Hypervolemic Hypotonic Hyponatremia

• True hyponatremia, or hypotonic hyponatremia, involves reduced sodium and osmolarity levels.

Volume-Based Classification of Hyponatremia

• Volume status divides hyponatremia into three categories.
• The first type is hypovolemic hypotonic hyponatremia.
• The second type starts in this text with hypervolemic hypotonic hyponatremia.

Hypervolemic Hypotonic Hyponatremia

• In hypervolemic hypotonic hyponatremia, water increase exceeds sodium increase. The extra water dilutes the sodium concentration.
• There are two ways to reach this condition.
• First is renal impairment where kidneys can't excrete water, leading to high urine sodium levels
• High urine sodium occurs because the kidneys cannot filter water effectively increasing sodium concentration.
• Second is conditions that avidly retain sodium including cirrhosis, nephrosis, and CHF, resulting in reduced effective circulating volume (ECV).
• In these cases, RAAS and ADH are activated leading to edema
• Aldosterone activation lowers urine sodium while those on diuretics may invalidate urine sodium tests

Clinical Diagnosis

• Diagnosing renal impairment clinically is possible because the patient has been suffering for a while.
• Nephrosis diagnosis may be challenging for doctors.
• Diagnosis is straightforward clinically with CHF and Cirrhosis
• Reminder: Hypotonic hyponatremia involves excessive free water intake and increased ADH activity

Hypervolemic Hypotonic Hyponatremia: Specific Causes

• Characterized by increases in both total body water and total body sodium, but the water increase is more pronounced.
• Diagnosing cause relies on concentration of the sodium based on urine
• Can be due to acute or chronic renal failure, uniquely raises urine sodium concentration.
• Renal insufficiency reduces ability to excrete free water, resulting in urine sodium concentration above 20 mmol/L.
• Also related to sodium-avid edematous disorders including heart failure, cirrhosis, and nephrotic syndrome.
• Pathophysiology is similar to hypovolemic hyponatremia.
• Effective circulating blood volume is reduced by etiologic factors rather than real loss.
• Radom Urine Na+ concentration is <20 mmol/L, often obscured by diuretics

Normovolemic Hyponatremia

• Involves decreased sodium concentration despite normal extracellular volume.
• Normovolemic patients drink a lot and amount of sodium in the body doesn't change
• Increased water dilutes sodium while volume signals for ADH remain normal
• Volume shifts as water distributes across compartments

Causes of Normovolemic Hyponatremia

• Nonhemodynamic stimuli cause nausea, cortisol deficiency, in secondary adrenal insufficiency.
• Disrupts ADH regulation and this state known as SIADH-like related to secondary adrenal insufficiency.
• Can result from primary osmoregulation defects.
• Can result from malignancy, stroke, or pneumonia.
• Condition known as Syndrome of inappropriate ADH (SIADH)

Normovolemic Hypotonic Hyponatremia: Water and Sodium Levels

• Expansion of total body water occurs due to excessive intake coupled with failure to dilute urine
• Impaired urine dilution results from defective osmotic suppression related to ADH activity.
• Nausea and cortisol deficiency stimulate conditions
• Another disorder known as Syndrome of inappropriate secretion of ADH also relates

SIADH

• Important topic with specified diagnostic criteria
• Hospital syndrome is overdiagnosed, where all criteria not followed to call it SIADH
• Doctors diagnose elevated ADH secretion without discerning cause
• On doctor's terms, hyponatremia cause is undetermined and called SIADH
• Coping mechanisms may mean SIADH patients do sometimes make improvement and management based on it

SIADH Diagnosis

• Requires strict adherence to all diagnostic criteria
• Edema rules out SIADH
• Patients drink too many water, causing hyponatremia
• Increase water intake, is a must in hyponatremia so ADH activation triggers this
• Restriction manages free water and limits hypovolemic shock as the natural ADH response will conserve water

SIADH: Key Diagnostic Factors

• Inability to regulate water loss and thus always lose some level of water through breathing, skin, gut, stool, even with ADH present
• In most cases of hyponatremia, obligatory water loss renders ADH ineffective to net any real changes because what you retain, you lose in other ways
• Even if increase ADH, unless net free water level is high, net effects of SIADH will be limited
• Only hyponatremia involves obligatory net free water losses
• Patients should be free water restricted

