electrolytes disturbances

ELECTROLYTES ELECTROLYTES DISTURBANCES DISTURBANCES

Oleh:Oleh:

Dr. Husnil Kadri, M.KesDr. Husnil Kadri, M.Kes

Bagian Biokimia Fakultas KedokteranBagian Biokimia Fakultas Kedokteran

Universitas AndalasUniversitas Andalas

PadangPadang

Change in [Electrolyte] Can Occur By…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

Sodium (NaSodium (Na++))

Key role (s): plasma osmolality and water balance

Regulation: ThirstKidneyNa+/K+ ATPase pumpsNa+/H+ pumpsBlood 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 disordersHyponatremiaHypernatremia

HyponatremiaHyponatremia

Sodium Water

Symptomsnausea/vomitinggeneralized weaknessmental confusionheadachelethargypossible coma if too low

and/or

Possible causes excessive renal loss of saltexcessive renal loss of salt

(aldosterone deficiency, kidney disease, diuretics)excessive ADH secretionexcessive ADH secretion (SIADH)water overloadwater overload

(congestive heart failure, cirrhosis, renal disease)

HypernatremiaHypernatremia

Sodium Water

Symptomsdehydrationincreased thirstfevertremorsaltered mental statuslethargyseizurescoma

and/or

Possible causesextrarenal lossextrarenal loss

(diarrhea, skin losses)renal lossesrenal losses

(diuretics therapy and water intake)impaired secretion or ability to respond to ADHimpaired secretion or ability to respond to ADH

(diabetes insipidus)excessive water lossexcessive water losshyperaldosteronismhyperaldosteronism

Potassium (KPotassium (K++))

Key role (s): Regulate cardiac contraction and rhythm, muscle contraction

Regulation: KidneysNa+/K+ -ATPase pumpAcid/Base balance (i.e., K+/H+ pumps) Aldosterone results in K+ excretion and shift

extracellular to intracellular.

Clinical: HypokalemiaHyperkalemia

HypokalemiaHypokalemia

Potassium Water

Symptomweaknessfatigueanorexianauseaarrhythmiapossible cardiac arrest

and/or

Possible Causesextra -> intracellular shiftsextra -> intracellular shifts

(alkalosis, diuretics) extrarenal lossesextrarenal losses

(excessive diarrhea, vomiting)renal lossesrenal losses

(renal disease, polyuria)hyperaldosteronismhyperaldosteronism

HyperkalemiaHyperkalemia

Potassium Water

Symptomsmuscular weaknesstinglingnumbnessconfusioncardiac arrhythmiaspossible cardiac arrest

and/or

Possible Causesintra -> extracellular shiftsintra -> extracellular shifts

(acidosis)renal failurerenal failure

(K+ secretion deficiency)adrenal failureadrenal failure

(hypoaldosteronism)leukemialeukemiapseudohyperkalemiapseudohyperkalemia

(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].

Calcium (CaCalcium (Ca2+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 homeostasisCalcitonin – 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%)

Magnesium (MgMagnesium (Mg2+2+))

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

Chloride (ClChloride (Cl--))

Key role (s): Maintains osmolality, blood volume, electric neutrality Regulation: kidneys (reabsorbed /w Na+ in the proximal tubules),

aldosterone

Clinical: Hypochloremia – similar causes ashyponatremia, prolonged vomiting, high [bicarbonate] associated metabolic alkalosis

Hyperchloremia – similar causes as hypernatremia, dehydration, low [bicarbonate] associated with prolonged diarrhea or metabolic acidosis

Bicarbonate (HCOBicarbonate (HCO33--))

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

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Disorders of Water Balance: Disorders of Water Balance: DehydrationDehydration

• 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

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Disorders of Water Balance: Disorders of Water Balance: DehydrationDehydration

