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Hematology > Anemias > Flashcards

Anemias Flashcards

1
Q

What are the stages of iron deficient anemia

A

storage iron depletion - stored iron is used up as there is a decrease of available iron
storage iron/pool exhaustion - storage pools are completely used up and serum iron continues to be used until it is also exhausted
iron deficient anemia - all iron stores and pools have been used and there is very little iron for incorporation into new RBCs

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2
Q

What are the symptoms of IDA

A

spooning of nails, sore tongue, muscle dysfunction, fatigue, blue sclera, cravings for non-nutritional items

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3
Q

What are the causes of anemia of chronic infection/disease

A

impaired iron kinetics - during infection available iron is removed from the serum and stored as ferritin
impaired erythropoiesis - inflammatory cytokines hinder the action of EPO
decreased RBC survival - body and immune system is on high alert

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4
Q

What are the features of warm auto-immune hemolytic anemia

A

usually of unknown cause or secondary to disease

IgG, reacts at 37, DAT IgG positive C3D variable, Complement activation variable, EVH, pan reactive Rh complex antibody

sphero, poly, nRBC, retic

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5
Q

What are the features of cold agglutin disease

A

can be non-pathogenic (will not react aboe 30) or pathogenic (will react at 37) usually idiopathic or secondary to lymphoproliferative disorders

IgM, reacts at 4, DAT C3D positive, activates compliment, EVH, anti- I, -i, -pr

autoagglutination, poly

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6
Q

What are the features of paroxysmal cold hemoglobinuria

A

idopathic or secondary to infection. Biphasic - bind at 4 and partially activate compliment then when 37 is achieved it will dissociate but complement will fully activate

IgG, reacts at 4, DAT C3D positive, activates compliment, IVH, anti-P

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7
Q

What are the expected hemoglobin levels in Beta Thalassemia Major

A

decreased/absent HGB A
normal-increased HGB A2
70-90% HGB F

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8
Q

What are the expected hemoglobin levels in Sickle cell trait

A

> /= 60% HGB A
Normal/increased HGB A2
<1% HGB F
</= 40% HGB S

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9
Q

What are the expected hemoglobin levels in sickle cell disease

A

Normal/increased HGB A2
20% HGB F
>/= 80% HGB S

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10
Q

What are the expected hemoglobin levels in hemoglobin C trait

A

> /= 60% HGB A
Normal HGB A2
Normal HGB F
30% HGB C

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11
Q

What are the expected hemoglobin levels in hemoglobin C disease

A

2% HGB A2
< 7% HGB F
>90% HGB C

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12
Q

What are the lab findings in IDA

A

micro/hypo
decreased HGB
decreased MCV
normal WBC
increased or decreased PLT
targets, eliptos, tears
normoblasts with ragged edges in BM
decreased M:E

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13
Q

What are the confirmation tests for IDA

A

decreased iron stores in BM
decreased serum iron
decreased serum ferritin
decreased transferrin
increased TIBC

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14
Q

What are causes of sideroblastic anemia

A

enzyme deficiency - ALA synthase
drugs - chemo drugs, isoniazid and chloramphenical
lead poisoning - inhibits ALA dehydratase and inhibits incorporation of iron into the protoporphyrin ring

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15
Q

What are lab findings in sideroblastic anemia

A

micro/hypo and normo/normo
decreased HGB
normal WBC
normal PLT
increased RDW
basophilic stippling, pappenheimers
ringed sideroblasts in BM
decreased M:E

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16
Q

What are the confirmation tests for sideroblastic anemia

A

increased iron stores in BM
increased serum iron
increased serum ferritin
increased transferrin
decreased TIBC

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17
Q

What are lab findings for anemia of chronic infection

A

micro/hypo or normo/normo
decreased HGB
decreased MCV
normal/increased WBC
normal/increased PLT
suppressed EPO
no erythroid hyperplasia
normal/increased M:E

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18
Q

What are confirmation tests for anemia of chronic infection

A

increased CRP
normal/increased iron stores in BM
decreased serum iron
increased serum ferritin
increased transferrin
decreased TIBC

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19
Q

What are causes of megaloblastic anemia

A

B12/folate deficiency due to diet, malabsorption, increased need, increased loss

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20
Q

What are lab findings for megaloblastic anemia

A

macro ovalocytes
hyper-segmented neuts
erythroid hyperplasia
nuclear-cytoplasm asynchrony
large precursors
HJ, tears, schistos, BC, nRBCs
decreased reticulocytes
decreased HGB
decreased RBC
decreased PLT
decreased WBC
increased MCH
increased MCV
decreased M:E

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21
Q

What are confirmation tests for megaloblastic anemia

A

normal iron studies

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22
Q

What are causes of non-megaloblastic anemia

A

liver disease, chronic alcoholism, post-splenectomy, BM failure

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23
Q

What are lab findings for megaloblastic anemia

A

macrocytes
erythroid hyperplasia
nuclear-cytoplasmic asynchrony
large precursors
decreased HGB
increased MCV
normal WBC
decreased M:E

