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OS2 > RBC Disorders > Flashcards

RBC Disorders Flashcards

1
Q

Results of renal papillary necrosis

A

Results in gross hematuria and proteinuria

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2
Q

Main cause of death in paroxysmal nocturnal hemoglobinuria

A

Thrombosis of the hepatic, portal or cerebral veins

*Destroyed platelts release cytoplasmic contents into circulation, inducing thrombosis

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3
Q

_____ inhibits dihydrofolate reductase.

A

Methotrexate

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4
Q

Why do cells sickle in sickle cell anemia?

A

HbS polymerizes when deoxygenated; polymers aggregate into needle-like structures, resulting in sickle cells

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5
Q

Blood smear in Hemoglobin C

A

HbC crystals in RBCs

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6
Q

What type of mutation is seen in B-thalassemia?

A

Point mutations in promotor or splicing sites

*Seen in individuals of African and Mediterranean descent

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7
Q
  • Microcytic, hypochromic RBCs with target cells and nucleated red blood cells
  • HbA2
  • HbF
A

B-thalassemia major

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8
Q
  • Macrocytic RBCs with hypersegmented neutrophils
  • Glossitis
  • Subacute combined degeneration of the spinal cord
A

B12 deficiency

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9
Q

What strain of malaria causes daily fever?

A

P. falciparum

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10
Q
  • Severe anemia
  • B chains form tetramers (HbH)
  • HbH seen on electrophoresis
A

Three gene delection in a-thalassemia

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11
Q

Most common type of anemia in hospitilized patients

A

Anemia of chronic disease

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12
Q

Enterocytes transport iron across the cell membrane into blood via _______. _____ transports iron in the blood. Stored intracellular iron is bound to _________.

A

Ferroportin; Transferrin; Ferretin

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13
Q

Under what conditions does IgG bind to RBCs?

A
  • In relatively warm temps of the central body

*Membrane of antibody-coated RBC is consumed by splenic macrophages, resulting spherocytes

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14
Q

Cause of paroxysmal nocturnal hemoglobinuria

A
  • Acquired defect in myeloid stem cells resulting in absent glycosylphosphatidylinositol
  • Cells are rendered desctructible by complement
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15
Q

Stored iron bound to ferritin prevents iron from forming free radicals via the _______ reaction.

A

Fenton

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16
Q

Presentation of a two gene deletion in a-thalassemia

A
  • Mild anemia with increase in RBC count
    • Cis: Asians; worse
    • Trans: Africans
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17
Q
  • Microcytic, hypochromic RBCs and target cells seen on blood smear
  • Slightly decreased HbA
  • Increased HbA2
  • HbF
A

B-thalassemia minor

*The mildest form of disease and is usually asymptomatic with an increased RBC count

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18
Q

Laboratory findings:

  • Increased ferritin
  • Decreased TIBC
  • Increased serum iron
  • Increased % saturation
A

Sideroblastic anemia

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19
Q

What is the most common congenital defect in sideroblastic anemia?

A

Defect in aminolevunilic acid synthetase (ALAS)

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20
Q

What is the relationship between ferritin and TIBC?

A

Inverse

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21
Q

What causes sickling in the medulla of people with sickle cell trait?

A
  • Extreme hypoxia and hypertonicity of the medulla
    • Results in microinfarctions leading to microscopic hematuria and, eventually decreased ability to concentrate urine
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22
Q

Complications of paroxysmal noctunal hemoglobinuria

A
  • Iron deficiency anemia
  • Aute myeloid leukemia (develops in 10% of patients)
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23
Q
  • Hemoglobinemia
  • Hemoglobinuria
  • Hemosiderinuria
  • Decreased serum haptoglobin
A

Intravascular hemolysis

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24
Q

________ screen causes cells with any amount of HbS to sickle.

A

Metabisulfite

*;positive in both disease and trait.

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25
Q

Most common cause of vitamin B12 deficienct

A

Pernicious anemia

*Autoimmune destruction of parietal cells leads to intrinsic factor deficiency

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26
Q

Which proteins are most commonly affected in hereditary spherocytosis?

A

Ankyin

Spectrin

Band 3

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27
Q

Aplastic anemia results from damage to ___________ .

A

Hematopoietic stem cells

*Results in pancytopenia (anemia, thrombocytopenia, and leukopenia)

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28
Q

Aside from pernicious anemia. What are some other causes of vitamin B12 deficiency?

