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Clin Med- Heme/Oncol > Anemia > Flashcards

Anemia Flashcards

1
Q

the WHO defines anemia as?

A

♀ Hct < 41% /Hg < 4,000,000/mm3

Different institutions will have slight variations to reference ranges

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2
Q

Anemia

A

an indication of an underlying disease process

It is characterized by a decrease in RBC Mass Leading to a Decrease in Oxygen Carrying Capacity

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3
Q

Which organ produces blood cells?

A

The Bone Marrow (BM)

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4
Q

To facilitate adequate RBC production, the BM must be able to Maintain Homeostatic balance of?

A

Macrophages that supply Fe++ for Hgb production
Fibroblasts to support BM integrity
Adipocytes that store energy as fat
Osteoblasts and osteoclasts supporting the boney trabeculae
Precursors of Blood Cell Production
Maintain vascular integrity as a conduit between BM and peripheral circulation
Maintain erythroid stem cells responsive to Erythropoietin

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5
Q

Erythropoietin

A

regulating hormone
Secreted by kidney
Governs day-today RBC production
O2 availability is main EPO stimulus
EPO binds to erythroid precursor receptors
EPO levels should increase in proportion to anemia severity

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6
Q

Erythropoietin is inversely related to?

A

HCT

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7
Q

What does Erythropoietin do?

A

Increases RBC production (4-5x) and speed maturity of RBCs

Iron, B12, folate are needed substrates

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8
Q

What is the lifespan of a RBC in peripheral blood?

A

Lifespan of an RBC in Peripheral Blood is 120 days

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9
Q

Epidemiology of Erythropoiesis

A

African Americans have relatively lower RBC mass
Older adults Have a Deceased RBC mass
20% have <12 g/dL
Tissue hypoxia and ↑ cardio output
Increased falls, confusion, frailty, muscle weakness

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10
Q

Athletes can present with?

A

“Dilutional Pseudoanemia”—increased energy demand, increases O2 demand—with initial Plasma Vol increase followed

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11
Q

Changes in Plasma Volume May Decreases or Increase RBC Concentration Regardless of RBC Mass

A

Acute Bleeding– Decrease Intra-vascular Volume– Normal Hgb and Hct (Concentration)
When Normal Volume is Restored the patient will demonstrate Anemia
Dehydration:
Pregnancy:

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12
Q

How does pregnancy cause changes in plasma volume?

A

Plasma volume increases faster that RBC mass, therefore the patient may appear falsely anemic.

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13
Q

How does dehydration cause changes in plasma volume?

A

presents with normal or elevated Hgb & Hct, but once hydrated the Hgb & Hct may Reveal the Patient to be Anemic ( Decreased RBC Mass)

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14
Q

Reticulocyte

A

immature RBC that is Stained with Methylene Blue and reveals residual Ribosomal RNA as beads of tiny deep blue precipitates.

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15
Q

What does the clinical presentation of anemia depend on? (4)

A

Rapidity of Onset
Severity
Patient’s Physiologic Age & Co-morbidities
Physiologic Responses e.g. increase in 2,3-diphosphoglycerate

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16
Q

What are some symptoms of anemia?

A 
DOE
Fatigue
Palpitations
Headache
Tinnitus
Chest pain (esp. in patients with CAD)
Esophageal rings: Schatzki’s rings in Chronic Fe Deficiency
Spooning of Nails (Fe Deficiency)
Picas (Fe Deficiency)
Neuropathies (B12 Deficiency)
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17
Q

What are some clinical signs of anemia?

A 
Tachycardia
Orthostatic hypotension
Hypotension if acute
Systolic ejection murmur
Pallor:
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18
Q

Where are you going to look for pallor in anemic patients?

A 
Palmar creases 
If lighter than surrounding skin Hg < 8g/dL
Best physical sign indicator
Palpebral conjunctiva
Skin
Oral mucous membranes 
Nail beds
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19
Q

What are 4 GI signs associated with anemia?

A

Jaundice
Positive stool guaiac
Splenomegaly
Hepatomegaly

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20
Q

What are 3 MSK signs associated with anemia?

A

Pale, cold extremities
Bone tenderness
Frontal Bossing

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21
Q

Microcytic (and hypochromic) Anemia

A

Mean Corpuscular Volume (MCV) < 80 mm3

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22
Q

Main Causes of microcytic anemia

A

Thalassemia minor/major

Iron Deficiency Anemia
Most common cause anemia

Anemia of Chronic Diseases/Inflammatory Diseases
Sideroblastic Anemias and Pb Poisoning

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23
Q

Iron deficiency anemia epidemiology

A

Accounts for 50% of Anemias Worldwide
Accounts for > 800,000 Deaths/year Worldwide
> 70% of Iron Deficiency Anemia Deaths are in Africa & Asia

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24
Q

Lab evaluations for iron deficiency anemia

A

Serum Iron, Fe: Iron Bound to Transferrin in the Serum

Total Iron Binding Capacity, TIBC: Total Transferrin in the Serum

Fe/TIBC is the % Saturation of Iron to Iron Binding Capacity (Transferrin)

Serum Ferritin: A Rough Estimate of Iron Stored in the Reticuloendothelial System

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25
Q

Causes (DDX) of Iron Deficiency Anemia

A 
GI Bleeding***
Excessive Menstruation
Malnutrition & Dietary Insufficiency
Celiac sprue
Crohn’s Disease
Subtotal gastrectomy
Pregnancy
Growth Spurts in Childhood
Blood Donation, Blood Loss in Dialysis & Factious Auto-phlebotomy
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26
Q

Specific Clinical Manifestations of Iron Deficiency Anemia

A 
Angular Cheilosis
PICA
Koilonychia (spoon nails)
Plummer-Vinson Syndrome
Fe++ def anemia, esophageal webs, dysphagia and atrophic glossitis
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27
Q

inital eval of someone you suspect is anemic?

A 
CBC
Ferritin level
Wright-stained Peripheral Smear
Degree of Anisocytosis and Poikilocytosis (Increased RDW)
decreased Fe  
increased TIBC  
Saturation < 10%
Ferritin < 20 ng/dL
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28
Q

Treatment of Iron deficiency

A

oral iron supplement
-ferrous sulfate = MC
can also be given IV or IM

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29
Q

Why would iron be given IM or IV?

A

Patients Intolerant to Oral Preparation
If More Rapid Correction of Fe Deficiency Anemia is Needed
If Patient Cannot Absorb Oral Iron
If Chronic Blood Loss  Fe Loss > Oral Repletion is Possible
Patients on Dialysis

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30
Q

Why can the treatment fail?

A 
Unidentified blood loss
Non-adherence
Incorrect diagnosis
GI malabsorption
Achlorhydria
PPIs
Crohn’s etc. 
S/P Gastrectomy
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31
Q

Side effects of iron supplements?

A

Constipation, black stools, nausea, bloating abdominal pain, & diarrhea

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32
Q

What increases iron absorption?

A

vit c–> orange juice

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33
Q

Alpha-Thalassemia:

A

↑prevalence in Malaria Regions:

Southeast Asia & China

34
Q

Beta-Thalassemia:

A

↑ prevalence in Mediterranean populations (Southern Italy, Greece & North Africa)

35
Q

Thalassemia Syndromes

A

Genetic disorder characterized by inadequate production of either the Alpha or Beta-globin chain of hemoglobin

36
Q

What are Heinz bodies?

A

Are precipitants of excess Alpha chains in Beta-Thalassemia
Are precipitants of excess Beta chains in Alpha-Thalassemia
They Impair DNA synthesis   RBC Production
They Damage RBC Membrane   RBC Destruction

37
Q

Thalassemia Clinical features

A

Positive family history
History of life-long hypochromic, microcytic anemia not responsive to Fe++
From silent carrier status to profound anemia:
Depends on genetic defects

38
Q

Complications of Beta-Thalassemia Major (Cooley’s Anemia)

A 
Growth retardation
Severe anemia
Abnormal facial structure
Pathologic fractures & Osteopenia
Hepatosplenomegaly
Jaundice and bilirubin gall stones
High out put CHF
Short life span (< 30 years)
39
Q

What lab findings confirm the diagnosis of Cooley’s anemia?

A

Hg electrophoresis
increase Hgb F (in both Thalassemias)
Hgb A decrease Beta Thal, but ↑ Hgb A2
Hgb H in severe Alpha Thalassemia

40
Q

What would be seen on peripheral smear for Cooley’s anemia?

A

Small, pale RBCs
Target cells
Nucleated erythroblasts
Basophilic stippling

41
Q

Thalassemia Treatment

A

Transfusions + deferoxamine (to prevent iron overload)
Keep Hgb >12 g/dL
Splenectomy
Experimental Allogeneic Hematopoietic Stem Cell Transplantation (BM transplant) in severe cases
Avoid Iron containing Supplements

42
Q

Iron Overload can cause what?

A 
Heart Failure
Liver Failure 
Pancreatic Failure with DM & Malabsorption 
Other Endocrine Abnormalities
Skin Pigmentation
43
Q

How do you treat iron overload?