Excessive loss of H2O from ECF

1 2 3ECF osmotic pressure rises

Cells lose H2O to ECF by osmosis; cells shrink

(a) Mechanism of dehydration

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• 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: Disorders of Water Balance: Hypotonic HydrationHypotonic Hydration

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Disorders of Water Balance: Disorders of Water Balance: Hypotonic HydrationHypotonic Hydration

Excessive H2O enters the ECF

1 2 ECF osmotic pressure falls

3 H2O moves into cells by osmosis; cells swell

(b) Mechanism of hypotonic hydration

Protein Imbalances

• Plasma proteins(especially albumin) are important determinants of plasma volume

• Hyperproteinemia is rare– Occurs with dehydration-induced

hemoconcentration

Hypoproteinemia

• Caused by – Anorexia– Malnutrition– Starvation– Fad dieting– Poorly balanced vegetarian diets

Hypoproteinemia

• Poor absorption d/t GI malabsorptive diseases

• Inflammation → protein can shift out of intravascular space

• Hemorrhage

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)

BioavailabilitasBioavailabilitas

• 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

Kalsium & FosforKalsium & 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

Interaksi yang MenghambatInteraksi yang Menghambat

• Beras mengandung asam fitat (P) sehingga mengikat Ca membentuk Ca-fitat.

• Sayuran & buah yang mengandung asam oksalat juga akan menghambat absorpsi Ca.

Fungsi PFungsi P

• Ikatan fosfat berenergi tinggi ATP, ADP, kreatin-P, PEP, dll.

• Komponen membran sel fosfolipid

• Membentuk hidroksiapatit pada tulang dan gigi

Defisiensi CaDefisiensi Ca

• Rickets pada anak-anak

• Osteomalacia (osteoporosis) pada dewasa

• Tetani / kejang

• Postmenopause (estrogen rendah)

Defisiensi PDefisiensi P

• Gangguan absorpsi di usus

• Ekskresi berlebihan melalui ginjal

• Sindrom Milkman

• Sindrom de Toni Fanconi

Penyakit yang BerhubunganPenyakit yang Berhubungandgn Na & Kdgn Na & K

• Penyakit Addison

- hipoaktif kelenjar kortek adrenal

- hiponatremia & hiperkalemia

• Penyakit Cushing

- hiperaktif kelenjar kortek adrenal

- hipernatremia & hipokalemia

Konsumsi NaCl berlebihanKonsumsi NaCl berlebihan

• Hipertensi

• Diabetes

• Gangguan ginjal kronik

BesiBesi

• Komponen penting pada:

hemoglobin, sitokrom, katalase,peroksidase

• Terdapat dalam makanan terutama daging sebagai ion Fe3+ (Ferri).

• Pengaturan absorpsi Fe dikenal sebagai mucosal block system

Mucosal Block SystemMucosal 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.

Mucosal Block SystemMucosal 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.

Mucosal Block SystemMucosal 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.

Defisiensi BesiDefisiensi Besi

• Anemia mikrositer hipokrom,

disebabkan oleh:

- infeksi cacing tambang

- perdarahan

• Pil KB meningkatkan pembuangan besi

Kelebihan BesiKelebihan Besi

• Hemosiderosis,

disebabkan oleh:

- Pemberian preparat besi

- Transfusi darah

• Bronze diabetikum (gangguan Mucosal Block System ).

Seng/ZincSeng/Zinc

• Berhubungan dengan fungsi enzim dan hormon;

- karbonat anhidrase

- laktat dehidrogenase

- glutamat dehidrogenase

- hormon insulin

Seng/ZincSeng/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

Fluor (F)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

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SourcesSources

1. Beaudoin, D. Electrolytes and ion sensitive electrodes. PPT. 2003.

2. Hardjasasmita, P. 1993. Ikhtisar: biokimia dasar B. Balai Penerbit FKUI. Jakarta: 50 - 6.

3. Marieb, EN. Fluid, electrolyte, and acid-base balance. PPT. Pearson Education, Inc. 2004