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elimination and detox - wk 3 > renal contribution to homeostasis > Flashcards

renal contribution to homeostasis Flashcards

1
Q

plasma proteins contribute greatly to the ____ pressure in the intravascular space

A

oncotic

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2
Q

what is osmolality

A

number of solutes dissolved in a kilogram of water

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3
Q

what is the most abundant ion in the ECF

A

sodium

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4
Q

how can plasma osmolality be estimated

A

by 2x the sodium concentration

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5
Q

what are some other factors contributing to osmolality

A
  • urea and glucose contribute 3-5% of the total
  • urea easily crosses membranes so it is not an effective osmole unless it it very high
  • glucose levels in patients that are normoglycemic do not significantly change osmolality
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6
Q

what are the two main mechanisms that are involved in regulating the concentration of sodium and osmolarity of ECF

A
  • osmoreceptor-ADH mechanism
  • thirst mechanism
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7
Q

what is the osmoreceptor-ADH system

A
  • feedback loop that ultimately leads to retention of water (dilution) when osmolarity is increased
  • the opposite effect occurs when there is a decrease in osmolarity
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8
Q

what are osmoreceptors

A

specialized neurons in the anterior pituitary that shrink when osmolarity is increased

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9
Q

how do changes in blood pressure/volume stimulate ADH

A
  • arterial baroreceptor reflex
  • cardiopulmonary reflex
  • rapid decrease in blood pressure/volume causes increased ADH secretion and increased water reabsorption to help restore blood pressure and blood volume back to normal
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10
Q

what regulated ADH secretion

A

osmolarity and blood volume

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11
Q

which stimulus is stronger: osmolarity or blood volume

ADH

A

osmolarity (~1% change triggers ADH release) (volume stimulus requires ~10% blood lost to stimulate ADH)

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12
Q

day to day stimulation is mediated by changes in:

A

osmolarity

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13
Q

many factors that increase ADH also trigger:

A

thirst

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14
Q

____ in the thirst center sense an increase in CSF osmolarity and stimulate drinking behavior

A

osmoreceptors

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15
Q

thirst is stimulated by:

A
  • increased ECF osmolarity
  • decreased ECF volume, decreased arterial blood pressure
  • angiotensin II
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16
Q

what helps regulate sodium reabsorption

A

angiotensin II and aldosterone

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17
Q

what does low sodium and high sodium cause

angiotensin II and aldosterone

A

increased hormone production; decreased hormone production

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18
Q

angiotensin II and aldosterone are more important in determining ____ of sodium, NOT _____

A

amount; concentration

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19
Q

effect of angiotensin II and aldosterone with amount of sodium reabsorption

A
  • increase ECF volume by increasing reabsoprtion of water with sodium
  • increased sodium reabsorption slightly increases ECF osmolarity, thirst mechanim is activated and ECF osmolarity is diluted back to normal
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20
Q

long-term regulation of arterial blood pressure is the ____ responsibility

A

kidney’s

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21
Q

arterial pressure is controlled by:

