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lecture Date 18/10/2011

Dr. Mahmmoud Ayish

(( ))

The lecture included what dr said and slides.
Doctor stressed out some notes about anaemia:
- In practice of medicine; the importance things we should concentrate on what is common of
- You Should take a good history from the patient to get a right diagnosis.
- Before treating anemia looks for the causes
- Dr will give us a blood film in exam to identify the diagnosis.

What is Anemia?
It is a reduction below normal in the mass of red blood cells in the circulation.
The impaired oxygen delivery ;
o Consequences secondary to tissue hypoxia
o Compensatory mechanisms to correct anoxia
It is reduction in; total RBC count, Hemoglobin concentration (HGB) ,and/or hematocrit
Men: HGB < 13.5 or HCT < 41%
Women: HGB < 12.0 or HCT < 36%
you should consider; the AGE and SEX (female HGB is less than male HGB)
example; 30 years old female her HGB is 12 we can accepted within normal range. BUT for 30
years old Male this is Not accepted as normal.
Anemia is NOT a diagnosis per say, always you should look for a CAUSES (e.g cancer, GI
bleeding, heavy menstruation .). So remember anaemia is a symptoms NOT a disease!
The most common cause of anaemia world wide is iron deficiency anaemia female and child
bearing age (Menses and pregnancy)
Remember that Vitamin B12 associated with neurological damage lead to neuropathy. So
Vitamin B12 deficiency anemia patient is different and we should care with them by giving Vit
B12 supplements to prevent neuropathy.
Microscopically : usually hypochromic microcytic anaemia.

Anemia and Volume Status:

Therefore dependent upon plasma volume
Acute bleeds not reflected for 24-36 hrs
Due to volume deficit being slowly repaired via movement of fluid from extravascular
space to intravascular
Anemic patients who are dehydrated will not appear anemic
Pregnant women expand RBCs 25% but plasma volume increases 50%, producing physiologic

Anemia: History
There are important questions should be kept in consideration
for patient with anaemia:
Age, Male or Female
Is the patient bleeding?
((most likely example ; 70 years old male was given NSAIDS;
aspirin after long time when check his CBC the HGB is 5.
Answer; most likely diagnosis is chronic GI bleeding.))

In physical examination; it is
important to do vital signs for
patient with bleeding on lying
and standing positions.
for example on lying BP= 100/80
but on standing will drop !! pulse
is tachycardia. this significant for

Past medical history of anemia? Family history ? ((genetic disease like thalassemia, hemolytic
anaemia, SCA .))
Some patient do a surgery like gastrointestinal surgery; ( ) actually they will
have iron defeciency or aplastic anaemia.
Alcohol, nutritional questions
Liver, renal diseases
Menstrual history if applicable
Hemolytic anaemia usually come
Environmental/work toxins (i.e lead)
with jaundice or changing of
Is he have Jaundice ((i.e in hemolytic anaemia))
urine color (tea color )

General clinical features/symptoms of Anemia;

Causes of sudden drop of Hb:
The Symotoms of anemia is depend on the severity of anemia
- Bleeding.
((patient with sudden drop of HGB with SOB, pallor.. important
- Hemolysis.
to look for bleeding !!))
- Aplastic crises:
Decreased O2 delivery
Hypovolemia if acute loss
Exertional dyspnea, wakness, malaise, easy fatigability , palpitations, bounding pulses
Headache, faintness, dimness of vision
In Severe cases or chronic anemia come with: heart failure, angina, MI
Pica craving for clay or paper products
Pagophagia craving for ice

Signs and pathologic features of Anemia;

Tachycardia, tachypnea, orthostasis

Thin and atropic skin
Koilonychia or Spoon nails
Splenomegaly, lymphadenopathy
BM hyperplasia (except aplastic anemia)
Extramedullary hematopoiesis in severe cases.
Petechiae, ecchymoses
Atrophy of tongue papillae

In hematology P/E ;
Clinical finding of anemia is
You need to practice how
to examine the spleen.

