recognize normal/abnormal results and understand their implications interpret abnormal results,...

Recognize normal/abnormal results and understand their implications

Interpret abnormal results, identify possible underlying disease states and perform additional evaluation

Identify critical results and take appropriate action

Series of tests used to evaluate the composition and concentration of various cellular components of blood› Red Cell Parameters

Hemoglobin, RBC, MCV, MCHC, MCH, RDW

› White Cell Parameters Differential Count

› Platelet Count

Automated instruments using anti-coagulated whole blood

Clots consume platelets and can trap other cells artificially decreasing values

Incomplete filling of tubes with blood can cause artifacts by exposing cells to toxic quantities of the tube’s anti-coagulants

WBC Parameters

RBC Parameters

Platelet Count

Red Cell Disorders› Anemia› Polycythemia

White Cell Disorders› Leukocytosis› Leukopenia

Platelet Disorders› Thrombocytosis› Thrombocytopenia

Biconcave disk Clinical significance:

transport hemoglobin, measure of the oxygen carrying capacity of blood

Regulated by erythropoietin

Life span of ~120 days

Hematocrit – packed cell volume› Ratio of volume of RBC to volume of blood

MCV (mean corpuscular volume)› Normal 80-100› Microcytic <80› Macrocytic >100

MCHC (mean corpuscular hemoglobin concentration)› Hemoglobin/RBC › Low = hypochromic

MCH (mean corpuscular hemoglobin)› Hemoglobin/Hematocrit

RDW (red cell distribution width)› Correlates with the degree of anisocytosis

Reticulocyte Count› Young RBC› Normal: 1-2%

Most common hematologic disorder Decrease in the number of circulating

red blood cells causing a decrease in oxygen carrying capacity of blood

Usually a secondary underlying cause

Shortness of Breath Chest Pain Tachycardia Skin/Mucosal Pallor Bleeding Fatigue

Blood Loss Anemia Anemia of Decreased RBC Production Anemia with Increased RBC Destruction

Microcytic: MCV <80 Normocytic: MCV 80-100 Macrocytic: MCV >100

Microcytic Anemias› Iron Deficiency Anemia› Thalassemia› Sideroblastic Anemia› Chronic Disease

Macrocytic Anemias Normocytic Anemias

Iron Deficiency Thalassemia Sideroblastic Chronic Disease

1. Dietary Deficiency› Meat deficient diets› Pregnancy

2. Malabsorption› Partial gastrectomy (hypochlorhydria)› Celiac › Chronic diarrhea

3. Chronic Blood Loss› GI Tract - Ulcerative disease, Gastritis,

Cancer, Hemorrhods, AV Malformations› Menorrhagia› Hematuria – Bladder/Kidney Cancers› Frequent blood donation/inpatient

phlebotomy

Diagnosis of Iron deficiency in an adult mandates an evaluation to rule out malignancy

Gold Standard: Bone Marrow Biopsy

Iron Studies (Fe, Ferritin, TIBC)

Iron

Iron Saturati

on

Ferritin

TIBC

Peripheral Smear

Low Low Low High Microcytic (low MCV) and Hypochromic (low MCHC) Red Cells

Oral Iron Replacement› Ferrous Sulfate 325mg PO TID› Ascorbic Acid can increase absorption› Can cause GI upset/constipation

Parenteral Iron› Indicated in cases of intolerance to PO Fe

or failure to respond to PO Fe Important to not only treat the iron

deficiency, but you must discover and treat the underlying disorder

Spectrum of diseases characterized by decreased or lack of production of one or more globulin chains

Normal hemoglobin contains four alpha and two beta chains

Alpha thalassemias – alpha chain production problem leading to an excess of beta globin chains

Beta thalassemias – beta chain production problem leading to excess alpha chains

More common in Mediterranean, African and Southeast Asian populations

Beta Thalassemia Major – complete lack of production of Beta Globin Chains

Beta Thalassemia Minor – loss of one of the two alleles coding for the Beta-globulin gene

Complete lack of hemoglobin A production Microcytic (low MCV) hypochromic (low

MCHC) red cells Complications:

› Bone deformities (EPO stimulated expansion of bone marrow)

› Hepatosplenomegaly (extramedullary hemoatopiesis)

› Secondary Iron Overload (increased iron absorption and repeated transfusions)

Asymptomatic condition Microcytosis and a normal RDW If anemia is present, usually mild

