Brainscape's Knowledge GenomeTM

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


See full index

Physiology, Josh > Exam 3: Control of Blood Flow Presentation > Flashcards

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.

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

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

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

A

Low O2 levels or lack of blood supply

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

What is vasomotion?

A

Cyclical opening and closing of precapillary sphincters.

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

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

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

What is the Metabolic theory of autoregulation?

A

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

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

What is the Myogenic Theory of Autogreulation?

A

Stretching of vessels → reactive vasculature constriction

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

What is the role of NO in vasodilation/vasoconstriction?

A

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

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

What is humoral circulation control?

A

What’s in the blood that can control circulation.

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

What four components of circulation control vasoconstriction?

A

Norepinephrine Epinephrine Angiotensin II Vasopressin

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

What components of circulation control vasodilation?

A

Bradykinins Histamine

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

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

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

A

Anterolateral Portions of upper medulla

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

What are vasoconstrictor tones?

A

Continual Firing of vasoconstriction area of brian

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

What are vasomotor tones?

A

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

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

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

A

Bilateral in the anterolateral portions of lower medulla.

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

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

What does the adrenal medulla secrete?

A

Epinephrine Norepinephrine

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

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

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

Describe Chemoreceptors.

A

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
Q

What are atrial reflexes?

A

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
Q

An increase in atrial stretch reflex results in….

A
  • 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
Q

What is the equation for atrial pressure?

A

Atrial Pressure = cardiac output x total peripheral resistance

29
Q

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?

A
  • Pressure diuresis
  • Pressure Natriuresis (Na+ in urine)
30
Q

What are four major causes of hypertension?

A
  • Renal causes
  • Endocrine Causes
  • Cardiovascular causes
  • Neurologic causes
31
Q

Primary hypertension usually has an unknown origin, what percentage of people who suffer from hypertension have Primary?

A

90- 95%

32
Q

What is atherosclerosis?

A

Type of arteriosclerosis that is characterized by lesions within tunica intima that protrude into lumen.

33
Q

A genetic variant in the renin-angiotensis system can lead to what pathology?

A

Hypertension.

34
Q

Factors resulting in decreased peripheral resistance (vessel dialtion) that can lead to decreased blood pressure would be categorized by what pathology?

A

Hypotension.

35
Q

What are some factors that can lead to hypotension?

A
  • ↑ production of NO
  • ↑ release of prostacyclin
  • ↑ release of kinins
  • ↑ in atrionatriuretic peptide (ANP)
  • ↓ neural factors (ß-adrenergic)
36
Q

What are non-modifiable risk factors associated with atherosclerosis?

A

age, gender, genetics

37
Q

List 3 humoral vasoconstrictiors

A
  • Angiotensin II
  • Catecholamines
  • Endothelin
38
Q

List 3 humoral Vasodilators

A
  • Kinins
  • Prostaglandins
  • Nitric oxide
39
Q

What are modifiable risk factors associated with atherosclerosis?

A
  • Hyperlipidemia
  • Hypertension
  • Cigarette Smoking
  • Diabetes
40
Q

Name 6 other factors contributing to atherosclerosis.

A
  • Inflammation
  • Hyperhomocystinemia
  • Metabolic syndrome
  • Lipoprotein (a)
  • Factors affecting hemostasis
  • Life Style
41
Q

Explain the accumulation of lipoproteins (esp LDL) in atherosclerosis.

A
  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
Q

What are the stages of atherosclerosis formation due to monocyte adhesion to endothelium?

A
  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
Q

What is a mature atheroma?

A

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
Q

What is the process of atherosclerosis Development?

A
  • 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
Q

What are the most common arterial sites for atherosclerosis?

A
  • Lower abdominal aorta
  • coronary arteries
  • popliteal arteries
  • internal carotid arteries
  • circle of willis
46
Q

How is short term arterial pressure controlled?

A
  • Via SNS on total peripheral vascular resistance and capacitance (cardiac pumping ability)
47
Q
A
48
Q

How is long-term arterial pressure controlled?

A
  • Via multiple nervous & hormonal controls
  • Via local controls in kidney that regulate salt and water excretion
    *
49
Q

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

A
  • Degree of pressure shift of the renal output curve for water/salt
  • level of water/salt intake
50
Q

Define chronic hypertension.

A

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

Normal = 90mmHg

Hypertensive 110 mmHg

51
Q

What is considered severe hypertension?

A

150-170 mmHg (250/130)

52
Q

What are 5 causes of lethal effects of chronic hypertension?

A
  • Early heart failure
  • coronary heart disease
  • heart attack
  • cerebral infarct
  • destruction of area of kidneys
53
Q

List 5 characteristics of primary hypertension

A
  • Increased cardiac output
  • increased SNS activity
  • Increase in angiotensin II & aldosterone levels
  • impairment of renal-pressure natriuresis mechanism
  • Inadequate secretion of water/salt

Physiology, Josh (9 decks)

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