Bems Rabia presentation
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INTRODUCTION
Name : Rabia Manzoor Roll No: 04Topic: ANEMIA
Department Of Eastern Medicine & SurgeryFaculty of Medical & Health SciencesUniversity of Poonch Rawalakot Aj&K
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What is ANEMIA?
Anemia is present when there is decreased Level of Hb in blood below the reference levelFor age ,sex and individuals
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Classification of ANEMIA Types of classification.
1. According to cause2. According to morpholology Cause:1. Blood loss2. Increase of red cell destruction3. Decrease of red cell production
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Morphological classification
According to shape and size
1. Hypo chromic microcytic with low MCV2. Norm chromic normacytie with normal MCV3. Macrocytic with high MCV
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S/S of Anemia
1. Pallor 2. Tachycardia 3. Breathlessness4. Head ache5. Fatigue6. faintness
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Microcytic anemiaRBCS become smallMCV<80
Causes of microcytic anemia•Iron low to iron deficiency Anemia•Iron normal to sedroblastic and Thalasemia
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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.
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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
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Etiology of iron deficiency
1. Dietary deficiency2. .Increase in iron demand 3. Malobsorption of iron4. Acute and chronic blood loss
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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.
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•S/S OF IRON DEFICIENCY ANEMIA•Pallor•Lethargy•Fatigue•Kolinchyia•Dysnea•Numbness•Joint pain•Vomiting•Body ache
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Investigation
Blood pictureBone marrow study
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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.
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Diagnosis: Microcytic cellsBone marrow show erythroblast with ring of iron granules around. The nucleus ring sidreoblasts.
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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.
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Types
1.Alpha 2.Beta
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Alpha
It occurs due to reduction or absence of alpha chain synthesis .There are four alpha gene1.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.
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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
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B Thalasemia intermediate
Electrophoresis which shows reduced HBA while HBA2 and F elevated (asymptomatic + moderate anemia)
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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,.
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Macrocytic Anemia]
1.Megloblastic anemia√.vita B12 deficiency√folic acid deficiency
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Megloblastic anemia
In this type of anemia RBC became enlarged and odd shape.
Causes
Vit B12 deficiencyFolic acid deficiency
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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
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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—↓↓
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s/s
•Pallor•Dysnea•Vibration sense loss•Neurological disorder•Tachycardia
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Investigation
Blood c/pBone marrowLow serum Vit. B12
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Folic acid
Causes: Decrease diet inakeIncrease demandMal absorption
InvestigationLow serum folic acidMacrocytic Blood c\p
ResultFolic and supplement 5mg readyMaintence dose 5mg/wk.
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NORMOCYTIC ANEMIA
CAUSES
•Chronic disease •Acute blood loss•Blood disorder
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CHRONIC DISEASE
Pathogenesis
Failure of transport of storage ironfrom bone marrow to plasma developing Erythrocytes→ decrease HB and cause anemia.
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Investigation
Increase iron in bone marrow.Increase serum iron level. Increase ferretin level.
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Anemia due to acute blood loss ?
Blood disorder
A plastic Anemia.Hemolytic Anemia.
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A plastic Anemia ?
C/FAnemia Infection Bleeding
InvestigationsBlood PictureBone marrow biopsy
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Hemolytic Anemia ?
Mechanism
Cell Membrane abnormalityAbnormal HBAbnormality of nasal walls
Inherited Hemolytic AnemiaHereditary spherocytosisSickle cell AnemiaThalassaemia
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Hereditary spherotosis?
Pathogenesis?
C/FAnemiaJaundiceSpleenomegelyA plastic crisesGallstoneLeg cancer
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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
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Pathogenesis?
C/F
AnemiaTissue infraction
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Investigations
Hb descreasedsickles erythrocytes