Bipolar disorder is characterized by alternating periods of depression and mania. It has genetic and environmental causes and is thought to involve neurotransmitter imbalances. Treatment involves mood stabilizers like lithium long-term combined with other drugs depending on the current mood state, such as antipsychotics for mania. Lifestyle changes and psychotherapy can also help manage symptoms. The goal of treatment is to prevent mood episodes and maintain good functioning.
In this slideshare we gonna discuss about Mania Disorder, a key component of Bipolar Disorder, is a mental health condition characterized by extreme mood swings, with episodes of mania at one end and depressive states on the other. This comprehensive presentation delves into the complexities of Mania Disorder, shedding light on its symptoms, underlying causes, and the range of treatment options available.
In this slideshare we gonna discuss about Mania Disorder, a key component of Bipolar Disorder, is a mental health condition characterized by extreme mood swings, with episodes of mania at one end and depressive states on the other. This comprehensive presentation delves into the complexities of Mania Disorder, shedding light on its symptoms, underlying causes, and the range of treatment options available.
This presentation is a credit presentation part of my M.Pharm 1st Semester review. It discuss about the Antidepressant primary in-vitro and in-vivo screening models.
A presentation about depressive disorder. The presentation composed of the definition, causes, types, clinical feature, diagnosis, prognosis, treatment and prevention of depression
Depression is a mental disorder and has become most common in recent years. This slide or presentation deals with all types of aetiologies of depression, theories that are involved in development of depression, pathophysiology of drepression, various classes anti-depressant their pharmacology with the adverse events or effects. This also gives a brief note on difference between depression and sadness.
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.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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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
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.
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.
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.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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
1. Bipolar disorder
Definition: Bipolar disorder is characterized by periods of deep, prolonged,
and profound depression that alternate with periods of an excessively elevated
or irritable mood known as mania.
Bipolar disorder is divided into four subtypes based on the identification of
specific mood episodes: bipolar I, bipolar II, cyclothymic disorder, and bipolar
disorder not otherwise specified
Etiologic theories of bipolar disorder:
The exact etiology of bipolar disorder is unknown. Bipolar disorder is
thought to be a complex genetic disease that is environmentally
influenced and caused by a wide range of neurobiologic abnormalities.
Stressfullife events, alcohol or substance use, and changes in the sleep-
wake cycle can elicit the expression of genetic or biologic vulnerabilities
that causedysregulationof neurotransmitters,neuroendocrinepathways
and second messenger systems.
Genetic factors:
Linkage studies suggest that certain loci on genes and the X chromosome may
contribute to genetic susceptibility of bipolar disorder
2. Nongenetic factors:
1.Perinatal insult
2.Head trauma
3.Environmental factors
Desynchronization of circadian or seasonal rhythms cause diurnal
variations in mood and sleep patterns and can result in seasonal
recurrences of mood episodes.
Changes in the sleep-wake cycle or light-dark cycle can precipitate
episodes of mania or depression.
Bright light therapy can be used for the treatment of winter depression
and can precipitate hypomania, mania, or mixed episodes.
4.Psychosocial or physical stressors
Stressful life events often precede mood episodes and can increase
recurrence rates and prolong time to recovery from mood episodes.
5.Nutritional factors
Deficiency of essential amino acid precursors in the diet can cause a
dysregulation of neurotransmitter activity (e.g., L-tryptophan deficiency
causes a decrease in 5-HTand melatonin synthesis and activity).
Deficiency in essential fatty acids (e.g., omega-3 fatty acids) can cause a
dysregulation of neurotransmitter activity
6.Neurotransmitter/neuroendocrine/hormonaltheories
Dysregulation between excitatory and inhibitory neurotransmitter
systems; excitatory: NE, DA, glutamate, and aspartate; inhibitory: 5-HT
and GABA.
7.Monoaminehypothesis
An excess of catecholamines (primarily NE and DA) cause mania.
Deficit of neurotransmitters (primarily NE, DA, and/or 5-HT) cause
depression.
8.Dysregulation of amino acid neurotransmitters
Deficiency of GABA or excessiveglutamate activity causes dysregulation
of neurotransmitters (e.g., increased DA and NE activity).
3. 9.Cholinergic hypothesis
Deficiency of acetylcholine causes an imbalance in cholinergic-
adrenergic activity and can increase the risk of manic episodes.
Increased centralacetylcholine levels can increasethe risk of depressive
episodes.
10.Secondary messenger system dysregulation
AbnormalG protein functioning dysregulates adenylatecyclase activity,
phosphoinositideresponses, sodium/potassium/calcium channel
exchange, and activity of phospholipases.
