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65 Cards in this Set
- Front
- Back
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ineffective osmoles
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Urea
glucose in presence of insulin |
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most important effective osmole
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Na
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Effect that a fluid has on cell volume
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tonicity
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formula to estimate plasma osmolality
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(2 x [Na]) + glucose/18 + BUN/2.8
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formula to estimate plasma tonicity
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2 x [Na]
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what regulates plasma osmolality
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vasopressin release or inhibition by the supraoptic nucleus of the hypothalamus
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what regulates plasma volume
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RAAS activation via JG cells
Cardiac receptors release/inhibit Natriuretic peptides Carotid sinus and atrial baroreceptors regulate vasopressin release via paraventricular nuclei of the hypothalamus |
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what happens when both plasma volume and osmolality drop
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plasma volume regulation overrides the drop in plasma osmolality and ADH is secreted via the paraventricular nucleus
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what determines urine osmolality
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ADH secretion, no the amount of Na excretion
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in what situation will urine osmolality and specific gravity no be similar
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when radiocontrast dyes are excreted into the urine causing a much larger increase in specific gravity than osmolality
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what happens to urine osmolality and Na excretion when a hypertonic saline is added to the ECF
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increase urine Na excretion - inhibit RAAS
increase urine osmolality - activate ADH |
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what happens to urine osmoality and Na excretion when a hypotonic saline is added to the ECF
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decrease plasma osmolality -inhibit ADH release
increase urine Na excretion - inhibit RAAS |
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what happens to urine osmoality and Na excretion when a hypertonic fluid is removed from the ECF
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increase urine osmolality - increase ADH
decrease urine Na excretion -activate RAAS |
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what happens to urine osmoality and Na excretion when a hypotonic fluid is removed from the ECF
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increase urine osmolality - increase ADH
decrease urine Na excretion - activate RAAS |
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define true hyponatremia
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characterized by sodium concentration less than 136 resulting from either massive water intake or impaired renal water excretion
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what are two examples of hyponatremias that are not "truely hyponatremia" and why
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isotonic hyponatremia - actually a pseudohyponatremia because the elevated serum lipids or proteins reduce the amount of water in plasma resulting in decreased amount of Na, but plasma osmolality is normal
hypertonic hyponatremia - result from poorly diffusible solutes (mannitol or glucose) accumulate in plasma causing water to shift from ICF to ECF |
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calculate how much plasma Na concentration decreases for every 100 mg/dL increase in plasma glucose above 100 mg/dL
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decrease by ~2 mEq/L for each 100 mg/dL increase in plasma glucose
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Gives examples of hypovolemic states in which there is high Na excretion
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aldosterone deficiency
sprionolactone and thiazide diuretics cerebral salt wasting osmotic and loop diuretics chornic kidney failure |
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differentiate SIADH from compulsive water drinking
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SIADH - urine osmolality (>100) indicating ADH is being release
compulsive water drinking - urine osmolality (<100) indicating ADH is inhibited **both are euvolemic hyponatremias |
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describe CNS adaptation that occur in response to chronic hyper/hyponatremias
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chronic hypotonic hyponatremia - brain cell export solute (K) and amino acids into the ECF compartment
chronic hypernatremia - brain cells manufacture idiogenic osmoles (glutamine and myoinositol) to raise the ICF osmolality |
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Describe the most appropriate therapy to resolve each of the different types of hyponatremias:
hypovolemic, isovolemic, and hypervolemic |
hypovolemic - isotonic saline
isovolemic - water restriction hypervolemic - Na and water restriction |
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Describe the most appropriate therapy to resolve each of the different types of hypernatremias:
hypovolemic, isovolemic, and hypervolemic |
hypovolemic - hypotonic saline
isovolemic - water replacement hypervolemic - diruetics and water replacement |
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Plasma BUN/C, Urine osmolality, and urine Na excretion in hypovolemic hyponatremia secondary to aldosterone deficiency, spironolacton, or thiazide-type diuretics
why? |
BUN/C > 20:1
Urine [Na] > 20 Urine osmo > 400 **because hypovolemia activated RAAS but the kidney cannot reabsorb enough Na due to block |
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What does cerebral salt wasting lead to and why
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hypovolemic hyponatremia because there is increased BNP release from head trauma resulting in increased urine Na excretion (>40). However the urine osmo is dilute because the increased GFR does not allow medullary interstitium to because hypertonic and water does not leave the tubule
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normal body reaction expected with hypovolemic hyponatremic patient
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increased RAAS and vasopression leading to:
BUN/C > 20:1 Urine [Na] < 10 Urine osmo > 400 **seen with persistent vomiting, secretory diarrhea, or excessive sweating |
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Two causes of SIADH
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IL-6 released during inflammation
small cell carcinoma |
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lab finding in SIADH
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BUN/C < 10
Urine [Na] > 20 (because small increase in ECF inhibits RAAS and stimulates natriuretic peptide) Urine osmo > 100 (should be < 100 if ADH wasn't being secreted abberenatly) |
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most common causes of hyponatremia
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hypervolemic states:
heart failure, cirrhosis, nephrotic syndrome |
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differentiate lab findings in hypervolemic hyponatremia due to (HF, cirrhosis, nephrotic syndrome) vs. (ATN and CKD)
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HF, C, NS - BUN/C > 20:1, urine osmo > 400, and urine [Na] < 10 because reduction in effective volume stimulates RAAS and vasopressin
ATN and CKD - BUN/C < 15:1, urine [Na] > 20, and urine osmo ~ 300 because kidney is impaired - cannot reabsorb urea or Na |
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Don't allow the kidney to reabsorb sufficient Na and H20 leading to a hypovolemic hypernatremic state
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osmotic or loop diruetics, CKD
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differentiate BUN/C ratio in loop diuretics vs. osmotic diuretics/CKD hypovolemic hypernatremic states
