NSE11 Lecture Notes - Lecture 6: Renal Function, Natriuretic Peptide, Adrenal Insufficiency
FLUID AND ELECTROLYTE BALANCE/IMBALANCE (Part 2)
Gould, Chapter 2, Kozier, Chapter 44
ELECTROLYTE IMBALANCES
Sodium Imbalance
Review of sodium
Definition -the primary cation (positively charged ion) in the ECF
-the primary regulator of the volume, osmolality and distribution
of ECF
Movement -sodium moves between the vascular and interstitial
compartments by diffusion
-sodium moves across the cell membrane controlled by the
sodium-potassium pump and active transport
-sodium levels are high in the extracellular fluid and low inside
the cell
Source -ingested in food and beverages
-500 mg per day is usually sufficient to meet the body’s needs
Excretion -sodium is primarily excreted by the kidneys
-a small amount is excreted through the skin and GI tract
Control of serum
sodium levels
-the kidney is the primary regulator of sodium balance in the
body
-the kidney excretes or conserves sodium in response to changes
in vascular volume
-if blood volume falls, the following mechanisms occur to
cause sodium and water retention:
-renin-angiotensin-aldosterone system
-release of ADH from the posterior pituitary
-if blood volume increases, sodium and water elimination by
the kidneys increases:
-glomerular filtration rate increases
-atrial natriuretic peptide (ANP) is released by the atria
and increase sodium excretion by the kidneys
-ADH release from the pituitary gland is inhibited
Functions -makes up 90% of the solute in the ECF and so maintains
extracellular fluid volume through its’ effect on osmotic
pressure
-essential in the conduction of nerve impulses
-essential in muscle contraction
Normal serum levels -135 - 145 mmol/L
-need to note the relative changes of electrolytes and fluids to put
the actual serum value in perspective, eg. excessive sweating
may result in a low sodium level if proportionately more sodium
is lost than water
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Hyponatremia (Figure 2-6 on page 23 in Gould)
Definition -a serum sodium concentration of < 135 mmol/L
Causes Net loss of sodium:
excessive sweating
vomiting
diarrhea
gastrointestinal suctioning
irrigation of GI tubes with water rather than with saline
repeated tap water enemas
use of diuretic drugs
adrenal insufficiency resulting in insufficient aldosterone
kidney disease
Net gain of water:
neurological disorders causing excess ADH secretion – explain why
hyponatremia would occur
systemic diseases such as heart failure, renal failure or cirrhosis of
the liver
excessive administration of hypotonic IV fluids
excessive water intake
Effects – signs
and symptoms
Review Table 2-5
on page 23 in
Gould
With hyponatremia, the ECF is _____________________ in relation to the
cells, therefore water will move from _________________ to
___________.
impaired nerve conduction and manifestations include:
fatigue
muscle cramps
abdominal discomfort
decreased osmotic pressure in the ECF, causing a fluid shift into
the cells; result is hypovolemia and decreased blood pressure
swelling of brain cells, causing confusion, headaches, seizures
Diagnostic Tests serum sodium levels < 135 mmol/L
24-hour urine specimen to evaluate sodium excretion
decreased in specific gravity of urine
2
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Document Summary
The primary cation (positively charged ion) in the ecf. The primary regulator of the volume, osmolality and distribution of ecf. Sodium moves between the vascular and interstitial compartments by diffusion. Sodium moves across the cell membrane controlled by the sodium-potassium pump and active transport. Sodium levels are high in the extracellular fluid and low inside the cell. 500 mg per day is usually sufficient to meet the body"s needs. A small amount is excreted through the skin and gi tract. The kidney is the primary regulator of sodium balance in the body. The kidney excretes or conserves sodium in response to changes in vascular volume. If blood volume falls, the following mechanisms occur to cause sodium and water retention: If blood volume increases, sodium and water elimination by the kidneys increases: Atrial natriuretic peptide (anp) is released by the atria and increase sodium excretion by the kidneys. Adh release from the pituitary gland is inhibited.