A
  • Pancreatic insufficiency
  • Damage to terminal ileum
    • Crohn’s disease
    • Diphyllobothrium latum
  • Dietary deficiency in vegans
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29
Q

Causes of aplastic anemia

A

Drugs or chemicals

Viral infections

Autoimmune damage

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30
Q

Absorption of iron occurs in the _______.

A

Duodenum

*Enterocytes have heme and non-heme (DMT1) transporters. The heme form is more readily absorbed

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31
Q

In people with sickle cell trait, RBCs with <50% HbS do not sickle in vivo except in the _________.

A

Renal medulla

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32
Q

Causes of anemia due to underproduction

A
  • Causes of microcytic and macrocytic anemia
  • Renal failure-decreased EPO production by peritubular interstitial cells
  • Damage of bone marrow presursor cells
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33
Q

Where is iron bound to transferrin delivered?

A

Luver and bone marrow macrophages for storage

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34
Q

Mutation in sickle cell anemia

A

Autosomal recessive mutation in B chain of hemoglobin; a signle amino acid change replaces normal glutamic acid (hydrophilic) with valine (hydrophobic)

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35
Q

In hemoglobin C, glutamic acid is replaced by ________.

A

Lysine

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36
Q

Dactylitis

A

Swollen hands and feet due to vaso-occlussive infarcts in bone (infants)

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37
Q

55% HbA, 43% HbS, 2% HbA2

A

Sickle cell trait

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38
Q

treatment for hereditary spherocytosis

A

Splenectomy

*Anemia resolves but spherocytes persist and Howell Jolly bodies emerge on blood smear

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39
Q
  • Macrocytic RBCs and hypersegmented neutrophils
  • Glossitis
  • Decreased serum folate
  • Increased serum homocysteine
  • Normal methylmalonic acid
A

Folate deficiency anemia

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40
Q

Why are spherocytes consumed by splenic machrophages?

A

Spherocytes are less able to maneuver through splenic sinusoids

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41
Q

In paroxysmal nocturnal hemoglobinuria, why does intravascular hemolysis occur episodically during the night?

A

Mild respiratory acidosis develops with shallow breathing during sleep and activates complement

*RBCs, WBCs, and platelets are lysed

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42
Q

________ confirms the presence and amount of HbS.

A

Hb electrophoresis

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43
Q

alpha2delta2

A

HbA2

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44
Q

What causes the round shape of RBCs in hereditary spherocytosis?

A

Loss of membrane, due to loss of cytoskeleton-membrane tethering proteins

*These cells are called sperocytes

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45
Q

Treatment for aplastic anemia

A
  • Cessation of any causative drugs and supportive care with transfusions
  • Marrow-stimulating factors (EPO, GM-CSF, and G-CSF)
  • Immunosuppression may be helpful
  • Bone marrow transplantation as a last resort
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46
Q

RC <3%

A

Overproduction, normocytic anemia

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47
Q

90% HbS, 8% HbF, 2% HbA2

A

Sickle cell disease

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48
Q

Treatment for hereditary spherocytosis

A

Splenectomy

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49
Q

Role of acid in iron absorption

A

Acid aids iron absorption by maintaining the Fe 2+ state. which more readily absorbed thatn the Fe 3+ state

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50
Q

__________ attaches protoporphyrin to iron to make heme. Where does this occur?

A

Ferrochelatase; mitochondria

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51
Q

Fanconi anemia can progress to what neoplasm?

A

AML (>10%)

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52
Q

target cells

A

Decreased Hb in cytoplasm

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53
Q

a2B2

A

HbA

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54
Q
  • Anemia with splenomegaly
  • Jaudice
  • Increased risk for bilirubin gallstones
  • RC count >3%
A

Extravascular hemolysis

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55
Q

Extravascular hemolysis and sickle cell anemia

A
  • Reticuloendothelial system removes RBCs with damaged membranes, leading to anemia, jaundice with unconjugated hyperbilirubinemia, and increased risk for bilirubin gallstone

*Cells continuously sickle and de-sickle while passing through the microcirculation, resulting in complications related to RBC membrane damage

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56
Q

IgG mediated immune hemolytic anemia is associated with which conditions?

A
  • SLE
  • CLL
  • Certain drugs
    • Penicillin and cephalosporins
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57
Q

4 alpha genes are pressent on chromosome _______. Two beta genes are present on chromosome ______.

