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B4W1 > PBL 2 > Flashcards

PBL 2 Flashcards

1
Q

what type of cell is the first precursor for blood cells? what does the differentiate in to?

A

long term multipoint haematopoietic stem cells

short term multipotent haematopoietic stem cells

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2
Q

what can short term haematopoietic stem cells differentiate in to?

A

multipoint progenitor cells

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3
Q

what can multipoint progenitor cells differentiate in to?

A

common myeloid progenitors and common lymphoid progenitors

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4
Q

what can common lymphoid progenitor cells differentiate in to?

A

dendritic cells, natural killer cells, B lymphocytes and T lymphocytes

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5
Q

what is the tissue equivalent of a B lymphocyte?

A

plasma cells

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6
Q

what can common myeloid progenitor cells differentiate in to?

A

megakaroycte and erythrocyte progenitors

or granulocyte and macrophage progenitors

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7
Q

what can megakaryocytic progenitors differentiate into?

A

megakaryocytic and then thrombocytes

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8
Q

what can erythrocyte progenitors differentiate into?

A

erythrocytes

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9
Q

what can granulocyte and macrophage progenitors differentiate into?

A

mast cells, basophils, neutrophils, eosinophils, monocytes

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10
Q

what can monocytes differentiate into?

A

macrophages and dendritic cells

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11
Q

describe erythropoiesis from the megakaryocyte and erythrocyte progenitor?

A

the megakaryocyte and erythrocyte progenitor differentiates into the proerythroblasts and then early erythroblasts in the bone marrow. the early erythroblast then differentiates into the late erythroblast which then develops into the normoblast. the normoblast extrudes its nucleus and develops into a reticulocyte which leaves the bone marrow and enters circulation. within the blood stream it matures into an erythrocyte.

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12
Q

when does haemoglobin develop?

A

when we see the early erythroblasts as this Is where ribsosome synthesis for haemoglobin begins.

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13
Q

how are the erythrocytes removed when they are old and damaged?

A

macrophages in the spleen, liver and bone marrow engulf the old erythrocytes and break them down.
haemoglobin is broken down into haem and globin which then breaks down into amino acids, bilirubin and iron.
The amino acids will enter back into the circulation and will
travel to the bone marrow for re-use in erythropoiesis. Iron re-enters circulation bound to transferrin, make its way back to the bone marrow for re-use in erythropoiesis. Bilirubin makes its way back to
the liver via an albumin transporter and is excreted as urine or faeces.

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14
Q

where are erythrocytes broken down?

A

spleen liver and bone marrow

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15
Q

in kidney failure why is it common to see anaemia?

A

as the kidneys produce erythropoietin which is required for erythropoiesis.

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16
Q

what is the structure of bone marrow?

A

its found in the marrow cavity of long bones as well as the small spaces in spongy bone. we have red marrow and yellow bone marrow

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17
Q

what do red and yellow bone marrow consist of?

A

red- haematopoietic stem cells and stromal cells

yellow-fat

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18
Q

what happens to the structure of our bone marrow as we age?

A

most of the red marrow turns into yellow, fatty marrow

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19
Q

what can the bone marrow do when you are really anaemic?

A

yellow marrow can turn back to red marrow in order to produce more erythrocytes

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20
Q

where is the spleen?

A

under our 9-11 ribs in the left upper quadrant under the diaphragm.

21
Q

what is the blood supply of the spleen?

A

the splenic artery off the coeliac trunk and the splenic vein that goes ion to the inferior mesenteric artery.

22
Q

where do vessels enter and leave the spleen?

A

the hilum

23
Q

describe the blood vessel structure within the spleen

A

the splenic artery enters the spleen and branches to form central arterioles and then branches again to form end arteries.

24
Q

describe the histology of the white pulp of the spleen

A

surrounding the end arteries is the periarteriole lymphatic sheath, surrounding this is the marginal zone and within this we get follicles.

25
Q

describe the histology of the red pulp of the spleen?