A

excretion of sodium and water

22
Q

pressure diuresis

A

urinary output increases as arterial pressure rises

23
Q

pressure natriuresis

A

urinary sodium excretion increases as arterial pressure rises

24
Q

what changes the long-term mean arterial pressure

A
  • degress of pressure shift of the renal output curve for water and salt - seen with impaired kidney function
  • level of water and salt intake
25
chronic changes in arterial pressure have a much greater effect on:
pressure natriuresis and pressure diuresis than acute changes
26
increased fluid volume causes and increase in
arterial pressure
27
autoregulation
when excess blood flows through a tisue, local tissue vasculature constricts and decreases blood flow back to normal
28
how do the kidneys respond to increased fluid volume and increased arterial pressure
respond immediately with pressure natriuresis and pressure diuresis - increased intrarenal vascular resistance
29
increases salt intake is more likely to increase arterial pressure than:
increased water intake
30
how does salt affect arterial blood pressure
* salt increases osmolality, which triggers the thirst mechanism * increased osmolality leads to ADH secretion, which causes water reabsorption in the kidneys and increased ECF volume
31
the renin-angiotensin-aldosterone system (RAAS) is a powerful tool for regulating:
blood pressure
32
____ is an enzyme produced by the JG cells of the juxtaglomerular apparatus
renin
33
JG cells
smooth muscle cells in the afferent arteriole next to the glomerulus
34
macula densa
cells of the distal tubule that sense sodium and chloride delivery
35
what are the three mechanisms that stimulate the release of renin from the JG cells
* pressure-sensitive baroreceptors in the JG cells that sense a drop in arterial pressure * decreased NaCl delivery to the macula densa * increased sympathetic nervous activity activates beta-adrenergic receptors in the JG cells
36
how does an increased sympathetic nervous activity activate beta-adrenergic receptors in the JG cells
* enhances sensitivity of JG baroreceptors and macula densa mechanisms * activates alpha-adrenergic receptors which increase renal NaCl reabsorption which decreases GFR with severe activation
37
how does renin release ultimately lead to production of angiotensin II
* renin works on angiotensinogen (liver) to create angiotensin I * angiotensin-converting enzyme (ACE) works on angiotensin I to create angiotensin II (most conversion occurs in the lungs as blood flows through the pulmonary capillaries)
38
what is angiotensin II and how is it inactivated
potent vasocontrictor, angiotensinases
39
what are the two ways that angiotensin II increases arterial blood pressure
* potent and rapid vasocontriction * decreased excretion of salt and water through the kidneys slowly increases the ECF volume and arterial pressure over hours to days
40
potent and rapid vasoconstriction effect
* all areas of body * arterioles > veins * increased total peripheral resistance * mild increase in venous return
41
decreased excretion of salt and water through the kidneys slowly increases the ECF volume and arterial pressure over hours to days, direct effect:
* vasoconstriction of the efferent arteriole decreases blood flow, through the kidney and reduces pressure in the peritubular capilarries, which increases reabsorption of fluid from the tubules * works on tubular cells in various segments to increase water and sodium reabsorption
42
decreased excretion of salt and water through the kidneys slowly increases the ECF volume and arterial pressure over hours to days, indirect effect:
* stimulates production of aldosterone from the adrenal cortex * aldosterone causes marked sodium reabsorption by the tubules
43
what happens when a person with healthy kidneys ingests a lot of salt
their blood pressure does not change * salt increases the ECF volume and arterial pressure * renin production is decreased which helps decrease ECF and blood pressure back to normal
44
what happens when a person with not healthy kidneys ingests a lot of salt
* blood pressure will increase * ex: give fluids that contain a supraphysiologic amount of sodium, a similar rise in blood pressure can occur - why use Na-restricted IV fluids in patients with kidney disease
45
why do patients with kidney disease become hypertensive
* some kidney diseases lead to ischemia (decreased blood flow) * decreased blood flow in this area leads to renin production, which acts on other areas of healthy kidney tissue, leading to salt and water retention * excessive levels of circulating angiotensin II reset the blood pressure to a higher point
46
triggered by and increase in plasma osmolality and decrease in ECF * ADH * Aldosterone * Angiotensin II
ADH
47
triggered by angiotensin II and hyperkalemia * ADH * Aldosterone * Angiotensin II
aldosterone
48
triggered by decrease delivery of Na and Cl to the macula densa * ADH * Aldosterone * Angiotensin II
aldosterone
49
inserts aquaporins in the CD and increases reabsorption of H2O and creates a concentrated urine * ADH * Aldosterone * Angiotensin II
ADH
50
causes potent vasoconstriction of the arterioles * ADH * Aldosterone * Angiotensin II
angiotensin II
51
increase Na reabsorption and K excretion in principal cells * ADH * Aldosterone * Angiotensin II
aldosterone

elimination and detox - wk 3 (6 decks)

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