Hypernatremia

40,958views

Hypernatremia

Nephrology

Nephrology

Renal system anatomy and physiology
Hydration
Body fluid compartments
Movement of water between body compartments
Renal clearance
Glomerular filtration
TF/Px ratio and TF/Pinulin
Measuring renal plasma flow and renal blood flow
Regulation of renal blood flow
Tubular reabsorption and secretion
Tubular secretion of PAH
Tubular reabsorption of glucose
Urea recycling
Tubular reabsorption and secretion of weak acids and bases
Proximal convoluted tubule
Loop of Henle
Distal convoluted tubule
Renin-angiotensin-aldosterone system
Sodium homeostasis
Potassium homeostasis
Phosphate, calcium and magnesium homeostasis
Osmoregulation
Antidiuretic hormone
Kidney countercurrent multiplication
Free water clearance
Vitamin D
Erythropoietin
Physiologic pH and buffers
Buffering and Henderson-Hasselbalch equation
The role of the kidney in acid-base balance
Acid-base map and compensatory mechanisms
Respiratory acidosis
Metabolic acidosis
Plasma anion gap
Respiratory alkalosis
Metabolic alkalosis
Horseshoe kidney
Potter sequence
Hyperphosphatemia
Hypophosphatemia
Hypernatremia
Hyponatremia
Hypermagnesemia
Hypomagnesemia
Hyperkalemia
Hypokalemia
Hypercalcemia
Hypocalcemia
Renal agenesis
Renal tubular acidosis
Minimal change disease
Diabetic nephropathy
Focal segmental glomerulosclerosis (NORD)
Amyloidosis
Membranous nephropathy
Lupus nephritis
Membranoproliferative glomerulonephritis
Poststreptococcal glomerulonephritis
Rapidly progressive glomerulonephritis
IgA nephropathy (NORD)
Alport syndrome
Kidney stones
Hydronephrosis
Acute pyelonephritis
Chronic pyelonephritis
Prerenal azotemia
Renal azotemia
Acute tubular necrosis
Postrenal azotemia
Renal papillary necrosis
Renal cortical necrosis
Chronic kidney disease
Polycystic kidney disease
Multicystic dysplastic kidney
Medullary cystic kidney disease
Medullary sponge kidney
Renal artery stenosis
Renal cell carcinoma
Angiomyolipoma
Nephroblastoma (Wilms tumor)
WAGR syndrome
Beckwith-Wiedemann syndrome
Posterior urethral valves
Hypospadias and epispadias
Vesicoureteral reflux
Bladder exstrophy
Urinary incontinence
Neurogenic bladder
Lower urinary tract infection
Transitional cell carcinoma
Non-urothelial bladder cancers
Congenital renal disorders: Pathology review
Renal tubular defects: Pathology review
Renal tubular acidosis: Pathology review
Acid-base disturbances: Pathology review
Electrolyte disturbances: Pathology review
Renal failure: Pathology review
Nephrotic syndromes: Pathology review
Nephritic syndromes: Pathology review
Urinary incontinence: Pathology review
Urinary tract infections: Pathology review
Kidney stones: Pathology review
Renal and urinary tract masses: Pathology review
Osmotic diuretics
Carbonic anhydrase inhibitors
Loop diuretics
Thiazide and thiazide-like diuretics
Potassium sparing diuretics
ACE inhibitors, ARBs and direct renin inhibitors
Pediatric urological conditions: Clinical
Elimination disorders: Clinical
Hyponatremia: Clinical
Hyperkalemia: Clinical
Hypokalemia: Clinical
Parathyroid conditions and calcium imbalance: Clinical
Metabolic and respiratory acidosis: Clinical
Metabolic and respiratory alkalosis: Clinical
Toxidromes: Clinical
Medication overdoses and toxicities: Pathology review
Environmental and chemical toxicities: Pathology review
Acute kidney injury: Clinical
Chronic kidney disease: Clinical
Urinary tract infections: Clinical
Nephritic and nephrotic syndromes: Clinical

Flashcards

Hypernatremia

0 of 10 complete

Questions

USMLE® Step 1 style questions USMLE

0 of 1 complete

A 2-year-old boy presents to the emergency department due to persistent vomiting and diarrhea over the past week. His parent states, “He just cannot seem to keep anything down, whenever I feed him he just vomits it right back up.” The patient attends daycare, and his parent is unsure of any sick contacts. He is otherwise healthy, vaccines are up to date, and birth history was uncomplicated. Temperature is 37.5°C (99.5°F), pulse is 160/min, respirations are 26/min, blood pressure is 84/40 mmHg, and O2 saturation is 96% on room air. On physical exam the patient is crying but consolable and is noted to have diminished tear production. Which of the following best describes the most likely electrolyte abnormality present?  