What is the first test help us to know if the patient have anaemia or not?
A complete blood count (CBC) test which including; number of RBCs, WBCs , hemoglobin ,
hematocrit, MCV, MCH, MCHC, and platelet count

How anaemias are classified?

By using CBC indices; which are part of CBC test. It used to help diagnose the CAUSE of
The CBC (or RBC) indices calculated by:
1- MCV = hematocrite RBC count
(NR= 80 100 fl)
(low microcytic, normal normocytic, high macrocytic )
2- MCH = hemoglobin RBC count
(NR= 27 31 pg)
( low hypochromic, normal normochromic, high hyperchromic)
3- MCHC = hemoglobin hematorcite (NR= 32 36 gm/dL)
4- RDW= the variation in cellular volume (cells differ in shape and size) of the RBC population
(NR = 11-15 %)
In iron deficiency anemia theres high variation in RDW but in thalasemia RDW is normal.

PCV = (Hematocrit or packed cell volume); fraction of whole blood volume that consists of red blood cells.
MCV = (Mean corpuscular volume); the average volume of the red.
MCH =( Mean corpuscular hemoglobin) ; the average amount of hemoglobin per red blood cell.
MCHC = (Mean corpuscular hemoglobin concentration); the average concentration of hemoglobin in the cells.
RDW = (Red blood cell distribution width)

To find out what disorder is causing the anaemia you need to know what type of anaemia it is!!
how anaemias are classified using RBC indices??
1. MCV, MCH and MCHC are all normal normocytic, normochromic anaemia (RBC's
size and hemoglobin content are within normal limits), most often caused by acute blood loss
2. MCV, MCH, and MCHC are all decreased - microcytic, hypochromic anaemia (RBC's are smaller
and their hemoglobin content is much less) - most often caused by iron deficiency (most common),
but sometimes by impaired production of hemoglobin; i.e thalassemia, sideroplastic anaemia,
Anemia of chronic diseases chronic renal failure, and multiple myeloma.
3. Increased MCV with variable MCH and MCHC - macrocytic anaemia (RBC's are larger ) - most
often caused by megaloblastic (vitamin B12 deficiency and folic acid deficiency) and nonmegaloblastic anaemia (myleodysplastic anaemia, liver diseases, and thyroid diseases)
In clinical practice; if you find patients have anaemia you should think:
1st common cause is Iron defeiciency anaemia
and the 2nd cause is thalassemia and chronic illness

The Classification of anaemia according to :

Morphologic: ((the easy way to classify of anaemia))
1- Decrease production
2- Increase destruction


Underlying Mechanism:
Impaired or decreased RBC production (proliferation/differentiation/ maturation)
Increased RBC destruction hemolytic
Blood loss
1- Decreased RBC production:
Lack of iron, B12, folate
Marrow is dysfunctional from myelodysplasia, tumor infiltration, aplastic anemia, etc.
Bone marrow is suppressed by chemotherapy or radiation
Low levels of erythropoeitin, thyroid hormone, or androgens
2- Increased RBC destruction:
RBCs live about 100 days
Acquired: autoimmune hemolytic anemia, TTP-HUS, DIC, malaria
Inherited: spherocytosis, sickle cell, thalassemia
3- RBC Loss:
Obvious vs occult
Iatrogenic: venesection e.g. daily CBC, surgical, hemodialysis

Approach to Anemia:

The BEST investigation of

anemia after CBC is BLOOD


FILM which is the most
Convenient to separate into three classes based on the size
important tool for diagnosis of
of the RBC
CBC; MCV (micro, macro) and RDW
Anemia Workup:
Reticulocyte count
Serum iron; low in IDA and high in chronic illness.
TIBC (Total Iron Binding Capacity)
Serum Ferritin (reflection for iron store); it is important than serum iron low in IDA,
and high in iron overload.

