B5.058 Prework 1 Electrolyte Abrnormalities Flashcards

1
Q

sources of electrolyte disbalances

A

glomerulus
tubules
mechanisms of regulation (RAA, ADH, ANP)

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2
Q

alterations in filtration with electrolytes and water accumulation

A

glomerular defects

-renal insufficiency from any origin

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3
Q

alteration in reabsorption and secretion of electrolytes and water

A

tubular defects

  1. acquired- injury or inflammatory processes
  2. genetic- mutation of renal transport systems in both dominant and recessive manner
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4
Q

precursors of renal insufficiency/glomerular damage

A
DM
hypertensive nephropathy
glomerulonephritis
renal artery stenosis
polycystic kidney disease
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5
Q

symptoms of glomerular damage

A

electrolyte retention

  • hypernatremia
  • hyperkalemia
  • calcium/phosphate imbalance
  • acidosis
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6
Q

reasons for acquired tubular injury

A

ischemic (interrupted blood flow)
toxic (drugs, dyes, gentamicin, heavy metals)
inflammatory

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7
Q

result of acute/chronic renal tubular injury

A

inability to concentrate urine
salt wasting
metabolic acidosis

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8
Q

variants of Bartters

A
  1. neonatal (NKCC)
  2. neonatal (ROMK1)
  3. classic (mutated Cl- channel)
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9
Q

pathophysiology of Bartter’s

A

malfunctions of NKCC, ROMK1, and Cl channels > solute diuresis and wasting of Na+, K+, and Cl-
malfunction of countercurrent mechanisms > polyuria and polydipsia, inability to concentrate urine
malfunction of juxtaglomerular apparatus > hyperreninemia, high aldosterone, alkalosis

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10
Q

why do you get alkalosis in Bartters

A

high aldosterone stimulates H+ secretion in the collecting ducts/distal tubules

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11
Q

clinical presentation of Bartters

A
tendency to volume depletion
excitability alterations
electrolyte disbalance
renin up regulation
pH problems
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12
Q

electrolyte disbalances in Bartters

A
hyponatremia
hypokalemia
hypochloremia
ECF volume contraction
hypercalciuria
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13
Q

what causes hypercalciuria in Bartters

A

reduced reabsorption of Cl-, Ca2+ and Mg2+ absorption is reduced

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14
Q

Bartters prognosis

A

non curable
variable outcome depending on mutation
significant morbidity and mortality

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15
Q

Bartters complications

A

cardiac arrhythmia and sudden death due to electrolyte disbalance
failure to thrive and developmental delay

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16
Q

diagnosis of Bartters

A

blood analysis of lytes, renin, and aldosterone

urine tests for lytes and PGE2

17
Q

why is PGE2 elevated in Bartters

A

intermediate for products of juxtaglomerular apparatus which is hyperactive

18
Q

treatment of BArtters

A
potassium supplements and liberal salt intake
aldosterone antagonists (spironolactone)
ACE inhibitors to counteract effects of angiotensin II and aldosterone
NSAIDs (indomethacin) to decrease PGE2
calcium a nd magnesium supplements
19
Q

extrarenal causes of hypokalemia

A

GI
skin
redistribution (insulin, B2 activity alkalosis)
neuromuscular symptoms

20
Q

renal causes of hypokalemia with metabolic acidosis

A

renal tubular acidosis (type 1 or 2)
diabetic ketoacidosis
carbonic anhydrase inhibitor therapy

21
Q

renal causes of hypokalemia with metabolic alkalosis

A

diuretics
mineralcorticoid excess
Gitelman and Bartters

22
Q

renal cause of hypokalemia without acid base disorder

A

osmotic diuresis