Transcript

Watch video only

With hypernatremia, hyper- means high, and -natrium is latin for sodium, often shortened to Na+, and -emia refers to the blood, so hypernatremia means a higher than normal concentration of sodium in the blood, generally above 145 mEq/L.

The concentration of sodium depends on both sodium and water levels in the body.

About 60% of our body weight comes from just water, and it basically sits in two places or fluid compartments—it either outside the cells in the extracellular fluid or inside the cells in the intracellular fluid.

The extracellular fluid includes the fluid in blood vessels, lymphatic vessels, and the interstitial space, which is the space between cells that is filled with proteins and carbohydrates.

One third of the water in the body is in the extracellular compartment, wheres two thirds of it is in the intracellular compartment.

Normally, the two compartments have the same osmolarity -- total solute concentration -- and that allows water to move freely between the two spaces.But the exact composition of solutes differs quite a bit.

The most common cation in the extracellular compartment is sodium, whereas in the intracellular compartment it’s potassium and magnesium.

The most common anion in the extracellular compartment is chloride, whereas in the intracellular compartment it’s phosphate and negatively charged proteins.

Of all of these, sodium is the ion the flits back and forth across cell membranes, and subtle changes in sodium concentration tilts the osmolarity balance in one direction or another and that moves water. This is why we say “wherever salt goes, water flows”.

So with hypernatremia, someone can have a high concentration of sodium in the extracellular fluid and therefore the blood, by either losing more water than sodium, or gaining more sodium than water. Either way this increases the sodium concentration in the extracellular fluid, draws water out of the cells.

When hypernatremia develops over a long period of time, the cells get time to adapt and they start generating osmotically active particle, which ends up preventing water from being lost via osmosis.

However, when hypernatremia develops acutely, the cells get no time to adapt, and the loss of water leaves them shriveled up and can cause them to die.

Now, there are several common causes of hypernatremia via water loss. All of us lose some free water everyday without even realizing it, for example through sweat as well as in the moisture breathed out during normal breathing.

Under normal conditions, this loss is replaced by the water we drink but this balance can be tipped when you have a high fever or exercise a lot on a hot summer day.

In those situations, you can have temporary hypernatremia which is easily fixed by drinking lots of water.

Another way that the body can lose free water is through the kidneys.

When the nephrons filter blood and form urine, some of the water in the filtrate is reabsorbed in the distal convoluted tubule and the collecting duct.

When you’re dehydrated, the hypothalamus releases antidiuretic hormone also called ADH or vasopressin, which acts on receptors on the nephron to boost its ability to reabsorb water.

So if there’s brain damage affecting the part of the hypothalamus that controls the release of ADH, then ADH levels could fall and the nephron wouldn’t reabsorb as much water, meaning more fluid gets lost and the urine becomes more dilute, and the sodium concentration in the blood gets more concentrated. This is called central diabetes insipidus because the fault lies centrally, in the hypothalamus.

Another possibility is that the hypothalamus makes ADH normally, but the receptors in the kidney stop responding to it. This time the fault is in the kidneys, so it’s known as nephrogenic diabetes insipidus.

Again the urine becomes dilute and the sodium concentration in the blood becomes concentrated.

Alternatively, there might be brain damage that only affects the thirst center in the hypothalamus rather than the ADH secreting part of the hypothalamus.

Here, the kidneys aren’t losing water, but the person is drinks too little water while still losing some through sweat, urination, and breathing, again resulting in hypernatremia.

Key Takeaways

Hypernatremia is a condition where the blood sodium levels are too high, specifically above 145 mEq/L. Having proper blood sodium levels is essential for the conduction of nerve impulses and the balance of water and minerals in the body. When the levels are too high, it can cause dehydration, seizures, coma, and even death.