RBCs Flashcards

1
Q

erythrocyte components of a CBC

A
  • Red Blood Cells (RBC) –> erythrocytes
  • Hemoglobin(Hgb)
  • Hematocrit (Hct)
  • Red Blood Cell Indices
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2
Q

hemoglobin

A

o Iron containing protein in RBCs that carries O2 from the lungs to the body’s tissues and CO2 back from the tissues to the lungs
o Composed of 2 subunits: beta globin and alpha globin

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3
Q

hematocrit

A

o Packed cell volume (the ratio of RBCs to total blood volume)
o Hint: Hemoglobin x 3 = estimate of hematocrit

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4
Q

mean corpuscular volume (MCV)

A

average size in volume of a RBC

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5
Q

mean corpuscular hemoglobin (MCH)

A

gives you the average amount of hemoglobin that is in each blood cell

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6
Q

mean corpuscular hemoglobin concentration (MCHC)

A

gives you the average weight of the hemoglobin based on the volume of RBCs

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7
Q

RBC Distribution Width (RDW)

A

this is a measurement that reflects the range of size in volume of RBCs; may be elevated in conditions like iron deficiency anemia, macrocytic anemia

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8
Q

Erythropoiesis

A
  • Aka hematopoiesis
  • Process of maturation of RBCs from the stem cell phase to full maturity
  • A functioning erythropoiesis feedback loop allows for the number of RBCs to maintain stable levels
  • When the body is in a diseased state, blood cells that are lost are replaced so sufficient oxygen levels are maintained
  • Erythropoietin levels in circulation increase as the levels of RBCs decrease
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9
Q

stages of maturation

A

**RBC is higher first 2 weeks after birth and then a dip from 6-12 months
**Prior to that the infant’s iron stores are reflecting the mother’s nutrition from the last trimester of pregnancy
**Definition of anemia in kids is a hemoglobin of less than the 5th percentile or a hemoglobin of less than 2 SD below the mean population for the same gender and age

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10
Q

anemia

A
  • The condition of having a lower-than-normal number of RBCs or quantity of hemoglobin (reduced RBC mass)
  • Anemia results in the diminished capacity of the blood to carry oxygen and often hypovolemia, resulting in:
    o Fatigue, weakness, pallor, palpitations, SOB, dizziness, chest pain, cold hand and feet
    o S/s hyperdynamic state, decreased CO
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11
Q

causes of anemia

A
  • Acute blood loss – overt, occult
  • Hemolytic Anemia
  • Anemia of Chronic Disease –> most common in pts with chronic kidney disease, hemodialysis, or heart failure
  • Malabsorption–> iron deficiency anemia, can be an issue in Celiac disease, H. pylori
  • Nutritional–>vegetarians are more likely to get anemias
  • Drug Induced Anemia
    o Oxidative stress–> hemolysis
    o Methemoglobinemia
    o Hemolytic anemia
  • Lead Poisoning
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12
Q

lead poisoning

A
  • Lead molecules are blocking iron absorption–> iron deficiency anemia
  • Perform lead exposure risk assessment at the following well-child visits: 6, 9, 12, 18, 24 mos, and 3, 4, 5 and 6 years of age.
  • If risk assessment is positive check blood lead level
  • Per AAP and CDC, universal screens or blood lead level tests are no longer recommended except for high prevalence areas with increased risk factors (i.e. older housing)
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13
Q

Definition of Anemia in Children: Hemoglobin

A

*Does vary by age and you have that dip from 6-12 months due to the mother’s iron stores
*At 12 months or older, if there is a Hgb of less than 11 that is considered anemic

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14
Q

screening in children

A
  • AAP recommends screening at 9 to 12 months of age
  • High risk groups should have more intensive screening premature infants, low birth weight infants
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15
Q

anemia screening in adults

A
  • Women during pregnancy??
    o USPSTF: Grade I (insufficient evidence) for routine screening of asymptomatic pregnant women
    o ACOG: screen at 1st prenatal visit
    o UTD: repeat at week 24-28
  • No routine screening in asymptomatic adults
    o Any individual with risk factors, symptoms or findings of IDA should be tested:
     Premenopausal women (heavy periods, prior pregnancies)
     Conditions with associated risk of blood loss or iron malabsorption
    o If CBC done for other reasons, review results including MCV
  • If IDA diagnosed in men or postmenopausal women – should have GI endoscopic testing
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16
Q

Classification of Anemia

A
  • Morphologic
    o Size
     Macrocytic–> abnormally large RBCs
     Microcytic –> abnormally small RBCs
     Normocytic–> normal RBCs
    o Amount of hemoglobin (color)
  • Pathologic
    o Blood loss
    o Hemolytic
    o Impaired production/underproduction
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17
Q

mean corpuscular volume (MCV): size

A
  • Normocytic: RBCs size and volume is normal
  • Microcytic: MCV is below normal range–> RBC size is below normal (small)
  • Macrocytic: MCV above normal range–> RBC size is above normal (large)
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18
Q

mean corpuscular hemoglobin (MCH)

