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ANAEMIA
2012.12.06
Paj sir’s lecture note

                         jumbz
 Anaemia- british style
 Anemia – american style
 Acording to WHO(1960) proposed a
  cut off value for hb content for
  anaemia.It is 12%
 How ever excluded from this group
  are
  1.pregnant(15-49years)
  2.children(6-59 months)
 For srilanka today,peak or the
  maximum apears around to 9-11
  months in children
 If you want to look at anaemia in
  pregnant,
  you find it 35%
 In children 6-60months – 33%
  anaemia
 At the time of birth we have sufficient
  iron storage . It lasts at in 6th month
 Breast milk is poor source of iron only
  help untill 6th month.iron in breast milk
  is in the form of heme iron.
 There are two types of iron
      1.mainly inorganic iron
      2.heme iron
 Of these two iron is absorbed through
  carrier system..The percentage of
  absorption is depend on body state.
 In anaemic condition it willl increase
  absorption.those people who are
  normal will absorb low amount relative
  to anaemic patients.
 So absorption is governed by body
  state.
 Iron is carried by a protein-
  transferrin,not as ferus state,but as
 When it is absorbed to enterocyte
  once,it is converted to Fe3+ by a
  protein,-ceruloplasmin.
 Fe2+           Fe3+
 Ceruloplasmin is a beautiful blue
  colour protein.
 So iron in ferus state absorbs and is
  converted to feric state and is loaded
  to transferin.(a protein)
   Apo-transferin-produce in liver


                    Fe3+ loaded.
 Can loaded 2 atoms,then it
  transported to sites where iron is
  required; principal site is bone
  marrow.liver is also a site.
 Erythroblast ae born in bone
  marrow,iron for synthesis of heme and
  then corperated into hemoglobin
 Also goes to other places where heme
  proteins are produced.
 1.myoglobin-in muscle.
  2.cytochroms-in mitochindria,electrone
  transport system on inner surface of
  mitochondria.
  (Mitochondria originates from maternal
  side,so genatic disorders from mother)
 Excess iron stored in liver as
  feritin.another form is hemosidarin.but
  most is in the form of feritin.
 Everyday on an average we relase
  1mg of iron to iron pool.
 Fe2+                    Fe3+
 why is this reaction is so important???
 If you have iron in ferrus state it will be
  more active and begins to produce
  oxygen free radicles.
 Oxygen free radicles are sometime
  important as to attack invading
  pathogens.
 Free radicles are caused to oxidation of
  sevarel components
      1.oxidation of nucleic acids-cause to
  cancer
      2.phospholipids-reduction in cell
  membrane function.
      3.protein-make an inactive condtion.
 Skin-wrinkling of the skin.in skin
  abundantly present protein is collagen.
 In wrinkling 2 sulper amino acids are
  oxidized forming disulfied linkage
  -SH-          -S-S-
 Free radicles oxidise
  protein,PUFA,nucleic acids.so they
  are toxic.ceruloplasmin is a protective
  agent makinf it less toxic.
 Iron is transported by apo-transferrin.
 what happen in iron deficiency???
 The body will try to bring as much as
   But we release only 1mg.so in growing
    child,adolecent and pregnant 1mg is
    insufficient.so become anaemia.
        Howrcome do we overcome this???
   1.liver starts to produce more an more
    apotransferrin.so in iron deficiency
    anaemia apotransferrin is increased.
   What about iron we put out into
    blood.they are carried by ferritin.infact
    level of ferritin in blood plasma is an
    indicator of iron store.
   What about heme??? Maximum
    percentage of heme iron absorption is
    30%.absorption of inorganic iron is 10%.
   Heme iron from animal sources.(liver
    o,organ meats).
   Fish – almost black colour is due to lot of
    heme iron.
    Myoblobin present in red colour.
   If you are a vegiterian maximum absorption is
    10%.but average value is 3%-5%.so have to
    provide vit.c.
   Iron deficiency is found in all over the world.
      Special reasons,
     1.iron is found in richly surface on the earth.
     2.plant-iron in ferric state.so it is unavailable.
