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- Contraindications and warnings for its use, including not taking it if you have breathing problems or a history of substance abuse.
- How to take zolpidem, including only taking it at bedtime for 2-4 weeks as prescribed by your doctor.
- Possible side effects and drug interactions to be aware of when taking zolpidem with other medications.
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This document is a patient information leaflet for Zolpidem Tartrate 5mg and 10mg tablets produced by Taj Pharmaceuticals. It provides information on:
- What zolpidem is and what it is used for, which is the short-term treatment of insomnia.
- Contraindications and warnings for its use, including not taking it if you have breathing problems or a history of substance abuse.
- How to take zolpidem, including only taking it at bedtime for 2-4 weeks as prescribed by your doctor.
- Possible side effects and drug interactions to be aware of when taking zolpidem with other medications.
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This document provides information on Haloperidol Oral Solution 5 mg/5 ml, including its:
1) Indications for treating various psychiatric conditions in adults and children.
2) Dosing guidelines which vary based on the condition, with most adult doses ranging from 2-10 mg/day and pediatric doses from 0.5-5 mg/day.
3) Contraindications for patients with certain cardiac conditions or those taking QT-prolonging medications.
4) Warnings about increased mortality in elderly patients with dementia, potential cardiovascular side effects, and recommendations for ECG monitoring and electrolyte management.
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8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the 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 lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
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. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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This document provides information on Haloperidol Oral Solution 5 mg/5 ml, including its:
1) Indications for treating various psychiatric conditions in adults and children.
2) Dosing guidelines which vary based on the condition, with most adult doses ranging from 2-10 mg/day and pediatric doses from 0.5-5 mg/day.
3) Contraindications for patients with certain cardiac conditions or those taking QT-prolonging medications.
4) Warnings about increased mortality in elderly patients with dementia, potential cardiovascular side effects, and recommendations for ECG monitoring and electrolyte management.
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8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the 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 lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
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. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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Hiranandani Hospital in Powai, Mumbai, is a premier healthcare institution that has been serving the community with exceptional medical care since its establishment. As a part of the renowned Hiranandani Group, the hospital is committed to delivering world-class healthcare services across a wide range of specialties, including kidney transplantation. With its state-of-the-art facilities, advanced medical technology, and a team of highly skilled healthcare professionals, Hiranandani Hospital has earned a reputation as a trusted name in the healthcare industry. The hospital's patient-centric approach, coupled with its focus on innovation and excellence, ensures that patients receive the highest standard of care in a compassionate and supportive environment.
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There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
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Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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According to research conducted by the National Family Health Survey of India, diabetic cases show a projection which might increase to 10.4% by 2030.
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BETAHISTINE
DIHYDROCHLORIDE
TABLETS
16MG
1.NAME OF THE MEDICINAL
PRODUCT
Betahistine Dihydrochloride 16 mg Tablets
2. QUALITATIVE AND
QUANTITATIVE COMPOSITION
Each tablet contains 16 mg of betahistine
dihydrochloride.
For the full list of excipients, see section 6.1.
3. PHARMACEUTICAL FORM
Tablet.
White, 8.5 mm, round, flat bevel edged tablet.
4. CLINICAL PARTICULARS
4.1 Therapeutic indications
Betahistine is indicated for the treatment of vertigo,
tinnitus, hearing loss and nausea associated with
Ménière's syndrome.
4.2 Posology and method of
administration
Posology
Adults (including the elderly)
Initial oral treatment is 8 mg to 16 mg three times
daily, taken with food. Maintenance doses are
generally in the range 24 - 48 mg daily. Dosage
can be adjusted to suit individual patient needs.
Paediatric population
Betahistine tablets are not recommended for use in
children below 18 years due to insufficient data on
safety and efficacy.
Geriatric population
Although there are limited data from clinical studies
in this patient group, extensive post marketing
experience suggests that no dose adjustment is
necessary in this patient population.
Patients with renal impairment
There are no specific clinical trials available in this
patient group, but according to post-marketing
experience no dose adjustment appears to be
necessary.
Patients with hepatic impairment
There are no specific clinical trials available in this
patient group, but according to post-marketing
experience no dose adjustment appears to be
necessary.
Method of administration
For oral use.
4.3 Contraindications
Phaeochromocytoma. As betahistine is a synthetic
analogue of histamine it may induce the release of
catecholamines from the tumour resulting in severe
hypertension.
Hypersensitivity to the active substance or to any
of the excipients listed in section 6.1.
Concurrent use with antihistamines (see section
4.5).
4.4 Special Warnings and precautions for
use
Caution is advised in the treatment of patients with
peptic ulcer or a history of peptic ulceration,
because of the occasional dyspepsia encountered
in patients on betahistine.
Caution should be exercised in patients with
bronchial asthma.
Patients with bronchial asthma (as clinical
intolerance has been seen in a relatively few
patients) and history of peptic ulcer need to be
carefully monitored during the therapy.
Caution is advised in prescribing betahistine to
patients with either urticaria, rashes or allergic
rhinitis, because of the possibility of aggravating
these symptoms.
Betahistine is not indicated for treatment of the
following diseases: benign paroxysmal vertigo and
vertigos in relation with a central nervous system
disease.
4.5 Interaction with other medicinal
products and other forms of interaction
No in vivo interaction studies have been
performed. Based on in vitro data, no in
vivo inhibition on Cytochrome P 450 enzymes is
expected.
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In vitro data indicate an inhibition of betahistine
metabolism by drugs that inhibit monoamino-
oxidase (MAO) including MAO subtype B (e.g.
selegiline). Caution is recommended when using
betahistine and MAO inhibitors (including MAO-B
selective) concomitantly.
As betahistine is an analogue of histamine,
interaction of betahistine with antihistamines may
in theory affect the efficacy of one of these drugs.
There is a case report of an interaction with ethanol
and a compound containing pyrimethamine with
dapsone and another potentiation of betahistine
with salbutamol.
4.6 Fertility, Pregnancy and lactation
Pregnancy
There are no adequate data from the use of
betahistine in pregnant women. Animal studies are
insufficient with respect to effects on pregnancy,
embryonal/foetal development, parturition and
postnatal development. The potential risk for
humans is unknown. Betahistine should not be
used during pregnancy unless clearly necessary
(see also section 5.3).
Breast-feeding
It is not known whether betahistine is excreted in
human milk. There are no animal studies on the
excretion of betahistine in milk. The importance of
the drug to the mother should be weighed against
the benefits of nursing and the potential risks for
the child.
4.7 Effects on ability to drive and use
machines
Vertigo, tinnitus and hearing loss associated with
Ménière's syndrome negatively affect the ability to
drive and use machines. In clinical studies
specifically designed to investigate the ability to
drive and use machines betahistine had no or
negligible effects.
However, rare reports of drowsiness associated
with betahistine have been made. Patients should
be advised that if they are affected in this way they
should avoid activities requiring concentration,
such as driving or operating machinery.
4.8 Undesirable Effects
Betahistine is generally well tolerated and relatively
few side effects have been reported.
The frequency categories assigned to the adverse
reactions below are estimates; as for most
reactions suitable data for calculating incidence are
not available. In addition the incidence of adverse
reactions associated with betahistine
dihydrochloride may vary according to the
indication.
Data from clinical trials were used to determine the
frequency of very common to rare undesirable
effects. The frequencies assigned to all other
undesirable effects (i.e. those occurring at
<1/1,000) were mainly determined using post-
marketing data, and refer to a reporting rate rather
than a true frequency.
The following convention has been used for the
classification of frequency:
very common (≥1/10), common (≥1/100 to <1/10),
uncommon (≥1/1,000 to <1/100), rare (≥1/10,000
to <1/1,000), very rare (<1/10,000), not known
(cannot be estimated from the available data;
reported spontaneously during post-marketing use
and in scientific literature)
MedDRA
system
organ
class
Very
common
Common Rare Very rare Not known
Blood and
lymphatic
system
disorders
thrombocyto
penia
Immune
system
disorders
hypersensitivity
reactions, e.g.
anaphylaxis
Nervous
system
disorders
headache somnolen
ce
Gastrointe
stinal
disorders
dry mouth,
diarrhoea
nausea
dyspepsi
a
mild gastric
complaints (e.g.
vomiting,
gastrointestinal
pain, abdominal
distension and
bloating). These
can normally be
dealt with by
taking the dose
during meals or
by lowering the
dose.
Skin and
subcutane
ous tissue
disorders
skin rashes,
cutaneous and
subcutaneous
hypersensitivity
reactions, in
particular
angioneurotic
oedema,
urticaria, rash
and pruritus.
General
disorder
and
administrat
ive site
conditions
asthenia
Investigatio
ns
increase of
transaminas
es
Reporting of suspected adverse reactions
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Reporting suspected adverse reactions after
authorisation of the medicinal product is important.
It allows continued monitoring of the benefit/risk
balance of the medicinal product.
4.9 Overdose
Symptoms
The symptoms of betahistine overdose are nausea,
vomiting, dyspepsia, ataxia and seizures at higher
doses.
A few overdose cases have been reported. Some
patients experienced mild to moderate symptoms
with doses up to 640 mg (e.g. nausea,
somnolence, abdominal pain). More serious
complications (e.g. convulsion, pulmonary or
cardiac complications) were observed in cases of
intentional overdose of betahistine, especially in
combination with other drugs.
Management
No specific antidote. Treatment of overdose should
include gastric lavage, symptomatic treatment and
standard supportive measures.
5. PHARMACOLOGICAL
PROPERTIES
5.1 Pharmacodynamic properties
Pharmacotherapeutic group: antivertigo
preparations
The mechanism of action of betahistine is only
partly understood. Single oral doses of betahistine
of up to 32 mg in normal subjects produced
maximal suppression of induced vestibular
nystagmus 3-4 hours post-dose, with larger doses
being more effective in reducing the nystagmus
duration.
