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

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Presentasi berjudul: "ELECTROLYTES DISTURBANCES Oleh: Dr. Husnil Kadri, M.Kes Bagian Biokimia Fakultas Kedokteran Universitas Andalas Padang."— Transcript presentasi:

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

5 Hypernatremia Sodium Water Symptoms  dehydration  increased thirst  fever  tremors  altered mental status  lethargy  seizures  coma and/or Possible causes  extrarenal loss (diarrhea, skin losses)  renal losses (diuretics therapy and  water intake)  impaired secretion or ability to respond to ADH  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 Water Symptom  weakness  fatigue  anorexia  nausea  arrhythmia  possible cardiac arrest and/or Possible Causes  extra -> intracellular shifts (alkalosis, diuretics)  extrarenal losses (excessive diarrhea, vomiting)  renal losses (renal disease, polyuria)  hyperaldosteronism

8 Hyperkalemia PotassiumWater Symptoms  muscular weakness  tingling  numbness  confusion  cardiac arrhythmias  possible cardiac arrest and/or 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 (Ca 2+ ) 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 = Ca 2+ ionized (45%) + Ca protein-bound (45%) + Ca complexed to anions (10%)

10 Magnesium (Mg 2+ ) Key role (s): enzyme cofactor; calcium and bone homeostasis Regulation: Kidney  PTH,  serum Mg 2+ 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 (HCO 3 - ) 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 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

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

15 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

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

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; Fe 3+ -transferin Cu 2+ -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 Berhubungan dgn 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 Fe 3+ (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 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 & dentin

38 38Sources 1.Beaudoin, D. Electrolytes and ion sensitive electrodes. PPT Hardjasasmita, P Ikhtisar: biokimia dasar B. Balai Penerbit FKUI. Jakarta: Marieb, EN. Fluid, electrolyte, and acid- base balance. PPT. Pearson Education, Inc. 2004


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