Lec 23 Flashcards
Hematopoiesis
Blood cell synthesis in the bone marrow
Hemostasis
blood clotting
blood is – percent of body weight
7
what kind of tissue is
connective
how many liters in male and female
5l and 4l
explain blood tissue compostion
1- watery ECM (plasma)
2- RBC (erythrocytes)
3- WBC (leukocytes)
4- Platelets
ecm bone vs blood
bone=rigid
blood=watery
RBC main function
gas transport
WBC main function
immune function
platelets main function
hemostasis
platelets are
cellular elements that used to be a giant cells
not cells
hematocrit
percentage of total blood volume that is occupied by RBC
hematocrit in males
40-54
hematocrit in female
37-47
plasma volume percentage
58%
white cells percentage
<1%
white cell physical function in blood
buffer layer
plateletes and white cells between plasma and rbc
whithin active bone marrow – become rbc and rest become wbc
25%
rbc lifespan
120 days
wbc lifespan
6-12 hours
—– smashes to produce platelets
megakaryocyte
hematopoietic stem cell can become
wbc
rbc
platelets
cytokines
proteins released from 1 cell that affect activity of others
cytokines involved in hematopoiesis
1- erythropoietin (ETO)
2- thrombopoietin (TPO)
erythropoietin site of production and influence growth on
produce in kidney
influence on growth rbc
thrombopoitenin site of production and influence growth on
produce in liver
influence on growth wbc
hypoxia
low level O2 in arterial blood
hypoxia sensed by
kidney
hypoxia sensing by kidney reaction
1- kidney mkes EPO
2- EPO act on progenitor cell in bone marrow to produce erythropoiesis
3- increase #of rbc
4- increase O2 transporting capability
RBC contain
hemoglobin
hemoglobin has – subunit
4
each subunit hemoglobin is
porphyrin ring with an iron atom in the center
Fe binds to
O2
FE binding to O2 is
cooperative
Anemia
low RBC count
result anemia
1-decreased hemoglobin content
accelerated RBC loss
reduce o2 carrying capacity
decreased RBC production
accelerated RBC loss
blood loss
hemolytic anemia
RBC degradation > production
Anemia reasons
1- genetic (sickle cell anemia)
2- malaria
Decreased RBC production
aplastic anemia
drug/radiation
dietery insufficiencies
iron/folic acid/vit B12
Malaria
infect normal RBC and kill it
malaria cannot infect sickle cell anemia
hemorrhage
loss of the blood from the vessels
hemostasis
keeping blood inside the blood vessel
4 step of hemostais
1- vasoconstriction
2- platlet plugformation
3- coagulation (forming of blood)
4- dissolution of clot (fibrinolysis)
plateletplug formation
collagen vessel wall exposed into lumen blood cell
1-exposed collagen binds together
2- activate platelets
3- release of platelet factor
4- factor attract more platelets (positive feedback)
5- platelets aggregation into platelet plug
Coagulation cascade change platelet plug to
fibrous clot
Coagulation cascade of reactions activate enzymes leading to production of
fibrin
coagulation pathway kinds
1- intrinsic pathway
2- extrinsic pathway
intrinsic pathway
involve plasma proteins
Initiated by exposure of collagen
extrinsic pathway
release tissue factor from damaged tissue
release factor is
protein and phospholipid
both pathways of coagulation will activate
factor X
factor X formation will make a positive feedback in
extrinsic pathway
factor x will activate
thrombin from thrombinogen
thrombin activate
fibrin(insoluble) from fibrinogen(soluble)
thrombin will make a positive feedback in
intrinsic pathway
active factor XIII will
produce fibrin cross-links forming mesh-like net
why stepwise reactions of coagulation happens
insures we make clot only when we really need clot
Vasoconstriction happens due to
paracrine signals from endothelium
blood type refers to
aantigens on rbc
antigens are
inherited surface proteins
antibodies will make against
antigens you don’t have
+/- sign in blood group refer to
carry rhesus (Rh) factor antigen
Rh- people only make anti-Rh antibodies if —-
explicitly exposed to Rh+ blood
universal donor is
O-
