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Clin Med III - Heme/Onc > Anemia > Flashcards

Anemia Flashcards

1
Q

WHO definition of anemia for females

A

Hct under 36%
Hgb under 12 g/dL
RBC under 4,000,000

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2
Q

WHO definition of anemia for males

A

Hct under 41%
Hgb under 13 g/dL
RBC under 4,000,000

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3
Q

What is the main hormone of erythropoiesis?

A

EPO

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4
Q

Describe EPO

A
  • Hormone that regulates RBC production and speeds maturity of RBCs
  • Secreted by kidney
  • Binds to erythroid precursor receptors
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5
Q

What is the main EPO stimulus?

A

O2 availability

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6
Q

How are EPO levels affected by anemia severity? HCT levels?

A
  • EPO levels increase in proportion to more severe anemia

- EPO levels are increased with LOW HCT

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7
Q

What substrates are needed for erythropoiesis?

A

Iron, B12, folate

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8
Q

RBC mass in African Americans? Elderly?

A

Decreased in both AAs and elderly

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9
Q

Describe volume status and anemia in acute bleeding

A
  • Acute bleeding causes decreased intravascular volume
  • Hgb and HCT are normal because of the decreased volume
  • When normal volume is restored, patient will demonstrate anemia
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10
Q

How does dehydration affect Hgb/HCT/anemic status?

A
  • Normal or elevated Hgb/HCT due to low volume

- Once hydrated, Hgb and HCT may reveal anemia

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11
Q

How does pregnancy status affect RBC mass?

A
  • Plasma volume increases faster than RBC mass

- Patient may appear falsely anemic

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12
Q

In a person with normal BM, reticulocyte production index should be:

A

At least 2.5% (less than this indicates impaired RBC production)

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13
Q

Define microcytic anemia

A

MCV under 80

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14
Q

Main causes of microcytic anemia

A

TICS

  • Thalassemia minor/major
  • Iron deficiency
  • Chronic/inflamm disease anemia
  • Sideroblastic anemias and Pb poisoning
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15
Q

MC cause of anemia

A

Fe deficiency (microcytic)

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16
Q

Where is Fe found in the body?

A

70% in hemoglobin of RBCs

30% in the form of ferritin and hemosiderin

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17
Q

What is the body’s source of iron?

A

Diet only (but only 10% absorbed and usable)

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18
Q

Etiology of Fe deficiency anemia

A
  • Insufficient iron intake
  • Inadequate gut absorption (Celiac, Crohns, etc)
  • Increased requirements/demands (children, pregnant women)
  • Loss of blood
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19
Q

Notable clinical s/s of Fe deficiency anemia

A
  • Angular cheilosis
  • PICA (eating non-nutritive things)
  • Koilonychia (spooning of nails)
  • Plummer-Vinson Syndrome (esophageal webs, dysphagia, atrophic glossitis)
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20
Q

Labs to evaluate Fe deficiency anemia

A
  • Serum Fe
  • Transferrin
  • TIBC
  • Fe/TIBC ratio
  • Serum Ferritin
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21
Q

Describe serum Fe

A

Amount of iron bound to transferrin in serum

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22
Q

Describe Transferrin

A

-Protein that binds iron and transports it to BM to be formed into Hgb
-Produced in liver
(reflection of liver function and nutrition)

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23
Q

Describe Total Iron Binding Capacity (TIBC)

A
  • Total Transferrin in serum available to bind iron

- Indicates level of transferrin

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24
Q

If Fe stores are low, how is TIBC affected?

A

Fe low = TIBC high

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25
Q

If Fe stores are high, how is TIBC affected?

A

Fe high = TIBC low/normal

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26
Q

How is Fe/TIBC ratio affected in iron deficiency anemia?

A

DECREASED

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27
Q

Describe serum ferritin

A

Rough estimate of stored iron (inside cells)

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28
Q

How do lab values present in Fe deficiency anemia (Hgb/Hct/MCV/serum Fe/TIBC/% transferrin saturation/ferritin)?

A 
Low Hgb/HCT
Low MCV
Low serum Fe
Low % transferrin saturation
Low ferritin
HIGH TIBC
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29
Q

Treatment of Fe deficiency anemia

A
  • ORAL Fe supplementation (ferrous sulfate 325 mg/65 mg elemental, 3x/day with meals)
  • Patient education regarding iron therapy
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30
Q

How long does it take to correct Fe deficiency anemia with oral Fe supplementation? How long does it take to replete bone marrow stores?

A

6 weeks

6 months

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31
Q

What to avoid taking ferrous sulfate with and why?

A

Milk/dairy/Ca supplements because it decreases absorption of Fe

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32
Q

Patient education regarding Fe supplementation therapy?

A
  • Side effects: constipation, black stools, nausea, bloating, abd pain, diarrhea
  • Do NOT take with TCAs, quinolones, antacids/PPIs and careful with Ca supplements
  • Vit C (OJ) increases absorption
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33
Q

What increases absorption of Fe supplements?

A

Vit C (OJ)

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34
Q

Causes of Fe deficiency anemia treatment failure

A
  • Unidentified blood loss
  • Non-adherence to treatment
  • Incorrect diagnosis
  • GI malabsorption
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35
Q

Indications for IM/IV Fe supplementation

A
  • Intolerant to oral Fe
  • Cannot absorb oral Fe
  • Rapid correction needed
  • Dialysis pt
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36
Q

Define Thalassemia syndromes

A
  • Hereditary
  • Characterized by inadequate production of either alpha or beta-globin chain of Hgb
  • Results in hypochromic microcytic anemia
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37
Q

Pathophys of Thalassemia syndromes

A
  • Genetic defect results in decreased/absent synthesis of Alpha or Beta Hgb chains
  • Leads to low Hgb synthesis (microcytic anemia)
  • RBCs are destroyed, BM does not respond to EPO
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38
Q

What happens with the imbalance of globin chains in Thalassemia?

A
  • Unaffected chain takes over, accumulates in RBC (Heinz bodies)
  • Leads to free radical production that induces hemolysis and anemia
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39
Q

What does normal adult hemoglobin consist of?

A
  • Hgb A (98%): 2 alpha, 2 beta
  • Hgb A2 (1-3%): alpha 2, delta 2
  • Hgb F (less than 1%): major Hgb of fetal life, alpha 2/gamma 1
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40
Q

What are the degrees of Thalassemia?

A
  • Trait (lab features of anemia w/o significant clinical repercussions)
  • Intermedia (occasional transfusion required or other moderate clinical impact)
  • Major (life threatening and pt is transfusion dependent)
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41
Q

Who is MC affected by Alpha Thalassemias?

A
  • SE Asia/China
  • Positive fam hx
  • Hx of life long hypochromic, microcytic anemia NOT responsive to Fe therapy
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42
Q

Degree of Alpha Thalassemia depends on what?

A

Number of genes affected (0 affected = normal, 4 affected = hydrops fetalis dies in utero)

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43
Q

What is required to make official diagnosis of Thalassemia?

A

Genetic testing

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44
Q

Who is MC affected by Beta Thalassemia?

A
  • Mediterranean

- Positive fam hx

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45
Q

Classification of Beta Thalassemia?

A
  • Minor (1 mutation resulting in mild anemia)

- Major (2 mutations resulting in severe transfusion dependent anemia)

46
Q

What does Hgb electrophoresis show in Beta Thalassemia Minor?

A

Increased Hgb A2 and slight increase in Hgb F

47
Q

What does Hgb electrophoresis show in Beta Thalassemia Major?

A

Predominant Hgb F, small amts of Hgb A2, little-no Hgb A

48
Q

What is Cooley’s anemia?

A

Beta Thalassemia Major

49
Q

Complications of Cooley’s anemia

A
  • Growth retardation
  • Severe anemia
  • Abnormal facial structure
  • Pathologic fractures
  • Hepatosplenomegaly
  • Jaundice
  • CHF
  • Short life span (under 30 yo)
50
Q

What differentiates Thalassemias from Fe deficiency anemia?

A
  • Lower MCV
  • Normal/elevated RBCs
  • Abnormal blood smear
  • Elevated retics
  • Iron studies are normal or transferrin sat/ferritin may be high
51
Q

How to treat alpha trait of Beta minor thalassemia?

A

None required

52
Q

Treatment of Alpha major thalassemia/Hemoglobin H disease?

A
  • Folic acid

- Avoid iron

53
Q

Treatment of severe Thalassemias

A
  • Regular transfusions
  • Folic acid
  • Iron chelation (to prevent organ damage from iron overload)
  • Splenectomy if hypersplenism results in increased transfusions/refractory symptoms
  • Allogenic stem cell transplant
54
Q

What is the treatment of choice for Beta Thalassemia Major?

A

Allogenic stem cell transplant

55
Q

Treatment of iron overload?

