It is a anti- hypertensive drug. It is non-selective beta blocker drug. Hence it is beta blocker drug so it has many side effect.Not only Propranolol but also Timolol,Atenolol are beta blocker drugs.
It is a anti- hypertensive drug. It is non-selective beta blocker drug. Hence it is beta blocker drug so it has many side effect.Not only Propranolol but also Timolol,Atenolol are beta blocker drugs.
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
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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
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
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
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.
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.
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.
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2. HYPERTENSIONHYPERTENSION
HYPERTENSIONHYPERTENSION is defined as either ais defined as either a
sustained systolic blood pressure (SBP) ofsustained systolic blood pressure (SBP) of
greater than 140 mm Hg or a sustainedgreater than 140 mm Hg or a sustained
diastolic blood pressure (DBP) of greater thandiastolic blood pressure (DBP) of greater than
90 mm Hg.90 mm Hg.
Hypertension results from increasedHypertension results from increased
peripheral vascular smooth muscle tone, whichperipheral vascular smooth muscle tone, which
leads to increased arteriolar resistance andleads to increased arteriolar resistance and
reduced capacitance of the venous system.reduced capacitance of the venous system.
6. ►►►► A.C.E. INHIBITOR ◄◄A.C.E. INHIBITOR ◄◄
A.C.E.(Angiostensin converting enzyme)A.C.E.(Angiostensin converting enzyme)
inhibitor is an agent which block the angiotensininhibitor is an agent which block the angiotensin
converting enzyme which ultimately inhibit theconverting enzyme which ultimately inhibit the
conversion of Angiotensin- from Angiotensin- .ɪɪ ɪconversion of Angiotensin- from Angiotensin- .ɪɪ ɪ
Classification of ACE InhibitorClassification of ACE Inhibitor
1. Direct action but internalized metabolite to1. Direct action but internalized metabolite to
disulfide group.Ex.disulfide group.Ex. captoprilcaptopril
2. Prodrug (ester dicarboxylic acid)2. Prodrug (ester dicarboxylic acid)
They have the effects when they are changed toThey have the effects when they are changed to
active metabolized .Exactive metabolized .Ex enalapril, benazepril,enalapril, benazepril,
3. Soluble in water and not change in the body3. Soluble in water and not change in the body
7. ►►►► A.C.E. INHIBITOR ◄◄A.C.E. INHIBITOR ◄◄
MECHANISM OF ACTION :MECHANISM OF ACTION :
The ACE inhibitors lower blood pressureThe ACE inhibitors lower blood pressure
by reducing peripheral vascular resistance.by reducing peripheral vascular resistance.
Block the ACE that cleaves angiotensin I toBlock the ACE that cleaves angiotensin I to
form the potent vasoconstrictor angiotensinform the potent vasoconstrictor angiotensin
II.II.
ACE inhibitors decrease angiotensin II andACE inhibitors decrease angiotensin II and
increase bradykinin levels.increase bradykinin levels.
ACE inhibitors also decrease the secretion ofACE inhibitors also decrease the secretion of
aldosterone, resulting in decreased sodiumaldosterone, resulting in decreased sodium
and water retention.and water retention.
10. ►►►► A.C.E. INHIBITOR ◄◄A.C.E. INHIBITOR ◄◄
ADVERSE EFFECT :ADVERSE EFFECT :
Dry cough, rash, fever,Dry cough, rash, fever,
altered taste, hypotension (in hypovolemicaltered taste, hypotension (in hypovolemic
states), and hyperkalemia, fatigue, angioedema,states), and hyperkalemia, fatigue, angioedema,
headache, dizziness.headache, dizziness.
CONTRAINDICATION & PRECAUTION :CONTRAINDICATION & PRECAUTION :
The ACE inhibitors areThe ACE inhibitors are
contraindicated in patients with:contraindicated in patients with:
Previous angioedema associated with ACEPrevious angioedema associated with ACE
inhibitor therapyinhibitor therapy
11. ►►►► A.C.E. INHIBITOR ◄◄A.C.E. INHIBITOR ◄◄
ACE inhibitors should be used with caution inACE inhibitors should be used with caution in
patients with:patients with:
Impaired renal function.Impaired renal function.
