L17 Electrolyte Disorders Flashcards
Regulation of Potassium?
Alkalemia: K+ Uptake by cells
Insulin Secretion: K+ Uptake by cells
Catecholamine Release: K+ Uptake by cells
Aldosterone Secretion (Principal Cells of Adrenal Cortex): Increased Urinary K+ Excretion (Na+ Reabsorption)
Increased Distal Urine Flow: Increased Urinary K+ Excretion
Causes of Hypokalemia?
Decreased K+ Intake: (rarely causes hypokalaemia on its own)
- Alcoholism
- Eating disorders
- Elderly
Increased Entry into cells
- Insulin (DKA treatment)
- Refeeding syndrome
- Alkalosis
Increased GI Losses
- Villous Adenoma
- Persistent Diarrhea
Increased Renal Losses
- Diuretics
- Increased mineralocorticoid (aldosterone) activity
- Polyuria (Excessive urine excretion)
- Hypomagnesaemia
Symptoms of Hypokalemia?
- Asymptomatic if mild
- Ileus (inhibition of peristalsis)
- Muscle weakness, cramps, rhabdomyolysis, paralysis
- Cardiac Arrhythmia (BIGGEST CONCERN)
Treatment of Hypokalemia?
Oral vs. IV?
Aim is to quickly bring K+ to a safe level with Potassium chloride, then replace the remaining deficit more slowly (Check Mg2+ level, correct if low)
ORAL Potassium Chloride: Capsule/tablet/liquid
- For mild/moderate hypokalemia
- More effective than replacing K+ by dietary adjustment
INTRAVENOUS Potassium Chloride: In saline solution
- Severe, symptomatic hypokalemia
- CAREFUL MONITORING: NEVER Give a bolus if too high an amount or rate can trigger a fatal arrhythmia
Electrolyte disorder that’s most likely to have fatal consequences?
HYPERKALAEMIA
1-10% of hospitalised patients
May cause ECG abnormalities, fatal arrhythmias & muscle weakness.
Causes of Hyperkalemia?
Drug-Induced Hyperkalaemia?
Management of ↑K+?
- What’s causing it? => Stop any drugs that may be causing or exacerbating it
- ECG
- Start Rx to lower K+:
- Stabilise the myocardium (Calcium directly antagonizes the membrane actions of hyperkalemia- doesn’t lower potassium, but prevents fatal arrhythmia)
- IV insulin to shift K+ into cells Give Insulin WITH SUGAR to drive K+ into cells without dropping blood sugar dangerously low
-
GI Cation Exchangers (Exchange bound Na+ or Ca2+ for cations (including K+) to enhance the elimination of K+ from the GIT)
Often cause GI upset (constipation)
Can bind other drugs in the GIT (e.g ciprofloxacin, thyroxine, metformin) - β2 agonist
- Sodium Bicarbonate if patient has CKD or severe metabolic acidosis
- Loop Diuretic
When to consider dialysis for hypercalcemia?
Consider DIALYSIS if…
1. Severe refractory hyperkalemia
- AKI
- Advanced CKD
Regulatory mechanisms of Sodium (& Water) Balance?
Most common electrolyte disturbance?
HYPONATRAEMIA
Extremes of age most vulnerable
Symptoms of Hyponatremia?
Threshold when seen?
Symptoms:
–Usually not seen until Na+ <125
–Fatigue, lethargy, gait or movement disorder
–Confusion, headaches, n+v
–Seizures & coma if severe (Na+ <110): Shift of water into the brain => uncal herniation as the brain swells and is pressed down=> can quickly lead to death
Causes/Categorization of Hyponatremia?
Categorised by VOLUME STATUS
Causes of Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)?
Important for Exam
CNS: Stroke, Haemorrhage, Trauma, Infection
Pulmonary: Malignancy, Pneumonia, TB
Drugs: MANY psychiatric & chemotherapeutic agents
Malignancy: SCC lung most commonly
MISCELLANEOUS: Hereditary, hypothyroidism, hypopituitarism, symptomatic HIV infection
MOA of ADH/Vasopressin?
Released in response to increased serum osmolarity => binds vasopressin V2 receptor (V2R) => insertion of aquaporin-2 (AQP2) water channels in the apical membrane, thereby allowing water reabsorption from the pro-urine to the interstitium=> also leads to a drop in concentration of sodium
Vaptins Indication/MOA/Drugs?
Indication: Treatment of SIADH (Rarely used due to risk of overshooting)
MOA: ADH binds to V2 receptors in the kidney=> Selective solute-free water diuresis
Adverse effects: polyuria, polydipsia, fatigue, thirst, headache
Conivaptan (IV): V1A/V2 antagonist
Tolvaptan (PO): V2 antagonist Safety concerns => liver dysfunction
