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Heme Path > Week 1 RR > Flashcards

Week 1 RR Flashcards

1
Q

hypoxic injury and infarction w/ severe pain in the affected organ

A

Pain crises (vaso-occlusive)–> sickle cell disease

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2
Q

Transfusion rxn: Fever, Chills, back pain and headache; hemoglobinuria, hemoglobinemia

A

Acute hemolytic transfusion reaction

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3
Q

G6PD recovery phase

A

reticulocytosis.

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4
Q

Sickle Cell Anemia inheritance

A

Autosomal recessive

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5
Q

PIG-A is x-linked; significance?

A

when PIG-A is INACTIVATED–> PNH PIG-A may be inactivated through lyonization causing PNH

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6
Q

hydrops fetalis pathogenesis

A

high output cardiac failure–> Liver dysfunction–> Dec albumin–> EDEMA

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7
Q

pre-renal azotemia: oliguria or anuria

A

Acute blood loss

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8
Q

s/s of HTLV‐1 and HTLV‐2

A

T‐Cell lymphoma Demyelinating neuropathy

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9
Q

“bite cells

A

G6PD

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10
Q

OLDER RBCs have more damage

A

G6PD

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11
Q

what are Heinz bodies and where found

A

seen in G6PD def. Sulfhydryl groups in Hb is oxidized and precipitates forming Heinz bodies

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12
Q

Seen in Middle Eastern ppl

A

Mediterranean variant G6PD

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13
Q

secondary hemosiderosis (iron overload)

A

Thalassemia (from the transfusion) Sickle Cell anemia Hereditary spher.

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14
Q

Megaloblastic Anemia retic count; MCV

A

macrocytic MCV>100 ↓ retic count

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15
Q

PNH mutation

A

INACTIVATING somatic mutation of PIG-A

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16
Q

acute vs. delayed Hemolytic transfus. rxn: intra/extravascular hemolysis

A

acute–> intra delayed–> extravascular

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17
Q

Pernicious anemia diagnosis

A

anti-IF antibody

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18
Q

NO levels in Sickle cell disease; significance?

A

it is depleted b/c Hb from lysed sickle cells bind it; Result–> more vasconstriction leading to INC transit time and more problems

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19
Q

Erythroblastosis fetalis retic count

A

INC. because it is hemolytic

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20
Q

the direct Coombs detects (1) and the indirect detects (2)

A
  1. antibodies on red cells 2. antibodies in serum or plasma
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21
Q

Drug induced: Sudden, severe hemolysis w/ Hburia

A

Cephalosporins.

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22
Q

associated w/ chronic inflammation

A

Anemia of Chronic Disease (ACD)

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23
Q

intravascular hemolysis

A

G6PD PNH Microangiopathic Hemolytic Anemia

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24
Q

IgG vs IgM in erythro. fetalis

A

IgG can cross placenta; IgM too large;

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25
Q

(a) ineffective erythropoiesis (b) extravascular hemolysis

A

β-thalassemia

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26
Q

RBCs susceptible to destruction by complement. *i.e. decreased inhibition of complement activation*

A

PNH

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27
Q

Acute blood loss lab values

A

↑ platelets (thrombocytosis) ↑ WBC esp. granulocyte (leukocytosis)

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28
Q

Pseudo‐Pelger –Huet cells–>

A

dumb-bell shaped neutrophils seen in Myelodysplastic syndrome

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29
Q

↑serum homocysteine; ↑ methylmalonic acid

A

Vit. B12 def.

