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Physiology I (Exam II material) > Control of blood flow > Flashcards

Control of blood flow Flashcards

1
Q

What are some acute controls for local blood flow

A

Rapid changes in local vasodilation/vasoconstriction

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2
Q

How quickly does acute control (rapid changes in local vasodilation/vasoconstriction) occur

A

seconds to minutes

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3
Q

What are the basic theories behind acute control (rapid changes in local vasodilation/vasoconstriction)

A

Vasodilator theroy

oxygen (nutrient) lack theory

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4
Q

What is a method of long-term local blood flow control

A

increase in sizes/numbers of vessels

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5
Q

how long does it take for long-term control (increase in sizes/numbers of vessels take to occur

A

over a period of days, weeks, or months

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6
Q

What does the vasodilator theory state

A

when we have an increase in metabolism we will have lower oxygen availability, which leads to the formation of vasodilators

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7
Q

Explain the oxygen (nutrient) lack theory

A

Low oxygen concentration leads to blood vessel relaxation, which leads to vasodilation. This is because the smooth muscles in the walls of blood vessels require oxygen to remain contracted

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8
Q

What is the definition of Vasomotion

A

Cyclical opening and closing of precapillary sphincters

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9
Q

Hyperemia can be _____ or _____

A

reactive, or active

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10
Q

Give an example of reactive hyperemia

A

Tissue blood flow blocked (from seconds to hours or more), when you unblock the blood flow increases 4-7x normal

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11
Q

Explain the Vasodilator theory

A

increased metabolism leads to decreased O2 and thus the formation of Vasodilators

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12
Q

Name some Vasodilators (6)

A 
Adenosine
Carbon Dioxide
Adenosine phosphate compounds 
Histamine
Potassium ions
Hydrogen ions
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13
Q

Explain the oxygen (nutrient) lack theory

A

Decreased Oxygen leads to blood vessel relaxation (because the smooth muscle that constricts around blood vessels needs oxygen to remain contracted) thus leading to vasodilation

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14
Q

What is the definition of Vasomotion

A

Cyclical opening and closing of precapillary sphincters

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15
Q

The number of precapillary sphincters open at any given time is roughly proportional to what

A

nutritional requirements of tissues

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16
Q

Vasomotion is a major component to what theory

A

oxygen (nutrient) theory

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17
Q

Vasomotion and the oxygen (nutrient) theory assume what

A

that smooth muscles require oxygen to remain contracted

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18
Q

What is hyperemeia

A

increase in bloodflow that is greater than normal

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19
Q

What are the two forms of hyperemia

A

reactive and active

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20
Q

What is reactive hyperemia

A

tissue blood flow is blocked (for seconds to hours or more)
once unblocked you get a blood flow increase of 4-7 times the normal for (seconds, minutes, or hours) it is the bodies attempt to reapy for hte lost oxygen and nutrients during the blockage

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21
Q

What is active hyperemia

A

When any tissue becomes active, rate of blood flow increases (ex. exercise)

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22
Q

Explain autoregulation

A

A rapid increase in arterial pressure leads to an increase in blood flow
within minutes, blood flow returns to normal even with elevated pressure

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23
Q

Autoregulation can occur in

A

any tissue but is more precise in some such as in the brain

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24
Q

What are two views that explain autoregulation

A

Metabolic theory and Myogenic theory

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25
Q

Explain the metabolic theory for autoregulation

A

increased blood flow leads to too much oxygen and nutrients which then wash out the vasodilators leading to a constriction of the vessel and a decrease in flow

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26
Q

Explain the myogenic theory for autoregulation

A

Stretching of the vessel walls leads to reactive vasculature constriction therefore decreasing blood flow

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27
Q

Where are three special acute blood flow control mechanisms found

A

Kidneys, Brain, and skin

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28
Q

How do the kidneys effect acute blood flow control

A

Tubuloglomerular feedback: composition of the fluid in the early distal tubule is detected by an epithelial structure of the distal tubule itself called the macular densa, located at the juxtaglomerular apparatus.
When too much fluid filters form the blood through the flomerulus into the tubular system, feedback signals form the macula densa cause constriction of the afferent arterioles, in this way reducing both renal blood flow and glomerular filtration rate back to nearly normal

