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CPRII > Hypo and Hyper Na+/K+ > Flashcards

Hypo and Hyper Na+/K+ Flashcards

1
Q

What is the most common form of RTA?

A

RTA Type 4

lack of aldosterone or failure to respond to it

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2
Q

What is the role of the NK2Cl transporter in the TAL?

A

helps give rise to dilute tubular fluid and hypertonic renal medullary interstitium in combo w/ water impermeability and direction of flow outside TAL

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3
Q

What transporter is target of loop diuretics?

A

NK2CL transporter in TAL

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4
Q

What is the role of insulin?

A

hormone primarily responsible for cell uptake of K+

can cause HYPOk w/ normal acid-base balance

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5
Q

What occurs in SIADH?

A

causes euvolemic hyponatremia

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6
Q

What is the role of the V2 receptor in the collecting duct?

A

mediates response to ADH

leads to insertion of AQ2 water channels in luminal membrane for water reabsorption

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7
Q

What electrolyte disturbance can be caused by vomiting episodes?

A

hypoNa, hypoK, hypovolemia

metabolic alkalosis w/ renal retention of K & Na

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8
Q

What is sensed by special sensors in brain?

A

body osmolality

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9
Q

What is DDVAP (desmopressin)?

A

V2 agonist used to tx central DI

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10
Q

What is tolvaptan?

A

V2 receptor antagonist that can be used orally to pts w/ persistent hyponatremia despite use of initial therapies

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11
Q

What is ADH?

A

hormone released by PP whose receptor-mediated water-retaining effects are blocked by vaptans

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12
Q

What is the effect of alcohol?

A

consumption decreases ADH secretion

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13
Q

What is given to pt w/ hypokalemia and acidosis?

A

potassium salt (formed w/ acetate)

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14
Q

What is an invasive method to tx life-threatening hyperkalemia?

A

dialysis

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15
Q

When would you consider RTA in a pt?

A

acidemia w/ normal AG and serum CR level and NO diarrhea

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16
Q

What can cause pseudohyponatremia?

A

large volume of LIPID in plasma

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17
Q

What occurs if give pt digoxin with a loop diuretic?

A

toxicity of digoxin is increased by K+ loss induced by loop diuretic

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18
Q

What is a toxicity of loop diuretic?

A

ototoxicity

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19
Q

What is mannitol?

A

osmotic diuretic used to eliminate excess intracellular volume

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20
Q

What type of solution is used to tx acute severe hyponatremia?

A

hypertonic solution (3% NaCl, causes cells to shrink)

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21
Q

What can cause pseudohyperkalemia?

A

cell lysis in a collected blood sample

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22
Q

What is the fxn of osmotic diuretics?

A

cause polyuria (excrete excess glucose in urine)

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23
Q

What acts @ proximal tubule?

A

osmotic diuretics and carbonic anhydrase inhibitors

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24
Q

What is affected @ prox tubule?

A

where can increase or decrease fraction of filtered load that is reabsorbed

determines Na+ excretion

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25
Q

What is route for Mg2+ and Ca2+ reabsorption?

A

both paracellular @ TAL; Ca2+ paracellular @ prox tubules

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26
Q

What is a potential AE of spironolactone used by males?

A

gynecomastia

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27
Q

What can influence stone formation?

A

increase risk w/ more Ca2+ in urinary pelvis by loop diuretics

decrease risk w/ less Ca2+ in urinary pelvis by thiazide diuretics

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28
Q

What is caused by both loop and thiazide diuretics?

A

hyperuricemia

can increase risk of gout

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29
Q

What is 1st line tx for symptomatic hospitalized pt w/ hyponatremia?

If fails, what is next used?

A

fluid restriction

if fails to tx, indication for vaptans

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30
Q

What is CI for loop diuretics and not good time for thiazides?

A

pregnancy

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31
Q

What is MOA and indication for acetazolamide?

A

inhibitor of carbonic anhydrase (causes Na+ HCO3 diuresis w/ hyperchloremic acidosis)

used for urinary alkalization to hasten elimination of weak acid toxins, tx of metabolic alkalosis, acute mtn sickness and glaucoma

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32
Q

What is MOA and indication for conivaptan?

A

V2 receptor antagonist to cause H2O excretion w/o solute excretion

used to tx euvolemic and hypervolemic hyponatremic if unresponsive to other tx

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33
Q

What are PE findings of hypovolemia?

A

thirst, tenting of skin, sunken eyes and oliguria

stronger stimulus for ADH release

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34
Q

What can cause hyperkalemia?

A

tissue necrosis

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35
Q

What is a common cause of hypervolemic hyponatremia?

A

heart failure

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36
Q

What portion of nephron increase K+ reabsorption when plasma levels are low?

A

distal nephron (esp collecting duct)

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37
Q

What are sxs of hyper aldsteronism?

A

hypervolemic hypernatremia

hypokalemia w/ metabolic alkalosis

urinary Cl- loss even w/ low plasma levels and HTN

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38
Q

What is an AE assoc w/ admin of tolvaptan for >30 days?

