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S2B5 MEDI > Hypernatremia > Flashcards

Hypernatremia Flashcards

1
Q

define hypernatremia

  • in what populations is it seen in most?
A
  • serum sodium > 145 mmol/L
  • hypernatremia is uncommon if one’s thirt response is intact and water is available. is it commonly seen in patients who
    • do not experience/respond to thirst
    • are unable to get water
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2
Q

what na/water imbalances lead to hypernatremia?

A
  • loss of free water
  • gain of sodium
  • combination of both
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3
Q

discuss the body’s normal resonse to an increase in plasma osmolality

A
  • increase in plasma osmolality stimulates:
    • release of ADH - minimizes water loss
    • thirst - increases water intake
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4
Q

how are neuronal cell schrinkage and and cerebral edema related to plasma osmolality?

A
  • unmitigated water loss can lead to neuronal cell shrinkage
  • on the other hand, too _rapid water replacemen_t can cause ceerebral edema
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5
Q

what are the risk factors for hypernatremia?

A
  • uncontrolled diabetes (glucosemia can cause osmotic diuresis –> polyuria)
  • other underlying polyuria disorder
  • diuretic therapies
  • circumstances that impair normal water intake:
    • mental/physical impairment
    • hospitazliation
    • nurisng home patients
    • infants
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6
Q

define hypervolemic hypernatremia

what circumstances/disease can lead to hypernatremia?

A
  • characterized by Na+ retention (and water retention, but to a lesser degree)
    • infusion of hypertonic saline
    • salt ingestion
    • mineracorticoid excess due to
      • conn’s syndrome: excess aldosterone secreted
      • cushing’s syndrome: excess cortisol secreted
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7
Q

define euvolemic hypernatremia

what circumstances/disease can lead to euvolemic natremia?

A
  • LOSS OF WATER and normal Na+. can be caused by
    • diabetes insipidus
    • hypodipisa: decreased water intake
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8
Q

define hypovolemic hypernatremia

what circumstances/diseases may lead to hypovolemic hypernatremia?

A
  • caused by a loss of Na+ and a greater loss of H20
    • ​note that the losses here can also cause hypovolemic hyponatremia. it dependens on the ratio of water:Na+ los from teh body
      • non renal losses: urine Na+ < 20
        • GI losses- vomitting/diarrhea
        • skin losses - burns, ing
      • renal losses: urina Na+ > 20
        • loop diuretics
        • osmotic diuretics
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9
Q

based on serum [Na+], volume status, and U[Na+] outline the diagnosis of the subsets of hypernatremia

A

hypernatremia = serum [Na+] over 145 mmol/L

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10
Q

presentation of infants/children with hypernatremia

A
  • irritability
  • high pitched cry
  • lethargy, somnolence, possible coma
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11
Q

patients with hypernatremia due to diabetes insipidis will likely have what symptoms?

A
  • polyuria - excessive urination
  • polydypsia - excessive thirst
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12
Q

diagnostic signs seen on physical exam of a hypernatremic patient

A
  • prolonged capillary refill (also seen in hyponatremia)
  • orthostatic hypotension (also seen in hyponatremia)
  • skin is:
    • doughy due to water loss
    • dry mucous membranes
  • tachycardia
  • sharp reflexes/myodonus
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13
Q

ADH (vasopressin)

  • where is it synthesized?
  • where is it store?
  • what are its primary functions?
A
  • synthesized in hypothalamus
  • stored in the vesicles in the posterior pituitary
  • main functions:
    • retains water by increasing water reabsorption at the collecting ducts
    • vasoconstriction
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14
Q

what defines diabetes insipidus (DI)?

what are the two types of diabetes insipidus?

