CPY-L7 Potassium Disorders PDF

14 CPY-L7 Potassium disorders Clinical features...

14 CPY-L7 Potassium disorders Clinical features d --- T Potassium disorder Clinical features Hypokalaemia Asymptomatic when mild Muscle weakness bexcitability of muscle ­risk of arrhythmia Hyperkalaemia Asymptomatic when mild Muscle weakness, paralysis epolarization block) X repolarize ---I Progressive abnormalities in ECG Approach to hypokalaemia Hypokalaemia K < 3.5 - kt Transcellular shift x6 True deficit ATPase 1 :: energy 1) Nat , in Insulin ↑ Nat/K + out Urine K - Adrenergic ↑ Nat/k ATPase (Estphrase :Pet = Theophylline (drug for asthma Renal loss Extrarenal loss ↑ E Renalty Thyrotoxic periodic paralysis TH ↑ Nat/K ATPase = hypo lit : - Urine K > 40 Urine K < 20 Anabolic surge (e.g. after B12 ↑ Nat/17 ATPase insulin - + losing Cretuxfromthenhousetories ↑ demands supp in megaloblastic anaemia) energy ABG blood arterial gas ?? M. acidosis: diarrhoea, laxative (Mg (OH) c) G M. alkalosis: Hx vomiting, Hx lose of gastric adid (Hsee ) & KT C1-JlossOC + , diuretics excreteNat Yaldosterone of Ls for Ho retention - Normal acid-base: poor intake Mg ↓ Diarrhea would also result in -omcrenal outer medullary k+ ( Normal acid-base Metabolic alkalosis Metabolic acidosis Sodium and chloride loss, but due ↓ GM HypoMg renal tubular acidosis RTA Crenal X reabsorb HCOs & excrete H ] to volume contraction, it activates + : : ROMK X H / K antiporter + + , aldosterone E Cisplatin (Chemotherapeutic agen a Drug: AmphoB, CAI the RAAS resulting in retention of amphotericin B carbonic anhydrase LnephrotoxicityMy reabsorption hypogoSo Nall inhibitor sodium in the expense of Saline responsive Saline resistant CA : ↑ reabsorption of HCO3 & Nat potassium U[Cl] < 10 U[Cl] > 20 Vomiting Gloss H +, Cli, K+ (NS can correct 11- but not kt) BP HTVHCO2K ↓ via renal compensation ↑ BP Normal BP 1 hyperald Conn's Syndrome. Mineralocorticoid excess < 2 hyperald. - RAAS Diuretics Check renin + aldosterone IRAAS] Channelopathy: Gitelman, Bartter 10 hyperald : ↓ renin channel in renal tube dysfunctional :on Renin Aldosterone Cause - RAAS - Haldosterone ↑ ↑ Tumour (renin, ACTH) RAAS :retan ↑ Nat reabsorption Se to ↓ ↓ Liddle syndrome (genetic disorder) reabsorption Licorice/ 11β-HSD deficiency cortisol cortisone - 3 AME inhibit dehydrogenasei ↑ cortisone ↓ ↑ CAH 11p-HSD mahydrosteroid - aldosterome los adrenal congenital hyperplasia Specific diseases ① ② Thyrotoxic periodic paralysis Common presentation: a Chinese young male cannot stand up from chair after a heavy meal or exercise Paralysis transient & self-limiting Treatment: K supplement, propranolol (to blunt Na-K ATPase), definitive anti-thyroid treatment Monitor: rebound hyperK, respiratory muscle involvement Hypomagnesemia ­renal excretion of K, ¯secretion and action of PTH [L12] Correct Mg before correcting K  15 Vomiting/ NG suction e. g. Toxic substance removal Contain Na 60mmol/L, K 30, Cl 120; pH 1.6 ① Generation phase: loss of H+ & Cl- à bicarbonaturia à ↑K+ (&Na+) loss – chloride-responsive alkalosis Maintenance phase: hypovolaemia-induced RAAS à paradoxical aciduria + kaliuresis + inappropriate HCO3 ② retention – contraction alkalosis NNat-H : aldosterone + exchange Licorice poisoning Glycyrrhetinic acids inhibits 11β-HSD2 (responsible for cortisol to cortisone) ↑Cortisol activates aldosterone receptors àapparent mineralocorticoid syndrome (AME) Approach to hyperkalaemia Hyperkalaemia K > 5.0 Pseudohyperkalaemia Transcellular release TTKG Massive cell lysis Insulinopenia (DKA) ↓ insulin HyperK periodic paralysis TTKG > 10 TTKG < 6 Drug: suxamethonium, digoxin CHF) NMBA ↑ depolarization : D ↓ WalkAiPase pump Normal K excretion K retention in cell membrane Excessive intake ↓ MC: check renin + aldosterone (decrease) Iatrogenic Drug: ACEI, NSAID, K-sparing ↓ > - aldosterone (inhibit K+ excretion) function normal renal diuretics prostagland coX : ↑ blood flow XNat ↓ : in , K excretion + Renal: AKI, CKD ↓ GFR GK+ excretion Trans-tubular potassium gradient (TTKG) assessabilityofrena - kalemical ( % ) +,- $$%& = ∗ ) % ( +,- cortical collecting tube Caldosterone ( Surrogate marker of mineralocorticoid activity at CCT o Urine-to-plasma osmolality ratio adjusts for the degree of medullary water reabsorption à TTKG estimates [K+] at a point where the fluid was last isotonic to plasma, i.e. CCT Only valid if: UOSm > 300 & U[Na] > 25 Normal: 6 – 8 Specific diseases Pseudohyperkalaemia Ex-vivo release from cells, e.g. overnight sample, traumatic damage RBC venepuncture, chilled sample (cold inhibition of Na/K ATPase), WBCM yell release It thrombocytosis (K+ release from platelet granules), leucocytosis (leukaemic cells more fragile à plasma K, but note reverse pseudohyperkalaemia) clotting process release It Drip arms supply K+1, body fluid K**, leak into blood CBC NaF potassium oxalate + anticoagulant > - Contamination during blood taking: EDTA tube (purple), fluoride tube (grey) more fragile chronic lymphocytic leukemia - Reverse pseudohyperkalaemia (plasma K > serum K): in CLL, neoplastic WBC membranes sensitive to heparin (anticoagulant used in plasma sample; plasma = serum + clotting factors) l of We  it after chemotherapy /radiation 16 Tumour lysis syndrome (TLS) Massive lysis of high burden tumour, e.g. lymphoma, leukaemia, metastatic CA Laboratory TLS: ≥2 of the following D-3 to D7 o HyperK cell break down o Hyperuricaemia curic acid 1) nucleic acid purine uric acid + -> o Hyperphosphataemia (POp3-1) phosphate containing molecule breakdown - secondary o Hypocalcaemia (complex depletion by phosphate) Clinical TLS = Lab TLS + ↑ Cr/ seizure/ arrhythmia/ sudden death Treatment: hydration, allopurinol, correct electrolytes & arrhythmia, dialysis uric acid ↑↑ Xanthine Oxidase A Crenal perfusion) inhibitorrid production Rhabdomyolysis Rapid lysis of skeletal muscle cells Features: o ↑K, ↑urate, ↑phosphate, ↓Ca2+ (~TLS) o Myoglobinuria: dark red urine without RBC Or binding protein in skeletal muscle myoglobin : o ↑muscle enzymes: CK, AST o AKI: free radical Fe release, myoglobin cast formation, urate cast, ischaemia Treatment: hydration, correct electrolyte, forced alkaline diuresis (to clear myoglobin) add NaHLOz to urine & make in alkaline Genetic channelopathy [L11] Pathophysiology Presentations Bartter Defect at TAL: NKCC2 (I), ROMK2 (II), etc Metabolic alkalosis RAAS *: Texcrete Hakt reabsorption of Nat , K+, 21- HypoK Gitelman Defective NCCT (Na-Cl cotransporter) at DCT Metabolic alkalosis HypoK Gordon (PHA II) pseudo hypoaldosteronism type I Overactive NCCT at DCT - Metabolic acidosis Nat Cl ↑ HyperK - , Pseudohypoaldosteronism (PHA I) Defective response to aldosterone at CCT Metabolic acidosis HyperK Liddle Overactive ENaC at CCT Metabolic alkalosis HypoK epithelial Nat channel ↑ Nat reabsorb Diuretics ↑H + * excrete HypoK: thiazides, loop diuretics o Thiazides: hyperCa block NCCT G NatCl reabsorption o Loop diuretics: hypoCa leg furosemide) block NKCC2 &Nat (1) 4. , + reabsorption My Ca't reabsorption HyperK: potassium-sparing diuretics o Aldosterone antagonist: spironolactone, eplerenone o ENaC blockers: amiloride, triamterene o (ACEI/ ARB)