Exam 3: Control of Blood Flow Presentation Flashcards

1
Q

Describe acute control of localized tissue regulation

A

Rapid changes in local vasodilation/vasoconstriction occurs in seconds to minutes.

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2
Q

Describe long-term control of local blood flow.

A

increase in sizes/number of vessels, and can occur over a period of days, weeks, or months.

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3
Q

Under what conditions would a vasodilator be released by the tissue?

A

Low O2 levels or lack of blood supply

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4
Q

What is vasomotion?

A

Cyclical opening and closing of precapillary sphincters.

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5
Q

What is hyperemia

A

an excess of blood in the vessels supplying an organ. Can increase to 4-7x’s the normal limits. Reperfusion can cause damage b/c of the large influx of O2

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6
Q

What is autoregulation?

A

Tissues control how much blood they get/need. So within minutes, blood flow returns to normal even with elevated pressure.

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7
Q

What is the Metabolic theory of autoregulation?

A

Increase in blood → Too much oxygen/nutrients → washes out vasodilators

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8
Q

What is the Myogenic Theory of Autogreulation?

A

Stretching of vessels → reactive vasculature constriction

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9
Q

What is the role of NO in vasodilation/vasoconstriction?

A

Damaged cells block production of NO which inhibits vasodilation creating vasoconstriction.

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10
Q

What is humoral circulation control?

A

What’s in the blood that can control circulation.

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11
Q

What four components of circulation control vasoconstriction?

A

Norepinephrine Epinephrine Angiotensin II Vasopressin

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12
Q

What components of circulation control vasodilation?

A

Bradykinins Histamine

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13
Q

T/F the sympathetic nervous system innervates all vessels except capillaries which primarily results in vasodilation.

A

False, It primarily results in vasoconstriction.

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14
Q

What part of the brain is the vasoconstriction area of the brain

A

Anterolateral Portions of upper medulla

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15
Q

What are vasoconstrictor tones?

A

Continual Firing of vasoconstriction area of brian

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16
Q

What are vasomotor tones?

A

Partial state of contraction of blood vessels due to vasoconstriction are of brain.

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17
Q

Where in the brain is the Vasodilation are of the brain?

A

Bilateral in the anterolateral portions of lower medulla.

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18
Q

How does the vasodilation area of the brain function?

A

It caused vasodilation by inhibiting vasoconstriction at vasoconstriction area of brain in upper medulla.

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19
Q

What does the adrenal medulla secrete?

A

Epinephrine Norepinephrine

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20
Q

Neural rapid control of arterial pressure is simultaneously caused by….

A

Constriction of most systemic arteries ( increases peripheral resistance) constriction of veins, Increased HR.

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21
Q

T/F The simultaneous changes that control neural rapid arterial pressure all increase blood pressure?

A

True, They are 1)Constriction of most systemic arteries 2) constriction of veins 3) Increased heart rate

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22
Q

What do baroreceptors do?

A

Sense pressure changes Stimulated by low arterial pressure Carotid sinus stimulated by pressure <30 mmHg

23
Q

What are the 4 main functions of Baroreceptors?

A

1) Inhibit vasoconstriction center 2) Excite vasodilator center 3) Signals cause ↑ or ↓ in arterial pressure. 4) 1º Function is to reduce the minute-by-minute variation in arterial pressure.

24
Q

What is the effective range of baroreceptors?

