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IPAP 21-2 Soph Semester > Anemia/ Heam > Flashcards

Anemia/ Heam Flashcards

1
Q

H&H low
MCV & MCHC Low
Iron Low

A

iron Deficiency

Anemia of Chronic Disease

Renal Disease

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2
Q

H&H low
MCV & MCHC low
IRON normal

A

Hemoglobin electrophoresis for thalassemias

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3
Q

H&H low
MCV & MHCH Low
IRON High

A

Bone Marrow Examination for sideroblastic anemia

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4
Q

H&H low

MCV & MCHC Normal

A

Hz of acute blood loss

Autoimmune hemolytic anemia

Anemia of Chronic Disease

Dyserthropoesis

Anemia of Infection

Aplastic Anemia

Congenital dyserthropoiesis anemia

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5
Q

H&H low
MCV High
Low B12

A

Pernicious anemia
Severe malnutrition
GI problem

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6
Q

H&H low
MCV High
Low folate

A

Folate Malnutrtion

GI Problem

Liver Disease

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7
Q

H&H low
MCV high
B12 and folate normal/high

A

Myleoproliferative dz

Liver Dz

Congenital dyserthropoesis anemia

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8
Q

Microcytosis + target cells

A

Thalassemia Minor

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9
Q

Severe microcytotic anemia, target cells, schistocytes, nucleated RBCs

A

Thalassemia Major

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10
Q

Is thalassemia minor symptomatic or asymptomatic?

A

Asymptomatic

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11
Q

How does thalassemia major present

A

Severe anemia w/ Severe microcytic anemia, targets, schistocytes, nucleated RBCs

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12
Q

How does Hemoglobin H disease present

A

Moderately severe anemia, with severe microcytic, hypo chronic anemia

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13
Q

How does hydrops fetalis present

A

Severe anemia, with severe microcytic hypo chronic anemia

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14
Q 
Microcytic Hypochromic 
Serum Iron high 
Ferretin High 
Iron Saturation high 
TIBC Low 
Transferring Low
A

Thalassemia

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15
Q 
Microcytic Hypochromic 
Iron Low 
Ferritin Low 
Iron Saturation Low 
TIBC high 
Transferrin High
A

Iron Def. Anemia

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16
Q 
Macrocytic Normochroomic 
Serum Iron High
Ferritin High 
Iron Sat High 
TIBC low 
Transferring low
A

B12 deficiency anemia

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17
Q

Hienz bodies correlate with…

A

G6PD deficiency

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18
Q

Beta 4 bands in hemoglobin electrophoresis are assoc. with

A

Hemoglobin H disease

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19
Q

Gamma 4 bands in hemoglobin electrophoresis is mostly assoc. w/

A

Hydrops Fetalis

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20
Q

complicated infectious mono affects what cells most

A

Lymphocytes

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21
Q

Where is vWF made

A

Endothelium of vessels

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22
Q

What is the aggregate plug made of

A

Platelets

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23
Q

What is the 1st stage of platelet plug formation

A 
Platelet adhesion to exposed collagen(GP Ia/IIa) 
and vWF(GPIb-V-IX)
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24
Q

What is the 2nd stage of platelet activation and degranulation

A 
Pseudopod formation w/ 
Alpha granules (vWF, fibrinogen)
And
Dense granules (Ca++, Serotonin, ADP)
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25
Q

What is the 3rd stage of platelet plug formation

A

Platelet aggregation

IIb/IIIa to fibrinogen

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26
Q

What effect does Asprin have on platelet function

A

Aspirin inhibits the cyclo-oxygenase enzyme in platelets leading to the reduced formation of prostaglandin

Prevents aggregation

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27
Q

Abnormalities in primary hemostasis result in…

A

hemorrhage from mucosal surfaces (epistaxis, hematuria), petechial or ecchymotic hemorrhages, and prolonged bleeding after venipuncture or wounds.

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28
Q

PFA 100 contains what chemicals

A

Collagen/Epinephrine

Collagen/ADP

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29
Q

If the 1st PFA 100 (Col/Epi) is abnormal then the second test (Col/ADP) corrects, what is the likely problem

A

aspirin-induced platelet dysfunction is most likely.

