Common Suffixes Or Prefixes For Drugs Flashcards

1
Q

What do PPI’s (proton pump inhibitors)
Commonly End in, what is its mechanism of action and some common drugs?

A

-Prazole

  • Mechanism of action
  • H+, K+-ATPase inhibition
  • Specific agents
  • Omeprazole, esomeprazole
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2
Q

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.

A

-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)
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3
Q

What do beta blockers commonly end in and what are there mechanism of action and some drugs?

A

-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

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4
Q

What do Angiotensin Converting Enzymes (ACE) Inhibitors commonly end in and what are there mechanism of action and some common drugs

A

-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

  1. inhibits ACE

lisinopril, enalapril, and captopril

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5
Q

What do antihistamine/h1 receptor antagonist commonly end in and what is it’s mechanism of action and common drug names?

A

-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)

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6
Q

What do cholesterol lowering drugs commonly end in and what are there mechanism of action and list some of the drugs?

A

-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)

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7
Q

What do Selective-norepinephrine- reuptake inhibitors (SNRIs) commonly end in and what is there mechanism of action and common names.

A

-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.

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8
Q

What do SSRIs commonly end in, and what are there mechanism of action and list some medications.

A

-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)

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9
Q

What are common name suffixes for Bisphosphonates and what are there mechanism of action and common drugs?

A

-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)

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10
Q

What are common suffix names for NSAIDs and what is it’s mechanism of action?

A

-profen

  1. 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.
  2. 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.
  3. 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.
  4. 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.
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11
Q

What do antifungals commonly end in and what are there mechanism of actions and what are some.

A

-azole

  1. Work by inhibiting an enzyme necessary for the synthesis of ergosterol which is necessary for fungal membrane function
  2. 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)

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12
Q

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

A
  1. -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.
  2. -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.
  3. -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.
  4. -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.
  5. -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.
  6. -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.
  7. 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.
  8. 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.
    ======================
    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.
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13
Q

What are common suffix for benzodiazepines and what is it’s mechanism of action and list some

A

-pam or -lam

  1. 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.
  2. 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.
  3. 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).
  4. 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)

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14
Q

What is the common name in gabapentin and what is its mechanism and name some

A

-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

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15
Q

What is the common suffix of Fluoroquinolones
(An antibiotic)

A
  • 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.

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16
Q

What is a common suffix for Alpha1-adrenergic Receptor Antagonists

A

-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
17
Q

What are common names for 5-Alpha-reductase Inhibitors

A

-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

18
Q

What is a common name for Phosphodiesterase Type 5 Inhibitors

A

-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.

19
Q

What are common names for Calcium Channel Blockers and what are the exceptions

A

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)

20
Q

What are common names for muscuranic agonist

A

chol or carb and some drugs have both

  • methacholine
  • carbachol
  • Bethanechol
  • ## Pilocarbine
21
Q

What are common names associated with indirect muscarinic agonist

A

-gmine

Neostigmine
Pyridostigmine
Rivastigmine:

Exceptions:
Donepezil
Galantamine
Edrophonium

22
Q

What are common names for Muscarinic Antagonist

A

-trop- is somewhere in the name

ATropine
TioTropium
IpraTropium
BenzTropine
Tropicamide

Exceptions:
Scopolamine
Glycopyrrolate
Oxybutynin
Dicyclomine
Propantheline
Methscopolamine
Trihexyphenidyl
Tolterodine
Darifenacin
Solifenacin
Fesoterodine

23
Q

What are common names for Nictonic M agonist

A

Succinylcholine- Stimulates in small doses
Hinders in Hi doses

24
Q

What are common names for Nicotinic M antagonist

A

-cur-, curonium, or curium

Generally used for anesthesiology

examples:
Vecuronium
Rocuronium
Cisatracurium
Pancuronium
Atracurium
Doxacurium
Mivacurium
Tubocurarine
Dimethyltubocurarine

exceptions:
Gallamine
Hexafluorenium
Decamethonium

25
Q

What are common names for short acting (SABA) and long acting Beta 2 adrenergic agonists (LABA) and there mechanism of action?

A

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.

26
Q

What is the common names for inhaled corticoid steroids?

A

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.

27
Q

Useful for SOB

What name is a common name amongst Phosphodiesterase-4 (PDE4) Inhibitors

A

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.

28
Q

What are the common names for Methylxanthines, please note this is a trick question?

A

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.