Hypernatremia & Hyponatremia Flashcards

1
Q

Normal serum sodium is between _ and _

A

Normal serum sodium is between 135-145 mEq/L

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2
Q

We care about the serum sodium levels because sodium is a major determinant of _

A

We care about the serum sodium levels because sodium is a major determinant of volume status and serum osmolality
* Normal 285 mOsm/kg

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3
Q

Serum osmolality equation

A

Serum osmolality equation = (2Na) + (Glucose/18) + (BUN/2.8)

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4
Q

Hypernatremia presents with symptoms such as _

A

Hypernatremia presents with symptoms such as dehydration, polyuria, polydipsia, seizures/coma

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5
Q

Hypernatremia is caused by either a _ in Na+ or a _ in H2O

A

Hypernatremia is caused by either an increase in Na+ or a decrease in H2O

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6
Q

Primary causes of hypernatremia include:

A

Primary causes of hypernatremia include:
1. Diabetes insipidus
2. Hyperaldosteronism
3. Decreased H2O intake
4. Increased H2O loss

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7
Q

Central diabetes insipidus is caused by _

A

Central diabetes insipidus is caused by lack of ADH

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8
Q

Nephrogenic diabetes insipidus is caused by _

A

Nephrogenic diabetes insipidus is caused by resistance to ADH
* Receptors are not responding

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9
Q

A patient has hypernatremia, excessive thirst and heavy urination; the first step in diagnosis is _

A

A patient has hypernatremia, excessive thirst and heavy urination; the first step in diagnosis is water deprivation
* If urine is still dilute: diabetes insipidus
* If urine is concentrated: psychogenic polydipsia

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10
Q

A patient has hypernatremia, excessive thirst and heavy urination; if the water deprivation reveals concentrated urine then it suggests _

A

A patient has hypernatremia, excessive thirst and heavy urination; if the water deprivation reveals concentrated urine then it suggests psychogenic polydipsia
* This is often seen in psychiatric patients

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11
Q

A patient has hypernatremia, excessive thirst and heavy urination; if the water deprivation reveals dilute urine then it suggests _

A

A patient has hypernatremia, excessive thirst and heavy urination; if the water deprivation reveals dilute urine then it suggests diabetes insipidus
* Next we administer ADH (desmopressin)

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12
Q

How can we differentiate between nephrogenic and central DI?

A

We differentiate between nephrogenic and central DI via ADH administration

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13
Q

If ADH is administered, we expect the urine to be (dilute/concentrated) in nephrogenic DI

A

If ADH is administered, we expect the urine to be dilute in nephrogenic DI
* Because we are still not responding to ADH

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14
Q

If ADH is administered, we expect the urine to be (dilute/concentrated) in central DI

A

If ADH is administered, we expect the urine to be concentrated in central DI
* The problem with central DI was that we were unable to make ADH to bring back free water and concentrate the urine
* Now, with the administration of ADH the urine is finally concentrated

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15
Q

How do we manage hypernatremia?

A

Hypernatremia is managed with:
* Fluid replacement
* Thiazide diuretics
* NSAIDs (nephrogenic DI)
* Desmopressin (central DI)

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16
Q

Thiazide diuretics work via _ to treat nephrogenic DI (in combination with NSAIDs)

A

Thiazide diuretics work via blocking the Na/Cl cotransporter to treat nephrogenic DI (in combination with NSAIDs)
* This blocks Na+ reabsorption in the DCT but also causes the sympathetic nervous system to increase reabsorption in the PCT

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17
Q

NSAIDs are used to treat nephrogenic DI via _ (in combination with thiazide diuretics)

A

NSAIDs are used to treat nephrogenic DI via blocking prostaglandin production (in combination with thiazide diuretics)
* Prostaglandins are ADH antagonists

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18
Q

Water balance in the body is maintained by:

A

Water balance in the body is maintained by:
1. The osmotic release or inhibition of release of ADH
2. The response of the kidney to ADH
3. Stimulation of thirst

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19
Q

We have an osmostat in the _ region of the brain that stimulates thirst

A

We have an osmostat in the hypothalamus that stimulates thirst

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20
Q

Explain the pituitary-renal feedback system that maintains the amount of water in the body

A

Loss of water –>
Rise in serum tonicity –>
ADH is released & Thirst initiated –>
ADH stimulates increased tubular reabsorption of water,
Thirst increases water intake –>
Both act to dilute the body fluid –>
Inhibition of ADH & inhibition of thirst –>
Loss excess water

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21
Q

What does it mean when the urine is maximally concentrated?

