Chemistry of Anti Anginal Drugs by Professor BeubenzProfessor Beubenz
This presentation will give you an idea about the chemistry of Anti-anginal drugs along with its classification, mechanism of action & Structural Activity Relationship.
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https://www.youtube.com/watch?v=-7yjQm4zzX8&t=1183s
Hypolipidemic agents, also known as cholesterol-lowering drugs or antihyperlipidemic agents, are a diverse group of pharmaceuticals that are used in the treatment of high levels of fats (lipids), such as cholesterol, in the blood (hyperlipidemia). They are also called lipid-lowering drugs.
Introduction.
Classification .
Drugs used in Coagulant and Anticoagulant Agents
Mechanism of action .
Structure
Synthesis
Adverse Drug Reactions .
Uses.
Reference
Chemistry of Anti Anginal Drugs by Professor BeubenzProfessor Beubenz
This presentation will give you an idea about the chemistry of Anti-anginal drugs along with its classification, mechanism of action & Structural Activity Relationship.
#Professor_Beubenz
For more such videos do
#Subscribe
#Share
#Like
to the Channel Professor Beubenz
Thank You.
https://www.youtube.com/watch?v=-7yjQm4zzX8&t=1183s
Hypolipidemic agents, also known as cholesterol-lowering drugs or antihyperlipidemic agents, are a diverse group of pharmaceuticals that are used in the treatment of high levels of fats (lipids), such as cholesterol, in the blood (hyperlipidemia). They are also called lipid-lowering drugs.
Introduction.
Classification .
Drugs used in Coagulant and Anticoagulant Agents
Mechanism of action .
Structure
Synthesis
Adverse Drug Reactions .
Uses.
Reference
ANTI HYPERTENSIVE AGENTS [MEDICINAL CHEMISTRY] BY P.RAVISANKAR, HYPERTENSION,...Dr. Ravi Sankar
ANTI HYPERTENSIVE AGENTS [MEDICINAL CHEMISTRY] BY P.RAVISANKAR, HYPERTENSION,TYPES,CAUSES OF HYPERTENSION, CLASSIFICATION, MECHANISM OF ACTION, SAR, ACE INHIBITORS, ARB , DIURETICS(WATER PILLS), TIPS TO STOP SILENT KILLER.
BY P. RAVISANKAR, VIGNAN PHARMACY COLLEGE, VADLAMUDI, GUNTUR,A.P, INDIA.
Introduction to diuretics.
Therapeutic approaches.
Normal physiology of urine formation.
Classification of drugs .
Mechanism of action of Acetazolamide.
Mechanism of action of Thiazides.
Mechanism of action of Loop diuretics.
Mechanism of action of potassium sparing diuretics &aldosterone antagonists.
Calcium channel blockers - Medicinal chemistry for B.Pharm.Purna Nagasree K
This ppt describes about the drugs used as calcium channel blockers, their mechanism of action, metabolism and Structure activity relationship of dihydropyridines
Overview of Discussion-
Anti-rheumatoid drugs
Classification of anti-rheumatoid drugs
Pharmacology of disease modifying anti-rheumatic drugs (DMARDs)
Pharmacology of adjuvant drugs
UAEU - CMHS - Hematology-Oncology Course - MMH 302 - HONC 320. Education material for medical students - It cover basic principles of hematology and oncology, including CAR-T and gene editing. It can be used for study and review. It illustrates main principles of hematology and oncology.
ANTI HYPERTENSIVE AGENTS [MEDICINAL CHEMISTRY] BY P.RAVISANKAR, HYPERTENSION,...Dr. Ravi Sankar
ANTI HYPERTENSIVE AGENTS [MEDICINAL CHEMISTRY] BY P.RAVISANKAR, HYPERTENSION,TYPES,CAUSES OF HYPERTENSION, CLASSIFICATION, MECHANISM OF ACTION, SAR, ACE INHIBITORS, ARB , DIURETICS(WATER PILLS), TIPS TO STOP SILENT KILLER.
BY P. RAVISANKAR, VIGNAN PHARMACY COLLEGE, VADLAMUDI, GUNTUR,A.P, INDIA.
Introduction to diuretics.
Therapeutic approaches.
Normal physiology of urine formation.
Classification of drugs .
Mechanism of action of Acetazolamide.
Mechanism of action of Thiazides.
Mechanism of action of Loop diuretics.
Mechanism of action of potassium sparing diuretics &aldosterone antagonists.
Calcium channel blockers - Medicinal chemistry for B.Pharm.Purna Nagasree K
This ppt describes about the drugs used as calcium channel blockers, their mechanism of action, metabolism and Structure activity relationship of dihydropyridines
Overview of Discussion-
Anti-rheumatoid drugs
Classification of anti-rheumatoid drugs
Pharmacology of disease modifying anti-rheumatic drugs (DMARDs)
Pharmacology of adjuvant drugs
UAEU - CMHS - Hematology-Oncology Course - MMH 302 - HONC 320. Education material for medical students - It cover basic principles of hematology and oncology, including CAR-T and gene editing. It can be used for study and review. It illustrates main principles of hematology and oncology.
Hemostasis is normal physiological mechanism by which blood in fluid state in vascular system normally and prevention of bleeding by Hemostasis by complex interactions of blood vessels wall, plasma proteins and platelets.
Anticoagulants, commonly referred to as blood thinners, are chemical substances that prevent or reduce coagulation of blood, prolonging the clotting time.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
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Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
2. Coagulation is the process of conversion of
Blood from a liquid form into a gel form and
formation of a blood clot.
Homeostasis is the process of Cessation of
blood loss from a damaged vessel and
followed by Repair.