Hemoglobin electrophoresis › Beta Thalassemia and Severe Alpha

Thalassemia

Mild alpha thalassemia detection› Alpha:Beta Ratio› Molecular testing› Neither test is widely available

Depends on the severity of the genetic defect and the clinical sequelae

Minor Thalassemias › Often asymptomatic and require no therapy

Major Thalassemias› Chronic transfusions› Iron chelation› Splenectomy

Avoid Routine Iron Supplementation

Characterized by ineffective erythropoiesis and presence of ringed sideroblasts in the bone marrow

“Ringed” – accumulation of iron in the mitochondria that surround the periphery of the nucleus

Hereditary Ideopathic Drug-Associated

› Alcohol, INH, Chloramphenicol Lead Poisoning

› Basophilic Stippling

No cure for hereditary condition Prevent iron overload/chelation Drug induced

› Often resolves when offending agent discontinued

Isoniazid associated – can be overcome with high dose pyridoxine supplementation › Can reverse anemia and allow for

continuation of drug

Microcytic Anemias Macrocytic Anemias

› Vitamin B12 Deficiency› Folate Deficiency› Drug Induced

Normocytic Anemias

MCV >100 Can be categorized based on features

seen on peripheral smear Megaloblastic – oval macrocytes;

hypersegmented polymorphonuclear lymphocytes (PMN)› >5 lobes

Non-Megaloblastic

Megaloblastlc

Vitamin B12 Deficiency

Folic Acid Deficiency Drug induced

Non-Megaloblastic

Liver Disease Hypothyroidism Alcohol Induced Reticulocytosis

(hemolysis)

Etiologies:› Pernicious Anemia› Gastrectomy/Gastric Bypass› Ileal disorders› Inadequate intake

Additional Symptoms:› Diarrhea/abdominal pain› Numbness/paresthesia› Glossitis› Motor weakness/spasticity› Decreased proprioception

Vitamin B12 level Serum Methylmalonic Acid and

Homocystine levels Anti-intrinsic Factor or Anti-parietal Cell

Antibodies Endoscopic evaluation Surgical History

Vitamin B12 1mg IM or SC › Daily x7 days, then› Weekly for 4 weeks, then› Monthly thereafter

Hematologic abnormalities take about 2 moths to resolve

Neurologic abnormalities can take up to 18 months to resolve; however, may be permanent

Inadequate intake Decreased absorption

› Celiac, bacterial overgrowth, drugs (dilantin) Increased requirement

› Hemolytic Anemia, Pregnancy, Hemodialysis Iatrogenic – Folic Acid Antagonists

› Methotrexate, Trimethoprim Appears similar to Vitamin B12 deficiency;

however, no neurologic symptoms

Folic Acid 1mg PO daily Hematologic abnormalities should

resolve in about 2 months

Important to rule out concurrent Vitamin B12 deficiency› Folic Acid may improve the hematologic

parameters in Vitamin B12 deficiency but wont correct any underlying neurologic symptoms

Purine Analogs (azathioprine)

Pyrimidine Analogs (5-FU, ARA-C)

Hydroxyurea Anticonvulsants

(dilantin, phenobarbital)

Treatment:› Stop offending

agent› Tolerate mild

anemia if therapeutic benefit of drug is justified

Microcytic Anemias Macrocytic Anemias Normocytic Anemias

› Hemolytic Anemias G6PD Deficiency Spherocytosis Microangiopathic Hemolytic Anemia

(DIC/TTP/HUS)› Malignancy/Bone Marrow Infiltration› Myelodysplastic Syndrome› Anemia of Chronic Kidney Disease

Elevated Reticulocyte Count› Hemolytic Anemia› Acute Bleeding

Decreased Reticulocyte Count› Malignancy/Marrow infiltration

Leukemia/lymphoma, Myeloma, Granulomatous Disease

› Stem Cell Disorders Myelofibrosis, Aplastic Anemia/Pure RCB Aplasia,

Myelodysplasia› Medical Conditions

Chronic Kidney Disease, Anemia of Chronic Disease

Anemias with increased RBC destruction Jaundice, splenomegaly, brown/red urine Laboratory abnormalities:

› Increased LDH› Decreased Haptoglobin› Increased unconjugated bilirubin› Increased reticulocyte count› Positive Direct Coombs Test

Disordered Hemoglobin Synthesis› Sickle Cell

RBC Membrane Disorders› Spherocytosis› Elliptocytosis

RBC Enzyme Disorders› G6PD Deficiency› Pyruvate Kinase Deficiency› Hexokinase Deficiency

