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(C) CM 1A: Heme/Onc/Endo > Lecture 3: Anemia I > Flashcards

Lecture 3: Anemia I Flashcards

1
Q

Why do females generally have a lower Hb?

A

Lower EPO stimulation due to more dilated kidneys from estrogen.

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2
Q

What anemias are classified as microcytic?

A

Iron deficiency
Thalassemias
Anemia of chronic disease
Lead toxicity
Zinc deficiency

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3
Q

What anemias are classified as normocytic?

A

Kidney disease
Non-thyroid endocrine heart failure
Copper deficiency
Mild form of most acquired microcytic or macrocytic etiologies of anemia

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4
Q

What anemias are macrocytic, specifically megaloblastic?

A

B12 deficiency
Folate deficiency
DNA synthesis inhibitors

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5
Q

What anemias are macrocytic, specifically non-megaloblastic?

A

Myelodysplasia
Liver disease
Reticulocytosis
Hypothyroidism
Bone marrow failure state (aplastic anemia, marrow infiltrative disorders, etc)
Copper deficiency

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6
Q

What does it mean if a hemolytic anemia is intravascular?

A

RBCs are being lysed within the BLOOD VESSELS.

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7
Q

Why is it significant if a hemolytic anemia is intravascular?

A

It is significant because large amts of Hgb are being released into circulation.

This will appear as a decrease in iron and haptoglobin.
This may appear as hemoglobinuria.
Iron will NOT be recycled.
Schistocytes will form.

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8
Q

What is a schistocyte?

A

A tripolar, popped balloon RBC.

It is like a shredded RBC.

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9
Q

Why does haptoglobin decrease in intravascular anemia?

A

A serum haptoglobin test measures FREE haptoglobin, so if there is a lot of Hgb circulating, then the FREE haptoglobin gets used up.

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10
Q

What does it mean if a hemolytic anemia is extravascular?

A

RBCs are being lysed within ORGANS.

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11
Q

Why is it significant if a hemolytic anemia is extravascular?

A

Minimal Hgb released into circulation.

This means little to no decrease in haptoglobin.
Iron should remain almost unchanged.

Spherocytes will form.

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12
Q

What is a spherocyte?

A

It is a smaller, darker, denser, hyperchromic cell.

It is essentially the formation of a damaged RBC repairing itself by collecting excess Hgb.

Excess Hgb = smaller RBC.

They are NOT biconcave and LACK central pallor.

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13
Q

Why does Iron remain unchanged in extravascular anemia?

A

Generally, the spleen is where most RBCs get caught, and it is able to recycle the Hgb from the lysed cells.

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14
Q

What is a key PE finding that may differentiate extravascular hemolytic anemia from intravascular?

A

Red-dark urine in intravascular anemia.

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15
Q

If I have a hemolytic anemia, what lab changes would I expect on:
Hgb
MCV
Reticulocyte count

A

Hgb would be normal or reduced.

MCV are often increased.

Reticulocytes are often increased.

Note:
Hgb changes little because bone marrow can up the production of RBCs.
Upping RBC production means increasing retic count and generally MCV.

Retic count can remain unchanged if it is a chronic anemia and the bone marrow is exhausted.

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16
Q

If I have a hemolytic anemia, what lab changes would I expect on:
Bilirubin
LDH
Haptoglobin

A

Bilirubin would increase, esp. unconjugated.

LDH would increase.

Haptoglobin would only markedly decrease in intravascular anemia.
Haptoglobin MAY decrease in extravascular anemia.

Note:
Haptoglobin changes are dependent on the severity of the anemia.

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17
Q

What can falsely elevate haptoglobin?

A

Chronic inflammation.

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18
Q

Which hemolytic anemia is structural?

A

Hereditary spherocytosis

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19
Q

What hemolytic anemias are related to Hgb pathologies?

A

Thalassemias
Sickle cell disease (SCD)

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20
Q

What hemolytic anemia is metabolic?

A

G6PD deficiency

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21
Q

What hemolytic anemias are immune-related?

A

Autoimmune hemolytic anemia (AIHA)
Paroxysmal nocturnal hemoglobinuria (PNH)
Hemolytic disease of the newborn (HDN)

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22
Q

What is hereditary spherocytosis and what causes it?

A

Abnormal formation of proteins in the RBC membrane.

It is a result of improper cytoskeleton formation and is mainly AUTOSOMAL DOMINANT inheritance.

