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Prob set 2
Terms in this set (37)
42. What is the approximate lifespan of RBC, WBCs, and Platelets?
RBC's = 120 days
WBC = 20 yrs - whole life
Platelets = 10-12 days
43. What is the term for white blood cell formation? If you had to invent a name for a hormone which caused this, what would you call it in order to maintain consistency of the bloodish hormones?
Hypothetical name: leukopoietin
44. Does the digestive system affect and/or regulate blood volume?
Digestive system is the volume input (we drink water to increase blood volume)
But this is not a regulated function (the kidney regulates appropriate volume)
45. What are the "big three" plasma proteins and what are the basic functions of each?
where are they produced?
Albumin = regulate osmotic pressure of capillaries, act as carrier proteins for hydrophobic hormones
Globulins = associated with immune system, act as carrier proteins
Fibrinogen = associated with coagulation
46. What are the three categories of formed elements and what is an approximate mean count for each? (per microliter)
Erythrocytes = 5 mill/microliter
Leukocytes = 10,000 cells/ microliter
Thrombocytes= 300,000 /microliter
47. What formed element of blood participates most in immune function?
48. Where is erythropoietin secreted from?
49. How and why would a liver disorder affect clotting, immune function, and osmotic balance?
A lot of coagulation factors + fibrinogen is made here, thus damage would result in underclotting
inability to produce globulins = immune dysfunction
inability to produce albumins = osmotic imbalance
51. How would autoimmune destruction of red blood cells affect the body and what is the response of the body to correct for this loss?
It would result in hemolytic anemia
Erythropoietin secretion is upregulated by the kidney and targets red bone marrow to increase rate of stem cell division - resulting in increased production of erythrocytes.
52. Where are leukocytes initially formed?
In red bone marrow
53. Describe the structure of thrombocytes and the cell from which they originate. Are they long lived? why or why not?
They are small plasma membrane bound to packets of cytoplasm, they are anucleate, have mitochondria
Originate from megakaryocytes
Short lived because they are anucleate
54. What is the difference between plasma and serum?
serum doesn't have platelets or any clotting factors
55. Technically, what does coagulation refer to?
fibrinogen activation & fibrin in hemostasis
56. What is a thrombus? What non-clotting element typically gets stuck within a thrombus?
A platelet clot
Formed elements get tangled up in a thrombus
57. What are the two ways most commonly utilized to "blood dope"?
Administration of erythropoietin
Injection of stored RBC's from oneself to others
How is blood doping beneficial for an athlete? How is it not beneficial?
Resultant polycythemia effectively increases levels of aerobic activity
increased viscosity of the blood will overwork the heart and cause long-term health problems
58. Would EPO therapy be beneficial for iron-deficiency anemia? Why or why not?
no, iron deficient anemia is a result of insufficient hemoglobin (O2) within red blood cells, so producing more red blood cells won't have an effect
59. Why might a red bone marrow disorder affect hemostasis?
It would decrease production of leukocytes and thrombocytes, thus blood would have a difficult time clotting in the event of a wound
60. How does prostacyclin affect platelet activation? When / where is it present?
It inhibits platelet activation within a healthy vessel.
Present within endothelium, which lines all vessels.
61. What specifically do both the instrinsic and extrinsic pathway cause to happen?
Both activate factor X of the common pathway
Microhemorrhages are primarily defined as damage to capillaries. Are platelet plugs sufficient to stop microhemmorhages? Are they sufficient to stop larger "macro" hemorrhages?
Yes, the typically are sufficient.
Macro hemorrhages will require coagulation of fibrin
62. What is the initial and thus "fastest" step in hemostasis? What stimulates it?
Damage to vessel → Endothelial cells release chemical factors resulting in vasoconstriction
63. If you cut yourself and "clot" is that considered an embolism?
No, this is a thrombus
64. What is the initial stimulus that typically first initiates platelet activation following some sort of tissue damage. What other stimuli can cause platelet activation?
Initial: exposure to collagen (not typically encountered by blood cells)
Other: thrombin, ADP, Ca++ ions, serotonin, thromboxane
65. What does activation of platelets cause to happen?
- positive feedback by secretion of chem. Mediators (ADP, Ca++, serotonin, thromboxane)
- platelets express pseudopods that adhere to other pseudopods = platelet plug
- positive feedback by thromboxane and serotonin
- positive feedback by platelet thromboplastin
- Von Willebrand Factor strengthens adhesion of platelet plug to the vessel wall
- activated platelets stick to activated fibrin (reinforcing bonds b/w platelet plug & fibrin
66. How do platelets "stick" to a wound before fibrinogen is activated?
via VonWillebrand Factor. it acts as the bridge between exposed collagen, activated platelets, and strengthens the adhesion of the platelet plug to the vessel wall
67. Where is thromboxane formed and what is it's effect?
In activated platelets
Effect = activation of more platelets (pos. feedback)
68. Is the instrinsic or extrinsic pathway more reliable to successfully close large hemorraghes? Why?
Intrinsic pathway because exposed collagen acts as a continuous stimulus, whereas released thromboplastin (w/in extrinsic) can be "washed away" by large hemorrhages
69. What is the basic pattern regarding the chemical factors responsible for coagulation of fibrin? What are these chemicals, where are they found, what do they cause when activated, and where are they mostly formed?
In common pathways, activation of one factor catalyzes the activation of a subsequent factor. each step is associated with amplification, resulting in an explosive process once initially activated.
These factors are soluble proteins that exist in an inactive form within the plasma until activated
They are formed in the liver
70. Describe the common pathway of coagulation. What is(are) the initial trigger(s)?
What is the final result?
Activation of Factor Xa causes prothrombin (F II) to become thrombin (IIa)
Thrombin causes the conversion of fibrinogen to fibrin
Fibrin binds to activated platelets = thrombus/coagulation
71. Compare and contrast the differing characteristics of fibrinogen and fibrin:
Fibrinogen consists of soluble monomers
Fibrin consist of insoluble polymers that precipitate out in a long sticky string
Name three things activated platelets "stick" to.
72. What pro-coagulant does collagen activate?
Factors XII, XI, and IX
73. What factors are most centrally involved in the extrinsic pathway (before the common pathway)?
Tissue Thromboplastin (F III) → F VII → F X of common pathway
74. What factors are most centrally involved in the intrinsic pathway (before the common pathway)?
Factors XII, XI, IX, VIII → F X
75. Which is more important, the intrinsic or extrinsic pathway? Which is faster and why?
Neither are more/less important, both are critical in assuring proper clotting
Extrinsic is faster b/c it requires fewer steps to activate Factor X
76. What characteristic of coagulation makes it a system which is clearly related to your genotype?
Chemical factors are proteins and have a gene that encodes for it, therefore can demonstrate mutations that result in improper coagulation
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