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Renal CPR 2 > Wolff Hyper-Hypokalemia Hyper-Hyponatremia Renal > Flashcards

Wolff Hyper-Hypokalemia Hyper-Hyponatremia Renal Flashcards

1
Q

routine dietary intake of this cation would increase its plasma levels to the toxic range if not for a means for rapid redistribution into cells

A

potassium

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2
Q

type of metabolic alkalosis seen with thiazide and loop diuretics secondary to K+ loss

A

hyperchloremic

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3
Q

this of body is monitored by special sensors in the brain, cannot be eye-balled but instead approx clinically by summing things that are measured (or measured directly via colligative properties of vapor point elevation or freezing point depression)

A

osmolality

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4
Q

characterizes the on and off-rate for drugs such as spironolactone that decrease protein expression with disappearance of existing proteins each having their own half-life (hours, days) to see the effects

A

slow

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5
Q

adverse effect associated with administration of tolvaptan for >30 days

A

hepatotoxicity

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6
Q

whether extracellular or intracellular, means that too much sodium is in this compartment (water compartment); extracellular location is a common indication for a loop diuretic

A

edema

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7
Q

prototype for the non-peptide V2 receptor antagonists that can be used judiciously to treat euvolemic and hypervolemic hyponatremia if unresponsive to other measures; causes water excretion w/o solute excretion

A

conivaptan

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8
Q

class of drugs that interferes with renin secretion and the ability of diuretics to cause a diuresis

A

NSAIDs

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9
Q

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

A

laxative

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10
Q

invasive means for treating life-threatening hyperkalemia

A

dialysis

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11
Q

increased by a step change in daily sodium intake

A

body weight

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12
Q

potential adverse effect of spironolactone use by females

A

hirsutism

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13
Q

caused by loop and thiazide diuretics, increases the risk of gout

A

hyperuricemia

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14
Q

contraindication for loop diuretics and not a good time to start thiazide diuretics

A

pregnancy

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15
Q

positive inotrope used in HF whose toxicity is increased by loop diuretic-induced K+ loss

A

digoxin

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16
Q

RTA with hypokalemia due to, for example, autoimmunity leading to fibrosis with impaired function in the cortical collecting duct

A

Type 1

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17
Q

among the neuromuscular manifestations of hypokalemia

A

constipation

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18
Q

occurs in liver disease due to impaired synthesis of plasma proteins and increased portal venous pressure, reason to administer loop diuretics

A

ascites

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19
Q

can cause hyperkalemia

A

tissue necrosis

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20
Q

tablets that are a treatment for hypovolemia hyponatremia

A

NA K2Cl

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21
Q

suggestive clues include hypovolemic hypernatremia, hypokalemia with metabolic alkalosis, significant urinary Cl- loss despite low plasma levels

A

hyperaldosteronism

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22
Q

hypo- and hyper- mean respectively that there is too much or too little water diluting the body’s sodium content

A

natremia

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23
Q

identified the forces that determine the net magnitude and direction of fluid movement across capillary barriers

A

starling

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24
Q

part of the coma cocktail, it is also often administered along with other agents to patients presenting with hyperkalemia

A

glucose

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25
Q

tablets that are a treatment for hypovolemic hyponatremia

A

salt

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26
Q

consequence of treating hyponatremia too rapidly

A

osmotic demyelination

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27
Q

well known toxicity of loop diuretics

A

ototoxicity

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28
Q

osmotic pressure is the driving force for water movement across this

A

cell membrane

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29
Q

organ that doesn’t have space for its cells to swell due to hyponatremia, lack of space leads to symptoms of encephalopathy and possible uncal herniation +/- death

A

brain

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30
Q

abbr. for hormone released by posterior pituitary whose receptor-mediated water-retaining effects are blocked by the vaptans

A

ADH

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31
Q

caused by a lack of ADH secretion or a failure of the kidneys to respond to it leads to euvolemic hypernatremia

