Electrolytes and ABG Flashcards

1
Q

Factors increasing renal K + loss

A

hyperkalemia, thiazides and loop diuretic, increased aldosterone (increased Na reabsorption and K+ excretion). Metabolic alkalosis, hypomagnesemia, increased non-reabsorbable anions in tubule lumen.

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2
Q

Hypokalemia def:

A

K+

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3
Q

SSx of hypokalemia

A

usually asymp if mild. N/V, fatigue, generalized weakness, myalgia, muscle cramps, constipation. if severe: arrhythmias, muscle necrosis, rarely paralysis.

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4
Q

ECG changes in hypokalemia

A

U wave (low amplitude wave following a T wave), depressed ST, prolonged QT intervall. inverted T wave.

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5
Q

Causes of hypokalemia

A

Decreased intake, increased loss (renal, GI), redistribution into cells (metabolic alkalosis, insulin, catecholamines, b2- agonist (ventoline) tocolytic agents, uptake into newly forming cells)

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6
Q

treatment of hypokalemia

A

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.

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7
Q

Hyperkalemia def:

A

> 5,0 mEq/L.

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8
Q

SSx in hyperkalemia

A

usually asymptomatic. may develop nausea, palpitations, muscle weakness, muscle stiffness, paresthesias, areflexia, ascending paralysis, hypoventilation.

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9
Q

ECG changes in hyperkalemia

A

peaked and narrow T waves. decreased amplitude and eventual loss of P wave. prolonged PR interval. AV block, widening of QRS. ventricular fib, asystole.

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10
Q

causes of hyperkalemia

A

sample hemolysis (MC), increased intake, cellular release (intravascular hemolysis, rhabdomyolysis, insulin deficiency, met acidosis, TLS, drugs: b-blocker, digitalis, succinylcholine), decreased excretion.

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11
Q

treatment of hyperkalemia

A

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

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12
Q

Nephrotic syndrome: def: and clinical

A

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)

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13
Q

Causes of nephrotic syndrome

A

Minimal change disease (MCD), FSGS, membranoproliferative glomerulonephritis, membranous glomerulopathy. Can also be secondary to another disease or drug.

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14
Q

treatment of nephrotic syndrome

A

steroid, and treat underlying cause if due to secondary causes.

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15
Q

acute kidney injury (AKI) def

A

Abrupt decline in renal function leading to increased nitrogenous waste products normally excreted by the kidneys

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16
Q

clinical features of AKI

A

azotemia (increased BUN and Cr), abnormal urine volume (anuria, oliguria, polyuria)

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17
Q

causes of AKI prerenal

A

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

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18
Q

Causes of AKI renal/intrinsic

A

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.

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19
Q

Causes of AKI: postrenal

A

caused by acute obstruction of urinary tract.
stones, blood clots, papillary necrotic tissue, urtehral disease, prostate disease. Bladder disease: cancer, neurogenic bladder.

20
Q

SSx of AKI

retention of nitrogenous waste products:

A

retention of nitrogenous waste products: NVD, foul taste, hiccup, dry crusted mouth, drowsiness, ALOC, neuropathy, pericardititis, GI bleed, coma

21
Q

SSx of AKI

Retention of salt and water

A

pulm edema, peripheral edema, ascites, pleural effusion.

22
Q

SSx of AKI

Retention of K +

A

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.

23
Q

SSx of AKI

retention of acid

A

Kussmaul resp, hyperreflexia, hypotension.

24
Q

treatment of AKI

preliminary measures

A

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.

25
Q

treatment of AKI

complications

A

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:

26
Q

Diff diagnosis in proteinuria

A

nephritic or nephrotic syndrome, enal failure, DM, amyloidosis, increased BP, intersititial nephritis, heavy metals, multiple myeloma, pregnancy.

27
Q

Indications for renal replacement therapy

A

oliguria(anuria, hyperammoniemia, hyperkalemia, severe acidemia or azotemia, plum edema, uremic complications, severe electrolyte abnormalitoes, rhabdomyolysis, anasarca.

28
Q

indication for dialysis (?)’

A

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

29
Q

Chronic kidney disease

A

progressive and irreversible loss of kidney function. GFR 3 months +- kidney pathology seen on biopsy or decreased renal size

30
Q

Chronic kidney disease: causes

A

glomerulonephritis, multisystem disease: DM, hypertensive nephropathy, acute pyelonephritis/tubulointersititial. Polycystic kidney disease, idiopathic, drugs, CT disease:

31
Q

clinical features of CKD

A

volume overload and htn, electrolyte and acid base balance disoders: metabolic acidosis, uremia

32
Q

Metabolic acidosis

A

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+,

33
Q

symptoms

Metabolic acidosis

A

headache, lethargy, N/V, diarrhea, coma, death

34
Q

Metabolic acidosis

compensation and treatment

A

increased ventilation, renal excretion of h+ ions, k + exchanges with excess H+ in ECF –> hyperkalemia.
Treatment: Iv lactate solution.

35
Q

Metabolic alkalosis

A

Bicarbonate excess. Inc CO2, inc HCO3-, inc pH.

36
Q

Metabolic alkalosis

causes

A

excessive vomiting = loss of stomach acid, excessive use of alkaline drugs, certain diuretics, endocrine disorders, heavy ingestion antacides, severe dehydration.

37
Q

Metabolic alkalosis

symptoms

A

respiration slow and shallow, hyperactive reflexes: tetany, often related to depletion of electrolytes, atrial tachycardia, dysarrthmias.

38
Q

Metabolic alkalosis

treatment

A

electrolytes to replace those lost ,IV cholride containing solution, treat underlying disorder

39
Q

Renal cell carcinoma

A

Presentation: hematuria, mass in abdomen, flank pain, Other: weight loss, fever, night sweats, malaise, htn, hypercalcemia.

40
Q

DX of RCC

A

usg, ct, mri,

41
Q

treatment RCC

A

surgical resection. Advanced stages: HD IL2, IFN-alpha, bavacizumab, temsirolimus

42
Q

pyelonephritis def

A

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

43
Q

pyelonephritis: clinical picture

A

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.

44
Q

pyelonephritis: TX

A

Antibiotics, fluids,

45
Q

Hypercalcemia

A

HyperPTH and maliganacy account for 90 %. lithium use,

symptoms: fatigue, depression, confusion, anorexia, N/V, pancreatitis.