1. Disorders of electrolytes and water and acid – base balance
- Hyper and Hyponatremia
- Hyper and Hypokalemia
- Syndrome of inappropriate secretion of
ADH
- Diabetes insipidus
Asst. Prof. Dr. Dalya Basil

2. Disorder of Electrolytes
Electrolytes are substances that dissociate in solution to form charged particles .
An electrolyte disorder is an imbalance of certain ionized salts (i.e., bicarbonate, calcium, chloride, magnesium, phosphate, potassium, and sodium) in the blood.
Electrolytes facilitate the passage of fluid between and within cells through a process known as osmosis and play a part in regulating the function of the neuromuscular, endocrine, and excretory systems.

3. Disorder of Electrolytes
Disorders of sodium concentration produce a change in the osmolality of the ECF with movement of water from the ECF compartment into the ICF compartment (hyponatremia) or from the ICF compartment into the ECF fluid compartment (hypernatremia).

4. Hypernatremia
Hypernatremia is an electrolytes imbalance and is indicates a serum sodium level above 145 mmol/L and a serum osmolality greater than 295 mOsm/kg.
The normal adult value for sodium is mmol/L.
Hypernatremia is a state of hyperosmolality, because sodium is the dominant extracellular cation and solute.

5. Causes of hypernatremia

6. Types of hypernatremia
1. hypovolemic hypernatremia = greater decrease total body water and a decrease total body sodium, caused by vomiting, diarrhea, excessive sweating, diuretics, acute renal failure or chronic renal failure.
2. euvolemic hypernatremia = decrease total body water, caused by prolonged rapid breathing, hyperventilation, high fever, diabetes insipidus, poor water intake.

7. Types of hypernatremia
3. hypervolemic hypernatremia = increase in total body sodium and lesser increase in total body water, caused by ingestion of large quantities of sodium, low potassium, high calcium, and some cases such as alcoholism.

8. Clinical manifestations
Extracellular fluid loss and cellular dehydration.
Body weight loss with proportion to the amount of water that has been lost.
Because blood plasma is roughly 90%-93% water, the concentration of blood cells increase as extracellular water decreases.
Thirst occurring when water losses are equal to 0.5% of body water.
Body temperature is elevated, and the skin becomes flushed.
The vascular volume decreases, the pulse becomes rapid and thready.

9. Clinical manifestations
The mouth becomes dry, the tongue becomes rough and fissured, and the swallowing becomes difficult.
Increase in serum osmolality leadings to water being pulled out of body cells, so the skin and mucous membrane become dry, and salivation and lacrimation are decreased.
And most significantly, water is pulled out of the cell in the CNS, causing decreased reflexes, agitation, headache, coma and seizures may develop as hypernatremia progresses.

10. Hyponatremia

11. Hyponatremia
Hyponatremia is defined as a serum sodium concentration of less than 135 mmol/L.
Low blood sodium occurs when water and sodium are out of balance: there is either too much water or not enough sodium.

12. Hyponatremia

13. Types of hyponatremia
In hyponatremia, the imbalance of water to salt is caused by one of three conditions:
Euvolemic hyponatremia -- total body water increases, but the body's sodium content stays the same. E.g., syndrome of inappropriate antidiuretic hormone secretion (SIADH) is characterized by excessive release of ADH. The increase in blood volume (hypervolemia) often results in dilutional hyponatremia in which the plasma sodium levels are lowered and total body fluid is increased.

14. Types of hyponatremia
Hypervolemic hyponatremia -- both sodium and water content in the body increase, but the water gain is greater. E.g., congestive heart failure and massive edema for any cause.
Hypovolemic hyponatremia -- water and sodium are both lost from the body, but the sodium loss is greater, in such as prolonged vomiting, decreased oral intake, severe diarrhea.

15. Causes of hyponatremia

16. Clinical manifestations
The manifestations of hyponatremia depend on the rapidity of onset and the severity of the sodium dilution.
The signs and symptoms may be acute (onset within 48 hrs) or more insidious in onset and less sever, as in chronic hyponatremia.

17. Clinical manifestations
Muscle cramps,weakness reflect the effect of hyponatremia on skeletal muscle function.
Brain and nervous system cells affected by increases in intracellular water, with symptoms of headache and lethargy.
Seizures occurs when serum sodium level reach extremely low level.

18. Hyperkalemia

19. Hyperkalemia
Hyperkalemia refers to an increase in serum levels of potassium in excess of 5.0 mmol/L.
Normal serum potassium levels are between mmol/L.
It rarely occurs in healthy persons because the body is extremely effective in preventing excess potassium accumulation in the extracellular fluid.

20. Hyperkalemia

21. Pseudohyperkalemia
A pseudohyperkalemia can occur secondary to release of potassium from intracellular stores after traumatic venipuncture, or prolonged application of a tourniquet during venipuncture.

22. Causes of Hyperkalemia
The three major causes of potassium excess are:
1- Decreased renal elimination, which is the most common cause of hyperkalemia:
A decrease in aldosterone-mediated potassium elimination can result from adrenal insufficiency, depression of aldosterone release due to a decerease in rennin or angiotensin II, or impaired ability of the kidney to respond to aldosterone.

23. Causes of Hyperkalemia
Potassium sparing diuretics can produce hyperkalemia.
Some antihypertensive drugs, the angiotensin converting enzymes inhibitors and angiotensin II receptor blockers can also produce an increase in serum potassium level because of their ability to decrease aldosterone levels.

24. Causes of Hyperkalemia
2- Movement of potassium from the intracellular fluids (ICF) to the extracellular fluids (ECF) compartment:
Acidosis tends to increase serum potassium by causing potassium to move from ICF to ECF (increase H+ concentration decreases the activity of Na+/K+ - ATPase pump).
Also tissue injury causes release of intracellular K+ for example, burns and crushing injuries that cause cell death.
Transient hyperkalemia may be induced during extreme exercise or seizures when muscle cells are permeable to K+.

