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
Cardiovascular pharmacology
Cardiovascular (=Circulatory) system – heart and blood vessels
Arteries – transport blood to tissues
Capillaries – sites of exchange, fluid O2, CO2, nutrients etc.
Venules – collect blood from capillaries
Veins – transport blood back to heart
Blood moves within vessels – higher pressure to lower pressure
Resistance to flow depends on vessel diameter, length and viscosity of blood
Cardiovascular pharmacology
Cardiovascular (=Circulatory) system – heart and blood vessels
Arteries – transport blood to tissues
Capillaries – sites of exchange, fluid O2, CO2, nutrients etc.
Venules – collect blood from capillaries
Veins – transport blood back to heart
Blood moves within vessels – higher pressure to lower pressure
Resistance to flow depends on vessel diameter, length and viscosity of blood
nitrates mechanism of action,overview of nitroglycerin[short acting], iso sorbide dinitrates, iso sorbide mononitrates, amyl nitrates and nitroprusside,
nitrates mechanism of action,overview of nitroglycerin[short acting], iso sorbide dinitrates, iso sorbide mononitrates, amyl nitrates and nitroprusside,
Pharmacology: Class Session 1 and 2 Introduction to PharmacologyMariaJose2001
This is an outline of the basics of Pharmacology. A discussion of how drugs are named, classified and its effects on the person's biochemical processes. It also included the factors influencing drug action and potential drug interactions. At the end, some commonly ysed terminologies were defined.
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
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
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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2. Angina
• Atherosclerotic disease, also known as coronary artery disease
(CAD) or ischemic heart disease (IHD), is the most common
cause of mortality worldwide.
• Atherosclerotic lesions in coronary arteries can obstruct blood
flow, leading to an imbalance in myocardial oxygen supply and
demand that presents as
– stable angina (ischaemic chest pain)
– an acute coronary syndrome
• unstable angina.
• myocardial infarction (MI) (heart attack): caused by the complete
occlusion of the coronary artery and associated death of tissue
• Spasms of vascular smooth muscle may also impede cardiac
blood flow, reducing perfusion and causing ischemia and
anginal pain.
23-May-16
3. Angina
• Is a characteristic sudden, severe, pressing-like substernal
chest pain radiating to the neck, jaw, back, and arms.
Patients may also present with dyspnea or atypical
symptoms such as indigestion, nausea, vomiting, or
diaphoresis.
• is caused by inadequate blood flow through the coronary
blood vessels, is a consequence of myocardial O2 demand
exceeding supply.
• Transient, self-limited episodes (15 seconds to 15 minutes)
of myocardial ischemia (stable angina) do not result in cellular
death; such as occurs in myocardial infarction (MI).
• however, acute coronary syndromes and chronic ischemia can
lead to deterioration of cardiac function, heart failure,
arrhythmias, and sudden death.
23-May-16
4. Types of Angina
Angina pectoris has three patterns:
1. stable, effort-induced, classic, or typical angina.
2. unstable angina, preinfarction or crescendo angina.
3. Prinzmetal, variant, vasospastic, or rest angina.
They are caused by varying combinations of increased
myocardial demand and decreased myocardial
perfusion.
23-May-16
5. Stable angina: the most common (90%)
is chest pain caused by a temporary inadequacy of
blood flow to the myocardium, The underlying cause is
usually occlusion of the coronary arteries by
atherosclerosis
Usually lasts 1-15 minutes, and is provoked by
exercise, stress, extreme cold or heat, heavy meals,
alcohol, or smoking.
Rx: is promptly relieved by rest or nitroglycerin (a
vasodilator).
Stable Angina
6. Unstable angina
(Acute coronary syndrome)
• lies between stable angina and MI.
• The pathology is similar to that involved in MI: a platelet-fibrin
thrombus associated with a raptured atherosclerotic plaque, but
without complete occlusion of the blood vessel.
1. chest pains occur with increased frequency, duration, and intensity.
2. precipitated by progressively less effort.
3. Any episode of rest angina longer than 20 minutes, any new-onset
angina, any increasing (crescendo) angina, or even sudden
development of shortness of breath is suggestive of unstable
angina.
4. The symptoms are NOT relieved by rest or nitroglycerin.
5. requires hospital admission and more aggressive therapy to prevent
death and progression to MI.
23-May-16
7. Prinzmetal's or variant or vasospastic angina
• is an uncommon pattern of episodic angina that occurs at rest
and is due to coronary artery spasm.
• Symptoms are caused by decreased blood flow to the heart
muscle from the spasm of the coronary artery.
• Although individuals with this form of angina may have
significant coronary atherosclerosis, the angina attacks are
unrelated to physical activity, heart rate, or blood pressure.
