STUDY - Technical - New Dacian's Medicine
Fluid
and Electrolyte Imbalances (2)
Translation Draft
I "broke" the post about incontinence (much bigger than a regular post of mine) and what about all the chemistry of "unbalances"... I hope I can recover the entire set of posts for today and put the "results" materials on facebook. But let's get to work!
Hypovolemia or actual volume loss generally refers to the situation where concomitant loss of water and salt exceeds ingestion, leading to contraction of the FEC volume. Renal, excessive urinary loss of NaCl and water occurs in many cases, one of which is the effect of diuretics.
Pharmacological diuretics specifically inhibit the reabsorption of Na+ along the nephron, leading to a consequent increase in na+ urinary excretion. Increased filtering of non-reabsorbing solvents, such as glucose and urea, can also alter tubular reabsorption of water and Na+ leading to osmotic diuresis. It often occurs in poorly controlled diabetes mellitus, as well as in patients receiving a hyperprotein diet.
Manitol is a diuretic that produces an osmotic diuresis, because the renal tube is impervious to mannitol. Many tubular and interstitial kidney disorders are associated with loss of Na+. Excessive loss of Na+ and water may occur during the diuretic phase of acute tubular necrosis (NTA) and as a result of removal of bilateral urinary tract obstruction. Natriumuse and aqueous diuresis associated with these two situations are usually short-lived and represent an appropriate response to an ecf volume expansion situation that occurs as a result of the previous oliguria.
However, continued loss in the absence of adequate fluid replacement may possibly lead to hypovolemia. Chronic renal failure is associated with decreased ability to adequately regulate renal excretion of salt and water. Therefore, patients with an RFG of less than 25 ml/ min have a mandatory renal loss of Na+, which may result in a progressive dissolution of the FEC volume if there are restrictions on Na+ ingestion.
Finally, the deficiency of mineralocorticoids (hypoaldosteronism) causes salt loss in the presence of normal intrinsic renal function. Massive water loss can also lead to hypovolemia. The decrease in FEC volume is usually less severe because two-thirds of the lost volume is intracellular. Situations associated with excessive urinary water loss include central insipid and nephrogenic diabetes. These two conditions are caused by alteration of AVP secretion and renal non-responsiveness to AVP respectively and are treated below.
Extrarenal causes of hypovolemia include loss of fluids through the gastrointestinal tract, skin and respiratory system and accumulation in space three (burns, pancreatitis, peritonitis). Approximately 9 liters of fluids enter the gastrointestinal tract daily, 2 liters by ingestion and 7 liters by secretion. Almost 98% of this volume is reabsorbed, so the loss of fluids through feces is only 100-200 ml/ day. Impairment of gastrointestinal reabsorption or increased secretion leads to loss of volume. Because gastric secretion has an acidic pH (increased concentration of H+), vomiting and diarrhoea are often accompanied by alkalose and metabolic acidosis respectively.
Evaporation of water from the skin and respiratory system contributes to thermoregulation. These insensitive losses reach up to 500 ml/ day. In febrile diseases, prolonged exposure to high temperatures or exercise, increased loss of salt and water through the skin in the form of perspiration can be significant and can lead to a volume deplation. the Na+ concentration of perspiration is normally 20-50 mmol/ l and decreases in profuse sweating due to the action of aldosterone.
Because sweating is hypotonic, the loss of water exceeds the loss of Na+. Water deficiency is reduced by increasing the feeling of thirst. However, the continuous loss of Na+ manifests itself as hypovolemia. Increased evaporative water loss in the respiratory system may be associated with hyperventilation, especially in febrile, mechanically ventilated patients.
Certain conditions lead to the seizure of liquids in space three. This compartment is extracellular, but is neither in balance with FRC nor with FIC. Liquids are actually lost from the FEC and can result in hypovolemia. Examples include intestinal lumen in gastrointestinal obstruction, subcutaneous tissues in severe burns, retroperitoneal space in acute pancreatitis and peritoneal cavity in peritonitis. Finally, severe bleeding from any source can cause volemic deplation.
From the point of view of physiopathology, the decrease in the volume of FEC is manifested as a decrease in plasma volume and hypotension. Hypotension is caused by decreased venous return (pre-pregnancy) and decreased cardiac output (baroreceptors in the carotid sinus and aortic arch are stimulated, thus stimulating the activation of the sympathetic nervous system and the renin-angiotensin system). The net effect is to maintain average arterial pressure and cerebral and coronary infusion.
