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INTRODUCTION
         Name : Rabia Manzoor
         Roll No:            04
        Topic:         ANEMIA
Department Of Eastern Medicine & Surgery
  Faculty of Medical & Health Sciences
  University of Poonch Rawalakot Aj&K
What is ANEMIA?



Anemia is present when there is decreased Level
of
Hb in blood below the reference level
For age ,sex and individuals
Classification of ANEMIA
 Types of classification.
 1. According to cause
 2. According to morpholology
 Cause:
 1. Blood loss
 2. Increase of red cell destruction
 3. Decrease of red cell production
Morphological classification
     According to shape and size

1. Hypo chromic microcytic with low MCV
2. Norm chromic normacytie with normal MCV
3. Macrocytic with high MCV
S/S of Anemia
1. Pallor
2. Tachycardia
3. Breathlessness
4. Head ache
5. Fatigue
6. faintness
Microcytic anemia
RBCS become small
MCV<80


Causes of microcytic anemia
•Iron low to iron deficiency Anemia
•Iron normal to sedroblastic and Thalasemia
Iron deficiency anemia

Iron deficiency is the most common cause of anemia
in world.
iron deficiency anemia is defined as when there is
Inadequate
Amount of iron for HB synthesis.
Daily Requirement. 2 to 4 gm

Source of iron.
Meat,   Egg, Vegetables, Milk , Spinach.


Storage of iron
•Liver 50 to 60 percent
•Muscles 20 percent
•Bone marrow
•Plasma
Etiology of iron deficiency

1. Dietary deficiency
2. .Increase in iron demand
3. Malobsorption of iron
4. Acute and chronic blood loss
Pathology
•Iron absorbed in intestine iron intake through diet to stomach to
where gastric secretion made complex with vitamin c and enter in
intestine where it combine with apotransferin and foam transferring
and then enter in circulation. In normal person this transferring in
about 33 percent saturated with iron.
•When iron in excessive amount :
•Lost in feces because transferring is already saturated.
•When there is iron deficiency this saturation decreases and
transferring accept more iron to iron balance. Excessive iron stored
in liver , spleen, bone marrow, skeletal muscles here it combine with
protein called apoferitin and foam ferretin storage iron.
•In iron deficiency initially depletion of stored iron. There follows a
decreased in circulating iron with low level of serum iron and rise in
serum transferring iron binding capacity.
•S/S OF IRON DEFICIENCY
ANEMIA
•Pallor
•Lethargy
•Fatigue
•Kolinchyia
•Dysnea
•Numbness
•Joint pain
•Vomiting
•Body ache
Investigation

Blood picture
Bone marrow study
Sedroblastic Anemia

It is an inherited or acquired disorder characterized by
dyserthropoesis inability of iron utilization and therefore
iron overload . There is a disordered accumulation of
iron in erythroblast because it can not be utilized due to
defect in enzymes involve in heam synthesis.
Diagnosis: Microcytic cells
Bone marrow show erythroblast with ring of
iron granules around. The nucleus ring
sidreoblasts.
Thalasemia


It is genetic disorder of hb synthesis characterized by
decreased synthesis of goblin chain .
Two alpha and 2 b chain of globins' polypeptide
combine with heam to foam HB therefore if synthesis
of globins' is reduced it will lead to decreased HB to
anemia.
Types



1.Alpha
2.Beta
Alpha

It occurs due to reduction or absence of alpha chain
synthesis .
There are four alpha gene
1.If one is deleted there is no clinical effect.
2.If two are deleted there is mild Hypochromic anemia.
3.If three are deleted pt has hb (hbh). It has functionally
unless →moderate anemia and spleenomegaly.
4.If four r deleted the baby is still born.
Beta

This occur due to reduction or absences
of alpha chain synthesis.
In normal (homozygote) both polypeptide
genes are normal and produce normal B
polypeptide chain in normal quantity.
In abnormal both B chain are abnormal
and do not produce B polypeptide chain→
B Thalasemia major
B Thalasemia intermediate


Electrophoresis which shows reduced HBA while HBA2
and F elevated (asymptomatic + moderate anemia)
Minors.
In heterozygote to one gene is normal and other is
abnormal which does not produced B polypeptide
chain . In this person normal gene produce enough
B chain to maintain HB level about to maintain.
This Thalasemia is asymptomatic and often
detected when iron therapy for mild microcytic
Hypo chromic anemia fails,.
Macrocytic Anemia]
1.Megloblastic anemia
√.vita B12 deficiency
√folic acid deficiency
Megloblastic anemia

In this type of anemia RBC became enlarged and
  odd shape.

