Day 5/18/15 Flashcards
Hypovolemic Hyponatremia
- dec. total body Na and dec total body water also, but to a lesser extent bc of appropriate ADH release
- hemorrhage
- 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
- thirst
- neuromuscular irritability with twitches, seizures
- altered mental status
- failure to thrive in infants
- high mortality rate
Causes of Hypernatremia
- renal or extrarent losses that exceed Na loss (hypovolemic hypernatremia)
- addition of hypertonic fluid (hypervolemic hypernatremia), usually iatrogenic
- lack of ADH effect: diabetes insipidus
Diabetes Insipidus 2 Causes
- 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
- pregnancy
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
TGF
-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
- aldosteron
- catecholamines
- vasopressin
Dec. Na Reabsorption
- natriuretic peptides
- prostaglandins
- bradykinin
- dopamine
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
volume

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
Thiazides
- 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
