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Cell Biology > hematology -rbc > Flashcards

hematology -rbc Flashcards

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1
Q

Where are the precursor stem cells for rbc produced?

A

hematopoietic stem cells (HSC) are produced in the bone marrow

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2
Q

What 2 lineages do the HSC differentiate into?

A
  • Myeloid: proerythroblast, myeloblast, monoblast, megakaryoblast
  • lymphoid: lymphoblast
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3
Q

What percentage of total blood volume is cellular components (RBC)?

A

about 45% of total blood volume is RBC (hematocrit)

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4
Q

Why is the structure of RBC bi-concave?

A
  • maximize surface area
  • maximize gas diffusion
  • Bi-concave shape also allows for equal access of hemoglobin to oxygen.
  • fold and squeeze through sinusoids.
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5
Q

Where is RBC produced through out life span?

A
  • middle trimester: RBC is produced in the liver/spleen
  • last month of gestation: rbc is produced in bone marrow
  • Birth to 5 yrs: rbc produced in all bones
  • age >20yrs: no rbc production in long bones. only produced in vertebrae, sternum, ribs, ilium
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6
Q

What is the process of rbc production/maturation?

A

pluripotent stem cell stimulated by IL-3 (inflammation) and EPO –> differentiation of HSC down the myeloid line to proerythroblast –> erythroblast cell –> basophil –> reticulocyte (no nucleus) –> erythrocyte (mature rbc) (100-120days life span)

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7
Q

Why do rbc have such a short life span?

A
  • Mature RBC contain cytoskeleton that holds the shape of the cell, but do not contain nucleus. So when the cytoskeleton eventually breakdowns, there is no way for the cell to replicate it as it lacks nucleus.
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8
Q

How much blood is made every day to maintain homeostasis?

A

1% of the blood needs to be made everyday as we lose 1% of blood everyday. So about 1% of reticulocytes are released everyday to make up for the blood loss.

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9
Q

Under what conditions do reticulocyte counts increase?

A

-increase: when there is lack of blood oxygen for example when I cut myself and lose blood. The local tissue will release IL factors (especially IL 3) to stimulate more EPO that will terminally differentiate more stem cells to become erythrocytes.

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10
Q

What are the functions of the erythropoietin (EPO)?

A
  • 90% of EPO is secreted by the kidney from the peritubular cells when there is decrease in tissue oxygen.
  • terminally differentiate HSC into proerythroblast
  • speed up the rbc development process
  • dump all the reticulocytes in the blood
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11
Q

What disease states might increase erythropoietin secretion?

A
  • sickle cell anemia (less oxygen carrying capacity)

- COPD (less oxygen, so more rbc will be produced in response to hypoxia)

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12
Q

What disease state might decrease EPO secretion?

A
  • ESRD

- chronic kidney disease

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13
Q

How does chronic kidney disease affect EPO secretion?

A
  • In CKD, there is more production of collagen in injured renal tubules which decreases the amount of EPO producing fibroblast therefore decreasing EPO secretion
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14
Q

What is the function of RBC?

A
  • pH buffer
  • CO2 transport
  • O2 transport
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15
Q

How does RBC transport Co2?

A
  • binding of Co2 to peptide of rbc decreases affinity of o2 binding to rbc.
  • Co2 is converted into H2CO3 (carbonic acid) which the dissociates into HCO3- (bicarbonate) and H+ ions through carbonic anhydrase. HCO3- is then diffused out into the plasma (buffer rbc by binding to acids) in exchange of chloride ions, while H+ binds to hemoglobin (act as a pH buffer)
  • 70% of Co2 is transported as HCO3-
  • CO2 can bind to Hg (23%) carbinohemoglobin
  • CO2 dissolves in plasma, interacts with water to form gases and water (7%)
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16
Q

How does hemoglobin transport O2?

A
  • 1 HGB molecule has 4 heme molecules containing iron and 4 hgb chains (alpha, beta, gamma, delta) that can each bind to oxygen molecule, resulting in 4 oxygen molecules binding to 1 hgb molecule and being transported throughout the body.
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17
Q

How is hgb affinity for o2 effected?

A
  • Affinity for o2 is affected by temp and pH level
  • low pH and high temp shifts the o2 affinity graph to the right (decreases the o2 affinity on hgb so more o2 is distributed to the tissue).
  • high pH and low temp shifts the graph to the left (increases o2 affinity of hgb so there is more o2 on hgb)
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18
Q

How does fetal hemoglobin o2 affinity affect mom’s hemoglobin o2 affinity?

A
  • fetal hgb has a high o2 affinity so it will take oxygen from the maternal hgb, resulting in left shift in curve for fetal hgb vs right shift in curve for maternal hemoglobin
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19
Q

How is hemoglobin S formed and what does it result in?

A
  • hemoglobin S mutation causes sickle cell disease.
  • genetic mutation in beta chain changes the charge on hgb’s surface and changing the shape of rbc into more rigid sickle like structure, resulting in aggregation and decrease o2 carrying and transport capacity.
20
Q

What is thalassemia?

A
  • genetic mutation to hemoglobin that results in loss of one or two beta chains, therefore decreasing O2 carrying capacity and resulting in anemia. Would see small target cells in the blood smear.
21
Q

What is Hgb F and why does it help in sickle cell disease?