Causes

Vit B12 deficiency
Folic acid deficiency
Vit b12 deficiency
This is type of anemia in which there is atrophy of
  gastric mucosa so failure of intrinsic factor
  production so Vit b12 not absorbed.




Causes
Pathogenesis

Tissue perforation need DNA.
DNA need VIT 12 and folic acid--- deficiency of both—
DNA not formed— cell division stop.
While cytoplasm progressive continuously — RNA
increase in amount — erthroyid tend to destroy marrow
—RBC—↓↓
s/s

•Pallor
•Dysnea
•Vibration sense loss
•Neurological disorder
•Tachycardia
Investigation

Blood c/p
Bone marrow
Low serum Vit. B12
Folic acid

Causes:
Decrease diet inake
Increase demand
Mal absorption
Investigation
Low serum folic acid
Macrocytic Blood cp
Result
Folic and supplement 5mg ready
Maintence dose 5mg/wk.
NORMOCYTIC ANEMIA

CAUSES
•Chronic disease
•Acute blood loss
•Blood disorder
CHRONIC DISEASE

    Pathogenesis
Failure of transport of storage iron
from bone marrow to plasma developing
Erythrocytes→ decrease HB and cause anemia.
Investigation


 Increase iron in bone marrow.
 Increase serum iron level.
  Increase ferretin level.
 Anemia due to acute blood loss ?

 Blood disorder
 A plastic Anemia.
 Hemolytic Anemia.
A plastic Anemia ?

C/F
Anemia
Infection
Bleeding

Investigations
Blood Picture
Bone marrow biopsy
Hemolytic Anemia ?

Mechanism

Cell Membrane abnormality
Abnormal HB
Abnormality of nasal walls

Inherited Hemolytic Anemia
Hereditary spherocytosis
Sickle cell Anemia
Thalassaemia
Hereditary spherotosis?

   Pathogenesis?

   C/F
   Anemia
   Jaundice
   Spleenomegely
   A plastic crises
   Gallstone
   Leg cancer
Sickle cell disease
 There is presence of abnormal
 HBS which upon low oxygen
 tension become crystal giving
 shape Rbcs as sickle and not
 passes through capillaries and
 destruct
Pathogenesis?

