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Block 3 Week 3 Dani > Ward Small and Large intestine (2) > Flashcards

Ward Small and Large intestine (2) Flashcards

1
Q

CIrcular concentric kirkrin folds (plicae), do what for the small intestine?

A

increase surface area 3X

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2
Q

What all increases the surface area of the small intestine?

A

plica (krikling) (3X)
villi (30X)
Microvilli on villi (600X)

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3
Q

Each enterocyte on the villi have (blank) increasing the surface area even further/

A

microvilli

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4
Q

enterocytes have what kind of border in the small intestine?

A

brush border

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5
Q

THe (blank) on the microvilli surface of enterocytes is the location of numerous enzymes that provide final stages of protein and carbohydrate breakdown for absorption.

A

glycocaylax

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6
Q

The presence of (blank) on the microvilli surface ensures that the final stages of intestinal content breakdwn occurs at the same point where contents are absorbed.

A

enzymes

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7
Q

The presence of enzymes on the microvilli surface ensures that the final stages of intestinal content breakdown occurs at the same point where contents are absorbed.
This reduces the possibility of (blank) and subsequently (blank) being established within the intestinal lumen.

A

osmotic gradients

osmotic diarrea

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8
Q

What does each villi of the intestine get?

A

its own blood supply and blind ended lacteals

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9
Q

Describe the mucosa of the small intestine.

A

has villi filled with blood, lacteals, lymph nodules, intestinal gland, underneath is muscularis mucosa

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10
Q

Describe the submucosa of the small intestine?

A

has blood vessels
submucosal plexus
lymphatic vessels

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11
Q

What is the muscularis externa made up of in the small intestine?

A

ICOL

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12
Q

Where do we find the myenteric plexus?

A

in between IC and OL

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13
Q

Does the small intestine have a serosa or a adventitia?

A

serosa

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14
Q

(blank) supply to the villi ensures the optimal removal of absorbed peptides, amino acids, sugars and fats.

A

Blood and lymphatic

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15
Q

To ensure maximal absorption the small intestine undergoes (blank) which ensure proper mixing of the lumenal contents, exposure of the contents to digestive enzymes and maximal exposure of the digestion products to the intestinal mucosa.

A

segmentation

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16
Q

How do we get movement of the contents of the lumen of the intestine in the aboral diection?

A

A gradient along the small intestine with the highest frequency in the duodenum and the lowest in the terminal ileum. This gradient ensures oral to aboral movement of the contents in the lumen of the intestine.

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17
Q

What are the three major sources of carbs as food sources?

A

disaccharides-sucrose/ lactose
polysaccharides or starches
Other-> usually ingested to lesser degree such as amylose, glycogen, alcohol, lactic acid etc.

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18
Q

(blank) is a carb that cannot be broken down for absorption in the GI tract.

A

cellulose

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19
Q

What does oral/salivary amylase?

A

hydrolysis of carbs (3-5%)

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20
Q

Hydrolysis of carbs continues into the stomach where in 1 hour, 30-40% of starches are hydrolyzed to (blank)

A

maltose

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21
Q

Pancreatic secretions contains a lot of (blank) that is identical in function to that found in saliva, but is several times more powerful.
What does this do?

A

alpha amylase

digests carbs/starches

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22
Q

Following neutralization of chyme that enters the proximal duodenum, by bicarb secretion, pancreatic secretion of amylase continues the digestion of carbs producing (blank,blank and blank)/

A

maltose, maltotriose, and alpha limited dextrins

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23
Q

What class of enzymes does the SI release?

A

enterokinases/enteropeptidase
disaccharidases
peptidases

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24
Q

What is enterokinase/enteropeptidase?

A

it is a serine protease that converts trypsinogen to trypsin

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25
Q

What are all the digestive enzymes that the pancreas secretes?

A 
Calling All Ladies, Please Try Cheap Ethiopian Cuisine
Cholesterol esterase
amylase
Lipase
Phospholipase A2
trypsin
chymotrypsin
Elastase
carboxypeptidase
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26
Q

What does somatostatin do?

A

it is an inhibitor of everything

i.e inhibits Gi hormones, inhibits glucagon, insulin etc.

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27
Q

The digestions products of starch and other disaccharides are further digested by enzymes located at the (blank)

A

brush border membrane

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28
Q

Where do we find the enzymes of the brush border membrane of the SI?

A

near the membrane transport carriers that bring glucose or galactose into the enterocyte.

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29
Q

How can you up regulate maltase and sucrase?

A

via consuming a diet high in sucrose and fructose

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30
Q

Epithelial cells lining the microvilli of mucosa of the small intestine contain what four disaccharidases?

