Title: Gao Qingping
1Anemia
Gao Qingping Department of Hematology
Renmin Hospital of Wuhan University
2Renmin Hospital of Wuhan University
3 4 5 Anemia is defined as a reduction in one or
more of the major RBC measurements Hb
(hemoglobin concentration) Hct
(hematocrit) or RBC (red blood cells count)
6 anemia is a symptom of underlying
disorders and is characterized by a lower than
normal hemoglobin value or a low red cell count
or low hematocrit
7 Hemoglobin (Hb) ,hematocrit
(Hct) or red blood cells count (RBC) is below the
normal range for age and sex
8- ??????????????,??????????????????(?)
- ???????????????????,??????(?)???????????,?????????
? - ??????
9Normal Blood
10 11- Adults
- Hblt120g/L in males
- Hblt110g/L in females
- Hblt100g/L in maternals
12- Children
- Hblt145g/L in babies 9d
- Hblt100g/L in babies 5m
- Hblt110g/L in babies infants 5y
- Hblt120g/L in children 14y
13- 3?Factors of Affecting Anemia
14- (1)increased plasma volume
- increased plasma volume (relative anemia)
- seen in pregnancy, hypoproteinemia,
congestive heart failure, splenomegaly,
macroglobulinemia - increasing plasma volume make blood
dilution,the concentration of hemoglobin is
decreased
15- (2)decreased plasma volume
- (2)decreased plasma volume (Dehydration and The
blood loss )bring about hemoconcentration,the
concentration of hemoglobin is decreased
16- ? ?Classification of Anemia
17- Classified according to
- progress
- erythrocyte morphological features
- the hemoglobin concentration
- degree of erythropoietic proliferation
- Etiology and pathogenesis
18- (?)Classified According to Progress
19- acute
- Sever aplastic anemia, acute hemolysis, Acute
Hemorrhage - chronic
- Iron deficient anemia, Not-severe aplastic
anemia, chronic hemolysis, and chronic blood loss
20- (?)Classified According to
- Erythrocyte Morphology
21- In the morphological approach, anemia is
classified by the size of red blood cells this
is either done automatically or on microscopic
examination of a peripheral blood smear
22- The size is reflected in the mean
corpuscular volume (MCV). If the cells are
smaller than normal (under 80 fl), the anemia is
said to be microcytic if they are normal size
(80-100 fl), normocytic and if they are larger
than normal (over 100 fl), the anemia is
classified as macrocytic
23- This scheme quickly exposes some of the
most common causes of anemia for instance, a
microcytic anemia is often the result of iron
deficiency
24- In clinical workup, the MCV will be one
of the first pieces of information available so
even among clinicians who consider the "kinetic"
approach more useful philosophically, morphology
will remain an important element of
classification and diagnosis
25Types MCV (fl) MCH (pg) MCHC (g/L) example
Macrocytic gt100 gt32 310-350 Megaloblastic, HA,MDS,Liver
Normocytic 80-100 26-32 310-350 AA,PRCA,HA
Microcytic lt80 lt26 310-350 Anemia of chronic disease
hypochromic microcytic lt80 lt26 lt310 IDA,MDS-RS, thalassemia
MCV mean corpuscular volume MCH mean
corpuscular hemoglobin MCHC mean corpuscular
hemoglobin concentration
26- The Criterion of Classified According to
Erythrocyte Morphology(2007)
Criterion MCV (fl) MCH (pg) MCHC (g/L) example
Macrocytic gt100 gt34 320-360 Megaloblastic, HA,MDS,Liver
Normocytic 80-100 27-34 320-360 AA,PRCA,HA
Microcytic lt80 lt27 320-360 Anemia of chronic disease
hypochromic microcytic lt80 lt27 lt320 IDA,MDS-RS, thalassemia
27Normocytic
Normal RBC's. They have a zone of central
pallor about 1/3 the size of the RBC.). A few
small fuzzy blue platelets are seen. In the
center of the field are a band neutrophil on the
left and a segmented neutrophil on the right
28Hypochromic Microcytic
The RBCs here are smaller than normal
and have an increased zone of central
pallor. This is indicative of a hypochromic
(less hemoglobin in each RBC) microcytic
(smaller size of each RBC) anemia. There is also
increased anisocytosis??????? (variation in size)
and poikilocytosis ?????(variation in shape)
29Microcytic
the average size of erythrocytes is smaller than
normal
30Macrocytic
Note the hypersegmented neurotrophil and also
that the RBC are almost as large as the
lymphocyte. Finally, note that there are fewer
RBCs.
