ST - Water

Disorders of Water metabolism
1. PATHOLOGY_Theory_Medical_Student_s_Libra.pdf - UNIT 16 pp.

154 161
2. Gyton - Physiology water metabolism
3. Robbins (Cumar, Cotran, Robbins) 5th edition - Pathophysiologic basis of
disease - Schemes of edema formation from chapter Heart failure - 541
-569
4. McCance, K.L., & Huether, S.E. - Pathophysiology: The biologic basis for
disease in adults and children. (St. Louis:, Mosby, Inc.). - Heart failure -
1032 1048
5. Goljan
Water Disorders
Fluid movement across a capillary/venule wall into the interstitial space is driven by
Starling pressures
ECF, extracellular fluid; ICF, intracellular fluid; POsm, plasma osmolality; TB,
total body; W, water.
Disordered water metabolism dyshydria:
- hypohydration (water loss) and
- hyperhydration (hyperhydria), i. e. edema.
On the basis of osmolality of extracellular fluid dyshydria are:

1. hypoosmolalic (with plasma osmolality under 280 mosm/kg H2O);
2. hyperosmolalic (with plasma osmolality above 300 mosm/kg H2O);
3. isoosmolalic.
Hypohydration - is the negative fluid balance

Hyperhydration - is the positive fluid balance
In hypoosmolalic hypo-hydration predominates the salt loss compared to

water losses.
In hyperosmolalic hypo-hydration predominats the water loss compared to
salt losses.
Isoosmolalic hypohydration involves an approximately equivalent reduction of
water and salt concentration in the organism.
Hypoosmolalic hyperhydration is characterized by excess extracellular fluid of
low osmolality.
Hyperosmolalic hyperhydration is characterized by increased osmolality of
extracellular fluid.
Isoosmolalic hyperhydration is characterized by the increased volume of
extracellular fluid of normal osmolality.
THE MECHANISMS OF COMPENSATION at HYP0-HYDRATION

Inhibition of diuresis (increase in aldosterone secretion, Na reabsorption,
vasopressin (ADH) synthesis and secretion).
THE MECHANISMS OF COMPENSATION at HYPER-HYDRATION

Stimulation of diuresis (decrease in vasopressin , ADH synthesis and secretion).
Hypo-hydration - negative fluid balance: predominates water loss

than intake.
Causes:
- insufficient water supply or its increased loss.
- mental disorders or traumas, reducing or eliminating the feeling of thirst.
- somatic diseases, resisting food and liquid intake (impaired swallowing,
esophageal occlusion etc.).
- continuous polyuria (renal failure, diabetes mellitus, administration of
improper doses of diuretics).
- gastrointestinal disorders (continuous profuse salivary discharge, recurrent
vomiting, chronic diarrhea).
- pathological processes, causing the heavy loss of lymph, severe blood loss.
- prolonged or profuse sweating.
- hyperthermic states of the organism - fever ( increase in body temperature
by 1 C results in 400-500 ml of liquid loss daily through sweating).
Hypo-osmolalic Hypo-hydration
Causes:
- Hypoaldesteronism (associated with decreased reabsorption of Na + ions in the
kidneys, decreased osmolality of blood plasma and water reabsorption).
- Continuous profuse sweating involving the discharge of a great amount of salts.
- Severe vomiting (causing Na+, K+ and Cl +
losses).
- Diabetes mellitus or diabetes insipidus (ADH deficiency) combined with the
excretion of K+ salts, Na+ glucose, albumins.
- Diarrhea (cholera or malabsorption syndrome) associated with the loss of
+ + 2+
intestinal juice containing K , Na , Ca .
- Improper dialysis (hemodialysis or peritoneal dialysis with low osmolality of
dialyzing solution).
Consequences and manifestations.

- Mucous and cutaneous dryness
- Decreased salivary secretion (hyposalivation)
- Decreased elasticity and tension (turgor) of skin, muscles
- Softening of eyeballs
- Reduced amount of daily excreted urine.
All these manifestations result from the organisms
hypohydration/dehydration, the reduced volume of intercellular fluid and the
volume of circulating blood, decreased perfusion and hemodymanic pressure in
arterioles and precapillaries.
It should be noted that patients with hypoosmolalic hypohydration do not
feel thirst due to low blood plasma osmolality and cell hyperhydration.
Hyper-osmolalic Hypo-hydration
Causes:
Insufficient water intake (in case of so called dry starvation when a person
refuses to drink water; when there is lack of drinking water supply in time of
hostilities, emergency situations etc.).
Hyperthermic states (fever), associated with heavy prolonged sweating.
Polyuria (at diabetes insipidus, diabetes mellitus due to osmotic polyuria in
combination with high hyperglycemia).
Prolonged artificial lung ventilation (ALV).
Drinking sea water in the conditions of the organisms hypohydration.
Parenteral Infusion of Solutions of Increased Osmolality
Results in (at failure of compensatory reactions attempting to increase secretion

