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MLSCI 330 > Anemia > Flashcards

Anemia Flashcards

1
Q

Anemia is classified either by …

A

retic count or MCV of red blood cells

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2
Q

Anemias caused by these… tend to have low retic count

A

defects in cell pathways and abnormal reproduction of RBCs

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3
Q

T or F. Anemia due to loss have decreased retics

A

F! INCREASED reticulocytes because body is trying to compensate by increasing production and also has the necessary components to do so

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4
Q

4 causes of anemia

A
  • ineffective erythropoiesis
  • insufficient erythropoiesis
  • excessive blood loss
  • hemolysis
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5
Q

describe ineffective erythropoiesis

A
  • defective erythroid precursor production
  • cells die before maturing
  • increased stimulation by EPO leading to high RBC production but RBC are defective
  • lack of critical molecules
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6
Q

anemia with ineffective erythropoiesis

A
  • megaloblastic anemia
  • thalassemia
  • sideroblastic anemia
  • IDA

lack of critical molecules

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7
Q

describe insufficient erythropoiesis

A
  • decrease in # of erythroid precursors in BM so low # of RBCs produced
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8
Q

common causes of insufficient erythropoiesis

A
  • IDA
  • decreased EPO
  • autoimmune diseases or infections
  • replacement of normal hematopoietic cells with malignant cells
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9
Q

stain used for iron studies

A

Prussian blue

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10
Q

osmotic fragility test

A
  • RBCs in 0.85 saline
  • normal patients will reach certain normality before RBCs burst (hypotonic)
  • spherocytes = increased fragility; don’t have excess membrane so hypotonic and burst FASTER
  • targets = excess membrane = so take longer to lyse; decreased OF
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11
Q

these factors can lead to IDA

A
  • inadequate intake
  • increased need (pregnancy, rapid growth periods, etc.)
  • impaired absorption (decreased stomach acid, inflam. bowel disease, gastrectomies)
  • chronic blood loss (menstrual bleeds, ulcers, etc.)
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12
Q

iron studies in IDA

A
  • decreased iron
  • decreased ferritin
  • increased TIBC
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13
Q

platelets in IDA

A

often increased esp. if IDA due to blood loss or in severe anemia; WBC usually normal

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14
Q

T or F. In IDA, normoblasts won’t be as blue

A

T! bc poorly hemoglobinized ; may also develop ragged cytoplasm

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15
Q

anemia due to sideroblasts

A

anemia results from ineffective production of heme
- protoporphyrin ring = failure to use iron
- or impaired insertion of iron to ring centre

without iron = cannot carry O2

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16
Q

cause of sideroblastic anemia

A
  • deficiency in ALA or heme synthase
  • decreased vit. B6 or interference by drugs
  • deficiency in other enzymes necessary for synthesis of heme (congenital)
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17
Q

iron studies in sideroblastic anemia

A
  • increased serum iron (may have enough, just can’t incorporate it)
  • increased ferritin
  • incr Tsat
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18
Q

PBS findings in sideroblastic anemia

A
  • dimorphic
  • basophillic (esp. w lead)
  • normal indices, RDW increased
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19
Q

how is sideroblastic anemia acquired?

A
  • hereditary
    or acquired
  • primary = myelodysplastic syndrome (chromosmal damage overtime)
  • secondary = more common; due to drugs (which inhibit ALA synthase, etc.)
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20
Q

BM findings for sideroblastic anemia

A

BM + Prussian Blue = siderocytes

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21
Q

anemia of chronic infection mechanisms

A

cytokines:

  1. disturb iron metabolism = incr hepcidin and decrease iron absorption and release; increase lactoferrin and serum ferritin
  2. diminished erythropoiesis = blunted response to EPO
  3. decreased red cell lifespan = macs clear minimally damaged RBCs quicker bc they’re on high alert
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22
Q

RBC indices for ACI

A

all decreased (MCV, MCHC, MCH)

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23
Q

BM findings for ACI

A
  • M:E ratio normal or slightly increased due to HYPOprolifeation of RBCs
    (BM suppressed due to inflammation)
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24
Q

iron studies for ACI

A
  • serum iron = decreased
  • serum ferritin = increased (sequestered in macs)
  • TIBC = decreased
  • Tsat = decreased
  • BM iron = normal to increased due to sequestration
  • elevated ESR and CRP bc of inflammation
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25
Q

If the anemia is caused by ineffective or insufficient erythropoiesis, there will be a __________in retics and the BM will show a _______ M:E ratio

A

decreased retics
decreased M:E ratio bc trying to ramp up RBC production

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26
Q

root cause of megaloblastic anemia

A

impaired DNA synthesis

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27
Q

without vitamin B12 or folate, we can’t make this

A

thymine, one of the nucleotide bases in DNA

28
Q

vitamin B12 role in NA synthesis

A

it is the coenzyme necessary for homocysteine to turn into methionine

29
Q

PBS findings fr megaloblastic anemia

A
  • oval macrocytes
  • ## HJ bodies
30
Q

BM findings for megaloblastic anemia

A
  • hypersegs
  • hypercellular; erythroid hyperplasia
  • megakaryocytes decreased lobulation
  • N:C asynchrony
  • pancytopenia
  • increased serum iron
  • enlarged precursors
31
Q

clinical presentation megaloblastic anemia

A
  • jaundice
  • glossitis
  • gastritis
  • nausea
  • ailments related to GI
32
Q

anemia caused by _________ causes increased homocysteine levels

A

folate
- thrombosis
- CV disease

33
Q

pernicious anemia

A
  • impaired absorption of B12 due to lack of IF
  • autoimmune (parietal cells destroyed), gastric bypass, chronic gastric issues
34
Q

non-megaloblastic anemia

A
  • normal newborn blood
  • postsplenectomy
  • liver disease
  • reticulocytosis
  • chronic alcoholism
  • bone marrow failure (MDS/AA)
35
Q

aplastic anemia results from…

A

bone marrow failure and subsequent decreased hematopoietic cells

36
Q

causes of aplastic anemia

A
  • acquired: idiopathic of secondary to toxic agents or viruses
  • inherited: Fanconi’s, Dyskeratosis congenita Shwachman-Diamond syndrome
37
Q

Damage to bone marrow can cause (4)

A
  • increased destruction of hem. stem cells (drugs, viruses, autoimmunity)
  • decreased self-renewal of hematopoietic stem cells
  • infiltration with abnormal cells
  • inadequate or impaired microenvironment (decreased growth factors, etc.)
38
Q

T or F. The majority of AA cases is inherited

A

F! acquired mostly - idiopathic

39
Q

Fanconi’s

A
  • AA
  • aut recessive
  • defect in DNA repair
  • increased fetal Hb (macros)
  • renal probs, absent/hypoplastic thumb
40
Q

Dyskeratosis Congenita

A
  • X-linked or autosomal dominant
  • abn skin, nail malformation, oral leukoplakia
  • dyskerin protein lacking = inability to assemble ribosomes and maintain telomeres
41
Q

Schwachman-Diamond syndrome

A
  • aut recessive
  • SBDS mutation = defect in ribosomal assembly
  • affects BM - neuts predominantly so prone to infections
  • pancreatic functions affected, skeletal abnormalities, etc.
42
Q

Pure Red Cell Aplasia

A
  • ACQUIRED through exposure to harmful substances
  • no ribosomal assembly and function
  • leads to Bm failure
43
Q

AA CBC and PBS

A
  • pancytopenia
  • neuts and PLTs critically low
  • low retics despite increased EPO
  • normo/mormo or macrocytossis
  • no poly or nRBCs
44
Q

AA BM findings

A
  • hypocellular
  • trephine biopsy needed
  • iron stores normal to increased
  • Tx: BM transplants or continued transfusions
45
Q

RBC indices in hemolytic anemia

A

usually N; can be increased due to reticulocytosis

46
Q

T or F. Iron stores in hemolytic anemia is decreased

A

F! it is increased due to recycling!!

47
Q

alpha thalassemia genetics

A

large deletion that removes one or more alpha genes; chr 16

48
Q

Hemoglobin H

A

alpha thal; 3 gene deletion; alpha thal major
- does not precipitate right away but is unstable
- when leave the BM = Heinz bodies
- leads to decreased RBC lifespan and EVH
- still not as severe as B thal

49
Q

Hb Barts

A

complete alpha deletion
excess gamma = incompatible with life

50
Q

Hb S

A
  • sickle cells
  • Glu replaced with Val at 6th
  • aut co-dom inheritance
  • HbS less soluble than HbA
    > polymerizes under deoxygenated conditions
    > elongate/sickle
    > RBCs less deformable
    > vasculature occluded; sticky
    > deformed RBCs hemolyzed; lifespan 10-20 days
51
Q

Screens for sickle

A

HbS solubility test: patient sample with alkaline buffer = Hb precipitates out; HbS = insoluble = turbid

Sickling test: blood + alkaline solution to slide = real time sickling observed under mic

52
Q

HbC

A
  • Glu to lysine at 6th of B chain
  • also polymerizes under low O2 = but less splenic sequestration and hemolysis, milder than HbS
  • crystals (in/extracellular), spheros, targets
53
Q

HbE

A
  • Glu to Lys at 26th
  • no clinical symptoms, mild anemia
  • problem when co-dom with other Hbinopathies
54
Q

HbM

A
  • predisposition to form methemoglobin (Fe 3+)
  • methemoglobin reductase CANNOT correct this oxidation
55
Q

G6Pd deficiency tests

A
  • negative DAT
  • blister cells
  • IVH indicators (incr LD, bili, hemoglobinuria, decrease hapto) or EVH
  • decreased G6PD activity
56
Q

what causes echinocytes in PK deficiency?

A
  • less ATP formed
  • Na/K pump fails
  • K+ and water leak out
  • cells rigid, shrink
57
Q

RBC indices in HE

A

normal

58
Q

T or F. In HE, the elliptos are made in the BM

A

F! they form like that overtime as they pass through vasculature

59
Q

T or F. 80-95% of HE are asymptomatic

A

T!

60
Q

three clinical findings of HS

A
  • jaundice
  • anemia
  • splenomegaly

** symptoms often appear early in life**

61
Q

screens vs confirmatory testing for HS

A
  • EMA (binds to band 3; HS is decreased fluorescence) and osmotic fragility test
  • molecular testing
62
Q

hereditary acanthocytosis

A
  • pts w liver disease may develop HA with acanthocytosis
  • excess free cholesterol; mutation in MTP; decreases fluidity in cells
  • spleen remodels cells into acanthocytes
  • low Hb; normal indices
  • EVH
  • autosomal recessive
63
Q

CBC for PNH

A
  • low Hb
  • decreased WBcs and PLTs
  • elevated MCV due to retics
  • loss of iron in urine => IDA?
64
Q

PNH

A

red cells lack GPI-anchored proteins = susceptible to spontaneous lysis by complement; also found in WBCs and PLTs

65
Q

T or F. PNH can lead to BM failure or AA

A

T

66
Q

tests for PNH

A
  • IVH tests
  • flow cytometry for CD55, CD59
67
Q

hemolysis markers

A
  • increased LDH (intravascular)
  • increased bilirubin (shows increased turnover of heme rings
  • decreased haptoglobin
  • decrease methemalbumin (occupied by Hb to transport to liver)

MLSCI 330 (9 decks)

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