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Electrolytes & Fluid HY Flashcards

1
Q

Hyposthenuria is the inability of the kidneys to concentrate urine and can occur in patients with ____. Patients have polyuria, low urine specific gravity, and normal serum sodium.

A

sickle cell disease and sickle cell trait

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2
Q

Treatment of Hypercalcemia in acute setting?
(weakness, GI distress, AMS)

A

Initial treatment: Normal Saline then calcitonin
Chronic tx: Bisphosphonates

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3
Q

The kidneys compensate for primary metabolic acidosis via increased HCO3− (bicarb) reabsorption and H+ (acid) excretion.
↑ bicarb reabsorption via → ↑ urinary _____
↑ acid excretion via → ↑ urinary ____

A

↑ chloride (Cl−) excretion
↑ ammonium (NH4+) excretion
(or dihydrogen phosphate (titratable acid))

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4
Q

_____ is necessary for HCO3− (bicarb) reabsorption in the renal proximal tubule; thus it is increased in response to metabolic acidosis.

A

Carbonic anhydrase
(Converts CO2 + H2O to/ from
H+ & HCO3-)

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5
Q

Bulimia (excessive vomiting) leads to volume depletion and metabolic ___.
Labs show: ↑ bicarb ↓K+ ↓Cl-
Treatment of electrolyte derangement is with what?

A

Alkalosis
Tx: normal saline

(restores intravascular volume & replenishes chloride, thus allowing renal elimination of bicarbonate)

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6
Q

Acetazolamide is a ____ that decreases proximal tubular reabsorption of sodium (Na+) and HCO3−, thereby promoting mild metabolic acidosis.

A

carbonic anhydrase inhibitor

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7
Q

Loss of HCO3− increases serum Cl− to maintain an electronegative balance. Due to this relationship, NAGMA is also referred to as ___.

A

hyperchloremic acidosis

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8
Q

high drain output of pancreatic fluid the patient is likely to develop primary metabolic acidosis (low pH, low bicarbonate) with a normal anion gap and compensatory ____.

A

respiratory alkalosis (low PaCO2)

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9
Q

Nonanion gap metabolic acidosis (NAGMA) results from the loss of ____.

A

bicarbonate (HCO3−)

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10
Q

Because exocrine pancreatic secretions are high in HCO3−, NAGMA is expected with large-volume fluid losses from the pancreas (pancreatic duct leak/fistula or high drain output) or ____.

A

small intestine:
high ileostomy output
enterocutaneous fistula

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11
Q

Excessive _____ causes hyperchloremic metabolic acidosis (formerly called dilutional acidosis).
Because an increase in chloride ions drives bicarbonate intracellularly to maintain electronegativity, which causes NAGMA (low pH & low bicarbonate).

A

infusion of normal saline
(NaCl)

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12
Q

a potassium-sparing diuretic that blocks the epithelial sodium channel (ENaC) in the renal collecting system.

A

amiloride

(Spironolactone is an MR antagonist)

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13
Q

Patients with asymptomatic mild or moderate hyperkalemia (<6.5) can usually be managed with medication or dietary changes.

A

Those with severe manifestations of hyperkalemia require urgent therapy (Calcium gluconate, insulin + dextrose).

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14
Q

Medications that cause Hyperkalemia (8)

A

ACE inhibitor
ARB
Cyclosporine
Digoxin
Nonselective β blockers
Potassium-sparing diuretic (amiloride, spironolactone)
Succinylcholine
Trimethoprim

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15
Q

The goal of hypertonic saline infusion is to correct hyponatremia levels by 4-6 mEq/L over a period of hours to reduce the risk of ____.

A

brain herniation (cerebral edema)

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16
Q

The maximum rate of correction for hyponatremia is __ mEq/L in 24 hours to prevent osmotic demyelination syndrome (ODS) aka Central Pontine Myelinolysis (CPM).

A

8

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17
Q

used for the treatment of patients with chronic hyponatremia due to SIADH

A

Vasopressin receptor antagonists

Tolvaptan

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18
Q

Occurs due to a combination of excessive hypotonic fluid intake and nonosmotically mediated release of inappropriately high levels of antidiuretic hormone causing hyponatremia.
In severe cases, patients may experience seizures, profound confusion, and even death.

A

Exercise-associated hyponatremia

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19
Q

Hypernatremia should then be corrected gradually ( __ mEq/L/hr) to prevent neurologic complications (cerebral edema) from excessive movement of water into brain cells.

