Please find the power point on Acute management of seizure. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Coma is defined and the anatomy of consciousness explained. The various levels of arousal, AVPU scale and Glasgow Coma Scale described. The differential diagnosis of coma discussed are coma with & without focal deficits and the meningitis syndrome.
The various aspects of history discussed in details. The examination part includes the general examination, Brainstem reflexes, motor functions with the signs of lateralisation and meningeal irritation signs.
The basic lab investigations, Imaging and special investigations like CSF examination, EEG discussed.
Elevated intracranial pressure and its management explained.
Please find the power point on Acute management of seizure. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Coma is defined and the anatomy of consciousness explained. The various levels of arousal, AVPU scale and Glasgow Coma Scale described. The differential diagnosis of coma discussed are coma with & without focal deficits and the meningitis syndrome.
The various aspects of history discussed in details. The examination part includes the general examination, Brainstem reflexes, motor functions with the signs of lateralisation and meningeal irritation signs.
The basic lab investigations, Imaging and special investigations like CSF examination, EEG discussed.
Elevated intracranial pressure and its management explained.
ATAXIA IN CHILDREN -CAUSES, MANAGEMENT, INVESTIGATIONS, TYPES, COMMONEST ATAXIA IN CHILDREN IN DETAIL, HOW WILL YOU FIND OUT THE CAUSE FOR ATAXIA IN CHILDREN FLOWCHART, DEFINITION, TREATMENT
Hello readers.................!!!!!!!!!!!!!!
This is my 32nd powerpoint.....its regarding a form of childhood epilepsy, known as "LENNOX-GASTAUT SYNDROME".
It has been dealt with in the Therapeutics way, and in precise format.
Do look into it and give your reviews!!!!
Thank you!!!!
@rxvichu-alwz4uh!!!!
:) :)
How to manage status epilepticus, what drugs should be used and when to use what to avoid and need to know
everything you should have about status epilepticus is here.
ATAXIA IN CHILDREN -CAUSES, MANAGEMENT, INVESTIGATIONS, TYPES, COMMONEST ATAXIA IN CHILDREN IN DETAIL, HOW WILL YOU FIND OUT THE CAUSE FOR ATAXIA IN CHILDREN FLOWCHART, DEFINITION, TREATMENT
Hello readers.................!!!!!!!!!!!!!!
This is my 32nd powerpoint.....its regarding a form of childhood epilepsy, known as "LENNOX-GASTAUT SYNDROME".
It has been dealt with in the Therapeutics way, and in precise format.
Do look into it and give your reviews!!!!
Thank you!!!!
@rxvichu-alwz4uh!!!!
:) :)
How to manage status epilepticus, what drugs should be used and when to use what to avoid and need to know
everything you should have about status epilepticus is here.
This slides contains all you need to know about "Status Epilepticus" in a nutshell. It includes definition, investigation, emergency management of status epilepticus. This educational material is suitable for med students, paramedics, nurses & neurology residents.
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.
HOT NEW PRODUCT! BIG SALES FAST SHIPPING NOW FROM CHINA!! EU KU DB BK substit...GL Anaacs
Contact us if you are interested:
Email / Skype : kefaya1771@gmail.com
Threema: PXHY5PDH
New BATCH Ku !!! MUCH IN DEMAND FAST SALE EVERY BATCH HAPPY GOOD EFFECT BIG BATCH !
Contact me on Threema or skype to start big business!!
Hot-sale products:
NEW HOT EUTYLONE WHITE CRYSTAL!!
5cl-adba precursor (semi finished )
5cl-adba raw materials
ADBB precursor (semi finished )
ADBB raw materials
APVP powder
5fadb/4f-adb
Jwh018 / Jwh210
Eutylone crystal
Protonitazene (hydrochloride) CAS: 119276-01-6
Flubrotizolam CAS: 57801-95-3
Metonitazene CAS: 14680-51-4
Payment terms: Western Union,MoneyGram,Bitcoin or USDT.
Deliver Time: Usually 7-15days
Shipping method: FedEx, TNT, DHL,UPS etc.Our deliveries are 100% safe, fast, reliable and discreet.
Samples will be sent for your evaluation!If you are interested in, please contact me, let's talk details.
We specializes in exporting high quality Research chemical, medical intermediate, Pharmaceutical chemicals and so on. Products are exported to USA, Canada, France, Korea, Japan,Russia, Southeast Asia and other countries.
Title: Sense of Taste
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 structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
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
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.
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
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
38. Initial choice of long acting anticonvulsants in SE Is patient an infant? Is patient already receiving phenytoin? Yes No At high risk for extravasation ? (small vein, difficult access etc.)? Phenobarbital Yes No Phenytoin Fosphenytoin
39.
