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Renal > Renal Physiology IV > Flashcards

Renal Physiology IV Flashcards

1
Q

Elevations do not directly control BP but can raise BP

-more profound in some people than others

A

Na+

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2
Q

In some individuals, increases in Na+ ingestion resets the renal function curve so that Na+ secretion is insufficient to maintain

A

Normal MAP

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3
Q

The brain possesses an RAAS that is upregulated by (the opposite of what occurs with renal RAAS)

A

NaCl

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4
Q

A modicum of Na+ (i.e. 1-3% of the remaining filtered load) can be reabsorbed by the

A

Collecting duct

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5
Q

Most commonly occurs in the very young and elderly and sometimes develops as a complication of neurosurgery or traumatic brain injury

A

Hypernatremia

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6
Q

Hypernatremia is caused by the disproportional loss in H2O relative to Na+ and/or hypertonic Na+ gain. It is defined as a plasma Na+ greater than

A

145 meq/L

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7
Q

The signs and symptoms of hypernatremia reflect the hyperosmolality that leads to an impediment of

A

Neuronal structure and function (i.e. disrupted APs)

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8
Q

In addition, the increased osmotic gradient present in hypernatremia favors the siphoning of intracellular fluid to the intravascular space. If severe enough, this can result in

A

Brain shrinkage resulting in cerebral bleeding and subarachnoid hemmorhage

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9
Q

Therefore, patients with hypernatremia can present with signs and symptoms reflecting structural and functional insult to neuronal and muscular tissue including

A

Muscle weakness, lethargy, restlessness, and if severe enough, coma and death

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10
Q

To treat hypernatremia, we have to carefully lower the

A

Hypertonicity

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11
Q

Defined as a plasma Na+ of less than 136 meq/L

A

Hyponatremia

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12
Q

In general, serum [Na+] of what concentration results in symptoms including: Lethargy, nausea, muscle weakness, irritability, and anorexia?

A

Less than 120 meq/L but greater than 110 meq/L

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13
Q

As hyponatremia progresses, the change in the intra-versus extracellular osmotic gradients will favor the translocation of H2O into the

A

Intracellular space

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14
Q

If profound enough, this translocation of H2O into the intracellular space will cause

A

Cellular swelling and damage

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15
Q

IF not corrected will result in drowsiness, confusion, depressed reflexes, seizures, coma, and ultimately death

A

[Na+] below 110 meq/L

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16
Q

Simply means that Na+ content has not changed and intravascular volume is fine. However, something has caused an inordinate amount of H2O retention leading to hyponatremia

A

Euvolemic hyponatremia

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17
Q

In euvolemic hyponatremia, since volume status is within normal limits, we would not expect changes

A

Cardiovascular function

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18
Q

Tachycardia, flat neck veins, and orthostatic hypotension are cardiovascular function changes associated with

A

Volume depletion

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19
Q

Ascites and peripheral or pleural edema are cardiovascular changes associated with

A

Volume overload

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20
Q

Some pathologies which can result in euvolemic hyonatremia include

A

Glucocorticoid deficiency, hypothyroidism, and SIADH

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21
Q

Exerts negative feedbac on AVP, so deficiency can cause euvolemic hyponatremia

A

Cortisol

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22
Q

Since euvolemic hyponatremia is due to some limitation in H2O excretion, we see an elevation in

A

Urine [Na+]

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23
Q

Part of the treatment protocol in a euvolemic hyponatremic patient is

A

H2O restriction

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24
Q

Results from a loss of total body water and Na+, whereby more Na+ is lost relative to H2O

A

Hypovolemic Hyponatremia

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25
Q

What are three intrarenal causes of hypovolemic hyponatremia

A
  1. ) Diuresis
  2. ) Osmotic diuresis
  3. ) Aldosterone deficiency
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26
Q

What would the urine chemistry show in a patient with an intrarenal cause of hypovolemic hyponatremia?

A

Increased urine [Na+]

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27
Q

Results from profound intravascular fluid loss such as that from diarrhea, vomiting, third space fluid shifts, and excessive sweating

A

Extrarenal hypovolemic hyponatresis

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28
Q

What signs do we expect to see in a patient with hypovolemic hyponatremia from extrarenal causes?

A

Tachycardia, flattened neck veins, and orthostatic hypotension

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29
Q

In an extrarenal cause of hypovolemic hyponatremia, what do we see in the urine chemistry?

A

Urine [Na+] is decreased and BUN is elevated (due to decreased renal perfusion)

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30
Q

How can we treat the hypovolemic hyponatremic patient?

