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Erythrocytes Flashcards

(49 cards)

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1
Q

Erythropoiesis

A

process of RBC formation

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2
Q

RBC made in

A

Bone marrow under influence of erythropoietin (EPO) produced by the kidneys

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3
Q

Characteristics of RBC

A

no nucleus (enucleate) or organelles (mitochondria, golgi, etc)
Packed with Hb (hemoglobin)
No DNA/RNA aka no cell division
Major role carries O2 and CO2 away from tissues

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4
Q

RBC shape

A

highly flexible biconcave disk

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5
Q

Flexibility of RBC is for

A

maximizing surface area for gas exchange and passage through small capilaries

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6
Q

Where are RBC produced

A

Bone Marrow; 7 days for maturation

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7
Q

How are RBC eliminated?

A

Spleen

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8
Q

Reticulocytes

A

immature RBC. They are bigger than normal RBC. Have a small amount of ribosomal RNA but no nucleus

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9
Q

Reticulocyte count

A

accurate way to assess body’s response to anemia

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10
Q

Low reticulocyte count

A

poor production in bone marrow

anemia due to decreased production of RBC

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11
Q

High reticulocyte count (Reticulocytosis)

A

more made in bone mature

anemia due to premature destruction of RBCs (hemolysis)

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12
Q

Hemoglobin (Hb)

A

RBCs packed with hemoglobin = o2 carrying protein

Large protein composed of 4 amino acid chains, global chains, each bound to an iron-containing heme group

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13
Q

Heme group

A

Consists of iron (Fe) which is the site of O2 binding

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14
Q

Where is the synthesis of heme?

A

mitochondria and cytoplasm of immature RBCs

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15
Q

Where is globin synthesis?

A

cytoplasm of ribosomes

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16
Q

During 3 -10 weeks gestation hemoglobin chains are

A

zeta and epsilon

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17
Q

As a fetus what HB is available?

A

Hb F alpha2 gamma 2

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18
Q

Has an adult what HB is available?

A

HBA- HB A1: alpha2beta2, HbA2 alpha2delta2; HB F

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19
Q

What is oxyhemoglobin?

A

Hemoglobin carrying O2

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20
Q

Carbaminohemoglobin

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A

Hb carrying Co2

21
Q

Abnormal Hv

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A

Carboxyhemoglobin: binds CO2 instead of O2

Methemoglobin Fe2+ to Fe3+; cano’t bind O2

22
Q

Erythrocytosis (polycythemia)

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A

increased number off RBC

23
Q

ANemia, erythropenia (erythrocytopenia)

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A

decreased number of RBC

24
Q

Poikilocytosis

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A

difference in shape of hemoglobin

25
Rouleaux
like stacks of coins; due to increase in high molecular weight plasma proteins
26
Red cell agglutination
due to antibody present in RBC surface forms irregular clumps
27
Howell-Jolly bodies
large round densely stained inclusions on edge of cell; nuclear reminants ALWAYS ON EDGE OF CELL
28
Increased destruction of RBCS
hemolytic anemia G6PD deficiency Sicle cell disease
29
Decreased production of RBC
Iron deficiency anemia | Thalassemia (A,Beta)
30
Polycythemia
increased # of RBC Absolute: primary or secondary Primary: overproduction of RBCS Secondary: caused by increased secretion due to hypoxia Relative: due to dehydration or fluid loss (looks like we have more RBC but really don't)
31
Polycythemia (Rubra) Vera (PV)
myeloproliferative disease; rare due to increased RBC proliferation in bone marrow Possible cause: JAK-2 gene
32
Anemia
Rate of RBC production does not equal rate of RBC destruction
33
Iron deficiency anemia
Insufficient iron stores due to poor diet, poor iron absorption, body iron stores are depleted by prolonged bleeding **most common Common in menstruating or pregnant women
34
Sideroblastic anemia
Abnormal incorporation of iron into the heme group of Hb | Toxic accumulation of iron in mitochondria = ringed sideroblasts
35
Microcytoic anemia
second most common anemia after iron deficiency anemia Cause: chronic infection, chronic inflammatory diseases (rheumatoid arthritis) Mechanism: blocked iron transport from storage sites to developing RBC in bone marrow
36
Microcytic anemias: Thalassemias
Inherited genetic disorader Reduced or absent production of normal Hb A 2 types: alpha thalassemia- caused by deletion of 1,2,3,4 alpha globin B thalassemia- caused by mutations in beta global gene cluster
37
Alpha Thalassemia
deficiency or no synthesis of alpha global chains | Asymptomatic and silent carriers
38
Alpha Thalassemia major- Hemoglobin Barts Hydrops Fetalis
No survival. Most severe form. Complete absence of alpha global chains. Anemia in utero. Hv F cannot be produced.
39
Alpha Thalassemia minor (trait)
mildest form; one B global gene is defection Moderately reduced Hv A1; increased HV A2 and HV F Low MCV and MCH but high RBCs no symptoms
40
Beta Thalassemia major (Cooley's anemia)
most severe form; both B global games are defection | Reduced or absent Hb A1; increased A2 and HF
41
Macrocytic anemias
elevated MCV Impaired DNA synthesis but normal RNA synthesis Usually due to B12 and folic acid deficiency which causes neural tube defects (spina bifida)
42
Hemolytic disorders
Reduction in RBC lifespan and compensatory increase in rate of erythropoiesis Cause: incompatible blood transfusions, cancer, drugs
43
Extravascular hemolysis
RBCs by macrophages in spleen, liver, BM
44
Intravascular hemolysis
RBCs within blood vessels
45
Intrinsic defect
structural or functional defect within the RBC Red cell membrane- hereditary spherocytosis Red cell metabolism- G6PD deficiency Hb- sickle cell disease and thalassemias
46
Extrinsic defect
abnomality in RBC environment immunologic abnomalities mechanical injury infectious organism that invade and destruct RBCs or produce toxins
47
Herditary spherocytosis
most common inherited RBC abnomality transmitted in autosomal dominant manner but autosomal recessive form also exists Defective gene encodes for the Red Cell cytoskeletal protein spectrum= rupture Major site of hemolysis= spleen
48
G6PD deficiency
The role of G6PD is to protect red cell proteins from endogenous or exogenous oxidant stress Mechanism: converts glucose --> ribose - 5- phosphate --> NADPH production NADPH prevents building up of free radicals within the cell Triggers: ingestion of lava beans -divicine Reason: production and release of free radicals
49
Sickle cell disease
genetic. Change in hemoglobin structure due to mutation of Hb gene Normal Hb: substitution of glutamic acid by valine Result: distortion of RBC shape from biconcave to half moon. Becomes inflexible rod Normal RBCS move freely but sickle RBCS get trapped in small capillaries and get destroyed. Damage organs: spleen, kidneys, liver

Basic Tissues (11 decks)

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