METABOLIC ALKALOSIS Flashcards
What causes hypochloraemic, hypokalaemic metabolic alkalosis? Explain the electrolyte disturbance
GI acid loss through vomiting or gastric suction
- Loss of stomach content causes alkalosis and chloride loss
- Hypokalaemia occurs from RAAS activation due to hypovolaemia
HIGH YIELD CONCEPT
Why does hypokalaemia cause alkalosis and vice versa?
Potassium and hydrogen shift in and out of cells
Describe what causes a contraction alkalosis and what happens
Loss of fluid with sodium and chloride for example haemorrhage, vomiting
→ Causes reduced effective circulating volume → RAAS + SNS activated → increased sodium and HCO3 reabsorption in proximal tubule
Increased hydrogen secretion in collecting duct due to aldosterone
► results in metabolic alkalosis
How are sodium and HCO3 reabsorption linked in the kidney?
Proximal tubule reabsorbs sodium from urine and pumps it out back into blood along with HCO3
This process is increased by sympathetic nervous system (fall in ECV)
Why does RAAS activation cause hydrogen excretion?
Aldosterone causes excretion of potassium and hydrogen ions
Give 4 common causes of contraction alkalosis
- Vomiting
- Diuretics
- Heart failure
- Cirrhosis
In a patient with a metabolic alkalosis plus hypokalaemia plus hypertension which condition should you consider? What investigation should you do?
Hyperaldosteronism: Adrenal overproduction of aldosterone
- Adrenal hyperplasia - most common cause
- Adrenal adenoma e.g. Conn’s syndrome
► serum potassium, aldosterone/renin ratio
What condition should you consider in someone with hypercalcaemia, metabolic alkalosis and deranged kidney function? Explain pathophysiology of this condition
Milk-alkali syndrome: increased ingestion of calcium and alkali
- Hypercalcaemia interferes with kidney function: inhibits Na/K/Cl pump in LOH AND water reabsorption in collecting duct
- Like taking a loop and aldosterone antagonist = diuresis = volume contraction
- Volume contraction → metabolic alkalosis + reduced eGFR
Hypovolaemia vs dehydration vs volume contraction
Hypovolaemia: loss of extracellular fluid
Dehydration: loss of water component of body fluid
Volume contraction: loss of body fluid including dissolved substances that maintain osmotic balance (osmolytes)
- What condition in childhood causes defective sodium reabsorption in thick ascending limb?
- What symptoms does it cause?
- What metabolic dysfunction does it cause? Explain why
- Which electrolyte would you expect to be raised in the urine?
Bartter syndrome: defective reabsorption in TAL
- Mimics administration of loop: polyuria, polydipsia, nocturia
- Volume depletion activates RAAS → metabolic alkalosis + hypokalaemia
- Children will have a high urinary calcium due to lack of reabsorption from TAL
What is an important differential diagnosis of Bartter syndrome? How would you differentiate?
Gitelman Syndrome → defective sodium reabsorption in DCT = Similar to giving thiazide
Same symptoms as Bartter (polyuria, polydipsia, cramps due to hypokalaemia, metabolic alkalosis)
Differentiating: low urine calcium in GS vs BS → DCT normally secretes calcium into urine and this fails to happen in GS
Which syndrome is associated with hypertension, hypokalaemia and metabolic alkalosis with a low aldosterone level?
How is this condition treated?
Liddle Syndrome Genetic disorder, increased activity of sodium channel normally activated by aldosterone
Presents in children
Treatment: amiloride (epithelial sodium channel inhibitor)
What happens in syndrome of apparent mineralocorticoid excess (SAME)?
Cortisol is converted to cortisone by renal cells to prevent it acting on aldosterone receptors
11-B-hydroxysteroid dehydrogenase is responsible for conversion
There is deficiency of enzyme in SAME → Cortisol produces aldosterone effects
Why can licorice cause hypertension, hypokalaemia and metabolic alkalosis?
Contains glycyrrhetinic acid (a steroid)
- Weak mineralocorticoid affect
- Inhibits real or 11 beta hydroxysteroid dehydrogenase
- Mimics clinical picture of SAME
