Ions, vitamins and minerals Flashcards

1
Q

What are some examples of primary active transporters?

A

Na/K ATPase

H/K ATPase

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2
Q

What are some examples of secondary active transporters?

A

SGLT-1 - uses Na gradient to take up glucose
HCO3-/Cl- counter-transport
Na+/H+ counter transport

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3
Q

What are some examples of facilitated transport/diffusion?

A

GLUT-5 -

GLUT-2

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4
Q

Where does the greatest amount of water get absorbed?

A
Jejunum
Small intestine absorbs 8 lirtes
- saliva
- gastric secretions
- pancreas
- bile
- water
- intestine
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5
Q

how is water abosrobed?

A

Standing gradient osmosis
the absorption of water is powered by absorption of ions
Na+ —-

It is then pumped out of the cells that it is in in exchange for K+ and this creates a high conc of Na+ near basement membrane. electrochem grad changes so Cl- and HCO3- move out as well, drives H2O absorption via both para and transcellular paths

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6
Q

How is Na+ absorbed?

A
  • counter transport with H+ bowel
  • cotransport with monosac - jej Cl- - ileum
  • ion channel colon
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7
Q

How are K+ and Cl- absorbed?

A
K+
diffuses via paracellular pathways - small intestine
transcellular in colon
Cl-
cotransport with na+ in the ileum
Exchanged for HCO3 in the colon
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8
Q

Where is calcium absorbed? What increases it?

A

In the duodenum and ileum
deficiency increases ability to absorb
PTH and Vit D increase absorption

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9
Q

How is calcium absorbed?

A

Intestinal calcium-binding protein
- fac diff

Ion channel

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10
Q

Why is ca2+ low in the cell? how is Ca2+ brought in while maintaining this low conc? how is it then pumped into the blood?

A

Acts as a signalling molecule
- Constant intake might cause loops of secondary messenger

calcium is bound to CALBINDIN to prevent action as intracellular signal and then moved into blood

Has to be pumped as against concentration gradient

  • plasma membrane Ca ATPase
    • High affinity but sklow but lowers conc in cell
  • Na/Ca exchanger
    • Low affinity, needs lots of Ca but v fast
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11
Q

Why is Vit D needed for Ca uptake?

A

Enhances transport of Ca2+ thru cytosol
Increases calbindin levels
Increases rate of extrusion on BM - increases levels of PMCA

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12
Q

Why is iron absorbed??

A

Needed as is e- donor, acceptor
Ox transport
Ox phos

but, is toxic in excess and no active excretion mechanism
- so, mediate it

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13
Q

How is iron present in the diet?

A

inorganic iron, haem group - Hb etc

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14
Q

Why must Ffe2+ be absorbed?

A

Fe3+ has to be reduced to Fe2+ because body can’t absorb Fe3+

This is done by Vit C

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15
Q

What does Fe3+ form

A

Insoluble salts with OH, Po4 and HCO3

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16
Q

How is haem absorbed?

A

Absorbed through haem carrier protein and endocytosis
Kept intact

Fe2+ is then liberated by haem oxygenase

17
Q

how can Fe3+ be utilised by ce;l;

A

Duodenal cytochrome b catalyses formation of Fe2+ from Fe3+

Fe2+ is then transported by divalent metal transporter 1 -DMT-1, a H+ co transporter

Fe2+ binds to factors, moves to BM and moves into blood via FERROPORTIN channel

18
Q

How is iron carried in the blood?

A

Reforms Fe3+ via Hephaestin

Fe3+ binds to apotransferrin, now in blood as transferrin

Regulated by hepcidin
- suppresses ability to pump fe2+ out into blood by ferroportin

19
Q

What might occur if iron is not required in the blood?

A

immobilised in cytosol by binding to apoferritin
Fe2+ gets oxidised, and then this complex is ferritin - forms crystallised micelle

this prevents too much absorption which would be toxic

  • irreversible
  • iron not available for blood
  • then gets lost in the lumen, excreted as faeces

stimulated by increased cytosolic iron concentration

20
Q

What is a vitamin?

A

ORGANIC MOLECULE THAT CANNOT BE MADE BY BODY

21
Q

How are vitamins taken up?

A

Passive diffusion
ADEK - brush border micelle - fat soluble
K - active transport

C, folic acid, B1, B12 by specific mechanisms

22
Q

Where is B12 stored andwhat are the problems if low

A

Liver, retards blood cell maturation

23
Q

When is it released? Describe its journey

A
Low pH and digestion of proteins
but gets denatured by HCl
- Prevented by binding to R protein - haptocorrin
   - released by parietal cells
   - broken down in duodenum
  • B12 is then bound to intrinsic factor, recognised by Cubilin and stopped from being digested
  • Then taken up into ileum after binding to cubilin receptor
    • endocytosis
  • This complex is then broken down inside and B12 binds to TRANSCOBALAMIN II, crosses BM
  • Then it travels to liver in blood where it is taken up after binding to TCII receptor
  • Proteolysis breaks TCII down in liver