Corticosteroids are a class of steroid hormones that are produced in the adrenal cortex of vertebrates, as well as the synthetic analogues of these hormones
Corticosteroids are a class of steroid hormones that are produced in the adrenal cortex of vertebrates, as well as the synthetic analogues of these hormones
Diabetes mellitus is a clinical syndrome characterized by an increase in plasma blood glucose (hyperglycemia).
Diabetes has many causes but is most commonly due to type 1 or type 2 diabetes
Diabetes mellitus is a clinical syndrome characterized by an increase in plasma blood glucose (hyperglycemia).
Diabetes has many causes but is most commonly due to type 1 or type 2 diabetes
Diabetic drugs is a very important topic for pg entrance.....so all about it has been discussed in detail as required for pg entrance....do make use of it...
Sulphonamides and co trimoxazole- A BRIEF OUTLOOK!!!RxVichuZ
Hello friends...........................this is me Vishnu..........
I am back with a ppt on SULPHONAMIDES and COTRIMOXAZOLE.............................Hope the ppt helps....................all precise details have been given with due commitment and syllabus for pharm.D kept in mind...................
For further details, do contact me anytime!!!!
Take care...read well.....cheez!!!
@rxvichu!!
:):)
Diabetes mellitus (DM):- It is a metabolicdisorder characterized by hyperglycaemia, (fasting plasma glucose ≥ 126 mg/dl and/or ≥ 200 mg/dl 2 hours after 75 g oral glucose),glycosuria, hyperlipidaemia, negative nitrogen balance and sometimes ketonaemia.
Diabetes mellitus, one of the major public health problems worldwide, is a metabolic disorder of multiple etiologies distinguished by a failure of glucose homeostasis with disturbances of carbohydrate, fat and protein metabolism as a result of defects in insulin secretion and/or insulin action.
According to International Diabetes Federation (IDF) report, elevated blood glucose is the third uppermost risk factor for premature mortality, following high blood pressure and tobacco use globally
Cardiovascular diseases, neuropathy, nephropathy, and retinopathy are among the major risks that are associated with diabetes.
These chronic complications may lead to hardening and narrowing of arteries (atherosclerosis) that could advance to stroke, coronary heart disease, and other blood vessel diseases, nerve damage, kidney failure, and blindness with time
Two major types of diabetes mellitus are
1. Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
2. Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
There is β cell destruction in pancreatic islets; majority of cases are autoimmune (type 1A) antibodies that destroy β cells are detectable in blood, but some are idiopathic (type 1B)-no βcell antibody is found.
2.Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Type 2 diabetes mellitus (T2DM) is the most prevalent metabolic disease worldwide.
There is no loss or moderate reduction in β cell mass: insulin in circulation is low. normal or even high. no anti-β -cell antibody is demonstrable: has a high degree of genetic predisposition: generally has a late onset (past middle age). Over 90% cases of diabetes are type 2 DM
Abnormality in gluco-receptor of β cells so that they respond at higher glucose concentration or relative β cell deficiency. In either way. insulin secretion is impaired: may progress to β cells failure.
Reduced sensitivity of peripheral tissues to insulin: reduction in number of insulin receptors, “down regulation” of insulin receptors.
Insulin history:
Insulin was discovered in 1921 by Banting and Best who demonstrated the hypoglycaemic action of an extract of pancreas prepared after degeneration of the exocrine part due to ligation of pancreatic duct.
It was first obtained in pure crystalline form in 1926 and the chemical structure was fully worked out in 1956 by Sanger.
Insulin is a two chain polypeptide having 51 amino acids and MW about 6000.
The A-chain has 21 while B-chain has 30 amino acids.
Insulin is synthesized in the β cells of pancreatic islets as a single chain peptide Preproinsulin (110 AA) from whic
Diabetes mellitus (DM):- It is a metabolicdisorder characterized by hyperglycaemia, (fasting plasma glucose ≥ 126 mg/dl and/or ≥ 200 mg/dl 2 hours after 75 g oral glucose),glycosuria, hyperlipidaemia, negative nitrogen balance and sometimes ketonaemia.
Diabetes mellitus, one of the major public health problems worldwide, is a metabolic disorder of multiple etiologies distinguished by a failure of glucose homeostasis with disturbances of carbohydrate, fat and protein metabolism as a result of defects in insulin secretion and/or insulin action.
