Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Physiology > [2] Lecture 12-Control Of Blood Flow > Flashcards

[2] Lecture 12-Control Of Blood Flow Flashcards

1
Q

Rapid changes in local vasodilation/vasoconstriction

A

Acute control of local blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Two basic theories of acute control of local blood flow:

A
  1. Vasodilator theory

2. oxygen (nutrient) lack theory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Increase in sizes/ number of vessels

Occurs over a period of days, weeks, or months.

A

Long-term control of local blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Increased metabolism = decreased O2 availability

Formation of vasodilator [adenosine, CO2, Adenosine P compounds, histamine, K+ ions H+ ions]

A

Vasodilator theory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Decreased O2 = blood vessel relaxation

[vasodilation]

A

Oxygen [nutrient] lack theory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Cyclical opening and closing of precapillary sphincters

A

Vasomotion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What controls the number of precapillary sphincters open at any given time?

A

Roughly proportional to nutritional[O2] req’ments f tissues.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Tissue blood flow blocked [s to hrs or more]

When unblocked, blood flow increases 4-7x normal

A

Reactive hyperemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

When any tissue becomes active rate of blood flow increases

A

Active hyperemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

When there is a higher rate of metabolism, what happens to blood flow rate

A

Increased blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

When arterial oxygenation desats, what happens to blood flow?

A

Blood flow increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Rapid increase in arterial pressure leads to increased blood flow

W/in minutes, blood flow returns to normal even with elevated pressure

What term would be used to describe this phenomenon

A

Autoregulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

2 theories/views to explain autoregulation:

A

Metabolic/myogenic theory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Increase in blood flow leads to:
Too much O2 or nutrients leads to:
Washes out vasodilators

A

Metabolic theory of autoregulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Stretching of blood vessels leads to reactive vasculature constriction

A

Myogenic theory of autoregulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Range that autoregulation typically operates at:

A

75 mmHg to 175 mm Hg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Higher arterial pressure has what effect on blood flow:

A

Increases blood flow [w/ higher arterial pressure]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the kidneys role in ACUTE blood flow control

Involves the macula densa / juxtaglomerular apparatus

A

Tubuloglomerular feedback

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

[CO2] increase and/or [H+] increase leads to:
Cerebral vessel dilation leads to:
Washing out of excess CO2/H+

A

Acute blood flow control mechanism: Brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Blood flow linked to body temperature
Sympathetic nerves via CNS
(3ml/min/100g tissue->7-8 L/min for entire body)

A

Acute blood flow control mechanism: skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What type of endothelial cells can help control blood flow to tissue?

A

Healthy Endothelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Sequence of Helathy endothelial cell blood flow control mechanism:

A

Endothelial cell->Nitric Oxide->cGTP becomes cGMP in vascular smooth muscle->activation of protein kinases->VASODILATION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What happens in damaged endothelial cells?

A

Damages cells-> endothelin->vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

21 AA peptide; effective in nanogram quantities

A

Endothelin-potent!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

If endothelial cells aren’t healthy, they can’t do what?

A

Secrete NO for vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Hormones for vasoconstriction:

A

NEVA

Norepinephrine
Epinephrine
Vasopressin
Angiotensin II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

WHich hormone typically acts to increase total peripheral resistance

A

Angiotensin II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Which hormone is a very powerful vasoconstrictor; major function is to control body fluid volume

A

ADH- vasopressin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Hormones that result in vasodilation:

A

Bradykinins

Histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Hormone that cause vasodilation and increased capillary permeability:

A

Bradykinin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Hormone that is a powerful vasodilator derived from mast cells and basophils

A

Histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Innervates all vessels except capillaries

Primarily results in vasoconstriction

A

Sympathetic system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What vessels do sympathetic innervation not apply to:

A

Capillaries;

Arteries, arterioles,
venules, veins do apply

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Vasomotor center in brain has 2 components:

A

Vasoconstrictor and vaso dilator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Anterolateral portions of upper medulla

Transmits continuous signals to blood vessels: continual firing results in sympathetic vasoconstrictor tone. Partial state of contraction of blood vessels

A

Vasoconstrictor area of vasomotor center of Brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Partial state of contraction of blood vessels

A

Vasomotor tone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Bilateral in the anterolateral portions of the medulla

Inhibits activity in vasoconstrictor area

A

Vasodilator area of vasomotor center of Brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Part of the medulla

Receives signals via: vagus nerve and glossopharyngeal nerves

A

Sensory area vasomotor center of Brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Cranial nerve X