31- (?)Classified According to
- the Hemoglobin Concentration
32mild 90g/L moderate
60-89g/L sever
30-59g/L extremely severe lt30g/L
33- (?)Classified According to
- Degree of Erythropoietic Proliferation
34hyperplastic anemia other anemia except
AA
and MA hypoplastic anemia
AA megaloblastic anemia
MA
35- (?)Classified According to
- Etiology and Pathogenesis
36- The "kinetic" approach to anemia yields
what many argue is the most clinically relevant
classification of anemia
37- This classification depends on evaluation
of several hematological parameters, particularly
the blood reticulocyte (precursor of mature RBCs)
count
38- This then yields the classification of
defects by decreased RBC production versus
increased RBC destruction and/or loss
39- Clinical signs of loss or destruction
include abnormal peripheral blood smear with
signs of hemolysis elevated LDH suggesting cell
destruction or clinical signs of bleeding, such
as guiaic-positive stool, radiographic findings,
or frank bleeding
40- 1?Decreased Production of RBCs
41Erythropoiesis depended on
three kinds of factors 1.hematopoietic cells
HSC HPC BFU-E CFU-E RBC 2.hematopoietic
regulatory SSC Lym HGF(SCF IL
G(M)- CSF Epo Tpo TNF
IFN) 3.hematopoietic elements Protein, Lipid,
Vitamin, Mineral
42Natural Killer cell(NK)
Hematopoiesis
T-cells
Eosinophil
Basophil
Lymphoid progenitor
B-cells
Neutrophil
femur
M-Mf
Hematopoietic Stem Cell(HSC)
Myeloid progenitor
Multipotential Stem cell
Platelets
RBC
Hematopoietic Support cell
Osteoblast
Pre-osteoblast
adipocyte
Osteocyte
Stromal Stem Cell
43The life cycle of a RBC a) Kidneys respond to a
lower than normal oxygen concentration in the
blood by releasing erythropoietin(Epo) b) Epo
travels to the red bone marrow(RBM) and
stimulates an increase in the production of red
blood cells (RBCs) c) RBM manufactures RBCs from
stem cells that live inside the marrow d) RBCs
squeeze through blood vessel membranes to enter
the circulation e) The heart and lungs work to
supply continuous movement and oxygenation of
RBCs f) The old RBCs are destroyed primarily by
the spleen
f
a
e
b
d
c
The RBC lifetime is about 120 days
44 The pictures shown the cells of
BFU-E (day 3), CFU-E (day 7), immature
erythroblast (day 11) and mature erythroblast
(day 15) in culture in vitro. Cells were stained
by the Romanowski water-based adaptation of
Wright-Giemsa
45- Erythropoiesis is the development of
mature red blood cells (erythrocytes) - Like all blood cells, erythroid cells
begin as pluripotential stem cells
46- The earliest erythroid progenitor, the
BFU-E (burst forming unit-erythroid), is small
and without distinguishing histologic
characteristics - The stage after the BFU-E is the CFU-E
(colony forming unit-erythroid) which is larger
and is the stage right before hemoglobin
production begins
47- The first cell that is recognizable as
specifically leading down the red cell pathway is
the proerythroblast
48- As development progresses, the
nucleus becomes smaller and the cytoplasm becomes
more basophilic, due to the presence of
ribosomes. In this stage the cell is called a
basophilic erythroblast
49- The cell will continue to become smaller
throughout development - As the cell begins to produce
hemoglobin, the cytoplasm attracts both basic and
eosin stains, and is called a polychromatophilic
erythroblast
50- The cytoplasm eventually becomes more
eosinophilic, and the cell is called an
orthochromatic erythroblast
51- This orthochromatic erythroblast will
then extrude its nucleus and enter the
circulation as a reticulocyte - Reticulocytes are so named because
these cells contain reticular networks of
polyribosomes
52- They become mature red blood cells as
reticulocytes loose their polyribosomes
53 54- A. Multipotential stem cells failure
- a. Aplastic anemia
- b. Anemia of leukemia
- c. Anemia of myelodysplastic syndrome
55- B. Unipotential stem cells failure
- a. Pure red cell aplasia
- b. Anemia of renal failure
- c. Anemia of chronic disorders
- d. Anemia of endocrine disorders
56- (2)Abnormal Regulation of Hematopoiesis
- Damaged bone marrow stromal cells
- bone marrow necrosis and
myelofibrosis - Abnormal function of lymphocytes
- T(apoptosis)
- B(immune damage)
- Abnormal hematopoietic regulatory factor
- Epo? TNF? IFN?
