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Digestion n Absorption Flashcards

1
Q

How is K+ absorbed in the colon

A

In general K+ reabsorption is by passive diffusion, the net movement begin determined by the potential difference between the lumen and intestinal capillaries. Note: Diarrhoea can result in severe hypokalaemia (loss of K+)

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2
Q

How is Cl- absorbed in the colon

A

Cl- is actively reabsorbed in exchange for bicarbonate - resulting in the intestinal contents becoming more alkaline

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3
Q

There are 2 functional states/periods the body undergoes in providing energy for cellular activities, these are

A

the absorptive & postabsorptive states

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4
Q

What happens during the absorptive state

A
  • During which ingested nutrients enter the blood from the GI tract
  • During this state, some of the ingested nutrients provide the energy requirements of the body and the remainder is added to the body’s energy stores to be called upon during the next postabsorptive state
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5
Q

What happens during the post absorptive state

A

During which the GI tract is empty of nutrients and the body’s ownstores must supply energy

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6
Q

What is the average daily lipid intake

A

Average daily intake of lipid is 70 to 100 per day - most in the form of triglycerides (glycerol with three fatty acids attached)

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7
Q

What are the 3 main important fatty acids we absorb

A

There are 3 main important fatty acids we absorb; Palmitic (most abundant), Stearic & Oleic acid

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8
Q

what is a triglyceride

A

Triglycerides (triglycerols): A glycerol molecule with 3 fatty acids attached

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9
Q

where does triglyceride digestion occur

A

Triglyceride digestion occurs to a limited extent in the mouth & stomach but it predominantly occurs in the small intestine.

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10
Q

What is the main fat digestive enzyme

where is it produced
‘
how does it work

A

The major digestive enzyme is lipase (synthesised in the PANCREAS) which catalyses the splitting of bonds linking fatty acids to the 1st & 3rd carbon atomsof glycerol, producing two free fatty acids & a monoglyceride as products:

Triglyceride —> Monoglyceride + 2 Fatty acids ,
under the action of lipase

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11
Q

lipids ingested in food are water insoluble so what happens to them

A

The lipids in ingested food are insoluble in water so aggregate into large lipid droplets in the upper portion of the stomach

-These lipid droplets are then converted into very small droplets (1mm in diameter) via the process of emulsification, which requires two things..

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12
Q

what does the process of emulsification require

A
  1. Mechanical disruption of the large droplets into smaller droplets - provided by the motility of the GI tract, in the lower portion of the stomach & in the small intestine, which grinds & mixes the luminal contents
  2. An emulsifying agent - provided by the phopho-lipids in food and by bile saltssecreted in bile:

Phospho-lipds are amphipathic (both hydrophilic & phobic) molecules (containing polar or ionised groups on one end of the molecule and non-polar groups on the other) consisting of 2 non polar fatty acid chains attached to glycerol with a charged phosphate group on one end

  • Bile salts are formed form cholesterol in the liver and are also amphipathic
  • The non-polar portion of the phospholipids and bile salts associate with the non polar interior of the lipid droplet - leaving the polar portions exposed at the water surface - here they repel other lipid droplets that are similarly coated with these emulsifying agents thereby prevents their reaggregation into larger fat droplets
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13
Q

two examples of emulsifying agents and how they work

A
  • Phospholipids
  • Bile salts

The non-polar portion of the phospholipids and bile salts associate with the non polar interior of the lipid droplet - leaving the polar portions exposed at the water surface - here they repel other lipid droplets that are similarly coated with these emulsifying agents thereby prevents their reaggregation into larger fat droplets

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14
Q

The coating of the lipid droplets with these emulsifying agents does what to lipase

so what happens

A

impairs the accessibility of the droplet for lipase

To overcome this issue, the pancreas secretes a protein called colipase which binds to the lipid droplet surface as well as binding to lipase - thereby holding it onto the surface of the lipid droplet

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15
Q

These small droplets are further converted into smaller droplets under the actions of what

what are these

A

under the further action of bile salts,called micelles (4-7 nm in diameter) - these consist of bile salts with fat soluble vitamins (A,D,E,K) and cholesterol, fatty acids, monoglycerides & phospholipids all clustered together with their polar ends facing outwards and their non-polar ends facing inwards

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16
Q

Despite the fact that fatty acids and monoglycerides have an extremely low solubility in water what can happen

