Pharmacology - Cancer Oncology drugs


Chapter 011: Antimicrobial Drugs
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Video lectures in clinical pharmacology (Arabic version) by Dr. Abdel-Motaal Fouda, associate professor of clinical pharmacology and therapeutics at Mansoura Faculty of Medicine, Egypt. 2016.
foudaamm@mans.edu.eg
------ Contents of this video -------------------
01:59- Antibacterial treatment
11:00- Classification of antibiotics
17:41- Bacterial resistance
24:35- Clinical approach to antimicrobial prescription (rule of the 5 rights)
25:46 1.The right patient (confirm the presence of infection)
33:51 2.The right drug (selection of drug)
48:19 3.The right dose (MIC)
55:28 4.The right route (route of administration)
56:07 5.The right duration
58:09- Antibiotic combination
1:06:52- Adverse effects of the antibiotics


Every year in Germany, 500,000 people are diagnosed with cancer. Only about half of these people can be cured. It’s no wonder that the pharmaceutical industry works tirelessly to deliver improved treatments. But how reliable are the new drugs?
Pharmaceutical cancer research is in full swing. New products are constantly entering the market, promising patients longer and more pain-free lives. Others even hold out the prospect of a cure.
Many of these treatments come to the market via an accelerated process. Often, they are accompanied by talk of major breakthroughs and new strategies: Targeted hormone therapy, antibody therapy, gene therapy. Spending on cancer drugs has risen by more than 50 percent in recent years - to more than 8.6 billion Euros in 2019.
It’s a profitable market for the pharmaceutical industry. But survival rates are not increasing as much as hoped. "We are in a situation where we have more and more fast-tracked drugs with less and less certainty about the actual benefit. And we're in a situation where we're spending a lot of money on them," says Prof. Wolf-Dieter Ludwig, Chairman of the German Medical Association’s Drug Commission.
So, what is really known about the new cancer drugs? Their side-effects, benefits and potential harm they may cause? How well-researched are they before they come to market? Who controls their usage in practice? This documentary looks for answers.
#documentary #dwdocumentary #pharma
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Today’s video is all about Antiplatelet vs Anticoagulant Blood Thinners for Nursing Students and NCLEX Review.
For your FREE quiz and access to more full-length videos, click here: http://bit.ly/3hzVHge
The difference between antiplatelet vs anticoagulant blood thinners is important – if you give the wrong one to a patient, it could be life-threatening.
Antiplatelets work by preventing blood platelets from sticking together and forming clots. Anticoagulants, on the other hand, keep your blood from clotting too much.
Blood thinners are often prescribed for patients with heart problems or other conditions requiring regular monitoring of blood flow throughout the body.
#NCLEX #pharmacology
#RegisteredNurse #Heparin #Warfarin