Serum Folate; we have serum folate and RBC folete (which is more accurate than serum
Serum B12; both folate and B12 for megaloblastic anemia.
LDH (Lactate dehydrogenase); high LDH in hemolytic anemia, MI, leukemia,
lymphoma, and any affect on muscles increase LDH.
Bilirubin; Total Bilirubin; direct and indirect.
high indirect bilirubin hemolytic anemia and Gilbert's syndrome
high direct bilirubin in obstructive diseases
Haptoglobin ; circulating protein which binds and clears free Hb low in hemolytic
Urine for hemosiderin; not important
Coombs Test
o Direct: (also called direct antiglobulin test) ; antibodies against RBCs destruction
RBCs (hemolysis) .
positive in patient with autoimmune hemolytic anaemia
o Indirect: in serum (antibodies against outside RBCs), this test done for patient who
repeated blood transfusion.
Hemoglobin electrophoresis; test for thalasemia & sickle cell anemia
Acid hemolysis; previously done for Paroxysmal nocturnal hemoglobinuria (PNH)
because blood acidity increases during sleep due to CO2 retention.
Osmotic fragility; increased in for hereditary spherocytosis.
Rx iron/folate/B12
Erythropoietin analogs
Type & Cross
Transfuse 2-4 units
GI Consult
Hematology Consult
Bone Marrow

Reticulocyte Count :

Nucleated RBCs form in marrow where they mature for 3 days and then spend 1 day in
circulation (before maturing to RBC)
Given avg life span of RBC of 100 days, 1% of RBCs are destroyed each day
Retics form 1% of circulating RBCs qd
Nl RBC count is 5million/uL so marrow makes 50,000 reticulocytes/uL blood qd
With epo, can increase to 250,000 retics/uL blood qd (given nl marrow and replete iron, folate,
Value = Retic % x RBC Count E.g 0.01 x 5x1012/l = 5x 1010/l
Normal up to 1.2x1011/l (120,000/l)
More accurate way to assess bodys response to anemia (BM is functioning or not)
If Retics count is high hemolytic anemia or patient taking iron therapy.
If Retics low hyporeproductive like aplastic anaemia.
Dr said; you have to know what is the test done for hemolytic anemia? Is reticulocyte count.
So if you found in the exam hemolytic anemia = reticulocytosis



Causes of IDA:
1. Common in females (pregnancy, menses)
2. The most common cause is bleeding; Chronic blood loss: GI and GU bleeding: gastric CA, peptic
ulcers colon CA, hemorrhoid, polyps, hematuria, epistaxis and intravascular hemolysis (common in
G6PD or prosthetic valve).
usually do endoscopy to know the cause.
3. nutritional causes; Poor diet, surgical like partial gastric or
duodenal or proximal bowel dissection.
4. Increase requirements: infant, children, pregnancy.

Celiac disease Tests:

Anti-Tissue transglutaminase
antibodies (tTGA)
anti-endomysium antibodies
Anti-gliadin antibodies
biopsy; villous atrophy is present

5. malabsorption : gastrectomy, celiac disease: very common

(usually cause IDA associated sometimes with folate & B12 dificiency).
How to diagnose IDA:
- Take a history and it is important to know the UNDERLINE CAUSES of IDA.
- CBC: Low Hb, MCV, MCH, MCHC and high RDW.
- Blood film: hypochromic microcytic, Elliptocytes (or
pencil cells), target cells. Anisocytosis and
- Low reticulocytes.
- Low serum iron, low ferritin, high TIBC, < 15%
saturation (( saturation =(serum iron/TIBC) *100% ))

The definitive test for IDA is serum

Low serum ferritin is diagnostic of iron
Although ferritin is an acute phase
reactant, it will still be low in iron
Low serum Fe is not in itself diagnostic
neither is marrow staining.