According to International Diabetes Federation (IDF) report, elevated blood glucose is the third uppermost risk factor for premature mortality, following high blood pressure and tobacco use globally
Cardiovascular diseases, neuropathy, nephropathy, and retinopathy are among the major risks that are associated with diabetes.These chronic complications may lead to hardening and narrowing of arteries (atherosclerosis) that could advance to stroke, coronary heart disease, and other blood vessel diseases, nerve damage, kidney failure, and blindness with time
Two major types of diabetes mellitus are
1. Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
2. Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
There is β cell destruction in pancreatic islets; majority of cases are autoimmune (type 1A) antibodies that destroy β cells are detectable in blood, but some are idiopathic (type 1B)-no βcell antibody is found.
2.Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Type 2 diabetes mellitus (T2DM) is the most prevalent metabolic disease worldwide.
There is no loss or moderate reduction in β cell mass: insulin in circulation is low. normal or even high. no anti-β -cell antibody is demonstrable: has a high degree of genetic predisposition: generally has a late onset (past middle age). Over 90% cases of diabetes are type 2 DM
Abnormality in gluco-receptor of β cells so that they respond at higher glucose concentration or relative β cell deficiency. In either way. insulin secretion is impaired: may progress to β cells failure.
Reduced sensitivity of peripheral tissues to insulin: reduction in number of insulin receptors, “down regulation” of insulin receptors.
Insulin history:
Insulin was discovered in 1921 by Banting and Best who demonstrated the hypoglycaemic action of an extract of pancreas prepared after degeneration of the exocrine part due to ligation of pancreatic duct.
It was first obtained in pure crystalline form in 1926 and the chemical structure was fully worked out in 1956 by Sanger.
Insulin is a two chain polypeptide having 51 amino acids and MW about 6000.
The A-chain has 21 while B-chain has 30 amino acids.
Insulin is synthesized in the β cells of pancreatic islets as a single chain peptide Preproinsulin (110 AA) from which
Diabetes mellitus (DM):- It is a metabolicdisorder characterized by hyperglycaemia, (fasting plasma glucose ≥ 126 mg/dl and/or ≥ 200 mg/dl 2 hours after 75 g oral glucose),glycosuria, hyperlipidaemia, negative nitrogen balance and sometimes ketonaemia.
Diabetes mellitus, one of the major public health problems worldwide, is a metabolic disorder of multiple etiologies distinguished by a failure of glucose homeostasis with disturbances of carbohydrate, fat and protein metabolism as a result of defects in insulin secretion and/or insulin action.
According to International Diabetes Federation (IDF) report, elevated blood glucose is the third uppermost risk factor for premature mortality, following high blood pressure and tobacco use globally
Cardiovascular diseases, neuropathy, nephropathy, and retinopathy are among the major risks that are associated with diabetes.
These chronic complications may lead to hardening and narrowing of arteries (atherosclerosis) that could advance to stroke, coronary heart disease, and other blood vessel diseases, nerve damage, kidney failure, and blindness with time
Two major types of diabetes mellitus are
1. Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
2. Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Insulin-dependent diabetes mellitus (IDDM) / juvenile onset diabetes mellitus
There is β cell destruction in pancreatic islets; majority of cases are autoimmune (type 1A) antibodies that destroy β cells are detectable in blood, but some are idiopathic (type 1B)-no βcell antibody is found.
2.Noninsulin-dependent diabetes mellitus (NIDDM) / maturity onset diabetes mellitus
Type 2 diabetes mellitus (T2DM) is the most prevalent metabolic disease worldwide.
There is no loss or moderate reduction in β cell mass: insulin in circulation is low. normal or even high. no anti-β -cell antibody is demonstrable: has a high degree of genetic predisposition: generally has a late onset (past middle age). Over 90% cases of diabetes are type 2 DM
Abnormality in gluco-receptor of β cells so that they respond at higher glucose concentration or relative β cell deficiency. In either way. insulin secretion is impaired: may progress to β cells failure.
Reduced sensitivity of peripheral tissues to insulin: reduction in number of insulin receptors, “down regulation” of insulin receptors.
