This interesting ppt deals with the Pharmacology of Antiepileptic drugs and the treatment of different types of seizures with beautiful illustrations....
Novel Drugs for Seizure disorder, Newer Drugs for seizure disorders, Recent Advances in treatment of seizure disorder, Recent Advances in Pharmacotherapy of sizure disorders, Recent Advances in Treatment of epilepsy, Newer Antiepileptics, Newer Anticonvulsants
Definition, types and Classification of Migraine according to severity
- Pathophysiology of Migraine (Vascular & Neurovascular)
- Drug Therapy of Acute Migraine attack & Prophylaxis according to SIGN & NICE guidelines
- Triptans & Ergots mechanism of action, side effects and drug interactions
- Management of Migraine in Woman (Menstrual, Hormonal contraception, Pregnancy)
It may contain a brief intoduction of disease, etiology, types of parkinson disease, clinical findings, dignosis, pathophysiology, treatment, drug classification and their mechanisms of actions.
by: Dr. Vishal Pawar, MD Pharmacology
All the recent updates regarding antiepileptics, composed into a single ppt presentation to make researching and learning easier
Novel Drugs for Seizure disorder, Newer Drugs for seizure disorders, Recent Advances in treatment of seizure disorder, Recent Advances in Pharmacotherapy of sizure disorders, Recent Advances in Treatment of epilepsy, Newer Antiepileptics, Newer Anticonvulsants
Definition, types and Classification of Migraine according to severity
- Pathophysiology of Migraine (Vascular & Neurovascular)
- Drug Therapy of Acute Migraine attack & Prophylaxis according to SIGN & NICE guidelines
- Triptans & Ergots mechanism of action, side effects and drug interactions
- Management of Migraine in Woman (Menstrual, Hormonal contraception, Pregnancy)
It may contain a brief intoduction of disease, etiology, types of parkinson disease, clinical findings, dignosis, pathophysiology, treatment, drug classification and their mechanisms of actions.
by: Dr. Vishal Pawar, MD Pharmacology
All the recent updates regarding antiepileptics, composed into a single ppt presentation to make researching and learning easier
New Treatment Devices and Clinical Trials jgreenberger
Dr. Kathryn Davis from Penn Epilepsy Center present on new treatment devices and clinical trials for epilepsy. From the 2014 Epilepsy Education Exchange.
Sedatives and Hypnotics
Pharmacology
Clinical uses
Sedation
Coping with stress and anxiety
Smoothing effects of stimulants
Potentiation of narcotics
Treatment of serious mental disorders
Pleasurable sensations, including intoxication
Classifications
Benzodiazepines
Diazepam, Clonazepam, Oxazepam, Clobazam, Clordiazepoxide, Midazolam
Barbiturates
Phenobarbitone, Amobarbital, Thiopental-Na
Newer drugs
Zolpidem, Zaleplon, Buspirone
Chloral hydrate
Paraldehyde
Diphenhydramine
Benzodiazepines
Properties
High therapeutic index (high LD50)
Relatively safe in overdose
Develop tolerance slowly
Less addiction liability
Benzodiazepines
Benzodiazepines
Most commonly prescribed Benzodiazepines
All Benzodiazepines are classified as Controlled Drugs in some countries.
Most are CD Schedule 4
Diazepam (Valium,Anxicalm)
Alprazolam (Xanax)
Bromazepam (Lexotan)
Clobazam (Frisium)
Lormetazepam (Noctamid)
Nitrazepam (Mogadon)
Clonazepam
Two are CD Schedule 3
Flurazepam (Rohypnol)
Temazepam (Nortem)
Structure Activity Relationship
In ring A an electron – withdrawing group such as Cl, Br, NO2 or CN at position 7.
A methyl Group is attached to the nitrogen atom in position 1 in ring B. However, substituents at position 1 that are metabolically are still clinically useful e.g. Flurazepam.
Replacement of the carbonyl function with two hydrogens in position 2 gives medazepam, less potent than diazepam.
Replacement of one of the hydrogen with a OH group on position 3 lower the activity on the one hand and aids elimination on the other.