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30
Q

If both tests of the PFA 100 are abnormal what is the likely Dz

A

Once anemia and thrombocytopenia have been excluded,

further evaluation to exclude von Willebrand disease and inherited/acquired platelet dysfunction such as renal failure storage pool disease, release defect, Bernard-Soulier disease, and Glanzmann thromboasthenia should be considered.

Long-term aspirin therapy may modestly prolong the Col/ADP.

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31
Q

What does the Bleeding time test focus on

A

BT tests focus on the number of platelets present and their ability to form a plug

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32
Q

What is primary hemostasis

A

Interaction between platelets and walls of injured blood vessels forming a platelet plug that assists in clot formation

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33
Q

What is secondary hemostasis

A

Is the formation of FIBRIN through the intrinsic, extrinsic, and common pathways of the coagulation cascade.

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34
Q

Secondary hemostasis defects result in what kind of bleeding

A

more serious bleeding than with primary hemostasis, including bleeding into cavities (chest, joints) and subcutaneous hematomas.

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35
Q

What is the final product of the coagulation cascade

A

Final product is a fibrin mesh or clot which completely stops bleeding

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36
Q

What factors are in the extrinsic pathway

A

III and VII

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37
Q

What factors are in the intrinsic pathway

A

XII, XI, IX, VIII

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38
Q

What factor unites both the intrinsic and extrinsic pathways and is the common pathway

A

Factor X

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39
Q

What factors are in the common pathway

A

X, V, II, I

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40
Q

What is Christmas Factor

A

Factor IX

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41
Q

A deficiency in Factor IX is called what

A

Deficiency = Hemophilia B (Christmas disease)

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42
Q

What is factor VIII is a complex with what other factor

A

vWF

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43
Q

What is a factor VIII deficient known as

A

Deficiency Factor VIII = Hemophilia A

(classic hemophilia), most common hereditary coagulation disorder

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44
Q

Why is vWF important

A

vWF is important in platelet adhesion

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45
Q

What is Factor X known as

A

Stuart Prower Factor

Common pathway

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46
Q

What is factor XI known as

A

Plasma Thromboplastin Antecedent

Antihemophiliac C factor

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47
Q

What is factor XII known as

A

Hageman Factor

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48
Q

What is the first factor activated in the intrinsic pathway

A

Factor 12

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49
Q

What activates factor XII

A

Proenzyme activated by contact with foreign (negatively charged) surfaces:

Collagen (damaged endothelial lining)
Glass

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50
Q

What is the only factor deficiency that causes no coagulation problems in vivo

A

Factor XII

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51
Q

What is factor XIII also known as

A

Fibrin Stablizing Factor

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52
Q

What activates factor XIII

A

Thrombin in the common pathway

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53
Q

What

A

Stabilizes the fibrin clot by crosslinking fibrin monomers

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54
Q

What are the vitamin K dependent factors

A

II, VII, IX, X

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55
Q

What are the three stages of secondary hemostasis

A

Intrinsic/ Extrinsic pathway to Factor X

Prothrmobinas (X-V complex) converts prothrombin (II) into thrombin

Thrombin coverings fibrinogen into fibrin

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56
Q

What are D-Dimers

A

Crossed linked Fibrin Degradation Products

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57
Q

Fibrin fragments still cross-linked by Factor XIIIa are referred to as

A

D-Dimers

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58
Q

How are FDPs normally cleared

A

By the liver and reticuloendothelial system

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59
Q

What is AT III

A

Antithrombin III is synthesized by the liver and binds Thrombin and Factor Xa partially neutralizing their activity (Protease)

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60
Q

What is the relationship of AT III and heparin

A

Heparin released by vascular subendothelial cells enhances ATIII activity

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61
Q

Where is heparin naturally produced

A

Basophils and mast cells

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62
Q

Does heparin directly dissolve clots ?

A

Heparin does not directly dissolve clots but it does stop clot propagation and allows natural fibrinolysis to occur

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63
Q

What is protein C

A

A vitamin K dependent enzyme produced by the liver

Circulates in plasma in an inactive form

In its active form it inactivates factors Va and VIIIa (inhibits both the Common and Extrinsic Coagulation Pathways)

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64
Q

What does Protein C inhibit

A

In its active form it inactivates factors Va and VIIIa (inhibits both the Common and Extrinsic Coagulation Pathways)

