Erythrocytes Flashcards
what is blood?
a specialized connective tissue in fluid, extracellular matrix
what comprises blood? (3)
water
electrolytes
protein
what percentage of blood is plasma?
~55%
what is serum?
plasma-clotting factors
what does blood transport? (4)
nutrients
O2/CO2
waste products
hormones
blood functions in both — and —
thermoregulation
homeostasis
what are the three plasma proteins?
albumins
globulins
fibrinogens
what is the bulk of the plasma proteins?
albumins
albumins are synthesized by the
liver
albumins function as transport proteins for
insoluble metabolites
albumins are responsible for maintaining
colloid osmotic pressure in blood vessels
globulins are used as transport proteins for (2)
lipids and heavy metal ions
what are the largest fraction of globulins?
immunoglobulins
what are immunoglobulins?
Ab’s synthesized by plasma cells
fibrinogens are the — proteins
largest
fibrinogens are —
soluble
fibrinogens are synthesized by the —
liver
fibrinogens polymerize to form insoluble
fibrin during clotting
what is fibrin formed from?
prothrombin then thrombin catalyzes fibrinogen into fibrin
what are formed elements?
cells in the blood
what are the three formed elements?
rbc
wbc
platelets
formed elements are formed in bone marrow via —
hemopoiesis
what is hematocrit?
the volume of rbc
why do males have a higher hemocrit?
males are slightly larger so their muscles need more o2
what is polycythemia vera?
genetic neoplasia, which leads to an increase in rbc production
what is the consistency of blood with polycythemia vera?
thick, sludging of blood
what is the buffy coat?
WBCs and platelets
PCV
packed cell volume
hemocrit is about equal to the
PCV, +/- the buffy coat
what is a blood smear?
when a drop of blood is smeared, air dried, stained with modified Romanovsky method
what is hemopoiesis?
the process by which mature blood cells develop from precursor cells
what is erythropoiesis?
red cell production
what is myelopoiesis?
white cell production
hemopoiesis is under the control of —, secreted by the kidney
erythropoietin
hemopoiesis process
begins with pluripotential stem cells which differentiates into several unipotential stem cell lines (CFU)
erythropoiesis stages (5)
stem cell (CFU-E) proerythroblast erythroblast/normoblast reticulocyte mature rbc
where does hemopoiesis occur in adult humans?
vascular sinuses of bone marrow of cert bones
especially flat bones of the skull, ribs, sternum, vertebrae, pelvis, and some long bones
is it estimated that we make about – billion rbc daily
2.5
in the fetus, hemopoiesis first occurs in the — — in the wall of the — — during the first trimester
blood islands
yolk sac
during second semester, hemopoiesis occurs in the – and — — and during the last month of pregnancy in the — —
liver and lymphatic tissue
bone marrow
at the time of birth, hemopoiesis is restricted primarily to the
marrow cavities
the number of active sites — with age
decrease
red bone marrow vs yellow bone marrow
red: active, contains large number of mature rbc
yellow: fatty, inactive
over trends in erythropoiesis (3)
progressive decrease in cell size
loss of nucleus and organelles
increase in hemoglobin
rbc — in mammals
enucleate (remove the nucleus from a cell)
before rbc are released into the blood stream, what must occur?
the nucleus must be extruded and all organelles must degenerate
mature rbc consist of an outer cell membrane containing (3)
cytoplasm, hemoglobin, and a few enzymes
because rbc lack —, they have a limited life span
mitochondria
rbc can only make ATP via
anaerobic glycolysis
senescent rbc are removed from circulation by the
liver and spleen
what are howell-jolly bodies?
occasional, basophilic nuclear remnants visible within the cytoplasm
what are reticulocytes?
immature rbcs with stippled cytoplasm; still have some rRNA
reticulocytes are slightly larger than
mature rbc
what is reticulocytosis?