Abnormalcyclic adenosine monophosphateand phosphoinositide
secondary messenger system activity.
Abnormalprotein kinase C activity and signalling pathways.
11.Hypothalamic-pituitary-thyroid axis dysregulation
Hyperthyroidismcan precipitate manic-like symptoms.
Hypothyroidismcan precipitate a depression and be a risk factor for
rapid cycling
Hormonalchanges during the female life cycle can cause dysregulation
of neurotransmitters (e.g., premenstrual, postpartum, and
perimenopause).
12.Membrane and cation theories
Abnormalneuronal calcium and sodium activity and homeostasis cause
neurotransmitter dysregulation.
Hypocalcemia has been associated with causing anxiety, mood
irritability, mania, psychosis, and delirium.
Hypercalcemia has been associated with causing depression, stupor, and
coma.
Extracellular and intracellular calcium concentrations may affect the
synthesis and release of NE, DA, and 5-HT, as well as the excitability of
neuronal firing.
13.Sensitization and kindling theories
Recurrences of mood episodes causebehavioralsensitivity and
electrophysiologic kindling (similar to the amygdala-kindling models for
seizures in animals) and can resultin rapid or continuous mood cycling.
4.
5. Evaluation and diagnosis of mood episodes:
The mood states are further separateinto four subcategories to differentiate
the currentor most recent mood episode: major depressive, manic,
hypomanic, or mixed.
1.Major depressive- DSM-IV-TR Criteria
>2-Week period of either depressed mood or loss of interest or pleasure in
normal activities, associated with
at least five of the following symptoms:
• Depressed, sad mood (adults); can be irritable mood in children
• Decreased interest and pleasurein normal activities
6. • Decreased appetite, weight loss
• Insomnia or hypersomnia
• Psychomotor retardation or agitation
• Decreased energy or fatigue
• Feelings of guilt or worthlessness
• Impaired concentration and decision making
• Suicidal thoughts or attempts
2.Manic
>1-Week period of abnormaland persistentelevated mood (expansiveor
irritable), associated with at least three
of the following symptoms (four if the mood is only irritable):
• Inflated self-esteem(grandiosity)
• Decreased need for sleep
• Increased talking (pressureof speech)
• Racing thoughts (flight of ideas)
• Distractible(poor attention)
• Increased activity (either socially, at work, or sexually) or increased motor
activity or agitation
• Excessiveinvolvement in activities that are pleasurablebut havea high risk
for serious consequences
(buying sprees, sexualindiscretions, poor judgmentin business ventures)
3.Hypomanic
At least 4 days of abnormaland persistentelevated mood (expansiveor
irritable); associated with at least three of the following symptoms (four if the
mood is only irritable)
4.Mixed
Criteria for both a major depressiveepisodeand manic episode (except for
duration) occur nearly every day for at least a 1-week period
5.Rapidcycling:
>4 Major depressiveor manic episodes (manic, mixed, or hypomanic) in 12
months
7. Treatment:
Desired outcomes:
The desired outcome for bipolar disorder is to preventan acute manic,
hypomanic, or depressiveepisode,
To maintain good functioning, and
To prevent further episodes of mania or depression.
8. General approach to treatment:
The treatment of bipolar disorder can vary depending on what type of episode
the patient is experiencing. Once diagnosed with bipolar disorder, patients
should remain on a mood stabilizer (e.g., lithium, valproate) for their lifetime.
During acute episodes, medications can be added and then tapered once the
patient is stabilized and euthymic.
For example, when treating a patient for mania with psychotic features, the
patient should be on a mood stabilizer and an antipsychotic.
If treating a patient for a severe depressive episode, a clinician may need to
maximize the dose of the mood stabilizer or add another medication (e.g.,
quetiapine).
Non pharmacological therapy:
1.Electroconvulsive therapy [ECT]
2.High-intensity bright light therapy
3.Repetitive transcranialmagnetic stimulation (rTMS)
4.Vagus nervestimulation (VNS) may also havea role in treatment-resistant
rapid-cycling bipolar disorder
Life style modifications:
Adequate nutrition, sleep, exercise, and stress reduction.
Adjunctive psychoeducational programs, supportive counseling, insight
oriented psychotherapy (individual or group), couples or family therapy,
cognitive behavioral therapy, and communication enhancement training.