A

Maximally concentrated urine (1200):
* The goal is to excrete solute in as small amount of urine as possible
* Low water intake
* Low urine volume
* High ADH levels

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22
Q

What does it mean when the urine is maximally dilute?

A

Maximally dilute urine (50-100):
* The goal is to excrete as much water as necessary
* Large water intake
* Large urine volume
* No ADH

23
Q

In order to concentrate the urine we must have _

A

In order to concentrate the urine we must have ADH

24
Q

Three physiologic stimuli for ADH release

A

Three physiologic stimuli for ADH release
1. Increased plasma osmolality
2. Decreased ECF
3. Decreased blood pressure

25
Q

Examples of pathologic, nonosmotic stimuli for ADH release

A

Examples of pathologic, nonosmotic stimuli for ADH release:
* Drugs
* Vomiting
* Stress
* SIADH

26
Q

If osmoreceptors sense hypotonicity while at the same time baroreceptors sense low blood pressure, ADH is (inhibited/secreted)

A

If osmoreceptors sense hypotonicity while at the same time baroreceptors sense low blood pressure, ADH is secreted
* Blood pressure regulation trumps tonicity
* ADH can still get released despite being in a hypotonic state

27
Q

In order to estimate our ICF, we must know _

A

In order to estimate our ICF, we must know effective osmolality
* ICF volume is inversely related to effective osmolality

28
Q

In order to estimate our ECF, we must evaluate _

A

In order to estimate our ECF, we must evaluate volume status by physical examination
* High ECF: edema, pulmonary (crackles), venous congestion (JVP)
* Low ECF: low BP, tachycardia, decreased capillary refill

29
Q

Most often, we can estimate ECF via the physical exam; however, the exception is _

A

Most often, we can estimate ECF via the physical exam; however, the exception is SIADH
* In SIADH, we have an increased ECF but overall euvolemic state

30
Q

Hyponatremia is defined as [Na+] < _

A

Hyponatremia is defined as [Na+] < 135 mEq/L

31
Q

[Na+] =

A

[Na+] = ECF Na+ / ECF H2O

32
Q

What will serum osmolality tell us about hyponatremia?

A

High serum osmolality ( > 295 mOsm/kg):
* Hypertonic hyponatremia: hyperglycemia

Low serum osmolality ( < 280 mOsm/kg):
* Hypotonic hyponatremia (what we should probably expect)

Normal serum osmolality (280-295 mOsm/kg):
* Hyperproteinemia, hyperlipidemia

33
Q

What does it mean if you have hyponatremia and high serum osmolality?

A

High serum osmolality must be from something other than Na+ in the serum –> hyperglycemia for example
* High glucose in the serum pulls water out of the cell and dilutes the Na+

34
Q

What does it mean if you have hyponatremia but normal serum osmolality?

A

What does it mean if you have hyponatremia but normal serum osmolality?
* You have a pseudohyponatremia (hyperproteinemia or hyperlipidemia)

35
Q

If you have hyponatremia and low serum osmolality, what do you do next?

A

Most commonly hyponatremia is associated with low serum osmolality –> next we need to check the volume status
* Is the patient hypovolemic, euvolemic, or hypervolemic?