A
  • Hgb F (fetal hemoglobin that is not susceptible to sickle cell disease) concentration increases in people with sickle cell disease, therefore increasing O2 affinity for hgb and more o2 being transported through the blood.
22
Q

How does RBC act as a pH buffer?

A
  • hgb on rbc is going to bind to plasma co2, and excreting it out of the cell, preventing the cell from becoming acidic.
23
Q

How much is the total body iron and where is it stored?

A
  • 4-5 grams (total)
  • 65% in hgb
  • 15-30% in liver as ferritin
  • 0.1% bound to transferrin
24
Q

What is a cause of iron deficiency anemia?

A
  • chronic blood loss
25
Q

How much of the iron intake is absorbed vs non-absorbed?

A
  • only about 3-15% of Fe intake is absorbed as it has to be modified in order to be absorbed
  • 85-97% of Fe intake is not absorbed and is excreted out in feces
  • mostly absorbed in the small intestine
26
Q

What is hepcidin and how does it affect iron absorption in the small intestine?

A
  • Hepcidin stops the ferroportin 1 from absorbing iron.
  • less iron in body –> liver down regulates hepcidin –> more iron is absorbed
  • too much iron –> liver up-regulates hepcidin –> prevents iron absorption.
  • increase in inflammation –> increase in hepcidin –> less iron released/absorbed in body –> secondary iron deficiency
27
Q

What results in abnormal iron loss?

A
  • hemolysis
  • acute blood loss
  • chronic blood loss
28
Q

How does inadequate iron levels affect rbc?

A
  • less iron –> hgb formation impaired –> small/microcytic rbc with low hgb concentration/pale looking (hypochromic)
29
Q

What does deficiency of B12 or folate leads to?

A
  • Macrocytosis cells in blood smear (leads to megaloblastic anemia) due to large nucleus because B12 is necessary for nuclear maturation in rbc
30
Q

What is vitamin B12 important for and where is it stored?

A
  • necessary for nuclear maturation in RBC

- stored in liver (3 yrs worth)

31
Q

How does spleen result in rbc death?

A
  • old rbc will be pushed out through small opening in endothelium and will burst. (“self destruct”)
  • new rbc will be able to pass through because they can deform as their cytoskeleton is intact
32
Q

How is rbc recycled?

A
  • rbc bursts
  • contents phagocytized by macrophages in spleen and liver
  • iron is recycled and carried by transferrin to liver
  • free hgb binds to H
  • porphyrin ring converted to bilirubin
33
Q

What is anemia?

A
  • defined as hemoglobin deficiency

- macrocytic, microcytic, normocytic

34
Q

What are the causes of microcytic anemia?

A 
(MCV <80)
(TAILS)
-THALASSMIA
-ANEMIA OF CHRONIC DISEASE (ACD)
-IRON DEFICIENCY ANEMIA  
-Lead poisoning
-Sideroblastic anaemia
35
Q

What are some of the causes of normocyctic anemia?

A 
MCV (80-100)
(ABCD)
- acute blood loss
- Bone marrow failure
- ANEMIA OF CHRONIC DISEASE
- destruction of rbc (HEMOLYSIS)
36
Q

What are the causes of macrocyctic anemia?

A 
MCV(>100)
(FATRBC)
- fetus (pregnancy)
- alcohol
- hypothyroidism 
- reticulocytosis
- B12/FOLATE DEFICIENCY  
- Cirrhosis
37
Q

How to tell if someone is developing new anemia?

A
  • red cell distribution width
    should increase because the size of new rbc will vary (increase in smaller/larger rbc amount suggests that someone is developing new anemia)
38
Q

What are the causes of iron deficiency anemia?

A
  • wasting of iron or poor absorption of iron
  • could be due to chronic blood loss
  • diet
  • results in smaller MCV
39
Q

What are the causes of aplastic anemia?

A
  • extrinsic factors such as radiation that could potentially damage the bone marrow, therefore reducing the amount of all blood cells production.
  • could be in normocytic anemia because there is no change in rbc size
  • treatment = bone marrow transplant
40
Q

How to differentiate between vitamin B12 deficiency anemia or folate deficiency anemia?

A
  • Vitamin B12 results in elevated methylmalonic acid and irreversible neurological damage
41
Q

What are the causes of anemia of chronic disease?

A
  • kidney disease –> no EPO –> no new rbc –> normocyctic anemia
  • inflammation –> increase hepcidin and inhibit EPO release –> inhibits iron release from liver and EPO from kidney –> limited iron
42
Q

What are the causes of hemolytic anemia?

A
  • destruction of rbc
  • hereditary (G6PD deficiency)
  • acquired (infections such as malaria, secondary due to liver or renal disease)
43
Q

What is polycythemia?

A
  • too many rbcs

- Hct >50%

44
Q

What is primary polycythemia?

A
  • polycythemia vera

increased production of rbc and all other cells in bone marrow but EPO levels LOW

45
Q

What is secondary polycythemia?

A
  • erythrocytosis

increase in RBCs in response to prolonged hypoxia to compensate by increasing oxygen transport, EPO levels HIGH

Cell Biology (9 decks)

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