- Increased hematopoietic cell apoptosis PNH
57- (3)Hematopoietic Elements Deficiency
- Folate and Vit B12 deficiency
- Iron deficiency and utilization obstacle
- IDA
- MDS-RAS RCMD-RAS
58- 2?Excessive Destruction of RBCs
59Hereditary Acquired
Membrane defects immunological(AIHA, blood group incompatibility)
Hemoglobin defects Angiopathic (Valvular Disease of Heart ,TTP,DIC, March hemoglobinuria)
Enzyne defects Biological (Venom, malaria)
physical and chemical factors (burns, The Change of plasma osmotic pressure , nitrite poisoning)
60 61- Hemorrhagic disorders
- (ITP, Hemophillia,
- Live disease)
- Non-hemorrhagic disorders
- (injury, tumor,
- bronchiectasis,
- cankerulcer)
62           Anemia Anemia Anemia Anemia Anemia Anemia Anemia Anemia Anemia Anemia Anemia Anemia Anemia Anemia Anemia Anemia      Â
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 No clinical findings consistent with hemolysis or blood loss pure disorder of production No clinical findings consistent with hemolysis or blood loss pure disorder of production No clinical findings consistent with hemolysis or blood loss pure disorder of production No clinical findings consistent with hemolysis or blood loss pure disorder of production No clinical findings consistent with hemolysis or blood loss pure disorder of production No clinical findings consistent with hemolysis or blood loss pure disorder of production No clinical findings consistent with hemolysis or blood loss pure disorder of production Clinical findings and abnormal MCV hemolysis or loss and chronic disorder of production  Clinical findings and abnormal MCV hemolysis or loss and chronic disorder of production  Clinical findings and abnormal MCV hemolysis or loss and chronic disorder of production  Clinical findings and abnormal MCV hemolysis or loss and chronic disorder of production  Clinical findings and abnormal MCV hemolysis or loss and chronic disorder of production  Clinical findings and abnormal MCV hemolysis or loss and chronic disorder of production  Clinical findings and abnormal MCV hemolysis or loss and chronic disorder of production  Clinical findings and abnormal MCV hemolysis or loss and chronic disorder of production  Clinical findings and abnormal MCV hemolysis or loss and chronic disorder of production  Clinical findings and abnormal MCV hemolysis or loss and chronic disorder of production  Clinical findings and abnormal MCV hemolysis or loss and chronic disorder of production  Clinical findings and abnormal MCV hemolysis or loss and chronic disorder of production  Clinical findings and abnormal MCV hemolysis or loss and chronic disorder of production  Clinical findings and abnormal MCV hemolysis or loss and chronic disorder of production  Clinical findings and abnormal MCV hemolysis or loss and chronic disorder of production  Clinical findings and normal MCV acute hemolysis or loss without adequate time for bone marrow production to compensate Clinical findings and normal MCV acute hemolysis or loss without adequate time for bone marrow production to compensate Clinical findings and normal MCV acute hemolysis or loss without adequate time for bone marrow production to compensate Clinical findings and normal MCV acute hemolysis or loss without adequate time for bone marrow production to compensate Clinical findings and normal MCV acute hemolysis or loss without adequate time for bone marrow production to compensate Clinical findings and normal MCV acute hemolysis or loss without adequate time for bone marrow production to compensate Clinical findings and normal MCV acute hemolysis or loss without adequate time for bone marrow production to compensate Clinical findings and normal MCV acute hemolysis or loss without adequate time for bone marrow production to compensate
 No clinical findings consistent with hemolysis or blood loss pure disorder of production No clinical findings consistent with hemolysis or blood loss pure disorder of production No clinical findings consistent with hemolysis or blood loss pure disorder of production No clinical findings consistent with hemolysis or blood loss pure disorder of production No clinical findings consistent with hemolysis or blood loss pure disorder of production No clinical findings consistent with hemolysis or blood loss pure disorder of production No clinical findings consistent with hemolysis or blood loss pure disorder of production Clinical findings and abnormal MCV hemolysis or loss and chronic disorder of production  Clinical findings and abnormal MCV hemolysis or loss and chronic disorder of production  Clinical findings and abnormal MCV hemolysis or loss and chronic disorder of production  Clinical findings and abnormal MCV hemolysis or loss and chronic disorder of production  Clinical findings and abnormal MCV hemolysis or