A

Despite the fact that fatty acids and monoglycerides have an extremely low solubility in water, some do exist in solution and are able to diffuse across the lipid portionof the luminal plasma membranes of the epithelial cells of the small intestine

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17
Q

The micelles are in equilibrium with these free fatty acids and monoglycerides meaning

A

the micelles are continuously breaking down & reforming - as the concentration of free lipids decreases since they are diffusing through the epithelial cellsmore lipids are released into solution by the breakdown of the micelles

NOTE: it is not the micelle which is absorbed but instead the individual lipid molecules released from the micelle, thus micelles can be regarded as holding stations for lipids

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18
Q

Once in the small intestine what happens to fatty acids and monoglycerides

why is this important

A

Once in the small intestine the fatty acids and monoglycerides are re-synthesised into triglycerides in the smooth endoplasmic reticulum where the enzymes for triglyceride synthesis are located.

important because …
This process decreases the cytosolic concentration of free fatty acids and monoglycerides and thus maintains a diffusion gradient for these molecules into the cell from the intestinal lumen

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19
Q

The resynthesises fat does what

what does this do

A

The resynthesises fat aggregates into small droplets coated by proteins that perform an emulsifying function similar to that of bile salts

The fat droplets then pinch off the endoplasmic reticulum in vesicles where they are then processed through the golgi apparatus where they are modified into CHYLOMICRONS, they then bud off the golgi in vesicles which then fuse with the plasma membrane and enter the interstitial fluid via exocytosis

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20
Q

what do chylomicrons contain

A

Chylomicrons contain not only triglycerides but other lipids such as phospholipids, cholesterol & FAT-SOLUBLE VITAMINS which have been absorbed in the same process as the fatty acids

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21
Q

what do chylomicrons do after they enter the interststitial fluid

A

The chylomicrons then enter the lacteals - lymphatic vessels in the intestinal villirather than into the blood capillaries - this is due to the fact that chylomicrons cannot enter the capillaries due to the basement membrane at the outer surface of the capillaries providing a barrier to diffusion

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22
Q

why cant chylomicrons enter blood capillaries

A

cannot enter the capillaries due to the basement membrane at the outer surface of the capillaries providing a barrier to diffusion

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23
Q

why can chylomicrons enter lacteals

A

The lacteals have large pores between their endothelial cells which enable the chylomicrons to pass through

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24
Q

what happens to the lymph from the small intestine

A

The lymph from the small intestines eventually empties into the systematic veins

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25
Q

what happens once chylomicrons enters the circulation

what enzyme causes this

A

Once the chylomicrons (containing triglycerides, phospholipids, cholesterol & fat soluble vitamins) have entered the circulation the processing of the triglycerides in chylomicrons in blood plasma is similar to that for VLDL’s produced by the liver

The fatty acids of plasma chylomicrons are released, mainly within adipose-tissue capillaries by the action of endothelial lipoprotein lipase (since it hydrolyses the triglyceride)

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26
Q

what happens to the fatty acids released from the chylomicrons in the adipose tissue capillaries

A

The released fatty acids then diffuse into adipocytes and combine with alpha-glycerol phosphate (produced from dihydroxyacetone phosphatein glycolysis), synthesised in the adipocytes from glucose metabolites to form triglycerides

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27
Q

why is Glucose is ESSENTIAL for triglyceride synthesis in adipocytes

A

Glucose is ESSENTIAL for triglyceride synthesis in adipocytes due to the fact that adipocytes do not have the enzyme required for phosphorylation of glycerol to alpha glycerol, so glycerol can only be produced by reducing dihydroxyacetone phosphate (from glycolysis) and NOT from glycerol or any other fat metabolites

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28
Q

In contrast to alpha glycerol there are 3 main sources of fatty acids for triglyceride synthesis;

any enzymes needed?

