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Physiology Block 6 > Special Circulations And Hemostasis > Flashcards

Special Circulations And Hemostasis Flashcards

1
Q

How can blood flow to organs change

A

Depending on metabolic demand

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2
Q

What are the two ways that blood flow can be controlled

A

Extrinsically

Intrinsically

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3
Q

Extrinsic blood flow control

A

Something else decides

Neural or hormonal

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4
Q

Intrinsic blood flow control

A

Organ decides

Loca control from tissue itself

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5
Q

Neural and hormonal autonomic innervation

A

SNS-a1 receptors constrict
SNS-B2 receptors-dilate
PNS-M3 receptors-dilate (via NO) primarily via drugs

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6
Q

Vasoconstriction hormones in neural and hormonal control

A 
Angiotensin II-constricts
Prostaglandins- variable
Histamine-dilates
Endothelin-constricts
NO-dilates
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7
Q

What is local control

A

Organ controlling its own blood control

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8
Q

What are the 3 examples of loca control

A

Autoregulation
Active hyperemia
Reactive hyperemia

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9
Q

Blood flow is maintained constant despite changing arterial pressure

A

Autoregulation

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10
Q

What organs use autoregulation method of local control

A

Kidney and Brian.

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11
Q

Blood flow changes as metabolic demand changes

A

Active hyperemia

Running-blood goes to legs

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12
Q

Periods of reduced blood flow are followed by supernormal flow

A

Reactive hyperemia

Goes above what it actually needs

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13
Q

What are the two main mechanisms of local control

A

Myogenic mechanism

Metabolic mechanism

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14
Q

Smooth muscle adjusts diamterer of vessels to maintain blood flow

A

Myogenic mechanism

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15
Q

What type of regulation is mygenic mechanism of local blood flow control

A

Autoregulation

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16
Q

What happens in myogenic mechanism

A
  • flow decreases, vessels dilate
  • flow increases, vessels constrict
  • based on maintaining wall tension of vessels
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17
Q

Metabolic by-products act as local signals to alter flow

A

Metabolic mechanism

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18
Q

What kind of local control is metabolic mechanism

A

Active or reactive hyperemia

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19
Q

Exercise increases metabolic activity means more metabolites. This causes dilation and more flow. Opposite is true

A

Active hyperemia

Exercise

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20
Q

During transient ischemia metabolites build up, excess blood flow is required to wash them out

A

Reactive hyperemia

Occlusion

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21
Q

Blood flow in the coronary vessels to feed heart

A

Coronary flow

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22
Q

What kind of control is coronary flow

A

Metabolic control- active hyperemia through hypoxia and adenosine MOST IMPORTANT

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23
Q

When does coronary flow have reactive hyperemia

A

Diastole because it pinches off blood supply during systole, increased metabolites

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24
Q

Coronary flow and neural control

A

Very little neural control. Brain cant kill the heart or brain wont get any blood

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25
Q

Local control of skeletal blood flow

A

Metabolic most important during times of exercise. K+, lactate, and adenosine

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26
Q

When does skeletal muscle local control use metabolic control

A

After exercise (K+, lactate, adenosine)

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27
Q

When does skeletal muscle local control use reactive hyperemia

A

After contraction (pinch caps during contraction, increases metabolites)

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28
Q

When is neural control of local control of skeletal muscles important

A

During rest

A1 and B1

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29
Q

Metabolic local control and blood flow to skin

A

Very little

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30
Q

Neural local control and blood flow to skin

A

Most important for body heat regulation

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31
Q

Hormonal regulation for local control of blood flow to skin

A

Histamine

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32
Q

Blood flow to what is heavily metabolic?

A

Coronary and skeletal bloo dflow

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33
Q

Blood flow to what has some neural control

A

Skeletal

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34
Q

Blood flow to what is heavily neural

A

Skin

35
Q

What kind of regulation in local control of blood flow to the brain

A

Myogenic autoregulation and metabolic control through CO2 and H+

36
Q

Neural and hormonal control to neural blood flow

A

Little to none. BBB stops the hormones

37
Q

Local control of blood flow to retina

A

Myogenic autoregulation and metabolic control through lactic acid

Some hormonal control through NO and endothelin-1 production (minor)

38
Q

Between neural and local control, what usually wins

A

Neural. Sympathetic usually well

39
Q

What are the last organs to lose blood flow during extreme hemorrhage

A

Brain, heart, lungs, kidneys because they have little neural control. The Brian will literally kill everything else to keep its own blood flow, but not these because they don’t have much neural control

