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MSS Renal Exam 2 > Regulation of Na/H2O Balance > Flashcards

Regulation of Na/H2O Balance Flashcards

1
Q

intracellular osmolarity?

A

K+

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2
Q

interstitial osmolarity?

A

Na+

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3
Q

plasma osmolarity

A

protein (usually albumin

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4
Q

ICF vs. ECF?

A

ECF: Na, Cl, HCO3-, Ca
ICF: K, protein (slightly lower pH)

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5
Q

osmotic equilibration

A

osmotic pressure determines distribution of body water

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6
Q

total body sodium content?

A

major in ECF

  • water and sodium are regulated independently
  • prevent large changes in plasma osmolality
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7
Q

increase sodium content?

A

water from ICF to ECF
also renal retention of water

increased ECF volume

increased sodium expands ECF and effective circulating volume

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8
Q

total body Na content

A

dietary intake - urinary excretion

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9
Q

plasma Na

A

regulated by changes in water balance

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10
Q

decreased ECF volume

A

increased Na conservation

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11
Q

increased ECF volume

A

increased Na excretion

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12
Q

reabsorption of Na

A

proximal tubule 65% and loop of henle 25%

fine tuning in distal nephron

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13
Q

thick ascending limb

A

co-transporter
-Na/K/Cl

important in establishing medullary hyperosmolarity

inhibited by loop diuretics

messes up medullary gradient
-can’t concentrate urine

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14
Q

promotion of Na reabsorption

A

renal sympathetics
RAAS
aldosterone

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15
Q

promote Na excretion

A

ANP, BNP
urodilatin
intrarenal prostaglandins

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16
Q

hypovolemia

A

increases sympathetics

  • stimulate Na and H2O reabsorption (aldosterone)
  • increased granular cell stimulation
  • leads to increased renin secretion

decreases GFR (therefore decreased fluid delivery to macula densa (increases renin)

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17
Q

promotion of renin secretion

A

renal sympathetics
-beta-1 in JG apparatus

decreased NaCl to macula densa (tubuloglomerular feedback)

intrarenal baroreceptor
-afferent arteriolar vasoconstriction leads to decreased pressure at granular cells

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18
Q

loop diuretics and renin?

A

renin secretion increases (senses hypoperfusion)

19
Q

ANG II

A

systemic arterial contsriction (increased BP)

renal constriction (efferent > afferent)

Na reabsorption in PCT (Na-H exchanger), TAL, CCD

thirst**

ADH and aldosterone secretion

contracts mesangial cell (decrease GFR)

decreased medullary blood flow (bc of efferent )

20
Q

ADH

A

secreted from pituitary

21
Q

aldosterone

A

secreted from adrenal cortex

22
Q

thirst

A

stimulated by ANG II

23
Q

ANG II arteriolar constriction affect?

A

decreased RBF
GFR maintained

because efferent > afferent

24
Q

ANG Ii and medullary blood flow?

A

decreased

25
Q

aldosterone

A

late distal convoluted tubule and collecting duct

  • stimulates sodium reabsorption
  • leaves lumen-negative potential
  • passive Cl- reabsorb and K/H secretion

stimulates K secretion (hypokalemia)
stimulates H secretion (H-ATPase)

26
Q

hyperkalemic patients?

A

can give diuretics

27
Q

hyperaldosteronism**

A

excessive K and H excretion

metabolic alkalosis
hypokalemia

28
Q

stimulation of aldosterone release?

A

hyperkalemia
high ACTH levels
ANG II

29
Q

feedback of aldosterone

A

increased pressure feeds back to inhibit aldosterone

30
Q

ANP

A

increases Na and H2O excretion

increases GFR
inhibits Na reabsorption
suppress renin and aldosterone and ADH
systemic vasodilator

31
Q

affect of ANP

A

afferent arteriolar dilation

efferent arteriolar constriction

32
Q

ANP release

A

stimulated by increased atrial pressure

33
Q

urodilatin

A

secreted by DCT and collecting duct in response to increased pressure and volume

suppresses Na and H2O reabsorption by medullary collecting duct

    • no effect on systemic circulation
  • unlike ANP BNP
34
Q

intrarenal prostaglandins

A

PGE2
-increased GFR by dilating renal arterioles

suppress Na reabsorption in thick ascending limb and cortical collecting duct

increased urinary Na excretion

to protect kidney from damage**
-ibuprofen be careful

35
Q

effect of prostaglandins on concentration in renal medullary tissue

A

solute concentration goes down

can’t concentrate urine (no good)

36
Q

ADH

A

released by hypothalamus (posterior pituitary)

stimulated by ANG II
also stimulated by osmoreceptors

37
Q

major stimuli for ADH release?

A

hyperosmolarity (major)***
volume depletion

hypothalamic more important than hepatic osmoreceptors

38
Q

volume depletion

A

potentiates ADH response to hyperosmolarity

-prevents inhibition of ADH release

39
Q

too much water

A

hyponatremia

40
Q

too little water

A

hypernatremia

41
Q

too much Na

A

edema

-fluid from vascular to interstitium

42
Q

too little Na

A

volume depletion

43
Q

hemorrhage response?

A

hypoperfusion

  • increased renin (RAAS increase)
  • increased sympathetic activity

constriction renal arterioles (sympathtic)
-constriction of efferent (ANG II)

increased Na and water reabsorption

MSS Renal Exam 2 (7 decks)

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