A

Vagus nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Cranial nerve IX

A

Glossopharyngeal nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Controlled by higher nervous centers than medulla (3)

A

Reticular substance (RAS)
Hypothalamus
Cerebral cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Continual firing of vasoconstrictor area:

A

Vasoconstrictor tone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Partial state of blood vessel contraction:

A

Vasomotor tone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Inhibit vasoconstrictor center/ stimulate vasodilator center

A

Baroreceptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Chemosensitive cells that are more important in resp control

A

Carotid bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Aortic arch baroreceptor vs. carotid baroreceptor:

A

Carotid: >60 mm Hg

Aortic: >30 mm Hg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How does the baroreceptor signal travel to glossopharyngeal nerve (CN IX)

A

Herings nerves ***

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Completely define and state How to decrease the continual firing of the vasoconstrictor area? *

A

The vasodilator area negatively impacts vasoconstrictor to decrease firing…so,

The vasoconstrictor is always active but in HTN states, the vasodilator area will kick on to compensate for the elevated BP..this is only activated by CN IX from hering’s nerves from carotid baraprecptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What 2 hormones come from Adrenal medulla?

A

Epinephrine and norepinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

3 simultaneous changes during rapid neural control of arterial pressure:

A

Constriction of most systemic arteries
Constriction of veins
Increased HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Within seconds

A

Rapid response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is increased BP during exercise accompanied w/?

A

Vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Alarm rxn

A

Fight or flight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Spinal anesthesia and norepinephrine chart:

A

Anesthesia dropped pressure and norepinephrine increased pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Located in carotid and aortic sinus:

A

Baroreceptors

56
Q

Stimulated by a pressure drop >60 mm Hg

A

Carotid sinus

57
Q

Stimulated by a pressure drop > 30 mm Hg:

A

Aortic sinus

58
Q

Besides the carotid and aortic sinus, what are the 2 others involved in detecting low pressure?

A

Vagus nerve (CN X)

Glossopharyngeal nerve (CN IX) via hering’s nerves [carotid baroreceptors]

59
Q

What are other baroreceptors?

A

Reticular substance (RAS)
hypothalamus
Cerebral cortex

60
Q

What are the signals from baroreceptors:

A
  • inhibit vasoconstrictor
  • excite vasodilator
  • increase/decrease arterial pressure
61
Q

What is primary function of baroreceptors:

A

To reduce the minute-by-minute variation in arterial pressure `

62
Q

Graph depicting clamping carotid arteries:

A

Pressure increased b/c there was no longer barorecptor control

63
Q

What is the necessity for baroreceptors:

A

Maintaining pressures at a steady rate

64
Q

Located in carotid bodies in bifurcation of the common carotid and in aortic bodies

A

Chemoreceptors

65
Q

Chemosenesitive means sensitive to what chemicals?

A

Lack of O2,
Increase in CO2,
Increase in H+ ion

66
Q

Chemoreceptors pass through what nerves? (2)

A

Vagus and hering’s

67
Q

Chemoreceptors play an important role in:

A

Respiratory control

68
Q

Located in the atria and pulmonary arteries and play an important role in minimizing arterial pressure changes in response to changes in blood volume

A

Low pressure receptors

69
Q

Increase in atrial stretch results in:

A

-reflex dilation of kidney afferent arterioles:
Increase FLuid loss(urine excretion) ad decrease blood volume
-increase in HR
-Signals to hypothalamus-drop [ADH]
-atrial natriuretic peptide (ANP)-kidneys:decrease Na+ reabsorption and increase GFR

-basically stop keeping fluid, pee it out including Na+

70
Q

Arterial pressure =

A

CO x Total peripheral resistance

71
Q

Arterial pressure rises when TPR is:

A

Increased

72
Q

Normal functioning kidneys return the arterial pressure back to normal w/in a day or 2 by 2 means:

A

Pressure dieresis and

Pressure Natriuresis

73
Q

Increased amt. of Na+ lost in urine

A

Natriuresis

74
Q

Increased urine output

A

Diuresis

75
Q

CO can be increased or decreased by certain conditions. What’re the 2 that cause decrease CO

A

Removal of limbs
And
Hypothyroidism…

Everything else has sympathetic effect

76
Q

With many conditions causing increased pressure, what compensatory mechanism helps to bring back to norm?

A

Norm kidney function.

