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Hem/Onc > Anemias- part 1 > Flashcards

Anemias- part 1 Flashcards

1
Q

What are the parameters of a male patient being anemic?

A

Hgb less than 13.6 g/dL
Hct less than 41%

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2
Q

What are the parameters of a female patient being anemic?

A

Hgb less than 12.0 g/dL
Hct less than 36%

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3
Q

What are the 3 major causes of anemia

A

Decreased production of red blood cells (RBCs)
Increased destruction of RBCs (hemolysis)
Increased RBC loss

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4
Q

Define intravascular hemolytic anemia

A

RBCs lyse within the blood vessels

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5
Q

With intravascular hemolytic anemia large amounts of _____ are released into circulation

A

Hgb

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6
Q

intravascular hemolytic anemia (increase/decrease) in haptoglobin

A

decrease

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7
Q

Schistocyte formation is seen in what kind of anemia?

A

intravascular hemolytic anemia

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8
Q

The retic count will (increase/decrease) with decreased production of RBCs

A

decrease

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9
Q

The retic count will (increase/decrease) with increased destruction of RBCs

A

increase

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10
Q

The retic count will (increase/decrease) with increased RBC loss

A

increase

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11
Q

In extravascular hemolytic anemia, what is haptoglobin doing?

A

Haptoglobin may or may not decrease

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12
Q

What kind of anemia are RBCs are destroyed within organs (spleen, liver)?

A

Extravascular hemolytic anemia

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13
Q

In (intra/extra)vascular hemolytic anemia, there will be a decrease in iron over time

A

intravascular

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14
Q

In (intra/extra)vascular hemolytic anemia, iron is recovered and stored

A

extravascular hemolytic anemia

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15
Q

In what kind of anemia, do you see spherocyte formation

A

Extravascular hemolytic anemia

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16
Q

In (intra/extra)vascular hemolytic anemia, it is more common to see splenic enlargement

A

extravascular

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17
Q

In (intra/extra)vascular hemolytic anemia, it is more common to see red-brown urine discoloration

A

Intravascular

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18
Q

In hemolytic anemias labs, what are Hgb, MCV and retic increasing or decreasing?

A

Hgb: normal or reduced
MCV: often increased
Retic: usually increased

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19
Q

In hemolytic anemias labs, what are Bilirubin, LDH and Haptoglobin doing increasing or decreasing?

A

Bilirubin - increased (esp. unconjugated)

LDH - increased

Haptoglobin - decreased (intravascular hemolysis)
Inflammatory marker - can lead to false elevations
May or may not be decreased in extravascular hemolysis

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20
Q

What is hereditary spherocytosis caused by? How common is it?

A

Inherited genetic defect; 1 in 5000 (northern Europeans)

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21
Q

Hereditary spherocytosis is considered ____ _____ disorders

A

autosomal dominant

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22
Q

Is hereditary spherocytosis intra or extra? Why?

A

extravascular, because the round cells (not biconcave discs) are destroyed by the SPLEEN

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23
Q

Hereditary spherocytosis PE will present with ????? (4 things)

A

Jaundice, enlarged spleen
+/- gallstones (50% of pts)
May acutely present after infection

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24
Q

What is a disorder that can cause ↑ MCHC in microcytosis/normocytosis

A

Hereditary spherocytosis

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25
Q

Why would you order a Coombs test if you are considering hereditary spherocytosis?

A

to r/o autoimmune hemolysis (should be negative)

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26
Q

What is the treatment for Hereditary spherocytosis?

A

All - Folic acid (1 mg daily)

Transfusions - If anemia becomes severe
—EPO - may reduce need for transfusion in infants

Definitive tx - Splenectomy (partial or full)
Delay until after 5 yrs of age, or until puberty if moderate
If mild - may observe
Antipneumococcal vaccination

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27
Q

Why do you need to wait until 5yrs old to perform a splenectomy in a hereditary spherocytosis pt?

A

kids need their spleen to fight infections

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28
Q

Hemoglobin A is made up of _____ and _____

A

2 alpha and 2 beta

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28
Q

Hemoglobin B is made up of _____ and _____

A

2 alpha and 2 Delta

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29
Q

Hemoglobin F is made up of _____ and _____

A

2 alpha and 2 gamma

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30
Q

______ 2 copies of alpha-globulin gene (4 total)

A

chromosome 16

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31
Q

_____ 1 copy of beta-globulin gene (2 total)

A

chromosome 11

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32
Q

What is alpha thalassemias caused by?

