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Clin Med2- Hematology > Anemias part 1 > Flashcards

Anemias part 1 Flashcards

1
Q

What does a CBC include

A

RBC count
Hgb/Hct (aka H&H)
Red cell indices
Reticulocytes (immature RBCs)
WBC count (with or without differential)
Platelets

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2
Q

what is Hgb

A

Hemoglobin - measure of total amount of hemoglobin in the peripheral blood

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3
Q

what is hemoglobin

A

oxygen carrying proteins
often a proxy for RBC amount/function
falsely reduced by dilution and vice versa
elevated in environments/conditions producing hypoxia (high altitudes, smokers, COPD,etc)

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4
Q

what is Hct

A

Hematocrit - measure of total blood volume made up of RBCs
expressed as a percentage

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5
Q

What is the RBC indices

A

look at specific properties of RBCs (size, shape, Hgb, ect)

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6
Q

what is included in the RBC indices

A

mean corpuscular volume (MCV)
mean corpuscular hemoglobin(MCH)
mean corpuscular hemoglobin concentration (MCHC)
Red cell distribution width (RDW) - how many different sizes are there? Range of sizes?

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7
Q

what are reticulocytes

A

total number of immature RBCs - used as a proxy for bone marrow function
RBC spit out their nucleus and RNA during maturation - reticulocytes haven’t spit out their RNA yet

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8
Q

what are the types of leukocytes

A

neutrophils
lymphocytes
monocytes
eosinophils
basophils

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9
Q

what are common causes of increased WBC

A

infection, trauma, malignancy, leukemias, tissue necrosis
WBC are an acute phase reactant

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10
Q

what is a CBC with diff used for

A

to identify underlying cause of leukocytosis

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11
Q

what are neutrophils

A

primarily for phagocytosis, indication of bacterial infections aka PMNs

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12
Q

what is the presence of immature neutrophils

A

“left shift”
gives indication that BM is pumping out WBCs before they are fully developed in response to some threat (real or perceived)

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13
Q

what are lymphocytes

A

T and B cells, responsible for antigenic immune response; chronic bacterial and viral infections

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14
Q

what are monocytes

A

similar function as PMNs, but are present longer in the blood
phagocytosis of bacterial infection

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15
Q

what are basophils and eosinophils

A

involved in allergic response (histamine) - also respond to parasitic infections

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16
Q

what is a platelet count sort of a proxy for

A

clotting function but sometimes even with normal number of platelets they can be dysfunctional

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17
Q

when can platelet levels be reduced

A

consumption (used up in clotting)
reduced production by BM
sequestration in the spleen
destruction (drugs, autoimmune, infections)
hemorrhage
dilution (blood replacement with platelet-poor fluids)

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18
Q

what is a normal absolute count of neutrophils

A

2500-8000

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19
Q

what is the normal absolute count of lymphocytes

A

1000 - 4000

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20
Q

what is the normal absolute count of monocytes

A

100-700

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21
Q

what is the normal absolute count of Eosinophils

A

50-500

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22
Q

what is the normal absolute count of basophils

A

20-100

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23
Q

what are signs of anemia

A

DOE (dyspnea on exertion)
Fatigue
bounding pulses
palpitations
muscle cramps
postural dizziness
syncope
headache
jaundice

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24
Q

what are history clues that may lead to anemia diagnosis

A

abdominal pain
melena - old/dark blood in stool
Pica - eating ice/dirt/cigarette butts
Menorrhagia - heavy period
NSAID/ASA use
pregnancy
hematochezia - bright red blood in stool
hematoemesis - blood in vomit
history of gastric bypass
+ FH of RBC disorder
history of ETOH abuse
dysphagia
malnutrition

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25
Q

how is anemia diagnosed

A

low number of circulating RBCs
low Hgb, low Hct or low absolute number of RBCs

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26
Q

what is the classification of anemia by Hgb status

A

mild: anything 10.0+
Moderate = 7.0-9.9
Severe = <7.0

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27
Q

how does elevated MCV present

A

RBCs larger than normal (aka macrocytic)

