Wolff Hyper-Hypokalemia Hyper-Hyponatremia Renal Flashcards
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
potassium
type of metabolic alkalosis seen with thiazide and loop diuretics secondary to K+ loss
hyperchloremic
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)
osmolality
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
slow
adverse effect associated with administration of tolvaptan for >30 days
hepatotoxicity
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
edema
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
conivaptan
class of drugs that interferes with renin secretion and the ability of diuretics to cause a diuresis
NSAIDs
abuse of this can cause extra-renal K+ losses leading to hypokalemia that can occur +/- concurrent metabolic acidosis
laxative
invasive means for treating life-threatening hyperkalemia
dialysis
increased by a step change in daily sodium intake
body weight
potential adverse effect of spironolactone use by females
hirsutism
caused by loop and thiazide diuretics, increases the risk of gout
hyperuricemia
contraindication for loop diuretics and not a good time to start thiazide diuretics
pregnancy
positive inotrope used in HF whose toxicity is increased by loop diuretic-induced K+ loss
digoxin
RTA with hypokalemia due to, for example, autoimmunity leading to fibrosis with impaired function in the cortical collecting duct
Type 1
among the neuromuscular manifestations of hypokalemia
constipation
occurs in liver disease due to impaired synthesis of plasma proteins and increased portal venous pressure, reason to administer loop diuretics
ascites
can cause hyperkalemia
tissue necrosis
tablets that are a treatment for hypovolemia hyponatremia
NA K2Cl
suggestive clues include hypovolemic hypernatremia, hypokalemia with metabolic alkalosis, significant urinary Cl- loss despite low plasma levels
hyperaldosteronism
hypo- and hyper- mean respectively that there is too much or too little water diluting the body’s sodium content
natremia
identified the forces that determine the net magnitude and direction of fluid movement across capillary barriers
starling
part of the coma cocktail, it is also often administered along with other agents to patients presenting with hyperkalemia
glucose
tablets that are a treatment for hypovolemic hyponatremia
salt
consequence of treating hyponatremia too rapidly
osmotic demyelination
well known toxicity of loop diuretics
ototoxicity
osmotic pressure is the driving force for water movement across this
cell membrane
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
brain
abbr. for hormone released by posterior pituitary whose receptor-mediated water-retaining effects are blocked by the vaptans
ADH
caused by a lack of ADH secretion or a failure of the kidneys to respond to it leads to euvolemic hypernatremia
diabetes insipidus
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
bradycardia
ion that exchanges with cellular K+ during acid-base maintenance and/or compensation; reason acidosis can cause hyperkalemia
hydrogen
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
metabolic alkalosis
blocks ENaC channels in the principal cells of the connecting tubule and and collecting duct, similar to amiloride
triamterene
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
osmotic
not a good time to take a loop or thiazide diuretic given the typical duration of action
bed time
potential adverse effect of spironolactone use by males
gynecomastia
hyperkalemic/most common form of renal tubular acidosis, caused by lack of aldosterone or failure to respond to it
type 4
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
GFR
hormone whose levels decrease in response to a dietary sodium load to help facilitate its renal elimination
aldosterone
hormone principally responsible for cellular uptake of K+, can cause hypokalemia with normal acid-base balance
insulin
problematic with diuretics presumably in part cuz of urgent need to urinate
non-adherence
type of acids that have less of an effect on plasma K+ than, for example, hydrochloric or sulfuric acids
organic
slowing the progression of this is a reason for continued administration of expensive tolvaptan
APKD
interval widened by hyperkalemia
QRS
loop diuretic that can be used by patients with sulfa allergy
ethacrynic acid
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
TRPM6
class of diuretics acting in the collecting duct to block Na+/K+ exchange, useful to counterbalance an adverse effect of loop and thiazide diuretics
K+ sparing
cells in the collecting duct that are the primary target of K+ sparing diuretics
principal cells
diuretic that blocks epithelial Na+ channels in principal cells of the collecting duct, effects are rapid when compared to spironolactone
amiloride
characteristic of urine excreted with maximally effective doses of furosemide, irrespective of plasma ADH levels
isotonic
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
proximal tubule
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
magnesium
3% NaCl is an example of this type of solution that causes cells to shrink, can be used to treat acute severe hyponatremia
hypertonic
receptors that sense body Na+ content via measurement of effective blood volume
stretch
can be a hidden source of excessive K+ intake
antibiotics
co-transporter in the DCT that acts to further dilute the tubular fluid; target of thiazide diuretics
NaCl
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
mannitol
