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.

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

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

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

68%

90%

3.6-7.8L/kg

Not metabolized

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

Urine (unchanged)

Urine and faeces

5.6-14.8hrs

1-2hours, metab upto 24hrs

↓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 - Thiazide

Diuretic – Aldosterone antagonist

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

related to the sulphonamides

A synthetic steroid

Level 3

Level 3

orange scored tablets of 25mg and combos

25/100mg tablets

PO. 12.5-200mg/day

PO. 25-200mg/day