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30
Q

IgM antibodies bind to RBCs at less than 37 deg. C

A

Cold AIHA

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31
Q

how is metabolic complications in blood transfusion occur

A

Blood unit is anticoagulated w/ citrate; Rapid infusion chelates calcium

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32
Q

Manifestations of post transfusion purpura

A

severe bleeding thrombocytopenia 1-3 weeks post transfusion

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33
Q

HbC (Lys for Glu) cells lose 1) and become dehydrated, sickling

A

1) salt and water

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34
Q

hyper-segmented (>5 nuclei) neutrophils

A

Megaloblastic Anemia

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35
Q

extravascular hemolysis

A

Hereditary spherocytosis Immune Hemolytic Anemia Thalassemia

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36
Q

1) inhibits HbS polymerization

A

1) HbF

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37
Q

P. pneumoniae and H. influenzae

A

Encapsulated organisms; seen in Sickle patients

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38
Q

Hypoalbuminemia Generalized edema

A

Fetal compensation in erythro. fetalis

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39
Q

(Paroxysmal Nocturnal Hburia) inheritance

A

ACQUIRED; not inherited

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40
Q

Febrile non hemolytic transfusion reactions are caused by (1) antibodies in the recipients plasma which react with (2) leading to the release of endogenous pyrogens (3)

A
  1. anti‐leukocyte or antiplatelet 2. donor WBC’s 3. IL‐1 ,IL‐6 , TNF‐alpha
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41
Q

non-transmembrane proteins that attach to the cell membrane through GPI

A

PIGA

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42
Q

peripheral nucleated RBC’s, polychromatophylia (indicates ↑turnover), thrombocytopenia and ↑bilirubin

A

Erythroblastosis fetalis

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43
Q

Sickle cell pathogenesis: Deoxygenated HbS polymerizes–> aggregate into long needle-like structures–> ↓pH–> 1)

A

1) RBC sickles

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44
Q

Hereditary Spherocytosis–> intravascular or extravascular

A

Extravascular

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45
Q

(CD55

A

Decay-accelerating factor–>inhibitor of complement

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46
Q

coats the Rh positive cells of fetus and prevents sensitization of mother

A

Rho-gam; only effective against Rh(D)

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47
Q

Direct Coomb’s test: (-) Anti-IgG (+) anti-C3d

A

Cold AIHA

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48
Q

decreased reticulocyte count

A

Iron def. anemia Thalassemia Megaloblastic anemia ACD Aplastic anemia

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49
Q

Sickle cell hallmark in children

A

Hand-foot syndrome–> swollen hands and feet

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50
Q

Myelodysplastic syndrome: (1) gene is located on chromosome 8 and trisomy 8 is commonly seen in a variety of (2)

A
  1. MYC 2. myeloid malignancies
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51
Q

Acute hemolytic transfusion reactions are most often from transfusion of (1

A
  1. ABO incompatible red blood cells
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52
Q

β0-thalassemia vs. β+-thalassemia

A

β0-thalassemia: Absent functional β-globin protein β+-thalassemia: ↓ β-globin protein.

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53
Q

Sickle cell MCHC

A

Increased due to intracellular dehydration

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54
Q

Transfusion complication: HTN; SOB, pul. edema, etec.

A

Circulatory overload

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55
Q

Antigen antibody reactions from infusion of plasma proteins

A

Allergic Rxns to blood transfusion

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56
Q

IgM vs. IgG

A

Erythroblastosis fetalis: IgM can’t cross placenta IgG can. Autoimmune Hemolytic anemia: warm–> IgG Cold–> IgM Drug Induced Hemolytic anemia:

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57
Q

Disposal of the oxidant H2O2 is dependent on reduced glutathione (GSH), which is generated by the action of 1); without G6PD, 1) cannot be generated

A

NADPH

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58
Q

SEVERE anaphylaxis due to transfusion

A

IgA deficient pts

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59
Q

This cytokine released during (1) binds to hemoglobin leading to renal vasoconstriction

A
  1. acute hemolytic transfusion reactions; cytokine is NO (EDFR)
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60
Q

Myelodysplastic syndrome: 5q vs. 7q

A

5q–> often good prognosis in older women 7q–>worse prognosis

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61
Q

Point mutation in beta globiin gene;

A

β-thalassemia

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62
Q

Sicke cell diagnosis

A

Positive sickling w/ metabisulfate; Hb electrophoresis shows High HbS

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63
Q

More severe. Markedly reduced ½ life (reduction in protein stability

A

Mediterranean variant G6PD

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64
Q

anti-leukocyte or anti-platelet Abs in host plasma which react with donor WBCs

A

Febrile non hemolytic transfusion reaction

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65
Q

Cold agglutinins are associated with

A

mycoplasm pneumonia, infectious mono (EBV, CMV)

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66
Q

Transfusion complication: pt on ACE inhibitor (unable to break down bradykinin)

A

Hypotensive rxn;

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67
Q

Erythroid hyperplasia in the bone marrow (“crewcut” on scalp), extramedullary hematopoiesis (in liver, spleen, and lymph nodes).