A

Iron chelation therapy (deferasirox)

56
Q

Define sideroblastic anemia

A

Abnormal iron metabolism in bone marrow

57
Q

Etiology of sideroblastic anemia

A
  • Acquired: primary (MDS), secondary (drugs, Pb poisoning, chronic ETOH)
  • Hereditary
58
Q

Pathophys of sideroblastic anemia

A
  • BM produces ringed sideroblasts instead of healthy RBCs

- Iron is available but it cannot incorporate into Hgb

59
Q

What is the diagnosis of sideroblastic anemia based on?

A

BM biopsy with Prussian blue stain

60
Q

Treatment of sideroblastic anemia

A
  • Remove toxic agents
  • Antidote: iron chelation
  • Vitamins (folic acid, pyridoxine)
61
Q

Define normochromic normocytic anemias

A
  • Low Hgb/HCT

- MCV 80-100

62
Q

Common causes of normochromic normocytic anemias

A
  • Anemia of chronic disease
  • Early Fe deficiency
  • Myelodysplasia or marrow failure
  • Acute blood loss
  • Anemia a/w renal failure
63
Q

Why do inflammatory conditions cause anemia? How are serum Fe levels?

A
  • Reduced iron uptake in the gut and transfer to BM
  • Reduced responsiveness to EPO
  • Serum Fe is low
64
Q

Why does organ failure cause anemia? How are serum Fe levels?

A
  • EPO levels are decreased and RBC mass decreases

- Serum Fe is normal

65
Q

Describe anemia in the elderly (how are serum Fe levels?)

A

Decreased EPO production due to RBC production resistant to EPO (serum Fe is normal)

66
Q

If anemia of chronic disease is severe enough, what is the treatment?

A

RBC transfusions or parenteral EPO (goal Hgb 10-12)

67
Q

Primary causes of macrocytic anemias

A

B12 deficiency

Folate deficiency

68
Q

What defines a macrocytic anemia?

A

MCV over 100

69
Q

Onset of B12 deficiency?

A

Takes over 3 years to occur if ALL intake and absorption of B12 stops

70
Q

Where does absorption of B12 occur? Where is B12 stored?

A

Absorption in terminal ileum, stored in liver

71
Q

Etiologies of B12 deficiency

A
  • Strict vegan diet
  • Pernicious anemia (MC)
  • Abd surgery
  • Pancreatic insufficiency
  • Severe Crohn’s
  • Tapeworm, GI bacterial or fungal overgrowth
72
Q

MC cause of B12 deficiency?

A

Pernicious anemia (auto-antibody destruction of intrinsic factor leading to atrophic gastritis)

73
Q

What is a notable clinical feature of B12 deficiency?

A

Complex neuro syndrome - peripheral nerves affected first (stocking like paresthesias, dementia)

74
Q

Lab findings of B12 deficiency

A
  • Macrocytic RBCs on blood smear
  • Low retics
  • Low serum B12
  • Low WBC/platelets (severe cases)
75
Q

How to confirm low serum B12?

A

Methylmalonic acid is HIGH

Homocysteine is HIGH

76
Q

Treatment for B12 deficiency anemia

A
  • Pernicious anemia: 1 mg B12 IM qd x 7 days then weekly for 4-8 wks, then monthly for life
  • Folate can reverse hematologic abnormalities but NOT neuro symptoms
77
Q

What may happen if treatment for B12 deficiency anemia is delayed for greater than 6 months?

A

Neuro problems may NOT respond to treatment (folate can reverse hematologic abnormalities but NOT neuro)

78
Q

Why is it essential to obtain both B12 AND folate levels in macrocytic anemias?

A
  • If treatment is delayed more than 6 months, neuro problems may not respond to treatment
  • Folate can reverse hematologic problems but not neuro symptoms
79
Q

Where is folic acid found? What are the daily requirements? How does the body store it?

A
  • Most fruits and veggies
  • Daily required 50-100 mcg
  • Body stores about 5 mg which is good for 2-3 months
80
Q

Causes of folate deficiency anemia?

A
  • Inadequate dietary intake
  • Reduced absorption (rare)
  • Increased requirements (pregnancy, malignancy, infants/children)
  • Meds (MTX, phenytoin, bactrim)
81
Q

Clinical presentation of folate deficiency anemia?

A
  • Onset can be seen in just a few months (FASTER than B12 deficiency)
  • Similar symptoms to B12 but NO NEURO SYMPTOMS
82
Q

What is diagnostic for folate deficiency anemia?

A

RBC folic acid level under 150 ng/mL (preferred over serum level - less than 5.0 ng/mL)

83
Q

Treatment of folate deficiency anemia

A
  • Oral folic acid 1 mg/day
  • Avoid ETOH and folic acid antagonist meds
  • Treat malabsorption, r/o B12 deficiency
84
Q

Total correction of folate deficiency anemia can occur in how long?

