Disorder of electrol Monday, September 28, 2020 Sodium - Total body Na+ 4000mmol ytes 12:35 PM © 70% freely exchangeable © 30% being complexes in bone 135-145mmol/I - Nat balance depends on ren Na excretion Renal regulation of sodium - Determined by intravascular Normal ECF Na concentration: al regulation of volume - Factors controlling renal handling of sodium ° ° system Glomerular filtration rate _ filtered Glomerular filtration rate Renin-angiotension-aldosterone Atrial natriuretic peptide (ANP) Determines amount of Na+ - Increased GFR © Greater amount of Na filtered © Greater flow through nephrons and reduces amount of Na reabsorbed ANP Causes Stimulated by distension of atria - Vasodilation of afferent and efferent arterioles © Increased GFR and renal blood flow - Suppress renin and aldosterone secretion - Direct inhi reabsorpti ibit Na ion in the collecting duct RAAS: reabsoprtion by Angiotensin II increases Na - Directly affecting renal tubules ~ Reduces GFR and renal blood flow (vasoconstriction) - Stimulates aldosterone secretion © Directly increases Nat reabsoprtion in the collecting ducts Hyponatremia - [Na+] < 135 Lethargy and confusion Muscle weakness Decreased deep tendon reflexes (DTRs) Diarrhea Respiratory problems - Evaluate © Hydration status = History Decreased excitability of cell membranes; brain does not function well with low levels of sodium Decreased excitability of cell membranes Decreased excitability of cell membranes Gi tract motility increases Late symptom; respiratory muscles become weak and can’t function properly Physical exminastion Plasma osmolality, urinary spot Na+ concentration Eutonic hyponatremia (Normal plasma osmolality) Hypertonic hyponatremia (high plasma osmolality) Hypotonic hyponatremia (low plasma osmolality) Adinical approach to hyponatraemia Pseudohyponatraemia High protein High lipid Nar loss Urinary sodium t ‘concentration Urinary osmolality amp ‘Treatment Normal saline Hypernatremia - Serum [Na+] > 145mmol/I Tachycardia Ory, sticky mucous membranes Thirst Changes in level of consciousness (LOC) Decreased heart contractility Seizure ‘Muscle twitching ‘Muscle weakness Decreased DIRs ‘Non-renal loss * Gastrointestinal tract *Skin Plasma urine and creatinine Pseudohyponat Hyperlipidemia, remia hyperproteinemia Hyperglycemia, mannitol, glycine Hypovolemia _Extrarenal (Urine [Na] <20mmol/L) - Gastrointestinal loss: Diarrhoea, vomiting ~ Skin loss: Excessive sweating Renal (Urine [Na] >20mmol/L) - Diuretic therapy, salt- losing nephritis, ‘Addison's disease Urine [Na] <20mmol/L - Acute water overload: Increased water intake PLUS: - Hypovolaemia: Haemorrhage, burns, drugs - Stress: Post- surgery, psychogenic - Endocrine: Hypothyroidism cortisol deficiency - Renal insufficiency Euvolemia Urine [Na] >20mmol/L - Chronic water overload: -SIADH - Drugs - Chronic renal failure - Endocrine: Hypothroidism, cortisol deficiency Urine [Na] <20mmol/L ~ Cardiac failure - Cirrhosis of liver - Nephrotic syndrome Hypervolemia (Oedematous states) j Hypo-osmatic hyponatraemia ‘Assess extracellular fluid (volume) status ‘jugular venous pressure ‘Postural blood pressure ‘= Presence of oedema Hyperglycaemia Mannitol Heart failure ver failure ‘Nephrotic syndrome Syndrome of inappropriate antidiuretic: hormone secretion Paychogenic Hypothyroid Onigs - Waterrestriction Heart is trying to pump what little fluid is left around the body to ensure adequate organ perfusion Decreased saliva Brain sending signals that fluids are needed to dilute the sodium Increased sodium interferes with brain function Late hypernatremia causes decreased excitability of muscles; high serum sodium decreases the movement of calcium into the cardiac cells, causing decreased contraction and cardiac output Early hypernatremia causes increased muscle excitability Early hypernatremia causes increased muscle excitability Late hypernatremia causes decreased muscle response Late hypernatremia causes decreased muscle response Causes of hypernatremia Pure water depletion Too old, too young or too sick to drink Access to water denied Esophageal obstruction Thirst center lesion Sodium and water _Extrarenal depletion (hypotonic - GIT: vomiting, fluid loss) diarrhea - Skin: excessive sweating Renal - Osmotic diuresis - Diabetes insipidus © Neurogenic ‘© Nephrogenic Salt gain (without proportional gain in water) latrogenic -1V hypertonic saline / NaBCO3 Salt ingestion Primary mineralocorticoid