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24
Q

What are confirmation tests for megaloblastic anemia

A

normal iron studies

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25
Q

What are lab findings for aplastic anemia

A

decreased HGB
decreased WBC
decreased PLT
pancytopenia
normo/normo or macro
increased yellow tissue in BM (dry tap)

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26
Q

What are lab findings for Beta Thalassemia

A

decreased HGB
decreased MCV
increased/normal retic
hypo/micro
targets, tears, schisto, sphero, elipto, HJ, BS, papenheimer
Heinz bodies in major
nRBC
erythroid hyperplasia
decreased M:E

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27
Q

What causes Beta Thalassemia

A

decrease in beta globin chains due to deletion or silencing of one or both genes
1 gene: minor
2 genes: major

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28
Q

What are confirmation tests for Beta Thalassemia

A

HPLC
HGB electrophoresis
increased iron stores in BM
normal serum iron
normal/increased serum ferritin
molecular genetics

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29
Q

What are lab findings for Alpha Thalassemia

A

decreased HGB
decreased MCV
micro/hypo
tears, schistos, spheros, targets, HJ, BS
erythroid hyperplasia

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30
Q

What are confirmation tests for Alpha Thalassemia

A

HPLC
HGB electrophoresis
normal serum iron
normal/increased serum ferritin

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31
Q

What are lab findings for Hemoglobin S

A

sickle cells
increased iron stores
targets, sphero, schisto, poly, nRBC, JH, BS, pappenheimer
decreased M:E

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32
Q

What are confirmation tests for Hemoglobin S

A

HGB electrophoresis
HPLC
sickling test
solubility test

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33
Q

What are lab findings for hemoglobin C

A

short, thick crystals
increased iron stores
normo/normo
targets, sphero, schisto, nRBC

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34
Q

What are confirmation tests for Hemoglobin C

A

HBG electrophoresis
HPLC

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35
Q

What are lab findings for hemoglobin E

A

micro
target cells
increased iron stores

often another hemoglobinopathy

36
Q

What are confirmation tests for hemoglobin E

A

HGB electrophoresis
HPLC

37
Q

What are confirmation tests for Hemoglobin M

A

HGB electrophoresis
HPLC

38
Q

What are lab findings for hemoglobin M

A

increased iron stores

39
Q

What does G6PD deficiency effect

A

the hexose monophosphate shunt in the ebdimeyerhoff pathway causing cells to be more prone to oxidative damage under stress

X-linked inheritance

40
Q

What are lab findings for G6PD deficiency

A

heinz bodies
bites, helmets, schistos
DAT neg

41
Q

What is the confirmation test for G6PD deficency

A

decreased G6PD assay

42
Q

What are lab findings for PK deficiency

A

poly
echinocytes

43
Q

What causes PNH

A

acquired stem cell disorder missing the GPI protein (CD 55, 59) these proteins are responsible for preventing cell lysis from complement

44
Q

What are lab findings of DIC

A

decreased HGB
thrombocytopenia
schistos
increased PT
increased PTT
decreased fibrinogen
increased D-dimers
poly

45
Q

What causes TTP

A

decrease om ADAMTS-13 which is responsible for cleaving VWF multimers. Without ADAMTS-13 the long multimers cause thrombi formation and blockages in the vasculature

it can be inherited, idiopathic or acquired

46
Q

What are lab findings in TTP

A

thrombocytopenia
schistos
increased LDH
poly

47
Q

What causes HUS

A

toxins from ecoli O1:5:7 or shigella. The toxins cause endothelial cell damage which creates a pro-coagulative environment and thrombi formation

atypical HUS can cause spontaneous activation of the alternate complement system leading to vascular injury and subsequent activation of the coagulation system. Increased damage leads to large multimers of VWF despite normal ADAMTS-13 activity

47
Q

What are the lab findings in HUS

A

thrombocytopenia
schistos
poly

48
Q

What are the lab findings in HELLP

A

increased liver enzymes
decreased platelets

49
Q

What is the confirmation test of PCH

A

donath-landsteiner test

50
Q

What are causes of anemia

A

ineffective erythropoiesis
insufficient erythropoiesis
excessive blood loss
hemolysis

51
Q

What are the microcytic anemias

A

IDA, Sideroblastic, ACI, Thalassemia

52
Q

What are the macrocytic anemias

A

megaloblastic, non-megaloblastic

53
Q

What are the normocytic anemias

A

hemolytic, aplastic, ACI

54
Q

What do vitamin B12 and folate have to do with erythropoiesis

A

they are vital to the production of thymine, without them thymine cannot be produced and DNA replication is slowed down. A place holder is used but never replaced causing the DNA to be broken during proof reading making unstable cells

55
Q

What is pernicious anemia

A

an autoimmune disorder that causes a lack of intrinsic factor due to destruction of parietal cells

56
Q

What causes aplastic anemia

A

bone marrow failure and decrease in hematopoietic cells due to damage or injury to the marrow

acquired - idiopathic, exposure to toxic agents or viruses
inherited - fanconcis anemia, duskeratosis congenita. schwachman-diamond syndrome

