Download 5 Hypernatremia

Lecture 5
Definition
 Serum Na concentration above reference range.
 (135-145 mmol/L).
 Water loss
decreased intake or excessive loss
 Sodium gain
food, drinks etc.
Water loss
 Pure water loss
 Decreased intake (elderly, unconscious)
 Excessive loss (decreased AVP secretion lead to diabetes
insipidus, while nephrogenic if the renal tubule don’t
respond to AVP)
 Water and sodium loss
 Water loss exceeds sodium loss
 Osmotic diuresis (Diabetes mellitus, excessive sweating
or diarrhoea can sometime lead to hypernatremia but in
most cases lead to hyponatramia)
Sodium gain (salt poisoning)
 Sodium bicarbonate (for correction of acidosis)
 Acidosis is excessive blood acidity caused by an overabundance of acid in
the blood or a loss of bicarbonate from the blood (metabolic acidosis), or
by a buildup of carbon dioxide in the blood that results from poor lung
function or slow breathing (respiratory acidosis).
 Near drowning in salt water
 Infants fed on high salt diet (1 tbs of salt raises upto 70
mmol/L of sodium.
 Primary hyperaldosteronism or Con’s syndrome (excessive
aldorsteron secretion lead to Na retention in the renal
tubule)
 Cushing’s disease. (excess cortisol production which has weak
mineralocorticoid activity)
Mineralocorticoids are a class of corticosteroids, which are a class of
steroid hormones. Mineralocorticoids influence salt and water balances
(electrolyte balance and fluid balance). The primary mineralocorticoid is
aldosterone.
Aldosterone acts on the kidneys to provide active reabsorption of sodium
and an associated passive reabsorption of water, as well as the active
secretion of potassium in the collecting tubule.
Cushing disease is caused by a tumor or excess growth (hyperplasia) of the
pituitary gland.
Clinical Manifestations
 Confusion
 Neuromuscular excitability
 Hyperreflexia (difficulty in reading, understanding etc
 Seizures (epileptic fits)
 coma
Other osmolality diordres
 Increased urea in renal diseases
 Hyperglycemia
 Ethanol
 Osmolal gap
 Common cause is presence of ethanol
 Comatosed patients
Hyperkalemia
 Important IC electrolyte
 Maintain resting membrane potential of the cells like nerve and muscle cells.
 Resting membrane potential can be defined as a relatively stable, ground value of
transmembrane voltage in animal and plant cells.
 Or it can also be defined as
 the relatively static membrane potential of quiescent cells is called the resting
membrane potential (or resting voltage).
 Membrane potential (also transmembrane potential or membrane voltage)
is the difference in electric potential between the interior and the exterior of a
biological cell. With respect to the exterior of the cell, typical values of membrane
potential range from –40 mV to –80 mV.
 The resting membrane potential of a neuron is about -70 mV (mV=millivolt) this means that the inside of the neuron is 70 mV less than the outside. At rest,
there are relatively more sodium ions outside the neuron and more potassium ions
inside that neuron.
Heart arrythmias
Serum potassium concentration
3.5- 5.5 mmol/L
Daily intake is
30 -100 mmol/L
loss through GIT
5 mmol
Loss through kidneys
20-100 mmol/L
 ˃ 7 mmol/L is life threatening
 Cardiac arrest
 ECG changes
 Tented of T-waves and
Widening of the QRS complex
 Muscle weakness
 Paraesthesiae
ECG readings
Causes of hyperkalemia
 Increased intake
 Redistribution
 Decreased excretion
Increased intake
 Patients with impaired renal functions
 Drugs as potassium salts
 Intra venous (not more than 20 mmol/hr)
 Blood products should be fresh
old RBCs releases K+
Redistribution out of cell
 Metabolic acidosis
 There lies a reciprocal relationship between K+ and H+ level inside the cell. Due to
acidosis, K+ inside the cell are replaced by H+ and thus causing hyperkalemia in serum
 Potassium release from damaged cells
 (140 mmol/L is K+ conc. Insdie the cell, so a breakdown of the cell will lead to
hyperkalemia e.g. in rhobdomylosis (skeletal muscle breakdown), trauma, tumor lysis
etc.
 Insulin deficiency (insulin stimulates cellular uptake of potassium)
 So hyperkalemia is an associated feature in insulin deficient patients
 Hyperkalemic periodic paralysis
 Rare familial disorder autosomal dominance
 Recurrent attacks of muscle weakness or paralysis
 Rest after exercise
 Pseudohyperkalemis
Decreased excretion
 Glomerular filtration rate (GFR) is a test used to check how well the kidneys
are working. Specifically, it estimates how much blood passes through the
glomeruli each minute. Glomeruli are the tiny filters in the kidneys that filter
waste from the blood.
 Renal failure
 Potassium can not be excreted out when GFR is low
 Hypoaldosteronism
is seen mainly with the use of
 ACE inhibitors (ACE stands for angiotensin-converting enzyme) for
hypertension
 Potassium sparing diuretics (medicine) also antagonize effect of
aldosterone
Pseudohyperkalemia
 Sampling errors
 Hemolysis (rbc, wbc and platlets)
 Check potassium in serum and plasma
 Chilled samples
Treatment
 Insulin infused along with glucose to enhance
muscular K+ uptake
 Calcium gluconate/chloride be given to counteract the
hyperkalemia
 Cation exchage resins orally
 Dialysis in refractory hyperkalemia