36
Q

Causes of hypotonic, hypovolemic hyponatremia

A

Causes of hypotonic, hypovolemic hyponatremia:
* Extrarenal salt loss like dehydration, diarrhea, vomiting
* You have likely rehydrated with pure water

37
Q

Causes of hypotonic, euvolemic, hyponatremia

A

Causes of hypotonic, euvolemic, hyponatremia:
* SIADH
* Thiazides
* Hypothyroidism
* Increased CRH
* Psychogenic polydipsia
* Endurance exercise

38
Q

Causes of hypotonic, hypervolemic, hyponatremia

A

Causes of hypotonic, hypervolemic, hyponatremia:
* Congestive heart failure
* Liver disease

39
Q

Hyponatremia with low serum osmolality (hypotonic) + low urine osmolality; ADH is (present/not present)

A

Hyponatremia with low serum osmolality (hypotonic) + low urine osmolality; ADH is not present
* Urine is dilute so ADH is not present
* Causes include primary polydipsia, low solute intake, beer potomania, tea and toast diet

40
Q

Hyponatremia with low serum osmolality (hypotonic) + high urine osmolality; ADH is (present/not present)

A

Hyponatremia with low serum osmolality (hypotonic) + high urine osmolality; ADH is present
* The urine is concentrated so ADH is present
* Multiple causes including true hypovolemia (volume loss), CHF/ cirrhosis (hypervolemic), and SIADH (euvolemic)

41
Q

Patient with hypotonic hyponatremia from vomiting, burns, diarrhea will have UNa+ of _

A

Patient with hypotonic hyponatremia from vomiting, burns, diarrhea will have UNa+ of < 20 mEq/L

42
Q

Patient with hypotonic hyponatremia due to CHF, cirrhosis, nephrosis will have UNa+ of _

A

Patient with hypotonic hyponatremia due to CHF, cirrhosis, nephrosis will have UNa+ of < 20 mEq/L

43
Q

Patient with hypotonic hyponatremia from SIADH will have UNa+ of _

A

Patient with hypotonic hyponatremia from SIADH will have UNa+ of > 40 mEq/L
* The concentration of Na+ in the urine will be high because water will be so low in the urine
* Volume expansion also induces pressure natriuresis which increases urine sodium

44
Q

Causes of SIADH

A

Causes of SIADH:
* Drugs (ecstasy)
* Pulmonary disorders
* Tumors
* CNS disorders
* HIV, pain, post-op, nausea, stress
* Vigorous exercise

45
Q

The consequence of rapid correction of hyponatremia is _

A

The consequence of rapid correction of hyponatremia is osmotic demyelination syndrome
* Also called central pontine myelinolysis
* “Low to High your pons will die”
* Causes locked in syndrome: paralysis

46
Q

_ is the consequence of rapid correction of hypernatremia

A

Cerebral edema is the consequence of rapid correction of hypernatremia

47
Q

Polyuria is defined as the excretion of more than _ L of urine per day

A

Polyuria is defined as the excretion of more than 3 L of urine per day

48
Q

What is on our differential when a patient presents with polyuria?

A

Patient is excreting over 3L of urine per day…
Is a solute pulling out water?
Is there a problem with ADH?
Is someone simply drinking too much?

49
Q

How does urine osmolality narrow our differential of polyuria?

A

If patient with polyuria has a low urine osmolality (< 200 mOsm/kg): ADH is not functioning; we are losing lots of water in the urine

If patient with polyuria has a high urine osmolality (> 300 mOsm/kg): osmotic or solute diuresis

50
Q

How does the water deprivation test help to narrow our differential?

A

Patient is now NPO:
* Uosm < 200: DI
* Uosm > 600: primary polydipsia

51
Q

How does desmopressin help to differentiate between DI?

A

Administering desmopressin means giving the patient a synthetic ADH:
* Uosm < 200: kidneys are still not responding to ADH; nephrogenic DI
* Uosm > 600: finally we are concentrating the urine; central or gestational DI

52
Q

Headache, N/V are more classically associated with (hypo/hyper) natremia

A

Headache, N/V are more classically associated with hyponatremia
* Depends on volume status though

53
Q

Addison’s disease is a possible cause of _ natremia

A

Addison’s disease is a possible cause of hypovolemic hyponatremia
* Addison’s is an adrenal insufficiency