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

Diuresis
Inhibition of active chloride ion reabsorption in PCT and ascending limb of LoH
↓ reabsorption of NaCl → ↓ tonicity in the renal medulla → ↓water reabsorption and diuresis.
Other effects are mediated by the induction of the COX-2 enzyme which assists in synthesis of prostaglandins.

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

Acts in the DCT.
It is a competitive antagonist of aldosterone at the receptors in the DCT.
Decreased Na reabsorption and increased K reabsorption
= Increased Na loss and Diuresis.

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

Pulmonary and systemic vasodilation
Diuresis ↑ RBF and ↑ corticomedullary blood flow
↓O₂ demand in the LoH (ischaemic
protection)

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

Sedation and muscle weakness (due to electrolyte abnm)
Antihypertensive,
Diuresis (in 3-4 days)
Potassium retention
Anti-androgenic effect- inhbn of ovarian androgen secretion
↑renal Ca excr, ↑plasma urea
Reversible hyperchloraemic MA

IV/PO
PO BA = 100%

PO/IV/SL/IM. PO BA 50% Onset PO/SL 30-60mins, IV 5 mins .
Dur PO/SL 6-8hrs, IV 2hrs

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

PO - BA 70%, extensive 1st pass metb. Onset 3-4hrs, dur upto 3 days

Lip sol: crosses BBB

70-90%

91-99% (Albumin)

68%

90%

0.1L/kg

3.6-7.8L/kg

Not metabolised

Renal to glucuronide
Minimal hepatic

Not metabolized

Hepatic: Rapidly and extensively metabolised by deacetylation and dethiolation. Active metab: canrenone and 7-alpha-spirolactone

Unchanged in urine

80% unchanged in urine

Urine (unchanged)

Urine and faeces

6-9hrs

0.5-2hrs. ESRF: 9hrs

5.6-14.8hrs

1-2hours, metab upto 24hrs

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

Tox: Rashes, renal stones

↓ K+/Na+/Cl-/Ca++, Hyper- urea/glu/chol, Metabolic alkalosis
Tox: Deafness, Pancreatitis
BM depression
Interstitial nephritis (worse with aminoglycoside)

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

↑K+(esp in renal failure). N/V and GI disturbances
Menstr irreg, Gynaecomastia
↑digoxin conc.
↓pressor response
↑effects of CVS depressants

Diuretic – Carbonic Anhydrase Inhibitor

Diuretic - Loop

Diuretic - Thiazide

Diuretic – Aldosterone antagonist

Glaucoma
Miniere’s disease
Altitude sickness
Adjunct in epilepsy

Oedema of cardiac, renal or hepatic origin, Renal insufficency
Hypertension
Raised ICP
Hypercalcaemia

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

Oedema – CHF, cirrhosis with ascites, refractory. HTN, Nephrotic syndrome. With loop/thiazide to conserve K+, diagn of Conn's syndr

Sulfonamide

Sulfonamide derivative

related to the sulphonamides

A synthetic steroid

Level 3

Level 1

Level 3

Level 3

250mg white tablets
500mg vials for reconstitution

Photosensitive solution 10mg/ml
20/40/500mg tabs, Syrup

orange scored tablets of 25mg and combos

25/100mg tablets

250-1000mg q6hrly
IV/PO

20-2000mg daily
PO/IV/SL/IM.

PO. 12.5-200mg/day

PO. 25-200mg/day