40.
41.
42.
43.
44.
45.
46.
47.
48.
49.
50.
51.
52.
53.
54. Suggested Reading 1. Fountain NB. Status epilepticus: risk factors and complications. Epilepsia 2000;41 Suppl 2:S23-30. 2. Treatment of convulsive status epilepticus. Recommendations of the Epilepsy Foundation of America's Working Group on Status Epilepticus. JAMA 1993;270(7):854-9. 3. Bassin S, Smith TL, Bleck TP. Clinical review: status epilepticus. Crit Care 2002;6(2):137-42. 4. Bleck TP. Management approaches to prolonged seizures and status epilepticus. Epilepsia 1999;40(1):S64-6. 5. DeLorenzo RJ, Towne AR, Pellock JM, et al. Status epilepticus in children, adults, and the elderly. Epilepsia 1992;33 Suppl 4:S15-25. 6. Haafiz A, Kissoon N. Status epilepticus: current concepts. Pediatr Emerg Care 1999;15(2):119-29. 7. Lowenstein DH, Bleck T, Macdonald RL. It's time to revise the definition of status epilepticus. Epilepsia 1999;40(1):120-2. 8. Orlowski JP, Rothner DA. Diagnosis and treatment of status epilepticus. In: Fuhrman BP, Zimmerman JJ, editors. Pediatric Critical Care. St. Louis: Mosby; 1998. p. 625-35.
Editor's Notes
SE and GCSE are the only abbreviations used during this presentation
This definition has been repeated in most articles and textbooks. However, there is nothing magic about 30 minutes. In fact, the likelihood for a tonic-clonic seizure to stop spontaneously decreases dramatically after 5 minutes. Where did the initial definition of 30 minutes come from?
This information however is not very helpful when trying to formulate a rational approach to the treatment of a child with GCSE.
The key questions for the physician treating a child with GCSE should be: - When does treatment for GCSE need to be initiated? - After what length of GCSE is it unlikely to stop spontaneously? - Should I wait ? How long?
The above statements are reviewed and referenced in the papers by Bleck and by the (British) Status Epilepticus Working Party. Bleck TP. Management approaches to prolonged seizures and status epilepticus. Epilepsia 1999;40(1):S64-6 Appleton R, Choonara I, Martland T, et al. The treatment of convulsive status epilepticus in children. The Status Epilepticus Working Party, Members of the Status Epilepticus Working Party. Arch Dis Child 2000;83(5):415-9
Lowenstein and Bleck review (with references) average duration of tonic-clonic seizures in children, i.e. usual length of seizure with high chance of spontaneous cessation. Lowenstein DH, Bleck T, Macdonald RL. It's time to revise the definition of status epilepticus. Epilepsia 1999;40(1):120-2.
They consequently present a revised definition of status epilepticus. They essentially use the term status epilepticus for GCSE in a child which - is unlikely to stop by itself, and - will require active intervention.
The fact that infants with SE have a higher mortality is likely due to the different etiologies of SE in infants, when compared to older children.
Nicely reviewed in : Fountain NB. Status epilepticus: risk factors and complications. Epilepsia 2000;41 Suppl 2:S23-30 Marked systemic and neurologic changes occur after about 30-60 minutes of seizure activity (see Fountain) and also: DeLorenzo RJ, Towne AR, Pellock JM, et al. Status epilepticus in children, adults, and the elderly. Epilepsia 1992;33 Suppl 4:S15-25 Bassin S, Smith TL, Bleck TP. Clinical review: status epilepticus. Crit Care 2002;6(2):137-42 Neurologic injury is likely to occur after 60 minutes of SE ( reviewed in: DeLorenzo.) There is also a nice graph with probable time relationship in: Haafiz A, Kissoon N. Status epilepticus: current concepts. Pediatr Emerg Care 1999;15(2):119-29
The priority is oxygenation! All actively seizing children have a significant respiratory (and usually moderate metabolic) acidosis. Most practitioners feel that, intubation (and ABG sampling) can be deferred until the seizures have been stopped, as long as the patient remains well oxygenated and is not completely apneic. See: Treatment of convulsive status epilepticus . Recommendations of the Epilepsy Foundation of America's Working Group on Status Epilepticus. JAMA 1993;270(7):854-9 Aminoff MJ, Simon RP. Status epilepticus. Causes, clinical features and consequences in 98 patients. Am J Med 1980;69(5):657-66 Any NMB agent given during SE should be very short acting, so that ongoing SE can be observed if it occurs. Termination of convulsive activity by muscular paralysis alone does not protect the brain from seizure induced hypermetabolism and risk of neuronal injury!