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29
Q

How does the brain effect acute blood flow control

A

increase in CO2 and/or H+ leads to cerebral vessel dilation and thus washes out the excess CO2/H+

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30
Q

Explain how the skin has acute blood flow control

A

Blood flow linked to body temperature, sympathetic nerves via CNS,
3 ml/min/100g tissue in cooler temps can increase to as high as 7-8 L/min for entire body in higher temperatures

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31
Q

Nitric Oxide is released by who

A

Endothelial cells

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32
Q

Explain endothelial-Derived mechanisms for vasodilation

A

Endothelial cells release NO which assists in the activation of cGTP to cGMP (in vascular smooth muscle cells), which then activates Protein kinases and dilates the vessel

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33
Q

What is endothelin

A

27 amino acid peptide; effective in nanogram quanities

released by damaged endothelial cells and results in vasocontriction

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34
Q

What is eNOS

A

Nitric oxide synthetase

enzyme in endothelial cells used with O2 and L-arginine to produce NO

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35
Q

What is the half life of NO

A

6 seconds

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36
Q

Humoral Vasoconstriction molecules

A

Norepiephrine, Epinephrine, Angiotensin II, Vasopressin

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37
Q

What is the function of angiotensin II

A

Normally acts to increase total peripheral resistance

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38
Q

What is Vasopressin

A

aka=ADH
very powerful vasoconstrictor
major function is to control body fluid volume

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39
Q

Humoral Vasodilators

A

Bradykinins, Histamine

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40
Q

What is the function of bradykinins

A

cause both vasodilation and increased capillary permeability

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41
Q

What is the function of histamine

A

Powerful vasodilator derived from mast cells and basophils

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42
Q

The sympathetic nervous system innervates all vessels except?

A

Capillaries

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43
Q

The sympathetic nervous system primarily results in _____

A

Vasoconstriction

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44
Q

Retrolental fibroplasia

A

abnormal proliferation of fibrous tissue immediately behind the lens of the eye, leading to blindness.
affected many prematutre babies in the 1950s, owing to the excessive administration of oxygen

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45
Q

What is meant by humoral control of circulation

A

control by substances secreted or absorbed into the body fluids, such as hormones and locally produced factors.

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46
Q

Epinephrine is normally a vasoconstrictor but can cause mild vasodilation in some areas such as the ___

A

coronary arteries during increased heart activity

this is because it has a beta-adrenergic receptor stimulatory effect

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47
Q

which is a stronger vasoconstrictor epinephrine or norepinephrine

A

norepinephrine

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48
Q

As little as one millionth of a gram of angiotensin II can increase the arterial pressure of a human being by

A

50mm Hg or more

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49
Q

Which is a stronger vasoconstriction ADH or Angiotensin II

A

ADH

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50
Q

Where is ADH formed

A

in the hypothalmus

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51
Q

Where is ADH secreted from

A

posterior pituitary gland

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52
Q

What are the 3 vasomotor centers in the brain called

A

vasoconstrictor area, vasodilator area, sensory area

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53
Q

Where is the vasoconstrictor area found

A

in the bilateral anterolateral portions of the upper medulla

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54
Q

What vasomotor center in the brain transmits continuous signals to the blood vessels

A

Vasoconstrictor area

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55
Q

The partial state o f contraction of blood vessels is referred to as

A

vasomotor tone

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56
Q

The Vasodilator area is located in what part of the brain

A

Bilateral in the anterolateral portions of lower medulla

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57
Q

What is the function of the vasodilator area

A

inhibits activity in vasoconstrictor area thus leading to dilation

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58
Q

Where is the sensory area of the vasomotor center of the brain located

A

Bilateral in tractus solitarius in posterolateral portion of medulla

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59
Q

The sensory area of the vasomotor center of the brain receives signals from where

A

vagus nerves (CN X) and Glossopharyngeal nerves (CN IX)

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60
Q

Where are some higher nervous centers that control arterial pressure

A

Reticular substance (RAS), Hypothalamus, Cerebral Cortex

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61
Q

The lateral and superior portions of the RAS cause what in the smooth muscles around vessels

