This document discusses drugs used for angina pectoris. It defines angina as chest pain caused by insufficient oxygen to the heart muscle. Angina has underlying causes like coronary heart disease and atherosclerosis. The document outlines four types of angina and discusses the mechanisms and pathophysiology of atherosclerosis. It then summarizes various drug classes used to treat angina, including nitrates, beta blockers, calcium channel blockers, nicorandil, aspirin, and clopidogrel. Specific drugs within each class are mentioned along with their mechanisms of action, indications, and side effects.
Angina pectoris is the medical term for chest pain or discomfort due to coronary heart disease. It occurs when the heart muscle doesn't get as much blood as it needs. This usually happens because one or more of the heart's arteries is narrowed or blocked, also called ischemia.
Angina usually causes uncomfortable pressure, fullness, squeezing or pain in the center of the chest. You may also feel the discomfort in your neck, jaw, shoulder, back or arm. (Many types of chest discomfort — like heartburn, lung infection or inflammation
This document discusses angina pectoris, or chest pain due to insufficient blood flow to the heart. It defines angina and lists its main types. It then covers the epidemiology, etiology, pathophysiology, clinical manifestations, diagnosis, and management of angina. Management involves both non-pharmacological approaches like lifestyle changes as well as pharmacological treatments including nitrates, beta blockers, and calcium channel blockers. Revascularization procedures like percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG) may also be used in some cases.
Principles of cell injury and cellular adaptation .pptMirza Anwar Baig
This document provides an overview of cell injury and adaptation. It discusses various causes of cell injury including hypoxia, infections, physical and chemical agents. The pathogenesis and morphology of reversible and irreversible cell injury is explained. Cellular adaptations such as atrophy, hypertrophy, hyperplasia, metaplasia and dysplasia are defined. Necrosis and apoptosis are compared as two types of cell death. Specific examples of cell injuries and adaptations in different organ systems are also presented.
Angina pectoris is a type of chest pain or discomfort that occurs when the heart muscle does not receive enough oxygen-rich blood. It is caused by an imbalance between the heart's oxygen supply and demand. There are several types of angina including stable angina, unstable angina, and variant angina. Risk factors that can trigger angina include atherosclerosis, coronary artery spasm, increased cardiac output from exercise or stress, and damaged heart muscle. Diagnosis involves taking a medical history, physical exam, ECG, blood tests, imaging tests like angiography, and exercise testing. Treatment focuses on lifestyle changes, medications like nitroglycerin, beta blockers, and calcium channel blockers, and procedures like
Angina pectoris is a medical condition resulting in chest pain or discomfort. Angina pectoris occurs when the heart is not getting enough blood supply. the pain related to angina is temporary, but if left untreated can make serious heart complications inevitable.
This document discusses cholinergic and anticholinergic drugs. Cholinergic drugs stimulate the parasympathetic nervous system by mimicking the effects of acetylcholine. They are classified as direct-acting or indirect-acting. Direct-acting cholinergic drugs bind directly to cholinergic receptors, while indirect-acting drugs inhibit the enzyme acetylcholinesterase. Anticholinergic drugs block the action of acetylcholine at muscarinic receptors. Cholinergic drugs have effects in the CNS, eyes, GI tract, and elsewhere, while anticholinergic drugs effects include decreasing secretions, relaxing smooth muscles, and impacts in the CNS, heart and respiratory system. Both drug types can
1. Angina pectoris is a clinical syndrome characterized by episodes of chest pain or pressure resulting from inadequate blood supply to the heart muscle.
2. Risk factors for angina include age over 55 for men or 65 for women, smoking, diabetes, high cholesterol, high blood pressure, obesity, physical inactivity, and family history of early heart disease.
3. There are several types of angina including stable angina brought on by exertion, unstable angina occurring at rest or with minimal exertion, and Prinzmetal or variant angina occurring during rest especially between midnight and dawn.
This document discusses congestive heart failure (CHF), which occurs when the heart cannot pump enough blood to meet the body's needs. It defines two types of CHF based on ejection fraction - systolic and diastolic dysfunction. Several causes of CHF are listed, including arrhythmias, myocardial infarction, hypertension, and obesity. The body compensates via the sympathetic nervous system and renin-angiotensin-aldosterone system. Drug classes used to treat CHF are discussed in detail, including cardiac glycosides like digoxin, beta blockers, ACE inhibitors, angiotensin receptor blockers, aldosterone antagonists, and vasodilators. Side effects of each class are
This document provides an overview of shock, including its pathophysiology and classification. It discusses the main types of shock: hypovolemic, cardiogenic, distributive, and obstructive. For each type, it describes the causes, characteristics, and treatment approaches. It also covers fluid resuscitation, vasopressors, inotropic drugs, and mechanical ventilation as general treatment strategies for shock.
1) Definition of PUD
2) Pathogenesis of PUD
3) Risk Factors for PUD
4) Morphology of PUD
5) Clinical features
6) Complications
7) Summary
This presentation was presented in MULTI SYSTEM SEMINAR by a 2nd year MBBS-2015 student of BPKIHS, Dharan, NEPAL.
Arteriosclerosis refers to the thickening, hardening, and loss of elasticity of the arterial walls. It is caused by aging, loss of the elastic protein elastin, and thickening of the arterial walls. Cholesterol deposits form beneath the artery endothelium and calcify to form atheromatous plaques, which narrow the arterial lumen. This reduces blood circulation and can lead to heart attack, stroke, hypertension, angina, and peripheral arterial disease.
This document provides an overview of ischemic heart disease (IHD). IHD is caused by reduced blood flow to the heart muscle and includes conditions like angina and myocardial infarction. The main causes are atherosclerotic lesions in the coronary arteries leading to plaque buildup and blockages. Over time, plaques can rupture, causing blood clots that fully or partially block blood flow to the heart. This leads to insufficient oxygen delivery and cell death. The document outlines the pathogenesis and morphological changes that occur during angina and myocardial infarction as well as risk factors, diagnosis, and complications of IHD.
Cellular adaptations like hyperplasia, hypertrophy, atrophy, metaplasia, and apoptosis allow cells to respond to physiological and pathological stimuli in their environment. These adaptations preserve cell viability by allowing cells to modify their growth patterns or metabolism. Certain adaptations like sustained hyperplasia can increase cancer risk by providing fertile ground for neoplastic changes if the stimuli are persistent. Clinical terminology around cellular adaptations is important for understanding disease processes and responses.
Cirrhosis is a late stage of scarring (fibrosis) of the liver caused by many forms of liver diseases and conditions, such as hepatitis and chronic alcoholism.