A

16;11

58
Q

Normal Hb males/females

A

Males: 13.5-17.5g/dL

Females: 12.5-16 g/dL

59
Q

Under what conditions does Igm bind to RBCs?

A

Relatively cold temps of the extremities

*Also fixes complement

60
Q

Stepwise synthesis of protoporphyrin

A
  1. Aminolevulinic acid synthesae converts succinyl CoA to aminolevulinic acid using vitamin B6 as a cofactor
  2. Aminolevulinic acid dehydratase converts aminolevulinc acid to porphobilinogen
  3. Porphobilongen to protoporphyrin
61
Q

Percentage of HbS in sickle cell anemia

A

>90%

62
Q

Treatment for anemia of chronic disease

A
  • Treat underlying condition
  • Exogenous EPO is useful in patients with cancer
63
Q

Plummer-Vinson syndrome

A

Iron deficiency anemia with esophageal web and atrophic glottis; presents with anemia, dysphagia, and beefy-red tongue

64
Q

Igm mediated immune hemolytic anemia is associated with what conditions?

A

Mycoplasma pneumoniae

Infectious mononucleosis

65
Q

a2y2

A

HbF

66
Q

Normocytic anemias predominantly associated with intravascular hemolysis

A
  • Paroxysmal nocturnal hemoglobinuria
  • Glucose-6-phosphate dehydrogenase deficiency
  • Immune hemolytic anemia
  • Microangiopathic hemolytic anemia
  • Malaria
67
Q

Causes of normocytic anemia

A
  • Increased peripheral destruction
  • Underproduction
68
Q

process by which B12 is absorbed

A
  • Salivary gland enyzymes liberate vitaming B12
  • B12 then bound to R-binder and carried to the stomach
  • Pancreatic proteases in the duodenum detach vitamin B12 from R-binder
  • Vitamin B12 binds intrinsic factor
  • Vitamin B12-intrinsic factor complex is absorbed in the ileum
69
Q

How is hereditary spherocytosis diagnosed?

A

by osmotic fragility test, which reveals increased spherocyte fragility in hypotonic solution

70
Q

Treatment for IgG mediated immune hemolytic anemia

A

Cessation of offending drug

Steroids

IVIG

Splenectomy (if necessary)

71
Q

Causes of macrocytic anemia without megaloblastic change?

A

Alcoholism

Liver disease

Drugs

72
Q
  • X-linked recessive disorder
  • Renders cells susceptible to oxidative stress
A

Gucose-6-Phosphate dehydrogenase deficiency

73
Q

Total iron binding capacity

A

Measure of transferrin molecules in the blood

74
Q

RC >3%

A

Peripheral destruction, normocytic anemia

*Marrow response (to increase RC in response to anemia) is good

75
Q
  • Hydrops fetalis
  • Hb Barts seen on electrophoresis
A

Four genes deleted causing a-thalassemia

76
Q
  • Increased serum homocysteine
  • Increased methylmalonic acids
  • Decreased serum vitamin B12
A

Anemia due to B-12 deficiency

77
Q

Which strain of malaria results in fevers every other day?

A

P.vivax and Povale

78
Q

Treatment for B-thalassemia major

A
  • Chronic transfusions
    • Leads to risk for secondary hemochromatosis
79
Q

Percentage of HbS in sickle cell trait

A

<50%

80
Q

Subacute combined degeneration

A

–Demyelination lateral and dorsal columns

–Paraesthesia, loss of vibration and position, gait, spasticity

*Seen in B12 deficiency

81
Q

malaria is transmitted by _________

A

Female anopheles mosquito

82
Q

MCV >100

A

Macrocytic

83
Q

a-thalassemia is usually due to ______________. B-thalessemia is due to _________.

A

Gene deletion; gene mutation

84
Q

Which conditions are predominantly associated with extravascular hemolysis?

A
  • Hereditary spherocytosis
  • Sickle cell anemia
  • Hemoglobin C
85
Q

Stages of iron deficiency

A
  • Storage iron deficiency
  • Serum iron is depleted
  • Normocytic anemia
  • Microcytic, hypochromic anemia
86
Q

Complications of extensive sickling

A

Vaso-occlusion

  • Dactylitis
  • Autosplenectomy
  • Acute chest syndrome
  • Pain crisis
  • Renal papillary necrosis
87
Q

Vitamin B6 deficiency can caused acquired sideroblastic anemia. When is this most commonly seen?

