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Hematology > Anemia > Flashcards

Anemia Flashcards

1
Q

anemia

A

reduction in Hb concentration or decrease in number or RBC/mm

-too low to deliver O2 to meet cellular demands

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2
Q

what type of anemia can be seen in the newborn period?

A

blood loss, hemolytic dz of the new born

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3
Q

what can cause the decreased production of RBC?

A

Hb synthesis

Fe deficiency

Thalassemia

Anemia of chronic dz

DNA synths

Aplastic anemia

myeloproliferative leukemia

Bone marrow infiltration

carcinoma

lymphoma

pure red cell aplasia

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4
Q

what can cause increased production of RBC?

A

blood loss

intrinsic hemolysis

hereditary spherocytosis

Elliptocytosis

Sickle cell

unstable hb

G6PD defi

extrinsic hemolysis

warm/cold antibody

TTP-HUS

mechanical cardiac valve

clostridial infxn

hypersplenism

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5
Q

how to you classify anemia?

A

decreased production of RBC (reticyocyte count low)

increasd destruction of RBC (hemolysis)

Red cell loss (reticuloctye count high)

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6
Q

early infancy anemia causes

A

pure red cell aplasia, physiologic anemia

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7
Q

6 mnth to 12 years anemia

A

nutritional anemias, acute inflammation (illness) bone marrow infiltration

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8
Q

signs and sx of anemia

A

** few physiologic distrubance < 7-8

decreased O2 transport- fatigue, dyspnea, syncope

decreased blood volume - pallor, postrual hyptension

increased cardiac OP_ congestive heart failure

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9
Q

what is the most usueful lab for anemai?

A

reticulocyte count for the cause of anemia

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10
Q

what are you looking at during a blood smear?

A
  • normocytic, microcytic, macrocytic
  • normochromic, hypechromic, hyop

+/- spherocytes, schistocytes,

maybe see polychromasia

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11
Q

direct coombs test

A

prenatal testing of pregnant women and in testing blood prior to a blood transfusion.

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12
Q

microcytic hypochromic anemia

A

Iron def
lead poisoning
thalassemia (minor-beta/alpa)
beta-thalassemia

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13
Q

Iron def anemia

A

the most common during childhood. Usually seen between 6-24 months, but not uncommon during adolescence. More common during periods of rapid growth and higher potential for inadequate dietary iron

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14
Q

if pt is chronically taking ASA/NSAids

A

maybe contributing to iron def

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15
Q

CF of iron def

A

o With moderate (Hgb 6-8 g/dL)  pallor, fatigue, irritability, tachycardia, cardiomegaly, systolic murmurs (LSB), pica, decreased appetite, decreased exercise tolerance
-Pica is the hallmark of iron deficiency
-Severe deficiency (Hct < 25%) :
brittle nails, cheilosis, smooth tongue, formation of esophageal webs (Plummer-Vinson syndrome

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16
Q

Plummer-Vinson Syndrome

A

“The Plumber Vincent DIGS a hole for the IRON pipie”

D= dysphagia from esophageal webs
I=Iron def anemoa
G=Glossitis
S= squamous cell carcinoma

IRON=tx

think severe deficiency!

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17
Q

lab findings in fe def anemai

A

 Decreased Hgb, MCV, ferritin

  • Increased TIBC
  • Hypochromic, microcytic RBC. Anisocytosis and poikilocytosis
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18
Q

anisocytosis

A

Anisocytosis is a medical term meaning that a patient’s red blood cells are of unequal size. Th

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19
Q

poikilocytosis

A

Poikilocytes are abnormally shaped red blood cells

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20
Q

management of Iron def

A

o Mild to moderate anemia
 Therapeutic trial of oral iron therapy
• Ferrous sulfate, 325 mg tid – given in slow escalating doses. Absorption enhanced by vitamin C
• Repeat hemoglobin after 1 month (should normalize)
• Continue iron replacement for 3-6 months after achieving a normal hemoglobin
• If patients are intolerant to oral iron, have GI disease, or continuing blood loss  parenteral iron. Sodium ferric gluconate is less likely than iron dextran to cause anaphylaxis
 Dietary modifications  limiting milk

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21
Q

microcytic anemia lead poisoning

A

lead poisoning

often concomitant w/ iron def.

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22
Q

lead poisoning

A

inhibition of sythetic enzymes necessary for production of hemoblobin

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23
Q

lab findiing on lead poisoning

A

Low MCV, basophilic stippling on smear

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24
Q

sideroblastic anemia?