   We can only absorb iron only in Fe2+ form.so
    bioavailability is low.
   If you are a vegan-no iron come from
    heme.so vitamin c should be 60mg per
    day.smokers should get 100mg per day,due
    to produce oxygen free radicles by
    components such as CO,arsenic.
   We usualy use in curries surviving
    agents(tamerin,lime,goraka,bilin). These
    agents give acidic ph helping in iron
    absorption.
   Never ever use aluminium pots.otherwise
    aluminium jump into them.So use clay pots.
   In green leaves vegitables also in legums iron
    is bound to phytic acid.so they are not
    bioavailable.
     How do we release them???
      Soaking them
    wtare absorbs.It triggers growth of
    seeds.(germination).so trace elmants are
    released.Bound to phytic acid is a self
    defence.
   There is an enzyme called phytase to release
   Are there any form of anaemias??? Yes!
   But the main thing is iron deficiency
    anaemia.
   If you have malaria,those parasite enter
    your body having a luxury day :D
   But people who are in anaemic
    condition,parasites can not grow.
   In addition toirion deficiency ther are also
    folate def and vit b 12 def.
    folate and vit.B12 are involve I DNA
    synthesis.when deficiency (one or both)
    dna replication will be affected.Without
    DNA replication no cell division.
    So reducing cell division.
 So what will happen???
  Number of enterocyte will be reduced
  and affect in absorption of nutrients.
  Malabsorption accures.
 So not only anaemia but also
  undernutrition condition occures.
 How do you know it???
 1.take a blood sample from finger
  pit.
    2.get a blood picture.can be seen
  macrocytic and microcytic RBCs.This
  says number of RBCs and Hb content
  is less.
   Clinical feature-involve with nerve
    transmission. In vit B12
    deficiency.Dismatching signals through
    nerves.It will damage the nerve covering-
    mayalin sheath.So what will happen???
    -Not proper covering the nerve fiber
    -signal will become weak and leak.
   Vitamin B 12 is most stable.can be in
    125c’
   Folic acid-
   50% of iron deficiency are also in folic
    acid deficiency.
   Folic acid deficiency is caused mainly
    due to poor processing.
   Folic acid is heat unstable.So it is called
    labile.acidic pH is good for it.
 What are the other bad affects???
    1.growth retardation        folate &
    2.malabsorption              B12 defi.
 Anaemic women
     placenta is large.But small
  fetus.Small for date babies.
  How do we define- infant is less than
  2.5kg
  These infant ,in their middle and old
  age will be affected in
     1.DM
     2.hypertension.
  Their imunity is reduced
 Children and workers as tea pluckers
  and ruber tappers-increased absence of
  days and reduced work output.
  School children-increased absence of
  school is due to illness.
     1.common cold
     2.cough              low immunity
     3.diarrhoea
 Fe-
 1.Need to transport oxygen.They
  require O2 and also for production in
  heme protein
    .Need for mitochondria for production
  of citochromefor energy production.
     2. mayoglobin in red muscle.
    Darker red in muscle.
    What is the reason???
    Continuos 24hr energy rquirement.
   In anaemia growth rate is reduced.
   Any other form of anaemia??? Yes !
   Thalassemia – commmonest form is
    beta thalassemia.Their Hb A amount is
    low.So how do they overcome-by Hb A2
    and Hb F.
   Also they will have alfa-4.they are not
    functional Hbs.Abnormal proteins.
         ‘’heinz bodies’’-dark pigment
 Sickle cell anaemia-sickling of RBCs
  giving hypoxia.
 Normally RBCs are rolled over and
  creeped through blood vessels.but
  due to sickle shape it damage blood
  vessles and blocks the blood flow.
 Sickling can be seen only in oxygen
  deficinecy.
 Maleria - patasites enter good helath
  peoplefor their multiplication.they
  would finaly burst RBCs.leading
  hemolysis anaemia.-hemolytic
  anaemia.
   Iron is something that retains in body
    strongly.
      How do we loss it???
      Skin,feces….
    No in urine
    no in bile.
          Only through removed of
    cells.dead cells.