A

<0.5

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20
Q

Acute treatment of Hyperkalemia with calcium gluconate to stabilize the cardiac membrane and insulin + glucose to shift serum potassium into cells.

Definitive removal of potassium via the stool (____), kidneys (___), and/or blood (____) should then be initiated.

A

patiromer
furosemide
hemodialysis

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21
Q

Sodium nitroprusside infusion can result in _____, particularly in patients with renal insufficiency. Clinical findings include:
metabolic acidosis and neurologic changes (headache, confusion, hyper-reflexia).

A

cyanide toxicity

(other sxs: flushed skin, respiratory distress, GI distress, arrhythmia)

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22
Q

Acute ____ intoxication should be suspected in patients with the triad of tinnitus, fever, and tachypnea.
It usually causes a mixed primary respiratory alkalosis and primary metabolic acidosis with arterial ____ pH

A

salicylate (Aspirin)

normal pH (no osmolal gap)

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23
Q

_____ should be considered in infants with a nonanion gap metabolic acidosis, particularly in the setting of children with growth failure and absence of gastrointestinal loss (diarrhea).

A

Renal tubular acidosis

A defect in either hydrogen excretion (type 1) or bicarbonate resorption (type 2) in the kidney.

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24
Q

_____ of HCO3− occurs with infusion of excess normal saline (NaCl) and leads to NAGMA.

A

Intracellular shift

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25
Q

The normal anion gap of 10-14 mEq/L is consistent with nonanion gap metabolic acidosis (NAGMA), which results from ____.

A

loss of HCO3− (bicarb)

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26
Q

Cause of NAGMA from net bicarb loss is likely due to _____.
A common complication of Sjögren syndrome.

A

type 1 renal tubular acidosis (RTA)
⎯
impaired H+ excretion
Hypokalemia
urine pH >5.5 (not acidic)

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27
Q

Cause of NAGMA from net bicarb loss.
Type 4 RTA results from reduced ___ activity, leading to impaired __ & __ excretion in the collecting duct. HYPERkalemia is typical.
The urine pH is usually <5.5 (normal).

A

aldosterone
impaired H+ and K+ excretion

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28
Q

Cause of NAGMA from net bicarb loss.
Type 2 (proximal) RTA results from impaired ___ in the proximal tubule.
Hypokalemia is typical.
Urine pH is variable & often <5.5 (normal).

A

HCO3− reabsorption

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29
Q

Cause of NAGMA from net bicarb loss.
Type 1 (distal) RTA results from impaired ____ by alpha-intercalated cells in the distal tubule.
Hypokalemia is typical (s/t reduced K+ reabsorption)
Urine pH ___ (s/t markedly impaired capacity to acidify the urine)

A

H+ excretion
>5.5 (basic)

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30
Q

Electrolyte abnormalities that can be induced by thiazide (chlorthalidone, hydrochlorothiazide) diuretics include (4)

A

hyponatremia
hypokalemia
hypomagnesemia
hyper calcemia

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31
Q

Adverse metabolic effects of thiazide diuretics are dose-dependent include (4)

A

hyperglycemia (glucose intolerance)
increased LDL cholesterol
increased triglycerides
Hyperuricemia (gout risk)

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32
Q

Patients with CKD taking ACE-I often develop chronic mild or moderate hyperkalemia.
Typically managed with a low-potassium diet and what medication?

A

an oral cation exchange agent
(patiromer, zirconium cyclosilicate)
binds to K+ in the colon to be pooped out

Kayexalate (Sodium Polystyrene) Potassium Binders

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33
Q

Hypokalemia or Hyperkalemia with
↑ Chloride
↓ Bicarb
= Hyperchloremic Metabolic Acidosis
List one cause that could cause either of this presentation

A

Renal Tubular Acidosis (RTA)
⎯
⬩Hypokalemia → RTA (1 or 2)
⬩Hyperkalemia → RTA (4)

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34
Q

Type 4 RTA (hyperkalemic RTA) is commonly seen in elderly patients who have poorly controlled ____ with damage to the juxtaglomerular apparatus,
which causes ↓ Renin & ↓ Aldosterone

A

diabetes

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35
Q

Although diarrhea most commonly causes metabolic ____,
diarrhea from laxative abuse often causes metabolic ___ & ___.

A

Acidosis
ALkaLosis (Laxative abuse) & hypokalemia

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36
Q

Loop diuretic use causes hypocalcemia, _____ and metabolic ____.

A

hypokalemia
aLkaLosis

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37
Q

Surreptitious vomiting causes a hypochloremic metabolic alkalosis due to loss of gastric HCl.
Hypokalemia may be seen due to increased _____ secretion caused by volume depletion.

A

aldosterone

38
Q

Severe _____ can cause weakness, gastrointestinal distress, and neuropsychiatric symptoms.

Patients are typically volume depleted due to polyuria or decreased oral intake.

A

hypercalcemia

Initial treatment = normal saline hydration
Second is calcitonin (tone down bone resorption)

Long term is Bisphosphonates

39
Q

_____ can be used to treat hypercalcemia due to
excessive vitamin D intake,
granulomatous diseases (eg, sarcoidosis),
and certain lymphomas.

A

Glucocorticoids
(inhibit the formation of 1,25-dihydroxyvitamin D by activated cells in the lungs and lymph nodes)

40
Q

An assessment of ____ is essential in diagnosing and before treating hyponatremia (serum sodium <135 mEq/L).

A

volume status

41
Q

Low ADH (Anti-Pee hormone) and low urine sodium (watery pee) may be observed in a patient with _____.

Presents with polyuria, polydipsia, and normal to high serum sodium levels (s/t peeing out all the body’s water).

A

central diabetes insipidus

(It’s central bc ↓ ADH versus nephrogenic where ↑ ADH)

42
Q

_____ is characterized by euvolemic, hypotonic hyponatremia.

Low serum osmolality (<275 mOsm/kg) → watery blood
high urine osmolality (>100 mOsm/kg) → concentrated pee
and an high urine sodium concentration (>40 mEq/L)

A

SIADH

Syndrome of inappropriate antidiuretic hormone secretion

43
Q

Renal resistance to ADH occurs in nephrogenic diabetes insipidus. The result is uncontrolled loss of free water by the kidneys and consequent (electrolyte abnormality).

A

hypernatremia

44
Q

Symptoms of Acute Hyponatremia

A

Mild: Headache, Nausea, Vomiting, Muscle weakness
Moderate: Confusion, Altered Mental Status, gait distrubances
Severe: Seizures, Coma, increased ICP

45
Q

Patients with chronic alcohol use disorder often present with multiple electrolyte abnormalities (hypokalemia, hypomagnesemia, hypophosphatemia).

___ can lead to refractory hypokalemia that’s difficult to correct.

A

Hypomagnesemia

(Replenish both at the same time)

46
Q

___ is the active form of vitamin D, normally made in the kidney. aka 1,25-dihydroxycholecalciferol (a hormone which binds to and activates the vitamin D receptor)

A

Calcitriol

47
Q

Calcitriol used to treat ____ in patients whose kidneys or parathyroid glands aren’t working.

A

Hypocalcemia

48
Q

Hypercalcemia in sarcoidosis occurs due to extrarenal ____ production in the lungs and lymph nodes and is independent of parathyroid hormone (PTH).

Labs show
____ serum calcitriol
___ PTH
___ urinary calcium

A

Calcitriol

↑ serum calcitriol
↓ PTH
↑ urinary calcium

49
Q

Increased serum calcitriol stimulates ___ absorption, causing hypercalcemia.

A

intestinal calcium

50
Q

Refeeding syndrome occurs after giving carbohydrates or fluids in chronic malnourished pts resulting in massive insulin release that shifts electrolytes intracellularly.

Labs show: ↓ ____, ↓ potassium, ↓ magnesium

± Clinical manifestations include:
muscle weakness, [__Reflex Finding__], Rhabdomyolysis , ______, or CHF

A

↓ phosphate
hyporeflexia/areflexia
Arrhythmia (Torsades)

51
Q

A mixed acid-base disorder involves ≥2 primary disturbances and may be suggested by either ____ or ____ despite significant abnormalities in serum bicarbonate (HCO3−) and PaCO2.

A

a very abnormal pH (ex: <7.2 or >7.6)
or
a near-normal pH

52
Q

Patient presents with
hypokalemia
metabolic alkalosis
low Urine Chlorine
and normotensive

(3)

A

Surreptitious vomiting (Bulimia)
NGT Aspiration
Diuretic abuse → (High, if acute)

53
Q

Patients with chronic diarrhea have metabolic ___ and hypokalemia.

A

acidosis
(due to the loss of bicarbonate in the stool)

54
Q

Patients with chronic diarrhea have metabolic ___ and hypokalemia.
DUPLICATE?

A

acidosis
(due to the loss of bicarbonate in the stool)

55
Q

Patients with primary ____ have hypokalemia, metabolic alkalosis and hypertension

A

hyperaldosteronism

56
Q

____ diuretics are frequently administered to cirrhotic patients with volume overload and ascites.

Potential side effects include:
hypokalemia
metabolic _____
_____

A

Loop diuretics

metabolic alkalosis
prerenal AKI

57
Q

Hypokalemia may be caused by:
increased intracellular shifting (via insulin, Beta agonist, hematopoiesis: G-CSF),
gastrointestinal losses, or
renal potassium wasting (2).

A

hyperaldosteronism
diuretics

58
Q

_____ can lead to primary respiratory alkalosis, which is indicated by high pH and low PaCO2. Serum HCO3− remains near normal in the acute setting because full renal compensation requires 2+ days to show.

A

hyperventilation

59
Q

Diuretic abuse leads to increased excretion of water and electrolytes by the kidneys.

Results in dehydration, weight loss, orthostatic hypotension,
& 2 electrolyte abnormalities

↑ urinary ___ & ___

A

hyponatremia
hypokalemia

sodium and potassium

60
Q

Familial hypocalciuric hypercalcemia
(s/t mutated calcium-sensing receptor)
Presents as

asymptomatic hypercalcemia
___ PTH levels
___ urinary calcium excretion.

vs.

Primary hyperparathyroidism which has
hypercalcemia
___ PTH levels
____urinary calcium excretion.

A

↑/– PTH
↓ Urinary calcium excretion (UCCR <0.01)
⎯
↑ PTH
↑ Urinary calcium excretion (UCCR >0.01)

61
Q

Acute, symptomatic hyponatremia (impaired mental status/seizures) is a medical emergency. It requires prompt treatment with 3% or hypertonic saline at a rate of no more than 0.5 mEq/L/hr to avoid causing _____.

A

osmotic demyelination syndrome
(Central pontine myelinolysis)

Symptoms develop several day after the correction of hyponatremia with AMS, COMA, or locked-in Syndrome.

62
Q

Rapid correction of hyponatremia results in excess water being moved by osmosis from the inside of neurons and glia to the outside/extracellular compartment. This in turn leads to ____.

A

osmotic demyelination syndrome (ODS)
or
central pontine myelinolysis

(Myelin Sheath Dmg)

63
Q

Rapid correction of hypernatremia results in excess water being moved by osmosis into the neurons from the outside compartment. This in turn leads to _____.

A

cerebral edema (herniation)

64
Q

Hyponatremia
+
Serum osmolality >290 mOsm/kg (Concentrated blood) →

(2)

A

hyperglycemia
advanced renal failure

65
Q

Hyponatremia
+ serum osmolality <290 mOsm/kg (Dilute blood)
+ urine osmolality <100 mOsm/kg (Dilute pee) →
(2)

A

primary polydipsia
malnutrition (beer potomania/ Tea & Toast diet)

66
Q

Hyponatremia
+ A serum osmolality <290 mOsm/kg (Dilute blood)
+ urine osmolality >100 mOsm/kg (Concentrated pee)
+ Urine Sodium <25 (low- kidneys retaining salt) →

(3)

A

Volume Depletion
CHF
Cirrhosis/Ascites

67
Q

Hyponatremia
+ serum osmolality <290 mOsm/kg (Dilute blood)
+ urine osmolality >100 mOsm/kg (Concentrated pee)
+ urine Sodium >20 (High- Kidneys wasting salt) → (3)

A

SIADH
Adrenal Insufficiency (↓ aldosterone = ↑K+/H+ = acidosis)
Hypothyroidism (Weight gain, bradycardia)

⎯
SIADH: ↑ ADH secretion → ↑aquaporin-2 (water retention) → ↑ urine Osm & ↓ serum osmolality + transient ↑ volume →
↓ aldosterone → ↑ urinary sodium excretion.

68
Q

Many drugs (3) can stimulate hypothalamic ADH production and SIADH.
____ can also cause SIADH (s/t ectopic ADH by the tumor cells)

Excess ADH → water retention → concentrated urine → hyponatremia.

Urine osmolality is higher than Serum osmolality

A

carbamazepine
SSRIs
cyclophosphamide

Lung cancer (small cell cancer)

69
Q

In hypernatremia, serum osmolality is always increased, resulting in a hypertonic state. This is either due to a ____ (due to low intake or loss) or increased sodium (due to high __ or __).

A

free water deficit
high intake or retention

70
Q

Causes of Hypovolemic hypernatremia
(4)

A

Gastrointestinal loss (diarrhea , vomiting)
Dermal fluid loss (burns, excessive sweating)
Diuretics
Osmotic diuresis (hyperglycemia, mannitol)

71
Q

Causes of Euvolemic hypernatremia

A

Central Diabetes insipidus

Nephrogenic Diabetes insipidus

72
Q

Causes of Hypervolemic hypernatremia
(3)

A

Iatrogenic: excessive infusion of NaCl or sodium bicarbonate
Primary hyperaldosteronism
Cushing syndrome

73
Q

Symptoms of Acute Hypernatermia

A

Mild: signs of dehydration

Moderate: Confusion, Irritability, restlessness, Lethargy, Muscle weakness, Hyperreflexia

Severe (> 160): Focal neurological deficits, AMS, Seizures, Coma

74
Q

Correcting natremias too rapidly:

Hyponatremia: From low → high → ____

Hypernatremia: From high → low → ____

A

Hyponatremia correction → your pons will die (ODS)

Hypernatremia correction → your brain will blow (cerebral edema)

75
Q

Patient presents with
hypokalemia
metabolic alkalosis
High Urine Chlorine
and normotensive

(2)

A

Barter’s
Gitelmann’s

76
Q

Patient presents with
hypokalemia
metabolic alkalosis
High Urine Chlorine
and Hypertensive

(3)

A

Primary Hyperaldosteronism

Cushing Disease (secondary Hypercortisolism s/t Pituitary adenomas → ACTH secretion )

Ectopic ACTH production (Lung /Renal cancer, Medullary Thyroid cancer, Pancreatic Tumors, Carcinoid tumors, Pheochromacytomas)

77
Q

_____ is a leading cause of euvolemic (normal vitals/ no dehydration) hypernatremia.

A

Diabetes insipidus (DI)

78
Q

Lithium-induced nephrogenic DI is treated with ____ and discontinuation of lithium.

A

salt restriction

79
Q

Lithium-induced nephrogenic DI results from lithium accumulation in the ______, which leads to ADH resistance and impaired renal water reabsorption.

A

renal collecting ducts

80
Q

A desmopressin challenge can differentiate central from nephrogenic DI (as desmopressin causes increased urine osmolality only in ___ DI).

A

central

81
Q

____ is a cause of daytime and nighttime urinary incontinence and should be suspected in a child with fatigue, hypertension, proteinuria, and/or a history of urinary tract infections.

A

Chronic kidney disease

(Get serum creatinine level and renal imaging)

82
Q

Nocturnal enuresis secondary to ____ should be considered in a child who has bed-wetting in addition to inattention, behavioral concerns, hypertension, and/or tonsillar hypertrophy. Evaluation is with _____.

A

obstructive sleep apnea
nocturnal polysomnography

83
Q

Vesicoureteral reflux (VUR) causes retrograde urinary flow and often presents with febrile UTIs in young children. IF severe VUR (kidney with structural damage) there is high risk for recurrent pyelonephritis and warrant ____ to decrease the risk for renal scarring and CKD.

A

prophylactic antibiotics

84
Q

The first step in evaluation of nocturnal enuresis is ____.

A

urinalysis
⎯
to exclude UTI, even if it sounds psychological

85
Q

Bilateral Flank Pain, HTN, CKD on labs, polyuria/nocturia in an adult suggests

A

ADPKD

86
Q

Exercise-induced hematuria is a benign condition that can occur in long-distance runners due to traumatic injury to the ___ mucosa from repeated collision.

A

bladder

87
Q

Present in newborn boys with bladder distension, decreased urine output, and respiratory distress (due to oligohydramnios and subsequent lung hypoplasia).

A

Posterior urethral valves
⎯
Initial evaluation → renal and bladder U/S & voiding cystourethrogram

88
Q

Oligohydramnios from urinary obstruction (ex: Posterior Urethral Valves, Vesicoureteral reflux) can lead to ____, which is characterized by pulmonary hypoplasia, flat facies, and limb deformities.

A

Potter sequence

89
Q

An autosomal dominant disorder resulting in multiple benign and malignant multiorgan tumors.

Cerebellar & retinal hemangioblastomas
Pheochromocytoma
Renal cell carcinoma (clear cell subtype)

A

Von Hippel-Lindau disease

90
Q

An autosomal dominant disorder associated with early onset malignant multiorgan tumors

Breast Cancer
Sarcomas
Adrenal carcinomas
Gliomas & Medulloblastomas

A

Li-Fraumeni syndrome

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