Ryan: Hyper/hypokalemia
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| Most abundant cation in the body | Potassium
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| Most body potassium is... | Intracellular
~150 mEq/L
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| Extracellular K level | ~3.5-5 mEq/L
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| Small changes in K... | Can have big changes in the body
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| Kidney excretes ___% of K | 90%
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| Where is K reabsorbed? | Proximal nephron
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| Aldosterone adds K back into the... | Distal tubular fluid
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| Actions of Angiotension II | Stimulates aldosterone production
Vasoconstricts arterioles
Stimulates proximal tubule exchange
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| Actions of Aldosterone | Stimulates Na resorption and K excretion in late distal
Stimulates ATPase pumps in late tubule
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| After 4 hours how much K is int he urine? | 4%
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| Remainder of K is transported.. | Intracellularly until it can be excreted
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| K shifts INTO cells during ____ and OUT of cells in _____ | Alkalemia
Acidosis
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| Signs of Hypokalemia | Serum K <3.5 mEq/L
Hypotension
Cardiac arrest
Brady/tachycardia
Premature atrial or ventricular beats
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| Causes of hypokalemia | Decreased intake
Internal K shifts
Extra-renal losses
Renal losses
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| Causes of hypokalemia Decreased intake | Kidney can conserve 2-25 mEq/day
Normally get 40-129 mEq/day
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| Causes of hypokalemia Internal K shifts | Alkalosis (K in)
Catecholamines
Insulin admin
Hypokalemic periodic paralysis:
intermittent episodes of muscle weakness (acute shifts K in)
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| Causes of hypokalemia Extrarenal Losses | Diarrhea: most common
Major cause of M&M in developing world
Skin losses: sweat/burns
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| Causes of hypokalemia Renal K losses High plasma renin | Renal artery stenosis
Malignant HTN
Renin-secreting tumors
Cushing's syndrome
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| Causes of hypokalemia Renal K losses Low plasma renin | Aldosterone secreting adenoma
Bilateral adrenal hyperplasia
Mineralocorticoid excess
Liddle syndrome
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| 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
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| Causes of hypokalemia Renal K Losses Normotensive renal K wasting | Bartter syndrome
Gitelman sundrome
Diuretic use
Distal RTA
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| 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
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| Gitelman's Syndrome | Autosomal resessive (Dx later)
Mimic thiazide diuretics
Polyuria and cramps
Not have high urine Ca, typically have low serum Mg
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| Hypokalemia on EKG | ST segment depression
Decreased T wave
Prominent U
Prolongation of QRS
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| Hypokalemia on EKG (cont) | Increase in amplitude and duration of p-wave
Cardiac arrhythmias and AV block
No prolongation of the QTc
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| 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
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| Symptoms for hyperkalemia occur when... | Serum K >6.5-7 mEq/L
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| Earliest manifestations of hyperkalemia are... | Cardiac
Peaked T wave
Prolonged QT
Widened QRS complex
Disappearance of P
Sine waves
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| True/False ECG changes predict the severity of hyperkalemia | False
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| Other symptoms of hyperkalemia | Weakness
Parasthesia
Respiratory paralysis
Cardiac standstill
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| Causes of hyperkalemia | Pseudohyperkalemia
Extracellular shifts
Increased intake/production
Impaired renal excretion
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| Causes of hyperkalemia Pseudohyperkalemia | Traumatic hemolysis
Thrombocytosis
Marked leukocytosis
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| Causes of hyperkalemia Extracellular shifts | Acidosis
Beta adrenergic blockage
Insulin deficiency
Digoxin toxicity
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| Causes of hyperkalemia Increased intake/production | Increased K in diet or K containing drugs
Rhabdomyolysis or hemolysis
Tumor lysis syndrome
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| 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
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| Gordon syndrome | Familial hyperkalemic HTN
Autosomal dominant
Suppressed renin activity
Short stature, stiff spine, defomities of hands and feet
Responds well to thiazide
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| Things to check first | Is the value accurate?
Are there EKG changes?
Evidence of hemolysis on lab specimen
Recheck blood
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| Treatment of hyperkalemia | Stabilize myocardial membrane
Drive extracellular K into the cells
Removal of K from the body
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| Treatment Stabilize the myocardial membrane | Increase plasma K, results in decrease in membrane excitability
Ca antagonizes the cellular effects of hyperkalemia
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| 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
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| 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
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| 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
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| 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
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| Removal of K from the body Loop diuretics | Inhibiting NKCC in the Loop of Henle
Need renal fxn and volume to get filtrate
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| 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
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| True/False You can not give Kayexalate to anyone and everyone | True
There are several complications with the drug
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