Bipolar disorder is a mood disorder with alternate episodes of mania and depression. the symptoms includes hyperexcitability, mood changes, psychological and behavioural affect, weight gain or weight loss, sleep disturbances, fatigue etc. Mania is a state with periods of great excitement or euphoria, delusions, and over activity. The presentation includes points about mania and treatment strategies of mania
antipsychotics history, managment of psychosis,side effect of antipsychotics, mechanism of antipsychotics, atypical antipsychotics,2nd generation antipsychotics.
Bipolar disorder is a mood disorder with alternate episodes of mania and depression. the symptoms includes hyperexcitability, mood changes, psychological and behavioural affect, weight gain or weight loss, sleep disturbances, fatigue etc. Mania is a state with periods of great excitement or euphoria, delusions, and over activity. The presentation includes points about mania and treatment strategies of mania
antipsychotics history, managment of psychosis,side effect of antipsychotics, mechanism of antipsychotics, atypical antipsychotics,2nd generation antipsychotics.
A compiled Power point presentation on "Antipsychotic drugs" suitable for Undergraduate level medical students and also PG students in the subject of Pharmacology.
Anxiety is an emotional state, unpleasant in nature, associated with uneasiness, discomfort and concern or fear about some defined or undefined future threat. It has several types. the presentation includes pharmacologic approach of anxiety disorder.
A compiled Power point presentation on "Antipsychotic drugs" suitable for Undergraduate level medical students and also PG students in the subject of Pharmacology.
Anxiety is an emotional state, unpleasant in nature, associated with uneasiness, discomfort and concern or fear about some defined or undefined future threat. It has several types. the presentation includes pharmacologic approach of anxiety disorder.
Psychopharmacologic Advances of the 1950s, Part 2: Imipramine, iproniazid and...Kevin Nasky
Grand rounds presentation reviewing the history of the development of the first antidepressants (imipramine and iproniazid) and the blockbuster anxiety medication, meprobamate (Miltown). Part two of a two-part presentation.
Antipsychotics, antipsychotic drugs, major tranquilizers, tranquilizersMuthu Venkatachalam
introduction, indication, contraindications and side effects of antipsychotic drugs are explained.
Antipsychotic drugs used in the treatment of schizophrenia including psychosis is described.
Chlorpromazine, Clozapine
Psychotherapeutic agents are a key component in the management of psychiatric disorders. Knowledge in this aspect of therapy goes a long way to help the health professional and the patient as well. However, care must be taken in administering these agents to pregnant women, and if possible stop, or consult your psychiatrist before taking these agents.
It may contain a brief intoduction of disease, etiology, types of parkinson disease, clinical findings, dignosis, pathophysiology, treatment, drug classification and their mechanisms of actions.
A disorder of the central nervous system that affects movement, often including tremors.
Nerve cell damage in the brain causes dopamine levels to drop, leading to the symptoms of Parkinson's.
Parkinson's often starts with a tremor in one hand. Other symptoms are slow movement, stiffness and loss of balance.
Treatment consists of medications to increase dopamine.
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.
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
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
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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.
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
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.
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.
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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.
2. History
Introduction
Different hypothesis for schizophrenia
Classification
Mechanism of action
Uses
Adverse effects
Recent advances
3. 1931 Sen and Bose – publish therapeutic effect of
reserpine in Hypertension and Insanity
Hans Laborit – note the antipsychotic effect of
chlorpromazine, which was being tried as
preanesthetic medication
1950 - Jean Delay and Piere Deniker conducted
trial
1960-1970: identification of D2 blockade as the
key mechanism, development of these first-
generation of antipsychotic agents
Janssen introduced Haloperidol & Pimozide
4. Neuroleptics/ Major tranquillisers/ Dopamine
antagonist
Psychoses and Neuroses
Psychotic disorders – Schizophrenia, severe forms of
depression and mania
5.
