Brainscape's Knowledge GenomeTM

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


See full index

Renal > Renal Physiology III > Flashcards

Renal Physiology III Flashcards

1
Q

Stimulates the secretion of adrenocorticotropic hormone (ACTH) by binding V1b

A

AVP

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

Secreted by atrial myocytes in response to increased right atrial pressure

A

Atrial natriuretic peptide

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

Exerts vasodilatory effects within afferent and efferent arterioles

A

ANP

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

ANP also decreases the sensitivity of the

A

TGF mechanism

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

Collectively, ANP increases

A

GFR and RBF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

In general, ANP increases diuresis. To complement this activity, ANP suppresses

A

Renin secretion

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

Renal autoregulation is mediated by

A

Prostaglandins

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

If renal perfusion pressure plummets below an autoregulatory range, the mobilization of locally produced vasoconstrictors stimulates

A

Constriction of the afferent arteriole

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

Constriction of the afferent arteriole results in which three things?

A
  1. ) Decreased glomerular P
  2. ) Drop in GFR
  3. ) Reduction in post-glomerular capillary pressures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Reduction in post glomerular capillary pressures creates gradients favorable for

A

Reabsorption

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

Can lead to ischemic acute renal failure

A

Renal hypoperfusion

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

The two most common examples of renal hypoperfusion leading to ischemic acute renal failure are

A
  1. ) Prerenal azotemia

2. ) Acute tubular necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

An extrarenal problem causing acute renal failure due to poor renal perfusion

-an increase in plasma urea

A

Azotemia

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

Include structural changes in renal arterioles and small arteries, impaired production of vasodilatory prostaglandins, afferent arteriolar vasoconstriction, or the inability to increase efferent arteriolar resistance due to failure/pharmacologic inhibition of the RAS in a normotensive patient

A

Factors leading to renal hypoperfusion

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

Structural changes in renal arterioles and small arteries are associated with

A

Old age, chronic hypertension, and chronic kidney disease

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

The impaired production of vasodilatory prostaglandins is induced by

A

NSAIDs and COX-2 inhibitors

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

Hypercalcemia, sepsis, or the use of cyclosporine, tacrolimus, or radiocontrast agents can cause

A

Pathologic Afferent arteriole vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

If you received labs that showed:

  1. ) Increased urinary specific gravity (greater than or equal to 1.015)
  2. ) Decreased Na+ and urea
  3. ) Elevated plasma BUN to Creatinine ratio (20:1 or higher)

than you would suspect

A

Renal hypoperfusion

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

The vast majority of filtered Na+ is reabsorbed by the

A

Tubule system (only 0.4% is excreted)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the two mechanisms by which Na+ (and everything else) can be reabsorbed?

A
  1. ) Transcellular

2. ) Paracellular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

When Na+ traverses the apical and basolateral plasma membranes via transporter and/or channel activity

A

Transcellular reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Requires metabolic energy to establish favorable electrochemical gradients and/or to directly power Na+ transporters

A

Transcellular reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

There is a cohort of hormonally regulated Na+ transporters and channels which enable Na+ reabsorption via transcellular reabsoption within the

A

Distal nephron (TAL and beyond)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Reabsorption where Na+ does not traverse the plasma membrane, but instead moves through extracellular pathways (tight junctions) between tubule epithelial cells

A

Paracellular reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

A passive mechanism of reabsorption and thus relies on electrochemical and/or concentration gradients to drive ion movement and not metabolic energy

A

Paracellular reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Solvent drag,i.e. the movement of Na+ without H2O occurs via

A

Paracellular reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

The vast majority of Na+ reabsorption (approximately 70%) occurs within the

A

1st half of the proximal tubule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

The mechanism in the 1st half of the proximal tubule centers around basolateral

A

Na+/K+ ATPases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

These ATPases establish a Na+ gradient that is favorable for the apical transport of Na+ from the forming urine (lumen) into the

A

Tubule epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Movement of Na+ across the apical membrane of the proximal tubule is mediated by

A

Na+-glucose cotransporters (SGLT1 and 2) and Na+-H+ exchangers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Transport of Na+ from the tubule epithelial cell cytosol into the renal intersitium is accomplished by

A

Na+/K+ ATPases and Na+-HCO3- symporters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Hydraulic and oncotic pressures within the peritubular capillaries that surround the proximal tubule will affect