A

hepatotoxicity

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39
Q

What class of diuretics act in collecting duct?

A

K+ sparing diuretics

block Na+/K+ exchange to counterbalance AE of loop and thiazide diuretics

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40
Q

What is spironolactone?

A

aldosterone antagonist

effects in principal cells of collecting duct to act as K+ sparing diuretic

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41
Q

What is MOA of triamterene?

A

blocks ENaC channels in principal cells of collecting tubule and duct

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42
Q

What is role of aldosterone?

A

hormone whose levels decrease in response to dietary Na+ load to help facilitate its renal elimination

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43
Q

What are some causes of hyperkalemia?

A

anything that interferes w/ normal renin secretion or angiotensin II generation or the actions of angio II/aldosterone

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44
Q

What type of solution is used to tx hypernatremia?

A

hypotonic (0.45% NaCl causes cells to swell)

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45
Q

What dz causes hyperkalemia despite nl GFR?

A

Addison dz

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46
Q

What organ does not have space for cells to swell?

A

BRAIN (in setting of hyponatremia)

lack of space leads to sxs of encephalopathy and possible uncal herniation +/-death

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47
Q

How do loop and thiazide diuretics cause hyponatremia?

A

excess loss of Na+ and H2O

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48
Q

What is a potential AE of spironolactone in females?

A

hirsutism

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49
Q

How is free water clearance related to urine osm?

A

free H2O clear is zero when urine is isotonic

+ when urine is dilute

  • when urinary solute returned to body
50
Q

What is Fanconi syndrome?

A

cause of type 2 RTA due to impaired ability to reabsorb filtered HCO3 in prox tubule

51
Q

What is a consequence of tx hyponatremia too rapidly?

A

osmotic demyelination

52
Q

What ion exchanges w/ cellular K+ during acid base maintenance?

A

HYDROGEN

reason acidosis can cause hyperkalemia

53
Q

What is administered to raise threshold potential when people present w/ hyperkalemia?

A

calcium

54
Q

What is significant about intercalated cells?

A

change phenotype and assoc w/ maintenance of acid-base balance

55
Q

What cells do thiazide diuretics target?

A

intercalated cells in distal nephron

56
Q

What is equivalent to infusing volume of distilled water?

A

administer 5% solution of dextrose

57
Q

Why is tolvaptan still used?

A

slow progression of APKD

58
Q

What is the aldosterone antagonist w/ greater selectivity?

A

eplerenone

59
Q

Describe GFR requirements for diuretics

A

thiazide do NOT work if GFR<30 ml/min

loop diuretics work if GFR<30 ml/min

can be cause of hyperkalemia if GFR<5

60
Q

What remains unchanged when excreting max dilute or max conc urine?

A

elimination of solute

61
Q

What is the most common electrolyte abnormality seen in clinical practice?

A

HYPOnatremia

Na+ conc <135

62
Q

What is the effect of licorice?

A

dose dependently potentiates aldosterone effects and increases systolic blood pressure

63
Q

What changes occurs with step change in daily sodium intake?

A

increase in body weight

64
Q

What cells are primary target of K+ sparing diuretics?

A

principal cells in collecting duct

65
Q

What receptors sense body Na+ content via measure effective blood volume?

A

stretch receptors

66
Q

What is the role of TRPV5 receptor?

A

Ca2+ reabsorption in DCT

major site of regulation w/ calcitriol (to increase synthesis) and PTH (regulate conductance)

67
Q

What increases K+ excretion from distal nephron?

A

increased tubular fluid flow rate

68
Q

What are K+ losing diuretics?

A

thiazides, loops, carbonic anhydrase inhibitors, osmotic diuretics

69
Q

What occurs with abuse of laxatives?

A

extra renal K+ losses leading to hypokalemia that can occur +/- concurrent metabolic acidosis

70
Q

What occurs in severe hypokalemia, DI and vaptan use?

A

polyuria

71
Q

What is glomerulotubular balance?

A

forces acting across proximal tubular epithelium that result in proportional amounts of isotonic fluid reabsorption from prox tubule

72
Q

What loop diuretic can be used in pts w/ sulfa allergy?

A

ethacrynic acid

73
Q

What defines hypokalemia and outcome?

A

plasma K+ <3.5

hyperpolarizes most cell membranes

can be caused by K+ losing diuretics

74
Q

Hypovolume v hypervolume

A

too little or too much sodium in body

75
Q

What is a cause of hyperosmolar hyponatremia?

A

hyperglycemia

76
Q

What prevents plasma potassium toxicity from dietary intake?

A

rapid redistribution of K+ into cells

77
Q

What is role of TPRV6 channel?

A

Mg2+ reabsorption in DCT which somewhat blocked in TAL by loop diuretics

will downregulate in presence of thiazides leading to more profound Mg2+ loss in urine

78
Q

What is an important indication for loop diuretics?

