nill

2.  One of the most common medical problems
 Most common cause of anemia
 Iron deficiency anemia is the last step ;
 Iron depletion: absent or decreased iron stores
 Iron deficiency: depletion of stores + low serum iron
and ferritin
 Iron deficiency anemia: Anemia developing in an
iron deficient patient

4.  Iron is located at the center of Hem
molecules of Hb (amount:1.5-2 gr)
and it is also;
 Part of the myoglobin
 Takes place in the tissue enzymes
 Storage forms are
 Ferritin
 Hemosiderin
 Location: Bone Marrow, Liver, Spleen
 Transport iron is by transferrin.

5.  Transferrin picks up iron from ;
1. The GI cells to deliver it to Hb forming cells
2. Storage parts as a step of iron recycling process
 Absorbtion + recycling provides the constant
iron supply of 1-2 mg/day necessary for Hb
synthesis

6. Male 1 mg
Adolesc. 2-3 mg
Women in repr.age 2-3 mg
Pregnant 3-4 mg

7.  Iron absorbtion is restricted to the needs of the
body
 1mg of iron is lost each day
 Menstruation and pregnancy/lactation are other
major causes of iron loss and incresed demand in
women

8.  Normal diet contains about 14 mg of
iron/day
 1/10 of ingested iron is absorbed
 Gastric acid releases iron from food
 Iron is absorbed in the reduced form
 Ascorbate increases absorbtion (by reducing)
 Phytates,phosphates , Tea,
infection,,antacids decrease absorbtion by
making complexes with iron

9.  Main sites of absorbtion are;
 Duodenum
 Upper jejunum
 Malabsorbtive states or gastrojejunostomy
prevent absorbtion.

10. Transport of iron
 Transferrin is the main iron carrier in plasma
 It is produced in liver cells with increased synthesis
in iron deficiency
 Transferrin binds 1-2 ferric iron molecules
 Transferrin-iron complex is endocytosed by Hb
producing cells after linking to receptors.

11.  Total iron binding capacity and iron
 Transferrin is measured by quantifying the iron
binding sites available
 This is also called “Total iron binding capacity”
 TIBC is 1/3 saturated under normal conditions

12.  Chronic blood loss
 Increased demand
 Malabsorbtion of iron
 Inadequate iron intake
 Intravascular hemolysis and
hemoglobinuria-hemosiderinuria
 Combinations

13.  Pregnancy
 Lactation
 Rapid growth

14.  Decreased iron in the diet
 Vegetarianism
 Decreased absorbtion
 Gastric surgery
 Achlorhydria
 Sprue
 Pica

15.  Menorrhagia
 GIS hemorrhagia
•Angiodysplasia
•Diverticulosis
•Meckel diverticula
•Colitis or imf. Bovel
disease
•Hemorrhoids
•NSAID use
•Parasites
•P.Ulcer
•Oesophagitis
•Varices
•Hiatal hernia
•Malignancy

16.  Bleeding disorder
 Pulmonary lesions with bleeding
 Hemoglobinuria – hemosiderinuria (chronic
intravascular hemolysis)
 Hemodialysis
 Hematuria (chronic)
 Frequent donation
 250 mg iron /unit-blood

17.  General symptoms of anemia
 Fatigue may be disproportional to the degree
of anemia due to deficiency of tissue enzymes
which also need iron
 Chlorosis
 Glossitis
 Angular stomatitis
 Paterson-Kelly (Plummer Vinson) syndrome
(oesephageal web leading to disphagia)

18.  Gastric atroph
 Nail changes
 Brittle/fragility
 Koilonchia/spooning
 Hair loss
 Splenomegaly

19.  Pica:Appetite for bizzare food/substances
 Geophagy (earth,clay)
 Pagophagia(ice)
 Amylophagia(starch)
 Developmental problems
 Splenomegaly
 Immun-deficiency

20.  Hb,Htc,RBC:Low
 MCV,MCH,MCHC:Low
 RDW: High
 Retics: Normal/Low
 Plt:Normal/Low/High
 WBC:Normal/Low
 Smear:
Hypochromia,anisocytosis,microcytosis,
poikilocytosis

21.  Serum Iron: 
 TIBC: 
 Serum Ferritin 

22.  Transferrin saturation (Fe/TIBC):  (<15%)
<5%:definitely indicates iron deficiency
 Serum Transferrin Receptor: 
 Free Erythrocyte Protoporphyrin  (17 – 27 μg/dL)
 Bone marrow :
 Erythroid hyperplasia,
 Absence of hemosiderin

23.  Microcytic anemias
 Iron deficiency anemia
 Thalassemia ,HbC,HbE etc
 Sideroblastic anemia
 Lead poisoning
 Anemia of chronic diseases (sometimes)

24.  The diagnostic procedure is not complete until
the underlying pathology is disclosed.

25.  Replace iron and treat underlying disease.
 Oral route is preferred for replacement.
 Response can be followed by retic. increase in
1-2 weeks (5-7 days)
 Hb response to treatment
 half normal by a month
 returns to normal by 2-4 months
 Replacement therapy is prolonged by 6-12
months to replenish stores of iron.
 Ongoing bleeding may cause indefinite
therapy.

26. Oral iron therapy:
dose (mg) elemental
iron(mg)
Fe fumarate 200 65
Fe gluconate 300 35
Fe sulphate 200 65

27. Oral iron therapy:
Total daily dose:150-200 mg elemental iron
Give in 3-4 divided doses,
Each one hour before meals.
Do not prefer enteric coated forms.
In case of GIS intolerance;
 Change the route of administration or
 Change the preparation or
 Reduce dose

28. Non responding patient:
 possible causes
 Misdiagnosis
 Patient does not take the medicine
 Continuing blood loss
 Malabsorbtion
 Change the drug
 Change the route of administration
 Underlying disease /comorbidity
 Combined deficiency

29.  Parenteral iron therapy:
Routine use is not justified,
Response is not faster than oral replacement.
Indications
 Malabsorbtion
 Intolerance to oral replacement
 Colitis/enteritis
 Needs in excess of amount that can be given
orally
 Patient uncooperative/poor compliance
 Autologous blood donation setting
 Hemodialysis

30. Treatment
Parenteral iron therapy:
Total iron dose: (15-patient Hb) x bw x 3
– Iron Dextran: 50 mg/ml (iv/im)
 Max daily dose is 100 mg im
– Ferric gluconate:
 A test dose of 25 mg elemental iron (2 mL) must be
given in 50 mL saline over 60 minutes
– Ferric-hydroxy-sucrose (100 mg/5mL)
– 2.5 ml first day
– 5ml third day
– 2x5 ml/week

31. Parenteral replacement therapy may cause
 allergic reactions,
 local pain or induration,
 serum sickness like disease,
 lymphadenomegaly,
 arthralgia,
 myalgia etc.
Treatment

32.  Pregnants ( at 20-24 weeks Hb< 11 g/dL,
Ferritin ).
 Lactation.
 Frequent blood donation.
 Autologous blood donation settings.
 Gastrectomised patients.
 High dose asprin treatment.