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1. UNIVERSIDAD TECNICA DE MACHALA
ACADEMIC UNIT OF CHEMICAL
SCIENCES AND HEALTH
MEDICINE SCHOOL
ENGLISH
ALTERATIONS
HIDROSALINE
METABOLISM
STUDENTS
William Cruz
Kevin Herrera
TEACHER:
Mgs. Barreto Huilcapi Lina Maribel
CLASS:
EIGHTH SEMESTER ‘’A’’
Machala, El Oro
2018

2. ALTERATIONS HIDROSALINE METABOLISM
The electrolytic alterations include, therefore, alterations in the osmoregulation and in
the distribution of body fluids
Characteristics and composition of body compartments.- Body water: In the
healthy adult, body water represents approximately 60% of its weight. And it is
distributed in the intracellular space (40% of the weight) and the rest (20%), in the
extracellular space; in which it is divided between the intravascular space (5%) and
the interstitial space (15%). Displacement of water between the intracellular and
extracellular spaces: Determined by the concentration difference of osmotically active
solutes on each side of the cell membranes. Plasma osmolality can be calculated
through the molar concentrations of the three major solutes, sodium, glucose and
urea, by the formula:
Also in the absence of hyperglycemia or renal failure, the osmolality of the
extracellular fluid can be estimated as twice the plasma concentration of sodium.
Hydrosaline balance and renal regulation.- Any solute added to the organism is
balanced by renal excretion or by endogenous use of a similar amount. The water
balance is adjusted very precisely by the variations in intake, controlled by the
mechanisms of thirst, and also by renal excretion. Regulation of the water balance.-
basically depends on the glomerular filtration (GFR), proximal tubular resorption,
active reabsorption of sodium and chlorine in the ascending branch of the loop of
Henle and the reabsorption of water in the collecting tubule under the influence of the
ADH. Regulation of natremia.- The renal excretion of sodium begins with the
filtration of 180 L / day of plasma water containing 25,000 mEq (mmol) of sodium
(FG × plasma sodium = 180 × 140). The tubules reabsorb almost all the filtered

3. sodium, to leave only 100-200 mEq (mmol) for its excretion under normal conditions
(less than 1% of the filtered sodium).
ALTERATIONS OF WATER METABOLISM (VARIATIONS IN VOLUME)
Reduction of extracellular
volume.- The intracellular
water deficit as a
consequence of a water
metabolism disorder and a
state of hypertonicity that
generates hypernatremia
itself. By contrast,
extracellular volume
depletion defines the loss of
total body sodium and a
reduction in intravascular
volume, and is caused by a
loss of blood or a reduction in the body's sodium content. Clinical picture: Initially
there is weakness, fatigue, thirst and, depending on the severity of the hypovolemia,
headaches, nausea, cramps, hypotension and postural dizziness. When the depletion
of extracellular volume is 10% -15%, renal hypoperfusion with oliguria and retention
of sodium and water appear. If the volume loss is greater than 25%, the onset of
hypovolemic shock is common. Diagnosis: If there are no blood losses, then the
urinary sodium will be determined, which will allow to distinguish if the origin of the
losses of sodium and water is renal (sodium higher than 20 mEq / L [mmol / L]) or
extrarenal (lower sodium) at 10-20 mEq / L [mmol / L]). The presence of metabolic
acidosis will suggest that the origin of hypovolemia is related to intestinal losses
(diarrhea), diabetic ketoacidosis, salt-losing nephropathies or hypoaldosteronism

4. states. Conversely, a metabolic alkalosis will lead to high digestive losses (vomiting
or nasogastric aspiration) or to the use of diuretics. Treatment: For the correction of
volemia disorders, isotonic solutions of crystalloids (0.9% saline or lactated Ringer's
solutions) and hypotonic solutions (glucose serum or glucosaline serum) are
available.
Increase in extracellular volume (Edema).- Consists of an excessive accumulation
of water in the interstitial space, and is basically due to an increase in hydrostatic
pressure or a decrease in the oncotic pressure of the capillary, to an increase in
capillary permeability or a lymphatic obstruction. Clinical Table.- In the states of
hypoproteinemia and renal failure, the distribution of edema tends to be more diffuse,
in the form of anasarca, while in heart failure interstitial fluid accumulates in
declining areas. In cases in which there is circulatory overload, this manifests itself in
the form of hypertension, increased cardiac preload, and pulmonary edema due to
increased cardiac filling pressures. Treatment.- The fundamental principles in the
treatment of generalized edema are: rest, restriction of sodium and water intake, and
the use of diuretics.
ALTERATIONS OF SODIUM METABOLISM.
Hyponatremia. - Plasma sodium concentration lower than 135 mEq / L (mmol / L).
Clinical Table.- Below 120 mEq / L or mmol / L, the manifestations are expressed as
cerebral edema (headache, nausea, lethargy, convulsions, coma), occasionally
patients may present pulmonary edema without cardiogenic. Treatment: symptomatic
acute hyponatremia: Plasma osmolarity should be rapidly increased with perfusion of
3% hypertonic saline ([Na] = 513 mEq / L). It is recommended to increase plasma
sodium by 4-6 mEq / L in about 6 h, with boluses of 100 mL, each one increases 2

5. mEq of plasma sodium. Chronic hyponatremia: Hyponatremia with decreased
extracellular volume is treated by administration of isotonic saline solutions (0.9%).
The required amount of milliequivalents of sodium is calculated according to the
following formula.
Hypernatremia.- Hypernatremia is considered to be a plasma sodium concentration
higher than 145 mEq / L. Its basic mechanism of production lies in the limitation in
urinary concentration capacity. Clinical picture: Neurological symptoms are
especially evident from natremias above 160 mEq / L (mmol / L). In the beginning
they can be manifested only by irritability and muscular hypertonicity, later sensory
alterations appear with seizures, coma and death.
BIBLIOGRAPHICAL REFERENCE
A. Martínez Vea, 2016 "alterations in hydrosaline metabolism", Valenti Farreras and
C Rozman. Internal Medicine Farreras / Rozman. Barcelona: Elsevier, 2016.