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Basic Tissues > Erythrocytes > Flashcards

Erythrocytes Flashcards

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

A

Hb carrying Co2

21
Q

Abnormal Hv

A

Carboxyhemoglobin: binds CO2 instead of O2

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

22
Q

Erythrocytosis (polycythemia)

A

increased number off RBC

23
Q

ANemia, erythropenia (erythrocytopenia)

A

decreased number of RBC

24
Q

Poikilocytosis

A

difference in shape of hemoglobin

25
Q

Rouleaux

A

like stacks of coins; due to increase in high molecular weight plasma proteins

26
Q

Red cell agglutination

A

due to antibody present in RBC surface forms irregular clumps

27
Q

Howell-Jolly bodies

A

large round densely stained inclusions on edge of cell; nuclear reminants

ALWAYS ON EDGE OF CELL

28
Q

Increased destruction of RBCS

A

hemolytic anemia
G6PD deficiency
Sicle cell disease

29
Q

Decreased production of RBC

A

Iron deficiency anemia

Thalassemia (A,Beta)

30
Q

Polycythemia

A

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
Q

Polycythemia (Rubra) Vera (PV)

A

myeloproliferative disease; rare
due to increased RBC proliferation in bone marrow

Possible cause: JAK-2 gene

32
Q

Anemia

A

Rate of RBC production does not equal rate of RBC destruction

33
Q

Iron deficiency anemia

A

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
Q

Sideroblastic anemia

A

Abnormal incorporation of iron into the heme group of Hb

Toxic accumulation of iron in mitochondria = ringed sideroblasts

35
Q

Microcytoic anemia

A

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
Q

Microcytic anemias: Thalassemias

A

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
Q

Alpha Thalassemia

A

deficiency or no synthesis of alpha global chains

Asymptomatic and silent carriers

38
Q

Alpha Thalassemia major- Hemoglobin Barts Hydrops Fetalis

A

No survival. Most severe form. Complete absence of alpha global chains. Anemia in utero. Hv F cannot be produced.

39
Q

Alpha Thalassemia minor (trait)

A

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
Q

Beta Thalassemia major (Cooley’s anemia)

A

most severe form; both B global games are defection

Reduced or absent Hb A1; increased A2 and HF

41
Q

Macrocytic anemias

A

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
Q

Hemolytic disorders

A

Reduction in RBC lifespan and compensatory increase in rate of erythropoiesis
Cause: incompatible blood transfusions, cancer, drugs

43
Q

Extravascular hemolysis

A

RBCs by macrophages in spleen, liver, BM

44
Q

Intravascular hemolysis

A

RBCs within blood vessels

45
Q

Intrinsic defect

A

structural or functional defect within the RBC

Red cell membrane- hereditary spherocytosis
Red cell metabolism- G6PD deficiency
Hb- sickle cell disease and thalassemias

46
Q

Extrinsic defect

A

abnomality in RBC environment
immunologic abnomalities
mechanical injury
infectious organism that invade and destruct RBCs or produce toxins

47
Q

Herditary spherocytosis

A

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
Q

G6PD deficiency

A

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
Q

Sickle cell disease

A

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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