Anemia Flashcards

1
Q

what does the Mean Corpuscular volume measure?

A

Size of RBC

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2
Q

Macrocytic anemia

A

MCV > 100 fL

  • 110-140 MCV (B12 AND FOLATE DEFFIECENT)
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3
Q

Microcytic anemia

A

MCV < 80 fL

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4
Q

Normocytic anemia

A

MCV 80-100 fL

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5
Q

what causes macrocytic anemia?

A

Vit B12 or folate deficiency

- with increased retics - hemolysis

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6
Q

what causes microcytic anemia?

A

Iron deficiency

Thalassemia

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7
Q

Signs and Sx of anemia

A
  • Exertional dyspnea, dyspnea at rest, varying
    degrees of fatigue, bounding pulses,
    palpitations, “roaring” sound in the ears

■ Acute bleeding with severe volume depletion may lead to fatigue, muscle cramps and can progress to postural dizziness, lethargy, syncope, hypotension, shock, and death

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8
Q

very severe anemia signs and sx

A

■ Severe anemia may cause lethary, confusion and can lead to congestive heart failure, angina, arrhythmias, MI

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9
Q

What Hx to ask when suspecting anemia?

A
  • Famil Hx
  • Pt Hx
  • Ethnicity
  • renal failure
  • PUD, CHF, Liver Dz
  • medication use? – Asprin, NSAID, hydroxyurea
  • toxic habits - Lead exposure, alcohol abuse, nutritional status
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10
Q

What to look at upon physical exam?

A
■ Organ or multisystem involvement 
■ Assess patient’s condition (sick or not)
 ■ Tachycardia, dyspnea, fever, postural
hypotension
 ■ Jaundice, pallor, petechiae 
■ Lymphadenopathy, HSM, bone tenderness 
■ Signs and symptoms of recurrent infxns
■ Stool occult blood
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11
Q

Diagnostic Studies for Anemia

A

■ CBC with platelets and WBC differential
■ Reticulocyte count
■ Peripheral blood smear
■ Specific tests to narrow the differential
diagnosis as indicated
– Iron, TIBC, transferrin saturation, ferritin
– LDH, indirect bilirubin, haptoglobin
– Folate, vitamin B12 levels
– TSH, other specific endocrine studies

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12
Q

when would the Reticulocyte count be helpful?

A

when you already know they have anemia and you want to know specific red cell count and what causes the anemia

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13
Q

why would you do a Peripheral blood smear?

A

to see shape of the cells, to see how red it is (MHC)

  • Morphology of RBC and other cells in the
    blood can be helpful in determining a diagnosis
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14
Q

what does the CBC include?

A

RBC, WBC, Hgb, Hct, MCV,

MCH, MCHC, RDW, platelet count

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15
Q

What does the MCHC tell?

A

concentration (color) of the Hgb

– Hypochromic, hyperchromic, normochromic

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16
Q

WBC count and differentials

Leukopenia + anemia

A

due to bone marrow suppression, hypersplenism, vitamin B12 or folate deficiencies

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17
Q

WBC count and differentials

Leukocytosis + anemia

A

indicates infection, inflammation, or hematologic malignancy

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18
Q

WBC count and differentials

Inc neutrophils in infxn (specific parts of differential)

A

inc monocytes in myelodysplasia;
inc eosinophils with parasites or allergic disease;
dec neutrophils s/p chemo; dec lymphocytes in HIV or steroid tx

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19
Q

Platelet count can be…

A

Thrombocytopenia with anemia: DDx includes
hypersplenism; malignancy involving bone marrow; autoimmune platelet destruction; sepsis; vitamin B12 or folate deficiency
– Thrombocytosis with anemia: DDx includes
myeloproliferative disease; chronic iron deficiency; inflammatory, infectious, or neoplastic disorders

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20
Q

what is the most common reason you see anemia?

A

GI bleeds

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21
Q

What is the most common cause of anemia world wide?

A

Iron Deficiency Anemia

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22
Q

How is Iron stored?

A

As Ferritin

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23
Q

Causes of Iron Deficiency

A
■ Deficient diet 
■ Decreased GI absorption
■ Increased iron requirements
– Pregnancy and lactation
 ■ Blood loss
– GI, menstrual, blood donation 
■ Hemoglobinuria - losing iron somewhere else 
 ■ Iron sequestration
– Pulmonary hemosiderosis
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24
Q

what is the clinical presentation in someone with IDA?

A

■ Easy fatigability, tachycardia, palpitations,
dyspnea with exertion; pica (craving dirt)
■ Skin and mucosal changes: smooth
tongue, brittle nails, cheilosis
■ Dysphagia due to esophageal webs
■ Stool positive for occult blood if GI
bleeding is the cause of IDA

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25
Q

Diagnostic test for IDA?

