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N 2440 > 5.1 - RBC's > Flashcards

5.1 - RBC's Flashcards

1
Q

What is hematopoiesis?

A
  • process by which blood cells are made
  • occurs in bone marrow
  • starts with hematopoietic stem cells that can differentiate into any type of cell
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2
Q

What 2 progenitor cells are made by hematopoietic stem cells?

A

1) myeloid progenitor
- cells involved in oxygen transport, immune responses, and blood clotting

2) Lymphoid progenitors
- produce lymphocytes (needed for adaptive immune response)

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3
Q

Blood Cell Lineages

A

1) Erythrocytes - RBC’s
- erythropoesis - production of RBC’s

2) Lymphocytes
- T cells, B cells, NK cells
- lymphopoiesis: lymphocyte production

3) Myeloid cells
1. granulocytes
- neutrophils, basophils,
eosiniphils
2. monocyte & macrophages
- do phagocytosis
4. megakaryocytes
- plateletes

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4
Q

How an HSC differentiates?

A

1) HSC develop into mulitipotent progenitor cell (MPP)

2) MPP becomes myeloid progenitor cells

3) Myeloid progenitor becomes granulocyte-monocyte progenitors

4) These become eosinophiloblasts (immature eosinophil)

5) Immature eosinphils produce granules to become mature

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5
Q

What controls the growth and differentiation of HSC’s?

A
  • Cytokines and growth factors
  • Colony stimulating factor: stimulates proliferation of progenitor cells

Hematopoiesis occurs in 2 pools:
1) Stem Cell Pool
- pluripotent stem cells; differentiate into any type of cell

2) Bone Marrow
- stores cells that are actively proliferating or maturing

Once mature blood cells enter circulation, they divide into 2 pools:
1) Circulating
- cells actively moving through bloodstream

2) Migrating
- neutrophils adhering to blood vessel walls

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6
Q

2 Types of Bone Marrow

A

Red
- produces blood cells
-active
-found in pelvis, vertebrae, cranium, ribs

Yellow
- contains fat
- inactive

2 Types of Bone Marrow Niches
1) Osteoblastic
- where HSC’s are inactive

2) Vascular
- where HSC’s proliferate and differentiate

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7
Q

Extra medullary

A

Medullary Hematopoiesis
- blood cell production occurs within BONE MARROW
- in fetus, hematopoiesis occurs within liver and spleen

Medullary HematoPAResis
- failure/suppression of this process
- can be caused by chemo radiation, and aplastic anemias: bone marrow stops producing new cells

Extra medullary Hematopoesis
- production of blood cells OUTSIDE of bone marrow
- occurs in liver, spleen and lymph nodes
- occurs when the body/bone marrow is unable to keep up with bodys demands for RBC production

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8
Q

What is involved in the lymphatic system?

A

Primary Organs
- bone marrow and thymus

Secondary Organs
- spleen, lymph nodes

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9
Q

Role of Spleen

A
  • reservoir for blood
    ex. in case of low BP, spleen can release stored blood to increase BP
  • where fetal RBC production occurs
  • filters blood and removes damaged/old blood cells

White pulp: T and B cells
Red pulp: filters RBC’s

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10
Q

Role in Lymph Nodes in the Immune Response

A

1) antigens encounter lymphocytes

2) lymphocytes (B and T cells) enter lymph nodes and interact with antigens

3) lymphocytes get processed by macrophages and dendritic cells

4) B cells proliferate into plasma

5) Macrophages filter lymph and debris

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11
Q

Erythropoiesis

A
  • kidneys stimulate erythropoiesis when they detect low oxygen in circulation
  • final immature stage of an RBC is a reticulocyte
  • RBC production is regulated by the hormone erythropoietin
  • tissue hypoxia increases production of EPO which triggers increases RBC production
  • in chronic kidney disease, kidneys fail ton produce EPO which then causes decreased RBC production = anemia
  • conditions that lower O2 (COPD triggers kidneys to produce EPO and stimulate RBC production
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12
Q

Process of Hemoglobin Synthesis

A
  • protophorphyrin + iron = heme
  • heme + globin chains = hemoglobin
    - each heme has 2 alpha and 2 beta globin chains
  • heme is made in the mitochondria and cytoplasm of RBC precursor cells
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13
Q

Role of Vit B12 in Erythroporeosis

A
  • b12 forms thymidine (needed for DNA replication)
  • low B12 = impaired DNA synthesis = abnormal RBC production
    • produces larger than normal erythrocytes: megaloblasts
  • B12 is absorbed with the help of intrinsic factor
  • low intrinsic factor = poor B12 absorption = pernicious anemia
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14
Q

Role of Iron in Erythroporeosis

A
  • iron is required to make heme
  • low iron = impaired hemoglobin synthesis (RBC can not properly transport oxygen) = abnormal RBC production = iron deficient anemia
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15
Q

Iron Cycle

A
  • iron is stored as ferritin
  • apoferritin - iron free version

Hemosiderin
- iron-storage complex that is deposited in tissues (esp when there is excess of iron)
- less accessible for immediate use

Transferrin
- transports iron in the blood (iron binds to transferrin receptors)
- once iron is absorbed, transferrin - now apotransferrin get released back into bloodstream

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16
Q

Role of Hepcidin

A

Hepcidin - regulates iron levels

  • hepcidin binds to ferroportin - iron exporter
  • when hepcidin binds to ferroportin, ferroportin breaks dow and stops iron from being released into blood
  • hepcidin levels increase when iron levels are high
  • low iron or ↑ erythropoesis = less hepcicin (body needs more iron when making RBC’s)
17
Q

