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Pathology > Midterm RBC Review > Flashcards

Midterm RBC Review Flashcards

1
Q

What stimulates RBC production?

A

EPO from kidney

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2
Q

Hemoglobin has what two parts

A

Heme protein + 2 pairs of globin chains

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3
Q

Heme has what two parts

A

Iron + protoporphryin

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4
Q

HbA is 95% and has what chains

A

Alpha and beta

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5
Q

HbA2 is 3.5% and has what chains

A

Alpha and delta

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6
Q

HbF is 1.0% and has what chains

A

alpha and gamma

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7
Q

Anemia definition

A

Decreased red blood cell mass

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8
Q

Normal HCT to HB ratio?

A

3:1

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9
Q

Anemia special title

A

Most common RBC abnormality

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10
Q

What is reticulocytosis

A

Increase in reticulocytes signaling marrow response to anemia

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11
Q

What is polychromasia

A

New immature RBC’s made in response to anemia are bigger and blue

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12
Q

Two GI losses causing anemia and their patient type

A
  1. Peptic Ulcer: Adult males

2. GI Neoplasm: Elderly

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13
Q

One GYN loss causing anemia and patient type

A

Woman with menorrhagia

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14
Q

Intravascular sees decrease in what two proteins

A

Hemopexin and Haptobloin due to binding Iron

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15
Q

Extravascular hemolysis is done by what two things?

A
  1. Spleen

2. Liver macrophages

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16
Q

What are the Hb and HCT level changes in extravascular hemolysis?

A

None

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17
Q

Intravascular hemolysis due to mechanical causes include?

A

Microangiopathic hemolytic anemias

Mechanical heart valves

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18
Q

What is the principal finding in microangiopathic hemolytic anemias

A

Schistocytes

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19
Q

Three types of microangiopathic hemolytic anemias?

A
  1. Disseminated Intravascular coagulation
  2. Hemolytic uremic syndrome
  3. Thrombotic thrombocytopenic purpura
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20
Q

Three things elevated in DIC only?

Common patient type

A

D-dimer
PTT
PT

Pregnant

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21
Q

Hemolytic uremic syndrome is what age?

Cause?

A

Children

Toxin damage

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22
Q

Thrombotic thrombocytopenic purpura is due to what?

Patient type?

A

Adams 13 mutation

Young women

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23
Q

Microangiopathic hemolytic anemias have what common cause?

A

Lumen narrows and injures RBC’s causing them to lyse and form schistocytes

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24
Q 
Hereditary spherocytosis
Heredity
Ethnic group
2 proteins affected
Mechanism of path
Characteristic cell shape
One sequelae to know
Diagnose how? 
Treatment?
Result of treatment
A 
Autosomal Dominant
Scandinavians
Ankyrin and Spectrin
Lose parts of membrane over time and become sphere
Spherical
Cholelithiasis
Osmotic fragility
Splenomegaly
Howell Jolly Bodies
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25
Q 
G6PD deficiency
What does G6PD normally make
Function of this product
Heredity
Moderate version ethnicity
Severe version ethnicity
Causes (3)
Typical histo finding in cells
Typical cell shape
A 
NADPH
Reduces glutathione to protect against ROS
Recessive X-linked
African = moderate
Mediterranean = Severe
Antimalarials, Sulfonamides, Fava beans
Heinz bodies
Bite cells
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26
Q 
Paroxysmal nocturnal hemoglobinuria
Congenital or acquired
Mutated gene
Loss of what proteins
Result of lost proteins
Most common cause of death
LAP score
Timing of hemolysis
A

Acquired
X-linked PIGA gene mutation
Loss of GPI proteins so no CD55/DAF or CD59/MIRL
Complement binds to RBC’s at night and lyses them.
THrombosis
Decreased
Episodic at night

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27
Q

Immune hemolytic anemias definitive tests (2)

A
  1. Positive antiglobulin test (DAT)

2. Direct Coomb’s test

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28
Q

Alloimmune hemolytic anemia definition

A

Make Ab’s against foreign RBC’s

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29
Q

3 times alloimmune occurs

A
  1. Immediate transfusion reaction
  2. Delayed transfusion reaction
  3. Hemolytic disease of newborn
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30
Q