A

Give isotonic saline

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31
Q

Results when an inordinate amount of H2O and some Na+ occurs such that plasma [Na+] is abnormally decreased

A

Hypervolemic hyponatremia

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32
Q

Hypervolemic hyponatremia is also called

A

Dilutional hyponatremia

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33
Q

One relatively common cause of hypervolemic hyponatremia is

A

Heart failure

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34
Q

What would we expect to see in the urine chemisty of a patient in heart failure resulting in hypervolemic hyponatremia?

A

Decreased urine [Na+]

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35
Q

Acute and chronic renal failure can also result in

A

Hypervolemic hyponatremia

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36
Q

Why would acute and chronic renal failure result in hypervolemic hyponatremia?

A

Because GFR is decreased triggering the GFR decrease chain reaction

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37
Q

What would we expect to see in the urine chemistry of a patient with hypervolemic hyponatremia due to acute or chronic renal failure?

A

Solute rich urine (i.e. increased urine [Na+]

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38
Q

How would we treat hypervolemic hyponatremia, regardless of the cause?

A

Restriction of both Na+ and H2O

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39
Q

In addition to causing hypertension, this condition is often characterized by hypokalemia, kaliuresis, metabolic acidosis, and decreased plasma [renin]

A

Mineralocorticoid hypertension

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40
Q

Mineralocorticoid hypertension results in decreased

A

Plasma renin concentration

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41
Q

A common cause of mineralocorticoid hypertension is a condition of

A

Aldosterone excess that hyperstimulates ENaC

42
Q

Can becaused by a primary or secondary hyperaldosteronism due to an aldosterone-secreting tumor, adrenal hyperplasia, or (rarely) adrenal carcinoma

A

Mineralocorticoid Hypertension

43
Q

Regardless of the specific cause, the mechanism for mineralocorticoid hypertension centers around heightened ENaC Na+ reabsorption at the expense of

A

Elevated K+ Excretion

44
Q

Aldosterone has been shown to induce the activation of several cell signaling mechanisms which are linked to inflammation and the development of

A

Fibrosis in cardiovascular tissues

45
Q

Fatal syndrome that will show in infants

-Causes salt waisting

A

Type I hypoaldosteronism (pseudohypoaldosteronism)

46
Q

Type I hypoaldosteronism (pseudohypoaldosteronism) may stem from mutations in

-The gene encoding ENaC protein

A

SCNN1

47
Q

A complex and mixed disorder that results from a disruption in the AVP system in which body H2O and often Na+ balances are severely disrupted

A

Diabetes Insipidus (DI)

48
Q

Caused by either a loss in AVP production or a mutation that disrupts the expression of V2R or AQP2

A

Diabetes insipidus (DI)

49
Q

Mutations which disrupt the expression of V2R or AQPs lead to a block in

A

AVP mediated H2O reabsorption within the tubules (nephrogenis)

50
Q

The AVP loss associated with DI can be either

A

Central or nephrogenic

51
Q

Under normal circumstances, promotes H2O reabsorption from the distal nephron and collecting ducts

A

AVP

52
Q

So what results then if AVP is lost?

A

Mass diuresis (polyuria) of dilute urine

53
Q

The formation of dilute urine is the hallmark of

A

DI

54
Q

The formation of solute rich urine is one of the hallmarks of

A

Diabetes Mellitus

55
Q

DI results in loss of ECF volume which will result in siphoning of H2O form plasma. The resulting reduced plasma volume stimulates Osmoreceptors that stimulate

A

Hypothalamic thirst centers

56
Q

Thus, many DI patients will also experience

A

Polydipsia (desire for increased fluid intake)

57
Q

The problem with this is that without AVP, all of the H2O that goes in, goes right out during urine. This is caused

A

Positive free H2O clearance

58
Q

Remember that any time there is a massive movement of H2O, what will likely follow?

A

Ions (Na+ and K+)

59
Q

Thus there is a high probability that DI patients will also present with one or more forms of

A

Ion imbalance

60
Q

Involves a problem with the AVP system such that improper free H2O balance occurs

A

Syndrome of Inappropriate ADH (SIADH) Secretion

61
Q

A defect at the level of hormone release is classified as

A

Neurogenic

62
Q

A defect in hormone responsiveness in the target tissue (nephron in this case) is classified as

A

Nephrogenic

63
Q

SIADH can be congenital or induced by a variety of stimuli including

A

Drugs, lesions, and neoplasms

64
Q

The congenital form of SIADH is present in the neonate and involves a mutation in the X-linked

A

V2 receptor (V2-R)

65
Q

This mutation is a gain of function mutation in which V2-R is constitutively activated in the absence of

A

AVP (Nephrogenic SIADH)