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28
Q

how does decreased MCV present

A

RBCs smaller than normal aka microcytiic

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29
Q

how does elevated MHC present

A

more Hgb per cell than normal (also hyperchromic) - darker

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30
Q

how does decreased/low MCH present

A

hypochromia (paler)

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31
Q

What is MCHC

A

mean corpuscular hemoglobin concentration
average Hgb concentration per RBC
percentage of RBC volume that is Hbg

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32
Q

what is the formula MCHC

A

MCHC = Hgb/Hct

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33
Q

what is anisocytosis

A

large variety of cell sizes; large, normal and smaller RBCs present
elevated RDW

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34
Q

what is Poikilocytosis

A

abnormally shaped RBCs

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35
Q

what is a peripheral smear

A

microscopic examination
tells us RBC color, shape, size, overall structure

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36
Q

how does a peripheral smear present with a B12 or folate deficiency

A

megaloblastic process
Macro-ovalocytes - ‘big’ and ‘oval’

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37
Q

what are schistocytes/helmet cells

A

fragmented RBCs
intravascular destruction (DIC, TTP, etc)

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38
Q

what is hyperchromia

A

loss of central pallor, spherocytes
hereditary spherocytosis
(circular and darker in color)

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39
Q

what is hypochromia

A

not enough hemoglobin, thalassemia, iron deficiency, sideroblastic

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40
Q

what are target cells

A

relative ‘membrane excess’; abnormal surface-to-volume ratio
liver disease, thalassemias

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41
Q

what are spiculated cells

A

liver disease, uremia
disorganization in cell membrane (lipids, proteins)
AKA echinocytes: Spiny

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42
Q

what are Burr cells assicated with

A

uremia

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43
Q

what is acanthocytes associated with

A

liver disease

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44
Q

what are Howell - Jolly Bodies

A

nuclear remnants
asplenia or hyposplenia (sickle cell)
seen on wright -giemsa stain

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45
Q

what are Heinz Bodies

A

denatured hemoglobin
‘inclusion bodies seen with crystal violet dye)

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46
Q

what are basophilic stippling

A

percipitation of ribosomes
*lead/heavy metal poisioning, thalaseemias, ETOH abuse

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47
Q

What are the Microcytic anemias

A

TIC
Thalassemias
Iron deficiency
Chronic disease
Siderobloastic

48
Q

What are thalassemias

A

group of hereditary anemias (autosomal recessive) - one of the most common autosomal recessive in the world
absent or defective synthesis of adult hemoglobin (alpha and beta chains)
results in RBC destruction in bone marrow or intravascular hemolysis due to damaged red cell membranes

49
Q

Where are thalassemias often seen/attributed with

A

historically regional: sub-saharan africa, mediterranean, middle east, india, southeast asia/china, central asia

conferred protection from malaria

50
Q

What is Hemoglobin H

A

4 beta chains
error in alpha chains - clumping of beta chains

51
Q

what is hemoglobin Barts

A

4 gamma chains
error in alpha chains early in life means more gamma chains ; not compatible with life

52
Q

what is Hemoglobin S

A

sickle; 2 alpha, 2 mutated beta

53
Q

what is Hemoglobin C

A

2 alpha, 2 differently mutated beta

54
Q

What are the different types of Thalassemias

A

Alpha (major and minor)
Beta (major and minor)
Hgb Barts

55
Q

what are alpha thalassemias

A

more common in AA, southeast asians or Chinese descent
most likely dx in pts <6months of age
gene deletion or mutation

56
Q

what is the presentation of alpha thalassemias

A

often found on incidental screening:
- maternal/paternal screening
- newborn screenings
-part of adult physical screening

57
Q

when and who do we see beta thalaseemia in

A

more common in AA and mediterranean pts
most likely diagnosed about 6+ months of age
-fetal Hgb (HbF) being replaced by adult Hgb