Pharmacological therapy:
Pharmacotherapy is crucial for the acute and maintenance treatment of
bipolar disorder and includes (mood stabilizers)
1.Lithium carbonate
2.Anti convulsants
3.AtypicalAntipsychotics
4.Adjunctiveagents like Antidepressants and Benzodiazepines
9. DRUG INITIAL DOSE
1.Lithiumsalts
Lithium carbonate 900-2400mg/day, TID
Lithium citrate -
2.Anticonvulsants
Divalproexsodium
(sodium valproate+
valproic acid)
750-3000mg/day, OD
Lamotrigine 50-400mg/day
Carbamazepine 200-1800mg/day, TID
3.Atypical antipsychotics
Olanzapine 5-20mg/day, OD
Quetiapine 50-800mg/day
Risperidone 0.5-6mg/day, OD
Ziprasidone 40-160mg/day
Aripiprazole 10-30mg/day, OD
1.Lithiumcarbonate:
Chronic lithium administration may modulate gene expression and have
neuroprotective effects
lithium has been found to have efficacy, but there can be a 6- to 8-week delay
for its antidepressant effects
Dosing is generally titrated up to achieve steady state serum lithium
concentrations of 0.6 to 1.2 mEq/L (mmol/L).
Lithium requiresregularassessmentofrenaland thyroid functioning and lithium
blood level monitoring to minimize adverse effects.
MOA:
1.Effecton Electrolytes and Ion Transport-
Lithium act by partially replacing the Na+
ions in the body. This leads to changes
in the ionic fluxes across the brain cells or in the properties of cell membranes.
2.Effect on Neurotransmitters-
Lithium decreases the release and action of neurotransmitters, such as
dopamine and norepinephrinein the brain, which may correct the imbalance in
the turnover of brain monoamines
10. 3.Effect on secondary messengers and intracellular enzymes-
In mania, these neuronal circuits become hyperactive which results in more IP3
and DAG production. Lithium selectively inhibits the hydrolysis of IP2 to IP1 and
IP1 to inositol. As a result, the levels of inositol decreases and this in turn
decreases IP3 and DAG levels
4.A specific isoform of protein Kinase-C may be effected by the lithium, which
leads to the altered protein Kinase-C mediated signalling. This results in altered
gene expression and production of proteins that ultimately prolong the
stabilization of mood.
5.Inhibition of adenylyl cyclase results in antidepressant and antimanic effects.
ADR:
- Nausea, Vomiting, Diarrhoea(Osmotic), Tremors, ataxia, oedema
(Osmotic), arrhythmias, blurred vision, glycosuria (Insulin like action),
polyuria (inhibits action of ADH on DCT), allergy
- Seizures, cerebralataxia, hypotension, ECG changes, hypothyroidism
(interferes with iodination of tyrosine), coma, leucocytosis.
- Ebstein’s anomaly in the foetus
Contraindications:
- Pregnancy (Foetalgoitre),
- lactating women (Lethargy, cyanosis and hepatomegaly in newborns)
- patient with low sodium or on diuretics (diuretics increases lithium
conc.)
- In sick sinus syndrome(Increased leucocytes)
11. 2.Anti convulsants:
MOA:
Effect on neurotransmitters of brain:
a. On Gamma Aminobutyric Acid (GABA)
GABA is a fast acting inhibitory neurotransmitter presentin the brain and spinal
cord. Several antiepileptic drugs act to increase the effect of GABA and thus
prevent the excitation of neurons
I. GABA facilitators:
These drugs elicit their action by binding to a specific site located on the GABAA
receptors in the brain. Once bound, these drugs facilitate the opening of
chloride channels, leading to the influx of more amount of chloride ions,
generation of high negative potential and hyperpolarization of the cell. Due to
this, the post synaptic nerve impulse transmission and thus excitation of the
neurons is inhibited
II. GABA reuptake inhibitors:
GABA is transported fromthe synaptic space into the neurons and glial cells for
its metabolism. This transportation of GABA is facilitated by specific GABA
transporter. Some of the antiepileptic drug bind to these transporters and
inhibit the transportation of GABA. This raises the levels of GABA in the synaptic
cleft, due to which inhibition of postsynaptic nerve impulse transmission and
excitation of neurons occurs
III. GABA Agonist:
GABA agonists act by increasing the concentrations of GABA by enhancing the
effect of enzymeGAD (glutamic acid decarboxylase), which converts glutamate
to GABA
IV. GABA-Transaminase inhibitors:
GABA-T is an enzyme responsiblefor the catabolism of GABA. Some drugs bind
irreversibly to GABA-T due to their structural similarity with GABA and inhibit
the action of the enzyme. Thus, the concentration of GABA increase with an
inhibition of postsynaptic nerve impulse transmission and excitation of the
neurons
12. b. On Glutamate
Glutamate is an excitatory neurotransmitter present in the brain. The different
receptors subtypes of glutamate are NMDA, AMPA, Kainate. Some drugs act by
binding to these receptors and inhibit influx of calcium and sodium ions and
efflux of potassium ions. Thus this preventexcitation of neurons and generation
of action potentials.
