Control of blood flow Flashcards

1
Q

What is acute control?

A

local blood flow control that is rapid (occurs in seconds to minutes). It includes the vasodilator theory and the oxygen (nutrient) lack theory.

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2
Q

What is long-term control?

A

local blood flow control that occurs over a long period. An increase in the size and numbers of vessels results.

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3
Q

What is the vasodilator theory?

A

Theory of SHORT TERM local blood flow control. As metabolism increases, oxygen availability to the tissues decreases, and vasodilators are formed.

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4
Q

When do vasodilators form?

A

under conditions of low oxygen (hypoxia).

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5
Q

What are some examples of vasodilators?

A

adenosine, CO2, histamine, K+, H+

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6
Q

What is the oxygen (nutrient) lack theory?

A

a decrease in oxygen causes blood vessel relaxation and dilation..

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7
Q

What is vasomotion?

A

the cyclical opening and closing of pre-capillary sphincters. They open in proportion to the needs of tissues.

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8
Q

What is hyperemia?

A

increased blood flow

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9
Q

What is reactive hyperemia?

A

increased blood flow after a blocked artery is no longer blocked. The flood flow increases 4 -7 x, which can be fatal.

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10
Q

What is active hyperemia?

A

When any tissue becomes active, the rate of blood flow increases.

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11
Q

An increase in blood flow is ____ proportional to the rate of metabolism.

A

directly

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12
Q

An increase in blood flow is ____ proportional to the rate of arterial oxygen saturation.

A

inversely

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13
Q

In tissues, autoregulation will decrease high blood flow, but it will not decrease what?

A

blood pressure; high blood flow is regulated by negative feedback.

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14
Q

What are two theories of autoregulation?

A

metabolic and myogenic

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15
Q

What is the metabolic theory of autoregulation?

A

increase in blood flow -> too much oxygen or nutrients -> vasodilators washed out

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16
Q

What is the myogenic theory of autoregulation?

A

stretching of vessels -> reactive vasculature constriction -> blood flow returned to normal.

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17
Q

Generally, when blood flow increases, ___ also increases.

A

blood pressure; an acute response increases in pressure more rapidly than a long-term response.

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18
Q

What three organs use special acute flow mechanisms?

A

kidney (tubuloglomerular feedback), brain and skin (blood flow linked to body temperature and is regulated by sympathetic nerves to the CNS).

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19
Q

What is the special acute flow control mechanism for the brain?

A

increase in CO2/H+ -> cerebral vessel dilation -> washing out of excess CO2/H+

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20
Q

In endothelial cells, what molecule initiates the process of vasodilation?

A

cyclic GTP (cGTP)

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21
Q

in endothelial cells, what molecule activates cGTP?

A

Nitrous oxide (NO)

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22
Q

In endothelial cells, cGMP activates what proteins?

A

protein kinases.

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23
Q

Protein kinases directly activate the blood vessels to do what?

A

dilate

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24
Q

In damaged endothelial cells, what protein is secreted?

A

endothelin; it causes vasoconstriction.

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25
Q

In damaged endothelial cells, what molecules is not released that would otherwise activate cGTP and hence vasodilation?

A

NO

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26
Q

What are some vasoconstrictors?

A

norepinephrine, epinephrine, angiotensin II, vasopressin (ADH)

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27
Q

What are some vasodilators?

A

bradkinins and histamine

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28
Q

What kind of vessel does the sympathetic nervous system not innervate?

A

capillaries

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29
Q

Innervation from the sympathetic nervous system causes the vessels to do what?

A

constrict

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30
Q

The vasocontrictor area in the upper medulla does what?

A

transmits continuous signals to blood vessels, which results in sympathetic vasoconstriction tone.

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31
Q

The vasodilator area in the lower medulla inhibits what other area?

A

vasoconstrictor area

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32
Q

Where is the sensory area in the brain?

