STUDY - Technical - New Dacian's Medicine
The
Edema (2)
Translation Draft
Strange is life... Yesterday we lost, irretrievably, the new medicine file that generated the pdf that we constantly update to readers on Facebook or dorinm.ro... That's it! I'm going to redo it, but it's going to be a little while before I can make it available again... This can also attract a severing of my efforts on this blog so... From today, I will start posting only on husband days (the days seems)... but... get to work and finish the edema presentations!
Other factors of influence in the appearance and evolution of edema are represented by aginin vasopressin (AVP) and endotelin. The secretion of AVP occurs in response to the increase in intracellular osmolar concentration and, by stimulating V2 receptors, increases the rearborption of free water in the distal contorted tube, thus increasing the total water in the body. Circulating AVP is increased in many patients with heart failure secondary to a non-osmotic stimulus that is not yet identified, which fails to produce normal reduction of AVP by decreasing osmolarity, thus contributing to fluid retention and edema formation.
Endotelin is a powerful vasoconstrictor peptide released by endothelial cells, its concentration being increased in heart failure and contributes to renal vasoconstriction, sodium retention and edema occurring in heart failure.
Let's move on to the natriumetic peptides now! Distance of atria and/ or a load of sodium causes a discharge into circulation of atrial natriuretic peptide (NAF), a polypeptide (a precursor, with a high molecular weight of PNA is stored in secretory granules in atrial myocytes).
The discharge of PNA causes: 1. sodium and water excretion by increasing glomerular filtration, inhibiting sodium rearbsorption in the proximal tube and inhibiting the discharge of renin and aldosterone and 2. arteriolar and venous dilation antagonizing the vasoconstrictor action of AII, AVP and sympathetic stimulation. Thus, THE NAP has the ability to oppose sodium retention and increase in blood pressure in hypervolemy states.
Cerebral natriuretic peptide (PNC), related to PNA, is stored primarily in the ventricular myocardium and is released into circulation when ventricular diastolic pressure increases. Its actions are similar to those of the NAP. Circulatory levels of PNA and PNC are increased in congestive heart failure, but obviously not enough to prevent the formation of edema. In addition, in edematous states (especially in heart failure) there is an abnormal resistance to the action of natriumetic peptides.
I will now address the clinical causes of edema, starting with obstruction of the venous (and lymphatic) circulation of a limb. Under these conditions, the hydrostatic pressure in the capillary bed downstream of the obstruction increases, so that the increased volume of fluids is transferred from the vessels to the interstitial spaces. As the alternative (i.e. lymphatic) pathway can often be obstructed, the volume of interstitial fluids in the limb, i.e. a build-up of fluid in that territory, at the expense of the blood olum in the rest of the body, thus reducing the volume of effective arterial blood, occurs.
When venous and lymphatic drainage are prevented, fluid accumulates in the interstitial spaces at the expense of plasma volume. The latter stimulates salt and water retention until the plasma volume deficiency is corrected. tissue tension increases in the affected limb until the primary alteration of Starling forces is counterbalanced, at which point no more fluid accumulates.
The net effect is a local increase in the volume of interstitial fluid. The same sequence occurs in ascites and hydrothorax, in which fluid is retained or accumulates in the cavitary space, with intravascular volume deletation, leading to secondary retention of salt and liquids, as has already been described.
In case of congestive heart failure, defective systolic emptying of the heart cavities and/ or inadequate ventricular relaxation leads to a build-up of blood in the heart and the aforementioned sequence of events is initiated. In mild heart failure, a small increase in total blood volume can compensate for the deficiency of the arterial volume and a new equilibrium situation is established because, through the action of the Starling Law, an increase in the volume of blood in the atria and ventricles causes a stronger contraction and thus can increase cardiac flow.
However, if heart disease is more severe, fluid retention cannot compensate for the deficit of the actual arterial volume. Growth occurs in the venous circulation, and increased capillary and lymphatic hydrostatic pressure causes the formation of edema. In heart failure, a decrease occurs in the baroreflex mediated inhibition of the vasomotor center, which produces activation of renal vasoconstrictor nerves and the RAA system, causing sodium and water retention. Incomplete ventricular emptying (systolic heart failure) and/ or inadequate ventricular relaxation (diastolic heart failure) both lead to an increase in diastolic ventricular pressure. if impaired cardiac function involves the right ventricle, pressure in the veins and systemic capillaries may increase, thereby increasing the transsweat of fluids into the interstitial space and increasing the likelihood of peripheral edema in the presence of sodium and water accumulation, as described above.