A

~60-110 mmHg

25
Describe Chemoreceptors.
They are located in common carotids and in aortic bodies. Sensitive to lack of O2, CO2 excess, and H+ ion excess. Play an important role in respiratory control.
26
What are atrial reflexes?
Low pressure receptors located in atria and pulmonary arteries that play important role in minimizing arterial pressure changes in response to changes in blood volume.
27
An increase in atrial stretch reflex results in....
* Reflex dilation of kidney afferent arteriols. * Increase in HR * Signal hypothalamus to decrease ADH. * Atrial Natriuretic peptide (ANP) →Kidneys * Kidneys ↑ GFR and ↓ Na+ reabsorption
28
What is the equation for atrial pressure?
Atrial Pressure = cardiac output x total peripheral resistance
29
Atrial pressure rises when total peripheral resistance is acutely increased. What are two ways normal kidneys return the arterial pressure back to normal within a day or two?
* Pressure diuresis * Pressure Natriuresis (Na+ in urine)
30
What are four major causes of hypertension?
* Renal causes * Endocrine Causes * Cardiovascular causes * Neurologic causes
31
Primary hypertension usually has an unknown origin, what percentage of people who suffer from hypertension have Primary?
90- 95%
32
What is atherosclerosis?
Type of arteriosclerosis that is characterized by lesions within tunica intima that protrude into lumen.
33
A genetic variant in the renin-angiotensis system can lead to what pathology?
Hypertension.
34
Factors resulting in decreased peripheral resistance (vessel dialtion) that can lead to decreased blood pressure would be categorized by what pathology?
Hypotension.
35
What are some factors that can lead to hypotension?
* ↑ production of NO * ↑ release of prostacyclin * ↑ release of kinins * ↑ in atrionatriuretic peptide (ANP) * ↓ neural factors (ß-adrenergic)
36
What are non-modifiable risk factors associated with atherosclerosis?
age, gender, genetics
37
List 3 humoral vasoconstrictiors
* Angiotensin II * Catecholamines * Endothelin
38
List 3 humoral Vasodilators
* Kinins * Prostaglandins * Nitric oxide
39
What are modifiable risk factors associated with atherosclerosis?
* Hyperlipidemia * Hypertension * Cigarette Smoking * Diabetes
40
Name 6 other factors contributing to atherosclerosis.
* Inflammation * Hyperhomocystinemia * Metabolic syndrome * Lipoprotein (a) * Factors affecting hemostasis * Life Style
41
Explain the accumulation of lipoproteins (esp LDL) in atherosclerosis.
1. Lipoprotiens accumulate in the intima & are oxidized by O2 free radicals from macrophages or endothelial cells 2. Macrophages ingest oxidized LDL = foam cells 3. Oxidized LDL stimulates release of growth factors, cytokines, and chemokines 4. Oxidized LDL is toxic to endothelial cells and smooth muscle cells.
42
What are the stages of atherosclerosis formation due to monocyte adhesion to endothelium?
1. Monocytes and T-cells are bound to endothelial cells through expression of VCAM-1 on endothelial cells. 2. Monocytes transform into macrophages and engulf lipoproteins 3. T-cells stimulate a chronic inflammatory response 4. Activated leukocytes and endothelial cells release growth factors that promote smooth muscle cell proliferation.
43
What is a mature atheroma?
a cap of smooth muscle cells, macrophages, foam cells (converted macrophages), and other extracellular components, overlying a necrotic center composed of cell debris, cholesterol, foam cells, and calcium. Garbage pile.
44
What is the process of atherosclerosis Development?
* Earliest lesions are fatty streaks * Plaques impinge on lumen of artery (yellow/white) * Plaques progressively enlarge * plaques often undergo clacificaiton * plaques may rupture, ulcerate, or erode.
45
What are the most common arterial sites for atherosclerosis?
* Lower abdominal aorta * coronary arteries * popliteal arteries * internal carotid arteries * circle of willis
46
How is short term arterial pressure controlled?
* Via SNS on total peripheral vascular resistance and capacitance (cardiac pumping ability)
47
48
How is long-term arterial pressure controlled?
* Via multiple nervous & hormonal controls * Via local controls in kidney that regulate salt and water excretion *
49
What are the primary determinants of long-term arterial pressure level?
* Degree of pressure shift of the renal output curve for water/salt * level of water/salt intake
50
# Define chronic hypertension.
One's mean arterial pressure is greater than the upper range of the accepted normal measure. Normal = 90mmHg Hypertensive 110 mmHg
51
What is considered severe hypertension?
150-170 mmHg (250/130)
52
What are 5 causes of lethal effects of chronic hypertension?
* Early heart failure * coronary heart disease * heart attack * cerebral infarct * destruction of area of kidneys
53
List 5 characteristics of primary hypertension
* Increased cardiac output * increased SNS activity * Increase in angiotensin II & aldosterone levels * impairment of renal-pressure natriuresis mechanism * Inadequate secretion of water/salt