3. CELLULAR (PLATELETS) PROTEIN (COAGULATION FACTOR)
Activation
Adhesion
Aggregation of platelets
Deposition and maturation of fibrin
By Activating,
Factor I - fibrinogen
Factor II - prothrombin
Factor III - tissue thromboplastin
(tissue factor)
Factor IV - ionized calcium ( Ca++ )
Factor V - labile factor or proaccelerin
Factor VI - unassigned
Factor VII - stable factor or
proconvertin
Factor VIII - antihemophilic factor
Factor IX - plasma thromboplastin
component, Christmas factor
Factor X - Stuart-Prower factor
Factor XI - plasma thromboplastin
antecedent
Factor XII - Hageman factor
Factor XIII - fibrin-stabilizing factor
5. Coagulation begins after injury to the Blood
vessel has damaged the Endothelium lining of
blood vessels.
Blood vessel Damage
Explosure of Blood to subendothelial
space
Explosure of subendothelial Tissue Factor to
Plasma factor VII &Change in Platelets.
6. PRIMARY HEMOSTASIS:
Platelets forms a plug at the site of
injury is called primary hemostasis.
SECONDARY HEMOSTASIS:
Additional coagulation factor/clotting
factors beyond Factor VII forms a Fibrin
strands to strengthen the platelet plug is
called secondary hemostasis.
7. Endothelium damage
Circulating platelets +underlying collagen
(via gp VI receptor)
Signal cascade &Activation of platelet Integrins
Tight binding of platelet to the extracellular matrix
Process of adhere platelet to the site of injury
8. Activated platelets release ADP , Serotonin, PAF,
Platelet factor 4, Thromboxane A2.
Activated platelets also activate other platelets.
Activated platelets changes its shape from
Spherical to Satellite.
Fibrinogen Cross-links between glycoprotein &
aggregation of adjacent platelets.
9. Activated platelet Release granular substances
Activate Gq-linked receptor
Increases the coc.of Calcium in the platelet’s cytosol
Activate protein kinase C
act
Phospholipase A2
Modify Integrin membrane glycoprotein &
Increases affinity to bind Fibrinogen
10.
11. 1.Calcium & phospholipids:
Require for tenase & prothrombinase
complexes to function.
2.Vitamin K:
Gamma-glutamyl carboxylase
add
-COOH group to glutamic acid residues
(F,II,VII,IX,X Protein S,C,Z)
12. Vitamin K
Vitamin K epoxide reductase
Active form
Maturation of Clotting Factors
13. Protein C:
Thrombin Act on Protein C
Activated Protein C
APC Protein + S Phospholipid (Co factor)
Degrade Fva &FVIIIa
18. It is the process of Desorption &
Reorganisation of Blood clot.
19. Anticoagulants also called as blood thinners.
These are chemical substances that prevent
or reduce coagulation of blood & prolonging
the clotting time.
20.
21. Heparin also known as unfractionated heparin
(UFH).
HISTORY::
1. Heparin was discovered by Jay
McLean and William Henry Howell in 1916.
2. In 1918, Howell coined the term 'heparin' for
this type of fat-soluble anticoagulant.
3. In the early 1920s, Howell isolated a water-
soluble polysaccharide anticoagulant, which he
also termed 'heparin',
CHEMISTRY:
1. Native heparin is a polymer with
a molecular weight ranging from 3 to
30 kDa and commercial heparin
preparations is in the range of 12 to 15 kDa.
2. [Heparin is a member of
the glycosaminoglycan family
of carbohydrates and consists of a variably
sulfated repeating disaccharide unit
MOA:
Binds with antithrombin III
Inactivate thrombin,factor Xa and protease
ANTODOTE:
1.Protamine sulfate
(1 mg per 100 units of heparin that had been
given over the past four hours).
21MEDICINAL CHEMISTRY II
22. Heparin (M.Wt- 5000 -40,000Da) is a
naturally occurring polysaccharide that
inhibits coagulation.
LMWHs are defined as heparin salts having
an average molecular weight of less than
8000 Da
ANTIDOTE:
1.Protamine
28. These are a class of anticoagulant drugs which act
directly upon Factor X in the coagulation cascade,
without using antithrombin as a mediator.
These compounds as substitutes for the currently
administered vitamin K antagonists or low
molecular weight heparin.
ADVANTAGES:
1.Rapid onset and offset of action.
31. These are agents which decrease platelet
aggregation and inhibit thrombus formation
They are effective in the arterial
circulation, where anticoagulants have little
effect.
34. Antifibrinolytics are a class of medication that are
inhibitors of fibrinolysis.
These drugs block the binding sites of the enzymes
or plasminogen respectively and thus
stop plasmin formation.
MECHANISM OF ACTION:
Plasminogen (plasma protein)
Tissue plasminogen activate(t-PA)
Plasmin
Block
Fibrin Fibrin degrade product
Anti Fibrinolytics
MEDICINAL CHEMISTRY II 34
36. Strokes – where a blood clot restricts the flow of
blood to your brain, causing brain cells to die and
possibly resulting in permanent brain damage or
death.
Transient ischemic attacks (TIAs) – also called "mini-
strokes", these have similar symptoms to a stroke,
but the effects usually last less than 24 hours.
Heart attacks– where a blood clot blocks a blood
vessel supplying your heart, starving it of oxygen and
causing chest pain and sometimes death.
Deep vein thrombosis (DVT) – where a blood clot
forms in one of the deep veins in your body, usually
your legs, causing pain and swelling.
Pulmonary embolism – where a blood clot blocks one
of the blood vessels around the lungs, stopping the
supply of blood to the lungs.