A
  1. Glucose that enters adipose tissue and is broken down to provide building blocks for the synthesis of fatty acids
  2. Glucose that is used in the liver to form VLDL triglycerides, which are transported in the blood and taken up by adipocytes
  3. Ingested triglycerides transported in the blood in chylomicrons and taken up by adipocytes

•2 & 3 require lipoprotein lipase to release the fatty acids from the circulating triglycerides

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29
Q

Fat-soluble vitamins such as vitamin A,D,E & K follow the pathway for fat absorption mentioned above in the ILEUM
•With one exception

A

water-soluble vitamins such as vitamin C & B are absorbed by diffusion or mediated transport in the JEJUNUM:

•The exception is vitamin B-12, which is a very large and charged vitamin. To be absorbed B-12 must first bind to the protein intrinsic factor (secreted by parietal cells of the stomach) - intrinsic factor whit bound B-12 then binds to specific sites on the epithelial cells in the LOWER PORTION OF THE ILEUM where vitamin B-12 is absorbed via endocytosis

.•Vitamin B-12 is needed for erythrocyte formationand a deficient in B-12 can lead to pernicious anaemia and is usually caused due to a deficiency in intrinsic factor

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30
Q

why is vitamin B12 needed

A

Vitamin B-12 is needed for erythrocyte formationand a deficient in B-12 can lead to pernicious anaemia and is usually caused due to a deficiency in intrinsic factor

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31
Q

How is Vitamin B12 absorbed

A

The exception is vitamin B-12, which is a very large and charged vitamin. To be absorbed B-12 must first bind to the protein intrinsic factor (secreted by parietal cells of the stomach) - intrinsic factor whit bound B-12 then binds to specific sites on the epithelial cells in the LOWER PORTION OF THE ILEUM where vitamin B-12 is absorbed via endocytosis

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32
Q

where does the digestion and absorption of protein mainly occur

A

duodenum

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33
Q

how much protein a day does a healthy adult require

A

A healthy adult only requires 40 to 50g of protein a day to supply essential amino acids and replace the nitrogen contained in amino acids that are converted to urea

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34
Q

how many essential AA do we need

A

8 are essential - we cannot manufacture them

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35
Q

how many AA are found in the proteins we use

A

20

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36
Q

Amino acids exist as optical isomers what form is in the proteins we use

A

only the L-forms are found in the proteins we utilise

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37
Q

what is a zwitterion

A

Amino acids start as very top picture but form zwitterions having bothpositive and negative groups on the same molecule

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38
Q

what is the basic building block for a protein

A

The basic building block of a proteinis the peptide bond - CONH (HN-C=O)

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39
Q

where does digestion of proteins begin

A

Begins in the stomach where the enzymepepsin (chief cells release pepsinogenwhich is rapidly activated by the low luminal pH) cleaves some of the peptide linkages - forming peptide fragments

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40
Q

where is pepsinogen I found

A

found only in the HCl secreting region (mainly the body) of the stomach

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41
Q

where is pepsinogen II found

A

found in the pyloric region

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42
Q

what do pepsins do to proteins

A

Pepsins hydrolyses the bonds between an aromatic amino acid (tyrosine or phenylalanine) and a second amino acid

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43
Q

optimum pH for pepsin

A

The optimum pH for pepsins is around pH 1.6 - 3.2 thus action is terminated on exit from the stomach

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44
Q

what is the pH in the duodenal cap

A

The pH in the duodenal cap is around pH 2 - 4

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45
Q

pH in the rest of the duodenum

A

The pH in the rest of the duodenum is around pH 6.5

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46
Q

what happens to peptides in the small intestine

A

In the small intestine these smaller peptides are further fragmented by enzymesproduced in the pancreas which can be divided into:

Endopeptidases
Exopeptidase’s

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47
Q

Example of endopeptidases

A

trypsin, chymotrypsin & elastase

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48
Q

example of Exopeptidase’s

A

carboxyl dipeptidases and the amino peptidases of the brush border (microvilli border)

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49
Q

Some di & tripeptides are absorbed and finally broken down by intracellular peptidases meaning final digestion of peptides occurs in three locations;

A
  • the intestinal lumen
  • the brush border
  • within the cell
50
Q

where does digestion and absorption of carbohydrates occur

A

occurs in duodenum

51
Q

what is a Monosaccharide

A

single sugars e.g. glucose, fructose & galactose

52
Q

What is a Oligosaccharide

A

several sugar molecules

53
Q

examples of Oligosaccharides

A
  • Lactose - forms beta linkages since OH groups lies above the plane of the molecule thus it requires its own enzyme to be broken down, can’t use the same one as sucrose since it has alpha linkages. People who are lactose-intolerant do not have sufficient amounts of beta enzymes
  • Sucrose (most common disaccharide)
  • Both are disaccharides - the important dietary ones
54
Q

what is Polysaccharide

A

many sugar containing molecules

55
Q

example of polysaccharide

A

starch & glycogen

56
Q

how do sugar molecules exist

which one is used in metabolism

A

Sugar molecules also exist as optical isomers - only the D-isomers are utilised in metabolism

