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Block 2 Week 3 > Local and Systemic Control > Flashcards

Local and Systemic Control Flashcards

1
Q

What is ohm’s law?

A

Q(flow)= pressure differences/ resistance

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2
Q

Blood flows when pressure exceeds (blank)

A

resistance

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3
Q

Flow =(blank)/resistance

A

MAP

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4
Q

(blank) can be changed by changing resistance of the vasculature or the pressure gradient in the circulation.

A

Blood flow

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5
Q

What is poiseuille’s law?

A

R =8nl/pir4
n=blood viscosity
l=blood vessel length
r=radius of the vessel

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6
Q

Blood flow is directly related to the pressure and the (blank)

A

4th power of the radius

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7
Q

blood flow is (blank) related to the length of the vessel segment and viscosity of the blood.

A

inversely

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8
Q

Changing the (blank) of a vessel will change the resistance of this vessel the most.

A

radius

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9
Q

What are the regulatory mechanisms of peripheral circulation?

A

adjustment of pump output
changes in diameter of resistance vessels
Alteration in capacitance of vessels (veins)
changes in extracellular fluid volume

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10
Q

What is the dual control of the peripheral circulation?

A

Local (intrinsic) mechanisms

Systemic (extrinsic) mechanisms

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11
Q

The peripheral circulation is under dual control: centrally through the (blank), and locally by the conditions in the (blank) of the blood vessels.

A

nervous system

immediate vicinity

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12
Q

In some areas of the body, such as the skin and splanchnic regions, (blank) predominates, whereas in others, such as the heart and brain, this mechanism plays only a minor role.

A

neural regulation of blood flow

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13
Q

What are the two types of local (intrinsic) mechanisms?

A

metabolic and myogenic

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14
Q

What are the two types of metabolic local (intrinsic) mechanisms?

A

release of vasodilators, nutrient deficiency for vascular smooth muscle

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15
Q

What are the two types of myogenic local (intrinsic) mechanisms?

A

sudden stretch and reduced stretch

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16
Q

What do local (intrinsic) mechanisms effect?

A

Pressure flow autoregulation
Active hyperemia
Reactive hyperemia

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17
Q

Can vascular smooth muscle maintain basal tone when there is nutrient deficiency?

A

no

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18
Q

(blank) is constant flow under varying pressures

A

autoregulation

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19
Q

(blank) of blood flow is the acute return of the flow back to normal shortly after the arterial pressure changes from normal.

A

Autoregulation

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20
Q

The myogenic theory of autoregulation invokes a role for (blank) as the controlled variable in the vasculature.

A

arteriolar wall tension

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21
Q

Sudden stretch of small blood vessels will cause the smooth muscle of the vessel wall to (blank) (possible mechanism – activation of stretch-activated cation channels that are permeable for Ca2+)

A

contract

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22
Q

The vascular smooth muscle contracts in response to an (blank) across the wall of a blood vessel. The resulting vasoconstriction will maintain a . (Without vasoconstriction, blood flow would increase as a result of the increased pressure).

A

increase in pressure difference

constant flow

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23
Q

(blank) is the maintenance of a constant blood flow in the presence of a change in arterial pressure

A

autoregulation

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24
Q

The changes in blood flow in response to overall homeostasis (e.g., the dilation of coronary arteries when the energy requirements of the heart increase during exercise) are not classified as (blank)

A

autoregulatory processes.

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25
Q

Blood flow is trying to be constant so (blank) is altered to maintain this

A

resistance

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26
Q

Autoregulation is only when you have (blank) , you do not utilize autoregulation when stressed via exercise (this is increased output, NOT changes in pressure)

A

increased or decreased pressure

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27
Q

Do you utilize autoregulation when stressed via exercise (increased output, not changes in pressure)?

A

no

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28
Q

(blank) cannot be maintained at extreme changes in mean arterial pressure.

A

Autoregulation

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29
Q

The safe range for blood flow is about 80-125% of normal and usually occurs at arterial pressure of (blank) due to active adjustments of vascular resistance.

A

60-160 mm Hg

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30
Q

(blank) is increased blood flow caused by increased tissue activity

A

ACTIVE HYPEREMIA

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31
Q

(blank) is blood flow above control level upon release of an arterial occlusion

A

REACTIVE HYPEREMIA

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32
Q

When would you have active hyperemia?

A

exercise

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33
Q

When would you have reactive hyperemia?

A

skeletal muscle contracts and compresses blood vessel, when contraction of skeletal muscle ends the blood is free to move through the vessel

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34
Q

Why do you want vasoconstriction in pressure flow autoregulation when you have high blood pressure?

A

Since you are sensing an increased difference in pressure than you need to increase resistance proportionally to maintain flow

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35
Q

WHat two things cause release of vasodilator substances?

A

deficiency of 02 and increased metabolism

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36
Q

Deficiency of 02 and nutrients in the vascular smooth muscle inhibits the ability of what?

