Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

STEP > Hem/Onc > Flashcards

Hem/Onc Flashcards

1
Q

Source of energy for erythrocytes

A

Glucose (90% glycolysis, 10% HMP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

RBC transporter that allows RBCs to export bicarb and transport CO2 from periphery to lungs

A

Cl-/HCO3- antiporter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

ANisocytosis

A

Varying sizes of RBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Pikilocytosis

A

Varying shapes of RBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Life span of plts

A

8-10 d

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Dense granule of plts contents

A

ADP, Ca2, Serotonin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Alpha granule of plts contents

A

vWF, fibrinogen, fibronectin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Storage of plt pool

A

1/3 in spleen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Low platelets/plt fxn –>

A

Petiechiae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

vWF receptor

A

GpIb (attach)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Fibrinogen receptor

A

GIIb/IIIa (aggregate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Blue color in retics…

A

Residual rRNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Neutrophil specific granule contents

A

Leuk Alk PHos, collagenase, lysozyme, lactoferrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Azurophilic granule contents

A

In neuts – proteinases, acid phos, MPO, b-glucuronidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Hypersegmented neuts in

A

Vit B12/folate def

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

More band cells means

A

More myeloid proliferation (CML, bacterial infxn)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Neutrophil chemotactic agents

A

C5a, IL8, LTB4, kallikrein, PAF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Activates macs

A

Gamma interferon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Lipid A binds…

A

From bacteria LPS binds CD14 on macs –> septic shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Eosinophils produce

A

Histaminase, MBP (helminthotoxin), eosinphil peroxidase, eosinophil cationic protein, eosinophil derived neurotoxin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Causes of eosinophilia

A

Neoplasia, Asthma, Allergic process, Chronic adrenal insufficiency, Parasites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Basophil granules contain

A

Heparin (anticoag), histamine (vasodilator)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Basophils can synthesize

A

Leukotrienes – not preformed!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Basophilia can mean

A

Myeloproliferative disease, like CML

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Mast cell from same precursor as

A

Basophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Mast cell releases

A

Histamine, heparin, tryptase, and eosinophil chemotactic factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Drug that prevents mast cell degranulation and use

A

Cromolyn sodium – asthma prophylaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

B cell markers

A

CD19, CD20,CD21

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

T cell markers

A

Tc: CD3, CD8
Th: CD3, CD4
T reg: CD3, CD28

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Majority of circulating lymphs are…

A

T cells (80%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Plasma cell cancer

A

Multiple myeloma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Fetal erythropoesis

A 
Yolk sac (3-8wks)
Liver (6wk-birth)
Spleen (10-28 wks)
Bone marrow (18wk-adult)
Young Liver Synthesizes Blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Embryonic globins

A

L and E

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Fetal hemoglobin

A

a2gamma2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Adult hemoglobin

A

a2b2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Why does HbF have a higher affinity of O2?

A

Less avid binding of 23 BPG –> can extract oxygen from maternal hemoglobin across placenta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

HbA2

A

a2d2 – small amounts in adult

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

ABO abs are

A

IgM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Rh abs are

A

IgG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Presentation of ABO hemolytic disease in newborn (rare)

A

Mild jaundice in neonate w/in 24 hrs of birth – tx phototherapy or exchange transfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Order of furthest migration on a gel for hemoglobins

A

A (normal hemoglobin B chain – HbA)
F (normal hg gamma chain – HbF)
S (sickle cell hemoglobin B chain – HbS)
C (Hemoglobin C B chain – HbC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Intrinsic (contact activation) pathway

A

Collagen/basement membrane/activated platelets –> 12>11>9 and 8…

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Tissue factor (extrinsic) pathway

A

7>…

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Combined pathway

A

X & V>2>1> cross linking via 13

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Require calcium/phospholipid

A 
9 to 9a, 
9a+8a to X-->Xa, 
7-->7a-->+cofactor to catalyze X-->Xa
Xa+Va to catalyze II-->IIa
13 to crosslink
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Kinin cascade