X-linked disorder that leads to hemolysis in the presence of an oxidative stress

Hemoglobin loses its ability to maintain a reduced state and precipitates within the RBC and cells lyse

Leads to Heinz Body formation and hemolysis

Bite cells

Precipitants of hemolysis: Infection – E. coli, salmonella, S.

pneumoniae, vital hepatitis Drug Induced

› Antimalarials (primaquine and chloroquine)› Antibiotics (sulfonamides, nitrofurantoin)

Fava Beans Napthalene

Diagnosis made by measuring G6PD activity level› Should be checked 3-4 weeks after

hemolytic episode for accurate results› Measuring during hemolytic episode will

give false negative results certain subtypes

Treatment is supportive› Transfusions/Folic Acid supplementation› Avoiding precipitants of hemolysis

Autosomal Dominant, mostly commonly in people of Northern European decent

Defect in a membrane cytoskeletal protein leading to spherocyte formation

Physical Examination: splenomegaly secondary to extravascular hemolysis

Peripheral blood smear: Spherocytes Diagnosis: Osmotic fragility test Treatment: splenectomy (corrects

anemia, not underlying defect) and supportive transfusions

Small, dark, dense, hyperchromic red blood cells lacking central pallor

Increased MCHC

Immune Related› Transfuision Reactions› Cold Agglutinin› Warm Auto Antibody

Non-immune related› Microangiopathic Hemolytic Anemia› Infection› PNH› Prosthetic Heart Valves

Potential Causes› TTP/HUS› DIC› Malignant Hypertension› Metastatic Malignancy

Malfunction of coagulation/secondary hemostasis Usually secondary (Infection, trauma, immune-

mediated reactions, obstetric complications) Inappropriate systemic thrombosis of small/mid-

sized vessles Depleted clotting factors leading to potential for

life-threatening hemorrhage Labs: in addition to anemia

› Thrombocytopenia› Abnormal coagulation tests› Elevated fibrin split products› Decreased fibrinogen

Peripheral Smear: Schistocytes Treatment aimed at underlying disorder

› Patients are usually gravely ill

Microangiopathic hemolytic anemia and thrombocytopenia

Neurologic changes, Fever, Renal Dysfunction (Predominates in HUS)

Involves microvascular damage and platelet destruction/aggregation; high shear stress and endothelial damage

Typically sporadic; HUS can be associated with verotoxin and E. coli O157:H7 (typically in children)

Classis Pentad of Findings› Thrombocytopenia (typically <40,000)› Microangiopathic Hemolytic Anemia

Elevated LDH, Decreased Haptoglobin, elevated reticulocyte count, peripheral smear schistocytes

› Neurologic Changes› Renal Dysfunction

Elevated Creatinine, Decreased Urine output› Fever

Bleeding › Coagulation studies typically normal

Abdominal Pain/Nausea/Vomiting/Diarrhea

Additional Potential Etiologies: › Drug exposure: Quinine, Mitomycin C,

Bleomycin, Cisplatin, Cyclosporine, Plavix› HIV infection› Systemic Lupus Erythematosis› Metastatic Adenocarcinoma

Treatment: Urgent Plasmapheresis

Metastatic Cancer to the Bone Marrow Leukemias/Lymphomas/Myelomas

Peripheral smear: Nucleated RBC, teardrop cells, immature WBC

Bone marrow biopsy core usually needed for diagnosis; often a “dry tap”

Heterogeneous group of clonal hematopoietic stem cell disorders with the presence of dysplastic changes in one or more cell line

Associated with inappropriate apoptosis and excessive bone marrow proliferation

Peripheral cytopenias and dysplastic changes in the bone marrow

Mean age of diagnosis: 68 Slight male predominance Environmental Links:

› Smoking, benzene, organic chemicals, herbicides, pesticides, fertilizers, petroleum and diesel derivatives

Prior Chemotherapy or Radiation› Melphalan, chlorambucil,

cyclophosphamide

Refractory cytopenias Anemia and fatigue

› Macrocytic or normocytic Infections, bleeding

Symptoms depend on cytopenias present and their severity

CBC: Macrocytic anemia (other cytopenias)

Low reticulocyte count Peripheral Smear: macrocytic red cells,

hypogranular granulocytes with pseudo-Pelger-Huët anomaly, giant platelets

Bone Marrow Biopsy

Type of MDS Peripheral Blood Blasts

OR

Bone Marrow Blasts

Refractory Anemia (RA) ≤1% <5%

Refractory Anemia with Ringed Sideroblasts (RARS)

