Antiplatelet medications

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Antiplatelet medications

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)

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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)

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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

Antiplatelet medications

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Antiplatelet medications

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External References

First Aid

2022

2021

2020

2019

2018

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2016

Abciximab p. 120

Glycoprotein IIb/IIIa inhibitors p. 445

thrombogenesis and p. 419

Antiplatelet antibodies p. 721

abciximab as p. 120

Transcript

Contributors

Sean Watts, MD

Elizabeth Nixon-Shapiro, MSMI, CMI

Sam Gillespie, BSc

Robyn Hughes, MScBMC

Antiplatelet medications prevent blood clot formation during hemostasis, where hemo means blood, and stasis means to halt or stop.

Hemostasis is divided into primary hemostasis, where circulating cell fragments called platelets form a plug at the site of an injured blood vessel, and secondary hemostasis, which involves multiple coagulation factors working together to form a fibrin mesh to stabilize the platelet plug.

Antiplatelet medications inhibit the steps of primary hemostasis to prevent the platelet plug from forming.

Primary hemostasis can be further divided into five steps: endothelial injury, exposure, adhesion, activation, and aggregation.

Endothelial injury is when the innermost layer of the artery, called the endothelium, gets damaged.

The second step is exposure, where the damaged endothelium exposes the underlying collagen.

The underlying collagen and endothelial cells then release a protein called Von Willebrand's factor, or vWF, that binds to this collagen.

The third step is adhesion where circulating platelets bind to the vWF via a surface protein called GPIB. The fourth step is activation, where platelets become active after binding to vWF.

First, the platelet changes shape and its membrane forms tentacle-like arms allowing it to grab onto other platelets.

Second, platelets release more vWF, as well as serotonin, a tiny molecule that attracts more platelets to the area.

Third, the platelets also release adenosine diphosphate or ADP, and thromboxane A2, or TXA2. These two molecules can activate other platelets that haven’t bound to vWF.

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. "Nomograms" D. Nicoll , C. Mark Lu, S.J. McPhee (Eds.), Guide to Diagnostic Tests, 7e. McGraw-Hill (2017)
  5. "Overview of hemostasis" J.C. Aster, H. Bunn (Eds.), Pathophysiology of Blood Disorders, 2e. McGraw-Hill. (2016)
  6. "Not all (N)SAID and done: Effects of nonsteroidal anti‐inflammatory drugs and paracetamol intake on platelets" Research and Practice in Thrombosis and Haemostasis (2019)
  7. "Assessment of platelet function in patients receiving tirofiban early after primary coronary intervention" Interventional Medicine and Applied Science (2016)
  8. "The first‐generation phosphodiesterase 5 inhibitors and their pharmacokinetic issue" Andrology (2019)
Elsevier

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