This document defines sedative and hypnotic drugs and describes their mechanisms of action and effects. It discusses different classes of sedative-hypnotics including benzodiazepines, barbiturates, and newer non-benzodiazepine hypnotics. Benzodiazepines potentiate GABA's effects by binding to GABA-A receptors. They are generally safe but can cause drowsiness, impaired coordination, and interaction risks with other CNS depressants. Barbiturates directly activate GABA receptors and carry greater overdose and dependence risks than benzodiazepines. Newer non-benzodiazepine hypnotics like zolpidem selectively target
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Neurohumoral transmission in CNS-
The term neurohumoral transmission designates the transfer of a nerve impulse from a presynaptic to a postsynaptic neuron by means of a humoral agent e.g. a biogenic amine, an amino acid or a peptide.
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Neurohumoral transmission in CNS-
The term neurohumoral transmission designates the transfer of a nerve impulse from a presynaptic to a postsynaptic neuron by means of a humoral agent e.g. a biogenic amine, an amino acid or a peptide.
This topic is pharmacology . More detail in sedative and hypnotics pharmacology and drug , and classification of drug or combination of drug and knowledge of drug dose ,
Notes are my best teacher DR . DIGVIJAYA SAINI
Introduction
What are Sedatives??
“A drug that subdue excitement and calms the patient without inducing sleep. Though the drowsiness may
be produced.”
► It also refers to the decrease in responsiveness to stimulation, along with this ,it also decrease the
alertness,ideation, and motor activities.
What are Hypnotics???
► “ These are the drugs that causes the sleep which resembles with the natural sleep”.
► These are having quicker action,shorter duration and steeper DRC while sedatives having slow on set of
action with flatter DRC
► Hypnotics at lower dose sedative
► There are different grades of CNS depressants
► Sedation Hypnosis General anaesthesia
Difference between Sedative &
Hypnotics
Sedative
► A drug that reduces excitement,calms the
patient without inducing sleep
► Sedative in therapeutic doses are
anxiolytics
► At larger doses causes hypnosis
► Site of action is on limbic system
► Examples- diazepam,lorazepam,etc.
Hypnotics
► Sleep producing drugs
► Used for inititation or maintain the sleep
► At high doses causes general anaesthesia
► Site of action is in midbrain & acending
RAS which maintains wakefullness
► Examples – zopiclone,phenobarbitone
DRC for two hypothetical
sedative - Hypnotics
• Drug A – An increase in dose higher than that needed for
hypnosis may lead to state of general anaesthesia.
• With higher doses , the durg will depresses the respiratory and
vasomotor centers which leads to coma.
• Steeper DRC, Narrow margin of safety
• Drug A is an example of alcohol and Barbiturates.
• Drug B – Needs greater dose to achieve CNS depression
• Drug B is an example of benzodiazepine and newer hypnotics
• Flatter DRc, greater margin of safety
► Sleep
1. NREM – In this there is no fast movement of eyes.It occurres between stage 0 to 4
2. REM – In this eye movements are very fast.
► Stage of NREM-
► Stage 0 [ awake]- It is condition from lying down to falling a sleep(1-2%)
► Stage 1 [dosing]– Eye movement decrease,body muscles relax (5-10%)
► Stage 2 [unequivocal sleep]– more decrease in eye movements, person may arousable.(50%)
► Stage 3 deep sleep transition]– Deeper sleep with minimum eye movements,not easily arousal.
► Stage 4[cerebral sleep] – deepest level of sleep, GH secretion increased, no eye movements, muscles are
fully relaxed, if awakened causes disorientation.(20%)
► REM – dreaming, HR,breathing rate, brain activity increases and relaxation of voluntary muscles.