Increased systemic venous pressure is transmitted to the thoracic duct with consecutive reduction of lymphatic drainage, further leading to increased fluid accumulation. if impaired cardiac function (incomplete ventricular emptying and/ or inadequate relaxation) mainly involves the left ventricle, venous and pulmonary capillary pressures increase, leading in some situations to pulmonary edema, as well as pressure in the pulmonary artery, which in turn interferes with systolic emptying of the right ventricle, leading to an increase in diastolic pressure of the right ventricle and central and systemic venous pressure, increasing the possibility of formation of peripheral edema. Pulmonary edema affects gas exchanges and can induce hypoxia, which also affects cardiac function, sometimes resulting in a vicious circle.
In the case of nephrotic syndrome and other hypoalbuminic states, the primary alteration is represented by a decrease in colloid-oncotic pressure due to massive loss of protein through the urine. This leads to a net movement of fluids between interstitial spaces, creates hypovolemia and initiates the edema formation sequence described above, including activation of the RAA system.
Due to severe hypoalbuminemia, the water and salt that are retained cannot be kept in the intravascular compartment, the volume of arterial blood effectively decreases and for this reason the stimuli that produce salt and water retention are not stopped. A similar sequence of events occurs in other situations leading to severe hypoalbuminemia, including states of severe nutritional deficiency, enteropathy with loss of protein, congenital hypoalbuminemia and severe chronic liver disease. However, in nephrotic syndrome impairment of renal function contributes to sodium retention.
Cirosis is characterized by blockage of liver venous flow, which produces the expansion of splanhnic blood volume and increased lymph formation in the liver. Intrahepatic hypertension appears to be responsible for sodium retention and systemic vasodilation as well as for the reduction of actual arterial blood volume. These alterations are frequently complicated by secondary hypoalbuminemia to reduce liver synthesis and further decrease the volume of actual arterial blood, leading to the activation of the RAA system of renal sympathetic nerves and other hydrosalin retention mechanisms.
The concentration of circulating aldosterone is increased by the inability of the liver to metabolize it. Initially, excess interstitial fluid is located preferentially upstream of the congested portal venous system and obstructed liver lymphatics, i.e. at the level of the peritoneal cavity.
In the final stages, especially when there is also severe hypoalbuminemia can develop and peripheral edema. Excessive production of prostaglandins (PGE2 and PGI2) in cirrhosis impairs renal sodium retention. When the synthesis of these substances is inhibited by nonsteroidal anti-inflammatory agents, renal function deteriorates and sodium retention increases.
Ready for today! We're not going to continue with the edema until the 24th... I've seriously typed that I'll post every two days...
Strange is life... Yesterday we lost, irretrievably, the new medicine file that generated the pdf that we constantly update to readers on Facebook or dorinm.ro... That's it! I'm going to redo it, but it's going to be a little while before I can make it available again... This can also attract a severing of my efforts on this blog so... From today, I will start posting only on husband days (the days seems)... but... get to work and finish the edema presentations!
Other factors of influence in the appearance and evolution of edema are represented by aginin vasopressin (AVP) and endotelin. The secretion of AVP occurs in response to the increase in intracellular osmolar concentration and, by stimulating V2 receptors, increases the rearborption of free water in the distal contorted tube, thus increasing the total water in the body. Circulating AVP is increased in many patients with heart failure secondary to a non-osmotic stimulus that is not yet identified, which fails to produce normal reduction of AVP by decreasing osmolarity, thus contributing to fluid retention and edema formation.
Endotelin is a powerful vasoconstrictor peptide released by endothelial cells, its concentration being increased in heart failure and contributes to renal vasoconstriction, sodium retention and edema occurring in heart failure.
Let's move on to the natriumetic peptides now! Distance of atria and/ or a load of sodium causes a discharge into circulation of atrial natriuretic peptide (NAF), a polypeptide (a precursor, with a high molecular weight of PNA is stored in secretory granules in atrial myocytes).
The discharge of PNA causes: 1. sodium and water excretion by increasing glomerular filtration, inhibiting sodium rearbsorption in the proximal tube and inhibiting the discharge of renin and aldosterone and 2. arteriolar and venous dilation antagonizing the vasoconstrictor action of AII, AVP and sympathetic stimulation. Thus, THE NAP has the ability to oppose sodium retention and increase in blood pressure in hypervolemy states.
Cerebral natriuretic peptide (PNC), related to PNA, is stored primarily in the ventricular myocardium and is released into circulation when ventricular diastolic pressure increases. Its actions are similar to those of the NAP. Circulatory levels of PNA and PNC are increased in congestive heart failure, but obviously not enough to prevent the formation of edema. In addition, in edematous states (especially in heart failure) there is an abnormal resistance to the action of natriumetic peptides.
