From Sensitivity to Tolerance: Understanding Aspirin Desensitisation

I was confused when I met a patient with documented aspirin sensitivity who was still taking low-dose aspirin every day. If aspirin can trigger bronchospasm, why would they continue using it? And how does this desensitisation process actually work?

This question opens the door to a critical intersection of pharmacology, immunology, and respiratory medicine. Aspirin sensitivity is common enough to matter clinically, yet nuanced enough that its mechanisms can be confusing when first studying the pharmacology of non-steroidal anti-inflammatory drugs (NSAIDs). Here is a concise guide to help you understand what’s going on and why desensitisation can be a life-changing intervention for some patients. Continue reading

Parabens, PABA, and Allergies to Local Anaesthetics

I learned that some people are allergic to benzocaine or procaine because they metabolise into PABA. But I also heard that parabens in topical creams and even in lidocaine vials can cause reactions. Are ester local anaesthetic allergies and paraben allergies related? And do they cross-react?

Understanding allergies to local anaesthetics can be surprisingly tricky. Patients can report being “allergic to all anaesthetics,” but the real culprit is frequently something far more specific, such as PABA from ester-type local anaesthetics or parabens used as preservatives. These substances share some structural features, but they behave very differently in the body. Because of this, you may hear mixed messages about cross-reactivity, preservative-free formulations, and whether lidocaine is truly “safe” in someone with a benzocaine allergy.

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The Unexpected Link Between Sunscreens and Local Anaesthetics

An auntie told me she reacts to both some older PABA-containing sunscreen brands and to the benzocaine lozenges you can buy at pharmacies. Are PABA-containing sunscreens actually related to ester local anaesthetic allergies, and why do these reactions happen?

When you hear the acronym PABA, you might think vaguely of “old-fashioned sunscreens.” But PABA is also a structural motif in ester-type local anaesthetics: a fact that connects dermatology, pharmacology, and anaesthesia in surprisingly meaningful ways. Understanding this link not only sharpens pharmacology knowledge but also helps you anticipate adverse reactions and counsel patients more confidently. Continue reading

Uroselectivity of Tamsulosin vs Alfuzosin vs Prazosin for BPH?

We always hear that tamsulosin is the go-to for BPH, but I’m confused about where alfuzosin and especially prazosin fit in. If prazosin is also an alpha-1 blocker, why is it basically never used for BPH unless the patient also has hypertension? Aren’t they all doing the same thing? And honestly, is this whole idea of ‘prostate selectivity’ real, or is it just a marketing story?

Lower urinary tract symptoms (LUTS) caused by benign prostatic hyperplasia (BPH) are among the most common issues you will encounter in older men. Two of the most frequently prescribed drugs for BPH, alfuzosin and tamsulosin, belong to the same class of α₁ (alpha-1)-adrenergic blockers but differ in receptor selectivity, side-effect profile, and clinical nuances. Another α₁-blocker, prazosin, sometimes enters the discussion but is used far more often for refractory chronic hypertension and PTSD-related nightmares than for BPH.

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Pasireotide: A Next-Generation Somatostatin Analogue

Pasireotide is a newer drug than octreotide? I don’t remember learning this drug in the GIT system block. Is pasireotide going to replace octreotide?

When students first learn about somatostatin analogues, the emphasis is usually on octreotide, a drug used in gastrointestinal (GIT) medicine for conditions such as secretory diarrhoea, carcinoid syndrome, variceal bleeding, and pancreatic fistulae. Octreotide’s role in suppressing endocrine and GI secretions makes it valuable in acute inpatient care.

Pasireotide, however, belongs to a newer generation of somatostatin analogues that were engineered with a very different purpose. Unlike octreotide, which is best at binding SSTR2 and controlling GIT hypersecretion, pasireotide targets multiple receptor subtypes, especially SSTR5, allowing it to treat endocrine disorders that octreotide often cannot. This makes pasireotide central to the modern management of Cushing’s disease and treatment-resistant acromegaly.

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Racedotril vs Loperamide: A Smarter Choice for Paediatric Diarrhoea?

What is the difference between racedotril and loperamide? Why is racedotril called an antisecretory?

When faced with a case of acute diarrhoea, clinicians often reach for anti-diarrhoeal agents, but not all drugs are created equal. Two options are loperamide, an opioid receptor agonist, and racedotril, an enkephalinase inhibitor. Though both reduce stool output, they differ in their mechanism of action, safety profile, and clinical applications.

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Domperidone vs. Metoclopramide: A Pharmacological Face-Off

What is the difference between domperidone and metoclopramide? Why is domperidone not always preferred, as it has less risk of CNS adverse effects? 

Gastrointestinal motility disorders and nausea are common clinical challenges, and two dopamine antagonists — domperidone and metoclopramide — are often used in their management. Although both act on dopamine D2 receptors, key differences in their pharmacokinetics, central nervous system penetration, and adverse effect profiles make the choice between them more than a matter of availability. Let’s unpack the differences.

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Can allopurinol be taken during acute gouty attacks?

Is it safe to continue allopurinol therapy during an acute gout attack, or does it risk worsening the flare?

Acute gout attacks are characterized by painful joint inflammation caused by immune cells attacking urate crystals. While chronic management to lower blood urate levels is crucial for preventing flare-ups, the approach to using urate-lowering therapies such as allopurinol during an acute gout attack continues to evolve. This blog will clarify some of the clinical considerations and evidence surrounding the use of allopurinol during acute gout episodes.

The Dilemma: Traditional Teaching vs. Emerging Evidence. Traditionally, initiating or adjusting allopurinol during an acute attack was discouraged, as altering uric acid levels can exacerbate symptoms. This concept led to a common recommendation of holding off allopurinol until the acute phase subsides. However, recent evidence has challenged this approach, suggesting that allopurinol, if already in use, should be continued during acute attacks to maintain steady uric acid levels and prevent rebound hyperuricaemia.

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Why does fingolimod have cardiac effects?

Fingolimod is prescribed as an immunosuppressant for managing multiple sclerosis, but why should clinicians be particularly cautious about its cardiovascular effects during initial dosing?

Fingolimod, an oral immunomodulatory drug approved for the treatment of multiple sclerosis (MS), has a unique mechanism of action that makes it highly effective in reducing MS relapses. However, like many medications, it comes with a specific set of adverse effects that need careful consideration, particularly its impact on the cardiovascular system. Here’s what you need to know.

How Does Fingolimod Work?
Fingolimod functions as a sphingosine-1-phosphate (S1P) receptor modulator. It sequesters lymphocytes in the lymph nodes, reducing their migration out, and preventing them from crossing into the central nervous system (CNS) where they would normally contribute to the inflammatory damage seen in MS. This modulation of S1P receptors is crucial to its therapeutic effect, but it also leads to unintended cardiovascular effects.

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The Difference Between Mycophenolate Mofetil (MMF) and Mycophenolate Sodium (MPS)

What is the difference between mycophenolate mofetil (MMF) and mycophenolate sodium (MPS)

Understanding the nuances between different formulations of a drug is crucial to ensuring optimal patient care. Mycophenolate mofetil (MMF) and mycophenolate sodium (MPS) are two formulations of the immunosuppressant mycophenolic acid, commonly used to prevent organ rejection in transplant recipients and to manage autoimmune conditions. Despite their similar purposes, there are important differences between them that influence their clinical use.

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