A

Gene deletions → reduced alpha-chain synthesis

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33
Q

What kind of anemia is caused by increased numbers of small, “pale” (low Hb) RBCs

A

Alpha thalassemias

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34
Q

______: Excess beta chains precipitate → damage to RBC membranes → hemolysis in marrow and in splenic vessels

A

alpha thalassemia

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35
Q

What is the MC type of demographic associated with alpha thalassemia?

A

southeast asian and Chinese descent
- mediterranean or african

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36
Q

a normal pt has _____ alpha-globulin gene

A

4

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37
Q

an alpha thalassemia minima (silent carrier) pt has _____ alpha-globulin gene

A

3

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38
Q

an alpha thalassemia minor pt has _____ alpha-globulin gene

A

2

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39
Q

Hemoglobin H disease pt has _____ alpha-globulin gene

A

1

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40
Q

hydrops fetalis pt has _____ alpha-globulin gene

A

0

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41
Q

Alpha thalassemia pts Hgb, RBC and MCV will be (increased/decreased)

A

Hgb/Hct - normal or decreased
RBC - increased
MCV - markedly decreased

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42
Q

Alpha thalassemia pts Retic, MCH, Hemoglobin electrophoresis will be (increased/decreased)

A

Reticulocytes - normal or increased

MCH - decreased

Hemoglobin electrophoresis
Normal in silent carriers and alpha thalassemia minor
Presence of HbH band in patients with HbH disease

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43
Q

What do you need to monitor an alpha thalassemia minor patient for?

A

iron overload- iron chelation if necessary

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44
Q

What is the treatment for Hemoglobin H disease?

A

folic acid supplementation (1 mg/day)

Avoid iron supplements and oxidative drugs (sulfa drugs, antimalarials, isoniazid, nitrofurantoin)

May require transfusions on a regular regimen (goal hemoglobin - 9.5-10.5 mg/dL)

May consider splenectomy if severe anemia or frequent transfusions needed

Must monitor for iron overload - iron chelation if necessary

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45
Q

If a fetus is diagnosed with hydrops fetalis in utero, what is the recommendation?

A

Recommended termination of pregnancy due to maternal morbidity

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46
Q

What is beta thalassemias caused by?

A

Gene point mutations → reduced beta-chain synthesis

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47
Q

What does beta+ mean?

A

reduced, but not absent, beta-chain synthesis

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48
Q

What does beta0 mean?

A

absent beta-chain synthesis

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49
Q

In a beta thalassemias pt, what does their Hb electrophoresis results look like?

A

Increased proportion of HbA2 and HbF

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50
Q

What is the MC demographic of a beta thalassemias pt?

A

MC in pts of Mediterranean descent
May be seen in pts of African and Asian descent as well

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51
Q

What kind of anemia has increased numbers of small, “pale” (low Hb) RBCs?

A

beta thalassemias

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52
Q

______: Excess alpha chains precipitate → damage to RBC membranes → hemolysis in marrow, spleen, liver

A

Beta thalassemias

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53
Q

what do the inclusion bodies present on RBCs lead to ?

A

damaged erythroid precursors

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54
Q

What kind of anemia?

A

beta-thalassemia minor

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55
Q

What kind of anemia?

A

beta- thalassemia intermedia

will need occasional blood transfusions

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56
Q

What kind of anemia?

A

(Cooley’s Anemia or
Beta-thalassemia major)

will be blood transfusion dependent

57
Q

What kind of anemia is associated with “chipmunk facies”. What causes it?

A

severe beta thalassemia

erythroid hyperplasia

58
Q

What kind of anemia would you find the hemoglobin electrophoresis with abnormal proportions of HbA, HbA2, HbF?

A

Alpha thalassemia

59
Q

Name some additional exam findings of beta thalassemia?

A

thinning of long bones, pathologic fracture, failure to thrive

60
Q

What would the lab findings be on a patient with beta thalassemia?

A

Hgb/Hct - decreased
RBC - increased
MCV - markedly decreased
Reticulocytes - normal or increased
MCH - decreased

61
Q

How do you treat thalassemia intermedia?

A

Avoid iron supplements (may need if secondary conditions causing iron deficiency arise)

May require transfusions, especially in times of physiologic stress

May consider splenectomy if severe anemia or frequent transfusions needed

Must monitor for iron overload - chelation if necessary

62
Q

What is the treatment for beta thalassemia major?