I will now address the clinical causes of edema, starting with obstruction of the venous (and lymphatic) circulation of a limb. Under these conditions, the hydrostatic pressure in the capillary bed downstream of the obstruction increases, so that the increased volume of fluids is transferred from the vessels to the interstitial spaces. As the alternative (i.e. lymphatic) pathway can often be obstructed, the volume of interstitial fluids in the limb, i.e. a build-up of fluid in that territory, at the expense of the blood olum in the rest of the body, thus reducing the volume of effective arterial blood, occurs.
When venous and lymphatic drainage are prevented, fluid accumulates in the interstitial spaces at the expense of plasma volume. The latter stimulates salt and water retention until the plasma volume deficiency is corrected. tissue tension increases in the affected limb until the primary alteration of Starling forces is counterbalanced, at which point no more fluid accumulates.
The net effect is a local increase in the volume of interstitial fluid. The same sequence occurs in ascites and hydrothorax, in which fluid is retained or accumulates in the cavitary space, with intravascular volume deletation, leading to secondary retention of salt and liquids, as has already been described.
In case of congestive heart failure, defective systolic emptying of the heart cavities and/ or inadequate ventricular relaxation leads to a build-up of blood in the heart and the aforementioned sequence of events is initiated. In mild heart failure, a small increase in total blood volume can compensate for the deficiency of the arterial volume and a new equilibrium situation is established because, through the action of the Starling Law, an increase in the volume of blood in the atria and ventricles causes a stronger contraction and thus can increase cardiac flow.
However, if heart disease is more severe, fluid retention cannot compensate for the deficit of the actual arterial volume. Growth occurs in the venous circulation, and increased capillary and lymphatic hydrostatic pressure causes the formation of edema. In heart failure, a decrease occurs in the baroreflex mediated inhibition of the vasomotor center, which produces activation of renal vasoconstrictor nerves and the RAA system, causing sodium and water retention. Incomplete ventricular emptying (systolic heart failure) and/ or inadequate ventricular relaxation (diastolic heart failure) both lead to an increase in diastolic ventricular pressure. if impaired cardiac function involves the right ventricle, pressure in the veins and systemic capillaries may increase, thereby increasing the transsweat of fluids into the interstitial space and increasing the likelihood of peripheral edema in the presence of sodium and water accumulation, as described above.
Increased systemic venous pressure is transmitted to the thoracic duct with consecutive reduction of lymphatic drainage, further leading to increased fluid accumulation. if impaired cardiac function (incomplete ventricular emptying and/ or inadequate relaxation) mainly involves the left ventricle, venous and pulmonary capillary pressures increase, leading in some situations to pulmonary edema, as well as pressure in the pulmonary artery, which in turn interferes with systolic emptying of the right ventricle, leading to an increase in diastolic pressure of the right ventricle and central and systemic venous pressure, increasing the possibility of formation of peripheral edema. Pulmonary edema affects gas exchanges and can induce hypoxia, which also affects cardiac function, sometimes resulting in a vicious circle.
In the case of nephrotic syndrome and other hypoalbuminic states, the primary alteration is represented by a decrease in colloid-oncotic pressure due to massive loss of protein through the urine. This leads to a net movement of fluids between interstitial spaces, creates hypovolemia and initiates the edema formation sequence described above, including activation of the RAA system.
Due to severe hypoalbuminemia, the water and salt that are retained cannot be kept in the intravascular compartment, the volume of arterial blood effectively decreases and for this reason the stimuli that produce salt and water retention are not stopped. A similar sequence of events occurs in other situations leading to severe hypoalbuminemia, including states of severe nutritional deficiency, enteropathy with loss of protein, congenital hypoalbuminemia and severe chronic liver disease. However, in nephrotic syndrome impairment of renal function contributes to sodium retention.
Cirosis is characterized by blockage of liver venous flow, which produces the expansion of splanhnic blood volume and increased lymph formation in the liver. Intrahepatic hypertension appears to be responsible for sodium retention and systemic vasodilation as well as for the reduction of actual arterial blood volume. These alterations are frequently complicated by secondary hypoalbuminemia to reduce liver synthesis and further decrease the volume of actual arterial blood, leading to the activation of the RAA system of renal sympathetic nerves and other hydrosalin retention mechanisms.
The concentration of circulating aldosterone is increased by the inability of the liver to metabolize it. Initially, excess interstitial fluid is located preferentially upstream of the congested portal venous system and obstructed liver lymphatics, i.e. at the level of the peritoneal cavity.
In the final stages, especially when there is also severe hypoalbuminemia can develop and peripheral edema. Excessive production of prostaglandins (PGE2 and PGI2) in cirrhosis impairs renal sodium retention. When the synthesis of these substances is inhibited by nonsteroidal anti-inflammatory agents, renal function deteriorates and sodium retention increases.
Ready for today! We're not going to continue with the edema until the 24th... I've seriously typed that I'll post every two days...
Understanding, love and
gratitude to all!
Dorin, Merticaru