A

diabetes insipidus

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32
Q

surprising consequence of hyperkalemia, occurs because hyperkalemia increases K+ conductance in SA nodal tissue enough to cause membrane hyperpolarization; other regions of heart do become hyperexcitable so arrhythmias likely

A

bradycardia

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33
Q

ion that exchanges with cellular K+ during acid-base maintenance and/or compensation; reason acidosis can cause hyperkalemia

A

hydrogen

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34
Q

occurs when K+ (and Cl-) are lost in urine due to, for example, diuretics; cells donate K+ while taking up H+ (and leaving behind HCO3-) in an effort to maintain hypokalemic plasm K+ levels closer to normal

A

metabolic alkalosis

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35
Q

blocks ENaC channels in the principal cells of the connecting tubule and and collecting duct, similar to amiloride

A

triamterene

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36
Q

gliflozin class of drugs lowers circulating glucose levels in diabetes by blocking its reabsorption in proximal tubule… this causes polyuria as does diabetes itself cuz glucose excreted in urine functions as this type of diuretic

A

osmotic

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37
Q

not a good time to take a loop or thiazide diuretic given the typical duration of action

A

bed time

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38
Q

potential adverse effect of spironolactone use by males

A

gynecomastia

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39
Q

hyperkalemic/most common form of renal tubular acidosis, caused by lack of aldosterone or failure to respond to it

A

type 4

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40
Q

when this is less than about 30 ml/min, thiazides no longer work but loop diuretics still work when treating HTN; can be cause of hyperkalemia when <~ 5 ml/min

A

GFR

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41
Q

hormone whose levels decrease in response to a dietary sodium load to help facilitate its renal elimination

A

aldosterone

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42
Q

hormone principally responsible for cellular uptake of K+, can cause hypokalemia with normal acid-base balance

A

insulin

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43
Q

problematic with diuretics presumably in part cuz of urgent need to urinate

A

non-adherence

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44
Q

type of acids that have less of an effect on plasma K+ than, for example, hydrochloric or sulfuric acids

A

organic

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45
Q

slowing the progression of this is a reason for continued administration of expensive tolvaptan

A

APKD

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46
Q

interval widened by hyperkalemia

A

QRS

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47
Q

loop diuretic that can be used by patients with sulfa allergy

A

ethacrynic acid

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48
Q

channel responsible for Mg2+ distal convoluted tubule, can compensate somewhat when Mg2+ reabsorption is blocked in TAL by loop diuretics but down-regulates in presence of thiazides leading to more profound Mg2+ loss in urine

A

TRPM6

49
Q

class of diuretics acting in the collecting duct to block Na+/K+ exchange, useful to counterbalance an adverse effect of loop and thiazide diuretics

A

K+ sparing

50
Q

cells in the collecting duct that are the primary target of K+ sparing diuretics

A

principal cells

51
Q

diuretic that blocks epithelial Na+ channels in principal cells of the collecting duct, effects are rapid when compared to spironolactone

A

amiloride

52
Q

characteristic of urine excreted with maximally effective doses of furosemide, irrespective of plasma ADH levels

A

isotonic

53
Q

nephron location where osmotic diuretics and carbonic anhydrase inhibitors exert their effects; increasing or decreasing the fraction of the filtered load absorbed here is a primary determinant of Na+ excretion

A

proximal tubule

54
Q

ionized form of this divalent cation is a crucial cofactor in many biological processes, plasma levels are maintained in normal range by regulation of reabsorption through TRPM6 channels in DCT in a poorly understood manner; both loop and thiazide diuretics cause it to be lost in urine, especially thiazides

A

magnesium

55
Q

3% NaCl is an example of this type of solution that causes cells to shrink, can be used to treat acute severe hyponatremia

A

hypertonic

56
Q

receptors that sense body Na+ content via measurement of effective blood volume

A

stretch

57
Q

can be a hidden source of excessive K+ intake

A

antibiotics

58
Q

co-transporter in the DCT that acts to further dilute the tubular fluid; target of thiazide diuretics

A

NaCl

59
Q

example of an osmotic diuretic administered in gram quantities to help eliminate excess intracellular volume (eg. causing elevated intracranial pressure), now often supplanted by hypertonic saline

A

mannitol

60
Q

substance that promotes free water clearance

A

aquaretic

61
Q

broad characterization of diuretics that includes thiazides, loop diuretics, carbonic anhydrase inhibitors and osmotic diuretics

A

K+ losing

62
Q

likelihood of formation from calcium in the urinary pelvis is increased by loop diuretics and decreased by thiazide diuretics due to their differing effects on its reabsorption

A

stones

63
Q

membrane potential that is determined by extracellular K+ levels

A

resting

64
Q

failure of this to treat hyponatremia in symptomatic hospitalized patients is an indication for vaptans

A

fluid restriction

65
Q

refers to factors such as Ang II, ANP, and SNS activity that modify the intrinsic renal relationship between arterial pressure and Na+ excretion

A

extrinsic

66
Q

irrespective of whether hypo- or hyper-natremia, if this word applies the rate of correction must be slow

A

chronic

67
Q

means plasma levels <1.7 mg/dL, often coexists with hypokalemia and hypocalcemia; contributes to clinical signs such as muscle weakness, tremors, tetany, seizures, parasthesias, nystagmus, torsades de pointes

A

hypomagnesemia

68
Q

this clearance is 0 when urine is isotonic, positive when urine is dilute, and negative when urine is hypertonic; negative means the water in which urinary solute was dilute has been returned to body to dilute to lower plasma osmolality

A

free water

69
Q

a potassium salt formed with this bicarbonate precursor can be administered to a person with hypokalemia and acidosis

A

acetate

70
Q

thirst, tenting of skin, sunken eyes and oliguria are signs of this, ultimately a more powerful stimulus of ADH release than increases in plasma osmolality

A

hypovolemia

71
Q

predictable consequence of severe hypokalemia, diabetes insipidus, and vaptan administration

A

polyuria

72
Q

V2 agonist used to treat central diabetes insipidus

A

DDAVP

73
Q

syndrome that is a cause of type 2 RTA due to impaired ability to reabsorbed filtered bicarb in the proximal tubule

A

Fanconi

74
Q

nephron cells that can change their phenotype and are normally associated with the maintenance of acid-base balance, they are also a target of thiazide diuretics

A

intercalated

75
Q

ability impaired in the kidney by loop diuretics, Bartter syndrome, and hypokalemia (here presumably due to need for K+ by Na+ K+ 2Cl- cotransporter) resulting in polyuria and nocturia

A

concentrating

76
Q

chicory, dandelion leaves, fennel, goldenseal, and others are diuretics of this type of alternative medicine with generally uncharacterized MOAs and uncertain efficacy

A

herbal

77
Q

loss of this in excess of water is why loop and thiazide diuretics can cause hyponatremia

A

sodium

78
Q

substance that promotes excretion of urine, potential cause of hypovolemic hyponatremia

A

diuretic

79
Q

causes include anything that interferes with normal renin secretion or Ang II generation or the actions of Ang II or aldosterone

A

hyperkalemia

80
Q

prototypical loop diuretic

A

furosemide

81
Q

refers to the channels directly blocked by amiloride and triamterene in collecting duct cells

A

ENaC

82
Q

real European form of this contains sweet glycrrhizic acid which dose-dependently potentiates aldosterone effects and increases systolic BP

A

licorice

83
Q

common term for diuretic class with “high-ceiling” effects exerted in the TAL

A

loop

84
Q

its blockade of carbonic anhydrase causes a sodium bicarb diuresis with hyperchloremic acidosis; principal uses include urinary alkalinization to hasten elimination of weak acid toxins (eg. aspirin), treatment of metabolic alkalosis, acute mountain sickness and glaucoma

A

acetazolamide

85
Q

healthy way to transiently raise extracellular K+ levels

A

exercise

86
Q

common cause of hypervolemic hyponatremia

A

heart failure

87
Q

caused by cell lysis in a collection of blood samples

A

pseudo-hyperkalemia

88
Q

this of Na+ increases as BP increases

A

urinary output

89
Q

refers to the fact that RBF and GFR are maintained approx. constant at MAP of ~100 mmHg +/- 40 cuz of myogenic mechanism and tubuloglomerular feedback