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23
Q

Is hereditary spherocytosis intravascular or extravascular? What does that mean?

A

Extravascular.

The spherocytes commonly get stuck in red pulp fenestrations in the spleen, so the spleen will bite them.

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24
Q

Describe the clinical presentation of spherocytosis.

A

Varying degrees…

It can go undetected for years but:

PE:
Jaundice
Splenomegaly
+/- gallstones in 50% of pts
Presents acutely after infection or stress.

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25
Q

Describe the peripheral blood smear of spherocytosis.

A

High counts of spherocytes.

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26
Q

Describe the lab findings in hereditary spherocytosis.

A

Variable decreases in Hgb/Hct
Increased reticulocytes
Increased MCHC (one of the few that can do this in micro/normocytic)
Normal to low MCV
Normal to low Haptoglobin (will drop more if inflammation present)
Peripheral blood smear: spherocytes
Coombs test: negative (ideally)

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27
Q

What is the general basic Tx for hereditary spherocytosis? Definitive?

A

General is folic acid 1mg daily.

Transfusions can be used for severe anemia.
EPO may be used in infants.

Definitive:
Splenectomy

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28
Q

Why is iron supplementation CI in hereditary spherocytosis?

A

It is an extravascular anemia, so it is not losing iron, but recycling it.

Iron supplementation will overload it.

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29
Q

What are the types of hemoglobin found naturally in the blood?

A

HbA: 97-99% of Hb in RBCs and considered adult Hb. (2 alpha, 2 beta)

HbA2: 1-3% of Hb in RBCs (2 alpha, 2 delta)

HbF: <1% of Hb in RBCs (Fetal Hb). (2 alpha, 2 gamma)

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30
Q

How many copies of each globulin gene do we have?

A

2 copies of alpha-globulin in chromosome 16. (4 total)

1 copy of beta-globulin in chromosome 11. (2 total)
Also includes delta and gamma.

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31
Q

What causes alpha thalassemia?

A

Gene deletions related to the alpha-globulin gene, resulting in reduced alpha-chain synthesis.

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32
Q

How does alpha thalassemia present on electrophoresis?

A

Equal proportions of all 3 hemoglobins.

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33
Q

What is the pathology of an alpha thalassemia?

A

Increased small, pale (hypochromic) RBCs.

Excessive beta chains will precipitate, causing hemoylsis and inclusion bodies to occur.

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34
Q

What demographic is most susceptible to alpha thalassemias?

A

SEA and Chinese

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35
Q

At what point does alpha thalassemia start to show lab changes?

A

With 2 gene deletions, aka alpha thalassemia minor/trait. Hct and MCV will begin dropping.

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36
Q

What are the two concerning types of alpha thalassemias?

A

HbH disease (1 normal gene)
Hydrops fetalis (0 normal genes)

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37
Q

What lab findings would I expect in alpha thalassemia?

A

Hb/Hct: normal or decreased
RBC: increased
MCV: Markedly decreased
Retic: Normal or increased
MCH: Decreased
Hb electrophoresis: Presence of HbH band means HbH disease. Normal otherwise.
Inclusion bodies: HbH

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38
Q

How would you describe alpha thalassemia morphologically?

A

Microcytic hypochromic anemia.

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39
Q

How does alpha thalassemia trait/minor present on peripheral smear?

A

Hypochromic, microcytic cells
Target cells (Ring appearance)

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40
Q

How does HbH disease present on peripheral smear?

A

Hypochromic, microcytic cells
Target cells
Poikilocytosis

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41
Q

How are the minor alpha thalassemias treated?

A

Minima/Silent carrier only require genetic counseling.
Minor/trait may rarely need transfusions.

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42
Q

Why do I need to monitor iron overload in transfusion patients and how do I treat it?

A

Extravascular anemias such as alpha thalassemias do not lose iron, so it would build up if transfused.
Treated via iron chelation.

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43
Q

How are HbH and hydrops fetalis treated?

A

HbH: folic acid 1mg/day
Avoiding iron supplements and oxidative drugs.
Consider splenectomy and transfusions regularly.

Hydrops fetalis: almost always lethal in utero :(
Recommended to terminate pregnancy.

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44
Q

What causes a beta thalassemia?

A

Gene point mutations resulting in reduced beta-chain synthesis.

Beta+ = reduced
beta0 = absent

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45
Q

How does beta thalassemia present on electrophoresis?

