Bio chapter 17 & 18
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239 Terms
intrinsic pathway
factors found in blood, begin cascade
Extrinsic Pathway
factors released by damaged blood begin cascade
Coagulation (clotting)
Last and most effective defense against bleeding
Procoagulants
clotting factors generated by liver
when are procoagulants in plasma
during inactive form
what is hemostasis
termination of bleeding
what do platelets release
seratonin and thromboxane
how long is the feedback cycle active during platelet plug formation
until the break in the vessel is sealed
what happens during platelet plug formation
broken vessels expose collagen causing platelets to stick together and to damaged vessel
What happens in vascular spasm
prompt constriction of the vessel
what causes vascular spasm
pain receptors cause blood vessels to constrict and platelets secrete vasoconstrictor
Effects of vascular spasm
constriction of broken vessel provides time for other clotting pathways
what order does hemostasis take place
vascular spasm, platelet plug formation, coagulation
what are platelets
cell fragments from bone marrow
platelets
secrete clotting factors
platelets
form a plug
platelets
secrete vasoconstrictor chemicals
platelets
attract neutrophils and macrophages
types of leukemia
myeloid, lymphoid, acute, chronic
what is myeloid leukemia
uncontrolled granulocyte production
what is lymphoid leukemia
uncontrolled lymphocyte or monocyte production
what is acute leukemia
appears suddenly, progresses rapidly and has short survival time
what is chronic leukemia
undetected for months, longer survival time
what is leukemia
cancer of hemopoietic tissue
what are the effects of leukemia
large numbers of immature leukocytes lead to impaired clotting and room for infection
when do monocytes increase
during viral infections
what are monocytes
the largest white blood cell
what do monocytes do
leave blood stream and transform into macrophages
what do monocytes do
phagocytize pathogens and debris
what do monocytes do
activate other immune cells
what are lymphocytes
the most abundant agranulocyte
when do lymphocytes increase
with infection
what do lymphocytes do
destroy bad blood cells
what do lymphocytes do
secrete antibodies
what do lymphocytes do
activate other immune cells
when do basophils increase
with viral infections
what do basophils do
secrete histamine- increase blood flow
what do basophils do
secrete heparin- promote leukocyte mobility
when do eosinophils increase
with parasitic infections
what do eosinophils do
phagocytize antigen antibody complexes and allergens
what do eosinophils do
release enzymes to destroy parasites
what are neutrophils
most abundant granulocyte
What do neutrophils do
phagocytize bacteria
how many lobes does a neutrophil nucleus have
3-5 lobes
what are leukocytes
white blood cells
leukocytes are
the least abundant blood cells
leukocytes can
leave blood and go into tissues
leukocytes have
an obvious nucleus
When would an rh- woman produce rh+ antibodies
during the placental tear in childbirth
during the second Rh+ pregnancy with and Rh- mother
antigen d can go through the placenta and cause agglutination in the baby
What happens when Rh- women are pregnant with an Rh+ baby
she is given immune globulin prior to birth to prevent the formation of antigen d
Anti D forms when
Rh- is exposed to Rh+
an Rh+ person
has antigen D
an Rh- Person
lacks antigen D
Type O blood
has neither A or B antigen
Type O has what antibodies
A and B
Type o blood is
the universal donor
what type of blood can type O recieve
type O
Type AB blood
has both A and B antigens
What antibodies does type AB blood have
no antibodies
Type AB blood is
the universal recipient
Type AB blood can donate to
type AB
Type B blood has
B antigens
What antibodies does type B have
anti A
Type B can receive
type O or B blood
Type B can donate to
type B and AB
Type A blood
has A antigens
Type A blood has
Anti B antibodies
Type A can receive
type O or A
Type A can conate to
A and AB
Agglutination
antibody molecules bind to antigens and mark them for destruction
agglutination cause
clumping of RBC
Agglutination happens when
incompatible blood is given in a transfusion
Agglutinins
antibodies against A and B
Agglutinis are present in
plasma
Blood types are
inherited Agglutinogens
antigens on RBCs that determine blood type
Anemia
bad blood synthesis cause
anemia
bleeding can cause
anemia
RBC destruction causes
anemia
where are RBCs broken down
the spleen and liver
what is separated in RBC breakdown
heme from the globin
in RBC breakdown, what do globins become
amino acids
what is removed from the heme in RBC breakdown
iron
what does heme pigment become
bilirubin
the liver removes bilirubin and
secretes into bile in the gallbladder
eythropoiesis
production of RBCs
what is the lifespan of red blood cells
120 days
erythropoiesis feedback
kidneys and liver detect low o2 so they produce erythropoietin which stimulates RBC procution
Sickle cell disease is
hereditary
what happens in sickle cell disease
RBCs become rigid and sticky, clump together and block blood vessels
sickle cell disease can lead to
kidney or heart failure and stroke or paralysis
hemoglobin is made of
4 chains of protein chains and 4 heme groups
hemoglobin makes up what percent of cytoplasm
33%
heme binds
o2 to ion in the center
globin chains are comprised of
2 alpha and 2 beta
globin chains bind to
co2
erythrocytes are
red blood cells