Digestion and absorption 1 Flashcards

1
Q

what is the main site for digesting CHO

A

site for carbohydrate digestion is the mouth and intestinal lumen

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2
Q

what are glycosidases ?

A

Group of enzymes responsible for digesting the CHO

Very specific to the bond that they product

Final product of digestion are MONOSACCHARIDES ( glucose, galactose , fructose )

cuz the intestinal cells lack transporters for disaccharides

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3
Q

what are glycosyltransferase ?

A

Enzyme that synthesizes glycosidic bonds

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4
Q

what amylase ?

A

salivary alpha amylase

BREAKS alpha 1,4 glycosidic bond

CANNOT hydrolyze :

Alpha 1-6 ( amylopectin and glycogen )

Beta 1-4 ( cellulose ) –> human cannot digest this

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5
Q

what is the result of amylase digestion ?

A

Dextrin ( branched and unbranched oligosaccharides )

Disaccharides ( some are resistant to amylase )

Disaccharides need to be disaccharidase enzyme to hydrolyze them into monosaccharides

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6
Q

what is the pancreas role in digestion?

A

when acidic stomach content reach the small intestine they are neutralized by bicarbonate secreted by pancreas

release Pancreatic amylase

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7
Q

what does pancreatic amylase do?

A

continue the process of starch digestion :

BREAK DOWN alpha 1-4 linkage

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8
Q

where does the last part of CHO digestion occur?

A

intestinal brush border

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9
Q

what are the enzymes in brush border?

A

Isomaltase 6 alpha

Maltase 4 alpha

Lactase 4 beta

Sucrase 2 alpha

Trehalase 1 alpha

I M LA S T
6 4 4 2 1

all of them break alpha except the middle one ( LA ) its B

all of them give 2 glucose except the middle one and sucrase

Lactase –> 1 glucose 1 galactose

Sucrase —> 1 glucose 1 fructose

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10
Q

whats special sucrase and isomaltase ?

A

its a single enzyme with 2 functional subunits

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11
Q

what is the difference between epimers and anomers?

A

Glucose and galactose are C-4 epimers

they differ in the configuration of 4th carbon

Alpha glucose and Beta glucose are anomers as they differ in the configuration at 1st anomeric carbon

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12
Q

describe monosaccharides absorption ?

A

occur at the duodenum and upper jejunum

Different monosaccharides have different hexose transporter

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13
Q

what do glucose and galactose transporters depend on ?

A

Sodium glucose linked transport -1

Na + / glucose co transporter

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14
Q

what does fructose transport depend on?

A

facilitated diffusion through GLUT5

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15
Q

How does sugar transport occur ?

A

Secondary active transport

they dont directly transport using ATP

they use Sodium-potassium pump NA/K atpase

The pump establishes a sodium gradient by actively pumping Na out of epithelial cell into bloodstream

This creates low Na inside the cell allowing sodium to come into the cell and when it comes in glucose will come with it

co transported into epithelial cell via SGLT-1 symporter

Since glucose concentration inside the cell is low compared to outside it needs active

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16
Q

what are types of active transport ?

A

Uniporter –> one substance across the membrane

Co- transporter : moves 2 substances together :

Symporter in the same direction

Antiporter : opposite directions

17
Q

why are sugars not transported passively ?

A

If glucose absorption relied on passive absorption

it will stop once it reaches equilibrium preventing further uptake

this would lead to excess glucose being lost in feces

18
Q

what are the glucose transport pathways?

A

from lumen to epithelial cell : via SGLT-1 symporter using sodium gradient

from epithelial cell to bloodstream - facilitated diffusion via GLUT-2

19
Q

describe lactase deficiency ?

A

Lactase deficiency results in lactose intolerance

Lactose is fermented by gut bacteria to gas

lactose accumulation leads to increase osmotic pressure in lumen preventing water absorption —> Diarrhea

20
Q

describe primary lactase deficiency?

A

Congenital deficiency of lactase

after ingestion of lactose an affected child will typically experience stomach cramps , bloating , excess gas production and diarrhea

These digestive problems can lead to failure to gain weight and grow at the expected rate —> failure to thrive and malnutrition

21
Q

what are the causes of secondary lactase deficiency ?

A

possible causes are :

Gastroenteritis - an infection of stomach and intestine

Celiac disease - chronic autoimmune disorder triggered by consuming gluten , a protein found in wheat , barely and rye
in genetically predisposed individual , the gluten ingestion causes the immune system to attack small intestine damaging intestinal villi which is essential for nutrient absorption —> malabsorption symptoms like diarrhea , bloating, pain

Crohn’s disease –> IBD - inflammation of lining of GIT

chemotherapy

long courses antibiotics

downregulation of lactase enzyme

22
Q

what are relevant tests to diagnose lactose intolerance ?