A

the bone marrow produces ringed sideroblasts rather than healthy red blood cells (erythrocytes).

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25
Q

thalassemia

A
  • Characterized by varying degrees of ineffective hematopoiesis and increased hemolysis, resulting in decreased or absent globin synthesis
  • The most prominent feature is microcytosis out of proportion to the degree of anemia
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26
Q

how is thalassemia dx

A

electrophoresis

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27
Q

CF of thalassemia?

A
  • Hemoglobin usually between 3-6 g/dL

- Serum iron and ferritin are usually normal (or elevated

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28
Q

what population has thalassemia

A

with African, Mediterranean (beta), Middle Eastern, Chinese (alpha) or Southeast Asian (alpha) ancestry

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29
Q

what causes Betat T

A

point

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30
Q

what causes alpha T

A

gene

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31
Q

beta thatlassemia major

A

a transfusion-dependent condition

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32
Q

a-thalassemia

A
  • Severity of clinical syndrome depends upon number of genes expressed
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33
Q

what happens w/ a single gene deletion in a thalaseemia

A

silent carrier

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34
Q

two gene deletion for alpha Two gene deletion in A. thalassemia

A

 Occurs in 1.5% African Americans
 Results in hypochromic, microcytic anemia (mild)
 Normal Hgb electrophoresis

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35
Q

what happens when there is a 3 gene deletion?

A

o Hemoglobin H disease (on electrophoresis)
o One α-globin chain
o Moderately severe chronic hemolytic anemia
o Variably symptomatic
o Need folic acid supplements and should avoid iron supplements and oxidative drugs (e.g., dapsone, primaquine, quinidine, sulfonamides, nitrofurantoin)

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36
Q

4 gene deletion or A. thal.

A

o Bart’s or Hydrops fetalis (and thus, still birth)

o Incompatible with life :severe anemia, tissue hypoxia, heart failure, hepatosplenomegaly, edema

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37
Q

B-Thalassemia (mino and major)

A

results from an abnormal beta gene in one or both of the genes, occasionally entire gene is deleted

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38
Q

BT minor

A

only one gene
-lifelong anemia
HgbA2 and HgbF

no tx needed

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39
Q

Cooley’s anemia

A

both gnese needed for beta globin production are affected

-ineffective erthyropoieses

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40
Q

CF of Cooley’s eanemai

A

o Severe anemia, organomegaly, growth failure (failure to thrive is prominent)
 Can get frontal bossing, maxillary hypertrophy with prominent cheekbones, overbite
o Basophilic stippling. Hemoglobin electrophoresis shows Hgb F and Hgb A2
o Problems begin at 4-6 months, when the switch from fetal hemoglobin (Hgb F) to adult hemoglobin (Hgb A) occurs.

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41
Q

tx of Cooley’s

A

life long transfusions of packed RBC

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42
Q

what is the main cause of death from Cooley’s?

A

cadiace disease!

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43
Q

what is the goal after blodd transfusions? (in cooley’s

A

(Goal 14.5g/dL)
• Allow improved growth and development
• Reduce hepatosplenomegaly
• Reduce bone deformities

44
Q

Macrocytic anemia

A

larger than avg RBC

*also acute hemorrhage and hemolysis

45
Q

Macrocytosis

A

MCV >100

  • down syndrome
  • normal newborn
  • folic acid def
  • vit b12 def
46
Q

how is macrocystosis subclassifed?

A

based on presence of absence of megaloblastosis

  • megaloblastic: vitamin B12 deficiency, folate deficiency, drugs, metabolic disorders
  • anemias w/ MCH > 125 almost always megaloblastic ex for those associated w. myelodysplastic syndrome
47
Q

what is non-megaloblastic

A

 bone marrow failure syndromes (Diamond-Blackfan, Fanconi), chronic liver disease, hypothyroidism

48
Q

what lab work ups should you use?

A
  • peripherla blood smear
  • B12 level
  • folate level
  • bone marrow bx
49
Q

vit b12 deficiency

A

pernicious anemia-leads to atrophic gastritis and increased risk of gastric carcinoma

50
Q

what food has vit b12 in it?

A

meat, fish, cheese, eggs

51
Q

where does vit b 12 absorption occur

A

terminal ileum and storage in the liver

52
Q

what can cause pernicious anemia?

