Elektrolytes and Homeostasis

Beim hyperosmolaren Koma sind noch geringe Mengen an Insulin vorhanden, so dass die Lipolyse nicht einsetzt.

->Keine Ketoazidose

z.B. bei Alkoholikern, die sich schlecht ernährt haben und gefastet haben

mit Captopril

und unter Therapie der Ketoazidose ( conversion of β-hydroxybutyrate(wird nicht angezeigt) back to acetone and acetoacetate)

• Decrease glucagon release from the pancreas
• Counteract the ketogenic actions of glucagon
• Inhibit lipolysis and deplete the substrate needed for ketogenesis
• Decrease plasma glucose by increasing tissue (muscle and fat) utilisation of glucose.

Verdopplung der Insulindosis!

Art.: Vasodilatation

Ven.: Vasokonstriktion

->Insulinresistenz

Beide setzen Anionen-GAP runter

Norm-AG = 0.2 (albumin g/L) + 1.5 (phosphate mmol/L).

Zweck: bei met.Azidose mit normalem Angionen-Gap kann die Ursache durch die "urine strong ion difference" herausgefunden werden:

Strong ions: Ionen in dissoziierter Form bei normalen pH-> Strong Cations  Na⁺ and K⁺

^{Strong anions:} include Cl⁻. The difference between strong cations and anions make the strong ion difference (SID).

In conditions of acidosis, the normally functioning kidney excretes more Cl⁻ than Na⁺ and K^+->the urine SID should be negative.

• In so-called chloride-responsive metabolic alkalosis, Cl⁻ losses in excess of Na⁺ increase the SID. The urine Cl⁻ concentration is usually <10 mmol/L. GI loss, post-diuretic use and post-hypercarbic states are chloride-responsive.
• Chloride-unresponsive alkalosis results in a urine Cl⁻ concentration >20 mmol/L and is caused by mineralocorticoid excess or active diuretic use.

• Schwerer Wassermangel führt zu einem Anstieg an Na und Cl. Since the concentration of Na⁺ > Cl⁻, the difference between them increases-> SID steigt an.
• Cl⁻ -Verlust über den GI-Trakt oder Urin (diuretic use or abuse)ist  mehr als Na⁺.
• Na⁺ wird mehr zugeführt als  Cl⁻.
• Schwerer Mangel an magnesium oder Kalium. Dies vermindert intracellulares Cl⁻ and secondarily total body Cl⁻.

• Diuretikagabe oder Missbrauch (am häufigsten)
• GI-Verluste von Cl⁻(vomiting, gastric drainage, and rarely, chloride wasting diarrhoea (villous adenoma)).
• Gabe von nichtcholrierten Salzen: massive blood transfusions (sodium citrate), parenteral nutrition (sodium acetate), plasma volume expanders (acetate or citrate), Ringer’s solution (sodium lactate) or overzealous use of sodium bicarbonate.
• Abklingen einer schwerer Hyperkapnie führt zu Alkalose.
• Mineralocorticoid excess: primary hyperaldosteronism (Conn’s syndrome), secondary hyperaldosteronism, Cushing’s syndrome, Liddle’s syndrome, Bartter’s syndrome, exogenous corticosteroids,Lakritze!

• New-onset arrhythmias, especially atrial fibrillation
• Acute confusional state
• Severe fever and persistent tachycardia
• Anxiety, tremors and palpitations
• Diarrhoea or unexplained weight loss
• Muscle weakness.

• Severe vasodilatory shock refractory to vasopressor therapy
• Persistent shock despite adequate resuscitation, antibiotics and source control in a septic patient
• Unexplained or recurrent hypoglycaemia
• Unexplained fever
• Protracted hyperkalaemia combined with hyponatraemia
• Overwhelming sepsis, HIV infection and severe stress if the patient has been previously exposed to corticosteroids.

• high fever
• delirium
• severe cardiac arrhythmias and failure
• seizures
• jaundice

•  Excess thyroxine from the thyroid gland
  • Grave's disease (M.Basdow->Rez.antikörper->TRAK)
  • Autonomous thyroid hormone production from the thyroid gland (adenoma, toxic multinodular goitre)
  • Increased thyroid hormone release (nur vorübergehend bei thyroiditis)
  • TSH secreting pituitary tumours
  • Ectopic TSH production (choriocarcinoma)
•  Excess thyroxine from non-thyroid source
  • Thyrotoxicosis factitia and deliberate overdose
  • Ectopic thyroxine  secretion (ovarian teratoma)

Propanolol, hemmt auch die Umsetzung von T4 in T3

60-80mg 4stdl.

propylthiouracil (PTU) , hemmt ebenfalls Umsetzung von T4 in T3

supranormale Dosis: 200mg /d

They reduce T4 to T3 conversion, and may have a direct effect on the underlying auto-immune process if the thyroid storm is due to Grave’s disease. Hydrocortisone is the usual drug of choice and is given at a dose of 100 mg intravenously every eight hours in patients with thyroid storm.

• Diuretic use (or abuse) is perhaps the most common cause of metabolic alkalosis.
• Gastrointestinal losses of Cl⁻ may be due to vomiting, gastric drainage, and rarely, chloride wasting diarrhoea (villous adenoma).
• Administration of non-chloride sodium salts can occur with massive blood transfusions (sodium citrate), parenteral nutrition (sodium acetate), plasma volume expanders (acetate or citrate), Ringer’s solution (sodium lactate) or overzealous use of sodium bicarbonate.
• For several hours (or longer) following recovery from chronic, renally compensated hypercarbia, metabolic alkalosis (chloride-responsive) will persist.
• Mineralocorticoid excess: primary hyperaldosteronism (Conn’s syndrome), secondary hyperaldosteronism, Cushing’s syndrome, Liddle’s syndrome, Bartter’s syndrome, exogenous corticosteroids, and excessive liquorice intake.