In contrast to cardiovascular response, renal response aims to restore the FEC volume by decreasing RFG and tubular Na+ filtering. Increased sympathetic tone increases proximal tubular reabsorption of Na+ and decreases RGFG by preferential vasoconstriction of the related arteriole. Sodium is also reabsorbed into the proximal contorted tube in response to both increased angiotensin II and alteration of peritubular capillary hemodynamics (decreases hydrostatic pressure and increases oncotic pressure).
Increased reabsorption of Na+ in the collector duct is an important component of renal adaptation to decreased FEC volume.
The "time" of clinical manifestations has come. Careful anamnesis is often useful in determining the etiology of the decrease in The volume of the FEC (e.g. vomiting, diarrhoea, polyuria, diaphoresis). Most symptoms are nonspecific and are secondary to electrolyte imbalance and tissue hypoperfusion and include fatigue, weakness, muscle cramps, thirst and postural vertigo. In more advanced stages of volume decrease can lead to ischemia of various organs manifested by oliguria, cyanosis, abdominal or chest pain and confusion or obnubilation.
The reduction of the skin turgor and the dryness of the oral mucosa are weak indicators of the decrease of the interstitial fluid. Signs of decreased intravascular volume include reduction of jugular venous pressure, hypotension and orthostatic tachycardia. A large and sudden loss of fluids leads to hypovolemic shock, manifested by hypotension, tachycardia, peripheral vasoconstriction and hypoperfusion (cold, wet and cyanotic extremities, oliguria and altered mental status).
In the case of diagnosis, a complete anamnesis and a careful objective examination are generally sufficient to diagnose the etiology of hypovolemia. Laboratory data usually confirm and support clinical diagnosis. Plasma concentrations of urea and creatinine tend to be increased reflecting a decrease in RFG. Normally, the urea/creatinine ratio is approximately 10/1. However, in prerenal nitrogenemia, hypovolemia causes increased reabsorption of urea, which leads to an increase in blood urea compared to plasma creatinine, with the urea/ creatinine ratio becoming 20/ 1 or higher.
An increase in urea (relative to creatinine) may also be caused by an increase in urea production that occurs through hypernutrition (with high protein content), glococorticoid therapy and gastrointestinal bleeding. Fluid loss may be associated with hyponatremia or a normal concentration of Na+ in plasma, depending on the tonicity of the lost liquids, the presence of thirst and access to water. Hypopotasemia is common in situations where there is an increased loss of K+, renal or gastrointestinal, and hypopotasemia occurs in renal failure, insufficiency of mineralocorticoids and various types of metabolic acidosis. Metabolic alkalose occurs in diuretic-induced hypovolemia and in the case of vomiting or nasogastric aspiration.
In contrast, metabolic acidosis is associated with renal failure, tubulointerstitial disorders, insufficiency of mineralocorticoids, diarrhea, diabetic ketoacidosis and lactic acidosis. Because albumin and erythrocytes are limited to intravascular space, the decrease in FEC volume often leads to a relative increase in hematocrit (hemoconcentration) and plasma albumin concentration. The appropriate response to hypovolemia is to increase renal reabsorption of Na+ and water, which is reflected in the composition of urine.
The concentration of Na+ in urine is normally less than 20 nmol/ l, except in situations associated with alteration of Na+ reabsorption, such as acute tubular necrosis. Another exception is hypovolemia given by vomiting, because associated metabolic alkalosis and increased HCO3- filtering affect the proximal reabsorption of Na+. In this case, the urinary chlorine is low (less than 20 nmol/ l). Osmolarity and urinary density in hypovolemic subjects are generally greater than 450 mosm/ kg and 1015, respectively, reflecting the increase in AVP production. However, in hypovolemia in insipid diabetes, osmolarity and urinary density are indicators of inadequate urine dilution.
For treatment, the therapeutic purposes are to restore normonolemy with liquids similar in composition to those lost and to replace the losses that continue. Symptoms and signs, including weight loss, may be helpful in assessing the degree of volemy decrease and may also be monitored to assess the response to treatment. An average volume decrease can be corrected per bone. A more severe hypovolemia requires intravenous therapy. The isotonic or normosalin solution is chosen in normotremic or moderately hyponatremic patients and should be given initially in those with hypotension or shock.
Severe hyponatremia requires hypertonic saline solution. Hypernatremia reflects a proportionally higher water deficiency compared to Na+ deficiency and its correction requires a hypotonic solution, such as hyposalin solution or 5% glucose solution in water. patients with significant haemorrhage, anaemia or intravascular volume deplation may require blood transfusions or colloidal solutions (albumin, dextran). Hypopotasemia may be present from the beginning or may occur as a result of increased urinary excretion of K+ (must be corrected by adding an adequate amount of KCl to replacement solutions).
Here I managed to recover (after almost 9 hours of work)... We'll continue tomorrow with hyponatremia, hypernatremia and whatever!