A

Increased HbA2 and HbF.

AKA low HbA since little to no beta chains present anymore.

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46
Q

What demographic is most susceptible to beta thalassemias?

A

Mediterranean

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47
Q

Describe the pathology of beta thalassemia.

A

Increased numbers of SMALL, PALE (low Hb) RBCs

Excess alpha chains = hemolysis.
Excess alpha chains = inclusion bodies & damaged precursors.
Surviving RBCs will have inclusion bodies and have shortened lifespans.

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48
Q

What are the 4 types of beta thalassemias and how are they broken down in terms of beta genes?

A

Normal

Minor: Normal Beta + Beta0 or +

Mild: 2 Beta+

Major/severe: Beta0 + Beta+ or 2 Beta0

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49
Q

How do lab findings change as the beta thalassemia gets worse?

A

Generally:
MCV decreases
Hct decreases
HbF and HbA2 increase

Transfusions start at mild/intermedia and progress to dependent if major.

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50
Q

What are the two types of beta thalassemia major?

A

Cooley’s anemia or beta-thalassemia major

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51
Q

What are the general lab findings for beta-thalassemia?

A

Hb/Hct decrease
RBC increase
MCV markedly decreased
Retic: increase
MCH: decrease
Hb electrophoresis: Decreased HbA

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52
Q

What are the most pertinent PE findings for mod-severe beta thalassemia?

A

Erythroid hyperplasia will lead to chipmunk facies, thinning of long bones, pathologic fx, and failure to thrive.

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53
Q

How does beta-thalassemia MINOR present on a peripheral smear?

A

Hypochromic, microcytic cells
Target cells

Note:
Similar to an alpha thalassemia.

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54
Q

How does beta-thalassemia Intermedia present on a peripheral smear?

A

Hypochromic, microcytic cells
Target cells
Poikilocytosis

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55
Q

How does beta-thalassemia Major present on a peripheral smear?

A

Hypochromic, microcytic cells
Target cells
Poikilocytosis
NUCLEATED RBCs

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56
Q

How is beta thalassemia minor treated?

A

Minor requires just genetic counseling and rare transfusions.

Note:
Monitor for iron overload just like alpha.

57
Q

How is beta thalassemia intermedia treated?

A

Genetic counseling

Avoid iron supplements
Transfusions
Splenectomy (consider)
Iron overload

58
Q

How is beta thalassemia major treated?

A

Genetic counseling
Transfusion-dependent
Avoid iron supplements and monitor iron overload.
Splenectomy
Luspatercept (Reblozyl)

DEFINITIVE TX: Allogeneic bone marrow transplant.

59
Q

What is Luspatercept? Who uses it?

A

It is an Activin-A-trap drug indicated for transfusion dependent ADULT beta thalassemia pts.

CI: Splenectomy, pregnancy, breastfeeding.

60
Q

What causes SCD?

A

It is an autosomal recessive inherited disease.

Abnormal beta-chain substitution results in a betaS chain.

It can appear as heterozygous (trait) or homozygous (anemia)

61
Q

What is HbS?

A

2 alpha chain, 2 betaS chain hemoglobin.

62
Q

What demographic is most susceptible to SCD?

A

African Americans (8% in US are carriers)

63
Q

Describe the pathology of SCD.

A

Unstable HbS polymerization results in sickle shaped cells.

Sickle shaped cells cause vaso-occlusion in all vessels and are sticky to endothelium.

This results in ischemia, pain, and end-organ damage.

64
Q

How does the spleen play a role in SCD?

A

It sequesters and destroys the sickle RBCs, but this can lead to hypoxemia, acidosis, infection, excessive exercise, abrupt temperature changes, and anxiety/stress.

65
Q

Is SCD extra or intravascular?

A

Extravascular.

66
Q

What is the only real change between normal and SCT?

A

Decrease in HbA and presence of HbS on electrophoresis.

67
Q

What changes between SCT and SCD?

A

Decreased Hct
Lack of HbA
Increased HbF
Highly increased HbS

68
Q

What lab findings would I expect in SCD?

A

Hgb/Hct: normal in trait, decreased in SCD.
MCV: normal
Retic: Minor increase
WBC: Elevated (12-15k)
Hb electrophoresis: Presence of HbS band + abnormal proportions of other Hgb.

69
Q

How does SCD present on peripheral smear?

