Iron metabolism and microcytic anaemia

Question 1

inflammatory

Answer 1

cytokines released like IL6 c ^hepciidin so v iron released from RES and v absorption of fe2+ because ferritin absorption reduced fe2+ for RBC also cytokines cause inhibition of EPO production kidney so inhibitor of eryhtopoiesis

Question 2

histology

Answer 2

haemosidirin

Question 3

on a blood film how do microcytic anaemia usually present and lab results

Answer 3

hypochromatic

microcytic

v MCV

Question 4

treatment

Answer 4

diet oral supplest (b side effects make them sick) IM or IV (should see 20g/L rise in 3 weeks) only b transfusion if emergency

Question 5

iron uses? and why is free iron dangerous?

Answer 5

• carries 02 in hb (RBC) and myoglobin (myocytes)
• cofacor for many enzymes
• eg. cytochromes (oxidative phosphorylation)
• Krebs cycle enzymes
• cytochrome p450 enzymes (detoxification)
• catalse

-free fe2+ dangerous b of Fenten cycle, toxic to cells

Question 6

f affects

Answer 6

NEGATIVE INFLUENCE -tannins in tea -PHYTATES (CHAPPTIIE ) -fibre (bind to fe2+) - antacids (need acid to reduce fe3+ to fe2+) POSITIVE \ -vit c and citrate b give e needed for the conversion of fe3+ to fe2+

Question 7

how is fe2+ stored

Answer 7

ferritin (soluble ) haemosiderin (insoluble ) aggregates and c denaturing of lipids and proteins , accumulate in macrophages particularly In liver spleen and marrow

Question 8

tst

Answer 8

ferritin (usually in cells ) but some in b and is constant level and v in b = iron defiicny - but don’t rule out normal deficiency b cancer/infalmmatio/liver disease -chR IS MORE RELIABLE SO USE HIS except for thalasmea

Question 9

state of existence of iron

where is iron absorbed?

how us iron excreted?

Answer 9

ferrous and ferric (not useful fe3+) - we use ferrous state

duodenum and upper jejenum

no mechanism for excretion

Question 10

absorption of iron

Answer 10

• from diet into chyme ham readily absorbed -nonhaem ferrous and ferric, but can only absorb fe2+ so /fe3+ is converted to fe2+ via REDUC/tase enzyme and used vit c as cofactor moves using DMT1 into enterocytes (co transported b fe2+ eve in and H+ out) fe2+ joins liable pool where stored a FERRTINor transported out the cell VIA FERROPORTIN out of the enterocyte b cant travel it b as fe2+ must be converted into fe3+(oxidase ) via hephaestin does this -hepcindin inhibits ferroporin controlling the amount of iron absorbed in our diet

Question 11

microcytic anaemia what is it and examples?

Answer 11

smaller RBC than normal due to reduced Hb synthesis tharn normal

<80fl

Thalassaemia

Anaemia of chronic disease

Iron defic.

Lead poisoning

Sideroblastic anaemia

Question 12

hepcidin

Answer 12

peptide hormone made my liver inhibits iron absorbed b causing ferroportin to be interlined and degraded so less fe2+ removed from ferritin stores of entroecytes and macrophages - so fe2+ inmacropages stored and not released c anaemia b cant use fe2+

Question 13

iron def st

Answer 13

ANGINA pica (craving to eat non nutrition food like dirt) cold hands nadfeet epithelialchange s|(b they need iron ) kol…

Question 14

heredity haemochromatosis

Answer 14

HFE gene defect on chromes 6 autosomal reccsiesibe usually interacts with transferring receptor c v affinity for it to fe2+ so more stored than released and has negative influence on hepcidin production so fe2+ not lost - symptoms same as before but bronze skin colour treated with venesection to remove that blood

Question 15

HOW IS REcycleing controlled

Answer 15

• ferroportin - receptor HFE -hepcidin and cytokines

Question 16

Haem vs non-haem iron?

how do interchange from NH to H?

what prevents absorption of iron and what promotes it?

Answer 16

H = fe2+ (meat)

non-haem fe3+ (veg/beans)

reduction which occurs at low pH in the stomach (as a result of the prescence of acid) fe3+ + e = fe2+

oxidation occurs at a high pH ; fe2+ = fe3+ + e

• inhibits; tannins (tea), phylates (pulses and chapattis) (because they bind to non-haem iron so inhibiting it ) antacids
• promotes ; vitamin c and citrates prevent the formation of insoluble iron compounds and also reduced ferric into ferrous as it donates e

Question 17

o b film?

Answer 17

microcytic v MCV vMCHC ^ platelet unknown reason ^WBC’’ v reticulocyte hypo chromic

Question 18

tranfusion asscaued haemosodierosis

Answer 18

soem conditons like tjalaksedm really rely o b trasnfeusoion as with every 400ml transfusion there’s 200mg iron stored and this builds up overtime as haemosiderin free radicals - diabets in pacnera -hyerpgonas -joints -liver cirrhosis -grey skin colour d build up

Question 19

at risk of groups

Answer 19

prgannt infant child geriatric

Question 20

cellular iron intake

Answer 20

fe3+ bound to transferrin travel in the b bind to receptor mediated endocytosis fe3+ then put into endosome and released into the acidic micorenvironemtns and reduced to fe2+ fe2+ transported to cytosol via DMT1 stored or move out via ferroportin

Question 21

iron recalling

Answer 21

most iron is recycled in our body instead of making it new only daily dietary requirement old RBC engulfed by macrophages via phagocyte mainly splenic macrophages but some kpufeer cells - macrophages metabolise the haem - aareused and iron exported to b via transferrin or returned to storage pool ferrtinin in macrophages HOW

Question 22

excess iron

Answer 22

insoluble haemosidrie , fedangerous because free radical in Fenton reaction

Question 23

how much iron needed daily?

§

Answer 23

10-15mg/day

Question 24

what is sideroblastic and lead poisoning anaemias , and how lead differ from the other types of microcytic anaemias

Answer 24

• S = inherited x-linked genetic defect of the ALA synthase gene, involved in the haem synthesis pathway
• presentations is sideroblastic cells in blood film
• L= aquired defect wheere you inhibit the enzymes involved in the haem synthesis pathway