Excess of hyperglycemic hormones (glucagon, ete. ) obesity: ; cause relative insulin deficiency the β cells Tag behind
Insulin history:
Insulin was discovered in 1921 by Banting and Best who demonstrated the hypoglycaemic action of an extract of pancreas prepared after degeneration of the exocrine part due to ligation of pancreatic duct.
It was first obtained in pure crystalline form in 1926 and the chemical structure was fully worked out in 1956 by Sanger.
Insulin is a two chain polypeptide having 51 amino acids and MW about 6000.
The A-chain has 21 while B-chain has 30 amino acids.
Announcement about my previous presentations - Thank youAreej Abu Hanieh
ANNOUNCEMENT Thank you for all of you, my followers who sent me messages with a lot of love and appreciations, I finally graduated after 6 years of studying in Birzeit University , In doctor of Pharmacy department I hope all of you benefited from all the presentations posted before Thank you a new PharmD GraduatedAreej ^^
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
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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.
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
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
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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.
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
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
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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
Evaluation of antidepressant activity of clitoris ternatea in animals
Drugs for diabetes - Pharmacology
1.
2. The pancreas is both:
◦ Exocrine gland that produces digestive enzymes
◦ Endocrine gland that produces peptide hormones: insulin,
glucagon, and somatostatin
The peptide hormones are secreted from cells
located in the islets of Langerhans
◦ β cells produce insulin
◦ α cells produce glucagon
◦ δ cells produce somatostatin
These hormones play an important role in
regulating the metabolic activities of the body
particularly the homeostasis of blood glucose
3. Hyperinsulinemia (due for example, to an
insulinoma) can cause severe hypoglycemia
The inadequate release of insulin is commonly
aggravated by an excess of glucagon
A relative or absolute lack of insulin, such as in
diabetes mellitus, can cause serious hyperglycemia
If diabetes is left untreated, retinopathy,
nephropathy, neuropathy, and cardiovascular
complications may result
Administration of insulin preparations or other
injectable or oral glucose lowering agents can
prevent morbidity and reduce mortality associated
with diabetes
4. Diabetes is heterogeneous group of syndromes
characterized by an elevation of blood glucose
caused by relative or absolute deficiency of insulin
There are four clinical classifications of diabetes:
◦ Type 1 diabetes (insulin dependent diabetes mellitus)
◦ Type 2 diabetes (non-insulin dependent diabetes mellitus)
◦ Gestational diabetes
◦ Diabetes due to other causes (genetic defects or
medications, etc)
5. Gestational diabetes is defined as carbohydrate
intolerance with onset or first recognition during
pregnancy
◦ It is important to maintain adequate glycemic control
during pregnancy
◦ Uncontrolled gestational diabetes can lead to fetal
macrosomia (abnormally large body), shoulder dystocia
(difficult delivery), and neonatal hypoglycemia
◦ Diet, exercise, and or insulin administration are effective
in this condition
◦ Glibenclamide (glyburide US)and metformin may be safe
alternatives to insulin therapy for gestational diabetes
6.
7. Most commonly affects individuals in puberty or
early adulthood
Some latent forms can occur later in life
8. Absolute deficiency of insulin caused by massive
β-cell necrosis
Loss of β-cell function is usually ascribed to
autoimmune- mediated processes against the β
cell
May be triggered by an invasion of viruses or the
action of chemical toxins
Due to β-cell destruction pancreas fails to respond
to glucose
9. Shows classic symptoms of insulin deficiency
(polydipsia, polyphagia, polyuria, and weight loss)
Require exogenous (injected) insulin to control
hyperglycemia and maintain blood glucose
concentrations as close to normal as possible
Treatment helps in avoiding the catabolic state that
results from Type II diabetes which is characterized
by hyperglycemia and life-threatening ketoacidosis
10. In a normal post-absorptive period, low basal
levels of circulating insulin are maintained through
constant β-cell secretion which suppresses
lipolysis, proteolysis, and glycogenolysis
A burst of insulin secretion occurs within 2
minutes after a meal, in response to transient
increases in circulating glucose and amino acids
This lasts for up to 15 minutes and is followed by
the postprandial secretion of insulin
11. Having non-functional β cells in T1DM can neither
maintain a basal secretion level of insulin nor
respond to variations in circulating fuels
The development and progression of neuropathy,
nephropathy, and retinopathy are directly related
to the extent of glycemic control (measured as
blood levels of glucose and/or HbA1c)
12. Most diabetic cases
Influenced by genetic factors, aging, obesity, and peripheral
insulin resistance, rather than autoimmune processes or
viruses
The metabolic alterations observed are milder than those
described for type 1
The long-term clinical consequences can be as devastating
The pancreas retains some β-cell function, but variable
insulin secretion is insufficient to maintain glucose
homeostasis
Frequently accompanied by the lack of sensitivity of target
organs to either endogenous or exogenous insulin
13. The pancreas retains some β-cell function, but variable
insulin secretion is insufficient to maintain glucose
homeostasis
The β-cell mass may become gradually reduced in type
2 diabetes
In contrast to patients with type 1, type 2 diabetes are
often obese
Frequently accompanied by the lack of sensitivity of
target organs to either endogenous or exogenous
insulin
14.