57
Q

what is Glycogen and whats it structure

A

the principal dietary polysaccharide from animal sources,

polymer of glucose molecules which are joined by alpha 1-4 glycosidic linkages and some chain branching by alpha 1-6 glycosidic linkages

58
Q

structure of starch

A

majority alpha 1-4 glycosidic linkages with some chain branching by alpha 1-6 linkages but LESS THAN IN GLYCOGEN

59
Q

structure of cellulose

A

only beta 1-4 glycosidic linkages

60
Q

how is starch initially degraded and where

what is the optimal pH of this

A

Starch is first degraded by ptyalin - the alpha amylase of saliva in the mouth only a small fraction of starch digestion occurs here

The optimal pH for this is pH 6.7 and activity is terminated by gastric acidity of the stomach

61
Q

once in the small intestine how is starch degraded

A

Once in the small intestine (responsible for 95% of starch digestion), pancreatic alpha amylase catalyses alpha 1-4 linkages

But NOT the alpha 1-6 linkage, the alpha 1-4 linkages next to branch points or the terminal alpha 1-4 linkages

62
Q

what are the end products of the initial digestion of starch in the small intestine

A

Thus the end products of this digestion are:
• the disaccharide maltose
•the trisaccharide maltotriose
•larger polymers of glucose with alpha 1-4 linkages
•branched polymers consisting of around 8 units called the alpha-limit dextrins

63
Q

what further digests the products of starch in the small intestine and where about

what are they broken down into

A

These are further digested by the oligosaccharidases located at the outer portionof the membrane of the microvilli (the brush-border):

  • maltase
  • lactase
  • sucrase
  • alpha-limit dextrinase

They are broken down into monosaccharide - glucose, galactose & fructose

64
Q

Hexoses & pentoses are rapidly absorbed across the intestinal mucosa, these then enter the capillaries which drain into what

A

to the HEPATICPORTAL VEIN

65
Q

how is glucose transported across the intestinal mucosa

A

Glucose and Na+ SHARE the SAMETRANSPORTER - sodium-glucose cotransporter (SGLT) thus a high Na+ concentration at the mucosal surface facilitates glucose absorption

66
Q

how is galactose transported from the lumen

A

Galactose, a glucose isomer, is transported from the lumen by the SGLT

67
Q

How is fructose transported across the intestinal mucosa

A

Fructose utilises a different carrier and its absorption is independent of luminal Na+ since it is absorbed by facilitated diffusion via a glucose transporter (GLUT)

68
Q

what happens to glucose, galactose and fructose once they have been transported across the intestinal mucosa

A
  • These monosaccharides then leave the epithelial cells and enter the interstitial fluid by way of facilitated diffusion via GLUT proteins in the basolateral membranes of the epithelial cells
  • From there, the monosaccharide diffuse into the blood through capillary pores

Most ingested carbohydrates are digested & absorbed within the first 20% of the small intestine - i.e duodenum

69
Q

What happens to the monosaccharides once they have been absorbed and are now in the blood

A

After entering the hepatic portal vein and thus the liver, the liver then converts these carbohydrates into glucose

70
Q

what is the major consumer of glucose in the body

A

Skeletalmuscle make up the majority of the body and so is the major consumer of glucose, even at rest

71
Q

what does skeletal muscle do with glucose

A

Skeletal muscle not only catabolises (breaks it down into smaller units) glucose in the absorptive phase but also converts some of the glucose to the polysaccharide glycogen, which is then stored in the muscle for future use

72
Q

when is there a net uptake of glucose by the liver

A

absorptive state

73
Q

What are two things the liver can convert glucose into

A
  • The LIVER also converts glucose into glycogen to be used at some point in the future
  • The LIVER can also convert the glucose into alpha-glycerol phosphate ( by reducing dihydroxyacetone phosphate via glycolysis) and fatty acids which are then used to synthesise triglycerides
  • NOTE: this process of converting glucose into alpha-glycerol phosphate (via glycolysis) and fatty acids also occurs in adipose-tissue cells (adipocytes) which can then be used to synthesise triglycerides which can be then stored in the adipocytes
74
Q

What are lipoproteins

A

Most of the fat synthesised from glucose in the liver is packaged along with specific proteins into molecular aggregates of lipids and proteins known as lipoproteins