Immediate transfusion reaction
Type of hemolysis
Antibody type

A

Intravascular

Preformed ABO IgM antibodies

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31
Q

Delayed transfusion reaction
Type of hemolysis
Timing
Antibody type

A

Extravascular
4-6 days after transfusion
IgG Ab’s against RBC’s

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32
Q 
Hemolytic disease of newborn
Antibody type
Type of hemolysis
Treatment
What to do before birth
Most common situation
A 
IgG against RBC's of newborn
Extravascular
Treat with Rhogam
Plasmapheresis
Mom's Anti-D Ab's against Fetal D antigen
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33
Q 
Warm AIHA 
Antibody
Temperature
Primary or secondary
Secondary causes (2)
Hemolysis type
RBC shape
A 
IgG
37 degrees
Primary 50%
RE neoplasm or Collagen vascular disease
Extravascular
Spherocytes
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34
Q

Cold AIHA
Antibody
Temperature
Normal Cold Auto Ab’s

A

IgM
4 degrees
Auto Ab’s: Anti-I, Anti-H, Anti-IH

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35
Q

Acute gold agglutinin AIHA

secondary to what?

A

Mycoplasma

36
Q 
Cold agglutinin syndrome 
Secondary to:
Common presentation
Specific antibody
Lab test:
A

Infection or lymph neoplasm
Elderly guy with lymphoma
Anti-I
DAT+

37
Q 
Paroxysmal COld hemoglobinuria
Common presentation
Specific AutoAb
Lab test
Name of this antibody:
A

Children with viral infection
Autohemolysin
Biphasic IgG Ab with Anti-P specificty
Donath-landsteiner antibody

38
Q

Drug induced hemolytic anemia
Antibody
Two drug types

A

IgG

  1. antigenic drugs
  2. Alpha-methyldopa
39
Q

Sickle Cell geography

A

Africa and Mediterranean

40
Q

Hemoglobin C location

A

West Africa

41
Q

Hemoglobin E location

A

SE asia

42
Q

Beta Thalassemia
Characteristic cell
Characteristic intracellular sign
Clinical features (2)

A

Target cells
Basophilic stippling
Crewcut X-ray
WIdened facial bones

43
Q

Beta minor hemoglobin change

A

Higher HgbA2

44
Q

Beta major hemoglobin change

A

Absent HgbA and Increased HbF

45
Q

How to distinguish between Beta minor and Fe deficiency?

A

Fe levels

46
Q

Alpha thalassemia
4 betas forms what
4 gammas forms what

A

4 Betas: HbH

4 gammas: Hb Barts

47
Q

Alpha thalassemia one gene deletion.

Only difference

A

Hb Barts at birth

48
Q

Alpha thal two gene deletion
Only difference
The mutation that is far more severe and what ethnic group

A

Hb barts at birth

Cis mutation (same chromosome) causes hydrops fetalis in Asians

49
Q

Three gene deletion alpha thal
Hb change?
Result?

A

Hemoglobin H disease (beta tetramers)

Extravascular hemolysis

50
Q

Four gene deletion alpha thal

A

Hydrops fetalis with hemoglobin barts

51
Q

How to determine alpha thal in lab? (3)

A
  1. Target cells
  2. Abnormal hemoglobins (barts and HbH)
  3. Hemoglobin H inclusions with cresyl blue stain
52
Q 
Hemoglobin S 
Inheritance
Mutation
Main population in US
Trait advantage
If infarction occurs what is result
One primary clinical finding
A 
Autosomal recessive
Valine to glutamine on Beta globin chain
Blacks
Malaria protection
Autosplenectomy
Salmonella osteomyelitis
53
Q

Sickle cell trait
Cell findings
Lab test
Hemoglobin changes

A

Target cells and sickle cells
Cloudy sickle solubility test
60% HbA and 40% HbS

54
Q 
Hemoglobin C 
Main lab finding in disease
Hb change  in Disease
Hb change in trait
Trait advantage
A

Hemoglobin C crystals
HbC 90% with increased HbF
HbA 60% and HbC 40%
Malaria protection

55
Q

Hemoglobin E
Trait advantage
Trait hb levels
Disease hb levels

A

Protective against malaria
equal HbA and HbE
No HbA and 95% HbE

56
Q

3 megaloblastic anemia causes

A
  1. Vitamin B 12 deficiency
  2. Folic acid deficiency
  3. Methotrexate
57
Q

First sign of defective DNA synthesis in megaloblastic?