A

Sickle cell

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68
Q

Drug induced: Direct or indirect Coombs’ test: Complement only

A

immune-complex type

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69
Q

PNH–> intravascular or extravascular

A

intravascular hemolysis

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70
Q

acute phase reactants such as ferritin and hepcidin ↑

A

Anemia of chronic disease (ACD)

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71
Q

INHERITED defect in RBC membrane

A

Hereditary Spherocytosis

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72
Q

Myelodysplastic syndrome has a high risk of transformation to (1)

A

Acute Myeloid Leukemia (AML).

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73
Q

Aplastic crises: RBC progenitors w/ parvovirus B19

A

Sickle cell disease

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74
Q

Antibodies against transfused leukocytes or platelets release endogenous pyrogens(IL‐1 ,IL‐6 , TNF‐alpha )

A

Febrile non hemolytic transfusion reaction:

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75
Q

hypocellular marrow with lots of fat; few erythroid progenitors

A

Aplastic Anemia

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76
Q

1 mutated β gene vs. 2 mutated

A

Thalssemia minor–> Mild anemia 2: Thalassemia major–> severe anemia; needs transfusion

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77
Q

PNH RBCs go through intravascular hemolysis caused by 1)

A

1) C5b-C9 MAC

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78
Q

small molecule that generates an immune response when attached to a larger molecule.

A

Hapten

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79
Q

↓haptoglobin.

A

Intravascular hemolysis

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80
Q

G6PD deficiency–> intravascular or extravascu

A

intravascular hemolysis

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81
Q

Splenomegaly

A

Extravascular

82
Q

colon polyps/carcinoma in elderly

A

Iron-Deficiency Anemia

83
Q

Sickle cell anemia s/s due to extravascular hemolysis

A

Bilirubin stones;

84
Q

seen in conditions such as Diabetes, RA, SLE, neoplastic disorders

A

Anemia of Chronic Disease (ACD)

85
Q

Poikilocytosis vs. aniscocytosis

A

aniScocytosis–> varying Sizes poikilocytosis–> varying SHAPES

86
Q

Iron-Deficiency Anemia lab

A

↓serum iron ↓Ferritin; ↑TIBC;

87
Q

Erythroblastosis fetalis LABS

A

Inc. UCB; Dec. platelets (thrombocytopenia)

88
Q

G6PD s/s

A

Intravascular hemolysis therefore: Hbemia; Hburia ANEMIA

89
Q

Myelodysplastic syndrome: Epigenetic factors

A

hyper methylation with silencing of tumor suppressor genes

90
Q

Sickle cell lab test

A

Mix blood with metabisulfate–>

91
Q

Mildly reduced ½ life of G6PD (protein misfolding)

A

African variant G6PD

92
Q

most common cause of death in adults with sickle cell disease

A

Acute Chest Syndrome

93
Q

Erythroblastosis fetalis: jaundice soon after birth. why not in utero

A

placenta handles the bilirubin in utero

94
Q

extravascular hemolysis s/s

A

Splenomegaly, jaundice ↑risk of pigmented gallstones.

95
Q

Hereditary Spherocytosis inheritance

A

AD; more severe when compound heterozygote

96
Q

associated w/ PNH

A

Aplastic Anemia

97
Q

Erythroblastosis fetalis direct coomb’s test

A

(+) direct Coombs test (IgG)

98
Q

Acquired antibody mediated RBC destruction

A

autoimm. hemolytic anemia

99
Q

MCV, Hb, Hct and MCH are all ↓.