Introduction of a carbonyl function in the 3 position increases the duration of action and also favours formation of water soluble salts.
e) α-pyridyl derivative and cycloalkyl substituent at 5 position give potent compounds.
f) Electronegative substituents such as Cl or F at the ortho and disubstituted in both ortho positions in ring C.
g) Derivatives with additional rings joining the diazepine nucleus at the 1 and 2 positions are generally more active than the corresponding 1-methylbenzodiazepines.
h) Replacement of the benzene ring by heteroaromatic (e.g. pyrazole) resulted in compounds with interesting anxiolytic properties ( e.g. ripazepam).
i) Saturation of the 4,5- double bond reduces potency, as does a shift of the unsaturation into the 3,4-position.
Barbiturates
Barbiturates
Barbiturates
Barbiturate poisoning
Treatment of Barbiturate poisoning
Buspirone
this ppt deals with different types of drug interactions with examples and highlights important principles in monitoring drug therapy....for better understanding of complexity of multiple drug usage (polypharmacy)
complete and detail study on the topic of anti epileptic drugs . the topic contain drugs of epilepsy with their uses, side effect, mechanism of action, classification of epileptic drugs.
basic information of receptors
This presentation consisits about antimanic agents, its mode of action, indication, contraindication, side-effects and nursing management. It also has details of Carbamazepine and Valporate.
Difference between seizures and convulsion, types of epilepsy,drugs used in epilepsy as per different mechanism of action,treatment of status epilepticus,guidlines for treatment of epilepsy
This interesting, illustrative presentation is a preliminary guide for preparing medical & paramedical teachers for effective teaching and enable them to conduct different courses for medical & paramedical students
This interesting and useful ppt highlights different pharmacokinetic concepts with illustrations for easy understanding - an overview for revision for medical and paramedical students
This is an excellent ppt on Dermatological pharmacology highlighting types of formulations, topical preparations and the treatment of individual skin disorders with illustrations...!!
This interesting ppt is the continuation of the Pharmacology of Opioid analgesics I... This impressive ppt highlight the pharmacology, advantages and disadvantages of opioid analgesics other than morphine with illustrations....!!
This interesting ppt is about the Pharmacology of morphine and acute morphine poisoning dealt with illustrative pictures, diagrams to facilitate learning for medical/paramedical students....
This is an Inspiring presentation on cultural diversities of india and how to work in cohesion.. mainly for medical students studying Foundation course in medicine...
This is an interesting and novel PPT on the Pharmacology of NSAIDs, on drugs other than aspirin ( for Aspirin check NSAIDs PART I ) illustrated with beautiful pictures and flowcharts....!!
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.
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.
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.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
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
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
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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.
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.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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.
4. Interesting Facts about Human Brain
∗ The human brain has about 100,000,000,000
(100 billion) neurons
∗ There are about 100,000 miles of blood
vessels in the brain.
5. The human brain is the fattest organ in the body
and may consists of at least 60% fat.
There are no pain receptors in the brain, so the brain
can feel no pain.
Neurons multiply at a rate 250,000 neurons/minute
during early pregnancy
15. Group of disorders of CNS
Affects 5-10/ 1000 population
2nd
most common CNS disorder after stroke
Known as disease of lightening
16.
17.
18.
19. Characterized by paroxysmal cerebral
dysrhythmia
Manifests as brief episodes of loss or
disturbance of consciousness
with or without convulsions, sensory or
psychiatric phenomena
20.
21.
22.
23.
24.
25. Stabilize membrane and prevent
depolarization by action on ion
channels
Increase GABAminergic transmission
Decrease EAA transmission
30. Action on Ion
Channels
Enhance GABA
Transmission
Inhibit EAA
Transmission
Na+
:
Phenytoin, Carbamazepine,
Lamotrigine, Topiramate
Valproic acid
Ca++
:
Ethosuximide
Valproic acid
Benzodiazepines
(diazepam, clonazepam)
Barbiturates (phenobarbital)
Valproic acid
Gabapentin
Vigabatrin
Topiramate
Felbamate
Felbamate
Topiramate
Na+
: For general tonic-
clonic and partial seizures
Ca++
:
For Absence seizures
Most effective in myoclonic but
also in tonic-clonic and partial
Clonazepam: for Absence
33. Act by Enhancing GABA A receptor mediated
synaptic inhibition
Increases seizure threshold, limits spread
Cause sedation, decrease intelligence, learning,
memory
Cheapest antiepileptic
Effective in GTCS, SPS, CPS
Less popular
34.