The document discusses peptic ulcers, including their causes, risk factors, symptoms, diagnosis, and treatment. Peptic ulcers are open sores in the lining of the stomach or small intestine caused by an imbalance of protective and damaging factors. Common treatments include H2 blockers, proton pump inhibitors, antacids, and antibiotics to treat Helicobacter pylori infections. These drugs help reduce acid production and promote healing of ulcers.
This document discusses antianginal drugs used to treat angina pectoris, or chest pain caused by reduced blood flow to the heart. There are three main classes of drugs used: organic nitrates, beta-blockers, and calcium channel blockers. Organic nitrates like nitroglycerin work by dilating blood vessels to increase blood flow to the heart and reduce its workload. Beta-blockers lower the heart rate and force of contraction to decrease oxygen demand. Calcium channel blockers inhibit calcium entry into heart and blood vessel cells to relax vessels and reduce workload. Each drug class is described in more detail regarding mechanisms, effects, pharmacokinetics, uses, and side effects.
Angina pectoris, or angina, is a type of chest pain caused by reduced blood flow to the heart. There are different types of angina that vary based on factors like when the pain occurs and how long it lasts. Risk factors include obesity, high cholesterol, smoking, and diabetes. Treatment involves medications like nitroglycerin to relieve symptoms as well as procedures like CABG to restore blood flow if needed. Nurses manage angina by addressing pain, activity tolerance, and providing patient education.
Arteriosclerosis and atherosclerosis are diseases that cause hardening and narrowing of arteries. Arteriosclerosis is thickening of arterial walls while atherosclerosis involves plaque buildup within artery walls from accumulation of lipids, calcium, and other substances. Major risk factors for atherosclerosis include age, smoking, diet, hypertension, diabetes, and stress. The formation of fatty streaks and plaques within artery walls can progress over decades and lead to complications when plaques rupture and form blood clots. Prevention focuses on lifestyle modifications like quitting smoking, regular exercise, healthy diet, weight control, and stress management.
This document provides an overview of drugs for congestive heart failure. It defines heart failure as the heart's inability to pump sufficient blood to meet the body's needs. Causes include diseases like atherosclerosis, heart attacks, and hypertension. Signs and symptoms include dyspnea, fatigue, edema, and confusion. Angiotensin receptor blockers work by competitively blocking angiotensin II receptors, reducing blood pressure, afterload, and remodeling of the left ventricle. Common drug classes discussed are ACE inhibitors, ARBs, diuretics, beta-blockers, and aldosterone antagonists. Stages of heart failure and appropriate therapies are also covered.
The document discusses shock, including its definition, types, pathophysiology, and stages. Shock is defined as a state of low tissue perfusion that is inadequate for normal cellular respiration, leading to hypotension and cellular hypoxia if left uncompensated. The types of shock discussed include hypovolaemic, cardiogenic, obstructive, distributive (septic, anaphylactic, neurogenic), and endocrine shock. The pathophysiology of shock is explained at the cellular, microvascular, and systemic levels. Shock is divided into three stages: non-progressive/compensated, progressive decompensated, and decompensated/irreversible shock. Compensatory mechanisms in the initial
The document discusses the use of organic nitrates and calcium antagonists to treat angina. It provides details on their mechanisms of action, pharmacological effects, and clinical uses. Specifically, it explains that organic nitrates act by relaxing smooth muscle and increasing cGMP, while calcium antagonists prevent the opening of voltage-gated calcium channels. Both drug classes are used to reduce cardiac oxygen demand and redistribute blood flow for the treatment of stable and unstable angina.
Angina is chest pain due to reduced blood flow to the heart muscle. There are three main types: atherosclerotic angina caused by plaque buildup, vasospastic angina occurring at rest from artery spasm, and unstable angina with increased attacks. Nitrates like nitroglycerin are used to treat angina by dilating blood vessels and reducing oxygen demand on the heart. They work by increasing nitric oxide which causes smooth muscle relaxation. While effective for angina relief, nitrates can cause side effects like headaches and low blood pressure, and tolerance can develop with regular use.
This document discusses the patterns of angina pectoris and their characteristics. It describes stable angina, which produces reproducible chest pain relieved by rest. Unstable angina occurs with less exertion or at rest and is less responsive to nitroglycerin. Prinzmetal angina is an uncommon variant occurring at rest, often in young individuals, triggered by substances like alcohol. The document also outlines various drug classes used to treat angina, including nitrates, calcium channel blockers, beta blockers, and other adjunctive therapies. It provides details on the mechanisms and side effects of these drug classes.
1) Angina pectoris is characterized by chest pain due to myocardial ischemia. There are three main types: typical (classical), variant, and unstable angina.
2) Typical angina is induced by exercise and associated with atherosclerosis. Variant angina occurs at rest and is caused by coronary vasospasm. Unstable angina involves coronary spasm and atherosclerosis with longer, worsening chest pain.
3) Treatment involves decreasing oxygen demand and increasing supply. Nitrates, calcium channel blockers, and beta blockers are commonly used either alone or in combination to relieve angina by reducing preload, afterload, heart rate, and contractility.
Anti-Angina & Anti arryhthias Drugs .pptssuser504dda
This document discusses drugs used to manage angina and arrhythmias, and current guidelines for managing acute coronary syndrome (ACS). It describes the classification and pathophysiology of angina, then focuses on pharmacological management including nitrates like nitroglycerin, calcium channel blockers like nifedipine, beta blockers like atenolol, and alpha/beta blockers like carvedilol. It provides details on their mechanisms of action, indications, interactions, and side effects in treating conditions like angina, heart failure and ACS.
PH1.28 Describe the mechanisms of action, types, doses, side effects, indicat...Dr Pankaj Kumar Gupta
PH1.28 Describe the mechanisms of action, types, doses, side effects, indications and contraindications of the drugs used in ischemic heart disease (stable, unstable angina and myocardial infarction), peripheral vascular disease
This document discusses angina pectoris, including its causes, risk factors, classifications, and treatments. Angina is chest pain due to an imbalance between myocardial oxygen demand and supply. It is classified into four types based on triggers and severity. Treatment includes short-acting nitrates for acute attacks and long-acting options like nitrates, calcium channel blockers, and beta-blockers for prophylaxis. Additional therapies discussed are potassium channel openers, fatty acid oxidase inhibitors, and antiplatelets/anticoagulants. Combination drug regimens and surgical options are also outlined for management of angina.