• Severe depletion of free water inducing a parallel increase in Na⁺ and Cl⁻. Since the concentration of Na⁺ > Cl⁻, the difference between them increases.
• Cl⁻ is lost from the GI tract or urine (diuretic use or abuse) in excess of Na⁺.
• Na⁺ is administered in excess of Cl⁻.
• There is a severe deficiency of intracellular cations such as magnesium or potassium. This decreases intracellular Cl⁻ and secondarily total body Cl⁻.

• For patients with diuretic-induced metabolic alkalosis, 0.45% saline is effective for reversing free water deficit and treating alkalosis. Also consider expanding the circulating volume and stopping diuretics.
• For patients with volume overload and metabolic alkalosis, KCl can be administered along with loop diuretics. Alternatively, K⁺ sparing diuretics (which will also spare Cl⁻) can be used.
• Acetazolamide (250–500 mg bid), inhibits carbonic anhydrase and can induce excretion of Na⁺ in excess of Cl⁻ and thus reduce the SID.
• For patients with renal failure and at risk of volume overload, dilute (0.1N) HCl acid can be administered through a central venous line. Each litre of this solution contains 100 mmol of Cl⁻, and it is advisable to recheck the acid-base status after each litre. However, it is important to remember this treatment has potential risks and may not be licensed in many jurisdictions.

• hypothyroidism
• cirrhosis
• chronic heart failure
• conditions known to cause the syndrome of inappropriate antidiuretic hormone secretion (SIADH)
• and adrenal insufficiency.

Bei hypertoner Hypo-Natriämie ist die osmotische Lücke >10 mosmol/L.

Eine häufige Ursache von hypertonen Hypo-Natriämien sind Hyperglykämien;

ein Anstieg der Blutglukosevon 100 mg/dL (5,5 mmol/L) über den Normwert führt zum Abfall des Serum-Natrium zwischen 1,4 und2,4 mmol/L

Die Differenz zwischen berechneter und gemessener Serum-Osmolarität wird als osmotische Lücke bezeichnet

und beträgt ≤ 10 mosmol/L.

Unterscheidung zwischen:

1. verminderter Wasserausscheidung (Urin-Osmolarität ist hoch)

2. Wasserausscheidung ist normal, aber im Verhältnis zur Einfuhr zu gering (Polydypsie, Urin-Osmolarität ist niedrig)

presence of ‘unmeasured osmoles’ in the plasma, like mannitol and alcohols

SIADH macht Wasser retention ->Hypourikämie

im Vgl. zu Wassermangel->erhöhte Harnsäurewerte und Ausscheidung

The only exception to this rule is that in patients with cerebral salt wasting, despite intravascular volume depletion, the serum uric acid levels stay low.

CNS disorders

Stroke

Cerebral haemorrhage
Neurotrauma
Meningitis

Tumours

Small cell cancer of the lung
Squamous cell cancer of lung
Cancer of pancreas and duodenum (rare)

Major surgery 

Pulmonary disorders

Pneumonia
Tuberculosis

Drugs

Cyclophosphamide
Carbamazepine
Cancer chemotherapeutic agents (vincristine, vinblastine)
Selective serotonin uptake inhibitors (fluoxetine)
Anti-psychotics (haloperidol, thioridazine, bromocriptine)

Hypovoläm: Herzinsuffizienz, Nephrotisches Syndrom

Euvoläm: SIADH, primäre psychogene Polydypsie

(kann durch Urinosmol. differentiert werden)

=Pseudohyponatriämie

falsch tiefes Plasma-Na bei Hyperprotein- oder lipidämie

Bei Hyperglykämie und Mannitol:

 both of which induce osmotic water movement out of the cells and lower the plasma sodium concentration by dilution.

Corrected PNa = Measured PNa + [Change in plasma glucose (mmol/L) / 3]

dysphagia, dysarthria, quadriparesis, lethargy, seizures and coma

Irreversibel!

hohe Plasmaosmolalität -> ADH-Ausschüttung->Konzentration des Urins

Keine ADH-Ausschüttung duch Hypothalamus

Renale Resistenz gegen ADH

Urin bleibt hypoton bei hypertonem Plasma

Durch Wasser- und Natrium-Verlust geht im Verhältnis mehr Wasser verloren->Hypernatriämie

z.B. Schleifendiuretika, Durchfall, Erbrechen

durch Zurfuhr von NaCl oder Nabic

Wasserverlust muss entweder gross sein oder Wasserzufuhr ist vermindert

central DI (brain death, neurotrauma, neurotumours and neurosurgery)

or nephrogenic DI of varied aetiology: congenital, hypercalcaemia, hypokalaemia and drugs such as lithium, demeclocycline and amphotericin B.

Wasserverlust muss entweder gross sein oder Wasserzufuhr ist vermindert

central DI (brain death, neurotrauma, neurotumours and neurosurgery)

or nephrogenic DI of varied aetiology: congenital, hypercalcaemia, hypokalaemia and drugs such as lithium, demeclocycline and amphotericin B.

durch Hpernatriämie geht Wasser aus den Zellen in das Intersitium->macht Hirnschrumpfung

Das Gehrin behilft sich mit idiogenen omotisch wirksamen Substanzen und macht dadurch den Effekt teilweise rückgängig.