35.
36.
37. A prodrug
Produce active metabolites
Efficacy similar to phenobarbitone
Useful in refractory epilepsy adjuvant to
phenytoin
38.
39. Barbiturate analogue
M.O.A prolong the inactivated state of
neuronal voltage dependent Na+ channels,
stabilize neuronal membrane
80-90% protein bound
Metabolism changes from 1st
order to zero
order
Monitoring is very helpful in tailoring dosage
75. A Prodrug of phenytoin
Given i.v. or i.m.
rapidly converted to phenytoin
Given i.v Avoids complications
associated with phenytoin: vein irritation,
tissue damage
Can be injected in drip
Alternative to phenytoin in status
epilepticus
76.
77.
78.
79.
80. Chemically related to imipramine
MOA – Similar to phenytoin
75% protein bound
Long half life
Autoinduction occur
81.
82. Hypersensitivity
Dose related neurotoxicity- drowsiness,
ataxia, vertigo
Hypersensitivity reactions- Hepatitis, lupus
like syndrome
Enhance ADH action
Aplastic anemia
Minor fetal malformations
83.
84.
85.
86.
87.
88.
89.
90.
91. Induce microsomal enzymes – OCP
failure
Metabolism Induced by phenytoin &
valproate
Metabolism Inhibited by erythromycin
92.
93. 1ST
choice in GTCS,CPS,SPS
1st
choice in Trigeminal neuralgia ,
post herpetic neuralgia
and other neuropathic pain
Manic depression
Acute mania
Dose : 200-400 mg TDS
94.
95.
96.
97.
98.
99.
100.
101. Less toxic than carbamazepine
Mild enzyme inducer – less drug
interactions
Less side effects
Cause hyponatremia
102.
103.
104.
105.
106.
107.
108.
109.
110. Broad spectrum anticonvulsant
MOA – prolongation of Na channel
inactivation
Attenuation of Ca ++ mediated T current
Inhibit GABA transaminase increase
GABA
Increase GABA synthesis
PK- 90% protein bound
111.
112. Drowsiness, ataxia, tremor –dose related
Alopecia, curling of hair, weight gain
Hypersensitivity
Fulminant hepatitis in children – rare but
serious
Young girls – menstrual irregularities,
polycystic ovarian disease
Monitor liver function
Neural tube defects in pregnancy
113.
114.
115.
116.
117.
118.
119.
120.
121. Displace phenytoin from
protein binding sites
Induce metabolism of
carbamazepine
Contraindicated with
carbamazepine,
clonazepam
122. Drug of choice for Absence seizures
Alternative/ adjuvant drug for GTCS,
SPS, CPS
1st
choice for myoclonic seizures, atonic
seizures
Prophylaxis in migraine
Mania
Bipolar depression
133. Not used for long term therapy
because of
Prominent sedative action
Rapid development of tolerance
134.
135.
136. Drug of choice for
status epilepticus
tetanus
Eclampsia
Convulsant poisoning
Rectally given for febrile
convulsions in children
137.
138.
139.
140.
141. Given i.v – can cause
marked fall in BP,
Respiratory depression
Cause sedation , tolerance
142.
143.
144. Benzodiazepine with prominent
anticonvulsant activity
Potentiate GABA induced Cl influx
ADR- sedation, lack of concentration,
irritability, ataxia
Uses – absence seizures, adjuvant in
myoclonic, akinetic seizures, infantile spasms
Limitation – tolerance in 6 months
145.
146.
147.
148.
149.
150.
151. Similar to clonazepam
Used as an adjuvant to other antiepileptic
drugs in Refractory epilepsy
ADR – sedation, psychomotor retardation
152.