A

muscle to contract

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37
Q

These are potential candidates for (blank)

  • (increase) CO2
  • lactic acid
  • (decrease) pH
  • K+
  • PO4
  • PgI2
  • adenosine
  • ATP
  • (decreased) O2
  • increased osmolarity
A

vasodilator metabolites

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38
Q

Large amounts of (blank) can cause vasoconstriction. Small amounts of (blank) can cause vasodilation.

A

Potassium

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39
Q

What does adensosin do and when is it released?

A

it is a vasodilator and it s released under hypoxia

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40
Q

What are EDRF? DO they have receptors?

A

relaxation factors secreted by endothelium

They each have their own receptors on endothelial cells

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41
Q

Endothelial cells can sense (blank) which will induced them to release (blank)

A

stress

relaxation factors

42
Q

There is a (blank) between endothelium and adjacent smooth muscle cells.

A

functional interaction

43
Q

Endotoxin cytoking, L-arg, shearing forces, acetycholine, bradykinin substance P insulin, NOS can induce what to be made?

A

NO (citrulline too)

44
Q

What does NO do?

A

it creates cGMP to cause relaxation

45
Q

Endothelium lines arterioles (and virtually all blood

vessels). So it experiences the (blank) associated with flow.

A

shear stress

46
Q

Where does autoregulation take place?

A

liver, brain and kidney

47
Q

With increased (blank) endothelium releases factors, in particular EDRF

A

flow (and increased shear stress)

48
Q

EDRF (=NO) activates (blank), which increases cGMP increases sequestering of intracellular Ca2+, less calcium means less contraction

A

GC

49
Q

Increased blood flow allows for release of factors from vessel endothelium which results in dilation and (blank) velocity through vessel.

A

decreased

50
Q

What are the two systemic (extrinsic) mechanisms?

A

Humoral (hormonal) and Neural

51
Q

What are the systemic (extrinsic) mechanisms of humoral function?

A 
Adrenal medullary hormones
RAAS
Endothelins
Kinins
Natriuretic peptides
52
Q

What are the systemic (extrinsic) mechanisms of neural function?

A

Sympathetic (heart and blood vessels)

Parasympathetic (heart&raquo_space; blood vessels)

53
Q

Stimulation of the nerves to the adrenal glands

causes release of both (blank) and (blank) in the systemic circulation.

A

epinephrine (80 %) and

norepinephrine (20 %)

54
Q

What do Alpha 1 receptors do?

A

-Vasoconstriction
-Increased peripheral
resistance
-Increased blood pressure

55
Q

What do Beta 1 receptors do?

A

-Tachycardia
-Increased myocardial
contractility

56
Q

What do Alpha 2 receptors do?

A

-Inhibition of NE release
-Vasoconstriction
(veins>arteries)

57
Q

What do Beta 2 receptors do?

A

-Vasodilatation
-Slightly decreased
peripheral resistance

58
Q

What is the most common way catecholamines cause vasoconstriction?

A

alpha 1 activation

59
Q

What are present at presynaptic junctional receptors that regulate release of norepinephrine

A

Alpha 2 activation

60
Q

(blank) adrenal medullar hormones effect all receptors but mostly the betas

A

epinephrine

61
Q

(blank) affects only A1, A2 and B1

A

norepinephrine

62
Q

(blank) affects only B1 and B2

A

isoproterenol

63
Q 
What causes this:
INCREASED Heart rate                   
Increase Stroke volume
Increase Cardiac contractility
Decrease Venous capacitance
Increase coronary flow
Increase muscle flow
Decrease kidney flow
Increase splachnic flow
A

Epinephrine

64
Q 
What causes this:
DECREASED Heart rate (vagal)                  
Increase Stroke volume
Increase Cardiac contractility
Decrease Venous capacitance
Increase coronary flow
Decrease muscle flow
Decrease kidney flow
Increase splachnic flow
A

Norepinephrine

65
Q

What causes this:

  • Vasoconstriction (veins > arteries)
  • Effect on blood pressure consists of initial depressor response (release of PgI2) followed by sustained increase in blood pressure due to vasoconstriction.
  • Positive inotropic and chronotropic effect.
  • Increase plasma levels of ANP, renin, aldosterone, and catecholamines.
  • Increase release of sympathetic transmission.
  • Produce bronchoconstriction.
  • Decrease glomerular filtration rate, renal blood flow, increases Na+ reabsorption.
A

Endothelins

66
Q

What is released form endothelial cells and causes vasoconstriction

A

endothelins

67
Q

Explain the renin-angiotensin-aldosterone system?

A

Angiotensin is produced from liver->coverts to angiotensin I-> epithelial cells of lungs produced angiotensin II->ADH (brain) + aldosterone (kidney)-> vasoconstriction + increased water absorbtion (Na and H20)

68
Q

Explain the Kinin pathway?

What does it do?

A

active factor XII + plasmin->plasma kallikrein + kininogens-> bradykinin and lyslbradykinin

vasodilation

69
Q

If you block ACE or Kinanase II you will cause (blank).