A

Iron-Deficiency Anemia

100
Q

Drug induced: penicillin

A

Hapten Mechanism

101
Q

Cause of death in PNH

A

venous Thrombosis–> platelet pieces destroyed by compliment clump together;

102
Q

What are the s/s of chelation of calcium?

A

Circumoral paresthesia and tingling of fingers

103
Q

dumb-bell shaped neutrophils with two nuclei

A

Pseudo‐Pelger –Huet celll–>Myelodysplastic syndrome

104
Q

Intravascular and extravascular hemolysis

A

Sickle Cell disease

105
Q

associate w/ ankyrin, band 4.2 and band 3.1; alpha and beta spectrin dimers

A

Hereditary Spherocytosis

106
Q

Which transfusion reactions are complement mediated?

A

Acute hemolytic transfusion reactions Delayed are not complement mediated

107
Q

an excess of α-globin chains causes problems

A

β-thalassemia (↓β-globin mRNA)

108
Q

Secondary to mycoplasma pneumoniae infection

A

Cold AIHA

109
Q

target cells, microcytic hypochromic cells

A

Sickle cell

110
Q

↑serum homocysteine; normal methylmalonic acid

A

Folate def.

111
Q

blood from multiparous woman can cause:

A

TRALI (Transfusion acute LUNG injurY)

112
Q

loss of central pallor

A

Hereditary Spherocytosis

113
Q

Inc. susceptibility to oxidative damage

A

G6PD

114
Q

myeloblasts in myelodysplastic syndrome vs. acute myeloid leukemia

A

Myelodys–> inc. but less than 20% AML–> myeloblasts less than 20%

115
Q

Transfusion complication: Hypotensive rxn; s/s

A

HYPOTENSION facial flushing and abdominal pain

116
Q

Acute Chest Syndrome s/s

A

chest pain, and pulmonary infiltrates; SOB; seen in Sickle cell pts

117
Q

fava beans

A

G6PD–> generates oxidants when metabolized

118
Q

hemoglobinemia, hemoglobinuria, hemosiderinuria

A

intravascular hemolysis

119
Q

Transfusion complication: HBV vs. HCV

A

HBV–> jaundice 2 mos after; very few become chronic carrier HCV–> non-icteric; HIGH percent becomes chronic carriers

120
Q

Transfusion complication in an IgA def. pt

A

anaphylaxis hypotension

121
Q

Thalassemia–> intravascular or extravascular

A

Extravascular

122
Q

Dec. pH on Sickle cell

A

INCREASES sickling

123
Q

β-Thalassemia major vs. minor genetics

A

Major–>Homozygous (some compound heterozygous) minor–> heterozygous

124
Q

vitamin B12 or Folic acid deficiencies

A

Megaloblastic Anemia

125
Q

Sickle cell on xray; why?

A

crewcut appearance due to compensatory erythroid hyperplasia in the bone marrow of SKULL

126
Q

Why should neonates get blood 7 day old or less for exchange transfusions?

A

To reduce the risk of a storage lesion in which potassium leaks out of RBC during storage

127
Q

Drug induced: Drug stimulates IgM production against RBCs

A

Immune Complex Mechanism

128
Q

If store blood for too long, what may occur?

A

Metabolic Complications: Storage lesion –> K+ leaks out of RBC during storage

129
Q

“Underhemoglobinized” hypochromic microcytic cells

A

β-thalassemia

130
Q

Transfusion related acute lung injury is due to antibodies in the donor plasma directed against the recipient’s (1); these are usually (2) antigens

A
  1. WBC’s 2. class I MHC
131
Q

Hburia in the morning that disappears in the afternoon

A

Paroxysmal Nocturnal Hburia

132
Q

Sulfhydryl groups in Hb is oxidized and precipitates forming 1)

A

1) Heinz bodies

133
Q

G6PD inheritance

A

X-linked recessive

134
Q

metabisulfate test

A

causes sickling in both sickle cell disease and trait

135
Q

Due to slow transit times, Sickled cells show increased adhesion 1)

A

1) to vascular endothelium

136
Q

Increased risk of sickling occurs w/

A

hypoxemia, dehydration and acidosis

137
Q

Drug induced: Direct or indirect Coombs’ test: IgG only

A

hapten type or autoantibody type

138
Q

What problem can occur as a result of a rapid infusion?

