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ELECTROLYTES DISTURBANCES

ELECTROLYTES DISTURBANCES. Oleh: Dr. Husnil Kadri, M.Kes Bagian Biokimia Fakultas Kedokteran Universitas Andalas Padang. Change in [Electrolyte] Can Occur By…. 1.) Increase/Decrease in amount of electrolyte 2.) Increase/Decrease in amount of water. Remember

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ELECTROLYTES DISTURBANCES

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  1. ELECTROLYTES DISTURBANCES Oleh: Dr. Husnil Kadri, M.Kes Bagian Biokimia Fakultas Kedokteran Universitas Andalas Padang

  2. Change in [Electrolyte] Can Occur By… 1.) Increase/Decrease in amount of electrolyte 2.) Increase/Decrease in amount of water Remember Concentration = amount of solute volume of solution

  3. Sodium (Na+) Key role (s): plasma osmolality and water balance Regulation: Thirst Kidney Na+/K+ ATPase pumps Na+/H+ pumps Blood volume status  ADH (saves water) when  blood volume or plasma osmolality  renin when  arteriolar pressure or  Na+  aldosterone (saves salt) when  Na+ ( renin) Clinical: Na disorders = water disorders Hyponatremia Hypernatremia

  4. Hyponatremia Sodium and/or Water Symptoms • nausea/vomiting • generalized weakness • mental confusion • headache • lethargy • possible coma if too low Possible causes • excessive renal loss of salt (aldosterone deficiency, kidney disease, diuretics) • excessive ADH secretion (SIADH) • water overload (congestive heart failure, cirrhosis, renal disease)

  5. Hypernatremia Sodium and/or Water • Symptoms • dehydration • increased thirst • fever • tremors • altered mental status • lethargy • seizures • coma • Possible causes • extrarenal loss (diarrhea, skin losses) • renal losses (diuretics therapy and  water intake) • impaired secretion or ability to respond to ADH (diabetes insipidus) • excessive water loss • hyperaldosteronism

  6. Potassium (K+) Key role (s): Regulate cardiac contraction and rhythm, muscle contraction Regulation: Kidneys Na+/K+ -ATPase pump Acid/Base balance (i.e., K+/H+ pumps)  Aldosterone results in  K+ excretion and shift extracellular to intracellular. Clinical: Hypokalemia Hyperkalemia

  7. Hypokalemia Potassium and/or Water • Symptom • weakness • fatigue • anorexia • nausea • arrhythmia • possible cardiac arrest • Possible Causes • extra -> intracellular shifts (alkalosis, diuretics) • extrarenal losses (excessive diarrhea, vomiting) • renal losses (renal disease, polyuria) • hyperaldosteronism

  8. Hyperkalemia Potassium and/or Water • Symptoms • muscular weakness • tingling • numbness • confusion • cardiac arrhythmias • possible cardiac arrest • Possible Causes • intra -> extracellular shifts (acidosis) • renal failure (K+ secretion deficiency) • adrenal failure (hypoaldosteronism) • leukemia • pseudohyperkalemia (hemolysis of sample, leukocytosis) Remember: About 98% K+ is intracellular leaving only 2% extracellular. Hence, a K+ shift from the ICF to the ECF of only 2% can double the [plasma].

  9. Calcium (Ca2+) Key role (s): primarily resides in bone, muscular contraction, neurotransmission, membrane transport, enzymes, and blood coagulation Regulation: Kidney (reabsorbed in the proximal tubules) Parathyroid hormone (PTH) Vitamin D – active form controls homeostasis Calcitonin – exact mechanism not known Clinical: Hypocalcemia – hypoparathyroidism, malabsorption of calcium or Vit. D, renal failure Hypercalcemia – hyperparathyroidism, excess Vit. D, tumors Serum Calcium = Ca2+ionized (45%) + Caprotein-bound (45%) + Cacomplexed to anions (10%)

