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Hematology
review
Mihaela Mates
PGY3 – Internal Medicine
Normal hematopoiesis
Hemoglobin
Approach to anemia
Definition (The WHO criteria):
Men: Hb <13.0 g/dL or Ht<40%
Women: Hb <12.0 g/dL or Ht<36%
Useful measurements:
Mean corpuscular volume (MCV): 80 to 100 fl
RDW (red cell distribution width): increased
RDW indicates the presence of cells of widely
differing sizes
Reticulocytes: suggestive of regeneration
Approach to Anemia
Microcytic:
MCV low, RDW high - iron deficiency
MCV low, RDW normal – thalassemia
Macrocytic:
MCV very high - B12 or folate deficiency
Normocytic:
MCV normal
Morphologic approach
Microcytic anemia – MCV < 80 fl
Reduced iron availability — severe iron deficiency, the
anemia of chronic disease, copper deficiency
Reduced heme synthesis — lead poisoning, congenital or
acquired sideroblastic anemia
Reduced globin production — thalassemic states, other
hemoglobinopathies
The three most common causes of microcytosis in
clinical practice are
iron deficiency (↓ iron stores)
alpha or beta thalassemia minor (often N or ↑ iron stores)
anemia of chronic disease (hepatoma, RCC)
Morphologic approach
Macrocytic anemia — MCV > 100 fL
Reticulocytosis
Abnormal nucleic acid metabolism of erythroid
precursors (eg, folate or vitamin 12 deficiency and
drugs interfering with nucleic acid synthesis, such
as zidovudine, hydroxyurea and Septra)
Abnormal RBC maturation (eg, myelodysplastic
syndrome, acute leukemia, LGL leukemia)
Other common causes:
alcohol abuse
liver disease
hypothyroidism
Morphologic approach
Normocytic anemia – MCV normal
Increased distruction
Reduced production (bone marrow
supression):
Bone marrow invasion (myelofibrosis, multiple
myeloma)
Myelodysplastic syndromes
Aplastic anemia
Acute blood loss
Chronic renal failure
Iron deficient anemia
Diagnosis:
↓ serum iron
↑ TIBC
↓ Transferrin saturation <20%
↓ Ferritin < 10
Iron replacement requires normalization of
the hemoglobin and the body stores
ALWAYS A SYMPTOM – LOOK FOR THE
CAUSE
Iron deficient anemia
Anemia of Chronic Disease
Common in patients with infection, cancer,
inflammatory and rheumatologic diseases
Iron can not be remobilized from storage
Blunted production of erythropoietin and
response to erythropoietin
Usually normocytic and normochromic but may
be microcytic if severe
TIBC ↓, Iron ↓, Transferrin saturation ↓, Ferritin↑
Anemia of Chronic Disease
Sideroblastic Anemia
Two common features:
Ring sideroblasts in the bone marrow (abnormal
normoblasts with excessive accumulation of iron in the
mitochondria)
Impaired heme biosynthesis
Produces a “dimorphic” blood film with
microcytes and macrocytes
Usually acquired:
Myelodysplastic syndrome
Drugs (Ethanol, INH)
Toxins (Lead, zinc)
Nutritional (Pyridoxine deficiency, copper deficiency)
Sideroblastic Anemia
Thalassemia
Anemia 2º reduced or absent production
of one or more globin chains
Poikilocytosis (variation in shape) and
basophilic stippling may be seen in the
blood film
Hemoglobin electrophoresis is only
diagnostic for beta-thalassemia and may
not be diagnostic if iron deficiency is also
present
Hb H (β-4) prep or DNA analysis is needed
to diagnose alpha-thalassemia
Basophilic stippling (ribosomal
precipitates)
Sickle Cell Disease
Inherited anemia (HbS)
Acute crisis management includes fluids,
oxygen and pain control +/- transfusion
Transfusion therapy, hydroxyurea, magnesium
and clotrimazole may reduce the frequency of
vaso-occlusive crises
Full vaccination program essential before
functional hyposplenism develops
Transplant may be curative
Sickle Cell Disease
B12 Deficiency
Megaloblastic anemia (macrocytosis,
hypersegmented neutrophils, abnormal
megakaryocytes)
Be aware of the neurological complications
Never treat possible B12 deficiency with
folate - the CNS lesions may progress
Schilling test distinguishes pernicious
anemia from other causes
Megaloblastic smear
Folic Acid Deficiency
The peripheral blood film and bone
marrow are identical to B12 deficiency
Women of childbearing age should take
supplemental folate to prevent neural tube
defects in their children
Folate supplementation lowers
homocysteine levels leading to less heart
disease and stroke
Hemolytic anemia
Extravascular hemolysis
Increased reticulocytes
Increased serum lactate dehydrogenase (LDH)
Increased indirect bilirubin concentration
Intravascular hemolysis:
RBC fragments, hemoglobinuria, urinary hemosiderin,
decreased haptoglobin
Immune (positive direct antiglobulin test)
Nonimmune (microangiopathic hemolytic anemia)
Hemolytic Anemia-Intravascular
Inherent RBC Defects:
Enzyme defects - G6PD
Acquired Causes: Non-immune
Drowning, burns, infections, PNH
RBC fragmentation
DIC
prosthetic heart valves
vasculitis
TTP
Hemolytic Anemia-Extravascular
Inherited RBC Defects:
Membrane defects - hereditary spherocytosis and
elliptocytosis
Hemoglobinopathy - Sickle Cell Disease,
Thalassemia
Immune causes:
Hemolytic transfusion reactions
AIHA- primary or secondary
Drugs eg. penicillin
Cold agglutinins
Approach to Bruising & Bleeding
Family history - bleeding or transfusion
Drugs - ASA, NSAIDS and alcohol, steroids
Other diseases - myeloma, renal or liver disease
Pattern - lifelong or recent, deep seated bleeds or
superficial bruising and petechiae
Check for the spleen, petechiae, purpura and
telangiectasia
Hemostasis Investigations
Platelet count and platelet function studies
INR, PTT, fibrinogen, FDP, bleeding time
Thrombin time and reptilase time
Euglobulin lysis time
Inhibitor studies
Factor assays
made in the liver, vitamin K dependent - 7
made in the liver, not vitamin K dependant - 5
made in endothelial cells -8
Platelets
Acquired dysfunction is common in ill patients
and DDAVP is often a valuable treatment
The blood film helps differentiate ITP from the
early phases of TTP. RBC fragments are present
in TTP but not in ITP.
