+CILINCAL BIOCHEMISTRY

Fluid and electrolyte balane

 Measuring body electrolytes gives an indicator on patients info about his renal function and fluid
state( hypovolemia/ hypervolemia)
 Sodium measuring conc: ratio of solute to solvent (mmol/L), its high in 135-145.
 Water content (60%) is devided to : ICF=2/3 total / ECF: 1/3 total devided to plasma and interstitial fuid.
 Kidney concerve water: - entery : from water and food and metabolism output: skin,lungs,urine,feces.
Total = zero.
 Electrolytes determin the chemical and physical reactions of fluids: main cations and anaions:
- ECF: Na+ , Cl-, HCO3-
- In ICF: k+, P-, negative proteins(buffering system)

Sodium and potassium conc. Are opposite in conc.

 Sodium Na+: preserve homostatic mechanism to maintain water levels. Most of it is exchangeable, only
25% is in bones. Excess is lost by urine and sweat.
- Sodium balance: directly affect osmolality; 2*[Na+] = osmolality of ECF.
- Hormones that regulate sodium conc. : 1. Aldosterone 2. Atrial natriuretic peptide (ANP). Controlled by
hypothalamus, kidney and adrenal glands. (also argenin).

1. Aldosterone regulation of sodium: In adrenal cortex, stimulated by volume of ECF (increasing K+

and falling Na+ levels in blood) , it increase reabsorption of na which increases osmolality, increase and
excretion of k+ and hydrogen. Water follows na+. When ECF is low the juxtaglomerlular of nephrons senses
this.
- Angeotensin is converted to Ang. 2 by ACE which is a vasoconstrictor stimulating adrenal cortex to release
aldosterone. Increasing sodium reabsorption increases osmolality, leading fpr hypothalamus to release ANP
secretion or arginine vasopressin (AVP), these increases water reabsorption when osmolality is high [low
blood volume].
- Aldosterone determins rate of na+ reabsorption and k+ loss along distal convoluted tubule. High
aldosterone levels lead kidney to conserve salt. This is in case of low na conc.
Low volume blood-> renin release- >ang-1 -- ang 2-- affect both adrenal cortex and blood vessel
then --- aldosterone released

2. Atrial natriuretic peptide ANP: released by cardiac muscle cells of right atrium of heart in response to
high blood pressure. Involved in homostatic control of body water, sodium and fat.
- It reduces thirst, blocks release of adh and aldosterone, causes diuresis, lowers blood pressure and blood
volume. Blocks action of aldosterone.

 Body senses and regulates serum osmolality, serum Na is surrogate marker for serum osmolality.
 Osmoreceptors stimulated adh secretion is not triggered by hyperosmolality due to BUN and BS.
(ineffective osmole).
  Hypernatremia
- etiology :
1. Water loss for diabetes insipidus due to polyuria.
2. Water loss exceeds sodium loss for osmotic diuresis(diabetes mellitus) excessive sweat and diarrhea
in children.
3. Increase sodium reabsorption such as in Cushing syndrome( increase cortisol production) and Conns
syndrome ( increase aldosterone hormone, hyperaldosteronism)
- Symptoms: depends on rise of osmolality pressure, chronic hypernatremia.
Lethargy, weakness, irritability, seizures, coma, death.
- Treatment : its not fast, treatment should be given orally, if chronic it should be given 5% dextrose i.v.

 Hyponatremia: albumin improves blood fluidity, if there is no albumin blood wont penetrate. Serum
sodium con less than 3.5
- Etiology:
1.Water retention: result from impared water excretion.
- non-edematus hyponatremia: SAID(syndrome of inappropriate antidiuresis), infections, malignancy,
gi or lung trauma.

-Edematous hyponatremia: heart failure, hypoalbuminemia, nephrotic syndrome.

2. sodium loss more than water loss: adisons disease, Spironolactone that antagonize aldosterone.

 Potassium K+: (determine resting membrane) serum k levels 3.5-5.5, regulated by aldosterone.
Depending on GFR. Potassium levels might lead to cardiac arrestor and muscle cramps.
K+ uptake is stimulated by insulin.
When H+ serum conc. Are high, k+ displaces the H+ to facilitate its uptake.
Hyperkalemia cause muscle weakness and cardiac arrests while hypokalemia causes cardiac
arrhythmia.
If serum k+ >=6 –> worrisome. If >7 cause
cardiac arrest. hyperkalemia
- Pseudo hyperkalemia: hemolysed blood
Cell
samples not stored in good conditions. Decreased urinary shift(redistributi
Intake of k on out of cell
K + excretion
Drained renal - Metabolic
function patients 24 hr urine K < 40
mmol: acidosis:
may have severe accumulation of
hyperkalemia if Renal failure (low
GFR) inability of acids in blood
increased k intake
glomerular to -
Drugs that have high filtrate serum. Hyperglycemia=
k conc. (insulin
Addison’s disease
IV containing k+ (hyperaldosteremia deficiency)
blood infusion such ) - β-blockers
as in Hemorrhage Aldosterone - Cell lysis due
patients antagonists to trauma,
malignancy
- Signs and symptoms of hyperkalemia: 1. Muscle weakness 2. ECG change ( t waves peaked, st
short, qrs widen, p wave loss) 3. Cardiac arrest

- Treatment :

• Stabilize membrane excitability (if ECG changes)

give Calcium chloride or Gluconate, 1 g IV(it kalate k to reduce its activity)
• Increase K+ entry into cells (rapid but transient)
Glucose +Insulin
β2-adrenergic agonist (Albuterol)
NaHCO3 in non-dialysis patients
• Removal of excess K+ (slow but definitive)
Cation exchange resin (Resonium A)
diuretics
Dialysis
• Dietary K+ restriction (chronically helpful)

- Factors effecting Hypokalemia balance:

1. Reduced intake : - GI loss - Severe Vomiting - Diarrhea - Low calory diet
2. Urinary K+ wasting 24 h urine K+ > 25 mmol
a) Thiazide diuretics
b) Corticosteroids
c) Carbenoxolone
d) Conn’s Syndrome: increased aldosterone
3. Cell shift(redistribution into the cell)
- Metabolic Alkalosis: low h+ outside so k+ remain inside cells
- Insulin excess: refeeding syndrome
Anorexia, cancer, prisoners etc..
- β-agonist( adrogenic agonist)
- Treatment of anemia
Sings and Symptoms of Hypokalemia
 • Muscle weakness
• Polyuria/Polydipsia (acquired nephrogenic DI)
• ECG changes:
– Depressed ST segment
– Flat T wave
– Prolonged QT interval
– U waves
• Cardiac arrhythmia
Treatment of Hypokalemia
• Oral KCl supplements
• IV KCl (no more than 10 mmol/hr through peripheral line, 40 mEq/hr through central line)
• Amiloride (K+ sparing diuretics) or spironolactone may be useful in patients with
hyperaldosteronism