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Hematology Exam I > Microcytic Anemia > Flashcards

Microcytic Anemia Flashcards

1
Q

Anemia

  1. Definition
  2. Symptoms
A
  1. Decrease in the number of RBCs in the blood, resulting in reduced oxygen-carrying capacity
  2. Symptoms: fatigue, dyspnea (on exertion), weakness

***With more severe anemia, may see confusion, tachycardia, hypotension, syncope, and death

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2
Q

Anemia

  1. How to categorize? (4)
A

Size, Color, Chronicity, Etiology

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3
Q
A

Hypochromic Microcytosis

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4
Q

What is a normal Hb in Males? Females?

A

Males = 14 to 17.5 g/dL

Females = 12 to 15 g/dL

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5
Q

What is a normal Hct in Males? Females?

A

Males = 42-50%

Females = 36-44%

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6
Q

What is a normal RBC count in Males? Females?

A

Males = 4.5 - 6.0 Million

Females = 4.0 to 5.0 Million

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7
Q

What is a normal MCV?

A

80-100 fL

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8
Q

What is a normal MCH?

A

30-34 pg

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9
Q

What is a normal MCHC? (i.e. Hgb/Hct x 100)

A

30-36%

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10
Q

What is a normal RDW? (Red Cell Distribution Width)

A

13-15%

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11
Q

What does a large RDW mean? small?

A

Large = Size is all over the map

Small = Uniform in size

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12
Q

Iron

  1. Absorption
    - Where is it absorbed?
    - Forms?
A

First and second portions of the duodenum

Forms:

  • Reduced +2 (Ferrous) or +3 (Ferric) state (Ferric is useless to us)
  • Heme Iron
  • Gluconate, sulfate
  • Role of pH, food (absorbed better in low pH/acidic)
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13
Q

Iron

  1. Dietary Sources
    - Most easily absorbed?
    - Plants/Vegetarians?
    - Geritol?
A
  • Heme iron is most easily absorbed
  • Plants are a poor source (have Fe 3+ if they do)
  • Vegetarians at risk for deficiency

Supplement with Geritol

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14
Q

Iron Absorption at the Enterocyte

  1. Describe the Process
A

***Heme Iron is absorbed by heme transporter then bound to Mucosal Ferritin (protects from redox reactions)

  • Fe 2+ leaves the enterocyte into the extracellular space via Ferroportin 1 (inhibited by Hepcidin), is oxidized by Hephaestin (copper containing molecule) to Fe 3+ (Ferric form)
  • Binds Plasma Transferrin in the blood

***Nonheme iron does the same, except is converted to Fe 2+ by Duodenal Cytochrome B first and then taken up by DMT 1

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15
Q

Hepcidin

  1. Role
  2. Upregulation
  3. Downregulation
A

Role: Reduces iron absorption by blocking ferroportin

Upregulated: by IL-6, high circulating ferritin

Downregulated: by low ferritin, hypoxia

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16
Q

Erythropoietin

  1. Produced where?
  2. Use in Anemias?
  3. Therapeutic Use
A

Produced by renal fibroblasts in response to hypoxia

Not useful in anemias that are already EPO-abundant (e.g. iron deficiency)

Should be co-administered with parenteral iron

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17
Q

Iron Distribution in the Body

4 parts

A

Circulating RBCs 2500 mg

Fe-containnig Proteins (e.g. Ferritin) 400 mg

Transferrin-bound 3-7 mg

Storage (marrow, RES) 1000 mg

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18
Q

Iron Loss

  1. Insensible loss
  2. Vascular loss
A

Insensible: sweat and endothelial sloughing

Vascular:

  • External loss (traumatic)
  • Sequestration (hematoma)
  • Menstrual
  • Internal loss (GI) –> Gastroduodenal (ulcer, espophageal varices), Colonic (tumors, diverticulitis)
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19
Q

Iron Deficiency Anemia

  1. Lab Values
    - Hgb/Hct
    - MCV
    - Ferritin
    - Transferrin Saturation
    - TIBC
    - Reticulocytosis
A

Hgb/Hct low

MCV low

Ferritin low (both intracellular (can’t be measured) and vascular)

  • Very accurate indirect measurement of total iron body stores
  • Ferritin of 10 or less is 99% sensitive/specific for ***Iron deficiency anemia***

Transferrin Saturation low (Transferrin itself will be high)

TIBC high (measures transferrin ^^^)

Reticulocytosis

20
Q
A

Reticulocytosis

21
Q

Normal Lab Values

  1. Serum Fe
  2. TIBC
  3. Saturation
  4. Ferritin
A

Serum Fe 60-150 mcg/dL

TIBC 300-360 mcg/dL

Saturation 20-50%

Ferritin 40-200 mcg/L ***Excellent indicator of total body iron***

22
Q

Iron Deficiency Anemia

  1. Common Causes
A
  • Detailed history is essential
  • > 50 y.o. GI malignancy until proven otherwise
  • IBD
  • Ulcer/esophagitis
  • Vascular malformations
  • Hematoma, sequestration (rare)
  • Gynecologic loss
23
Q

Iron Deficiency

  1. Signs and Symptoms (5)
A

Pica (chewing ice)/Pagophagia (chewing on/eating clay)

Restless Legs Syndrome

Pallor/Pale palmar creases/Pale Conjunctiva

Glossitis

Nail Changes

24
Q

How much iron can be absorbed per day if given orally?

