Digestion n Absorption Flashcards

(120 cards)

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
what happens once chylomicrons enters the circulation what enzyme causes this
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)
26
what happens to the fatty acids released from the chylomicrons in the adipose tissue capillaries
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
27
why is Glucose is ESSENTIAL for triglyceride synthesis in adipocytes
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
28
In contrast to alpha glycerol there are 3 main sources of fatty acids for triglyceride synthesis; any enzymes needed?
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
29
Fat-soluble vitamins such as vitamin A,D,E & K follow the pathway for fat absorption mentioned above in the ILEUM •With one exception
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
30
why is vitamin B12 needed
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
31
How is Vitamin B12 absorbed
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
32
where does the digestion and absorption of protein mainly occur
duodenum
33
how much protein a day does a healthy adult require
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
34
how many essential AA do we need
8 are essential - we cannot manufacture them
35
how many AA are found in the proteins we use
20
36
Amino acids exist as optical isomers what form is in the proteins we use
only the L-forms are found in the proteins we utilise
37
what is a zwitterion
Amino acids start as very top picture but form zwitterions having bothpositive and negative groups on the same molecule
38
what is the basic building block for a protein
The basic building block of a proteinis the peptide bond - CONH (HN-C=O)
39
where does digestion of proteins begin
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
40
where is pepsinogen I found
found only in the HCl secreting region (mainly the body) of the stomach
41
where is pepsinogen II found
found in the pyloric region
42
what do pepsins do to proteins
Pepsins hydrolyses the bonds between an aromatic amino acid (tyrosine or phenylalanine) and a second amino acid
43
optimum pH for pepsin
The optimum pH for pepsins is around pH 1.6 - 3.2 thus action is terminated on exit from the stomach
44
what is the pH in the duodenal cap
The pH in the duodenal cap is around pH 2 - 4
45
pH in the rest of the duodenum
The pH in the rest of the duodenum is around pH 6.5
46
what happens to peptides in the small intestine
In the small intestine these smaller peptides are further fragmented by enzymesproduced in the pancreas which can be divided into: Endopeptidases Exopeptidase’s
47
Example of endopeptidases
trypsin, chymotrypsin & elastase
48
example of Exopeptidase’s
carboxyl dipeptidases and the amino peptidases of the brush border (microvilli border)
49
Some di & tripeptides are absorbed and finally broken down by intracellular peptidases meaning final digestion of peptides occurs in three locations;
- the intestinal lumen - the brush border - within the cell
50
where does digestion and absorption of carbohydrates occur
occurs in duodenum
51
what is a Monosaccharide
single sugars e.g. glucose, fructose & galactose
52
What is a Oligosaccharide
several sugar molecules
53
examples of Oligosaccharides
- 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
what is Polysaccharide
many sugar containing molecules
55
example of polysaccharide
starch & glycogen
56
how do sugar molecules exist which one is used in metabolism
Sugar molecules also exist as optical isomers - only the D-isomers are utilised in metabolism
57
what is Glycogen and whats it structure
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
structure of starch
majority alpha 1-4 glycosidic linkages with some chain branching by alpha 1-6 linkages but LESS THAN IN GLYCOGEN
59
structure of cellulose
only beta 1-4 glycosidic linkages
60
how is starch initially degraded and where | what is the optimal pH of this
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
once in the small intestine how is starch degraded
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
what are the end products of the initial digestion of starch in the small intestine
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
what further digests the products of starch in the small intestine and where about what are they broken down into
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
Hexoses & pentoses are rapidly absorbed across the intestinal mucosa, these then enter the capillaries which drain into what
to the HEPATICPORTAL VEIN
65
how is glucose transported across the intestinal mucosa
Glucose and Na+ SHARE the SAMETRANSPORTER - sodium-glucose cotransporter (SGLT) thus a high Na+ concentration at the mucosal surface facilitates glucose absorption
66
how is galactose transported from the lumen
Galactose, a glucose isomer, is transported from the lumen by the SGLT
67
How is fructose transported across the intestinal mucosa
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
what happens to glucose, galactose and fructose once they have been transported across the intestinal mucosa
- 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
What happens to the monosaccharides once they have been absorbed and are now in the blood
After entering the hepatic portal vein and thus the liver, the liver then converts these carbohydrates into glucose
