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Hematology/Oncology > Anemias > Flashcards

Anemias Flashcards

1
Q

The who defines anemia for females as

A

Hct<4,000,000

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2
Q

The who defines anemia for woman as

A

Hct<4,000,000

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3
Q

Macrophages supply what?

A

supply Fe++ for Hgb production

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4
Q

what is the function of fibroblasts in maintaining homeostatic balance

A

support bone marrow integrity

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5
Q

what is the function of adipocytes in maintaining homeostasis?

A

store energy as fat

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6
Q

What is the function of osteoblasts and osteoclasts in maintaining homeostasis

A

support the boney trabeculae

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7
Q

what regulates erythropoiesis?

A

erythropoietin

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8
Q

where is erythropoietin secreted from

A

the kidney

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9
Q

what is the function of erythropoietin

A

governs day to day RBC production

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10
Q

what is the main stimulus for EPO

A

O2 availability

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11
Q

How should EPO levels change in relation to an anemia

A

they should increase in proportion to the severity of the anemia

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12
Q

what substrates are needed for RBC production

A

Iron,B12,Folate

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13
Q

what is the normal lifespan of an RBC

A

120days

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14
Q

what does hypoxia do to RBC’s

A

Increases RBC’s

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15
Q

Which types of people have relatively lower RBS mass?

A

African americans and older adults

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16
Q

there is an increased mortality with Hgb of what?

A

Hgb of <12g/dL

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17
Q

What would the plasma and erythrocytes look like in an athlete?

A

increase in both plasma and erythrocytes

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18
Q

what are examples of volume and anemia concept

A

Acute bleeding, When normal volume is restored, dehydration and pregnancy

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19
Q

what would a reticulocyte with an index<2.5 be classified as?

A

hypoproliferative

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20
Q

what would a reticulocyte index >2.5 be classified as?

A

hyperproliferative

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21
Q

what is a reticulocyte?

A

an immature RBS that is stained with methylene blue and reveals residual Ribosomal RNA as beads of tiny deep blue precipitates

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22
Q

what happens to the retic count with blood loss?

A

the marrow should be able to increase production by 3 to 4 times normal over a 10day period

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23
Q

Anemia symptoms

A

DOE, Fatigue, Palpitations, H/A, Tinnitus, Chest pain, Esophageal rings, Nail spooning, Picas, Neuropathies

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24
Q

Clinical signs of Anemia

A

Tachycardia, Orthostatic hypotension, Systolic ejection murmur, Pallor

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25
Q

GI signs of anemia

A

Jaundice, Positive stool guaiac, splenomeagly, hepatomegaly, Petechiae, glossitis, Koilonychia, neurologic, musculo-skeletal

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26
Q

what is the definition of microcytic and hypochromic anemia

A

MCV<80mm3

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27
Q

what are causes of microcytic anemia (TICS)

A

Thalassemia major/minor
Iron deficiency
Chronic dz/Inflammatory dz
Sideroblastic anemia and Pb poisoning

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28
Q

Iron deficiency anemia accounts for what % of anemias

A

50% of anemias worldwide

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29
Q

serum irons is measured how?

A

Iron bound to transferrin in the serum

norm 40-140uG/dL

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30
Q

total iron binding capacity

A

total transferrin in the serum

norm 200-400uG/dL

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31
Q

Fe/TIBC

A

is the % saturation of iron binding capacity

norm should be 25-50%

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32
Q

Serum ferritin

A

is a rough estimate of iron stored in the reticuloendothelial system
norm. 30-250ng/ml

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33
Q

what are causes of Iron deficiency anemia

A 
GI bleeding
Excessive Menstruation
Malnutrition and Diet Insufficiency
Malabsorption
Increased demand (pregnancy&growth spurts)
Blood donation,blood loss in dialysis
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34
Q

what are specific clinical manifestations of Iron Deficiency Anemia

A

Angular Cheilosis
PICA
Koilonychia
Plummer-Vinson Syndrome

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35
Q

How do you treat Iron Deficiency Anemia

A

6wks to correct anemia
6 months to replete bone marrow stores
Ferrous Sulfate 325mg 3x/day, avoid milk/dairy products/calcium simultaneously
-Can be given IV or IM

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36
Q

When should you give IV or IM iron treatment

A 
intolerant to oral preparation
If more rapid correction of Fe deficiency anemia is neded
Patients can not absorb oral Iron
Chronic blood loss
Pt on Dialysis
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37
Q

what are causes for treatment failure

A

Unidentified blood loss
non-sdherence
Incorrect diagnosis
GI malabsorption

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38
Q

What would you want to educate your patient on with Fe++ side effects

A

Constipation, black stools, nausea, bloating, abdominal pain and diarrhea
-do not take with tetracyclines/fluoroquinolones and antacids/PPI’s and be careful with calcium supplements
Vitamin C

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39
Q

Where is alpha-thalassemia most prevalent?