• generally responds promptly to coronary vasodilators, such as
nitroglycerin and calcium-channel blockers.
• but β-blockers are contraindicated???
23-May-16
8. Determinants of the volume of oxygen required by the heart.
23-May-16
Determinant of myocardial O2 demand
Preload- diastolic filling pressure (blood volume and venous tone)
Afterload-peripheral vascular resistance
Heart rate
Wall tension
Ejection time
9. Angina-precipitating factors:
exercise, emotional stress, sex
↑sympathetic activity ↑HR, Contraction
force, wall tension, TPR ↑ work of the
heart
↑ myocardial O2 demand ≠ myocardial O2 supply
23-May-16
Ischemia
10. 1. Increase blood flow to ischemic heart muscle and/or
2. Decrease myocardial oxygen demand
Four types of drugs, used either alone or in combination,
are commonly used to manage patients with stable
angina: β-blockers, CCBs, organic nitrates, and the
sodium channel blocking drug, ranolazine. These agents
help to balance the cardiac oxygen supply and demand equation by
affecting blood pressure, venous return, heart rate, and contractility.
Lipid lowering drugs, particularly statins, can be given if
elevated plasma cholesterol levels are detected
Antiplatelet drugs, especially low-dose (75mg) aspirin to reduce the
possibility of thrombosis.
Fibrinolytic drugs (e.g. heparin) are used in unstable angina
Therapeutic strategies
11. A newer Therapeutic strategies
• Trimetazidine: Partial fatty acid oxidation inhibitors (pFOX
inhibitors). A newer strategy attempts to increase the
efficiency of oxygen utilization by shifting the energy
substrate preference of the heart from fatty acids to
glucose.
• Ranolazine: inhibition of late sodium current.
• Ivabradine: selectively reduces heart rate with no other
detectable hemodynamic effects, act by inhibition of the SA
pacemaker current, If.
• Nicorandil, Potassium channel activators,
23-May-16
13. Organic nitrates
Nitroglyserin, Isosorbid dinitrat, Isosorbid mononitrate
• They are effective in all types of angina pectoris.
at therapeutic doses :has 2 major effects
a) Dilation of the large veins resulting in pooling of blood
in the veins which diminish the preload and reduces the
work of the heart
b) Dilates the coronary vasculature providing increased
blood supply to the heart muscle
↓ Preload
↓ Afterload
Relieving vasospasm
Redistribution blood flow
• The total effect is a decrease in myocardial oxygen consumption
because of decreased cardiac work
23-May-16
14. A. Mechanism of action
• relax vascular smooth muscle
by their intracellular
conversion to nitrite ions, to
nitric oxide,
• activates guanylate cyclase
(GC) and increases the cGMP.
• dephosphorylation of the
myosin light chain, vascular
smooth muscle relaxation.
23-May-16
15. Pharmacokinetics of Nitroglycerin
• Prototype: nitrate
• significant first-pass effect metabolism of nitroglycerin occurs
in the liver with PO forms
• Therefore, it is common to take the drug either sublingually or
via a transdermal patch,
• The time to onset of action varies from 1 minute for
nitroglycerin to more than 1 hour for isosorbide mononitrate.
• Isosorbide mononitrate owes its improved bioavailability and
long duration of action to its stability against hepatic
breakdown.
• Oral isosorbide dinitrate undergoes denitration to two
mononitrates, both of which possess antianginal activity.
23-May-16
16. Time to peak effect and duration of action
23-May-16
17. Common nitrate preparations
Glyceryl trinitrate can be taken by sublingual tablet or
spray
The effects start within minutes and last ~30 min
Transdermal patches and I.V preparations are also
available
Isosorbide mononitrate is a longer acting preparation
which is given orally (half-life 4hrs), and slow release
preparations are available.
Side effects: nitrates can cause
Headache in about 30% - 60% of patients because of
the pronounced vasodilation.
High doses can cause postural hypotension, flushing &
tachycardia
18. Nitrate Tolerance
• Tolerance develops rapidly. The blood vessels become
desensitized to vasodilation. providing a daily “nitrate-free
interval” to restore sensitivity to the drug.
• This interval is typically 10 to 12 hours, usually at night,
because demand on the heart is decreased at that time.
• Nitroglycerin patches are worn for 12 hours then removed for
12 hours.
• However, variant angina worsens early in the morning,
perhaps due to circadian catecholamine surges. Therefore, the
nitrate-free interval in these patients should occur in the late
afternoon.