excess * Clinically patient is hypervolemic * Complications: © Pulmonary edema © Circulatory overload Hypernatremia " Ecry 2202809. Sait excess = salt ingestion = hypertonic NaCl “hypertonic Na bicarb Insufficient water intake | ECFV Hypotonic fluid deficit Pure water deficit | | Urine sodium Urine osmolality Urine osmolality 20 mEq/L < 10 mEq. < 700 mOsmit, > Extrarenal hypotonic Renal water loss Extrarenal water loss 700 mOsmit_ Renal hypotonic fluid loss fluid loss nephrogenic DI ‘or hypodipsia - diuretics ~ skin - contral DI - insensible loss ‘osmotic diuresis -GIT = primary hypodipsia = secondary hypodipsia Potassium - Human body contain 3000-3500mmol K+ in total Most are intracellular Predominant intracellular cation Only 2% total body K+ is located in the extracellular compartment Important for the maintenance of cell membrane polarization Majority of K+ excretion is in the kidney © Others: feces, sweat Homeostasis © K+ distribution between ECF and ICF is maintained by membrane associated Na+K+-ATPase pump © Factors affecting K+ transfer = Insulin (stimulate cellular uptake) Cathecolamines (stimulate cellular uptake) Hydrogen ion ©. Inalkalosis, H+ ion move across the cell membrane in exchange with K+ Aldosterone © Increases uptake of ECF K+ © Renal handling >90% K+ that pass through glomerulus - reabsorbed in proximal tubules Majority excretion occur in distal tubules Movements of K+ and H+ from tubular cells into lumen neutralize membrane potential generated by active reabsoprtion of Nat Factors affecting K+ excretion © Increased by aldosterone Hydrogen ion Increased K+ load Increase urine flow rate Diuretic, osmotic diuresis, increased Na load o o o Hypokalemia - Serum [k#] <3.5mmol/I rope oir * Alkalosis % Shallow Respirations % Irritability % Confusion, Drowsiness * Weakness, Fatigue % Arrhythmias - Irregular rate, Tachycardia » Lethargy % Thready Pulse % | Intestinal Motility Nausea Vomiting lleus - Causes Decreased Normal plasma Inadequate IV uptake (HCO3-],, therapy Chronic alcoholism Anorexia nervosa urinary [K+] <20 Transcellular shift Transient - Stress ~ Post carbohydrate meal Therapy - Insulin - Salbutamol ~ Vitamin B12 Familial periodic paralysis Barium toxicity Low plasma [HCO3-] - Acute diarrhea - Pancreatic fistula High plasma [HCO3-] - Laxative abuse -Villous adenoma of colon Low plasma [HCO3-] = Respiratory alkalosis ~ Renal tubular acidosis - Ureteral diversion High plasma [HCO3-] - Current diuretic therapy ~Mineralocortico id excess - Metabolic alkalosis, vomiting and chloride diarrhea Normal plasma [HCO3-], urinary [K+] <20 Extrarenal loss Urinary [K+] <20 Renal loss Urinary [K+] > 20mmol/! Misc Gentamicin (and other aminoglycosides) therapy Leukemia Osmotic diuresis Post-obstructive nephropathy Magnesium depletion Evaluation of hypokalaemia Hyperkalemia - Serum [K+] >5.0mmol/I vere Gcesan * Muscle Twitches —> Cramps —> Pa tT * Irritability & Anxiety *4ePr * EKG Changes * Dyerhythmias - Irregular Rhythm * Abdominal Cramping * Diarrhea - Laboratory © Exclude pseudohyperkalemia = Hemolysos, leucolysis, thrombocytosis © Acid-base status © Renal function test © Anion gap © Urinary spot [K+] - Causes Extrarenal Pseudohyperkal Hemolysis emia - Delayed separation of serum / prolonged tourniquet cause seepage of K+ from red cells Leucolysis Thrombocytosis - Release of K during clottig Increase intake to ECF Extragenous - oral /IV therapy Endogenous ~ Tissue necrosis (crush injury, burns, malignancy) Intravascular hemolysis Disturbed intracellular / extracellular distribution Acidemia Insulin deficiency / DM Drugs: ~ Digoxin toxicity - Succinylcholine Hypertonicity - Glucose = Sodium Hyperkalemic periodic paralysis Acute chronic Renal - Renal failure decreased renal potassium excretion Diuretics Prostaglandin inhibitors - Indomethacin - Ibuprofen Others: = Captopril and other ACE-I - heparin Drugs Mineralocortico id deficient syndromes Hypocorticolism, hypoaldosteronism (high renin) - Addison's disease, adrenal C21- hydroxylase defects Selective aldosterone deficiency (low renin) - Syndrome of hyporeninaemi c hypoaldosteron ism ~ Prostaglandin inhibition Selective aldosterone deficiency (high renin) - Heparin therapy = Corticosteroid methyl oxidase deficiency Mineralocortico id resistant syndromes High renin and aldosterone = Intersitial nephritis; obstructive nephropathy; amylodosis; systemic lupus erythematosus; sickle cell disease; pseudohypoald osteronism