A

HMWK > activates 12

via kallikrien–>bradykinin –> vasodilation, permeability and pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Inhibited by Warfarin

A

2,7,9,10 C,S

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Hemophilia A def

A

Factor 8 – XR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Hemophilia B

A

Factor 9 – XR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Hemophilia C

A

Factor 11 –AR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Vit K in coagulation

A

Reduced via epoxide reductase to become cofators in gamma glutamyl carboxylation to make mature/active coag cascade components

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

VIt K def

A

Low fact II, 7, 9, 10, pC, pS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

vWF carries/protects

A

Factor 8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Protein C cleave and inactivates

A

Va and 8a w/ help of pS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Antithrombin inhibits activated

A

2,7,9,10,11,12; principal targets are thrombin and Xa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Heparin acts by

A

Enhancing activity of antithrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Factor V leiden mutation

A

Factor V that cannot be inhibited by protein C –> hypercoagulability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Plasminogen–>

A

via tPA to plasmin –> fibrinolysis – cleavage of fibrin mesh, destruction of coag factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Platelet plug formation

A

Endothelial damage –> transient vasoconstriction (neural stim reflex and endothelin released) –> vWF binds exposed collagen (from Weibel Palade bodies of endothelial cells and a granules of plts –> plts bind vWF via GpIb and undergo conformational change –> release ADP (helps plts adhere, binds P2Y12 receptor to induce GpIIbIIIa expresion on plt), Ca, and TXA2 –> Fibrinogen binds GpIIb/IIIa receptors to link platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Proaggregation factors

A

TXA2 from plts, slower blood flow, increased platelet agg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Antiaggregation factors

A

PGI2 and NO from endothelial cells, faster blood flow, less platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

How does aspirin cause anticoag?

A

Irreversible inhib of COX in plts –> no TXA2 synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

These inhibit GpIIb/IIIa direction

A

Abiciximab, eptifibatide, tirofiban

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Action of ristocetin

A

Activates vWF to bind GpIb – failure of assay with vWD and Bernard Soulier syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Inhibit P2Y12 receptor

A

Clopidogrel, prasugrel, ticlodipine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Deficiency of GpIb on plt –>

A

Bernard-Soulier syndrome

67
Q

Def of vWF

A

vWD

68
Q

Inside endothelial cells

A

vWF and factor 8, thromboplastin, tPA, PGI2

69
Q

Acanthocytes seen in

A

Liver disease, abetalipoproteinemia (states of cholesterol dysregulation)

70
Q

Basophilic stippling seen in

A

Lead poisoning, sideroblastic anemias, myelodysplastic syndromes

71
Q

Basophilic stippling sample

A

Periperal smear

72
Q

Ringed sideroblast sample

A

Bone marrow

73
Q

Basophilic stippling is

A

Aggregation of residual ribosomes

74
Q

Dacrocyte aka

A

Teardrop cell

75
Q

Acanthocytes aka

A

Spur cell

76
Q

Dacrocyte seen in

A

Bone marrow infilitration (myelofibrosis) – due to mechanical squeezing out of its home

77
Q

Degmacyte aka

A

Bite cell

78
Q

Degmacyte seen in

A

G6PD def

79
Q

Echinocyte aka

A

Burr cell

80
Q

Echinocyte seen in

A

ESRD, liver disease, PK def

81
Q

Ddx from acanthocyte to echinocyte

A

Echinocyte has more uniform and smaller projections

82
Q

Elliptocyte seen in

A

Mereditary elliptocytosis, usually asymptomatic – caused by mutations in genes encoding RBC membrane proteins (spectrin)

83
Q

Macroovalocytes seen in

A

Megaloblastin anemia (w/ hypeseg PMNs)

84
Q

Ringed sideroblast seen in

A

Sideroblastic anemia, excess iron in mitochondria

85
Q

Schistocyte seen in

A

Microangiopathic hemolytic anemias (DIC,TTP/HUS, HELLP), mechanical hemolysis

86
Q

Schitocyte is a

A

Fragmented RBC, eg helmet cell

87
Q

Sickle cell seen in/caused by

A

Sickle cell anemia – occurs w/ dehydration, deoxygenation, and high altitudes

88
Q

Spherocytes seen in

A

Hereditary spherocytosis, drug/infxn induced hemolytic anemia

89
Q

Target cells seen in

A

HbC disease, Asplenia, Liver disease, Thalassemia (HALT)