A

As a side effect of isoniazid treatment for TB

88
Q

Aquired caused of sideoblastic anemia

A
  • Alcoholism-mitochondrial poison
  • Lead poisoning- inhibits ALAD and ferrochelatase
  • Vitamin B6 deficiency
89
Q

_________ is needed to regenerate reduced glutathione

A

NADPH

*By-product of G6PD

90
Q

Biochem of folate B12, and methionine

A
  • Methylytetrahydrofolate donates a methyl group to B12 and becomes folate
  • B12 donates methyl grouo to homocysteine and becomes methionine
91
Q

Clinical findings of B-thalassemia major

A
  • Crewcut appearance on X-ray
    • erythroid hyperplasia
    • Expansion of hematopoiesis into the skull
  • Chipmuck facies
    • Hematopoiesis in facial nones
  • Hepatosplenomegaly
92
Q

Causes of microangiopathic hemolytic anemia

A
  • Microthombi
    • TTP-HUS
    • DIC
    • HELLP
  • prostetic heart valves
  • Aortic stenosis

*When prsent, microthrombi produce shistocytes on blood smear

93
Q

Laboratory findings:

  • Increased ferritin
  • Decreased TIBC
  • Decreased serum iron
  • Decreased %saturation
  • Increased free erythrocyte protoporphyrin
A

Anemia of chronic disease

94
Q

Causes of macrocytic anemia with megaloblastic change

A

Folate and B12 deficiency

95
Q

Methylmalonic builds up in ______ in spinal cord.

A

Myelin

96
Q

What conditions lead to an increased risk of sickling?

A

Hypoxemia

Dehydration

Acidosis

97
Q

Biopsy of aplastic anemia

A

Emplty, fatty marrow

98
Q

Cause of immune hemolytic anemia

A

Antibody-mediated destruction of RBCs

99
Q

B-thalassemia presents with a risk of aplastic crisis with __________ infection of erythroid precursors.

A

Parvovirus B19

100
Q

What are the consequences of autosplenectomy seen with extensive sickling?

A
  • Increased risk of infection with encapsulated organisms such as S. pneumonia and H. influenza
  • Increased risk of Salmonella paratyphi osteomyelitits
  • Howell-Jolly bodies on blood smear
101
Q

Which vitamin is deficient in sideoblastic anemia?

A

B6

102
Q
  • Increased RDW
  • Increased mean corpuscular hemoglobin concentration (MCHC)
  • Splenomegaly, jaudice with unconjugated bilirubin
  • Spherocytes with loss of central pallor
A

Hereditary spherocytosis

103
Q

What is the confirmatory test for paraoxysmal nocturnal hemoglobinuria?

A

Acidified serum test or glow cytometry to detect lack of CD55 (DAF) on blood cells

104
Q

Organs of reticuloendothelial system

A

Macrophages of spleen

Liver

Lymph nodes

105
Q

MCV <80

A

Microcytic

106
Q

Hb Barts

A

Gamma chains form a tetramer

107
Q

Causes of folate deficiency

A
  • Poor diet
  • Increased demand (pregnancy, cancer, and hemolytic anemia)
  • Folate antagonists (methotrexate)
108
Q

Oxidative stress precipitates Hb as ___________.

A

heinz bodies

*heinz bodies are removed from RBCs by splenic macrophages, resulting in bite cells

109
Q

________ on the surface of blood cells protects against complement-mediated damge by inhibiting C3 convertase.

A

Decay accelerating factor (DAF)

*DAF is secured to the membrane by GPI

110
Q

Common cause of iron deficiency in the elderly?

A

Colon polyps/ carcinoma in the western world

Hookworm (Anyclostoma duodenale and Nectar americanus) in the developing world

111
Q

parvovirus B19 infects __________.

A

Progenitor red cells

*Temporary halts erythropoiesis

112
Q

Folate is absorbed in the ___________.

A

Jejunum

113
Q

______ is used to diagnose immune hemolytic anemia

A
  • Coombs test (direct or indirect)
114
Q

Causes of oxidative stress

A

infections

drugs (primaquine, sulfa drugs, and dapsone)

Fava beans

115
Q

Laboratory findings:

  • Microcytic, hypochromic RBCs with increase in RDW
  • Decreased ferritin
  • Increase TIBC
  • Decreased serum iron
  • Decreased % saturation
  • Increased free erythrocyte protoporphyrin
A

iron-deficiency anemia

116
Q

What are the results of consumption of RBCs by macrophages?

