Hematology

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Hematology
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  1. Anemia is?
    • •A decrease in one or both:
    •    –Hemoglobin
    •    –Hematocrit
    •     •General rule, Hct = 3 X Hgb value 
    •      HGB 10 then HCT=30
    • •Multiple Causes
    • •<RBC  = < O2 carrying capacity
    •      •Symptoms depend on age, severity and compensation capability of CV and Pulm systems
    • •Treatment
    •     – underlying causes
  2. Criteria for anemia
    • WHO criteria
    •     –Males
    •         •Hgb < 13 g/dL or Hct < 41 %
    •     –Females (menstrating)
    •         •Hgb < 12 g/dL or Hct < 36 %

    • CDC more age specific criteria in 1998 (summary)
    •   –Males
    •      •Aged 12 to < 15, Hgb <12.5 and Hct< 37.3
    •      •Aged 15 and up, Hgb <13.5 and Hct <39.9
    •    –Females (menstrating)
    •      •Aged 12 to < 15, Hgb <11.8 and Hct <35.7
    •      •Aged 15 and up, Hgb <12 and Hct <35.9
    • –excluding smokers and those living at high altitudes ( this increases hemegolobin)
  3. Who are prone for anemia and why?
    •Infants, adolescents, menstrating women, and pregnant and lactating women are more likely to become anemic due to increased nutritional needs
  4. What is Mean Corpuscular Volume (MCV)
    • Measures size of cell
    •     •Microcytic or Macrocytic
  5. What is Mean Corpuscular Hemoglobin Concentration (MCHC and MCH)
    • –Amount of pigment
    • –Average amount of Hgb/RBC
    •     •Microchromic or Macrochromic
  6. What is the implication of
      MCV
      MCH
      MCHC
    • •Average red blood cell size (MCV)
    • Hemoglobin amount per red blood cell (MCH)
    • •The amount of hemoglobin relative to the size of the cell (hemoglobin concentration) per red blood cell (MCHC)
  7. Norm range of MCV and typing
    • MCV: 80 to 100 femtoliter
    •    -•machine measured
    • MCV less than lower limit of normal: microcytic anemia=<80
    • •MCV within normal range: normocytic anemia
    • •MCV greater than upper limit of normal: macrocytic anemia=>100
  8. What is  norm range of MCH
    • –MCH: 27 to 31 picograms/cell
    •    •MCH = Hgb/RBC count

    • MCH less than lower limit of normal: hypochromic anemia
    • MCH within normal range: normochromic anemia
    • MCH greater than upper limit of normal: hyperchromic anemia
  9. What is norm range of MCHC
    • –MCHC: 32 to 36 grams/deciliter
    •       •MCHC = Hgb/Hct
  10. Serum Ferritin level
    • •Serum Ferritin 2-20 mcg/dL
    •      –Measures iron stores
    •      –First to drop during blood lost
  11. Serum Iron
    • •Serum Iron 50-150 mcg/dL
    •     –Measures circulating iron
    •     –Drops after serum ferritin
  12. Total iron binding capacity (TIBC)
    • –Ability of cells to bind to iron
    •     •What the iron would be if all transferrin were saturated
  13. Causes of anemia
    • •Blood Loss
    • •Inadequate Production
    • •Excessive Destruction
  14. Microcytic Etiology
    • Iron deficiency (late)
    • Anemia of chronic disease
    • Thalassemias*
    • Sideroblastic anemias
    • Hemoglobinopathies
    • Plumbism   (lead poisoning)
  15. Normocytic etiology
    • Acute bleeding
    • Hemolytic anemias
    • Chronicrenal failure or Anemia of chronic disease(early)
    • Aplastic anemia
    • Hypothyroidism
    • Sickle cell anemia*
    • Marrow   infiltration (neoplasm, fibrosis, or granulomas)
    • Iron deficiency (early)
    • B12 or folate deficiency (early)
  16. Macrocytic etiology
    • B12 or folate deficiency (late)
    • Hemolytic anemias (more severe)
    • Chronic liver disease
    • Alcohol excess (elevated GGT)
    • Aplastic anemia
  17. Anemia Classification
    • •Mild–Hgb 10-14 g/dl
    • •Moderate–Hgb 7-9 g/dl
    • •Severe–Hgb 4-6 g/dl
  18. S/S ofd anemia
    • •Mild
    •   –Asymptomatic
    • •Moderate
    •    –Fatigue
    •    –Dyspnea on exertion
    • •Severe
    •    –Exhausted
    •    –Severe palpitations
    •    –Sensitive to cold
    •    –Anorexia
    •    –Dizziness
    •    –Headache
  19. Type of Anemia
    • •Acute (blood loss) Normcytic
    • •Iron Deficiency=mircocytic
    • •Vitamin B12 Deficiency/Macrocytic Anemia
    • •Anemia of Chronic Disease=micrcytic
  20. Acute blood lost
    • •Blood loss
    • Normocytic Anemia
    • •Hgb/HCT abnormal
    • •Other endices are normal