A

allogeneic bone marrow transplant
Splenectomy
Regular transfusions (goal hemoglobin 9.5-10.5 mg/dL); frequently transfusion-dependent
Avoid iron supplements

63
Q

What is Luspatercept (Reblozyl) indicated for? What must you NOT be actively doing?

A

transfusion-dependent adult beta thalassemia patients

Must not have not had splenectomy, must not be pregnant or breastfeeding

64
Q

_____ autologous hematopoietic stem cells are transduced with the BB305 lentiviral vector to have a functional beta-globin gene

A

Betibeglogene autotemcel (Zynteglo, Beti-cel)

65
Q

_____ autologous hematopoietic stem cells undergo gene editing with CRISPR/Cas9 to disrupt the BCL11A gene, leading to increased HbF production instead of HbA

A

Exagamglogene autotemcel (Casgevy, Exa-cel)

66
Q

Which of the beta thalassemia treatment is more precise and has less risk of metagenesis?

A

Exagamglogene autotemcel (Casgevy, Exa-cel)

67
Q

_____ pyruvate kinase activator; may help improve ATP production; helped with alpha-thalassemia and beta-thalassemia

A

mitapivat

68
Q

____ HDAC inhibitors, decitabine, JAK2 inhibitors , drugs acting on hepcidin, stem cell factor drugs

A

improved erythropoiesis

69
Q

_____ increased HbF production, but not found to be especially helpful in beta-thalassemia, possibly due to decreased erythropoietin efficiency in this population

A

hydroxyurea

70
Q

_____ is autosomal recessive inherited disease

A

sickle cell disease

71
Q

_____ is caused an abnormal substitution of an amino acid in the beta chain (betaS)

A

sickle cell disease

72
Q

What is hemoglobin S composed of?

A

Hb composed of 2 alpha chains and 2 betaS chains

73
Q

What is the MC demographic associated with sickle cell?

A

MC in African Americans (8% in US are carriers)

1 in 400 black children in US will be born with sickle cell anemia

Also seen in pts of Mediterranean, Latin, and Native American descent

74
Q

What anemia is associated with unstable HbS polymerizes → abnormally shaped RBCs

A

sickle cell disease

75
Q

What are some s/s of vasoocclusion episode?

A

ischemia, pain,
end-organ damage

76
Q

What are some triggers for sickle cell episode?

A

hypoxemia, acidosis, infection, excessive exercise, abrupt temperature changes, anxiety/stress

77
Q

What does a patient with this B-globulin genes called? What is their percent breakdown of hemoglobin?

A

Sickle cell trait

60% HbA
40% HbS

78
Q

What does a patient with this B-globulin genes called? What is their percent breakdown of hemoglobin?

A

Sickle cell anemia

HbA: 0%
HbA2: 1-3%
HbF: 5-15%
HbS: 86-98%

79
Q

What is the lab findings of a patient with sickle cell disease?

A
80
Q

What kind of inclusions are commonly found on a peripheral smear of a sickle cell pt?

A

Howell- Jolly inclusion body

81
Q

Why is the WBC usually elevated in a pt with sickle cell disease?

A

because of the low levels of chronic inflammation

82
Q

When might a patient with sickle cell trait experience symptoms?

A

May have s/s during physical stress (high altitudes, heavy exercise, dehydration)

83
Q

When do the s/s of sickle cell disease begin to appear?

A

start around 6 months old

84
Q

Name some common s/s associated with sickle cell disease?

A

General - often appear chronically ill

Skin - jaundice, pallor, poorly healing ulcers of LE (>10 y/o)

Extremities - pain and swelling, dactylitis (“sausage fingers/toes”)

Eyes - vision changes, retinopathy, retinal detachment

Abdomen - splenomegaly (<3 y/o), hepatomegaly, gallstones

Chest - cardiomegaly, hyperdynamic precordium

85
Q

What is the clinical presentation of a sickle cell crisis?

A

Sickled RBCs obstruct microcirculation = ischemic injury to 1+ organs

**Pain - sudden, lasts from hours to weeks, resolves spontaneously

Fever, tachycardia, tenderness, anxiety

86
Q

Where is the most common place for a child less than 18 months old to have a sickle cell crisis?

A

hands/feet

87
Q

Where is the most common place for a child/teen to have a sickle cell crisis?

