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Whitney - Physiology Test 2 > Lecture 11 Control of Blood Flow > Flashcards

Lecture 11 Control of Blood Flow Flashcards

1
Q

Describe Acute Control

A

Rapid changes in local vasodilation/vasoconstriction

Occurs in seconds to minutes

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2
Q

Describe Long-term Control

A

Increase in sizes/numbers of vessels

Occurs over a period of days, weeks, or months

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3
Q

Basic theories of Acute Control

A

Vasodilator Theory

Oxygen (nutrient) lack theory

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4
Q

Vasodilator theory

A

Increase Metabolism –> decrease O2 availability –> formation of vasodilators (adenosine, carbon dioxide, adenosine phosphate compounds, histamine, potassium ions, hydrogen ions)

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5
Q

Oxygen (nutrient) lack theory

A

Decrease [O2] –> BV relaxation –> Vasodilation

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6
Q

Define Vasomotion

A

Cyclical opening and closing or precapillary sphincters

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7
Q

Number of precapillary sphincters open at any given time is roughly proportional to:

A

nutritional requirements of tissues

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8
Q

Hyperemia - Reactive

A

Tissue blood flow blocked –(unblocked)–> Blood flow increases 4-7x normal

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9
Q

Hyperemia - Active

A

When any tissue becomes active, rate of blood flow increases

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10
Q

Autoregulation

A

Rapid increase in arterial pressure leads to increased blood flow.
Within minutes, blood flow returns to normal even with elevated pressure.

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11
Q

Theories that explain autoregulation

A

Metabolic theory

Myogenic theory

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12
Q

Metabolic theory

A

Increase in blood flow –> Too much O2 or nutrients –> Washes out vasodilators

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13
Q

Myogenic theory

A

Stretching of vessels –> reactive vasculature constriction

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14
Q

Special Acute Blood Flow in the Kidneys

A

Tubuloglomerular feedback: involves the macula densa/juxtaglomerular apparatus

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15
Q

Special Acute Blood Flow in the Brain

A

Increase [CO2] and/or [H+] –> cerebral vessel dilation –> washing out of excess CO2/H+

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16
Q

Special Acute Blood Flow in the Skin

A

Blood flow linked to body temp.
Sympathetic nerves via CNS
3 ml/min/100 g tissue –> 7-8 L/min for entire body

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17
Q

Review endothelial-derived mechanisms for control of tissue blood flow

A

Slides 16 and 17

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18
Q

Vasoconstrictors

A

Norepinephrine
Epinephrine
Angiotensis II
Vasopressin

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19
Q

Vasodilators

A

Bradykinins

Histamine

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20
Q

Angiotensin II normally acts to _______ total peripheral resistance

A

Increase

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21
Q

Vasopressin

A

aka ADH
Very powerful vasoconstrictor
Major function is to control body fluid volume

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22
Q

Bradykinins

A

Causes both vasodilation and increased capillary permeability

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23
Q

Histamine

A

Powerful vasodilator derived from mast cells and basophils

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24
Q

Sympathetic System

A

Innervates all vessels except capillaries

Primarily results in VASOCONSTRICTION

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25
Q

What is the function of the vasoconstrictor area of the brain?

A

Transmits continuos signals to BVs:

  • continual firing results in sympathetic vasoconstrictor tone
  • partial state of contraction of BVs = vasomotor tone
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26
Q

What is the function of the vasodilator area of the brain?

A

Inhibits activity in vasoconstrictor area

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27
Q

What is the function of the sensory area of the brain?

A

Receives signals via Vagus Nerves and Glossopharyngeal Nerves & transmits the signals to the motor areas

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28
Q

Higher nervous centers that control the vasomotor centers of the brain:

A

Reticular substance (RAS)
Hypothalamus
Cerebral Cortex

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29
Q

Adrenal Medulla Secretes:

A

Epinephrine and Norepinephrine

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30
Q

Neural Rapid Control of Arterial Pressure Simultaneous Changes:

A

Constriction of most systemic arteries
Constriction of veins
Increased HR

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31
Q

Where are Baroreceptors located?

A

In Carotid sinuses and aortic sinuses

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32
Q

Baroreceptors are stimulated by:

A

Low arterial pressure

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33
Q

Baroreceptors in the carotid sinuses are stimulated by:

A

Pressure > 60 mmHG

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34
Q

Baroreceptors in the aortic sinuses are stimulated by:

A

Pressure > 30 mmHg

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35
Q

Signals from Baroreceptors:

A

Inhibit vasoconstrictor center
Excite vasodilator center
Signals cause either increase or decrease in arterial pressure
Primary function is to reduce the minute-by-minute variation in arterial pressure

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36
Q

Where are chemoreceptors located?

