Objective 1 pt 2 Flashcards
cytoplasmic fragments of extraordinarily large cells
megakaryocytes
blue-staining outer region, purple granules
granules contain serotonin, Ca2+, enzymes, ADP, and platelet-derived growth factor
platelets
what is the function of platelets?
form temporary platelet plug that helps seal breaks in blood vessels
platelet formation is regulated by hormone …
thrombopoietin
plateleets are formed in myeloid line from…
megakaryoblast
sends cytoplasmic projections into lumen of capillary
projections break off into platelet fragments
stage IV megakaryocyte
fast series of reactions for stoppage of bleeding
requires clotting factors and substances released by platelets and injured tissues
hemostasis
what are the 3 steps involved in hemostasis?
vascular spasm
platelet plug formation
coagulation
damaged vessel constricts through _________
most effective in smaller blood vessels
can significantly reduce flow until other mechanisms can kick in
step 1: vascular spasm
what are vascular spasms triggered by?
direct injury to vascular smooth muscle
chemical released by endothelial cells and platelets
pain reflexes
platelets stick to collagen fibers that are exposed when vessel is damaged
the plasma protein von Willebrand factor helps to stabilize platelet-collagen adhesion
platelets become activated and swell, become spiked and sticky and release chemical messengers
postitive feedback cycle occurs
platelet plugs are fine for small vessel tears
step 2: platelet plug formation
as more platelets stick, they release more chemicals, which cause more platelets to stick and release more chemicals
positive feedback cycle
reinforces platelet plug with fibrin threads that act as a glue
blood is transformed from liquid to gel
series of reactions use clotting factors, mostly plasma proteins
step 3: coagulation
what are the 3 phases of coagulation?
Phases 1: two pathways to prothrombin activator
Phase 2: pathway to thrombin
phase 3: common pathway to the fibrin mesh
initiated by either intrinsic or extrinsic pathway
triggered by tissue-damaging events
involves a series of clotting factors
the intermediate steps of each pathway cascade toward a common intermediate, factor X
once factor X is activated, it complexes with Ca2+, PF3, and factor V to form prothrombin activator
Phase 1: two pathways to prothrombin activator
because clotting factors are present within the blood
triggered by negatively charged surfaces such as activated platelets, collagen, or even glass of a test tube
slow process
intrinsic pathway
because factors needed for clotting are located outside blood
triggered by exposure to tissue factor, also called factor III
bypasses several steps of intrinsic pathway, so faster pathway
extrinsic pathway
prothrombin activator speeds up the transformation of prothrombin to activate enzyme thrombin
phase 2: pathway to thrombin
thrombin converts soluble fibrinogen to fibrin
fibrin strands form structural basis of clot
fibrin causes plasma to become a gel-like trap catching formed elements
thrombin activates factor XIII, which:
cross-links fibrin
strengthens and stabilizes clot
Phase 3: common pathway to the fibrin mesh
factors that normally dominate in blood to prevent coagulation
anticoagulants
actin and myosin in platelets contact within 30-60 mins
contraction pulls on fibrin strands, squeezing serum from clot
draws ruptured blood vessel edges together
clot retraction
released by platelets
stimulates division of smooth muscle cells and fibroblasts to rebuild blood vessel wall
platelet-derived growth factor
stimulates endothelial cells to multiply and restore endothelial lining
vascular endothelial growth factor
process whereby clots are removed after repair is completed
begins within 2 days and continues for several days until clot is dissolved
fibrinolysis
plasma protein that is trapped in clot is converted to plasmin
plasminogen
a fibrin-digesting enzyme
plasmin
factor XIII, and thrombin all play a role in conversion process
tissue plasminogen activator
what are the factors limiting normal clot growth?
two homeostatic mechanisms limit clot size
other mechanisms block the final step in which fibrinogen is polymerized into fibrin
swift removal and dilution of clotting factors
inhibition of activated clotting factors
two homeostatic mechanisms limit clot size
fibrin binds thrombin, preventing clot from getting too big or escaping into bloodstream
Heparin in basophil and mast cells inhibits thrombin by enhancing
antithrombin III
other mechanisms block the final step in which fibrinogen is polymerized into fibrin
inactivates any unbound thrombin that escapes into
bloodstream
antithrombin III
what are the factors preventing platelet adhesion?
Smooth endothelium of blood vessels prevents platelets from
clinging
Endothelial cells secrete antithrombic substances
such as nitric oxide and prostacyclin
Vitamin E quinone, formed when vitamin E reacts
with oxygen, is a potent anticoagulant
how does the cardiovascular system minimize effects of blood loss?
reducing volume of affected blood vessels stepping up production of RBCs
what must volume be replaced immediately with?
normal saline or multiple-electrolyte solution that mimics plasma electrolyte composition
are used only when blood loss is rapid and substantial
whole-blood transfusions
these are preferred to restore oxygen-carrying capacity
packed red blood cells
anything perceived as foreign that can generate an immune response
antigen
RBC antigens are referred to as…
because they promote agglutination
agglutinogens
have at least 30 naturally occurring RBC antigens
presence or absence of each antigen is used to classify blood cells into different groups
human blood groups
cause most vigorous transfusion reactions; therefore, they are major groups typed
antigens of ABO and Rh blood groups
based on presence or absence of two agglutinogens on surface of RBCs
blood may contain performed anti-A or anti-B antibodies
ABO blood groups
only has A agglutinogen
type A
only has B agglutinogen
type B
has both A and B agglutinogens
type AB
has neither A nor B agglutinogens
type O
52 named Rh agglutinogens
C, D, and E are most common
Rh+ indicates presence of D antigen
second exposure to Rh+ blood will result in typical transfusion reaction
Rh blood groups
are not spontaneously formed in Rh- individuals
form Rh- individual receives Rh+ blood, or Rh- mom is carrying Rh+ fetus
Anti-Rh antibodies
occur if mismatched blood is infused
donor cells are attacked by recipient’s plasma agglutinins
blood clots and clog small vessels
rupture and release hemoglobin into bloodstream
transfusion reactions
what do transfusion reactions result in?
diminished oxygen-carrying capacity
decreased blood flow beyond blocked vessel
hemoglobin in kidney tubules can lead to renal failure
what are symptoms of transfusion reactions?
fever, chills, low BP, rapid HR, nausea, vomiting
how to we treat transfusion reactions?
preventing kidney damage with fluids and diuretics to wash out hemoglobin
no A or B antigens
type O universal donor
no anti-A or anti-B antibodies
type AB universal recipient
pt predonates own blood that is stored and available if needed
autologous transfusions
donor blood is mixed with antibodies against common agglutinogens
blood is typed for ABO and Rh factor in same manner
blood typing
typing between specific donor and specific recipient
cross matching
what can examination of blood yield about info on persons health?
low hematocrit seen in cases of anemia
blood glucose tests check for diabetes
leukocytosis can signal infection
looks at relative proportions of each WBC
increases in specific WBC can help with diagnosis
differential WBC count
assess hemostasis
prothrombin time and platelet counts
blood chemistry profile that checks various blood chemical levels
abnormal results could indicate liver or kidney disorders
CMP
checks formed elements, hematocrit, hemoglobin
complete blood count
