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CRRAB II Week 4 - WLB > Natremic - Popham > Flashcards

Natremic - Popham Flashcards

1
Q

What is the normal serum sodium?

A

135-145 mEq/L

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2
Q

What level of serum sodium classifies as HYPOnatremia?

A

sodium less than 135

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3
Q

What level of serum sodium classifies as HYPERnatremia?

A

sodium greater than 145

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4
Q

What is the normal plasma/serum osmolality?

A

285 - 300

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5
Q

How can you estimate the serum osmolality with known values of sodium, BUN, and glucose?

A

Equation:

Osmolality = 2(Na) + BUN/2.8 + Glucose/18

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6
Q

What solute is the main contributor to serum osmolality?

A

Sodium

(obviously)

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7
Q

Fill in the blank:

Hyponatremia/Hypernatremia is almost always a ______ problem, not a ______ problem!

A

Hyponatremia/Hypernatremia is almost always a WATER problem, not a SALT problem!

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8
Q

In the case of Hyponatremia & Hypernatremia, what are symptoms due to?

A

Alterations in plasma osmolality and subsequent changes in brain cells.

  • Hyponatremia
    • extracellular hypoosmolality → subsequent brain cell swelling
  • Hypernatremia
    • extracellular hyperosmolality → causes brain cell dehydration/shrinkage
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9
Q

Although reversible, what are common symptoms of hyponatremia (Na+ <125mEq/L, Na+ 115-120 mEq/L, Na+ < 115 mEq/L)?

A
  • Na+ <125mEq/L: nausea/malaise
  • Na+ 115-120 mEq/L: headache/lethargy
  • Na+ < 115 mEq/L: obtundation, seizures, coma
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10
Q

Although most are reversible, what are common symptoms of HYPERnatremia?

A
  • Lethargy
  • Weakness
  • Irritability
  • Twitching
  • Seizures
  • Coma
  • Death
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11
Q

When do clinically significant water shifts occur in HYPERnatremia?

A
  • 30-35 mOsm/kg osmolar gradient between plasma & brain
  • Or a Na+ elevation of 17 mEq/L
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12
Q

What is ADH released in response to?

A
  • Osmotic stimuli
    • increases in plasma osmolality
  • Non osmotic stimuli
    • Non-osmotic signals from baroceptors → indicating hypovolemia or decreased ECV
    • Pain, esophageal stimuli (intubation, NG tube, esophageal ca), various medications
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13
Q

What happens to urine osmolality and serum osmolality if ADH is present?

A
  • If ADH present →water channels present:
    • urine osmolality will be high as water is returned to the blood
    • lowering serum osmolality
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14
Q

What happens to urine osmolality and serum osmolality if ADH is absent?

A
  • If ADH absent → water channels absent
    • urine osmolality will be low as water is excreted in the urine
    • raising serum osmolality
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15
Q

Considering the plasma osmolality is maintained within 1%, what happens when the Posm becomes high?

A
  • thirst
  • ADH released
  • collecting tubule permeable to water (water channels inserted) free water reabsorbed
  • free water reabsorbed → production of concentrated urine
  • high Uosm
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16
Q

Considering the plasma osmolality is maintained within 1%, what happens when the Posm becomes low?

A
  • no thirst
  • no ADH released
  • collecting tubules impermeable to water (no water channels)
  • loss of free water → production of dilute urine
  • low Uosm
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17
Q

If high Urine osmolality, is ADH present or absent?

A

ADH present, kidney reabsorbing water

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18
Q

If low Urine osmolality, is ADH present or absent?

A

ADH low or absent, kidney excreting water

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19
Q

What does urine [Na+] generally tell you about the kidneys?

A

Urine Na+ generally tells you what the kidney thinks about the body’s volume status (effective circulating volume, ECV).

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20
Q

What does the kidney think if there is high urine Na+?

A

kidney behaving as if body is volume expanded, getting rid of excess sodium

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21
Q

What does the kidney think if there is low urine Na+?

A

kidney behaving as if body is volume depleted, reabsorbing/reclaiming sodium

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22
Q

What does a Urine Osmolality <100 indicate?

A

no ADH present, and urine is maximally dilute

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23
Q

What does a Urine Osmolality of >100 indicate?

A
  • varying degrees of ADH activity
    • the higher the Uosm → the more ADH is present
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24
Q

What is the normal urine osmolality range in a normal kidney?

A

50-1400 mOsm/L

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25
Q

What is the minimum volume of water excreted daily (with working kidneys) based on a daily osmolar load of 500 mOsm and maximal urine osmolarity of 1000 mOsm?

A

500 / 1000 = 0.5 L

(qualifies as oliguria)

26
Q

What is the minimum volume of water excreted daily (with working kidneys) based on a daily osmolar load of 750 mOsm and maximal urine osmolarity of 1000 mOsm?

A

750 / 1000 = 0.75 L

27
Q

What is the maximum volume of water excreted daily (with working kidneys) based on a daily osmolar load of 500 mOsm and maximal urine osmolarity of 50 mOsm?

A

500 / 50 = 10 L

28
Q

What is the maximum volume of water excreted daily (with working kidneys) based on a daily osmolar load of 750 mOsm and maximal urine osmolarity of 50 mOsm?

A

750 / 50 = 15

29
Q

In a steady state, what is the amount of dietary intake of sodium vs. the excretion of sodium?

A

dietary intake of sodium = urinary excretion of sodium

30
Q

How do the renal tubules handle sodium if volume depleted?

A

kidney responds to hormones (Angiotension II, aldosterone) to retain sodium

31
Q

What percent of Na+ is reabsorbed in each section of the nephron tubules?

A
  • Proximally: 65%
  • Loop: 25%
  • Distally: 5%
  • Collecting Duct: 4%
32
Q

What influences regulate the amount of Na+ reabsorption in the Proximal Tubule?

A
  • Neurohumoral regulation
    • Influenced by:
      • hemodynamics
      • Angiotension II
      • dopamine
      • Norepinephrine
33
Q

What influences regulate the amount of Na+ reabsorption in the Loop of Henle?

A
  • Flow dependent
    • Generates dilute urine in ascending limb d/t water impermeability
34
Q

What influences regulate the amount of Na+ reabsorption in the Distal Tubule?

A
  • Flow dependent
    • Distal and loop diuretics work best to help you get rid of Na+
35
Q

What influences regulate the amount of Na+ reabsorption in the Collecting duct?

A
  • Neurohumoral regulation
    • Aldosterone
    • Atrial natriuretic peptide (ANP)
36
Q

HYPOnatremia usually reflects what type of osmolality?

A

HYPOosmolality!

  • Posm = Na x 2 + glucose/18 + BUN/2.8 = 285-300
  • BUN is ineffective osmole
    • crosses membranes so doesn’t contribute to osmotic gradient
  • If glucose normal, doesn’t add much
  • So effectively → Posm = Na x 2 if glucose normal
37
Q

What is pseudohyponatremia?

A
  • Hyponatremia with normal Posm (pseudo)
    • Due to:
      • Hyperlipidemia
      • Hyperproteinemia
  • Lipids/protein take up more plasma space, and reduces plasma water space, but Na+ still measured in total plasma space
38
Q

How does hyponatremia develop if mechanisms are in place to maintain plasma osmolarity within 1%?

A
  • Osmotic stimuli to ADH would maintain plasma osmolarity within 1% by itself, without regard to ECV status
  • Non-osmotic stimulus (from baroreceptors in kidney/carotid/heart) for ADH secretion maintain effective circulating volume (ECV) at expense of plasma osmolarity
    • Better to have brain perfusion than perfect plasma osmolarity
39
Q

How does hyponatremia occur in the setting of an elevated Posm?

A
  • hyperglycemia
  • hypertonic mannitol
    • Water shifts out of cells to reestablish osmotic equilibrium, so Na+ is now more dilute in plasma water
40
Q

What does the clinical evaluation for hyponatremia consist of?

A
  1. Check Posm → confirm true hypoosmolar hyponatremia
  2. Check Uosm → is ADH acting?
    • Uosm < 100: little or no ADH, appropriate if hypoosmolar
    • Uosm > 100: ADH is present despite hypoosmolarity – either appropriately to volume status or inappropriately
  3. Check UNa+ → what is kidney’s perception of ECV?
  4. Check patient/H&P → what is volume status/clinical status?
  5. History: volume losses (bleeding, vomiting, diarrhea, diuretics), medications, pain, surgery
  6. Physical Exam for volume status: neck veins, edema, rales, S3, orthostatic vital signs, skin turgor
  7. Labs: electrolytes for metabolic alkalosis/acidosis, K+, renal failure, Posm, Uosm, UNa+
41
Q

What is the DDx for Hyponatremia with Uosm < 100?