an increase in reticulocytes in circulation associated with chronic blood loss (hemolytic anemia) aka left shift
older cells are lost quicker than they can be replaced so immature rbc are released more than usual
macrocytes
red blood cells that are larger than normal, immature
when do you see macrocytes?
with vitamin B12 & B9 deficiency
what is megaloblastic anemia?
large numbers of erythrocyte precursors in the peripheral blood
diameter of erythrocytes
6-8 nm
why are erythrocytes biconcave disc shape?
deformability because capillaries are 3-4 nm in diameter, so rbc have to fold in half in order to fit through
what is the primary structural protein in rbc that allows them to unfold?
spectrin
spectrin provides both (2)
resiliency and deformability
spectrin binds to the inner surface of the
plasma membrane
biconcave shape has increase the surface area for
gas exchange
erythrocytes are involved in CO2 and O2 transport, so they contain large amounts of
hemoglobin
Fe containing pigment
what is the hemoglobin structure?
4 polypeptide chains associated with 4 fe-containing heme groups
anemia is a decrease in
fe or blood
it is more difficult to carry o2 because of the lack of blood
with fe deficient anemia, rbc are (2)
microcytic and hypochromic
microcytic
small
hypochromic
pale staining
what causes sickle cell anemia?
a signle amino acid substitution
what is the single amino acid substitution?
valine for glutamic acid
sickle cell anemia results in a conformational change in the cell, so it looks
sickle shaped
frail, easily damaged
the single amino acid substitution changes the 3D structure of the — molecule
hemoglobin
sickle shaped rbc can also cause damage to
endothelial cells of capillary walls due to rough edges
sickle cell anemia confers resistance to — because
malaria
because with malaria, you remove damaged rbc in from the bloodstream often enough to remove intracellular parasite populations
malaria is caused by the intracellular blood parasite
plasmodium spp
what are platelets/thrombocytes?
small, non-nucleated cells containing organelles (cell fragments)
platelets are formed from
megakaryocytes
megakaryocyte nucleus
single, multilobed
platelets develop from pleated — — in the cytoplasm, platelets “tear off”
demarcation channels
platelets function in — — to form physical plugs at the site of vascular damage
blood clotting
what drug impairs platelet function? why?
aspirin
inhibits clotting
— is a result of cascade interactions between plasma proteins and coagulation factors
coagulation
coagulation occurs only if the endothelial lining of vessel is
injured
extrinsic pathway vs intrinsic pathway
faster
slower
extrinsic pathway is initiated by the release of the tissue — as a result of tissue damage
thromboplastin
the intrinsic pathway is initiated by the exposure of
collagen
found everywhere, when you have a cut there is almost always collagen present
intrinsic pathway requires
numerous clotting factors and a longer cascade reaction
serotonin is a potent
vasoconstrictor
coagulation mechanism
when the wall of a blood vessel breaks, tissue injury results. this releases thromboplastin, which initiates the extrinsic pathway and also exposes collagen, which initiates the intrinsic pathway. platelets mechanically adhere to exposed collagen and release serotonin. this constricts the smooth muscle in the damaged blood vessel to minimize blood loss.
both — are triggered to damage of blood vessels
pathways
the extrinsic and intrinsic pathways converge to form a — pathway
common
at the point where factor X is activated
the common pathway results in conversion of
prothrombin to thrombin, which converts soluble fibrinogen into insoluble fibrin
coagulation traps (2)
platelets and rbc
what stops blood clotting?
exhaustion of fibrinogen and removal of thrombin from blood during the conversion of fibrinogen to fibrin
antithrombin 3 and heparin are examples of
anticoagulants
inappropriate clot formation can lead to (3)
heart attack
stroke
DIC
hemophilia is a deficiency in — —, so blood cannot —
clotting factors
clot
hemophilia is a result of a defect in the
intrinsic pathway
how is hemophilia sex linked?
it is present in males on the X chromosome
hemophilia A is a deficiency of
clotting factor 8
hemophilia B is a deficiency of
factor 9
hemophilia C is a deficiency of
factor 11
von willebrands disease
?