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65
Q

Protein C requires what cofactors

A

Protein S

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66
Q

A decrease in Protein C or S increases the risk of

A

ntravascular coagulation

67
Q

What does prothrombin time (PT) asses

A

Assesses the Extrinsic (and common) Coagulation Pathways

Screens for deficiencies of Factors I, II, V, VII, and X

68
Q

What tube top is PT pulled in

A

Light blue, citrates plasma

69
Q

What is added to the patients plasma in a PT test

A

Calcium + tissue thromboplastin (tissue factor) are added to the patient’s plasma and the time necessary for clot formation is measured

70
Q

What test is used to monitor Coumadin/ Warfarin therapy

A

PT

71
Q

What conditions is Coumadin/warfarin used for

A

Atrial fibrillation/flutter
Deep vein thrombosis
Heart valve replacement

Medication given orally to patients with certain medical conditions to prevent development of very small “micro” blood clots

72
Q

What does the INR measure

A

Coumadin therapy

The INR value is a “normalized” PT time test result that provides a workable reference range that all laboratories can report (and clinicians can use!) to monitor patients on Coumadin therapy

73
Q

Increases in the INR correspond to

A

Increases in the INR corresponds to increased anticoagulation

74
Q

What is a mixing study

A

Performed on blood plasma to distinguish factor deficiencies from factor inhibitors, such as lupus anticoagulant

75
Q

What does a correction or failure of a mixing study indicate

A

a correction with mixing indicates factor deficiency; failure to correct indicates an inhibitor.

76
Q

What should be ordered when the aPTT is prolonged and not corrected with mixing studies

A

Lupu anticoagulant study

77
Q

What is the presence of lupus anticoagulant associated with

A

Is associated with an INCREASED formation of thrombi in vivo (misnomer)

78
Q

What is a aPTT (activated partial thrmboplastin time)

A

Used to:
Monitor heparin anticoagulant therapy

Screen for coagulation disorders

Evaluate liver function (synthesis of liver produced coagulation factors)

79
Q

What part of the coagulation cascade does aPTT monitor

A

The intrinsic and common pathways

80
Q

What is added to the patients blood in a aPTT test

A

Calcium + phospholipid + a contact activator (e.g. kaolin) are added to the patient’s plasma and the time necessary for clot formation is measured

81
Q

What does a Thrmobin Time test measure

A

Measures the rate of formation of fibrin and assesses the fibrinogen to fibrin conversion

82
Q

What is added to a PTs blood for a thrombin time test

A

Calcium + thrombin are added to the patient’s plasma and the time necessary for clot formation is measured

83
Q

What does a Thrombin Time test detect

A

Detect deficiency of fibrinogen as well as the presence of circulating inhibitors of fibrinogen function:

Fibrin Degradation Products interfere with fibrin monomer polymerization

Circulating natural anticoagulants (e.g. heparin)

84
Q

What does a factor VIII assay detect

A

von Willebrand’s disease

Hemophilia A
Classic hemophilia

85
Q

What does a D dimer assay indicate

A

Indicates active intravascular clot formation is occurring

Indicates active fibrinolysis is also occurring

Used mainly to assess a patient for the presence of:

Deep vein thrombosis (DVT)

Pulmonary embolism (PE)

Disseminated intravascular coagulation (DIC)

86
Q

Can a D-Dimer rule in a specific clot?

A

NO

High Negative Predictive Power, i.e. can rule out, but not rule in

87
Q

What causes deficient platelet production

A

Bone marrow infiltrative processes:
Leukemia, lymphoma

Aplasia:
Aplastic anemia
Drug effect(Chemotherapy)

Leads to a quantitative thrombocytopenia

88
Q

how can hypersplenism affect platelet distribution

A

When spleen enlarges, more platelets can be sequestered in the spleen

Leads to a quantitative thrombocytopenia

89
Q

What is a primary immune quantitative thrombocytopenia

A

Idiopathic Thrombocytopenic purpura

Or

Post transfusion purpura

90
Q

What is a secondary immune quantitative thrombocytopenia

A

Systemic lupus erythematosus

Or

Viral infection(mononucleosis, HIV)

91
Q

What are nonimmune quantitative thrombocytopenia

A

Hemolytic uremic syndrome

Disseminated intravascular coagulation (DIC)

