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Renal > Disorders of Volume Balance > Flashcards

Disorders of Volume Balance Flashcards

1
Q

What are the following normal values in the blood plasma?

[Na+]

[K+]

[Cl-]

[protein]

osmolality

A

[Na+] = 142 mM

[K+] = 4.4 mM

[Cl-] = 102 mM

[protein] = 1 mM

osmolality = 290 mOsm

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2
Q

What are the following normal values in the interstitial fluid?

[Na+]

[K+]

[Cl-]

[protein]

osmolality

A

[Na+] = 145 mM

[K+] = 4.5 mM

[Cl-] = 116 mM

[protein] = 0 mM

osmolality = 290 mM

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3
Q

What are the following normal values in the intracellular fluid?

[Na+]

[K+]

[Cl-]

[protein]

osmolality

A

[Na+] = 15 mM

[K+] = 120 mM

[Cl-] = 20 mM

[protein] = 4 mM

osmolality = 290 mOsm

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4
Q

effective arterial blood volume (EABV)

A

the part of the extracellular fluid that is in the arterial system and is effectively perfusion the tissues (~700 cc in a 70 kg person)

in physiological terms, EABV is the pressure perfusion the arterial baroreceptors in the carotid sinus and glomerular afferent arterioles

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5
Q

What are the high pressure volume receptors?

A

carotid sinus

aortic arch

left ventricle

juxtaglomerular apparatus

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6
Q

What are the low pressure volume receptors?

A

cardiac atria

right ventricle

pulmonary vessels

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7
Q

What is normal serum sodium? What is a good measure of? And what does it mean when it is high? Low?

A

normal value - 140 mEq/L

best measure of relative proportion of solute to water ratio in the body

low values indicate relative water excess

high values indicate relative water deficit

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8
Q

volume regulation vs. osmoregulation

A

volume regulation is the renal handling of salt, and thereby volume

(volume is sensed (EABV) with multiple regulators and urine sodium excretion is primarily affected)

osmoregulation is the measurement of plasma osmolality and the subsequent response to high or low osmolality

(sensed by hypothalamic osmoreceptors, stimulating either thirst or water excretion, plasma osmolality is change dthrough water balance)

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9
Q

causes of low volume hyponatremia

A

GI losses

diuretics

salt losing nephropathy

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10
Q

causes of euvolemic hyponatremia

A

hyperthyroidism

glucocorticoid def.

ADH release

SIADH

polydipsia

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11
Q

causes of high volume hyponatremia

A

CHF

cirrhosis

nephrosis

renal failure

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12
Q

effectors of osmoregulation

A

ADH

thirst

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13
Q

effectors of volume regulation

A

RAA

sympathetic nerves

ANP

ADH

pressure natriuresis

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14
Q

What is the body’s response to a high osmolality?

A

stimulates release of ADH and stimulates thirst

water intake and ADH water retention by the kidneys causes plasma osmolality to decrease

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15
Q

What is the body’s response to a low osmolality?

A

little or no ADH would be released, and there would be no thirst stimulation

lack of ADH would allow for the excretion of dilute urine and therefore water loss from the body and an increase in the serum osmolality

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16
Q

What are the effector mechanisms integral for volume regulation?

A

RAAS

sympathetic nervous system

atrial natriuretic peptide (ANP)

ADH

pressure natriuresis

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17
Q

At the extremes is osmolality or volume more important to the body?

A

volume statis is more important

at the extremes, the body will retain or release ADH despite the osmolality stimulus

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18
Q

What are the criteria for successful urinary concentration?

A

intact medullary osmotic gradient

ADH is present and cells can respond

slow flow to allow osmotic equilibrium

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19
Q

What are the criteria for successful urinary dilution?

A

sufficient delivery of fluid through nephron

optimal solute transport out of urinary space in thick ascending limb

no ADH present

fast flow through tubules

20
Q

How is GFR releated to sodium load?

A

in the steady state, sodium intake is equal to output (~100 mEq/day)

therefore the kidney filters > 20,000 mEq/day, but only 100 mEq are excreted in the urine in one day

21
Q

Describe the distribution of sodium reabsorption in the nephron.

A

67% filtered in the proximal tubule

25% filtered in the TAL

5% filtered in the DCT

3% filtered in the CCD

urinary excretion is ~100 mmole/day

0.4% filtered load remaining

22
Q

What is the equation for the fractional excretion of sodium?