A

Target cells
Sickled RBCs
Howell-Jolly inclusion body (tiny very dark purple spot in a cell)

70
Q

How does SCT present clinically?

A

Asymptomatic generally unless under heavy physical stress.

71
Q

How does SCD present clinically?

A

Starts around 6mo.

Chronically ill
Jaundice, pallor, poor healing LE ulcers >10 yo
Pain/swelling, dactylitis
Vision changes, retinopathy, retinal detachment
Splenomegaly > 3yo, hepatomegaly, gallstones
Cardiomegaly, hyperdynamic precordium

72
Q

How does sickle cell crisis present clinically?

A

Ischemic injury to organ, causing sudden pain that may resolve spontaneously.

Fever, tachycardia, tenderness, anxiety

Main locations of ischemia:
<18m = hands/feet
Child/teen = long bones of arm and legs
Adults = vertebrae

Triggers are stress.

Note:
Fever appears bc of RBC death, which trigger inflammation.

73
Q

What retinal signs would I expect on someone with sickle cell anemia?

A

Retinal hemorrhage
Cotton wool spots
Venous tortuosity

74
Q

Why is sickle cell anemia more dangerous than thalassemia and spherocytosis?

A

Sickle cell anemia blocks blood vessels, whereas the spleen is the only place the other two get stuck in.

75
Q

How is sickle cell anemia treated in terms of lifestyle adjustments?

A

Avoiding triggers:

Hypoxemia
Temperature changes
Dehydration
Acidosis
Stress

76
Q

How is sickle cell anemia treated pharmacologically?

A

Folic acid supplement

Vaccines
ACE inhibitors
Omega-3 fatty acids
Transfusions PRN
Pain management
Abx prophylaxis until age 5 to protect the spleen

77
Q

What medication is given for pts with multiple pain crises a year in sickle cell anemia?

A

Hydroxyurea

78
Q

What is the function of hydroxyurea?

A

Increases HbF levels, prolonging pt survival.

Suppresses bone marrow as a MAJOR SE. Increased risk of cancer!

79
Q

What MAB is given in sickle cell treatment and why?

A

Crizanlizumab (Adakveo).

Alternative to hydroxyurea, decreases vaso-occlusive episodes by reducing RBC interaction with endothelium.

EXPENSIVE and IV only. No major SE.

80
Q

What supplement is given in sickle cell treatment that must be pharmaceutical-grade?

A

L-glutamine (endari).

Alternative to hydroxyurea, decreases vaso-occlusive epsides by reducing oxidative stress.

EXPENSIVE, minimal SE since it is only a supplement.

81
Q

What is the main protocol for treatment of an acute sickle cell crisis?

A

HOP
Hydration
Oxygenation
Pain control

82
Q

What is an exchange transfusion?

A

Exchanging sickle blood out for donor blood.

Commonly used in vaso-occlusive crises, pain crises, priaprism, stroke, and severe sequelae

83
Q

What is a splenic sequestration crisis? How do I recognize and treat it?

A

Disproportionate amount of blood being sequestered in the spleen.

Presentation: Rapidly enlarging spleen + Hgb drop of >2g/dL below baseline.

Treated via splenectomy. 10-15% mortality if not addressed.

84
Q

What is the definitive treatment for sickle cell anemia?

A

Allogeneic hematopoietic stem cell transplantation.

Curative in 80% of cases prior to end-organ damage.

85
Q

What demographic is most susceptible to a G6PD deficiency?

A

African-American MALES

X-linked recessive genetic defect.

86
Q

Describe the pathology of a G6PD deficiency.

A

RBCs vulnerable to oxidative stress, which will cause them to denature and form precipitate known as a Heinz body.

Heinz bodies damage the RBC’s membrane, so the spleen will recognize them as injured and destroy them.

RBCs can also pop spontaneously.

87
Q

How does a G6PD deficiency present?

A

Asymptomatic.

It is an episodic hemolytic anemia triggered by 3 major things.

Acute episodes include malaise, weakness, abd/lumbar pain, jaundice, and dark urine.

88
Q

What are the 3 major triggers in G6PD deficiencies?

A

Abx: sulfa, quinolones, nitrofurantoin/macrobid
aspirin & Phenazopyridine (Azo)
Foods: FAVA BEANS, soy, red wine, other beans, blueberries.

89
Q

If I have jaundicing or dark urine, what does that suggest about the hemolysis characteristic?