This document discusses angina pectoris, also known as stable angina. It defines angina as chest pain or discomfort that occurs due to decreased blood flow to the heart muscle. It then describes the different types of angina and their causes. The main causes are atherosclerosis, coronary artery spasm, traumatic injury, and embolic events which can all restrict blood flow to the heart. The document outlines the goals of treatment which are to prevent heart attacks and death while reducing angina symptoms. It then discusses the various pharmacological treatments used including nitrates, beta blockers, calcium channel blockers, antiplatelet agents, ACE inhibitors, and ranolazine. Non-pharmacological options like percutaneous coronary
This document discusses various drugs used to treat angina pectoris. It begins by defining angina and describing its causes as inadequate blood flow through the coronary arteries. It then discusses the different types of angina - stable, unstable, and Prinzmetal's variant angina. The main drugs used to treat angina are described - nitrates, beta-blockers, calcium channel blockers, and newer drugs like ranolazine. Nitrates work by dilating blood vessels to reduce preload and afterload. Beta-blockers reduce heart rate and contractility. Calcium channel blockers inhibit calcium entry to arteries and heart muscle. Ranolazine inhibits sodium channels to reduce oxygen demand. Combinations of these drugs
This document provides information on antianginal drugs used to treat angina pectoris. It discusses the different types of angina, how myocardial oxygen demand is determined, and classifications of angina. The mechanisms and uses of various antianginal drug classes are summarized, including nitrates, beta-blockers, calcium channel blockers, nicorandil, aspirin, clopidogrel, and thrombolytics. Newer antianginal drugs such as niludipine, prasugrel, brilinta, and bivalirudin are also mentioned along with their indications. References used in compiling the document are listed at the end.
Antianginal ppt brief description and informationDevoratsingh1
This document discusses drugs used to treat angina pectoris, a chest pain syndrome caused by inadequate blood flow to the heart. It describes two main types of angina - classical, brought on by exertion and relieved by rest, and variant which occurs at rest. Nitrates like glyceryl trinitrate are first-line treatments that work by dilating blood vessels and reducing workload on the heart. Beta-blockers also lower heart rate and workload while calcium channel blockers and nicorandil relax blood vessels. Other options include isosorbide dinitrate, trimetazidine, and dipyridamole. All work to prevent or terminate angina attacks by increasing oxygen supply or decreasing demand
An interesting ppt on antianginal drugs and drug therapy of myocardial infarction with illustrations for better understanding of concepts and grasping facts...
This document discusses various drugs used to treat angina pectoris, which is chest pain due to myocardial ischemia. It describes several classes of antianginal drugs that work by either increasing oxygen supply to the heart or decreasing oxygen demand. These include organic nitrates like glyceryl trinitrate, beta-blockers, calcium channel blockers, and ACE inhibitors. The document provides details on the mechanisms and sites of action of these drug classes as well as their adverse effects. Alternative treatment methods for ischemic heart disease like rotational atherectomy are also mentioned.
This document discusses angina pectoris, its causes, symptoms, diagnosis and management. It provides details on:
- Angina is caused by transient myocardial ischemia due to an imbalance of oxygen supply and demand in the heart. The most common cause is atherosclerosis.
- Risk factors, symptoms, and physical exam findings for angina are described. Management involves identifying and treating risk factors, introducing anti-anginal drugs, and considering revascularization if drugs do not control symptoms.
- Five main classes of anti-anginal drugs are discussed - nitrates, beta-blockers, calcium channel blockers, potassium channel activators, and ivabradine. Their mechanisms of action and usage guidelines are
This document discusses anti-ischemic agents used to treat ischemia, which is an imbalance between the supply and demand of oxygen to tissues like the heart. It summarizes several classes of anti-ischemic drugs including nitrates, calcium channel blockers, beta blockers, potassium channel openers, antiplatelet drugs, cholesterol lowering drugs, and ACE inhibitors. For each drug class, it describes the mechanism of action, pharmacological effects, adverse effects, and clinical uses in treating conditions like angina, myocardial infarction, and ischemic stroke.
Drugs used for the treatment of myocardial ischemiask-yasmeen
This document provides information on drugs used for the treatment of myocardial ischemia. It discusses the types of myocardial ischemia including stable, unstable, and variant angina. It then describes the heart and coronary arteries and risk factors for myocardial ischemia. The main drug classes used for treatment are discussed in detail, including nitrates, calcium channel blockers, beta blockers, potassium channel activators, antiplatelet drugs, ACE inhibitors, and cholesterol lowering medications. Adverse effects, pharmacokinetics and contraindications are summarized for each drug class. Additional treatments beyond medications are also mentioned.
The document discusses clinical pharmacy in cardiology and ischemic heart disease. It describes the three main risk factors for ischemic heart disease as hypercholesterolemia, arterial hypertension, and smoking. It defines angina and unstable angina, and describes their symptoms. The document also summarizes various antianginal drugs used to treat angina, including nitrates like nitroglycerin, beta-blockers, and calcium channel blockers like nifedipin. It explains the mechanisms of action and side effects of these different classes of antianginal drugs.
These slides contain detailed description of antianginal drugs including : Introduction, Definition of Angina, Types of Angina, Classification of antianginal drugs - nitrates, beta adrenergic blockers, calcium channel blockers, potassium channel openers, ( with their classification, pharmacological action, mechanism of action, available forms, therapeutic uses, pharmacokinetics, adverse effects, and contraindications ) Nursing responsibility, Summary.
principle action of drugs,types of angina classification of drugs ,nitrates,calcium channel blockers pharmacological actions ,combination therapy and its sid effects
Angina pectoris is chest pain due to ischemia of the heart muscle. It is usually felt as a tightness or pressure in the middle of the chest that may spread to the neck, jaw, or arm. There are three main types - stable angina brought on by exertion, unstable angina that occurs at rest, and Prinzmetal or variant angina caused by coronary artery spasm. Treatment involves medications to relieve symptoms like nitrates, beta blockers, calcium channel blockers, and newer drugs that open potassium channels or have a cytoprotective effect. Combination therapy with two or more classes is often used for better management of angina.
This document provides guidelines for the pharmacological management of heart failure. It defines heart failure and classifies it based on ejection fraction into heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF). For patients with HFrEF (stage C), it recommends using ACE inhibitors, ARBs, beta-blockers, aldosterone antagonists, hydralazine/isosorbide dinitrate, and diuretics. For patients with HFpEF (stage C), evidence-based pharmacological therapies have not been identified. The document also provides dosing recommendations for common heart failure medications like loop diuretics, ACE inhibitors, and beta-blockers
Hormone replacement therapy (HRT) involves prescribing estrogen, often along with progesterone, to treat symptoms of menopause. It helps relieve hot flashes and vaginal dryness, prevents osteoporosis, and maintains quality of life. HRT is generally safe for most women, especially when taken for short durations at low doses, but does increase risks of blood clots, breast cancer, stroke and heart disease for some. Proper screening and monitoring is important for safe administration of HRT.