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loop - BUN/C > 20:1
osmotic/CKD - BUN/C < 15:1 - because the kidney cannot reabsorb Na and urea |
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how would you know if excessive sweating or diarrhea would result in hyponatremia or hypernatremia, we know that both result in hypovolemia
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enough water intake would result in hyponatremia, while inadequate results in hypernatremia
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what is the only way in which a hypernatremic state occurs
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inadequate water intake
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Cause of isovolemic hypernatremia
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diabetes insipidus
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Causes of nephrogenic diabetes insipidus
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chronic hypokalemic, chronic hypercalcemia, lithium, demenclocycline
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Causes of isovolemic hyponatremia
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SIADH
glucocorticoid deficiency hypothyroidism carbamazepine chlorpropamide NSAIDs primary psychogenic polydypsia |
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Treatment of SIADH
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canivaptan
tolvaptan demenclocycline lithium |
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Differentiate administration of isotonic saline vs. primary hyperaldosteronism as causes of hypervolemic hypernatremias
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isotonic saline - BUN/C < 15:1, urine osmo > 600, and urine [Na] > 40 because increased osmolality stimulated vasopressin release
primary hyperaldosteronism - BUN/C < 15:1, urine osmo <100, and urine [Na] > 20 because intravascular expansion expansion inhibited vasopressin release |
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two prerequisites for edema formation
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alternation in capillary starling forces
renal sodium and water retention |
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is edema a disorder of water or sodium balance
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sodium
*hypo/hypernatremia is a disorder of water balance |
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cause of edema formation in myocardial systolic dysfunction
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RAAS activation and systemic venous hypertension contribute to increase in capillary hydrostatic pressure
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cause of edema formation in nephrotic syndrome when albumin concentration > 2g/dL
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reduced GFR results in decreased response to ANP and increased ENaC activity leading to increased capillary hydrostatic pressure
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cause of edema formation in nephrotic syndrome when albumin concentration < 2g/dL
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decreased oncotic pressure contributes
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cause of edema formation in cirrhosis
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increased capillary hydrostatic pressure (venous hypertension and vasodilation) along with decreased intravascular oncotic pressure
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cause of edema formation in chronic obstructive bronchitis
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accumulation of PaCO2 leading to vasodilation resulting in RAAS activation and increased capillary hydrostatic pressure
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cause of myxedema formation in patients with hypothyroidism
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decrease in osmotic reflection coefficient results in increased capillary permeability
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why is myxedema non-pitting
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sluggish lymph flow unable to clear mucopolysaccharide that accumulate in subcutaneous tissue
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cause of edema formation in at risk patients with NSAID therapy
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decreased GFR from decreased prostaglandin synthesis results in increased capillary hydrostatic pressure
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cause of edema formation in patients with idiopathic edema
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decease in osmotic reflection coefficient resulting in increased capillary permeability
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cause of dependent edema vs. generalized edema
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dependent - increased venous pressure (CHF)
generalized - hypoproteinemia |
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3 causes for pitting edema
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increased systemic venous pressure
increased capillary permeability hypoalbunemia |
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a decrease in effective volume initiates activation of RAAS resulting in increased Na and H20 reabsorption
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vascular underfill
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increased intravascular volume results in increased capillary hydrostatic pressure
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vascular overfill
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what causes systemic vasodilation is perceived by the kidneys as a fall in effective intravascular volume resulting in stimulation of RAAS
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chronic obstructive bronchitis
cirrhosis |
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40 second rule for causes of pitting edema if less than 3 months
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more than 40 seconds - systemic venous hypertension or decreased capillary integrity
less than 40 seconds - hypoalbunemia (nephrotic syndrome) |
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causes dilating of precapillary shpincters throughout the systemic circulation
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dihydropyridine calcium channel blockers
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drug that causes edema by enhancing renal Na reabsorption through aldosterone sensitive Na channels
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Thiazolidinediones
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how can estrogens result in edema
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increase capillary permeability and aldosterone secretion
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two strategies effective against edema
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spironolactone - diuretic of choice since if blocks secondary hyperaldosteronism
ACE inhibitors |
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why would some patients with cirrhosis and a GFR < 30mL/min have BUN and serum creatinine concentrations within the normal reference range
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becuase cirrhosis impairs BUN synthesis and creatinine production is reduced from muscle atrophy
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differentiate JVP in patients with edema due to CHF, Cirrhosis, and Nephrotic syndrome
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CHF - elevated JVP
Cirrhosis - normal or low JVP Nephrotic syndrome (albumin > 2) - elevated JVP Nephrotic syndrome (albumin < 2) - low-normal JVP |
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clinical manifestations of vasodilation in patients with cirrhosis
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spider angiomas
palmar erythema |
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4 changes in capillary starling forces
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1. increased capillary hydrostatic pressure
2. decreased capillary oncotic pressure 3. increased interstitial oncotic pressure 4. increased capillary permeability |
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causes of increased interstitial oncotic pressure
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local inflammation
decreased lymph flow -central venous pressure increased -myxedema |
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inhibits the natriuretic and diuretic effects of loop and thiazide diuretics
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NSAIDs
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