Miscellaneous protein synthesis inhibitors

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Miscellaneous protein synthesis inhibitors

Medical and surgical emergencies

Cardiology, cardiac surgery and vascular surgery

Advanced cardiac life support (ACLS): Clinical (To be retired)

Supraventricular arrhythmias: Pathology review

Ventricular arrhythmias: Pathology review

Heart blocks: Pathology review

Coronary artery disease: Clinical (To be retired)

Heart failure: Clinical (To be retired)

Syncope: Clinical (To be retired)

Pericardial disease: Clinical (To be retired)

Valvular heart disease: Clinical (To be retired)

Chest trauma: Clinical (To be retired)

Shock: Clinical (To be retired)

Peripheral vascular disease: Clinical (To be retired)

Leg ulcers: Clinical (To be retired)

Aortic aneurysms and dissections: Clinical (To be retired)

Cholinomimetics: Direct agonists

Cholinomimetics: Indirect agonists (anticholinesterases)

Muscarinic antagonists

Sympathomimetics: Direct agonists

Sympatholytics: Alpha-2 agonists

Adrenergic antagonists: Presynaptic

Adrenergic antagonists: Alpha blockers

Adrenergic antagonists: Beta blockers

ACE inhibitors, ARBs and direct renin inhibitors

Loop diuretics

Thiazide and thiazide-like diuretics

Calcium channel blockers

cGMP mediated smooth muscle vasodilators

Class I antiarrhythmics: Sodium channel blockers

Class II antiarrhythmics: Beta blockers

Class III antiarrhythmics: Potassium channel blockers

Class IV antiarrhythmics: Calcium channel blockers and others

Positive inotropic medications

Antiplatelet medications

Dermatology and plastic surgery

Blistering skin disorders: Clinical (To be retired)

Bites and stings: Clinical (To be retired)

Burns: 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)

Parathyroid conditions and calcium imbalance: Clinical (To be retired)

Adrenal insufficiency: Clinical (To be retired)

Neck trauma: Clinical (To be retired)

Insulins

Mineralocorticoids and mineralocorticoid antagonists

Glucocorticoids

Gastroenterology and general surgery

Abdominal pain: Clinical (To be retired)

Appendicitis: Clinical (To be retired)

Gastrointestinal bleeding: Clinical (To be retired)

Peptic ulcers and stomach cancer: Clinical (To be retired)

Inflammatory bowel disease: Clinical (To be retired)

Diverticular disease: Clinical (To be retired)

Gallbladder disorders: Clinical (To be retired)

Pancreatitis: Clinical (To be retired)

Cirrhosis: Clinical (To be retired)

Hernias: Clinical (To be retired)

Bowel obstruction: Clinical (To be retired)

Abdominal trauma: Clinical (To be retired)

Laxatives and cathartics

Antidiarrheals

Acid reducing medications

Hematology and oncology

Blood products and transfusion: Clinical (To be retired)

Venous thromboembolism: Clinical (To be retired)

Anticoagulants: Heparin

Anticoagulants: Warfarin

Anticoagulants: Direct factor inhibitors

Antiplatelet medications

Thrombolytics

Infectious diseases

Fever of unknown origin: Clinical (To be retired)

Infective endocarditis: Clinical (To be retired)

Pneumonia: Clinical (To be retired)

Tuberculosis: Pathology review

Diarrhea: Clinical (To be retired)

Urinary tract infections: Clinical (To be retired)

Meningitis, encephalitis and brain abscesses: Clinical (To be retired)

Bites and stings: Clinical (To be retired)

Skin and soft tissue infections: Clinical (To be retired)

Protein synthesis inhibitors: Aminoglycosides

Antimetabolites: Sulfonamides and trimethoprim

Antituberculosis medications

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

Anthelmintic medications

Antimalarials

Anti-mite and louse medications

Nephrology and urology

Hypernatremia: Clinical (To be retired)

Hyponatremia: Clinical (To be retired)

Hyperkalemia: Clinical (To be retired)

Hypokalemia: Clinical (To be retired)

Metabolic and respiratory acidosis: Clinical (To be retired)

Metabolic and respiratory alkalosis: Clinical (To be retired)

Toxidromes: Clinical (To be retired)

Medication overdoses and toxicities: Pathology review

Environmental and chemical toxicities: Pathology review

Acute kidney injury: Clinical (To be retired)

Kidney stones: Clinical (To be retired)

Adrenergic antagonists: Alpha blockers

Neurology and neurosurgery

Stroke: Clinical (To be retired)

Seizures: Clinical (To be retired)

Headaches: Clinical (To be retired)

Traumatic brain injury: Clinical (To be retired)

Neck trauma: Clinical (To be retired)

Lower back pain: Clinical (To be retired)

Spinal cord disorders: Pathology review

Anticonvulsants and anxiolytics: Barbiturates

Anticonvulsants and anxiolytics: Benzodiazepines

Nonbenzodiazepine anticonvulsants

Migraine medications

Osmotic diuretics

Antiplatelet medications

Thrombolytics

Opioid agonists, mixed agonist-antagonists and partial agonists

Opioid antagonists

Pulmonology and thoracic surgery

Asthma: Clinical (To be retired)

Chronic obstructive pulmonary disease (COPD): Clinical (To be retired)

Venous thromboembolism: Clinical (To be retired)

Acute respiratory distress syndrome: Clinical (To be retired)

Pleural effusion: Clinical (To be retired)

Pneumothorax: Clinical (To be retired)

Chest trauma: Clinical (To be retired)

Bronchodilators: Beta 2-agonists and muscarinic antagonists

Pulmonary corticosteroids and mast cell inhibitors

Rheumatology and orthopedic surgery

Joint pain: Clinical (To be retired)

Anatomy clinical correlates: Clavicle and shoulder

Anatomy clinical correlates: Axilla

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

Assessments

Miscellaneous protein synthesis inhibitors

Flashcards

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Flashcards

Miscellaneous protein synthesis inhibitors

of complete

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

Transcript

Content Reviewers

Yifan Xiao, MD

Contributors

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

  1. "Katzung & Trevor's Pharmacology Examination and Board Review,12th Edition" McGraw-Hill Education / Medical (2018)
  2. "Rang and Dale's Pharmacology" Elsevier (2019)
  3. "Goodman and Gilman's The Pharmacological Basis of Therapeutics, 13th Edition" McGraw-Hill Education / Medical (2017)
  4. "Chloramphenicol: A Review" Pediatrics in Review (2004)
  5. "Clarithromycin: Review of a New Macrolide Antibiotic with Improved Microbiologic Spectrum and Favorable Pharmacokinetic and Adverse Effect Profiles" Annals of Pharmacotherapy (1992)
  6. "New Macrolide Antibiotics: Azithromycin and Clarithromycin" Annals of Internal Medicine (1992)
  7. "Macrolides and ketolides: azithromycin, clarithromycin, telithromycin" Infectious Disease Clinics of North America (2004)
  8. "Enhancement of opsonophagocytosis of Bacteroides spp. by clindamycin in subinhibitory concentrations" Journal of Antimicrobial Chemotherapy (1989)
  9. "Linezolid versus Vancomycin for the Treatment of Methicillin‐ResistantStaphylococcus aureusInfections" Clinical Infectious Diseases (2002)
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