   Synthesis of heme.
   1.succinyl CoA+glycine
              rate limitting step
   Delta.amino lenolenic acid
              inhibited by heme     (surplace free)


 Porphobilinogen
 There is a feedback type inhibition
 Transferrin – loaded with iron.maximux is
  2 atoms of iron.
 There is a normal saturated rate of
  transferrin.In iron deficiency this rate will
  be reduced.

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Anaemia paj sir lec note

  • 2.  Anaemia- british style  Anemia – american style  Acording to WHO(1960) proposed a cut off value for hb content for anaemia.It is 12%  How ever excluded from this group are 1.pregnant(15-49years) 2.children(6-59 months)  For srilanka today,peak or the maximum apears around to 9-11 months in children
  • 3.  If you want to look at anaemia in pregnant, you find it 35%  In children 6-60months – 33% anaemia  At the time of birth we have sufficient iron storage . It lasts at in 6th month  Breast milk is poor source of iron only help untill 6th month.iron in breast milk is in the form of heme iron.  There are two types of iron 1.mainly inorganic iron 2.heme iron
  • 4.  Of these two iron is absorbed through carrier system..The percentage of absorption is depend on body state.  In anaemic condition it willl increase absorption.those people who are normal will absorb low amount relative to anaemic patients.  So absorption is governed by body state.  Iron is carried by a protein- transferrin,not as ferus state,but as
  • 5.  When it is absorbed to enterocyte once,it is converted to Fe3+ by a protein,-ceruloplasmin.  Fe2+ Fe3+  Ceruloplasmin is a beautiful blue colour protein.  So iron in ferus state absorbs and is converted to feric state and is loaded to transferin.(a protein)
  • 6. Apo-transferin-produce in liver Fe3+ loaded.  Can loaded 2 atoms,then it transported to sites where iron is required; principal site is bone marrow.liver is also a site.  Erythroblast ae born in bone marrow,iron for synthesis of heme and then corperated into hemoglobin  Also goes to other places where heme proteins are produced.
  • 7.  1.myoglobin-in muscle. 2.cytochroms-in mitochindria,electrone transport system on inner surface of mitochondria. (Mitochondria originates from maternal side,so genatic disorders from mother)  Excess iron stored in liver as feritin.another form is hemosidarin.but most is in the form of feritin.  Everyday on an average we relase 1mg of iron to iron pool.
  • 8.  Fe2+ Fe3+  why is this reaction is so important???  If you have iron in ferrus state it will be more active and begins to produce oxygen free radicles.  Oxygen free radicles are sometime important as to attack invading pathogens.  Free radicles are caused to oxidation of sevarel components 1.oxidation of nucleic acids-cause to cancer 2.phospholipids-reduction in cell membrane function. 3.protein-make an inactive condtion.
  • 9.  Skin-wrinkling of the skin.in skin abundantly present protein is collagen.  In wrinkling 2 sulper amino acids are oxidized forming disulfied linkage -SH- -S-S-  Free radicles oxidise protein,PUFA,nucleic acids.so they are toxic.ceruloplasmin is a protective agent makinf it less toxic.  Iron is transported by apo-transferrin.  what happen in iron deficiency???  The body will try to bring as much as
  • 10. But we release only 1mg.so in growing child,adolecent and pregnant 1mg is insufficient.so become anaemia.  Howrcome do we overcome this???  1.liver starts to produce more an more apotransferrin.so in iron deficiency anaemia apotransferrin is increased.  What about iron we put out into blood.they are carried by ferritin.infact level of ferritin in blood plasma is an indicator of iron store.  What about heme??? Maximum percentage of heme iron absorption is 30%.absorption of inorganic iron is 10%.  Heme iron from animal sources.(liver o,organ meats).
  • 11. Fish – almost black colour is due to lot of heme iron. Myoblobin present in red colour.  If you are a vegiterian maximum absorption is 10%.but average value is 3%-5%.so have to provide vit.c.  Iron deficiency is found in all over the world. Special reasons, 1.iron is found in richly surface on the earth. 2.plant-iron in ferric state.so it is unavailable.  We can only absorb iron only in Fe2+ form.so bioavailability is low.  If you are a vegan-no iron come from heme.so vitamin c should be 60mg per day.smokers should get 100mg per day,due to produce oxygen free radicles by components such as CO,arsenic.