A

It is intravascular.

90
Q

Why is splenomegaly not present in G6PD deficiencies?

A

It is episodic and has no infarcts, so the spleen is fine.

91
Q

What lab findings would I expect in a G6PD deficiency?

A

Hgb/Hct: normal, but low during episodes.
MCV: normal
Retic: Normal, but high during episodes or post-episode.
MCH: normal
G6PD Assay: Decreased, but normal/increased after an episode.

92
Q

How does G6PD deficiency present on peripheral smear?

A

Bite cells
Blister cells
Polychromataphils/Reticulocytes

93
Q

How does G6PD deficiency present on a specially green-stained peripheral smear?

A

Heinz bodies (little freckles)

94
Q

What preventative measures should a G6PD deficient person take?

A

Avoiding oxidant drugs
Avoiding trigger foods
Genetic counseling

95
Q

What is a supportive therapeutic measure a G6PD deficient person should take?

A

Folic acid supplement.

96
Q

What is autoimmune hemolytic anemia? (AIHA)

A

it is when an antibody forms against surface RBC antigens.

50% of cases are idiopathic.

97
Q

What are the two types of immune hemolytic anemias?

A

Drug-induced
Autoimmune.

98
Q

What causes drug-induced immune hemolytic anemia?

A

ABX (Cephalosporins, PCNs, quinolones)
Methyldopa
Levodopa
NSAIDs

99
Q

What diseases commonly cause AIHA?

A

SLE
CLL (chronic lymphocytic leukemia)
Lymphoma

100
Q

How does AIHA present?

A

Abrupt and rapid onsets.

Fatigue, jaundice, splenomegaly

10% mortality

101
Q

Describe the pathology of AIHA.

A

RBCs are tagged for destruction by the immune system.

This results in splenic macrophages removing portions of the RBC’s membrane, making them into spherocytes. Spherocytes get stuck in the spleen and destroyed.

Second way is that complements tag the RBCs and they are destroyed by Kupffer cells in the liver.

IgM can also help facilitate MAC-induced direct intravascular hemolysis.

102
Q

What are the two types of AIHA?

A

Warm and cold.

Warm occurs at normal body temp.

Cold activates cold agglutinins.

103
Q

What kind of anemia is AIHA? (Morphologically)

A

Normocytic normochromic anemia.

104
Q

What lab findings would I expect in AIHA?

A

Hb/Hct: decreased
RBC: decreased
MCV: normal
Retic: normal
MCH: normal
Platelets: 10% will have immune thrombocytopenia
Dx test: Coombs test, either direct or indirect.

105
Q

What are the two Coombs tests?

A

Coombs test, aka antiglobulin test, has a direct and indirect version.

106
Q

Describe the direct coombs test.

A

The Coombs reagent is added to a blood sample with AIHA.
The AIHA blood should have antibodies already attached to the RBC’s antigens.

107
Q

Describe the indirect coombs test.

A

Serum is obtained containing just antibodies.

Donor blood is added to the serum.

The serum antibodies should target the blood antigens, forming the complex.

Coombs reagent is added.

108
Q

When do I use a direct vs indirect coombs test?

A

It is used to check for hemolytic disease of the newborn.

The fetus will have a positive DIRECT coombs test, since the fetus has the antigens on its blood.

The mother will have a positive INDIRECT coombs test, since her serum contains antibodies. Her blood cells lack the antigens.

109
Q

How does AIHA present on peripheral smear?

A

Marked MICROspherocytosis
Polychromataphils/reticulocytes

110
Q

What is the main medication used to treat AIHA? Secondary?

A

Prednisone.

Sometimes rituximab (Rituxan)

111
Q

What treatment is done for severe AIHA?

A

Splenectomy

112
Q

Why is type/cross matching not required for transfusing an AIH patient?

A

new RBCs will be attacked by the immune system regardless.

113
Q

What is hemolytic disease of the newborn also known as?

A

Erythroblastosis fetalis

114
Q

What is the cause of erythroblastosis fetalis?

A

Maternal IgG binds to antigens of the surface of fetal RBCs.

This is caused by 3 things:
Fetal-maternal hemorrhage, aka exposure of placenta to maternal blood.
Maternal transfusion
Maternal pre-existing anti-A or anti-B antibodies

Essentially, maternal blood must be exposed to fetal blood.

115
Q

Describe the pathology of erythroblastosis fetalis.