≤1% <5%

Refractory Anemia with Excess Blasts (RAEB)

<5% 5-20% (1:5-9%; 2:9-19%)

Refractory Anemia with Excess Blasts in Transformation (RAEB-T)

≥5% 21-30%

Chronic Myelomonocytoc Leukemia (CMML)

<5% ≤20% with >1000 Monocytes/microL

Usually supportive Dependent on degree/severity of

findings

Erythropoietin support Transfusion support Chemotherapy Bone Marrow Transplantation

Due to Erythropoietin Deficiency Generally anemia begins when the

creatinine clearance in <45 mL/min and worsens with increasing renal failure

Treat underlying CKD and cause Can support with subcutaneous

erythropoietin with adjustment in dose based on response

Laboratory finding of increased RBC number and subsequently hemoglobin and hematocrit

Can be primary (Polycythemia Vera) or secondary

Initial evaluation: determine underlying cause and minimize potential complications

Hypertension Thrombosis Pruritus Erythromelalgia Joint Pain Headache Weakness Visual disturbance Weakness

Palpable splenomegaly

Gout/Kidney stones (increased cellular turnover)

Suspected when hematocrit elevated Can also have associated elevation in

platelets or white blood cells Erythropoietin level

› Low in Polycythemia Vera› High in Secondary Polycythemia

Oxygen saturation› Low levels can suggest secondary causes

JAK-2 Mutation Status› JAK2 V617F mutation is identified in >90% PV

Complete evaluation for secondary causes

Hypoxemia leading to EPO overproduction› Lung disease, high altitude, smoking, right-to-

left heart shunts, sleep apnea, obesity hypoventilation

EPO overproduction› Tumors – renal, hepatoma, fibroids,

pheochromocytoma Androgen Therapy Relative Erythrocytosis (decreased plasma

volume)› Diuretics, blood doping

Most common myeloproliferative disease

Diagnosis requires either Both Major and 1 Minor or 1st Major and 2 Minor Criteria

Major Criteria

Hemoglobin >18.5/16.5g/dL

Presence of JAK2 mutation

Minor Criteria

Bone Marrow Biopsy: Hypercellularity for Age with prominent erythroid proliferation

Low EPO level

Endogenous erythroid colony formation in vitro

Goal: reduce blood volume to normal and prevent complications (thrombosis)

Phlebotomy to a goal Hematocrit of <45% for men; <42% for women

Aspirin Therapy If refractory to Phlebotomy: hydroxyurea Can progress to myelofibrosis and/or

acute leukemia

Immune system cells involved in protecting the body from infectious disease and foreign invaders

Derived from a mulitpotent stem cell in bone marrow (hematopoietic stem cell)

Several types of leukocytes with different primary functions

When evaluating abnormalities in WBC number must also consider which sub-type of WBC is involved

Neutrophil – mature WBC of the Granulocyte series; part of the innate immune system

Lymphocyte – facilitate humoral and cellular immunity against foreign proteins and pathogens.

Monocyte – Large phagocytic WBC; serves as part of the innate immune system

Eosinophil – WBC implicated in inflammatory/allergic response

Basophil – WBC that is active in the inflammatory response


White Cell Disorders› Leukocytosis

Neutrophilia Lymphocytosis Monocytosis Eosinophilia

› Leukopenia Platelet Disorders

› Thrombocytosis› Thrombocytopenia

Primary› Myeloproliferative

Disorders (CML, PV, ET)

› Chronic Idiopathic Neutrophilia

› Down’s Syndrome

Secondary› Infection› Stress (physical or

emotional)› Drugs – steroids,

lithium, G-CSF› Non-hematologic

malignancy› Asplenia

Uncontrolled proliferation of mature and maturing granulocytes

Associated with the fusion of two genes:› BCR on chromosome 9› ABL1 on chromosome 22

Reciprocal translocation creates the fusion protein BCR-ABL

Up to 50% can be asymptomatic

Malaise/Fatigue Weight Loss Night sweats Splenomegaly/Andominal discomfort

Leukostasis – Headache, neurologic deficits (usually with WBC>300,000)

High leukocyte count Hypercellular marrow Basophilia PCR/Chromosome analysis for BCR-ABL

Peripheral smear: Left shifted WBC (myeloblasts, myelocytes, metamyelocytes and band forms) and Basophilia

Phase Symptoms/Signs

Chronic Gradual rise in WBC, splenomegaly, hyperleukocytosis<15%/20% blasts PB/BM<20% Basophils

