- The document describes the case of a 28-year-old woman who experienced rapid deterioration with 9 hospitalizations for psychosis over the course of a year. She had been diagnosed with a prolactin-secreting pituitary tumor.
- Treatment of her conditions was complex due to the counteractive nature of medications used to treat psychosis (dopamine antagonists) versus those used to treat her prolactinoma (dopamine agonists).
- After her most recent hospitalization, her cabergoline treatment for the prolactinoma was discontinued due to concerns about potential psychotic side effects. Clozapine was also initiated for her psychosis. Her condition improved after getting off cabergoline and starting clozap
Cognitive changes have been a defining feature of Sz since onset. A lot of research has been done in understanding these changes and its implication in developing novel methods of treatments. This ppt summarises the cognitive changes occurring in the brain.
Narcolepsy is a chronic disorder of the central nervous system characterized by the brain's inability to control sleep-wake cycles. At various times throughout the day, people with narcolepsy experience irresistible and sudden bouts of sleep, which can last from a few seconds to several minutes.
Neurocognitive disorders includes : Delirium and Dementia.
This presentation focuses on causes, risk factors, management and how to prevent its complication
Cognitive changes have been a defining feature of Sz since onset. A lot of research has been done in understanding these changes and its implication in developing novel methods of treatments. This ppt summarises the cognitive changes occurring in the brain.
Narcolepsy is a chronic disorder of the central nervous system characterized by the brain's inability to control sleep-wake cycles. At various times throughout the day, people with narcolepsy experience irresistible and sudden bouts of sleep, which can last from a few seconds to several minutes.
Neurocognitive disorders includes : Delirium and Dementia.
This presentation focuses on causes, risk factors, management and how to prevent its complication
Antipsychotics, also known as neuroleptics,[1] are a class of psychotropic medication primarily used to manage psychosis (including delusions, hallucinations, paranoia or disordered thought), principally in schizophrenia but also in a range of other psychotic disorders.[2][3] They are also the mainstay together with mood stabilizers in the treatment of bipolar disorder.[4]
Antipsychotic
Drug class
Zyprexa.PNG
Olanzapine, an example of a second-generation (atypical) antipsychotic
Class identifiers
Synonyms
Neuroleptics, major tranquilizers[1]
Use
Principally: Schizophrenia, Schizoaffective disorder, Dementia, Tourette syndrome, Bipolar disorder, irritability in autism spectrum disorder
Clinical data
Drugs.com
Drug Classes
External links
MeSH
D014150
In Wikidata
Prior research has shown that use of any antipsychotic is associated with smaller brain tissue volumes,[5][6] including white matter reduction[7] and that this brain shrinkage is dose dependent and time dependent.[5][6] A more recent controlled trial suggests that second generation antipsychotics[8] combined with intensive psychosocial therapy[9] may potentially prevent pallidal brain volume loss in first episode psychosis.[10][7]
The use of antipsychotics may result in many unwanted side effects such as involuntary movement disorders, gynecomastia, impotence, weight gain and metabolic syndrome. Long-term use can produce adverse effects such as tardive dyskinesia, tardive dystonia, and tardive akathisia.
Prevention of these adverse effects is possible through concomitant medication strategies including use of beta-blockers. Currently, treatments for tardive diseases are not well established.
First-generation antipsychotics (e.g. chlorpromazine), known as typical antipsychotics, were first introduced in the 1950s, and others were developed until the early 1970s.[11] Second-generation antipsychotics, known as atypical antipsychotics, were introduced firstly with clozapine in the early 1970s followed by others (e.g. risperidone).[12] Both generations of medication block receptors in the brain for dopamine, but atypicals tend to act on serotonin receptors as well. Neuroleptic, originating from Greek: νεῦρον (neuron) and λαμβάνω (take hold of)—thus meaning "which takes the nerve"—refers to both common neurological effects and side
Mood disorders:major depressive and bipolar disorderNandu Krishna J
a basic description about mood disorders mainly MDD and bipolar disorder. Can be made useful in presentations and theory exams. Subject was imbibed from different presentations and DSM IV manual. Thanks for viewing.
Understanding Bipolar Disorder: Biopsychosocial Approaches to Mind Body HealthMichael Changaris
Explores psychological, medical and primary care treatment and self-care for bipolar disorder from the biological bases of brain function and medication management to the psychological integrated care and treatment plan for health complexity and bipolar treatment needs.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
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
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
DISSERTATION on NEW DRUG DISCOVERY AND DEVELOPMENT STAGES OF DRUG DISCOVERYNEHA GUPTA
The process of drug discovery and development is a complex and multi-step endeavor aimed at bringing new pharmaceutical drugs to market. It begins with identifying and validating a biological target, such as a protein, gene, or RNA, that is associated with a disease. This step involves understanding the target's role in the disease and confirming that modulating it can have therapeutic effects. The next stage, hit identification, employs high-throughput screening (HTS) and other methods to find compounds that interact with the target. Computational techniques may also be used to identify potential hits from large compound libraries.