A

Increase in malaria regions: Southeast Asia & China

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40
Q

where is beta-thalassemia most prevalent?

A

in mediterranean populations

Southern Italy, Greece and North Africa

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41
Q

What is the definition of Thalassemia

A

genetic d/o characterized by inadequate production of either alpha or beta globin chain of hemoglobin.
There is an ineffective erythropoiesis and increase hemolysis

42
Q

what happens when there is a defective alpha or beta globin chain production?

A

an imbalance of globin chains
The unaffected chain takes over-accumulates in the RBC interfering with normal maturation of the RBC
Leads to free radical production that induces hemolysis and anemia

43
Q

what are heinz bodies

A

are precipitants of excess alpha chains in beta-thalassemia
are precipitants of excess beta chains in alpha thalassemia
-they impair DNA synthesis and decrease RBC production
-they damage RBC membrane and increase RBC destruction

44
Q

what are the clinical features of thalassemia

A

positive family history
history of life-long hypochromic microcytic anemia not responsive to Fe++
From silent carrier statues to profound anemia
-depends on genetic defects

45
Q

Beta-thalassemia minor contains how many gene mutations?

A

one gene mutation

results in mild anemia

46
Q

beta-thalassemia major contains how many gene mutations?

A

two gene mutations
results in severe transfusion dependent anemia-Iron overload
If transfusions is delayed growth retardation ensues in children

47
Q

What are complications of beta-thalassemia major (cooley’s anemia)

A 
growth retardation
Severe anemia 
abnormal facial structure
pathologic fractures and osteopenia
hepatosplenomegaly
jaundice and bilirubin gall stones
high out put CHF
short life span <30yrs
48
Q

what are the laboratory findings for thalassemia

A 
Hg electrophoresis (confirms diagnosis)
Inc
Increase in fetal hemoglobin 
decrease in Hgb beta thal but increase in Hgb A2
HgbH in severe alpha thalassemia
49
Q

what will thalassemia look like in a peripheral smear

A

small, pale RBC
target cells
nucleated erythroblasts
basophilic stippling

50
Q

other laboratory findings in thalassemia

A 
high serum iron and ferritin
Hgb level 3-6g/dl
Marked microcytosis
Heinz bodies in beta-thalassemia
increase retic count with hemolysis
51
Q

what is the treatment for thalassemia?

A

transfusion + deferoxamine (to prevent iron overload)
Splenectomy
Experiment allogeneic hemtaopoietic stem cell transplantation in severe cases
avoid iron containing supplements

52
Q

Transfusion complications

A 
Iron overload
-heart failure
-liver failure
pancreatic failure w/DM & malabsorption
-Other endocrine abnormalities
-skin pigmentation
Tx iron overload with chelation
53
Q

Thalassemia patient education

A

genetic counseling
testing of parents
prenatal diagnosis for severe forms of thalassemia

54
Q

what is the definition of normochromic normocytic anemia

A

MCV 80-100

55
Q

what are the causes of a normochromic normocytic anemia

A 
anemia of chronic disease
Early Fe deficiency
Myelodysplasia or marrow failure
Acute blood loss
Anemia associated with renal failure
56
Q

what is the pathophysiology of chronic/inflammatory disease

A 
impaire iron utilization and metabolism
-retic prod is low
norm or incr. ferritin
norm Fe/TIBC
low transferrin and low serum iron
Iron remain sequestered in RE system 
Controlled by hepcidin which is released by liver and controls Fe absorption
57
Q

what is the most important hormone regulating the Fe release from cells

A

Hepcidin.

As hepcidin levels increase there is a decrease in iron availability.

