Information includes:
- Name and class of medication
- Indications for use
- Mechanism of action
- Side effects and interactions
- Route of administration
RENAL DRUGS
Name Class Clinical Indications Receptor Action Mechanism of Action Adverse Effects and Interactions Administration + PK
Agonises V2 receptors eliciting the same mechanism of action as ADH. Causes insertion Usually sublingual or
Rapid or short term control of of aquaporin into the DCT and collecting ducts allowing more water to leave the lumen Fluid retention, hyponatraemia, oral tablet
Synthetic ADH Desmopressin Hormone V2 receptor agonist
bed wetting in children down its concentration gradient. Leads to a decrease in urine production and therefore a headaches, nausea and vomiting
decrease in enuresis. Excreted in the urine
Oxybutynin Hydrochloride Competitively inhibits postganglionic M1, M2 and M3 receptors which inhibits the Oral
Postganglionic M1, M2 Blurry vision, dry mouth, urinary
Antimuscarinic Antimuscarinic Overactive bladder muscarinic action of acetylcholine on smooth muscle and not skeletal muscle. In the
and M3 receptor inhibitor retention, and constipation
Tolterodine Tartrate detrusor muscle this inhibits contractions decreasing urination urgency and frequency. Excreted in the urine
Overactive bladder if Agonises beta 3 receptors in the detrusor smooth muscle of the bladder. This causes
Selective beta 3 receptor Excreted in the urine
Beta Agonist Mirabegron Beta agonist antimuscarinic is relaxation of the bladder and therefore decreased urination urgency and frequency UTI, headache, tachycardia, nausea
agonist and faeces
contraindicated
Inhibits alpha 1 receptors in the prostate and bladder neck. Activation of these receptors
Doxazosin Alpha Urinary obstruction due to Hypotension (usually postural), Most is excreted in the
Alpha Antagonist Alpha 1 receptor inhibitor would usually cause contraction of nearby muscular tissue preventing urine flow. By
Tamsulosin antagonist benign prostatic hyperplasia arrhythmias faeces
inhibiting this receptor, urine is allowed to flow more easily.
Inhibition of type II 5a-reductase blocks the conversion of testosterone to DHT resulting in a
5a-Reductase 5a-Reductase Symptomatic benign prostatic Type II 5a-reductase significant decrease in serum and tissue DHT. DHT is the principal androgen responsible for 57% excreted in
Finasteride Sexual dysfunction, breast tenderness
Inhibitor inhibitor hyperplasia competitive inhibitor stimulation of prostatic growth, the prostate will begin to decrease in size relieving faeces, 39% in urine
symptoms.
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