Consider a bone marrow if platelet count is very
low
Approach to thrombocytopenia
Increase distruction (ITP, TTP, HIT)
Decreased production (amegakaryocytic
thrombocytopenia, aplastic anemia, acute
leukemia, etc)
Idiopathic (ITP)
Secondary:
Drug toxicity
Connective tissue diseases
Infections: HIV
Hypersplenism
Thrombotic thrombocytopenic
purpura
Diagnosis:
Microangiopathic hemolytic anemia
=nonimmune hemolysis (negative direct
antiglobulin test) with prominent red cell
fragmentation (>1%)
Thrombocytopenia
Acute renal insufficiency
Neurological abnormalities (fluctuating)
Fever
Microangiopathic blood
smear
Immune Thrombocytopenic
Purpura
Acquired: postviral infections in children
(history of infection in the several weeks
preceding the illness)
Immune/Idiopathic:
Mainstem of treatment: steroids (response in
up to 2 weeks)
If no response to steroids after 2 weeks
consider splenectomy
In severe bleeding treat with IvIg (rapid
response)
Disorders of Secondary Hemostasis
Hereditary
Hemophilia A (factor VIII deficiency) and
Hemophilia B (factor IX deficiency) are X-
linked and produce hemarthroses and
hematomas and are treated with
recombinant factor concentrates and
DDAVP (prolonged PTT)
von Willebrand’s disease (prolonged
bleeding time and prolonged PTT)
Disorders of Secondary Hemostasis
Acquired
Vitamin K deficiency (factors II, VII, IX
and X)
Liver disease (all factors other than VIII)
Circulating anticoagulants (lupus
anticoagulant)
DIC
DIC
DIC = uncontrolled THROMBIN and
PLASMIN
Excess thrombin leads to clotting, excess
plasmin leads to bleeding
Numerous disorders can trigger DIC ie.
Sepsis, trauma, cancer, fat or amniotic
fluid emboli, acute promyelocytic leukemia
DIC
Can be acute or chronic
Produces RBC fragmentation, confusion or
coma, focal necrosis in the skin, ARDS,
renal failure, bleeding and
hypercoagulability
Management of DIC
Treat the underlying cause
Give cautious replacement therapy with
FFP, cryoprecipitate and platelets
Avoid products with activated factors
In exceptional cases use low dose heparin
Approach to Neutropenia
History - drugs, toxins, recurring mouth
sores
Physical - splenomegaly, bone pain
Blood film - are granulocytic precursors or
blasts present
Bone marrow
Approach to Neutropenia
Congenital
Acquired
Immune Neutropenia
Neonatal Alloimmune Neutropenia
Primary Autoimmune Neutropenia
Secondary Autoimmune Neutropenia
Felty’s syndrome (Rheumatoid arthritis,
Splenomegaly, Neutropenia)
SLE-associated neutropenia
Drugs
Drug-Induced Neutropenia
Antithyroid
medications:
Carbamizole,
Methimazole,
Thiouracil
Antibiotics:
Cephalosporins,
Penicillins,
Sulfonamides,
Chloramphenicol
Ticlopidine
Anticonvulsants:
Carbamazapine,
Valproic acid
Antipsychotics:
Clozapine,
Olanzapine
Antiarrythmics:
Procainamide
Sulpha drugs:
Sulfasalazine,
Sulfonamides
Leukemoid Reactions
CML mimicked by acute bacterial infection
inflammatory reactions, severe marrow
stress such as bleeding, underlying tumors
and treatment with G-CSF and GM-CSF
CLL mimicked by pertussis, TB and mono
CMML and acute monoblastic leukemia
mimicked by TB
Febrile Transfusion Reactions
The most common reaction, non-immune
Within 1-6 hours of transfusion
Most often due to cytokines in the product
Become more common as the product
ages
Treatment - Acetaminophen, Demerol and
the transfusion of young products, washed
products or leukodepleted products. The
value of corticosteroids is less clear
Other Transfusion Reactions
Urticaria (soluble plasma substances react with
donor IgE) - treat with antihistamines
Anaphylaxis (sec-min) 2o IgA deficiency -
HISTORY! – only transfuse washed blood
products
Acute hemolytic (ABO mismatch)- recheck blood
group and crossmatch - usually due to clerical
error
Delayed hemolytic (2-10 days) - mimics AIHA
Citrate toxicity (hypocalcemia)- give calcium
gluconate
Approach to pancytopenia
Central
Peripheral
Central causes
Empty marrow: Aplastic anemia,
