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WBCs (leukocytes)
produced in nucleus (same RBCs)
function: protection (immunity, etc.)
most are capable of movement becaus ethya re in-tact cells
2 categories of WBCs
granulocytes
neutrophils, eosinophils, basophils
agranulocytes
lymphocytes, monocytes
granulocytes
granules found in the cytoplasm of these
the granules contain proteins
multi-lobulated nucleus - easiest to find nucleus in these
phils
neutrophils
granules in these do’’t show up in cytoplasm - clear
nucleus is obvious because no granules covering; funky
in blood for 10-12 hours, then move to tissues
attract to wounds, breaks in skin, etc.
phagocytosis
signaled by autocrine symbols
dying neutrophils create pus
splinter
only live for a few days in the blood - die for the cause
high count = fever, pain, etc.
phagocytosis
eat anything that doesn’t belong in tissue
neutrophils perform
eosinophils
produce red granuoles
high count when parasites and allergies
basophils
rarest type of WBC
blue/purple
agranulocytes
w/o granules
specific responders for immune system
lymphocytes and monocytes
lymphocytes
smallest of WBCs
round
aka B cells (make antibodies) and T cells (recognize antigens as not self)
involved in transfusion reaction (tissue rejection)
monocytes
stay in circulation for a few days, go out to tissue
macrophages - eat things that don’t belong
clean up cells
hang in the tissues for a long time, can even mitosis
plasma
connection for all body fluids
liquid part of blood
thrombocytes (PLTs/platelets)
fibrinogens (plasma protein) to clot blood
NOT in tact cells when in circulation
megakaryocytes fragment to become these
its sticky because of its glycoproteins
stickiness helps its job (clotting)
platelets are viable/functional for how long
5-9 days
why you stop taking aspirin 1 week before surgery
why are adults recommended to take aspirin every day
it prevents clotting, makes platelets permanently less sticky
prevents strokes
why old people bruise often, less clotting = more bruising/bleeding
hemostasis
the process of stopping blood loss/clotting
coagulation (NOT AGGLUTINATION)
clotting factors
fibrinogen
the 3 steps of hemostasis
vascular spasm
platelet plug formation
coagulation
act as a cascade - one after another
vascular spasm
immediate/temporary
smooth muscle at the site of injury has a spasm and contracts
makes any BV in the damaged area smaller to reduce bleeding
platelet plug formation
process where a platelet plug forms to prevent further loss of blood from a damaged vessel
“primary homeostasis”
fibrinogens
“clotting factors”
produce fibrin —> already present in plasma, but must be activated (by injury) to form the fibrin
makes the blood clot stronger - holds everything in place for the healing to occur
intrinsic cascade
responds to spontaneus, intravascular damage
extrinsic clotting pathway
begins in the tissues, activated secondary to external trauma
both depend on where injury occurs
hemophilia
no genes or clotting factors
there are many types because there are different genes for each clotting factors
liver requires what nutrient to make these clotting proteins
vitamin K
warfarin
drug given to people to prevent them from clottng too much and having strokes
lowers vit. K in liver, therefore lowering clotting proteins
“rodenticide” because causes rodents to bleed to death internally
fibrinolysis
once blood clot is formed and structurally sound, it starts breaking down blood clot so blood flow can occur again and the tissue can continue its function
serum
plasma without the fibrinogens → fluid part of blood that is left after the blood is clotted
easier to measure this because less sticky
doesn’t test for clotting speed./fcn. because it has no fibrinogens
whole blood transfusion
do a type and cross match
cross match
give donor RBCs and mix it with recipient antibodies (plasma/serum)
give donor antibodies (plasma/serum) and mix with recipient RBCs
do BOTH - why whole blood transfusion is much harder to do
hematocrit
percent of RBCs in your blood - gives you a quick screen if someone has anemia