A

hydrogen breath test

helps to diagnose :

Intolerance to sugars

Small intestinal bacterial overgrowth ( SIBO )

the test measures the amount of hydrogen present in your breath changes after consuming sugar solution

usually theres little hydrogen in breath

but if u have higher level than usually it indicates a problem either intolerance or bacterial overgrowth

23
Q

describe congenital sucrase isomaltase deficiency ? CSID

A

become apparent after an infant is weaned and starts to consume fruit , juices, grains

24
Q

how is congenital sucrase isomaltase deficiency diagnosed?

A

Small bowel biopsy

sucrose intolerance hydrogen breath test

13C sucrose breath test – -> person consumes a sugary drink of sucrose that contains carbon 13 —-> if one has little or no working sucrase isomaltase enzymes in their intestine , there will be less 13 CO2 gas exhaled than if working sucrae - isomaltase enzymes were present

The carbon 13 breath test is thought to directly measure sucrase activity

444 oral sucrose challenge test :

simple test that may indicate the possible presence of CSID

fating patient drinks a well dissolved solution of 4 tablespoons of table sugar in a 4 ounce of glass of water

IF sucrase isomaltase activity is diminished or absent within 4 hours the patient will experience the GI symptoms associated with CSID such as gas , bloating , abdominal distention swelling or diarrhea

Test is not appropriate for infants , young children, geriatric patients, those with comorbid condition like diabetes , patients may have severe symptoms if very sensitive to sugar

auto antibodies in celiac disease

25
what is a polysaccharide that cannot be digested by human GI?
Fiber is a type of carbohydrate that the body cant digest though most carbohydrates are broken down into sugar molecules fibers cannot be broken down into sugar molecules and instead it passes through the body undigested
26
what bond is between amino acids?
peptide bonds Formed by condensation reaction
27
where does the digestion of protein start?
starts in the stomach intestinal lumen
28
what happens in stomach that digest protein ?
HCL - PH 1.5-3.5 HCl is used to convert the enzyme pepsinogen into pepsin ( active ) pepsin denatures protein Proteases generally the proteases are secreted inactive ( Zymogens ) They get active by cleavage by HCL or other proteases Specific to certain amino acid
29
describe pepsin ?
Pepsin is secreted by chief cells Secreted as inactive pepsinogen Activated by H of HCL in endopeptidase : hydrolyses peptide bonds Specific for tyrosine and glutamate The result of pepsin digestion is polypeptide
30
what are the enzymes in the small intestine secreted by pancreas ?
Trypsin Chymotrypsin --> aromatic amino acid Elastase ---> small neutral aliphatic Carboxy peptidases Aminopeptidase : secreted by intestinal mucosa Dipeptidases --> brush border Tripeptidases ---> brush border
31
how are di-tri peptides are absorbed ?
co- transport mechanism internalized peptides hydrolyzed by intra-cellular peptidase Faster rate of absorption than free amino acids H dependent co transporter - gradient generated by Na/H exchanger --> relay on Na gradient made by na/k atpase pump Symporter ( so both are going in the same direction )
32
how are amino acids are absorbed ?
sodium linked secondary to transport
33
describe hartnup's disease ?
defect in transporter of non polar amino acids which are not absorbed Particularly TRYPTOPHAN Defect in the apical brush border membranes of the small intestine and in kidney proximal tubules Symptoms of hartnup disorder may begin in infancy or early childhood but sometimes they begin as late as early adult hood Since tryptophan is affected : serotonin , niacin and melatonin is affected some patients develop : Pellagra like manifestation which include rash , ataxia, neuropsychiatric symptoms Treatment is niacin
34
describe iminoglycinuria ?
defect in transporter of proline , hydroxyproline , glycine autosomal recessive disorder of renal tubular transport affecting reabsorption of amino acid glycine and the imino acids proline and hydroxyproline ---> EXCESS URINARY EXCRETION OF ALL 3 ACIDS
35
what is Cystinuria ?
defect in transporter inability to transport cystine and other basic amino acids ( lysine, arginine and ornithine ) in urine --> COAL ( CYSTINE, ORNITHINE, ARIGININE , LYSINE ) Inherited autosomal recessive disease characterized by high concentration of amino acids cystine in the urine leading to formation of cystine stones in the kidney , ureter and bladder Type of aminoaciduria Cystine is the one implicated in this disease NOT CYSTEINE which is a dimer
36
what are the causes cystinuria ?
Mutation in the SLC3A1 and SLC7A9 genes these changes prevent reabsorption of basic amino acids ( COAL ) disturb the ability to reabsorb and make them concentrate in urine when cystine is high in urine it forms cystine crystals in kidney stones the stones can be seen via microscope only cystine forms crystals the other amino acids who are in the urine dont form crystals