58
Q

what decreases the response to erythropoietin

A

IL-1, IL-6 & TNF

59
Q

What is the treatment for anemia of chronic disease

A

treatment of the underlying condition is the most important
Fe++ supplement may or may not help
There is a decrease response to EPO

60
Q

Anemia due to chronic renal failure is common and severe due to

A

EPO deficiency
Uremic toxins interfere with RBC production and survival
Hemodialysis
Responds well to EPO and Iron

61
Q

What are intrinsic causes of hemolytic anemia (RBC defects)

A

G6PD deficiency
Sickle cel
Hereditary spherocytosis

62
Q

what are the extrinsic causes?

A 
immune hemolytic anemia
Drug induced hemolytic anemia
TTP
hemolytic uremic syndrome
DIC
mechanical hemolysis d/t cardiac valve dysfunction
hyperslpenism
63
Q

what are general clinical features with hemolytic anemias

A

may be associated with jaundice

may have symptoms consistent with tissue hypoxia, similar to other anemia related syndrome: pallor, SOB, Tachycardia

64
Q

what is sickle cell anemia

A

point mutation of the beta-globin chain of Hb-A molecule- with replacement of glutamine with valine-Hbs
short arm of chromosome 11 mutation

65
Q

what is the pathophys of sickle cell anemia

A

HbS become sickled when doxygenated- producing structural cellular damage
sickle cell HgB can return to its normal configuration when reoxygentated

66
Q

what is sickle cells disease defined as in terms of genetics

A

homozygous hemoglobin S

67
Q

what is sickle cell trait defined as

A

heterozygous for Hgb A and HgbS

little tendency to sickle unless there is severe hypoxia usually asymptomatic

68
Q

sickle cell demographics

A

affects .1-.2% african american
about 10% of african american carry sickle cell
positive fam. hx

69
Q

symptoms of sickle cell anemia

A

due to deformed RBC’s causing hemolysis, splenic sequestration and microvascular occlusion

70
Q

what happens during painful crisis with sickle cell anemia?

A 
bone infarctions
osteomyelitis part w/salmonella
pneumococcal and other infx due to autoslpenectomy
acute chest syndrome- pulmonary infarcts, hypoxia, fever
slpenic sequestration crisis
arthropathy
renal papillary necrosis
priapism-impotence
retinal hemorrhage
71
Q

what are complications of sickle cell?

A

infections d/t splenic infarction causes overwhelming infection by encapsulated organmism (strep, hemo,kleb,sal)
parvo B19 causing hemolysis
aplastic crisis due to viral infx.
transient arrest in Erythropoiesis with marked decreased in retic

72
Q

how is sickle cell diagnosed

A 
Hg electrophoresis
-will detect HbS
Smear
-sickled cells, hemolysis, reduced RBC count
-reticulocytes
-nucleated RBC
-Target Cells
-Howell jolly bodies d/t autosplenectomy
73
Q

what is the treatment for sickle cell anemia

A

prevent sickle cell crisis by monitoring condition that demand O2 from RBC’s
-infection
-exercise
-climate extremes
-dehydration during periods of physiologic/emotional distress
When patient with Hgb AS or SS presents with paint and distress this is a sickle cell crisis until proven otherwise
-Consider BM transplant
-hydroxyurea given PO chronically, this increases Hbf which decreases Hbs and painful crisis and acute chest syndrome
WBC and Retics which may worsen symptoms

74
Q

how to treat sickle cell crisis

A

IV hydration, Supplemental O2, Analgesics-morphine, transfusion for Hct<30%
R/O occult infx, MI or PE

75
Q

what are supportive cares treatments for sickle cell

A

folic acid
pneumococcal and H flu vac.
Penicillin prophylaxis
Opthalmological monitoring against retinopathy
Orthopedic care
careful monitoring of renal,pulm and cardiac function
paint management

76
Q

what is the definition of autoimmune hemolytic anemias

A

acquired antibody mediated toward RBC membrane antigens, mostly non-specific but occasionally against Rh
Types IgM or IgG

77
Q

what is warn AIHA

A

IgG mediated
more common than cold AIHA
IgG binds to RBC at >37C
results in extravascular hemolysis- especially in spleen and liver