92
Q

What is Bernard Soulier Syndrome

A

Congenital Qualitatitve DO of adhesion

giant platelets;
decreased or absent expression of GPIb and or GPIX

93
Q

What is the platelet type vWF Dz

A

defective platelet adhesion;

reduced factor VIII levels
MOST COMMON

94
Q

WHat is Glanzmann Thrombasthenia

A

autosomal recessive disorder; decreased or absent for either GPIIb or GPIIIa

Disorder of Aggregation

95
Q

What condition presents with platelets that look empty or gray

A

Alpha granule disorder;
lack of alpha granules

AKA Storage pool disorder

96
Q

What is a Dense granule disorders or delta granule deficiency

A

Congenital Storage pool DO

97
Q

What is a defective TXA2 pathway classified as

A

Congenital Qualitative DO of secretion

98
Q

What are the acquired platelet defects

A

Chronic Renal Failure

Myeloproliferative DO

Acute Luekemia

Drugs

  • Asprin
  • alcohol
  • abx
99
Q

How does Chronic renal failure present on PFA and BT

A

Prolonged

Decrease aggregation with collagen

100
Q

Describe hemophilia A

A

(Classic Hemophilia):

X-linked recessive disorder in which there is a deficiency of Factor VIII

101
Q

Describe Hemophilia B

A

(Christmas Disease):

X-linked recessive disorder in which there is a deficiency of Factor IX

102
Q

If you suspect your patient has hemophilia (patient history + prolonged aPTT), order a…

A

Factor VIII assay

103
Q

What is the first factor affected in a Vitamin K def.

A

Factor VII is the first coagulation factor to become deficient (the only vitamin K dependent factor in the Extrinsic pathway and the deficiency causes a prolonged PT only)

104
Q

What are the earliest indications of impaired hemostasis

A

The earliest indicators of impaired hemostasis are prolonged PT and aPTT tests (the vitamin K dependent factors are affected first)

105
Q

What disease is Characterized by hyper-stimulation of all coagulation and fibrinolytic activity simultaneously
And The condition is diffuse (affects the entire body)

A

DIC

106
Q

What is the progression of DIC

A

Diffuse small thrombi are formed followed by blood ooze from many sites (i.e., surgical sites, IV sites, venipuncture sites)

Patients then develop petechiae indicating the presence of microthrombi

The patient then develops organ failure

107
Q

What is often used to monitor Therapy in DIC

A

D-dimer assay

108
Q 
How does DIC present with 
PT
APTT 
BT
Platelet count
A

PT- prolonged
aPTT- Prolonger
BT-Prolonged
Platelets- decreased

109
Q 
How does Vit. K present in 
PT 
APTT
BT/PHA100 
Platelets
A

PT- Prolonged
aPTT- normal to mild prolonged
PFA100- unaffected
Platelets- unaffected

110
Q 
How does vWF DZ present with 
PT 
APTT
PFA 100
Platelets
A

PT-unaffected
aPTT- pROlonged
PFA100- prolonged
Platelets -unaffected

111
Q 
How does hemophilia present on 
PT 
APTT 
PFA100 
Platelets
A

Pt-unaffected
APTT- prolonged
PFA100-unaffected
Platelets unaffected

112
Q 
How does thrombocytopenia present on 
PT 
APTT
PFA100 
Platelets
A

PT-unaffected
APTT- unaffected
PFA100- prolonged
Platelets- decreased

113
Q 
How does early liver failure present on 
PT 
APTT 
PFA100 
platelets
A

PT- prolonged
APTT- unaffected
PFA100- unaffected
Platelets- unaffected

114
Q 
How does late liver failure present on 
PT 
APTT
PFA100
Platelet count
A

All are prolonged with platelet count decreased

115
Q

IF only the PT is abnormal then what could be the cause

A

Factor VII or III (DEAD) def.

Warfarin ingestion

Mild Vit K def.

Or lupus anticoagulant

116
Q

What is the difference between Glazmanns and Bernads

A

Platelet count is normal in Glanzmanns

Both have normal PT and APTT
Both have prolonged PFA100

117
Q

Restore or maintain oxygen-carrying capacity or hemoglobin. Best achieved by..

A

utilizing packed red blood cells (pRBCs)

118
Q

How are ABO blood group antigens formed

A

ABO blood group antigens are formed when transferases add specific sugars to the H substance on the membrane.

119
Q

What are the 9 ABO blood groups of clinical significance

A 
ABO, 
Rhesus, 
Kell, 
Kidd, 
Duffy,
 MNS, 
P, 
Lewis,
 and Lutheran
120
Q

What is the Antihuman globulin test

A

Anti-human Globulin (AHG or Coombs reagent) is used to detect the presence of antibodies coating the surface of RBCs.