    • •Treatment
    •     –Stop the Bleeding
    •     –Depends on Hgb/HCT
    •           –Possible blood transfusion
  21. IronDeficiency Anemia
    • •Microcytic Anemia
    • •Prevalence:
    •     –20%Women
    •     – 3% men
    •     –50% Pregnant women
    •     –17% elderly (>75 years)

    • •Most adults consume enough iron so etiology is often:
    •      –Chronic, occult blood loss
    •      – usually from GI tract or menses
    •      –Malabsorption
    •            •Gut issues
    • >abd pain/ 40 and older think rectal exam.  r/o GI bleeding

    • Two reason of <iron level
    •    Blood lost
    •    Poor absortion
  22. Symptoms IronDef.  Anemia
    • •Blue color to whites of the eyes
    • •Brittle nails/up turned (koilonychia)
    • •Decreased appetite
    • •Fatigue
    • •Headache
    • •Cracks in corners of mouth (Cheilitis)
    • •Irritability
    • •Pale skin color
    • •Shortness of breath
    • •Sore tongue
    • •Pica
    • •Weakness
    • •Tongue enlarged (atropic glossitis)
  23. History
    • •Menstrual Cycles ask when LMP
    • •Change in stool pattern/color
    • •Dietary intake/ can have do a 24 hr diet
    • •Medications
    •      –OTC meds 
    •      – NSAIDS/Kidney and GI
    •      –Coumadin/Plavix, ASA
    •      -Herbal (ginesing, garlic)
  24. Iron total
    • Total body 3 to 4 g
    • Hemogoblin 2g
    • protien/enzymes 400mg
    • transferrin 3 to 7 mg
    • ferritin/hemosiderm 1g

    • Adult males loses 1g daily/easily replace via diet
    • Women iro loss is 1.5g with additioanl 700mg during pregnnacy.
  25. Type of stored iron
    • Ferrintin
    •    stored in bone marrow or liver.
    •    Used as marker for iron deficiency or        overload. (total body store) 
    •    <15ug/L is dx of iron deficiency
    •    erythrocyte zinc protoporphyrin also used as marker for iron deficiency
    •    
    • Hemosiderm
    •    Iron stored in macrophage
    •   
  26. Total iron binding capacity (TIBC)
    Increase with iron deficiency. 
  27. What are the stages of iron deficiency anemia
    • 1.negative iron blanace (comp by stored iron) serum lvl normal. ferritin decrease. Pulling from stored iron (ferritin)
    • 2.Iron defienct erythropoiesis: TIBC may elevate.  If transferrin sat < 15% hemo systhesis stops.
    • 3.Iron defiency anemia: HH falls.  Bone Marrow hypoproliferate, RBC are mirocytic and hypochronic.
  28. Diagnostic testing for anemia
    • CBC
    • •MCV
    • •MCH
    • •Serum ferritin
    •     –1st to drop
    • •Serum Iron
    •     –2nd to drop
    • •TIBC
    •    –Normal
    •    - High
  29. Serum value of iron deficiency
    • serum ferrtin <
    • serum iron <
    • transferrin sat % <
    • total iron binding capcity(TIBC) >
    • mean corpuscular volume < mircocytic/ hypochromic
  30. Beta thalassemia anemia
    • serum ferrtin =
    • serum iron = or >
    • transferrin sat % = or >
    • total iron binding capcity(TIBC) >
    • mean corpuscular volume < mircocytic/ hypochromic
  31. Anemia of chronic inflammtion
    • serum ferrtin = or >
    • serum iron = or <
    • transferrin sat % <
    • total iron binding capcity(TIBC) = or <
    • mean corpuscular volume = or < microcytic
  32. Treatment for anemia
    • • Must Identify cause (men and post-menopausal women mandate GI eval to r/o CA
    •     –Diet
    •      –Blood lost =Occult blood/ urine analysis
    • •Try diet first
    • •Supplemental Iron
    •      –Ferrous Sulfate 325 mg po TID
    •             •On an empty stomach
    •             •3 - 6 months
    • –Recheck MCV 2 – 4 wks to ensure working
    •                       micro to norm
    • Failure to improve 
    •    failure to absorb
    •    excessive blood lost
    •     noncompliant
    •    incorrect diagnosis

