BL 2 Flashcards
Define reticulocyte count + absolute reticulocyte count
- Reticulocyte count: % of reticulocytes when 1000 RBCs are counted
- Absolute reticulocyte: %of reticulocyte x RBC count
What anemias are going to be associated w/ decrease in exercise tolerance?
Any of them, but mainly Iron deficiency, Anemia due to renal dysfunction
How is hepcidin regulated, and what does it do?
Hecidin is released from hepatic cells during high iron intake or infection/inflammation –> increased accumulation of ferritin –> lower plasma iron
(save it for a rainy day or keep away from bad guys)
Where does absorption of Iron from diet take place? What form of Fe is it in?
duodenum
Ferric iron arrives at duodenum -> converted to Ferrous iron (via surface reductase) -> gets absorbed as Ferrous ion (via DMT1 transport) then
Which anemia is associated with sore tongue?
B12 and folate deficiency
Erythropoietin (EPO) made by what in response to what?
Made by kidney cells in response to hypoxia and promotes erythropoiesis
Granulopoiesis makes what 3 types of granulocytes? Via what growth factor?
Neutrophils, Eosinophils, Basophils
via G-CSF or GM-CSF
*GM = Granulocyte-monocyte
IL-5 Promotes production of which granulocytes?
eosinophils
*count fingers
IL-3 Promotes production of which granulocytes?
basophils
*count fingers
order of progression of the different precursor and mature cell types in erythroid maturation
HSC -> CFU-GEMM (pluripotent stem cell) -> BFU-E (progenitor) -> CFU- E (progenitor) -> Pronormoblast -> basophilic normoblast -> polychromatophilic normoblast -> orthochromatic normoblast -> reticulocyte -> erythrocyte
order of progression of the different precursor and mature cell types in granulocytic maturation
HSC > CFU-GEMM > CFU-GM/G > myeloblast > promyelocyte > myelocyte > metamyelocyte > band > granulocyte (basophil, neutrophil, or eosinophil)
order of progression of the different precursor and mature cell types in monocytic maturation
HSC > CFU-GEMM > CFU-GM/M > Monoblast > Promonocyte > Monocyte > Macrophage
order of progression of the different precursor and mature cell types in megakaryocytic maturation.
HSC > CFU-GEMM > CFU-Meg > Megakaryoblast > Promegakaryocyte > megakaryocyte > platelet
When looking at a bone marrow biopsy, what is the normal myeloid:erythroid ratio around?
2:1 - 4:1
Does BM hyperplasia indicate increased destruction or decreased production?
increased destruction
- Growth factors should signal marrow to make more of what is being destroyed
What would CML and leukemoid rxns indicate in peripheral blood smears?
increased blood neutrophils indicating hyperplasia
Would MCV be high or low in B12/Folate deficiency anemias?
High
deficiency -> impaired DNA synth > cell cannot progress from G2 to M stage. So cell continues to grow w/o division
examples of PMN cells
Neutrophils, basophils, eosinophils
(granulocytes) - cell whos nucleus is lobulated due to granules
What is the opposite of an immunogen?
Toleragen
delivered antigen that does not = immune response AND furthermore prevents immune response to subsequnt exposure to immunogen.
How must the antigenic determinant of an antigen fit the lymphocyte receptor (at hypervariable region) to be activated? (3 things must happen)
- Fit must be specific
- Nearby receptors simultaneously bound by antigen
- Other cell surface molecules costimulated
humoral vs cell mediated immunity
a. Humoral: this is the antibody mediated response,
i. Occurs extracellularly where all the bacteria etc. live.
ii. B lymphocytes are the main cells involved.
iii. B cells transform into plasma cells which secrete antibodies. Cytokines are also released.
iv. Can be transferred by serum.
b. Cell mediated immunity:
i. T lymphocytes become activated → activate macrophages, NK cells, and cytotoxic T lymphocytes.
ii. Cytokines are released when the T cells become activated. Not transferred by serum.
How can malignancies/sepsis result in anemia?
which cytokines are involved?
-Malignancy/sepsis > TNF > ↓ iron store availability > ↓ production of EPO > ↓ Erythropoiesis
–Malignancy/sepsis > INF-β ↓ erythropoiesis
How can chronic infection/inflammation result in anemia?
which cytokines are involved?
- IL-1 ↓ iron mobilization -> ↓ production of EPO
- IL-6 > high hepcidin
- INF-γ -> ↓ erythropoiesis
How can renal insufficiency result in anemia?
↓ EPO made in juxtaglomerular region of kidneys -> ↓RBC production = anemia