6. Positive symptoms: the presence of inappropriate
behaviors
Delusions
Hallucinations
Disorganized talking
Movements
Negative symptoms: the absence of appropriate behaviors
Flat affect
Anhedonia
Catatonia
7. Excessive dopaminergic activity:
• Drugs which increase dopamine activity
• Postmortem – receptor density high in nucleus
accumbens, caudate, putamen
• Imaging studies – amphetamine – high
dopamine in striated areas
Diminished dopaminergic activity
• Cortical/hippocampal – cognitive and negative
• Postmortem – cortical, limbic, nigral, striatal
8. 5HT2A and 5HT2C – hallucination
5HT2A- depolarization of glutamate receptors
stabilization of NMDA
5HT 2C- inhibition of cortical dopamine release
5HT1C- anxiolytic effect, exert procognitive effects in
schizophrenia
9. Hypofunctioning of NMDA receptors located on
GABAergic interneurons, leading to diminished
inhibitory influence on neuron function
GABA ergic activity induce disinhibiton of
downstream glutamate activity
hyperstimulation of cortical neuron through non
NMDA receptor
NMDA requires glycine
In schizophrenia, glycine site is not fully occupied
11. Phenothiazines
With aliphatic
tertiary amine side
chain
Chlorpromazine
With piperadine
moiety in side chain
Thioridazine
With piperazine
moiety in side chain
Trifluperazine,
fluphenazine
13. Typical or first generation
antipsychotics (FGA)
Atypical antipsychotics or
second generation
antipsychotics (SGA)
D2 receptor blockade 5HT and Dopamine receptor
block
Less effective against negative
symptoms
More effective against
negative symptoms
Not effective in refractory
cases
Effective in refractory cases
More side effects (EPS) Less side effects profile
Clozapine
Olanzapine
Quetiapine
Zotepine
Risperidone
Ziprasidone
Paliperidone
Aripiprazole
Sertindole
14. Increased
dopamine
Rise in Number
of brain D2
receptors
Receptor
supersensitivity
Excess
availability of
dopamine due
to over
production
Reduced
destruction
through
enzyme
deficiency
SCHIZOPHRENIA
15. Typical/ FGA – D2 antagonist
Initially – increased synthesis of DA – later
decreases
HVA and DOPAC level in blood & urine
Molindone, loxapine, sulpiride and amisulpiride
In between typical and atypical antipsychotics
16.
17. Most of the antipsychotics are given orally but
incompletely absorbed.
Significant first-pass metabolism.
Bioavailability is 25-65%.
Most are highly lipid soluble.
Most are highly protein bound (92-98%).
High volumes of distribution (>20 L/Kg).
18. Plasma half life
• Quetiapine – 7h
• Clozapine – 12h
• Fluphenazine- 20h (depot – 14.3days)
• Haloperidol – 24-48h (depot – 21days)
• Olanzapine – 33h
Depot preparation – 2-4 weeks
Measurable plasma concentration with I.M route
is seen within 15-30min
19. Most antipsychotics are almost completely
metabolized- phase 1 and subsequent phase 2
Exceptions are asenapine(phase 2),
ziprasidone(aldehyde oxidase system) and
paliperidone(oxidized metabolite)
Most metabolites- inactive.
Chlorpromazine – 160 metabolites, 70 have been
identified.
21. • Drug induced psychoses –LSD , amphetamine
• Schizo-affective disorder – schizo part – antipsychotic,
affective part – anti depressant or lithium
Neuro psychiatric indication
• Tourette’s syndrome – haloperidol or pimozide
• Huntington’s disease – haloperidol or chlorpromazine
Non psychiatric indication:
• Antiemetic – D2 block at CTZ,GIT – prochlorperazine,
domperidone
• Preanaesthetic medication - promethazine
• Intractable hiccups – parenteral haloperidol, CPZ
22. CNS side effects:
• Behavioral effects – sedation more with
phenothiazines, thioxanthenes, olanzapine
Less with butyrophenones, pimozide
• Tolerance and dependence – tolerance
develops to sedation and autonomic side
effects
31. Raloxifene Exhibit agonistic and protective
action on the brain by modulating the
monoaminergic neurotransmission of dopamine,
serotonin and GABA
Addition of Raloxifene (60 mg/day) to regular
antipsychotic treatment ↓ negative, positive &
general psychopathological symptoms in
comparison with women receiving antipsychotic
medication alone (Usall et al., 2011)
32. *Short term Rapid membrane effects by altering
functional activity in the dopaminergic synapse (Di
Paolo, 1994)
*Long term Modifies synthesis in dopamine receptors
(Di Paolo, 1994)
*Estrogen alters serotonergic system (Moses et al., 2000)
*Estrogen promotes neuronal regeneration & blocks
mechanisms of neuronal death (DonCarlos et al., 2009)
33. Glutathione is a major antioxidant that protects
cells against oxidative stress (Meister and
Anderson, 1983)
Glutathione potentiates NMDA receptors (Choi
and Lipton, 2000)
34. * Targeted gene therapy Dysbindin, Neurogelin 1,
COMT, DISC1
* Enhancement of BDNF
* Targets GSK 3, PKC , GABAA receptor
* PDE inhibitors (particularly at PDE1B)
*Cannabinoid receptor antagonist
*Currently glycine transport inhibitors are in trials
*Preliminary study with LY2140023 (agonist at
glutamate receptor) is also been tried