A

Carotid bodies in bifurcation of the common carotids and in aortic bodies

37
Q

Chemosensitive cells sensitive to:

A

lack of O2, CO2 excess, and H+ excess

38
Q

Chemoreceptor signals pass through:

A

Herring’s nerves and vagus nerves

39
Q

Chemoreceptors play an important role in:

A

respiratory control

40
Q

Where are low pressure receptors located?

A

In the atria and pulmonary arteries

41
Q

Low pressure receptors play an important role in:

A

Minimizing arterial pressure changes in response to changes in blood volume

42
Q

Increase in atrial stretch results in:

A

Reflex dilation of kidney afferent arterioles
Increase in Heart Rate (via CN X)
Signals to hypothalamus –> dec. [ADH]
Atrial natriuretic peptide (ANP) –> kidneys –> inc. [GFR] & dec. Na+ reabsorption
Decrease Na+ reabsorption

43
Q

Arterial Pressure = ?

A

Cardiac Output x Total Peripheral Resistance

44
Q

Arterial pressure rises when:

A

Total Peripheral Resistance is acutely increased

45
Q

Normal functioning kidneys return the arterial pressure back to normal within a day or two:

A

Pressure diuresis

Pressure natriuresis

46
Q

Primary Hypertension Characteristics

A

Increased cardiac output
Increased sympathetic nerve activity
Increase in angiotensin II and aldosterone levels
Impairment of renal-pressure natriuresis mechanisms
Inadequate secretion of salt and water

47
Q

Primary hypertension is of ______ origin

A

unknown, 90-95% of hypertension

48
Q

Major factors of primary hypertension

A

Weight gain characterized by: increased cardiac output, increased sym. nerve activity, increased angiotensin II and aldosterone levels, impaired renal-pressure natriuresis mechanisms.
Sedentary life style

49
Q

Secondary Hypertension

A

Hypertension second to some other cause: Tumor affecting renin-secreting juxtaglomerular cells, renal artery constriction, coarctation of the aorta, preeclampsia, neurogenic hypertension, genetic causes

50
Q

Renal causes of hypertension:

A 
Chronic renal disease
Renal artery stenosis
Renin-producing tumors
Acute glomerulonephritis 
Polycystic disease
Renal vasculitis
51
Q

Endocrine causes of hypertension:

A 
Cushing syndrome
Exogenous hormones
Pheochromocytoma 
Acromegaly
Hypothyroidism 
Hyperthyroidism
Pregnancy induced
52
Q

Cardiovascular causes of hypertension:

A 
Coarctation of the aorta
Polyarteritis nodosa 
Increased intravascular volume
Rigidity of the aorta 
Increased Cardiac Output
53
Q

Neurologic causes of hypertension

A

Psychogenic
Increased intracranial pressure
Sleep apnea
Acute stress

54
Q

Contributing factors to hypertension:

A 
Genetic factors
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
55
Q

Factors resulting in decreased peripheral resistance (vessel dilation) leading to decreased blood pressure:

A 
^ production of NO
^ release of prostacyclin 
^ release of kinins 
^ in atrionatriuretic peptide (ANP)
Decreased neural factors (beta-adrenergic)
56
Q

Factors resulting in decreased cardiac output leading to decreased blood pressure:

A

Decreased blood volume
Decreased HR
Decreased contractility

57
Q

Factors resulting in increased cardiac output leading to increased blood pressure:

A

^ HR
^ Contraction
^ Blood Volume (due to aldosterone)

58
Q

Factors resulting in increased peripheral resistance leading to increased blood pressure:

A

^ angiotensin II
^ catecholamines
^ thromboxane
^ neural factors (alpha-adrenergic)

59
Q

Humoral Vasoconstrictors:

A

Angiotensin II
Catecholamines
Endothelin

60
Q

Humoral Vasodilators:

A

Kinins
Prostaglandins
Nitric Oxide

61
Q

Lethal effects of chronic hypertension:

A

Early heart failure & coronary artery disease
Cerebral infarct
Kidney Failure

62
Q

Atherosclerosis

A

Type of arteriosclerosis (“hardening of the arteries”)