70
what is the major consumer of glucose in the body
Skeletalmuscle make up the majority of the body and so is the major consumer of glucose, even at rest
71
what does skeletal muscle do with glucose
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
when is there a net uptake of glucose by the liver
absorptive state
73
What are two things the liver can convert glucose into
- 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
What are lipoproteins
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
how do lipoproteins enter the blood
These aggregates are secreted by hepatocytes and enter the blood
76
why are they called very-low-density lipoproteins (VLDL’s)
since they contain more fatthan protein and fat is less dense than protein
77
What is the process of VLDL synthesis similar to
The synthesis of VLDL’s in hepatocytes occurs by a similar process as that ofchylomicrons by intestinal mucosa cells(see above)
78
Why can't VLDL's penetrate capillary walls what happens to them instead
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
where is lipoprotein lipase located
Lipoprotein lipase is located on the on the blood-facing surface of capillary endothelial cells, especially those in adipose tissue
80
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
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
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
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
Amino acids, triglyceride & glucose are transported to the liver for what conversion to storage molecules Then to the storage areas such as:
- Adipose tissue for fats | - Muscle for glycogen
83
LOOK AT PHOTO FOR METHOD OF STORAGE
AND FOR HOW THESE FUELS ARE USED
84
BMI
body mass index
85
BMI equation
Weigh (Kg)/ Height2 (m)
86
what is normal BMI range
18.5 < BMI < 25 = normal
87
what is an obese BMI
BMI > 30 = obese
88
What is underweight BMI
BMI < 18.5 = underweight
89
what is overweight BMI
BMI > 25 = overweight
90
Glycogen stores for a resist adult male are roughly sufficient to last Lipid stores are sufficient to last
12 hours 3 months
91
Tissue protein as a source of energy supply only becomes significant when
in times of prolonged starvation
92
Different tissues have very different energy requirements - the brain & liver represent about 4.6% of body weight yet consume around
40% of energy requirement at rest
93
what fuels are used by the brain
glucose, ketone bodies
94
what fuels are used by muscle
glucose, ketone bodies (in starvation), triacyglycerol & branched-chain amino acids
95
what fuels are used by the liver
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
why can't liver use ketone bodies as fuel
they do not have the enzyme thiolase
97
what fuels are used by kidney
glucose & ketone bodies (cortex), only glucose (medulla)
98
what fuels are used by small intestine
ketone bodies (mainly in starvation), glutamine (amino acid)
99
what fuels are used by large intestine
short-chain fatty acids, glutamine
100
what is the BMR
basal metabolic rate Minimum amount of energy required to keep the body alive
101
how is BMR usually measured
Usually measured by O2 consumption in a person who is awake, restful and faster for 12 hours
102
what happens to BMR with Age
decreases
103
what units is BMR measured in
Measure in kcal expended/hr/m^2
104
what is malabsorption
The inadequate absorption of nutrients from the intestines | •Failure to absorb certain vitamins, minerals, carbohydrate, proteins or fats
105
what is the most common cause of malabsorption
Chiefly cause by disease of the small bowel
106
Giardiasis
infection which causes the villi to atrophy thus reducingabsorption capacity
107
what is Coeliac disease
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
who does coeliac disease occur in
Occurs in genetically disposed individuals
109
What can coeliac disease cause
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
What is cystic fibrosis and what causes it
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
The exocrine portion of the pancreas secretes HCO3- and a number of digestive enzymes e.g how do these enter the duodenum
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
whats the difference between the secretion of HCO3 and the digestive enzymes
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
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
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
How is HCO3- produced
produced from CO2 & H2O using carbonic anhydrase
115
what happens to H+ when its enters the pancreatic capillaries
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
the energy for the secretion of HCO3- is provided by what
The energy for secretion of HCO3- is provided by Na+/K+ - ATPase pumps on the basolateral membrane.
117
why does Cl- no normally accumulate in the cell
Cl- normally does not accumulate within the cell because these ions are recycled into the lumen through the CFTR
118
how do Na+ & H20 move into the ducts
Via a paracellular route, Na+ & H20 move into the ducts due to the electrochemical gradient established by chloride movement through the CFTR
119
However in cystic fibrosis, the CFTR is faulty meaning what
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
in people with cystic fibrosis the lack of normal water movement leads to
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