A

long bones of the arms and legs

88
Q

Where is the most common place for an adult to have a sickle cell crisis?

A

vertebrae

89
Q

Name some common triggers for a sickle cell crisis

A

physical stressors (hypoxia, dehydration, infection, acidosis)
change in temperature (fever or environment)
fatigue; pregnancy; alcohol; psychosocial stress

90
Q

_____ ischemia manifested by acute pain and
tenderness, fever, tachycardia, and anxiety

A

sickle cell crisis

91
Q

Name some supportive treatments for sickle cell anemia

A

Folic Acid - supplement 1 mg/day, every day

Vaccines - Pneumococcal, Meningococcal, Influenza, COVID, all standard childhood vaccines

ACE inhibitors - pts with proteinuria due to kidney damage

Omega-3 Fatty Acids - may reduce vaso-occlusive crises

Transfusions - PRN for aplastic or hemolytic crises

Pain Management

Antibiotics

92
Q

Why, what and until what age do you a child with sickle cell anemia?

A

prophylactically give PCN daily until age 5 because their immune system is compromised and easily susceptible to disease

93
Q

What is considered the mainstay for sickle cell anemia treatment?

A

Hydroxyurea (Doxia, Hydrea, Siklos)

94
Q

How does Hydroxyurea (Doxia, Hydrea, Siklos) work?

A

Increases HbF levels; and reduces vaso-occlusive episodes and hospitalizations

95
Q

What is the major SE of increased hydroxyurea?

A

MAJOR bone marrow suppression, specially WBC/neutrophils

96
Q

What are additional SE associated with hydroxyurea?

A

May cause vasculitic skin ulcers
May see increased cancer risk (leukemia, skin CA) with prolonged use
Teratogenic - should not take if possibility of pregnancy

97
Q

_____ monoclonal antibody against P-selectin proteins on endothelial cells and platelets.

A

Crizanlizumab (Adakveo)

sickle cell anemia

98
Q

When is Crizanlizumab (Adakveo) mainly used?

A

Mainly used in patients who do not tolerate or respond to hydroxyurea

99
Q

______ Decreases vasoocclusive episodes by reducing interaction between RBCs and endothelium

A

Crizanlizumab (Adakveo)

100
Q

______ Decreases vasoocclusive episodes possibly by reducing oxidative stress that promotes sickling

A

L-glutamine (Endari)

101
Q

Crizanlizumab (Adakveo) is given in what form?

L-glutamine (Endari) is given in what form?

A

Given as IV every 2-4 weeks; expensive

Must be pharmaceutical-grade powder, mixed with food or water; expensive

102
Q

What do you do in an acute sickle cell crisis?

A

Exchange transfusions

103
Q

______ disproportionate amount of blood sequestered in spleen

A

splenic sequestration crisis

104
Q

When can a splenic sequestrian crisis happen in a sickle cell pt? What is the mortality rate? What do you usually do after the crisis has resolved?

A

when the hgb drop of more than 2 g/dL below baseline

10-15% mortality rate

splenectomy: to prevent recurrence

105
Q

What is the definitive treatment to sickle cell anemia?

A

allogeneic hematopoietic stem cell transplantation

106
Q

Name some emerging/investigational treatments to sickle cell anemia

A

Activating pyruvate kinase - mitapivat, etavopivat

Increasing RBC hydration - senicapoc, memantine

Increasing tissue oxygen delivery - sanguinate (pegylated bovine carboxyhemoglobin)

Decreasing inflammation and cell adhesion - several interventions, including IVIG

Decreasing oxidative stress - cathepsin B inhibitors, L-arginine

107
Q

What is Lovotibeglogene autotemcel (lovo-cel, Lyfgenia) gene therapy targeting?

A

artificial anti-siclking beta globin gene

108
Q

What is Gamma-globulin upregulation (exa-cel, Casgevy) gene therapy targeting?

A

increased Hb F production

109
Q

What anemic disease is x-linked recessive genetic defect?

A

G6PD deficiency

110
Q

What does G6PD deficiency mean?

A

Deficit in glucose-6-phosphate dehydrogenase enzyme

111
Q

What is the MC enzyme deficiency in humans - 400 million people worldwide

A

G6PD deficiency mean?

112
Q

What is the MC demographic for G6PD deficiency?