Hypovolemia or dehydration.Hypovolemia or dehydration.
THERPEUTIC USES :Used in patients withTHERPEUTIC USES :Used in patients with
cardiac failure, renal disease or systemiccardiac failure, renal disease or systemic
sclerosis .It also used to treat diabeticsclerosis .It also used to treat diabetic
nephropathy and left ventricularnephropathy and left ventricular
hypertrophy.hypertrophy.
12. ▶▶▶▶ STUDY OF DRUGS UNDERSTUDY OF DRUGS UNDER
ACE INHIBITORS ◄◄ACE INHIBITORS ◄◄
CAPTOPRIL :CAPTOPRIL :
Mechanism of action:Mechanism of action:
Captopril prevents the conversion of angiotensinCaptopril prevents the conversion of angiotensin
I to angiotensin II by inhibition of ACE.I to angiotensin II by inhibition of ACE.
Decreased plasma angiotensin II.Decreased plasma angiotensin II.
Increased plasma renin activity (PRA) resultingIncreased plasma renin activity (PRA) resulting
from loss of negative feedback on renin release.from loss of negative feedback on renin release.
Decreased aldosterone secretion.Decreased aldosterone secretion.
small increases in serum potassium with sodiumsmall increases in serum potassium with sodium
and fluid loss.and fluid loss.
13. CAPTOPRILCAPTOPRIL
Adverse effectsAdverse effects : Cough due to increase in the
plasma levels of bradykinin, angioedema,
agranulocytosis, proteinuria, hyperkalemia, taste
alteration, teratogenicity, acute renal failure and
leukopenia..
Contraindication :Contraindication : Hypersensivity,stenosis,renal
impairment,pregnancy..
Precaution :Precaution : Lactation, severe CHF.Lactation, severe CHF.
Dose :Dose : 25 mg BD or 50 mg TDS.25 mg BD or 50 mg TDS.
Clinical use:Clinical use: vasodilation and inhibition of somevasodilation and inhibition of some
renal function activities .Used inrenal function activities .Used in
Hypertension,Cardiac conditions such as postHypertension,Cardiac conditions such as post
myocardial infarction and congestive heart failure.myocardial infarction and congestive heart failure.
14. ENALAPRILENALAPRIL
Enalapril, an angiotensin-converting enzymeEnalapril, an angiotensin-converting enzyme
(ACE) inhibitor, is a prodrug which, when(ACE) inhibitor, is a prodrug which, when
hydrolyzed by estarases to its active Enalaprilat.hydrolyzed by estarases to its active Enalaprilat.
Mechanism of action:Enalaprilat competesMechanism of action:Enalaprilat competes
with angiotensin I for binding at the angiotensin-with angiotensin I for binding at the angiotensin-
converting enzyme, blocking the conversion ofconverting enzyme, blocking the conversion of
angiotensin I to angiotensin II.angiotensin I to angiotensin II.
As angiotensin II is a vasoconstrictor and aAs angiotensin II is a vasoconstrictor and a
negative-feedback mediator for renin activity,negative-feedback mediator for renin activity,
lower concentrations result in a decrease in bloodlower concentrations result in a decrease in blood
pressure. Enalaprilat may also act on kininasepressure. Enalaprilat may also act on kininase
II,that degrades the vasodilator bradykinin.II,that degrades the vasodilator bradykinin.
15. ENALAPRILENALAPRIL
Pharmacokinetic data :Pharmacokinetic data :
Bioavailability - 60% (oral), Metabolism -Bioavailability - 60% (oral), Metabolism -
hepatic (to enalaprilat), Half-life - 11 hourshepatic (to enalaprilat), Half-life - 11 hours
(enalaprilat), Excretion - renal.(enalaprilat), Excretion - renal.
Clinical uses :Management of hypertension.Clinical uses :Management of hypertension.
In hypertensive patients with heart failure,In hypertensive patients with heart failure,
postmyocardial infarction, high coronarypostmyocardial infarction, high coronary
disease risk etc.disease risk etc.
16. ENALAPRILENALAPRIL
Adverse effects :Adverse effects : Hypotension, dizziness whenHypotension, dizziness when
standing up, and dry cough etc.standing up, and dry cough etc.
