Hemostatic Systems Flashcards
what is a hemostatic system
a balance between procoagulant and anticoagulant forces maintains blood in fluid state and flowing through the vasculature to deliver oxygen to tissues systematically and remove CO2 and toxic waste products
what are the 3 main stages of the hemostatic system
-vasoconstriction of blood vessels
- formation of a platelet plug with collagen fibers
- blood clotting which reinforces the platelet plug with a fibrin mesh
what are the 2 homeostatic pathways when BP and blood volume decrease
endocrine mechanism and neural mechanism
what is the endocrine mechanism of homeostasis
ADH, angiotensin II, aldosterone, EPO are released which increases blood volume
what is the neural mechanism of homeostasis
baroreceptors and chemoreceptors stimulated, cardiovascular centers stimulated, sympathetic activation, release of norepinephrine and epinephrine. this increases CO and BP
what do sympathetic nerves trigger
contraction of smooth muscle in vessels
what does serotonin do
vasoconstricts in high concentrations. indirectly can act as a vasodilator when it stimulate NO release by cells
what synthesizes serotonin
platelets at NMJs
what makes and releases endothelin-1
damaged endothelial cells
what can happen if endothelin-1 is overexpressed
high BP, heart disease, lung kidney and brain disease
what does histamine bind to
histamine GPCRs on GI, uterus, lung, vascular SM cells
what does histamine do
vasodilation of vasculature and vasoconstriction of airways
what produces and released histamine
basophils in circulation and mast cells in tissue
what does prostacylin (PGI2) do
inhibits platelet activation and is a vasodilator
what does PGI2 counteract
TXA2
what is the mechanism of action of PGI2
binds to PGI2 receptor (GPCR) which signals adneylyl cyclase to produce cAMP which activates PKA which leads to vascular smooth muscle relaxation and vasodilation
what is thromboxane A2 made and released by
platelets and endothelial cells
what is TXA2
a prostaglandin
what doeos TXA2 do
stimulates activation of new platelets and increases platelet aggregation by increasing expression of GPIIb/IIIa (fibrinogen receptor) on platelet membranes
what do PGI2 and TXA2 have in common
they both have a short half life and are potent acting locally not systemically
what are the intrinsic factors of vascular tone
myogenic, endothelial, local substances, and metabolic byproducts
what are the extrinsic factors of vascular tone
sympathetic nerves and circulating factors
how do constrictor influences affect vascular tone
increase vascular tone
how do dilator influences affect vascular tone
decrease vascular tone
what do myogenic mechansims do
arise from vascular smooth muscle and constrict vessels, increasing tone
what are endothelial factors
nitric oxide (vasodilator) and endothelin (vasoconstrict- increase tone)
what are local factors
arachidonic acid metabolites, histamine, bradykinin (vasodilator or vasoconstriction)
what do metabolic byproducts or hypoxia do
decrease tone (vasodilation)
what does angiotensin II do
increase vascular tone
what does ANP do
vasodilation- decrease tone
what does ischemia do (pathway)
activate phospholipase A2 which cleaves arachidonic acid from phospholipids and uses COX1 and COX 2 to form prostaglandins
what can a pluripotenital hematopoietic stem cell differentiate into
a lymphoid cell or myeloid cell
what does the common lymphoid progenitor differentiate into
B cell, T cell and NK cell which mature into plasma cell, activated T cell and activated NK cell
what does the common myeloid progenitor differentiate into
granulocyte/macrophage progenitor or megakaryocyte/erythrocyte progenitor
what does the granulocyte/macrophage progenitor differentiate into
neutrophil, eosinophil, basophil,precursor of mast cell, monocyte. in tissues the mast cell matures and the monocyte becomes a macrophage
what does the megakaryocyte/erythrocyte progenitor differentiate into
megakaryocyte or erythroblast
what does the megakaryocyte differentiate into
platelets
what does the erythroblast differentiate into
erythrocyte
what do macrophages do
phagocytosis and bacteria kill and antigen presentation
what do neutrophils do
phagocytosis and activation of bactericidal mechanisms, important in innate immune response
what are the primary cells recruited to the site of acute inflammation
neutrophils
what do mast cells do
release granules containing histamine and active agents
how does histamine work
causes vasodilation and permits entry of cells and proteins into site of infection to engage invading pathogens. also a mediator of itching
what happens in each of the 3 stages in erythropoiesis
1- ribosome synthesis
2- hemoglobin accumulation
3- ejection of nucleus
what are the sites of hematopoiesis in fetus
first trimester-yolk sac
second trimester- liver and spleen
third- bone marrow
what are platelets
anuclear membrane limited bags filled with granules and vesicles from megakaryocytes
what is in the dense granules of platelets
-epinephrine
- histamine
- serotonin
- Ca2+ ions
- ADP
- PDGF
what happens when platelets are activated
forms temporary plug to seal breaks in vessels
what are the 5 cardinal signs of inflammation
pain, heat, redness, swelling, loss of function
what are the 3 major componenets to acute inflammation
- vascular changes - increased blood flow and vascular permeability
- cellular events - migration of leukocytes into the site of injury
- mediators - derived from plasma cells and proteins
what are the temporal events of self-limited acute inflammation
edema -> PMN -> monocytes/macrophages -> tissue repair and regeneration
when does the inflammation stage of healing occur
48 hour post injury
when does the proliferation stage of healing occur
3-10 days post injury
when does the remodeling stage of healing occur
21 days post injury
what is exudate
high protein ( >1.02)
- fluid and protein leakage, increased interendothelial spaces
what is transudate
low protein (<1.01)
- increased hydrostatic pressure
- decreased colloid osmotic pressure
what is pus
enriched in neutrophils
what counteracts hydrostatic pressure
colloid osmotic pressure
what is a type 1 inflammation and hypersensitivity disease and examples
anaphylactic, allergy
ex: hayfever, bee sting, asthma, penicillin
what is a type 2 inflammation and hypersensitivity disease and what happens
antibody dependent
- cell membrane is altered to non self
ex: graves disease
what is a type 3 inflammation and hypersensitivity disease
immune complex type
- involves antibody-antigen complex cause tissue damage
what is a type 4 inflammation and hypersensitivity disease
cell mediated ( delayed type hypersensitivty)
- protect against intracellular pathogens
- mediated by T-cells
ex: poison ivy
