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Physio > Control Of Extracellular Fluid Volume And Osmolality > Flashcards

Control Of Extracellular Fluid Volume And Osmolality Flashcards

1
Q

Hypoatremia

A

. Normal PNa = 135-145 mEq/L so less than 135 is hypoatremia
. Most common disorder of electrolytes encountered in clinical practice
. Typically result of H2O retention in excess of solute but doesn’t mean that the patient is hypervolemic

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2
Q

Pseudohypoatremia

A

. [Na] in plasma H2O is normal
. [Na] in total plasma fractions is low due to hyperlipidemia, hyperproteinemia
. Directly measured plasma osmolality is normal

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3
Q

Isotonic or hypertonic hypoatremia

A

. Due to presence of unmeasured effective osmoles initiating fluid shift from IVF to ECF
. Hyperglycemia, mannitol, radiographic contrast agents
. Removal of additional effective osmoles will correct it

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4
Q

True hypotonic hypoatremia

A

. Effective osmolality of plasma is low

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5
Q

Hypovolemic hypotonic hypoatremia

A 
. Clinical signs of volume depletion
. Orthostatic intolerance
. Dry mucous membranes 
. Dry armpits
. Dec. skin turgor 
. Low spot urine [Na] under 30 
. Treatment: infusion of 0.5-1.0 L normal saline will begin to correct hypoatremia w/o initiating signs of volume overload
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6
Q

Euvolemic hypotonic hypoatremia

A

. Modest change in ECFV can’t be detected clinically
. Assume euvolemia in absence of clinical or biochemical signs of other volemias
. Spot urine [Na] around 30

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7
Q

Hypervolemic hypotonic hypoatremia

A 
. Clinical signs of volume expansion
. SubQ edema 
. Ascites
. Pulmonary edema 
. Elevated BNP 
. Spot urine [Na] over 30 or FENa is low
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8
Q

Hypoatremia

A

. Normally is plasma osmolality dec., plasma AVP would dec. and free H2O clearance would inc. to correct imbalance
. Hypoatremia is secondary to a defect in renal water excretion

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9
Q

Psychogenic (primary) polydipsia

A

. Compulsive water drinking
. Hypoatremia assoc. w/ this condition
. Also accompanied by reduced renal ability to excrete free water and plasma AVP regulation is dysfunctional due to organic causes or secondary to meds for the psych part of disorder

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10
Q

Syndrome of inappropriate ADH (SIADH)

A

. Common cause of hypoatremia
. Usually euvolemic
. Plasma AVP is too high relative to plasma osmolality
. Due to persistent secretion from pituitary or ectopic tumor or due to reset osmostat for release of AVP, antidepressant or morphine can also cause enhanced AVP release
. Intake of water sufficient to overwhelm the reduced renal capacity to excrete free water
. Reduction in plasma Na is gradual and patients do not show signs right away, but will eventually have hypoatremia, urine osmolality over 100 mOsm and may exceed plasma osmolality, free water clearance may be neg.

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11
Q

SIADH treatment

A

. Water restriction

. Pharmacological blockade of action of AVP at collecting duct (V2R receptor antagonists like tolvaptan)

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12
Q

Nephrogenic syndrome of inappropriate antidiuresis

A

. Consistent w/ SIADH but had undetectable AVP levels

. Caused by mutations causing constitutive activation of receptor and likely cause the SIADH-like clinical picture

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13
Q

Exertional hypoatremia

A

. Symptoms: confusion, nausea, cramping, headache, seizure, pulmonary edema
. Persons undergoing prolonged exertion (over 4 hrs) who drink large amounts of electrolyte free water and have lowered ability to excrete free water (non-osmotic stimulation of AVP secretion)
. Electrolytes lost in sweat but inc. in hypotonic fluids causes hypoatremia

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14
Q

Hyperatremia

A

. Plasma Na over 145 mEq/L
. Always assoc. w/ hyperosmolality
. Often result of unreplaced H2O losses
. Could also be due induced by infusion of IV solution of hypertonic saline

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15
Q

Physiologic defense against net water loss

A

. AVP

. Thirst

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16
Q

Diabetes insipidus

A

. Excretion of large volumes of hypotonic urine due to defect in AVP function or release

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17
Q

Central diabetes insipidus (CDI)

A

. Dec. in production or release of AVP from pituitary

. Causes: stroke, tumor, drug-induced, genetic

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18
Q

Nephrogenic diabetes insipidus (NDI)

A

. Kidney unable to respond to AVP
. Drug-induced
. Defect in V2 receptor or aquaporin structure