A

lactase
sucrase
maltase
alpha-dextrinase

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31
Q

glucose and fructose =?

A

sucrose

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32
Q

How do we move glucose and galactose into an enterocyte and out into the blood stream?

A

Na+ moves down its concentration gradient and bring glucose or galactose with it.

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33
Q

How do we keep from overloading an enterocyte with Na+ if it is constantly going down its gradient and bringing sugars with it.

A

The sugars increase the activity of a Na+/K+ ATPase which pumps the sodium back out of the enterocyte

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34
Q

What is another name for the sodium-glucose co transport mechanisM?

A

SLGT1

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35
Q

How do we get glucose or galactose out of the cell?

What about fructose?

A

GLUT2

GLUT5

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36
Q

What are the two ways glucose can be absorbed?

A

some can be absorbed passively, but most is absorbed actively

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37
Q

Can people with celiac disease absorb glucose and fructose?

A

barely

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38
Q

If you have glucose malabsorbption, will this affect your fructose absorption?

A

yes (it wont be as good)

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39
Q

What ethnicities are most effected by lactose deficiency?

A

blacks, orientals, and eskimos

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40
Q

Why do some people get malabsorption of carbs?

A

because they are lacking membrane bound proteins necessary for carb uptake

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41
Q

undigested (blank) causes osmolality changes.

A

lactose

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42
Q

Why does lactose intolerance cause diarrea?

A

Undigested lactose causes osmolality changes. Osmolality is further increased by the production of lactic acid by intestinal bacteria acting on the lactose. Osmolality increases in the intestinal lumen cause water to enter the lumen. Increases in luminal water cause distension and increased propulsion in the intestine producing a watery diarrhea.

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43
Q

The enzymatic deficiency of lactose intolerance can be genetic or by factors such as (blank) which results in diarrhea, flatulence and distention

A

viral infections

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44
Q

How do you test for lactose intolerance?

A

fast->take blood sample-> look to see if you have a flat curve (no glucose rises pat 25)-> if low then lactose intolerance

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45
Q

What do dietary fibers that are not absorbed do? WHy is this important?

A

add to the bulkiness in stool
decreases transit time. (may decrease colon cancer due to lack of time for carcinogenic bile acids AKA lithocholic acid to hang out)

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46
Q

How does lithocholic acid form?

A

via decongugation of chendeoxycholic acid by bacteria in the lumen

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47
Q

Almost all proteins require (blank) before absorption. What is the one exception?

A

digestion

newborns can absorb y-globulins from milk

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48
Q

Besides eating protein, how can we get protein?

A

1) intestinal mucosa gets sleuthed off into the lumen and used as protein
2) Enzymatic proteins get degraded and reabsorbed (pancreatic enzymes can be absorbed without digestion via pinocytosis back into pancreas)

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49
Q

Proteins are almost entirely absorbed in the (blank)

A

jejunum

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50
Q

When and how can you absorb basic proteins?
neutral?
Acidic?

A

(i) Basic: Actively absorbed at concs. less than 3 mM.
(ii) Neutral: Requires concs. of 20 mM to be absorbed.
(iii) Acidic: Are significantly metabolized prior to absorption.

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51
Q

Explain breakdown of proteins?

A

proteins get digested via pancreatic proteases and by brush border enzymes-> get absorbed via active transport into cells-> get moved to blood via facilitated diffusion

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52
Q

How often are proteins absorbed as single amino acids?

A

70% of the time

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53
Q

Absorption is dependent on the (blanK)

A

sodium glucose cotransporter

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54
Q

Where do we find enterokinase/enteropeptidase?

A

on the brush border of duodenal enterocytes

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55
Q

The activity of enterokinase is stimulated by the presence of (blank)

A

trypsinogen (remember it turns trypsinogen into trypsin)

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56
Q

How does enterokinase activate trypsinogen?

A

it releases a hexapeptide from N-terminal of trypsinogen

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57
Q

What does active trypsin do?

A

it activates trypsinogen and other peptidase precursors from the pancreas

58
Q

Trypsin makes active what 5 molecules?

A 
trypsinogen
chymotrypsinogen
proelastase
procarboxypeptidase A
procarboxypeptidase B
59
Q

Which of the enzymes that trypsin activates are endopeptidases?

A

trypsin
chymotrypsin
elastase

60
Q

What is this:

Attacks peptide bonds involving basic amino acid ends - products with basic C terminal ends.

A

Trypsin

61
Q

What is this:

Attacks peptide bonds involving aromatic amino acid ends - products with aromatic C terminal ends.