Classification
► Benzodizepines1. Hypnotics-Diazepam,flurazepam,Nitrazepam,Alprazolam,Lorazepam,Templepatrick,Triazolam
2. Antianxiety-Diazepam, Chlordiazeperoxide, Oxazepam, Lorazepam, Alprazolam, Clonazepam
3. Anticonvulsant- Clonazepam, clobazam, Diazepam, Loranzepam
► Barbiturates1. Long acting- phenobarbitone
2. Short acting- butobarbitone, Phenobarbitone
3. Ultrashort acting- Thiopentone, Methohexitone
Non- benzodiazepines- Zopiclone, Eszopiclone, Zolpidem, Zaleplon, Etisalat
► Other Hypnotics- Triclofos, Melatonin, Ramelteon, Suvorexant
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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
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2. Objectives
Define sedative and hypnotics.
Different stages of CNS Depressants.
Name benzodiazepines and pharmacological actions.
Name their adverse effects and indications.
Name two barbiturates ,
PATKI2
9. Different phases of sleep and their characteristics
NREM sleep
Stage 0 (awake)
From lying down to falling asleep and occasional nocturnal
awakenings – constitutes 1-2% of sleep time
eye movements are irregular or slowly rolling
Stage 1 (dozing)
Eye movements are reduced but there may be bursts of rolling
Neck muscles relax - occupies 3-6% of sleep time
Stage 2
Little eye movement, subjects are easily arousable
This comprises 40-50% of sleep time
10. Stage 3 (deep sleep transition)
Eye movements are few, subjects are not easily arousable
This comprises 5-8% of sleep time
Stage 4 (cerebral sleep)
Eyes are practically fixed, subjects are difficult to arouse.
Night terror may occur at this time
This comprises 10-20% of sleep time
slow wave sleep: physical restoration process
REM: consolidation of learning
During stage 2, 3 and 4 – HR, BP and respiration are steady and
muscles are relaxed
11. There are marked, irregular eye movements; dreams and night-
mares occur, which may be recalled if the subject is aroused
HR, BP – fluctuate, respiration irregular
Muscles are fully relaxed, DREAMS
Erection occurs in males
About 20-30% of sleep time is spent in REM
Normally stages 0-4 and REM occurs in succession over a
period of 80-100 min. Then stages 1-4-REM repeated cyclically
A normal 8 hrs sleep consists of 4 or 5 cycles of quite sleep
alternating with REM sleep
REM sleep (paradoxical sleep)
13. Insomnia
It is defined as inadequate sleep and may be
manifested as difficulty in falling asleep or
difficulty in maintaining sleep with
intermittent wakening during sleep
Exhaustion, tension, anxiety, depression,
caffeine, jet lag, etc…
18. Benzodiazepines (BZD)
Mechanism of action:
BZD act on midbrain ascending reticular formation and
Limbic system
Bind to BZD receptor (integral part of GABAA receptor –Clˉ channel
complex)
19. Mechanism of action:
Benzodiazepines
Increase in chloride conductance
No GABA mimetic action
Potentiates the inhibitory effects of GABA
Increase the frequency of opening of Cl-
channel
Binds to specific site on GABA-A receptor
Membrane Hyperpolarization
CNS depression
21. Pharmacological actions of BZD
1. Sedation and hypnosis:
Reduces sleep latency
Reduces intermittent awakening
Time spent in stage II ↑ and stage III & IV ↓
Shortens REM phase
Body movements during sleep ↓
Sleep quality similar to natural sleep
Tolerance develops gradually
22. Pharmacological actions of BZD
2. Anxiolytic - ↑ depressant effect
3. Muscle relaxant – medullary site action
4. Anticonvulsant – ↑ seizure threshold
5. Amnesia
6. Other actions – analgesia and ↓ nocturnal
gastric secretion
25. Pharmacokinetics
Highly lipid soluble – two phase plasma concentration
decay curve
Metabolised in the liver – dealkylation and hydroxylation
Excreted in urine
Diazepam undergoes enterohepatic circulation
Cross placenta and are secreted in milk
27. D- Diagnostic and Minor operative procedures
I. Insomnia
A- Alchohol withdrawal syndrome
Z-
E- Epilepsy
P- Preanesthetic Medication
A- Anxiety
M- Muscle relaxation in tetanus,
cerebral palsy
28. Long term treatment with hypnotics:
Rebound insomnia
Change in sleep architecture
Reduced effectiveness due to blockade of slow wave sleep
Blocks the slow wave sleep – it is important for physical
restoration process
Suppression of REM sleep
29. Adverse effects of BZD
BZD – relatively safe drug with a wide margin of
safety
Dizziness, vertigo, disorientation, muscle
weakness, impaired motor coordination,
prolongation of reaction time, hangover (less
common).