- Thrombocytosis
-BM (not done in IDA) : erythroid hyperplasia and absence of storage iron.

angular cheilitis: fissures at the

corners of mouth in advanced IDA

Dr ;
I knew a 60 years old patient his HGB is = 7 and ferritin is very low , he was complaining of chronic
constipation, when I ask him to do a colonoscopy I found that he has colon cancer!! So you have to
look for the cause not only treat the IDA !!
The normal amount of iron needed per day :
o in pregnant about 3.5 mg
o menstruating females about 2mg
o least for males and children which is about 1mg per day.
10-15% absorbed from the duodenum.
Total stores : 2-4g
Intake=10-15mg per day!
Found into two forms:
1. Functional (80%): Hb,myoglobin,transferrin and enzymes.
2. Storage(20%): ferritin and hemosiderin.
*transferrin is 33% saturated with iron.
*transferrin is synthesized in the liver.

1. Treat the underlying cause.
2. Then administer iron orally.
3. IV iron for patient with malabsorption or can't tolerate oral iron.
4. Restore iron stores (treat for several months); continue treatment therapy by iron for 3 months

after patient Hb returns back to normal.

Differential Diagnosis of Hypo chromic Microcytic Anemia:

Iron Deficiency Anemia (if ferritin is low ).

Anemia of chronic disease (esp. RA and lymphoma)
Sideroblastic anemia (myelodysplastic syndromes)


Decreased production of either -globin or -globin chains

Abnormal hemoglobin electrophoresis
Polychromasia, basophilic stippling, target cells
Normal/increased RBC mass

Heme (iron) + globin chain = Hemoglobin


2 alpha and 2 beta chains 96-98 % adults

2 alpha and 2 delta chains < 3.5 %
2 alpha and 2 gamma chains 1%
(predominant at age one or less)
Heterogenous group of mandelian disorders, all characterized by a lack of or decreased synthesis of
either the alpha or beta globin chain of HbA1
Types: Alpha or beta thalassemia
Decreased HbA1 and relative excess of other chain
Ineffective erythropoiesis and/or hemolysis

Beta thalassemia
Total lack of or reduction in the synthesis of structurally normal
Beta globin chains with unimpaired synthesis of
alpha chains
Defect: point mutation
+ or 0 Homozygous or heterozygous
Beta thalassemia major
Beta thalassemia intermedia
Beta thalassemia minor

Ineffective erythropoiesis and hemolysis

Low MCV, microcytic hypochromic, normal RDW, basophilic stippling, target cells
Increased reticulocytes
Serum iron and ferritin normal or increased
TIBC normal or decreased
basophilic stippling
BM iron storage is normal or increased
Saturation normal or increased
Hemoglobin electrophoresis
Treatment; blood transfusion, iron chelators,
stem cell transplant

How to diagnose Beta thalassemia minor:

Mild anemia
Low MCV, normal RDW, erythrocytosis
Basophilic stippling
Electrophoresis: Normal HbA1, slight increase in HbA2, HbF
may or not be increased
Beta thalassemia minor is difficult to diagnose in the presence
of iron deficiency anemia.

Ferritin is a reflection of iron store:

Low ferritin: IDA.
High ferritin: Thalassemia, iron overload, and ACD

blood Transfusion in case of :

Coronary artery disease (CAD) : Hgb < 10
All pts: if Hgb <7.0

Complication of thalassemia major:

Systemic iron overload and secondary Hemochromatosis: (HIGH FERRITIN): which will cause:
1. Grey or brown color.
2. Deposition of iron in pituitary gland growth failure (e.g: hypogonadism).
3. Deposition of iron in pancreas diabetes mellitus.
4. deposition of iron in liver cirrhosis
5. skeletal deformities because of marrow expansion due to:
Anemia tissue anoxia erythropoietin release erythroid hyperplasia & expansion.

Alpha thalassemia:

Two genes from each parent

Deletion of genes most common
Reduced synthesis or absent synthesis of alpha globin chains
Excess beta Hb H
Excess gamma- Hb Bart

How to alpha thalassemia diagnose:

Exclude other causes of microcytic anemia.

Low MCV, erythrocytosis, normal RDW.
Hb elecrophoresis is normal in silent carriers and trait.
HbH and Barts(fast).
HbH inclusions: precipitate upon oxidation because it is unstable .
Treatment: similar to thalassemia.