Hypoplastic MDS, myelofibrosis
Infiltration by abnormal cells: leukemia,
lymphoma, solid tumors, TB
Deranged marrow: Myelodysplastic
syndrome
Starved marrow: B12, folic acid
Drug-induced: chemotherapy, antibiotics
(sulpha), alcohol
Peripheral causes
Hypersplenism
Autoimmune
Severe Sepsis
Aplastic Anemia
Pancytopenia with ”empty” marrow
Most idiopathic cases are due to abnormal T cell
inhibition of hematopoiesis
Treatment:
Immunosuppression (Cyclosporin and antithymocyte
globulin)
Allogeneic BMT
Give irradiated, CMV negative blood products
until CMV status is known
Myeloproliferative Disorders
All are disorders of the pluripotent stem
cell
Acute Myelogenous Leukemia and Acute
Lymphoblastic Leukemia
Chronic Myeloproliferative Disorders
Myelodysplastic Syndromes
Acute Myelogenous Leukemia
Usually seen in adults
Intensive, toxic treatment is needed to
produce a complete remission
Marrow transplantation may be curative
Blasts are large with abundant cytoplasm
Auer rods are diagnostic and granules are
common
Auer Rods
Acute Lymphoblastic Leukemia
Usually seen in children and adolescents
Complete remission and cure rates are
high
Clinically: lymphadenopathy, hepato-
splenomegaly
Blasts are small, have scant cytoplasm, no
granules and few nucleoli
Some cases require marrow
transplantation
Myelodysplastic Syndromes
Refractory anemia
Refractory anemia with ring sideroblasts
Refractory anemia with excess blasts
Refractory anemia with excess blasts in
transformation
Chronic myelomonocytic leukemia
MDS
Chronic Myeloproliferative Disorders
Polycythemia rubra vera (tx: phlebotomy,
hydroxyurea)
Chronic myeloid leukemia (tx: Gleevec,
BMT)
Idiopathic Myelofibrosis
Essential thrombocythemia
Chronic Lymphocytic Leukemia
Common in the elderly
The blood film shows a lymphocytosis that
may be extreme and smudge cells
Lymphadenopathy and splenomegaly
Autoimmune anemia and
thrombocytopenia
Treatment is observation, alkylating
agents, fludarabine, steroids or radiation
CLL
Multiple Myeloma
A monoclonal immunoglobulin in the serum or a
single light chain in the urine is found (SPEP,
UPEP) and marrow plasmocytosis
Hypercalcemia and renal failure are frequent
Lytic bone lesions are classical but osteoporosis is
more common (alk phos is normal)
The blood film shows rouleaux
High ESR
MGUS
Characteristics:
Presence of a monoclonal immunoglobulin
< 3g/l (in 1% of people)
Normal marrow (<10%plasma cells), normal
chemistry (no anemia, hypercalcemia, no renal
failure) and no lytic lesions
The M-protein remains stable
May transform to myeloma
Macroglobulinemia
Monoclonal IgM protein
Clinically:
Lymphadenopathy
Hepatosplenomegaly
Hyperviscosity syndrome
ESR may be very low
Treat the hyperviscosity with
plasmapheresis
Hodgkin’s Disease
The Reed-Sternberg cell is diagnostic
The cure rate is high
Long term complications are heart
disease, hypothyroidism and secondary
malignancies
Reed-Sternberg cell
Non-Hodgkin’s Lymphoma
Numerous classification systems
Low grade: Radiation +/- gentle chemotherapy
does not cure but does produce long survival
Intermediate and high grade: Radiation ±
chemotherapy is used. Cure is possible
Autoimmune hemolytic anemia and
thrombocytopenia are common
Hypersplenism is common
Immunosuppression is frequent
never give live vaccines
Deep Vein Thrombosis and
Pulmonary Embolism
1859 Rudolph Virchow described the
major pathogenic determinants:
1) Blood stasis
2) Changes in the vessel wall
3) Hypercoagulability
Thrombophilia
Antiphospholipid antibodies
Factor V Leiden
G20210A prothrombin gene mutation
Deficiency of protein C, protein S, and
antithrombin
Hyperhomocysteinemia
DVT/PE treatment
Start LMWH (superior to UFH) if no
contraindications
Start Warfarin with LMWH
Stop LMWH after 2 consecutive days of
therapeutic INR (2-3)
Thrombolytics indicated if circulatory
collapse (shock)
Duration of anticoagulation
Major transient risk factor (recent
surgery): 3 months AVK
Minor transient risk factor
