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Digestion > Absorption > Flashcards

Absorption Flashcards

1
Q

what disaccharidases are localised to the membrane of enterocytes

A
  • Maltase (breaks down maltose), sucrase (splits sucrose into glucose and fructose) as they can cleave internal and terminal 1-4
  • isomaltose (can cleave alpha limit dextrin’s as it cleaves 1-6)
    Lactase which breaks down lactose
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2
Q

what are the 2 stages of carbohydrate digestion?

A

Intraluminal digestion (salivary enzymes and pancreatic enzymes in the GI tract) and membrane digestion (microvilli on the brush border convert oligosaccharides to monosaccharides)

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3
Q

where are the disaccharidases in the small intestine concentrated?

A

jejunum

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4
Q

how does intraluminal digestion occur for proteases?

A

Intraluminal digestion occurs via proteases excreted by the gastric and pancreatic cells (secreted as proenzymes activated by low PH and enterokinases on the brush border respectively)

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5
Q

what are the 2 types of peptidases?

A

endopeptidases (cleave after specific amino acids within polypeptide chain)
exopeptidase (cleave specific peptide bond adjacent to the C terminus)

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6
Q

how are neonates an exception to protein absorption?

A

can absorb intact antibodies from mothers breast milk via endocytosis
otherwise peptides have to be oligopeptides or amino acids to be absorbed

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7
Q

where are peptidases present?

A

secreted from chief cells in the stomach, or acinar cells in the pancreas where they are activated in the small intestine, membrane of enterocytes (membrane digestion)

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8
Q

give 3 examples of proteins transporters in enterocytes?

A

PepT1- H+ cotransporter (oligopeptides and H+ into cells), Na+ cotransporter of AA, Na+ independent AA transporters on the basal side

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9
Q

what is cystinuria?

A

cysteine stone formation in renal system due to mutated channels leading to deficient cysteine uptake in the intestine

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10
Q

what is vitamin A for?

A
  • Retinol (animal form), Beta Carotene (Plants)
  • Needed to form rhodopsin a key component of the eye for detecting light
    Deficiencies lead to light blindness
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11
Q

explain vitamin E

A
  • Also know as alpha-tocopherol
  • Major source is oily food
  • Antioxidant, turn of oxidants produced by immune cells to kill pathogens
  • Deficiencies damage caused in many areas of the body / poor immune system function due to the build-up of oxidants
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12
Q

Explain vitamin D source and effects of poor vitamin D

A
  • Can get it from sunlight, if lack sufficient sunlight need to consume it in our diet
  • Vitamin D deficiency = bone softening also known as osteomalacia also have demineralisation
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13
Q

explain vitamin K

A
  • Green leafy vegetables are a major source
  • Produced by macrobacteria in the gut
  • Deficiencies are uncommon but supplements are given to babies
  • Needed for prothrombin formation so deficiencies = excessive bleeding
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14
Q

how are vitamins absorbed?

A

dissolved within micelles in the small intestine to aid adsorption

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15
Q

what are the functions of dietary lipids?

A

energy storage molecule that provides a large source of energy and insulation
essential for membrane formation as essential fatty acids cannot be endogenously produced

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16
Q

what are the 3 sources of lipases?

A

There are lingual, gastric (from chief cells) and pancreas lipases

17
Q

how does bile aid lipid digestion?

A

emulsifies fat globules (micelle) this gives a large surface area for lipase to work
provides optimum PH for lipases

18
Q

explain the action of colipase

A

come from the pancreas and anchors the lipase to the micelle so catalytic activity can occur without the lipase being washed off by bile salts

19
Q

when are lingual lipases most active?

A

at low PH’s they work more optimally when they reach the stomach
they work minimally in the mouth at neutral PH

20
Q

how are triglycerides broken down

A

diglycerides = single fatty acids and monoacylglycerol

21
Q

how are short medium fatty acids absorbed?