A

malabsorption, strict vegan diet, gastric surgery, pancreatic insufficiency, Crohn’s disease

53
Q

what are CF of pernicious anemai

A
  • Glossitis, pale icterus, diarrhea, weight loss, vitiligo, possible neuro manifestations (stocking-glove paresthesias, loss of position, fine touch, and vibratory sensation, clumsiness, dementia, and ataxia
54
Q

what other lab results are associated w/ pernicious anemia?

A

hypersegmented neutrophils,

serum LDH and indirect bilirubine

decreased reticuloctyes count

55
Q

Folate deficiency causes?

A

poor dietary intake- alos defective absorption, prego, hemolyytic anemia, alcohol abuse, and consumption of of folic acid antagonists (i.e., phenytoin, TMP/SMX, sulfasalazine)

56
Q

CF of folate def

A

sore tongue (glossiltis) and vague GI sx

57
Q

lab finding in folate def

A

macro-ovalocytes and hypersegmented polymorphonuclear cells

dx: <150 mg/nL

58
Q

what are other findings in folate def?

A

Howell-Jolly bodys (nulear DNA remnants)

59
Q

tx of folate def

A

1 mg folate

60
Q

Diamond-Blackfan anemia

A
  • Congenital pure red cell aplasia
  • May have congenital anomalies  short stature, web neck, cleft lip, shield chest, triphalangeal thumb
  • Macrocytosis and reticulocytopenia
  • Treat with oral corticosteroids or transfusion if necessary (maybe even bone marrow transplant)
61
Q

Fanconi Anemia

A
  • autosomal recessive, results in pancytopenia

- what is the mean agor of onset? 8yrs

62
Q

what are some clinical features of fanconia anemia?

A
  • Hyperpigmentation and café au lait spots, microcephaly, microphthalmia, short statue, horseshoe or absent kidney, absent thumbs
63
Q

how do you tx fanconi anemia

A

transfusions, even stem cell transplant

64
Q

normocytic anemia

A

associated w/ chronic inflammatory dz

  • caused by organ failure or impaired marrow fxn resulting from systemic dz
  • upregulation of hepcidin in response to inflammatory mediators

*** LOW reticulocyte response

65
Q

types of normocytic anemia

A

Anemia of inflammation (results from chronic inflammatory dz- such as JRA)

-congenital pure red cell aplasia

  • Transient erythroblastopenia of childhood
  • acquired pure red cell aplasia
  • gradual onset of pallor
  • self-limited w/in 1-2 mnths
66
Q

hemolytic anemia

A

-episodic or continuous RBC destruction

67
Q

what is hallmark of the hemolytic

A

elevated reticuloctye count in the present of a falling or stable hematocrit

68
Q

peripheral smear of hemolytic anemai?

A

immature red cells, nucleated red cells, or morphologic changes

69
Q

Intrinsic hemolytic anemia

A
  • intrinsic membrane defect
  • RBC enzyme defects
  • Hemoglobinopathes
70
Q

acquired hemolytic anemaia?

A

fragmentation hemolysis

-immune-medicated hemolytic anemia

71
Q

Hereditary hemolytic anemia

A
  • Intrinsic membrane defects
  • RBC Enzyme Defects
  • Hemoglobinopathes
72
Q

intrinsic membrane defects

A

o Conditions caused by abnormalities of the RBC cytoskeleton which produces accelerated RBC destruction in the spleen

o Elasticity is what makes red cells able to deform reversibly
o If they cannot reshape to biconcaved discs, then there is an destruction of erythrocytes through the spleen

73
Q

Hereditary spherocytosis

A
  • Autosomal dominant
  • Elevated MCHC
  • Spherocytes on peripheral smear-Hemolysis occurs in the extravascular compartment and the spleen (possible splenectomy if severe)
  • May have indirect hyperbilirubinemia
74
Q

how do you dx herediarty spherocytosis?

A

osmotic fragility test

75
Q

hereditary elliptocytosis

A

benign dominantly inherited disorder

elliptocytes on peripheral smear
-significant hemolysis 10% pt

76
Q

RBC ezyme defects

A

G6PD def

common worldwide

gene is X-lined recessive disorder

oxidative drugs (ASA, dapsone, primaquine, quindine, sulfonamides, macrobid)

77
Q

what will you see on a blood smear of someone who has G6PD def?