A

This is extravascular hemolysis

  • Hemoglobin is broken down
  • Globin broken down into amino acids
  • Heme is broken down to iron and protoporphyrin,
    • Iron is recycled
    • Protoporphyrin is broken down in unconjugated bilirubin, which is bound to serum albumin and delivered to the liver for conjugation and excretion into bile
117
Q

Larger cells with bluish cytoplasm

A

Reticulocytes

*Due to residual RNA

118
Q

Clinical feautres of iron deficiency

A

Anemia, koilonychia, and pica

119
Q

___ (IgG/IgM)- mediated disease usually involves extravascular hemolysis. ____ (IgG/IgM) can lead to intravascular hemolysis.

A

IgG, IgM

120
Q

intravascular hemolysis and sickle cell anemia

A
  • RBCs with damaged memnranes dehydrate, leading to hemolysis with decreased haptoglobin and target cells on blood smear

*Target cells are due to dehydration

121
Q

__________ is a inherited defect of RBC cytoskleton-membrane tethering proteins.

A

Hereditary spherocytosis

122
Q

Plasmodium affects ______ and the ______.

A

RBCs ; liver

*RBCs rupture as a part of the Plasmodium life cycle

123
Q

_________ is used to screen for paroxysmal nocturnal hemoglobinuria.

A

Sucrose test

*Sucrose activates complement

124
Q

Role of hepcidin

A

Acute phase reactant that sequesters iron in storage sites by:

  • Limiting iron transfer from macrophages to eythroid precursors
  • Suppressing erythropoietin production

*Aims to prevent bacteria from accessing iron, which is necessary ofr their survival

125
Q

What attributes to the production of spherocytes in IgM mediated immune hemolytic anemia?

A
  • IgM binds to RBCs and fixes complement
  • RBCs inactivate complement but residual C3b serves as an opsonin for splenic macrophages resulting in spherocytes

*Extreme activation of complement can lead to intravascular hemolysis

126
Q

Cause and symptoms of acute chest syndrome

A

Cause: vaso-occlusion in pulmonary microcirculation

Symptoms

  • Chest pain, shortness of breath, and lung infiltrates
  • Precipitated by pneumonia
  • Most common cause of death in adult patients
127
Q

HbH

A

B chains forming a tetramer

*Damage RBCs

128
Q

Types of microcytic anemias

A
  • iron deficiency anemia
  • Anemia of chronic disease
  • Sideorblastic anemia
  • Thalassemia
129
Q

Treatment with _________ increases levels of HbF.

A

Hydroxyurea

130
Q

What happens to iron is protoporphyrin is deficient?

A

Iron is trapped in the mitochondria

*iron-laden mitochondria form a ring around the nucleus of erythroid precursors called ringed sideroblasts

131
Q

Frequent pigment gall stones

A

Hereditary spherocytosis

132
Q

Against protein based antigens

A

IgG

133
Q

Against carbohydrate based antigens

A

IgM

134
Q

Indications for packed red blood cells

A
  • (Restoration of red cell oxygen carrying capacity)
  • Improve Tissue Oxygen Delivery
  • Alleviation of signs & symptoms of anemia
135
Q

Guidelines for packed red cells

A

General Guidelines:

  • Maintain Hgb > 7mg/dl
    • Increased mortality when Hgb drops to < 5 mg/dl
  • Need to keep higher HCT in CAD, pulmonary disease (Hgb > 8mg/dl)
  • Important to maintain normovolemia even with acute blood loss
136
Q

Contraindications for Platelet Transfusion

A
  • Thrombotic thrombocytopenic purpura (TTP)
  • Heparin induced thrombocytopenia (HIT)
  • Immune mediated thrombocytopenic purpura (ITP)
137
Q

Cryoprecipitated AHF components

A

contains fibrinogen, Factors VIII and XIII,

von Willebrand factor

138
Q

Cryoprecipitated AHF indications

A
  • Hypofibrinogenemia/Dysfibrinogenemia
  • Uremic bleeding
  • Second-line treatment of Hemophilia A, Factor XIII deficiency and von Willebrand disease
139
Q

Treatment for allergic transfusion reactions

A

diphenylhydramine

140
Q

RBC receptors for Malaria

A

Glycophorin A for P. falciparum and Duffy antigen for P. vivax

141
Q

Mode of transmission for leishmania

A

Sandlfy

142
Q

Treatment for leishmania

A

Sodium stibogluconate

OS2 (10 decks)

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