The document discusses the anatomy and electrophysiology of the heart. It explains that the electrocardiogram (ECG or EKG) detects the heart's electrical activity as it travels through the heart muscle. Sodium, calcium, and potassium ions are responsible for initiating electrical charges that cause the heart muscle to contract. The heart consists of four chambers - the two upper atria collect blood and deliver it to the two lower ventricles, which pump blood out of the heart.
This document discusses medication errors, including definitions, types, contributing factors, detection, reporting processes, and prevention. The key points are:
- Medication errors are preventable events that may harm patients and are caused by mistakes in prescribing, dispensing, or administering drugs.
- Common types of errors include prescription errors, dispensing errors, administration errors, and transcription errors.
- Factors like look-alike drug names, poor communication, and environmental distractions contribute to errors.
- Errors can be detected through methods like medical rounds, medication administration records, and analyzing returned doses.
- Reporting helps identify root causes and improve safety, but relies on voluntary participation and protecting confidentiality
Medication errors are preventable events that can harm patients. They occur frequently due to look-alike and sound-alike drug names, improper dosing, and other issues. Reporting medication errors is important to identify root causes and improve safety. High alert medications require extra precautions like independent checks and labeling to prevent harmful errors. Reducing distractions, improving communication, and ensuring proper training can help reduce medication errors.
THYROID AND ANTITHYROID DRUGS PRESENTATION.pptxJhansi Uppu
Iodine is essential for thyroid hormone production. The recommended daily iodine intake varies by age group from 50 μg in infants to 200 μg in pregnant and lactating women. Thyroid hormones regulate growth, metabolism, and heart function. Hypothyroidism is defined as deficient thyroid hormone production and is most often caused by iodine deficiency, autoimmune disease, or treatment for hyperthyroidism. Levothyroxine is the drug of choice for replacement therapy in hypothyroidism due to its stability, uniformity, and ability to produce T3 and T4 hormones. Dosage is individualized and adjusted based on factors like age, weight, and concurrent conditions.
Hypertension is defined as blood pressure above 140/90 mmHg. It can be essential (95% of cases, no identifiable cause) or secondary (5% of cases, due to an underlying condition like kidney disease). Lifestyle modifications like weight loss, reduced salt intake, exercise, and moderation of alcohol can help control hypertension. If lifestyle changes are not enough, medications may be prescribed. Common classes of medications include diuretics, beta-blockers, ACE inhibitors, calcium channel blockers, and ARBs, which work to lower blood pressure by different mechanisms like reducing fluid volume or relaxing blood vessels. Controlling high blood pressure helps prevent damage to organs like the heart, brain, and kidneys that can
Principles of Cleaning
Nonsurgical root canal treatment is a predictable method of retaining a tooth that otherwise would require extraction. Success of root canal treatment in a tooth with a vital pulp is higher than that of a tooth that is necrotic with periradicular pathosis. The difference is the persistent irritation of necrotic tissue remnants, and the inability to remove the microorganisms and their by-products. The most significant factors affecting this process are tooth anatomy and morphology, and the instruments and irrigants available for treatment. Instruments must contact and plane the canal walls to debride the canal.
Morphologic factors such as lateral and accessory canals, canal curvatures, canal wall irregularities, fins, cul-de-sacs, and isthmuses make total debridement virtually impossible. Therefore the goal of cleaning not total elimination of the irritants but it is to reduce the irritants.
Currently there are no reliable methods to assess cleaning. The presence of clean dentinal shavings, the color of the irrigant, and canal enlargement three file sizes beyond the first instrument to bind have been used to assess the adequacy; however, these do not correlate well with debridement. Obtaining glassy smooth walls is a preferred indicator. The properly prepared canals should feel smooth in all dimensions when the tip of a small file is pushed against the canal walls. This indicates that files have had contact and planed all accessible canal walls thereby maximizing debridement (recognizing that total debridement usually does not occur).
Principles of Shaping
The purpose of shaping is to
1) facilitate cleaning and
2) provide space for placing the obturating materials.
The main objective of shaping is to maintain or develop a continuously tapering funnel from the canal orifice to the apex. This decreases procedural errors when cleaning and enlarging apically. The degree of enlargement is often dictated by the method of obturation. For lateral compaction of gutta percha the canal should be enlarged sufficiently to permit placement of the spreader to within 1-2 millimeters of the corrected working length. There is a correlation between the depth of spreader penetration and the apical seal.5 For warm vertical compaction techniques the coronal enlargement must permit the placement of the pluggers to within 3 to 5 mm of the corrected working length.6
As dentin is removed from the canal walls the root is weakened.7 The degree of shaping is determined by the preoperative root dimension, the obturation technique, and the restorative treatment plan. Narrow thin roots such as the mandibular incisors cannot be enlarged to the same degree as more bulky roots such as the maxillary central incisors. Post placement is also a determining factor in the amount of coronal dentin removal.
Hemodialysis: Chapter 11, Venous Catheter - Basics, Insertion, Use and Care -...NephroTube - Dr.Gawad
- Video recording of this lecture in English language: https://youtu.be/QeWTw_fYPlA
- Video recording of this lecture in Arabic language: https://youtu.be/fUWI9boFc7w
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Introduction to Dental Implant for undergraduate studentShamsuddin Mahmud
Introduction to Dental Implant
Dr Shamsuddin Mahmud
Assistant Professor, Department of Prosthodontics
Nortth East Medical College (Dental Unit)
Definition of Dental Implant
A prosthetic device
made of alloplastic material(s)
implanted into the oral tissues beneath the mucosal and/or periosteal layer and
on or within the bone
to provide retention and support for a fixed or removable dental prosthesis.
Classification of Dental Implant
According to placement within the tissue
Blade/Plate form implant
According to Material Used
A) METALLIC IMPLANTS
Commercially pure Titanium
Cobalt chromium molybdenum
Titanium aluminum vanadium
Stainless steel
B) NON-METALLIC IMPLANT
Zirconium
Ceramic
Carbon
According to the ability of implant to stimulate bone formation
A) Bio active
Hydroxyapatite
Tri Calcium Phosphate
B) Bio inert
Metals
Parts of Dental Implant
Implant fixture
Implant mount
Cover screw
Gingival former/healing screw/healing abutment/permucosal extension
Impression post/impression transfer abutment
Implant analogue
Abutment
Fixation screw
Implant Fixture
Implant Mount
Connected to the fixture
Function: used to carry implant from its vital to the prepared osteotomy site either by hand or with a ratchet/ handpiece adaption
Cover Screw
component that is used to cover the implant connection during the submerged healing of the implant
Function: preserves the patency of the connection by preventing any soft tissue ingrowth in the connection
Gingival former/ Healing Abutment/ Healing screw
Screw/ abutment used to create the soft tissue emergence profile around the implant.
Time of placement:
During 1st surgery – One step surgery
After Osseointegration – Two step/stage surgery
Gingival former/ Healing Abutment/ Healing screw
Placed in the site 2-3 weeks for soft tissue healing
Function:
Create gingival emergence profile
Formation of biological width
Impression post/impression transfer abutment
component that is used to trans- fer the implant Hex position and orientation from the mouth to the working cast.
Types
Closed tray
Open tray
Implant analogue/
component which has a different body but its platform and connection are exactly similar to the implant. The analogue is used to replicate the implant platform and connection in the laboratory mode.
Abutment
Abutments
Advantages of Dental Implant Retained Prosthesis
Maintain bone height and width by preventing bone resorption
Maintain facial esthetics
Improve masticatory performance
Improve stability and retention of prosthesis
More esthetics
Increase survival times of prostheses
There is no need to alter adjacent teeth
Improve psychological health
Disadvantages of Dental Implant Retained Prosthesis
Very expensive.
Cannot be used in medically compromised patients who cannot undergo surgery.
Longer duration of treatment
Requires a lot of patient co-operation because of repeated recall visits are essential
INDICATION OF DENTAL IMPLANT
Dental implants can successfully restore all
This Presentation provides information on hyperlipidemic drugs. It begins with an introduction to hyperlipidemia and its causes. It then discusses various drug classes for treating hyperlipidemia, including their mechanisms of action, effects on lipid levels, pharmacokinetics, therapeutic uses, adverse effects and interactions. The major drug classes discussed are HMG-CoA reductase inhibitors (statins), bile acid sequestrants, fibrates, and niacin. For each class, specific drugs are highlighted and their properties compared.
Factors influencing growth & development:
Growth & development depend upon multiple factors or determinants. They influence directly or indirectly by promoting or hindering the process.
The determinants can be grouped as Heredity & environment..
Heredity or genetic factors are also related to sex, race, & nationality. Environment includes both pre natal & post natal factors.
These lecture slides, by Dr Sidra Arshad, offer a simplified description of the physiology of insulin and glucagon.
Learning objectives:
1. Describe the synthesis and release of insulin
2. Explain the mechanism of action of insulin
3. Discuss the metabolic functions of insulin
4. Elucidate the effects of insulin on adipose tissue, skeletal muscle, and liver
5. Enlist the factors which stimulate and inhibit the release of insulin
6. Explain the mechanism of action of glucagon
7. Discuss the metabolic functions of glucagon
8. Elucidate the role of insulin and glucagon in glucose homeostasis during the fasting and fed states
9. Discuss the role of other hormones in the glucose homeostasis
10. Differentiate between the types of diabetes mellitus
11. Explain the pathophysiology of the features of diabetes mellitus
12. Discuss the complications of diabetes mellitus
13. Explain the rationale of oral hypoglycemic drugs
14. Describe the features of hyperinsulinemia
Study Resources:
1. Chapter 79, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 24, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 39, Berne and Levy Physiology, 7th edition
4. Chapter 19, Human Physiology, From Cells to Systems by Lauralee Sherwood, 9th edition
5. Chapter 3, Endocrine and Reproductive Physiology, Bruce A. White and Susan P. Porterfield, 4th edition
6. Insulin and Insulin Resistance, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1204764/
7. Complications of diabetes mellitus,
https://pdb101.rcsb.org/global-health/diabetes-mellitus/monitoring/complications
Definition of mental health nursing, terminology, classification of mental disorder, ICD-10, Indian Classification, Personality development, defense mechanism, etiology of bio psychosocial factors,
an huge problem we are facing about the anaemia , we slight our contribution to aware with one of its class , with detailed description. it is usefull for health , medicine , pharmacy , nursing.
The Revolutionary Nature of Needleless Double Transfer Spikes in HealthcareNanchang Kindly Meditech
It's likely that you have witnessed medical personnel using needles to transmit fluids or medicines if you have ever visited a hospital or other healthcare facility. But as technology advances, needleless double transfer spikes are becoming more and more common and revolutionizing the delivery of healthcare.
CASE PRESENTATION ON ACUTE GASTROENTERITIS.Bhavana
This is a case presentation of a 72 year old female patient who was admitted in the hospital with the chief complaints of loose stools since 6 Days and generalised weakness and history of one episode of vomiting (one day back).
कायाकल्प क्लिनिक: पटना के अग्रणी सेक्सोलॉजिस्ट और स्किन केयर विशेषज्ञ
पटना का एक शानदार स्वास्थ्य सेवा प्रदाता, कायाकल्प क्लिनिक, आपके स्वास्थ्य और त्वचा की देखभाल में विशेषज्ञता प्रदान करता है। हमारे नवीनतम तकनीकी समाधानों और अनुभवी विशेषज्ञों के साथ, हम पुरुष और महिलाओं के स्वास्थ्य सम्बंधित मुद्दों को हल करते हैं। यहां पर हम प्रदान करते हैं:
Expert Treatment for Sex Issues at Kaya Kalp Clinic in Patna -best sexologist in patna
Dealing with sex-related problems? Find effective solutions at Kaya Kalp Clinic in Patna. Our experienced sexologist doctors are here to help.
Experienced Doctors
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Phone: 93342 00215
Discover the Best Sexologist in Patna: Expert Care at Kayakalp Clinic
Kayakalp Clinic - Best Sexologist in Patna
Kayakalp Clinic - Best Sexologist in Patna
When it comes to sexual health, finding the right expert is essential for effective diagnosis and treatment. At Kayakalp Clinic in Patna, we pride ourselves on providing exceptional care for a wide range of sexual health issues. If you’re searching for the best sexologist in Patna, look no further. Our team of highly skilled professionals is here to help you navigate and resolve your concerns with confidentiality and compassion.
Why Choose Kayakalp Clinic?
1. Experienced Professionals
Our sexologists are highly trained and experienced in dealing with various sexual health issues. They stay updated with the latest advancements in the field to provide the best care possible.
