Common Suffixes Or Prefixes For Drugs and how to calculate half life Flashcards
What do PPI’s (proton pump inhibitors)
Commonly End in, what is its mechanism of action and some common drugs?
-Prazole
- Mechanism of action
- H+, K+-ATPase inhibition
- Specific agents
- Omeprazole, esomeprazole
The mechanism of action of Proton Pump Inhibitors (PPIs) involves the inhibition of the gastric H+/K+ ATPase enzyme, also known as the proton pump, which is located on the parietal cells of the stomach lining.
Steps of Action:
Activation in Acidic Environment:
PPIs are prodrugs that are activated in the acidic environment of the stomach.
Once ingested, PPIs pass through the bloodstream and concentrate in the secretory canaliculi of parietal cells, where they are activated by the acidic pH.
Irreversible Binding to the Proton Pump:
The active form of PPIs covalently binds to the cysteine residues on the H+/K+ ATPase enzyme.
This binding irreversibly inhibits the proton pump, preventing the exchange of hydrogen ions (H⁺) with potassium ions (K⁺) across the gastric parietal cell membrane.
Reduction in Gastric Acid Secretion:
By blocking the final step of acid secretion, PPIs suppress both basal (resting) and stimulated (meal-induced) gastric acid production.
The reduction in stomach acidity helps manage conditions caused by excess acid.
What do H2-Blockers/Histamine receptor-2 antagonist commonly end in and what are there mechanism of action and some of the drugs?
Please remember there is another class for receptor 1 that does different things. DO NOT GET CONFUSED another way to remember is which is most important the 1 or 2 there in lies your answer if you know what 1 works on.
-tidine; Remember the T In the suffix means H2 and H1 usually ends in -ine
- Competitive block of H2-R on parietal cells
- Ranitidine (brand name: Zantac)
Famotidine (brand names: Pepcid, Pepcid AC)
Cimetidine (brand name: Tagamet)
Nizatidine (brand name: Axid)
What do beta blockers commonly end in and what are there mechanism of action and some drugs?
-lol 🤣😂, although nothing is funny if you need this
They block beta-adrenergic receptors. Moreover, they also block the effects of adrenaline (epinephrine) and related hormones. But many are selective as beta 2 adrenergic blockers would case bronchoconstriction which is why most are selective
metoprolol, propranolol, and atenolol.
hint letters
A-M is selective for B1
Atenolol
Betaxolol
Bisoprolol
Esmolol
Metoprolol
Nebivolol
N-Z is non selective
Nadolol
Pindolol
Propranolol
Sotalol
Timolol
exception of Carteolol
This is a general observation always check to confirm
What do Angiotensin Converting Enzymes (ACE) Inhibitors commonly end in and what are there mechanism of action and some common drugs
-Pril; to help remember this think of productive cough although there is no productive cough that occurs it’s just a cough due to its mechanism
- inhibits ACE
lisinopril, enalapril, and captopril
What do antihistamine/h1 receptor antagonist commonly end in and what is it’s mechanism of action and common drug names?
-zine, -dine, -tine or -amine. Be wary that SSRIs have similar endings but specifically in the amine has an ox in front of the amine
Also H1 is noted with 1 because it works on more impartant receptors as it deals with breathing over H2 the stomach.
Mechanism of action
Blocks action at the H1 receptor located on various cells throughout the body, including blood vessels, respiratory tract, skin, and nerves.
histamine triggers a series of cellular responses that contribute to allergic symptoms. These responses include vasodilation (widening of blood vessels), increased vascular permeability (leakage of fluid from blood vessels), smooth muscle contraction (bronchoconstriction in the airways), and stimulation of sensory nerves (resulting in itching and pain).
Loratadine (brand name: Claritin)
Cetirizine (brand name: Zyrtec)
Fexofenadine (brand name: Allegra)
Desloratadine (brand name: Clarinex)
Levocetirizine (brand name: Xyzal)
Diphenhydramine (brand names: Benadryl, Unisom)
Hydroxyzine (brand names: Vistaril, Atarax)
Promethazine (brand names: Phenergan, Promacot)
What do cholesterol lowering drugs commonly end in and what are there mechanism of action and list some of the drugs?
-statin
inhibits HMG-CoA reductase, an enzyme involved in cholesterol synthesis.
Atorvastatin (brand name: Lipitor)
Simvastatin (brand name: Zocor)
Rosuvastatin (brand name: Crestor)
Pravastatin (brand name: Pravachol)
Lovastatin (brand name: Mevacor)
Fluvastatin (brand name: Lescol)
Pitavastatin (brand name: Livalo)
What do Selective-norepinephrine- reuptake inhibitors (SNRIs) commonly end in and what is there mechanism of action and common names.
-venlafaxine or -oxetine; Duloxetine and Vortioxetine or think DV or F is after D just like SSRI is after SNRI so alphabetically D would belong to this group. Also -venlafaxine has a n in its name to help differentiate SNRI from SSRI
inhibit the reuptake of both serotonin and norepinephrine in the synaptic clefts of neurons. This means that after these neurotransmitters are released, SNRIs prevent them from being quickly reabsorbed by the presynaptic neuron.
Venlafaxine (Effexor)
Duloxetine (Cymbalta)
Desvenlafaxine (Pristiq)
Levomilnacipran (Fetzima)
Milnacipran (Savella)
Vortioxetine (Trintellix) - While primarily classified as an Serotonin Modulator and Stimulator (SMS), it also has some SNRI activity.
What do SSRIs commonly end in, and what are there mechanism of action and list some medications.
-aline, -oxetine, -opram or -oxamine. 👀 for the a line of O’s to help remember associate but - pram is the correct suffix. You get it 😂. And Fluoxetine is exclusive for SSRI
selectively blocking the reuptake of serotonin in the brain, leading to increased serotonin levels in key mood-regulating areas. This action enhances serotonin signaling, which contributes to the therapeutic effects of SSRIs in managing depression, anxiety disorders, and related conditions. While primarily acting within the central nervous system, SSRIs can also influence serotonin signaling in peripheral tissues, leading to a range of effects beyond the brain, including gastrointestinal, cardiovascular, and peripheral nervous system effects.”
PMDD-premenstrual dysphoric disorder
Fluoxetine (Prozac commonly OCD, bulimia nervosa)
Sertraline (Zoloft commonly OCD, PTSD, OCD, PMDD and panic disorders)
Paroxetine (Paxil usually Depression, GAD, OCD, PTSD, PMDD)
Fluvoxamine (Luvox usually OCD)
Escitalopram (Lexapro usually GAD)
Citalopram (Celexa usually Depression)
What are common name suffixes for Bisphosphonates and what are there mechanism of action and common drugs?
-dronate
the presence of the bisphosphonate functional group in these drugs, which is essential for their ability to inhibit bone resorption and treat conditions like osteoporosis.
Alendronate (brand name: Fosamax)
Risedronate (brand name: Actonel)
Ibandronate (brand name: Boniva)
Zoledronic acid (brand name: Reclast, Zometa)
Etidronate (brand name: Didronel)
Pamidronate (brand name: Aredia)
What are common suffix names for NSAIDs and what is it’s mechanism of action?
-profen
- inhibition of enzymes called cyclooxygenases (COX enzymes), specifically COX-1 and COX-2. These enzymes play a key role in the synthesis of prostaglandins, which are lipid compounds that regulate inflammation, pain sensation, and fever.
- Reduce the production of prostaglandins particularly those derived from arachidonic acid. Prostaglandins play a crucial role in mediating inflammatory responses, sensitizing pain receptors, and promoting vasodilation, leading to increased blood flow and swelling at the site of injury or inflammation.
- Anti-inflammatory and Analgesic Effects: The reduction in prostaglandin levels results in anti-inflammatory effects, as NSAIDs help decrease swelling, redness, and heat associated with inflammation. Additionally, NSAIDs provide analgesic (pain-relieving) effects by decreasing the sensitization of pain receptors and lowering pain perception.
- Antipyretic Effects: NSAIDs also exhibit antipyretic effects by reducing fever. Fever is often mediated by prostaglandins acting on the hypothalamus to increase body temperature. By lowering prostaglandin levels, NSAIDs help normalize body temperature in individuals with fever.
What do antifungals commonly end in and what are there mechanism of actions and what are some.
-azole
- Work by inhibiting an enzyme necessary for the synthesis of ergosterol which is necessary for fungal membrane function
- Depletion of ergosterol leads to increased membrane permeability and possibly interferes with membrane-bound enzyme systems
Clotrimazole (Lotrimin, Canesten)
Fluconazole (Diflucan)
Ketoconazole (Nizoral, Extina)
Miconazole (Monistat, Lotrimin AF)
Terbinafine (Lamisil)
Itraconazole (Sporanox)
Amphotericin B (Fungizone)
Ciclopirox (Loprox)
Nystatin (Mycostatin, Nystop)
What are common endings of antibiotics and what class do they belong too? P.S. Sulfa drugs and cephalosporins are different just in case you did not know
- -cillin: Penicillin-based antibiotics, e.g., amoxicillin, penicillin. Class Beta Lactam
Common Adverse Effects:
Allergic reactions: Ranging from mild (rash, hives) to severe (anaphylaxis).
GI upset: Diarrhea, nausea, vomiting.
Superinfections: Overgrowth of non-susceptible organisms, e.g., C. difficile.
Contraindications:
Penicillin allergy: Life-threatening reactions in individuals allergic to beta-lactams.
Generally safe during pregnancy and breastfeeding. - -floxacin: Class Fluoroquinolone antibiotics, e.g., ciprofloxacin, levofloxacin.
Common Adverse Effects:
Tendinitis and tendon rupture: Particularly in older adults or those on corticosteroids.
QT prolongation: Increased risk of arrhythmias.
Peripheral neuropathy: Can cause lasting nerve damage.
CNS effects: Dizziness, headache, insomnia, hallucinations and confusion, especially in the elderly.
Contraindications:
Pregnancy and children: Associated with cartilage damage and joint issues.
Myasthenia gravis: Can exacerbate muscle weakness. - -mycin or -micin: Class Aminoglycoside antibiotics, e.g., gentamicin, amikacin.
Common Adverse Effects:
Ototoxicity: Hearing loss or balance issues (can be irreversible).
Nephrotoxicity: Kidney damage, especially with prolonged use or high doses.
Neuromuscular blockade: Can cause muscle weakness or paralysis.
Contraindications:
Pregnancy: Risk of fetal hearing loss (ototoxic).
Use cautiously in individuals with kidney disease or neuromuscular disorders. - -cycline: Class Tetracycline antibiotics, e.g., doxycycline, minocycline.
Common Adverse Effects:
Photosensitivity: Increased risk of sunburn.
GI upset: Nausea, vomiting, esophagitis.
Tooth discoloration: Particularly in children under 8 and during pregnancy (permanent staining of developing teeth).
Contraindications:
Pregnancy and children: Affects bone and teeth development, crosses the placenta, causing possible stunting of bone growth.
Renal impairment: Should be used cautiously due to risk of toxicity. - -thromycin: Class Macrolide antibiotics, e.g., azithromycin, erythromycin
Common Adverse Effects:
GI upset: Nausea, vomiting, diarrhea (erythromycin especially causes significant GI motility).
QT prolongation: Can lead to serious arrhythmias.
Hepatotoxicity: Elevated liver enzymes and rare liver injury.
Contraindications:
Liver disease: Use with caution in patients with hepatic impairment.
Safe in pregnancy but avoid high doses due to potential risks. - -nidazole do not be confused with the –azole which is for antifungals. Class nitroimidazole of antibiotics
Common Adverse Effects:
GI upset: Nausea, metallic taste in the mouth.
Neurotoxicity: Dizziness, seizures, peripheral neuropathy (especially with prolonged use).
Disulfiram-like reaction: Severe nausea and vomiting if alcohol is consumed.
Contraindications:
First trimester of pregnancy: Teratogenic effects, though metronidazole is used in later pregnancy if necessary.
Alcohol consumption: Strict avoidance required. - Sulfa: Class Sulfonamides e.g. Sulfamethoxazole (often combined with trimethoprim as trimethoprim-sulfamethoxazole or TMP-SMX; brand name: Bactrim, Septra)
Sulfadiazine (brand name: Silvadene)
Sulfasalazine (brand name: Azulfidine)
Sulfacetamide (brand name: Bleph-10)
Sulfadoxine (used in combination
Common Adverse Effects:
Allergic reactions: Rashes, Stevens-Johnson syndrome, toxic epidermal necrolysis.
Crystalluria: Precipitation in the urine can cause kidney stones or damage.
Bone marrow suppression: Can lead to anemia, leukopenia, thrombocytopenia.
Contraindications:
Pregnancy (late/ third trimester): Risk of kernicterus in the newborn due to displacement of bilirubin.
G6PD deficiency: Can cause hemolytic anemia. - Cef- or Ceph-: Cephalosporin class drugs. Class Beta Lactam
- cephalexin
- ceftriaxone
Common Adverse Effects:
Allergic reactions: Cross-reactivity with penicillin in a small percentage of patients.
GI upset: Diarrhea, nausea, vomiting.
Superinfection: Risk of C. difficile infection.
Contraindications:
Penicillin allergy: Cross-reactivity in ~10% of patients.
Generally safe during pregnancy and breastfeeding.
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OVerall Summary
* Similarity in mechanism: Antibiotics generally work by targeting specific aspects of bacterial metabolism, such as cell wall synthesis (e.g., penicillins), protein synthesis (e.g., macrolides), DNA replication (e.g., fluoroquinolones), or other essential bacterial processes.
What are common suffix for benzodiazepines and what is it’s mechanism of action and list some
-pam or -lam
- Enhancement of GABA Binding: Benzodiazepines bind to a specific site on the GABA-A receptor, which is distinct from the GABA binding site. This binding enhances the affinity of the receptor for GABA, leading to increased binding of GABA molecules to their binding sites on the receptor.
- Increased Chloride Ion Influx: When GABA binds to its receptor, it opens chloride ion channels within the receptor complex. This allows chloride ions (Cl-) to flow into the neuron, leading to hyperpolarization of the cell membrane and inhibition of neuronal activity.
- Enhanced Inhibitory Neurotransmission: By enhancing GABA binding and chloride ion influx, benzodiazepines potentiate the inhibitory effects of GABA in the central nervous system. This results in increased inhibitory neurotransmission, leading to effects such as muscle relaxation, anxiolysis (anxiety reduction), sedation, anticonvulsant activity, and hypnotic effects (sleep induction).
- Selective Effects: Benzodiazepines have varying degrees of selectivity for different subtypes of GABA-A receptors, which can contribute to differences in their pharmacological effects. For example, some benzodiazepines may have more pronounced anxiolytic effects, while others may be more effective as muscle relaxants or anticonvulsants.
Diazepam (brand name: Valium)
Lorazepam (brand name: Ativan)
Alprazolam (brand name: Xanax)
Clonazepam (brand name: Klonopin)
Temazepam (brand name: Restoril)
Chlordiazepoxide (brand name: Librium)
Oxazepam (brand name: Serax)
Midazolam (brand name: Versed)
Flurazepam (brand name: Dalmane)
Triazolam (brand name: Halcion)
What is the common name in gabapentin and what is its mechanism and name some
-gab-
involves modulating the activity of neurotransmitters, particularly gamma-aminobutyric acid (GABA), in the central nervous system. However, unlike many other anticonvulsant medications that directly interact with GABA receptors, gabapentin’s exact mechanism is not fully understood.
Pregabalin, Tiagabine, Vigabatrin
What is the common suffix of Fluoroquinolones
(An antibiotic)
- ends in floxacin
Ciprofloxacin, levofloxacin, norfloxacin
These medications are widely used for treating various bacterial infections and are recognizable by their “-floxacin” suffix. However, it’s important to note that not all antibiotics with the “-floxacin” suffix are fluoroquinolones, so it’s essential to consult healthcare professionals for accurate information about specific medications and their uses.
Should be reserved for patients who do not have alternative options
Concerns related to resistance and serious adverse effects – tendon, joint and muscle pain, tingling, confusion, hallucination
Contraindicated in pregnancy and children
For further information:
Tendon, joint, and muscle pain (tendinopathy and tendon rupture):
Reason: Fluoroquinolones can disrupt collagen synthesis and induce oxidative stress, leading to tendon damage. The Achilles tendon is particularly susceptible to rupture. The exact mechanism isn’t fully understood, but it is believed that fluoroquinolones cause changes in the extracellular matrix of tendons, which weakens the structure.
Risk factors: Increased risk is seen in older adults, those on corticosteroids, and patients with renal disease.
Tingling (peripheral neuropathy):
Reason: Fluoroquinolones can cause nerve damage, leading to peripheral neuropathy. This manifests as tingling, numbness, and sometimes pain in the extremities. The mechanism may involve mitochondrial damage or altered nerve conduction, but the exact pathway is unclear.
Confusion, hallucinations (central nervous system effects):
Reason: Fluoroquinolones can cross the blood-brain barrier and affect the central nervous system (CNS). These drugs may disrupt GABA receptors (inhibitory neurotransmitter pathways) in the brain, leading to overexcitation, which can cause symptoms like confusion, agitation, and even hallucinations. Older adults and patients with a history of seizures are particularly vulnerable to CNS side effects.
Contraindicated in pregnancy and children:
Reason: Fluoroquinolones are contraindicated in pregnancy and children because they can affect cartilage and bone development. Studies in animals have shown that fluoroquinolones can cause damage to the developing musculoskeletal system, leading to arthropathy (joint problems) and impaired cartilage formation.
In pregnancy, these drugs could potentially harm the developing fetus, and their use in children is restricted due to the risk of irreversible musculoskeletal damage.
Concerns about resistance:
Reason: Fluoroquinolones are broad-spectrum antibiotics, meaning they target a wide range of bacteria. Overuse can lead to the emergence of antibiotic-resistant strains, making future infections harder to treat. Due to this rising resistance, healthcare providers are advised to reserve fluoroquinolones for cases where no other effective alternatives are available.
What is a common suffix for Alpha1-adrenergic Receptor Antagonists
-zosin for the nonselective; block a broader range of alpha-1 receptor subtypes.
* alfuzosin, doxazosin, terazosin
-losin for the selective; more specific to alpha-1A receptors, providing targeted therapy for conditions like BPH with potentially fewer side effects on blood pressure.
* silodosin and tamsulosin
All five have equal clinical effectiveness but differ in their adverse effect profiles
Choice depends on tolerance to adverse effects and patient comorbidities
Maximal response is seen within a few weeks of use
commonly used to treat conditions such as high blood pressure (hypertension), benign prostatic hyperplasia (enlarged prostate), and certain circulatory disorders. They work by blocking the effects of adrenaline (epinephrine) and related hormones at alpha1 adrenergic receptors, leading to relaxation of blood vessels and improved blood flow.
- Doxazosin and terazosin are known to cause first-dose syncope and should be started at a low dosage and gradually increased until symptomatic improvement or intolerance occurs
What are common names for 5-Alpha-reductase Inhibitors
-steride ; think as smoother flow of urine
Finasteride inhibits type 2 and dutasteride inhibits type 1 and 2
Neither is approved for the prevention of prostate cancer in Canada; however, both agents have been shown to reduce the overall risk of prostate cancer
On the other hand, patients taking a 5-alpha-reductase inhibitor who are diagnosed with prostate cancer may be more likely to be diagnosed with a high-grade cancer
The prediagnostic use of 5-alpha-reductase inhibitors appears to be associated with delayed prostate cancer diagnosis and increased mortality risk
What is a common name for Phosphodiesterase Type 5 Inhibitors
-fil
as in what you are about to do to her
Sildenafil (brand name Viagra)
Tadalafil (brand name Cialis)
Vardenafil (brand name Levitra, Staxyn)
Tadalafil is the only PDE5 inhibitor indicated for the daily management of erectile dysfunction, LUTS associated with BPH, or both
Mechanism of action:
These medications work by inhibiting the enzyme phosphodiesterase type 5 (PDE5), which leads to increased levels of cyclic guanosine monophosphate (cGMP) in the smooth muscle cells of the penis. This relaxation of smooth muscle allows for increased blood flow, resulting in improved erectile function.
What are common names for Calcium Channel Blockers and what are the exceptions
Dihydropyridines (typically end in “-dipine”):
Amlodipine (brand name: Norvasc)
Nifedipine (brand names: Procardia, Adalat)
Felodipine (brand name: Plendil)
Nicardipine (brand name: Cardene)
Isradipine (brand name: Dynacirc)
Nimodipine (brand name: Nimotop)
Clevidipine (brand name: Cleviprex)
Non-Dihydropyridines:
- Verapamil (brand names: Calan, Isoptin, Verelan)
- Diltiazem (brand names: Cardizem, Dilacor, Tiazac)
What are common names for muscuranic agonist
chol or carb and some drugs have both
- methacholine
- carbachol
- Bethanechol
- ## Pilocarbine
What are common names associated with indirect muscarinic agonist
-gmine
Neostigmine
Pyridostigmine
Rivastigmine:
Exceptions:
Donepezil
Galantamine
Edrophonium
What are common names for Muscarinic Antagonist
-trop- is somewhere in the name
ATropine
TioTropium
IpraTropium
BenzTropine
Tropicamide
Exceptions:
Scopolamine
Glycopyrrolate
Oxybutynin
Dicyclomine
Propantheline
Methscopolamine
Trihexyphenidyl
Tolterodine
Darifenacin
Solifenacin
Fesoterodine
What are common names for Nictonic M agonist
Succinylcholine- Stimulates in small doses
Hinders in Hi doses
What are common names for Nicotinic M antagonist
-cur-, curonium, or curium
Generally used for anesthesiology
examples:
Vecuronium
Rocuronium
Cisatracurium
Pancuronium
Atracurium
Doxacurium
Mivacurium
Tubocurarine
Dimethyltubocurarine
exceptions:
Gallamine
Hexafluorenium
Decamethonium
What are common names for short acting (SABA) and long acting Beta 2 adrenergic agonists (LABA) and there mechanism of action?
For short acting as of 2024 there are only 2 short-acting beta 2 adrenergic agonist:
– salbutamol and terbutaline
FYI
- Indicated for all stages of disease severity
- Rapid onset with a duration of 4-6 hours
For long acting beta 2 adrenergic agonist it ends in -terol:
Formoterol, Salmeterol, Indacaterol (Arcapta Neohaler),
Olodaterol (Striverdi Respimat), Vilanterol (often combined with fluticasone as in Breo Ellipta), Arformoterol (Brovana)
FYI
Think Formoterol is formal
Formoterol has a rapid onset of action compared to salmeterol (<3 min vs. 20–120 min in COPD)
* Both have a 12-hour duration of action
Mechanism of Action
Short-Acting Beta2-Adrenergic Agonists (SABA)
Mechanism: SABAs stimulate beta2-adrenergic receptors on bronchial smooth muscle, leading to the activation of adenylate cyclase and an increase in cyclic AMP (cAMP) levels. Elevated cAMP causes relaxation of the bronchial smooth muscle and bronchodilation, helping to relieve acute bronchospasm.
Onset: Rapid (within minutes), making SABAs ideal for quick relief or “rescue” in cases of acute bronchoconstriction.
LABA Mechanism: Similar to SABAs, LABAs also stimulate beta2-adrenergic receptors, resulting in increased cAMP and bronchodilation. However, LABAs have a longer duration of action due to their slower release from the receptor sites, which helps to maintain sustained bronchodilation.
Onset and Duration: Onset is slower than SABAs, and they have a longer duration (usually 8-24 hours). LABAs are not used for acute symptoms but rather for maintenance therapy in chronic respiratory diseases.
Adverse reaction:
Hypokalemia: Mechanism: Beta2-adrenergic agonists stimulate beta2 receptors on cells throughout the body, including muscle and liver cells. When these receptors are activated, they increase the activity of the sodium-potassium ATPase pump, which drives potassium into cells in exchange for sodium.
Clinical Relevance: This effect is more pronounced with higher doses or frequent use of beta2 agonists and can lead to symptoms like muscle weakness, cramps, or even heart rhythm disturbances if potassium levels drop significantly.
Hyperglycemia: 2. Hyperglycemia (High Blood Glucose Levels)
Mechanism: Beta2-adrenergic receptors are also present in the liver, where they stimulate glycogenolysis (the breakdown of glycogen into glucose) and gluconeogenesis (the production of new glucose). When beta2 receptors are activated, they promote these processes, leading to an increase in blood glucose levels.
Clinical Relevance: Monitoring blood glucose is particularly important in diabetic patients using beta2 agonists, as their blood sugar levels could be elevated by these medications, requiring potential adjustments in their diabetes management.
in a fight or flight situation this is great which provides an immediate energy supply that would theoretically support increased physical activity or stress response. However, long-term or frequent use could potentially exacerbate blood glucose control issues in diabetic individuals.
What is the common names for inhaled corticoid steroids?
Often end in “-sone” or “-nide”
Examples: Budesonide, Fluticasone
other examples:
Beclomethasone (Qvar)
Mometasone (Asmanex)
Ciclesonide (Alvesco)
Triamcinolone (Azmacort)
Flunisolide (AeroBid)
Mechanism of Action:
Mechanism: Inhaled corticosteroids work by binding to glucocorticoid receptors in the airway epithelial cells, leading to a reduction in inflammation. They inhibit the release of pro-inflammatory cytokines and decrease the activity of inflammatory cells (like eosinophils and mast cells) in the airways. This results in reduced airway hyper-responsiveness, decreased mucus production, and prevention of airway remodeling.
Use: ICSs are primarily used for long-term control of asthma and, in some cases, severe COPD. They do not provide immediate relief but are essential for reducing chronic inflammation and preventing exacerbations.
Adverse effects:
Oral Thrush (Candidiasis): Suppression of local immune response in the mouth can allow fungi like Candida to grow, causing thrush.
Hyperglycemia:
Mechanism: Although ICS are inhaled, some of the drug inevitably enters the systemic circulation, particularly if inhaler technique is suboptimal. Systemic corticosteroids are known to increase blood glucose levels by promoting gluconeogenesis (new glucose production) and glycogenolysis (breakdown of glycogen) in the liver.
Explanation: Glucocorticoids stimulate pathways that increase glucose production in the liver and reduce glucose uptake in peripheral tissues. This effect on glucose is part of the body’s normal response to stress or injury, as it helps make energy readily available. Consequently, ICS at high doses or with long-term use can increase blood glucose levels, which may be a concern in patients with diabetes or glucose intolerance.
Suppression of the Hypothalamic-Pituitary-Adrenal (HPA) Axis:
Mechanism: Long-term exposure to corticosteroids can suppress the body’s natural cortisol production by inhibiting the hypothalamic-pituitary-adrenal axis. The body reduces its production of endogenous cortisol as it “senses” that sufficient levels are available from the corticosteroid therapy.
Bone Density Loss (Osteoporosis):
Mechanism: Glucocorticoids can inhibit bone formation by decreasing osteoblast (bone-forming cell) activity and increasing osteoclast (bone-resorbing cell) activity. They also reduce calcium absorption in the gut and increase calcium excretion in the kidneys, leading to bone loss over time.
Clinical Impact: This can lead to adrenal insufficiency, where the body cannot produce enough cortisol in response to stress. Symptoms may include fatigue, weakness, and, in severe cases, adrenal crisis if corticosteroid therapy is suddenly stopped.
Growth Suppression in Children:
Mechanism: Systemic absorption of ICS can interfere with growth hormone and bone formation pathways, potentially slowing growth in children and adolescents.
Clinical Impact: Although the effect is usually mild, it is more noticeable in children using high-dose ICS. Growth should be monitored in pediatric patients on long-term ICS therapy.
Useful for SOB
What name is a common name amongst Phosphodiesterase-4 (PDE4) Inhibitors
Phosphodiesterase-4 (PDE4) Inhibitors
Typically end in “-last”
Example: Roflumilast
Mechanism: PDE4 inhibitors specifically inhibit the phosphodiesterase-4 enzyme in immune and inflammatory cells, which increases cAMP levels, leading to reduced inflammation. Unlike bronchodilators, PDE4 inhibitors mainly target the inflammatory process in COPD.
Use: Used as an anti-inflammatory agent in severe COPD with chronic bronchitis, particularly to reduce the risk of exacerbations.
What are the common names for Methylxanthines, please note this is a trick question?
there is none, the main example is Theophylline
Mechanism: Theophylline is thought to inhibit phosphodiesterase (PDE) enzymes, leading to an increase in cAMP, similar to beta2-agonists, resulting in bronchodilation. Additionally, theophylline has mild anti-inflammatory effects and may reduce immune cell infiltration in the airways.
Use: Methylxanthines are less commonly used today due to narrow therapeutic ranges and potential side effects, but they can be used in some cases of asthma and COPD.
What are the common suffix for cancer drugs/ prefix for cancer drugs?
A. Alkylating Agents
Examples:
Nitrogen mustards: Cyclophosphamide, ifosfamide, melphalan.
Nitrosoureas: Carmustine, lomustine.
Platinum-based agents: Cisplatin (overlaps with platinum compounds).
Others: Busulfan, dacarbazine, temozolomide.
Mechanism of Action:
Alkylating agents transfer alkyl groups to DNA at specific sites, most commonly at the N7 position of guanine bases. This causes:
DNA cross-linking: Creates covalent bonds between DNA strands or within a single strand, blocking DNA separation during replication and transcription.
DNA strand breakage: The cross-linked DNA becomes brittle, leading to strand breaks.
Cell cycle arrest and apoptosis: Damage to DNA triggers p53-mediated apoptosis pathways.
These drugs are generally not cell cycle-specific, but their effects are most pronounced in rapidly dividing cells.
B. Platinum Compounds
Examples:
Cisplatin, carboplatin, oxaliplatin.
Mechanism of Action:
Platinum compounds bind to DNA bases, predominantly guanine, forming platinum-DNA adducts. This results in:
Intrastrand cross-links: Covalent bonds between adjacent guanine bases or guanine and adenine bases on the same strand.
Interstrand cross-links: Covalent bonds between guanine bases on opposite DNA strands, preventing strand separation.
Inhibition of DNA replication and transcription: Cross-links disrupt the unwinding of DNA required for these processes.
Induction of apoptosis: Persistent DNA damage activates apoptotic pathways.
These drugs are cell cycle nonspecific, meaning they can act on cells in any phase of division.
C. Inhibitors of Ribonucleotide Reductase
Examples:
Hydroxyurea, gemcitabine (also inhibits DNA polymerase).
Mechanism of Action:
These drugs target ribonucleotide reductase, an enzyme responsible for converting ribonucleotides (RNA precursors) into deoxyribonucleotides (DNA precursors). This leads to:
Depletion of dNTPs: Without deoxyribonucleotides, DNA synthesis cannot proceed.
Cell cycle arrest in the S phase: Cells fail to replicate DNA, halting division.
Hydroxyurea is also used to increase fetal hemoglobin levels in sickle cell anemia.
D. Inhibitors of Thymidylate Synthase
Examples:
5-Fluorouracil (5-FU), capecitabine (prodrug of 5-FU), floxuridine.
Mechanism of Action:
These drugs act as antimetabolites by interfering with pyrimidine biosynthesis, specifically targeting thymidylate synthase, the enzyme converting dUMP to dTMP (a precursor for thymidine).
Competitive inhibition: 5-FU is converted to its active form, 5-FdUMP, which forms a stable complex with thymidylate synthase and its cofactor (tetrahydrofolate).
Thymidine depletion: Without dTMP, DNA synthesis is interrupted, causing cell death.
Selective toxicity: These drugs are most active in cells undergoing rapid DNA synthesis (S phase).
what are common suffixes for anticancer medications -mab. -mab stands for monoclonal antibody. These are lab-created antibodies that mimic the natural antibodies produced by your immune system to fight infections or target specific cells, like cancer or immune system targets.
Rules for Naming -mab Drugs (Made Easy)
Rule 1: Source of the Antibody
The letters just before -mab tells you the source:
-o-: Mouse-derived (100% mouse).
-xi-: Chimeric (part human, part mouse). (i.e. Rituximab)
-zu-: Humanized (mostly human, small part mouse). (i.e. Trastuzumab)
-u-: Fully human.
Rule 2: Target in the Body
The letters before the source tell you what the antibody is targeting:
-c(i)-: Circulatory system (e.g., targets blood vessels).
-k(i)-: Interleukins (messengers in the immune system).
-l(i)-: Immune system.
-t(u)-: Tumors (e.g., cancer cells).
Rule 3: Prefix
The part of the name before the target and source (e.g., “tra-“ in trastuzumab) doesn’t follow a strict rule. It’s chosen to make the name sound good.
Examples of -mab Drugs
Rituximab
xi: Chimeric (part human, part mouse).
li: Immune system.
Targets B cells (used in autoimmune diseases and cancers like lymphoma).
Bevacizumab
zu: Humanized.
ci: Circulatory system.
Blocks blood vessel growth (used in cancer).
Adalimumab
u: Fully human.
li: Immune system.
Treats autoimmune conditions (e.g., rheumatoid arthritis).
What Do B Cells Do? (Simplified)
B cells are white blood cells (a type of lymphocyte) that play a key role in your immune system.
They make antibodies, which are proteins that attach to invaders like bacteria or viruses and help destroy them.
Types of B Cells
Naive B Cells: These haven’t encountered an invader yet. They patrol your body, waiting to be activated.
Plasma Cells: Once activated, B cells become plasma cells, which are antibody factories. They make lots of antibodies to target a specific invader.
Memory B Cells: After an infection, these cells “remember” the invader. If it shows up again, they react faster.
Why Are -mabs Important?
Monoclonal antibodies (-mabs) are designed to either:
Boost the immune system by targeting specific immune pathways.
Directly target and kill harmful cells, like cancer cells.
Block harmful processes (e.g., inflammation in autoimmune diseases).
The name of a monoclonal antibody tells you:
It’s a monoclonal antibody because it ends in -mab.
What it’s made from (e.g., human, mouse, or a mix of both).
What part of the body it targets (e.g., immune system, tumors, interleukins).
Here’s how to decode the name:
-c(i)-: Circulatory system
Example: Bevacizumab (blocks blood vessel growth in tumors by targeting VEGF).
-k(i)-: Interleukins (messengers in immune communication).
Example: Anakinra (targets interleukin-1 receptor).
-l(i)-: Immune system
Example: Rituximab (targets CD20 on B cells).
-t(u)-: Tumors
Example: Trastuzumab (targets HER2 in breast cancer).
-c(i)-: Circulatory system
Example: Bevacizumab (blocks blood vessel growth in tumors by targeting VEGF).
-k(i)-: Interleukins (messengers in immune communication).
Example: Anakinra (targets interleukin-1 receptor).
-l(i)-: Immune system
Example: Rituximab (targets CD20 on B cells).
-t(u)-: Tumors
Example: Trastuzumab (targets HER2 in breast cancer).
In some on these drugs like Rituximab it is the i in front of -man that lets you know it is for the immune system
What are Common Suffixes and Prefixes for Tricyclic Antidepressants (TCAs)
Common Suffixes: of TCA’s
“-ipramine” (e.g., imipramine, clomipramine, desipramine)
“-triptyline” or “-tyline” (e.g., amitriptyline, nortriptyline, protriptyline)
Common TCAs and Their Uses:
Imipramine – Used for depression, anxiety, and bedwetting (enuresis) in children.
Clomipramine – Primarily used for obsessive-compulsive disorder (OCD).
Amitriptyline – Used for depression, neuropathic pain, and migraines.
Nortriptyline – Used for depression and nerve pain.
Desipramine – Primarily used for depression.
- Why Do TCAs Cause Anticholinergic Effects?
TCAs block muscarinic (M1) acetylcholine receptors, which are responsible for parasympathetic nervous system functions like saliva production, gut motility, and bladder contraction.
🛑 When muscarinic receptors are blocked:
Dry mouth (decreased saliva production)
Blurred vision (affects ciliary muscles of the eye)
Constipation (slows down peristalsis in the gut)
Urinary retention (prevents bladder contraction)
Cognitive impairment (blocking acetylcholine in the brain affects memory and focus)
💡 Why do TCAs block acetylcholine?
TCAs do not just act on serotonin and norepinephrine reuptake transporters—they also bind to other receptors, including muscarinic acetylcholine receptors, histamine receptors (H1), and α1-adrenergic receptors.
This “dirty drug” effect leads to many of their side effects.
Mechanism of Action:
TCAs block the reuptake of serotonin and norepinephrine, increasing their levels in the brain, which helps improve mood.
Common Side Effects:
Anticholinergic effects: Dry mouth, constipation, blurred vision, urinary retention.
Sedation: Due to histamine receptor blockade.
Weight gain: Common with prolonged use.
Cardiovascular effects: Risk of arrhythmias and orthostatic hypotension.
Seizures: Can lower the seizure threshold.
Overdose risk: Can cause cardiotoxicity (QT prolongation, fatal arrhythmias).
** TCAs and the Heart:**
TCAs block cardiac sodium channels, similar to class I antiarrhythmic drugs, which can slow conduction through the heart, leading to arrhythmias and QT prolongation.
High doses of TCAs can cause fatal ventricular arrhythmias.
Why Do TCAs Lower the Seizure Threshold?
🔹 TCAs lower the seizure threshold by multiple mechanisms:
1️⃣ Inhibiting GABAergic Activity:
GABA is the brain’s main inhibitory neurotransmitter, preventing excessive neuronal firing.
TCAs reduce GABAergic inhibition, making neurons more excitable and increasing seizure risk.
2️⃣ Increasing Norepinephrine and Serotonin:
Higher levels of these neurotransmitters can increase cortical excitability, making the brain more prone to seizures.
3️⃣ Blocking Sodium Channels (at high doses):
TCAs block sodium channels in neurons, which can disrupt normal electrical activity and increase seizure risk.
4️⃣ Anticholinergic Effects:
Acetylcholine is involved in modulating seizure activity, and blocking muscarinic receptors (anticholinergic effects of TCAs) may contribute to increased excitability in the brain.
💡 Who is at higher risk?
Patients with epilepsy or a history of seizures.
Overdose situations (TCA overdoses are highly toxic and can cause seizures, arrhythmias, and coma).
What are Common Suffixes and Prefixes Monoamine Oxidase Inhibitors (MAOIs)
Common Suffixes:
Not really but some are
MAOI irreversible = -zin, -zid, -mine
reversible = - clobemide
“-zine” (e.g., phenelzine)
“-giline” (e.g., selegiline, rasagiline)
“-carbazide” (e.g., isocarboxazid)
Moclobemide (RIMA) - reversible
Common MAOIs and Their Uses:
Phenelzine – Used for depression, social anxiety disorder, and panic disorder.
Tranylcypromine – Used for treatment-resistant depression.
Isocarboxazid – Used for major depressive disorder.
Selegiline – Used for depression and Parkinson’s disease.
Mechanism of Action:
MAOIs inhibit monoamine oxidase, an enzyme that breaks down serotonin, dopamine, and norepinephrine, thereby increasing their levels.
Common Side Effects:
Hypertensive crisis: Can occur if taken with tyramine-rich foods (cheese, wine, cured meats).
Orthostatic hypotension: Dizziness or fainting when standing up.
Weight gain and sedation: More common with older MAOIs.
Sexual dysfunction: Reduced libido, erectile dysfunction.
Serotonin syndrome: If combined with SSRIs, SNRIs, or other serotonergic drugs.
How TCAs Cause Orthostatic Hypotension:
TCAs block α1-adrenergic receptors in blood vessels.
Normally, when you stand up, norepinephrine stimulates α1 receptors to constrict blood vessels, preventing blood from pooling in the legs and keeping blood pressure stable.
With TCAs blocking α1 receptors, blood vessels do not constrict properly, leading to a sudden drop in blood pressure when standing (orthostatic hypotension).
Symptoms: Dizziness, lightheadedness, fainting.
How MAOIs Cause Orthostatic Hypotension:
MAOIs inhibit the breakdown of norepinephrine, which might seem like it would increase blood pressure, but in reality:
Over time, MAOIs deplete norepinephrine stores in nerve terminals (because MAO is responsible for recycling neurotransmitters).
With less norepinephrine available, the body struggles to increase blood pressure when needed (e.g., when standing).
This leads to low resting blood pressure and a greater risk of orthostatic hypotension.
What is Tyramine and How Does it Affect MAOIs?
🔹 Tyramine is a naturally occurring monoamine found in aged, fermented, or cured foods (e.g., aged cheese, red wine, cured meats, soy products).
🔹 Normally, tyramine is broken down by monoamine oxidase (MAO) in the gut and liver before it enters circulation.
(monoamine - for more information refer the Diagnosis and treatment; Neurotransmitters and what do they do)
🔹 When someone is taking an MAOI:
MAO is inhibited, so tyramine is not broken down.
Tyramine then enters the bloodstream in high amounts and displaces norepinephrine from nerve terminals.
This causes a sudden surge in norepinephrine, leading to intense vasoconstriction and severe hypertension (hypertensive crisis).
Symptoms of Hypertensive Crisis:
⚠️ Severe headache, high blood pressure, blurry vision, chest pain, nausea, stroke risk.
Key Mechanism:
Tyramine acts like norepinephrine by forcing stored norepinephrine into circulation.
Since MAOIs prevent the breakdown of norepinephrine, the body cannot regulate blood pressure properly.
Extreme vasoconstriction raises blood pressure to dangerous levels.
Why MAOI Users Must Avoid Tyramine-Rich Foods:
🚫 Aged cheese, cured meats, fermented foods, alcohol (especially red wine, beer), fava beans, soy sauce, pickled foods.
what are common suffixes and prefixes of Noradrenergic and Specific Serotonergic Antidepressants (NaSSA’s) and some names of the drugs also is the above all or most of there general mechanism of actions?
Common Suffixes & Prefixes:
NaSSAs do not follow a strict suffix pattern like SSRIs (-oxetine) or TCAs (-triptyline), but some names share similarities:
Mirtazapine (most well-known NaSSA)
Setiptiline (less common, used in Japan)
There are very few NaSSA drugs available, making pattern recognition difficult.
Common NaSSA Drugs:
Mirtazapine (widely used)
Setiptiline (rare, mainly in Japan)
Mianserin (older, used in Europe, but not widely prescribed due to blood-related side effects)
Mechanism of Action
- α₂-Adrenergic Antagonism (Main Effect)
- Blocks α₂-autoreceptors → Increases norepinephrine (NE) release
- Blocks α₂-heteroreceptors → Increases serotonin (5-HT) release - Serotonin Receptor Modulation (Selective Action)
- Blocks 5-HT2A and 5-HT2C receptors → Reduces anxiety, improves sleep, reduces sexual dysfunction
- Blocks 5-HT3 receptors → Reduces nausea & GI side effects (this is a major difference from SSRIs, which often cause nausea) - Histamine (H1) Receptor Blockade
Causes sedation & weight gain
Used for patients who struggle with insomnia or low appetite - No Direct Reuptake Inhibition
Unlike SSRIs and SNRIs, NaSSAs do not inhibit serotonin or norepinephrine reuptake
Instead, they enhance neurotransmission through receptor modulation
What are common prefixes and suffixes for Norepinephrine Dopamine Reuptake Inhibitors (NDRIs) and there mechanism of action?
Examples of NDRI:
1. Bupropion
2. Amineptine (Rarely used)
3. Nomifensine (Withdrawn)
Mechanism of Action of NDRIs (Norepinephrine-Dopamine Reuptake Inhibitors)
NDRIs increase the levels of norepinephrine (NE) and dopamine (DA) in the brain by blocking their reuptake transporters (NET & DAT). This leads to:
Increased dopamine activity, improving motivation, energy, and focus.
Enhanced norepinephrine signaling, reducing fatigue and improving alertness.
Minimal serotonin effects, leading to lower risks of sexual dysfunction and weight gain compared to SSRIs/SNRIs.
Example: Bupropion (Wellbutrin, Zyban)
Inhibits NET and DAT, increasing NE & DA.
Used for depression, smoking cessation, and ADHD (off-label).
NET & DAT Explained
1. NET (Norepinephrine Transporter)
Function: NET is a protein that removes norepinephrine (NE) from the synaptic cleft and transports it back into the presynaptic neuron.
Effect of Blocking NET:
Increases norepinephrine levels in the brain.
Enhances alertness, energy, and focus.
Used in antidepressants (NDRIs, SNRIs), ADHD medications, and some pain medications.
2. DAT (Dopamine Transporter)
Function: DAT removes dopamine (DA) from the synaptic cleft, recycling it back into the presynaptic neuron.
Effect of Blocking DAT:
Increases dopamine levels, improving motivation, reward, and attention.
Used in antidepressants (NDRIs), ADHD medications, and stimulants (e.g., cocaine, amphetamines).
What are common prefixes, suffixes for amphetamines and there mechanism of action?
Suffix
- amphetamine
Common Drug Names:
- Dextroamphetamine (Dexedrine)
- Amphetamine/Dextroamphetamine (Adderall)
- Lisdexamfetamine (Vyvanse)
- Methamphetamine (Desoxyn)
Effects of Amphetamines
✅ Positive Effects:
Increased focus, energy, motivation (useful for ADHD & narcolepsy).
Improved alertness and wakefulness.
Enhanced dopamine levels, leading to a sense of reward and pleasure.
⚠️ Potential Risks & Side Effects:
Insomnia, anxiety, agitation.
Increased heart rate & blood pressure (risk of cardiovascular issues).
Appetite suppression, weight loss.
Risk of dependence and addiction (especially with misuse).
What Are Amphetamines?
Amphetamines are stimulant drugs that increase activity in the central nervous system (CNS). They enhance alertness, focus, and energy by boosting levels of dopamine (DA) and norepinephrine (NE) in the brain.
- Mechanism of Action
Amphetamines work by:
Blocking DAT & NET: Prevent dopamine and norepinephrine from being reabsorbed, increasing their levels in the synaptic cleft.
Reversing DAT & NET: Force dopamine and norepinephrine out of neurons, further increasing their availability.
Inhibiting VMAT2 (Vesicular Monoamine Transporter 2): Increases dopamine release into the synapse.
Does “Reversible” and “Irreversible” Mean the Same for Other Drug Types?
Not always! The concept of reversible vs. irreversible inhibition applies to other drugs, but the time frame and effects depend on the enzyme and drug class.
For example:
Acetylcholinesterase inhibitors (AChEIs):
Irreversible inhibitors (e.g., organophosphates like sarin gas) cause long-lasting effects and require the body to synthesize new enzymes.
Reversible inhibitors (e.g., donepezil for Alzheimer’s) temporarily block the enzyme and wear off quickly.
Proton Pump Inhibitors (PPIs) vs. H2 Blockers (acid reducers):
PPIs (e.g., omeprazole) irreversibly inhibit proton pumps and take days to wear off.
H2 blockers (e.g., ranitidine) reversibly inhibit histamine receptors and wear off within hours.
Summary:
For MAOIs, “irreversible” means permanent enzyme inactivation, requiring longer washout (~2 weeks).
“Reversible” MAOIs detach from the enzyme, so washout is much shorter (~5 days).
This concept applies to other drug classes, but the time frames depend on the drug and enzyme involved.
What are common suffixes or prefixes for atypical antipsychotics and list some common medications?
they end in -pine
Some common atypical antipsychotics are
1. Quetiapine
2. Asenapine
3. Olanzapine
4. Clozapine
These drugs block dopamine (D2) and serotonin (5-HT2A) receptors, making them effective for mania, schizophrenia, and sometimes bipolar depression.
However, not all drugs ending in “-pine” are antipsychotics. For example:
Nifedipine (Calcium Channel Blocker for blood pressure), by now you should know - dipines are CCB’s
Atropine (Anticholinergic for bradycardia), by now you should recognize the -trop and is a muscarinic antagonist
So, while “-pine” is common for atypical antipsychotics, it’s not a universal rule.
Atypical Antipsychotics (Second-Generation Antipsychotics)
Mechanism of Action:
Dopamine (D2) receptor blockade → Reduces manic symptoms & psychosis.
Serotonin (5-HT2A) receptor blockade → Enhances mood stabilization & reduces EPS (extra-pyramidal symptoms).
Some also partially activate dopamine (D2) receptors (e.g., aripiprazole) to balance dopamine levels instead of completely blocking it.
If a drug clears the body within 1 week, what is its half-life?
A drug’s half-life (t₁/₂) is the time it takes for 50% of the drug to be eliminated from the body. Complete clearance is typically estimated using 5 half-lives (since by then, ~97% of the drug is gone).
tclearance =5×t1/2
𝑡1/2=7days/5 =1.4days ≈ 34hours
So, the half-life of doxycycline is about 16-22 hours, while tetracycline has a shorter half-life of ~8-11 hours. If referring to a longer elimination process, it could suggest a half-life closer to 1-2 days for certain formulations.
1) What Information Do You Need to Calculate Half-Life?
To calculate the half-life (t₁/₂) of a drug, you typically need:
Elimination rate constant (k) – The rate at which the drug is removed from the body.
Formula:
𝑡1/2= 0.693/𝑘
Plasma concentration at two different times – Helps determine how quickly the drug decreases.
Clearance (CL) and Volume of Distribution (Vd) – Related to drug elimination:
t₁/₂ = (0.693 × Vd) / CL
Larger Vd = longer half-life, higher CL = shorter half-life.
2) How Long Until a Drug is Considered “Cleared”?
Drugs are generally considered “cleared” after 5 half-lives, meaning ~97% is eliminated from the body.
If 3.5% remains, that means 96.5% is eliminated, which is very close to the 5 half-life rule.
In practical terms, 3.5% would still be considered “cleared” because it’s near the threshold where drug effects are negligible.
What are common suffixes or prefixes for Retinoids and list some common medications?
They often have the root -retin- in their name
Key Takeaway:
Oral isotretinoin: 1 month before, during, and 1 month after therapy
Acitretin: Must be stopped at least 3 years before pregnancy
Topical retinoids: Minimal absorption; generally advised to avoid in pregnancy but not as strictly regulated
Examples of Retinoids
Isotretinoin – (Accutane, Claravis, Absorica)
Tretinoin – (Retin-A, Renova)
Adapalene – (Differin)
Alitretinoin – (Panretin)
Bexarotene – (Targretin)
Acitretin – (Soriatane)
Topical Retinoids (e.g., Tretinoin, Adapalene, Alitretinoin, Bexarotene)
Local irritation: redness, peeling, dryness
Increased sun sensitivity (phototoxicity)
Mild burning, tingling, or stinging
Common Side Effects of Retinoids (Including Isotretinoin)
Systemic Retinoids (Oral) - e.g., Isotretinoin, Acitretin
Skin & Mucous Membranes:
Dry skin, lips (cheilitis), and eyes
Mucocutaneous effects (e.g., nosebleeds, dry nasal passages)
Increased skin sensitivity and peeling
Gastrointestinal (GI) Effects:
Elevated liver enzymes (possible hepatotoxicity)
Increased triglycerides (risk of pancreatitis)
Neurological & Musculoskeletal:
Myalgia (muscle pain)
Arthralgia (joint pain)
Headaches
Rare risk of benign intracranial hypertension (especially with tetracyclines)
Psychiatric Effects (controversial but monitored):
Depression
Mood changes
Suicidal ideation (rare but a concern)
Teratogenicity (Pregnancy Risk Category X):
Causes severe birth defects (craniofacial, cardiac, central nervous system malformations)
Strict pregnancy prevention programs (two forms of birth control required)
Mechanisms Behind Increased Photosensitivity:
Thinner Stratum Corneum (Outer Skin Layer)
Retinoids promote rapid exfoliation and skin cell turnover, making the outermost layer of the skin thinner.
This reduces the natural UV-protective barrier, leading to increased sun sensitivity.
Reduced Melanin Protection
Retinoids can decrease melanin production, which is responsible for absorbing UV radiation.
Less melanin means higher susceptibility to UV-induced damage, including sunburn and hyperpigmentation.
Altered DNA Repair Mechanisms
Retinoids impact the way skin cells respond to UV damage by altering DNA repair pathways.
This can make cells more vulnerable to UV radiation, increasing the risk of sunburn and skin irritation.
Increased Vascular Reactivity
Retinoids increase blood flow to the skin, which can lead to redness and flushing when exposed to the sun.
This effect is particularly relevant in rosacea, where isotretinoin is sometimes used.
How to Reduce Photosensitivity While on Retinoids:
✅ Use broad-spectrum sunscreen (SPF 30+ or higher)
✅ Apply retinoids at night to minimize UV exposure
✅ Wear protective clothing (hats, sunglasses, etc.)
✅ Avoid prolonged sun exposure, especially midday
✅ Use gentle, hydrating skincare to support skin barrier