Iron Absorption

A
  • if iron is low, iron is absorbed rapidly in intestine and transported to plasma
  • if iron is sufficient, excess iron gets stored as ferritin
18
Q

RBC Destruction

A
  • when hemoglobin from RBC’s breaks down, heme is converted to bilirubin
  • bilirubin gets sent to liver where it gets processed and then excreted in bile
  • in intestines, bilirubin gets converted into urobilin
  • if too much RBC’s are destroyed, there are increases levels of unconugated bilirubin which can increase gallstones
19
Q

Role of Blood

A
  • removes waste products
  • delivers nutrients and oxygen to tissues
  • defends against injury
20
Q

Layers of blood

A

1) Erythrocyte - bottom
- carries oxygen

2) Buffy coat layer - middle
- contains leukocytes and thrombocytes

3) Plasma - top
- contains nutrients, waste products, hormones, gases, proteins, electrolytes

21
Q

Plasma

A

1) Albumin
- maintains oncotic pressure
- decreased albumin = fluid imbalance and swelling

2) Globulin
- provides immune defence in the form of antibodies

3) Fibrinogen (clotting)

4) Transferrin (for transporting iron)

22
Q

RBC Count

A

Erythrocytosis - elevated RBC count
- ex. in chronic hypoxia where the body compensates for low O2 by increasing RBC production

Decreased RBC
- occurs due to blood loss, bone marrow suppression (chemo)

23
Q

What is Hematocrit

A
  • % of RBC’s in proportion to plasma volume

-

24
Q

Interpretations of Hematocrit Value

A

Elevated
- can be elevated in cases of chronic hypoxia where body is producing RBC’s to compensate
- can be FALSELY elevated
ex. in dehydration, there is less plasma volume, which increase Hct (but there is not an increased amount of RBC’s)

Decreased
- can have true decreased (in anemia) where there is less RBC production
- can have false decrease
ex. when overhydrated, plasma volume increases which makes Hct appear low (but there are not actually fewer RBC’s)

25
Q

Always interpret hemoglobin levels in relation to ___________?

A

hematocrit; hydration status can affect hgb levels and make them appear falsely high or low

26
Q

Polycythemia Vera (elevated RBC)

A

Cause
- mutations in JAK 2 gene which causes uncontrollable RBC proliferation

  • results in high # of RBC’s, WBC’s, and plts

Structural Changes
- increased blood viscosity
- hyperactive bone marrow

S&S
- fatigue, headache dizziness; slowere circulation due to thicker blood
- red/flushed skin - due to a lot of RBC’s

Complications
- thrombosis: thick blood can clot
- Splenomegaly: spleen has to filter out increased # of RBC’s; it is overworked and enlarged

27
Q

Anemias

A
  • decreased total # of RBC’s

Caused by:
- increased RBC destruction
- blood loss
- impaired RBC production

cytic - cell size
chromic - hbg/colour

28
Q

Pernicious Anemia (macrocytic; noromochromic)

A

Cause
- deficient B12 and intrinsic factor

Patho
- DNA synthesis impaired = impaired RBC production = magaloblasts

Changes
- large and abnormal RBC

S&S
- weakness, fatigue, paraesthesia, loss of appetitie, abdominal pain, sore tongue
- ↓ RBC, ↓ Hbg, ↓ Hct, ↑ MCV (large size)

29
Q

Iron Deficiency Anemia (microcytic; hypochromic) ; marissa

A

Cause
- insufficient iron

Patho
- inadequate iron to bone marrow = iron deficient RBC’s

Changes
- microcytic - small
- hypochromic: pale

S&S
- fatigue, weakness, SOB, irritability, headache

↓ Hbg, ↓ Hct, ↓ MCV (small), ↓ MCHC, ↓ MCH

30
Q

Beta Thalassemia (microcytic; hypochromic)

A

Cause
- mutation in the HBB gene = reduced or absent globin chain production

Patho
- accumulation of unpaired glob chains = ineffective RBC production

Changes
- microytic
- hypochromic - pale
- bone marrow produced fewer RBC’s
- RBC’s are deformed/dysfunctional

S&S
- minor: asymtompatic
- major - trasnfusion-depednent

31
Q

Sickle-Cell Anemia (normocytic; normochromic)

A

Cause
- mutation in HBB gene = abnormal hemoglobin (hemoglobin S)

Patho
- low oxygen = hemoglobin S polymerizes = causes sickle shape = sticks to vessel walls = vasoocclusion

Changes
- sickle cell shaped
- bone marrow hyperplasia; there is increased demand for RBC production to compensate

S&S
- Chronic: pallor, fatigue, SOB
- Vaso-occlusion: tissue/organ ischemia
- Infetcion risk bc of spleen damage

32
Q

Aplastic Anemia (normocytic, normochromic)

A

Cause
- bone marrow fails to produce enough RBC’s
- due to bone marrow suppression: chemo, radiation

Patho
- damage to bone marrow = stem cell destruction

Changes
- bone marrow is replaced with fat = decrease in HSC cells
- pancytopenia: decreased RBC’s, WBC’s, and platelets

S&S
- Low RBC’s: fatigue, dizziness, SOB
- Low WBC’s: infection risk
- Low plts: bleeding risk

N 2440 (26 decks)

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