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TREATMENT RESISTANT DEPRESSION IS A AREA THAT IS NOT EXPLORED MUCH, BUT IT REALLY NEEDS LOT OF ATTENTION AS IT IS ONE OF THE MOST COMMON OBSTACLE IN ACHIEVING COMPLETE REMISSION IN DEPRESSION
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WEIL FELIX test very Specific
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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
1. Drug Interactions In Psychiatry
PRESENTER: DR.PJ.CHAKMA,PGT,AMCH
MODERATOR: DR.R.U.ZAMAN,ASSOC. PROF.
AMCH
21/06/2013
2. Plan of presentation
• Introduction
• Importance of drug interaction
• Risk factor
• Type of interaction
• Different drug interaction in psychiatry
• Clinical consequences
• Management
• Conclusion
• bibliography
3. introduction
• A drug interaction, defined as the modification
of the action of one drug by another, can be
beneficial or harmful, or it can have no
significant effect.This action can be synergistic
or antagonistic
• The risk that a pharmacological interaction will
appear increases as a function of the no of
combinations of drugs administered to a patient
at the same time
4. importance
Recognition of beneficial effects and
Recognition and prevention of adverse drug
interactions
Basic principles of drug-drug interactions in
planning a therapeutic regimen.
5. Risk factor
– Old age
– Polydrug misusers
– Polypharmacy
– Psychiatric patients taking high doses ofmedication
– people in developing countries in which there is a
high prevalence of self-medication
– Irresponsible dispensing by a small minority of
pharmacists
6. Role of Genetics
• An individual's genetic makeup can alter their
response to a drug.
• A common example is the metabolism of ethanol
.There are ethnic differences in the metabolism of
ethanol by alcohol dehydrogenase.
7. Presentation of drug interactions
A multitude of different types of serious adverse events (SAEs),
such as sudden death, seizures,cardiac rhythm disturbances,delirium
Poor tolerability (ie, patient is “sensitive” to adverse drug effect)
Lack of efficacy (ie, patient is “resistant” to beneficial drug effect)
Symptoms that mimic or lead to a misdiagnosis of a new disease
The apparent worsening of the disease being treated
Withdrawal symptoms or drug-seeking behavior on the part of the
patient
8. Epidemiology of Drug Interactions
• The overall prevalence of drug interactions is 50% to
60%.
• Those that affect pharmacodynamics or
pharmacokinetics have a prevalence of approximately
5% to 9%.
• About 7% of hospitalizations are due to drug
interactions.
9. Challenges in Anticipating Interactions
Drug potency, strength, dose
Drug purity – contaminants, adulterants
Research studies lacking, inconclusive, unethical
Drug interaction information based on unproven
theory or case reports with incomplete data
Clients not forthcoming
Over-the-counter drugs, herbal products and grapefruit
juice not often reported by clients
15. Pharmaceutical
When drugs are mixed outside the body prior to administration.
For example, mixing chemically incompatible drugs
before intravenous infusion can result In precipitation or inactivation.
16. Pharmacokinetic Interactions
• One drug changes how the body handles other drugs,
either increasing or decreasing blood levels of one or
both drugs
Absorption: (gut,skin)
– drug movement from administration site to bloodstream
(P-Glycoproteins, protein binding)
Distribution
– drug movement from bloodstream to the rest of the body
– psychotropics must cross the blood brain barrier to reach their site of action
Metabolism
– transformation of drug by chemical processes(phase 1 metabolism= CYP450)
PHASE II= conjugation
Excretion or Elimination(urine,bile,gut)
– routes of leaving the body for drug and drug metabolites
17. Effect of interaction at absorption
• Delay n the rate of absorption- Antacid can decrease the
rate of absorption of chlordizapoxide by increasing the pH
• Alteration of dissolution of tablets
• Elevation of gastric PH with antacids above the Pka of
chlordiazepoxide (4.8) may reduce the dissolution rate
• Change in the amount of drug absorbed
– Decreased serum concentration
– Increased serum concentration
– Precipitation of the drug
18. • Precipitation :Iron may decrease the antibacterial
efficacy of tetracycline by chelation
• Enzymatic reaction : Monoamine oxidase inhibitor
and tyramine.(drugs-food interactions)
19. Pharmacodynamic Interactions:
• Based on the way the drug works on
the body
Additive / Synergistic - two drugs with the same effect
– increased drug effects (e.g. euphoria, relaxation)
– increased side effects (e.g. drowsiness, nausea, overdose)
Opposing – two drugs with opposite effects
– do not necessarily ‘cancel each other out’
Counterproductive – drug exacerbates underlying condition;
more of a disease/drug interaction than true drug interaction
20. Pharamacodynamics:
Where Drugs Act
Four sites of action
Receptors (those sites to which a
neurotransmitter can specifically adhere to
produce a change in the cell membranes)
Ion channels
Enzymes
carrier Proteins
Biological action depends on how
its structure interacts with a
receptor
21. Receptors
Types of Action
Agonist: same biologic action
Antagonist: opposite effect
Interactions with a receptor
Selectivity: specific for a receptor
Affinity: degree of attraction
Intrinsic activity: ability to produce a biologic
response once it is attached to receptor
23. Protein Binding
• Not as clinically relevant as previously believed.