40
Q

Increasing skeletal muscle CO2 production would _______ blood flow

A

Increase

41
Q

Increasing skeletal muscle CO2 production would increase blood flow. This is an example of _______ regulation

A

Active hyperemia

42
Q

If blood volume stays the same and there are increased metabolites what kind of regulation comes into play

A

Active hyperemia

43
Q

If there is a loss of blood and gain of metabolites, what kind of regulation is this

A

Reactive hyperemia

44
Q

Process of forming clots on vessel walls in response to injury and prevents further blood loss

A

Hemostasis

45
Q

What are the 3 stages of hemostasis

A
  1. Vascular constriction
  2. Formation of a platelet plug
  3. Clot formation-coagulation
46
Q

What stages of hemostasis require platelets

A

All stages

47
Q

What are platelets?

A

Not true cells. Bags of enzymes

  • megakaryocytes shed them
  • full of clotting proteins, vasoconstrictors, and platelet activating molecules
48
Q

When does the vessel constrict in hemostasis

A

Immediately after damage

Slows flow to damaged area

49
Q

What does damaged endothelium do

A

Releases vasoactive compounds that cause vasoconstriction (adenosine, calcium, etc)

50
Q

What does pain do in hemostasis?

A

Causes vasoconstriction

51
Q

Platelet plug formation

A

Collage exposed-binds to Von Willebrand facrot-grabs platelets-platelets activate- ADP and TXA2 dump causes more platelets to come and do the same thing over and over-forms platelet plug

52
Q

What kind of feedback is platelet plug formation

A

Positive feedback mechanism

53
Q

Collagen binds to _______factor in platelet plug formation

A

Von Willebrand

54
Q

What protein is responsible for platelet plug formation

A

Von Willebrand factor

55
Q

Enzymatic cascade that converted fibrinogen into fibrin

A

Coagulation

56
Q

What is a thrombus?

A

A fibrous clot made during coagulation in a place you don’t really need one

57
Q

What happens if a thrombus breaks off

A

Embolus

58
Q

Where do venous emboli originate?

A

Legs (Deep vein thrombosis)

59
Q

Where do venous emboli usually get stuck

A

Lungs

60
Q

What do venous emboli cause

A

Pulmonary embolism (pulmonary HTN, and right sided heart failure)

61
Q

Where do arterial emboli originate

A

Atria or carotids

62
Q

Where do arterial thrombi normally get stuck

A

Cerebral or ocular vessels

63
Q

What does arteriolar emboli cause

A

Stroke and retinal ischemia

64
Q

What are the two pathways of clot formation

A

Intrinsic and extrinsic

65
Q

What is intrinsic clot formation caused by

A

Initiated by exposed collagen

66
Q

What is extrinsic clot formation initiated by

A

Release of tissue factor

Turns on platelets

67
Q

What are the Vit K dependent factors in clot formation

A

2 (prothrombin)
7 (stable factor)
9 (Christmas factor)
10 (Stuart prower factor)

68
Q

What factor is the most sensitive to vitamin K

A

7 (stable factor)

69
Q

Where do the extrinsic and intrinsic pathways of clot formation both merge together

A

Factor 10

70
Q

What happens during hemostasis after one hour

A

Clot retraction

71
Q

Clot retraction

A

Pulls damaged vessel walls together, takes a lot of platelets

72
Q

Fibrinolysis

A

Clot dissolution

73
Q

In fibrinolysis, what digests the fibrin

A

Plasmin

74
Q

Why do we want fibrinolysis?

A

Re establish blood flow to that area

75
Q

What is the clot buster

A

Tissue plasminogen activator (tPA)

76
Q

What do we use in strokes to try and break clot up?

A

Tissue plasminogen activator

77
Q

What kind of strokes do we use tPA for

A

Ischemic strokes. If we use them on hemorrhagic strokes, you will kill the person

78
Q

What does aspirin do

A

Blocks TXA2 production which keeps the platelets from sticking together

An aspirin a day keeps the clots away

79
Q

What does heparin inhibit

A

Factor 2 and 10

Inhibits where intrinsic and extrinsic come together!!!
TEST

80
Q

What does warfarin (Coumadin) do

A

Inhibits vitamin K production

Inhibits factor 7!!
TEST

81
Q

Which anti platelet drug is fast acting

A

Heparin

82
Q

Which anti platelet drug is slow acting

A

Warfarin (Coumadin)

83
Q

When starting someone on clot prevention therapy, what do you normally do

A

Start them on heparin and coumadin together and then ween them off of heparin. Just want it in the beginning because it is fast acting

Physiology Block 6 (7 decks)

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