Treatment of SIADH

• Those with SIADH improve with controlled free H2O intake since content reduced despite ADH is present
• One criteria related to lab levels is improvement in plasma osmolarity with biochemical measures because it shows results as you follow restriction is applied

Syndrome of Inappropriate Secretion of ADH (SIADH): Key Features

• Defined by hyponatremia (low sodium) and low plasma osmolality (dilution).
• Results from the body retaining water despite low blood osmolality levels leading to impaired excretion of the water.
• Most frequent cause of Normovolemic Hyponatremia.
• Exclusion diagnosis: rule out other causes before confirming.
• Edema is not a typical feature.
• Excess water is evenly distributed.
• Distribution is insufficient to cause edema.
• SIADH requires excess water in order to observe the syndrome

Importance of Water Intake in SIADH

• Hyponatremia is driven by excess of water and not loss of sodium
• ADH concentration helpful but can raise concerns based on levels so don't rely solely on this factor

Second Case

• Cause is defect with inappropriate ADH secretion- leads body to misunderstand and not regulate ADH
  • ADH being released during problem with body's ability to regulate its handling of water
  • Triggers drugs that stimulate ADH excretion, like diuretics
  • ADH being released by body and functioning like ADH triggers certain effects

ADH with Ectopic Secretion

• Tumors stimulate SIADH that relates to specific area of brain
• Posterior pituitary gland, pulmonary and cerebral disease all linked to oxytocin and cerebral vascular system issues which result from this
• Oxytocin functions much like ADH at a high DOSE such as given at birth

Oxytocin

• Does not stimulate ADH even though it is also has ADH
  • Vasopressin 2 binds to H20 and reabsorbs in tubules

Normovolemic Hyponatremia

To recap the causes of normovelemia where water intake may play an imbalance,

• Nonhemodynamic from naseauea
  • cort defincincy stimulate
  • 'SIADH' symptoms start but high intake is still the central Primary cause: ADH by other disorders

Acute Hyponatremia

• Encephalopathy from overwhelmed water is acute cerebral- vomiting, nausea and headache often occur

Chronic Hyponatremia

• After effect of loss of osmolytes can leave damage that does not resolve
• VHA- can make full protection even after symptoms of vomiting

Hypernatremia

• Caused by excess sodium in the system related to losing liquids
  • Main concern: inability to drink Often people unable to request for it

Additional Notes

• The kidneys are not able to treat this
• Common for people with a mental condition. coma, change in mental states

Hypernatremia Clinical Signs: Alteration of Mental Status & Damage to Tissues and Hypertension

• Alteration to metal states (coma and lethargy often)
• Damage to cell membranes (Rhabdo-) from muscle groups
• Volume change causes dehydration related or volume where sodium related causes fluid expansion
• Also to mention Anorexia or vomiting will also start

Hypernatremia Causes: Extrarenal and Renal Losses

• Extrarenal factors like over hydration are primary reasons like fever, hyperventilates
• Often lead to reduced volumes from bodies and large sodium losses
• Renal failure from renal failures: Polyuria is the hallmark.
• 3/L in 24 hours.
• Cannot conserve properly.

Hypernatremia: Diagnostic Approach

To summarize Hypernatremia needs to check Extracellular fluid volume, volume and more

• Look for other items. 1 Volume minimum but concentrated = ADH on
  • Body holds much and in tubules
• 2 Large urine/ not max is water theuosis - Problem with ADH

DI

• Polyeria volume to test
• Also note for electrolyte losses and if they did have sugar issues
• Urine gravity to check the osmo
• And plasma and for anti- diuretics

Tubules and Osmosis

• Di uses that then become high in water- tubules absorb too much

More on this concept

Two types-

• Central does not release the water while nephrogenic doesn't
• If a closure- after the closure we fix issue water is released- make diuresis as well

Also mention

• If dialysis also works normally in order to get this done- may be able to treat diabetes

A Few More Important Concepts

For Hyperkalemia

• The first thing to check after if all is ok must test test for ECG is good because if damage has been done

• Next steps treat to reduce levels
• But important side is it will cause the ECGs to give issues

The other hand Hyperkalemais happens as other levels that don't work- other

• Check the levels

Hyperkalemais

• With heart changes- ECG does not function.