Electrolytes and ABG Flashcards
Factors increasing renal K + loss
hyperkalemia, thiazides and loop diuretic, increased aldosterone (increased Na reabsorption and K+ excretion). Metabolic alkalosis, hypomagnesemia, increased non-reabsorbable anions in tubule lumen.
Hypokalemia def:
K+
SSx of hypokalemia
usually asymp if mild. N/V, fatigue, generalized weakness, myalgia, muscle cramps, constipation. if severe: arrhythmias, muscle necrosis, rarely paralysis.
ECG changes in hypokalemia
U wave (low amplitude wave following a T wave), depressed ST, prolonged QT intervall. inverted T wave.
Causes of hypokalemia
Decreased intake, increased loss (renal, GI), redistribution into cells (metabolic alkalosis, insulin, catecholamines, b2- agonist (ventoline) tocolytic agents, uptake into newly forming cells)
treatment of hypokalemia
treat underlying cause, K+IV(KCl) or oral, K-sparing diuretics (spironolactone), restore Mg2+ if necessary,
NB k + replacement in diabetics, elderly, and patients with decreased renal function.
Hyperkalemia def:
> 5,0 mEq/L.
SSx in hyperkalemia
usually asymptomatic. may develop nausea, palpitations, muscle weakness, muscle stiffness, paresthesias, areflexia, ascending paralysis, hypoventilation.
ECG changes in hyperkalemia
peaked and narrow T waves. decreased amplitude and eventual loss of P wave. prolonged PR interval. AV block, widening of QRS. ventricular fib, asystole.
causes of hyperkalemia
sample hemolysis (MC), increased intake, cellular release (intravascular hemolysis, rhabdomyolysis, insulin deficiency, met acidosis, TLS, drugs: b-blocker, digitalis, succinylcholine), decreased excretion.
treatment of hyperkalemia
treat underlysing cause, shift K+ into cells: insulin, b-agonist, NaHCO3´:, calcium gluconate: protect the heart, no effect on serum K+. Enhance K+ removal from body: furosemide, dialysis, kayexalate
Nephrotic syndrome: def: and clinical
syndrome caused by different diseases (constalation of symptoms). Clinically characterized by heavy proteinuria (>3,5g/d) hypoalbuminemia, edema, hyperlipidemia, hypercoagulable state (due to loss of antothrombin III and protein C and S)
Causes of nephrotic syndrome
Minimal change disease (MCD), FSGS, membranoproliferative glomerulonephritis, membranous glomerulopathy. Can also be secondary to another disease or drug.
treatment of nephrotic syndrome
steroid, and treat underlying cause if due to secondary causes.
acute kidney injury (AKI) def
Abrupt decline in renal function leading to increased nitrogenous waste products normally excreted by the kidneys
clinical features of AKI
azotemia (increased BUN and Cr), abnormal urine volume (anuria, oliguria, polyuria)
causes of AKI prerenal
caused by acute renal hypoperfusion. Intravscular volume depletion: bleeding, GI loss, renal loss, skin loss. decreased CO: CHF. Renal vasoconstriction: liver disease, sepsis, hyperca2+. Renal artery stenosis
Causes of AKI renal/intrinsic
caused by an acute disease of renal parenchyma. Vascular: vasculitis, malignant HTN, thrombotic microangiopathy, cholesterol emboli, large vessel disease. Glomerular: GN, Interstitial: AIN, Tubular: ATN MC: ischemic or toxic.