Miscellaneous protein synthesis inhibitors
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Miscellaneous protein synthesis inhibitors
Medicine and surgery
Allergy and immunology
Antihistamines for allergies
Glucocorticoids
Cardiology, cardiac surgery and vascular surgery
Coronary artery disease: Clinical (To be retired)
Heart failure: Clinical (To be retired)
Syncope: Clinical (To be retired)
Hypertension: Clinical (To be retired)
Hypercholesterolemia: Clinical (To be retired)
Peripheral vascular disease: Clinical (To be retired)
Leg ulcers: Clinical (To be retired)
Adrenergic antagonists: Alpha blockers
Adrenergic antagonists: Beta blockers
ACE inhibitors, ARBs and direct renin inhibitors
Thiazide and thiazide-like diuretics
Calcium channel blockers
Lipid-lowering medications: Statins
Lipid-lowering medications: Fibrates
Miscellaneous lipid-lowering medications
Antiplatelet medications
Dermatology and plastic surgery
Hypersensitivity skin reactions: Clinical (To be retired)
Eczematous rashes: Clinical (To be retired)
Papulosquamous skin disorders: Clinical (To be retired)
Alopecia: Clinical (To be retired)
Hypopigmentation skin disorders: Clinical (To be retired)
Benign hyperpigmented skin lesions: Clinical (To be retired)
Skin cancer: Clinical (To be retired)
Endocrinology and ENT (Otolaryngology)
Diabetes mellitus: Clinical (To be retired)
Hyperthyroidism: Clinical (To be retired)
Hypothyroidism and thyroiditis: Clinical (To be retired)
Dizziness and vertigo: Clinical (To be retired)
Hyperthyroidism medications
Hypothyroidism medications
Insulins
Hypoglycemics: Insulin secretagogues
Miscellaneous hypoglycemics
Gastroenterology and general surgery
Gastroesophageal reflux disease (GERD): Clinical (To be retired)
Peptic ulcers and stomach cancer: Clinical (To be retired)
Diarrhea: Clinical (To be retired)
Malabsorption: Clinical (To be retired)
Colorectal cancer: Clinical (To be retired)
Diverticular disease: Clinical (To be retired)
Anal conditions: Clinical (To be retired)
Cirrhosis: Clinical (To be retired)
Breast cancer: Clinical (To be retired)
Laxatives and cathartics
Antidiarrheals
Acid reducing medications
Hematology and oncology
Anemia: Clinical (To be retired)
Anticoagulants: Warfarin
Anticoagulants: Direct factor inhibitors
Antiplatelet medications
Infectious diseases
Pneumonia: Clinical (To be retired)
Urinary tract infections: Clinical (To be retired)
Skin and soft tissue infections: Clinical (To be retired)
Protein synthesis inhibitors: Aminoglycosides
Antimetabolites: Sulfonamides and trimethoprim
Miscellaneous cell wall synthesis inhibitors
Protein synthesis inhibitors: Tetracyclines
Cell wall synthesis inhibitors: Penicillins
Miscellaneous protein synthesis inhibitors
Cell wall synthesis inhibitors: Cephalosporins
DNA synthesis inhibitors: Metronidazole
DNA synthesis inhibitors: Fluoroquinolones
Herpesvirus medications
Azoles
Echinocandins
Miscellaneous antifungal medications
Anti-mite and louse medications
Nephrology and urology
Chronic kidney disease: Clinical (To be retired)
Kidney stones: Clinical (To be retired)
Urinary incontinence: Pathology review
ACE inhibitors, ARBs and direct renin inhibitors
PDE5 inhibitors
Adrenergic antagonists: Alpha blockers
Neurology and neurosurgery
Stroke: Clinical (To be retired)
Lower back pain: Clinical (To be retired)
Headaches: Clinical (To be retired)
Migraine medications
Pulmonology and thoracic surgery
Asthma: Clinical (To be retired)
Chronic obstructive pulmonary disease (COPD): Clinical (To be retired)
Lung cancer: Clinical (To be retired)
Antihistamines for allergies
Bronchodilators: Beta 2-agonists and muscarinic antagonists
Bronchodilators: Leukotriene antagonists and methylxanthines
Pulmonary corticosteroids and mast cell inhibitors
Rheumatology and orthopedic surgery
Joint pain: Clinical (To be retired)
Rheumatoid arthritis: Clinical (To be retired)
Lower back pain: Clinical (To be retired)
Anatomy clinical correlates: Clavicle and shoulder
Anatomy clinical correlates: Arm, elbow and forearm
Anatomy clinical correlates: Wrist and hand
Anatomy clinical correlates: Median, ulnar and radial nerves
Anatomy clinical correlates: Bones, joints and muscles of the back
Anatomy clinical correlates: Hip, gluteal region and thigh
Anatomy clinical correlates: Knee
Anatomy clinical correlates: Leg and ankle
Anatomy clinical correlates: Foot
Acetaminophen (Paracetamol)
Non-steroidal anti-inflammatory drugs
Glucocorticoids
Opioid agonists, mixed agonist-antagonists and partial agonists
Antigout medications
Non-biologic disease modifying anti-rheumatic drugs (DMARDs)
Osteoporosis medications
Assessments
Miscellaneous protein synthesis inhibitors
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Memory Anchors and Partner Content
External References
First Aid
2022
2021
2020
2019
2018
2017
2016
Anemia
chloramphenicol p. 189
Aplastic anemia p. 429
chloramphenicol p. 189
Chloramphenicol p. 189
aplastic anemia and p. 251, 429
gray baby syndrome p. 251
mechanism (diagram) p. 184
protein synthesis inhibition p. 188
Gray baby syndrome
chloramphenicol and p. 189, 201, 251
Haemophilus influenzae p. , 140
chloramphenicol p. 189
Haemophilus influenzae type B
chloramphenicol p. 189
Meningitis
chloramphenicol p. 189
Neisseria meningitidis
chloramphenicol p. 189
Rickettsia rickettsii p. , 148
chloramphenicol p. 189
Rocky Mountain spotted fever p. 148
chloramphenicol p. 189
Streptococcus pneumoniae p. , 134
chloramphenicol p. 189
External Links
Transcript
Content Reviewers
Yifan Xiao, MDContributors
Kaia Chessen, MScBMC
Sam Gillespie, BSc
Evan Debevec-McKenney
Protein synthesis inhibitors include many different classes of medications that prevent bacterial ribosomes from synthesizing proteins.