(immobilization): 6 months AVK
Unprovoked thrombosis: longterm AVK
Active cancer: longterm LMWH
Prophylaxis of VTE
General surgery
Anticoagulant prophylaxis is
recommended routinely
UFH 5000 U administered 3 times daily
is similarly effective as LMWH
(Enoxaparin 40mg sc daily or Dalteparin
5000U sc daily)
Fondaparinux - superior to other LMWH
for DVT prophylaxis in orthopedic
surgery
Prophylaxis of VTE
Central venous catheters
Based on recent data, the overall
thrombotic risk of catheter-related
thrombosis is low and probably insufficient
to warrant routine prophylaxis
Case 1
63y F with severe fatigue and bruising
O/E: T°=38.9°C, pale and slightly jaundiced, rest of
examination normal
PMHx: hypothyroidism
Meds: thyroxine
WBC=1.9 x 109/l
Hb=53 g/l
MCV=142 fl
Plt=15 x 109/l
Retics=10 x 109/l
Neut=1.0 x 109/l
Ly=0.7 x 109/l
Mono=0.2 x 109/l
Film: Hypersegmented polymorphs. Oval macrocytes
List 3 diagnosis in order of likelihood
Macrocytic anemia
Case 2
45y F on routine annual physical examination found to have
following blood count (previously healthy, on no meds):
WBC: 7.5
Hb=61
MCV=58
Plt=345
Retics=10
Neut=4.3
Ly=2.7
Mono=0.5
Film: Hypochromia. Microcytosis.
What is the most likely hematologic diagnosis?
List 3 alternative possibilities.
What tests would you order?
Outline a management plan.
Hypochromic microcytic
anemia
Microcytosis found in:
Iron deficiency anaemia
Thalassaemia
Sideroblastic anaemia
Lead poisoning
Anaemia of chronic disease
Hypochromia found in:
Iron deficiency
Thalassaemia
And any of the conditions leading
to microcytosis
Found in:
Iron deficiency
Thalassaemia
And any of the
conditions leading to
microcytosis
Case 3
59y F feeling “washed out”. Spleen palpable 4 cm BCM,
jaundiced. Blood counts as follows:
WBC=8.5
Hb=61
MCV=110
Retics=560
Plt=156
Neut=4.5
Ly=3.0
Mono=0.8
Eo=0.2
Film: Spherocytes. Polychromasia.
State the two most likely diagnoses, in order of probability
Outline a plan of investigation and management
Hemolytic anemia
Spherocytosis found in:
Hereditary spherocytosis
Immune haemolytic anaemia
Zieve's syndrome
Microangiopathic haemolytic
anaemia
Polychromasia found in:
Any situation with reticulocytosis
- for example bleeding,
haemolysis or response to
haematinic factor replacement
Case 4
Black 56y M with splenomegaly (5cm BCM), no
lymphadenopathy, non-drinker. Always had ‘low blood’, tx
with several courses of iron with no difference on his health
or blood counts. Upper and lower endoscopy – normal
WBC=8.5
Hb=106
MCV=72
Plt=254
Retics=100
Neut=4.5
Ly=3.0
Mono=0.8
Eo=0.2
Film: Target cells
List the differential diagnosis
Target cells
Found in:
Obstructive liver
disease
Severe iron deficiency
Thalassaemia
Haemoglobinopathies
(S and C)
Post splenectomy
Case 5
62y M on routine physical examination has a palpable spleen at
12cm BCM, no lymphadenopathy. He feels perfectly well, drinks a
bottle of red wine every day for 10years. No signs suggestive of
chronic liver disease
WBC=2.5
Hb=102
MCV=93
Plt=95
Retics=60
N=1.0
Ly=2.0
Mono=0.1
Other: myelocytes 0.2, nucleated RBC 0.1, tear drop poikylocytes
List the three most likely diagnoses
Outline a plan of investigation
Erythroleukoblastic smear
Found in:
Bone marrow fibrosis
Megaloblastic anaemia
Iron deficiency
Thalassaemia
Case 6
Patient with fatigue and bruising, present over the last 6-8weeks.
Otherwise well, on no medications. Has a history of CABG 3y ago,
and at that time found to have AAA, 3cm in diameter. Chest x-ray
shows a widened mediastinum
WBC=4.6
Hb=82
MCV 101
Plt=20
Retics=390
N=2.5
Ly=1.8
Mono=0.3
Film: Schistocytes++
What is the hematological diagnosis
List 3 differential diagnoses
Outline a plan of investigation and management
Schistocytosis
Schistocytes found in:
DIC
Micro angiopathic hemolytic
anemia
Mechanical hemolytic anemia
Case 7
65y F has headaches for about 3 weeks and gradually worsening
drowsiness for 1 week. She comes to ER, is rousable, but sleepy.