2. Comprehensive Services
At Kayakalp Clinic, we offer a wide range of services, including:
- Treatment for erectile dysfunction
- Solutions for premature ejaculation
- Counseling for low libido
- Infertility treatment
- Management of sexual pain disorders
- STI screening and treatment
- Relationship and intimacy counseling
3. Personalized Treatment Plans
We understand that every individual is unique, and so are their health concerns. Our sexologists take the time to understand your specific needs and create personalized treatment plans to ensure the best outcomes.
As a leading rheumatologist in Chandigarh, Dr. Aseem specializes in the diagnosis and management of a wide range of rheumatic conditions, including but not limited to:
Rheumatoid Arthritis: An autoimmune disorder that causes chronic inflammation of the joints.
Osteoarthritis: A degenerative joint disease characterized by the breakdown of cartilage.
Lupus: A systemic autoimmune disease that can affect the skin, joints, kidneys, and other organs.
Ankylosing Spondylitis: A type of arthritis that primarily affects the spine, causing pain and stiffness.
Gout: A form of arthritis characterized by sudden, severe attacks of pain, redness, and tenderness in the joints.
Psoriatic Arthritis: A type of arthritis that affects some people with psoriasis.
Vasculitis: An inflammation of the blood vessels that can cause a variety of symptoms.
Sjogren’s Syndrome: An autoimmune disorder characterized by dry eyes and mouth.
Accurate diagnosis is crucial for effective treatment. Dr. Aseem Goyal utilizes advanced diagnostic techniques to identify the underlying causes of rheumatic conditions. Our state-of-the-art facility is equipped with the latest technology to provide comprehensive diagnostic services, including:
Blood Tests: To check for markers of inflammation and autoimmune activity.
Imaging Studies: Such as X-rays, MRI, and ultrasound to assess joint and soft tissue damage.
Joint Fluid Analysis: To examine the fluid in the joints for signs of inflammation or infection.
Biopsy: In certain cases, a small tissue sample may be taken for further examination.
Treatment Approaches
Dr. Aseem Goyal adopts a holistic and patient-centered approach to treatment. Depending on the specific condition and its severity, treatment options may include:
Medications
Nonsteroidal Anti-Inflammatory Drugs (NSAIDs): To reduce inflammation and relieve pain.
Disease-Modifying Antirheumatic Drugs (DMARDs): To slow the progression of rheumatic diseases.
Biologic Agents: Targeted therapies that block specific pathways in the immune system.
Corticosteroids: To control severe inflammation quickly.
Prakinsons disease and its affect on eye.Riya Bist
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2. Angina is chest pain or discomfort caused when your heart
muscle doesn't get enough oxygen-rich blood.
Angina is not a disease. It is a symptom of an underlying
heart problem, usually coronary heart disease (CHD).
Angina happens when one or more of the coronary arteries is
narrowed or blocked, also called ischemia.
4. Mechanism include:
Atherosclerosis (plaque-related epicardial coronary
obstruction)
focal or diffuse spasm of normal or atheromatous
arteries
microvascular dysfunction
left ventricular dysfunction secondary to previous
acute myocardial necrosis/hibernation (ischaemic
cardiomyopathy)
left ventricular hypertrophy (hypertension, aortic
stenosis, hypertrophic cardiomyopathy).
7. Mechanisms of atherosclerosis
The pathophysiology of atherosclerosis, development of
symptomatic angina and subsequent acute coronary
syndrome (ACS) is well characterised.2,3 The microscopic
development of atherosclerotic plaque involves:
endothelial dysfunction
sub-endothelial accumulation and oxidation of low-density
lipoprotein (LDL)
increased expression of adhesion molecules and chemokine
secretion
immune cell infiltration and development of foam cells
development of fibroatheromatous plaque involving
positive remodelling, neovascularisation, and development
of necrotic core with overlying fibrous cap formation and
calcification.
8. Endothelial dysfunction and nitric oxide
The endothelium is a single layer of cells lining blood
vessels and performs multiple functions, including:
the regulation of coronary blood flow
a barrier to toxic substrates
regulation of thrombosis and inflammation
control of angiogenesis.
9. Endothelial dysfunction is characterised by a reduction in the bioavailability of
vasodilators, such as NO, as a result of reduced production and increased
consumption of NO, and an increase in endothelium-derived contracting factors,
such as endothelin and angiotensin II (AII) (figure 1). This is seen as the blood
vessel being unable to dilate. In addition, endothelial dysfunction promotes
platelet and leukocyte activation and the release of cytokines, which increase
vessel permeability. This enables the sub-endothelial infiltration of oxidised
lipoproteins and inflammatory cells.
10. Endothelial dysfunction has been referred to as “the risk of the risk factors”,4 since it has been
shown to occur in the presence of conventional, modifiable risk factors (e.g. cigarette smoking,
high blood pressure, hyperlipidaemia and diabetes). These risk factors are, in turn, associated
with a state of increased oxidative stress and the overproduction of reactive oxygen species. This
all contributes to the complex interplay of endothelial dysfunction since reactive oxygen species
can themselves lead to abnormal NO metabolism (figure 2).
11. Fatty streaks: A fatty streak marks the earliest macroscopic
atherosclerotic lesion. Beginning in early life, these fatty streaks
comprise a focal build-up of various substrates e.g. lipid-rich
macrophages (foam cells), extracellular matrix, smooth muscle cells,
intracellular and extracellular lipid deposits, and T lymphocytes, to
form a minor thickening of the intimal surface.
19. Unstable angina:
•Also called “Crescendo angina”
•Acute coronary syndrome in which angina worsens
•Occurs at rest
•Severe and of acute onset
•Crescendo pain- pain increases every time
20. Unstable angina:
•Increased frequency , severity or duration of pain
in a apatient of stable angina.
•Pain occurs with less exertion or at rest.
•Myocardial contraction may occur in 10-20%
patients
22. Microvascular angina:
•Also called Syndrome X
•Cause unknown
•Probably due to poor functioning of the small blood
vessels of the heart, arms and legs
•No arterial blockage
•Difficult to diagnose because it does not have arterial
blockage
•Good prognosis
23. Prinzmetal’s angina or variant angina
•Prinzmetal’s angina is a variant form of angina with
normal coronary vessels or minimal atherosclerosis
•It is probably caused by spasm of coronary artery
30. Immediate pre exertional prophylaxis of angina:
Sublingual Nitroglycerine 0.5mg or Isosorbide
dinitrate 5mg should be taken within 5 minutes.
For long term prophylaxis:
Long acting nitrates, calcium channel blockers,
beta blockers or combination of these drugs.
Antiplatelet therapy:
Aspirin small dose 75mg – 150mg once daily orally
or Dipyridimole 75mg orally.