15. Treatment:
◦ The goal in treating T2DM is to maintain blood glucose
concentrations within normal limits and to prevent the
development of long-term complications of the disease
◦ Weight reduction, exercise, and dietary modification
decrease insulin resistance and correct the hyperglycemia
of type 2 diabetes in some patients
◦ Most patients are dependent on pharmacologic
intervention with oral glucose-lowering agents
◦ As the disease progresses, β-cell function declines and
insulin therapy is often required
16.
17. Insulin is a storage hormone:
◦ it promotes anabolism
◦ inhibits catabolism of carbohydrates, fatty acids and
protein
In the absence of insulin:
◦ most tissues cannot use glucose
◦ fats/proteins are broken down to provide energy
18. Mechanism of action :
Insulin binds to insulin receptors on the plasma
membrane and activates tyrosine kinase – primarily
in adipose tissue, liver and skeletal muscle
19. Liver :
Insulin increase the storage of glucose as
glycogen in the liver
◦ It inserts the GLUT-2 glucose transport molecule in
the cell membrane
It inhibits gluconeogenesis – thus significantly ↓
glucose output by the liver
It decreases the protein catabolism
20. Muscle :
Insulin stimulates glycogen synthesis and protein
synthesis
◦ Glucose transport into the cells is facilitated by GLUT-4
into the cell membrane
Insulin inhibits the protein catabolism
21. Adipose tissue :
Insulin facilitates the storage of triglyceride by:
◦ Activating plasma lipoprotein lipase
◦ Inhibiting intracellular lipolysis
It increases the glucose uptake by GLUT-4
insertion into the cell membrane
22. Insulin is a polypeptide hormone consisting of two
peptide chains connected by disulfide bonds
Synthesized as a precursor (proinsulin) that
undergoes proteolytic cleavage to form insulin and
C-peptide, both of which are secreted by the β
cells of the pancreas
Insulin undergoes significant hepatic extraction,
circulating plasma insulin levels may not accurately
reflect insulin production
Measurement of circulating C-peptide provides a
better index of insulin levels
23. Insulin secretion is regulated by blood glucose levels, certain
amino acids, other hormones, and autonomic mediators
Secretion is most commonly triggered by high blood glucose,
which is taken up by the glucose transporter into the β cells
of the pancreas
In the pancreas, glucose is phosphorylated by glucokinase,
which acts as a glucose sensor
The products of glucose metabolism enter the mitochondrial
respiratory chain and generate ATP
The rise in ATP levels causes a block of K+ channels, leading
to membrane depolarization and an influx of Ca2+
The increase in intracellular Ca2+ causes pulsatile insulin
exocytosis
25. Glucose given by injection has a weaker effect on
insulin secretion than oral glucose
When given orally, glucose stimulates production of
incretin hormones by the gut, which, in turn, stimulate
insulin secretion by the pancreas
26. Human insulin is produced by recombinant DNA
technology using E. coli or yeast altered genetically
to contain the human insulin gene
Modifications of the amino acid sequence of
human insulin have produced insulins with
different PK properties
◦ The 3 insulins lispro, aspart, and glulisine have a faster
onset and shorter duration of action than regular insulin,
because they do not aggregate or form complexes
◦ Insulins glargine and detemir are long-acting and show
prolonged flat levels following injection
27. Insulin is degraded in the GIT if taken orally
Insulin is administered by subcutaneous injection
In a hyperglycemic emergency, regular insulin is
injected IV
Continuous subcutaneous insulin infusion (insulin
pump) does not require multiple daily injections
28. Insulin preparations vary in their onset of activity
and in duration of activity due to differences in
their amino acids
Dose, site of injection, blood supply, temperature,
and physical activity can affect the duration of
action of the various preparations
Insulin is inactivated by insulin-degrading enzyme
(insulin protease) which is found mainly in the liver
and kidney
29. Symptoms of hypoglycemia in excessive
dose
◦ Long-term diabetic patients do not produce
adequate amounts of the counter-regulatory
hormones (glucagon, epinephrine, cortisol, and
growth hormone) which normally provide an
effective defense against hypoglycemia
Weight gain
Lipodystrophy
Allergic reactions
Local injection site reactions
Diabetics with renal insufficiency may
require adjustment of the insulin dose
30. Caution should be paid when making any change
in insulin treatment and dose
31. Rapid acting and short acting insulin
Intermediate acting insulin
Long acting insulin
Insulin combinations
34. Lispro, aspart and glulisine forms are classified as
rapid-acting insulins because of their rapid onset
and short duration of action
Rapid acting insulins offer more flexible treatment
regimens and may lower the risk of hypoglycemia
35. Regular insulin, insulin lispro, and insulin aspart
are pregnancy category B
Insulin glulisine is pregnancy category C
36. Peak levels of insulin lispro are seen at 30 to
90 minutes after injection, as compared with
50 to 120 minutes for regular insulin
Insulin lispro also has a shorter duration of
activity than regular insulin
37. A short-acting, soluble, crystalline zinc insulin
Given subcutaneously
Given IV in emergencies
Rapidly lowers blood glucose
38. Insulin lispro is more rapidly absorbed after
subcutaneous injection than regular insulin
Insulin aspart and insulin glulisine have
pharmacokinetic and pharmacodynamic properties
similar to those of insulin lispro
Administered to mimic the prandial (mealtime)
release of insulin
Usually not used alone but with a longer-acting
insulin to ensure proper glucose control
Administered SC
39. Insulin lispro is usually administered 15 minutes
prior to a meal or immediately following a meal
Insulin glulisine can be taken either 15 minutes
before a meal or within 20 minutes after starting a
meal
Insulin aspart should be administered just prior to
the meal or up to 15 minutes following the meal
40. All of the rapid-acting formulations are suitable for
IV administration, although regular insulin is most
commonly used when the IV route is needed
Insulin lispro, insulin aspart, and insulin glulisine
may also be used in external insulin pumps
41. Neutral protamine Hagedorn (NPH) insulin suspension
of crystalline zinc insulin combined at neutral pH with
the positively charged polypeptide protamine
Insulin NPH is also called insulin isophane (Humulin N
NPH®)
Its duration of action is intermediate because of the
delayed absorption from its conjugation with
protamine forming a less-soluble complex
NPH insulin should only be given subcutaneously
(never IV)
42. Useful in treating all forms of diabetes except diabetic
ketoacidosis and emergency hyperglycemia
Used for basal control and is usually given along with
rapid- or short-acting insulin for mealtime control
A similar compound called neutral protamine lispro
(NPL) insulin has been prepared and is used only in
combination with insulin lispro (Humalog Mix ®)
43. Insulin glargine (Lantus®)
◦ It is slower in onset than NPH insulin and has a flat,
prolonged hypoglycemic effect with no peak
◦ Given SC
Insulin detemir
◦ Has a fatty-acid side chain which enhances association
to albumin
◦ Slow dissociation from albumin results in long-acting
properties
Insulin detemir and insulin glargine should not be
mixed in the same syringe with other insulins
44. Various premixed combinations of human insulins
are available
◦ 70% NPH insulin plus 30% regular insulin (Humulin
70/30®)
◦ 50% NPH insulin plus 50% regular insulin
◦ 75% NPL insulin plus 25% insulin lispro (Humalog Mix®)
45.
46. Standard treatment involves injection of insulin
twice daily
Intensive treatment seeks to normalize blood
glucose through more frequent injections of insulin
(three or more times daily in response to
monitoring blood glucose levels)
47. Normal mean blood glucose ≤ 115 mg/dL with
HbA1c content ≤ 5.7
For patients with diabetes:
◦ Target mean blood glucose levels ≤ 154 mg/dL
◦ HbA1c ≤ 7%
This is more likely to be achieved with intensive
treatment
48. The frequency of hypoglycemic episodes, coma, and
seizures is higher with intensive treatment
Patients on intensive therapy show a significant
reduction in long-term complications of diabetes as
retinopathy, nephropathy, and neuropathy
Intensive therapy has not been shown to significantly
reduce the macrovascular complications of diabetes
Intensive therapy is not recommended for patients with
longstanding diabetes, significant microvascular
complications, advanced age, and hypoglycemic
unawareness
49.
50. Used as an adjunct to mealtime insulin therapy in
patients with type 1 and type 2 diabetes
Acts as amylinomimetic, delaying gastric emptying,
decreasing postprandial glucagon secretion, and
improving satiety
Administered SC and should be injected immediately
prior to meals
When pramlintide is initiated, the dose of rapid- or
short-acting insulin should be decreased by 50% prior
to meals to avoid a risk of severe hypoglycemia
Pramlintide may not be mixed in the same syringe with
any insulin preparation
51. Adverse effects
◦ Nausea
◦ Anorexia
◦ Vomiting
Pramlintide should not be given to patients with
diabetic gastroparesis, cresol hypersensitivity, or
hypoglycemic unawareness
52. Oral glucose results in a higher secretion of
insulin than occurs when an IV glucose “incretin
effect”
Incretin effect is markedly reduced in type 2
diabetes
The incretin effect occurs because the gut
releases incretin hormones, notably GLP-1 and
glucose dependent insulinotropic polypeptide
after a meal
Incretin hormones are responsible for 60%-70%
of postprandial insulin secretion
53. Exenatide (Bydureon®, Byetta®)
Liraglutide (Victoza®)
Injectable incretin mimetics are used for the
treatment of patients with type 2 diabetes
These agents may be used as adjunct therapy in
patients who have failed to achieve adequate
glycemic control on a sulfonylurea, metformin, a
glitazone, or a combination of them
54. Mechanism of action
The incretin mimetics are analogs of GLP-1 that
act as GLP-1 receptor agonists
Improve glucose- dependent insulin secretion
Slow gastric emptying time, decrease food
intake
Decrease postprandial glucagon secretion
Promote β-cell proliferation
Weight gain and postprandial hyperglycemia are
reduced
HbA1c levels decline
55. Administered subcutaneously
Liraglutide is highly protein bound and has a
long half life allowing for once-daily dosing
Exenatide should be injected twice daily within
60 minutes prior to morning and evening meals
Exenatide should be avoided in patients with
severe renal impairment
56. Adverse effects
Nausea, vomiting, diarrhea, constipation
Patients may form antibodies to these agents, in
most cases the antibodies do not result in
adverse effects
Exenatide and liraglutide have been associated
with pancreatitis
57. Useful in the treatment of patients who have type 2
diabetes and cannot be managed by diet alone
Patients who have developed diabetes after age 40 and
have had diabetes less than 5 years are most likely to
respond well to oral glucose-lowering agents
Patients with long-standing disease may require
combination of glucose-lowering drugs/ insulin
Insulin is added because of the progressive decline in β
cells that occurs due to the disease or aging
Oral glucose-lowering agents should not be given to
patients with type 1 diabetes
59. Insulin secretagogues: Promote insulin release
from the β cells of the pancreas
◦ Sulfonylureas
Glibenclamide (Glucocare®, Gluconil®, Declamide®,
Daonil®)
Glimepiride (Amaryl®)
Glipizide(Gluco-Rite®)
◦ Glinides
Repaglinide (Novonorm®)
Nateglinide
60. Promote insulin release from the β cells of the
pancreas
The primary drugs used today are the second-
generation drugs glibenclamide, glipizide, and
glimepiride
Mechanism of action:
1) Stimulation of insulin release from the β cells of the
pancreas by blocking the ATP-sensitive K+ channels,
resulting in depolarization and Ca2+ influx
2) Reduction in hepatic glucose production
3) Increase in peripheral insulin sensitivity
61. Adverse eff ects:
Weight gain
Hyperinsulinemia
Hypoglycemia
Should be used with caution in patients with hepatic or
renal insufficiency, because drug accumulation may cause
hypoglycemia
Renal impairment is a particular problem in the case of
agents metabolized to active compounds like glibenclamide
Glibenclamide has minimal transfer across the placenta and
may be a safe alternative to insulin therapy in pregnancy
62.