A

Heinz body (denatured hb), bite cells

78
Q

what is the type A variant of G6PD

A

10% of AA males

  • Hemolysis can occure w. antimalarial agents
  • can be protective agains malaria
79
Q

Hemoglobinopathies

A

Sickle Cell Dz

HgB S gene-carried by 8% of AA population

Homozygous SS, SC, SB thal are clinically significant syndromes
• Lifelong anemia
• Acute and chronic tissue damage related to sickling
• Increased susceptibility to encapsulated organisms
• SA is sickle cell trait

80
Q

how do you dx hemogobinopathies

A

Hb electrophoresis

81
Q

HbSC dz?

A
  • HEP  SC
  • Hgb 9.0 – 12.0 gm/dL
  • MCV 60 – 80 fL (normal)
  • Retics 3 – 5%
  • Smear: microcytosis, hypochromia, target cells
82
Q

HbSS dz?

A

most common and severe form

  • HEP: SF
  • Hgb 6.5 – 8.5 gm/dL
  • MCV 80 – 100 fL (normal)
  • Retics 5 – 15%
  • Lifespan shorted to 10-20 days (normal is 120)
  • Smear : sickled cells, polychromasia, Howell-Jolly bodies, poikilocytes, target cells

• Sickling is increased by red cell dehydration, acidosis, and hypoxemia

83
Q

what are howell-Jolly bodies are indicative of?

A

hyposplenism

84
Q

what can make sickling worse?

A

red cell dehydration, acidosis, hypoxemia

85
Q

Sickle Cell Dz

A

hypchromic, microcytic

86
Q

what are acute clinical manifestations of SCD

A

-Acute vasoocculusive episodes (pain crises, stroke, acute chest syndrome)

87
Q

what is the first sign of SCD?

A

dactylitis “sausage fingers”

88
Q

Actue anemic episodes

A

splenic sequestration, aplastic crises (human parvovirus)

89
Q

Infection and SCD

A

increased susceptibility secondary to fxn asplenia

  • PCN prophylaxis
  • Pneumovax
90
Q

what is asplenia

A

absence of normal spleen function and is associated with some serious infection risks.

91
Q

Chronic clinical manifestations

A

CNS, CVD respiratory, hepatobiliary, ocular, skeletal, nutritional, GU, growth and development

92
Q

what other issues may pple w/ SCD present w/

A

unconjugated hyperbilirubinemia, elevations of LDH and AST

93
Q

Transfusion Indications in sickle cell dz

A
  • pre-anesthesia prep
  • stroke prophylaxis
  • sever acute chest syndrome
  • aplastic crisis w/ severe anemia
  • splenic sequestration crisis
  • elevated TCD velocity
94
Q

Hydroxyurea Therapy in scd

A

-improves hematological values
-increases fetal Hb which decreases sickling
-results in fewer:
painful events, episodes of acute chest syndrome, erythrocyte transfusion,

95
Q

hematopoietic stem cell transplantation and SCD

A

the only potential cure for SCD

-limited by lack of donor availabiltiy and toxicides or procedure

96
Q

acquired hemolytic anemias

A
  • HIGH reticulocyte response
  • fragmentation Hemolysis
  • immune-mediated hemolytic anemia
97
Q

Types of Fragmentation hemolysis

A 
TTP
HUS
giant hemangioma
artifical heart valves
Sepsis
DIC
98
Q

Immune-mediated Hemolytic Anemia

A
  • hemolytic dz of the newborn

- autoimmune hemolytic anemia

99
Q

Aplastic anemia

A

an acquired failure or hematopoietic stem cells that result in pancytopenia
-injury or abnormal expression of the pluripotent hematopoietic stem cell
-

100
Q

what infxn may cause an aplastic crisis?

A

parvovirus B19

101
Q

Clinical features of aplastic anemia?

A

fatigue, pallor, thrombocytopenia (bleeding, easy bruising)
Weakness, petechia,

***Hepatosplenomegaly, lymphadenopathy, and bone tenderness suggest an alternative diagnosis

102
Q

dx features of aplastic anemia

A

**Pancytopenia

  • microcytosis
  • bone marrow replaced by fat (hypocellular bone marrow)
103
Q

what can cause aplastic anemia?

A
  • idiopathic in developed countries

- may be induced by certain druges or infx (hepatitis and mononucleosis)

104
Q

how to tx severe cases

A

HSCT w. sib

105
Q

mild cases of aplastic anemia?

A

supportively w/ transfusion of red cells and platelets

Hematology (5 decks)

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