A

Excitation

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62
Q

The medial and inferior portions of the RAS have what effect on vessels

A

They inhibit excitation of smooth muscles around them

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63
Q

The posterolateral portions of the hypothalmus mainly has what effect on vessels

A

excitation of the smooth muscles around them

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64
Q

The anterior portion of the hypothalmus mainly has what effect on vessels

A

causes inhibition of smooth muscles around it

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65
Q

Baroreceptors in the internal carotid arteries are stimulated by pressures

A

Greater than 60 mm Hg

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66
Q

Baroreceptors in the Aorta is stimulated by pressures

A

greater than 30 mm Hg

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67
Q

The aortic baroreceptors send signals to

A

CN X and then to the sensory area

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68
Q

Baroreceptors in the internal carotid send signals to the ___ via ____

A

Sensory area, via Hering’s nerves which then jump onto CN IX

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69
Q

Once the baroreceptors get there signal to the sensory area what happens

A

it positively acts on Vasodilator area which then inhibits vasocontrictor area

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70
Q

The Adrenal Medulla secretes what

A

Epinephrine and Norephinephrine

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71
Q

What are three rapid neural controls of arterial pressure

A

Simultaneous changes of

  • constriction of most systemic arteries
  • constriction of veins
  • Increased heart rate
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72
Q

The neural rapid control of arterial pressure occurs in

A

seconds

73
Q

The neural rapid control of arterial pressure is seen during exercise and leads to

A

increased blood pressure, (accompanied by vasodilation)

74
Q

is fight or flight (alarm reaction) an example of neural rapid control of arterial pressure

A

Yes

75
Q

Baroreceptors are located wher

A

in interal carotid sinuses and aortic sinus

76
Q

baroreceptors are stimulated by what

A

high arterial pressures

77
Q

The carotid sinus baroreceptors are stimulated by pressures

A

greater than 60mm Hg

78
Q

The arotic Baroreceptors are stimulated by pressure

A

greater than 30 mmHg

79
Q

Baroreceptors inhibit what

A

Vasoconstriction center

80
Q

Baroreceptors excite the

A

vasodilator center

81
Q

Signals from the Baroreceptors either cause

A

increase or decrease in arterial pressure

82
Q

What is the primary function of Baroreceptors

A

to reduce the minute by minute variation in arterial pressure to about one third that which would occur if they weren’t present

83
Q

Baroreceptors work as a pressure _____ system

A

buffer

84
Q

Baroreceptors reset every

A

1 to 2 days

85
Q

Where are chemoreceptors located

A

In carotid bodies of bifurcation of the common carotids and in aortic bodies

86
Q

Chemoreceptors are sensitive to

A

lack of oxygen, carbon dioxide, and hydrogen ion excess

87
Q

Signals from chemoreceptors pass from

A

herring’s nerves and vagus nerves

88
Q

Chemoreceptors play an important role in what

A

respiratory control

89
Q

The atrial reflexes are controlled by

A

low pressure receptors located in the atria and pulmonary arteries

90
Q

What is the main function of low pressure receptors in atria and pulmonary arteries

A

play an important role in minimizing arterial pressure changes in response to changes in blood pressure

91
Q

Increase in atrial stretch is sensed by low pressure receptors and results in what

A

reflex dilation of kidney afferent arterioles
increase in heart rate
signals to hypothalamus to decrease ADH secretion
ANP is released and acts on Kidneys to extreme fluid in urine—- increase GFR and decrease NA reabsorption

92
Q

Atrial pressure is equal to what

A

cardiac output x total peripheral resistance

93
Q

Arterial pressure rises when total peripheral resistance is

A

acutely increased

94
Q

Normal functioning kidneys return the arterial pressure back to normal within

A

a day or two

95
Q

What is pressure diuresis

A

effect of increased blood pressure to raise urinary volume excretion

96
Q

What is pressure natriuresis

A

rise in sodium excretion that occurs with elevated blood pressure

97
Q

What are the two methods that kidneys return arterial pressure back to normal in a day or two

A

Pressure diuresis, Pressure natriuresis

98
Q

Characteristics of primary HTN

A

Increased cardiac output, increased sympathetic nerve activity, increase in angiotensin II and aldosterone levels, impairment of renal-pressure natriuresis mechanism, inadequate secretion of salt and water

99
Q

Primary HTN is also known as

A

Essential HTN

100
Q

Primary HTN is what percentage of HTN

A

90-95%

101
Q

Primary HTN has what origin

A

unknown

102
Q

What are the major factors of primary HTN

A

weight gain characterized by
- increased CO
- Increased sympathetic nerve activity
- Increased Angiotensin II and aldosterone levels
- Impaired renal-pressure natriuresis mechanism
sedentary life style