  • 12. We usualy use in curries surviving agents(tamerin,lime,goraka,bilin). These agents give acidic ph helping in iron absorption.  Never ever use aluminium pots.otherwise aluminium jump into them.So use clay pots.  In green leaves vegitables also in legums iron is bound to phytic acid.so they are not bioavailable.  How do we release them??? Soaking them wtare absorbs.It triggers growth of seeds.(germination).so trace elmants are released.Bound to phytic acid is a self defence.  There is an enzyme called phytase to release
  • 13. Are there any form of anaemias??? Yes!  But the main thing is iron deficiency anaemia.  If you have malaria,those parasite enter your body having a luxury day :D  But people who are in anaemic condition,parasites can not grow.  In addition toirion deficiency ther are also folate def and vit b 12 def. folate and vit.B12 are involve I DNA synthesis.when deficiency (one or both) dna replication will be affected.Without DNA replication no cell division. So reducing cell division.
  • 14.  So what will happen??? Number of enterocyte will be reduced and affect in absorption of nutrients. Malabsorption accures.  So not only anaemia but also undernutrition condition occures.  How do you know it???  1.take a blood sample from finger pit. 2.get a blood picture.can be seen macrocytic and microcytic RBCs.This says number of RBCs and Hb content is less.
  • 15. Clinical feature-involve with nerve transmission. In vit B12 deficiency.Dismatching signals through nerves.It will damage the nerve covering- mayalin sheath.So what will happen??? -Not proper covering the nerve fiber -signal will become weak and leak.  Vitamin B 12 is most stable.can be in 125c’  Folic acid-  50% of iron deficiency are also in folic acid deficiency.  Folic acid deficiency is caused mainly due to poor processing.  Folic acid is heat unstable.So it is called labile.acidic pH is good for it.
  • 16.  What are the other bad affects??? 1.growth retardation folate & 2.malabsorption B12 defi.  Anaemic women placenta is large.But small fetus.Small for date babies. How do we define- infant is less than 2.5kg These infant ,in their middle and old age will be affected in 1.DM 2.hypertension. Their imunity is reduced
  • 17.  Children and workers as tea pluckers and ruber tappers-increased absence of days and reduced work output. School children-increased absence of school is due to illness. 1.common cold 2.cough low immunity 3.diarrhoea  Fe-  1.Need to transport oxygen.They require O2 and also for production in heme protein .Need for mitochondria for production of citochromefor energy production.
  • 18. 2. mayoglobin in red muscle. Darker red in muscle. What is the reason??? Continuos 24hr energy rquirement.  In anaemia growth rate is reduced.  Any other form of anaemia??? Yes !  Thalassemia – commmonest form is beta thalassemia.Their Hb A amount is low.So how do they overcome-by Hb A2 and Hb F.  Also they will have alfa-4.they are not functional Hbs.Abnormal proteins. ‘’heinz bodies’’-dark pigment
  • 19.  Sickle cell anaemia-sickling of RBCs giving hypoxia.  Normally RBCs are rolled over and creeped through blood vessels.but due to sickle shape it damage blood vessles and blocks the blood flow.  Sickling can be seen only in oxygen deficinecy.  Maleria - patasites enter good helath peoplefor their multiplication.they would finaly burst RBCs.leading hemolysis anaemia.-hemolytic anaemia.
  • 20. Iron is something that retains in body strongly. How do we loss it??? Skin,feces…. No in urine no in bile. Only through removed of cells.dead cells.
  • 21. Synthesis of heme.  1.succinyl CoA+glycine  rate limitting step  Delta.amino lenolenic acid  inhibited by heme (surplace free)  Porphobilinogen  There is a feedback type inhibition  Transferrin – loaded with iron.maximux is 2 atoms of iron.  There is a normal saturated rate of transferrin.In iron deficiency this rate will be reduced.