       C/F
     Anemia
Tissue infraction
Investigations

   Hb descreased
sickles erythrocytes

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Rabia presentation

  • 1.
  • 2. INTRODUCTION Name : Rabia Manzoor Roll No: 04 Topic: ANEMIA Department Of Eastern Medicine & Surgery Faculty of Medical & Health Sciences University of Poonch Rawalakot Aj&K
  • 3. What is ANEMIA? Anemia is present when there is decreased Level of Hb in blood below the reference level For age ,sex and individuals
  • 4. Classification of ANEMIA Types of classification. 1. According to cause 2. According to morpholology Cause: 1. Blood loss 2. Increase of red cell destruction 3. Decrease of red cell production
  • 5. Morphological classification According to shape and size 1. Hypo chromic microcytic with low MCV 2. Norm chromic normacytie with normal MCV 3. Macrocytic with high MCV
  • 6. S/S of Anemia 1. Pallor 2. Tachycardia 3. Breathlessness 4. Head ache 5. Fatigue 6. faintness
  • 7. Microcytic anemia RBCS become small MCV<80 Causes of microcytic anemia •Iron low to iron deficiency Anemia •Iron normal to sedroblastic and Thalasemia
  • 8. Iron deficiency anemia Iron deficiency is the most common cause of anemia in world. iron deficiency anemia is defined as when there is Inadequate Amount of iron for HB synthesis.
  • 9. Daily Requirement. 2 to 4 gm Source of iron. Meat, Egg, Vegetables, Milk , Spinach. Storage of iron •Liver 50 to 60 percent •Muscles 20 percent •Bone marrow •Plasma
  • 10. Etiology of iron deficiency 1. Dietary deficiency 2. .Increase in iron demand 3. Malobsorption of iron 4. Acute and chronic blood loss
  • 11. Pathology •Iron absorbed in intestine iron intake through diet to stomach to where gastric secretion made complex with vitamin c and enter in intestine where it combine with apotransferin and foam transferring and then enter in circulation. In normal person this transferring in about 33 percent saturated with iron. •When iron in excessive amount : •Lost in feces because transferring is already saturated. •When there is iron deficiency this saturation decreases and transferring accept more iron to iron balance. Excessive iron stored in liver , spleen, bone marrow, skeletal muscles here it combine with protein called apoferitin and foam ferretin storage iron. •In iron deficiency initially depletion of stored iron. There follows a decreased in circulating iron with low level of serum iron and rise in serum transferring iron binding capacity.
  • 12. •S/S OF IRON DEFICIENCY ANEMIA •Pallor •Lethargy •Fatigue •Kolinchyia •Dysnea •Numbness •Joint pain •Vomiting •Body ache
  • 14. Sedroblastic Anemia It is an inherited or acquired disorder characterized by dyserthropoesis inability of iron utilization and therefore iron overload . There is a disordered accumulation of iron in erythroblast because it can not be utilized due to defect in enzymes involve in heam synthesis.
  • 15. Diagnosis: Microcytic cells Bone marrow show erythroblast with ring of iron granules around. The nucleus ring sidreoblasts.
  • 16. Thalasemia It is genetic disorder of hb synthesis characterized by decreased synthesis of goblin chain . Two alpha and 2 b chain of globins' polypeptide combine with heam to foam HB therefore if synthesis of globins' is reduced it will lead to decreased HB to anemia.
  • 18. Alpha It occurs due to reduction or absence of alpha chain synthesis . There are four alpha gene 1.If one is deleted there is no clinical effect. 2.If two are deleted there is mild Hypochromic anemia. 3.If three are deleted pt has hb (hbh). It has functionally unless →moderate anemia and spleenomegaly. 4.If four r deleted the baby is still born.
  • 19. Beta This occur due to reduction or absences of alpha chain synthesis. In normal (homozygote) both polypeptide genes are normal and produce normal B polypeptide chain in normal quantity. In abnormal both B chain are abnormal and do not produce B polypeptide chain→ B Thalasemia major
  • 20. B Thalasemia intermediate Electrophoresis which shows reduced HBA while HBA2 and F elevated (asymptomatic + moderate anemia)
  • 21. Minors. In heterozygote to one gene is normal and other is abnormal which does not produced B polypeptide chain . In this person normal gene produce enough B chain to maintain HB level about to maintain. This Thalasemia is asymptomatic and often detected when iron therapy for mild microcytic Hypo chromic anemia fails,.
  • 22. Macrocytic Anemia] 1.Megloblastic anemia √.vita B12 deficiency √folic acid deficiency
  • 23. Megloblastic anemia In this type of anemia RBC became enlarged and odd shape. Causes Vit B12 deficiency Folic acid deficiency
  • 24. Vit b12 deficiency This is type of anemia in which there is atrophy of gastric mucosa so failure of intrinsic factor production so Vit b12 not absorbed. Causes
  • 25. Pathogenesis Tissue perforation need DNA. DNA need VIT 12 and folic acid--- deficiency of both— DNA not formed— cell division stop. While cytoplasm progressive continuously — RNA increase in amount — erthroyid tend to destroy marrow —RBC—↓↓
  • 28. Folic acid Causes: Decrease diet inake Increase demand Mal absorption Investigation Low serum folic acid Macrocytic Blood cp Result Folic and supplement 5mg ready Maintence dose 5mg/wk.
  • 30. CHRONIC DISEASE Pathogenesis Failure of transport of storage iron from bone marrow to plasma developing Erythrocytes→ decrease HB and cause anemia.
  • 31. Investigation Increase iron in bone marrow. Increase serum iron level. Increase ferretin level.
  • 32.  Anemia due to acute blood loss ? Blood disorder A plastic Anemia. Hemolytic Anemia.
  • 33. A plastic Anemia ? C/F Anemia Infection Bleeding Investigations Blood Picture Bone marrow biopsy
  • 34. Hemolytic Anemia ? Mechanism Cell Membrane abnormality Abnormal HB Abnormality of nasal walls Inherited Hemolytic Anemia Hereditary spherocytosis Sickle cell Anemia Thalassaemia
  • 35. Hereditary spherotosis? Pathogenesis? C/F Anemia Jaundice Spleenomegely A plastic crises Gallstone Leg cancer
  • 36. Sickle cell disease There is presence of abnormal HBS which upon low oxygen tension become crystal giving shape Rbcs as sickle and not passes through capillaries and destruct
  • 37. Pathogenesis? C/F Anemia Tissue infraction
  • 38. Investigations Hb descreased sickles erythrocytes