erythropoiesis Flashcards
hematocrit definition
Relative vol of RBC out of total blood vol
Erythrocytes (out of whole blood)
Ht in Male
46%
Ht in female
42%
RBC function
- Resp gas transport
- Contain Hb, transport O2
- Contain carbonic anhydrase, transport CO2
- Buffer pH in blood
shape of RBC
- Biconcave
- Diameter: 7.5um
- Thickness: 2-1um
feature of RBC
○ Large SA/vol ratio
○ Easy diffusion of O2
○ Flexible (cap 3-4um)
○ Smooth flow through stack formation
other values of RBC??
- 99.9% of formed elements
- ~45% of blood vol
○ M: 5.2 x 10* 9 RBC/mL
○ F: 4.7 x 10* 9 RBC/mL - RBC lifespan: 100-120 days
RBC composition and numbers
- 97% Hb
- 25-30 x 10* 12 RBC/ human
- 2.5 x 10* 8 Hb molecules/ RBC
○ 1 RBC transport 10*9 O2 molecules
globin
4 folded pp chains
2 α chains
2 β chains
Aa seq determine affinity to O2
Heme
a. Pigment
b. Each heme grp 1 Fe, bind 1 O2 molecule
c. Weak, reversible binding (easy to diffuse)
number of O2 binding 1 Hb
1 Hb = 4 chains = 4 heme = 4 Fe = 4 o2
colour of bood
name of Co2 bound Hb
oxyHb: bright red
deoxyHb: dark red
CARBAMINOHb
Erythropoiesis rate
- Generate erythrocytes 25-30x10*12 RBC/human
- Replace RBC: 2-3X10*6 RBC/s
fetus erythropoiesis
yolk sac —-> liver, spleen, lymph node
<5yo erythropoiesis
all bone marrow
5-20 yo erythropoiesis
bone marrow of ribs, sternum, vertebrae, proximal ends of long bones
> 20 yo erythropoiesis
bone marrow in ribs, sternum, vertebrae
erythropoietin release (hormone)
○ Release and RBC prod regulated by tissue oxygenation
- Decr O2 delivery to kidney
- Decr blood flow to kidney
- Incr tissue demand for O2
- Anemia
- Blood donation
○ Release hormone, incr rate of erythropoiesis - Once O2 delivery to kidney is sufficient, kidney decr output
effect of erythropoietin
- Growth factor
- Enhance proliferation rate of proerythroblasts and erythroblasts
- Enhance Hb synthesis
- Incr RBC production (30x10*6/s)
- 90% secreted by kidneys, 10% in liver
WHY Androgen (M) enhance erythropoietin
higher RBC conc than F
how does erythropoiesis process work
- Stimulate hematopoietic stem cells to form proerythroblast
- Ribosome synthesis in early erythroblast
- Hb accumulation in late erythroblast & normoblast
- Eject NUCLEUS from normoblast = form reticulocytes
a. 0.8-1% reticulocyte
b. (indicative of erythropoiesis) - Continue Hb synthesis, leave bone marrow, complete differentiation to mature erythrocytes in blood
when is RBC broken down
- Self destruct, lifespan of 100-120days
- worn-out
how is RBC broken down
- Lack protein synthesis, makes mem fragile + Hb degrade
- Rupture in spleen tiny vessels (3um diameter)
- Macrophage take up dying RBC/ components
what is recycled in RBC and where
Fe recycled. Reused in BONE MARROW/ stored in LIVER
what is metabolised from RBC and where
Hb split –> 4 heme + 4 globulin (a,b chains)
○ Globulin metabolised into AA, released into circ
○ Heme grp degraded to yellow pigment, bilirubin
- Excreted via liver and bile –> urine and feces
- Excess bilirubin = jaundice
end pdt of rbc
heme – degraded into bilirubin
globulin – meta into aa
Fe – recycled, liver, bone marrow
Anemia
reduction of Hb/ erythrocytes below normal capacity of blood to carry O2
sx of anemia
blood O2 lvls cannot support normal metabolism, leads to
○ Fatigue, pale, SOB, chills
○ Low RBC, more lq blood, rush too fast into tissues, release little O2 ○ Hypoxia: widens blood vessels and reinforce effect ○ Incr workload for heart, cardiac arrest risk
types of anemia
HARN TES
nutritional
aplastic
renal
hemorrhagic
sickle cell
Erythroblastosis fetalis
thalassemia
nutritional
Dietary deficiencies of factors needed for erythropoiesis
□ Fe, folic acid, B12
Pernicious anemia: lack of vit B12, intrinsic factor
Aplastic
Failure of bone marrow to make adequate number of RBC
- Radiation damage or chemo
Renal
Kidney disease, lack of erythropoietin
- Not responsive/ unable to produce
Hemorrhagic
Due to loss of sig amt of blood vol and RBC
malaria
Plasmodium falciparum amplify in RBC, ruptures them. Offspring invades new RBC
sickle cell
Mutation in b-globin gene, cause Hb to aggregate in low O2 conditions
Erythroblastosis fetalis
Rh+ RBC of fetus are destroyed by anti-Rh antibodies of a Rh- mother
- mother’s second or later pregnancies. If she is ever carrying another Rh+ positive child, during birth, Rh- antibodies attack child
Thalassemia
blood disorder, genetic
Low production of Hb
excess RBC
Polycythemia/ erythremia
Excess RBC in circulating erythrocytes, elevated hematocrit
effect of polycythemia
cause viscous blood, potentially plug capillaries, insuff O2 delivery to tissues
caused by primary, secondary polycythemia, dehydration
primary causes of polycythemia
§ Tumour or tumour-like condition in bone marrow
7-8 X 10*9 RBC/mL
secondary causes of polycythemia
§ Erythropoietin-induced, adaptive mechanism to improve O2 carrying capacity blood
□ People living at high altitudes.
6-7 x 10*9 RBC/mL