A

2 months

85
Q

Describe hemolytic anemias

A

Frequently normochromic and normocytic (BUT may be macrocytic)

86
Q

Intrinsic causes of hemolytic anemias

A

RBC defects

  • G6PD deficiency
  • Sickle cell
  • Hereditary spherocytosis
  • Thalassemia
87
Q

Extrinsic causes of hemolytic anemia

A

Extracellular causes

  • Immune
  • Drug induced
  • TTP
  • HUS
  • DIC
  • Infection
  • Burns
  • Hypersplenism
88
Q

Define G6PD deficiency

A

Hereditary enzyme defect that causes episodic hemolytic anemia in response to oxidative stress

89
Q

Pathophys of G6PD deficiency

A
  • Excess oxidized glutathione that forces Hgb to denature and form Heinz bodies
  • Heinz bodies cause RBC membrane damage which leads to extravascular hemolysis (in spleen)
90
Q

Who is MC affected by G6PD deficiency?

A

American black men

91
Q

Treatment of G6PD deficiency

A
  • Self limiting: older RBCs are removed and replaced with younger RBCs w/adequate enzyme levels
  • Treat underlying cause
92
Q

Describe sickle cell disease

A
  • Autosomal recessive (Valine for glutamine in beta chain of Hgb)
  • Hgb becomes sickled from deoxygenation
  • Hgb S is formed (unstable and polymerizes under stress)
93
Q

What is the genetic makeup of sickle cell disease?

A

Homozygous Hgb S

94
Q

What is the genetic makeup of sickle cell trait?

A

Heterozygous for Hgb A and S

little tendency to sickle unless there’s severe hypoxia

95
Q

How is sickle cell disease diagnosed?

A

Confirmed by Hgb electrophoresis

96
Q

What is the MC complication of sickle cell disease?

A

Vaso-occlusive complications (specifically, pain crisis)

  • Pain in long bones, back, chest, abd
  • 2 to 6 days duration
97
Q

Treatment of sickle cell disease

A
  • Supportive
  • Prevent sickle cell crises by monitoring for conditions that demand O2 from RBCs
  • Consider BM transplant
98
Q

When to assume Sickle Crisis until proven otherwise?

A

Patient with Hgb AS or SS presents with pain and distress

99
Q

Define autoimmune hemolytic anemias (AIHA)

A

Acquired disorder resulting from autoantibodies targeted toward RBC membrane antigens (resulting in extravascular hemolysis in spleen/liver)

100
Q

Types of AIHA

A
  • IgG mediated = warm

- IgM mediated = cold

101
Q

Describe warm AIHA

A
  • IgG mediated

- MC than cold/IgM AIHA

102
Q

Causes of warm AIHA

A
  • Primary/idiopathic

- Secondary to lymphoid malignancies, SLE, viral infections, drugs

103
Q

Describe cold AIHA

A
  • IgM binds to RBC in temps under 37 C

- Produces complement fixation and activation leading to intravascular hemolysis (within RBCs)

104
Q

Causes of cold AIHA

A
  • Idiopathic
  • Lymphoproliferative diseases (Waldenstroms, lymphoma, CLL)
  • Post-infectious (EBV, measles, mumps, CMV)
105
Q

Clinical signs of warm AIHA

A
  • Rapid onset/life threatening
  • Fatigue
  • Dyspnea
  • Angina/heart failure
106
Q

Clinical signs of cold AIHA

A
  • Occurs on exposure to cold
  • Mottled/numb fingers or toes
  • Acrocyanosis
  • Episodic low back pain
  • Dark colored urine
107
Q

Lab findings of AIHA

A
  • Positive Direct Coombs test
  • High reticulocyte count
  • High indirect (unconjugated) bilirubinemia
  • High serum LDH
  • Immature RBCs
  • Free serum Hgb
108
Q

Treatment of warm AIHA

A
  • Prednisone taper (1st line)
  • Transfusion maybe
  • Splenectomy maybe
  • Treat underyling disorder
109
Q

If rapid hemolysis in warm AIHA, what is the treatment?

A

Therapeutic plasmapheresis (rituximab, Danazol, IVIG)

110
Q

Treatment of cold AIHA

A
  • Symptomatic
  • Rituximab (IV weekly x4 wks)
  • If severe, cyclosporine
111
Q

Prednisone and splenectomy are INEFFECTIVE for which type of AIHA?

A

Cold

Clin Med III - Heme/Onc (8 decks)

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