31. CORONARY ARTERY REVASCULARIZATION
For patients not responding to medical
therapy
Percutaneous Transluminar Coronary
Angioplasty (PTCA).
Coronary Artery bypass grafting (CABG)
36. NITRATES
MODE OF ACTION :
ACTS DIRECTLY ON VASCULAR SMOOTH MUSCLE TO
PRODUCE ARTERIAL AND VENOUS DILATATION
EFFECT DURING ANGINA
1.REDUCES MYOCARDIAL OXYGEN DEMAND (LOWERS
PRE-LOAD AND AFTER LOAD)
2. INCREASES MYOCARDIAL OXYGEN SUPPLY
(CORONARY VASODILATATION)
40. DURATION OF ACTION OF SOME NITRTATE PREPARATIONS
PEAK ACTION
DURATION OF
ACTION
Sublingual GTN(Tablet 300-
500µg or metered dose
aerosol 400µg/spray)
4-8 minutes 10-30 minutes
Buccal GTN (1-5 mg tablet 6
hourly)
4-10 minutes 30-300 minutes
Transdermal. GTN (5-10
daily)
1-3 hours Up to 24 hours
Oral isosorbidedinitrate.(10-
20 mg 8 hourly)
45-120 hours 2-6 hours
Oral isosorbide mononitrate
( 20-60 mg once or twice a
day)
45-120 hours 6-10 hours
41. SUBLINGUAL GTN- Administered
a.as a tablet – 300-500 µg to disolve under the tongue
b.As metered-dose aerosol (400 µg per spray)
RELIEVES AN ATTACK OF ANGINA IN 2-3 MINUTES
UNWANTED EFFECTS
HEADACHE
SYMPTOMATIC HYPOTENSION –DIZZINESS, POSTURAL GIDDINESS,
BLURRING OF VISION
RARELY SYNCOPE – FAINTING
ASK PATIENT TO SPIT TABLET IF ABOVE EFFECTS OCCUR
NOT HABIT FORMING
TEACH PATIENTS TO USE PROPHYLACTICALLY e.g. Before exerting
VIRTUALLY INEFFECTIVE IF SWALLOWED DUE TO EXTENSIVE FIRST PASS
METABOLISM IN THE LIVER
CONTINUOUS USE CAUSES PHARMACOLOGICAL TOLERANCE
THERFORE ATTEMPT TO INCLUDE A ‘NITRATE-FREE’ PERIOD OF 6-8 HOURS
A DAY
43. Beta Blockers are effective in Stable and Unstable
Angina.
In contrast they are not useful in variant angina may
worsen the condition. This deleterious effect is likely
due to the increase in the coronary resistance caused by
the unopposed effects of catecholamines acting at alpha
adrenoreceptors.
44. • Heart rate
• Contractility
• Preload
• Afterload
• Coronary flow
• Regional
myocardial blood
flow
O2
D
e
m
a
n
d
O2
S
u
p
p
l
y
-Blockers/Ca2+ channel
blockers
Nitrates/Ca2+ channel
blockers
Nitrates/Ca2+ channel
blockers/antithrombotics/
statins
HEART
47. CALCIUM CHANNEL BLOCKERS
MODE OF ACTION
1.DECREASES MYOCARDIAL OXYGEN DEMAND BY REDUCING BLOOD
PRESSURE AND MYOCARDIAL CONTRACTILITY
Mechanism of Action
1.Calcium channel blockers block voltage-gated L-type calcium channels, the calcium
channels most important in cardiac and smooth muscle.
By decreasing calcium influx during action potentials in a frequency and voltage
dependent manner, these agents reduce intercellular calcium concentration and muscle
contractility.
USED IN ALL TYPES OF ANGINA
Verpamil 80-160mg/8hr
Diltiazem 60-120mg/8hr
Nifedipine 10-40mg/8hr
Amlodipine 5mg/day
49. VERAPAMIL AND DILITIAZEM-SUITABLE FOR PATIENTS
WHO ARE NOT RECEIVING BETA BLOCKERS AS THEY
DECREASE THE HEART RATE ( DANGEROUS ADDITIVE
EFFECT
Adverse Drug reactions:
Facial puffiness
Pedal edema
Flushing
Headache
Contraindications: Heart failure, Bradycardia
50. POTASSIUM CHANNEL ACTIVATORS
MODE OF ACTION: DILATES ARTERIES AND VEINS
DOES NOT EXHIBIT TOLERANCE SEEN WITH NITRATES
NICORANDIL- 10-30 mg 12 hourly
Caution in:
hypovolaemic patients
Patients with pulmonary oedema
Side effects:
a.Headache
b.Flushing
c.Dizziness
d.Weakness
e.May cause a dose dependent increase in heart rate
f.Myalgia
g.Angioedema
51. Potassium channel openers:
Types of potassium channels: Voltage gated, calcium
activated, ATP acyivated
Nicorandil is a newer agent activates ATP sensitive
potassium channel and hyperpolarises vascular
smooth muscles.
Decreases pre and after load and produce coronary
dilation
52. Ranolazine
Reserve agent for chronic, resistant angina
Inhibits cardiac late Na Current influx ,
there by reducing calcium flow into the cells
thus help the heart to relax improve the
blood flow
Decreases cardiac contractility
No change in Heart rate and BP
Prolongs QT interval so it is containdicated
with drugs that prolong QT interval.
Dose: 500mg, 1000mg
54. IVABRADINE
Direct Bradycardic agent or pure HR lowreing agent
Blocks hyperpolarazation activated if current through Na
channel present in SA node which get activated during early part
of slow diastolic depolarization durring ischemic episodes.
