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Pathophysiology of kidney. Kidney insufficiency

Pathophysiology of kidney. Kidney insufficiency. Violation of the fundamental functions of the kidneys. Filtering (reduction mechanisms and increase filtration, azotemia, renal glomerular acidosis, proteinuria, hematuria);

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Pathophysiology of kidney. Kidney insufficiency

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  1. Pathophysiology of kidney. Kidney insufficiency

  2. Violation of the fundamental functions of the kidneys • Filtering (reduction mechanisms and increase filtration, azotemia, renal glomerular acidosis, proteinuria, hematuria); • Reabsorption (sodium and water, protein, glucose, amino acids, phosphate and calcium, Fanconi syndrome); • Secretion (renal tubular acidosis) - in violation of water homeostasis (change in volume extrcellular fluid, hyper-and hipohidriya; violation of osmotic homeostasis and hyper hipoosmiya; violation of acid-base status at nongasacidosis, and changes the chemical composition of blood in azotemia, hypoproteinemia, hypoglycemia.

  3. Renal insufficiency Renal insufficiency - a pathological condition in which disturbed the constancy of internal environment from the failure of the kidneys to perform their functionsClassification of renal failure1. Over the clinical course: acute and chronic;2. By origin: prerenal, renal, postrenalna, arenal3. In terms of dysfunction: total and partial4. With the development of mechanisms: glomerular and tubular

  4. Acute renal failure

  5. Chronic renal failure

  6. The main syndromes and kidney disease • Uraemic syndrome • Anemia • Hypertension • Edema • Violation of acid-base balance • Violation blood clotting • Renal osteodystrophy • Acute and chronic glomerulonephritis • Pyelonephritis • Nephrolithiasis • Nephrotic syndrome

  7. Uremia • As the blood accumulated wastes that would have normally preasent in the urine (uria, uric acid, creatine, creatinine, metylhuanidyn, dymetylhuanidyn, phenols, indoles, amino compounds, low molecular compounds - the total of 200 substances). • Pathological changes in the body due to intoxication in renal failure is characterized as uremic syndrome. • Clinical manifestations of uremic syndrome associated with lesions of all organs and systems in the first place - the nervous system (nausea, vomiting, mental disorders, peripheral nerve lesions, uremic coma), and disruption of water and electrolyte metabolism.

  8. Anemia in chronic renal failure • Anemia in chronic renal failure is revealed at glomerular filtration rate below 40 ml / min. • Pathogenesis of anemia due to inhibition of erythropoiesis by reducing the formation of renal erythropoietin and increased elaboration of inhibitors of hematopoiesis, injury to hematopoietic cells and mature erythrocytes of uremic toxins, loss of transferrin by proteinuria and red blood cells and iron deficiency due to chronic blood loss. • Blood loss arising from hematuria, the formation of ulcers in the stomach and intestines, hemorrhagic diathesis.

  9. Hypertension • Hypertension is one of the manifestations of chronic renal failure.Hypertension, dependent on the amount resulting from the reduction of glomerular filtration rate, reduced output of blood sodium and water and increased blood volume. • Hypertension with high renin resulting from renal blood flow and hypoxia yukstaglomerular cells. Activation of the renin-angiotensin system leads to hypertension.Hypertension, regardless of volume reduction occurs through the formation of renal prostaglandins (E), a neutral peptide, reducing the activity of kallikrein-kinin system.

  10. Edema • Reduced glomerular filtration rate leads to sodium and water retention in the vascular bed, there is hypervolemia. • Violation of glomerular filter causes massive proteinuria, so the reduced oncotic pressure of blood and fluid from the vascular tissue becomes, developing edema.

  11. Acidosis • Acidosis - a shift to the acid-base balance internal environment in the acidic side, which leads to atsydotychnoho damage cells, inhibition of contractile function of the heart and in extreme cases - coma acydotyc. • Kidneys normally compensate for an excess of hydrogen in the blood, increasing bicarbonate reabsorption in proximal tubules of the nephron and forming an additional amount of bicarbonate in the distal tubules. Renal tubules and absence of compensatory mechanisms leads to a decrease in blood pH.In compensated acidosis pH of blood does not go beyond the norm due to compensatory mechanisms and of buffer systems.

  12. Alkalosis • Alkalosis - a shift to the acid-base balance internal environment in the alkaline side, leading to cellular alkalosis (dysfunction of enzymes, oxidative phosphorylation, swelling of the cells) and hipokaltsiemiyi. • In normal kidneys compensate for alkalosis by reducing the reabsorption of bicarbonate in the proximal tubules of the nephron. • When compensated alkalosis pH of blood does not go beyond the norm due to compensatory mechanisms and of buffer systems.

  13. In renal failure there are violations of hemostasis • Hypercoagulation arises because of the shortage urokinaze, which is a plasminogen activator, the loss in the urine of antithrombin III and in violation of synthesis and deposition of heparin in the kidneys. • Hipocoagulation (hemorrhagic diathesis) is associated with thrombocytopenia due to uremic toxic effects on hematopoietic cells and loss of urine, blood clotting factors for proteinuria.

  14. Renal osteodystrophy • Renal osteodystrophy is a set of degenerative disorders of bone, arising from disorders of calcium and phosphorus metabolism in kidney damage. • Degenerative changes in bones can occur due to bone resorption (with hyperparathyroidism), osteomalacia, followed by deformation of the bones (if hipocalciemia in children), osteoporosis (reduced bone density without deformation of the bones); osteosclerosis (increased bone density).

  15. Glomerular disease • Glomerulonephritis - kidney disease is a diffuse allergic nature. • Acute glomerulonephritis has a rapid start, during or after infection, most often due to hemolytic streptococcus group A. Also found relationship with viral and parasitic factors, cooling, diffuse lesions of connective tissue (lupus, rheumatoid arthritis), burn disease, vaccination. As a result of damage to the glomerular membrane of developing oliguria, proteinuria, azotemia, hypertension, edema, hematuria, abnormalities of the central nervous system. • Chronic glomerulonephritis - progressive diffuse bilateral renal inflammatory disease.

  16. Pyelonephritis • Pyelonephritis - infection-inflammatory diseases of the mucous membrane of the urinary tract and renal parenchyma of the primary lesion of the interstitial tissue. • The most common cause of disease is spreading coccal infection Escherichia coli or by hematogenous or ascending direction of the urinary tract. Favorable conditions for disease is a violation of the outflow of urine, trophic disorders, reduced reactivity.

  17. Urolithiasis

  18. Nephrotic syndrome

  19. Change of acid-base status in the gas acidosis

  20. Change of acid-base status in the nongas acidosis

  21. Change of acid-base status in the gas alcalosis

  22. Change of acid-base status in the nongas alcalosis

  23. Dehydration • Dehydration (ehsiccosis; son.: Dehydration, eksikoz) - pathological condition caused by a decrease in water content in the body. The loss of water corresponding weight loss of 10-20%, life-threatening, withdrawal of water initially healthy adult leads to death within 7-10 days, and in a hot dry atmosphere - 3-5 days.

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