77
Q

Increased CO
Increased sympathetic nerve activity
Increased Angiotensin II and aldosterone
Impairment of renal-pressure natiuresis mechanism
Inadequate secretion of salt and water

A

Primary HTN

78
Q

90-95% of HTN
HTN of unk origin
Major factors:
Weight gain and sedentary life

A

Primary HTN

79
Q

HTN second to another cause:

A

Secondary HTN

80
Q

Ex of 2 HTN

A

Tumor affecting renin-secreting cells

Renal artery constriction

Carctation of aorta

Preeclampsia

Neurogenic HTN

Genetic causes

81
Q

Renal causes of HTN:

A 
Chronic renal disease
Renal artery stenosis
Renin-producing tumors 
Acute glomerulonephritis
Polycystic disease 
Renal vasculitis
82
Q

Endocrine causes of HTN:

A 
cushing syndrome
Exogenous hormones
Pheochromocytoma 
Acromegaly
Hypothyroidism
Hyperthyroidism 
Pregnancy induced
83
Q

CV causes of HTN:

A 
Coarctation (narrowing) aorta
Polyarteritis nodosa
Increased intravascular volume 
Rigidity of aorta
Increased CO
84
Q

Neurological causes HTN:

A

Psychogenic
Increased ICP
Sleep apnea
Acute stress

85
Q

Contributing factors to HTN:

A 
Genetics 
Single-gene disorders that alter NA reabsorption in kidney
Renin-angiotensin system
Stress
Smoking 
Physical inactivity 
Heavy consumption Na+
86
Q

Factors in decreased peripheral resistance (vessel dilation) = decreased BP

A

Increased: production of NO, release of prostacyclin, release of kinins, atrionatriuretic peptide (ANP)

Decreased: neural factors [ß-adrenergic]

87
Q

Factors resulting in decreased CO leading to decreased BP:

A

Decreased: blood volume, HR, contractility

88
Q

Factors resulting in increased CO leading to increased BP:

A

Increased HR, contraction, blood volume

89
Q

Factors resulting in increased peripheral resistance leading to increased BP

A

Increased: angiotensin II, catecholemines, thromboxane, neural factors (alpha-adrenergic)

90
Q

Vasoconstrictors:

A

Angiotensin II
Catecholemines
Endothelin

91
Q

Vasodilators

A

Kinins
Prostaglandins
NO

92
Q

Lethal effects of chronic HTN:

A

Early heart failure/ CAD
Cerebral infarct
Kidney failure

93
Q

Hardening of the arteries

A

Atherosclerosis

94
Q

Major characteristic of atherosclerosis:

A

Presence of lesions w.in the intima of the vessel wall that produce into the vessel lumen.

95
Q

Non-modifiable risk factors for atherosclerosis: (3)

A

Age [risk increased 40-60, death rate increases w/ each decade]

Gender [increases after menopause]

Genetics [mendelian disorders asso. W/ atherosclerosis]

96
Q

Modifiable risk factors of atherosclerosis: (4)

A

Hyperlipidemia [high cholesterol-major risk factor-high levels of LDL]

HTN [increases risk of IHD by 60%][most important cause L ventricular hypertrophy]

Cig smoking
Diabetes

97
Q

Other risk factors for Atherosclerosis:

A

Inflammation:
[linked w/ atherosclerotic plaque formation- CRP c reactive, synthesized by liver, play important role in opsonizing complement, inflammation correlated w/ high levels of LDL (not HDL)]

Hyperhomocytinemia [inborn error of metabolism, asso. W/ premature vascular disease]

Metabolic syndrome: asso. W/ insulin resistance [obesity,fasting hyperglycemia, increased lipid triglycerides, low HDL, HTN]

98
Q

Other risk factors atherosclerosis:

A

Lipoprotein A

Factors affecting hemostasis

Lifestyle: lack of exercise, stressful lifestyle, obesity

99
Q

Pathogensis of atherosclerotic Dz:

A

Results in intimate thickening after endothelial injury or dysfunction, may lead to formation of atheroma in presence of hyperlipidemia

Same factors cause atherosclerosis are r.t endothelial injury

100
Q

Accumulation of lipoproteins in pathogenesis of atherosclerosis:

A

Result chronic hyperlipidemia
Lipoproteins accumulate in intima and are oxidized by O2 free radicals generated by macrophages or endothelial cells
Oxidized LDL:
Ingested by macrophages=foam cells, stimulate growth factors, cytokines, chemokines, is toxic to endothlial cells and smooth muscle cells

101
Q

Ozxidzed LDL is ingested by macrophages which becomes:

A

Foam cells

102
Q

Consists of a cap of smooth muscle cells, macrophages, foam cells, and other Extracellular components, overlying a necrotic center composed of cell debris, cholesterol, foam cells and Ca+

A

Atheroma

103
Q

Common sites for arterial sites in atherosclerosis:

A 
Lower abd aorta
Coronary arteries
Popliteal arteries 
Internal carotid arteries 
Circle of willis
104
Q

Monocyte adhesion to endothelium

A

Endothelial cells express VCAM-1 adhesion molecules that bind monocytes and T cells to endothelium
Monocytes transform into macrophages and engulf lipoproteins
T cells stimulate a chronic inflammation response
Activated leukocytes and endothelial cells realease growth factors that promote smooth muscle cell proliferation

105
Q

Short term control of pressures:

A

Via sympathetic NS:
Total PV resistance and c capacitance
Cardiac pumping ability

106
Q

Long term control of pressures:

A

Via multiple Nervous and hormonal controls

And local controls in kidney that regulate Na and water excretion

107
Q

More arterial pressure r/t urinary output?

A

Higher pressure. = higher urinary output

108
Q

SMooth muscle proliferation

A

Intima smooth muscle cell proliferation and ECM deposition converts a fatty streak into a mature atheroma.

109
Q

Earliest detection atherosclerosis:

A

Fatty streaks- these are also seen al all children older than 10.

110
Q

Developmental stages of atherosclerosis:

A

Fatty streaks
Atherosclerotic plaques impinge on lumen of artery grossly appear yellow/white
Plaques progressively enlarge d/t cell death and degeneration and synthesis/degradation of ECM
Plaques often undergo calcification and may rupture, ulcerated, or erode.

111
Q

Kidney compensation for increasing blood volume:

A

Output to compensate for increased volume

112
Q

Increase in arterial pressure=

A

Increased urine and Na+ output

113
Q

Terms for increased urine output and Na+ output

A

Pressure diuresis and natriuresis

114
Q

Return of the arterial pressure always back to the equilibrium point=

A

Near infinite feedback gain principle

115
Q

PRimary determinants of long term arterial pressure level:

A

Degree of pressure shift of renal output curve for water/ salt

Level of water/salt intake

116
Q

Ways to increase arterial pressure:

A

Increase intake of salt and water

Retain water and salt- norm output and high arterial pressure

117
Q

Increased salt intake causes only small changes in arterial pressure

A

Chronic renal output

118
Q

Increased salt intake causes larger changes in arterial pressure

A

Acute renal output

119
Q

Feedback mechanism of extracellular fluid volume increases arterial pressure

A

NEgative feedback mechanism: increased blood volume=increased CO= higher arterial pressure=increased urine output (negatively affects the increased blood volume)

120
Q

One’s mean arterial pressure is > the upper range of accepted norm measure

A

Chronic HTN

121
Q

Norm arterial pressure

A

90 mm Hg (110/70)

122
Q

Hypertensive arterial measure

A

110 mm Hg (135/90)

123
Q

Severe HTN arterial:

A

150/170[mean arterial pressure] / 250/130

124
Q

Lethal effects of Chronic HTN:

A 
Early heart failure
Coronary heart disease 
MI
Cerebral infarct 
Destruction of areas of kidney-kidney failure-uremia-death
125
Q

Ex of vasoconstrictor:

A

Renin-angiotensin mechanism

126
Q

Role of renin-angiotensin mechanism

A

To increase BP if it goes low

127
Q

Effects of Renin-angiotensin:

A

Retention of salt and water and vasoconstriction

= increased arterial pressure

128
Q

Angiotensinogen is produced in what organ

A

Liver

129
Q

Precursor to angiotensin I

A

Angiotensinogen

130
Q

What converts Angiotensin I to II?

A

Angiotensin converting enzyme

131
Q

ACE enzyme comes from:

A

Many tissues including the lungs

132
Q

Angiotensin II acts on:

A

Kidney [Na and water reabsorption]

Adrenal gland [by means of aldosterone]

133
Q

Higher the arterial pressure=

A

Higher the urinary output

134
Q

2 results of increased arterial pressure:

A

Pressure diuresis and natriuresis

135
Q

Return to arterial pressure always back to the equilibrium point

A

Near infinite feedback gain principle

136
Q

Why is here an initial decrease in TPR after adding fluid w/ Na+?

A

Barorecptor mechanisms- recalculation

137
Q

What can assist if half blood volume is drained?

A

Renin-angiotensin system compensates by increasing arterial pressure

Physiology (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions