Hypernatremia

Question 1

define hypernatremia

• in what populations is it seen in most?

Answer 1

• 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

Question 2

what na/water imbalances lead to hypernatremia?

Answer 2

• loss of free water
• gain of sodium
• combination of both

Question 3

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

Answer 3

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

Question 4

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

Answer 4

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

Question 5

what are the risk factors for hypernatremia?

Answer 5

• 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

Question 6

define hypervolemic hypernatremia

what circumstances/disease can lead to hypernatremia?

Answer 6

• 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

Question 7

define euvolemic hypernatremia

what circumstances/disease can lead to euvolemic natremia?

Answer 7

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

Question 8

define hypovolemic hypernatremia

what circumstances/diseases may lead to hypovolemic hypernatremia?

Answer 8

• 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

Question 9

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

Answer 9

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

Question 10

presentation of infants/children with hypernatremia

Answer 10

• irritability
• high pitched cry
• lethargy, somnolence, possible coma

Question 11

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

Answer 11

• polyuria - excessive urination
• polydypsia - excessive thirst

Question 12

diagnostic signs seen on physical exam of a hypernatremic patient

Answer 12

• 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

Question 13

ADH (vasopressin)

• where is it synthesized?
• where is it store?
• what are its primary functions?

Answer 13

• synthesized in hypothalamus
• stored in the vesicles in the posterior pituitary
• main functions:
  
  • retains water by increasing water reabsorption at the collecting ducts
  • vasoconstriction

Question 14

what defines diabetes insipidus (DI)?

what are the two types of diabetes insipidus?

Answer 14

• 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

Question 15

what symptoms and findings aid the diagnosis

Answer 15

• 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

Question 16

what labs/values to collect to diagnose diabetes insipidus?

Answer 16

• 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

Question 17

define neurogenic (central) DI?

what are its common causes?

Answer 17

• 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

Question 18

define nephrogenic ID

what are its common causes?

Answer 18

• 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

Question 19

diabetes melitus vs diabetes insipidus

*need to confirm this

Answer 19

• 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

Question 20

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

Answer 20

• neurogenic DI:
  
  • ethanol
  • phenytoin
• nephrogenic DI:
  
  • lithium
  • demeclocyline

Question 21

primary polydipsia (psychogenic polydipsia)?

• cause, sympoms and presentation

Answer 21

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

Question 22

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

Answer 22

• 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

Question 23

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

(demsopressin = ADH)

Answer 23

• 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

Question 24

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

Answer 24

Question 25

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

Answer 25

* 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!!

Question 26

treatment of _chronic hypernatremia with no/mild symptoms_ * what is the rate of correction? * what percautions to take?

Answer 26

* 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

Question 27

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

Answer 27

* 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)

Question 28

* desmopressin can be used to treat what cause of hypernatremia? * what is its MOA

Answer 28

* 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

Question 29

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

Answer 29

* these pharmacuetical agents can be used to treat _partial_ central DI * they all work by increasing circulating ADH * chloropropamide * clofibrate * carbamzepine

Question 30

* thiazide diuretics can be used to treat what types of hypernatremia?

Answer 30

* 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

Question 31

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

Answer 31

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

Question 32

summary of pharmaceutical treatments for central (neurogenic) DI

Answer 32

* desmopressin * chlorpromade * clofibrate * carbazepine

Question 33

summary of pharmaceutical treatments for nephrogenic DI

Answer 33

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