The ones that target the 50S subunit of the ribosome include chloramphenicol, macrolides, lincosamides, and oxazolidinones.
Okay, first, let’s look at how genes become proteins. There’s two steps: transcription and translation.
During transcription, a specific gene on the DNA is “read” and a copy is made called a messenger RNA, or mRNA, which is like a blueprint with instructions on what protein to build.
Translation is also known as protein synthesis, and it’s when organelles called ribosomes assemble the protein from amino acids within the cytoplasm.
Now, prokaryotic cells, like bacteria, have smaller ribosomes than eukaryotic cells, like those found in humans.
Bacterial ribosomes are made up of a 50S subunit and a 30S subunit which combine to form a 70S ribosome.
Eukaryotic ribosomes are made up of a 60S and a 40S subunit that form an 80S ribosome.
Since these proteins are different, we can create medications that selectively interfere with the bacterial ones.
Protein synthesis involves initiation, elongation, and termination.
In bacteria, initiation occurs when the 50S and 30S subunits bind to the mRNA sequence to form a ribosome-mRNA complex, also called the initiation complex.
The mRNA serves as a blueprint for the protein that will be synthesized.
It’s made up of three nucleotide-long sequences, called codons, on top of which transport RNA, or tRNA, carrying amino acids can bind with their matching anticodon.
The complete ribosome has 3 sites where tRNA can enter and bind. These are called the A, or aminoacyl site, the P, or peptidyl site, and the E, or exit site.
Elongation starts when the first tRNA, carrying a formylmethionine amino acid, enters the P site and binds to the start codon. This causes a conformational change which unlocks the A site for the next tRNA.
The next tRNA binds at the A site, the amino acid detaches from the tRNA in the P site, and a peptide bond is formed by an enzyme called peptidyl transferase between the amino acids in the P and A sites, a process known as transpeptidation.
Now, the A site has the newly formed peptide chain dangling from it, while the P site has an empty tRNA with no amino acids.
Summary
Protein synthesis inhibitors are a class of antibiotics which prevent bacterial ribosomes from synthesizing proteins. They include drugs like chloramphenicol, macrolides, lincosamides, and oxazolidinones.
Most of these drugs act on the 50S subunit of the ribosome, but their mechanisms can be very different. For example, oxazolidinones like linezolid stop the initiation complex from forming. Both the macrolides and lincosamides prevent translocation. Chloramphenicol inhibits peptidyl transferase which is the enzyme that creates the peptide bonds.
Sources
- "Katzung & Trevor's Pharmacology Examination and Board Review,12th Edition" McGraw-Hill Education / Medical (2018)
- "Rang and Dale's Pharmacology" Elsevier (2019)
- "Goodman and Gilman's The Pharmacological Basis of Therapeutics, 13th Edition" McGraw-Hill Education / Medical (2017)
- "Chloramphenicol: A Review" Pediatrics in Review (2004)
- "Clarithromycin: Review of a New Macrolide Antibiotic with Improved Microbiologic Spectrum and Favorable Pharmacokinetic and Adverse Effect Profiles" Annals of Pharmacotherapy (1992)
- "New Macrolide Antibiotics: Azithromycin and Clarithromycin" Annals of Internal Medicine (1992)
- "Macrolides and ketolides: azithromycin, clarithromycin, telithromycin" Infectious Disease Clinics of North America (2004)
- "Enhancement of opsonophagocytosis of Bacteroides spp. by clindamycin in subinhibitory concentrations" Journal of Antimicrobial Chemotherapy (1989)
- "Linezolid versus Vancomycin for the Treatment of Methicillin‐ResistantStaphylococcus aureusInfections" Clinical Infectious Diseases (2002)
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