A

Rapid infusion results in chelation of calcium by citrate (which is used as an anticoagulant for blood)

139
Q

↑ LDH

A

seen in hemolysis

140
Q

Direct Coomb’s Test: (+) anti-IgG, (+) anti-C3d or both.

A

Warm AIHA

141
Q

Sickle cell: polymers aggregate and RBCs lose 1) and have 2)pH;

A

1) intracellular K+ and h2O 2) ↓

142
Q

Erythroblastosis fetalis s/s

A

ANEMIA hepato-splenomegaly; jaundice soon after birth; Generalized edema;

143
Q

common infection in Sickle cell

A

Osteomyelitis w/ salmonella or other encapsulated organisms

144
Q

CD59

A

inhibits C3 convertase and activation of the alternative complement pathway.

145
Q

HPA-1a; what is it?

A

if pt lacks this, after transfusion, develops post transfusion purpura;

146
Q

Fever; urticaria, pruritus, erythema after transfuion

A

allergic reaction

147
Q

↑RDW

A

Iron def. anemia Hereditary spherocytosis

148
Q

cell is expanding in size but nucleus is not dividing—hence macrocytic

A

Megaloblastic Anemia

149
Q

Transfusion complication: pt LACK platelet antigen HPA-1a

A

post transfusion purpura

150
Q

affect of pH on sickling

A

dec. pH reduces the oxygen affinity of hemoglobin, thereby increasing the fraction of deoxygenated HbS at any oxygen level increasing sickling

151
Q

Pernicious anemia lab

A

↓ Intrisic factor ↓ Vitamin B12 therefore ↑serum homocysteine; ↑ methylmalonic acid

152
Q

↑ risk of parvovirus–> aplastic crisis

A

Thalassemia Hereditary Spher. Sickle Cell

153
Q

IgG abs opsonize RBCs at body temperature

A

warm AIHA

154
Q

Pt with CHF or heart failure–> what transfusion complication?

A

Circulatory overload

155
Q

Splicing mutations –> create an “ectopic” cryptic splice site within the intron

A

β+-thalassemia

156
Q

Sickle Cell Anemia: amino acid change

A

Glutamic acid replaced by Valine

157
Q

Destruction of splice donor or splice acceptor sites.

A

β0-thalassemia

158
Q

hyper cellular bone marrow with ringed sideroblasts,

A

Myelodysplastic syndrome:

159
Q

Structurally abnormal hemoglobin; quantity fine

A

Sickle Cell Anemia

160
Q

Increased LDH and UCB, decreased Hct and haptoglobin; Hemoglobin normal!

A

Delayed hemolytic transfusion rxn

161
Q

Promotor mutations–> ↓ transcription (i.e. affects pre-mRNA)

A

β+-thalassemia

162
Q

conditions that decrease the MCHC (alpha thalassemia) reduce the disease severity

A

Sickle cell

163
Q

Hand-foot syndrome: Dactylitis of bones—happens in children

A

Sickle cell

164
Q

Hereditary Spherocytosis s/s

A

extravascular hemolysis therefore: ↑ UCB–> jaundice Bilirubin gallstone ANEMIA ↑LDH

165
Q

att birth w/ marked jaundice and require transfusions.

A

compound heterozygote Hereditary Spherocytosis

166
Q

Hereditary Spherocytosis treatment:

A

Splenectomy

167
Q

compound heterozygote Hereditary Spherocytosis

A

birth w/ marked jaundice and require transfusions.