    • Parenteral iron
    •    iron sucrose
    •    iron dextran - potential severe reaction
    •    sodium ferric gluconate

    PRBC is not ideal treatment for iron anemia
  33. Anemiaof Chronic Disease
    • •Microcytic
    • •Inflammatory diseases
    •       –Infection
    •       –Malignancy
    • •Unknown Etiology
    •       –Blocks the transfer of iron from stores to bone marrow
    •        = decrease  erythropoesis
    • •Note–Not destruction of RBC’s
  34. Diagnosis of Anenia of chronic origin
    • •History
    •     –Infectious or inflammatory process
    • Serum Ferritin
    •      –Normal to high
    • •Serum Iron
    •     –Low
    •  •TIBC
    •     –High
  35. Anemia of chronic disease
    • •Microcytic
    • •Inflammatory diseases
    •       –Infection
    •       –Malignancy
    • •Unknown Etiology
    •       –Blocks the transfer of iron from stores to bone marrow
    •        = decrease  erythropoesis
    • •Note–Not destruction of RBC’s
  36. treatment for Anemia of chronic origin
    • Transfusion
    •       –HCT falls below 27%
    • •Hgb would be ____9=x3 of __27__?
    • Erythropoietin
    • Hematology Consult
  37. Thalassemia
    • Inherited disorder of the hemoglobin chains2 a and 2b chains
    •     –Relative deficiency
    •           •Thalassemia minor
    •           •Thalassemai trait
    •      –Complete deficiency
    •           •Thalassemia major
  38. Chains of Thalassemia
    • Alpha thalassemia minor (surive)
    • Beta thalassemia minor (surive)
    • Alpha thalassemia major
    •      –Fetus always dies in utero
    • Beta thalasemia major
    •        –Major anemia
    •        –Most die very early
    • Mediterranean descent
    •       –Asians and Africans also
  39. Diagnositic Trait of thalessemia
    • •Electrophoresis of Hgb A2 and F
    •      –a minor or trait
    •            •Normal Hgb A2 and F
    •       –B minor
    •            •Elevated A2 and/or F–b major
    •            •Hgb F is primary found–Variable
    •                amounts of A2
  40. Treatment of thalessemia
    • Trait and minor
    •     –Mostly dietary
    •          •Folic Acid
    •          •Vitamin C
    • Major
    •      –Blood transfusions
    •      –Supplement
    •           •Folic Acid
    •           •Vitamin C
  41. What is the etiology of megalobastic anemia
    • Impaired DNA synthesis.
    • RBC will be Macrocystic

    • No B12(cobalamin) or folate acid available for DNA synthesis = macrocytic RBC
    • Normally B12 deficiency develops over a long period.

    In the stomach B12 bind to Intrinic Factors (secreted by partietal cells).  Then IF releases B12 at ileum where it is then absorbed. 

    Any surgical or pathological changes of GI can disrupt this process and cause decrease absorption (B12 deficiency).
  42. VitaminB12 Deficiency Anemia
    • Macrocytic Anemia
    • Not dietary deficiency (adult only require 1-2ug daily)
    •        –Liver stores enough for years
    • Hereditary
    •       –Pernicious anemia
    •            •Deficiency of intrinsic factor from    parietal cells in the gastric mucosa.
    • Autoantibodies to gastric parietal cell causes gastritis and decrease IF production.  It also interference with B12 binding sites. 