Accelerated Escape of blood counts from treatment controlMyelofibrosis>15-30%/>20-50% blasts PB/BM>20% basophils

Blastic Weight loss, B symptoms, bone pain, increased blastsMarrow Failure : thrombocytopenia and anemia>30%/>50% blasts PB/BM

Drugs targeting BCR-ABL tyrosine kinase Can provide long term disease control Supplanted previous standard therapies

such as bone marrow transplant

Imatinib mesylate (Gleevec) was the initial targeted therapy developed for this indication

Several additional second and third generation TKI drugs are available and can be used in firs or subsequent lines of therapy

Reactive› Viral infections:

EBV, CMV, VZV, influenza

› Other infections: pertussis, toxo.

› Stress: trauma, smoking

› Autoimmune: LGL, RA

Malignant› ALL› CLL› Follicular

Lymphoma › Marginal Zone

Lymphoma› Hairy cell› Other Lymphomas

Evaluation: Blood Lymphocyte Morphology Peripheral Blood Flow Cytometry

Neoplasm of small mature lymphocytes Can involve peripheral blood, bone

marrow, organs or lymph nodes (SLL) Most common leukemia in United States Diagnosed by the demonstration of an

absolute lymphocytosis and a clonal population of lymphocytes expressing CD5, CD19, CD20 and CD23 along with low levels of surface immunoglobulins

Lymphocytosis on screening blood test Asymptomatic lymphadenopathy

Abdominal fullness Fatigue/decreased exercise tolerance Other constitutional symptoms

Most patients with early CLL are asymptomatic and have a relatively good long term prognosis

Historically several trials of early chemotherapy did not demonstrate survival benefit

Deferral of treatment/Watch and Wait is the standard of care for early stage disease with monitoring every 3-6 months

Treatment is reserved for symptomatic or rapidly progressive disease

Usually <10% of total WBC Relatively non-specific finding

Asplenia Inflammation (sarcoid, IBD) Autoimmune Disorders Steroids Infections (VZV, TB, malaria) Malignancy (Hodgkins, CMML)

Numerous allergic, infectious and neoplastic disorders

Allergic – Atopic, Medications (NSIDS, ASA, allopurinol, PCN, cephalosporins)

Infectious – parasitic, fungal Specific organ disease – eosinophilic

esophagitis, asthma, skin disease, renal/vascular disease

Hematologic Neoplasm – Hypereosinophilic syndrome, tumor associated, mastocytosis


White Cell Disorders› Leukocytosis› Leukopenia –

Neutropenia: ANC <1500 Lymphopenia: ALC <1000


Widely variable implications; life-threatening to benign

Benign (familial) Neutropenia› African, W Indian, Sephardic Jews, Yemenites, Arab

Jordans Acquired Neutropenia

› Post infectious (bacterial, viral, paracytic)› Drug-induced – within 3 months› Autoimmune/Collagen Vascular Disorders› Immune Mediated

Hospitalized Patient› Drugs, Toxins, Sepsis, Virus› Bone marrow failure (rarely isolated neutropenia)

Infections: TB, HIV, hepatitis, malaria Congenital Immune Deficiencies Immunosuppressive therapy: Rituxan,

steroids Chemotherapy/Radiation Autoimmune disorders Lymphoma Sarcoid Alcohol Abuse Malnutrition

Laboratory finding of elevated platelets >450,000/microL

Can be primary (essential thrombocytosis) or secondary

Is the thrombocytosis reactive or a result of bone marrow overproduction?

Is there any immediate risk to the patient?

Asymptomatic Laboratory Finding Vasomotor symptoms: Visual

disturbance, Lightheadedness, Headaches, Palpitations, Atypical Chest Pain, Erythromlealgia, Paresthesias

Thrombosis (15% at presentation) Major Hemorrhage (5-10% of patients

over disease course) Splenomegaly (less than 50%)

Iron Deficiency Severe Trauma/Burns Post-Splenectomy or CABG Metastatic Malignancy Acute Pancreatitis Chronic Infections (TB) Rheumatologic Disorders/Vasculitis IBD/Celiac Disease

Careful patient history to exclude reactive causes of thrombocytosis

Iron Studies, CRP/ESR, Peripheral Smear

JAK-2 Mutation (present in 55-60% of essential thrombocytosis cases)

Bone Marrow Biopsy (increased Megakaryocytes)

