Atherosclerosis - Definition - Risk Factors - Lesser and Non Quantitated risk factors - Arterial wall - The development of Atherosclerosis - Many Features of the injury Hypothesis - The process of Atherogenesis - Pathogenesis in short - Morphology of Atheroma - Components of Atheromatous Plaque (MP) - Complications and clinical significance - Cardiovascular risk and its assessment.
Congestive heart failure (CHF) is a chronic progressive condition that affects the pumping power of your heart muscles. While often referred to simply as “heart failure,” CHF specifically refers to the stage in which fluid builds up around the heart and causes it to pump inefficiently. You have four heart chambers.
Cardiomyopathy, or heart muscle disease, is a type of progressive heart disease in which the heart is abnormally enlarged, thickened, and/or stiffened. As a result, the heart muscle's ability to pump blood is less efficient, often causing heart failure and the backup of blood into the lungs or rest of the body. The disease can also cause abnormal heart rhythms.
Arteriosclerosis is the most common disease of the arteries; the term means “hardening of the arteries”.
It is the diffuse process whereby the muscle fibers and the endothelial lining of the walls of small arteries and arterioles become thickened.
Arrhythmia is also known as irregular heart beats. If SA node is not the pacemaker, any other part of the heart such as atrial muscle, AV node and ventricular muscle becomes the pacemaker. the beats may be fast, slow or miss beats.
Definition of diabetes - introduction - classification of diabetes - etiology of diabetes type 1 and type 2- risk factors for diabetes - diagnosis of diabetes - clinical manifestations of diabetes type 1 and type 2- investigations for diabetes - treatment of diabetes - non-pharmacological treatment and pharmacological treatment - pharmacotherapy of type 1 and type 2 - acute complications of diabetes and treatment
Chronic Stable Angina- Diagnosis & management
By Dr Awadhesh Kumar Sharma
Dr. Awadhesh kumar sharma is a young, diligent and dynamic interventional cardiologist. He did his graduation from GSVM Medical College Kanpur and MD in Internal Medicine from MLB Medical college jhansi. Then he did his superspecilisation degree DM in Cardiology from PGIMER & DR Ram Manoher Lohia Hospital Delhi. He had excellent academic record with Gold medal in MBBS,MD and first class in DM.He was also awarded chief ministers medal in 2009 for his academic excellence by former chief minister of UP Smt Mayawati in 2009.He is also receiver of GEMS international award.He had many national & international publications.He is also in editorial board of international journal- Journal of clinical medicine & research(JCMR).He is also active member of reviewer board of many journals.He is also trainee fellow of American college of cardiology. He is currently working in NABH Approved Gracian Superspeciality Hospital Mohali as Consultant Cardiologist.
Atherosclerosis - Definition - Risk Factors - Lesser and Non Quantitated risk factors - Arterial wall - The development of Atherosclerosis - Many Features of the injury Hypothesis - The process of Atherogenesis - Pathogenesis in short - Morphology of Atheroma - Components of Atheromatous Plaque (MP) - Complications and clinical significance - Cardiovascular risk and its assessment.
Congestive heart failure (CHF) is a chronic progressive condition that affects the pumping power of your heart muscles. While often referred to simply as “heart failure,” CHF specifically refers to the stage in which fluid builds up around the heart and causes it to pump inefficiently. You have four heart chambers.
Cardiomyopathy, or heart muscle disease, is a type of progressive heart disease in which the heart is abnormally enlarged, thickened, and/or stiffened. As a result, the heart muscle's ability to pump blood is less efficient, often causing heart failure and the backup of blood into the lungs or rest of the body. The disease can also cause abnormal heart rhythms.
Arteriosclerosis is the most common disease of the arteries; the term means “hardening of the arteries”.
It is the diffuse process whereby the muscle fibers and the endothelial lining of the walls of small arteries and arterioles become thickened.
Arrhythmia is also known as irregular heart beats. If SA node is not the pacemaker, any other part of the heart such as atrial muscle, AV node and ventricular muscle becomes the pacemaker. the beats may be fast, slow or miss beats.
Definition of diabetes - introduction - classification of diabetes - etiology of diabetes type 1 and type 2- risk factors for diabetes - diagnosis of diabetes - clinical manifestations of diabetes type 1 and type 2- investigations for diabetes - treatment of diabetes - non-pharmacological treatment and pharmacological treatment - pharmacotherapy of type 1 and type 2 - acute complications of diabetes and treatment
Chronic Stable Angina- Diagnosis & management
By Dr Awadhesh Kumar Sharma
Dr. Awadhesh kumar sharma is a young, diligent and dynamic interventional cardiologist. He did his graduation from GSVM Medical College Kanpur and MD in Internal Medicine from MLB Medical college jhansi. Then he did his superspecilisation degree DM in Cardiology from PGIMER & DR Ram Manoher Lohia Hospital Delhi. He had excellent academic record with Gold medal in MBBS,MD and first class in DM.He was also awarded chief ministers medal in 2009 for his academic excellence by former chief minister of UP Smt Mayawati in 2009.He is also receiver of GEMS international award.He had many national & international publications.He is also in editorial board of international journal- Journal of clinical medicine & research(JCMR).He is also active member of reviewer board of many journals.He is also trainee fellow of American college of cardiology. He is currently working in NABH Approved Gracian Superspeciality Hospital Mohali as Consultant Cardiologist.
Angina pectoris is a clinical syndrome usually characterized by episodes of pain or pressure in the anterior chest . The cause is usually insufficient coronary blood flow which results in a decreased oxygen supply to meet an increased myocardial demand for oxygen in response to physical exertion or emotional stress.
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Ischemic heart disease is a condition of recurring chest pain or discomfort that occurs when a part of the heart does not receive enough blood. This condition occurs most often during exertion or excitement, when the heart requires greater blood flow.
Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
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.
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
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
5. What is Angina pectoris ?
Symptom of Cardiac ischemia
Definition:Transient reversible cardiac ischemia
characterized by central chest pain or discomfort may
be radiating to,
• One or both arms
• Neck
• Jaw
• Epigastrium
or not radiating at all
6. Duration of chest pain
15 sec to 15 min
Generally if chest pain remains for
more than 20 min, than that severe
ischemic condition is recognised as
myocardial infarction
7. Epidemiology
Nearly 2,400 Americans die of CVD each day, or an
average of 1 death every 33 seconds
The syndrome of angina pectoris is reported to occur
with an average annual incidence rate (number of
new cases per time period/total number of persons in
the population for the same time period) of
approximately 1.5% (range: 0.1 to 5/1,000)
depending on the patient’s age, gender, and risk-
factor profile
8. Epidemiology
The presenting manifestation in women is
more commonly angina, whereas men more
frequently have myocardial infarction as the
initial event
Given the projection of large increases in IHD
throughout the world, IHD is likely to become the
most common cause of death worldwide by 2020
11. Classification of Angina
1. Stable (Typical/ classical/ exertional)
2. Prinzmetal (Varient)
3. Unstable (Crescendo)
Note: Remember all names, u will be
asked a Q. By any name.
13. Pathophysiology of stable angina
Atherosclerotic plaque formation in coronary artery of
heart ( a plaque covers approx. ≥70% diameter of the
lumen)
Obstruct blood supply in coronary artery
This less blood supply is enough during resting
condition
But when there is an exertion/ emotional stress, there
will be more work load of the heart
14. Pathophysiology of stable angina (Cont.)
This increased workload can’t be full fulfilled as
there would be no dilation of sclerotic point
Decreased blood supply to myocardium – Ischemia
Less oxygen supply
More oxygen demand at the time of exertion can’t be
fulfilled
Resulting into chest pain at the time of exertion
(Note: Draw a figure of atherosclerotic plaque
in coronary artery)
15. Pathophysiology of variant angina
Vasospasm in coronary artery
Decreased blood supply to myocardium – Ischemia
Less oxygen supply
Myocardial demand wont be fullfilled
Resulting into chest pain
(Note: Draw a figure of vasospasm in coronary
artery)
17. Clinical Presentation
Stable angina: Pain at the time of exertion
Unstable angina: Has symptoms even at rest and
the severity and duration of pain is very high
Variant angina: More likely to experience pain at
rest and early morning hours
18. Symptoms
Pattern of pain: It mainly causes squeezing,
tightness, pressure, constriction, fullness in the
chest, band-like sensation, heavy weight on
chest
Other symptoms may include nausea,
indigestion, diaphoresis, dizziness, light
headedness, and fatigue
19. Diagnosis
Clinical presentations
ECG: ST segment elevation/
depression & or T wave inversion
Stress Testing: Using treadmill, chest
discomfort, dyspnea, ST segment
depression, SBP, v. tachycardia
Cardiac Imaging: Thallium 201 and
technetium 99 for perfusion defect
21. Goals of therapy
The major goals of the therapy are as
follows:
To prevent angina pains as much as
possible, and to ease pain quickly if it
occurs
To limit further deposits of atheroma as
much as possible. This prevents or delays
the condition from getting worse
To reduce the risk of having a heart attack
22. Concept of therapy
Classical: reduce work, will reduce O2
demand – Nitrates
Prinzmetal: vaso-spasm, use coronary
vaso-dilators – CCB
25. Note: The algorithm in previous slide
was for the management of angina
(esp. Stable) Study and understand it
26. Nitrates
Rapidly absorbed orally
Nitroglycerine undergoes extensive first
pass metabolism
Isosorbide dinitrate is metabolised
extensively in the liver to isosorbide-5-
mononitrate and 2-mononitrate
5-mononitrate when used as a drug is
completely absorbed.