A 
Iron chelation therapy extends life expectancy by reducing iron overload
IV Desferal (deferoxamine)
44
Q

Thalassemia Patient Education

A

Genetic counseling
Testing of parents
Prenatal diagnosis for severe forms of Thalassemia

45
Q

Normochromic Normocytic Anemias causes?

A 
Causes:
Anemia of Chronic Disease
Early Fe++ deficiency 
Myelodysplasia or Marrow Failure
Acute Blood Loss
Anemia Associated with Renal Failure
46
Q

Normochromic Normocytic Anemias

A

Definition:

MCV 80-100 mm3

47
Q

Anemia of Chronic/Inflammatory Disease

A

Reticulocyte Production Index is Low
Normal or Increased Ferritin
“Normal” Fe/TIBC (Transferrin Saturation) BUT….
Low Levels of Transferrin ( Low TIBC) &
Low serum iron
decreased Fe++ release to BM from storage sites
Iron Remains Sequestered in the RE System:

48
Q

Treatment of Anemia of Chronic Disease

A

Treatment of the Underlying condition is Most Important
Fe++ supplements +/- help

Erythropoietin
There is decreased response to Erythropoietin

49
Q

Anemia of Renal Failure: a Normocytic Normochromic Anemia

A

Erythropoietin deficiency
Uremic toxins interfere with RBC production and survival
Hemodialysis (causes hemolysis and blood loss)
Responds well to Erythropoietin & Iron

50
Q

Hemolytic Anemias intrinsic causes?

A

RBC defects)
G6PD deficiency
Sickle Cell
Hereditary spherocytosis

51
Q

Hemolytic Anemias extrinsic causes?

A 
Immune hemolytic anemia**
Drug-induced hemolytic anemia**
Thrombotic thrombocytopenic purpura
Hemolytic Uremic Syndrome
Disseminated intravascular coagulation
Mechanical hemolysis d/t cardiac valve difunction
Hypersplenism
52
Q

Hemolytic anemia clinical features?

A

May Be Associated with Jaundice, Gallstones or Splenomegaly

May Have Symptoms Consistent with Tissue Hypoxia, similar to other anemia related syndromes: Pallor, SOB, Tachycardia

53
Q

Sickle Cell Anemias?

A

Point mutation of the Beta-globin chain of Hb A molecule—with abnormal replacement of glutamine (hydrophilic) with valine (hydrophobic)  HbS

Short arm of chromosome 11 mutation

54
Q

Pathophys of sickle cell anemia?

A

HbS becomes sickled when deoxygenated—producing structural cellular damage
Sickled Hgb can return to Its Normal Configuration when re-oxygenated

55
Q

Sickle Cell disease vs sickle cell trait?

A

Sickle Cell Disease
Homozygous Hemoglobin S

Sickle Cell Trait:
Heterozygous for Hgb A & Hgb S
Little tendency to sickle unless there’s severehypoxia—usually asymptomatic

56
Q

Sickle cell anemia complications?

A 
hemolysis 
splenic sequestration 
microvascular occlusion
bone infarcts
osteomyelitis
priaprism
blindness
57
Q

How do you diagnose sickle cell anemia?

A

Hg Electrophoresis
Will detect Hb S
Trait will have 40% Hb S
Disease >95% Hb S

Smear
Sickled cells, hemolysis, reduced RBC count
Reticulocytosis
Nucleated RBCs
Target Cells
Holly Jolly Bodies due to Autosplenectomy

58
Q

Treatment of sickle cell anemia?

A

Prevent Sickle Cell crises by monitoring for conditions that demand O2 from RBCs
Infection
Exercise
Climate extremes
Dehydration during periods of physiologic/emotional distress
Bone marrow transplant**

59
Q

Treatment for sickle cell crisis?

A

IV Hydration
Supplemental oxygen
Analgesics—Morphine
Transfusion for Hct < 30% ( Hgb < 10 g/dL)
R/O Occult Infections, MI or Pulmonary Emboli

60
Q

Supportive care for sickle cell anemia?

A

Folic acid qd
Pneumococcal and H. flu vaccination
Penicillin prophylaxis
Ophthalmological monitoring against retinopathy
Orthopedic Care
Careful Monitoring of Renal, Pulmonary and Cardiac Function
Pain Management

61
Q

Autoimmune Hemolytic Anemias

A

occurs when antibodies directed against the person’s own red blood cells (RBCs) cause them to burst (lyse), leading to insufficient plasma concentration

62
Q

2 types of Autoimmune Hemolytic Anemias

A

IgG or IgM mediated have different disease courses

63
Q

Warm AIHA—IgG mediated

Autoimmune Hemolytic Anemias

A

More common than cold AIHA
IgG binds to RBC at > 37⁰C
Results in extravascular hemolysis—especially in spleen or liver

64
Q

Cold AIHA—IgM mediated

Autoimmune Hemolytic Anemias

A

IgM binds to RBC in temperatures < 37⁰C

Produces complement fixation & activation leading to intravascular hemolysis—within blood vessels

65
Q

Causes of Warm AIHA- IgG mediated?