One of the myeloproliferative disorders

WHO Criteria for Diagnosis of ET

Sustained Platelet Count >450,000

Bone Marrow showing proliferation of Megakaryocytes

Does not meet the criteria for the diagnosis of another MPD

JAK2 mutation positive or, if JAK2 negative, an unrevealing evaluation for secondary causes of thrombocytosis

Decision to treat is based on risk stratification

Low Risk Age <60No CV Risk FactorsPLT <1,500,000No prior thrombosis

Consider ASA

Intermediate Risk

Not High or Low Risk Consider ASA

High Risk Age >60Prior thrombosis

Consider ASA and Cytoreductive therapy

Patients >60 years, Aspirin should not be used if platelets >1,500,000 because of increased risk of bleeding

Low and Intermediate Risk patients should be observed and cytoreductive therapy initiated when platelets are >1,500,000

Myelosuppressive Agents – Hydroxyurea (usually the first agent of choice)

Maturation Modulators – Anagrelide Antiplatelet Agents Plateletpheresis – in extreme, acute

situations

Goal of cytoreductive treatment should be a sustained platelet count <400,000

Platelet count less than the lower level of normal (130-150,000/microL)

Surgical Bleeding (solely due to low platelets) starts with <50,000/microL

Spontaneous Bleeding <10-20,000/microL

Decreased Platelet Production› Infection: HIV, hepatitis C, parvovirus› Chemotherapy/Radiation› Alcohol› Congenital/Acquired Bone Marrow Failure

Increased Platelet Destruction› Drugs: heparin, Valproic Acid, quinine, Bactrim,

Digoxin, Amiodarone, H2-blockers› Autoimmune Platelet Destruction: ITP, TTP/HUS› DIC

Pseudothrombocytopenia› Platelet Clumping

Inadequately anti-coagulated or incompletely mixed samples can form a clot that traps platelets

Exposure of blood to the anti-coagulant EDTA may induce platelet clumping; platelet clumps are counted as leukocytes instead of platelets› 0.1% of people have EDTA dependent

agglutinins

If observed platelet count should be repeated using heparin (green top tube) or sodium citrate (blue top tube) as the anticoagulant

If citrate is used as the anticoagulant the platelet count should be adjusted based on a correction factor to account for dilution

Acquired thrombocytopenia caused by autoimmune destruction of platelets

Typical presentations:› Markedly reduced platelet counts and

mucocutaneous bleeding› Asymptomatically with mildly decreased

platelets found incidentally Generally idiopathic but can be

associated with disorders of immune dysregulation or lymphoproliferation

No single test is diagnostic of ITP; primarily a diagnosis of exclusion

New onset isolated thrombocytopenia with no other readily identifiable cause

Requires careful review of patient’s medications, peripheral smear review and screen for viral causes

Initial Management: Corticosteroids› 60-75% initial response rate

Additional Treatments:› IVIG 1gm/kg x2 days› Anti-D 75 mcg/kg/day (Rh+, non-anemic

patients only)› Rituxan 375mg/m2 IV weekly x4 doses› TPO Agonists

Romiplostim (N-plate) Eltrombopag (Promacta)

Aplasia Acute leukemia, myelodysplasia,

myeloma Infiltration with lymphoma, solid

tumours, tuberculosis Megaloblastic anemia Paroxysmal nocturnal hemoglobinuria Myelofibrosis

Group of disorders characterized by uncontrolled proliferation of myeloid or lymphoid progenitor cells that gradually replace normal hematopoiesis in the bone marrow› Acute Myeloid Leukemia (AML)› Acute Lymphoblastic Leukemia (ALL)

Several subtypes exist based upon the specific cell type which has become malignant

Usually present with bone marrow failure and pancytopenia

Tissue infiltration by leukemic blasts Fatigue, dyspnea, fever, infection,

bleeding, bone pain Anemia, thrombocytopenia,

neutropenia, DIC, hyperuricemia, elevated LDH

Elevated peripheral blood WBC with increased blast population

Therapy is individualized based on patient factors (age, co-morbidities) and disease factors (sub-type, molecular mutations, cytogenetics)

High dose chemotherapy Bone Marrow Transplant Palliative chemotherapy Primary palliative care

Lichtman, M. et.al. Williams Hematology, seventh edition. McGraw-Hill Medical. 2006

Rodgers, G. and Young, N. The Bethesda Handbook of Clinical Hematology, second

edition. Lippincott, Williams and Wilkins. 2010. Images from UptoDateOnLine as sited.

recognize normal/abnormal results and understand their implications interpret abnormal results,...

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