75
Q

how do lipoproteins enter the blood

A

These aggregates are secreted by hepatocytes and enter the blood

76
Q

why are they called very-low-density lipoproteins (VLDL’s)

A

since they contain more fatthan protein and fat is less dense than protein

77
Q

What is the process of VLDL synthesis similar to

A

The synthesis of VLDL’s in hepatocytes occurs by a similar process as that ofchylomicrons by intestinal mucosa cells(see above)

78
Q

Why can’t VLDL’s penetrate capillary walls

what happens to them instead

A

Due to their large size, VLDL’s in the blood do not readily penetrate capillary walls,

instead, their triglycerides are hydrolysed mainly to monoglycerides (i.e glycerol linked to one fatty acid) and fatty acids by the enzyme lipoprotein lipase

79
Q

where is lipoprotein lipase located

A

Lipoprotein lipase is located on the on the blood-facing surface of capillary endothelial cells, especially those in adipose tissue

80
Q

why do most of the fatty acids in VLDL triglycerides originally synthesised from glucose in the liver end up being stored in triglyceride in adipose tissue

A

In adipose-tissue capillaries the fatty acids generated by the action of lipoprotein lipase diffuse from the capillaries into the adipocytes - there they combine with alpha-glycerol phosphate, supplied by glucose metabolites to form triglycerides once again. As a result, most of the fatty acids in VLDL triglycerides originally synthesised from glucose in the liver end up being stored in triglyceride in adipose tissue

81
Q

Some of the monoglycerides produced by the break down of triglycerides by lipoprotein lipase in the blood in adipose-tissue capillaries are also taken up by what

what happens to them here

A

Some of the monoglycerides produced by the break down of triglycerides by lipoprotein lipase in the blood in adipose-tissue capillaries are also taken up by adipocytes where enzymes can then reattach fatty acids to the two available carbon atoms of the monoglyceride and thereby form a triglyceride

Some of the monoglycerides travel via the blood to the liver to be metabolised

82
Q

Amino acids, triglyceride & glucose are transported to the liver for what conversion to storage molecules

Then to the storage areas such as:

A
  • Adipose tissue for fats

- Muscle for glycogen

83
Q

LOOK AT PHOTO FOR METHOD OF STORAGE

A

AND FOR HOW THESE FUELS ARE USED

84
Q

BMI

A

body mass index

85
Q

BMI equation

A

Weigh (Kg)/ Height2 (m)

86
Q

what is normal BMI range

A

18.5 < BMI < 25 = normal

87
Q

what is an obese BMI

A

BMI > 30 = obese

88
Q

What is underweight BMI

A

BMI < 18.5 = underweight

89
Q

what is overweight BMI

A

BMI > 25 = overweight

90
Q

Glycogen stores for a resist adult male are roughly sufficient to last

Lipid stores are sufficient to last

A

12 hours

3 months

91
Q

Tissue protein as a source of energy supply only becomes significant when

A

in times of prolonged starvation

92
Q

Different tissues have very different energy requirements - the brain & liver represent about 4.6% of body weight yet consume around

A

40% of energy requirement at rest

93
Q

what fuels are used by the brain

A

glucose, ketone bodies

94
Q

what fuels are used by muscle

A

glucose, ketone bodies (in starvation), triacyglycerol & branched-chain amino acids

95
Q

what fuels are used by the liver

A

amino acids, fatty acids (including short chain acids), glucose & alcohol.

NOTE: ketone bodies are not used by the liver, although they are produced herethey are then sent to extrahepatic tissue to buy used there, the liver cannot use ketone bodies for fuel due to the fact they do not have the enzyme thiolase

96
Q

why can’t liver use ketone bodies as fuel

A

they do not have the enzyme thiolase

97
Q

what fuels are used by kidney

A

glucose & ketone bodies (cortex), only glucose (medulla)

98
Q

what fuels are used by small intestine

A

ketone bodies (mainly in starvation), glutamine (amino acid)

99
Q

what fuels are used by large intestine

A

short-chain fatty acids, glutamine

100
Q

what is the BMR

A

basal metabolic rate

Minimum amount of energy required to keep the body alive

101
Q

how is BMR usually measured

A

Usually measured by O2 consumption in a person who is awake, restful and faster for 12 hours

