Hyponatremia and Hypernatremia Flashcards
1
Q
Hypertonic Hyponatremia
A
If high glucose or mannitol inc tonicity of serum –> water out of cells and into serum –> dilutes Na conc in serum
2
Q
Katz Conversion
A
- Can decide if dec serum Na is actually due to inc serum glucose
- Can correct for Na conc during hyperglycemia (add 1.6 mEq/L of Na for every extra 100 mWq/L of glucose above 100)
3
Q
Iso-osmotic Hyponatremia
A
Pseudohyponatremia
- Lab artifact when using indirect ion-selective electrode to measure serum Na conc
- Indirect method looks at Na in both the aqueous and non-aqueous parts of serum; so if high levels of lipid/protein then the non-aqueous part increases and displaces some of the aqueous part of serum –> so less overall water content in blood/reflected as less overall Na conc in blood
- FALSE LOW NA
4
Q
5 Scenarios of Hypotonic Hyponatremia (+ what labs distinguish them)
A
- 1- Normal Na content - inc water content (polydipsia)
- *low urine Osm
- 2- Dec Na content - less dec in water content (volume loss - more Na lost than water b/c vasopressin)
- *High urine Osm/low urine Na (RAAS) but hypovolemic
- 3- Inc Na content - greater inc in water content (HF or liver cirrhosis w/ RAAS act)
- *High urine Osm/low urine Na (RAAS) but hypervolemic
- 4- Dec Na content - inc water content (SIADH)
- *High urine Osm/HIGH urine Na (just ADH)
- 5- Dec Na content - normal water content
- *Does not occur in real life b/c when Na is lost so is water - lost together
5
Q
SIADH (causes, early and late pathophysiology, labs)
A
Syndrome of inappropriate ADH secretion (SIADH)
- Can be from pneumonia, lung cancer, CNS tumors, encephalitis/meningitis, nausea or pain and some drugs (SSRIs, carbamazepine, cyclophosphamide)
- Pathophysiology - ADH secreted in absence of low effective arterial blood vol or hypertonicity –> water retention and not making up for water intake –> elevated water
- Compensatory natriuresis (get rid of Na to make up for high volume); “ADH escape”
- Clinical - high urine Osm (retain water) but high urine Na (comp natriuresis), euvolemia (high at first when water retention - inc water in ECF but evens out w/ comp and body becomes resistant to vasopressin/ADH)
6
Q
Acute v. Chronic Hyponatremia and the Brain
A
- If dec plasma tonicity then water leaves IV space –> brain edema (risk herniation)
- Adapts by dec solute to dec ICF Osm to stop gradient (takes 48 hrs)
- So acute hyponatremia (<48 hrs) = more brain edema b/c less time to adapt
- Chronic hyponatremia (>48 hrs) = less brain edema b/c more time to adapt - Symptoms of cerebral edema
- If severe… seizures, coma, brain herniation (“hyponatremic encephalopathy”)
- If moderate… lethargy, disorientation, confusion
- If mild … fatigue, nausea, headache
7
Q
Proper Na Correction in Hyponatremia
A
- Want to inc Na but not too much (avoid ODS)
- Inc 6 mEq/L in 6 hrs if severe/moderate or in 24 hrs if more mild
- ODS (osmotic demyelination syndrome)
- Unclear mechanism but rapid correction of chronic hyponatremia leads to demyelination at multiple sites in brain (BBB breakdown and glial cell damage)
- Risk if alcoholism, malnutrition, adv liver disease, liver transplant, hypokalemia
- Symptoms (delayed - several days or wk) - altered mental status, quadriparesis, dysphagia, dysarthria
- No effective tx - maybe re-lowering Na
8
Q
How to treat each cause of hyponatremia
A
Polydipsia - fluid restriction
Hypovolemia - volume expansion (IV w/ some NaCl)
Heart fail/liver cirrhosis - fluid restriction and loop diuretics (to get rid of excess water) then Vaptans (V2 receptor antagonists)
SIADH - treat underlying cause; fluid restriction/loop diuretic w/ salt tablet (to get rid of excess volume caused by inc ADH), Vaptans (block ADH), Demeclocycline (prevent new AQP2)
9
Q
Vaptans v. Demeclocycline
A
- Demeclocycline - inhibit adenylyl cyclase in principal cells –> dec cAMP so no new AQP2 channels in ducts
- Vaptans (V2 receptor antagonists); expensive
10
Q
When does hypernatremia occurs?
A
- Occurs if less water intake along w/ high Na, normal water loss or abnormal water loss
- If thirsty then this will compensate so only occurs when not thirsty/not drinking
- Water unavailable (lost in desert)
- Unconscious (not awake to drink)
- Altered thirst mechanism so pt not thirsty
11
Q
5 Scenarios of Hypernatremia
A
- 1- High Na - normal water content
- *Does not occur in real life
- 2- Higher Na - high water (if give hypertonic IV and cannot drink)
- *High urine Osm/hypervolemia
- 3- Normal Na - dec water (normal water loss but cannot drink) **High urine Osm/euvolemia OR (diabetes - insipidus or nephrogenic) **Low urine Osm/euvolemia
- 4- Inc Na - dec water
- *Does not occur in real life
- 5- Dec Na - more dec water (inc extra-renal loss w/o drinking)
- *High urine Osm/hypovolemia
12
Q
Diabetes Insipidus v. Neprhogenic Diabetes
A
- Can be Diabetes Insipidus
- Idiopathic (most common)
- Genetic - dysfunctional ADH (ADH gene mutation), Wolfran syndrome, congenital hypopituitarism
- Acquired - neurosurgery, brain tumor, head trauma, infiltrative disorders
- Responds to desmopressin
- Can be Nephrogenic Diabetes
- Genetic - inactive V2 mutation or inactive AQP2 gene
- Acquired - renal disease, electrolyte abnormalities or drugs (lithium, demeclocycline, vaptans, ifosamide)
- Does not respond to desmopressin
13
Q
Clinical Manifestations of Hypernatremia
A
- Brain Adaptation
- Water leaves brain –> brain shrinkage
- Adapts by inc ICF osm to stop water movement out (RVI - regulatory vol inc - start by gaining NaCl then organic solutes)
- Acute (<48 hr) = less time to adapt
- Chronic (>48 hr) = more time to adapt; more common
- Symptoms
- Mild - irritable and restless
- Moderate - stupor, muscle twitch, hyper-reflexive
- Severe - seizure, coma, death
14
Q
Tx of Hypernatremia
A
- Admin water or hypotonic IV (correct free water deficit)
- Target underlying disorder
- Diuretics if excess Na
- Diabetes Insipidus - desmopressin
- Nephrogenic Diabetes - thiazide diuretics
- Goal = dec Na conc by no more than 10 mEq/L in 24 hr
