Absorption of iron and gastrointestinal disease Flashcards

1
Q

What is the role of iron in human biology?

A

Oxygen transport and storage
electron transport
plethora of enzymes
cell cycle control

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2
Q

Why is control of iron important?

A

There is no active excretory mechanism

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3
Q

Iron- physiological processing

A
very small amount of iron absorbed
stored in the liver
very small amount lost
Iron circulates in plasma
RBC made in bone marrow
RBCs engulfed by macrophages
haem broken down into bilirubin and ion is liberated
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4
Q

What is the purpose of Dcytb?

A

ferric reductase

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5
Q

What is DMT1?

A

divalent metal transporter responsible for ferrous uptake

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6
Q

What is Ferritin?

A

inert iron storage

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7
Q

What is the purpose of ferroportin?

A

Cellular iron efflux

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8
Q

What is hephaestin?

A

Ferroxidase

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9
Q

What is transferrrin?

A

essential for iron binding in blood

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10
Q

Why do patients who have had gastrectomies develop iron defieciency anaemia?

A

Acids can reduce Fe3+ to Fe2+- a form that is more readily absorbed in the duodenum. Removal of stomach often leads to decrease production of acid

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11
Q

Why is PPI used for hereditary haemochromatosis?

A

PPI decrease acid production. This decreases the reduction of Fe3+ to Fe2+ which is more readily abdorbed

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12
Q

How does non-enterocyte iron transport occur?

A

Transferrin receptor mediated endocytosis. Cells that are iron deficient would express more transferrin receptors on its cell surface

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13
Q

What does transferrin receptor mediated endocytosis involve?

A

Transferrin receptor, DMT-1 and the ferric reductase STEAP-3

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14
Q

How does haem transport occur?

A

Via HCP-1 at brush border of enterocyte

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15
Q

Once inside cell, what happens to haem?

A

Haem is broken down into haem-oxygenase -1 (HO-1). This releases free iron and biliverdin. Iron enters the labile iron pool within the cell and gets exported by ferroportin or stored by ferritin.

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16
Q

Haem biosyntheis

A

Complex lots of steps. lots of enzymes

Defects can therefore lead to disease

17
Q

What is hyperbilirubinaemia a consequence of?

A

Too much break down of biliverdin to bilirubin by biliverdin reductase

18
Q

What is the cause of PCT- porphyria cutanea tarda?

A

mutation in uroporphyrinogen decarboxylase.
Build up of precursor as enzyme doesn’t work properly
Build up of substrate

19
Q

What are the clinical manifestations of PCT?

A

Vampires and werewolfs
pathological sensitivity of skin to light
hypertrochosis- excess hair
changes in urine colour

20
Q

What are the major stores of iron?

A

liver, spleen and bone marrow

21
Q

What is the master regulator of iron metabolism?

A

Hepcidin- communicates with the small bile