90
Q

Heinz bodies seen in

A

G6PD def (precipitated hemoglobin due to SH grp reduction to S-S – phagocytes eat leading to bite cells

91
Q

Howell Jolly bodies seen in

A

Fxnal hyposplenia or asplenia

92
Q

HJ bodies are made up of

A

Basophilic nuclear remnants in RBCs –normally removed by splenic macrophages

93
Q

Causes microcytic anemia

A 
Sideroblastic anemia (cause be caused by Cu def)
ACD
Lead poisoning
Thalassemias
Iron def (late)
SALTI
94
Q

Causes megaloblatic macrocytic anemia

A

Folate def
B12 def
Orotic aciduria

95
Q

Causes nonmegaloblastic macrocytic anemia

A

Liver disease
Alcoholism
Diamond-BLackfan anemia

96
Q

Causes nonhemolytic normocytic anemia (normal or low retic)

A

Iron def (early)
ACD
Aplastic anemia
CKD

97
Q

Causes intrinsic hemolytic normocytic anemia

A

RBC membrane defect (hereditary spherocytosis), RBC enzyme def (G6PD, pyruvate kinase), HbC disease, Paroxysmal nocturnal hemoglobinuria, Sickle cell anemia

98
Q

Causes extrinsic hemolytic normocytic anemia

A

Autoimmune, microangiopathic, macroangiopathic, infxns

99
Q

Iron def causes

A

Chronic bleeding (GI loss, mnorrhagia), malnutrition, absorption disrders, GI surg, increased demand (e.g. preg), –> lowers the final step in heme synth

100
Q

Labs in iron def anemia

A

Low iron, high TIBC, low ferritin, high free erythrocyte protophyrin; microcytosis, hypochromasia (central pallor)

101
Q

Sx of IDA

A

Fatigue, conjunctival pallor, pica, spoon nails (koilonychia); glossitis, cheliosis

102
Q

Plummer Vinson

A

IDA, esophageal webs, dysphagia

103
Q

Alpha thalassemia caused by

A

Alpha globin deletions –> less alpha synthesis

104
Q

Alpha thalassemia genetics

A

Cis – Asian pops
Trans – African pops
4 allele deletion –> no alpha globin, excess gamma globin –> Hb Barts (gamma4) –> hydrops fetalis
3 allele delition –> HbH disease – very little alpha globin –> excess b globin makes HbH
2 allele deletion –> less clinically severe anemia
1 allele deletion –> no anemia (clinically silent)

105
Q

HbH disease sx

A

Hemolytic anemia, jaundice (hyperBR), high LDH, low hapto

106
Q

B thalassemia genetics

A

Point mutations in splice sites and promoter sequences –> less B globin synthesis (esp in Mediterranean pops)

107
Q

B thalassemia minor

A

Heterozygote – less B change produced, usually asymptomatic – diagnosis by high HbA2 (>3.5%) on EP

108
Q

B thalassemia major

A

Homozygote – no B chain –> severe mycrocytic hypochromic anemia w/ target cells and increased anisopoikilocytosis req blood transfusion (2o hemochromatosis) –>
a. marrow expansion (crew cut on xray) –> skeletal deformities, chipmunk facies,
b. extramedullary hematopoesis -_> hepatosplenomegaly, higher risk of parvo aplastic crisis
High HbF (alpha2g2) – protective in infant so only symptomatic after 6 mths when fetal hb declines

109
Q

HbS/B thalassemia heterozygote

A

Mild-mod sickle cell depending on amt of B globin prodxn

110
Q

Lead poisoning inhibs

A

Ferrochetalase and ALA DHase –> less heme synth and increased RBC protophyrin;
also inhib rRNA degradation –> retaining aggregates of rRNA –> basophilic stippling

