ch 17- blood lecture 1/23 Flashcards
how does the body compensate for blood loss
decreasing blood volume and increasing RBC production
% of blood loss and the issues it causes
15-30% lose muscle function, 30% + can be severe shock and die
what kind of blood transfusion is the most common
red cell transfusions
why can transfusions between 2 different people with 2 different antigens not work?
immune system recognizes what antigens are ours vs what is foreign. will destroy foreign antigen
what two antigens are medical professionals most concerned with
ABO and Rh
ABO blood groups and what cells they have
A- A antigen
B- B antigen
O- no antigen (most common)
AB- A and B antigens (least common)
agglutinins
immune system antibodies that will attack mismatched blood cells (identifiers)
what types of blood will have what antibodies
A- anti-B antibody
B- anti-A antibody
AB- neither antibody
O- both anti A and B antibodies
Rh blood groups antigens
C,D,E,c,e
D is Rh+ (85%)
C,E,c,e is Rh- (15%)
rules for Rh donation
Rh- must be only Rh- donor, Rh+ can be either Rh+ or Rh-
is ABO or Rh more important when it comes to donation
ABO, immune system reacts worse to mismatched ABO
agglutination
if foreign donor blood enters, these form- foreign erythrocytes that are large and can block circulation. can break free and release hemoglobin
what happens if foreign blood cells lyse, releasing free hemoglobin
hemoglobin doesn’t carry oxygen unless its inside a cell, free hemoglobin can decrease oxygen transport and damage kidneys (they will stop filtering blood)
Blood type O
universal donor, neither antigen is present (anti A/B antigens have judgment on if a cell can belong) , can only receive from other type O
Blood type AB
universal recipient, neither antibody is present, can’t donate A or B or O but can receive any- only matching Rh groups
leukocyte
responsible for defending the body
characteristics of leukocytes
can leave blood vessels to go anywhere in the body, this is good bc they can go straight to sight of infection and stop it from entering the body. also produced fast, live 13-20 days, can double in 2-3 hrs
2 leukocyte types
granulocytes and agranulocytes
granulocytes
spherical, big, granule inside- there are 3 types. neutrophils, eosinophils, basophils
neutrophils
type of granulocyte, kills bacteria, makes up 50-70% of leukocyte population, have defensins (punch holes in bacteria membrane)
defensins
antimicrobial proteins, water rushes inside to make bacteria explode, chemically attracted to inflammation site, can be phagocytic (eat the bacteria)
eosinophils
parasite killer, 2-4% leukocyte population, lysosomes in the cell has digestive enzymes, that will digest body wall of parasitic worms, very specific
basophils
.5-1% of the leukocyte population, nonspecific and do not search for foreign things, and have histamine granules, which will increase diameter of blood vessels.
why is histamine important
increases diameter, enlarges vessels, brings more leukocytes for more defense.
agranulocytes
no visible granules, 2 types that are lymphocytes and monocytes.
lymphocytes
25% of leukocyte population, migrates in and out continuously, 3 types (T,B,NK)
T-lymphocytes (T cells)
acts against virus infected cells and tumor cells, immunity in nature
B-lymophocytes (B cells)
produces antibodies released to blood, flagger, immunity in nature
NK natural killer lymphocyte cells
natural defense against cancer, acts against virus infected cells and tumor cells
monocytes
3-8% leukocyte population, once they leave they will specialize, differentiates into macrophages as it leaves bloodstream and enters damaged tissues, a phagocyte
leukopoiesis
production of leukocytes (WBC) from red bone marrow, stimulated by interleukins and colony stimulating factors.
order of leukocyte differentiation
hematopoetic stem cell (not differentiated) to either myeloid stem cell or lymphoid stem cell. myeloid stem cell has either myeloblast or mono blast, lymphoid will turn into ether B or T lymphocyte precursor cell. then goes to granular or Agranular leukocytes (granular is eosinophils, basophils, or neutrophils.) (agranular will be B or T lymphocytes or monocyte)
stem cells
hematopoietic stem cell, myeloid, and lymphoid
committed cells
myeloblast, monoblast, B or T lymphocyte
granular and agranular eukocyte types
granular- eosinophil, basophil, neutrophils
agranular- monocyte, B or T lymphocyte
leukemia
a cancer resulting in over production of leukocytes, extra cells come from one abnormal cell. unspecialized, proliferate extensively. they don’t know what to defend, so they defend nothing
leukemia goes hand in hand with
anemia, wbc overcrowds rbc and platelets and causes bleeding issues. blood won’t clot as well bc no platelets.