A
  • Primary Polydipsia
    • excessive water intake (psych)
    • Tx by restricting fluid intake
  • Beer Potamania
    • low daily osmolar intake
    • Tx by giving protein
  • Tea & Toast Syndrome
    • low daily osmolar intake
    • Tx by giving protein
42
Q

What is the biggest question in diagnosing a patient with Hyponatremia and Uosm > 100?

A

Whether ADH release is appropriate to volume depleted status or if ADH release is inappropriate to both osmolality and volume status?

  • ADH release when plasma hypoosmotic is “inappropriate” from the standpoint of osmotic stimuli, but not if ECV depletion present
43
Q

Given the UNa+ is <10, how do you evaluate a patient that is volume depleted?

A
  • UNa+ < 10 & volume depleted
    • Kidney reabsorbing Na+ in effort to reexpand vascular space
    • Hyponatremia develops because non-osmotic stimuli to ADH secretion overwhelm desire to keep Posm in range
      • GI losses (n/v/diarrhea), skin losses (burns), diuretics (late), poor cortisol deficiency
44
Q

Given the UNa+ is <10, how do you evaluate a patient that is volume expanded?

A
  • UNa+ <10 & volume expanded, but with ECV depletion
    • Kidney is receiving wrong signals → edematous states
      • CHF/cirrhosis/nephrosis
    • Non-osmotic stimuli to ADH secretion cause reabsorption of free water, without regard to Posm
45
Q

Given the UNa+ is >10, how do you evaluate a patient that is volume expanded?

A
  • volume appropriate or expanded (brain or kidney confused)
    • excess ADH production → reset osmostat (body set to different osm state)
      • CKD
      • SIADH: Syndrome of Inappropriate ADH secretion
46
Q

Given the UNa+ is >10, how do you evaluate a patient that is volume depleted?

A
  • kidney is receiving wrong signals
    • adrenal insufficiency
    • salt wasting renal nephropathy
    • diuretics (early)
    • hypokalemia w/ metabolic acidosis after vomiting (obligate Na+ loss w/ bicarb loss)
    • hypothyroidism
47
Q

How do you treat Hyponatremia with UNa+ less than 10?

A
  • Volume depleted → give NS to replenish volume and turn off ADH
    • Giving them Na+ so they can clear free water (get them above daily osm load)
  • Volume neutral or expanded → restrict free water intake, or treat states of poor perfusion
  • Severe hyponatremia not related to pure volume depletion or with neurologic symptoms may require hypertonic saline (3% saline) to get out of danger zone
  • ADH antagonist (Tolvaptan, Conivaptan) can be used in states of volume expanded hypoNa+
48
Q

What is the guideline for correcting hyponatremia?

A
  • If hyponatremia developed rapidly
    • ​less risk of complications from rapid correction and more likely to have symptoms from hyponatremia
  • If hyponatremia developed slowly → brain has had time to adjust (idiogenic osmoles)
    • Usually less symptomatic
    • more at risk for complications with rapid correction
49
Q

In was situations should you use 3% NaCl emergently?

A
  • To quickly bring serum Na+ out of danger range
    • 3% NaCl = 513 meq Na+/L
  • Hyponatremic seizures → 100 cc 3% NaCl over 10 minutes, IV (about 51 meq Na+)
  • Neurologic symptoms (not seizures) → 30-50 cc/hour for several hours
  • Treat underlying problem causing hyponatremia
50
Q

When is it appropriate to give ADH antagonists?

A
  • Indicated for hypervolemic hyponatremia – 3% NS contraindicated
    • can’t use Tolvaptan long term for CHF
    • cannot be used more than 30 days → risk of liver failure
51
Q

When do you see cases of Hypernatremia?

A
  • Due to excessive water losses and inadequate intake
    • Usually see problems with hypernatremia in the young, elderly, or pt with altered mental status (unable to access free H2O)
52
Q

What three things cause Hypernatremia?