30. Precautions and counselling points for
nitrates
Contra-indicated with Sildenafil (or other
PDE-5 inhibitors)
Nitrate tolerance – to avoid it keep nitrate free
interval, use beta-blockers
Prophylactic use of nitrare- before exercise
Storage precautions (deteriorates in direct
exposure to air, moisture and sun-light)
31. Beta blockers
Reduce myocardial oxygen demand by
decreasing the increase in heart rate, arterial
pressure and myocardial contractility caused
by adrenergic stimulation
Action most prominent during exercise; only
small reductions in variables at rest
32. Drug Dosage ADR
Propranolol Initially 40mg 2-3 times daily;
maintenance 120-240mg daily
Bradycardia, heart failure,
hypotension, bronchospasm,
conduction disorders,
peripheral vasoconstrictionAtenolol 100 mg daily in 1 or 2 doses
Acebutolol Initially 400mg once daily or
200mg twice daily
Bisoprolol Usually 5-10mg once daily, max.
20mg daily
Carvedilol Initially 12.5 twice daily, increased
after 2 days to 25mg twice daily
Metoprolol 50-100 mg 2-3 times daily
Nadolol 40mg daily, increased at weekly
intervals if required; usual max.
160mg daily
Pindolol 2.5-5mg upto 3 times daily
33. CI of beta-blockers
Chronic lung disease (Use
cardioselective)
Atrioventricular conduction disturbances
Severe bradycardia
Raynaud’s phenomenon
H/o mental depression
Diabetic patient on insulin therapy
34. DDIs
Verapamil: Left ventricular dysfunction
(decreased myocardial contractility)
Nifedipine (CHF, severe hypotension)
Increased beta blocking action by
cimetidine, oral contraceptives,
furosemide and hydralazine
Smoking: decreasd Propranolol level
Clonidine: Rebound hypertension
35. Alternative in CI
Use Esmolol: 50-300 mcg/kg per min
(IV)
Ultra short acting, rapid onset, less side
effects
36. Other option
Ivabradine
Act on If current
Initially 5mg twice daily, increasing to
7.5mg twice daily after 3-4 weeks
depending on therapeutic response
Used when Beta-blockers are CI
ADRs: Visual symptoms
(transient enhanced brightness)
37. Calcium channel blockers
Act on slow calcium channels (voltage-
gated L-type) – Arterial smooth muscle
and nodal tissue of the heart
Verapamil – nodal tissue & h. muscles
Nifedipine – arteriolar smooth muscles
Diltiazem - intermediate
40. Drug Dosage ADR
Verapamil 80-120 mg 3 times
daily
Constipation, facial flushing, headache,
dizziness, rarely pain the gums, facial
pain, epigastric pain etc.
Diltiazem 30-80 mg 6 hourly Headache, dizziness, ankle edema,
occassionally skin rash, exfoliative dermatitis,
gingival hyperplasia, sinus bradycardia,
hypotension, palpitations
Amlodipine 2.5-5 mg daily, max.
10 mg daily
Headache, edema, fatigue, nausea, gum
hyperplasia, dry mouth, sweating,
palpitations, myalgia, etc.
Felodipine Initially 5 mg daily in
the morning, increased
if necessary to 10 mg
once daily
Flushing, headache, palpitations,
dizziness, fatigue, gravitational edema,
gum hyperplasia, urinary frequency
Nifedipine
(*long acting)
20-40 mg OD/BD Bilateral ankle edema, flushing,
headache, tachycardia, renal failure,
muscle cramps, myalgia, gingival
hyperplasia
41. Contra-indications and
precautions
Sick sinus syndrome (Verapamil and
diltiazem)
Second and third degree AV blocks and
hypotension (Verapamil and diltiazem)
Hypersensitivity: Nifedipine
Withdrawal syndrome of nifedipine
Cautious with beta blockers
42. ADRs
Verapamil: constipation (most
commom)
Other: headache, vertigo, weakness,
nervousness, pruritus, flushing and
gastric disturbances
Orthostatic hyypotension, AV block,
CHF, pedal and pulmonary edema,
53. Non pharmacological
management
Mainly involves identification and modification of
risk factors to ischaemic heart disease.
Weight reduction: Reduction in weight may be
achieved by dietary modification and exercise.
Increased physical activity: Physical exercise
can enhance good cholesterol and reduce the risk
of bad cholesterol and heart disease and
contribute to improvement of overall health. The
patients with angina however have to be
careful and must know the level of
exercising above which it can precipitate
chest pain
54. Quitting smoking:
Tobacco use lowers HDL cholesterol. This could
lead to an increased risk for heart disease.
Smoking one or more packs of cigarettes per day
for several years increases the death rate by
ischaemic heart disease by 200%.
Smoking cessation reduces the risk of heart attack
to about 15-25% of that associated with continued
smoking.
Some of the techniques of smoking cessation
which are helpful include using nicotine substitutes
or some group programs or self-help programs.
55. Limiting alcohol consumption: Moderation in
alcohol consumption must be adopted. Ingestion of
alcohol in large amounts increases the risk of
coronary artery disease.
Stress reduction: Stress results in
hypercholesterolemia and therefore increased risk
of angina pectoris. Stress reduction with yoga and
medication is helpful.
Avoiding certain drugs: Certain drugs like
thiazide diuretics increase the risk of
cardiovascular disorders by increasing the
cholesterol levels in the body.
56. Note: For unstable angina; antiplatelets,
anti-coagulants and fibrinolytics classes
have been discussed in ppt of MI