103
Q

Secondary HTN is second to some other causes like what

A 
Tumor affecting renin-secreting juxtaglomerular cells
Renal artery constriction
Coarctation of the aorta
Preeclampsia
Neurogenic HTN
Genetic causes
104
Q

What are some renal causes of HTN

A 
CRD
Renal artery stenosis
Renin-producing tumor 
Acute glomerulonephritis 
polycystic disease
renal vasculitis
105
Q

Endocrine causes of HTN

A

Cushings syndrom (adrenocortical hyperfunction)
Exogenous hormones (glucoricooids, estrogen)
Pheochromocytoma
Acromegaly
Hypothyroidism (myxedma)
Hyperthyroidism (thyrotoxicosis)
Pregnancy induced

106
Q

Cardiovascular causes of HTN

A 
Coarctation of the aorta  (stenosis of aorta)
Polyarteritis nodosa
Increased intravascular volume
Rigidity of the aorta
Increased cardiac output
107
Q

What is polyarteritis nodosa

A

systemic vasculitis of small or medium sized muscular arteries

108
Q

Neurologic causes of HTN

A

Psychogenic
Increased intracranial pressure
Sleep apnea
Acute Stress

109
Q

What are some contributing factors to HTN

A

Genetic factors (essential hypertension is a complex multifactorial disorder)
other single-gene disorders that alter sodium reabsorption by the kidneys
Genetic variants in the renin-angiotensin system
Stress
Obesity
Smoking
Physical inactivity
Heavy consumption of salt

110
Q

What are some factors resulting in decreased peripheral resistance (vessel dilation) leading to decreased blood pressure

A

Increased production of NO
Increased release of prostacyclin
Increased release of kinins
Increase in atrionatriuretic peptide (ANP)
Decreased neural factors (Beta-adrenergic)

111
Q

Factors resulting in decreased cardiac output leading to decreased blood pressure

A

Decreased blood volume
Decreased heart rate
decreased contractility

112
Q

Factors resulting in increased cardiac output leading to increased blood pressure

A

Increased HR
increased contraction
increased blood volume (due to aldosterone)

113
Q

Factors resulting in increased peripheral resistance leading to increased blood pressure

A

Increased angiotensin II
Increased catecholamines
Increased Thromboxane
Increased neural factors (alpha adrenergic)

114
Q

Humoral vasoconstrictors

A

Angiotensin II
Catecholamines
Endothelin

115
Q

Humoral vasodilators

A

Kinins
Prostaglandins
Nitric Oxide

116
Q

What are three lethal effects of chronic HTN

A

early heart failure and CAD
Cerebral infarct
Kidney failure

117
Q

What is atherosclerosis

A

is a type of arteriosclerosis (hardening of the arteries)

118
Q

What is the major characteristic of atherosclerosis

A

presence of lesions within the intimate of the vessel wall that protrude into the vessel lumen

119
Q

Give 3 non-modifiable (constitutional) risk factors for atherosclerosis

A

Age, Gender, Genetics

120
Q

The risk of atherosclerosis increases between the ages of ___ and ___-

A

40 and 60

121
Q

The death rates from ischemic heart disease secondary to atherosclerosis increase with each what

A

decade

122
Q

Atherosclerosis is uncommon in ______ women without other risk factors

A

premenopausal

123
Q

The risk of atherosclerosis increases after ______ in women and eventually _______ that of men

A

menopause, exceeds

124
Q

There are some medelian disorders associated with atherosclerosis but mostly _____-

A

multifactorial

125
Q

What are four modifiable risk factors for atherosclerosis

A

Hyperlipidemia, HTN, Cigarette smoking, Diabetes

126
Q

Hyperlipidemia is a ______ risk factor of atherosclerosis

A

major

127
Q

hyperlipidemia is correlated with high levels of ____ (carries cholesterol to peripheral tissues) as opposed to _____ (carries cholesterol to the liver)