A

the medulla; it receives signals from the vagus nerves and glossopharyngeal nerves.

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33
Q

What is the sensory area controlled by?

A

reticular substance, hypothalaus and cerebral cortex

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34
Q

What is the function of basoreceptors?

A

They inhibit vasoconstrictor areas and activate vasodilator centers. They are found in the common carotid arteries and the aorta.

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35
Q

The glossopharyngeal nerve sends signals to what area of the brain?

A

sensory area

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36
Q

Signals from the sensory area in the brain are send to which region?

A

Vasodilator area

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37
Q

The vagus nerve sends signals to what area of the brain?

A

sensory area.

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38
Q

What are carotid bodies?

A

chemosensitive sells that sense hydrogen ion concentration. They are important for respiration.

39
Q

What does the adrenal medulla secrete?

A

epinephrine and norepinephrine (sympathetic)

40
Q

The rapid neural control of arterial pressure includes what simultaneous changes to vessels?

A

constriction of the arteries and veins and increasd heart rate. The response is rapid and leads to decreased cardiac output.

41
Q

loss of vasomotor tone (e.g. sympathetic innervation) results in a _____ of blood pressure?

A

decrease

42
Q

When are baroreceptors stimulated?

A

when arterial pressure is low.

43
Q

Baroreceptors send signals where?

A

cerebral cortex, hypothalamus and reticular substance (e.g. the sensory area)

44
Q

Baroreceptors function to do what?

A

activate vasodilator area, which can cause an increase or decrease in pressure. Barorecepors function to reduce the minute-by-minute variation in arterial lpresure.

45
Q

As baroreceptors are activated, what happens to blood pressure?

A

the pressure increases , then levels off at around 240 mm Hg

46
Q

When the vagus nerve has been cut, what happens to blood pressure?

A

It increases by 50%

47
Q

When baroreceptors are denervated, what happens to blood pressure?

A

the pressure is highly variable.

48
Q

What do low pressure atrial reflexes do?

A

minimize arterial pressure changes in response to blood volume.

49
Q

Increase of atrial stretch results in what?

A

the kidneys will dilate, which causes an increase of kidney fluid loss and decreased blood volume. Heart rate increases, ADH and Na+ reabsorption decrease in the kidneys.

50
Q

What is the formula for arterial pressure?

A

cardiac output x total peripheral resistance.

51
Q

Arterial pressure rises when what kind of resistance is acutely increased?

A

total peripheral resistance

52
Q

How do kidneys return arterial pressure back to normal?

A

pressure diuresis or pressure natriuresis

53
Q

What is primary hypertension?

A

increased blood pressure. It results in increased cardiac output, sympathetic stimulation, angiontensin II & aldosterone, and impariment of natriuses and secretion of salt & water

54
Q

What are major factors that cause primary hypertension?

A

weight gain and sendentary lifestyle.

55
Q

What are causes of secondary hypertension?

A

kidney tumors, kidney vessel constriction, preeclampsia, neurogenic hypertension, genetics

56
Q

Secondary hypertension can be caused by many abnormalities in what organ?

A

kidney

57
Q

Hypertension can be caused by the endocrine system. What are some disorders of the endocrine system that cause hypertension?

A

hyperthroidism/hypothyroidism, pregnancy

58
Q

What are some cardiovascular causes of hypertension?

A

increased intravascular volume, increased cardiac output, rigid aorta

59
Q

What are some neurologic causes of hypertension?

A

increased intracranical pressure, sleep apnea, acute stress, psychogenic factors

60
Q

What are some general contributing factors to hypetension?

A

genetics, stress, obesity, smoking, physical inactivity, heavy consumption of salt.

61
Q

Factors that lead to decreased resistance and blood pressure include what?

A

nitric oxide, prostacyclin, kinins, ANP, decreaed beta-andrenergic factors.

62
Q

What are some cardiac factors that lead to decreased cardiac output?