No neurological signs, generalized lymphadenopathy, up to approx
3cm in size. The spleen is felt at 7cm BCM
WBC=3.1
Hb=88
MCV=87
Plt=134
Retics=27
N=1.0
Ly=2.0
Mono=0.1
Film: Rouleaux+++. Blue background staining
What is the most likely diagnosis
Outline a plan of investigation
Outline a management plan
Rouleaux
Found in:
Hyperfibrinogenaemia
Hyperglobulinaemia
Case 8
76y F has an incidental blood count performed
WBC=2.9
Hb=88
MCV=102
Plt=75
Retics=20
N=1.0
Ly=2.5
Mono=0.4
Film: dimorphic red blood cells
What is the most likely diagnosis?
How should it be investigated and managed?
Myelodysplasia
Dimorhic cells:
Two distinct populations of red cells.The populations may
differ in size, shape or haemoglobin content.
Found in:
Anemic patient after transfusion
Iron deficiency patient during therapy
Combined B12 / folate and iron deficiency
Sideroblastic anaemia

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Hematology review1

  • 4. Approach to anemia Definition (The WHO criteria): Men: Hb <13.0 g/dL or Ht<40% Women: Hb <12.0 g/dL or Ht<36% Useful measurements: Mean corpuscular volume (MCV): 80 to 100 fl RDW (red cell distribution width): increased RDW indicates the presence of cells of widely differing sizes Reticulocytes: suggestive of regeneration
  • 5. Approach to Anemia Microcytic: MCV low, RDW high - iron deficiency MCV low, RDW normal – thalassemia Macrocytic: MCV very high - B12 or folate deficiency Normocytic: MCV normal
  • 6. Morphologic approach Microcytic anemia – MCV < 80 fl Reduced iron availability — severe iron deficiency, the anemia of chronic disease, copper deficiency Reduced heme synthesis — lead poisoning, congenital or acquired sideroblastic anemia Reduced globin production — thalassemic states, other hemoglobinopathies The three most common causes of microcytosis in clinical practice are iron deficiency (↓ iron stores) alpha or beta thalassemia minor (often N or ↑ iron stores) anemia of chronic disease (hepatoma, RCC)
  • 7. Morphologic approach Macrocytic anemia — MCV > 100 fL Reticulocytosis Abnormal nucleic acid metabolism of erythroid precursors (eg, folate or vitamin 12 deficiency and drugs interfering with nucleic acid synthesis, such as zidovudine, hydroxyurea and Septra) Abnormal RBC maturation (eg, myelodysplastic syndrome, acute leukemia, LGL leukemia) Other common causes: alcohol abuse liver disease hypothyroidism
  • 8. Morphologic approach Normocytic anemia – MCV normal Increased distruction Reduced production (bone marrow supression): Bone marrow invasion (myelofibrosis, multiple myeloma) Myelodysplastic syndromes Aplastic anemia Acute blood loss Chronic renal failure
  • 9. Iron deficient anemia Diagnosis: ↓ serum iron ↑ TIBC ↓ Transferrin saturation <20% ↓ Ferritin < 10 Iron replacement requires normalization of the hemoglobin and the body stores ALWAYS A SYMPTOM – LOOK FOR THE CAUSE
  • 11. Anemia of Chronic Disease Common in patients with infection, cancer, inflammatory and rheumatologic diseases Iron can not be remobilized from storage Blunted production of erythropoietin and response to erythropoietin Usually normocytic and normochromic but may be microcytic if severe TIBC ↓, Iron ↓, Transferrin saturation ↓, Ferritin↑
  • 12. Anemia of Chronic Disease
  • 13. Sideroblastic Anemia Two common features: Ring sideroblasts in the bone marrow (abnormal normoblasts with excessive accumulation of iron in the mitochondria) Impaired heme biosynthesis Produces a “dimorphic” blood film with microcytes and macrocytes Usually acquired: Myelodysplastic syndrome Drugs (Ethanol, INH) Toxins (Lead, zinc) Nutritional (Pyridoxine deficiency, copper deficiency)
  • 15. Thalassemia Anemia 2º reduced or absent production of one or more globin chains Poikilocytosis (variation in shape) and basophilic stippling may be seen in the blood film Hemoglobin electrophoresis is only diagnostic for beta-thalassemia and may not be diagnostic if iron deficiency is also present Hb H (β-4) prep or DNA analysis is needed to diagnose alpha-thalassemia
  • 17. Sickle Cell Disease Inherited anemia (HbS) Acute crisis management includes fluids, oxygen and pain control +/- transfusion Transfusion therapy, hydroxyurea, magnesium and clotrimazole may reduce the frequency of vaso-occlusive crises Full vaccination program essential before functional hyposplenism develops Transplant may be curative
  • 19. B12 Deficiency Megaloblastic anemia (macrocytosis, hypersegmented neutrophils, abnormal megakaryocytes) Be aware of the neurological complications Never treat possible B12 deficiency with folate - the CNS lesions may progress Schilling test distinguishes pernicious anemia from other causes
  • 21. Folic Acid Deficiency The peripheral blood film and bone marrow are identical to B12 deficiency Women of childbearing age should take supplemental folate to prevent neural tube defects in their children Folate supplementation lowers homocysteine levels leading to less heart disease and stroke
  • 22. Hemolytic anemia Extravascular hemolysis Increased reticulocytes Increased serum lactate dehydrogenase (LDH) Increased indirect bilirubin concentration Intravascular hemolysis: RBC fragments, hemoglobinuria, urinary hemosiderin, decreased haptoglobin Immune (positive direct antiglobulin test) Nonimmune (microangiopathic hemolytic anemia)
