Académique Documents
Professionnel Documents
Culture Documents
(( ))
ANAEMIA
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
diseases.
- 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
ANEMIA IS NEVER NORMAL
It is reduction in; total RBC count, Hemoglobin concentration (HGB) ,and/or hematocrit
(HCT)
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.
1
Anemia: History
There are important questions should be kept in consideration
for patient with anaemia:
Age, Male or Female
Is the patient bleeding?
NSAIDs, ASA, GI
((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
bleeding.
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
Ethnicity
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 )
In hematology P/E ;
Clinical finding of anemia is
spleenomegaly.
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
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)
3
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
123-
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:
Bleeding!
Obvious vs occult
Iatrogenic: venesection e.g. daily CBC, surgical, hemodialysis
Retroperitoneal
Approach to Anemia:
Serum Folate; we have serum folate and RBC folete (which is more accurate than serum
folate)
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
anaemia.
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,
b12)
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
6
TYPES OF ANAEMIA:
- Thrombocytosis
-BM (not done in IDA) : erythroid hyperplasia and absence of storage iron.
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 !!
IRON :
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.
Treatment:
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
THALASSEMIA :
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
Asymptomatic
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.
Alpha 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
11
Serum iron
Saturation
IDA
Thalassemia
TIBC
/Normal
/Normal
BM stores
Abscent
/Normal
/Normal
ACD
TIBC usually increased when saturation decreased but in ACD it is decreased coz ferroportin is
inhibited.
MYELODYSPLASTIC SYNDROME:
Primary bone marrow disorder, often found in elderly
Macrocytosis, anemia
Pseudo-Pelger-Huet abnormality the bilobed nucleus
12
MEGALOBLASTIC ANEMIA:
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
drugs.
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
bodies.
Cobalamin
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.
13
Etiology: impaired absorbtion (like in crohns disease which affects the terminal ileum,
gastritis), increased requirements and inadequate diet like in vegetarians.
14
Lab findings:
o
o
o
o
o
15
FOLATE DEFICIENCY:
16
Alcoholism.
Hypothyroidism.
Liver disease.
Myelodysplastic syndrome (MDS)
Lab findings:
high MCV and normal RDW
Blood film: round macrocytes (not oval), absence of hypersegmented
neutrophils.
Nutritional anemias:
Iron deficiency and B12/folate deficiency can present with normocytic anemia esp. if both deficiencies are
concurrent.
Check iron studies and B12, folate levels.
17
APLASTIC ANEMIA:
bone marrow does not produce sufficient
new cells to replenish blood cells and replaced by
fat.
Intrinsic abnormality of stem cells.
Causes:
- 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
failure)
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
deficiency)
7. BM failure
8. Leukemias
9. Drugs; chemotherapy
10. Autoimmune disease ; SLE
HAEMOLYTIC ANAEMIA:
Shortened RBCs life span.
The normal survival for RBC is 100120 days.
On a blood smear one Reticulocyte
per 100, RBC = 50,000
reticulocyte/UL.
causes:
- immune: +ve coomb test (direct
antiglobulin test)
18
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).
Haemosidrinuria
MCV: normal or high (because the size of reticulocytes is high)
19
hemolysis
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)
21
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
21