    Macrocytosis anemia can also occur with folate deficiency, liver diseas, alcohol ingestion ( cells abosorb cholestrol)
  43. Pernicious Anemia
    • More prodominate in elderly
    • Associated with other autoimmune disorder like subacute Thyorditis.
    • Higher risk of gastric CA in this population 8%
    • Testing of anti-intrinsic factor antibodies= + result indicates (Pernicious anemia)
  44. VitaminB12 Deficiency Anemia
    • •Decreased absorption
    •       –Gastric mucosal disease/Chron’s disease
    •       –Gastric resection/Bypass–Inflammatory bowel disease
    • •Women > Men 5:1
    • ->40 years
  45. S/S B12 deficiency anemia
    • •Hematologic abnormalities often develop before onset of neurologic disease
    • Physiological presentation
    •    Pallor
    •    dyspnea
    •    dizziness
    •    high out HF
    •    syncope
    •    Smooth beefy red tongue
    • Neurological changes
    • •Paresthesias
    • •Numbness
    • •Ataxia
    •   hypoflexia
    •   impaired vibration and position sense

    Remember neuro changes think B12 deficiency
  46. Folate Deficiency
    • Macrocytic Anemia
    • Nutritional deficiency 
    •       -Requires high folate intake, body has low storgage
    •       –ETOH Abuse (check GGT) 
    •               •alcohol inhibits conversion to active folate 
    •       –pregnancy Develops quickly due to high demands
    •        –lactation  high demand
    • Malabsorption
    •       –Chron’s disease
    •       –Intestinal parasites/ if folate low Medication 
    •       Impair folate metabolism
    •         Phenytoin, Bactrim, methotrexate

    Unresponsive person to give 3 drug Narcain, dextrose, thiamine.
  47. S/S of Folate deficient anemia
    • Similar to B12 deficiency
    • No Neurologic symptoms
  48. Physical exam of  B12 deficient anemic tougue
    • Tongue
    •    •Shiny
    •    •Glazed
    •    •Beefy Red
  49. physical exam of Anemia for either B12 or Folate deficiency
    • Toungue=glosstitis
    • Skin/eye=Icterus (RBC destruction)
    • •Abdomen
    •     –Tenderness
    •      –Organomegaly/ spleenmegaly/   
    •           hepaticmegaly 
    • •Neurologic
    •    –May have peripheral nerve weakness
    •          •Vitamin B12 Deficiency
  50. Diagnosis Anemia
    • B12 deficiency
    •      –Low  Serum B12
    •       –Normal Folate
    •       -elevated MMA (methymalonic acid)
    • Folate Deficiency
    •      Normal Serum B12
    •      –Low Folate
    •      - No MMA
    • Liver enzymes elevated
    •       •In ETOH abuse/ liver disease anemia
    • -Homocysteine level are increase in both deficiency.
    • Methylmalonic acid (MMA)
    •      serum/urine elavtion only with B12 deficiency
    • Pernicious Anemia
    •     -antiantibodies IF (intrnic factor)
    •     - Schilling test