A
  • defined as the passage of large volumes of DILUTE urine (low osmoarlity) due ADH defect (either lack of ADH/irresponsiveness to ADH)
    • > 3L / 24 hrs constitutes a large volume
      • 800 - 2000 ml (or 8.-2 L) in 24 hrs is considered normal
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15
Q

what symptoms and findings aid the diagnosis

A
  • symptoms:
    • polydispsia - excessive thirst (due to hypernatremia detected by osmoreceptors)
    • polyuria/nocuturia - due to high urine volume
      • polyuria - frequent urination
      • nocturia - urination throughout the night
  • findings:
    • hypernatremia
    • high urine volume
    • low urine osmolality
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16
Q

what labs/values to collect to diagnose diabetes insipidus?

A
  • a 24 hr urine volume (have they excreted more than 800-2000 mL in 24 hrs)
  • serum: electrolytites, glucose levels
  • urinary sodium [Na+]: should be low
  • simultaneous plasma and urinary osmolality
    • plasma osmolality will be high
    • urinary osmolality will be low
  • plasma ADH level
17
Q

define neurogenic (central) DI?

what are its common causes?

A
  • neurogenic DI caused by a decreased secretion of ADH. ADH is not released in response to perceived thirst
    • causes:
      • pathologies that damage the CNS:
        • pituitary injury/head trauma
        • anuerysms
        • menengitis/encephalitis/tuberculosis
        • recent brain surgery
        • brain cancer/metastasis
      • drugs: ethanol, phenytoin
      • genetic
18
Q

define nephrogenic ID

what are its common causes?

A
  • characterized by a decrease of responsivness to ADH
    • ​causes:
      • most involve damage to/inflammation of kidney/UGI system
        • urinary tract obstruction
        • sickle cell neuropathy
        • tublointerstitial disease
          • medullary cystic disease
          • polycistic kidney disease
          • Sjogrens syndrome
          • lupus
          • sarcoidosis
        • distal tubular acidosis
      • medications: lithium, demeclocycline
19
Q

diabetes melitus vs diabetes insipidus

*need to confirm this

A
  • diabetes mellitus
    • unresponsivness to insulin leads to hyperglycemia.
      • high blood glucose pulls water into the blood and dilutes serum [Na+] –> hyponatremia
  • diabetes ispididius:
    • characterized by unresponsiveness to/lack of ADH.
      • inability to reabsorb water at collecting ducts –> high [Na+] in serum –> hypernatremia
20
Q

what drugs can cause neurogenic (central) DI? what about nephrogenic (peripheral) DI?

A
  • neurogenic DI:
    • ethanol
    • phenytoin
  • nephrogenic DI:
    • lithium
    • demeclocyline
21
Q

primary polydipsia (psychogenic polydipsia)?

  • cause, sympoms and presentation
A
  • remember that this is a cause of hyponatremia
    • ​(euvolemic hypontramia)
  • but like DI (a hypernatremic state), patients with pysychogenic polydipsia have
    • dilute urine
    • polyuria
22
Q

what is the purpose of the water test and how is it done?

A
  • water test differentiates between neurogenic DI, nephrogenic DI and psychogenic polydipsia
    • since all diagnoses present with excessive water consumption, dilute urine and polyuria
  • technique:
    • 1st phase: polydipsia vs DI
      • fluid restrict patient (deprive them of water)
      • monitor serum osmolality until it reaches steady state
        • if patient’s urine osmolality normalizes (increases) –> psychogenic polysipsia
        • if urine osmolality does NOT normalize –> DI
    • 2nd phase: what kind of DI?
      • administer endogenous ADH either by:
        • intranasal ddAVP: 10 ug
        • subcutaneous route: vasopressin 5 units
      • measure serum osmolality 1 hr after ADH administered
        • if urine osm. normalizes –> neurogenic DI
          • neurogenic DI due to lack of ADH synthesis. supplementing ADH will not fix problem
        • if urine osm. does NOT normalize –> nephrogenic DI
          • nephrogenic DI due to a lack of responsivess to ADH, supplementing with ADH will not fix problem
23
Q

indicate if urine osmolality would be corrected (increased) or not corrected in each situation.