CT indications clearly are not exclusive. Other patients also need to be considered. On the other hand, not every child with established seizure disorder need a CT for each episode of GCSE. MRI will give a more detailed image, and may show changes not seen on CT.
Lorazepam is for most practitioners the preferred benzodiazepine in SE, mostly because it has a longer lasting anticonvulsant effect. Both midazolam and lorazepam can be given i.m. . Although some reviews suggest i.m. medications in case of impossible i.v. access, rectal diazepam followed by intraosseus access are recommended by most
Rectal administration of undiluted diazepam was simple, safe, and effective in the treatment of seizures when intravenous access could not be obtained (Seigler, 1990). A 1 cc disposable insulin syringe, inserted 4 to 5 cm into the rectum was recommended as the means to administer the 0.5 to 1 milligram/kilogram diazepam dose. Alternatively, a small feeding tube attached to the syringe can be absorbed rectally. Prior to the advent of Diastat (quite expensive!!), many practitioners routinely used iv diazepam rectally with excellent results. Seigler RS. The administration of rectal diazepam for acute management of seizures. J Emerg Med 1990;8(2):155-9.
Chamberlain JM, Altieri MA, Futterman C, et al. A prospective, randomized study comparing intramuscular midazolam with intravenous diazepam for the treatment of seizures in children. Pediatr Emerg Care 1997;13(2):92-4. Towne AR, DeLorenzo RJ. Use of intramuscular midazolam for status epilepticus. J Emerg Med 1999;17(2):323-8.
The main difference between phenytoin and fosphenytoin in children is the pH. Fosphenytoin will not cause the severe tissue damage seen with phenytoin in case of infiltration. In most markets, fosphenytoin is significantly more expensive
Phenobarbital is usually the preferred long-acting anticonvulsants in infants , as it can be easily maintained later with oral administration. Intestinal phenytoin absorption is very erratic in infants. Otherwise, many recommend phenytoin as first choice, as it may alter mental state less severely.
The finding of any of the above does not necessarily suggest non-convulsive SE. Clonus, Babinski and some posturing are often found just after termination of SE, especially when touching/handling the patient
Reasonable indication to give intramuscular midazolam (0.2 mg/kg) or rectal diazepam (0.3 - 0.5 mg/kg), either as gel or iv solution, using a tuberculin syringe, r a small syringe with attached feeding tube. Continue attempts at iv access.
Continue oxygen and airway maintenance Labs, including rapid blood sugar Lorazepam 0.1 mg/kg i.v., readily repeat after 5 minutes if still seizing Needs long-acting anticonvulsant, phenytoin probably preferred over phenobarb in this 3 year old. As he has a small peripheral iv catheter only, he has a good indication to use the more expensive fosphenytoin. Give 20 mg/kg phenytoin-equivalent Start glucose containing iv fluid
Respiratory and metabolic acidosis very common while actively seizing. ABG does not help with management. There is no indication to intubate, as pt is now oxygenating well, and is not apneic. Unresponsiveness likely will improve soon, as his postictal state lightens. No need to repeat ABG. No indication for bicarbonate.
The usual: Oxygen, airway, circulation Monitor Start iv access Possible causes include hyponatremia/ - glycemia, and/or viral encephalitis or bacterial meningitis. Important to check electrolytes and blood sugar early.
First intervention should be manual ventilation with a bag. As it is - quite likely for the chest wall rigidity/hypoventilation to resolve as the seizure stops, and as - intubation of the actively seizing child is near impossible without significant trauma, Intubation should be postponed if possible. If oxygenation can not be maintained with manual ventilation, the patient should be intubated using a short acting muscle relaxant (rocuronium, or even succinylcholine).
Assume ongoing electrical seizure activity, treat seizures as urgently as if there were ongoing, visible convulsions. Waiting for blood sugar and sodium.
SE is likely due to acute, severe hyponatremia. SE is persisting, pt has only received one dose of lorazepam so far! Give more lorazepam. Load with 20 mg/kg phenobarbital (or phenytoin; but phenobarb is probably preferred drug for this age) As hyponatremia is symptomatic (and history suggests recent development), need to treat hyponatremia with hypertonic saline. Would suggest to raise Na rapidly to about 125 mEq/L. 125 - 118 = 7 In order to raise serum Na by 1 mEq/L, 0.6 mEq/kg Na are required 3% NaCl contains 0.5 mEq/ml 7 x 1.2 x weight (kg) = ml of 3% NaCl required