  51. ShillingTest
    • Differentiates Pernicious anemia from malabsorption syndrome
    •    –Radioactive cyanocobalamin given orally 
    •    –Then a parenteral flushing dose of the nonradioactive vitamin,
    •    – the percentage of radioactivity is determined in the urine excreted over a 24-hour period.
  52. SchillingTest
    • •The test is usually done three times
    •    – first with added  intrinsic factor (glycoprotein)
    •    –then without it,
    •     –and then after antibiotic therapy.
    •     –The results are used in the diagnosis of pernicious anemia and other disorders of vitamin B12 metabolism.
  53. B12 and folate anemia treatment
    • •Monthly B12
    •     –1000 micrograms IM
    •     -Oral B12
    •     –Continue treatment throughout lifetime
    •     –Common with malabsop/chronic diseased state. 
    • Folic Acid (dietary problem)
    •      –1-5 mg/day until normal Hct
    • Dietary counseling
    • -Pernicious Anemia
    •       treated with B12 injections
    •       high dose or oral B12
  54. SickleCell Anemia
    • Autosomal Recessive
    •    -•0.3% of African Americans are homozygotes
    •     –Abnormal Hgb SSickle Shape
    •     -Chromo change of valine for glutamine at 6th amino acid of beta chain
    •     -Sickle shape stiff=vaso occulsion = ischemia
    •    -10-20 day hemolyze (norm 120) anemia
    •    -vasco occlussion (hallmark symptom), infections, hemo crisis, also stokes, hematutia, leg ulcer, splenomegaly
    •     -anemia and > risk of bilary complication due to rapid hemolyzing.
    •     -first presentation in childhood(10) pain of extremities (dactylitis) most common initial sign.
    •  - Age of pain (20-40). True crisis usually dont live pass 30-40
    •  -Most common tissue of pain=bone, chest, abdomen, extremties, back
    •  -exacerbation of pain=stress, dehydration, infection, alcohol, menes, hypoxia
    • - Kidney 50% abnorm due to Renal infract= isosthenuria (< urine concentration) 
    •  
    • •13% of African Americans are
    • heterozygotes (Siclkle cell trait) SCT
    •     –Carriers/ Can be symptomatic but mostly asymptomatic
  55. DX SCD
    • Anemia Hgb (8-10) mild
    • Reticulocystosis (3-15%)
    • MCV (high) due to high MCV
    • high unconjugated indirect bilrubin
    • elevated lactate dehydrogennase
    • low haptogolbin

    Reticulocyte and Howell-jolly bodies indicates hyposplenism
  56. SickleCell Crissis
    • Sickling of cells causing vaso-occlusive disease
    • •Precipitated by
    •     –Heat
    •     –Cold
    •     –Infection


    Why morphine is important= it dilate vessel increasing fluid viscosity=O2 assist with tissue perfussion. Hydration also importanbt
  57. Sickle cell pain site
    • Lumbar Spine
    • Hips
    • •Knees
    • Femurs
    • Rib/Sternum
    • •Abdomen
    •    –Difficult to r/o surgical abdomen
    • -Priapism 35% > 3hrs emergency
  58. Treatment of pyrexia for Sickle cell
    • Broad-spectrum antibiotics
    •     –Start while searching for cause
    • Aggressive fever control
    • Pneumo- cocci and Haemophilus influenzae cause high mortality
    • Fever needs to be aggressive in treatment = Tylenol, culture then antibiotic.Must reduce fever= > fever increase slicking of cells
  59. Increased Bilirubin in Sickle cell
    • •Secondary to increased RBC destruction
    • Cholelithiasis is common (75%).

    increase RBC rupture due to sickle
  60. AcuteChest Syndrome
    • •Occurs in 40% of patients with sickle cell anemia
    • •“Pleuritic" chest pain
    • -Vaso occulssion or pulm fat embolism of lung  causing infarction.
    •     –s/s Fever, hypoxia, cough, dyspnea, rales, and rhonchi 
    •   Rapid decrease in Hgb with increased platelets and WBC
    • Platelet > due to clotting ; WBC > trauma
    •  -New lung infiltrate/ rapid onset think bact, fat, or vaso
    • -RHF or chronic Pulm HTN= chronic pulm artery vaso occ.
    • Major source of mortality

    Must r/o ACS
  61. AcuteChest Syndrome
    • Delayed development of infiltrates on CXR
    •     –Difficult to differentiate from pneumonia
    •     –This is a Inflammatory response
    •       =decrease HGB result rapid hypoxia
    • Rapid cycling of deterioration
  62. aplstic crisis in SCD
    • Sudden decrease of hemoglobin and reticulocyte count. 
    •   -Insult to Bone marrow
    •       Parvovirus B19 infection
    •       Folate deficiency
    •       
    •     
  63. Infection crisis of SCD
    • due to asplenia
    •  -low IgM
    •  -impaired opsonization pathyway
    •  -defective immunity to encapsulated Bact
    •     H. influ
    •     strep pneu
    •  Increase subsceptibility  to
    •    Mycoplasm Pneu
    •    Salmon typhim
    •    Staph aure
    •    E coli