111
Q

Sx of lead poisoning (and Tx)

A

Lead lines on gingivae (Burton lines) and metaphyses of long bones on Xray
Encephalopathy and Erythrocyte basophilic stippling
Abdominal colic and sideroblastic Anermia
Drops – wrist/food; Dimercaprol and EDTA are 1st line tx

112
Q

In kids tx

A

Succimer

113
Q

Siderblastic anemia causes

A

Genetics (x linked defect in ALA synthase), acquired (myelodyslastic syndromes), reversible (EtOH, lead, B6 def, Cu def, isoniazid)

114
Q

Labs in sideroblastic anemia

A

Increased iron, normal or low TIBC, high ferritin; ringed sideroblasts w/ iron laden Prussian blue stained mitochondria in bone marrow; peripheral smear –> basophilic stippling of RbCs

115
Q

Tx of sideroblastic anemia

A

Pyridoxine (B6 – cofactor for ALA synthase)

116
Q

Megaloblastic anemia

A

Impaired DNA synth –> maturation of nucleus of precursor cells in bone marrow delayed relative to maturation of cytoplasm
See RBC macrocytosis, hyperseg neuts, glossitis

117
Q

Folate deficiency causes

A

Malnutrition (alcoholics), malabsorption, drugs (methotrexate, TMP, phenytoin), increased req (e.g. hemolytic anemia, preggers)

118
Q

Labs in folate def

A

High homocystein, normal MMA; NO NEURO SYMPTOMS

119
Q

Vitamin B12 def causes

A

Insufficient intake (veganism), malabsoprtion (Crohns), pernicious anemia, Diphyllobothrium latum (fish tapeworm), gastrectomy

120
Q

Vit B12 def labs

A

High homocysteine, high MMA

121
Q

Vit B12 sx

A

NEURO! REversible dementia, SCD due to involvement in fatty acid pathways and myelin synth –> spinocerebellar tract, LCST, dorsal column

122
Q

Schilling test

A

Dietary vs malabsorption

123
Q

Liver can store folate or B12 longer

A

B12 – takes several years

124
Q

Orotic aciduria mechanism

A

Inability to convert orotic acid to UMP (de novo pyrimidine synth pathway) due to defect in UMP synthase

125
Q

Orotic aciduria genetics

A

AR

126
Q

Orotic aciduria presentation

A

In children – failure to trive, developmental delay, megaloblastic anemia refractory to folate and B12
NO HYPERAMMONEMIA! (vs OTC def!)

127
Q

Orotic aciduria lab

A

Orotic acid in urine

128
Q

Tx of orotic aciduria

A

Uridine triacetate to bypass mutated enzyme

129
Q

Nonmegaloblastic anemia

A

Macrocytic anemia where DNA synth is unimpaired –> RBC macrocytosis w/o hyperseg neuts

130
Q

Nonmegaloblastic anemia causes

A

EtOH, liver disease

131
Q

Diamond Blackfan anemia mechanism

A

Rapid onset anemia w/in first year of life due to intrinsic defect in erythroid progenitor cells (build up–> disrupt bone formation)

132
Q

Diamond blackfan labs

A

High %HbF, but low total Hb

133
Q

Diamond blackfan presentation

A

Short stature, craniofacial abnormalities, upper extremity malformations (triphalangeal thumbs)

134
Q

Intravascular hemolysis findings

A

Low hapto, high schistocytes, hemoglobinuria, hemosiderinuria, urobilinogen in urine, high unconj bili

135
Q

Causes of intravascular hemolysis

A

Mechanical, paroxysmal nocturanl hemoglobinuria, microangiopathic hemolytic anemia

136
Q

Extravascular hemolysis findings

A

Macs in spleen clear RBCs – spherocytes in peripheral smear; no hemoglobinuria or hemosiderinura but may have urobilinogen in urine

137
Q

Most common causes of extravascular hemolysis

A

Hereditary spherocytosis and autoimmune hemolytic anemia

138
Q

Anemia of chronic disease mechanism

A

Inflamm –> high hepcidin (binds ferroportin on intestine cells and macs to inhib iron transport –> less release of iron from macs and less iron absorption in gut