63. Repaglinide
Nateglinide
Mechanism of action:
Like the sulfonylureas, their action is dependent on
functioning pancreatic β cells
They bind to ATP-sensitive potassium channels
leading to release of insulin
Categorized as postprandial glucose regulators; they
are particularly effective in early release of insulin
after a meal
64. The glinides have a rapid onset and a short duration
of action
Combined therapy of these agents with metformin
or the glitazones is better than monotherapy in
improving glycemic control
Glinides should not be used in combination with
sulfonylureas (overlapping MOA)
65. Well absorbed orally after being taken 1 to 30
minutes before meals
Metabolized to inactive products by CYP3A4
Excreted through the bile
66. Drugs that inhibit CYP3A4 (ketoconazole, itraconazole,
fluconazole, erythromycin, and clarithromycin) may
enhance the glucose-lowering effect of repaglinide
Drugs that increase levels of CYP3A4 (barbiturates,
carbamazepine, and rifampin) may decrease their
glucose lowering effect
Repaglinide concurrent use with gemfibrozil is
contraindicated due to reports of severe hypoglycemia
67. Adverse effects
Hypoglycemia
(lower incidence than sulfonylureas)
Weight gain
(less than with sulfonylureas)
Must be used with caution in patients with hepatic
impairment
68. Insulin sensitizers improve insulin action
Lower blood sugar by improving target-cell
response to insulin without increasing pancreatic
insulin secretion
Biguanides
Thiazolidinediones
69. Metformin (Glucomet®, Glucophage®, Diamet®)
Increases glucose uptake and use by target tissues,
decreasing insulin resistance
Does not promote insulin secretion
(hyperinsulinemia is not a problem)
The risk of hypoglycemia is less than with
sulfonylureas
70. Mechanism of action:
Reduces hepatic glucose output by inhibiting
hepatic gluconeogenesis
Slows intestinal absorption of sugars and improves
peripheral glucose uptake and utilization
Reduce hyperlipidemia
(LDL and VLDL cholesterol concentrations fall, and
HDL cholesterol rises)
The patient commonly loses weight because of loss
of appetite
71. The ADA recommends metformin as the drug of
choice for newly diagnosed type 2 diabetics
Metformin may be used alone or in combination
with one of the other agents as well as with insulin
Hpoglycemia may occur when metformin is taken
in combination with insulin
72. Metformin is well absorbed orally
Not bound to serum proteins
Not metabolized
Excreted via the urine
73. Adverse effects:
GI adverse effects
Metformin is contraindicated in diabetic patients
with renal and/or hepatic disease and in those with
diabetic ketoacidosis
Should be discontinued in cases of acute MI,
exacerbation of CHF, and severe infection
Rarely fatal lactic acidosis has occurred
Long-term use may interfere with vitamin B12
absorption
74. Metformin is effective in the treatment of
polycystic ovary disease
Its ability to lower insulin resistance in these
women can result in ovulation and possibly
pregnancy
75. Insulin sensitizers
Insulin is required for their action
Do not promote insulin release
Hyperinsulinemia is not a risk
Troglitazone (withdrawn after deaths from
hepatotoxicity)
Pioglitazone (Actos®)
Rosiglitazone (Avandia®)
76. Mechanism of action
The exact mechanism by which the TZDs lower insulin
resistance is unknown
TZDs target the PPARγ
Ligands for PPARγ regulate adipocyte production and
secretion of fatty acids and glucose metabolism, resulting in
increased insulin sensitivity in adipose tissue, liver, and
skeletal muscle
Hyperglycemia, hyperinsulinemia, hypertriglyceridemia, and
elevated HbA1c levels are improved
LDL levels are not affected by pioglitazone
LDL levels have increased with rosiglitazone
HDL levels increase with both drugs
77. Pioglitazone and rosiglitazone can be used as
monotherapy or in combination with other glucose-
lowering agents or insulin
The dose of insulin required for adequate glucose
control in these circumstances may have to be
lowered
ADA recommends pioglitazone as a tier 2 alternative
for patients who fail or have contraindications to
metformin therapy
Rosiglitazone is not recommended due to concerns
regarding cardiac adverse effects