58
Q

what is the presentation of beta thalassemia

A

asymptomatic (beta thalassemia minor)
beta thalassemia intermedia - mildly symptomatic, mild anemia, occasional transfusions
beta thalassemia major - severe anemia, transfusion

59
Q

what are the clinical symptoms of thalassemia

A

fatigue
dizziness
dyspnea
tachycardia
HA
Leg cramps
difficult concerntration
pallor/jaundice
ulcerations
arrhythmias
heart failure
splenomegaly
immunocompromise
cholelithiasis
cirrosis or chronic liver failure
slow growth rate
delayed puberty

60
Q

what are the clinical bone presentation of thalassemias

A

bone expansion
bone fragility and pathologic fractures
iron in the joints - arthropathies

61
Q

what are shown on thalassemia labs

A

modest reduction in HCT - mild anemia
significantly reduced MCV - small RBC (microcytic)
normal RBC #
normal RDW
Normal iron studies
peripheral smear results: hypochromia, microcytosis, target cells, acanthocytes (spur cells)

62
Q

what is the definitive diagnosis test for thalassemia

A

hemoglobin analysis (electrophoresis, genotypic, HPLC)

63
Q

what is the treatment for mild thalassemia

A

asymptomatic do not need treatment
do not give iron - it can be damaging

64
Q

what are the treatment options for thalassemia

A

folic acid supplementation
avoid oxidative drugs
TRANSFUSIONS
IRON CHELATION THERAPY
+/- splenectomy
BMT in severe cases

65
Q

What is the number one cause of anemia worldwide

A

iron deficiency anemia

66
Q

what are the main causes of iron deficiency anemia

A

blood loss (most common): GI bleeding (usually occult), NSAID induced, menorrhagia, malabsorption
Inadequate dietary intake: more likely in peds and females

67
Q

what is the spectrum of iron deficiency

A

iron depletion (no stored iron)
iron deficient erythropoiesis (no storage and transport and functional iron being used)
iron deficiency anemia (no storage and transport and functional iron being used)

68
Q

what are the general anemia complaints

A

Pica, brittle nails, spoon shaped nails, cheilosis, smooth tongue, esophageal webs

69
Q

how does iron deficiency anemia present on peripheral smear

A

hypochromia, microcytic cells, target cells, nucleated red cells

70
Q

what iron studies confirm iron deficiency anemia

A

serum ferritin
serum iron
serum transferrin aka total iron binding capacity (TIBC)
transferrin saturation (Tsat)

71
Q

what is the treatment for menstruating females with AUB with iron deficiency anemia

A

emperic treatment

72
Q

What needs to be done prior to beginning treatment for iron deficiency anemia

A

search for the source of the anemia (usually source of bleeding)

73
Q

what are the treatment options for iron deficiency anemia

A

empiric iron treatment OR no evidence of non-dietary cause
120-200mg ELEMENTAL iron per day over 2-3 doses
typically ferrous sulfate 325mg PO TID, titrate up

74
Q

what are the Adverse effects of Ferrous sulfate

A

constipation, black stools, GI upset

75
Q

what should the result of iron deficiency anemia treatment be

A

Hgb increases 1mg/dL over 1 month
continue for minimum of 3 months
most sources recommend continuing for 6-12 months
will take several months for labs to normalize and stores to replenish

76
Q

what are dietary iron sources

A

heme iron comes from animal food source - beef, lamb, pork, poultry, eggs, fish
non-heme iron comes from plant based foods - fruits, nuts, vegetables, grains, legumes
cast iron cookware increases dietary iron

77
Q

what vitamin improves the absorption of iron

A

vitamin C

78
Q

what is another name for anemia of chronic disease

A

anemia of inflammation

79
Q

what is anemia of chronic disease

A

many etiologies - dependent on underling disease state
chronic inflammation - iron use ineffective, iron absorption impaired, decreased responsiveness to erythropoietin (Epo)
organ failure - decreased EPO production
any active malignancy
older adults - reduced sensitivity to EPO, reduced EPO production, chronic inflam
impaired marrow function