Following hit identification, the hits are optimized to improve their efficacy, selectivity, and pharmacokinetic properties, resulting in lead compounds. These leads undergo further refinement to enhance their potency, reduce toxicity, and improve drug-like characteristics, creating drug candidates suitable for preclinical testing. In the preclinical development phase, drug candidates are tested in vitro (in cell cultures) and in vivo (in animal models) to evaluate their safety, efficacy, pharmacokinetics, and pharmacodynamics. Toxicology studies are conducted to assess potential risks.
Before clinical trials can begin, an Investigational New Drug (IND) application must be submitted to regulatory authorities. This application includes data from preclinical studies and plans for clinical trials. Clinical development involves human trials in three phases: Phase I tests the drug's safety and dosage in a small group of healthy volunteers, Phase II assesses the drug's efficacy and side effects in a larger group of patients with the target disease, and Phase III confirms the drug's efficacy and monitors adverse reactions in a large population, often compared to existing treatments.
After successful clinical trials, a New Drug Application (NDA) is submitted to regulatory authorities for approval, including all data from preclinical and clinical studies, as well as proposed labeling and manufacturing information. Regulatory authorities then review the NDA to ensure the drug is safe, effective, and of high quality, potentially requiring additional studies. Finally, after a drug is approved and marketed, it undergoes post-marketing surveillance, which includes continuous monitoring for long-term safety and effectiveness, pharmacovigilance, and reporting of any adverse effects.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
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).
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
2. • People with Brain Tumors and Pituitary Tumors may sometimes experience
emotional problems and changes in thinking abilities.
• such tumors sometimes affect thinking (or cognitive) processes such as
memory, language and concentration.
• The pituitary gland, although strictly speaking is not part of the brain, is closely
connected to the hypothalamus in the brain, which has an important role in
coordinating different brain functions
• The Pituitary Gland is attached to, and receives, chemical messages in the
bloodstream from the Hypothalamus.
• The pituitary gland is divided into two sections known as lobes, the anterior lobe
and the posterior lobe, and each lobe releases different hormones.
3. • The Anterior Pituitary Gland secretes:
1. Growth Hormone which promotes growth Prolactin
2. Adrenocorticotropic which stimulates the adrenal glands
3. Thyroid-Stimulating Hormone which stimulates the thyroid gland and in turn
the metabolic rate
4. Follicle-Stimulating Hormone and Luteinizing Hormone, which influence the
production of hormones from the ovaries and testes
• The Posterior Pituitary Gland secretes
1. Vasopressin, which causes the kidneys to retain water, and also regulates
blood vessels
2. Oxytocin, which facilitates childbirth and the production of milk for breast-
feeding.
4. • Pituitary tumors arise from the pituitary gland within the base of the skull.
• These tumors are almost always benign.
• Symptoms arise when these tumors secrete hormones or become large enough
to compress adjacent structures.
• As these tumors enlarge, the normal pituitary function is destroyed.
• This destruction produces various hormonal deficiencies.
• Pressure on nearby structures can produce double vision and facial numbness.
• The nerves of vision, the optic nerves, are directly above the pituitary gland and
upward growth of pituitary tumors frequently causes progressive visual loss.
5. • Types ofTumors
• Generally, these tumors can be subdivided in to
1. non-hormone producing tumors of the pituitary gland
2. hormone producing tumors
3. other intra-sellar tumors
4. para-sellar tumors.
Prolactinomas are the most common pituitary tumor
6. • Neurological Symptoms
1. headaches
2. double vision
3. loss of peripheral vision leading to blindness
4. facial pain or numbness
7. Other symptoms
• Hypopituitarism
• lack of energy
• weight loss, nausea, vomiting, constipation
• amenorrhea and infertility
• dry skin, increased pigmentation of the skin
• cold intolerance
• mental status changes: sleepiness, psychosis, collapse, depression
• Individuals with a brain tumour or pituitary tumour sometimes experience depression
or anxiety.
• People often report physical symptoms and changes to their behaviour.
8. mental status changes with pituitary tumors
• Apathy, a lack of feeling or expression of your emotions.
• Euphoria, a feeling of great happiness or well being which is usually exaggerated
and not appropriate to the individual's current life situation.
• experience sudden mood changes and feel like on an emotional rollercoaster, one
minute feeling high and the next minute feeling down.