A

Primary or Idiopathic

Secondary to lymphoid malignancies, collagen vascular disease (SLE), viral infections, or drugs

66
Q

Causes of Cold AIHA- IgM mediated?

A

Idiopathic
Lymphoproliferative diseases, e.g. Waldenstrom’s Macroglobulinemia
Mycoplasma pneumoniae
Infectious mononucleosis (EBV infection)

67
Q

Clinical signs of Autoimmune Hemolytic Anemia

A

Jaundice
Splenomegaly
Fatigue
Pallor

68
Q

Diagnosis of Autoimmune Hemolytic Anemias (6)

A 
Positive Direct Coombs Test
Elevated reticulocyte count
Blood smear reveals immature RBCs
Free serum hemoglobin (hemoglobinemia) and hemoglobinuria—indicates intravascular hemolysis
Unconjugated (indirect) bilirubin is high
Total bilirubin can rise to 4 mg/dL
Elevated serum LDH indicates hemolysis
Low or Absent Haptoglobin
69
Q

Treatment of AIHA (6)

A 
Treat Underlying Disease
Lymphoma, Mycoplasma pneumonia, EBV
Immunosuppressive medications
Steroids: Prednisone
Cyclophosphamide
Rituximab (Anti-CD 20 Ab)
RBC transfusions
Folate
Splenectomy
70
Q

Vitamin B12 deficiency

A

Most common cause is of B12 deficiency is impaired GI absorption due to lack of intrinsic factor produced by gastric parietal cells

71
Q

Pernicious Anemia

A

is lack of Intrinsic Factor (IF) due to auto-antibody destruction of Gastric Parietal Cell

72
Q

Clinical Presentation of Vitamin B12 deficiency

A 
Can take >3 years to show up 
Macrocytic Hypoproliferative Anemia
Weakness, faintness, pallor of skin and mucous membranes
Dyspnea after slight exertion
Atrophic Glossitis and stomatitis
Neuropathy
73
Q

Lab Findings for Vitamin B12 deficiency anemia

A

Blood smear shows marked macrocytic RBCs (MCV >100 mm3)
Low serum B12 (< 250 pg/mL)
High methylmalonic acid (high only in B12 def.)
High homocysteine (elevated in both B12 and folate def.) levels
Anisocytosis, poikilocytosis, macro ovalocytes and hypersegmented PMNs
Low Reticulocyte Count
Elevated LDH and indirect bilirubin

74
Q

Deficiency in Erythropoiesis will result in

A

Ineffective RBC Production
Defective and fragile RBCs
Asynchronous maturation between cytoplasm and nucleus

75
Q

Treatment for B12 deficiency anemia

A

1mg B12 (cyanocobalamin) IM qd x 7 days then q wk x 4-8 weeks then monthly for life—for pernicious anemia

If treatment is delayed greater than 6 months neurological problems may not respond to treatment

Folate can reverse hematologic abnormalities of B12 deficiency, but not neurologic symptoms
It is therefore Essential to obtain BOTH B12 & Folate Levels in Macrocytic Anemias.

76
Q

Causes of Folate def anemia?

A 
Inadequate Folate intake
Alcoholics
anorectic persons
elderly 
diet low in meat, fruit and vegetables (leafy green vegetables—do not over cook veggies)
77
Q

Folate deficiency anemia?

A

Body stores sufficient for 2-3 months

Decrease folic acid causes impaired RBC maturation and early destruction

78
Q

when are times the body requires an increase in folate?

A 
Pregnancy
Chronic Hemolytic Anemias
Malignancy
Dialysis
infants and children
79
Q

Clinical Presentation of Folate def anemia?

A

Symptoms from dietary deficiency can be seen in a few months—quicker than B12 deficiency

Atrophic Glossitis and Angular cheilosis

anemia symptoms related to poor tissue oxygenation

80
Q

Lab findings for folate def anemia?

A

Macro-ovalocytes
Hypersegmented PMNs
B12 levels are normal
Low Levels of Serum folate ( < 5.4 ng/ml)

81
Q

Treatment for folate definciency anemia?

A

1-5 mg/day Folic Acid usually PO
Avoidance of alcohol and folic acid antagonists
Treat causes of malabsorption
Must rule out B12 deficiency
Deficiency can cause spontaneous abortion or fetal neurologic defects

Clin Med- Heme/Oncol (10 decks)

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