    Must have pnuemo vaccine.
  64. AcuteSplenic Sequestration Syndrome
    • •Causes Hgb to drop from 3 to 6 gdl due to acute massive pooling of erythrocytes=-hypovolemic shock
    • •Many have spleen removed
    •    -increase risk of infection
  65. SickleCell Trait
    • •Sloughing of papilla
    •     –Trouble concentrating urine
    • •Extremely rare to have Sickle Cell Crisis

    Lost of concentration of urine=dehydration > sickle
  66. Treatment of Sickle cell crisis and acute chest syndrome
    • •Sickle crisis and acute chest syndrome
    •     –Pain Control
    •        •Morphine IV dilated
    •     –Hydradtion
    •     –Transfusion
    •         •Cardiopulmonary failure
    •         •Hgb < 5mg/dl
    •    –Admit for fever >38o C (>101 F)
    •         •Tylenol
    •    –IV Hydration
    •    –IV ABX
  67. Chronic/ProphylacticTX plan
    • •Infection Prophylaxis
    •     –Vaccines
    •        •Pneumoccocal and H. influenzae
    •        •PCN daily – especially in children
    •  •Folic Acid–1 mg/day
  68. Hydroxyurea
    • •Reduced by half
    •     –Painful sickle cell episodes or crises
    •     –Hospitalizations for painful episodes
    •     –Episodes of acute chest
    •     –Units of blood that patients receive
    • •The first agent approved for the prevention of painful episodes in adult patients with sickle cell disease.
  69.  Prognosis
    • •Bone marrow transplant has be successful in small groups of people
    • •Life expectency has increased to 40–50 years
    • •Leading cause of death
    •    – all ages
    •    –Stroke–MI/Cardiac Arrest
    •     –Renal Failure
  70. WBCs
    • •Granulocytes
    •     –Neutrophils
    •           •Bands
    •           •Segs
    • –Basophils
    • –Eosinophils
    • •Agranulocytes
    •      –Lymphocytes
    •           •B and T Cells
    • –Monocytes
  71. What is left shift in WBC
    Left shift are seg and band = bacterial infection Viral infection results in increase of lymphocytes.
  72. WBCDifferential
    • •Neutrophils: 40% to 60%
    • •Bands: 0% to 3%
    • •Eosinophils: 1% to 4%
    • •Basophils: 0.5% to 1%
    • •Lymphocytes: 20% to 40%
    • •Monocytes: 2% to 8%
  73. Elevated Neutrophils
    • •Acute infection
    • •Eclampsia
    • •Gout
    • •Myelocytic leukemia
    • •Rheumatoid arthritis
    • •Rheumatic fever
    • •Acute stress
    • •Thyroiditis
    • •Trauma
  74. Decrease of Neutrophils
    • •Aplastic anemia
    • •Chemotherapy
    • •Influenza
    • •Widespread bacterial infection
    • •Radiation therapy or exposure
  75. Increased Lymphocytes
    • •Chronic bacterial infection
    • •Infectious hepatitis
    • •Infectious mononucleosis
    • •Lymphocytic leukemia
    • •Multiple myeloma
    • •Viral infection
    •      –Including mumps, measles
    • •Recovery from a bacterial infection

    Right shift, Left side still within range and > lympho.  If one side is depleted, than the shift is to opposited. 
  76. Decreased Lymphocytes
    • •Chemotherapy
    • •HIV infection
    • •Leukemia
    • •Radiation therapy or exposure
    • •Sepsis
  77. Increase Monocytes
    • •Chronic inflammatory disease
    • •Parasitic infection
    • •Tuberculosis
    • •Viral infection
    •     –infectious mononucleosis, 
    •     –mumps,
    •     –measles
  78. Increased Eosinophils
    • •Immunologic and allergic events
    •    –Allergic reaction
    •    –Cancer –Parasitic infection 
    •    –Hodgkin's disease
  79. Elevated Methymalonic acid (MMA) in serum and/or urine with elevated homocystenine
  80. Homocystine elevated in both B12 and Folate but MMA is only present in B12.  Early sign of B12 defiency before CBC indicates anemia.
  81. Decreased Basophils
    •Acute allergic reaction

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