102
Q

what happens to BMR with Age

A

decreases

103
Q

what units is BMR measured in

A

Measure in kcal expended/hr/m^2

104
Q

what is malabsorption

A

The inadequate absorption of nutrients from the intestines

•Failure to absorb certain vitamins, minerals, carbohydrate, proteins or fats

105
Q

what is the most common cause of malabsorption

A

Chiefly cause by disease of the small bowel

106
Q

Giardiasis

A

infection which causes the villi to atrophy thus reducingabsorption capacity

107
Q

what is Coeliac disease

A

Auto-immune condition whereby gluten is partially degraded triggering an immune response whereby the system attacks the villi & microvilli resulting in a loss of intestinal brush border surface area resulting in decreased absorption of many nutrients

108
Q

who does coeliac disease occur in

A

Occurs in genetically disposed individuals

109
Q

What can coeliac disease cause

A

Muscular atrophy
Abdominal Distention
Can prevent the absorption of vitamin D which ultimately results in the decrease in calcium absorption in the GI tract - resulting is osteoporosis

110
Q

What is cystic fibrosis and what causes it

A

Caused by an autosomal recessive mutation in an epithelial channel called the cystic fibrosis transmembrane conductance regulator (CFTR).

This results in problems with salt & water movement across cell membranes, which leads to thickened secretions & a high incidence of lung infection. The airways secrete a watery fluid upon which mucus can ride freely, in CF suffers the production of this fluid is impaired causing the mucous layer to become thick & dehydrated thereby obstructing the airways

111
Q

The exocrine portion of the pancreas secretes HCO3- and a number of digestive enzymes e.g

how do these enter the duodenum

A

The exocrine portion of the pancreas secretes HCO3- and a number of digestive enzymes e.g. lipase, colipase & alpha amylase (see further up) into the ducts that converge into the pancreatic duct which joins the common bile duct from the liver before it enters the duodenum at the duodenal papillae.

112
Q

whats the difference between the secretion of HCO3 and the digestive enzymes

A

The enzymes are secreted by gland cells at the pancreatic end of the duct system whereas HCO3- is secreted by the epithelial cells lining the ducts.

113
Q

The pancreatic duct cells secrete HCO3- (produced from CO2 & H2O using carbonic anhydrase) into the duct lumen via what

what happens to the H+ produced

A

The pancreatic duct cells secrete HCO3- (produced from CO2 & H2O using carbonic anhydrase) into the duct lumen via an apical membrane Cl-/HCO3- exchanger, while the H+ produced (from the dissociation of H2CO3) is exchangedfor extracellular Na+ on the basolateral side of the cell.

114
Q

How is HCO3- produced

A

produced from CO2 & H2O using carbonic anhydrase

115
Q

what happens to H+ when its enters the pancreatic capillaries

A

The H+ enters the pancreatic capillaries to eventually meet up in portal vein bloodwith the HCO3- produced by the stomach during the generation of luminal H+.

116
Q

the energy for the secretion of HCO3- is provided by what

A

The energy for secretion of HCO3- is provided by Na+/K+ - ATPase pumps on the basolateral membrane.

117
Q

why does Cl- no normally accumulate in the cell

A

Cl- normally does not accumulate within the cell because these ions are recycled into the lumen through the CFTR

118
Q

how do Na+ & H20 move into the ducts

A

Via a paracellular route, Na+ & H20 move into the ducts due to the electrochemical gradient established by chloride movement through the CFTR

119
Q

However in cystic fibrosis, the CFTR is faulty meaning what

A

meaning Cl- will build up in the gland cells thereby preventing the movement of HCO3- into the duct this means that less HCO3- enters the small intestine, its secreted to act as a buffer to raise the pH in the small intestine, since the contents have just been thought the low pH stomach - at low pH the digestive enzymes of the pancreas are not active - HCO3-is used as a buffer to increase intestinal pH so that the digestive enzyme can be active

Thus less HCO3- in the small intestine will result in a decrease in digestion and thus absorption

120
Q

in people with cystic fibrosis the lack of normal water movement leads to

A

Furthermore the lack of normal water movement leads to a thickening of pancreatic secretions - resulting in the clogging of the pancreatic ducts and thus enzymes and HCO3- cannot be released resulting in a decrease in digestion and thus absorption. Furthermore the digestive enzymes begin clogged in the duct can result in pancreatic damage resulting in the pancreas eventually not being able to produce digestive enzymes

Thus CF suffered are given pancreatic enzyme replacements to aid their digestionand thus absorption47KP

GI (7 decks)

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