There are several plausible hypotheses that are
supported by animal studies and human data:
• Betahistine affects the histaminergic system:
Betahistine acts both as a partial histamine H1-
receptor agonist and histamine H3-receptor
antagonist also in neuronal tissue, and has
negligible H2-receptor activity. Betahistine
increases histamine turnover and release by
blocking presynaptic H3-receptors and inducing H3-
receptor downregulation.
Pulmonary epithelial permeability in man is
increased by betahistine. This is derived from a
reduction in the time of clearance from the lung to
blood of a radioactive marker. This action is
prevented by oral pre-treatment with terfenadine, a
known H1 receptor blocker.
Whilst histamine has positive inotropic effects on
the heart, betahistine is not known to increase
cardiac output and its vasodilator effect may
produce a small fall in blood pressure in some
patients.
• Betahistine may increase blood flow to the
cochlear region as well as to the whole brain:
Pharmacological testing in animals has shown that
the blood circulation in the striae vascularis of the
inner ear improves, probably by means of a
relaxation of the precapillary sphincters of the
microcirculation of the inner ear.
Betahistine was also shown to increase cerebral
blood flow in humans.
• Betahistine facilitates vestibular compensation:
Betahistine accelerates the vestibular recovery
after unilateral neurectomy in animals, by
promoting and facilitating central vestibular
compensation; this effect characterised by an up-
regulation of histamine turnover and release, is
mediated via the H3-Receptor antagonism. In
human subjects, recovery time after vestibular
neurectomy was also reduced when treated with
betahistine.
• Betahistine alters neuronal firing in the vestibular
nuclei:
Betahistine was also found to have a dose
dependent inhibiting effect on spike generation of
neurons in lateral and medial vestibular nuclei.
The pharmacodynamic properties as demonstrated
in animals may contribute to the therapeutic benefit
of betahistine in the vestibular system.
The efficacy of betahistine was shown in studies in
patients with vestibular vertigo and with Ménière's
disease as was demonstrated by improvements in
severity and frequency of vertigo attacks.
5.2 Pharmacokinetic properties
Absorption
Orally administered betahistine is readily and
almost completely absorbed from all parts of the
gastro-intestinal tract. After absorption, the drug is
rapidly and almost completely metabolised into 2-
pyridylacetic acid. Plasma levels of betahistine are
very low. Pharmacokinetic analyses are therefore
based on 2-PAA measurements in plasma and
urine.
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Under fed conditions Cmax is lower compared to
fasted conditions. However, total absorption of
betahistine is similar under both conditions,
indicating that food intake only slows down the
absorption of betahistine.
Distribution
The percentage of betahistine that is bound by
blood plasma proteins is less than 5 %.
Biotransformation:
After absorption, betahistine is rapidly and almost
completely metabolised into 2- PAA (which has no
pharmacological activity).
After oral administration of betahistine the plasma
(and urinary) concentration of 2- PAA reaches its
maximum 1 hour after intake and declines with a
half-life of about 3.5 hours.
Elimination
2-PAA is readily excreted in the urine. In the dose
range between 8 and 48 mg, about 85% of the
original dose is recovered in the urine. Renal or
faecal excretion of betahistine itself is of minor
importance.
Linearity
Recovery rates are constant over the oral dose
range of 8 – 48 mg indicating that the
pharmacokinetics of betahistine are linear, and
suggesting that the involved metabolic pathway is
not saturated.
5.3 Preclinical safety data
Repeated oral dose toxicity studies in dogs and
rats for 6 and 18 months respectively revealed no
clinically relevant adverse effects.
Betahistine was not mutagenic in conventional in
vitro and in vivo studies of genotoxicity.
Histopathological examination in the 18 months
chronic toxicity study indicated no carcinogenic
effects. However, specific carcinogenicity studies
were not performed with betahistine.
Limited studies of reproductive toxicity in rats and
rabbits showed no teratogenic effects.
6. PHARMACEUTICAL
PARTICULARS
6.1 List of excipients
Cellulose, microcrystalline
Mannitol (E421)
Citric acid monohydrate (E330)
Silica, colloidal anhydrous
Talc (E553b)
6.2 Incompatibilities
Not applicable
6.3 Shelf life
2 years.
6.4 Special precautions for storage
Do not store above 25°C. Store in the original
container in order to protect from light and moisture
6.5 Nature and contents of container
PVdC (285 mm)/Aluminium (20 mm) blister strips.
Available in packs of 20, 28, 30, 56, 84, 90, 100,
112, 120, 168 and 180 tablets.
Polypropylene tablet containers sealed with
polyethylene caps with optional polyethylene ullage
filler. Available in packs of 5, 7, 10, 15, 20, 21, 25,
28, 30, 50, 56, 60, 84, 90, 100, 112, 120, 168, 250,
500 and 1000 tablets.
Not all pack sizes may be marketed.
6.6 Special precautions for disposal and
other handling
No special instructions.
7. MANUFACTURER:
Manufactured in India by:
TAJ PHARMACEUTICALS LTD.
Mumbai, India
At:388/34, Changodar Industrial Estate
Changodar- 382 210
Dist- Ahmedabad. Gujarat (India)
MFG. LIC NO: G/25A/4795-A
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