Effect on Ion channels:
a. Sodium channel inhibitors:
Antiepileptic drugs block the use-dependent or voltage-gated sodium channels
which are responsible for carrying the current required to generate an action
potential. Thus, repetitive firing of the neurons is inhibited
b. Calcium channel inhibitors:
Antiepileptic drugs act by blocking the calcium channels or calcium-dependent
potassium channels. Due to such blockade, influx of calcium currents and
ultimately the generation of action potential is inhibited. Thisfurther inhibits the
further excitation of neurons.
Drug ADRs Contraindications
Valproic acid Nausea, vomiting,
anorexia, heart burn,
tremors, ataxia, hairloss
and hepatotoxicity
In pregnancy and
lactation
Carbamazepine Ataxia, dizziness,
vertigo, diplopia, NVD,
rashes, hepatitis,
aplastic anemia
-In pregnancy and
lactation
-patients having bone
marrow depression,
hepatic disorders
-Patient having AV heart
block (CBZ block Na+
influx)
Lamotrigine Drowsiness,asthenia,
diplopia, ataxia,
agitation, skin rashes
-
13. 3.Atypical Antipsychotics:
MOA:
High affinity towards5-HT2,NA(α2)and Muscarinicand Histamine(H1)receptors
Very low affinity towards D2-receptors and inhibits these receptors.
DRUG ADRs
Olanzapine Sedation, priapism, postural
hypotension, dry mouth,
constipation, weight gain
Risperidone Postural hypotension, fewer
Aripiprazole Extrapyramidal symptoms
Clinical usage of drugs:
Hypomania:
Step 1:
Initiate mood stabilizing medication
-Consider adding a benzodiazepine(lorazepam or clonazepam) for shortterm
adjunctivetreatment of agitation or insomnia if needed, if responseis
inadequate
Step 2:
Consider a two-drug combination
i.Lithium+Anticonvulsant/Antipsychotic
ii.Anticonvulsant+Anticonvulsant/Antipsychotic
Mania:
Step 1:
Consider a two-drug combination
Lithium/Anticonvulsant/Antipsychotic+Benzodiazepine (lorazepam)
-Consider adding an antipsychotic for short-term adjunctivetreatment of
agitation or insomnia
-Do not combine antipsychotics, if responseis inadequate
14. Step2:
consider a three-drug combination
-Lithium+Anticonvulsant+Antipsychotic
- Anticonvulsant+Anticonvulsant+Antipsychotic, if responseis inadequate
Step3:
Consider ECT for mania with psychosis or catatonia
Mildtomoderate depressive episode:
Initiate mood stabilizing medication/Alternative fluoxetine+olanzapine
combination
Severe depressiveepisode:
Step:
Initiate mood stabilizing medication/Alternative fluoxetine+olanzapine
combination
-If psychosis is present, initiate an antipsychotic in combination with above, if
responseis inadequate
Step2:
Consider carbamazepineor adding antidepressant, if responseis inadequate
Step3:
consider a three drug combination:
-Lithium+Anticonvulsant(lamotrigine)+Antidepressant
-Lithium+Antipyschotic(quetiapine)+Antidepressant, if responseis inadequate
Step4:
Consider ECT for treatment-refractory illness and depression with psychosis or
catatonia
15. Special population:
Pregnancy/Lactation:
Based on Risk benefit ratio must be weighed
If using lithium during pregnancy, doseadjustments and closemonitoring of
serumlevels will beneeded due to changes in glomerularfiltration rates and
renal perfusion rates during pregnancy and immediately after delivery
The use of anticonvulsants also poses a teratogenic risk when used during
pregnancy. Neural tube defects cause the most concern for clinicians
treating pregnant patients during their first trimester of pregnancy
Administration of folate can reduce the risk of neural tube defects
Caution should be used when prescribing antipsychotics during pregnancy
Treatment of catatonia also varies from standard treatment in that mood
stabilizers and antipsychotics have minimal effect. Catatonic features such
as mutism, motor excitement, stereotypic movements, waxy flexibility,
negativism, echopraxia, and echolalia are best treated with
benzodiazepines, specifically lorazepam. The use of antipsychotics in
catatonia should be minimized because of an increased risk of neuroleptic
malignant syndrome.