Warning! DNA! Deoxyribonucleic acid? No!
Do not administer!
The triple whammy can lead to bad effects on the kidneys.
Dornase alfa is a mucolytic medication used in the treatment of cystic fibrosis. By cutting apart extracellular DNA, it makes mucus thinner.
Do topical NSAIDs increase the risk of skin cancer? After all, NSAIDs dampen inflammation and immune suppression is a factor that can promote malignancy. The answer is no!
For, on the contrary, research focuses more on the potential of using NSAIDs in the fight against cancer. How can this be?
Think of the mechanism of NSAIDs. They’re non-steroidal anti-inflammatory drugs, meaning they’re medications that reduce inflammation without being from the corticosteroid class.
NSAIDs indirectly inhibit prostaglandin synthesis by directly inhibiting COX enzymes. This provides anti-inflammatory effects and analgesia.
Prostaglandins play a starring role in situations such as fever.
In contrast, other things that are associated with increased malignancy risk have different ways of working.
For example, HIV impacts CD-4 T cells.
Meanwhile, chemotherapy agents have different mechanisms. For example, vincristine disruptively acts on microtubules.
Let’s not forget UV rays, which wreak havoc on the DNA process by inducing mutations.
These are just some of the villains of medicine. Thankfully, there are emerging medications that meet them in combat. But that’s a story for another day!
Let’s learn about a good friend: ACE inhibitors!
Renin (from those pesky organs called kidneys) turns angiotensinogen (also known as renin substrate) into angiotensin I.
ACE (whose full title is angiotensin-converting enzyme) turns angiotensin I into angiotensin II.
Angiotensin II has numerous magical properties: vasoconstriction, stimulating aldosterone release and more…so magical!
Angiotensin II normally clears bradykinin. When ACE inhibitors block that, bradykinin builds up and makes the person cough.
Aldosterone retains sodium and kicks out potassium. Take that, distal kidney parts! That’s where it acts.
Spironolactone, a medication well-known for its alluring gynaecomastia properties, is an aldosterone antagonist. It’s a potassium-sparing diuretic, which means it helps pass more urine without destroying the person’s blood potassium level to low, low amounts.
Let’s return to aldosterone itself, however. Aldosterone is like a vindictive, electrolyte-discriminating landlord that takes in sodium but evicts potassium from the rental property. It’s the excessively muscly security guard who stops that drunken, disorderly potassium from trying to enter the blood club.
Given the above, inhibition of aldosterone causes the opposite of its normal effects: not ejecting as much potassium from the system. Too much potassium is in the nightclub of your blood! That means hyperkalaemia!
Therefore, anything that stops the triggering of aldosterone creates a risk of hyperkalaemia.
But an ACE inhibitor stops angiotensin II from being formed! And that indirectly reduces the triggering of aldosterone that otherwise would have occurred! Hyperkalaemia might ensue! Chaos everywhere!
That explains one of the potential side effects of ACE inhibitors.
If an ACE inhibitor triggers this, the patient can be switched to an ARB, which is an angiotensin II receptor blocker. It achieves a similar effect without as much risk of the side effects of ACE inhibitors.
Well, well, well, ACE inhibitors. We’ve figured you out now!