  • 23. Hemolytic Anemia-Intravascular Inherent RBC Defects: Enzyme defects - G6PD Acquired Causes: Non-immune Drowning, burns, infections, PNH RBC fragmentation DIC prosthetic heart valves vasculitis TTP
  • 24. Hemolytic Anemia-Extravascular Inherited RBC Defects: Membrane defects - hereditary spherocytosis and elliptocytosis Hemoglobinopathy - Sickle Cell Disease, Thalassemia Immune causes: Hemolytic transfusion reactions AIHA- primary or secondary Drugs eg. penicillin Cold agglutinins
  • 25. Approach to Bruising & Bleeding Family history - bleeding or transfusion Drugs - ASA, NSAIDS and alcohol, steroids Other diseases - myeloma, renal or liver disease Pattern - lifelong or recent, deep seated bleeds or superficial bruising and petechiae Check for the spleen, petechiae, purpura and telangiectasia
  • 26. Hemostasis Investigations Platelet count and platelet function studies INR, PTT, fibrinogen, FDP, bleeding time Thrombin time and reptilase time Euglobulin lysis time Inhibitor studies Factor assays made in the liver, vitamin K dependent - 7 made in the liver, not vitamin K dependant - 5 made in endothelial cells -8
  • 27. Platelets Acquired dysfunction is common in ill patients and DDAVP is often a valuable treatment The blood film helps differentiate ITP from the early phases of TTP. RBC fragments are present in TTP but not in ITP. Consider a bone marrow if platelet count is very low
  • 28. Approach to thrombocytopenia Increase distruction (ITP, TTP, HIT) Decreased production (amegakaryocytic thrombocytopenia, aplastic anemia, acute leukemia, etc) Idiopathic (ITP) Secondary: Drug toxicity Connective tissue diseases Infections: HIV Hypersplenism
  • 29. Thrombotic thrombocytopenic purpura Diagnosis: Microangiopathic hemolytic anemia =nonimmune hemolysis (negative direct antiglobulin test) with prominent red cell fragmentation (>1%) Thrombocytopenia Acute renal insufficiency Neurological abnormalities (fluctuating) Fever
  • 31. Immune Thrombocytopenic Purpura Acquired: postviral infections in children (history of infection in the several weeks preceding the illness) Immune/Idiopathic: Mainstem of treatment: steroids (response in up to 2 weeks) If no response to steroids after 2 weeks consider splenectomy In severe bleeding treat with IvIg (rapid response)
  • 32. Disorders of Secondary Hemostasis Hereditary Hemophilia A (factor VIII deficiency) and Hemophilia B (factor IX deficiency) are X- linked and produce hemarthroses and hematomas and are treated with recombinant factor concentrates and DDAVP (prolonged PTT) von Willebrand’s disease (prolonged bleeding time and prolonged PTT)
  • 33. Disorders of Secondary Hemostasis Acquired Vitamin K deficiency (factors II, VII, IX and X) Liver disease (all factors other than VIII) Circulating anticoagulants (lupus anticoagulant) DIC
  • 34. DIC DIC = uncontrolled THROMBIN and PLASMIN Excess thrombin leads to clotting, excess plasmin leads to bleeding Numerous disorders can trigger DIC ie. Sepsis, trauma, cancer, fat or amniotic fluid emboli, acute promyelocytic leukemia
  • 35. DIC Can be acute or chronic Produces RBC fragmentation, confusion or coma, focal necrosis in the skin, ARDS, renal failure, bleeding and hypercoagulability
  • 36. Management of DIC Treat the underlying cause Give cautious replacement therapy with FFP, cryoprecipitate and platelets Avoid products with activated factors In exceptional cases use low dose heparin
  • 37. Approach to Neutropenia History - drugs, toxins, recurring mouth sores Physical - splenomegaly, bone pain Blood film - are granulocytic precursors or blasts present Bone marrow
  • 38. Approach to Neutropenia Congenital Acquired Immune Neutropenia Neonatal Alloimmune Neutropenia Primary Autoimmune Neutropenia Secondary Autoimmune Neutropenia Felty’s syndrome (Rheumatoid arthritis, Splenomegaly, Neutropenia) SLE-associated neutropenia Drugs
  • 40. Leukemoid Reactions CML mimicked by acute bacterial infection inflammatory reactions, severe marrow stress such as bleeding, underlying tumors and treatment with G-CSF and GM-CSF CLL mimicked by pertussis, TB and mono CMML and acute monoblastic leukemia mimicked by TB
  • 41. Febrile Transfusion Reactions The most common reaction, non-immune Within 1-6 hours of transfusion Most often due to cytokines in the product Become more common as the product ages Treatment - Acetaminophen, Demerol and the transfusion of young products, washed products or leukodepleted products. The value of corticosteroids is less clear
  • 42. Other Transfusion Reactions Urticaria (soluble plasma substances react with donor IgE) - treat with antihistamines Anaphylaxis (sec-min) 2o IgA deficiency - HISTORY! – only transfuse washed blood products Acute hemolytic (ABO mismatch)- recheck blood group and crossmatch - usually due to clerical error Delayed hemolytic (2-10 days) - mimics AIHA Citrate toxicity (hypocalcemia)- give calcium gluconate
  • 44. Central causes Empty marrow: Aplastic anemia, Hypoplastic MDS, myelofibrosis Infiltration by abnormal cells: leukemia, lymphoma, solid tumors, TB Deranged marrow: Myelodysplastic syndrome Starved marrow: B12, folic acid Drug-induced: chemotherapy, antibiotics (sulpha), alcohol