loss and chronic disorder of production  Clinical findings and abnormal MCV hemolysis or loss and chronic disorder of production  Clinical findings and abnormal MCV hemolysis or loss and chronic disorder of production  Clinical findings and abnormal MCV hemolysis or loss and chronic disorder of production  Clinical findings and abnormal MCV hemolysis or loss and chronic disorder of production  Clinical findings and abnormal MCV hemolysis or loss and chronic disorder of production  Clinical findings and abnormal MCV hemolysis or loss and chronic disorder of production  Clinical findings and abnormal MCV hemolysis or loss and chronic disorder of production  Clinical findings and abnormal MCV hemolysis or loss and chronic disorder of production  Clinical findings and abnormal MCV hemolysis or loss and chronic disorder of production  Clinical findings and abnormal MCV hemolysis or loss and chronic disorder of production  Clinical findings and normal MCV acute hemolysis or loss without adequate time for bone marrow production to compensate Clinical findings and normal MCV acute hemolysis or loss without adequate time for bone marrow production to compensate Clinical findings and normal MCV acute hemolysis or loss without adequate time for bone marrow production to compensate Clinical findings and normal MCV acute hemolysis or loss without adequate time for bone marrow production to compensate Clinical findings and normal MCV acute hemolysis or loss without adequate time for bone marrow production to compensate Clinical findings and normal MCV acute hemolysis or loss without adequate time for bone marrow production to compensate Clinical findings and normal MCV acute hemolysis or loss without adequate time for bone marrow production to compensate Clinical findings and normal MCV acute hemolysis or loss without adequate time for bone marrow production to compensate
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Macrocytic anemia (MCVgt100)Â Macrocytic anemia (MCVgt100)Â Macrocytic anemia (MCVgt100)Â Macrocytic anemia (MCVgt100)Â Macrocytic anemia (MCVgt100)Â Macrocytic anemia (MCVgt100)Â Macrocytic anemia (MCVgt100)Â Normocytic anemia (80ltMCVlt100) Normocytic anemia (80ltMCVlt100) Normocytic anemia (80ltMCVlt100) Normocytic anemia (80ltMCVlt100) Normocytic anemia (80ltMCVlt100) Normocytic anemia (80ltMCVlt100) Normocytic anemia (80ltMCVlt100) Normocytic anemia (80ltMCVlt100) Normocytic anemia (80ltMCVlt100) Normocytic anemia (80ltMCVlt100) Normocytic anemia (80ltMCVlt100) Normocytic anemia (80ltMCVlt100) Normocytic anemia (80ltMCVlt100) Normocytic anemia (80ltMCVlt100) Normocytic anemia (80ltMCVlt100) Normocytic anemia (80ltMCVlt100) Normocytic anemia (80ltMCVlt100) Normocytic anemia (80ltMCVlt100) Microcytic Anemia (MCVlt80)Â Microcytic Anemia (MCVlt80)Â Microcytic Anemia (MCVlt80)Â Microcytic Anemia (MCVlt80)Â Microcytic Anemia (MCVlt80)Â Â
63 64- (?)Decreased Oxygen Consumption
The activation of genes coding for
glycolytic enzynes wiil save oxygen but at the
expense of using less-efficient metabolic pathways
65- (?) Decreased Oxygen Affinity
The earliest and least costly adjustment
of oxygen delivery This permits
increased oxygen extraction without jeopardizing
oxygen pressure The red cells generate
increased amounts of 2,3-bisphosphoglycerate
66- (?)Increased Tissue Perfusion
Performed selectively with blood shunted
from presumably nonvital donor areas to
oxygen-sensitive recipient organ
67- (?)Increased Cardiac Output
To decrease the fraction of oxygen that
needs to be extracted during each circulation and
thereby keep the oxygen pressure high To
bring out tachycardia, increased arterial and
capillary pulsation, and many hemodynamic murmurs
68- (?)Increased Pulmonary Function
Exertional dyspnea and orthopnea are
characteristic clinical manifestations of severe
anemia
69- (?)Increased Red Cell Production
The most appropriate response to anemia
is a compensatory increase in the rate of red
cell production In anemia this may reach
6 to 10 times normal and is powered by an
increased synthesis of renal erythropoietin
70- (?)Uncorrected Tissue Hypoxia
Some of this contributes the necessary
driving force to sustain cardiovascular and
erythropoietic adjustments But tissue hypoxia
per se (itself) cause disturbing and even
disabling symptoms
71 72- Clinical manifestation depends on
- Etiology of anemia
- The degree of delining of oxygen carrying
capacity in blood which caused by anemia - The degree of the decrease of blood volume in
patients with anemia - The rate of resulting in anemia
- The capacity of compensation and resistance of
hematology, circulation and respiratory system to
anemia
73- Presentation
- dizzy ,headache, vertigo, syncope,
tinnitus, sleepiness, insomnia, dreaminess,
hypomnesia, inattention, dysphoria(???????????????