153.
154. Alternative to diazepam in status epilepticus
And emergency control of other convulsions
Action is more sustained than diazepam
155.
156. Like carbamazepine Blocks Na channels
stabilizes presynaptic membrane
blocks high voltage dependent Ca channels
Prevents release of excitatory
neurotransmitters
Broad spectrum action
Used as monotherapy and add on drug
157.
158. Sedation,
ataxia,
diplopia,
RASH –sometimes life threatening
Negative effect on cognitive function not
reported
159.
160.
161.
162.
163. GABA derivative
Increases GABA release
Add on drug in SPS, CPS
Pain due to diabetic neuropathy, post herpetic
neuralgia
Migraine
Manic depression
ADR- sedation, tiredness
164.
165.
166.
167.
168.
169.
170. Inhibit GABA transaminase increases
synaptic GABA
ADR – can cause behavioral changes –
(drawback),
drowsiness, amnesia,
TUNNEL VISION
Adjuvant medication for refractory epilepsy
171.
172.
173.
174. Broad spectrum anticonvulsant
Has Risk of aplastic anemia, hepatic failure
Reserved for use in refractory epilepsies
175.
176.
177. Recent drug
Prevents GABA uptake Potentiates GABA
mediated synaptic inhibition
ADR – sedation, tiredness
Add on drug for partial seizures
178.
179. Weak Carbonic anhydrase inhibitor
Broad spectrum anticonvulsant
Act by antagonizing glutamate,
GABA potentiation, prolonging Na channel
prolongation
Useful as supplementation in refractory SPS,
CPS, GTCS
Approved for prophylaxis of migraine
ADR – sedation, ataxia, psychiatric
symptoms
180.
181.
182.
183. Adjuvant drug in refractory partial seizures
Mechanism unknown
ADR- tiredness, drowsiness
184.
185.
186. Sulfonamide derivative
Has broad spectrum action
Has Long half life
May cause kidney stones, oligohydrosis
192. Acquired epilepsy
Physical insult to the brain
50% of patients with severe head injuries will develop a seizure
disorder
Brain tumors,
stroke,
CNS infections,
febrile seizures
Initial seizures cause anatomical events that lead to future
vulnerability
Latent period occurs
193.
194.
195.
196.
197. A drug which decreases the frequency and/or
severity of seizures in people with epilepsy
Treats the symptom of seizures, not the
underlying epileptic condition
198.
199. Goal—maximize quality of life by
minimizing seizures and adverse drug
effects
Currently no “anti-epileptogenic” drugs
available
223. Medical emergency
Continuous epilepsy without intermission >
30min
Diazepam 10 mg i.v bolus 2mg/ minute or
clonazepam or (Now - LORAZEPAM 4mg i.v
preferred)
Phenobarbitone or phenytoin act slowly
Fosphenytoin i.v
224. I.V midazolam/ propofol/ thiopentone
with or without muscle relaxants with
positive pressure ventilation
225.
226. Airway
Oxygen
Fluid & electrolytes
BP
Cardiac rhythm
Glucose
Care of the unconscious
227.
228.
229.
230. Focal with minimal spread of abnormal
discharge
Patient often exhibits abnormal activity of
single limb
normal consciousness and awareness are
maintained
231.
232. Carbamazepine, phenytoin 1st
line
Valproate second line, hepatotoxic
Young girls carbamazepine
Lamotrigene, gabapentin, topiramate –
good alternatives
Newer drugs – as add-on therapy
Post head injury – phenytoin, valproate
233.
234. Local onset, then spreads
Impaired consciousness
Clinical manifestations vary with site of origin and degree
of spread
Presence and nature of aura
Automatisms
Other motor activity
Temporal Lobe Epilepsy most common
235.
236. Difficult to control
Relapses common
Drug of choice – carbamazepine
If not controlled – add phenytoin, valproate
Refractory cases- lamotrigene, gabapentin,
clobazam, topiramate
237.