Cathy begins her coverage of nursing precautions, nursing care, and patient teaching associated with cancer treatment. She discusses nursing precautions for patients receiving chemotherapy and internal radiation. She explains important education to provide patients receiving external radiation. She then discusses nursing care and patient teaching for malnutrition and mucositis, which are 2 common complications associated with chemotherapy.
Our Medical-Surgical video tutorial series is taught by Cathy Parkes BSN, RN, CWCN, PHN and intended to help RN and PN nursing students study for their nursing school exams, including the ATI, HESI and NCLEX.
#NCLEX #Cancer #Chemotherapy #Mucositis #HESI #Kaplan #ATI #NursingSchool #NursingStudent #Nurse #RN #PN #Education #LPN #Nursingcare
0:00 What to expect with Cancer
0:20 Nursing precautions
2:24 Patient Teaching
3:48 Malnutrition
5:05 Mucositis
6:14 What’s Next?
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"Cyclophosphamide is a powerful immunosuppressant with a rapid onset of action (days to weeks). Cyclophosphamide is a popular chemotherapy agents used to treat lymphoma, multiple myeloma and leukaemia. In rheumatology it has a role in the treatment of vasculitis, life threatening complication of systemic lupus erythematosus and interstitial lung disease. Cyclophosphamide is an alkylating agent and works by disrupting the cell cycle targeting rapidly dividing cells such as cancer cells and immune cells because it is an immunosuppressant"
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(USMLE topics) Non-steroidal anti-inflammatory drugs (NSAIDs) - Aspirin and non-aspirin, non-selective NSAIDs and COX-2 specific. Mechanisms of action and toxicity. This video is available for instant download licensing here: https://www.alilamedicalmedia.....com/-/galleries/imag
Voice by: Ashley Fleming
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All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition.
Nonsteroidal anti-inflammatory drugs, NSAIDs, are the most widely used anti-inflammatories.
NSAIDs inhibit production of prostaglandins, a group of compounds that contribute to inflammatory response and are responsible for signs such as fever and pain. NSAIDs are very effective, and unlike other anti-inflammatories, they have no immunosuppressive effect.
Prostaglandins are synthesized from arachidonic acid by the action of cyclooxygenase (COX) enzymes. COX metabolizes arachidonic acid to prostaglandin H2, PGH2, which is then converted to different isoforms in different tissues, where they fulfill different functions.
Physiological prostaglandins act to maintain local homeostasis such as temperature regulation, bronchial tone, uterine tone, gastric mucosal barrier, among others. Some prostaglandins exert opposing effects to maintain balance. For example, platelet’s TXA2 constricts blood vessels and promotes platelet aggregation, while endothelial PGI2 dilates blood vessels and inhibits platelet aggregation. Together they modulate the interaction between activated platelets and blood vessel wall.
Physiological levels of prostaglandins are generally very low, but they go up drastically immediately upon acute inflammation, with PGE2 involved in most of its cardinal signs.
There are 2 known COX enzymes: COX-1 and COX-2.
COX-1 is expressed constitutively in most cells and is the major source of physiological prostaglandins. COX-2 is selectively induced by inflammatory stimuli and is the predominant source of inflammatory prostaglandins. But COX-2 also has some physiological functions in some tissues.
NSAIDs can be classified as non-selective, meaning they inhibit both COX-1 and COX-2, albeit with different efficiencies; and COX-2 selective.
All non-selective NSAIDs, except aspirin, act as reversible COX inhibitors. They compete with arachidonic acid for binding to the enzyme. Aspirin, on the other hand, covalently modifies and permanently destroys COX enzymes. The irreversible action of aspirin is most notable in blood platelets, which cannot synthesize new enzymes because they have no nucleus. Once the enzyme is inactivated by aspirin, no production of TXA2, and hence no platelet aggregation, is possible for the entire lifespan of the platelets. This makes aspirin stand out as a potent anti-thrombotic agent. In fact, aspirin is commonly prescribed to reduce risk of blood clot formation, as a preventive measure for heart attacks and ischemic strokes. For maximum effect, aspirin should not be taken together with other nonselective NSAIDs as these will compete with aspirin for a common binding site on the platelet’s COX-1.
Being anti-thrombotic, aspirin prolongs bleeding and is therefore contra-indicated in patients with bleeding risks or hemorrhagic disorders. Aspirin is also linked to Reye’s syndrome.
COX-1-dependent prostaglandins suppress gastric acid secretion and help maintain gastric mucosal barrier, providing protection to the stomach lining. Because non-selective NSAIDs inhibit COX-1, they may cause gastric irritation, peptic ulcer disease, and gastrointestinal bleeding.
The newer COX-2-specific NSAIDs, coxibs, are designed to reduce this gastrointestinal toxicity, but their use is controversial, as they appear to increase cardiovascular occlusive events. A possible explanation is that coxibs selectively inhibit COX-2-dependent PGI2, which is vasodilatory and anti-thrombotic, while having no effect on COX-1-dependent TXA2, which is pro-thrombotic and vasoconstrictory, and thus tipping the scales of homeostasis in favor of blood clot formation and vasoconstriction.
Some non-selective NSAIDs also exhibit various levels of cardiovascular toxicity depending on their COX-2 versus COX-1 inhibition ratio.
Suppression of physiological vasodilatory prostaglandins by NSAIDs may increase the risk for hypertension, edema, and exacerbate pre-existing heart failures.
Inhibition of renal vasodilatory prostaglandins, in the context of circulatory stress, may reduce renal blood flow and glomerular filtration rate, and ultimately cause renal ischemia or failure.


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#cancer #chemotheraphy
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