• experience a decrease in self-esteem, Lack of confidence. For example, changes in
body shape or weight may occur with some Pituitary and Brain Tumours, and this
can lead to problems with self-image
9. mental status changes with pituitary tumors
• thinking problems such as poor memory or distractibility.
• many factors are associated with such problems including the size of the tumour
and where it is located in the brain.
• Attention and Concentration Becoming distracted easily and having trouble
sustaining focus on a task over a longer period of time are common symptoms.
For example, loosing the thread of conversations
• not being able to concentrate when more than one thing
• Sometimes individuals have difficulty learning new information
• People may have difficulty remembering conversations, events or names
although their memory for events many years ago is well preserved.
• People may also have difficultly remembering to do something
10. pituitary tumor and psychosis
• There is not an extensive literature on patients with both psychosis and a pituitary
tumor.
• Acute psychosis has been reported in a woman with a known prolactinoma.
• also cases were reported of patients with psychoses and concomitant prolactin-
secreting pituitary tumors.
• A review of the literature on bromocriptine and psychosis concluded that
confusion, hallucinations, and delusions have often been reported with the use of
bromocriptine, .
• In addition, cabergoline-induced psychotic exacerbation in schizophrenic patients.
11. pituitary tumor and psychosis
• Some authors have reported prolactinoma growth with risperidone treatment and
suggest using other antipsychotic medications, which do not affect prolactin
secretion .
• It has been reported that psychotic patients treated with aripiprazole showed a
lower liability toward hyperprolactinemia .
• Others have recommended the use of clozapine
• A successful treatment of schizophrenia with no elevation of serum prolactin levels
using a combination of olanzapine and quetiapine was reported in a patient who
could not tolerate clozapine (Sigman and Drury., 2011)
12. Diagnosis
• The clinical diagnosis depends upon the combination of symptoms and signs
resulting from the size of the tumor and/or the type of hormone produced.
• Pituitary adenomas may be imaged with CT or MR scans.
• Evaluation of pituitary function is possible by measuring hormone levels in the
blood and urine.
• Occasionally, the measurement of ACTH levels in the venous blood draining the
pituitary.
• Formal evaluation of the visual fields are useful in outlining peripheral visual loss
before and after surgery .
13. Treatment
Medical therapy is useful in treating some hormone secreting adenomas:
• Prolactinomas: Dopamine agonists which effect the D2 receptors for dopamine
effectively treat prolactin tumors. About 80% to 90% of patients will normalize
their serum prolactin levels. Parlodel (bromocriptine) has been used for many
years. A new drug, Dostinex (carbergoline), may be more effective with fewer
side effects. It can be given by mouth twice a week.
• Cushing's disease
• Acromegaly
14. Surgery:
• transphenoidal approach and transcranial operations for pituitary tumors.
• Today, pituitary surgeons utilize the transsphenoidal approach for most
pituitary tumors. It is safe, effective, and requires a short stay in the hospital.
• For small tumors (less than 10 mm in diameter), the cure rate is greater than
50%
RadiationTherapy:
• Gamma Knife radiosurgery has become increasingly more important in the
control of pituitary adenomas. This technique allows for focused, high-dose
treatment of pituitary adenomas and results in greater rate of control of tumor
growth and better rates of normalization of increased hormone secretion
16. • A 28-year-old woman who, over a decade, had 9 hospitalizations for psychosis
in psychiatry, the final four in a one-year period. This rapid deterioration led us
to uncover potential interactions between her medication for a prolactin-
secreting pituitary tumor and those she was receiving for psychosis. The clinical
effects of increased prolactin levels are poorly understood; however, there is
some evidence that increases in serum prolactin may be associated with
several psychiatric disorders , and conventional neuroleptic medications may
cause an increase in serum prolactin levels.
• Dopamine antagonists are used to treat psychotic symptoms, while dopamine
agonists are used to treat prolactinomas. As a result of the potential
counteractive nature of the treatments, effective management of individuals
who present with both problems is extremely difficult. A lack of guidelines
regarding the monitoring for hyperppatients receiving antipsychotics only
serves to exacerbate the problemrolactinoma in.
17. • Ms. L was first hospitalized at the age of 18. She was in a catatonic state, her
chin was hairy, and she was circling her fingers repetitively. The following day
she was able to speak but was bizarre and inappropriate, believing she had been
admitted because she was cruel to animals as a child. Ms. L reconstituted
quickly, and after two weeks on the antipsychotic drug olanzapine 10 mgs at
bedtime, she gave the following history.