Normocytic Anemia:
Large and complicated group of disorders!
Hemolytic Anemias
Anemia of chronic disease
Bone marrow disorder
Nutritional (Fe deficiency)
Anemia of Renal Insufficiency


most common among hospitalized patients.
Thought to be a cytokine mediated process which inhibits red blood cell production or interferes
with action of erythropoietin.
Seen with; chronic infection, chronic renal disease ,malignancy, immune disorders,
diabetes, rheumatologic diseases.
Insufficient erythropoiesis, block in release of iron from RES
(reticuloendothelial system) to erythroid precursors and decreased
RBC survival.


How to diagnosis ACD:

Normochromic normocytic or hypochromic microcytic.

Low serum iron.
Low saturation.
Normal or increased ferritin.
Normal or increased storage iron in BM.

Treatment : treat the underlying cause.

Serum iron






BM stores




TIBC usually increased when saturation decreased but in ACD it is decreased coz ferroportin is

Macrocytic Anemia (MCV>100)

Drug Induced (hydroxyurea, AZT, MTX, chemotherapy)
B12 / folate deficiency
Myelodysplastic syndrome
Liver disease, alcohol abuse
Reticulocytes in the setting of hemolytic anemia
Spurious (i.e. cold agglutinins, etc)

Primary bone marrow disorder, often found in elderly
Macrocytosis, anemia
Pseudo-Pelger-Huet abnormality the bilobed nucleus


Defective DNA synthesis and normal RNA\protein synthesis.
Rapidly proliferating cells are affected.
Ineffective hematopoiesis, RPI <2.0 (Reticulocyte
body store of folate is 3 months
production index)
while vit B12 is 3 years
Etiology: vitamin B12 and\or folate deficiencies and
Clinical signs and symptoms; yellow discoloration of the skin ,dyspepsia, glossitis,
neurological symptoms (only in vit B12 def).
Retics count is low
peripheral blood film : pancytopenia, macroovalocytes (megaloblasts),
hypersegmented neutrophils (by enlargement of myeloid precursors), howell-jolly

Hypersegmentation neutrophil and macroovalocytes RBCs

BM : erythroid hyperplasia with megaloplastic changes, giant

bands(giant metamyelocytes as in the following picture) ,this
is the difference from aplastic anemia because in both we have


exclusive source is dietary animal proteins
70% absorbed and 30% synthesized by normal flora.
We need 2-3 g/day.
Stores=5000g mostly in the liver, kidney and heart,
enough for several years, about 3 years.
Absorbtion: binds to IF released from parietal cells,in bound
state IF binds to receptors on brush border of terminal ileum,
vitB12 absorbed by pinocytosis and transported to blood and
then to target organs by transcobalamine2.

The most common

causes of vitamin B12
deficiency worldwide is
So you should ask for
nutritional history to
know patient is vegetarian
or not.


Etiology: impaired absorbtion (like in crohns disease which affects the terminal ileum,
gastritis), increased requirements and inadequate diet like in vegetarians.

*THF=tetrahydropholate(active form),dUMP and dTMP=uridine and thymidine

monophosphate,conversion of dUMP to dTMP is the rate limiting step in DNA

Diagnosis of B12 defeiciency anaemia:

Normal or high MCV, high RDW, RPI<2.
Triad: macroovalocytes (megaloblasts), Holly- Jolly bodies and hypersegmented
neutrophils (by enlargement of myeloid precursors),
Ineffective erythropoiesis: increased indirect bilirubin ,increased LDH so resembles
HI but low retic count.
Low serum B12 levels.
Increased urinary excretion of methylmalonic acid.


Lack of intrinsic factor(IF).

Most important and common cause of vitB12 def.
90% have nonspecific (antiparietal Abs).
50% have specific (anti IF Abs).
So it can be associated with Addisons disease which is primary adrenal insufficiency
characterized by hyperpimentation, hypotention and hashimotos thyroiditis .