30. Adverse effects of BZD
Blurred vision, nausea, dry mouth, urinary
incontinence.
irritability & sweating
Tolerance to sedative effects
Not teratogenic ; flaccidity & respiratory
depression in neonate
31. Drug interactions- BZD
Alcohol & CNS depressants-Potentiate depressant action
Enzyme inhibitors like Cimetidine, ketoconazole, erythromycin -
↓ metabolism
Caffeine inhibits anxiolytic effect of BZD
32. Tolerance and dependence
Less
Tolerance to sedative effects develops slowly
Withdrawal symptoms are mild and slow in onset
Symptoms include anxiety, nervousness, tremor,
dizziness and anorexia
33. Acute over dosage of BZD
Induces sleep; respiratory depression is
mild
Specific antagonist - flumazenil
34. Flumazenil
BZD analogue
Compete with BZD agonist and inverse agonist
and reverses their effects
I.V - action starts in seconds and lasts for 1-2
hours
Elimination t1/2 is 1 hour
Uses:
1. To reverse BZD anesthesia
2. BZD overdosage
37. Advantages of BZD over barbiturates
1. Induce sleep- natural
2. No hang over
3. High therapeutic index – 20 hypnotic doses x endanger life
4. Hypnotic dose – does not affect Resp / CV function
5. No action on other systems
6. No Microsomal enzyme induction
7. withdrawl syndrome are less marked
38. Advantages of BZD over barbiturates
8. Less dependence
9. Lower abuse liability
10. Do not produce hyperalgesia
11. Amnesia without automatism
12. Do not produce generalized CNS depression
13. Less distortion of sleep and rebound phenomena
14. Specific BZD antagonist available
39. Mechanism of action:
Barbiturates
Increase in chloride conductance
Potentiates the inhibitory effects of GABA
Increase the DURATION of opening of Cl-
channel
Binds to specific site on GABA-A receptor
Membrane Hyperpolarization
CNS depression
51. Produces Hypnotic effect with minimal anticonvulsant
and muscle relaxant properties
It produces natural sleep without alteration of REM
sleep.
Minimal hangover effects
Short duration of action
Less likely to produce Tolerance and dependence
52. Short acting agents Long acting agents
Preferred in patients with sleep
onset insomnia
No REM suppression
Less hangover
Less tolerance and dependence
Less respiratory depression
Preferred in patients with daytime
anxiety, who can tolerate sedation
on next day and with depression.
Disadvantages:
Early morning awakening
Rebound anxiety
Amnesic episodes
Disadvantages:
Next day confusion
Cognitive impairment on next day
Delayed cognitive impairment
53. NMDA receptor
(N-methyl-D-aspartate)
Mediate slow excitatory responses
Long term adaptive changes in the brain
Normal stimulation – learning and memory(synaptic
plasticity)
Over stimulation – excitotoxicity in brain
(neurodegenaration and apoptosis
54. NMDA receptor BLOCKERS
Ketamine: IV general anesthetic
Phencyclidine: Psychedelic drugs
Memantine: Alzheimer's disease
Topiramate and Felbmate: Anti epileptic drugs
61. Melatonin
It is a mediator that is synthesized from 5-HT in the pineal
gland.
Melatonin receptors are mainly found in the retina
and brain.
Melatonin secretion is high at night and low by day, therefore it
is important in the regulation of circadian rhythm
Melatonin is medicinally used to control “jet-lag”
Ramelteon
62. Melatonin
Hormone of the pineal gland secreted at night
Synchronizing action – sleep-wakefulness cycle with circadian
rhythm
Treatment of jet-lag, elderly hypnotic dependent insomniacs and
shift workers
RAMELTEON
It is a selective agonist at the MT1 and MT2 R of melatonin
Used in insomnia – difficulty in falling asleep