Special Circulations And Hemostasis Flashcards by Sarah Heath

How can blood flow to organs change

Depending on metabolic demand

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What are the two ways that blood flow can be controlled

Extrinsically

Intrinsically

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Extrinsic blood flow control

Something else decides

Neural or hormonal

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Intrinsic blood flow control

Organ decides

Loca control from tissue itself

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Neural and hormonal autonomic innervation

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

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Vasoconstriction hormones in neural and hormonal control

Angiotensin II-constricts
Prostaglandins- variable
Histamine-dilates
Endothelin-constricts
NO-dilates

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What is local control

Organ controlling its own blood control

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What are the 3 examples of loca control

Autoregulation
Active hyperemia
Reactive hyperemia

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Blood flow is maintained constant despite changing arterial pressure

Autoregulation

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What organs use autoregulation method of local control

Kidney and Brian.

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Blood flow changes as metabolic demand changes

Active hyperemia

Running-blood goes to legs

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Periods of reduced blood flow are followed by supernormal flow

Reactive hyperemia

Goes above what it actually needs

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What are the two main mechanisms of local control

Myogenic mechanism

Metabolic mechanism

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Smooth muscle adjusts diamterer of vessels to maintain blood flow

Myogenic mechanism

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

Autoregulation

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What happens in myogenic mechanism

flow decreases, vessels dilate
flow increases, vessels constrict
based on maintaining wall tension of vessels

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Metabolic by-products act as local signals to alter flow

Metabolic mechanism

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What kind of local control is metabolic mechanism

Active or reactive hyperemia

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

Active hyperemia

Exercise

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

Reactive hyperemia

Occlusion

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Blood flow in the coronary vessels to feed heart

Coronary flow

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What kind of control is coronary flow

Metabolic control- active hyperemia through hypoxia and adenosine MOST IMPORTANT

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When does coronary flow have reactive hyperemia

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

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Coronary flow and neural control

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

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Local control of skeletal blood flow

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

When does skeletal muscle local control use metabolic control

After exercise (K+, lactate, adenosine)

When does skeletal muscle local control use reactive hyperemia

After contraction (pinch caps during contraction, increases metabolites)

When is neural control of local control of skeletal muscles important

During rest | A1 and B1

Metabolic local control and blood flow to skin

Very little

Neural local control and blood flow to skin

Most important for body heat regulation

Hormonal regulation for local control of blood flow to skin

Histamine

Blood flow to what is heavily metabolic?

Coronary and skeletal bloo dflow

Blood flow to what has some neural control

Skeletal

Blood flow to what is heavily neural

Skin

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

Myogenic autoregulation and metabolic control through CO2 and H+

Neural and hormonal control to neural blood flow

Little to none. BBB stops the hormones

Local control of blood flow to retina

Myogenic autoregulation and metabolic control through lactic acid Some hormonal control through NO and endothelin-1 production (minor)

Between neural and local control, what usually wins

Neural. Sympathetic usually well

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

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

Increasing skeletal muscle CO2 production would _______ blood flow

Increase

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

Active hyperemia

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

Active hyperemia

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

Reactive hyperemia

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

Hemostasis

What are the 3 stages of hemostasis

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

What stages of hemostasis require platelets

All stages

What are platelets?

Not true cells. Bags of enzymes - megakaryocytes shed them - full of clotting proteins, vasoconstrictors, and platelet activating molecules

When does the vessel constrict in hemostasis

Immediately after damage | Slows flow to damaged area

What does damaged endothelium do

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

What does pain do in hemostasis?

Causes vasoconstriction

Platelet plug formation

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

What kind of feedback is platelet plug formation

Positive feedback mechanism

Collagen binds to _______factor in platelet plug formation

Von Willebrand

What protein is responsible for platelet plug formation

Von Willebrand factor

Enzymatic cascade that converted fibrinogen into fibrin

Coagulation

What is a thrombus?

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

What happens if a thrombus breaks off

Embolus

Where do venous emboli originate?

Legs (Deep vein thrombosis)

Where do venous emboli usually get stuck

Lungs

What do venous emboli cause

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

Where do arterial emboli originate

Atria or carotids

Where do arterial thrombi normally get stuck

Cerebral or ocular vessels

What does arteriolar emboli cause

Stroke and retinal ischemia

What are the two pathways of clot formation

Intrinsic and extrinsic

What is intrinsic clot formation caused by

Initiated by exposed collagen

What is extrinsic clot formation initiated by

Release of tissue factor | Turns on platelets

What are the Vit K dependent factors in clot formation

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

What factor is the most sensitive to vitamin K

7 (stable factor)

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

Factor 10

What happens during hemostasis after one hour

Clot retraction

Pulls damaged vessel walls together, takes a lot of platelets

Fibrinolysis

Clot dissolution

In fibrinolysis, what digests the fibrin

Plasmin

Why do we want fibrinolysis?

Re establish blood flow to that area

What is the clot buster

Tissue plasminogen activator (tPA)

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

Tissue plasminogen activator

What kind of strokes do we use tPA for

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

What does aspirin do

Blocks TXA2 production which keeps the platelets from sticking together An aspirin a day keeps the clots away

What does heparin inhibit

Factor 2 and 10 Inhibits where intrinsic and extrinsic come together!!! TEST

What does warfarin (Coumadin) do

Inhibits vitamin K production Inhibits factor 7!! TEST

Which anti platelet drug is fast acting

Heparin

Which anti platelet drug is slow acting

Warfarin (Coumadin)

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

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

Special Circulations And Hemostasis Flashcards

(83 cards)