A

chymotrypsin

62
Q

What is this:

Attacks peptide bonds involving neutral aliphatic AA ends - products with neutral C terminal ends.

A

elastase

63
Q

WHich of the enzymes that trypsin activates are exopeptidases?

A

carboxypeptadase A

carboxypeptadase B

64
Q

What is this:

Attacks peptides with aromatic and neutral aliphatic amino acids at the C terminus.

A

Carboxypeptidase A

65
Q

What is this:

Attacks peptides with basic amino acids at the C terminus.

A

Carboxypeptidase B

66
Q

Many amino acids are taken into enterocytes by the proton coupled symporter called (blank)

A

PEPT1

67
Q

Gastric pepsin and pancreatic peptidases digest proteins into (blank) which are readily absorbed across the brush border of mucosal cells

A

di and tripeptides

68
Q

Once di and tripeptides get into enterocytes, how do they get further cleaved into amino acids?

A

the cytosol of eptihelial cells contain peptidases that break the remaining linkages

69
Q

The absorption of amino acids is coupled to the transport of (blank) similiar to that described for the absorption of monosaccharides

A

Na+

70
Q

Amino acids are (blank) at different rates therefor 2 carrier systems are involved and can work in parallel with one another.

A

absorbed

71
Q

Lumenal digestion of proteins results in 40% free AAs and 60% small peptides. What happens to these?

A

the free AAs and di and tripeptides get absorbed by the the larger peptides are acted on by brush border peptidases to produce AAs or smaller peptides for absorption. Once the di and tri are absorbed, peptidases in cytoplasm break them down into AAs

72
Q

What is this:
a specific fraction of wheat protein attacks the microvilli of the mucosa, denuding it of these cells. Patients with this are thought to lack certain peptidases and the consequent incomplete digestion of gluten results in the production of toxic substances. In unaffected individuals, gluten hydroxylase breaks down the toxic wheat peptide.

A

celiac sprue

73
Q

What disease is this:

May lead to a decrease or absence of trypsin leading to poor absorption of protein.

A

Cystic fibrosis and hereditary pancreatitis

74
Q

What disease is this:

Characterized by defective transport of cystine in the proximal renal tubule and small bowel.

A

Cystinuria

75
Q

What disease is this:
Hereditary condition in which the active transport of several neutral AA’s is deficient in both the renal tubules and small bowel. When patients are fed dipeptides these are readily abosorbed, just not free AA’s.

A

Hartnup disease

76
Q 
What are these:
phospholipids
sterols
hydrocarbons
waxes
A

Complex organic substances

77
Q

how do you absorb lipids?

A

you put them through processes that places them into micelles that are able to passively diffuse through the brush border

78
Q

Little or no absorption of fats in the (blank) except for some short chain fatty acids.

A

stomach

79
Q

(blank) slows gastric motility and emptying when fats are in the S.I

A

CCK

80
Q

(blank) stimulates the pancreas to secrete lipase

A

CCK

81
Q

(blank) also stimulates gallbladder contraction and sphincter of Oddi relaxation

A

CCK

82
Q

The process of absorption of dietary lipids depend on four major events……. which are?

A

1) secretion of bile and various lipase
2) emulsification
3) enzymatic hydrolysis of ester linkages
4) solubilization of lipolytic products within bile salt micelles

83
Q

Emulsification is a suspension of fat droplets, that are held apart by (blank, blank, blank) and other agents.

A

lecithin, bile salts, fatty acids

84
Q

What do the 1 um emulsified fat droplets do?

A

increase surface area of lipids to prepare for their enzymatic hydrolysis

85
Q

How big are micelles and what do you call the point where they form?

A

3-10nm

Critical micellar concentration

86
Q

Pancreatic lipase is secreted in (blank) form

A

active!!!

87
Q

Pancreatic lipase is inhibited by (blank) which displaces lipase at the fat to water interface.

A

bile salts

88
Q

Since we need lipase to interact with bile salts in order to break down lipids, how do we achieve this?

A

we acheive this through the activation of Colipase

89
Q

What does colipase do and how do we activate it?

A

it is a cofactor that complexes lipase to bile salts and lowers pH optimum of lipase to 6-7. It is secreted by pancreas as pro-colipase and is activated to colipase by trypsin hydrolysis

90
Q

Once co-lipase attaches to the fat droplet, lipase will bind to the (blank) molecule in a 1:1 ratio and carry out its catalytic function.

A

colipase

91
Q

Why are micelles cool and what is the importance of micellar solubilzation?