80
Q

what is often co-occurring with anemia of chronic disease

A

iron or folate deficiency - worsens anemia
blood loss of hemolysis - also worsens anemia

81
Q

what is EPO

A

erythropoietin

82
Q

what is the lab presentation of anemia of chronic disease

A

variable
often mild-moderate anemia (Hgb >8)
normochronic, normocytic OR hypochromic, microcytic
normal or increased iron stores
normal or decreased TIBC, serum iron
peripheral smear is normal

83
Q

what is the treatment of anemia of chronic disease

A

treat underlying cause/disease process
correct complicating factors (blood loss, folate deficiency, iron deficiency)
IV iron supplementation if warranted
EPO administration = must be Hgb <10, attempt to avoid transfusion
Transfusion - failure of other treatment - ongoing blood loss

84
Q

what is the etiology of aplastic anemia

A

aka ‘bone marrow failure’ - anemia PLUS reduction in all other cell lines (pancytopenia)
more prevalent in asian and middle eastern populations
peak incidence: bimodal (15-25 and 65-69)

85
Q

what are the causes of aplastic anemia

A

idiopathic
SLE
Chemotherapy
Radiation
Toxins
Drug induced
Hereditary

86
Q

what is the presentation of aplastic anemia

A

often symptoms/consequences in reduction of other cell lines
increase incidence of infections
purpura/petechiae and abnormal bruising
abnormal bleeding
anemia symptoms: weakness, fatigue, pallor

87
Q

what is diagnostic of aplastic anemia

A

pancytopenia
- low hemoglobin
- low absolute reticulocyte
- low neutrophil count
- low platelet counts

88
Q

what does a biopsy show for aplastic anemia

A

hypocellular marrow with fatty infiltration
+/- abnormal or malignant cells or fibrosis

89
Q

what are the treatment options for aplastic anemia

A

d/c any potential inciting agents
if mild = supportive care
- RBC and platelet transfusions
- treatment of infections
if severe and younger than 40 with compatible sibling donor - BMT from sibling donor
if sever and >40 OR <40 with no compatible sibling donor - immunosuppression

90
Q

what is the prognosis of aplastic anemia

A

in severe: median survival of 3 month without treatment - 20% survive 1 year
in young adults (<20) with related BMT - 80-90% complete response rate
with pharmacologic treatment about 90% get partial response
patients treated without BMT are at increased risk for other marrow disorders

91
Q

what is sideroblastic anemia

A

rare in practice
impaired heme synthesis - iron accumulation

92
Q

what causes sideroblastic anemia

A

myelodysplasia
chronic alcoholism
hereditary
copper/B6 deficiencies
drug induced
LEAD POISONING UNTIL PROVEN OTHERWISE

93
Q

what are the labs for sideroblastic anemia

A

normal or hypochromic cells on peripheral smear
basophilic stippling is likely lead poisoning

94
Q

how is sideroblastic anemia definitively diagnosed

A

bone marrow eval - “ringed sideroblasts on Prussian blue staining”

95
Q

what is the treatment of sideroblastic anemia

A

treat underlying cause
transfusion PRN, ban be lead to iron overload

96
Q

What are the normocytic anemias

A

ABCD
Acute blood loss
Bone marrow failure
Chronic disease
Destruction (hemolysis)

97
Q

acute blood loss anemia

A

pts will be bleeding
obvious of occult
GI tract most common site of occult bleeds - if you have a pt >50 yo with unexplained or new anemia YOU MUST RULE OUT COLON CANCER

98
Q

what is the treatment of acute blood loss anemia

A

stop the bleeding
replace the blood

99
Q

what is hemolytic anemias

A

episodic or continuous RBC destruction
classified by intrinsic or extrinsic cuases
characterized by elevated reticulocyte count with stable or falling Hgb/Hct