A
start with CBC
■ Low serum ferritin is the initial abnormality 
■ TIBC rises as iron stores become
increasingly depleted
■ Serum iron and transferrin saturation
levels decline as iron stores are depleted 
■ RBC level decreases, and RBC become
microcytic and hypochromic 
■ Peripheral smear also may show
anisocytosis and poikilocytosis
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26
Q

Treatment of IDA

A
  • ID and treat the cuase
  • replace the iron!
  • take with vitamin C not CALCIUM - it blocks absorption
  • talk to them about diet counseling and how to attain iron from foods
27
Q

Oral Iron therapy

A

– FeSO4 325mg po tid is preferred Rx
– Should see return to baseline in H/H in 2 mos
- Continue 3-6 mos after achieving normal labs to replenish iron stores

28
Q

SE of iron

A

constipation and nausea in many pts - mostly GI SE - dark stool

29
Q

Parenteral iron therapy

A

– Intolerance to oral iron, refractory(very low) IDA, GI disease, uncorrectable continued blood loss
- can cause local itching, etythemia (must refer)

30
Q

Anemia of Chronic Dz - normocytic mild

A
  • d/t many chronic systemic Dz
  • RBC survival is <120 days
  • bone marrow can’t keep up for shorter RBC lifespan
  • usually a normocytic anemia - mild
31
Q

Causes of anemia of chronic Dz

A

– Chronic infection or inflammation
– Cancer
– Liver disease
– Chronic renal failure - is more severe
▪ Somewhat different pathophysiology
▪ Decrease in EPO - can replace
▪ More severe anemia than other chronic diseases

32
Q

Presentation of anemia of chronic Dz

A
  • s/sx of causative illness
  • fatigue
  • tachycardia
  • palpitations
  • DOE
  • May have coexistant iron or folic acid
    deficiencies that complicate the diagnosis
33
Q

Diagnostic study for anemia of chronic Dz (ACD)

A
■ Low Hgb/Hct 
■ Normal or slightly decreased MCV 
■ Normal reticulocyte count and smear 
■ Low serum iron, TIBC, transferrin
saturation; Normal or increased serum
ferritin 
■ Low serum EPO in renal failure
34
Q

Treatment of ACD

A
  • not usually necessary
  • purified epo for renal failure
  • hemodialysis - also for renal failure
  • Treat any coexistant iron or folate
    deficiency
35
Q

Thalassemias -

A
  • hereditary disorder
  • Microcytosis out of proportion to the
    degree of anemia
    -
36
Q

Alpha-Thalassemia - Affects primarily people from SE Asia and
China

A

■ α-Thalassemia is due primarily to a gene
deletion causing reduced α-globin chain
synthesis
■ No change in percentage distribution of
Hgb A, A2, and F
■ Hemoglobin H disease is a severe form with excess β-chains that form a β4
tetramer

37
Q

Silent Carrier

A

α-globin genes

  • normal HCT
  • MCV (60-75)
38
Q

Hemoglobin H Disease - type of alpha thalassemia

A
  • will have a chronic hemolytic anemia of variable severity, pallor and splenomegaly
  • only one normal alpha gene - the other 3 are normal
  • Hemoglobin electrophoresis shows a fast
    migrating abnormal Hgb H as 10-40% of Hgb
39
Q

Diagnostic study for Thalassemias

A

Hemoglobin electrophoresis

40
Q

Beta-Thalassemia - mainly Mediterranean origin

A
  • This group of anemias usually caused by
    point mutations → premature chain
    termination or problems with transcription
    of RNA → reduced or absent β-globin
    chain synthesis
    ■ Results in a relative increase in the
    percentages of Hgb A2 and Hgb F
    compared to Hgb A
    ■ Excess α-chains are unstable and lead to
    damaged RBC membranes → hemolysis
    ■ Bone marrow becomes hyperplastic
41
Q

MCV in someone with Thalassemia?

A

low (55-75fL)

42
Q

Treatment for Thalassemia

A

■ Mild thalassemias do not usually require
treatment
■ Hemoglobin H disease treated with folate
supplements and regular transfusions; iron
chelation therapy often used; splenectomy
■ β-thalassemia major is primarily treated
with allogenic bone marrow transplant

43
Q

What causes megaloblastic anemias? (Macrocytic)

A
■ Folic acid (folate) deficiency and
cyanocobalamin (vitamin B12) deficiency 
■ Macrocytic anemia with macro-ovalocytes
and hypersegmented neutrophils on
peripheral blood smear
44
Q

What would you see on serum levels for macrocytic anemia?

A

■ Low serum levels of serum folate or

vitamin B12 levels

45
Q

Where is vitmain B12 bound? Where is it absorbed? And where is it stored?

A

Bound to intrinsic factor in the gut and
absorbed in the terminal ileum; stored in
the liver –> usually develops more than 3 years after absorption stops bc the liver is able to have a build up of B12

46
Q

What causes decreased production in intrinsic factor?