A

end arteries have no walls so fluid flows into surrounding tissues and are picked up by the venous sinus system. between the end arterioles and the venous sinuses there are cords containing macrophages. the venous sinuses then join up with collective veins which drain into the splenic vein.

26
Q

what is found in the periarteriole lymphatic sheath, marginal zone and follicles?

A

periarteriole lymphatic sheath- T cells and macrophages
marginal zone- macrophages
follicles- inactive B cells

27
Q

What is the function of the red pulp of the spleen?

how?

A

destroying and filtering abnormal, unhealthy or old RBCs.
the slits between the endothelial cells of the venous sinus only allow healthy RBCs through as they are the correct shape.

28
Q

what is the function of the white pulp of the spleen?

A

fighting infections, producing an immune response and producing antibodies.

29
Q

what is co-stimulation?

A

when B and T cells activate each other. e.g. when B cells pick up a pathogen in the follicle and present it to the T cell in the periarteriole lymphatic sheath.

30
Q

what do activated B cells become?

A

plasma cells

31
Q

what is the spleens role with platelets?

A

1/3rd of platelets stay in the spleen so its an important organ for maintaining efficient levels of platelets in the blood

32
Q

what is the mononuclear phagocyte system?

what are the functions?

A

part of the immune system that consists of phagocytic cells in reticular connective tissue.
formation of new RBCs and WBCs, destruction of old RBCs and WBCs, formation of plasma proteins, formation of bile pigments, storage of iron.

33
Q

where is iron stored? what is it stored as?

A

if excess due to catabolism of haem then in the liver.

it is stored as ferritin

34
Q

what is thrombopoietin?

A

a glycoprotein hormone produced by the liver and kidneys that regulates the production of platelets. it stimulates the production and differentiation of megakaryocytes.

35
Q

what are colony-stimulating factors?

A

a family of cytokines for stimulating WBC formation

36
Q

what are 4 causes of bone marrow failure?

A

haematopoietic cell damage, maturation defects, differentiation defects, bone marrow infiltration

37
Q

what is polycythemia? what is an implication? what is the main cause?

A

an increase in the number of RBCs in the blood. this causes the blood to be thicker so can cause clots
a mutation in the JAK-2 protein

38
Q

what is a venesection? what is it used to treat?

A

taking blood to reduce the RBC count. polycythemia

39
Q

what is hydroxycarbamide? what is it used to treat?

A

an orally administered drug for chemotherapy treatment that can lower the RBC and platelet count.
it is used to treat polycythemia
it uses cytotoxic drugs to destroy immature blood cells so it prevents growth and division of new cells

40
Q 
what is P-32? 
what is it used to treat?
how does it work?
how is it administered?
is it commonly used?
A

radioactive form of sodium phosphate, a type of internal radiotherapy
polycythemia
the bone marrow absorbs the radioactive phosphorous and receives a dose of radiation which slows down the blood cell production
administered as an injection
only used when other drugs/methods of treatment aren’t working or are causing side effects

41
Q

describe the role of the JAK-2 gene?

A

when EPO reaches the bone marrow it locks onto a receptor site on the surface of the stem cell which in turn locks onto the JAK-2 protein. this allows the JAK/STAT pathway to happen which tells the nucleus to grow and produce more RBCs.

42
Q

what are myeloproliferative disorders?

how do they come about?

A

when the body makes too many blood cells in the bone marrow so it can create problems for blood flow. often due to a mutation in the JAK-2 gene.
the JAK-2 gene results in a mutation which causes an amplification of the signal that EPO brings to the receptor. this excessively strong signal causes the body to produce too many blood cells

43
Q

what are macrophages of the CNS called?

A

microglia

44
Q

what is iron stored as when it is in an over-load state?

A

hemosiderin

45
Q

describe the point JAK-2 mutation?

A

valine is replaced for phenylalanine

46
Q

can folic acid worsen a vitamin B12 deficiency?

A

yes

47
Q

what can hydroxocobalamin treat?

A

cyanide poisoning and polycythemia

48
Q

what is the main immune cell found in the tonsils?

A

B cells

B4W1 (10 decks)

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