1) Ischemic heart disease results from an imbalance between the heart's demand for oxygenated blood and the supply delivered by the coronary arteries, usually due to atherosclerotic plaque buildup.
2) It manifests as stable angina, unstable angina, myocardial infarction, or sudden cardiac death.
3) Myocardial infarction occurs when a blockage in a coronary artery results in prolonged ischemia and cell death in the heart muscle.
Cardiomyopathy is a group of disease that affect the heart muscle. Early on there may be few or no symptoms. As the disease worsens, shortness of breath, feeling tired, and swelling of legs may occur, due to the onset of heart failure. An irregular heart beat and fainting may occur.
Cardiomyopathy is a disease of the heart muscles that makes it harder for your heart to pump blood to the rest of your body. Cardiomyopathy can lead to heart failure.
According to the structural and functional abnormalities of the heart muscle
Dilated cardiomyopathy
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
Arrhythmogenic right ventricular cardiomyopathy
Unclassified cardiomyopathy
Cardiomyopathy is a group of disease that affect the heart muscle. Early on there may be few or no symptoms. As the disease worsens, shortness of breath, feeling tired, and swelling of legs may occur, due to the onset of heart failure. An irregular heart beat and fainting may occur.
Cardiomyopathy is a disease of the heart muscles that makes it harder for your heart to pump blood to the rest of your body. Cardiomyopathy can lead to heart failure.
According to the structural and functional abnormalities of the heart muscle
Dilated cardiomyopathy
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
Arrhythmogenic right ventricular cardiomyopathy
Unclassified cardiomyopathy
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.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
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Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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
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.
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
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
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
2. ISCHEMIC HEART DISEASES ( IHD )
Resulting from myocardial ischemia [ imbalance
between supply (perfusion), and demand of heart
for oxygenated blood]
In 90% of cases, the cause is reduction in coronary
blood flow due to atherosclerotic coronary arterial
obstruction.
Thus, IHD is often termed coronary artery disease
(CAD) or coronary heart disease (CHD).
3. IHD divided into:-
o Angina pectoris: ( stable, Prinzmetal , unstable ):
ischemia is less severe and does not cause death
of cardiac muscle.
o Myocardial infarction (MI) : duration and severity of
ischemia is sufficient to cause death of heart muscle.
o Chronic IHD with heart failure.
o Sudden cardiac death.
Acute myocardial infarction, unstable angina,
and sudden cardiac death are referred to
acute coronary syndrome.
4. ANGINA PECTORIS:
Three patterns :
( 1 ) Stable ( typical ) angina:
most common form.
caused by chronic stenosing coronary atherosclerosis.
Occur whenever there is increased heart demand
(by physical activity, or emotional excitement).
relieved by rest or nitroglycerin (strong vasodilator).
5. ( 2 ) Prinzmetal ( variant ) angina:
uncommon pattern.
occurs at rest and is due to coronary artery spasm.
there is elevated ST segment on electrocardiogram
(ECG) indicative of transmural ischemia.
anginal attacks are unrelated to physical activity,
but responds to vasodilators such as nitroglycerin.
6. ( 3 ) Unstable ( crescendo ) angina:
precipitated with less effort, often occurs at rest,
and tends to be of more prolonged duration.
induced by disruption of an atherosclerotic plaque
with superimposed partial thrombosis and possibly
embolization or vasospasm (or both).
is often the prodrome of subsequent acute MI.
Thus sometimes referred to preinfarction angina.
7. MYOCARDIAL INFARCTION (MI):
Is the death of cardiac muscle resulting from
ischemia.
Transmural versus Subendocardial Infarction:
Transmural:
o Most MI are transmural.
o ischemic necrosis involves full or nearly full
thickness of ventricular wall in distribution of
a single coronary artery.
o usually associated with coronary atherosclerosis,
acute plaque change, and superimposed thrombosis.
8. Subendocardial (non-transmural) infarct:
o limited to inner one third or one half of
ventricular wall.
o occur as a result of plaque disruption followed by
coronary thrombus that becomes lysed before
myocardial necrosis extends across the major
thickness of the wall.
o can also result from prolonged and severe reduction
in systemic blood pressure (as in shock)
superimposed on chronic, otherwise noncritical,
coronary stenoses.
9. Incidence and Risk Factors:
MI may occur at any age.
Frequency rises with increasing age.
Predispositions to atherosclerosis are :
hypertension, cigarette smoking, diabetes mellitus,
and hypercholesterolemia
Blacks and whites are equally affected.
Men are at greater risk of MI than women.
The decrease of estrogen following menopause
can permit rapid development of CAD.
10. Pathogenesis:
Coronary arterial occlusion: sequence of events:-
o disruption in atheromatous plaque, manifest as
intraplaque hemorrhage, erosion or ulceration, or
rupture or fissuring.
o Platelets, which exposed to subendothelial collagen
and necrotic plaque contents, undergo adhesion,
aggregation, activation, and release of potent
aggregators ( thromboxane A2, serotonin, and
platelet factors 3 and 4).
o Vasospasm is stimulated by platelet aggregation.
o Frequently within minutes, the thrombus evolves to
completely occlude the lumen of coronary vessel.
11. In 10% of cases, transmural acute MI is not
associated with atherosclerotic plaque thrombosis.
other mechanisms may be involved:
• Vasospasm: isolated, intense, perhaps in association
with platelet aggregation (cocaine abuse).
• Emboli: from:- left atrium in atrial fibrillation;
vegetative endocarditis; paradoxical emboli from
right side of heart or peripheral veins .