I "broke" the post about incontinence (much bigger than a regular post of mine) and what about all the chemistry of "unbalances"... I hope I can recover the entire set of posts for today and put the "results" materials on facebook. But let's get to work!
Hypovolemia or actual volume loss generally refers to the situation where concomitant loss of water and salt exceeds ingestion, leading to contraction of the FEC volume. Renal, excessive urinary loss of NaCl and water occurs in many cases, one of which is the effect of diuretics.
Pharmacological diuretics specifically inhibit the reabsorption of Na+ along the nephron, leading to a consequent increase in na+ urinary excretion. Increased filtering of non-reabsorbing solvents, such as glucose and urea, can also alter tubular reabsorption of water and Na+ leading to osmotic diuresis. It often occurs in poorly controlled diabetes mellitus, as well as in patients receiving a hyperprotein diet.
Manitol is a diuretic that produces an osmotic diuresis, because the renal tube is impervious to mannitol. Many tubular and interstitial kidney disorders are associated with loss of Na+. Excessive loss of Na+ and water may occur during the diuretic phase of acute tubular necrosis (NTA) and as a result of removal of bilateral urinary tract obstruction. Natriumuse and aqueous diuresis associated with these two situations are usually short-lived and represent an appropriate response to an ecf volume expansion situation that occurs as a result of the previous oliguria.
However, continued loss in the absence of adequate fluid replacement may possibly lead to hypovolemia. Chronic renal failure is associated with decreased ability to adequately regulate renal excretion of salt and water. Therefore, patients with an RFG of less than 25 ml/ min have a mandatory renal loss of Na+, which may result in a progressive dissolution of the FEC volume if there are restrictions on Na+ ingestion.
Finally, the deficiency of mineralocorticoids (hypoaldosteronism) causes salt loss in the presence of normal intrinsic renal function. Massive water loss can also lead to hypovolemia. The decrease in FEC volume is usually less severe because two-thirds of the lost volume is intracellular. Situations associated with excessive urinary water loss include central insipid and nephrogenic diabetes. These two conditions are caused by alteration of AVP secretion and renal non-responsiveness to AVP respectively and are treated below.
Extrarenal causes of hypovolemia include loss of fluids through the gastrointestinal tract, skin and respiratory system and accumulation in space three (burns, pancreatitis, peritonitis). Approximately 9 liters of fluids enter the gastrointestinal tract daily, 2 liters by ingestion and 7 liters by secretion. Almost 98% of this volume is reabsorbed, so the loss of fluids through feces is only 100-200 ml/ day. Impairment of gastrointestinal reabsorption or increased secretion leads to loss of volume. Because gastric secretion has an acidic pH (increased concentration of H+), vomiting and diarrhoea are often accompanied by alkalose and metabolic acidosis respectively.
Evaporation of water from the skin and respiratory system contributes to thermoregulation. These insensitive losses reach up to 500 ml/ day. In febrile diseases, prolonged exposure to high temperatures or exercise, increased loss of salt and water through the skin in the form of perspiration can be significant and can lead to a volume deplation. the Na+ concentration of perspiration is normally 20-50 mmol/ l and decreases in profuse sweating due to the action of aldosterone.
Because sweating is hypotonic, the loss of water exceeds the loss of Na+. Water deficiency is reduced by increasing the feeling of thirst. However, the continuous loss of Na+ manifests itself as hypovolemia. Increased evaporative water loss in the respiratory system may be associated with hyperventilation, especially in febrile, mechanically ventilated patients.
Certain conditions lead to the seizure of liquids in space three. This compartment is extracellular, but is neither in balance with FRC nor with FIC. Liquids are actually lost from the FEC and can result in hypovolemia. Examples include intestinal lumen in gastrointestinal obstruction, subcutaneous tissues in severe burns, retroperitoneal space in acute pancreatitis and peritoneal cavity in peritonitis. Finally, severe bleeding from any source can cause volemic deplation.
From the point of view of physiopathology, the decrease in the volume of FEC is manifested as a decrease in plasma volume and hypotension. Hypotension is caused by decreased venous return (pre-pregnancy) and decreased cardiac output (baroreceptors in the carotid sinus and aortic arch are stimulated, thus stimulating the activation of the sympathetic nervous system and the renin-angiotensin system). The net effect is to maintain average arterial pressure and cerebral and coronary infusion.
In contrast to cardiovascular response, renal response aims to restore the FEC volume by decreasing RFG and tubular Na+ filtering. Increased sympathetic tone increases proximal tubular reabsorption of Na+ and decreases RGFG by preferential vasoconstriction of the related arteriole. Sodium is also reabsorbed into the proximal contorted tube in response to both increased angiotensin II and alteration of peritubular capillary hemodynamics (decreases hydrostatic pressure and increases oncotic pressure).
