Diuresis
Reversible, non-competitive inhibitor of carbonic anhydrase
PCT: ↓H+ and HCO3- prodn
↓ cytosol H+ → ↓Na+ reabs in PCT→ ↑H2O loss
↓cytosol HCO3→↑luminal HCO3→ H2O diffusion with HCO3 ,Na, K to urine
Eye: ↓Na pump, ↓AH formation

inhibit Na+ reabsorption in the early portion of the distal tubule by
blocking the Na+.Cl- symporter in the apical membrane of these cells. Naturesis
occurs with thiazide diuretics is 5-10% of the filtered load

Metabolic: Acidosis via ↑ excretion of bicarb (and reabsorption of Cl)
Resp: ↑MV → comp resp alk
CNS: anticonvulsant properties, ↓ CSF and IOP by ↓d formation GIT: ↓ Pancreatic and gastric
GU: mild diuresis, Na retention

Anti-HTN: (↓TPR, ↓plasma volume)
↓RBF → ↓GFR
↓K+,Na+,Mg.
Hyperchloremic MA
↑Ca++ (↓excretion)
↑Glu: (↓glycogenolysis, ↓insulin)

IV/PO
PO BA = 100%

PO- BA ~50-80%. Onset 2hrs Dur 6-12hrs.

Lip sol: crosses BBB

70-90%

68%

3.6-7.8L/kg

Not metabolised

Not metabolized

Unchanged in urine

Urine (unchanged)

6-9hrs

5.6-14.8hrs

metabolic acidosis, urinary alkalinisation, parathesias, fatigue,
hypokalaemia, N+V, abdo pain

Tox: Rashes, renal stones

↓K+/Na+/Mg++, ↑Ca++/urea/glu/chol.
indiosyncratic blood
dyscrasias. Rash, photsensitivity. Interactions may prolong action of NDMBs. NSAIDs antagonise the action

Diuretic – Carbonic Anhydrase Inhibitor

Diuretic - Thiazide

Glaucoma
Miniere’s disease
Altitude sickness
Adjunct in epilepsy

heart failure and hypertension. Used in combination. mostly bound to plasma prot, and gain access to the tubule via secretion in the PCT.

Sulfonamide

related to the sulphonamides

Level 3

Level 3

250mg white tablets
500mg vials for reconstitution

orange scored tablets of 25mg and combos

250-1000mg q6hrly
IV/PO

PO. 12.5-200mg/day