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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
Q

chronic changes in arterial pressure have a much greater effect on:

A

pressure natriuresis and pressure diuresis than acute changes

26
Q

increased fluid volume causes and increase in

A

arterial pressure

27
Q

autoregulation

A

when excess blood flows through a tisue, local tissue vasculature constricts and decreases blood flow back to normal

28
Q

how do the kidneys respond to increased fluid volume and increased arterial pressure

A

respond immediately with pressure natriuresis and pressure diuresis - increased intrarenal vascular resistance

29
Q

increases salt intake is more likely to increase arterial pressure than:

A

increased water intake

30
Q

how does salt affect arterial blood pressure

A
  • 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
Q

the renin-angiotensin-aldosterone system (RAAS) is a powerful tool for regulating:

A

blood pressure

32
Q

____ is an enzyme produced by the JG cells of the juxtaglomerular apparatus

A

renin

33
Q

JG cells

A

smooth muscle cells in the afferent arteriole next to the glomerulus

34
Q

macula densa

A

cells of the distal tubule that sense sodium and chloride delivery

35
Q

what are the three mechanisms that stimulate the release of renin from the JG cells

A
  • 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
Q

how does an increased sympathetic nervous activity activate beta-adrenergic receptors in the JG cells

A
  • 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
Q

how does renin release ultimately lead to production of angiotensin II

A
  • 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
Q

what is angiotensin II and how is it inactivated

A

potent vasocontrictor, angiotensinases

39
Q

what are the two ways that angiotensin II increases arterial blood pressure

A
  • 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
Q

potent and rapid vasoconstriction effect

A
  • all areas of body
  • arterioles > veins
  • increased total peripheral resistance
  • mild increase in venous return
41
Q

decreased excretion of salt and water through the kidneys slowly increases the ECF volume and arterial pressure over hours to days, direct effect:

A
  • 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
Q

decreased excretion of salt and water through the kidneys slowly increases the ECF volume and arterial pressure over hours to days, indirect effect:

A
  • stimulates production of aldosterone from the adrenal cortex
  • aldosterone causes marked sodium reabsorption by the tubules
43
Q

what happens when a person with healthy kidneys ingests a lot of salt

A

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
Q

what happens when a person with not healthy kidneys ingests a lot of salt

A
  • 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
Q

why do patients with kidney disease become hypertensive

A
  • 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
Q

triggered by and increase in plasma osmolality and decrease in ECF

  • ADH
  • Aldosterone
  • Angiotensin II
A

ADH

47
Q

triggered by angiotensin II and hyperkalemia

  • ADH
  • Aldosterone
  • Angiotensin II
A

aldosterone

48
Q

triggered by decrease delivery of Na and Cl to the macula densa

  • ADH
  • Aldosterone
  • Angiotensin II
A

aldosterone

49
Q

inserts aquaporins in the CD and increases reabsorption of H2O and creates a concentrated urine

  • ADH
  • Aldosterone
  • Angiotensin II
A

ADH

50
Q

causes potent vasoconstriction of the arterioles

  • ADH
  • Aldosterone
  • Angiotensin II
A

angiotensin II

51
Q

increase Na reabsorption and K excretion in principal cells

  • ADH
  • Aldosterone
  • Angiotensin II
A

aldosterone

elimination and detox - wk 3 (6 decks)

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