23-May-16
19. Beta Blockers
• Atenolol, metoprolol, propranolol, bisoprolol
• Are used only for prophylactic therapy of angina; they are of no
value in an acute attack
• Effective in preventing exercise-induced angina
• But are ineffective against the vasospastic form
• Cardioselective β-blockers, such as metoprolol or atenolol, are
preferred. Thus, Propranolol is not preferred
• Agents with intrinsic sympathomimetic activity (for example,
pindolol) are less effective and should be avoided in angina.
• The dose should be gradually tapered off over 5 to 10 days to avoid
rebound angina or hypertension.
• Side Effects:?
23-May-16
20. Mechanism of Action
• Suppress the activation of the heart by blocking B1 receptors
I. Decrease the HR, resulting in:
1. decreased myocardial oxygen demand.
2. increased oxygen delivery to the heart.
II. Decrease myocardial contractility, helping to conserve energy or
decrease demand
III. Reduce the work of the heart by decreasing COP and causing a
slight decrease in BP
• ↓ HR,
• ↓contractility,
• ↓systolic wall tension,
• ↑perfusion time
23-May-16
21. Reasons for Using Nitrates and β-Blockers in
Combination in Angina
• β-Blockers prevent reflex tachycardia and contractility
produced by nitrate-induced hypotension.
• Nitrates prevent any coronary vasospasm produced by β-
Blockers.
• Nitrates prevent increases in left ventricular filling pressure or
preload resulting from the negative inotropic effects produced
by β-Blockers .
23-May-16
22. Calcium Channel Blockers (CCBs)
ex : amlodipine, diltiazem, felodipine, nicardipine, nifedipine, verapamil
Mechanism of Action
• Calcium is essential for muscular contraction.
• The CCBs protect the tissue by inhibiting the entrance of Ca+2
into cardiac and smooth muscle cells of the coronary and
systemic arterial beds.
• All CCBs are therefore arteriodilators that cause a decrease in
vascular resistance. Cause peripheral arterial vasodilation
• Reduce myocardial contractility (-ve inotropic action)
• Result: decreased myocardial oxygen demand
23-May-16
24. calcium-channel blockers
1. Verapamil mainly affects the myocardium,
2. whereas nifedipine exerts a greater effect on smooth muscle
in the peripheral vasculature.
3. Diltiazem is intermediate in its actions.
They lower blood pressure may worsen heart failure due to their -
ve inotropic effect.
23-May-16
All
• ↓ afterload,
• coronary vasodilation
Verapamil & deltiazem:
• ↓HR,
• ↓contractility→↓O2
demand
25. Calcium Channel Blockers
a dihydropyridine derivative
A- Nifedipine
• a dihydropyridine derivative.
• functions mainly as an arteriolar vasodilator.
• This drug has minimal effect on cardiac conduction or heart
rate.
• Used in variant angina caused by spontaneous coronary
spasm
• Other members of this class, amlodipine, nicardipine, and
felodipine, have similar cardiovascular characteristics except
for amlodipine, which does not affect heart rate or cardiac
output.
23-May-16
26. Calcium Channel Blockers
B- nondihydropyridine derivative/ Verpamil
• The diphenylalkylamine
• slows cardiac atrioventricular (AV) conduction directly,
• and decreases HR, contractility, BP, and oxygen demand.
• causes greater -ve inotropic effects than nifedipine, but it is
a weaker vasodilator.
• is extensively metabolized by the liver.
• is contraindicated in patients with preexisting depressed
cardiac function or AV conduction abnormalities.
• Drug Interaction: verapamil increases digoxin levels.
• It also causes constipation.
23-May-16
27. Calcium Channel Blockers
C- nondihydropyridine derivative/ Deltiazem
• Its cardiovascular effects similar to verpamil
• Reduce the HR but lesser than verpamil
• Reduce BP
• Relieve coronary artery spasm so used in variant angina
• Can be used in angina in patients with concomitant diseases
I. First-line agents for treatment of:
1. angina,
2. hypertension,
3. supraventricular tachycardia
II. Short-term management of atrial fibrillation and flutter
Very acceptable side effect and safety profile, May cause:
• hypotension, palpitations, tachycardia or bradycardia, constipation,
nausea, dyspnea
23-May-16
28. Newer Antianginal Drugs
Sodium Channel Blocker, Ranolazine
• Ranolazine inhibits the late phase of the sodium current (late
INa), improving the oxygen supply and demand equation.
• Inhibition of late INa reduces intracellular sodium and calcium
overload, thereby improving diastolic function.
• It has antianginal as well as antiarrhythmic properties.
• Ranolazine is extensively metabolized, mainly by the CYP3A
family and also by CYP2D6. It is also a substrate of P-
glycoprotein. As such, ranolazine is subject to numerous drug
interactions.
• ranolazine can prolong the QT interval.
23-May-16