  10. Magnesium (Mg2+) Key role (s): enzyme cofactor; calcium and bone homeostasis Regulation: Kidney  PTH,  serum Mg2+ aldosterone Clinical: hypomagnesemia – decreased intake (malabsorption, malnutrition), increased loss (renal disease, hyperaldosteronism, hyperparathyroidism) hypermagnesemia – usually increased intake of magnesium or renal disease

  11. Chloride (Cl-) Key role (s): Maintains osmolality, blood volume, electric neutrality Regulation: kidneys (reabsorbed /w Na+ in the proximal tubules), aldosterone Clinical: Hypochloremia – similar causes as hyponatremia, prolonged vomiting, high [bicarbonate] associated metabolic alkalosis Hyperchloremia – similar causes as hypernatremia, dehydration, low [bicarbonate] associated with prolonged diarrhea or metabolic acidosis

  12. Bicarbonate (HCO3-) Key role (s): determines pH (along with H+); buffering the blood and maintaining acid/base equilibrium Regulation: kidneys (reabsorption in the tubules) lungs Clinical: Acid/Base disorders

  13. Disorders of Water Balance: Dehydration Water loss exceeds water intake and the body is in negative fluid balance Causes include: hemorrhage, severe burns, prolonged vomiting or diarrhea, profuse sweating, and diuretic abuse Signs and symptoms:thirst, dry flushed skin, and oliguria Other consequences include hypovolemic shock and loss of electrolytes 13

  14. Disorders of Water Balance: Dehydration 2 ECF osmotic pressure rises Cells lose H2O to ECF by osmosis; cells shrink Excessive loss of H2O from ECF 3 1 (a) Mechanism of dehydration 14

  15. Amount of water ingested quickly can lead to cellular overhydration or water intoxication ECF is diluted – sodium content is normal but excess water is present The resulting hyponatremia promotes net osmosis into tissue cells, causing swelling Disorders of Water Balance: Hypotonic Hydration 15

  16. Disorders of Water Balance: Hypotonic Hydration 3 H2O moves into cells by osmosis; cells swell ECF osmotic pressure falls 2 1 Excessive H2O enters the ECF (b) Mechanism of hypotonic hydration 16

  17. Protein Imbalances • Plasma proteins(especially albumin) are important determinants of plasma volume • Hyperproteinemia is rare • Occurs with dehydration-induced hemoconcentration

  18. Hypoproteinemia • Caused by • Anorexia • Malnutrition • Starvation • Fad dieting • Poorly balanced vegetarian diets

  19. Hypoproteinemia • Poor absorption d/t GI malabsorptive diseases • Inflammation → protein can shift out of intravascular space • Hemorrhage

  20. Hypoproteinemia: Clinical Manifestations • Edema (b/c insufficient oncotic pressure to “hold” water in vascular space) • Slow healing • Anorexia • Fatigue • Anemia • Muscle loss • Ascites (same reason as edema)

  21. Bioavailabilitas • Dalam makanan, mineral terdapat dalam bentuk garam yang sukar larut, kecuali K & Na. • Absorpsinya pada usus halus & besar. • Transportasi & penyimpanan memerlukan protein pengemban spesifik, contoh; Fe3+-transferin Cu2+-albumin

  22. Kalsium & Fosfor • Keduanya membentuk garam appatite didalam tulang & gigi (80-90%). • Absorpsi paling baik jika perbandingan dalam lumen usus Ca : P = 1 : 1 s/d 1 : 3 • Bila perbandingan > 3, maka absorpsi Ca terhambat (Rachitis). • Makanan penyebabnya disebut rachitogenik

  23. Interaksi yang Menghambat • Beras mengandung asam fitat (P) sehingga mengikat Ca membentuk Ca-fitat. • Sayuran & buah yang mengandung asam oksalat juga akan menghambat absorpsi Ca.

