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physiology > Rec blood cells etc chapter 33 > Flashcards

Rec blood cells etc chapter 33 Flashcards

1
Q

Functions of rbc

A

its function is to transport hemoglobin. Which in turn trasports oxygen from lungs to the tissues of the body
It has carbonic anhydrase, at enzyme that catalyses the reversible reaction between co2 and water, allows co2 to be carried in rbc as bicarbonate ions and diffuse out of blood
It act as an acid base buffer

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2
Q

Shape and size of RBC

A

shape is biconcave

Diameter is 7.8 micrometer, thickness is 2.5 micrometers and volume is 90-95 cubic micrometers

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3
Q

Concentration of rbc in blood

A

5200000 in male and 4700000 in female (-/+300000)

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4
Q

Quantity of hemoglobin in blood

A

rbc can concentrate hemoglobin in their cell upto 34g/100ml
When hematocrit and the quantity of hemoglobin in each respective cell in normal, men have 15g hemoglobin /100ml and 14 for women

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5
Q

Quantity of hemoglobin in connection with O2

A

each gram of hemoglobin can combine with 1.34 ml of O2

Which means 20milimleters of oxygen can be carried with hemoglobin in 100milileetrs of blood and 19 for woman

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6
Q

Production of rbc

A

Early embryonic stage it is produced in yolk sac, middle trimester of gestation it is produced in liver and also in spleen and lymph nodes, last month of gestation and after birth to is made in bone marrow

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7
Q

What bones stop making rbc after 20 and except

A

Long bones except proximal part of humeri and tibiae all long bone marrow stops making rbc cause it becomes fatty

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8
Q

What bone marrow produce rbc aftef 20

A

Bone marrow of membranous bone like sternum, ribs , vertebra, ilia

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9
Q

Multipotential hematopoietic stem cells

A

the blood cells originate in the home marrow from one kind of cells which are multipotential hematopoietic stem cells

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10
Q

Committed stem cells ?

A

Cells reproduced from MHSCm differentiate to form other type of cells, their intermediate stage cells are exactly like multipotential stem cells, even though they are committed to a particular line of cells they are called committed stem cells

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11
Q

Growth inducers

A

growth and reproduction of committed stem cells are controlled by proteins called growth inducers

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12
Q

Example of growth inducers

A

interleukin-3

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13
Q

Differentiation inducers

A

only growth and reproduction is controlled by growth inducers but differentiation is controlled by differentiation inducers. Which differentiate only one type of committed stem cells

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14
Q

Genesis of rbc

A 
proerythoblast 
Basophil erythroblast 
Polychromatophil erythroblast 
Orthrochromatic erthroblast 
Reticulocyte 
Mature erythroblast
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15
Q

Tissue oxygenation describe

A

the conditions which decrease the amount of oxygen transported to tissues increases the rate of RBC productions

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16
Q

Eg of tissue oxegenation

A

people who are anemic or destruction of major part of bone marrow due to xray therapy
Or people living in High altitude areas
People who have prolonged cardiac failure of lung diseases
Any tissue hypoxia case

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17
Q

Stimulus for rbc profuction is a circulating hormone called

A

erythropoietin, a glycoprotein with a molecular weight 34k

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18
Q

where are 90% of erythropoietin are formed

A

mainly in the kidneys and the rest are formed in liver

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19
Q

studies shows the erythropoietin is made in what cellsf

A

fibroblast like interstitial cells surrounding the tubules in cortex and outer medulla . renal epithelial cells also produce erythropoietin.

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20
Q

renal tissue hypoxia leads to?

A

increases tissue level of hypoxia induced factor-1 which serves as a transcription factor for a large number of hypoxia induced genes that includes erythropoietin gene.

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21
Q

explain briefly erythropoietin synthesis from the gene?

A

hypoxia induced factor binds to hypoxia response element, inducting transcription of messenger RNA and ultimately making erythropoietin.

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22
Q

important effects of erythropoietin?

A

it induces the formation of proerhythroblast from hemopoietic stem cells
it increases the speed of the process of formation of mature erythroblast.

23
Q

defecincy of virtamin B12 or Folic acid causes what and why?

A

it leads to maturation failure in the process of erythropoiesis. IT is because vitamin B12 and folic acid are essential for the synthesis of DNA, as they play a role in the formation of thymidine triphosphate.

24
Q

pernicious anemia is causes by what?

A

basic abnormality in an atrophic gastric mucosa that fails to produce normal gastric secretions.
the parietal cells of gastric glands fail to produce a glycoprotein called intrinsic factor which joins with the B12 make it available for absorption.