A

decreased blood volume, heart rate and contractility.

63
Q

What cardiac conditions lead to incresed blood pressure?

A

increased heart, volume, and contraction.

64
Q

What factors cause incresed resistance and blood pressure?

A

increased angiotensin II, catecholaimnes, thromboxane, alpha-adrenergic factors.

65
Q

What are the humoral vasoconstrictors?

A

angiotensin II, catecholamines, endothelin

66
Q

Wht are the huoral vasodilators?

A

kinins, prostagalandins, nitric oxide.

67
Q

What does chronic hypertension lea to?

A

early heart failure, cerebral infarct, kidney failure

68
Q

What is the major characteristic of atherosclerosis?

A

the presence of lesions within the intima of the vessel wall that protrude into the vessel lumen.

69
Q

What are risk factors (non-modifiable) for athersclerosis?

A

age (old), gender (post-menopausal women), genetics

70
Q

What are modifiable risk factors for athersclerosis?

A

hyperlipidemia (high cholesterol), hypertension, smoking diabetes, inflammation (correlated with high cholesterol), hyperhomocystinemia (errors in metabolism), metabolic syndrome (obesity & insulin ressitance)

71
Q

What is hyperhomocystinemia

A

A disorder in which metabolism is affected; it causes hypertension and premature vascular disease.

72
Q

What is metabolic syndrome?

A

Syndome associated with insulin resistance. It causes obseity, increased lipids and cholesterol levels and hypertension.

73
Q

Hypertension can be caused by what types of injury to the vessel?

A

Endothelial injuries. The intima thickens and an atheroma may result.

74
Q

The accumulation of lipoproteins, especially oxidized LDL, can cause what?

A

hypertension

75
Q

When monocytes adhere to damaged vessel epithelium, what do leukocytes and endothelial cells release?

A

growth factors that promote smooth muscle cell proliferation.

76
Q

Smooth muscle proliferation converts fatty streaks into what?

A

matura atheroma

77
Q

What is an atheroma?

A

a cap of smooth muscle cells, macrophages and foam cells that overlie a necrotic center composed cell debris, foam cellsa nd calcium.

78
Q

What are the earliest lesion in vessels called?

A

fatty streaks

79
Q

After plaques are deposited in the lumen and apoptose, what process do they undergo?

A

calcification

80
Q

Where is athersclerosis most common?

A

lower abdominal aorta and the coronary arteries.

81
Q

Where is athersclerosis leas common?

A

popliteal arteries, interal carotid arties and the circle of willis.

82
Q

Short term control of arterial pressure results in what?

A

sympathetic control of the vascular resistance, capaacitance and cardiac pumping ability.

83
Q

Long term control of arterial pressure is controlled by what?

A

nervous and hormonal controls, as well as local controls in the kidney that regulate salt and water excretion.

84
Q

As arterial pressure increases, what happens to urinay output?

A

it also increases

85
Q

An increase in arterial pressure results in an increase of what to things?

A

increased urine output and sodium output.

86
Q

Pressure diuresis is associated with what?

A

increased urine output.

87
Q

Pressure natriuresis is associated with what?

A

increased sodium output.

88
Q

What are the primary determinants of long-term arterial pressure lvel?

A

degree of the pressure shift of the renal output curve and the level of water/salt intake.

89
Q

How does increased salt intake affect arterial pressure?

A

Pressure is not greatly changed by salt intake.

90
Q

What is chronic hypertension?

A

Blood pressure is greater than 110 mm Hg (135/90)

91
Q

What are the lethal effects of chronic hypertension?

A

early heart failure, coronary heart disease, heart attack, cerebral infarct, destruction of areas of the kidney

92
Q

When the renin-angiotensin curve is blocked, what happens to arterial pressure?

A

it decreases

93
Q

What is “one-kidney” Goldblatt hypertension?

A

hypertension that results from the removal of one kidney and the constriction of the remaining renal artery.