Red cell coating may occur in vivo or in vitro

121
Q

What is the DAT

A

The DAT is an important diagnostic serologic technique used for the detection of antibody binding to RBC membranes in vivo.

122
Q

What are the clinical indications for a DAT

A

Clinical indications include

Testing cord cells for Hemolytic Disease of Fetal Newborn(HDFN)

Hemolytic Transfusion Reactions (HTR)

Autoimmune Hemolytic Anemia (AIHA) studies

123
Q

What is a IAT

A

The IAT is an important diagnostic serologic technique used for the detection of antibody binding to RBC membranes in vitro.

124
Q

What are the uses of a IAT

A

Laboratory indications include
Antibody detection
(crossmatch and antibody screening)

Antibody identification
Antibody titration
RBC phenotyping

125
Q

How long is a pre transfusion sample good for

A

72 hours

126
Q

What is the most important step in administration of blood products

A

Correctly identifying the donor unit and recipient is the most important step in the safe administration of blood products.

127
Q

What is the specimen of choice for pre transfusion testing

A

Specimen of choice: EDTA-anticoagulated blood specimen (lavender/pink top tube).

128
Q

How is an antibody screen preformed

A

Antibody Screen: the patient’s serum is screened for unexpected antibodies using IAT.

129
Q

Explain the cross-match procedure

A

Crossmatch Procedure: before blood can be administered, the recipient’s SERUM must be tested against donor RBCs.

130
Q

What temp must all pre transfusion samples be stored at

A

1-6 degrees C
For at least 7 days

along with at least one representative segment from each of the donor units crossmatched on the recipient.

131
Q

Describe a major cross match

A

The antiglobulin (AHG) crossmatch:

Major crossmatch
Performed when antibody is present
(Positive antibody screen).

3 steps:
-It starts with an immediate spin crossmatch followed by an incubation of the patient’s serum at 37º C and an indirect antiglobulin test.

-Crossmatch is incompatible if agglutination is observed during any of the three steps of testing.

132
Q

When should a type and screen be performed

A

For surgical cases where blood usage is infrequent, yet possible, the patient should be should be tested using a Type and Screen procedure.

ABO, Rh testing, and a screen for unexpected antibodies are performed on the patient’s blood.

133
Q

When is a type and cross performed

A

For surgical cases where blood usage is probable or whenever transfusion of blood is required, a Type and Cross is ordered.

ABO, Rh testing, and a screen for unexpected antibodies are performed on the patient’s blood.

The number of packed Red Blood Cell (pRBCs) units requested are then crossmatched with the patient’s serum

134
Q

Can Rh positive receive Rh negative blood ?

A

Yes

135
Q

Should Rh negative patients received Rh positive blood

A

No, should be avoided

136
Q

Plasma from blood type AB can be given to who

A

Plasma from blood type AB individuals may be given to patients of any type.

137
Q

What can lead to rare RhD alloimmunization in the recipient

A

Although platelets do not express Rh antigens, they contain small numbers of intact red blood cells or fragments, which can lead to rare RhD alloimmunization in the recipient.

138
Q

Which coag factors are Labile

A

Factors V and VIII are labile and are significantly decreased after 7 days (or sooner).

139
Q

Washed RBCs must be given within

A

24 hrs

140
Q

What can reduce Graft vs Host Dz

A

Lueke reduced RBCs

And Gamma Irradiated Blood components

141
Q

What is the shelf life of Gamma irradiated products

A

28 days

142
Q

When should CMV negative RBCs be used

A

Indications - CMV negative blood products are indicated for patients in the following categories, regardless of CMV status of the mother:

Premature infants.

Infants under four weeks of age.

Patients requiring intrauterine transfusion.

CMV negative blood products are indicated for CMV negative patients in the following categories:

Bone marrow or organ transplant recipients
(if the marrow or the organ donor is also CMV negative).

Potential candidates for transplant.

AIDS or HIV infected patients.

Patients who have congenital immune deficiency.

Patients undergoing splenectomy.

Pregnant women.

143
Q

When should FFP be transfused

A

Indications - FFP is indicated for patients with documented coagulation factor deficiencies who are actively bleeding or who are about to undergo an invasive procedure.