25
How the intrinsic factor make the vitamin B12 available ?
it binds with the vitamin and protects it from getting digested by GIT secretions Still bounded with The vitamin it binds to specific receptors on the brush border membrane of iliac It is then transported to the liver where it is stored
26
People who cannot absorb folic acid of intestinal disease called
sprue leads to maturation failure of RBCs.
27
Basic chemical steps in the formation of hemoglobin?
Succinyl-CoA made in the kerbs metabolic cycle joins with a Glycine to make pyrrole molecule 4 of these pyrrole molecule join together to form protoporphyrin IX, which then joins with iron to form heme This heme joins with a polypeptide chain called globin synthesized by ribosomes to form hemoglobin chain which 4 of these join together to form hemoglobin
28
Sickle cell anemia
the valine is substituted by glutamic acid in each of the two beta chains at one point, makes crystals inside rbc when exposed to low level of o2 which are spiked and rupture the cell membrane leading to sickle cell anemia
29
How oxygen combines with o2
it does not combined with the two positive bonds of iron but combined with the so called coordination bond loosely. Also it joins in its molecular form
30
Total quantity of iron in body and % found at different area of body
4-5 grams is present in body 65% is in the form if hemoglobin 4% is in myoglobin 1% in other heme compounds for intracellular oxidation 0.1% is found combined with protein transferrin in blood plasma 15-30 % Store in the reticuloendothelial system and liver parenchymal cells in the form of ferritin
31
How iron is stored
- in the form of transferrin in blood plasma - stored in liver hepatocytes and reticuloendothelial cells of bone marrow - storage iron which is stored in the form of ferritin - insoluble form hemosiderin
32
What happens when iron falls low in blood
The ferritin pool is removed easily and transported in the form of transferrin in the blood plasms to the place where it is needed
33
Special characteristic of transferrin
it binds to the receptors on the cell membrane of erythroblast in the bone marrow, and endocytosed by the erythroblast.
34
Hypochromic anemia
people who doesn't have transferrin in their body cannot transfer iron like this to erythroblast
35
absorption of iron in interstitial tract
Liver secretes apo transferrin though bile into the duodenum which binds with iron and hemoglobin and myoglobin. This combination is called transferrin, it binds with receptions on intestinal epithelial cells, pinocytosis occurs and releases into blood as plasma transferrin
36
Rbc of enzymes which do what function
maintains the pliability of the membrane Maintains membrane ion transport Keep the iron if ferrous form not ferric Prevents oxidization of protein inside the rbc
37
Destruction if hemoglobin
The hemoglobin is phagocytosed by macrophages mostly Kupffer cells of liver or macrophages of sleep and bone marrow. The iron is returned back to blood for new rbc formation or stored in ferritin form Porphyrin is changed into bilirubin
38
what other hormones stimulate the formation of erthypoietin
norepinephrine, epinephrine and prostaglandin
39
microcytic, hypochromic anemia,
When chronic blood loss occurs, a person frequently cannot absorb enough iron from the intestines to form hemoglobin as rapidly as it is lost. RBCs that are much smaller than normal and have too little hemoglobin inside them are then produced, giving rise to microcytic, hypochromic anemia
40
anemia due to blood loss
After rapid hemorrhage, the body replaces the fluid portion of the plasma in 1 to 3 days, but this response results in a low concentration of RBCs. If a second hemorrhage does not occur, RBC concentration usually returns to normal within 3 to 6 weeks
41
what is bone marrow aplasia
lack of functioning of bone marrow
42
causes of aplastic anemia
- radiation and chemotherapy - toxic chemicals like insecticides and benzene in gasoline - autoimmune disease called lupus erythematosus
43
idiopathic aplastic anemia
half of aplastic anemia causes doesnt know the cause a condition called idiopathic aplastic anemia
44
megaloblastic anemia
Thus, atrophy of the stomach mucosa, as occurs in pernicious anemia, or loss of the entire stomach after surgical total gastrectomy can lead to megaloblastic anemia. Also, megaloblastic anemia often develops in patients who have intestinal sprue, in which folic acid, vitamin B12, and other vitamin B compounds are poorly absorbed
45
what is hemolytic anemia
hereditary disease that make rbc fragile so they get ruptured easily specially when going through splenic red pulp
46
hereditary spherocytosis
the RBCs are very small and spherical rather than being biconcave disks. These cells cannot withstand compression forces because they do not have the normal loose, baglike cell membrane structure of the biconcave disks. Upon passing through the splenic pulp and some other tight vascular beds, they are easily ruptured by even slight compression.
47
sickle cell anemia is present in what people and what %
0.3 to 1% of west africans and american blacks
48
sickle cell anemia has what type of hemoglobin
abnormal hemoglobin called hemoglobin S with faulty beta chains
49
what happens in sickle cell anemia
When this hemoglobin is exposed to low concentrations of oxygen, it precipitates into long crystals inside the RBC. These crystals elongate the cell and give it the appearance of a sickle rather than a biconcave disk. The precipitated hemoglobin also damages the cell membrane, so the cells become highly fragile, leading to serious anemia.
50
sickle cell disease crisis
when rbc is exposed to low o2 level, the sickling happens which inturn decreases the oxygen to low level and rbc rupture and it goes on
51
erythroblastosis fetalis
when rh positive RBC are attacked by antibodies from Rh negative mother so the rh positive positive rbc become fragile and rapidly rupture in this case the baby is born anemic
52
secondary polycythemia
in the sate of hypoxia like in people living at high altitudes or in cardiac failure, rbc producing organs make rbcs more than the normal amount which is 6-7 million/mm2 30% more than normal
53
common type of secondary polycythemia
called as physiological polycythemia in which people living at high altitude 14000 to 17000 feet have large quantities of rbc in their blood
54
polycythemia vera
the RBC count may be 7 to 8 million/mm3 and the hematocrit may be 60 to 70 percent instead of the normal 40 to 45 percent. Polycythemia vera is caused by a genetic aberration in the hemocytoblastic cells that produce the blood cells. The blast cells no longer stop producing RBCs when too many cells are already present

physiology (25 decks)

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