A

Reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Results in a low hydraulic P in the efferent arteriole and the peritubular capillaries which it supplies

A

Filtration from the glomerulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

This P gradient then provides a driving force for the reabsorption of H2O and Na+ from filtrate within the

A

Proximal tubule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

As GFR changes, hydraulic and oncotic P within the efferent arteriole and peritubular capillaries will be altered and reabsorption from the proximal tubule will respnd

A

Accordingly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

For example, at normal GFR, the peritubular capillaries possess a relatively high oncotic P and low hydraulic P, these forces favor

A

Reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

However, as GFR increases, we see an increase in

A

Filtration fraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Once again, blood entering the peritubular capillaries has a relatively high oncotic P and low hydraulic P, and

A

Reabsorption is favored

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

This relationship helps to prevent excessive

A

H2O and Na+ loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Na+ is actively reabsorbed from the

A

Thin Ascending Limb (TnAL)

41
Q

Na+ reabsorption from TAL is a vital component of the counter-current multiplier mechanism that maintains

A

Tonicity within the renal intersitium

42
Q

Contains Na+-H+ exchangers and Na+/K+/Cl cotransporters (NKCC); each of which translocate Na+ from the lumen into the epithelium

A

The apical membrane of TAL cells

43
Q

Important because it is the target of loop diuretics (e.g. furosemide)

A

NKCC

44
Q

Maintains the favorable gradient that drives the NKCC symporter

A

Renal Outer Medullary K+ transporter (ROMK2)

45
Q

Translocation of Na+ from the cytosol into the interstitium is accomplished by the

A

Basolateral Na+/K+ ATPase

46
Q

The TAL is impermeable to

-but actively resorbs a number of ions

A

H2O

47
Q

For this reason, the tonicity of the forming urine is relatively low in this region and this segment is referred to as the

A

Diluting segment

48
Q

Secreted from blood into the proximal tubule transporters

A

Loop Diuretics

49
Q

Make note that since loop diuretics are bound to plasma albumin, they can not be freely filtered through the

A

Glomerular capillaries

50
Q

Once in the tubule, the loop diuretic uses the forming urine as the vehicle to reach and block

A

NKCC

51
Q

With this in mind, heavy proteinuria (i.e. hyperalbuminuria) will interfere with the efficacy of a

-Not ineffective but a higher dose will be required

A

Loop diuretic

52
Q

Suppresses Na+ reabsorption from the TAL

A

Loop diuretics

53
Q

Since NKCC mediates K+ reabsorption concaminant with Na+, Loop diuretics promote the elimination of

A

NaCl, H2O, and K+

54
Q

Thus loop diuretics can be referred to as

A

K+ wasting diuretics (also Ca2+ wasting)

55
Q

Essentially all Na+ movement in the Distal Convoluted Tubule (DCT) occurs

A

Transcellularly

56
Q

Apical Na+/Cl- cotransporters (NCC) of the DCT are blocked by

A

Thiazide diuretics

57
Q

Local changes in lumenal potential of the DCT actually make thiazide diuretics

A

Ca2+ sparing

58
Q

However, due to increased flow, thiazides enhance

A

K+ secretion in distal nephrons

59
Q

The principal cells within the CCT perform a modest amount of

A

Na+ reabsorption

60
Q

Although the absolute molar amount of Na+ reabsorption in this region appears to be

A

Relatively low (possibly because there is not much Na+ left in the forming urine by this point)

61
Q

Is Cortical collecting tubule (CCT) Na+ reabsorption an important regulatory point?

A

No

62
Q

Principal cells are targeted by

A

AVP, Aldosterone, and An-II

63
Q

Since aldosterone exerts effects in this region, this is commonly referred to as the

A

Aldosterone-sensitive distal nephron (ADSN)

64
Q

AVP stimulates the recruitment of Na+/K+ ATPases into the basolateral membrane and also activates the

A

Amiloride-sensitive apical Na+ channel protein ENaC

65
Q

ENaC is also stimulated by

A

An-II

66
Q

Na+ diffuses through the apical membrane of the CCT via

A

ENaC

67
Q

The translocation of Na+ by ENaC creates a lumen-negative charge in the CCT which, in this region, favors the recretion of

A

K+

68
Q

Hyperpolarizes the apical membrane by blocking ENaC, and in doing so disrupts the electrochemical gradient that would favor K+ secretion