  • 46. Aplastic Anemia Pancytopenia with ”empty” marrow Most idiopathic cases are due to abnormal T cell inhibition of hematopoiesis Treatment: Immunosuppression (Cyclosporin and antithymocyte globulin) Allogeneic BMT Give irradiated, CMV negative blood products until CMV status is known
  • 47. Myeloproliferative Disorders All are disorders of the pluripotent stem cell Acute Myelogenous Leukemia and Acute Lymphoblastic Leukemia Chronic Myeloproliferative Disorders Myelodysplastic Syndromes
  • 48. Acute Myelogenous Leukemia Usually seen in adults Intensive, toxic treatment is needed to produce a complete remission Marrow transplantation may be curative Blasts are large with abundant cytoplasm Auer rods are diagnostic and granules are common
  • 50. Acute Lymphoblastic Leukemia Usually seen in children and adolescents Complete remission and cure rates are high Clinically: lymphadenopathy, hepato- splenomegaly Blasts are small, have scant cytoplasm, no granules and few nucleoli Some cases require marrow transplantation
  • 51. Myelodysplastic Syndromes Refractory anemia Refractory anemia with ring sideroblasts Refractory anemia with excess blasts Refractory anemia with excess blasts in transformation Chronic myelomonocytic leukemia
  • 52. MDS
  • 53. Chronic Myeloproliferative Disorders Polycythemia rubra vera (tx: phlebotomy, hydroxyurea) Chronic myeloid leukemia (tx: Gleevec, BMT) Idiopathic Myelofibrosis Essential thrombocythemia
  • 54. Chronic Lymphocytic Leukemia Common in the elderly The blood film shows a lymphocytosis that may be extreme and smudge cells Lymphadenopathy and splenomegaly Autoimmune anemia and thrombocytopenia Treatment is observation, alkylating agents, fludarabine, steroids or radiation
  • 55. CLL
  • 56. Multiple Myeloma A monoclonal immunoglobulin in the serum or a single light chain in the urine is found (SPEP, UPEP) and marrow plasmocytosis Hypercalcemia and renal failure are frequent Lytic bone lesions are classical but osteoporosis is more common (alk phos is normal) The blood film shows rouleaux High ESR
  • 57. MGUS Characteristics: Presence of a monoclonal immunoglobulin < 3g/l (in 1% of people) Normal marrow (<10%plasma cells), normal chemistry (no anemia, hypercalcemia, no renal failure) and no lytic lesions The M-protein remains stable May transform to myeloma
  • 58. Macroglobulinemia Monoclonal IgM protein Clinically: Lymphadenopathy Hepatosplenomegaly Hyperviscosity syndrome ESR may be very low Treat the hyperviscosity with plasmapheresis
  • 59. Hodgkin’s Disease The Reed-Sternberg cell is diagnostic The cure rate is high Long term complications are heart disease, hypothyroidism and secondary malignancies
  • 61. Non-Hodgkin’s Lymphoma Numerous classification systems Low grade: Radiation +/- gentle chemotherapy does not cure but does produce long survival Intermediate and high grade: Radiation ± chemotherapy is used. Cure is possible Autoimmune hemolytic anemia and thrombocytopenia are common Hypersplenism is common Immunosuppression is frequent never give live vaccines
  • 62. Deep Vein Thrombosis and Pulmonary Embolism 1859 Rudolph Virchow described the major pathogenic determinants: 1) Blood stasis 2) Changes in the vessel wall 3) Hypercoagulability
  • 63. Thrombophilia Antiphospholipid antibodies Factor V Leiden G20210A prothrombin gene mutation Deficiency of protein C, protein S, and antithrombin Hyperhomocysteinemia
  • 64. DVT/PE treatment Start LMWH (superior to UFH) if no contraindications Start Warfarin with LMWH Stop LMWH after 2 consecutive days of therapeutic INR (2-3) Thrombolytics indicated if circulatory collapse (shock)
  • 65. Duration of anticoagulation Major transient risk factor (recent surgery): 3 months AVK Minor transient risk factor (immobilization): 6 months AVK Unprovoked thrombosis: longterm AVK Active cancer: longterm LMWH
  • 66. Prophylaxis of VTE General surgery Anticoagulant prophylaxis is recommended routinely UFH 5000 U administered 3 times daily is similarly effective as LMWH (Enoxaparin 40mg sc daily or Dalteparin 5000U sc daily) Fondaparinux - superior to other LMWH for DVT prophylaxis in orthopedic surgery
  • 67. Prophylaxis of VTE Central venous catheters Based on recent data, the overall thrombotic risk of catheter-related thrombosis is low and probably insufficient to warrant routine prophylaxis
  • 68. Case 1 63y F with severe fatigue and bruising O/E: T°=38.9°C, pale and slightly jaundiced, rest of examination normal PMHx: hypothyroidism Meds: thyroxine WBC=1.9 x 109/l Hb=53 g/l MCV=142 fl Plt=15 x 109/l Retics=10 x 109/l Neut=1.0 x 109/l Ly=0.7 x 109/l Mono=0.2 x 109/l Film: Hypersegmented polymorphs. Oval macrocytes List 3 diagnosis in order of likelihood
  • 70. Case 2 45y F on routine annual physical examination found to have following blood count (previously healthy, on no meds): WBC: 7.5 Hb=61 MCV=58 Plt=345 Retics=10 Neut=4.3 Ly=2.7 Mono=0.5 Film: Hypochromia. Microcytosis. What is the most likely hematologic diagnosis? List 3 alternative possibilities. What tests would you order? Outline a management plan.