A

Maternal IgGs cross placenta to fetal circulation and bind to their RBCs.

This causes hemolysis of the affected RBCs and causes fetal anemia.

116
Q

What demographic is most susceptible to erythroblastosis fetalis?

A

An Rh- mother with an Rh+ father/fetus.

MC: anti-ABO antibodies.
Most severe: Anti-Rh antibodies.

117
Q

Why is the second fetus most susceptible to hemolytic disease of the newborn?

A

The first fetus would cause the sensitization and cause mom to produce the antibodies. However, the first fetus would not be exposed.

118
Q

How does hemolytic disease of the newborn present?

A

Severe jaundice
Anemia at birth
Positive DIRECT coombs test
Hepatosplenomegaly
Edema (fetal hydrops possible)
HF (if severe)

119
Q

How does hemolytic disease of the newborn get tested maternally?

A

INDIRECT coombs test

120
Q

How is hemolytic disease of the newborn treated before birth?

A

Intrauterine fetal transfusions
Early induction of labor
Maternal plasma exchange (reducing circulating Ig levels)

121
Q

How is hemolytic disease of the newborn treated post-birth?

A

Transfusion
Supportive care

122
Q

Why is RhoGAM given?

A

Prevents an immune response in an Rh- mother to Rh+ blood.

RhoGAM should be given even if fetus #1 was fine.

123
Q

How does paroxysmal nocturnal hemoglobinuria present initially?

A

Dark red urine in the morning.

124
Q

What causes paroxysmal nocturnal hemoglobinuria?

A

Acquired genetic defect leading to the lysis of RBCs.

Specifically, it is a deficit in complement-regulating cell membrane proteins CD55 and CD59. (These keep complements calm)

125
Q

What demographic is most susceptible to PNH?

A

young adults

Both genders

No evidence of heritability. It is acquired.

126
Q

Describe the pathology of PNH.

A

RBCs vulnerable to lysis by complement leads to MAC formation and RBC destruction.

Free Hb depletes NO, which eventually leads to esophageal spasms, ED, renal damage, and thrombosis.

Free Hb is toxic, hence why NO must stop it.

127
Q

How does PNH present?

A

Episodically, with dark-red urine in the morning due to an overnight blood pH drop with gradual improvement throughout the day.

S/S of thrombosis, especially in mesenteric veins, liver, skin, and CNS.

Life expectancy: 10-15 years.

Sometimes has S/S of anemia also.

128
Q

What kind of anemia is PNH? (Morphologically)

A

Normocytic, normochromic anemia.

129
Q

What lab findings would I expect in PNH?

A

Hb/Hct: variable reductions.
Retic: normal/increased
MCV: normal
MCH: normal
Iron: normal or decreased
WBC: normal or decreased
Platelets: normal or decreased

130
Q

What diagnostic lab test can I run for PNH?

A

Urine hemosiderin, which can be + even after the urine Hb clears.

Flow cytometry: gold standard

131
Q

What causes decreased iron in PNH?

A

The loss of Hb in the urine.

132
Q

How is PNH treated if severe?

A

Allogeneic hematopoietic stem cell transplant for severe/aplastic anemia.

Eculizimab (C5 MAB) for severe hemolysis or thrombosis.

133
Q

What supportive therapy is done for PNH?

A

Transfusions PRN
Iron replacement therapy
Corticosteroids to reduce hemolysis.

134
Q

What are causes of anemia due to acute blood loss?

A

Posthemorrhagic anemia

Trauma, post-partum hemorrhage.
GI bleed, ruptured ectopic pregnancy, ruptured spleen, sub-arachnoid hemorrhage.

135
Q

What can cause chronic anemia?

A

Iron deficiency anemia.

136
Q

How does hypovolemia hide anemia?

A

Proportionate drops in plasma cause Hct to look normal.

137
Q

How does the body compensate for hypovolemia but result in anemia?

A

Movement of fluid into intravascular spaces.

CBC will now show anemia relative to the severity of blood loss.

138
Q

How does the body attempt to correct anemia?

A

Bone marrow production can ramp up to 8x.
Transient reticulocytosis.

139
Q

If the cause of the anemia due to blood loss is unknown, what can be done?

A

Investigative studies: EGD, colonoscopies, US, etc.

Transfusions PRN
Fluid replacement PRN
Supplemental iron PRN

(C) CM 1A: Heme/Onc/Endo (28 decks)

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