Hemostatic Systems Flashcards

1
Q

what is a hemostatic system

A

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

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2
Q

what are the 3 main stages of the hemostatic system

A

-vasoconstriction of blood vessels
- formation of a platelet plug with collagen fibers
- blood clotting which reinforces the platelet plug with a fibrin mesh

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3
Q

what are the 2 homeostatic pathways when BP and blood volume decrease

A

endocrine mechanism and neural mechanism

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4
Q

what is the endocrine mechanism of homeostasis

A

ADH, angiotensin II, aldosterone, EPO are released which increases blood volume

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5
Q

what is the neural mechanism of homeostasis

A

baroreceptors and chemoreceptors stimulated, cardiovascular centers stimulated, sympathetic activation, release of norepinephrine and epinephrine. this increases CO and BP

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6
Q

what do sympathetic nerves trigger

A

contraction of smooth muscle in vessels

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7
Q

what does serotonin do

A

vasoconstricts in high concentrations. indirectly can act as a vasodilator when it stimulate NO release by cells

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8
Q

what synthesizes serotonin

A

platelets at NMJs

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9
Q

what makes and releases endothelin-1

A

damaged endothelial cells

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10
Q

what can happen if endothelin-1 is overexpressed

A

high BP, heart disease, lung kidney and brain disease

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11
Q

what does histamine bind to

A

histamine GPCRs on GI, uterus, lung, vascular SM cells

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12
Q

what does histamine do

A

vasodilation of vasculature and vasoconstriction of airways

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13
Q

what produces and released histamine

A

basophils in circulation and mast cells in tissue

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14
Q

what does prostacylin (PGI2) do

A

inhibits platelet activation and is a vasodilator

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15
Q

what does PGI2 counteract

A

TXA2

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16
Q

what is the mechanism of action of PGI2

A

binds to PGI2 receptor (GPCR) which signals adneylyl cyclase to produce cAMP which activates PKA which leads to vascular smooth muscle relaxation and vasodilation

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17
Q

what is thromboxane A2 made and released by

A

platelets and endothelial cells

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18
Q

what is TXA2

A

a prostaglandin

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19
Q

what doeos TXA2 do

A

stimulates activation of new platelets and increases platelet aggregation by increasing expression of GPIIb/IIIa (fibrinogen receptor) on platelet membranes

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20
Q

what do PGI2 and TXA2 have in common

A

they both have a short half life and are potent acting locally not systemically

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21
Q

what are the intrinsic factors of vascular tone

A

myogenic, endothelial, local substances, and metabolic byproducts

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22
Q

what are the extrinsic factors of vascular tone

A

sympathetic nerves and circulating factors

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23
Q

how do constrictor influences affect vascular tone

A

increase vascular tone

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24
Q

how do dilator influences affect vascular tone

A

decrease vascular tone

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25
Q

what do myogenic mechansims do

A

arise from vascular smooth muscle and constrict vessels, increasing tone

26
Q

what are endothelial factors

A

nitric oxide (vasodilator) and endothelin (vasoconstrict- increase tone)

27
Q

what are local factors

A

arachidonic acid metabolites, histamine, bradykinin (vasodilator or vasoconstriction)

28
Q

what do metabolic byproducts or hypoxia do

A

decrease tone (vasodilation)

29
Q

what does angiotensin II do

A

increase vascular tone

30
Q

what does ANP do

A

vasodilation- decrease tone

31
Q

what does ischemia do (pathway)

A

activate phospholipase A2 which cleaves arachidonic acid from phospholipids and uses COX1 and COX 2 to form prostaglandins

32
Q

what can a pluripotenital hematopoietic stem cell differentiate into

A

a lymphoid cell or myeloid cell

33
Q

what does the common lymphoid progenitor differentiate into

A

B cell, T cell and NK cell which mature into plasma cell, activated T cell and activated NK cell

34
Q

what does the common myeloid progenitor differentiate into

A

granulocyte/macrophage progenitor or megakaryocyte/erythrocyte progenitor

35
Q

what does the granulocyte/macrophage progenitor differentiate into

A

neutrophil, eosinophil, basophil,precursor of mast cell, monocyte. in tissues the mast cell matures and the monocyte becomes a macrophage

36
Q

what does the megakaryocyte/erythrocyte progenitor differentiate into

A

megakaryocyte or erythroblast

37
Q

what does the megakaryocyte differentiate into

A

platelets

38
Q

what does the erythroblast differentiate into

A

erythrocyte

39
Q

what do macrophages do

A

phagocytosis and bacteria kill and antigen presentation

40
Q

what do neutrophils do

A

phagocytosis and activation of bactericidal mechanisms, important in innate immune response

41
Q

what are the primary cells recruited to the site of acute inflammation

A

neutrophils

42
Q

what do mast cells do

A

release granules containing histamine and active agents

43
Q

how does histamine work

A

causes vasodilation and permits entry of cells and proteins into site of infection to engage invading pathogens. also a mediator of itching

44
Q

what happens in each of the 3 stages in erythropoiesis

A

1- ribosome synthesis
2- hemoglobin accumulation
3- ejection of nucleus

45
Q

what are the sites of hematopoiesis in fetus

A

first trimester-yolk sac
second trimester- liver and spleen
third- bone marrow

46
Q

what are platelets

A

anuclear membrane limited bags filled with granules and vesicles from megakaryocytes

47
Q

what is in the dense granules of platelets

A

-epinephrine
- histamine
- serotonin
- Ca2+ ions
- ADP
- PDGF

48
Q

what happens when platelets are activated

A

forms temporary plug to seal breaks in vessels

49
Q

what are the 5 cardinal signs of inflammation

A

pain, heat, redness, swelling, loss of function

50
Q

what are the 3 major componenets to acute inflammation

A
  • 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
51
Q

what are the temporal events of self-limited acute inflammation

A

edema -> PMN -> monocytes/macrophages -> tissue repair and regeneration

52
Q

when does the inflammation stage of healing occur

A

48 hour post injury

53
Q

when does the proliferation stage of healing occur

A

3-10 days post injury

54
Q

when does the remodeling stage of healing occur

A

21 days post injury

55
Q

what is exudate

A

high protein ( >1.02)
- fluid and protein leakage, increased interendothelial spaces

56
Q

what is transudate

A

low protein (<1.01)
- increased hydrostatic pressure
- decreased colloid osmotic pressure

57
Q

what is pus

A

enriched in neutrophils

58
Q

what counteracts hydrostatic pressure

A

colloid osmotic pressure

59
Q

what is a type 1 inflammation and hypersensitivity disease and examples

A

anaphylactic, allergy
ex: hayfever, bee sting, asthma, penicillin

60
Q

what is a type 2 inflammation and hypersensitivity disease and what happens

A

antibody dependent
- cell membrane is altered to non self
ex: graves disease

61
Q

what is a type 3 inflammation and hypersensitivity disease

A

immune complex type
- involves antibody-antigen complex cause tissue damage

62
Q

what is a type 4 inflammation and hypersensitivity disease

A

cell mediated ( delayed type hypersensitivty)
- protect against intracellular pathogens
- mediated by T-cells
ex: poison ivy