(demsopressin = ADH)

A
  • this particular chart defines correction as urine > 800 mOsm and a lack of as urine < mOsm
  • ignore primary polydispsia after ADH box - not a thing
24
Q

what defines acute vs chronic hypernatrewhat is the key difference in their treatment management?

25
Q

outline the treatment of acute symptomatic hypernatremia

  • what is the optimum rate of serum [Na+] corrected ?
  • what is the max change in serum [Na+] permited per day?
  • how often to montitor serum/urine electrolytes
  • what cautions to take
  • any other details
A
  • acute can be corrected more rapidly than chronic
    • decreased serum [Na+] at an initial rate of 2-3 mEq/L per hour for 2-3 hrs
      • max total correction per day: drop of 12 mEq/L
    • monitor serum/urine electrolytes every 1-2 hrs
    • decrease rate of correction with improvement of symptoms
  • perform serial neurological examinations throughout!!
26
Q

treatment of chronic hypernatremia with no/mild symptoms

  • what is the rate of correction?
  • what percautions to take?
A
  • correct at a maximum rate of 0.5 mEq/L decrease per hour
    • total decrease of 8-10 mEq/day permitted
  • if the case of volume deficit hypernatremia:
    • supply isotonic sodium chloride - will correct hypernatremia and restore normal volume
  • correct more slowly is there is a risk of cerebral edema
27
Q

what general treatment approaches are used to hypervolemic, euvolemic, and hypovolemic hypernatremia?

A
  • hypervolemic hypernatremia (Na+ retention)
    • diruetics
  • euvolemic hypernatremia (loss of PURE water)
    • water replacement
  • hypovolemic (loss of water AND Na+, with greater water loss)
    • give saline: either normal saline (145 mEq/L) or a ringer (135 mE1/L)
      • this restores both volume and Na+, while diluting the patient’s hypernatremic serum (you can’t use a hypertonic saline - i.e, anything over 145 mEq/L)
28
Q
  • desmopressin can be used to treat what cause of hypernatremia?
    • what is its MOA
A
  • desmopressin an ADH analog is used to treat central DI
    • MOA:
      • increases cAMP in renal tubules –> this increases water permeability of tubules –> increasing water reabsorption –> decreases urine volume + increasing urine osmolality
29
Q

other than desmopressin (DDAVP) what drugs are used to treat and how do they work?

A
  • these pharmacuetical agents can be used to treat partial central DI
    • they all work by increasing circulating ADH
      • chloropropamide
      • clofibrate
      • carbamzepine
30
Q
  • thiazide diuretics can be used to treat what types of hypernatremia?
A
  • hypervolemic hypernatemia (Na+ retention)
    • diuretics lead to –> excretion of Na+
  • nephrogenic DI:
    • thiazide diuretics act on the the NaCl cotransporter in the distal convoluted tubule to inhibit Na+ reabsorption. since the DCT Is i_mpermeable to water,_ Na+ leaves the blood but water does not follow, which dilutes the blood and concentrates the urine, correcting nephrogenic DI
31
Q

NSAIDS can be used to treat what kind of hypernatremia? how?

A

NSAIDS can be used to treat nephrogenic hypernatremia:

  • NSAIDS inhibit COX enzymes, lowering prostaglandin synthesis. some prostaglandins mediate contraction of detrusor muscle, leading to urination. lowering circulating prostaglandins limits bladder contraction, leading to better urinary retention
    • decreases polyuria
32
Q

summary of pharmaceutical treatments for central (neurogenic) DI

A
  • desmopressin
  • chlorpromade
  • clofibrate
  • carbazepine
33
Q

summary of pharmaceutical treatments for nephrogenic DI

A
  • diruetics (like thiazide)
  • NSAIDS
  • stop any medication that might cause nephrogenic DI: lithium, demeclocycline

S2B5 MEDI (7 decks)

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