A

because they put all the hydrophobic stuff inside them and push all the hydrophilic stuff on the outside so it can move through the unstirred water layer like butter–>then the micelle presents fatty acids and monoglycerides to the apical membrane of enterocyte

92
Q

Once fats get to enterocyte, what kinds of processes lets them go across the enterocyte?

A

carrier dependent processes and simple diffusion (majority done this way)

93
Q

Bile salts are not absorbed across the unstired layer with micelles, so where do they go?

A

they are recycled to the lumen where they form new micelles

94
Q

Bile salts are actively reabsorbed into the (blank) in the distal ileum

A

enterohepatic circulation

95
Q

Where do bile salts get actively reabsorbed into the enterohepatic circulation?

A

in the distal ileum

96
Q

What are the 2 pathways involved in re-synthesis of triglycerides and what is the major pathway and what is the minor pathway?

A

(i) Monoglyceride acylation – Major.

(ii) Phosphatadic acid – Minor.

97
Q

(blank) secrete chylomicrons and very-low-density lipoproteins

A

enterocytes/intestine

98
Q

How do enterocytes secrete chylomicrons and VLDL?

A

they reassemble triglycerides, cholesterol, and cholesterol esters and package them into lipoproteins and transport them out of the enterocyte

99
Q

Are fat-soluble vitamins absorbed the same as water soluble vitamins?

A

NO

100
Q

What are the four major fat-soluble vitamins?

A

Vitamin A
Vitamin D3
Vitamin E
Vitamin K

101
Q

How are fat soluble vitamins absorbed?

A

passively via micelles, same way as lipids

102
Q

What are the 5 water soluble vitamins?

A 
Vit C
Vit B1
B2
B6
Folic acid
103
Q

How are water soluble vitamins absorbed?

A

via an active process

104
Q

How do we get B12 released from dietary protein?

A

gastric acid and pepsin make this happen

105
Q

What does B12 bind to in the saliva?

Intially, most of the B12 is bound to what?

A

IF and R protein

R protein!!

106
Q

So we eat some protein, and gastric acid and pepsin pull all this B12 out of it. This B12 loves R so it binds to it. So we got a lot of B12 all bound to R protein and its traveling down into the intestines, and something happens, what is it?

A

In the intestine, pancreatic enzymes cleave the complexes and the free B12 now binds to IF.

107
Q

So we eat some protein, and gastric acid and pepsin pull all this B12 out of it.This B12 loves R so it binds to it. So we got a lot of B12 all bound to R protein and its traveling down into the intestines, and something happens, it suddenly gets its R cleaved off!!! OH no, but its all good because IF comes and binds (B12 hates being alone). So now what happens?

A

B12 and IF bind to a receptor on the ileum and gets absorbed and transported to the tissues by another B12-binding protein, transcobalamin II

108
Q

Let me preface this story with B12 hates being alone…….
So we eat some protein, and gastric acid and pepsin pulls all this B12 out of it.This B12 is like OH no I am all alone so it falls in love with R and binds to it. So we got a lot of B12 all bound to R protein and its traveling down into the intestines, and something happens, it suddenly gets its R cleaved off!!! OH no,R has left B12, but its all good because a new fella comes along named IF and IF comes and binds. IF and B12 feel like taking a trip so they go to the ileum and when they get inside, someone greats them and takes them to other tissues. Who is this mysterious person?

A

it is transcobalamin II

109
Q

Failure to secrete vitamin B12, in cases such as chronic gastritis, can result in the development of (blank) (failure of maturation of RBCs occurs in the absence of vitamin B12 stimulation of the bone marrow).

A

pernicious anemia

110
Q

WHere do we get a huge amount of water and electrolyte absorption?

A

Small intestine

111
Q

Only (blank) percent of the absorptive capacity of the colon is regularly utilized

A

10-25

112
Q

Over 24 hours 7-10L of fluid can enter the small intestine of which only (blank) enters the colon

A

1-2L

113
Q

Water absorption is achieved by the simple process of (blank), which then passively draws along anions and water.

A

active Na+ transport

114
Q

25-30g of Na is ingested and must be (blank) each day, as little as 0.5% of the sodium is lost each day.

A

absorbed

115
Q

From the duodenum to colon the Na+ and Cl- ions become progressively (blank) in the GI lumen than plasma concentrations

A

lower

116
Q

Na+ that is approx. 140mM in the duodenum decreases to (blank) in the colon

A

35-40

117
Q

There is an increased effectiveness in absorbing ions along the GI tract that is partially attributable to the (blank) permeability to ions.

A

decreased….. this prevents back diffusion in the terminal parts of the GI tract

118
Q

(blank) ions are extremely well conserved (i.e reabsorbed very nicely), and can be exchanged for HCO3- ions.