Contraindication :Contraindication : Hypersensitivity , pregnancy,Hypersensitivity , pregnancy,
children.children.
Special precaution :Special precaution :Impaired renal failure,Impaired renal failure,
hyperkalaemiahyperkalaemia
Doses :Doses : The recommended initial dose in patientsThe recommended initial dose in patients
is 5 mg OD & should be adjusted according to bloodis 5 mg OD & should be adjusted according to blood
pressure response.pressure response.
The usual dosage range is 10 to 40 mg per dayThe usual dosage range is 10 to 40 mg per day
administered in a single dose or two divided doses.administered in a single dose or two divided doses.
17. RAMIPRILRAMIPRIL
RAMIPRIL : It is An inactive prodrug,RAMIPRIL : It is An inactive prodrug,
ramipril is converted to ramiprilat in the liverramipril is converted to ramiprilat in the liver
and is used to treat hypertension and heartand is used to treat hypertension and heart
failure, to reduce proteinuria and renalfailure, to reduce proteinuria and renal
disease and to prevent stroke, myocardialdisease and to prevent stroke, myocardial
infarction.infarction.
Mechanism of action:Mechanism of action:
•Ramiprilat competes with angiotensin IRamiprilat competes with angiotensin I
for binding at the angiotensin-convertingfor binding at the angiotensin-converting
enzyme. blocking the conversion ofenzyme. blocking the conversion of
angiotensin I to angiotensin II.angiotensin I to angiotensin II.
18. RAMIPRILRAMIPRIL
As angiotensin II is a vasoconstrictor and aAs angiotensin II is a vasoconstrictor and a
negative-feedback mediator for reninnegative-feedback mediator for renin
activity Lower concentrations result in aactivity Lower concentrations result in a
decrease in blood pressure and an increasedecrease in blood pressure and an increase
in plasma reninin plasma renin..
• Ramiprilat may also act on kininase II, anRamiprilat may also act on kininase II, an
enzyme identical to ACE that degrades theenzyme identical to ACE that degrades the
vasodilator bradykinin.vasodilator bradykinin.
19. RAMIPRILRAMIPRIL
Pharmacokinetic data:Pharmacokinetic data:
Bioavailability : 28%, Protein binding :73%Bioavailability : 28%, Protein binding :73%
(ramipril)(ramipril)
56% (ramiprilat), Metabolism : Hepatic, to56% (ramiprilat), Metabolism : Hepatic, to
ramiprilat Half-life : 2 to 4 hours, Excretion :ramiprilat Half-life : 2 to 4 hours, Excretion :
Renal (60%) and fecal (40%).Renal (60%) and fecal (40%).
Contrindication :Contrindication :
Renovascular disease, severe renal impairment,Renovascular disease, severe renal impairment,
volume-depleted patients, history of angioedemavolume-depleted patients, history of angioedema
while on an ACE inhibitor, pregnancy,while on an ACE inhibitor, pregnancy,
hypotension.hypotension.
20. RAMIPRILRAMIPRIL
Adverse effects:Adverse effects: low blood sugar, drylow blood sugar, dry
cough ,dizziness and light-headedness, mouthcough ,dizziness and light-headedness, mouth
dryness, tiredness and fatigue,nausea,dryness, tiredness and fatigue,nausea,
vomiting, diarrhea.vomiting, diarrhea.
Doses :Doses : Initial dose of 2.5 mg OD for 1Initial dose of 2.5 mg OD for 1
week, 5 mg OD for the next 3 weeks, and thenweek, 5 mg OD for the next 3 weeks, and then
increased as tolerated. Maintenance dose :10increased as tolerated. Maintenance dose :10
mg OD.mg OD.
21. RAMIPRILRAMIPRIL
• As angiotensin II is a vasoconstrictor and aAs angiotensin II is a vasoconstrictor and a
negative-feedback mediator for reninnegative-feedback mediator for renin
activity.activity.
• Lower concentrations result in a decreaseLower concentrations result in a decrease
in blood pressure and an increase in plasmain blood pressure and an increase in plasma
renin.renin.
• Ramiprilat may also act on kininase II, anRamiprilat may also act on kininase II, an
enzyme identical to ACE that degrades theenzyme identical to ACE that degrades the
vasodilator bradykinin.vasodilator bradykinin.