• She had been feeling ill only during the past year when her mother, who suffers
from schizophrenia, had a long hospitalization following a divorce from Ms. L’s
father. Ms. L was not a substance abuser. She had lived with her father who, she
explained, had previously physically, sexually, and emotionally abused her. Ms. L
had had severe hirsutism for two years. Her prolactin level was 125.1 units
(normal range: 20–25 ng/mL). Her diagnosis at this point was psychotic episode,
post traumatic episode had to be ruled out. Magnetic resonance imaging (MRI)
of the brain was ordered and revealed a pituitary tumor. An endocrinologist
prescribed 5 mg bromocriptine to shrink the microneuroadenoma.
18. • Ms. L’s second admission was 6 months later when she expressed feelings of
suicidality to the occupational therapist at her group home. An interview with a
consultant revealed no Axis 1 diagnosis. She was discharged with a diagnosis of
troubled grief reaction and prescribed olanzapine 20 mg qhs, paroxetine 20 mg
daily (qd), procyclidineHCl 5 mg twice a day (bid), and, in addition,
bromocriptine 5 mg qhs to treat the pituitary tumor. She was to go to a
rehabilitation program and see a therapist in the youth service. Some time later,
she left for the Middle East, where she had one admission to hospital for a
psychotic state.
• On her return to North America, she was diagnosed by our outpatient
department with schizophrenia and treated with risperidone. She continued to
have hbromocriptine.
• irsutism and to be treated by her endocrinologist with
19. • On Ms. L’s fourth hospital admission, she was preoccupied with religious ideas
and had minimal insight and judgment. She was prescribed 16 mg risperidone
and quetiapine 200 mg in the morning for her psychosis. The following year Ms.
L was again admitted psychotic and anxious, hyperventilating, showing poor
eye contact, and moving her fingers in a circular motion. She had told her
parents she had felt paranoid and suicidal. Again her insight and judgment were
poor. She had not complied with the psychiatric follow-up treatment as her
mother, in her own psychotic state, had cancelled it. In hospital, Ms. L remained
psychotic on 100 mg of loxapine and 500 mg quetiapine. She was given
electroconvulsive therapy, and this seemed to help her. She agreed to
placement in a group home and to take her medications on discharge. Ms. L was
prescribed flupenthixoldecanoate 75 mg 2 weeks I.M., divalproex sodium
500 mg and loxapineHCl 25 mg. A year later, in 2005, her endocrinologist
prescribed cabergoline to treat the pituitary adenoma to replace the
bromocriptine she had been receiving for five years.
20. • Ms. L’s next hospitalization five years later was the first of four in one year. She
was sad and tearful, felt her psychiatric medications were not working, and had
stopped them. Her last dose of flupenthixoldecanoate had been several months
prior. She was experiencing impaired concentration, memory, and energy. She
had cut her hair bizarrely, felt she had psychic abilities, and reported that her
vision was impaired. Ms. L was highly regressed, initially refusing treatment, but
once restarted on her oral medications, she re-compensated quickly. She
remained with behaviors such as rocking and circular hand movements and
returned to the group home never having remembered or understood why she
had suddenly left it. She was discharged on divalproex sodium 500 mg thrice
daily , procyclidine HCl 5 mg and loxapineHCl 25 mg for her psychosis and
continued cabergoline 0.5 mg twice weekly for the pituitary adenoma.
21. • Three weeks after discharge, Ms. L was picked up by the police in an apartment
lobby where she had spent the night. Ms. L was confused and catatonic, again
suffering impaired insight, judgment, and memory. She spoke of being
possessed, hearing voices, and having visual hallucinations. She was discharged
with ziprasidone 40 mg added to her prescription and a follow up with her
endocrinologist. An MRI showed that her microadenoma had shrunk. Four
weeks later, without apparent provocation, Ms. L quietly walked out of her
group home during dinner. She was found by police roaming barefoot. She
again had serious memory problems and disorganized thinking. Her ziprasidone
was increased to 60 mg, the loxapine decreased to 12.5 mg, and
electroencephalography (EEG) was suggested to rule out seizures in an effort to
explain her memory loss which was normal.
22. • Her doctor had concerns about the possible psychotic side effects of the
dopamine agonist cabergoline used to treat the pituitary tumor and
hyperprolactinemia. The general physician to the psychiatric ward had been
encouraged to consult the involved endocrinologist on this issue, and this
resulted in the cabergoline being discontinued. Ms. L was reorganized enough
to begin to eat and participate in milieu treatment. She had trials of both
ziprasidone and aripiprazole but remained psychotic in her thinking, for
example, getting orders from the devil. Clozapine was started, and the
psychosis began to remit. The endocrinologist felt Ms. L could be kept off the
cabergoline if it impaired her mental status. Ms. L continued to improve and
has not been hospitalized since. Was it getting off the cabergoline or starting
the Clozaril that ultimately led to her improved state, or, as we believe, a
combination of both?