• Properties of a drug that predict clinically relevant
displacement by protein binding:
– Low clearance drugs
– Low therapeutic index
– Small volume of distribution
– Examples: warfarin, tolbutamide, phenytoin
24. Protein Binding and Urinary Excretion of
SRIs
The Pharmacological Basis of Therapeutics; Goodman & Gilman; 10th Edition; 2001
*From Physician’s Desk Reference; 2004; page 1302
25. Protein Binding of Atypical
Antipsychotics
2005 Physicians’Desk Reference
26. Distribution of drug
When the drug leaves the systemic circulation and
moves to various parts of the body
• Drugs in the bloodstream are often bound to
plasma proteins; only unbound drugs can leave
the blood and affect target organs
• Low serum albumin can increase availability of
drugs and potentiate their effects
27. Factors affecting volume of distribution
Lipid solubility
Degree of plasma protein binding
Affinity for different tissue
eg duration of action of thiopental, first dose
lorazepam and diazepam.
28. Drug metabolism
• Primarily in the liver; cytochrome P-450 enzyme
system facilitates drug metabolism; metabolism
generally changes fat soluble compounds to
water soluble compounds that can be excreted
– Enzyme mediated biotransformation
– Cytochrome P450
29. Elimination
Clearance: Total amount of blood, serum, or plasma from which a
drug is completely removed per unit time
Half-life: Time required for plasma concentrations of the drug to be
reduced by 50%
kidneys (responsible for excreating all water soluble substances)
Some excreted via the liver,urine,faeces,saliva& sweat,milk, bile and
delivered to the intestine
may be reabsorbed in intestine and “re-circulate” (up to 20%)
30. Elimination Interactions
– Glomerular filtration: Chloral derivatives
– Tubular re-absorption:
• Alkalizing agent may enhance the excretion of Lithium or
Tranylcypromine
• Urinary acidifier such as may enhance excretion of
imipramine, amitriptyline or amphetamines
• (NSAIDs), angiotensin-converting enzyme (ACE)
inhibitors, or angiotensin II receptor blockers (ARBs)
should be used cautiously, if at all, in patients already
receiving lithium.
31. Cytochrome P450
– Oxidase system
– Metabolize endogenous compounds such as steroids and
neuropeptides
– Contain red pigmented heme
– Absorb light at a wave length of 450 nm if bound to CO
– Encoded by one particular gene
– Grouped into families and subfamilies on the basis of amino
acid sequences
32. Cytochrome P450
• Largest class of enzymes catalyzing oxidation of organic substances
in all living things
11,550+ identified ; 57 in humans
High affinity for fat-soluble drugs
Involved in metabolism of most psychiatric medications
Inactivate drugs (or in some cases activate them)
Chemicals may increase or decrease CYP activity
Example:
SSRIs inhibitors of the subfamily CYP2D6
Compounds in grapefruit juice inhibit CYP3A4
Tobacco induces CYP1A2
33. Cytochrome P450
Category meaning Examples
Family numeral CYP450 1
Subfamily numeral + capital letter CYP450 1A
Single gene or protein Arabic numeral + capital
letter + numeral for
individual gene
CYP450 1A2
35. cytochrome p450
• Substrate
– any drug metabolized by P450 enzymes
• Inhibitor
– any drug that inhibits the metabolism of a P450
substrate (strong, moderate, weak)
• Inducer
– anything that increases the amount of P450 enzymes
(strong, moderate, weak)
36.