168
Q

protected against P. falciparum malaria

A

Sickle Cell anemia Thalassemia G6PD

169
Q

Febrile non hemolytic transfusion reaction labs

A

normal; no inc. LDH, UCB, Retic, count, no decrease in haptoglobin or Hct

170
Q

monnuclear megakaryocytes with no platelets in periphery

A

Myelodysplastic syndrome:–> dysmegakaryopoiesis

171
Q

How does transfusion related acute lung injury appear on chest x-ray?

A

diffuse bilateral pulmonary infiltrates which are unresponsive to diuretics

172
Q

Oxidant drugs –> antimalarials, sulfonamids, and nitrofurantoins.

A

G6PD

173
Q

Target cells

A

Thalassemia Sickle cell

174
Q

decreased synthesis of the globin chains of Hb

A

Thalassemia

175
Q

Thalassemia retic count

A

↑ Reticulocyte count (extravascular hemo)

176
Q

Nonsense or frameshift mutations–> early stop codon

A

β0-thalassemia

177
Q

Homozygous for HbS but also has coexistent 1), which reduces Hb synthesis and has milder disease

A

1) α-thalassemia

178
Q

Drug induced: Drug stimulates IgG production against RBCs

A

Autoantibody Mechanism

179
Q

Hereditary Spherocytosis diagnosis:

A

Osmotic fragility test: red cells lyse in hypotonic sln

180
Q

microcytic, hypochromic RBCs, target cells, and basophilic stippling

A

β-thalassemia

181
Q

Complement mediated RBC lysis, platelet aggregation, and hypercoagulability

A

PNH

182
Q

Iron-Deficiency Anemia RBC indices

A

MCV, Hb, Hct and MCH are all ↓.

183
Q

Vascular obstruction, particularly stroke (CVA)

A

Sickle cell disease

184
Q

INACTIVATING somatic mutation of PIG-A

A

PNH

185
Q

increased reticulocyte count

A

Immune Hemolytic Anemia Hereditary Spherocytosis G6PD deficiency PNH

186
Q

Sickle cells s/s due to vasoocclusion

A

vascular necrosis of the femur renal infarcts Not comprehensive

187
Q

PNH diagnosis

A

Deficient: Decay-accelerating factor (CD55 Membrane inhibitor of lysis (CD59) C8 binding protein

188
Q

acquired clonal stem cell disorder; DYSMORPHIC blood cells and precursors

A

Myelodysplastic syndrome:

189
Q

Sickling of RBCs either cause:

A

(a) Hemolysis: extravascular (spleen) (b) Microvascular occlusion (due to sickle shape)

190
Q

Transfusion complication: Acute hemolytic transfusion rxn: what cytokines?

A

Pro inflammatory cytokines (IL‐1 ,IL‐6 ,IL‐8 ) TNF alpha NO (EDFR )

191
Q

Sickle Cell Trait vs. disease inheritance

A

Sickle Cell Trait –> heterozygous Sickle Cell Disease –> homozygous

192
Q

asymptomatic—only sickle on profound hypoxia

A

Sickle Cell Trait

193
Q

Autoimmune Hemolytic Anemia intra/extravascular

A

EXTRAvascular; both warm and cold

194
Q

Intravascular hemolysis s/s

A

Hbemia, Hburia, Hemosiderinuria, and ↓haptoglobin

195
Q

Delayed hemolytic transfusion rxn lab

A

lack of expected rise in Hb;

196
Q

ACD RBC indices

A

Normocytic normochromic

197
Q

Drug induced: Mild to moderate hemolysis, w/ slow onset developing over days to weeks

A

• Penicillin • Methyldopa

198
Q

Erythroblastosis fetalis complication

A

kernicterus due to Inc. UCB (fat soluble)

199
Q

β-thalassemia Hb electrophoresis

A

↑in HbA2 (α2δ2)

200
Q

Sickle cell: 1) in the sixth codon of β-globin that leads to the replacement of a glutamate with a valine residue.

A

1) point mutation

201
Q

β-Thalassemia: ___ is temporarily protective

A

HbF

Heme Path (21 decks)

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