66
Q

In fact, these babies will most likely have undetectable levels of serum AVP, yet the mutant receptor maintians

A

AVP-like bioactivity

67
Q

Can assume one of several types which involve the inappropriate regulation of AVP secretion that results in erratic and unpredictable elevations in serum AVP

A

Induced SIADH

68
Q

Interestingly, patients with SIADH continue to drink despite the decreased

A

Free- H2O clearance and resultant hyponatremia

69
Q

Patients with SIADH can not excrete the proper free H2O load that is required to maintain normal

A

Plasma osmolality

70
Q

Part of the diagnostic criteria for SIADH

A

Euvolemia

-many of these patients have euvolemic hyponatremia

71
Q

The underlying problem of the euvolemic hyponatremia in SIADH, and the condition that needs to be corected is the

A

Hyponatremia

72
Q

What are the 4 defining characteristics of SIADH?

A
  1. ) Highly concentrated urine (osmolality greater than 100)
  2. ) Urine Na+ greater than 40 meq/L
  3. ) Euvolemic hyponatremia (serum Na+ below 136 meq/L)
  4. ) Hypoosmolality
73
Q

All of the hallmarks of SIADH present with the

A

Exclusion of glucocorticoid and thyroid hormone deficiency

74
Q

What are 3 treatments of SIADH?

A
  1. ) fluid limitation
  2. ) Treatment with loop diuretic
  3. ) Restoration of eunatremia
75
Q

Which two compounds can be used to treat the nephrogenic form of SIADH?

A

Democycline and lithium

76
Q

Target the signaling molecules that orchestrate the V2-R-mediated activation of AQP2

A

Demeclocycline and lithium

77
Q

The principle extracellular anion

-Vital with Na+ in setting tonicity

A

Chloride (Cl-)

78
Q

Alterations in plasma Na+ and Cl- usually move in paralle and to the

A

Same degree

79
Q

What is the likely result of changes in plasma Cl- tht are opposite to those of Na+ or changes that are disproportionate in magnitude?

A

Acid-base disorder

80
Q

Unless specifically indicated otherwise, assume that Na+ movement means

A

NaCl movement

81
Q

Thus, like Na+, Cl- is overwhelmingly reabsorbed within the

A

Nephron

82
Q

Unlike with Na+, changes in chloremic state are not as associated with body fluid balance. However, elevated plasma Cl- can be induced by

A

Dehydration (as with Na+)

83
Q

However, hyperchloremia can also be induced as a compensatory mechanism during

A

Metabolic acidosis

84
Q

Hyperchloremic metabolic acidosis can be identified as

A

Normal AG metabolic acidosis

85
Q

When perturbations in plasma volume, pH, etc occur. the precedence is to restore the

A

Euvolemic State

86
Q

Describes the ability of the nephron to maintain an effective Na+ resorptive capacity in the face of changing tubular Na+ load

A

Glomerular-Tubule (GT) balance

87
Q

Through this mechanism, as more Na+ is filtered, comparably more Na+ will be reabsorbed

A

GT balance

88
Q

Changes in peritubular capillary oncotic and hydraulic pressures, alterations in the constituents of the filtrate, and the TGF system collectively provide the feedback that supports

A

GT balance

89
Q

An-II up-regulates Na+ conservation by stimulating Na+-H+ exchange within the

A

Proximal tubule

90
Q

This causes the reabsorption of Na+ and the secretion of

A

H+

91
Q

An-II also stimulates ENaC, thereby supporting Na+ reabsorption from the

A

Distal nephron

92
Q

Recall, AII induces aldosterone secretion. Aldosterone stimulates Na+ reabsorption from the

A

ASDN (and to a lesser degree from the collecting ducts)

93
Q

The trade-off for aldosterone directed Na+ reabsorption is an increase in the excretion of both

A

K+ and NH4+

94
Q

Increased renal SNS tone dampens

A

GFR and RBF

95
Q

SNS post-ganglionics also synapse within the JG

apparatus: norepi stimulates the RAS via

A

Type B1 adrenoreceptors

96
Q

What stimulates aldosterone secretion:

  1. ) Directly
  2. ) Indirectly
A
  1. ) An-II

2. ) SNS activity

97
Q

Activates α adrenoreceptors within the tubule epithelium

A

Norepinephrine

98
Q

These α adrenoreceptors are coupled to the activation of

A

Na+-H+ exchangers and Na+/K+ ATPases

99
Q

Thus the renal α adrenergic response induces

A

Na+ reabsorption and H+ secretion

100
Q

Impairs Na+ reabsorption

-Secreted by atrial myocytes

A

Atrial Natriuretic Peptide (ANP)

Renal (10 decks)

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