78. Extensively bound to serum albumin
Both undergo extensive metabolism by CYP450
Some metabolites of pioglitazone have activity
Elimination of pioglitazone and its metabolites is
mainly in the bile
The metabolites of rosiglitazone are primarily
excreted in the urine
79. Adverse effects
Very few cases of liver toxicity with rosiglitazone or
pioglitazone
Because of deaths due to hepatotoxicity from troglitazone it is
recommended that liver enzyme are periodically checked
Weight increase can occur
Osteopenia and increased fracture risk
Increased risk of myocardial infarction and death from
cardiovascular causes with rosiglitazone
Headache
Anemia
May cause resumption of ovulation in some women who have
been anovulatory
Premenopausal women should be counseled about the need
for adequate contraception while taking TZDs
80. Acarbose (Acrose®, Prandase®)
Miglitol
Oral drugs for the treatment of patients with type 2
diabetes
81. Mechanism of action
Taken at the beginning of meals
Act by delaying the digestion of carbohydrates
lowering postprandial glucose levels
Reversible inhibitors of membrane-bound α-
glucosidase in the intestine
This enzyme is responsible for hydrolysis of
oligosaccharides to glucose and other sugars
Acarbose also inhibits α-amylase, interfering with the
breakdown of starch to oligosaccharides
The postprandial rise of blood glucose is blunted
82. Adverse effects
Flatulence, diarrhea, and abdominal cramping
Patients with IBD, colonic ulceration, or intestinal
obstruction should not use these drugs
No hypoglycemia if used alone
Hypoglycemic patient should be treated with
glucose rather than sucrose, because sucrase is
also inhibited by these drugs
83. Sitagliptin (Januvia®)
Saxagliptin (Onglyza®)
Vildagliptin (Galvus®)
Linagliptin (Tradjenta®)
Orally active DPP-4 inhibitors used for the
treatment of patients with type 2 diabetes
Combinations with metformin are available
◦ Sitagliptin + metformin (Januet®)
◦ Vildagliptin + metformin (Eucreas®)
84. Mechanism of action
Inhibit the enzyme DPP-4, which is responsible
for the inactivation of incretin hormones such as
GLP-1
Prolonging the activity of incretin hormones
results in increased insulin release in response
to meals and reduction in glucagon secretion
85. DPP-4 inhibitors may be used as monotherapy or
in combination with a sulfonylurea, metformin,
glitazones, or insulin
Sitagliptin and saxagliptin are excreted in urine
◦ Dosage adjustments for both DPP-4 inhibitors are
recommended for patients with renal dysfunction
Saxagliptin is metabolized by CYP450
◦ Strong inhibitors of CYP3A4/5, such as nelfinavir,
atazanavir, ketoconazole, and clarithromycin, may
increase levels of saxagliptin
88. Dapagliflozin (Forxiga®)
Canagliflozin
Mechanism of action:
SGLT2 is responsible for reabsorbing filtered
glucose in the tubular lumen of the kidney
By inhibiting SGLT2, these agents decrease
reabsorption of glucose, increase urinary glucose
excretion, and lower blood glucose
Decreases reabsorption of sodium and causes
osmotic diuresis reducing systolic blood pressure
89. Given once daily in the morning
Canagliflozin should be taken before the first meal
of the day
Metabolized by glucuronidation to inactive
metabolites
Should be avoided in patients with renal dysfunction
90. Adverse effects:
Female genital mycotic infections urinary tract
infections, and urinary frequency
Hypotension
91. Bromocriptine and colesevelam produce modest
reductions in HbA1c
The mechanism of action of glucose lowering is
unknown
Indicated for type 2 diabetes
Modest efficacy, adverse effects limit their use in
clinical practice
92.
93.
94. Glucagon :
Uses
First aid in cases of severe hypoglycemia when the
victim is unconscious or for other reasons cannot
take glucose orally
Treatment of overdose with beta blockers
It has positive inotropic action and chronotropic
action on the heart
95. A nondiuretic thiazide that promptly increases blood
glucose levels by direct inhibition of insulin secretion
Activates potassium channels
Useful in cases of insulinoma or leucine-sensitive
hypoglycemia
Diazoxide may cause sodium retention, GI irritation,
and changes in circulating white blood cells