of aldosteron and vasopressin ):
- Unbearable suffering from thirsty
- Hypovolemia
- Decreased stroke volume
- Increased blood viscosity
- Impaired microhemocirculation
- Generalized hypoxia
- Brain hypoxia accompanied by acidosis leading to convulsions, hallucinations
and coma
- Azotemia due to decreased glomerular filtration and increased reabsorption
of urea due to disorders of tubular epithelium.
Iso-osmolalic hypo-hydration
Causes:
- Immediately after acute blood loss (i.e. before the compensatory mechanisms
are brought into action)
- Profuse recurrent vomiting
- Profuse diarrhea
- Extensive burns
- Polyuria due to high doses of diuretics
Consequences and manifestations of iso-osmolalic hypo-hydration are

conditioned by the reduced volume of extracellular fluid:
- Hypovolemia
- Increased blood viscosity
- Disorders of general and microhemocirculation
- Alteration of pH balance
- Hypoxia (especially after severe blood loss)
Hyperhydration - positive fluid balance: predominates water intake than

water excretion and losses
Hypo-osmolalic Hyper-hydration
Causes:
- Intake of water with low salt content
- Intake of great amount of water water poisoning at psychotic
disturbances, etc.
- ADH hyper-production
- Renal failure (with considerable excretory hypofunction)
Results in:
- Hypervolemia (oligocytemic)
- Hemodilution
- Poliuria
- Hemolysis
- Nausea and Vomiting
- Release of ions and substances from damaged cells (due to cell swelling)
leading to psychoneurotic disorders (fatigue, apathy, convulsions,
unconsciousness).
Hyper-osmolalic Hyper-hydration
Causes:
- Forced intake of sea water
- Infusion of the solutions with increased concentration of salts
- Hyperaldosteronism causing excessive reabsorption of Na+
- Renal failure associated with decreased salt excretion (at renal tubulo-
and/or enzymopathies).
Results in:
- Hypervolemia
- Increased stroke volume
- Increased arterial and venous pressure
- Hypoxia (due to heart failure)
- Neuro-psychotic disturbances
- Thirsty
- Sometimes brain or pulmonary edema may develop (due to intracellular
hyperhydration as well as the increased volume of intercellular fluid (edema)
due to cardiac insufficiency).
Iso-osmolalic Hyper-hydration
Causes:
- Infusion of a great amount of isotonic solutions (sodium chloride,
potassium chloride, sodium hydrocarbonate).
- Heart failure, Insufficient hemocirculation (leading to increased volume of
extracellular fluid due to increased filtration pressure and decreased
efficiency of liquid reabsorption).
Consequences and manifestations:

Increased blood volume (oligocytemic hypervolemia)
Increased arterial blood pressure (due to hypervolemia, increased cardiac
output and peripheral vascular resistance)
Cardiac insufficiency/Heart failure development especially in prolonged
hypervolemia
Edema
Edema
Presence of increased fluid in the interstitial space of the ECF compartment
Pathophysiology of edema
1. Alteration in Starling pressure
a. Produces a transudate
b. Increased vascular hydrostatic pressure:
i. Pulmonary edema in left-sided heart failure
ii. Peripheral pitting edema in right-sided heart failure
iii. Portal hypertension in cirrhosis producing ascites
c. Decreased vascular plasma oncotic pressure (hypoalbuminemia):
i. Malnutrition with decreased protein intake
ii. Cirrhosis with decreased synthesis of albumin
iii. Nephrotic syndrome with increased loss of protein in urine (>
3.5 g/24 hours)
iv. Malabsorption with decreased reabsorption of protein
d. Renal retention of sodium and water
i. Increases hydrostatic pressure (increased plasma volume)
ii. Decreases oncotic pressure (dilutional effect on albumin)
iii. Examples-acute renal failure, glomerulonephritis
2. Increased vascular permeability
a. Produces an exudate
b. Example-acute inflammation (e.g., tissue swelling following a bee
sting)
3. Lymphatic obstruction
a. Produces lymphedema
b. Examples
i. Lymphedema following modified radical mastectomy and
radiation
ii. Scrotal and vulvar lymphedema due to lymphogranuloma
venereum
iii. Breast lymphedema due to blockage of subcutaneous
lymphatics by malignant cells
Diseases leading to edema formation:

Heart failure
Renal edema
- Acute glomerulonephritis
- Nephrotic syndrome
Malnutrition
Inflammatory and Allergic edema
Pulmonary edema
Brain hypoxia

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Disorders of Water metabolism

1. PATHOLOGY_Theory_Medical_Student_s_Libra.pdf - UNIT 16 pp.

On the basis of osmolality of extracellular fluid dyshydria are:

Hypohydration - is the negative fluid balance

In hypoosmolalic hypo-hydration predominates the salt loss compared to

THE MECHANISMS OF COMPENSATION at HYP0-HYDRATION

THE MECHANISMS OF COMPENSATION at HYPER-HYDRATION

Hypo-hydration - negative fluid balance: predominates water loss

Consequences and manifestations.

Results in (at failure of compensatory reactions attempting to increase secretion

Consequences and manifestations of iso-osmolalic hypo-hydration are

Hyperhydration - positive fluid balance: predominates water intake than

Consequences and manifestations:

Diseases leading to edema formation:

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