acute leukemia
derived from stem cells, original stem cell, fast development, primarily affects children.
chronic leukemia
derived from a cell in a later stage, primarily elderly affecting, slow development
myeloid leukemia
myeloid stem cell defendants, T/B cells is where it involved
lymphocyte leukemia
involves lymphocyte cell
thrombocytes
platelets, helps clotting and stops blood loss. fragments of megakarocytes (larger cells), the smaller fragments break off and are released into blood. live 10 days if unused, shorter if actually used.
thrombocyte functions
initiate blood clot formation after damage, stick to each other and the injury site in damaged vessel, we do not want this to happen in undamaged vessel bc clot leads to issue in circulation.
what prevents platelets from sticking together
prostacyclin and nitric oxide, released all the time to stop sticking.
what hormone regulates platelet formation
thrombopoietin, released by liver
platelet formation stages
hematopoietic stem cell (hemocytoblast), megakyrocyte (stage IV), then platelets (the fragments)
hemostasis
when bleeding is stopped after blood vessel rupture occurs, localized response that is very fast. we only form clots at site of damage, if it goes elsewhere can cause a problem
three steps to hemostasis (blood clotting)
vascular spasm, platelet plug formation, coagulation
vascular spasm
rapid constriction of damaged blood vessel, smooth muslce tissue is injured then chemicals are released by damaged cells and reflexes from local pain receptors make this happen.
why are we benefitted from vascular spasm
diameter of blood vessel is quickly decreased, therefore we can’t prevent blood from just not flowing, narrowing allows less blood to flow and minimizes initial blood loss
platelet plug formation
platelets stick to each other and to fibers in vessel wall, form plug in damaged vessel. in response to injury, platelets release ADP and serotonin and thromboxane A2
what does ADP/serotonin and thromboxane do In platelet plug formation
causes more platelets to stick to site of injury, then increases vascular spasm and platelet aggregation
what can you use platelet plugs for
general wear and tear, smaller injuries
coagulation
severe mechanism preventing blood flow, a true blood clot, need clot factors 1-13 to form prothrombin activator (need all 13 for it to work) fibrinogen is dissolved in blood until this is needed for clotting
prothrombin activator
catalyzes plasma conversion protein prothrombin into thrombin (needed for clotting)
third step of coagulation
thrombin catalyzes transformation of soluble clotting factor fibrinogen into fibrin molecules, so its no longer soluble in blood, factor 13 finally binds fibrin strands together to create a mesh work of bridging one end of injury to another. fibrin also traps platelets and RBCs in to forma clot, a true clot has many fibrin strands and RBC/platelets, its rly strong. `
blood clot retraction
pulling damaged edges of blood vessel close together, further stabilizes clot to prevent tearing, platelets can contract and pull fibrin strands together to repair injury
fibrinolysis
gets rid of blood clot, too many clots would be bad for circulation. plasmin is an enzyme that digests the fibrin, breaking down fibrous strands- happens 2 days within clot formation. localized af
thromboembolic disorder
formation of undesired blood clots, thrombus is the formation of blood clot in unbroken vessel (remains stuck to vessel wall). this will block circulation.
embolus
thrombus breaks free and enters circulation, detaches from vessel wall, enters circulation. small not issue, large can affect circulation. example, pulmonary embolism which prevents oxygen uptake
thrombocytopenia
low platelet count in circulation, limited ability to form platelet plug so even small breaks can be deadly, caused by anything that will decrease red bone marrow.
hemophilia
hereditary bleeding disorder, a genetic blood loving, deficiency’s of clot factors, a lot of bleeding to small injury. symptom is prolonged bleeding and painful joints.
A- no factor 8
B- no factor 9
C- no factor 11
most serious type of hemophilia
A and B, C is not too serious. treatment to hemophilia is plasma transfusions or injections of absent clot factor.
