rabia presentation

38

Upload: aamir-sharif

Post on 31-May-2015

596 views

Category:

Health & Medicine


0 download

TRANSCRIPT

Page 1: Rabia presentation
Page 2: Rabia presentation

INTRODUCTION

Name : Rabia Manzoor Roll No: 04Topic: ANEMIA

Department Of Eastern Medicine & SurgeryFaculty of Medical & Health SciencesUniversity of Poonch Rawalakot Aj&K

Page 3: Rabia presentation

What is ANEMIA?

Anemia is present when there is decreased Level of Hb in blood below the reference levelFor age ,sex and individuals

Page 4: Rabia presentation

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

Page 5: Rabia presentation

Morphological classification

According to shape and size

1. Hypo chromic microcytic with low MCV2. Norm chromic normacytie with normal MCV3. Macrocytic with high MCV

Page 6: Rabia presentation

S/S of Anemia

1. Pallor 2. Tachycardia 3. Breathlessness4. Head ache5. Fatigue6. faintness

Page 7: Rabia presentation

Microcytic anemiaRBCS become smallMCV<80

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

Page 8: Rabia presentation

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.

Page 9: Rabia presentation

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

Page 10: Rabia presentation

Etiology of iron deficiency

1. Dietary deficiency2. .Increase in iron demand 3. Malobsorption of iron4. Acute and chronic blood loss

Page 11: Rabia presentation

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.

Page 12: Rabia presentation

•S/S OF IRON DEFICIENCY ANEMIA•Pallor•Lethargy•Fatigue•Kolinchyia•Dysnea•Numbness•Joint pain•Vomiting•Body ache

Page 13: Rabia presentation

Investigation

Blood pictureBone marrow study

Page 14: Rabia presentation

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.

Page 15: Rabia presentation

Diagnosis: Microcytic cellsBone marrow show erythroblast with ring of iron granules around. The nucleus ring sidreoblasts.

Page 16: Rabia presentation

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.

Page 17: Rabia presentation

Types

1.Alpha 2.Beta

Page 18: Rabia presentation

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.

Page 19: Rabia presentation

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

Page 20: Rabia presentation

B Thalasemia intermediate

Electrophoresis which shows reduced HBA while HBA2 and F elevated (asymptomatic + moderate anemia)

Page 21: Rabia presentation

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,.

Page 22: Rabia presentation

Macrocytic Anemia]

1.Megloblastic anemia√.vita B12 deficiency√folic acid deficiency

Page 23: Rabia presentation

Megloblastic anemia

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

Causes

Vit B12 deficiencyFolic acid deficiency

Page 24: Rabia presentation

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

Page 25: Rabia presentation

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—↓↓

Page 26: Rabia presentation

s/s

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

Page 27: Rabia presentation

Investigation

Blood c/pBone marrowLow serum Vit. B12

Page 28: Rabia presentation

Folic acid

Causes: Decrease diet inakeIncrease demandMal absorption

InvestigationLow serum folic acidMacrocytic Blood c\p

ResultFolic and supplement 5mg readyMaintence dose 5mg/wk.

Page 29: Rabia presentation

NORMOCYTIC ANEMIA

CAUSES

•Chronic disease •Acute blood loss•Blood disorder

Page 30: Rabia presentation

CHRONIC DISEASE

Pathogenesis

Failure of transport of storage ironfrom bone marrow to plasma developing Erythrocytes→ decrease HB and cause anemia.

Page 31: Rabia presentation

Investigation

Increase iron in bone marrow.Increase serum iron level. Increase ferretin level.

Page 32: Rabia presentation

Anemia due to acute blood loss ?

Blood disorder

A plastic Anemia.Hemolytic Anemia.

Page 33: Rabia presentation

A plastic Anemia ?

C/FAnemia Infection Bleeding

InvestigationsBlood PictureBone marrow biopsy

Page 34: Rabia presentation

Hemolytic Anemia ?

Mechanism

Cell Membrane abnormalityAbnormal HBAbnormality of nasal walls

Inherited Hemolytic AnemiaHereditary spherocytosisSickle cell AnemiaThalassaemia

Page 35: Rabia presentation

Hereditary spherotosis?

Pathogenesis?

C/FAnemiaJaundiceSpleenomegelyA plastic crisesGallstoneLeg cancer

Page 36: Rabia presentation

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

Page 37: Rabia presentation

Pathogenesis?

C/F

AnemiaTissue infraction

Page 38: Rabia presentation

Investigations

Hb descreasedsickles erythrocytes