This document discusses the management of acute ischemic stroke. It begins by outlining the magnitude of stroke as a problem in India and defines what constitutes a stroke. It then discusses the concepts of penumbra and the importance of short door-to-needle times for thrombolysis. The standard of care for acute ischemic stroke involves rapid evaluation, neuroimaging, ruling out contraindications to thrombolysis, and administration of IV alteplase within 4.5 hours of symptom onset. Barriers to effective stroke treatment in India include delays in recognition of symptoms, reaching care, and administering thrombolysis. Public education on stroke signs and rapid evaluation and treatment are needed to improve outcomes.
STROKE is also known as CVA. (cerebrovascular accident). it is a medical emergency. damage to the brain from interruption of its blood supply .early action can reduce brain damage and other complication.
signs and symptoms slur words or difficulty understanding speech.
Acute management of patients with stroke is to stabilize the patient and to complete initial evaluation and assessment, including imaging and laboratory studies, within 60 minutes of patient arrival.
Critical decisions focus on the need for intubation, blood pressure control, and determination of risk/benefit for thrombolytic intervention.
STROKE is also known as CVA. (cerebrovascular accident). it is a medical emergency. damage to the brain from interruption of its blood supply .early action can reduce brain damage and other complication.
signs and symptoms slur words or difficulty understanding speech.
Acute management of patients with stroke is to stabilize the patient and to complete initial evaluation and assessment, including imaging and laboratory studies, within 60 minutes of patient arrival.
Critical decisions focus on the need for intubation, blood pressure control, and determination of risk/benefit for thrombolytic intervention.
Remote Ischaemic Conditioning: A Paper Review & Uses in Paramedic Practicebgander23
A 2 part presentation. Part 1 reviews a paper on the long-term clinical outcomes of STEMI patients undergoing remote ischaemic perconditioning prior to primary percutaneous coronary intervention. The 2nd part looks at how this technique can be used in Paramedic practice.
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
Remote Ischaemic Conditioning: A Paper Review & Uses in Paramedic Practicebgander23
A 2 part presentation. Part 1 reviews a paper on the long-term clinical outcomes of STEMI patients undergoing remote ischaemic perconditioning prior to primary percutaneous coronary intervention. The 2nd part looks at how this technique can be used in Paramedic practice.
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
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.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
5. • STROKE
• Magnitude of problem
• Penumbra
• Window period
• Door to needle times
• Road blocks
• Stroke unit
6. What is Stroke?
• An abrupt onset of a neurological deficit that
is attributable to a focal vascular cause.
7. Actilyse® • Emergency Physician Slide Kit
Where are we now ?
• The stroke epidemic has arrived in India.
• While we were busy combating the scourge of
infections and deficiency diseases, non-communicable
diseases (NCDs) including stroke stealthily crept up on
us.
8. • Most common life-threatening neurologic disease
• Third most common cause of death globally
• Prevalence 500/ 1,00,000 per year
• Incidence 180/ 1,00,000 per year
• Incidence in India: 73/ 1,00,000 per year
• Burden likely to ↑ aging, smoking, dietary patterns
Stroke 1998;29:1730-36; Neurol India 2002;50:279-81
Epidemic
9.
10. Stroke awareness in India
• Far from satisfactory.
• 1/4th of the urban and 1/3rd of rural
respondents who were unaffected had no
knowledge of any warning symptom of stroke.
• There is an urgent need for stepping up
awareness drive in our country.
11. Actilyse® • Emergency Physician Slide Kit
The "Five Sudden, Severe Symptoms" of stroke include
• Sudden numbness or weakness of the face,
arm, or leg on one side of the body.
• Sudden confusion, difficulty talking or
understanding.
• Sudden trouble seeing on one side.
• Sudden, severe difficulty walking, dizziness,
loss of coordination or balance.
• Sudden, severe headache for no known
reason.
15. Code Stroke
• Initial evaluation
• Stroke team intimation (activation)
• Urgent Neuro-imaging
• Interpretation of Neuro-imaging
• Ruling out C/I of thrombolysis
• Drug/Intervention
16. Initial evaluation
• In ER/ICU
• Symptoms criteria: FAST (BEFAST)
• Time criteria present
Activation of CODE STROKE
17. • Secure 2 large bore venous access
• Labs: BSL, CBC, Blood urea, creatinine, electrolytes, PT (INR),
aPTT
• 12 lead ECG (should not hold patient from going to CT scan)
• Neurological assessment and NIHSS assessment and
documentation
To be completed within 10 minutes of arrival
to hospital
Initial evaluation
18. Activation of code stroke
Urgent
Phone call (and whattsapp group message)
Neurologist, Radiologist,
Intensivist
Intimate radiology technician for neuroimaging
Intimate lab processing samples
Intimate pharmacy for actilyse
Stroke team to arrive within
15 minutes of arrival of patient
19.
20. Code Stroke
• Initial evaluation
• Stroke team intimation (activation)
• Urgent Neuro-imaging
• Interpretation of Neuro-imaging
• Ruling out C/I of thrombolysis
• Drug/Intervention
28. Potential to Reverse Neurologic Impairment With Thrombolytic
Reperfusion when done in time
Saver. Stroke 2006;37:263-266.
González. Am J Neuroradiol 2006;27:728-735.
Donnan. Lancet Neurol 2002;1:417-425.