??????????? ????????????) - Causes
- brain anoxia
- hypovolemia or blood pressure drop
- hyperbilirubinemia or increasing of free
hemoglobin - complication for patients with anemia
neuritis
74- Presentation
- pallor, roughness, jaundice, ulcer
- Causes
- blood redistribution
- Folacin, VitB12,and iron deficiency
- Autoimmunity
- hemolysis
75- Presentation
- dyspnoea and orthopnea
- ???????
- Causes
- hypoxia
76- Presentation
- palpitation and tachycardia
- ???????
- Causes
- anemia
- hemochromatosis
77- Presentation
- anorexia, nausea, vomiring, abdominal
distension , cholelithiasis, - sense of eyewinker in swallowing, glossitis,
mirror-like tongue - ?????????????????? ????????????
- Causes
- reduction of digestive fluid
- hemolysis
- iron deficiency
- Folacin, or VitB12 deficiency
78- Presentation
- oliguria or anuria?????
- bilirubinuria, high uro-bilinogen,
hematuria and proteinuria - Causes
- hemolysis
- TTP and HUS
- AA
- MM
- hypovolemia that hemorrhage cauces
79- Presentation
- endocrine dyscrasia???????
- Causes
- Sheehanssyndrome
- hypothyroidism
- hypogonadism
- hypoadrenalism
- decrudescence of pancreatic function
80- Presentation
- weakened male characteristics
- increasing or decreased amount of
menstruation?????????????? - hypaphrodisia????
- don juanism??????
- masculinization?????
- Causes
- anemia
- treatment of androgen
81- Presentation
- immunologic decline
- Causes
- effect of anemia on immune function
- immune resulting in anemia
- inhibition of drug on immune function
82- Presentation
- Change of blood cell number
- Morphologic Changes of Blood Cells
- Changes of blood cells biochemistry
- Abnormal plasma component (M protain,
Free hemoglobin, hyperbilirubinemia , electrolyte
disturbance, Abnormal Coagulation and
Fibrinolysis System ) - Causes
- Etiopathogenisis of anemia
- Complication(hypersplenia?DIC?drugs)
83 84- To understand the degree, type and
etiology of anemia - 1 ask disease history in detail
- 2 careful medical examination
- 3 correlated laboratory tests
85 86- 1 History of Present Illness
- occurrence time of fatigue
- Cause and Inducement
- rate of occurrence
- accompany symptoms
- diagnosis and treatment
- time and therapeutic effects
- outcome of anemia
87- drug history
- occupational exposure
- exposed to special chemical substance
- hemorrhage history
- chronic disease history
88- History of anemia in grandparents, parents and
children
89- dietary constitution
- diet habit
- food preference
- With ot without digestive tract disease
90- 5 Menstrual and Reproductive History
- increasing amount of menstruation
- severe postpartum hemorrhage
91- Mucocutaneous color
- Scleral color????
- lymph node
- sternal tenderness????