A

passive diffusion through enterocytes

22
Q

explain the degradation of micelles

A

as triglycerides are broken down longer fatty acids remain with the lipid droplet shorter ones can diffuse into the solution and across the gastric mucosa
a new core lipid will replace what is lost to be broken down and the micelle will get smaller and smaller

23
Q

how are the longer FA remaining in the micelles absorbed?

A

protonated at the low PH of the enterocyte brush border
then absorbed by diffusion, carrier mediated transport or integrated into the cell membrane

24
Q

how is the low PH at the brush border created?

A

Na+/H+ antiporter in the enterocyte

25
Q

what happens to FA once inside the enterocytes

A

fatty acids are converted back into triglycerides in the smooth ER, leading to the formation of fat droplets
Apoproteins are then made in the rough ER and they associate with the lipids in the SER
This forms chylomicrons and VLDL (very low density lipoproteins)

26
Q

what happens to chylomicrons and VLDL?

A

The VLDL and chylomicrons leave via exocytosis, they enter the lymphatic system and then blood via the thoracic duct
Once in the blood, chylomicrons are broken down into FA and glycerol by lipoprotein lipase present on endothelial cells surface
Glycerol can be absorbed by the cell, FA can go to muscle or adipocyte cells to store fat

27
Q

what are the 5 types of cell in the small intestine?

A

goblet, stem, Paneth cells (produce antibacterial proteins e.g. lysosomes for protection), villous enterocytes (absorptive function), crypt enterocytes (secretory function)

28
Q

describe the fold structure of the small intestine

A

covered in circular folds called plicae of circulares which have microvilli present on them to increase surface area for absorption

29
Q

what are the 2 main routes of ion and water absorption?

A

transcellular and paracellular

30
Q

how is paracellular movement into enterocytes driven?

A

Paracellular transport is driven by the pumping of the ions (mainly Na,Cl into the interstitial fluid, making it hypertonic near the apical membrane and drawing water through tight junctions into the gut, a similar process occurs for transcellular movement

31
Q

what are the 4 mechanisms of sodium absorption?

A

SGTL1 sodium glucose transporter
AA / galactose symporters also exist
H+/Na antiporter (often coupled with HCO3/Cl antiporter to maintain PH)
ENaC (epithelial channels absorb Na+ against conc particularly in colon )

32
Q

how do mineralocorticoids effect sodium reabsorption?

A

e.g. Aldosterone bind to the cells causing increased opening of ENaC channels, increased fusing of channels from vesicles to the membrane and increased synthesis of Na channels and Na/K pumps

33
Q

how does E.coli act on sodium pumps?

A

it binds to the enterocytes and releases toxins that they take-up via endocytosis. This interacts with G proteins increasing the cAMP levels
This causes increased Cl- secretion and it block Cl and Na uptake, this results in low electrolytes being absorbed and osmotic diarrhoea

34
Q

when is CL/HCO3 transporter uncoupled from the Na/H+ transporter?

A

small intestine and ileum to neutralise stomach acid and combat the effects of bacteria making faeces more acidic

35
Q

what is Congenital chloridorrhea

A

absence of CL-HCO3 exchanger, results in diarrhoea, dehydration, low electrolyte levels and failure to thrive

36
Q

which 2 ways can calcium be absorbed?

A

paracellular (passively) and transcellularly

37
Q

how is Ca absorbed via the transcellular route?

A

binds to TRVP6 receptor, Calbindin-D 9K binds to Ca2+ to reduce it toxicity,
Calcium Is removed from enterocyte via Na/Ca antiporter and the PCMA Ca membrane transporter

38
Q

how is vitamin D linked to Ca absorption?

A

Binding of Vitamin D to the VD nuclear receptor increases transcription of the TRPV6 gene, promoting Ca uptake. Therefore deficiencies in VD have the same symptoms / cause calcium deficiency

39
Q
A

Digestion (8 decks)

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