Special Circulations And Hemostasis Flashcards
How can blood flow to organs change
Depending on metabolic demand
What are the two ways that blood flow can be controlled
Extrinsically
Intrinsically
Extrinsic blood flow control
Something else decides
Neural or hormonal
Intrinsic blood flow control
Organ decides
Loca control from tissue itself
Neural and hormonal autonomic innervation
SNS-a1 receptors constrict
SNS-B2 receptors-dilate
PNS-M3 receptors-dilate (via NO) primarily via drugs
Vasoconstriction hormones in neural and hormonal control
Angiotensin II-constricts Prostaglandins- variable Histamine-dilates Endothelin-constricts NO-dilates
What is local control
Organ controlling its own blood control
What are the 3 examples of loca control
Autoregulation
Active hyperemia
Reactive hyperemia
Blood flow is maintained constant despite changing arterial pressure
Autoregulation
What organs use autoregulation method of local control
Kidney and Brian.
Blood flow changes as metabolic demand changes
Active hyperemia
Running-blood goes to legs
Periods of reduced blood flow are followed by supernormal flow
Reactive hyperemia
Goes above what it actually needs
What are the two main mechanisms of local control
Myogenic mechanism
Metabolic mechanism
Smooth muscle adjusts diamterer of vessels to maintain blood flow
Myogenic mechanism
What type of regulation is mygenic mechanism of local blood flow control
Autoregulation
What happens in myogenic mechanism
- flow decreases, vessels dilate
- flow increases, vessels constrict
- based on maintaining wall tension of vessels
Metabolic by-products act as local signals to alter flow
Metabolic mechanism
What kind of local control is metabolic mechanism
Active or reactive hyperemia
Exercise increases metabolic activity means more metabolites. This causes dilation and more flow. Opposite is true
Active hyperemia
Exercise
During transient ischemia metabolites build up, excess blood flow is required to wash them out
Reactive hyperemia
Occlusion
Blood flow in the coronary vessels to feed heart
Coronary flow
What kind of control is coronary flow
Metabolic control- active hyperemia through hypoxia and adenosine MOST IMPORTANT
When does coronary flow have reactive hyperemia
Diastole because it pinches off blood supply during systole, increased metabolites
Coronary flow and neural control
Very little neural control. Brain cant kill the heart or brain wont get any blood
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
- Vascular constriction
- Formation of a platelet plug
- 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
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