A
  • Average amount of hemoglobin within an RBC
  • Normal adult value: 27.0-33.0 pg/cell
  • Average percentage of hemoglobin within a single RBC
  • Normal adult value: 31.0-36.0 g/dL
  • Low MCH indicates that the amount of hemoglobin per cell is abnormally decreased; often seen with iron deficiency anemia or thalassemia
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19
Q

RBC Distribution Width (RDW)

A
  • Indication of variation in RBC size
  • Normal adult value: 11-15%
  • Normally RBCs are the same size and shape
  • High RDW implies that there is a large variation in RBC size
  • RDW might be elevated in condition such as iron deficiency anemia, myoplastic syndromes, hemoglobinopathies, pts who have recently had a transfusion
20
Q

elevated RDW

A
  • Variation in size: anisocytosis
21
Q

Reticulocytes

A
  • Newly produced, immature red blood cells
  • Reflection of recent bone marrow activity
  • An increased number of reticulocytes may be seen in response to bleeding or hemolysis
  • Abnomally decreased or increased Retic Count suggest hypo- or hyperproliferative anemia
22
Q

mechanisms of anemia

A
  • Blood loss anemia—> trauma, acute GI bleed, PPH; greater than 100,000
  • Hemolytic anemia–> greater than 100,000; due to premature destruction of RBCs
  • Hypoproliferative anemia—> hallmark is a low reticulocyte count of less than 75,000
23
Q

blood loss anemia

A
  • Ask about: dizziness, falls, blood thinners, hematemesis, hematuria, melena, rectal bleeding, vaginal bleeding, menses, hemoptysis, hemorrhoids
  • Check for: hypotension/orthostatic hypotension, ecchymosis, tachycardia, trauma
  • Typical etiology: GI bleed
    o Can be hemorrhagic or slow, occult or overt
  • Slow GI bleeds present as Iron Deficiency Anemia
  • Monitor hematocrit
  • Acute vs. Chronic
    o Patients can tolerate lower HCT in chronic anemia
24
Q

hemolytic anemia

A

premature destruction of RBCs

25
Q

hemolytic anemia: can be congential or acquired

A

Congenital
o G6PD deficiency
o Sickle Cell
o Thalassemia
o Hereditary spherocytosis

Acquired
o Autoimmune (secondary to autoimmune disorders, malignancy, drugs, transfusion reactions), microangiopathy, infection

26
Q

hemolytic anemia: intravascular vs extravascular hemolysis

A

o Intravascular: destruction of RBCs in the circulation (less common) caused by mechanical trauma and infectious agents
o Extravascular: removal and destruction of RBCs by macrophages of the spleen and liver

27
Q

s/s hemolytic anemia

A

o Typical signs of anemia +
o Dark urine
o +/- back pain
o Pale or jaundiced skin
o Lymphadenopathy or hepatic splenomegaly

28
Q

diagnostic test findings: hemolytic anemia

A

o Characteristic feature = normocytic with a marked reticulocytosis
o Sometimes macrocytic due to increased volume of reticuloctyes
o Increased unconjugated bilirubin and lactic dehyrogenase – released into the blood stream when RBCs are destroyed
o Decreased Haptoglobin – binds to liberated hemoglobin and is quickly cleared by the liver

29
Q

oHyperproliferative

A

 Appropriate response of the bone marrow
 Seen in blood loss and hemolytic anemias and following replacement in deficiency anemias
 Normal in pregnancy

30
Q

o Hypoproliferative

A

 Bone marrow is unable to respond
 Seen in nutritional deficiencies, aplastic anemia, radiation, bone marrow failure, severe kidney disease, alcoholism

31
Q

Hypoproliferative Anemia

A
  • Bone marrow is unable to adequately produce RBCs (impaired/underproduction)
32
Q

Hypoproliferative Anemia: hallmark

A
  • Hallmark is low reticulocyte count
33
Q

Hypoproliferative Anemia

A
  • Check the MCV to determine etiology
    Microcytic anemias
    **o Iron deficiency
    o Thalassemia
    o Lead exposure
    **
    Normocytic anemias
    **o Anemia of chronic dz
    o Early iron deficiency
    o Bleeding, hemolytic
    o Bone marrow suppression
    o Mixed macro & microcytic anemia
    **
    Macrocytic anemias
    o Megaloblastic anemia
    **Folate deficiency
     Vitamin B12 deficiency
     Antimetabolite drugs (chemo)
    **o Non-megaloblastic
    ** Etoh
     Liver dz
     Hypothyroidism
     Myelodysplasia
34
Q