An untreated patient loses
approximately 1.9 million
neurons every minute in the
ischaemic area
Reperfusion offers the
potential to reduce the
extent of ischaemic injury
Ischaemic core
(brain tissue
destined to die)
Penumbra
(salvageable
brain area)
29.
30. “Time is brain”
Saver. Stroke 2006;37:263-266.
Neurons Lost Synapses Lost Myelinated Fibres Lost Accelerated Aging
Per Stroke 1.2 billion 8.3 trillion 7140 km 36 y
Per Hour 120 million 830 billion 714 km 3.6 y
Per Minute 1.9 million 14 billion 12 km 3.1 wk
Per Second 32,000 230 million 200 m 8.7 h
Minutes Hours Days
Inflammation
Peri-infarct
depolarisations
Excitotoxicity
Impact
Apoptosis
Time
31. CT scan performed on the day after thrombolysis
showing no hemorrhagic change and no enlargement
of the ischemic area
32. Code Stroke
• Initial evaluation
• Stroke team intimation (activation)
• Urgent Neuro-imaging
• Interpretation of Neuro-imaging
• Ruling out C/I of thrombolysis
• Drug/Intervention
33. IV rt PA
• The only approved therapy for better clinical
outcome in stroke has its effects strongly
dependant on time
• Principle behind the time dependency of
thrombolysis is that of penumbrA.
34. IV Alteplase
• Improves functional outcome in 3-6 months
• More patients are sent home independent
• Near complete recovery- 38% Vs 21%
• 3 month mortality- Same for both groups
• Symptomatic ICH- 6.8% Vs 1.3%
• Fatal bleed- 2.7% Vs 0.4%
• Severe systemic bleed < 1%
35. rtPA for Acute Ischemic Stroke
Indication
• Clinical diagnosis of stroke
• Onset of symptoms to time of drug
administration ≤4.5 h
• CT scan showing no hemorrhage
• Age ≥ 18 years
• Consent by patient or surrogate
36. Contraindication
• Sustained BP >185/110 mmHg despite
treatment
• Glucose <50 or >400 mg/dL
• Use of heparin within 48 h and prolonged
PTT, or elevated INR>1.7
• Rapidly improving symptoms
37. Cont..
• Prior stroke or head injury within 3 months;
prior intracranial hemorrhage
• Major surgery in preceding 14 days
• Minor stroke symptoms
• Gastrointestinal bleeding in preceding 21 days
• Recent myocardial infarction
• Coma or stupor
38. Administration of rtPA
• Administer 0.9 mg/kg IV (maximum 90 mg) IV
as 10% of total dose by bolus, followed by
remainder of total dose over 1 h
• Frequent cuff blood pressure monitoring
• No other antithrombotic treatment for 24 h
• For decline in neurologic status or
uncontrolled blood pressure, stop infusion,
give cryoprecipitate, and reimage brain
emergently
40. NIH-recommended Emergency Department Response
Times
NINDS NIH website. Stroke proceedings. Latest update 2008.
DTN ≤60 min: the “golden hour” for evaluating and treating acute stroke
T=0
Suspected
stroke patient
arrives at
stroke unit
≤10 min
Initial MD evaluation
(including patient
history, lab work
initiation, & NIHSS)
≤ 15 min
Stroke team
notified
(including
neurologic
expertise)
≤ 25 min
CT scan
initiated
≤ 45 min
CT & labs
interpreted
≤ 60 min
rt-PA
given if patient
is eligible
IDEALLY performed
prehospital
41. Thrombolysis: Number of Patients Needed to
Treat (NNT) to Achieve Excellent Recovery (mRS 0-1)
Lees et al. Lancet 2010;375:1695-1703.
3 - 4.5 h NNT=14
90 min - 3 h NNT=9
mRS, modified Rankin Scale
≤ 90 mins NNT=4 to 5
42. Barriers to stroke treatment - India
42
Reach
24 x 7 Diagnostic services
Confident Stroke physician
Fight vs . Time
43. Why Under-used?
Failure
to recognise
stroke symptoms
and act
appropriately
Prolonged
delays from
symptom onset
to FMC to treatment
Poor infrastructure
for on-going
monitoring and
evaluation of
patients post
rt-PA4
Inability to manage
potential post rt-PA
complications
(neurosurgery,
neuro-intensive
care)
44. Hospitalization and transportation
• Poor recognition of early stroke symptoms
• low perception of threat
• Only 1/4th arrive within 6 h.
• In a major urban centre, the median time to
casualty arrival was 7.66 h.
• A rural-based study, it was 34 ± 6 h.
45. Stroke Chain of Survival
• Recognition of stroke signs and symptoms
Detection
• Call Emergency Medical Services and dispatch
Dispatch
• Prompt transport and pre-hospital notification to hospital
Delivery
• Immediate ED triage
Door
• ED evaluation, prompt laboratory studies, and CT imaging
Data
• Diagnosis and decision about appropriate therapy
Decision
• Administration of appropriate drugs or other interventions
Drug
Disposition • Timely admission to stroke unit, intensive care unit, or transfer
46. Take Home Message
Remember: ACT Fast Time is brain!
Early recognition of stroke symptoms, by public, attendants, ambulance
service providers, and paramedics.
Public education of 5 “Sudden”.
Prioritisation and direct transfer to specialised stroke centres
or stroke units
Management by multidisciplinary teams
Act fast to initiate treatment with thrombolysis as early as possible
Earlier the action, better the result.