substance that promotes free water clearance
aquaretic
broad characterization of diuretics that includes thiazides, loop diuretics, carbonic anhydrase inhibitors and osmotic diuretics
K+ losing
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
stones
membrane potential that is determined by extracellular K+ levels
resting
failure of this to treat hyponatremia in symptomatic hospitalized patients is an indication for vaptans
fluid restriction
refers to factors such as Ang II, ANP, and SNS activity that modify the intrinsic renal relationship between arterial pressure and Na+ excretion
extrinsic
irrespective of whether hypo- or hyper-natremia, if this word applies the rate of correction must be slow
chronic
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
hypomagnesemia
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
free water
a potassium salt formed with this bicarbonate precursor can be administered to a person with hypokalemia and acidosis
acetate
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
hypovolemia
predictable consequence of severe hypokalemia, diabetes insipidus, and vaptan administration
polyuria
V2 agonist used to treat central diabetes insipidus
DDAVP
syndrome that is a cause of type 2 RTA due to impaired ability to reabsorbed filtered bicarb in the proximal tubule
Fanconi
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
intercalated
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
concentrating
chicory, dandelion leaves, fennel, goldenseal, and others are diuretics of this type of alternative medicine with generally uncharacterized MOAs and uncertain efficacy
herbal
loss of this in excess of water is why loop and thiazide diuretics can cause hyponatremia
sodium
substance that promotes excretion of urine, potential cause of hypovolemic hyponatremia
diuretic
causes include anything that interferes with normal renin secretion or Ang II generation or the actions of Ang II or aldosterone
hyperkalemia
prototypical loop diuretic
furosemide
refers to the channels directly blocked by amiloride and triamterene in collecting duct cells
ENaC
real European form of this contains sweet glycrrhizic acid which dose-dependently potentiates aldosterone effects and increases systolic BP
licorice
common term for diuretic class with “high-ceiling” effects exerted in the TAL
loop
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
acetazolamide
healthy way to transiently raise extracellular K+ levels
exercise
common cause of hypervolemic hyponatremia
heart failure
caused by cell lysis in a collection of blood samples
pseudo-hyperkalemia
this of Na+ increases as BP increases
urinary output
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
autoregulation
selective non-peptide V2 receptor antagonist that can be cautiously administered orally to patients with persistent hyponatremia despite use of initial therapies
tolvaptan
typical route for KCl administration to a person with hypokalemia
oral
administered to raise the threshold potential when people present with hyperkalemia
calcium
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
V2
a large volume of this in plasma can cause pseudo-hyponatremia
lipid
with worsening hyperkalemia, may have muscle twitching/weakness and numbness/prickling sensation gave way to this type of paralysis
flaccid
whether excreting a maximally dilute or maximally concentrated urine, the elimination of this is approx. unchanged
solute
becomes prominent in severe hypokalemia
U wave
K+ excretion is increased when this is increased in the distal nephron
tubular fluid flow rate
disease that causes hyperkalemia despite adequate GFR
Addison’s
administering a 5% solution of this is ultimately equivalent to infusing approx. that volume of distilled water
dextrose
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)
vomiting
aldosterone antagonist with greater selectivity than spironolactone, also much more expensive
eplerenone
cause of euvolemic hyponatremia
SIADH
major pathway for Mg2+ reabsorption in TAL, Ca2+ is also reabsorbed here in addition to its major reabsorption via this pathway in proximal tubule
paracellular
cause of hyperosmolar hyponatremia
hyperglycemia
volume expanded by infusion of 0.9% NaCl solution
extracellular
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
thiazide
hypo- or hyper- means there is too little or too much Na+ in the body
volemia
0.45% NaCl solution is an example of this type of solution that causes cells to swell, can be administered to treat hypernatremia
hypotonic
hypovolemic form of this sign of neglect in nursing home
hypernatremia
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
balance
classical aldosterone antagonist, its effects in the principal cells of the collecting duct cause it to act as K+ sparing diuretic
spironolactone
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
hyponatremia
consuming this decreases ADH secretion
alcohol
refers to form of diabetes insipidus when kidney fails to respond to ADH
nephrogenic
along with massive, this adjective characterizes the fluid removal response to loop diuretics
rapid
administration of this to treat bipolar disorder is the most common cause of nephrogenic diabetes insipidus, treated with amiloride
lithium
means of plasma K+ concentration is <3.5(ish), hyperpolarizes most cell membranes; can be used by K+ losing diuretics
hypokalemia
generic term for the portion of the nephron that increases K+ reabsorption when plasma levels are low
distal