Lab findings:

features of vitB12 def.

achlorhydria; low acidity because parietal cells are affected (by AutoAbs).
autoantibodies (anti-IF and antiparital Abs)
positive schilling test:
patient is given radioactive labeled vitB12 orally followed within two hours by IM
injection of unlabeled vitB12, urine is collected for 24 hours and radioactivity of
urine is determined:
- if excretion is <7.5% (urineB12/oral B12)
Shilling test:
this indicates pernicious anemia and
Help determine the
malabsorbtion and here we give the pt oral
etiology of megaloblastic
dose of B12 and IF to know the cause and
then we measure again.
Dietary deficiency
Absence of IF or
- If excretion >7.5% indicates PA
- If excretion <7.5% indicates malabsorbtion.
* why to give IM B12 in this test? to block
transcobalamin binding sites to ensure that all
radio- labelled B12 absorbed from the gut will be excreted in the urine.

Treatment: IM injection of vitB12: loading dose then maintenance dose, if we have

neurological damage we give it daily for 1 or 2 weeks.

In outpatient clinic; 67 years old male presented with general

weakness, numbness, Hb=5, MCV= 110, pancytopenia, high
LDH, high unconjugated billirubin, almost zero reticulocyte
and high LDH & billirubin, low WBC low, and platelets is
35,000, low serum vit B12. We also should do Schilling test to
know the causes of absorption (this test not available in
Patient had positive anti-IF and antiparital Abs. Patient did an
endoscopy atropy gastritis
He diagnosed as pernicious anemia, after treatment with
vitamin B12 and folic acid the patient improved.
**But Unfortunately later he came with; cold intolerance!!
why? Patient got autoimmune disease (Hashimoto's thyroditis
hypothyroidism ), and skin changes (Vitiligo).

smooth and beefy red (sore

tongue) in PA



Same characteristics as vitB12 def but without the neurological changes.

Pteroylglutamic acid.
Green leafy vegetables, liver, milk, egg, yeast, microorganisms
destroyed by heat.
50-70% absorbed from proximal ileum.
Stored in liver (5-10mg\good for 3-6 months)
Etiology: decreased intake, increased requirement, malabsorbtion and impaired
Associated with hemolytic anemia and pregnancy(so the pregnant given folic acid for
fetal demand and to prevent neural tube defect).
Therapeutic doses of folate can partially correct B12 def anemia but no effect on
neurological manifestation
Lab findings:
- Normal or high MCV, high RDW. RPI<2.
- Features of ineffective erythropoiesis (increase indirect bilirubin and increase LDH)
- Low serum and red cell folate, (both must decreased to diagnose folate def)
- red cell folate is better indication of folate stores.
- low serum folate usually indicates an imminent folic acid def and precedes red cell
folate def.
- neither serum nor red cell folate is good indicator of folate stores in the presence of
cobalamin def.
- in cobalamin def serum folate may be falsely increased and red cell folate falsely
decreased. this is because cobalamin is necessary to keep conjugated form of folate
within the cell.
- Increased urinary excretion of formiminoglutamic acid(FIGLU).

Glossitis in folate def.


Macrocytic anemia without megaloblastosis: (non megaloblastic macrocytic anemia):

called nonmegaloblastic coz we have normal vit B12 and folate levels.

Liver disease.
Myelodysplastic syndrome (MDS)

Lab findings:
high MCV and normal RDW
Blood film: round macrocytes (not oval), absence of hypersegmented

Gum hypertrophy in lymphoproliferative disorders like acute myelomonocytic leukemia

Nutritional anemias:
Iron deficiency and B12/folate deficiency can present with normocytic anemia esp. if both deficiencies are
Check iron studies and B12, folate levels.

