Diuretics are a class of drugs that cause the kidneys to produce more urine. They help the body eliminate excess fluid and salt. The main types are loop diuretics, thiazide diuretics, carbonic anhydrase inhibitors, potassium-sparing diuretics, and osmotic diuretics. Diuretics are used to treat conditions like heart failure, liver cirrhosis, and hypertension by removing extra fluid from the body. Common side effects include impotence, rashes, nausea, dizziness and fatigue.
3. Pharmacokinetics: Diuretics may be given orally or by slow intravenous
injection or IV infusion. Thiazides are absorbed from the
gastrointestinal tract with an onset of action of between one and three
hours. They are metabolized in the liver and excreted in urine.
PHARMACOLOGICAL ACTION
1.HIGH CEILING/LOOP DIURETICS
• High ceiling diuretics may cause a substantial decrease up to 20% of
the filtered load of NaCl and water.
• Loop diuretics such as FUROSEMIDE inhibit the body's ability to
reabsorb sodium at the ascending loop in NEPHRON.
2. THIAZIDES
• Thiazide diuretics such as Hydrochlorothiazide act on the distal
convoluted tubule and inhibit the sodium chloride symporter
leading to retention of water in the urine.
• Frequent urination is due to the increased loss of water.
• The long term anti -hypertensive action is based on the thiazides
which decrease preload and blood pressure. THIAZIDES.
4. 3.CARBONIC ANHYDRASE INHIBITORS
• Carbonic anhydrase inhibitors inhibits the enzyme carbonic anhydrase
which is found in proximal convoluted tubule.
• This results in several effects including bicarbonate retention in the
urine.
• Potassium retention in urine.
• Decreased sodium absorption.
E.g.: Acetazolamide.,Methazolamine.
4. POTASSIUM-SPARING DIURETICS
• These are diuretics which do not promote the secretion of potassium
into the urine. ⚫ Potassium is retained and not lost as much as with
other diuretics.
• The term potassium sparing refers to an effects rather than a
mechanism or location.
E.g.: Aldosterone antagonists Spironolactone
• Which is a competitive antagonist of aldosterone
• Aldosterone adds sodium channels in the cells of collecting duct and
late distal tubule of the Nephron.
5. • Spironolactone prevents aldosterone from entering the cells, and
preventing sodium reabsorption. E.g.: Eplerenone, Potassium
canrenonate.
• Epithelial sodium channel blockers
E.g.: Amiloride. Triamterene.
5.OSMOTIC DIURETICS
• The compounds as Mannitol are filtered in the glomerulus, but cannot
be reabsorbed. Their presence leads to increases in the osmolality of
the filtrate.
• To maintain osmotic balance, water is retained in the urine.
• Glucose like mannitol behaves as an osmotic diuretic. Glycosuria causes
a loss of hypotonic water & Na+, leading to a hypertonic state with
signs of volume depletion. Such as Hypotension, Tachycardia.
6.LOW CEILING DIURETICS
• The low celling diuretics are used to indicate an diuretic has a rapid
flatting dose effect curve.
• It refers to a pharmacological profile, not a chemical structure.
6. MEDICINAL USES
Diuretics are used to treat
Heart failures
Liver cirrhosis.
Hypertension.
Certain kidney diseases,etc
ADVERSE DRUG REACTION:
Impotence, skin rashes, nausea, dizziness and lethargy as well as
subjective side effects.
7. ANTIHYPERTENSIVE DRUG
Definition: A type of drug used to treat high blood pressure.
There are many different types of antihypertensive agents, and they
work in different ways to lower blood pressure. Some remove extra fluid
and salt from the body. Others relax and widen the blood vessels or
slow the heartbeat.
9. PHARMACOLOGY:
Antihypertensive drugs act centrally (methyldopa, clonidine,
guanabenz), peripherally (prazosin, guanadrel, guanethedine,
hydralazine, minoxidil), centrally and peripherally (beta-adrenergic
blocking drugs) and systemically [angiotensin converting enzyme
(ACE) inhibitors and diuretics]. Centrally-acting antihypertensives
decrease blood pressure by diminishing sympathetic outflow from the
vasomotor centre.
Peripherally-acting antihypertensives act by depleting or inhibiting
the release of catecholamines from the peripheral nerve ending or
altering the response at alpha 1- and alpha 2-receptor sites. Beta-
adrenergic blocking drugs act through a variety of mechanisms by
either decreasing cardiac output, decreasing renin release, inhibiting
prejunctional release of norepinephrine or through central
mechanisms.
Diuretics act as indirect vasodilators by depleting salt and water not
only within the intravascular compartment but within the intramural
portion of the arteriole, thereby diminishing its responsiveness to
catecholamine and angiotensin II stimulation.
ACE inhibitors such as captopril and enalapril act by inhibiting the
conversion of angiotensin I to angiotensin II thereby decreasing the
vasoconstrictor effect of angiotensin II and the aldosterone
production secondary to angiotensin II stimulation. The main
12. 𝛃-Adrenoceptor blockers: evidence for use of β-blockers in NSTE-ACS is
limited, but they are prescribed routinely to relieve ischaemia.
Contraindications include airways disease, acute heart failure and
impaired cardiac conduction.
Calcium channel blockers: small randomized trials suggest that calcium
channel blockers relieve symptoms in patients with NSTE-ACS. Calcium
channel blockers include dihydropyridines (e.g. amlodipine), diltiazem (a
benzothiazepine) and verapamil (a phenylalkylamine). Dihydropyridines
cause reflex tachycardia, but diltiazem and verapamil depress cardiac
contractility and conduction and should not be given to patients with
heart block or in combination with a β-adrenoceptor blocker.
Nitrates: small observational studies suggest that intravenous nitrate
relieves ischemia in patients with NSTE-ACS. Adverse effects include
headache and hypotension; continuous administration can induce
tolerance. Nitrates are contraindicated after recent use of
phosphodiesterase type 5 inhibitors (e.g. sildenafil).