Why most of the proton pump inhibitors are formulated as enteric coated

capsules?

Proton pump inhibitors (PPIs) are often formulated as enteric-coated capsules for several
reasons:

1. Acid Stability: PPIs are sensitive to stomach acid, which can degrade them before they
reach their target site in the small intestine. Enteric coatings protect the drug from
stomach acid, allowing it to pass through the stomach intact.
2. Site of Action: PPIs work by inhibiting acid secretion in the stomach’s parietal cells. To
be effective, they need to reach the small intestine, where they can be absorbed into the
bloodstream and then transported to the parietal cells. Enteric coatings ensure that the
drug is released in the small intestine, near its site of action.
3. Patient Comfort: PPIs can cause irritation or discomfort if they are released in the
stomach, as they are meant to act in the small intestine. Enteric coatings help prevent this
irritation, making the medication more tolerable for patients.
4. Improved Bioavailability: Enteric coatings can enhance the bioavailability of PPIs by
protecting them from degradation and enhancing their absorption in the intestines. This
can lead to more consistent and effective therapy.
5. Delayed Release: Enteric coatings are designed to dissolve or disintegrate at a higher pH
(less acidic) environment, such as the small intestine. This allows for delayed release of
the medication, providing a sustained effect over time.

Overall, the enteric-coated formulation of PPIs is intended to optimize their effectiveness,

reduce side effects, and enhance patient comfort during treatment for conditions like
gastroesophageal reflux disease (GERD) and peptic ulcers.

How the aldosterone antagonist work for the conservation of K+?

Aldosterone antagonists that work to conserve potassium (K+) by inhibiting the actions of
aldosterone, an adrenal hormone. An important part in controlling the body’s sodium and
potassium balance is played by aldosterone.

Aldosterone antagonist’s functions are as follows:

1. Aldosterone typically increases sodium (Na+) reabsorption while encouraging potassium
(K+) excretion in the distal tubules and collecting ducts of the kidneys. This causes
potassium loss and sodium retention.
2. Aldosterone antagonists bind to the renal tubule aldosterone receptors. They do this to
prevent aldosterone from attaching to its receptors.
3. Potassium is preserved and sodium reabsorption is decreased when aldosterone is
suppressed. As a result, more potassium is stored in the body and less sodium is
reabsorbed into the bloodstream.
4. Aldosterone antagonists therefore aid in redressing sodium and potassium imbalances.
They are frequently used in circumstances where excessive aldosterone secretion causes
salt retention and potassium depletion, such as in heart failure or several renal disorders.

Aldosterone antagonists work to raise blood potassium levels by reducing the effects of
aldosterone, which is beneficial for preserving healthy heart and muscle function. Patients
who take these medications need to be properly watched, though, as they may also result in
difficulties and side effects.

Why diuretics acting at site 1are less efficacious?

 Since they predominantly target the proximal convoluted tubules (PCT) in the kidneys,
diuretics that act at site-1 in the renal tubules are less effective. The distal tubules and
more distal portions of the nephron, including the loop of Henle, reabsorb most of the
filtered sodium and water, but the proximal convoluted tubules are less controlled and
have a higher capacity for reabsorption. Because a significant amount of reabsorption
takes place downstream from site 1, diuretics operating at this site may only have a
limited effect on lowering salt and water retention in the body.
 Because they target areas of the nephron where salt reabsorption is strictly controlled and
significant, loop diuretics (acting at site-2) and thiazide diuretics (acting at site-3) are
frequently more effective.
 Diuretics that act at site 1, specifically in the proximal convoluted tubules of the nephron
in the kidneys, are less efficacious compared to diuretics acting at other sites, like the loop
of Henle or distal tubules, for several reasons:
1. Reabsorption Levels: In the proximal tubules, a significant portion of filtered sodium and
water is reabsorbed, typically around 65-70%. Diuretics acting at site-1 target this early
 reabsorption process. Since a substantial amount of sodium and water is still reabsorbed
downstream, the impact of inhibiting reabsorption in the proximal tubules alone is
limited.
2. Compensatory Mechanisms: When diuretics block sodium reabsorption in the proximal
tubules, the body can activate compensatory mechanisms in other parts of the nephron to
increase sodium reabsorption. This reduces the net diuretic effect and can limit the
efficacy of site-1 diuretics.
3. Limited Sodium Load: The proximal tubules handle a smaller proportion of the sodium
load compared to the loop of Henle and distal tubules. Therefore, inhibiting sodium
reabsorption in the proximal tubules has a smaller overall impact on sodium and water
excretion.
4. Shorter Action: Diuretics acting at site-1 tend to have a shorter duration of action because
they are quickly metabolized or reabsorbed downstream in the nephron. This limits their
ability to provide sustained diuretic effects.

In clinical practice, diuretics acting at site 1, such as carbonic anhydrase inhibitors like
acetazolamide, are used for specific medical conditions like glaucoma and altitude sickness
but are not typically employed as primary diuretics for managing conditions like hypertension
or edema where more efficacious diuretics are preferred.