57
Q

What is fanconis anemia

A

an autosomal recessive disorder or X-linked that causes abnormal chromosomal fragility and a predisposition to leukemia and cancer

58
Q

What is dyskeratosis congenita

A

X-linked autosomal dominant or autosomal recessive mutations that reduce telomerase activity

59
Q

What is scheachman-diamond syndrome

A

a mutation in the SBDS gene similar to Fanconies anemia with additional pancreaticfunction and malabsorption

60
Q

What is pure red cell aplasia

A

a severe decrease of RBC precursors with no other bone marrow abnormalities

61
Q

What are lab findings for pure red cell aplasia

A

low HGB
low PLT
low WBC
normo/normo or macro
increased yellow tissue in the marrow

62
Q

What causes alpha thalassemia

A

defects in alpha globin chain production

minor - deletion of two genes
intermedia (hemoglobin H) - deletion of three genes
major (hemoglobin barts) - deletion of all four genes (not compatible with life)

63
Q

What are the clinical complications of hemoglobin S

A

oxidative damage to RBC membrane which induces adherence of RBCs to the surface of capillaries and arterioles as well as RBC aggregation

adhesion of RBCs could activate the coagulation cascade

64
Q

What is the benefit of sickle cell trait

A

malarial resistance

65
Q

What causes hemoglobin S

A

a substitution in the 6th position of the beta chain causing replacement of glutamic acid with valine

66
Q

What causes hemoglobin C

A

a substitution in the 6th position of the beta chain causing replacement of glutamic acid with lysine

67
Q

What causes hemoglobin E

A

a substitution in the 26th position of the beta chain causing lysine to be replaced by glutamic acid

68
Q

What causes hemoglobin M

A

different mutations in any chain that causes the formation of methemoglobin that has a structural abnormality in the globin portion. This causes heme iron to oxidize and cannot transport oxygen

69
Q

What does pyruvate kinase deficiency effect

A

the embden-meyerhof pathway causing the cell to not produce enough ATP. This effects membrane permeability and causes the cell to become rigid and less deformable

autosomal recessive inheritance

70
Q

What is hereditary eliptocytosis

A

autosomal dominant disorder with defects in the spectrin and protein 4.1 genes

RBC lack horizontal structural protein interactions causing them to form elliptocytes

71
Q

What are the variants of hereditary elliptocytosis

A

hereditary pyropoikolocytosis - sever form with increased poik (sphero, micro, schisto, ellipto) and increased thermal sensitiivity

southeast asian ovalocytosis - band 3 gene mutation causing increased rigidity of membrane. Causes resistance to malaria. Looks like pig nose

72
Q

What is hereditary spherocytosis

A

defects in vertical interactions of transmembrane protiens and cytoskeleton

mutations may occur in ankyrin. protein 4.3, band 3 or spectrin

due to lack of support RBC lose lipid membrane leading to formation of spherocytes as well as higher concentrations of Na and lower concentrations of K inside the cell

73
Q

What is hereditary acanthocytosis

A

autosomal recessive disease caused by mutations in the microsomal triglyceride transfer protein

causes an absence of VLDL, LDL and chylomicrons decreasing membrane fluidity

severe liver disease can be an acquired form of the disease

74
Q

What is the malaria lifecycle

A
  1. female anopheles mosquito acquires malaria from an infected source
  2. malaria reproduces and the zygote enters the stomach lining of the mosquito forming a cyst
  3. new parasites are produced and travel to the salivary gland of the mosquito
  4. malaria enters new host when bitten and travels to the liver
  5. parasites mature in the liver and then enter the blood stream and infect RBCs
75
Q

How does malaria cause anemia

A

lysing infected cells, inhibited/ineffective erythropoiesis, causing immune cells to attack infected cells

76
Q

What is the most severe form of malaria

A

plasmodium falciparum

77
Q

Why is plasmodium falciparum the most severe form of malaria

A

it can affect all stages of the RBC and adheres to endothelial cells in organs and microvasculature to avoid removal via spleen

78
Q

How is malaria confirmed once seen in smear

A

PCR

79
Q

What are differentiating features of falciparum

A

small delicate ring forms with two chromatin dots, banana shaped gametes, multiple rings in a single cell

80
Q

What is babesiosis

A

a parasite that is transmitted by Ixodes scapularis (tick)

81
Q

What is the presentation of babeiosis

A

extracellular or as a maltese cross in RBCs

82
Q

How does clostridium effect RBCs

A

releases alpha-toxins and phospholipase C as well as sphingomyelinase activity that all work together to alter the membrane causing spherocytes

83
Q

What is seen in blood smears of burn patients

A

schistocytes and spherocytes for ~24 hours after incident

84
Q

What are the methods of drug induced hemolytic anemias

A

autoimmune, drug adsorption, immune complex, drug induced non-immunologic protein adsorption

85
Q

What is seen in blood smears of drug-induced hemolytic anemias

A

spherocytes and poly

Hematology (7 decks)

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