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Physpharm Semester 2 > Blood Flow through the body > Flashcards

Blood Flow through the body Flashcards

1
Q

In what direction does blood flow in during circulation?

A

High pressure to low pressure

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2
Q

Organization of blood vessels in order from leaving the heart

A

Arteries - arterioles - capillaries - venules - veins

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3
Q

Characteristics of arteries

A
  • Large diameter
  • Thin walls (relative to the diameter)
  • Very elastic
  • Low resistance
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4
Q

Characteristics of arterioles

A
  • small diameter
  • thick walls (relative to the diameter)
  • lots of smooth muscle (innervated by SNS)
  • CONTROLS BLOOD FLOW
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5
Q

MAP = ?

A

TPR x CO

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6
Q

Characteristics of capillaries

A
  • one cell thick
  • extremely thin walls - allows for gas exchange (diffusion)
  • low blood pressure
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7
Q

Two types of capillaries

A
  • Continuous capillary (less permeable)
  • Fenestrated capillary (more permeable due to pores connecting it straight to the tissue)
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8
Q

What are Starling forces?

A
  • forces which dictate filtration and reabsorption in the capillaries
  • many different forces due to different molecules and gradients
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9
Q

What is edema?

A
  • swelling due to excess fluids accumulating in tissue
  • due to excess filtration from capillaries
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10
Q

Characteristics of veins

A
  • large diameter
  • very thin walls compared to diameter
  • very low blood pressure
  • smooth muscle innervated by SNS
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11
Q

What is the skeletal muscle pump in veins?

A
  • smooth muscle in veins constrict in order to bring blood back to the heart
  • special valves prevent back flow
  • SNS can cause these smooth muscles to contract faster/harder
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12
Q

How does the SNS increase blood flow through venous return?

A
  • innervates smooth muscles in veins (alpha adrenergic receptors)
  • faster/stronger contractions = higher EDV (preload)
  • higher EDV = increased stroke volume = increase CO
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13
Q

What are the three types of mechanisms used to regulate blood flow?

A
  • Neural mechanisms (SNS and PNS)
  • Humoral mechanisms (substances in blood)
  • Local (tissue environment)
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14
Q

True/False - The PNS innervates blood vessels and slows blood flow using direct blood vessel control

A

False

  • Only SNS innervates blood vessels (alpha adrenergic receptors)
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15
Q

What are 4 humoral molecules which regulate blood flow?

A

Vasoconstrictors (stimulus is a decrease in BP)
- ADH
- Angiotensin ll

Vasodilators (stimulus is an increase in BP)
- Atrial natriuretic peptide
- Histamine

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16
Q

Can epinephrine cause vasoconstriction AND vasodilation?

A

Yes

Vasoconstriction - by binding to alpha adrenergic receptors on blood vessels

Vasodilation - by binding to Beta 2 adrenergic receptors on heart, increasing blood flow indirectly causing blood vessels to dilate due to increased blood flow

17
Q

The two local mechanisms that control blood flow

A

Myogenic Theory - increased blood pressure means arterioles stretch, so arterioles contract back after stretching to original state or smaller to control blood flow

Metabolite Theory - change in metabolic needs/metabolites in the blood = higher/lower blood flow

18
Q

What are the receptors which detect changes in MAP and send signals to the CV centre in the medulla called?

A
  • baroreceptors (mechanoreceptors)
19
Q

Where are the mechanoreceptors that regulate MAP located?

A
  • walls of aortic arch and the carotid arteries
20
Q

How does the nervous system adjust the MAP when the it decreases?

A
  • SNS activation
  • heart pumps faster and harder = more CO
  • Blood vessels constrict = higher TPR
21
Q

How does the nervous system adjust the MAP when it increases?

A
  • PNS activation
  • Heart pumps slower and weaker = lower CO
  • PNS activated = no SNS activation on vessels meaning vasodilation = lower TPR
22
Q

What is hypertension?

A
  • high blood pressure
    Blood pressure >140 mm Hg
23
Q

Targets for treating hypertension

A
  • lowering TPR
  • lowering CO
24
Q

Treatments for hypertension

A
  • beta blockers (block SNS activity on heart)
  • Calcium channel blockers
  • Angiotensin-converting enzyme inhibitors (ACE inhibitors)
  • Angiotensin ll receptor blockers (ARBs)
25
Q

How do calcium channel blockers help treating hypertension?

A
  • Calcium channel blockers block calcium from entering smooth muscle on arteries = no vasoconstriction and decreased BP
26
Q

How do ACE inhibitors help treat hypertension?

A
  • prevents angiotensin l going to angiotensin ll
  • angiotensin ll leads to high BP by narrowing vessels
  • angiotensin 2 stimulates aldosterone production which increases blood pressure
  • therefore, stopping this reaction from taking place will decrease BP
27
Q

What are the two types of calcium channel blockers?

A
  • dihydropyridines (less effect on heart) and non-dihydropyridines (more effect on heart)
28
Q

How do angiotensin receptor blockers help treat hypertension?

A
  • blocks angiotensin ll from binding to its receptor
  • usually, angiotensin ll binding to the receptor causes vasoconstriction, so stopping that from happening will lower blood pressure
29
Q

What are the three mechanisms of hemostasis?

A
  • vasoconstriction around site of injury
  • platelet aggregation to stop bleeding (primary hemostasis)
  • coagulation cascade to form stable blood clot (secondary hemostasis)
30
Q

Why do platelets aggregate at a site of injury?

A
  • platelets adhere to collagen, which is exposed when a vessel is injured
  • when platelets contact collagen, they become active, sending chemical mediators (important one is called thromboxane) to recruit other platelets to the site of injury
31
Q

What is the final and most important product of the coagulation cascade?

A
  • Fibrin
32
Q

How can aspirin prevent a heart attack or a dangerous blood clot?

A
  • aspiring blocks enzyme responsible for release of thromboxane
  • results in less platelets activated and congregated
  • smaller/no blood clot formed
33
Q

What is Warfarin?

A

-Vitamin K important for synthesis of some clotting factors
- antagonist drug for vitamin K
- therefore, it stops clotting by blocking vitamin K from binding to receptors, inhibiting clotting to continue

Physpharm Semester 2 (11 decks)

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