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19
Q

How to test ability of kidney to concentrate urine

A

. H2O deprivation test
. Normal person: AVP release as plasma osmolality inc. due to H2O losses resulting in urine conc.
. CDI or nephrogenic DI: little change in urine osmolality even as plasma osmolality rises and urine osmolality will remain below plasma osmolality

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20
Q

How to test ability of kidneys to response to AVP

A

. Give exogenous AVP
. CDI: patients will response to it by concentrating urine (400 from 200 as urine osmolality)
. Nephrogenic DI: Urinary osmolality stays low
Then it is complete nephrogenic DI (200 urine osmolality)

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21
Q

Primary polydipsia

A

. Little response to exogenous AVP after H2O deprivation

. Difference btw normal and primary polydipsia would be level of urine conc. Reached (primary = 600, normal = 1000)

22
Q

Mechanisms of Na reabsorption regulation under euvolemic conditions at prox. Tubule and loop of Henle

A

. Autoregulation of GFR
. Glomerulotubular balance
. Load-dependent Na transport in loop of Henle (thick ascending limb)

23
Q

Autoregulation of GFR in Na regulation

A

. Small changes in GFR have large consequences in filtered load of Na
. Changes occur w/ posture, eating/drinking and physical activity
. Under euvolemic conditions, excessive loss or retention of Na is a valid w/ minute-to-minute alterations in tubular Na reabsorption and GFR autoregulation
. Limits alteration in filtered load of Na despite normal fluctuations in arterial pressure

24
Q

Tubuloglomerular feedback

A

. macula densa senses [NaCl] and provides neg. feedback control to afferent arteriole
. High NaCl = dec. GFR (opposite for low)
. Myogenic control of afferent arteriolar resistance also autoregulatory

25
Q

Glomerulotubular balance

A

. Spontaneous changes in GFR could happen
. Balance helps dampen the impact of GFR fluctuations on Na and H2O excretion when body Na is normal
. mechanisms: Na-solute cotransport and starling forces in peritubular capillaries

26
Q

Na-solute cotransport

A

. If GFR inc., then filtered load of glucose, AA, and co-transported solutes also inc.
. Inc. transport of these substances w/ Na inc. absolute rate of Na and H2O moving out of tubules and into interstitial space
. Enhances Na reabsorption
. Opposite for GFR dec.

27
Q

Starling forces in peritubular capillaries affecting H2O and Na reabsorption

A

. Favor bulk flow of H2O and solute from interstitial space into capillaries due to inc. peritubular oncotic pressure and lower capillary hydrostatic pressure
. Extent of the changes in starling forces will affect reabsorptive rate (filtration fraction effects forces)
. If fraction inc. then GFR inc. out of proportion to RPF, net reabsorptive pressure in peritubular capillaries is higher then usual inc. net reabsorptive pressure resulting in less backleak of Na into tubule and more interstitial Na and H2O diffuses into capillaries inc. net Na reabsorption
. Opposite for fraction dec.

28
Q

Load dependent Na transport in loop of Henle

A

. More Na delivered, the greater the Na reabsorption
. Constant amount of Na is sent to distal tubule and collecting duct (have limited ability to deal w/ large Na load variations)

29
Q

Regulatioin of renal Na and H2O excretion when Na balance and ECF volume is perturbed

A

. AVP
. Renal SNS
. RAAS
. ANP

30
Q

Renal sympathetic n. Activity when Na is perturbed

A

. Inc. renin release via beta-1 receptors
. Activates RAAS
. Directly inc. Na reabsorption in prox. Tubule
. Na reabsorptive effect is present at low levels at basal SNS activity
. Important during Na deprivation
. Overall effect is small in normal conditions

31
Q

AII major effects

A

. Inc. Na reabsorption directly via AT1 receptors (Na-H antiport insertion into apical membrane)
. Stimulates aldosterone synthesis and release from adrenal cortex
. Inc. filtration fraction (keeps GFR from going too low) by constricting efferent arteriole
. Systemic arteriolar vasoconstriction to raise bp
. Inc. H2O retention and intake (stimulates AVP release and thirst)
. Neg. feedback effect on renin release

32
Q

ADH release stimuli

A

. Osmolality: inc. AVP as plasma osmolality inc. (suppressed when dec.)
. AII releases
. Cardiac and arterial baroreceptors (dec. stretch)
. Mechanisms activated when ECF volume and/or BP dec.
. At any given plasma osmolality, volume contraction enhances AVP secretion
. Nausea, pain, morphine inc. AVP
. Surgery inc. AVP

