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Flashcards in Day 5/18/15 Deck (29):
1

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

2

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)

3

Euvolemic Hyponatremia

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

4

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

5

Tx of Euvolemic Hyponatremia

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

6

Sxs of Hypernatremia

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

7

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

8

Diabetes Insipidus 2 Causes

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

9

Acquired Nephrogenic Diabetes Insipidus Definition

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

10

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

11

Effective Arterial Blood Volume

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

12

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

13

Location of Low Pressure Baroreceptors

-venous side of circulation

14

Location of High Pressure Baroreceptors

-atrial side of circulation

15

Renal Autoregulation

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

16

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

17

Glomerulo-tubular Balance

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

18

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

Inc. Na Reabsorption
-angiotensin II
-aldosteron
-catecholamines
-vasopressin

Dec. Na Reabsorption
-natriuretic peptides
-prostaglandins
-bradykinin
-dopamine

19

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

20

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

21

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

22

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

23

Urinary Indices of Volume Contraction (dec.)

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

24

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

25

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

26

Thiazides

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

27

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

28

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

29

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