A

LDL, HDL

128
Q

What is the most important cause of left ventricular hypertrophy

A

HTN

129
Q

HTN increases the risk of ischemic heart disease by what

A

60%

130
Q

What are 6 other risk factors of atherosclerosis

A

Inflammation, Hyperhomocystinemia, Metabolic syndrome, Lipoprotein (a), Factors affecting hemostasis,
Life style: lack of exercise, competitive (stressful life style), Obesity

131
Q

Inflammation in the vessels is intimately linked with what

A

atherosclerotic plaque formation

132
Q

What is a major maker for vessel inflammation

A

C-reactive protein (CPR)

133
Q

Where is C-reactive protein (CPR) synthesized

A

Liver

134
Q

What is the function of C-reactive protein

A

Plays important role in opsonizing bacteria and activating complement

135
Q

Inflammation is correlated with high levels of

A

LDL (carries cholesterol to the peripheral tissues)

136
Q

Hyperhomocystinemia is what

A

inborn error of metabolism

associated with premature vascular disease

137
Q

What is metabolic syndrome

A 
Associated with insulin resistance 
characteristics:
  - Obesity ( esp. abdominal fat)
  - Insulin Resistance
  - Fasting hyperglycemia
  - Increased lipid triglycerides
   - Decreased HDL (carries cholesterol to the liver)  levels 
   - Hypertension
138
Q

What is the pathogenies of Atherosclerosis

A

Endothelial injury or dysfunction of any kind
- results in intimal thickening
- may lead to formation of atheroma in presence of hyperlipidemia
Accumulation of lipoproteins
Monocyte adhesion to endothelium and then enters intima. It is now a macrophage and engulfs the oxidized lipoprotein, thus forming a foam cells. this leads to the release of growth factors and inflammation.
smooth muscle proliferation

139
Q

What are some factors related to endothelial dysfunction and atherosclerosis

A 
HTN
Hyperlipidemia
Cigarette smoke
Homocysteine
Infectious agents
Hemodynamic disturbances
Hypercholesterolemia
140
Q

What is the result of chronic hyperlipidemia

A

Accumulation of lipoproteins (esp. LDL) thus leading to atherosclerosis

141
Q

Lipoproteins accumulate in the ____ and are oxidized by oxygen free radicals generated by ___ or ____

A

intima, macrophages, endothelial cells

142
Q

Oxidized LDL is ingested by macrophages which become what

A

Foam cells

143
Q

Oxidized LDL stimulates the release of ____ , ____, and ___

A

growth factors, cytokines, and chemokines

144
Q

Oxidized LDL is toxic to_____ and ________

A

Endothelial cells and smooth muscle cells

145
Q

Endothelial cells express _____ adhesion molecules that bind monocytes and T cells to the endothelium

A

VCAM-1

146
Q

Endothelial cells express VCAM-1 adhesion moleucules that bind ___ and ___ to endothelium

A

Moncytes and T cells

147
Q

When monocytes bind to endothelial cells they transform into ___ and engulf ____

A

macrophages, lipoproteins

148
Q

When T-Cells bind to the endothelium they stimulate what

A

Chronic inflammatory response

149
Q

Activated leukocytes and endothelial cells release growth factors that promote _________ and lead to atherosclerosis

A

smooth muscle proliferation

150
Q

intimal smooth muscle proliferation and extracellular matrix deposition converts a _____ into a ____

A

fatty streak into a mature atheroma

151
Q

An atheroma consist of what

A

cap of smooth muscle cells, macrophages, foam cells (converted macrophages), and other extracellular component, overlying a necrotic center composed of cell debris, cholesterol, foam cells, and calcium

152
Q

The earliest lesion of atherosclerosis are

A

fatty streaks: note these are also seen in all children older than 10

153
Q

Fatty streaks are seen in who

A

all children older than 10

154
Q

Describe the developmental stages of atherosclerosis

A

fatty streaks
atherosclerotic plaques impinge on the lumen of the artery and grossly appear white or yellow
- plaques progressively enlarge due to cell death and degeneration and synthesis/degradation of extracellular matrix
- Plaques often undergo calcification
- plaques may rupture, ulcerate, or erode

155
Q

What are the 5 most common arterial sites for atherosclerosis (most involved to least)

A
  • lower abdominal aorta
  • coronary arteries
  • Popliteal arteries
  • internal carotid arteries
  • Circle of Willis
156
Q

The sympathetic nervous system has short term control on arterial pressure by effecting what