• Unexplained: caused by coronary vasculitis,
hemoglobinopathies, amyloid deposition in vascular
walls.
12. Morphology:
Time Gross Features Light Microscope Electron Microscope
Reversible Injury
0–½ hr None None
Relaxation of myofibrils; glycogen
loss; mitochondrial swelling
Irreversible Injury
½–4 hr None
Usually none; variable waviness
of fibers at border
Sarcolemmal disruption;
mitochondrial amorphous
densities
4–12 hr Occasionally dark mottling
Beginning coagulation necrosis;
edema; hemorrhage
12–24 hr Dark mottling
Ongoing coagulation necrosis;
pyknosis of nuclei; myocyte
hypereosinophilia; marginal
contraction band necrosis;
beginning neutrophilic infiltrate
1–3 days
Mottling with yellow-tan infarct
center
Coagulation necrosis, with loss of
nuclei and striations; interstitial
infiltrate of neutrophils
3–7 days
Hyperemic border; central
yellow-tan softening
Beginning disintegration of dead
myofibers, early phagocytosis of
dead cells by macrophages at
infarct border
7–10 days
Maximally yellow-tan and soft,
with depressed red-tan margins
Well-developed phagocytosis of
dead cells; early formation of
fibrovascular granulation tissue at
margins
10–14 days
Red-gray depressed infarct
borders
Well-established granulation
tissue with new blood vessels and
collagen deposition
2–8 wk
Gray-white scar, progressive
from border toward core of infarct
Increased collagen deposition,
with decreased cellularity
>2 mo Scarring complete Dense collagenous scar
13.
14.
15.
16.
17.
18. Healed myocardial infarct. The necrotic fibers have been replaced by dense
collagenous scar (pink areas filling the right lower quadrant of the image).
This healed area will have decreased contractility compared to the adjacent
preserved myocardium.
19. Clinical Features:
MI is diagnosed by typical symptoms, biochemical
evidence, and ECG pattern.
Patients have rapid weak pulse and sweating
profusely (diaphoretic).
Dyspnea due to impaired contractility of ischemic
myocardium and the resultant pulmonary congestion
and edema.
In 10% to 15% of MI patients:
asymptomatic and discovered only later by ECG
changes(new Q waves).
Such "silent" MIs are common in patients with
diabetes mellitus and in elderly patients.
20. Lab. evaluation:
Based on measuring blood levels of intracellular
macromolecules that leak out of injured myocardial
cells.
These include myoglobin, cardiac troponins T and I
(TnT, TnI), creatine kinase (CK), and lactate
dehydrogenase.
TnI and TnT : are not normally detectable in
circulation, after acute MI levels of both rise at
2 to 4 hours and peak at 48 hours ,remain elevated
for 7 to 10 days after acute event.
21. Creatine kinase:
o Enzyme that is highly concentrated in brain,
myocardium, and skeletal muscle.
o Composed of two dimers "M" and "B “.
o Isoenzyme CK-MM is derived from skeletal muscle
and heart ; CK-BB from brain, lung, and many other
tissues ; and CK-MB principally from myocardium.
o Total CK activity is sensitive but not specific.
o CK-MB rise within 2 to 4 hours of onset of MI, peaks
at 24 hours, and returns to normal within 72 hours.
Absence of change in levels of CK and CK-MB during
first 2 days of chest pain , and of troponin in days
following essentially excludes diagnosis of MI.
22. C-reactive protein (CRP) : predict the risk of (M.I)
in patients with angina, and the risk of new infarcts
in patients who recover from infarcts.
Other diagnostic modalities :
Echocardiography (for visualization of abnormalities
of regional wall motion).
Radioisotope studies such as radionuclide
angiography (for chamber configuration).
Perfusion scintigraphy (for regional perfusion).
Magnetic resonance imaging- M.R.I (for structural
characterization).
23. Consequences and Complications of MI:
Half of deaths occur within 1 hour of onset.
Factors associated with poor prognosis include
advanced age, female gender, diabetes mellitus ,
and previous MI.
Three-fourths of patients have one or more
complications which include:
o Left ventricular failure.
o Severe pump failure (cardiogenic shock).
o Arrhythmias :- sinus bradycardia, heart block ,
sinus tachycardia, ventricular tachycardia, and
ventricular fibrillation.
24. o Myocardial rupture:-
(1) rupture of ventricular free wall.
(2) rupture of ventricular septum.
(3) papillary muscle rupture.
o Pericarditis.
o Mural thrombus.
o Ventricular aneurysm.
25. CHRONIC ISCHEMIC HEART DISEASE :
Describe cardiac findings in patients, often elderly,
who develop progressive heart failure as
a consequence of ischemic myocardial damage.
Morphology:
o Hearts are usually enlarged and heavy secondary
to left ventricular hypertrophy and dilation.
o Moderate to severe stenosing atherosclerosis of
coronary arteries .
o Microscopic findings: myocardial hypertrophy,
diffuse subendocardial vacuolization, and
scars of previously healed infarcts.
26. SUDDEN CARDIAC DEATH:
Unexpected death from cardiac causes.
A complication and often the first clinical
manifestation of IHD.
With decreasing age of victims, the following
non- atherosclerotic causes become probable:
o Congenital structural or coronary arterial
abnormalities.
o Aortic valve stenosis.
o Mitral valve prolapse.
o Myocarditis.
o Dilated or hypertrophic cardiomyopathy.
o Pulmonary hypertension.
o Hereditary or acquired abnormalities of cardiac
conduction system.