A
  • Sodium Retention (rare) – infusion of hypertonic NaCl or NaHCO3, salt water drinkers
  • Water Losses with Inadequate Water Intake
    • Insensible losses: sweating, fevers, exercise, respiratory
    • Renal loss: central nephrogenic diabetes insipidus, nephrogenic diabetes insipidus, osmotic diuretic
    • GI losses/osmotic diarrhea: lactulose, malabsorption, infectious diarrhea
    • Water loss into cells: seizures, severe exercise, rhabdomyolysis
  • Primary Inadequate Water Intake – hypothalamic dysfunction
    • Primary hypodipsia, reset osmostat due to mineralcorticoid excess, essential hypernatremia
53
Q

What is the difference between Central Diabetes Insipidus and Nephrogenic Diabetes Insipidus?

A
  • Central Diabetes Insipidus:
    • hypothalamus/pituitary axis not releasing ADH, so kidney can’t reabsorb free water
  • Nephrogenic Diabetes Insipidus:
    • collecting tubules don’t respond to ADH, so kidney can’t reabsorb free water
      • Can be partial or complete
54
Q

How do you diagnose the different causes of hypernatremia?

A
  • If Na>145, POsm will be >290, check UOsm
  • At POsm > 295, ADH release should be maximal and UOsm should be 800-1400 (urine SG 1.025 – 1.030)
    • UOsm > 800 – primary hypodipsia, increased insensible/GI losses, or Na+ overload
    • UOsm <300 – severe CDI or NDI
    • UOsm 300-800 – partial DI, volume depletion with DI, or osmotic diuresis
55
Q

What are possible causes of Central Diabetes Insipidus?

A
  • Idiopathic/familial
  • Craniopharyngioma, transsphenoidal surgery
  • Head trauma, hypoxic or ischemic encephalopathy
  • Pituitary tumor or metastases
  • Sarcoidosis/Histiocytosis X
  • Cerebral aneurysm
  • Encephalitis/meningitis
  • Anorexia nervosa
56
Q

What are possible causes of Nephrogenic Diabetes Insipidus?

A
  • Congenital: x-linked, recessive
  • Hypercalcemia
  • Hypokalemia
  • Lithium (damage is permanent, will always have NDI, need hypotonic fluids post-op), demeclocycline
  • Sjogren’s syndrome, amyloidosis
  • Osmotic diuretics, loop diuretics
  • Sickle cell anemia
  • Pregnancy
  • Ifosfamide, propoxyphene overdose, methoxyflurane
57
Q

What is the treatment for Diabetes Insipidus?

A
  1. Low Na+ diet and thiazide diuretic: induce mild volume depletion, can decrease urine output by 50%
  2. Moderate protein restriction to decrease osmolar load, and therefore minimize amount of free water that can be cleared
  3. Chlorpropamide/Clofibrate/Carbamazepine can enhance effects of ADH
  4. NSAID’s can decrease effects of renal prostaglandins, which normally impair response to ADH
  5. DAVP (ADH) for Central Diabetes insipidus–also used for bed wetters (watch for hyponatremia)
58
Q

How should you correct chronic hypernatremia?

A
  • Correct chronic hypernatremia slowly, to allow brain to readjust
    • brain develops idiogenic osmoles to prevent cellular dehydration
    • Safe rate = 0.5 meq/hour or 12 meq in 24 hours (same as for hyponatremia)
59
Q

How do you calculate free water deficit?

A
  • Body water adults: male usually 60%, female 50% (higher in younger children/babies)
    • 70 kg male, with serum sodium 170
    • Use body water volume of 0.5 x LBW due to volume depletion
    • 0.5 (70kg) x {(170/140) -1}= free water deficit of 7.5 liters
  • Replace this over 60 hrs or 125 cc/hr with additional fluid for “maintenance” & other obvious losses
60
Q

How do you decide which fluid composition to administer when treating Hypernatremia?

A
  • Free water orally or D5W IV (can’t give sterile water IV)
  • ¼ NaCl for hypernatremia due to volume depletion, as patient is also Na+ depleted
  • NS if patient is hypoTN with fluid losses, then switch to hypoosmotic fluids once tissue perfusion improved
  • Follow Na+ levels frequently, as patients and their kidneys don’t always respond as calculated

CRRAB II Week 4 - WLB (9 decks)

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