100
Q

what are intrinsic causes

A

problem is with the RBC

101
Q

what are extrinsic causes

A

problem outside of the RBC (often autoimmune)

102
Q

what are the lab values for hemolytic anemias

A

peripheral smear consistent with compensation for increased RBC loss. - blasts, nucleated red vells, various morphologic changes
elevated unconjugated bilirubin
+/- serum LDH
Low Haptoglobin
Coombs test - checking for agglutination

103
Q

what does a + Coombs test mean

A

autoimmune hemolytic anemia

104
Q

What is hereditary spherocytosis

A

most common genetic hemolytic disease
autosomal dominant
also likely many undiagnosed
RBC membrane defect with results in RBC shape changing from concave to spherical - less malleable, get stuck more often, decreased survival

105
Q

what is the presentation of hereditary spherocytosis

A

most patients asymptomatic
may or may not be associated with anemia
peripheral smear: microcytosis, spherocytes - loss of central pallor

106
Q

what is the treatment of hereditary spherocytosis

A

blood transfusions
chronic folic acid supplementation to sustain erythropoesis
treatment of choice = splenectomy

107
Q

what is the etiology of G6PD deficiency

A

glucose - 6 - phosphate dehydrogenase deficiency
herediatary, x-linked recessive disorder (M>F)
primarily a single amino acid substitution
more common in AA, mediterranean and ashkenazi jewish pts (aka Favism)

108
Q

what is G6PD deficiency

A

related to deficiency in the G6P enzyme
important in glulconeogenesis/glycolysis
also acts as natural antioxidant
deficiency results in episodic hemolytic anemia
stress caused by: infection, certain foods (fava beans) certain medications

109
Q

what is the presentation of G6PD

A

most are asymptomatic
episodic symptoms related to triggers:
-pallor
-jaundice
-bilirubinuria
- fever
-weakness, dizziness, confusion
-fatigue
-dyspnea
-splenomegaly and/or hepatomegaly
-tachycardia, heart murmur

110
Q

what is the lab presentation of G6PD

A

denatured hgb precipitates out - heinz bodies
also see ‘bite’ cells and ‘blister cells’

111
Q

what is the definitive diagnosis of G6PD

A

enzyme assay - reduced levels of G6PD

112
Q

what is the treatment of G6PD

A

avoid certain foods, meds, environmental exposures
Hemolytic episodes self limited with production of new RBCs

113
Q

what is the etiology of sickle cell anemia

A

inherited anemia - autosomal recessive
RBCs with Hgb S SICKLE UNDER STRESS
most common in AA pts
symptoms start around 6 months of age - Hgb F levels declining

114
Q

what is the presentation of sickle cell anemia

A

vascular occlusions - painful crises (organ swelling, dysfunction, infractions)
delayed growth/puberty
splenic sequestration

115
Q

what are pts with sickle cell anemia at risk for

A

cholelithiasis
splenomegaly
leg ulcers
infections with encapsulated organisms
stroke
AVN
Priapism
retinopathy - blindness
osteomyelitis
hematuria, poorly concentrated urine (renal infarcts)

116
Q

how is sickle cell anemia diagnosed

A

low Hgb, normal MCV
elevated reticulocyte count, elevated LDH, elevated indirect bilirubin
coombs test negative
sickles cells on peripheral smear
nucleated RBCs/Howell-Jolly bodies +/- target cells
Hgb electrophoresis >50% Hgb S

117
Q

what is the treatment of sickle cell anemia

A

pain: analgesics, fluids, O2, rest
Prevention of crisis: hydroxyurea (increases Hgb F production)
prevention of complications: low dose PCN from dx until 6 years old, pneumococcal vaccine with booster every 10 years, chronic folate supplementations, PFTs screening, transcranial doppler screening
possible BMT transplant in kids PRIOR to organ damage
genetic counseling/prenatal testing

Clin Med2- Hematology (8 decks)

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