-Thus is a K+ sparing diuretic

A

Amiloride

69
Q

Also functions as a K+ sparing diuretic by blocking aldosterone bioactivity

A

Spirolactone

70
Q

Similar to other components of the nephron, relies on basolateral Na+/K+ ATPases to establish and maintain the driving force for Na+ influx from the forming urine

A

Cortical Collecting Tubule (CCT)

71
Q

CCT Na+ influx also depends upon membrane potential that is maintained via

A

ROMK2-mediated K+ secretion

72
Q

A steroid hormone that is produced and secreted by cells within the adrenal cortex (Zona glomerulosa)

A

Alosterone

73
Q

Stimulated by elevated plasma [K+]

-express AT1

A

Adrenal glomerulosa cells

74
Q

Therefore, the secretion of aldosterone is stimulated by both

A

An-II and hyperkalemia

75
Q

Binds to and activates the mineralcorticoid type steroid receptor within principal cells as well as a specific isoform in vascular smooth muscle

-The predominant mineralcorticoid that is produced in humans

A

Aldosterone

76
Q

Competitive inhibitor of aldosterone binding to the mineralocorticoid receptor

-an ldosterone antagonist

A

Spirolactone

77
Q

What effect does Aldosterone have in vascular smooth muscle?

A

Vasoconstriction

78
Q

When you think of a steroid, think changes in

A

Gene transcription

79
Q

The intrarenal effects of aldosterone can be divided into

A
  1. ) Acute (early, 1-4 h)

2. ) Late (chronic, greater than 4 h)

80
Q

During the ACUTE phase, aldosterone activates signal transduction motifs which stimulate

A

ENaC activity

81
Q

Many of the acute actions of aldosterone are believed to be

A

Non-genomic (i.e. do not change gene transcription)

82
Q

The acute effects of aldosterone on ENaC results in

A

Increased Na+ reabsorption through this channel

83
Q

Involves an up-regulation in the expression of ENaC and Na+/K+ ATPase proteins, and their import into the principal cell plasma membranes

A

The chronic effects of Aldosterone

84
Q

Trades Na+ reabsorption for K+ secretion within the distal nephron

A

Aldosterone

85
Q

By conserving Na+, aldosterone maintains body Na+ content and builds a favorable osmotic gradient for

-the way aldosterone combats volume depletion

A

H2O reabsorption

86
Q

During volume depletion, the RAAS is mobilized, and together An-II and aldosterone induce Na+ reabsorption by actions within the

A
  1. ) Proximal nephron (An-II via NHE3)

2. ) Distal nephron (An-II via NCC and aldosterone via NCC and ENaC)

87
Q

Whereas in the event of euvolemic hyperkalemia, excessive K+ causes changes within the distal nephron of which aldosterone sensitive kinases?

A

WNK1, WNK4, and SGK1

88
Q

Recall that K+ increases aldosterone secretion without a rise in

A

An-II

89
Q

This occurs via direct stimulation of adrenal zona glomerulosa cells by

A

K+

90
Q

Thus, in the absence of An-II, aldosterone increases ROMK activity resulting in a more profoud effect on promoting

A

K+ secretion over Na+ reabsorption

91
Q

Occurs as aldosterone-induced colume expansion proceeds

A

Pressure natriuresis (urinary excretion of Na_)

92
Q

Pressure natriuresis is an increase in the excretion of Na+ and H2O in order to compensate for

A

Volume expansion (i.e. elevated MAP)

93
Q

This renal counter measure (pressure natriuresis) to aldosterone dependent Na+ retention is known as

A

Aldosterone escape

94
Q

Because of this escape, we can say that patients with the pathologic state of hyperaldosteronism are not generally

A

Hypernatremic (but are often hypokalemic)

95
Q

Within a few minutes of elevated or decreased BP, e see activation of the

A

RAAS vasoconstrictor component

96
Q

Activation of the RAAS vasoconstrictor component is followed by fluid shifts between

A

Extra- and intravascular volumes (within hours)

97
Q

Within days of BP changes, we see

A

Hormone-mediated changes in renal volume conservation/elimination

98
Q

Has vascular volume contributions of diuresis, antidiuresis w/ Na+ conservation (supported by An-II, aldosterone, and AVP), and vasomotor control

A

RAAS

99
Q

Innervate the afferent and efferent arterioles, JG apparatus, and basement membrane of tubule. This exerting control over GFR as well as volume and composition of excreted urine

A

SNS fibers

Renal (10 decks)

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