A

African-American males
Also seen in pts of Asian and Mediterranean descent

rarely seen in the females

113
Q

What inclusion body is seen in G6PD deficiency?

A

Heinz bodies

114
Q

What disease are RBCs especially vulnerable to oxidative stress?

A

G6PD deficiency

115
Q

Is G6PD deficiency (intra/extra)vascular?

A

both can be intra and extravascular

116
Q

What will G6PD deficiency present like in a newborn?

A

prolonged jaundice

117
Q

What are the three major triggers of G6PD deficiency?

A

Antibiotics - sulfas, quinolones, nitrofurantoin

Phenazopyridine (Azo), aspirin

Foods - **fava beans, soy, red wine, other beans, blueberries

118
Q

What will an acute episode of G6PD deficiency present as?

A

malaise, weakness, abdominal or lumbar pain, jaundice, dark urine

119
Q

What are some therapeutic measures of G6PD deficiency?

A

Removal of offending agent
Dietary restrictions - fava beans (including falafel)
Supportive - folic acid supplementation
Transfusions may rarely be needed

120
Q

______ Antibody forms against surface RBC antigens (mostly IgG)

A

Autoimmune hemolytic anemia

121
Q

What diseases can cause autoimmune hemolytic anemia?

A

systemic lupus erythematosus, chronic lymphocytic leukemia, lymphoma

122
Q

What drugs are commonly associated with drug-induced hemolytic anemia?

A

ABX (cephalosporins, PCNs, quinolones), methyldopa or levodopa, or NSAIDs

123
Q

______ RBCs “tagged” for destruction by immune system

A

autoimmune hemolytic anemia

124
Q

What anemia is associated with Splenic macrophages remove portions of RBC membrane → spherocyte formation results?

A

Autoimmune Hemolytic Anemia

125
Q

Complement can also tag RBC for destruction by _____ in liver

A

Kupffer cells

126
Q

____ can help facilitate MAC-induced direct intravascular hemolysis

A

IgM

127
Q

What is the difference between warm and cold autoimmune hemolytic anemia?

A

Warm - happens at normal body temperatures (more common)

Cold - only becomes active at colder temperatures (“cold agglutinins”)

128
Q

Describe what is happening in a direct Coombs test?

A

Reagent (IgM against human IgG or complement) mixed with pt RBCs

Agglutination = Ig, complement, or both on RBC surface

129
Q

Describe what is happening in an indirect Coombs test

A

Pt serum is mixed with RBCs (type O or donor); reagent is added
Agglutination = Ig in serum against RBCs

130
Q

What is the treatment for autoimmune hemolytic anemia?

A

Prednisone 1-2 mg/kg/day orally in divided doses

possible folic acid supplementation

transfusions: may be given without matching blood types

131
Q

What is another name for Hemolytic Disease of the Newborn?

A

Erythroblastosis fetalis

132
Q

_____ is Maternal IgG to antigens on surface of fetal RBCs

A

Hemolytic Disease of the Newborn

133
Q

Maternal ____ to fetal RBCs cross placenta to fetal circulation and bind to fetal RBCs

A

IgGs

Hemolytic Disease of the Newborn

134
Q

What is the classic example of hemolytic disease of the newborn?

A

classic case is Rh- mother and Rh+ father/fetus
MC type - anti-ABO antibodies; Most severe - anti-Rh antibodies

135
Q

What are the common s/s of a newborn born with Hemolytic Disease of the Newborn?

A

Severe jaundice
Anemia at birth
Positive direct Coombs test (indirect combs test will negative)
Hepatomegaly
Splenomegaly
Edema possible
Ranging from mild to fetal hydrops
Heart failure possible
If severe anemia/hydrops present

136
Q

A mother whose baby was just born with Hemolytic Disease of the Newborn her indirect coombs test will be _____ and direct coombs test will be _____

A

Indirect: positive

Direct: negative

137
Q

Before birth, what is the treatment for Hemolytic Disease of the Newborn?

A

Intrauterine fetal transfusion

Early induction of labor (once fetus is old enough to survive)

Maternal plasma exchange (reduces circulating Ig levels)

138
Q

After birth, what is the treatment for Hemolytic Disease of the Newborn?

A

Transfusion
Supportive care - phototherapy, IVIG to reduce hemolysis, synthetic EPO agents

139
Q

_____ prevents immune response to Rh+ blood in Rh- mother

A

RhoGAM

140
Q
A

Hem/Onc (14 decks)

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