The Absorption of Iron and Intestinal Disease Flashcards

1
Q

Which ion is ferrous iron and which is ferric?

A
ferrous = 2+
ferric = 3+
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2
Q

Where is dietary iron absorbed by?

What is it transported around the blood with/

A

duodenal enterocytes

transferrin

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3
Q

Where can iron by transported to and what does it do in each place?

A

bone marrow - added to Hb with RBC’s
liver/spleen - storage
muscle - stored in myoglobin
cells - utilises iron for enzymes, and other cellular functions

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4
Q
There are no mechanisms in the body to remove iron, although a few milligrams are lost daily in:
-
-
-
-
-
A
blood - menstruation
faeces - cells 
urine - cells
skin - cells
sweat - more in athletes
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5
Q

What are the two types of dietary iron?

A

inorganic iron = Fe3+

haem = Fe2+

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6
Q

Both forms of dietary iron are found highly bound to food proteins and are firstly released from them and kept soluble by …….. …… and ………

A

gastric acid

pepsin

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7
Q

How does haem enter the enterocyte?

What happens to it then?

A

via the transporter HAEM CARRIER PROTEIN (HCP1).

it is subsequently degraded by haem oxygenase to liberated Fe2+

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8
Q

What has to happen to inorganic iron before it can absorbed by enterocytes? Why?
How does it then enter the enterocyte?

A

Fe3+ is non-absorbable
It needs to be reduced to Fe2+, this is achieved by DcytB (ferric reductase). This can also be aided by gastric acid.
It enters the enterocyte via the transporter DMT1 (divalent metal transporter-1)

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9
Q

What 3 things does the Fe2+ do once inside the enterocyte?

A

stored as ferritin (Fe3+)
used by the cell
converted to Fe3+ by hephaestin, transported out by ferroportin, incorporated into transferrin

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10
Q

What effect does hepcidin have on iron levels?

When is it produced?

A

it decreases them

released when iron is high

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11
Q

Where does hepcidin act?

What effects does hepcidin have?

A

It internalises and degrades ferroportin so the iron cannot be transported out of the cells.
Ferroportin is found on, and hence hepicidin acts on:
- macrophages, enterocytes, hepatocytes

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12
Q

What is hepcidin synthesis suppressed by?

When is hepcidin synthesis induced?

A
  • iron deficiency, anaemia, hypoxaemia, accelerated erythropoesis
  • high iron stores, inflammation
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13
Q

Describe the basis of anaemia of chronic inflammation

A

During inflammation interleukin-6 levels are raised
This is a stimulator for hepcidin synthesis
Ferroportin transporters are degraded
Iron transport is decreased.
Iron levels decrease

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14
Q

Describe how hypoxaemia leads to increased iron levels.

A

Low O2 surpasses hepcidin synthesis

There is an increased uptake of dietary iron, iron is released from hepatocytes and macrophages

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15
Q

What 2 things occur when iron levels are low?

A
  • hepcidin levels low, so ferroportin is rich on the basolateral surface to permit more iron release
  • DMT1 is rich on the apical surface to permit more iron absorption
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16
Q

What 3 things occur when iron levels are high?

A

hepcidin levels are high, ferroportin is low on basolateral surface, reduces iron release
DMT-1 is down regulated
Iron is stored as ferritin

17
Q

How can a gastrectomy cause anaemia?

Which types of anaemia’s are these?

A

Lack of acid means ferric iron cannot be converted to the absorbable ferrous iron. This is iron deficiency anaemia.
Lack of intrinsic factor (released by stomach), Vitamin B12 cannot be transported and absorbed in the ileum. B12 is important in RBC maturation. This is megaloblastic or pernicious anaemia.

18
Q

How could a gastrectomy remedy the presence of anaemia.

A

obesity –> low grade chronic inflammation
IL-6, stimulates hepcidin synthesis, decreases iron
anaemia of chronic disease

19
Q

What are hepcidin levels like in anaemia of chronic disease and iron deficiecny anaemia?

A

ACD –> high hepcidin

IDA –> low hepcidin

20
Q

What is hereditary haemochromotosis?

A

Cannot make hepcidin

Excess storage of iron

21
Q

What is coeliac disease?

What is the test of coeliac disease?

A
autoimmune disorder, gluten sensitive enteropathy
inflammatory reaction
villous atrophy 
anti-tissue transglutaminase ab 
small bowel biopsy