25. Causes of Hyperkalemia
3- excessively rapid rate of administration:
Excess K+ can result from excessive oral ingestion or intravenous administration of K+.
The intravenous K+ solution can be fatal when infused too rapidly.

26. Clinical manifestations
Weakness, which can progress to flaccid paralysis and hypoventilation.
Secondary to prolonged partial depolarization from the elevated K+ , which impairs membrane excitability.
Metabolic acidosis, which further increases K+.
Secondary to hyperkalemia impairing renal ammoniagenesis and absorption, and thus net acid excretion.
Altered electrical activity of heart, cardiac arrhythmias.

27. Clinical manifestations
Gastrointestinal manifestations
Anorexia, nausea, vomiting, intestinal cramps, diarrhea.
Cardiovascular manifestations
Ventricular fibrillation and cardiac arrest.
Neuromuscular manifestations
Weakness
Muscle cramps.

28. Hypokalemia

29. Hypokalemia: It refers to a decrease in serum potassium levels below 3
Hypokalemia: It refers to a decrease in serum potassium levels below 3.5 mmol/L.

30. Causes of Hypokalemia
1- Inadequate intake: Is a frequent cause of hypokalemia. Insufficient dietary intake (typically <40 mmol/day) may result from the inability to obtain or ingest food or from a diet that is low in potassium containing foods. The kidneys lack the homeostatic mechanisms needed to conserve K+ during periods of insufficient intake. 2- Excessive loss of potassium: Approximately 80%-90% of K+ losses occur in the urine.

31. Causes of Hypokalemia
3- Redistribution between the ICF and ECF compartments:
Hypokalemia can also be caused by transcellular shifts in K+. Because of large difference between extracellular and intracellular potassium levels, a redistribution of K+ from the ECF to the ICF can produce marked decrease in the serum K+.
A wide varieties of β₂- adrenergic agonist drugs (e.g., decongestants and bronchodilators) shift K+ into cells and cause transient hypokalemia.

32. Clinical Manifestations
Neuromuscular manifestations
Muscle flabbiness, weakness and fatigue
Muscle cramps and tenderness
Paresthesia and paralysis.
Impaired kidney’s ability to concentrate the urine
polyuria, urine with low osmolality, polydipsia (ECF osmolality↑).

33. Clinical Manifestations
Gastrointestinal manifestations
Anorexia, nausea, vomiting,
Constipation, abdominal distension, paralytic ileus.
Cardiovascular manifestations
Arrhythmias.
Metabolic alkalosis

34. Diabetes Insipidus

35. Diabetes Insipidus
Diabetes insipidus is caused by abnormality in the functioning or levels of antidiuretic hormone (ADH), also known of as vasopressin. Manufactured in the hypothalamus and stored in the pituitary gland, ADH helps to regulate the amount of fluid in the body.
Diabetes insipidus characterized by polyuria and excessive thrist.

36. Types of Diabetes Insipidus
There are two forms of diabetes insipidus:
Central (cranial) diabetes insipidus, in which the production or release of ADH is too low to stop the kidneys from passing dilute urine, which results in an increased loss of water and therefore more thirst.

37. Types of Diabetes Insipidus
Nephrogenic insipidus:
People with nephrogenic diabetes insipidus, however, have adequate amounts of ADH in the body but the kidneys fail to respond it, and again the urine is still not concentrated.

38. Causes of diabetes insipidus
Some of the causes of cranial diabetes insipidus include:
Genetic inheritance of a mutation in the vasopressin gene, AVP-NPII.
Brain tumors such as pituitary adenoma and craniopharyngiomas.
Head injury causing damage to the pituitary gland or hypothalamus. Injury may also result after brain surgery.

39. Causes of diabetes insipidus
Meningitis and encephalitis or brain infections may also affect the pituitary gland and the hypothalamus.
Blood vessel complications such as those during pregnancy where the blood supply to the hypothalamus and pituitary gland may be compromised.
Stroke or sudden loss of oxygen to the brain (e.g. during anesthesia) may also result in diabetes insipidus.

40. Causes of diabetes insipidus
Causes of nephrogenic diabetes insipidus
Familial or genetic causes resulting from mutation in the AQP2 gene that codes for the aquaporin-2 protein.
Metabolic causes such as high blood sugar, high blood calcium and low potassium.
Diseases such as amyloidosis, obstructive uropathy, chronic kidney disease and polycystic kidney disease.

41. Clinical manifestation of diabetes insipidus
There are two main symptoms of diabetes insipidus:
Excessive thirst or polydipsia. The throat may feel parched, a sensation that may persist despite drinking water repeatedly.
Frequent passing of large amounts of urine or polyuria. The urine is usually pale, and passed in large volumes of up to 20 litres every 15 to 20 minutes.

42. Syndrome of Inappropriate Antidiuretic Hormone

43. Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
The syndrome of Inappropriate Antidiuretic Hormone (SIADH) results from a failure of the negative feedback system that regulates the release and inhibition of ADH. It is characterized by excessive release of ADH from the posterior pituitary gland.
In persons with this syndrome, ADH secretion continuous even when serum osmolality is decreased.

44. Causes of SIADH
Causes of SIADH include conditions that dysregulate ADH secretion in the central nervous system, tumors that secrete ADH, drugs that either increase ADH secretion, and many others, lung tumors, chest lesions, and CNS disorders.

45. Clinical manifestation of SIADH
Urine output decreases
coma from cerebral edema
Generalized muscle weakness
Lethargy
Confusion
Seizures