A

fractional excretion = amount excreted x 100%/filtered load

(Ux/Px) / (Ucr/Pcr)

23
Q

Describe the channels in the proximal tubule cell.

A
24
Q

Describe the channels in the thick ascending limb cell.

A
25
Q

Describe the channels in the distal convoluted tubule cell.

A
26
Q

Describe the channels in the principal cell.

A
27
Q

What is considered low urine Na? What are the exceptions?

A

low urine Na is less than 15-20 mEq/L

this suggests decreased EABV in the appropriate clinical setting

exceptions include low sodium diet in a steady state, renal ischemia

28
Q

What does low FeNa (<1%) suggest?

A

a prerenal state (decreased EABV) or normal physiology

29
Q

What are the effects of angiotensin II?

A

sympathetic activation

smooth muscle vasoconstriction

decreased bradykinin

Na/H2O retention (via aldosterone)

30
Q

What is the effect of increased sympathetic signals on the kidneys?

A

increased renin, angiotensin II, and aldosterone

increased Na+ reabsorption both directly and thorugh AGII and Aldo

increased EABV/ECV and cardiac output as a result

31
Q

natriuretic peptide

A

peptide released from the cardiac atria, activates guanylyl cyclase through attachment to membrane receptor

stimulus for release is atrial stretch

acts as vasodilator and promotes urinary Na+ and water excretion through increased GFR and inhibition of Na+ reabsorption in the medullary collecting tubule

32
Q

What is pressure natriuresis?

A

a backup physiological phenomenon that does not rely on humoral or neural control

unclear mechanism

probably does not play a large role in day to day volume balance, when the other effector systems are in place

33
Q

How does hypertension affect pressure natriuresis? Hypotension?

A

in the absence of neurohumoral factors, hypertension promotes Na+ excretion and hypotension promotes Na+ retention

34
Q

underfilling theory

A

as plasma leaks out of the capillaries, the kidney senses an “underfilled” vascular tree (a decreased EABV) and holds onto salt and water

can result in edema over time

treating with diuretics may decrease perfusion

35
Q

overfilling theory

A

the kidney inappropriately holds onto salt and water, creating an “overfilled” vascular system and edema

treatment with diuretics is usually safe

36
Q

What are the clinical features of nephrotic syndrome?

A

proteinuria

edema - periorbital, peripheral

37
Q

mechanism of edema in nephrotic syndrome

A

overfilling secondary to abnormal kidney retaining Na+

underfillying if capillary hemodynamics are altered by hypoalbuminemia

protein in urine creates a low plasma oncotic pressure and fluid movement into the interstitium

the result is a response to retain additional volume

38
Q

treatment of edema in nephrosis

A

cure the underlying disease

restrict NaCl intake

ACE-inhibitors may decrease proteinuria, improve cardiac function

diuretics to improve symptoms of edema

39
Q

mechanisms of edema in heart failure

A

increase in venous (hydrostatic pressure) behind the heart

lack of forward force to appropriately stimulate the high pressure receptors

low EABV results, the kidney retains Na+

40
Q

treatment options for heart failure

A

ACE inhibitors - reduce afterload (DM)

beta-blockers (DM)

spironolactone - antagonizes aldo (DM)

digoxin - improves cardiac function

diuretics - remove fluid

salt and water restriction for edema

41
Q

bradykinin

A

a vasodilator that results from angiotensin II release

42
Q

clinical features of cirrhosis

A

ascites

lower extremity edema (below the diseased liver)

43
Q

mechanism of edema in liver cirrhosis

A

splanchnic vasodilation and decreased systemic vascular resistance make the kidney perceive a decreased EABV due to the increased diversion of blood to the other abdominal organs, and retain salt and water

primary sodium retention (overfiling) - observed early in cirrhosis

decreased EABV, and resultant underfilling found later

44
Q

treatment of liver cirrhosis

A

fix the liver

restrict NaCl intake

water restriction if hyponatremic

diuresis if needed

45
Q

What is hepatorenal syndrome? How is it treated?

A

primary liver failure, renal failure, and low urine Na+ in the settin gof eu- or hypervolemia

treatmet - combination of midodrine (an oral alpha1 adrenergic stimulator) and octreotide (a splanchnic vassoconstrictor)

Renal (28 decks)

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