33
Q

ANP

A

. Peptide released from heart
. Vasodilator
. Inc. Na excretion and H2O excretion
. BNP released from ventricular cells in response to inc. ventricular volume and has similar effects on kidney
. Stimulated release w/ hypertension and/or expanded ECF
. Important when it is severely expanded, not in daily Na balance

34
Q

ANP inc. Na excretion through ____

A

. Vasodilatory effects inc. GFR (inc. Na filtered load)
. Inhibition of renin and aldosterone secretion
. Reduction in tubular Na reabsorption in collecting duct system (direct effect and indirectly via reduction in aldosterone secretion

35
Q

Osmolality is maintained at the expense of ___

A

. ECF volume
. Dec. in total body Na content = eventual ECF contraction
. Gain in total body Na = eventual ECF expansion
. ECF will only return to normal or the starting level when excess Na is either lost from the body or regained via eating/drinking

36
Q

An acute change in H2O intake or output can cause an acute change in ___

A

Plasma osmolality

37
Q

How changes in total body Na are reflected in changes in ECF

A

. Changes in ECF alter blood volume and bp

. Hemodynamic alterations are detected by arterial baroreceptors, atrial stretch receptors, and the kidney

38
Q

Mechanisms for renal response to changes in ECF

A

. RAAS
. Renal SNS activity
. ANP
. AVP

39
Q

Main steps in renal response w/ high ECF volume

A

. Inc. GFR which inc. filtered load of Na and H2O
. Dec. Na reabsorption in prox. Tubule
. Dec. Na reabsorption in collecting duct (principal cell)
. Inc. H2O excretion

40
Q

Main steps in renal response w/ low ECF volume

A

. Dec. GFR which dec. filtered lad of Na and H2O
. Inc. Na reabsorption in prox. Tubule
. Inc. Na reabsorption in collecting duct
. Dec. H2O excretion

41
Q

Role of kidney in edema formation

A

. Inc. netfiltration pressure in systemic vasculature
. Inc. fluid movement from vascular space into interstitium
. Dec. effective circulating volum e
. Detected by arterial baroreceptors, renal baroreceptor, and/or cardiopulmonary volume receptors
. Inc. Na and H2O reabsorption by kidney’s
. Replenish effective circulating volume (goes back to inc. fluid movement from vascular space into interstitium)

42
Q

Pressure-natriuresis relationship

A

. Inc. in arterial pressure inc. Na excretion
. Dec. in arterial pressure dec. Na excretion
. Powerful controller of ECF volume and long term bp

43
Q

Effective pressure-natriuresis hormone systems

A

. AII amplifies the basic pressure-natriuresis relationship
. Suppression of AII synthesis in response to sustained inc. in arterial pressure allows enhanced excretion of Na and H2O
. Activation of AII synthesis in response to sustained dec. in arterial pressure allows enhanced reabsorption of Na and H2O
. Allows large daily swings in Na and H2O intake to be accommodated by only slight changes in ECF volume, BV, CO, and arterial pressure

44
Q

T/F change in MAP cannot be maintained long term

A

T, the renal reaction inc. Na and H2O excretion to bring MAP back to a more normal level

45
Q

How can equilibrium point for arterial pressure be shifted

A

. Chronic inc./dec. in Na intake
. Shifting curve along x-axis (parallel shift)
. Altering slope of curve

46
Q

Factors that shift the pressure-natriuresis relationship

A

. Loss of kidney mass from renal disease
. Dec. in glomerular capillary Kf due to glomerular injury
. Inc. in tubular reabsorption (excess aldosterone or AII)
. Inherited functional alterations in renal Na handling
. Subtle alterations in renal medullary blood flow
. Inc. in preglomerular (afferent) resistance (renal a. Stenosis, excessive vasoconstriction)

47
Q

Alterations in pressure-natriuresis that lead to chronic hypertension

A

. Chronic hypertension is compensatory response for impaired renal pressure-natriuresis
. Initiating event shifts curve towards higher MAP at same Na intake
. Dec. renal Na and H2O excretion (intake more than output)
. MAP inc.
. Reestablishment of Na and H2O balance at the new setpoint

48
Q

DSH diet effect on pressure-natriuresis slope

A

. DSH diet inc. slope

. Similar to what is seen in diuretics (natriuretic effect)

49
Q

Hyperaldosteronism

A

. Assoc. w/ hypertension, inc. ECF, but normal Na excretion (patients in Na balance)

50
Q

Why does hyperaldosteronism have normal Na excretion?

A

. Kidney “escapes” from chronic Na retaining effects of aldosterone after a few days
. This is primarily caused by inc. in arterial pressure
. Pressure-natriuresis mechanism limits the Na and fluid retaining effects of chronically elevated aldosterone

Physio (62 decks)

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