A

total peripheral vascular resistance and capacitance

Cardiac pumping ability

157
Q

What are some examples of long term control of arterial pressure

A

via multiple nervous and hormonal controls

via local controls in kidney that regulate salt and water excretion

158
Q

what leads to pressure diuresis and pressure natriuresis

A

increased arterial pressure

159
Q

The goal of pressure diuresis and pressure natriuresis is what

A

Return of the arterial pressure always back to the equilibrium point= near infinite feedback gain principle

160
Q

What is the near infinite feedback gain principle

A

The kidneys are able to get the arterial pressure almost always back to the equilibrium point. this means that they have little error and are thus close to making an infinite gain when using the gain=corrected/error equation

161
Q

What are the primary determinants of the long-term arterial pressure level

A

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

162
Q

What are two ways of increasing arterial pressure

A

the renal output curve is shifted to the right to increase arterial pressure
The salt wan water intake shows that an increase in intake will result in an increase in arterial pressure

163
Q

what is chronic HTN

A

one’s mean arterial pressure is greater than the upper range of the accepted normal measure

164
Q

What is the normal blood pressure and mean

A

110/70 mean of 90 mmHg

165
Q

What is hypertensive blood pressure and mean

A

135/190 and a mean of 110mmHg

166
Q

What is severe HTN and mean

A

250/130 and a mean of 150-170mmHg

167
Q

What are 5 lethal effects of chronic HTN

A 
Early heart failure
CAD
Heart attack
Cerebral infarct
Destruction of areas of kidney---> kidney failure---> uremia ---> death
168
Q

What is uremia

A

a raised level in the blood of urea and other nitrogenous waste compounds that are normally eliminated by the kidneys

169
Q

Describe the Renin-Angiotensin system

A

Decreased arterial pressure—-> kidney, releases renin—-> renin acts on the substrate angiotensinogen (form the liver) thus forming Angiotensin I (has mild vasoconstrictive properties but not enought to cause significant changes in circulatory functions——> ACE (angiotensin converting enzyme released form endothelium in many tissues including the lungs) converts angiotensin I to angiotensin II (which is a strong vasoconstrictor)——> acts acutely within 20 minutes by constricting arteries (thus increasing peripheral resistance) and to a lesser extent constricting veins (thus leading to increased venous return), it also acts directly on the kidneys to increase salt and water reabsorption as well as on the adrenal gland to release aldosterone and thus leads to more sodium and water reabsorption and extened blood pressure control.

170
Q

What is Renin

A

a protein enzyme released by the kidneys when the arterial pressure falls too low. it is an enzyme and not a vasoactive substance

171
Q

Renin is synthesized and stored in an inactive form called ______ in the _________ of the kidney

A

Prorenin, Juxtaglomerular cells

172
Q

How long does the renin-angiotensin vasoconstrictor system require to become fully active

A

20 minutes

173
Q

The effect of angiotensin to cause renal retention of salt and water can have a powerful effect in promoting what

A

chronic elevation of the arterial pressure

174
Q

The renin-angiotensin system is a ______ mechanism that helps maintain the arterial pressure at or near the normal level even when salt intake is increased

A

automatic feedback

175
Q

Increased salt intake leads to what

A

increased extracellular volume—-> increased arterial pressure—-> decreased renin and angiotensin—> decreased renal retention of salt and water—-> Return of extracellular volume almost ot normal —> return of arterial pressure almost to normal

176
Q

what is the body’s most powerful system for accommodating wide variations in salt intake with minimal changes in arterial pressure

A

Renin-angiotensin system

177
Q

Renin-angiotensin system is powerful enough to return the arterial pressure at least ________ within a few minutes after severe hemorrhage

A

At least haflway back to normal

178
Q

Explain “one-kidney” Goldblatt hypertension

A

occurs when one kidney is removed an remaining renal artery of the other kidney is constricted. The immediate effect is greatly reduced pressure in the renal artery beyond the constrictor. Systemic pressure will rise for several days due to a large release of renin. This leads to increase of angiotensin II and aldosterone in the blood. secretion of renin rises to a peak in an hour or so but returns nearly to normal in 5 to 7 days because renal arterial pressure by that time has also risen back to normal, so the kidney is no longer ischemic. The second rise in arterial pressure is caused by the retention of salt and water .

Physiology I (Exam II material) (9 decks)

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