139
Q

ACD assc

A

SLE, RA, neoplastic disorders, CKD

140
Q

ACD findings

A

Low iron, low TIBC, high ferritin

141
Q

Tx of ACD

A

Address underling cause, can consider transfusion or stimulation

142
Q

Aplastic anemia causes

A

Failure/destruction of myeloid stem cells due to
Radiation and drugs (benzene, chloramphenicol, alkylating agents, antimetabolites)
Viral agents (parvovirus B19, EBC, HIV, hepatitis)
Fanconi anemia (DNA repair defects –> bone marrow failure, macrocytosis may be seen on CBC, also short statures, high incidence of tumors/leukemia, cafe au lait spots, thumb/radial defects
Idiopathic

143
Q

Findings in aplastic anemia

A

Low retic, high EPO; pancytopenia w/ severe anemia, leukopenia, thrombocytopenia; normal cell morph but hypocellular bone marrow w/ fatty infiltration
DRY BONE MARROW TAP!

144
Q

Sx of aplastic anemia

A

Fatigue, malaise, pallor, purpura, mucosal bleeding, petechiae, infxn

145
Q

Tx of aplastic anemia

A

W.drawal of offending agent, immunosuppressive regiments (antithymocyte globulin, cyclosporine), bone marrow allograft, RBC/plt transfusion, bone marrow stim (GM-CSF)

146
Q

Hereditary spherocytosis

A

A type of intrinsic hemolytic anemia – extravascular hemolysis due to defect in proteins interacting w/ RBC membrane skeleton and plasma membrane (anykyrin band 3, protein 4.2, spectrin) –> small, round RBCs w/ less surface area and no central pallor (high MCHC)–>premature removal by spleen

147
Q

Hereditary spherocytosis genetics

A

AD

148
Q

Sx and labs in hereditary spherocytosis

A

Sx: splenomegaly, aplastic crisis (parvoB19 infxn)
Labs: Osmotic fragility test pos (put in saline), NL/low MCV w/ abundance of cells

149
Q

Tx of hereditary spherocytosis

A

Splenectomy

150
Q

Most common enzymatic disorder of RBCs

A

G6PD def

151
Q

Genetics of G6PD def

A

XLr

152
Q

G6PD def mechanism

A

Extravascular and intravascular hemolysis due to defect in G6PD –> low glutathione -> high RBC susceptibility to oxidant stress -> hemolytic anemia under that stress (sulfa drugs, antimalarials, infxns, fava beans)

153
Q

Sx of G6PD def

A

Back pain, hemoglobinuria a few days after oxidant stress

154
Q

Labs in G6PD def

A

Heinz bodies and bite cells on blood smear

155
Q

Pyruvate kinase

A

PEP–> Pyruvate and ATP

156
Q

Pyruvate kinase def genetics

A

Ar

157
Q

Pyruvate kinase def mechanism

A

Less PKase–> less ATP –> rigid RBCs–>extravascular hemolysis
Increases levels of 23 BPG–>lower Hb affinity for O2

158
Q

Presentation of pyruvate kinase def

A

Hemolytic anemia in a newborn

159
Q

Paroxysmal nocturnal hemoglobinuria pathophys and associations

A

Compliment mediated intravascularRBC lysis due to impaired synth of GPI anchor for DAF (protects RBC membrane from compliment)
Is an acquired mutation in hematopoetic stem cell
–> increased incidence of acute leukemias, assc w/ aplastic anemia

160
Q

PNH fx

A

Red or pink urine (hemoglobinuria), Coombs neg hemolytic anemia, pancytopenia, venous thrombosis

161
Q

PNH labs

A

CD55/59 neg RBCs on flow cyto

162
Q

PNH tx

A

Eculizumab (terminal compliment inhibitor)

163
Q

Sickle cell anemia mutation

A

HbS point mutation –> single amino acid replacement in beta chain (glutamic acid –> valine)

164
Q

Type of hemolysis in sickle cell

A

Intra and extravascular

STEP (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions