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Flashcards in Day 5/18/15 Deck (29):

Hypovolemic Hyponatremia

-dec. total body Na and dec total body water also, but to a lesser extent bc of appropriate ADH release
-plasma volume and EC fluid losses (GI loss, sweating)
-tx: restore plasma volume by giving normal saline


Hypervolemic Hyponatremia

-excess total body Na (edema) and even more excess total body water
-can be due to heart failure, liver cirrhosis, kidney disease
-effective blood volume is so low that ADH is stimulated and released
-thiazide diuretics impair dilution and are frequent cause
-edema, ascites, pleural effusions, weight gain
-tx: water restriction and loop diuretics and tx of underlying condition (note: do NOT give salt)


Euvolemic Hyponatremia

-syndrome of inappropraite ADH secretion (hypothyroidism, adrenal insufficiency, nausea, pain, psychosis, meds)
-will have urine that is not maximally diltute


Sx of Hyponatremia

-depend on speed of development (acute/chronic) and on severity
-anorexia, nausea, vomiting
-weakness, lethargy, confusion, seizures, death
-sx likely due to cerebral edema


Tx of Euvolemic Hyponatremia

-hypertonic saline for seizures
-water restriction and correction of underlying disorder
-ADH antagonists


Sxs of Hypernatremia

-neuromuscular irritability with twitches, seizures
-altered mental status
-failure to thrive in infants
-high mortality rate


Causes of Hypernatremia

1. renal or extrarent losses that exceed Na loss (hypovolemic hypernatremia)

2. addition of hypertonic fluid (hypervolemic hypernatremia), usually iatrogenic

3. lack of ADH effect: diabetes insipidus


Diabetes Insipidus 2 Causes

1. no ADH is secreted
2. kidneys do not respond to ADH


Acquired Nephrogenic Diabetes Insipidus Definition

-chronic kidney disease causes a concentrating defect due to tubular dysfunction as well as ADH resistance


Causes of Acquired Nephrogenic Diabetes Insipidus

-sickle cell anemia and polycystic kidney disease cause early concentrating defects by disrupting medulla
-urinary obstruction causes ADH resistance


Effective Arterial Blood Volume

-that amount of arterial blood volume required to adequately “fill” the capacity of arterial circulation


Components of the Homeostatic Response

Afferent Limb- volume receptors:
-low-pressure baroreceptors
-high-pressure baroreceptors
-intrarenal sensors
-hepatic and central nervous system sensors

Efferent Limb- effector elements:
-glomerular filtration
-physical factors at level of proximal tubule
-humoral effector mechanisms
-renal sympathetic nerves


Location of Low Pressure Baroreceptors

-venous side of circulation


Location of High Pressure Baroreceptors

-atrial side of circulation


Renal Autoregulation

-an ability of the kidney to keep renal blood flow and GFR constant by the contraction of the vascular smooth muscle



-phenomenon whereby increased distal delivery of sodium chloride to the macula densa increases afferent arteriolar tone and returns the RBF and GFR towards normal values


Glomerulo-tubular Balance

-property of the kidney whereby changes in GFR automatically induce a proportional change in the rate of proximal tubular sodium reabsorption


Humoral Effector Mechanisms
(Inc. and Dec. Na Reabsorption)

Inc. Na Reabsorption
-angiotensin II

Dec. Na Reabsorption
-natriuretic peptides


Function of Renal Sympathetic Nerves

} Sympathetic nervous system innervates the afferent and efferent arterioles of the glomerulus

} Activation of these nerves has an anti-natriuretic effect

} Nerve stimulation enhances the release of renin from the JGA


Na Reabsorption in Proximal Tubule

} The proximal tubule reabsorbs about 60% of the glomerular filtrate, including the sodium
} Sodium reabsorption occurs by both passive and active mechanisms
} Occurs down the electrochemical gradient of sodium
} Gradient is maintained by the action of the sodium pump
(Na/K/ATPase) at the basolateral membrane
} Active mechanism of sodium transport is through the Na/ H antiporter


Na Reabsorption in Loop of Henle

} About 30% of the filtered sodium is reabsorbed in TALH
} Impermeable to water but highly permeable to sodium
} Tubular fluid: dilute with a low NaCl concentration
} Reabsorption of sodium at the apical membrane occurs by Na/K/2Cl co-transporter, an active transport process


Serum Indices of Renal and Extrarenal Volume Contraction (Loss)

} Increased BUN: plasma creatinine ratio
} Metabolic alkalosis during upper GI loss of fluid
} Metabolic acidosis during lower GI loss of fluid
} Increased hematocrit and serum albumin because of hemoconcentration


Urinary Indices of Volume Contraction (dec.)

 Urinary sodium > 20 mEq/L=Renal losses
 Urinary sodium 1.010
 Urine osmolality > 300 mOsm/Kg


Tx of Fluid Contraction (Loss)

} Objective: is expansion of the ECF volume
} Replacement fluid should resemble the lost fluid
} Rate, amount, and route of replacement will depend on the situation
} Blood, albumin and dextran solutions contain large molecules preferentially expand the intravascular volume
} Isotonic normal saline (which is comprised of 0.9% NaCl or 154 mEq/L of NaCl) preferentially expands the ECF


Pathophysiology of Nephrotic Syndrome

} Loss of albumin in the urine and hypoalbuminemia
} Fall in the capillary oncotic pressure
} Flux of fluids from the vascular space into the interstitium and a fall in effective arterial blood volume



-work in distal tubule
(1) Inhibit the sodium/chloride transporter
(2) They increase calcium reabsorption and decrease urinary calcium excretion


Carbonic Anhydrase

-work in proximal tubule
(1) Should be used to mobilize edema
(2) Improve cardiac and respiratory function
(3) Excessive use: worsen kidney function
(4) Several classes of diuretics are available


K+ Sparing Diuretics

-works in distal tubule/collecting duct?
(1) Triamterene and amiloride are sodium channel blockers
(2) Sspironolactone is a competitive inhibitor of aldosterone


Loop Diuretics

-works in thick portion of asc. loop of henle?
(1) Inhibits the coupled entry of sodium, potassium, and chloride across the apical membrane in TALH (at the Na/2Cl/K co- transporter)
(2) Metabolic alkalosis, hypokalemia, hypocalcemia, and hypomagnesemia