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.
Causes of AKI: postrenal
caused by acute obstruction of urinary tract.
stones, blood clots, papillary necrotic tissue, urtehral disease, prostate disease. Bladder disease: cancer, neurogenic bladder.
SSx of AKI
retention of nitrogenous waste products:
retention of nitrogenous waste products: NVD, foul taste, hiccup, dry crusted mouth, drowsiness, ALOC, neuropathy, pericardititis, GI bleed, coma
SSx of AKI
Retention of salt and water
pulm edema, peripheral edema, ascites, pleural effusion.
SSx of AKI
Retention of K +
weakness, ecg change: peaked and narrow T waves. decreased amplitude and eventual loss of P wave. prolonged PR interval. AV block, widening of QRS. ventricular fib, asystole.
SSx of AKI
retention of acid
Kussmaul resp, hyperreflexia, hypotension.
treatment of AKI
preliminary measures
prerenal: correct prerenal factors: optimize volume status and cardiac performace using fluids that will stay in the plasma
renal: adress reversible renal causes
postrenal: foley catheter, steting, nephrostomy, remove stones or strictures.
treatment of AKI
complications
fluid overload: nacl restriction, high dose loop diuretics. adjust dosage of medications cleared by kidneys. definitive tx depends of etiology. renal transplant IS NOT a therapy for AKI:
Diff diagnosis in proteinuria
nephritic or nephrotic syndrome, enal failure, DM, amyloidosis, increased BP, intersititial nephritis, heavy metals, multiple myeloma, pregnancy.
Indications for renal replacement therapy
oliguria(anuria, hyperammoniemia, hyperkalemia, severe acidemia or azotemia, plum edema, uremic complications, severe electrolyte abnormalitoes, rhabdomyolysis, anasarca.
indication for dialysis (?)’
Ccr 10,0 mg/dl. relative indication: ccr8 mg/d + accompanied SSx: chf/pulm edema, bleeding tendency, drug resistant hyper K+, uremic pericardititis, neurological symp, drug resistant metabolic acidosis, drug-resistant N and V
Chronic kidney disease
progressive and irreversible loss of kidney function. GFR 3 months +- kidney pathology seen on biopsy or decreased renal size
Chronic kidney disease: causes
glomerulonephritis, multisystem disease: DM, hypertensive nephropathy, acute pyelonephritis/tubulointersititial. Polycystic kidney disease, idiopathic, drugs, CT disease:
clinical features of CKD
volume overload and htn, electrolyte and acid base balance disoders: metabolic acidosis, uremia
Metabolic acidosis
deficient bicarbonate. (dec CO2, dec HCO3-, Dec pH,
Causes: loss of HCO3 through diarrhea or renal dysfunction, accumulation of acids (latic acid or ketones), failure of kidneys to excrete H+,
symptoms
Metabolic acidosis
headache, lethargy, N/V, diarrhea, coma, death
Metabolic acidosis
compensation and treatment
increased ventilation, renal excretion of h+ ions, k + exchanges with excess H+ in ECF –> hyperkalemia.
Treatment: Iv lactate solution.
Metabolic alkalosis
Bicarbonate excess. Inc CO2, inc HCO3-, inc pH.
Metabolic alkalosis
causes
excessive vomiting = loss of stomach acid, excessive use of alkaline drugs, certain diuretics, endocrine disorders, heavy ingestion antacides, severe dehydration.
Metabolic alkalosis
symptoms
respiration slow and shallow, hyperactive reflexes: tetany, often related to depletion of electrolytes, atrial tachycardia, dysarrthmias.
Metabolic alkalosis
treatment
electrolytes to replace those lost ,IV cholride containing solution, treat underlying disorder
Renal cell carcinoma
Presentation: hematuria, mass in abdomen, flank pain, Other: weight loss, fever, night sweats, malaise, htn, hypercalcemia.
DX of RCC
usg, ct, mri,
treatment RCC
surgical resection. Advanced stages: HD IL2, IFN-alpha, bavacizumab, temsirolimus
pyelonephritis def
is an inflammation of the kidney tissue, calyces, and renal pelvis. It is commonly caused by bacterial infection that has spread up the urinary tract or travelled through the bloodstream to the kidneys
pyelonephritis: clinical picture
fever, dysuria, tachycardia, abdominal pain radiating to the back, nausea, and tenderness at the costovertebral angle on the affected side. Pyelonephritis that has progressed to urosepsis may be accompanied by signs of septic shock, including rapid breathing, decreased blood pressure, violent shivering, and occasionally delirium.
pyelonephritis: TX
Antibiotics, fluids,
Hypercalcemia
HyperPTH and maliganacy account for 90 %. lithium use,
symptoms: fatigue, depression, confusion, anorexia, N/V, pancreatitis.
