True volume depletion or hypovolemia generally refers to a combined salt and water loss exceeding intake, leading to ECF volume contraction. Many condition are associated with excessive urinary tract NaCl and water losses, including diuretics. Many tubular and interstitial renal disorders are associated with NA+ wasting.
History of recurrent vomiting, diarrhoea, polyuria, diaphoresis.
• Fatigue, weakness, muscle cramps, thirst and postural dizziness are some secondary to electrolytes imbalance.
• Severe degree leads to end-organ ischaemia manifest as oliguria, cyanosis, abdominal and chest pain
• Confusion and obtundation
• Diminished skin turgor and dry oral mucous membrane
A plasma Na+ concentration <135m mol/L usually reflects a hypotonic state. However , plasma osmolarity may be normal or increased in some cases of hyponatremia.
Isotonic or slightly hypotonic hyponatremia may complicate transurethral resection of prostate or bladder because large volumes of iso-osmotic or hypo-osmotic bladder irrigation solution can be absorbed or result in dilution hyponatremia. Hypotonic hyponatremia is usually due to hypoglycemia or occasionally intra-venous administration of mannitol. During poorly controlled Diabetic mellitus, glucose is an effective osmole and draws water from muscle cells resulting in hyponatremia.
COMMON SYMPTOMS :
Hyponatremia related to osmotic water shift leading to increased ICF vol.
• Brain cell swelling or oedema symptoms are primarily neurologic.
• Asymptomatic or complaint of nausea and malaise.
• Headache, lethargy, confusion and obtundation.
3. HYPERNATREMIA –
When plasma Na+ concentration >145m mol/L.
Majority of cases of hypernatremia result from loss of water. The two causes of hypernatremia are
• Increase water intake stimulated by thirst.
• Excretion of the minimum vol of maximally concentrated urine reflecting AVP section in response to osmotic stimulus.
The degree of hyperosmolarity is typically mild unless the thirst mechanism is abnormal or access water is limited later occurs in infants, physical handicapped and patient with impaired mental status ,in postoperative state.
COMMON SYMPTOMS :- Subarachnoid or intracerebral hemorrhage
• Neurologic or altered mental status
• Weakness, neuromuscular irritability
• Focal neurologic deficits, coma or seizures.
• Patient also complain of polyuria or thirst .
• Patient with polydipsia from CDI tend to prefer Ice- cold water.
• History of excessive sweating, diarrhoea or an osmotic diuresis
4.HYPOKALEMIA – When plasma K+ concentration <3.5m mol/L may result
from once (or more) of the following decreased net intake, shift into cells,
increased net loss. Diminished intake of is seldom the sole cause of K+
depletion. With the exception of urban poor and certain cultural groups, the
amount of K+ in the diet almost always exceeds that excreted in urine.
However dietry K+ restriction may exacerbate the hypokalemia secondary to
increased gastrointestinal or renal loss.
LIDDLE SYNDROME :- Rare familial disease characterized by hypertension,
hypokalemia, metabolic alkalosis, renal K+ wasting & suppressed rennin and
BARTTER’S SYNDROME:- Is a disorder characterized by hypokalemia,
metabolic alkalosis, hyperreninemic and juxtaglomerular apparatus hyperplasia.
COMMON SYMPTOMS:- Depends on individual patients and their severity depend on degree of hypokalemia
• Fatigue, Malaise, Myalgia and muscular weakness of lower extremities are common complaints.
• Severe form lead to weakness, hypoventilation(due to respiratory muscle involvement) and eventually complete paralysis.
• Smooth muscle function may also be affected and manifest as paralytic ileus.
• Severe hypokalemia increased risk of ventricular arrhythmias especially in patient with myocardial ischaemia or ventricular hypertrophy
• Glucose intolerance may also occur.
5. HYPERKALEMIA:- Defined as plasma K+ concentration >5.0m mol/L occurs as a result of either K+ release from cells or decreased renal loss. Increase K+ intake is rarely sole cause of hyperkalemia.
• Renal failure
• Decreased distal flow (i.e decreased effective circulating arterial volume)
• Decreased K+ secretion.
A. IMPAIRED Na+ REABSORPTION:
• Primary hypoaldosteronism – Adrenal insufficiency adrenal enzyme deficiency
• Secondary hypoaldosteronism – Hyporeninemia, drugs (NSAID’S, Heparin, Ace inhibitors)
• Resistance to aldosteron- Pseudohypoaldosteronism, Tubulointerstitial disease, drug (trimethoprin,pentamidines)
B.ENHANCED Cl- :
* Reabsorption ( chloride shunt)
* Gordon’s syndrome
COMMON SYMPTOMS:- Weakness due to prolonged depolarization.
• May also causes flaccid paralysis and hypoventilation if respiratory muscles involved.
• Metabolic acidosis occur’s due to impaired acid excretion
• Most serious effect of hyperkalemia is cardiac toxicity.
6. HYPERCALCEMIA:- Excess PTH productions, which is not appropriately suppressed by increased Serum Calcium Concentration and occur in primarily neoplastic disorders of Parathyroid Glands (Parathyroid adenomas, hyperplasia or rarely, Carcinoma) that are associated with increased parathyroid cell mass and impaired feedback inhibition by calcium.
Disorders that directly increase calcium mobilization from bone, such as hyperthyroidism or osteolytic metastasis also lead to hypercalcemia with suppressed PTH secretions, as does exogenous calcium overload as in milk-alkali syndrome,or total parenteral nutrition with excessive calcium supplementation.
COMMON SYMPTOMS:- Mild Calcemia (11-1105mg/dl) is usually asymptomatic.
• Some patients complaint of vague neuropsychiatric symptoms, including trouble concentrating, personality changes, or depression.
• Peptic Ulcer or nephrolithiasis and fracture risk maybe increased.
• More severe Hypercalcemia (>12-13mg/dl) develops acutely may results lethargy, stupor or coma as well as GIT symptoms (anorexia, coma, constipation or pancreatitis).
• Hypercalcemia decrease renal concentrating ability, which may cause polyuria and polydipsia.
• With long standing Hyperparathyroidism, patient may present with bone pain or pathologic fractures.
7. HYPOCALCEMIA:- Causes of Hypocalcemia can be differentiated according to whether Serum PTH levels are low (Hypothyroidism) or high (Secondary Hyperparathyroidism). Although there are many potential causes of Hypocalcemia, impaired PTH or VITAMIN D production are most common etiologies. Hypocalcemia may also occur in conclusion associated with severe tissue injury such as Burns, rhabdomyolysis, tumourlysis or pancreatitis. The cause of hypocalcemia in these settings may include a combination of low albumin, hyperphosphatemia, tissue deposition of calcium and impaired PTH secretion.
COMMON SYMPTOMS:- Mostly asymptomatic but, if decrease in Serum Clcium are relatively mild and chronic, there maybe life threatening complications.
• Moderrate to severe associated with paresthesias, usually of fingers, toes and circumoral regions and caused by neuro-muscular irritability.
• Severe hypocalcemia induce seizures, carpopedal spasm, brochospasm, laryngospasm and prolongation of QT-interval.