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Renal 19 hyper/po K
Ryan: Hyper/hypokalemia
| Question | Answer |
|---|---|
| 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
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