78
Q

what are the causes of warm AIHA

A

primary or Idopathic

Secondary to lymphoid malignancies, collagen vascular dz, viral infx or drugs

79
Q

cold AIHA

A

IgM mediated
IgM binds to RBC in temp <37C
produces complement fixation and activation leading to intravascular hemolysis within blood vessels

80
Q

what causes cold AIHA

A

Idiopathic
lymphoproliferative dz
mycoplasma pneumonia
Infectious mono EBV

81
Q

what are clinical signs of autoimmune hemolytic anemia

A

jaundice
splenomegaly
fatigue
pallor

82
Q

what are the lab findings like for AIHA

A 
sine qua non: positive direct coombs test
elevated retic count
blood smear shows immature RBC
free serum hemoglobin and hemoglobinuria
high unconjugated bilirubin
elevated LDH
low or absent haptoglobin
83
Q

Tx of AIHA

A 
treat underlying disease
-Lymphoma, Mycoplasma pneumonia, EBV
Immunosuppressive meds
RBC transfusions
Folate
splenectomy-to reduce hemolysis and destruction/sequestration
84
Q

What is a macrocytic anemia

A

MCV>100

85
Q

what is the cause of a B12 macrocytic anemia

A

most common cause if of B12 is impaired GI absorption due to lack of intrinsic factor produced by gastric parietal cells

86
Q

what is a pernicious anemia

A

is a lack of intrinsic factor due to auto-antibody destruction of gastric parietal cells

87
Q

what are causes of B12deficiency

A 
Bariatric Surgery
Gastrectomy
Poor diet-alcoholic
Vegetarians
Terminal ileal resection
Crohns
celiac
competing organism
-tape worm, GI or fungal growth
88
Q

what is the clinical presentation of B12 deficiency?

A

can take >3yrs to show up
Macrocytic hypoproliferative anemia
Weakness, faintness, pallor of skin and mucous membranes
Dyspnea after slight exertion
Atrophic glossitis and stomatitis
Neuropathy-distinguishes between B12 and Folate
Important causes of dementia

89
Q

what are the lab findings in B12 deficiency

A

blood smear shows marked macrocytosis >100mm
low serum B12<250pg/ml
high methylmalonic acid (high only in B12)
high homocysteine (elevated in both B12 and folate)
macro ovalocytes and hypersegmented PMN
low retic count
elevated LDH and Indirect bilirubin

90
Q

what are the co-factors for DNA synthesis

A

B12 and folate

91
Q

what happens with there is a deficiency in erythropoiesis

A

Ineffective RBC production
defective and fragile RBC
Asynchronous maturation between cytoplasm

92
Q

What is the importance of B12 in terms of neurons

A

B12 maintains neuronal myelin integrity

deficiency predisposes to myelin breakdown with resulting neurological symptoms=peripheral neuropathy

93
Q

what is the treatment for B12 deficiency anemia

A

1mg B12 (cyanocobalamin) IM/PO x7days then q wkx 4-8 wks (IM for pernicious anemia)
If tx is delayed >6mths neurological prob may not respond to tx
Folate can reverse hematologic abnormalities of B12 but not neurologic symptoms
IT IS ESSENTIAL TO GET B12 & FOLATE in MACROCYTIC ANEMIA

94
Q

what is the pathophys for folate deficiency

A

body stores sufficient 2-3 months

decrease folic acid causes impaired RBC maturation and early destruction

95
Q

what are the causes for folate deficiency

A 
inadequate folate intake
alcoholics
anorectic persons
elderly
diet low in meat, fruit, and vegetables(leafy green veggies)
96
Q

what are reasons for increased requirement of folate

A 
pregnancy
chronic hemolytic anemias
malignancy
dialysis
infants and children
defective absorption
Celiac sprue
97
Q

meds that can cause folate deficiency

A

methotrexate
trimethoprim
anticonvulsants

98
Q

what are clinical presentations of folate deficiency

A

symptoms from dietary deficiency can be seen in a few months-quicker than B12
atrophic glossitis and angular chelosis
anemia symptoms

99
Q

what are the lab findings for folate deficiency

A

macro-ovalocytes
hypersegmented PMNs
B12 levels are normal
low levels of serum folate

100
Q

what is the Tx for folate

A

1-5mg/day folic acid PO
avoid alcohol and folic acid antagonist
treat malabsorption
rule out B12 deficiency

Hematology/Oncology (7 decks)

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