A

Pernicious anemia; gastrectomy

  • H. Pylori
  • Pancreatic insufficiency
  • dec. ileal absorption
  • Surgical resection/ Crohn’s Dz
47
Q

what is the clinical presentation in someone with macrocytic anemia? (folate has no neuro findings)

A
■ Changes in mucosal cells leading to
glossitis; vague GI complaints including
anorexia, diarrhea 
■ (STOCKING GLOVE PATTERN) - Peripheral nerves affected leading to
paresthesias, dysequilibrium, dementia
and other neuropsychiatric changes
– Reversible if treated within 6 months 
■ Pale, mildly icteric; decreased position or
vibration sense on PE
48
Q

Treatment for someone with B12 Difeicnecy

A

Replacement of vitamin B12
– Parenteral therapy is most commonly used
▪ PA: 100mcg IM daily x 1 week then weekly x 1
▪ 1000mcg IM monthly (
– Oral therapy may also be used monthly then monthly for life
▪ 1000mcg po qd continued indefinitely – Hypokalemia may occur at the onset of treatment – Hematologic findings normalize in 2 months

49
Q

How is Folic Acid Deficiency different than B12?

A

no neurological findings

50
Q

What are the causes of Folic Acid Deficiency?

A

– Dietary deficiency
skin disorders
▪ Alcoholics, anorexia, malnutrition, overcook foods
– Decreased absorption
▪ Tropical sprue; drugs (phenytoin, sulfasalazine)
– Increased requirement
▪ Chronic hemolytic anemia; pregnancy; exfoliative
– Loss of folic acid through dialysis – Inhibition of reduction to active form
▪ Methotrexate

51
Q

Tx for the Folic acid deficiency?

A

▪ Replacement of folic acid (1 mg po qd)
▪ rapid improvements within 2 mo
▪ tx underlying illness

52
Q

Causes of Hemolytic Anemia

A
  • Intrinsic RBC defects
  • Intravascular destruction of RBC
  • Extrinsic RBC defects - liver dz, hypersplenism, infections, burns, leukemia
53
Q

Diagnostic studies for Hemolytic Anemia

A
  • dec serum haptoglobin
  • increased indirect bilirubin in blood
  • elevated serum LDH levels
  • SCHISTOCYTES
  • Heinz Body
54
Q

clinical presentation of someone with Hemolytic Anemia

A
  • varies; depends on cause

- Sx of anemia Fatigue, Tachycardia, Palpitations, DOE

55
Q

What DNA base change occurs in Sickle Cell Anemia?

A

substituting valine for glutamine in the 6th position on the Beta-globin chain - HgB S

56
Q

Genotypes for Sickle Cell

AA
AS
SS

A

AA - normal
AS - Sickle Cell trait
SS - sickle cell anemia - 86-98% Hgb S - crescent-shaped blood cells - sticky = inflammation and clumping - not well functioning

57
Q

What factors influence RBC sickling?

A
  • [Hgb S in the RBC]
  • RBC Dehydration
  • Other types of Hgb in the cell (Hgb F)
  • Stress
  • Cold
  • Infection
  • Anything leading to deoxyhemoglobin state (acidosis, hypoxemia)
58
Q

Presentation of Sickle Cell

A
  • chronic hemolytic anemia - jaundice, pigmented gallstones, hepatosplenomegaly
  • poor healing
  • poor growth and development
  • aplastic crisis
  • attack of severe pain and hypoxemia
59
Q

Sickle Cell Crisis presentation

A
  • Acute painful episodes due to acute
    vaso-occlusion; associated low-grade fevers – Clusters of sickled cells occlude the
    microvasculature of the organ(s) involved
    ▪ Bones and chest most often affected
    – Last hours to days
    – Occur spontaneously or due to infection,
    dehydration, hypoxia
60
Q

Diagnostic test of choice

A

Hgb electrophoresis

  • can see sickle cells on the smear
  • WBC elevated
  • thrombocytosis
  • increased bilirubin
  • usually Dx in small children (by 1st yr of life)
61
Q

Tx for Sickle Cell Dz

A
  • no specific tx
  • maintain w/ folic acid supplements
  • blood transfusions for aplastic hemolytic crisis
  • acute - tx with oxygen, fluid, treat underlying infections
62
Q

what drug can you use for sickle cell?

A

Hydroxyurea (500-750 mg/ d PO) – helps decrease frequency of pain crisis

  • bone marrow txp
  • splenectomy - need PNA vaccine
63
Q

when would you need RBC transfusion?

A
  • 10/30 rule = Hgb < 10 or Hct < 30%
  • estimated blood loss volume >30%
  • sx anemia (dizzy, SOB, fatigue)
  • each unit rasies blood volume by 200mL RBC
64
Q

When would you do a bone marrow biopsy?

A
  • unexplained anemia
  • unexplained anything
  • not improving on iron replacement
  • plasma disroders