Heart rate decreased and Oxygen demand decreased
No fall in BP
Dose: 5mg
56. ASPIRIN
ANTIPLATELE T EFFECT BY INHIBITION OF THROMBOXANE A 2
NSAID, INHIBITS COX-1 AND COX -2 WHICH LEADS TO
DECREASED PROSTAGLANDIN SYNTHESIS
USES
THROMBO-EMBOLIC CVA, ISCHAEMIC HEART DISEASE-
PROPHYLAXIS (75MG/DAY) AND ACUTE TREAMENT (375 MG)
CONTRAINDICATIONS
1.THOSE UNDER AGE OF 16Y-CAN INCREASE INCIDENCE OF
REYE’S SYNDROME, LIVER/BRAIN DAMAGE
2.GASTRO-INTESTINAL ULCERS
3.BLEEDING DISORDERS
4.GOUT
5.HYPERSENSITIVITY TO ANY NSAID
6.GFR <10ML/MIN
58. ASPIRIN
CAUTION
1.ASTHMA
2.UNCONTROLLED HYPERTENSION
3.ANY ALLERGIC DISEASE
4.G6PD DEFICIENCY
5.DEHYDRATION
OTOTOXIC IN OVERDOSE
MAY INCREASE EFFECTS OF SULPHONYL UREAS AND OF METHOTREXATE
FOR ANALGESIA- 300-900 MG 4-6 HPOURLY –MAXIMUM DOSE4G/DAY
STOP 7 DAYS BEFORE SURGERY IF SIGNIFICANT BLEEDING IS EXPECTED
IF CARDIAC SURGERY OR PATIENT HAS ACUTE CORONARY SYNDROME-
CONSIDER CONTINUING
59. CLOPIDOGREL
ANTIPLATELET AGENT- The active metabolite of clopidogrel
selectively inhibits the binding of adenosine diphosphate (ADP) to
its platelet P2Y12 receptor and the subsequent ADP- mediated
activation of the glycoprotein GPIIb/IIIa complex, thereby
inhibiting platelet aggregation. This action is irreversible
USE
PROPHYLAXIS OF ANTI-THROMBOTIC EVENTS IN NON—ST
ELEVATIONMYOCARDIAL INFARCTION AND IN ST ELEVATION
MYOCARDIAL INFARCTION-IN COMBINATION WITH ASPIRIN
MYOCARDIAL INFARCTION (WITHIN A ‘FEW’ TO35 DAYS)
ISCHAEMICCEREBROVASCULAR ACCIDENT- WITHIN 7 DAYS TO 6
MONTHS
PERIPHERAL ARTERIAL DISEASE
CONTRAINDICATION
ACTIVE BLEEDING
NOT RECOMMENDED WITH WARFARIN
60. CLOPIDOGREL
SIDE EFFECTS
HAEMORRHAGE (ESPECIALLY GASTRO-INTESTINAL OR
INTRA-CRANIAL
GASTRO-INTESTINAL UPSET
PEPTIC ULCER
PANCREATITIS
HEADACHE
FATIGUE
DIZZINESS
PARAESTHESIA
RASH/PRURITUS
MONITOR FULL BLOOD AND FOR SIGNS OF OCCULT BLEEDING
61. STREPTOKINASE
THROMBOLYTIC AGENT
INCREASES PLASMINOGEN CONVERSION TO PLASMIN WHICH
INCREASES FIBRIN BREAKDOWN
USES
1.ACUTE MYOCARDIAL INFARCTION -1.5 MILLION UNITS
INTRAVENOUS INFUSION OVER 60 MIN
2.THROMBOEMBOLISM OF ARTERIES
3.PULMONARY EMBOLISM
4.CENTRAL RETINAL ARTERY THROMBOSIS
5.DEEP VEIN THROMBOSIS
OTHER DOSES-250,000 UNITS INTRAVENOUS INFUSION OVER
30 MIN, THEN 100,000 UNITS EVERYHOUR FOR UPTO12-72
HOURS
62. ALTEPLASE
(RECOMBINANT) TISSUE-TYPE PLASMINOGEN ACTIVATOR.
RECOMBINANT FIBRINOLYTIC
USE
ACUTE MYOCARDIAL INFARCTION (TOTAL DOSE 100MG-
REGIMEN DEPENDS ON TIME SINCE ONSET OF PAIN
0-6HOURS: 15 MG INTRAVENOUS BOLUS,FOLLOWED BY 50 MG
INTRAVENOUS INFUSION OVER 30 MINUTES AND 35 MG INTRAVENOUS
INFUSION OVER 60 MINUTES
6-12 HOURS-10 MG INTRAVENOUS BOLUS FOLLOWED BY 50 MG
INTRAVENOUS INFUSION OVER 60 MIN, AND FOUR FURTHER 10 MG
INTRAVENOUS INFUSIONS, EACH OVER 30 MIN)
DECREASE DOSE IF PATIENT WEIGHS LESS THAN 65 KG
RETEPLASE
RECOMBINANT PLASMINOGEN ACTIVATOR; THROMBOLYTIC
USED ONLY FOR MYOCARDIAL INFARCTION
DOSE-10 UNITS AS SLOW INTRAVENOUS INJECTION OVER 2 MINUTES,
REPEAT AFTER 30 MIN
63. Newer Drugs
A) Ranolazine appears to act mainly by reducing a late,
prolonged sodium current in myocardial cells.
1.The decrease in intracellular sodium causes an increase in
calcium expulsion via the Na/Ca transporter and a reduction in
cardiac force and work.
2.Ranolazine is moderately effective in angina prophylaxis.
B) Dipyridamole
1.It is a powerful coronary dilator;
increases total coronary flow by preventing
uptake and degradation of adenosine.
2.It dilates resistance vessels and abolishes autoregulation.
3.Inhibit platelet aggregation.
4.Not useful as an anti-anginal drug but used for prophylaxis of
Coronary and cerebral thrombosis in post-MI and post stoke
patients.
Editor's Notes
The principal mechanism by which the endothelium modulates coronary perfusion is by regulating coronary vascular tone through the production of nitric oxide (NO). NO is synthesised from the amino acid L-arginine by means of the enzyme endothelial NO synthase (e-NOS). Endothelial cells express e-NOS, producing a low level of NO, which is under the control of regulatory factors. NO has paracrine effects by readily permeating cell membranes where it activates the synthesis of cyclic guanylate cyclase (cGMP). Through this intracellular signalling pathway, it has a number of effects including vasodilation, angiogenesis, and reducing platelet adhesion and vascular smooth muscle proliferation.
Relieving pain is one of the main goals of treating coronary microvascular disease (MVD). Treatments also are used to control risk factors and other symptoms. Treatments may include medicines, such as:
ACE inhibitors and beta blockers to lower blood pressure and decrease the heart’s workload
Aspirin to help prevent blood clots or control inflammation
Nitroglycerin to relax blood vessels, improve blood flow to the heart muscle, and treat chest pain
Statin medicines to control or lower your blood cholesterol.
Causes of Variant (Prinzmetal) Angina: The pain from variant angina is caused by a spasm in the coronary arteries (which supply blood to the heart muscle).The coronary arteries can spasm as a result of:Exposure to cold weather
Stress
Medicines that tighten or narrow blood vessels
Smoking
Cocaine use
Symptoms of Variant (Prinzmetal) Angina: The pain or discomfort:Usually occurs while resting and during the night or early morning hours
Are usually severe
Can be relieved by taking medication
Treatment of Variant Angina | Prinzmetal's AnginaMedicines can help control the spasms. Drugs such as calcium antagonists and nitrates are the mainstays of treatment.