A

autoregulation

90
Q

selective non-peptide V2 receptor antagonist that can be cautiously administered orally to patients with persistent hyponatremia despite use of initial therapies

A

tolvaptan

91
Q

typical route for KCl administration to a person with hypokalemia

A

oral

92
Q

administered to raise the threshold potential when people present with hyperkalemia

A

calcium

93
Q

receptors in collecting duct that mediate the response to ADH (aka arginine vasopressin) leading to insertion of aquaporin 2 water channels in luminal membrane for water reabsorption

A

V2

94
Q

a large volume of this in plasma can cause pseudo-hyponatremia

A

lipid

95
Q

with worsening hyperkalemia, may have muscle twitching/weakness and numbness/prickling sensation gave way to this type of paralysis

A

flaccid

96
Q

whether excreting a maximally dilute or maximally concentrated urine, the elimination of this is approx. unchanged

A

solute

97
Q

becomes prominent in severe hypokalemia

A

U wave

98
Q

K+ excretion is increased when this is increased in the distal nephron

A

tubular fluid flow rate

99
Q

disease that causes hyperkalemia despite adequate GFR

A

Addison’s

100
Q

administering a 5% solution of this is ultimately equivalent to infusing approx. that volume of distilled water

A

dextrose

101
Q

recent episodes of this can give rise to hyponatremia, hypokalemia, hypovolemia, and metabolic alkalosis with renal retention of K+ and Na+ (eg. <20 and 30 mEq/L respectively)

A

vomiting

102
Q

aldosterone antagonist with greater selectivity than spironolactone, also much more expensive

A

eplerenone

103
Q

cause of euvolemic hyponatremia

A

SIADH

104
Q

major pathway for Mg2+ reabsorption in TAL, Ca2+ is also reabsorbed here in addition to its major reabsorption via this pathway in proximal tubule

A

paracellular

105
Q

cause of hyperosmolar hyponatremia

A

hyperglycemia

106
Q

volume expanded by infusion of 0.9% NaCl solution

A

extracellular

107
Q

class of diuretics with medium Na+ losing ability due to effects that include blockade of a transporter in distal convoluted tubules; treatment for nephrogenic diabetes insipidus

A

thiazide

108
Q

hypo- or hyper- means there is too little or too much Na+ in the body

A

volemia

109
Q

0.45% NaCl solution is an example of this type of solution that causes cells to swell, can be administered to treat hypernatremia

A

hypotonic

110
Q

hypovolemic form of this sign of neglect in nursing home

A

hypernatremia

111
Q

glomerulotubular ___ refers to forces acting across proximal tubular epithelium that result in proportional rather than absolute amounts of ~isotonic fluid reabsorption from the proximal tubule

A

balance

112
Q

classical aldosterone antagonist, its effects in the principal cells of the collecting duct cause it to act as K+ sparing diuretic

A

spironolactone

113
Q

means plasma Na+ concentration is <135 mEq/L; seen in 15-20% of hospitalized patients, it is the most common electrolyte abnormality seen in clinical practice

A

hyponatremia

114
Q

consuming this decreases ADH secretion

A

alcohol

115
Q

refers to form of diabetes insipidus when kidney fails to respond to ADH

A

nephrogenic

116
Q

along with massive, this adjective characterizes the fluid removal response to loop diuretics

A

rapid

117
Q

administration of this to treat bipolar disorder is the most common cause of nephrogenic diabetes insipidus, treated with amiloride

A

lithium

118
Q

means of plasma K+ concentration is <3.5(ish), hyperpolarizes most cell membranes; can be used by K+ losing diuretics

A

hypokalemia

119
Q

generic term for the portion of the nephron that increases K+ reabsorption when plasma levels are low

A

distal

Renal CPR 2 (1 decks)

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