FFP is also indicated in treatment of Thrombotic Thrombocytopenic Purpura (TTP), usually in conjunction with plasma exchange.

The FFP specifically replaces a missing enzyme found in these patients.

Both FFP and FP24 are thawed at 37°C and must be transfused within 24 hours.

144
Q

What is the indication of cryoprecipitaite

A

Indication – Cryo is used mainly as a source of fibrinogen. CRYO is indicated for bleeding or imminent invasive procedures for patients with significant hypofibrinogenemia (<100 mg/dL).

To limit exposure to transfusion related pathogens commercial clotting factor concentrates made with viral inactivation methods are preferred over CRYO for Hemophilia A and von Willebrand treatment.

145
Q

What factors are present in CRYO

A

VIII, XIII, vWF

146
Q

What is the indication for platelets

A

Indications - Platelet transfusions are indicated for patients with bleeding due to either thrombocytopenia, platelet dysfunction or some combination of the two conditions.

147
Q

What are the admin time frames for Rhogam

A

Used for the prevention of Rh HDN:
Antepartum dose given at 28 weeks.

Postpartum dose given within 72 hours of delivery.

Postpartum sample from mother is obtained/screened for feto-maternal hemorrhage.

148
Q

In HDN what is the DAT of cord blood

A

Cord blood will have a positive DAT

149
Q

What is the Kleihauer-Betke test

A

Fetal Hemoglobin (Hb F) is evaluated in the mother’s blood to estimate volume of fetal hemorrhage into maternal circulation.

150
Q

When should septic testing be ordered

A

Should be done if suggested by clinical data, for example:

a) Temperature greater than 102 F
b) Temperature increase greater than a specified amount (2 or 3 degrees F)

151
Q

What is the most common cause of Acute Hemopytic Transfusion Reactions

A

Clerical errors (both in transfusion service and at bedside) are most common cause

152
Q

What are schistocytes

A

Intravascular hemolysis

153
Q

What are spherocytes

A

Extra vascular hemolysis

154
Q

Febrile non hem transfusion reaction is most common with

A

Platelet transfusions

155
Q

How doe Transfusion related sepsis present

A

Signs/symptoms: Rapid onset high fever (often greater than 4oF/2C), Rigors (true shaking chills with rigidity), Abdominal cramping, nausea/vomiting, Hypotension/shock, DIC

Lab findings:

1) Discolored RBC product (+/-); contaminated RBCs may turn dark or purple
2) May have hemoglobinemia/uria (non-immune)
3) DAT negative
4) Gram stain positive in only half to 2/3 of proven cases!
- Remember to also culture associated IV fluids and consider that an indwelling IV catheter may be a source of contamination
5) Culture is proof positive (when same organism is cultured from both unit and recipient)

156
Q

How does graft v host present

A

Patients present with:
a) Fever 7-10 days post-transfusion

b) Face/trunk rash that spreads to extremities
c) Mucositis, nausea/vomiting, watery diarrhea

d) Pancytopenia and subsequent marrow aplasia
- This is what leads to the fatal consequences, with most patients dying from overwhelming infections

157
Q

What is the common culprit in Post transfusion purpura

A

Anti-HPA-1A

158
Q

What is a major risk in chronically infused pts

A

Iron overload

159
Q

What is the culprit in the pathology of TRALI

A

Neutrophils

160
Q

What kind of blood collection can be used to treat Thrombotic Thrombocytopenic Purpura

A

Hemapheresis

161
Q

What is hereditary elliptocytosis

A

Mutations in red cell membrane proteins spectrin, protein 4.1, or glycophorin C

Lab findings:

Very mild anemia that is compensated
Slight reticulocytosis
MCV: normal, slighty elevated
MCHC: normal
Decreased haptoglobin
Increase osmotic fragility
162
Q

What is hereditary stomatocytosis

A

Marked increase in the passive permeability of sodium into the cell and potassium out of the cell. Defect greater for sodium permeability resulting in water influx and formation of hydroctyes

LAb findings:

Mild anemia
MCV: Elevated
MCHC: Decreased
Decreased haptoglobin
Increased osmotic fragility
163
Q

What characterizes sickle cell

A

Characterized by production of HbS

Beta chain abnormality; Single amino acid substitution of valine for glutamic acid in the sixth position from the NH2-terminal end of the β chain

IPAP 21-2 Soph Semester (20 decks)

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