- hepatosplenomegaly
- Other system
92 93 94- Generally, clinicians request complete
blood counts in the first batch of blood tests in
the diagnosis of an anemia
95- Apart from reporting the number of red
blood cells and the hemoglobin level, the
automatic counters also measure the size of the
red blood cells by flow cytometry, which is an
important tool in distinguishing between the
causes of anemia
96 97- Examination of a stained blood smear
using a microscope can also be helpful, and is
sometimes a necessity in regions of the world
where automated analysis is less accessible
98 99- Reticulocyte counts, and the "kinetic"
approach to anemia, have become more common than
in the past in the large medical centers, in part
because some automatic counters now have the
capacity to include reticulocyte counts
100- A reticulocyte count is a quantitative
measure of the bone marrow's production of new
red blood cells. The reticulocyte production
index is a calculation of the ratio between the
level of anemia and the extent to which the
reticulocyte count has risen in response
101- Reticulocyte Production Index is
calculated as follows - Ret IndexRet Count(hematocrit/normal
hematocrit) - A value of 45 is usually used as a normal
hematocrit
102- If the degree of anemia is significant,
even a "normal" reticulocyte count actually may
reflect an inadequate response
103 104- In manual examination, activity of the
bone marrow can also be gauged qualitatively by
subtle changes in the numbers and the morphology
of young RBCs by examination under a microscope
105- Newly formed RBCs are usually slightly
larger than older RBCs and show polychromasia.
Even where the source of blood loss is obvious,
evaluation of erythropoiesis can help assess
whether the bone marrow will be able to
compensate for the loss, and at what rate
106 107RBC production RBC destruction RBC Loss
Ferritin osmotic fragility test Stool-ROB
Serum iron methemoglobin reduction test Urine-R
Transferrin Coombs test
Folate Free hemoglobin
Vit B12 haptoglobin
Hb electrophoresis autohemolysis test
Liver function CD55,CD59
Renal function Urine-R
Chest X rays Urine-Rous test
Abdomenal CT Hb electrophoresis
Bone marrow Bone marrow
Hemosiderin X rays, CT
108 109- Etiological Treatment
- Therapy Against Pathogenesis
- Symptomatic Treatment
110 111- (?) Therapy Against Pathogenesis
- Supply hemopoietic elements
- Immunosuppressive therapy
- Application of hemopoietic growth factor
- Splenectomy
- Chemoradiotherapy
- Hemopoietic stem cell transplantation
112- 1? Iron deficiency anemia
113Iron deficiency anemia
- This form of anemia is treated with iron
supplements, which you may need to take for
several months or longer. If the underlying cause
of iron deficiency is loss of blood other than
from menstruation the source of the bleeding
must be located and stopped. This may involve
surgery
114- 2? Vitamin deficiency anemias
115Vitamin deficiency anemias
- Pernicious anemia is treated with
injections often lifetime injections of
vitamin B-12 - Folic acid deficiency anemia is treated
with folic acid supplements
116- 3? Anemia of chronic disease
117Anemia of chronic disease
- There's no specific treatment for this
type of anemia. Doctors focus on treating the
underlying disease. Iron supplements and vitamins
generally don't help this type of anemia
118Anemia of chronic disease
- If symptoms become severe, a blood
transfusion or injections of synthetic
erythropoietin, a hormone normally produced by
the kidneys, may help stimulate red blood cell
production and ease fatigue
119 120Aplastic anemia
- Treatment for this serious anemia may include
blood transfusions to boost(??) levels of red
blood cells. You may need a bone marrow
transplant if your bone marrow is diseased and
can't make healthy blood cells
121Aplastic anemia
- You may need immune-suppressing medications to
lessen your immune system's response and give the
transplanted bone marrow a chance to start
functioning again
122- 5? Anemias associated with bone marrow disease
123Anemias associated with bone marrow disease
- Treatment of these various diseases can
range from simple medication to chemotherapy to
bone marrow transplantation. Treatment of these
types of anemia usually involves a consultation
from a blood specialist (hematologist)
124 125Hemolytic anemias
- Managing hemolytic anemias includes
avoiding suspect medications, treating related
infections and taking drugs that suppress your
immune system, which may be attacking your red
blood cells
126Hemolytic anemias
- Short courses of treatment with steroids
or gamma globulin can help suppress your immune
system's attack on your red blood cells. If the
condition has caused an enlarged spleen, you may
need to have your spleen removed
127Hemolytic anemias
- The spleen a small organ below your rib
cage on the left side filters out and stores
defective red blood cells. Certain hemolytic
anemias can cause the spleen to become enlarged
with damaged red blood cells
128- Transfusion
- Hemostasis
- Liver-protection
- Anti-infective
- Others
129Thanks