Increased reabsorption of Na+ in the collector duct is an important component of renal adaptation to decreased FEC volume.
The "time" of clinical manifestations has come. Careful anamnesis is often useful in determining the etiology of the decrease in The volume of the FEC (e.g. vomiting, diarrhoea, polyuria, diaphoresis). Most symptoms are nonspecific and are secondary to electrolyte imbalance and tissue hypoperfusion and include fatigue, weakness, muscle cramps, thirst and postural vertigo. In more advanced stages of volume decrease can lead to ischemia of various organs manifested by oliguria, cyanosis, abdominal or chest pain and confusion or obnubilation.
The reduction of the skin turgor and the dryness of the oral mucosa are weak indicators of the decrease of the interstitial fluid. Signs of decreased intravascular volume include reduction of jugular venous pressure, hypotension and orthostatic tachycardia. A large and sudden loss of fluids leads to hypovolemic shock, manifested by hypotension, tachycardia, peripheral vasoconstriction and hypoperfusion (cold, wet and cyanotic extremities, oliguria and altered mental status).
In the case of diagnosis, a complete anamnesis and a careful objective examination are generally sufficient to diagnose the etiology of hypovolemia. Laboratory data usually confirm and support clinical diagnosis. Plasma concentrations of urea and creatinine tend to be increased reflecting a decrease in RFG. Normally, the urea/creatinine ratio is approximately 10/1. However, in prerenal nitrogenemia, hypovolemia causes increased reabsorption of urea, which leads to an increase in blood urea compared to plasma creatinine, with the urea/ creatinine ratio becoming 20/ 1 or higher.
An increase in urea (relative to creatinine) may also be caused by an increase in urea production that occurs through hypernutrition (with high protein content), glococorticoid therapy and gastrointestinal bleeding. Fluid loss may be associated with hyponatremia or a normal concentration of Na+ in plasma, depending on the tonicity of the lost liquids, the presence of thirst and access to water. Hypopotasemia is common in situations where there is an increased loss of K+, renal or gastrointestinal, and hypopotasemia occurs in renal failure, insufficiency of mineralocorticoids and various types of metabolic acidosis. Metabolic alkalose occurs in diuretic-induced hypovolemia and in the case of vomiting or nasogastric aspiration.
In contrast, metabolic acidosis is associated with renal failure, tubulointerstitial disorders, insufficiency of mineralocorticoids, diarrhea, diabetic ketoacidosis and lactic acidosis. Because albumin and erythrocytes are limited to intravascular space, the decrease in FEC volume often leads to a relative increase in hematocrit (hemoconcentration) and plasma albumin concentration. The appropriate response to hypovolemia is to increase renal reabsorption of Na+ and water, which is reflected in the composition of urine.
The concentration of Na+ in urine is normally less than 20 nmol/ l, except in situations associated with alteration of Na+ reabsorption, such as acute tubular necrosis. Another exception is hypovolemia given by vomiting, because associated metabolic alkalosis and increased HCO3- filtering affect the proximal reabsorption of Na+. In this case, the urinary chlorine is low (less than 20 nmol/ l). Osmolarity and urinary density in hypovolemic subjects are generally greater than 450 mosm/ kg and 1015, respectively, reflecting the increase in AVP production. However, in hypovolemia in insipid diabetes, osmolarity and urinary density are indicators of inadequate urine dilution.
For treatment, the therapeutic purposes are to restore normonolemy with liquids similar in composition to those lost and to replace the losses that continue. Symptoms and signs, including weight loss, may be helpful in assessing the degree of volemy decrease and may also be monitored to assess the response to treatment. An average volume decrease can be corrected per bone. A more severe hypovolemia requires intravenous therapy. The isotonic or normosalin solution is chosen in normotremic or moderately hyponatremic patients and should be given initially in those with hypotension or shock.
Severe hyponatremia requires hypertonic saline solution. Hypernatremia reflects a proportionally higher water deficiency compared to Na+ deficiency and its correction requires a hypotonic solution, such as hyposalin solution or 5% glucose solution in water. patients with significant haemorrhage, anaemia or intravascular volume deplation may require blood transfusions or colloidal solutions (albumin, dextran). Hypopotasemia may be present from the beginning or may occur as a result of increased urinary excretion of K+ (must be corrected by adding an adequate amount of KCl to replacement solutions).
Here I managed to recover (after almost 9 hours of work)... We'll continue tomorrow with hyponatremia, hypernatremia and whatever!
A week of the most spornic
possible, either at the spore, or at the fun, or at all
together!
Dorin, Merticaru