A

TRUE

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41
Q

How does trypsinogen get activated to trypsin?

A

brush border enzyme enterokinase (initially only a small amount then it autocatalyzes itself)

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42
Q

How do all the other “precursor” proteases get activated?

A

tryspin activates all the other inactive precursors to their active forms

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43
Q

True or false: pancreatic proteases break down all proteins completely to amino acids.

A

FALSE: break the protein down into amino acids, dipeptides, tripeptides, and larger peptides (oligopeptides)

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44
Q

True or false: in order to be absorbed, protein must be in the form of free amino acids.

A

FALSE: must be in the form of free amino acids or di-/tri-peptides

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45
Q

What breaks down oligopeptides into smaller forms for absorption?

A

brush border peptidases

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46
Q

Which is more efficient, the free AA cotransporter or the dipeptide/ tripeptide cotransporter?

A

dipeptide/tripeptide cotransporter

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47
Q

What does free AA transport depend on?

A

cotransported with Na+ so depends on gradient established for Na+/K+ ATPase

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48
Q

True or false: There are different transporters for neutral, acidic, basic and imino amino acids

A

TRUE

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49
Q

What does dipeptide/tripeptide transport depend on?

A

cotransported with H+ along H+ gradient created by Na+/H+ exchanger in apical membrane

50
Q

What happens to dipeptides and tripeptides within small intestine epithelial cells?

A

most are hydrolyzed by cystoplasmic peptidase within intestinal epithelial cells to amino acid form be transported into the blood (though a very small amount are absorbed into the blood unchanged)

51
Q

True or false: most instances where an amino acid transporter is absent result in serous sequelae.

A

FALSE: if you are missing a carrier for amino acids, it is probably not clinically significant (because these can still be absorbed as di- and tripeptides).

52
Q

Why does cystinuria occur?

A

lack of cysteine transporter so you cannot reabsorb cysteine from kidney –> stones

53
Q

True or false: the diet composes a major fraction of the daily fluids that enter the small intestine

A

false, most is from secretions

54
Q

List the fat soluble vitamins.

A

A, D, E, K

55
Q

How does absorption of fat soluble vitamins differ from water soluble vitamins?

A

fat soluble uses diffusion, water soluble uses active mechanisms

56
Q

What is an example of a water soluble vitamin with a very complicated uptake system?

A

Vitamin B12 (cobalamin)

57
Q

Where is dietary B12 released?

A

in the stomach (by pepsin)

58
Q

What does free vitamin B12 bind to (excreted by salivary juice)?

A

R proteins

59
Q

What happens to the R-protein/cobalamin complex?

A

In the duodenum, pancreatic proteases break down R proteins→ shifting VitB12 over to intrinsic factor (from the gastric parietal cells)

60
Q

Is IF/VitB sensitive to pancreatic proteases?

A

NO

61
Q

Where does the IF/VitB complex get absorbed?

A

ileum

62
Q

IF someone is missing intrinsic factor, how do you treat them to prevent pernicious anemia?

A

get vitamin B12 injections

63
Q

How does vitamin D stimulate calcium absorption?

A

promotes calcium absorption from the small intestine by inducing the transcription of calbindin D-28K (transporter) to carry calcium from the lumen to the basolateral membrane

64
Q

In what forms is iron absorbed from the intestine?

A

free ferous iron (Fe2+)

heme iron

65
Q

What is responsible for conversion of ferric iron to ferrous iron for uptake?

A

gastric acid

66
Q

What happens if heme iron is taken up by intestinal epithelial cells?

A

acted upon by lysosomal enzymes within cells to release free iron

67
Q

What binds to free iron in epithelial cells and transports it to the basolateral membrane?

A

ferritin

68
Q

What releases iron into the blood?

A

ferroportin (when stimulated by hepcidin)

69
Q

What does iron travel in the blood bound to?

A

transferrin

70
Q

What happens when iron in the blood is high?

A

ferritin is upregulated (store iron) and ferroportin is down-regulated (so no more iron is put into blood)

71
Q

Are water and electrolytes absorbed more transcellularly or paracellularly?

A

paracellularly

72
Q

Because the colon absorbs more water than electrolytes, how does isotonicity remain present?

A

bacterial breakdown products

73
Q

What ions are mainly reabsorbed in the colon?

A

sodium and H+

74
Q

What do you lose in diarrhea?

A

K+ and HCO3- (leading to hypokalemia and metabolic acidosis)

75
Q

List the 4 types of transporters that bring Na+ into epithelial cells.

A

Na+ apical membrane pores
Na+/solute cotransporter
Na+/K+/2Cl- cotransporter
Na+/H+ exchanger

76
Q

How do Cl- and water get reabsorbed in the smal intestine?

A

paracellularly along the electrochemical gradient set up by sodium absorption

77
Q

How does Cl- get reabsorbed in the terminal ileum and colon?

A

Bicarbonate/chloride transporters send Cl- in for every HCO3- (made by Carbonic Anhydrase from products of oxidative metabolism) out—explains why stool water is alkaline.

78
Q

Why is K+ secreted into colonic lumen which Na+ is avidly reabsorbed?

A

sodium/potassium ATPase on the basolateral membrane

79
Q

How does aldosterone alter sodium absorption in the colon?

A

Aldosterone works on colon epithelial cells to increase Na+/K+ ATPases and to place more Na+ channels into the apical membrane

80
Q

How do sodium and water get secreted by the intestines?

A

Opening of Cl- channels (CFTR) initiates Cl-Secretion. Sodium and water follow Cl- through paracellular pathways.

81
Q

Why do apical membrane Cl-channels (CFTR) get activated?

