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Anemias Flashcards

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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
What are lab findings for aplastic anemia
decreased HGB decreased WBC decreased PLT pancytopenia normo/normo or macro increased yellow tissue in BM (dry tap)
26
What are lab findings for Beta Thalassemia
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
27
What causes Beta Thalassemia
decrease in beta globin chains due to deletion or silencing of one or both genes 1 gene: minor 2 genes: major
28
What are confirmation tests for Beta Thalassemia
HPLC HGB electrophoresis increased iron stores in BM normal serum iron normal/increased serum ferritin molecular genetics
29
What are lab findings for Alpha Thalassemia
decreased HGB decreased MCV micro/hypo tears, schistos, spheros, targets, HJ, BS erythroid hyperplasia
30
What are confirmation tests for Alpha Thalassemia
HPLC HGB electrophoresis normal serum iron normal/increased serum ferritin
31
What are lab findings for Hemoglobin S
sickle cells increased iron stores targets, sphero, schisto, poly, nRBC, JH, BS, pappenheimer decreased M:E
32
What are confirmation tests for Hemoglobin S
HGB electrophoresis HPLC sickling test solubility test
33
What are lab findings for hemoglobin C
short, thick crystals increased iron stores normo/normo targets, sphero, schisto, nRBC
34
What are confirmation tests for Hemoglobin C
HBG electrophoresis HPLC
35
What are lab findings for hemoglobin E
micro target cells increased iron stores often another hemoglobinopathy
36
What are confirmation tests for hemoglobin E
HGB electrophoresis HPLC
37
What are confirmation tests for Hemoglobin M
HGB electrophoresis HPLC
38
What are lab findings for hemoglobin M
increased iron stores
39
What does G6PD deficiency effect
the hexose monophosphate shunt in the ebdimeyerhoff pathway causing cells to be more prone to oxidative damage under stress X-linked inheritance
40
What are lab findings for G6PD deficiency
heinz bodies bites, helmets, schistos DAT neg
41
What is the confirmation test for G6PD deficency
decreased G6PD assay
42
What are lab findings for PK deficiency
poly echinocytes
43
What causes PNH
acquired stem cell disorder missing the GPI protein (CD 55, 59) these proteins are responsible for preventing cell lysis from complement
44
What are lab findings of DIC
decreased HGB thrombocytopenia schistos increased PT increased PTT decreased fibrinogen increased D-dimers poly
45
What causes TTP
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
What are lab findings in TTP
thrombocytopenia schistos increased LDH poly
47
What causes HUS
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
What are the lab findings in HUS
thrombocytopenia schistos poly
48
What are the lab findings in HELLP
increased liver enzymes decreased platelets
49
What is the confirmation test of PCH
donath-landsteiner test
50
What are causes of anemia
ineffective erythropoiesis insufficient erythropoiesis excessive blood loss hemolysis
51
What are the microcytic anemias
IDA, Sideroblastic, ACI, Thalassemia
52
What are the macrocytic anemias
megaloblastic, non-megaloblastic
53
What are the normocytic anemias
hemolytic, aplastic, ACI
54
What do vitamin B12 and folate have to do with erythropoiesis
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
What is pernicious anemia
an autoimmune disorder that causes a lack of intrinsic factor due to destruction of parietal cells
56
What causes aplastic anemia
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
What is fanconis anemia
an autosomal recessive disorder or X-linked that causes abnormal chromosomal fragility and a predisposition to leukemia and cancer
58
What is dyskeratosis congenita
X-linked autosomal dominant or autosomal recessive mutations that reduce telomerase activity
59
What is scheachman-diamond syndrome
a mutation in the SBDS gene similar to Fanconies anemia with additional pancreaticfunction and malabsorption
60
What is pure red cell aplasia
a severe decrease of RBC precursors with no other bone marrow abnormalities
61
What are lab findings for pure red cell aplasia
low HGB low PLT low WBC normo/normo or macro increased yellow tissue in the marrow
62
What causes alpha thalassemia
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
What are the clinical complications of hemoglobin S
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
What is the benefit of sickle cell trait
malarial resistance
65
What causes hemoglobin S
a substitution in the 6th position of the beta chain causing replacement of glutamic acid with valine
66
What causes hemoglobin C
a substitution in the 6th position of the beta chain causing replacement of glutamic acid with lysine
67
What causes hemoglobin E
a substitution in the 26th position of the beta chain causing lysine to be replaced by glutamic acid
68
What causes hemoglobin M
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
What does pyruvate kinase deficiency effect
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
What is hereditary eliptocytosis
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
What are the variants of hereditary elliptocytosis
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
What is hereditary spherocytosis
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
What is hereditary acanthocytosis
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
What is the malaria lifecycle
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
How does malaria cause anemia
lysing infected cells, inhibited/ineffective erythropoiesis, causing immune cells to attack infected cells
76
What is the most severe form of malaria
plasmodium falciparum
77
Why is plasmodium falciparum the most severe form of malaria
it can affect all stages of the RBC and adheres to endothelial cells in organs and microvasculature to avoid removal via spleen
78
How is malaria confirmed once seen in smear
PCR
79
What are differentiating features of falciparum
small delicate ring forms with two chromatin dots, banana shaped gametes, multiple rings in a single cell
80
What is babesiosis
a parasite that is transmitted by Ixodes scapularis (tick)
81
What is the presentation of babeiosis
extracellular or as a maltese cross in RBCs
82
How does clostridium effect RBCs
releases alpha-toxins and phospholipase C as well as sphingomyelinase activity that all work together to alter the membrane causing spherocytes
83
What is seen in blood smears of burn patients
schistocytes and spherocytes for ~24 hours after incident
84
What are the methods of drug induced hemolytic anemias
autoimmune, drug adsorption, immune complex, drug induced non-immunologic protein adsorption
85
What is seen in blood smears of drug-induced hemolytic anemias
spherocytes and poly

Hematology (7 decks)

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