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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
Environmental and chemical toxicities: Pathology review
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Maria Emfietzoglou, MD
Sam Gillespie, BSc
Tina Collins
Robyn Hughes, MScBMC
Kristen is a 47 year old female who showed up at the ER due to vomiting and diarrhea. Kristen works as a farmer, and tells you that her symptoms started right after she sprayed her crops with insecticides using her bare hands. On clinical examination, her pupils appear constricted. And a few minutes later, Kristen has a seizure.
Next comes Federico, a 9 year old boy who is brought to the ER by his parents after accidentally consuming a bottle of insecticide. His parents mention that he complained of stomach ache, and had repeated episodes of vomiting and diarrhea. Upon clinical examination, you first notice that Federico's breath has a characteristic garlic-like odor.
Lastly, you see Richard and Lucy, a 60 year old couple that arrived at the ER, both complaining of a dull headache and nausea. They seem confused, but they mention that their symptoms started more or less at the same time, while they were both relaxing next to the fireplace. Upon clinical examination, you realize that their skin looks cherry red, so you decide to run a blood test, which reveals high carboxyhemoglobin levels.
Based on their history and presentation, all cases seem to have some form of environmental and chemical toxicity. Toxicity refers to the extent of poisoning or damage to the body due to exposure to a toxic substance. For your exams, the most high yield toxic substances include acetylcholinesterase inhibitors; methanol and ethylene glycol; heavy metals, including arsenic, iron, lead, and mercury; cyanide and carbon monoxide; as well as methemoglobin, which is an endogenous substance that can become toxic at high levels.
Let’s start with acetylcholinesterase inhibitor poisoning. Okay, normally, acetylcholinesterases are enzymes that break down the neurotransmitter acetylcholine, so that it can’t activate the cholinergic receptors in the peripheral and central nervous system. And there are two types of cholinergic receptors, called muscarinic and nicotinic receptors. Now, acetylcholinesterase inhibitors are substances that can irreversibly inhibit the acetylcholinesterases at the neuromuscular junction. As a result, acetylcholine builds up in the neuromuscular junction, leading to overstimulation of its receptors.
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