Other cell finding later

A

Hypersegmented neutrophils

Oval macrocytes

58
Q

Vitamin B 12 deficiency results in what symptoms? (2)

A
  1. Glossitis

2. Subacute combined degeneration of spinal cord

59
Q

Pernicious anemia
Path mech
Ethnic group

A

Auto antibodies against B-12-IF binding

Scandinavians

60
Q

Common B 12 deficiency causes 3

A
  1. Impaired absorption
  2. Parasites
  3. Removal of GI (gastrectomy or ileal)
61
Q

Folate deficiency cause 3

A

Decreased intake
Impaired absorption
Blocked activation by Methotrexate

62
Q

Only diet patient type to be concerned with B12 deficiency?

A

Vegans

63
Q

Malabsorption symptoms make you think what anemia?

A

Folate deficiency

64
Q

Neurologic symptoms make you think what anemia?

A

B12 deficiency

65
Q

Schilling test
First part
Second part

A

Irradiated B 12 only

Irradiated B12 with Intrinsic factor

66
Q

Methylmalonic acid increase, think what?

A

B12 deficiency

67
Q

Iron is stored how

A

Ferritin

68
Q

Iron is transferred how

A

Transferrin

69
Q

Absorption of iron occurs where?

What regulates

A

Duodenum

Hepcidin

70
Q

When is hepcidin made?

Function

A

When liver iron stores are high.

Block absorption

71
Q

Most common cause of iron deficiency

A

Chronic blood loss

72
Q

Iron deficiency symptoms? (3)

A
  1. Koilonychias
  2. Pica
  3. Alopecia
73
Q 
Iron deficiency anemia iron studies
Serum iron
TIBC
Percent saturation
Ferritin
A

Serum iron: Decreases
TIBC increases
Percent saturated decreases
Ferritin decreases

74
Q 
Anemia of chronic disease
Common patient type
Serum iron
TIBC
Saturation
Ferritin
EPO
A 
Hospitalized patients
Low serum iron
Low TIBC
Normal saturation
High ferritin
EPO low
75
Q

Aplastic anemia
What cell lines involved
2 drug causes

A

Pancytopenia

Chloramphenicol and Dilantin

76
Q

Pure red cell aplasia causes (4)

A
  1. Drug/virus
  2. Thymoma
  3. Large granular lymphocytic leukemia
  4. Autoimmune disorders
77
Q 
SIderoblastic anemias
Cell finding 
Primary hereditary cause
Acquired primary cause
Secondary cause
A

Ringed sideroblasts (iron accumulating in mito)
Congenital sideroblastic anemia
Myelodysplastic disorder
Drugs like Tb and alcohol

78
Q 
Primary hemochromatosis
Inheritance
Defective gene
Chromosome 
Main manifestation
A

Autosomal recessive
HFE gene
Chromosome 6
Adult bronze diabetes

79
Q

Lead poisoning two main findings

A

Lead lines in bone and teeth

Basophilic stippling

80
Q

Myelophthisic anemia

Main histo finding

A

Teardrop cells = Dacrocytes

81
Q

Icterus suggests what

A

Hemolytic anemia

82
Q

subacute combined degeneration suggests what

A

Pernicious anemia

83
Q

Helmet cells/Schistocytes suggests what?

A

Hemolytic anemia

84
Q

Target cell suggests what? (2)

A
  1. Hemoglobinopathies

2. Iron deficient anemia

85
Q

Heinz bodies suggest what?

A

G6PD deficiency

86
Q

Basophilic stippling suggests what?

A

Lead poisoning or thalassemia

87
Q

Location for bone marrow exam?

A

Posterior superior iliac spine

Pathology (36 decks)

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