A

vasodilation

70
Q

(blank) is a 28-amino acid peptide that is synthesized, stored, and released by atrial myocytes in response to atrial distension, ANG II stimulation, endothelin and sympathetic stimulation (b-adrenoceptor-mediated).

A

Atrial natriuretic peptide (ANP)

71
Q

Elevated levels of ANP and BNP are typically found during (blank)

A

hypervolemic states (elevated blood volume) and congestive heart failure.

72
Q

Will you find CNP in the heart? Will you find ANP or BNP in the heart?

A

No,

Yes

73
Q

What serves as a counter-regulatory system for the RAAS?

A

natriuretic peptides

74
Q

What causes vasodilation and renal effects that lead to natruiresis and diuresis?

A

natriuretic peptides

75
Q

(blank) directly dilate veins and thereby decrease central venous pressure, which reduces cardiac output by decreasing ventricular preload.

A

Natriuretic peptides

76
Q

(blank) also dilate arteries, which decreases systemic vascular resistance and systemic arterial pressure. Vasodilatation is achieved by the increased cGMP levels (but by a different mechanisms of NO).

A

natriuretic peptides

77
Q

(blank) affect kidneys by increasing glomerular filtration rate (GFR) and filtration fraction, which produces natriuresis (increased sodium excretion) and diuresis (increased fluid excretion).

A

natriuretic peptides

78
Q

A second renal action of (blank) is that they decrease renin release, thereby decreasing circulating levels of angiotensin II and aldosteron. This leads to further natriuresis and diuresis (water and sodium loss). Decreased ANGII also contributes to systemic vasodilatation and decreased systemic vascular resistance.

A

Natriuretic peptides

79
Q

What are the two main action of natriuretic peptides?

A

Vasodilatation

Renal effects that lead to natriuresis and diuresis

80
Q

What are the 5 main effects of natriuretic peptides?

A 
Decreased blood volume
Decreased arterial pressure
Decreased central venous pressure
Decreased pulmonary capillary wedge pressure
Decreased cardiac output
81
Q

What doesnt have B2 receptors?

A

skin and mucosa
cerebral
salivary glands
veins (systemic)

82
Q

What are the two feedback loops?

A

autonomic feedback loop and hormonal feeback loop

83
Q

the (blank) directly influences the four major variables, peripheral vascular resistance, heart rate, contractile force of the heart, and venous tone.

A

sympathetic autonomic nervous system

84
Q

The (blank) directly influences heart rate.

A

vagus

85
Q

(blank) directly increases peripheral vascular resistance.

A

Angiotensin II

86
Q

an increase in (blank) causes an increase in renal blood flow; an increase in renal blood flow causes a decrease in renin release; an increase in plasma renin causes an increase in angiotensin production, etc.

A

mean arterial pressure

87
Q

Circulatory homeostasis for the whole organism is met by a balance between (blank)

A

metabolic, hormonal and neural influences.

88
Q

What are the extrinsic factors that effect arterioles?

A

neural and hormonal

89
Q

What are the intrinsic factors that effect arterioles?

A

tissue metabolits
local hormones
myogenic
endothelial factors

90
Q

There is no (blank) in smooth muscle; instead, Ca2+ regulates myosin on the thick filaments.

A

troponin

91
Q

(blank) plays a central role in the excitation-contraction coupling in vascular smooth muscle cell.

A

Calcium

92
Q

the (blank) is responsible for the control of total peripheral resistance, arterial and venous tone, and the distribution of blood flow throughout the body.

A

The Vascular Smooth Muscle

93
Q

How do you excited vascular smooth muscle and elicit contraction?

A

Ca++ + calmodulin
activates MLCK, which
phosphorylates myosin LC20, resulting in cross-bridge cycling.

94
Q

Vascular smooth muscle lacks (blank) in contrast to skeletal muscle. Ca2+ plays a central role on excitation-contraction coupling in vascular smooth muscle.

A

troponin and fast sodium channels

95
Q

(blank) coupling is the predominant mechanism for eliciting contraction of vascular smooth muscle

A

Pharmaco-mechanical

96
Q

The activation of Receptor/G protein/PLC/IP3/DAG/PKC pathway leads to (blank)

A

vasoconstriction and muscle contraction

97
Q

How does Ca elicit muscle contraction?

What is the clinical focus of this?

A

Calcium-> MLCK->Myosin + Actin-> contraction
-a1, AT, ET, 5HT receptor blockers
as antihypertensive drugs.

98
Q

The inhibition of cAMP/AC/PKA pathway leads to what?

A

vasoconstriction

99
Q

Activation of cAMP/AC/PKA pathway causes what?

What is the clinical focus of this?

A

vasodilation

  • isoproterenol induced vasodilatation
  • ischemia/adenosine/vasodilatation
100
Q

Activation of cGMP/GC/PKG pathway causes
what?
What is the clinical focus of this?

A

Vasodilation (relaxation)
shear stress
-ET, thrombin, atrial distension
and ANP release

Block 2 Week 3 (9 decks)

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