37. P450 Variations
• Some people have more than normal amounts
of certain P450 enzymes (ultra-rapid
metabolizers)
• Some people have normal amounts (extensive
metabolizers)
• Some people have less than normal amounts
(poor metabolizers
38. Effects of Drug Interaction
Different types of serious adverse effects
Poor tolerability
Lack of efficacy
Symptoms that mimic or lead to a misdiagnosis of
a new disease
The apparent worsening of the disease being
treated
Withdrawal symptoms or drug-seeking behavior
on the part of the patient
46. contd
• others common interaction
antacids
dopamine agonists or antiparkinson”s Rx
CNSdepressants such as analgesics, anxiolytics,
and hypnotics
47. Antidepressants and the Cytochrome P450
System
• Antidepressants and mood stabilizers may be inhibitors,
inducers or substrates of one or more cytochrome P450
isoenzymes
• Knowledge of their P450 profile is useful in predicting
drug-drug interactions
• When some isoenzymes are absent of inhibited, others
may offer a secondary metabolic pathway
• P450 1A2, 2C (subfamily), 2D6 and 3A4 are especially
important to antidepressant metabolism and drug-drug
interactions
51. Monoamine Oxidase Inhibitors
• The combination of MAOIs and narcotics,
particularly meperidine may cause a fatal
interaction
• With SSRIs can cause the serotonin syndrome.
71. Drug-Drug Interactions: approach
• Take a medication history
• Remember high risk patients
• Evaluate therapeutic alternative
– Dose spacing
– Decreasing dose
– Discontinue the drug
– Add another agent to counter the interaction
72. Management of Drug Interactions
• Inform all prescribers about current medications - GP’s,
psychiatrists, dentist
• When possible take all prescriptions to one pharmacy so there is
one computer record
• Ask pharmacist about OTC meds & check ingredient list on
combination products (will sometimes change!!)
• Scheduling different dosing times can sometimes minimize
interaction (but not always)
• Some interactions cannot be avoided, so close monitoring and
dosage adjustment is essential
73. contd
• Some websites have drug interaction programs, but significance
of each interaction needs to be assessed and put in proper
context by MD or pharmacist
• Some interactions are more theoretical, and may not have clinical
significance
• Some drug interactions are good
– Using a 2nd drug to decrease a “bad” metabolite of the first
drug
• Not all combinations can be anticipated or tested, so new drug
interactions are being discovered every day!!
74. How to avoid drug interaction
• Beware and follow good clinical practice
• Avoid multi target medication
• Use available literature
• When in doubt start low and go slow
• Monitor for adverse out come
75. conclusions
• Drug Interactions are inevitable .There is also a lack of
knowledge of the size of the problem and of the many
pharmacological and host factors that determine whether or
not an individual will have a particular interaction
• Future research has been carried out into potentially
hazardous interactions with different drugs, yet there is
much that remains unknown.
76. bibliography
• Kaplan and Sadock’s Comprehensive Textbook of Psychiatry
vol.1 by Benjamin J. Sadock and Virginia A Sadock 9th edition
2005, Williams and Wilkins
• Textbook of Postgraduate Psychiatry, Vol.1 by J.N. Vyas and
Niraj Ahuja, 2nd edition 2003 Jaypee Brothers Medical
Publishers (P) Ltd
• The south london and maudsley NHS foundation trust
prescribing guidelines 10th edition
• Jerald kay,Allan Tasman,wiley essentials of psuchiatry,2006
Richard A Harvey, Pamela C. Champe (2006) Lippincott’s
Illustrated Reviews: Pharmacology: 3rd Edition. Lippincott
Williams & Wilkins
77. contd
• New Oxford Textbook of Psychiatry vol.1 by M.G.
Gelder, Juan J. Lopez-Ibor Jr, Nancy C. Andreasen
• Dr. Brunton, Parker, and Lazo: Goodman Gillman’s
The Pharmacological Basis of Therapeutics, 10th
edition. McGraw Hills
• B.J.Sadock”s,V.A.Sadock”s,Kaplan & sadock”s
synopsis of psychiatry,10th edition
• Psychopharmacology treatment of psychiatric
disorders,(late) jambur anant,2007,jaypee publisher
• Wikipedia
• Googleimages.com