A

Ach or VIP bind to the basolateral receptor, activate adenylyl cyclase→ cAMP→ opens the Cl- channels (CFTR)

82
Q

Is metabolic acidosis in diarrhea normal anion gap?

A

yes (because Cl- is retained)

83
Q

What type of diarrhea is caused by impaired absorption or the presence of non-absorbable solutes in the lumen of the intestine?

A

osmotic diarrhea

84
Q

List 4 reasons for osmotic diarrhea.

A
  • Lack of enzymes (ex. lactase)
  • Decreased absorptive surface (ex. celiac disease)
  • Precipitation of bile salts (leads to steatorrhea)
  • Faster motility (less time for absorption
85
Q

What type of diarrhea is caused by excessive secretion of fluid by crypt cells?

A

secretory diarrhea

86
Q

List 2 causes of secretory diarrhea.

A

Bacteria

Verner Morrison syndrome

87
Q

What type of bacteria cause secretory diarrhea?

A

Vibrio cholera

88
Q

How does the vibrio cholera toxin work?

A

Catalyze ADP ribosylation of the alpha-s subunit of the Gs protein that is coupled to adenylyl cyclase. This permanently activates adenylyl cyclase and leads to high cAMP levels and constant opening of the Cl- apical membrane transporter. Cl- flows out, accompanied by Na+ and H2O leading to high volume of diarrhea.

89
Q

What is Verner Morrison syndrome?

A

tumor produces VIP allowing for constant activation of adenylyl cyclase and secretory diarrhea

90
Q

Where are the signals for hunger and satiety integrated?

A

arcuate nucleus of the hypothelamus

91
Q

What receives long term signals that stimulate alpha-MSH to stimulate metabolism and inhibit food intake?

A

POMC

92
Q

What stimulates POMC?

A

insulin and leptin

93
Q

What leads to decreased metabolism and increased food intake and is inhibited by metabolic and satiety signals?

A

NPY

94
Q

What inhibits NPY?

A

leptin

PYY (a bit)

95
Q

What stimulates NPY?

A

ghrelin

96
Q

What works to inhibit the alpha-MSH pathway to promote food intake and decreased metabolism; stimulated by hunger?

A

AgRP

97
Q

What inhibits AgRP?

A

leptin

PYY

98
Q

What stimulates AgRP?

A

Ghrelin

99
Q

When is Ghrelin relased?

A

released from stomach before you eat to stimulate food intake

100
Q

How does CKK alter appetite and metabolism?

A

decreases appetite and decreases metabolism

101
Q

Where does lipid digestion start?

A

mouth (lingual lipase) and stomach (gastric lipase)

102
Q

What do lipases do?

A

Break down TGs into glyceros and FFAs

103
Q

Why is it important that the stomach releases chyme slowly into the small intestine?

A

allows enough time for pancreatic enzymes to digest lipids

104
Q

What controls gastric emptying?

A

CCK

105
Q

How doe lipid digestion products get emulsified to dietary lipid?

A

bile salts and lysolecithin surround them and produce small droplets of lipid dispersed int he aqueous solution of hte intestinal lumen

106
Q

What activates procolipase to coplipase?

A

trypsin

107
Q

What is the role of colipse?

A

has a binding site for pancreatic lipase (binds to fat and displaces bile salts to allow the lipase to digest fat)

108
Q

What is the role of pancreatic lipase?

A

hydrolyzes TGs into 1 monoglyceride and 2 FAs

109
Q

What enzyme hydrolyzes cholesterol ester to free cholesterol and fatty acids (and also breaks down monoglyceride into glycerol and FFA)?

A

cholesterol ester hydrolase

110
Q

What enzyme is activated by trypsin and hydrolyzes phospholipids to lysolecithin and FAs?

A

phospholipase A2

111
Q

What is the exception to the statement that all breakdown products of lipid digestion are hydrophobic and not soluble in water?

A

glycerol

112
Q

How do all digestive products (minus sorbitol) become solubilized int he intestinal lumen?

A

in mixed micelles

113
Q

What is a micelle?

A

cylindrically shaped disks with a core of lipid digestive products and an exterior of bile salts (ampipathic)

114
Q

True or false: micelles enter intestinal epithelial cells.

A

FALSE: Micelles diffuse to apical membrane of intestinal epithelial cells and lipids are released from the micelle and diffuse down concentration gradient into the cell.

115
Q

What happens to the products of lipid digestion within the intestinal epithelial cells?

A
  • Bound by FA binding proteins

- Reesterified with FFAs on smooth ER to form original lipids, TGs, cholesterol, ester, and phospholipids

116
Q

What happens to the re-esterified products?

A

packaged with apoproteins into chylomicrons

117
Q

What is a chylomicron?

A

shell of phospholipids (80%) and apoproteins (20%) with a core of triglycerides and cholesterol

118
Q

What condition leads to a failure of patients to absorb chylomicrons?

A

abetalipoproteinemia

119
Q

Because chylomicrons are too big to enter the blood at capillaries, how do they get into the circulation?

A

enter lymphatic capillaries (lacteals) by moving between the endothelial cells that line the lacteals. Lymphatic circulation empties these into thoracic duct→ blood.

120
Q

What would lead to TGs in stool?

A
  • pancreatic insufficiency (not enough lipid digestion due to lack of pancreatic enzymes)
  • overly acidified duodenum
121
Q

What would lead to presence of FAs and monoglycerides in the stool?

A
  • bile salt deficiency (unable to solublize lipid digestion products)
  • bacterial overgrowth
  • decreased pH
  • celiac disease

GI (21 decks)

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