A

ASCITES that occurs in liver dz due to impaired synthesis of plasma proteins and increased portal venous pressure

79
Q

What is indication for salt tablets?

A

tx for hypovolemic hyponatremia

80
Q

What volume is expanded by infusion of 0.9% NaCl solution?

A

extracellular volume

81
Q

What drives water movement across cell membranes?

A

osmotic pressure

82
Q

What promotes excretion of urine and can cause hypovolemic hyponatremia?

A

diuretic

83
Q

What sx is among neuromuscular manifestations of hypokalemia?

A

constipation

84
Q

What type of paralysis is seen in worsening hyperkalemia?

A

FLACCID paralysis

twitching/weakness and numbness/prickling sensation

85
Q

What occurs when K+ (and Cl-) are lost in urine due to diuretics?

A

metabolic alkalosis due to cells donating K+ while taking up H+ to maintain plasma K+ levels near normal

86
Q

Where do loop diuretics act?

A

high ceiling effects exerted in TAL

87
Q

What becomes prominent in severe hypokalemia?

A

U waves

88
Q

What acids have less effect on plasma K+?

A

organic acids

89
Q

Hyponatremia v hypernatremia

A

too much or too little WATER diluting body Na+ content

90
Q

What can be hidden source of excessive K+ intake?

A

antibiotics

91
Q

What is a healthy way to transiently raise extracell K+ levels?

A

exercise

92
Q

What is most common cause of nephrogenic DI?

A

lithium to tx bipolar disorder

93
Q

How to tx nephrogenic DI due to lithium toxicity?

A

amiloride

94
Q

What is MOA of thiazide and indication?

A

medium Na+ losing ability b/c block of transporter in DCT

tx nephrogenic DI

95
Q

What is furosemide?

A

LOOP diuretic

96
Q

What is caused by lack of ADH secretion or failure of kidneys to respond to ADH?

A

diabetes insipidus

can lead to euvolemic hypernatremia

97
Q

What change in HR is consequence of hyperkalemia?

A

BRADYCARDIA

b/c hyperkalemia increases K+ conductance in SA node tissue to cause membrane hyperpolarization

higher risk of arrhythmia

98
Q

What is impaired in Bartter syndrome, use of loop diuretics, and hypokalemia?

A

concentrating ability of kidneys

results in polyuria, nocturia

99
Q

What type of metabolic alkalosis is seen w/ thiazide and loop diuretics?

A

HYPOchloremic secondary to K+ loss

100
Q

What is problematic with diuretics?

A

nonadherence due to urgent need to urinate

101
Q

What interval is widened by hyperkalemia?

A

QRS interval

102
Q

What is administered as the coma cocktail?

A

GLUCOSE in pts presenting w/ hyperkalemia

103
Q

How does urinary output of Na+ change as BP increases?

A

increased sodium urinary output

104
Q

What is nephrogenic diabetes insipidus?

A

form of DI when kidney fails to respond to ADH

105
Q

What is osm of urine when use max dose of furosemide?

A

ISOTONIC urine (irrespective of plasma ADH levels)

106
Q

What is autoregulation?

A

myogenic mechanism and tubuloglomerular feedback that maintains RBF and GFR at range of MAP

107
Q

What is hypomagnesemia?

A

plasma level <1.7

often seen w/ hypoK and Ca2+

clinical sxs of muscle weakness, tremors, tetany, seizures, paresthesias, torsades de pointes

108
Q

What is role of magnesium?

A

crucial cofactor in many biological processes

normal level regulation via reabsorb through TRPM6 channels in DCT

109
Q

What extrinsic factors modify intrinsic renal relationship btwn arterial pressure and sodium excretion?

A

Ang II
ANP
SNS activity

110
Q

What is a sign of neglect in nursing homes?

A

hypovolemic hypernatremia

111
Q

What is MOA of amiloride?

A

diuretic that blocks epithelial Na channels in principal cells of collecting ducts

rapid onset of action

112
Q

When is not a good time to take loop or thiazide diuretic?

A

bedtime

113
Q

What characterizes fluid removal response to diuretics?

A

rapid and massive

114
Q

What signifies that too much sodium is in 1 compartment?

A

EDEMA

indication for loop diuretic

115
Q

What promotes free water clearance?

A

aquaretic

116
Q

What is RTA type 1?

A

RTA w/ hypokalemia due autoimmunity (causes fibrosis w/ impaired fxn in cortical collecting duct)

117
Q

What channels are blocked by amiloride and triamterene in collecting duct cells?

A

ENaC

118
Q

What is determined by extracellular K+ levels?

A

resting membrane potential

119
Q

What defines tx of chronic hyponatremia or hypernatremia?

A

SLOW rate of correction

120
Q

What drugs interfere w/ renin secretion and ability of diuretics to cause diuresis?

A

NSAIDs

121
Q

What co-transporter in DCT further dilutes tubular fluid?

A

NaCl

target of thiazide diuretics

122
Q

What is typical route for KCl administration for pt w/ hypokalemia?

A

ORAL

CPRII (4 decks)

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