lecture 50 - Hypernatremia Flashcards

1
Q

What is the most influential drier behind ADH secretion?

A

Hypovolemia&raquo_space; Hyperosmolarity

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2
Q

defense of ECF Volume

how is volume sensed?

3 Players involved

A

Baro-receptors of the atrium and carotid sinus

Catecholamines – increase Na reabsorption

RAS –

ADH

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3
Q

defense of Osmolality

how is osmolality detected?

2 Players in the defense of osmolality

A

anterior hypothalamus (SON)

Central Axis – thirst

ADH -

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4
Q

where is ADH made?

where is it stored ?

A

Synthesis: made in the SON and PVN

Stored: Posterior Pituitary

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5
Q

Non osmotic regulators of ADH

A

Nausea, Post operative pain, pregnancy

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6
Q

Hypovolemic Hypernatremia -

describe the scenario-

How do you differentiate between renal vs non renal losses of H2O?

A

scenario: Patient has lost Na, but has lost even more Water;

The patient is dehydrated and Intravascular volume depleted

UNa –
If the kidney is working appropriately, in the setting of hypovolemia, it should be reabsorbing Na and H2O

Renal Losses: UNa > 20

Non Renal: UNa < 20

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7
Q

Causes of Non Renal Losses leading to Hypovolemic Hypernatremia

A

® Excessive sweating, burns, fevers, diarrhea, fistulas

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8
Q

Causes of Renal Losses leading to Hypovolemic Hypernatremia

A

Diurectics, Intrinsic renal disease

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9
Q

○ Euvolemic Hypernatremia

describe the scenario:

what will be the Una

A

Loss of water with normal Body Sodium;

U NA will be variable

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10
Q

○ Euvolemic Hypernatremia

  • renal losses
  • extra renal losses
A

Renal Losses: Nephrogenic DI (kidney unable to respond to ADH)

Extra renal losses: 
Insensible losses (water vapor loss through skin and breath) 

Hypodipsia

Central DI

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11
Q

HyperVolemic Hypernatremia

describe the scenario

causes:

A

Excess Na in the setting of normal or only slight gain of water

Hypertonic Infusion – Normal Saline or Na Bicarb

Hypertonic Dialysis

Patient is eating a lot of salt tablets

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12
Q

Patients at risk for developing hypernatremia

A

Inability to respond to sense of thirst — CNS Lesions (CVA or Tumor)

Physically unable to respond and get water – Obtunded, Intubated, Infant

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13
Q

Clinical manifestations of Hypernatremia

A

Change in mentation – slight confusion to an overt coma

§ Metabolic encephalopathy —

(pt should have an absence of a new focal or lateralizing neurologic sign)

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14
Q

• Treatment of Hypernatremia –
—- acute setting

time frame?
what is the body doing?
- what is the treatment?

A

acute setting (<24 hours)

body attempts to even out the tonicity of the environments of the intra and extra cellular spaces by pumping the cells full of electrolytes; but this is perturbing to the CNS

Treatment: Rehydrate the patient

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15
Q

• Treatment of Hypernatremia –
—- acute setting

time frame?
what is the body doing?
- what is the treatment?

A

> 24 hours

the body extrudes perturbing electrolytes and replaces them with Idiogenic Osmoles (Betaine, phosphorycholine, sorbitol, myoinositol)

Treatment: slow hydration so as not to induce cerebral edema

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16
Q

what are the idiogenic Osmoles

A

(Betaine, phosphorycholine, sorbitol, myoinositol)

17
Q

how do you calculate the amount of water to rehydrate with in the setting of acute hypernatremia ?

A

Calculate the electrolyte free water deficit

.6 x Weight in Kg) x ((Plasma Na - 140)/140