How much can be given IV?

A

Absorbed Orally: 25 mg

IV: 500 mg

25
Q

Anemic of Chronic Disease

  1. Hepcidin
    - What is it?
    - Effects?
    - Induced/Stimulated by?
A

Hepcidin

  • An acute phase reactant
  • Has an antibacterial effect (presumably by limiting Fe-dependent electron transport)
  • IL-6 is a potent stimulator of hepcidin production
  • TNF, IFa, IFy also induce hepcidin (elevated in anemias of autoinflammation, cancer)
26
Q

What is this and what disease does this patient have?

A

Microcytic Hypochormic Anemia

(with Rouleaux formation (i.e. clumping of cells))

Seen in Rheumatoid Arthritis (i.e. Anemia of Chronic Disease)

27
Q

Anemia of Renal Disease

  1. Type of Anemia
  2. Mechanism
A

Usually a normochromic anemia

Increased RBC destruction (lysis with azotemia (minor contribution))

Anemia unrecognized by diseased renal fibroblasts

NO erythropoietin surge

NO marrow stimulation

28
Q

Thalassemia

  1. Alpha-like globins (1 major)
  2. Beta-like globins (4 major)
A

Alpha-like: alpha, zeta, and xi

Beta-like: beta, gamma, delta, epsilon

29
Q

***Important***

How many alpha alleles do we have and on which chromosome?

A

Two alpha alleles per chromosome (4 total)

Chromosome 16

***only one copy of all Betas on chromosome 11***

30
Q

How are Thalassemias named?

A

For the gene that is deficient

31
Q

a+-thalassemia

  1. Missing one allele
  2. Missing two alleles
  3. Missing three alleles
A

Missing…

One: a2B2 –> Silent carrier —> asymptomatic

Two: 85-95% a2B2 –> a+-thal trait –> mild anemia (no tx. required)

Three: 5-30% Hgb H (B4) “Hgb H disease”

32
Q

a0-thalassemia

A

(no alpha chains) B4, Y4 –> a0-thal –> Fetal Hydrops (Lethal)

33
Q

What is a hallmark for Thalassemias on PBS?

A

Target Cells

34
Q
A

alpha-thalassemia trait

35
Q
A

Hemoglobin H Disease ( –/-a, B4)

36
Q
A

Hemoglobin Bart’s Fetal Hydrops (NO functional hemoglobin)

37
Q

B-Thalassemia

  1. B+-Thalassemia
  2. B0-Thalassemia
A

B+-Thalassemia: B-thal trait or B-thalassemia minor

B0-Thlassemia: B-thalassemia major

  • No Hb A, Mostly Hb F and some Hb A2
  • Severe, transfusion-dependent

***B-Thalassemia tends to be more severe, as there are only 2 B genes***

38
Q

B-Thalassemia

  1. Thalassemia Intermedia
A

Two defective but partially functional B genes

***Severity is between Minor and Major***

39
Q

B-Thalassemia

  1. Disease
A

Increased RBC destruction

Iron (Fe) overload

Anemia, hypermetabolic marrow

Therapeutic phlebotomy (bleeding)

Transfusion Requirement

40
Q

Sideroblastic Anemias

  1. Marrow Effects?
  2. Iron Stores?
  3. Cause
A
  1. All sideroblastic anemias produce ringed sideroblasts in the marrow
  2. Irone stores are sufficient, usually high
  3. Not making porphyrin
41
Q
A

Bone Marrow with Ringed Sideroblasts

42
Q

Sideroblastic Anemias

  1. Congenital
  2. Acquired (primary vs secondary)
A
  1. X-linked and involve ALA synthase deficiency
  2. Primary (myelodysplastic syndrome - pre-malignant)

Secondary (alcohol abuse, drug induced (isoniazid, chloramphenicol), lead poisoning, copper deficiency)

43
Q

Sideroblastic Anemias

  1. Characteristics
A

May be normocytic

May have a dimorphic appearance

May demonstrate hemolytic changes

May show iron deposits (***Pappenheimer Bodies***)

***Transfusion to treat anemia, therapeutic phlebotomy to treat iron overload***

44
Q
A

Pappeheimer Body (precipitated iron granules)

45
Q
A

Sideroblastic Anemia

  • Dimorphism
  • Hypochromic
  • Teardrop shapes
46
Q

Sideroblastic Anemia

  1. Summary
  2. Treatment
A
  1. Total body iron overload, insufficient heme iron
  2. Treated with Pyridoxine, Transfusion, Phlebotomy, Chelation, Marrow Transplantation
47
Q

Summary of Anemia Testing

A

Hematology Exam I (12 decks)

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