Microytic Anemia

A
  • Most commonly iron deficiency anemia (IDA)
    o Microcytic and hypochromic
  • Check iron studies
    o Start with Ferritin - major iron storage protein
    o Low ferritin rules in IDA but normal levels do not rule it out
     Ferritin is an acute phase reactant – can be elevated with inflammatory disease, infection, neoplasms
    o Normal ferritin level: add TIBC, total iron and transferrin saturation
    o Elevated ferritin level: rules out IDA
35
Q

iron studies

A
  • Transferrin: serum iron transport protein – brings iron to the bone marrow
    o Can be measured directly with a transferrin level, however more commonly measured by looking at TIBC
     Total Iron Binding Capacity: Measures the amount of transferrin available to bind to iron
     Increased TIBC means you are not carrying as much iron as you could
  • Serum iron level – measures the total amount of iron in the blood – nearly all of which is bound to transferrin
  • Transferrin saturation
    o Serum iron x100%/TIBC
  • Normal reference ranges:
    o Serum iron: 60–170 μg/dL (10–30 μmol/L)
    o Total iron-binding capacity: 240–450 μg/dL
    o Transferrin saturation: 15–50% (males), 12–45% (females)
36
Q

hemocrhomatosis

A
  • Genetic disorder that disrupts the body’s regulation of iron
  • Most common in white populations of northern European origin
  • Often asymptomatic
  • Symptoms may include
    o weakness,
    o lethargy,
    o arthralgias,
    o impotence
37
Q

thalassemia

A
  • Inherited blood disorder characterized by abnormal hemoglobin production
  • 2 main types
    o Alpha – Deletion of some or all of the HBA genes cause reduced levels of alpha globulin
    o Beta – mutations in the HBB gene cause reduced levels of beta globulin
    ** Hypochromic, microcytic anemia
    **
    Certain ancestries increase risk
    o African American, Mediterranean, Southeast Asian
38
Q

Beta Thalassemia

A
  • Heterozygous – carrier and have Beta thalassemia trait
    o May have mild anemia with microcytosis
  • Homozygous – Beta thalassemia major (Cooley anemia)
    o Life threatening, requires frequent transfusions
39
Q

Alpha Thalassemia

A
  • 2 genes (HBA1 and HBA2), each with 2 copies
  • Degree of condition related to how many gene copies are lost and in which combination
40
Q

microcytic with increased RDW=

A

iron deficiency anemia

41
Q

microcytic with normal RDW=

A

thalassemia

42
Q

Anemia of Chronic Disease

A

*** Typically normocytic, normochromic
**o May be microcytic – don’t mistake for IDA!
o Low reticulocyte count, normal/elevated ferritin, low/normal serum iron
* Think about in patients which chronic immune or infectious processes or neoplasm
o The chronic inflammation and immune system stimulation produces cytokines that alter the bodies ability to store and transport iron
* Chronic renal disease – decreased production of erythropoeitin leads to decreased production of RBCs

43
Q

Megaloblastic Anemia

A
  • Macrocytosis + presence of hypersegmented neutrophils and macroovalocytes on peripheral smear
  • Vitamin B12 or Folate deficiency
    o Essential for DNA synthesis
    o Related to:
     Inadequate intake
  • Folate (lack of fresh veggies)
  • B12 (lack of meat and dairy)
     Increased requirement – pregnancy, infancy, chronic inflammatory diseases, malignancies
     Medications
     Malabsorption
  • Folate: small bowel disease
  • B12: pernicious anemia, gastrectomy, chrohn’s, ileal resection
  • Check B12 and Folate levels
    o B12 deficiency:
     CBC can be normal for a long time
     Don’t miss diagnosis – can lead to:
  • Adults: irreversible neuro sx
  • Kids: growth retardation, seizures
    o B12 levels can be difficult to interpret:
     B12 “falsely” low: pregnancy, OCP use, folate deficiency
     B12 “falsely” normal: liver disease, bacterial overgrowth syndromes
     B12 “falsely” high: Etoh, liver disease, cancer
    o B12 <150 diagnostic
  • If suspect B12 deficiency but levels don’t support: check MMA and homocysteine
  • Methylmalonic Acid (MMA)
    o Vitamin B12 promotes the conversion of methylmalonyl CoA (a form of MMA) to succinyl Coenzyme A.
    o If there is not enough B12 available, then the MMA concentration begins to rise, resulting in an increase of MMA in the blood and urine.
    o Increased MMA = decreased B12
    o Can also be elevated in chronic kidney disease
    o Levels >1.0 are highly indicative of B12 deficiency
  • Homocysteine
    o Amino acid that requires B6, B12 and folate for its metabolism to methionine
    o Increased levels of homocysteine can indicate B12 or folate deficiency
    o Also plays a role in inflammation – marker in MI, stroke, blood clot
    o Nonspecific
44
Q

folate deficiency

A
  • Serum levels vary greatly based on diet
  • Better to check RBC folate level
  • Will see elevated Homocysteine but normal MMA with folate deficiency
45
Q

pernicious anemia

A
  • B12 deficiency due to lack of intrinsic factor related to autoimmune destruction of parietal cells or gastrectomy
  • Suspect in persons with B12 deficiency and other autoimmune disorders
  • Schilling Test – no longer available in the US
  • Test for anti-intrinsic factor antibodies
46
Q

what if the Hgb and Hct are elevated?

A
  • Polycythemia vera
    o Myeloproliferative disease
     Hyperviscosity  thrombosis
     Tx: low dose aspirin and therapeutic phlebotomy
  • Secondary Polycythemia
    o Chronic hypoxia leads to increased erythropoietin production
     OSA
     Smoking
     Altitude
     Chronic pulmonary disease
     Erythropoeitin secreting tumors