  • 71. Hypochromic microcytic anemia Microcytosis found in: Iron deficiency anaemia Thalassaemia Sideroblastic anaemia Lead poisoning Anaemia of chronic disease Hypochromia found in: Iron deficiency Thalassaemia And any of the conditions leading to microcytosis Found in: Iron deficiency Thalassaemia And any of the conditions leading to microcytosis
  • 72. Case 3 59y F feeling “washed out”. Spleen palpable 4 cm BCM, jaundiced. Blood counts as follows: WBC=8.5 Hb=61 MCV=110 Retics=560 Plt=156 Neut=4.5 Ly=3.0 Mono=0.8 Eo=0.2 Film: Spherocytes. Polychromasia. State the two most likely diagnoses, in order of probability Outline a plan of investigation and management
  • 73. Hemolytic anemia Spherocytosis found in: Hereditary spherocytosis Immune haemolytic anaemia Zieve's syndrome Microangiopathic haemolytic anaemia Polychromasia found in: Any situation with reticulocytosis - for example bleeding, haemolysis or response to haematinic factor replacement
  • 74. Case 4 Black 56y M with splenomegaly (5cm BCM), no lymphadenopathy, non-drinker. Always had ‘low blood’, tx with several courses of iron with no difference on his health or blood counts. Upper and lower endoscopy – normal WBC=8.5 Hb=106 MCV=72 Plt=254 Retics=100 Neut=4.5 Ly=3.0 Mono=0.8 Eo=0.2 Film: Target cells List the differential diagnosis
  • 75. Target cells Found in: Obstructive liver disease Severe iron deficiency Thalassaemia Haemoglobinopathies (S and C) Post splenectomy
  • 76. Case 5 62y M on routine physical examination has a palpable spleen at 12cm BCM, no lymphadenopathy. He feels perfectly well, drinks a bottle of red wine every day for 10years. No signs suggestive of chronic liver disease WBC=2.5 Hb=102 MCV=93 Plt=95 Retics=60 N=1.0 Ly=2.0 Mono=0.1 Other: myelocytes 0.2, nucleated RBC 0.1, tear drop poikylocytes List the three most likely diagnoses Outline a plan of investigation
  • 77. Erythroleukoblastic smear Found in: Bone marrow fibrosis Megaloblastic anaemia Iron deficiency Thalassaemia
  • 78. Case 6 Patient with fatigue and bruising, present over the last 6-8weeks. Otherwise well, on no medications. Has a history of CABG 3y ago, and at that time found to have AAA, 3cm in diameter. Chest x-ray shows a widened mediastinum WBC=4.6 Hb=82 MCV 101 Plt=20 Retics=390 N=2.5 Ly=1.8 Mono=0.3 Film: Schistocytes++ What is the hematological diagnosis List 3 differential diagnoses Outline a plan of investigation and management
  • 79. Schistocytosis Schistocytes found in: DIC Micro angiopathic hemolytic anemia Mechanical hemolytic anemia
  • 80. Case 7 65y F has headaches for about 3 weeks and gradually worsening drowsiness for 1 week. She comes to ER, is rousable, but sleepy. No neurological signs, generalized lymphadenopathy, up to approx 3cm in size. The spleen is felt at 7cm BCM WBC=3.1 Hb=88 MCV=87 Plt=134 Retics=27 N=1.0 Ly=2.0 Mono=0.1 Film: Rouleaux+++. Blue background staining What is the most likely diagnosis Outline a plan of investigation Outline a management plan
  • 82. Case 8 76y F has an incidental blood count performed WBC=2.9 Hb=88 MCV=102 Plt=75 Retics=20 N=1.0 Ly=2.5 Mono=0.4 Film: dimorphic red blood cells What is the most likely diagnosis? How should it be investigated and managed?
  • 83. Myelodysplasia Dimorhic cells: Two distinct populations of red cells.The populations may differ in size, shape or haemoglobin content. Found in: Anemic patient after transfusion Iron deficiency patient during therapy Combined B12 / folate and iron deficiency Sideroblastic anaemia