  24. Fungsi P • Ikatan fosfat berenergi tinggi ATP, ADP, kreatin-P, PEP, dll. • Komponen membran sel fosfolipid • Membentuk hidroksiapatit pada tulang dan gigi

  25. Defisiensi Ca • Rickets pada anak-anak • Osteomalacia (osteoporosis) pada dewasa • Tetani / kejang • Postmenopause (estrogen rendah)

  26. Defisiensi P • Gangguan absorpsi di usus • Ekskresi berlebihan melalui ginjal • Sindrom Milkman • Sindrom de Toni Fanconi

  27. Penyakit yang Berhubungandgn Na & K • Penyakit Addison - hipoaktif kelenjar kortek adrenal - hiponatremia & hiperkalemia • Penyakit Cushing - hiperaktif kelenjar kortek adrenal - hipernatremia & hipokalemia

  28. Konsumsi NaCl berlebihan • Hipertensi • Diabetes • Gangguan ginjal kronik

  29. Besi • Komponen penting pada: hemoglobin, sitokrom, katalase,peroksidase • Terdapat dalam makanan terutama daging sebagai ion Fe3+ (Ferri). • Pengaturan absorpsi Fe dikenal sebagai mucosal block system

  30. Mucosal Block System • Dalam lumen lambung, reduktor (asam askorbat, HCl, dll) mereduksi ferri menjadi ferro. • Ferro akan diabsorpsi mukosa usus. • Dalam sel usus, ferro dioksidasi kembali menjadi ferri. • Ion ferri diikat apoferritin membentuk ferritin.

  31. Mucosal Block System • Bila tubuh tidak membutuhkan Fe, apoferritin menjadi jenuh. • Akibatnya ion ferro di lumen usus tidak bisa masuk ke dalam sel usus. • Fe akan dibuang bersama feses. • Bila tubuh butuh Fe, ferritin melepas ferri, • Ferri direduksi menjadi ferro.

  32. Mucosal Block System • Dalam sirkulasi darah, ferro dioksidasi lagi oleh peroksidase (dalam ceruloplasmin). • Ion ferri kemudian diikat oleh apotransferin membentuk transferin. • Transferin ditranspor ke berbagai jaringan yang membutuhkan besi. • Dalam jangka panjang, besi disimpan sebagai hemosiderin jaringan.

  33. Defisiensi Besi • Anemia mikrositer hipokrom, disebabkan oleh: - infeksi cacing tambang - perdarahan • Pil KB meningkatkan pembuangan besi

  34. Kelebihan Besi • Hemosiderosis, disebabkan oleh: - Pemberian preparat besi - Transfusi darah • Bronze diabetikum (gangguan Mucosal Block System ).

  35. Seng/Zinc • Berhubungan dengan fungsi enzim dan hormon; - karbonat anhidrase - laktat dehidrogenase - glutamat dehidrogenase - hormon insulin

  36. Seng/Zinc • Faktor pengikat Zn dari sekret pankreas membantu absorpsi Zn di usus. • Absorpsi Zn berkompetisi dengan Cu. • Ekskresi melalui ; - empedu untuk keluar dengan feses - keringat - urine

  37. Fluor (F) • Komponen jaringan keras, tu gigi. • Melindungi email gigi. • Fluor bersifat racun thd enolase (glikolisis) • Air PAM mengandung fluor 1 -2 ppm. • Defisiensi fluor --> karies dentis. • Kelebihan fluor --> fluorosis (mottled enamel) = cekungan-cekungan kuning kecoklatan pada email & dentin

  38. Sources • Beaudoin, D. Electrolytes and ion sensitive electrodes. PPT. 2003. • Hardjasasmita, P. 1993. Ikhtisar: biokimia dasar B. Balai Penerbit FKUI. Jakarta: 50 - 6. • Marieb, EN. Fluid, electrolyte, and acid-base balance. PPT. Pearson Education, Inc. 2004

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