238. Sudden onset of impaired consciousness
associated with staring
Usually Less than 30 seconds
Ethosuximide
Valproate – more commonly used , superior
in mixed absense and GTCS
LAMOTRIGENE good alternative
Clonazepam 2nd
line
clobazam
239.
240.
241. Sudden, brief, shock like contraction of
muscles
Valproate
lamotrigene
242. Sudden loss of postural tone and the head
may drop or the person may drop
Valproate
lamotrigene
243.
244. Some children especially under 5 Develop
convulsions during fever
Don’t allow temperature to rise
External cooling
Paracetamol
Treatment - Rectal diazepam 0.5 mg/kg
i.v preparation can be used
Prophylaxis with rectal or oral diazepam at
the onset of fever
250. K+ channels have important inhibitory control
over neuronal firing in CNS
K+ channel agonists would decrease hyper
excitability in brain
valproate
Retiagabine is a novel AED in clinical trials
251.
252.
253. A mechanic was removing a cylinder head
from the motor of a motorcycle when he
spotted a well-known heart surgeon in his
shop.
The mechanic shouted across the garage,
"Hey, Doc, can I ask you a question?“
254. The surgeon a bit surprised, walked over to the
mechanic .
The mechanic asked, "So Doc, look at this engine. I
open its heart, take valves out, fix 'em, put 'em back
in, and when I finish, it works just like new.
So how come I get such a small salary and you get
the really big bucks, when you and I are doing
basically the same work?“
255.
256. The surgeon paused, smiled
and leaned over,
and whispered to the mechanic...
"Try doing it with the engine running."
Editor's Notes
Top. Facial features of the fetal hydantoin syndrome; note broad, flat nasal bridge, epicanthal folds, mild hypertelorism, strabismus, and wide mouth with prominent upper lip. Bottom. Hypoplasia of distal phalanges and nails
Figure 1: Left hand was edematous and had purplish-blue discoloration without blisters
Mentions: Phenytoin is a nonsedative, broad-spectrum anticonvulsant drug that has been used in the treatment and prevention of seizures for decades. Intravenous (IV) administration of phenytoin with or without extravasation can result in a devastating complication called as “Purple Glove Syndrome (PGS)” for its characteristic purplish-black discoloration accompanied by edema and pain distal to the site of injection.[1] Here we report a case of PGS following extravasation of phenytoin so as to alert clinicians on this potentially serious injury and suggest the ways to prevent it. A 60-year-old woman was admitted in a peripheral hospital for frontal bone fracture following road traffic accident (RTA) with normal brain parenchyma and generalized tonic-clonic seizure, for which she received 900 mg of loading dose of phenytoin dissolved in 100 ml of normal saline through a 22-gauge peripheral intravenous catheter kept in her left dorsum of the hand over 45 minutes. Two hours later, the patient's left hand was swollen and became bluish in color. The patient complained of severe pain at the site of injection, which soon spread throughout the left hand. On examination, the patient's left hand and forearm were edematous and had purplish-blue discoloration without blisters, cool to the touch [Figure 1] and tender. The radial pulse was feeble and the capillary refill was sluggish and pulse oximeter applied showed a good trace. Duplex ultrasound of the upper limb showed normal flow. A working diagnosis of PGS, possibly due to the extravasation of intravenous phenytoin, was made. Compartment syndrome was ruled out.
Carbamazepine allergy. Extensive rash over the back and arms of a 74-year-old woman due to an allergic reaction to carbamazepine. Carbamazepine is an anticonvulsant drug used in the long term treatment of epilepsy and to relieve neuralgia. A reaction to the drug has caused a rash consisting of numerous circular or irregular red spots which may be itchy. The rash may be accompanied by fever, sore throat, headache or diarrhoea. Treatment of such allergic reactions involves withdrawal of the causative drug. Corticosteroid drugs can be given to reduce inflammation and irritation.
Craniofacial features of a one-and-a-half-year-old child exposed in utero to both sodium valproate and carbamazepine. She has cherubic facies, a tall forehead, broad nasal root and flat nasal bridge, blunt nasal tip, smooth philtrum, and thin vermilion border to the upper lip.