Anemia of renal insufficiency:

Unremarkable peripheral blood smear

Inappropriately normal erythropoietin level
Anemia usually severe and symptomatic when Cr > 3.0
Mild to moderate anemia found in Cr 1.5-3.0
Treatment: Epogen or similar, Fe (oral, IV)


Anemia due to Primary Bone Marrow Disorder:

Myelodysplastic syndrome
Bone marrow infiltration: nucleated red blood cells
found in circulation
Might see rouleaux formation in multiple myeloma
WBC, plts often abnormal
Bone marrow biopsy

bone marrow does not produce sufficient
new cells to replenish blood cells and replaced by
Intrinsic abnormality of stem cells.
- Inherited: fanconis syndrome.
- Acquired: most common : idiopathic,
drugs, infections, chemicals, radiation
Pancytopenias (i.e., anemia, leukopenia, thrombocytopenia
.), absent reticulocytosis, no splenomegaly
(hypersplenism) , Hypocellular marrow (BM
Identify and remove the cause if known.
The diagnosis can only be confirmed on bone
marrow examination.
Immunosuppressive therapy and
stem cell transplantation.

Causes of pancytopenias:
(very important):
1. Aplastic anemia
2. Ineffective hematopiosis
3. Myelodysplastic syndrome (MDS)
4. Hypersplenism
5. Pernicious anemia
6. Megaloplastic anemia
(Severe Folate or vitamin B12
7. BM failure
8. Leukemias
9. Drugs; chemotherapy
10. Autoimmune disease ; SLE

Shortened RBCs life span.
The normal survival for RBC is 100120 days.
On a blood smear one Reticulocyte
per 100, RBC = 50,000
- immune: +ve coomb test (direct
antiglobulin test)

nonimmune: like in hemoglobinopathies(sickle cell anemia and thalassemia), toxicity,

trauma, hypersplenism, enzyme def like G6PD, hereditary spherocytosis
(splenomegaly+high unconjugated bilirubin+high LDH+anemia+positive family history
coz autosomal dominant).

Pictures showed Hemolytic Anemia: Intrinsic causes Spherocytosis, Sickle Cell

Physical findings:
Jaundice (the first) .
Splenomegaly (by palpation or ultrasound, it means if palpable it is twice its
normal size)
Ankle ulcers.

Lab findings:
Reticulocytes count is high.
Indirect bilirubin is high but remember Gilbert disease (asymptomatic indirect
hyperbilirubinemia), No bilirubinuria.
Low Hb.
Peripheral blood smears;
LDH: high.
Haptoglobin :low
Coombs test (to know if HA is immune or non-immune, if +ve so it is
autoimmune HA which can be primay or secondery like in SLE).
MCV: normal or high (because the size of reticulocytes is high)


FINDINGS Consistent with Hemolysis

(problems with sensitivity and specificity; none
define cause)
Reticulocyte count Increased
Cr51-RBC lifespan Decreased
Urine urobilinogen Increased
Urine hemosiderin Present ; present for
intravascular, absent for extravascular hemolysis!
Urine hemoglobin Present
Serum haptoglobin Decreased
Serum LDH (and LDH1:LDH2) Increased
Serum unconjugated (indirect) bilirubin Increased
(because increased Hgb catabolism)

Tests to define the cause of

Hemoglobin electrophoresis
Hemoglobin A2 (beta-thalassemia trait)
RBC enzymes (G6PD, PK, etc)
Direct & indirect antiglobulin tests (immune)
Cold agglutinins
Osmotic fragility (spherocytosis)
Acid hemolysis test (PNH)
Clotting profile (DIC)

Treatment of all autoimmune diseases:

1st line treatment is steroids --> if failed splenectomy

G6PD deficiency occurs when a person is

missing or doesn't have enough of an enzyme
called glucose-6-phosphate dehydrogenase,
which helps red blood cells work properly.
Too little G6PD leads to the destruction of red
blood cells. This process is called hemolysis.
Red blood cell destruction can be triggered by
beans , , infection,
Symptoms; sudden drop of Hb; dark color of
urine, jaundice, Shortness of breath.
Dx lab finding; as HA*
*LDH is high, Retics count usually high, but
sometime normal, we need to repeat G6PD
test every 4 months low


Mission Accomplished
Done By:

Hind S. Al-Otaibi

GG luck to all
specially all group "C" and my great group C2
Safa'a, Hala, Lina, Leen