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Medical and surgical emergencies
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
Blistering skin disorders: Clinical (To be retired)
Bites and stings: Clinical (To be retired)
Burns: Clinical (To be retired)
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
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
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
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
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
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
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
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
Miscellaneous protein synthesis inhibitors
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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
chloramphenicol and p. 189, 201, 251
chloramphenicol p. 189
chloramphenicol p. 189
chloramphenicol p. 189
chloramphenicol p. 189
chloramphenicol p. 189
chloramphenicol p. 189
chloramphenicol p. 189
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.
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.
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