A

Cl-

119
Q

What are the four models for sodium absorption in the small intestine?

A

1) Movement via restricted diffusion through water filled
2) co-transport of Na+ with sugars/AAs
3) co transport of Na+ with Cl-
4) Counter-transport of Na+ for H+

120
Q

When you are in the colon, how will you absorb NaCl?

What is this under control of?

A

1) Restricted diffusion becomes very important
2) Co-transport is absent (co-transport with AA’s and glucose specifically)
3) Na is still absorbed through Na/Cl co-transport and Na+ for H+ counter transport
4) Cellular junctions are less leaky

aldosterone

121
Q

What is this:

Occurs in response to the osmotic forces established with solute and ion transport.

A

3 compartment model for fluid absorption

122
Q

What are the 3 compartments of the 3 compartment model for fluid absorption

A

1st. Compartment: Is when solutes are moved from the lumen into and then out of the epithelial cell.

2nd Compartment: Creates a local osmotic gradient causing water to move into the intercellular space.

3rd. Compartment: The increase in hydrostatic pressure in the intercellular space, causing a flow of water through the basement membrane into capillaries.

123
Q

About 1g of calcium is taken orally, of which approximately (blank) is absorbed and is an important component in the regulation of whole body Ca2+.

A

40%

124
Q

The transepithelial movement of Ca2+ occurs (blank) an electrochemical potential gradient

A

against

125
Q

THe process of calcium absorption is localized in the (blank) and occurs in 4 steps.

A

proximal intestine

126
Q

The process of calcium absorption is localized in the proximal intestine and occurs in 4 steps. What are these four steps.

A

Ca enters the brush border
regulation of intracellular Ca2+
Vitamin D effects absorption
Ca2+ exits at basolateral side of membrane

127
Q

Calcium transport is initiated by (blank)

A

D3

128
Q

Where do we get D3?

A

the sun (uV rays)

129
Q

Vit D is converted into what enzyme for the initiation of Ca2+ and how do we make this enzyme for Vit D3?

A

1,25-dihydroxyvitamin D3
Vit D3 made from sun->transferred to liver and is turned into 25-OH-D3->then to kidney and becomes 25-OH-D3 (step regulated by parathyroid hormone)->gets taken up by enterocytes and is now 1,25-dihydroxyvitamin D3

130
Q

What are inserted into the brush border to allow for calcium entry down a concentration gradient?

A

binding proteins

131
Q

In the cytoplasm, calcium concentrations are minimized by (blank) on the endoplasmic reticulum and golgi.

A

CaBP

132
Q

How do we get calcium to exit at the basolateral side since it is against its chemical gradient?

A

utilize calcium ATPase and a Na+/Ca2+ exchanger (which is used when calcium ATPase is saturated)

133
Q

As calcium absorption increases and plasma concentrations increase, the rise in calcium concentration in the plasma inhibits the secretion of (blank) and the subsequent formation of 1,25 dihydroxyvitamin D3 leading to the waning of calcium absorption.

A

parathyroid hormone

134
Q

What step in 25-dihydroxyvitamin D3 does paraythroid hormone regulate?

A

The conversion of 25-OH-D3 to 1,25 dihydroxyvitamin D3 in the kidneys

135
Q

What are the 2 ways iron absorption can occur?

A

1) iron found in heme can be absorbed by endocytosis and digested by lysoenzymes to release free iron
2) Non-heme iron will be absorbed by enterocytes of the proximal small intestine which release an iron bind protein called transferrin. transferrin binds with the iron and becomes a complex which binds to the brush border by specific enzymes. The complex (including the receptor, transferrin and iron) is absorbed and the receptor is recycled and transferrin-iron complex transported to basolateral side of membrane

136
Q

Iron + apoferritiin=?

A

ferritin

137
Q

A small amount of iron can bind to an intracellular protein called (blank) and be taken up slowly, however the iron is though to be lost when the enterocytes slough off.

A

ferritin

138
Q

How is iron uptake regulated?

A

by brush border receptors and by the

ratio of ferritin to transport protein (transferrin), formation of ferritin is greatest when body iron levels are high

139
Q

Iron appears in the blood bound to (blank)

A

plasma transferrin

140
Q

(blank) is the most common genetic disease in white populations, has a prevalence of 1:200, not generally recognized. This disease of unregulated iron absorption leads to generalized iron overload that can eventually impair organ systems and lead to cirrhosis, diabetes, and cardiomyopathy.

A

hemochromatosis

Block 3 Week 3 Dani (10 decks)

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