63
Q

Major characteristics of Atherosclerosis

A

Presence of lesions within the intima of the vessel wall that protrude into the vessel lumen

64
Q

Non-modifiable risk factors of Atherosclerosis:

A

AGE - risk ^ between 40-60, death rates from ischemic heart disease ^ w/ each decade
GENDER - uncommon in premenopausal women w/o other risk factors, increase after menopause & eventually exceeds men
GENETICS - some mendelian disorders associated w/ atherosclerosis but mostly multifactorial

65
Q

Modifiable risk factors of Atherosclerosis:

A

Hyperlipidemia (esp. hypercholesterolemia) - major risk factor; high levels of LDL
Hypertension - increases risk of IHD by 60%; most important cause of left ventricular hypertrophy
Cigarette Smoking
Diabetes

66
Q

Other risk factors of atherosclerosis:

A 
Inflammation
Hyperhomocystinemia 
Metabolic Syndrome
Lipoprotein
Factors affecting hemostasis 
Life style: lack of exercise; competitive stressful life style; obesity
67
Q

Inflammation

A

Intimately linked w/ atherosclerotic plaque formation
Correlated with high levels of LDL
C-reactive protein

68
Q

C-reactive protein (CRP)

A

Major marker for inflammation
Synthesized by liver
Plays important role in opsonizing bacteria and activating complement

69
Q

Hyperhomocystinemia

A

Inborn error of metabolism

Associated with premature vascular disease

70
Q

Metabolic Syndrome

A

Associated with insulin resistance

71
Q

Characteristics of Metabolic Syndrome

A 
Obesity (abdominal fat)
Insulin 
Fasting hyperglycemia 
Increased lipid triglycerides 
Decreased HDL levels
Hypertension
72
Q

Endothelial injury or dysfunction of any kind:

A

Results in intimal thickening

May lead to formation of atheroma in presence of hyperlipidemia

73
Q

Factors related to endothelial dysfunction:

A 
Hypertension
Hyperlipidemia
Cigarette smoke
Homocysteine
Infectious agents
Hemodynamic disturbances
Hypercholesterolemia
74
Q

Accumulation of lipoproteins (esp. LDL) is the result of:

A

Chronic hyperlipidemia (esp. hypercholesterolemia)

75
Q

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

A

intima
macrophages
endothelial cells

76
Q

Oxidized LDL:

A

Is ingested by macrophages –> foam cells
Stimulates release of growth factors, cytokines, & chemokines
Is toxic to endothelial cells & smooth muscle cells

77
Q

Monocyte adhesion to endothelium:

A

Endothelial cells express VCAM-1 that bind monocytes & T cells to endothelium
Monocytes transform into macrophages & engulf lipoproteins
T cells stimulate chronic inflammatory response
Activated leukocytes & endothelial cells release factors that promote smooth muscle cell proliferation

78
Q

Smooth muscle proliferation:

A

Intimal smooth muscle cell proliferation and extracellular matrix deposition converts a fatty streak into a mature atheroma

79
Q

An atheroma 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 calcium

80
Q

In the developmental stages of atherosclerosis, the earliest lesions are ____ ______.

A

Fatty streaks

Also seen in all children older than 10

81
Q

In the developmental stages of atherosclerosis, atherosclerotic plaques impinge on the lumen of the artery and grossly appear _____ or _____.

A

White or yellow

82
Q

In the developmental stages of atherosclerosis, plaques progressively enlarge due to:

A

Cell death & degeneration and synthesis/degradation of extracellular matrix

83
Q

Atherosclerosis Plaques:

A

Often undergo calcification

May rupture, ulcerate, or erode

84
Q

Most common arterial sites for atherosclerosis (most involved to least):

A 
Lower abdominal aorta
Coronary arteries 
Popliteal arteries 
Internal carotid arteries 
Circle of Willis
85
Q

Short term control of arterial pressure:

A

Via sympathetic nervous system effects on:

  • Total peripheral vascular resistance & capacitance
  • Cardiac pumping ability
86
Q

Long term control of arterial pressure:

A

Via multiple nervous & hormonal controls
Via local controls in the kidney that regulate:
- salt & water excretion

87
Q

Relation of kidney output and arterial pressure:

If Arterial Pressure Increases then:

A

Increase in urine output –> pressure diuresis

Increase in sodium output –> pressure natriuresis

88
Q

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

Whitney - Physiology Test 2 (8 decks)

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