exam 1 lecture 7 Flashcards

1
Q

hyperemia

A

oxygen deficiency, vasodilation, carbon dioxide, hydogen ions, lactic acid account for

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2
Q

active hyperemia

A

skeletal muscle, heart and cerebral and splanchnic circulations, blood flow increases with increases metabolic activity. Because of accumulation of vasodilators coupled with initial reduce oxygen tension and nutrient supply

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3
Q

reactive hyperemia

A

when blood supply to tissue is clamped and then restored, flow through tissue increase by as much as five fold times, accumulation of vasodilators, reduced oxygen tension and depletion of nutrients (BUT can also lead to hypoxic pulmonary vasoconstriction)

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4
Q

autoregulation

A

when tissues maintain a fairly constant blood flow over a perfusion pressures ranging from 70-175 mmHg. Manly in renal, cerebral and coronary circuits

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5
Q

explanations for autoregulation

A

flushing vasodilators metabolites out of tissue when flow increases causes vasoconstriction and increase in R, myogenic mechanism: bayliss hypothesis, sudden stretch of the vessels walls provoke arterial and arteriolar smooth muscle to contract, causing vasoconstriction-> decrease flow

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6
Q

fast myogenic response is 50% responsible for renal blood flow autoregulation how?

A

Tubuloglomerular feedback (NaCl, macula densa, extraglomerular mesangial cells and afferent arterioles) complements the myogenic response.

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7
Q

vasoconstrictors

A

THE CATECHOLAMINES: Norepinephrine and epinephrine bind β1 adrenergic receptors in the heart,, alpha1 adrenergic receptors in the smooth muscle cells of the media of most blood vessels.Low E concentrations= vasodilator (beta 2)
high E concentrations= vasoconstrictor (alpha 1)

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8
Q

Dopamine

A

vasoconstrictor: Vasodilator at low concentrations (dopamine receptors), vasoconstrictor at high concentrations
(alpha1 adrenergic receptors). Acts on the heart at moderate doses (β1 adrenergic receptors )

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9
Q

dobutamine

A

sysnthetic catcholamine primarily with beta 1 activity, inotropic support in cardiogenic shock

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10
Q

Angiotensin II

A

Octapeptide, amount in the circulation controlled
by renin secreted by the JG cells
Low concentrations= Constricts the renal arteries and stimulates adrenal cortex to secrete aldosterone
High concentrations: Generalized vasoconstriction

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11
Q

angiotensin II blockers

A

ACE inhibitors used for anti-hypertensive therapies

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12
Q

ADH, or vasopressin

A

increased water permeability in collecting ducts of kidney, high concentrations= vasoconstictor.

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13
Q

ADH release when

A

high osmotic pressure, reduced blood volume, and reduced MAP

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14
Q

thromboxane A2

A

prostaglandin vasoconstrictor, causes platelet aggregation and vasoconstriction

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15
Q

endothelin

A

ET-1 split from ET-1 by endothelin converting enzyme, long lasting vasoconstrictor

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16
Q

Beta 2 adrenergic receptors

A

vasodilation when bind E

17
Q

Bradykinin

A

A nonapeptide that acts by stimulating nitric oxide and prostacyclin formation by the vascular endothelium.
Involved in inflammation
Destroyed by angiotensin-converting enzyme

18
Q

serotonin

A

In platelet granules.
Concentration can increase locally after platelet activation.
Effects complex, depending on dose, experimental conditions, animal species and vascular state.

19
Q

histamine

A

Can be a powerful dilator of arterioles, except in the lungs,where it increases PVR
Increases capillary permeability (e.g. to proteins)
Important in inflammation and anaphylactic shock,
where it is released by mast cells.

20
Q

prostacyclin

A

produced by the vascular endothelium by prostacyclin synthase used to treat PHT
antagonistic to thromboxane A2

21
Q

NO

A

Apart from its action on the vasculature, it also inhibits platelet adhesion, NO is continually produced by nitric oxide synthase in the vascular endothelium,

22
Q

vascular endothelium source of

A

prostacyclin (vd), NO (vd) and endothelin (vc)

23
Q

Parasympathetics

A

Heart (mainly rate)
Blood vessels: vasodilation in the blush areas and genitals (penile erection is via the intermediary nitric oxide).

24
Q

sympathetic branch

A

Controls distribution of cardiac output by vasoconstriction, mainly in the splanchnic and cutaneous circulations.
Regulates mean arterial pressure by acting on the:
a. Heart (cardiac output) (beta 1)
b. Blood vessels (SVR,
capacity) (alpha 1)
c.Volume, via the kidneys
(affects cardiac output)

25
Q

Angiogenesis

A

formation of new blood vessels: ischemic tissue, hypoxic wounds, embryogenesis, menstrual cycle.

26
Q

unregulated angiogenesis

A

tumor growth, arthritis, diabetic retinopathy, retinopathy of prematurity.

27
Q

endogenous angiogenesis inhibitors

A

prevent corneal neovascularization.

28
Q

angiogenic factors

A

Synthesis and release of angiogenic factors is driven by low oxygen – high oxygen suppresses them.

29
Q

MAP regulated by sympathetics (raise MAP)

A

cardiac output (beta 1), total peripheral resistance (arterioles, alpha 1), capacity (veins and venules alpha 1) and blood volume (renin-angiotensin II-ADH)

30
Q

baroreceptor reflex (volume depletion)

A

activator of sympathetic nervous system. critical for
blood pressure homeostasis.Stretch receptors in the carotid sinuses (less importantly the aortic arch) communicate via Hering’s nerve (branch of IX) with neurons in the nucleus tractus solitarius.
NTS is the integrating hub, and modulates the activity of sympathetic and parasympathetic (vagal) neurons in the medulla.

31
Q

baroreceptor reflex protect against

A

FALL in MAP, does provide against protection for hypertension

32
Q

when blood pressure rises….?

A

impulses from baroreceptor increases in frequency, reducing sympathetic vasoconstriction tone

33
Q

when blood pressure decreases?

A

baroreceptor reduce their firing rate , increasing vasomotor tone and causes constriction of veins and arterioles

34
Q

Shy-Drager

A

Multiple system atrophy with orthostatic hypotension.A progressive disorder of the CNS and ANS for which there is no cure. Orthostatic hypotension is the first sign of autonomic system failure

35
Q

orthostatic hypotention patient

A

supine: 120/74, sitting: 98/54, standing: 84/48

36
Q

Bainbridge reflex (volume loading)

A

sometimes called the atrial reflex, is an increase in heart rate and renal vasodilation due to an increase in central venous pressure operating on receptors located on the low pressure side of the circulation.

37
Q

atrial natriuretic peptide

A

secretion caused from atrial distension from increased venous pressure. inhibits ADH, renin and aldosterone secretion

38
Q

renin-aldosteron-angiotensin system

A

Most important action to control plasma volume. Takes several hours for pathophysiological expression, as might occur in the setting of hemorrhage or MI
Antidiuretic, vasoconstriction

39
Q

aldosterone

A

prevents sodium from excretion by promoting sodium reabsorption in distal and collecting tubules of kidneys, causes water retention in response to reduced systemic arterial pressure