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Renal 19 hyper/po K

Ryan: Hyper/hypokalemia

Most abundant cation in the body Potassium
Most body potassium is... Intracellular ~150 mEq/L
Extracellular K level ~3.5-5 mEq/L
Small changes in K... Can have big changes in the body
Kidney excretes ___% of K 90%
Where is K reabsorbed? Proximal nephron
Aldosterone adds K back into the... Distal tubular fluid
Actions of Angiotension II Stimulates aldosterone production Vasoconstricts arterioles Stimulates proximal tubule exchange
Actions of Aldosterone Stimulates Na resorption and K excretion in late distal Stimulates ATPase pumps in late tubule
After 4 hours how much K is int he urine? 4%
Remainder of K is transported.. Intracellularly until it can be excreted
K shifts INTO cells during ____ and OUT of cells in _____ Alkalemia Acidosis
Signs of Hypokalemia Serum K <3.5 mEq/L Hypotension Cardiac arrest Brady/tachycardia Premature atrial or ventricular beats
Causes of hypokalemia Decreased intake Internal K shifts Extra-renal losses Renal losses
Causes of hypokalemia Decreased intake Kidney can conserve 2-25 mEq/day Normally get 40-129 mEq/day
Causes of hypokalemia Internal K shifts Alkalosis (K in) Catecholamines Insulin admin Hypokalemic periodic paralysis: intermittent episodes of muscle weakness (acute shifts K in)
Causes of hypokalemia Extrarenal Losses Diarrhea: most common Major cause of M&M in developing world Skin losses: sweat/burns
Causes of hypokalemia Renal K losses High plasma renin Renal artery stenosis Malignant HTN Renin-secreting tumors Cushing's syndrome
Causes of hypokalemia Renal K losses Low plasma renin Aldosterone secreting adenoma Bilateral adrenal hyperplasia Mineralocorticoid excess Liddle syndrome
Liddle Syndrome Autosomal dominant HTN Plasma renin and aldosterone levels are suppressed Defect is in the regulation of salt absorption and NOT some unidentified mineralocorticoid
Causes of hypokalemia Renal K Losses Normotensive renal K wasting Bartter syndrome Gitelman sundrome Diuretic use Distal RTA
Bartter's Syndrome Dx in childhood Associated with growth and mental retaration Defect in impaired Na.Cl reabsorption in the look Findings similar to loops
Gitelman's Syndrome Autosomal resessive (Dx later) Mimic thiazide diuretics Polyuria and cramps Not have high urine Ca, typically have low serum Mg
Hypokalemia on EKG ST segment depression Decreased T wave Prominent U Prolongation of QRS
Hypokalemia on EKG (cont) Increase in amplitude and duration of p-wave Cardiac arrhythmias and AV block No prolongation of the QTc
Hypokalemia Tx Correct to 3.5 K=3 10 mEQ to raise by 0.1 K=2-3 20 mEq to raise by 0.1 K=1-2 30 mEq ro raise by 0.1
Symptoms for hyperkalemia occur when... Serum K >6.5-7 mEq/L
Earliest manifestations of hyperkalemia are... Cardiac Peaked T wave Prolonged QT Widened QRS complex Disappearance of P Sine waves
True/False ECG changes predict the severity of hyperkalemia False
Other symptoms of hyperkalemia Weakness Parasthesia Respiratory paralysis Cardiac standstill
Causes of hyperkalemia Pseudohyperkalemia Extracellular shifts Increased intake/production Impaired renal excretion
Causes of hyperkalemia Pseudohyperkalemia Traumatic hemolysis Thrombocytosis Marked leukocytosis
Causes of hyperkalemia Extracellular shifts Acidosis Beta adrenergic blockage Insulin deficiency Digoxin toxicity
Causes of hyperkalemia Increased intake/production Increased K in diet or K containing drugs Rhabdomyolysis or hemolysis Tumor lysis syndrome
Causes of hyperkalemia Impaired renal excretion Oligoanuric renal failure Problem with RAAS -↓ renin production -↓ conversion of AI to AII -↓ action of AII -Primary adrenal insufficiency
Gordon syndrome Familial hyperkalemic HTN Autosomal dominant Suppressed renin activity Short stature, stiff spine, defomities of hands and feet Responds well to thiazide
Things to check first Is the value accurate? Are there EKG changes? Evidence of hemolysis on lab specimen Recheck blood
Treatment of hyperkalemia Stabilize myocardial membrane Drive extracellular K into the cells Removal of K from the body
Treatment Stabilize the myocardial membrane Increase plasma K, results in decrease in membrane excitability Ca antagonizes the cellular effects of hyperkalemia
Types of Ca available Ca Gluconate given central or peripherally Ca Chloride Only given via central line High potential to cause local sclerosis and gangrene
Drive ECF K into the cells β2 Agonists Drives K into cells by increasing Na-K ATPase in skeletal muscle Effects in 20-30 min Must Monitor for palpatations/arrhythmia
Drive ECF K into the cells Insulin and Glucose Drives K in by increasing Na-K ATPase in skeletal muscle Effects in 30 min with peak in 60 Duration is several hours Monitor for hypoglygemia
Drive ECF K into the cells NaHCO3 Causes an alkalosis leading to K wasting Only works if hyperkalemia is secondary to severe met. acid Onset in few minutes, effects are not long lasting
Removal of K from the body Loop diuretics Inhibiting NKCC in the Loop of Henle Need renal fxn and volume to get filtrate
Removal of K from the body Sodium Polystyrene Sulfonate (Kayexalate) Exchanges Na for K and binds it in the gut K removed 8-12 hours after administration via stool Given PO/PR Monitor for GI necrosis/gangrene
True/False You can not give Kayexalate to anyone and everyone True There are several complications with the drug
Created by: bcriss