This document discusses tetanus, including its causative organism, clinical presentation, diagnosis, management, and prevention. Tetanus is caused by Clostridium tetani bacteria and presents with muscle rigidity, painful spasms, and autonomic dysfunction known as the tetanus triad. It is diagnosed clinically and managed by controlling spasms, neutralizing toxin, preventing further release, and supporting respiration. Active immunization through tetanus toxoid vaccines is important for prevention.
Sudden temporary change in PHYSICAL movement, SENSATION, BEHAVIOUR because of abnormal discharged of electrical impulses from nerve cells.
CLASSIFICATION
PARTIAL SEIZURE / FOCAL SEIZURE
>> Aimed to determine:
Type of seizure
Frequency
Severity
Aura
LOC
Dyspnea
Fixed and dilated pupil
Incontinence
Factors that precipitate them.
Developmental history taking (events of pregnancy and childbirth)
Questioned about illnesses or head injury
Tetanus an neurological disease characterized by an acute onset of hypertonia, painful muscular contractions (usually of the muscles of the jaw and neck), and generalized muscle spasms without other apparent medical causes.
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
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
Sudden temporary change in PHYSICAL movement, SENSATION, BEHAVIOUR because of abnormal discharged of electrical impulses from nerve cells.
CLASSIFICATION
PARTIAL SEIZURE / FOCAL SEIZURE
>> Aimed to determine:
Type of seizure
Frequency
Severity
Aura
LOC
Dyspnea
Fixed and dilated pupil
Incontinence
Factors that precipitate them.
Developmental history taking (events of pregnancy and childbirth)
Questioned about illnesses or head injury
Tetanus an neurological disease characterized by an acute onset of hypertonia, painful muscular contractions (usually of the muscles of the jaw and neck), and generalized muscle spasms without other apparent medical causes.
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
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
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
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.
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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.
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
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2. OBJECTIVES
At the end of presentation you will be able to learn
• about tetanus
• its causative organism
• its Diagnosis
• Pathophysiology of tetanus
• Incubation period of tetanus
• Clinical features and tetanus triad
• Generalized tetanus & Localized tetanus and their features
• Cephalic Tetanus
• neonatal tetanus
3. • complications of tetanus
• Classification of tetanus severity
• Management of tetanus
• Prevention of tetenus
4. SCENARIO
• A 35 yr old female P1 with a history of SVD with episiotomy 10 days
back presented with a complaint of generalized body stiffness,
breathing difficulty as well as an inability to chew and swallow food
for 4 days. the woman experienced neck pain and numbness in her
face. Her symptoms got worse over the next 24 hours — her neck and
jaw became stiff, and she had difficulty swallowing and breathing and
presented in emergency with following vitals
• BP 101/63mmHg
• PR 110 bpm
• RR 25 /min
• SPO2 90% at Room air
5. EXAMINATION
• Slurred speech
• Stiffness of neck and back present
• Limited mouth opening due to the mild facial muscle spasm
• rest of the examination was un remarkable
6. INVESTIGATIONS
LABS LABS
HB 11 T Bil 0.4 mg/dl
TLC 20 PH 7.35
PLT 200 PaCO2 38
UREA 25 mg/dl Pa O2 65 mmHg
CRET 0.5mg/dl HCO3 25
Na 145 BLOOD CULTURES neg
k 4.5 URINE CULTURES neg
ECG CXR
NORMAL SINUS RHYTHM UNREMARKABLE
7. What is your differential diagnosis?
• Tetanus
• Strychnine poisoning
• Dental infections
• Hysteria
• Malignant hyperthermia
• Hypocalcemia
• Local infections
• Intracranial hemorrhage
• Sepsis
• Seizure disorder (partial or
generalized)
• Serotonin syndrome
• Stroke, ischemic (cephalic
tetanus)
• Meningitis
• TMJ Dislocation
8. WHAT IS TETANUS?
Bacterial infection characterized by acute onset of hypertonia, painful
muscle contractions and spasms without any medical cause .
TETANOS- Greek word means stretch
9. WHAT ARE TYPES OF TETANUS?
LOCALIZED GENERALIZED
NEONATAL CEPHALIC
TYPES
10. WHAT IS THE CAUSATIVE ORGANISM?
• gram-positive bacillus - Clostridium tetani
• found in soil ,animal or human faeces
• motile, spore forming, obligate anaerobe
• Spores are not destroyed by boiling
• eliminated by autoclaving at 120°C for 15 min 1 (at one atmosphere
pressure)
12. CAN YOU NAME TETANI EXOTOXINS?
• TETANOSPASMIN
• Enter peripheral nerves
• Binds to gangliosides of neurons
• Axonal retrograde transport to cell body of neurons
• Transport occurs first in motor, and later in sensory and autonomic
nerves
• in the cell body the toxin can diffuse out, affect and entering
nearby neurons.
• spinal inhibitory interneurones are affected, symptoms occur.
• Further retrograde intraneural transport occurs with toxin
spreading to the brainstem and midbrain.
13. • Inhibit GABA & Glycine from presynaptic vesicles
• relative deficiency of synaptic acetylcholine (similar to botulinum
toxin) causes flaccid paralysis
• Disinhibition of motor & autonomic neurons
• Cause rigidity , spasm , autonomic dysfunction
• High toxin load diffusion via blood to nerves
16. WHAT ARE ROUTES OF TRANSMISSION?
BURNS
IM /IV
INJECTIONS
SURGERY
SEPTIC
ABORTION
SNAKEBITE
GANGRENE
ULCERS
CHILD BIRTH
17. WHAT ARE ITS CLINICAL FEATURES?
Muscle
rigidity
Spasms
TETANUS
TRIAD
Autonomic
dysfunction
18. WHAT ARE THE CLINICAL FEATURES?
• MUSCLE RIGIDITY
• First week
• Reduce after 2 , 3 week
• Autonomic disturbance
• occurs in 1 week
• Occurs several weeks after spasm
• Persists 1-2 weeks
• SPASM
20. • EARLY SYMPTOMS
• Neck stiffness
• Sore throat
• Poor mouth opening
• Increased muscle tone
• Pharyngeal and laryngeal spasm
• Rigidity of the neck muscles leads to retraction of the head
• Mimic convulsions
• Continuous spasm – RESPIRATORY FAILURE
21. WHAT ARE SIGNS OF GENERALIZED TETANUS?
TRISMUS
LOCK JAW
• Masseter muscle
spasm
RISUS
SARDONICUS
• Facial expression
• Facial muscle spasm
• Sarcastic smile
OPISTHOTONUS
• Truncal rigidity
• Extensor muscles
spasm
• Arched back
32. ABLETT CLASSIFICATION OF SEVERITY
GRADE SEVERITY SYMPTOMS
I MILD • Mild trismus ,
• general spasticity
• no respiratory embarrassmen
• no spasms, no dysphagia
II MODERATE • Moderate trismus, rigidity
• short spasms
• mild dysphagia,
• respiratory rate > 30,
• mild dysphagia
III SEVERE • Severe trismus
• generalized spasticity,
• prolonged spasms,
33. • prolonged spasms,
• respiratory rate > 40,
• apnoeic spells
• severe dysphagia,
• pulse > 120
IV VERY SEVERE • Grade 3 plus severe autonomic
disturbances
• cardiovascular system involvement
34. WHAT IS THE MANAGEMENT?
PREVENT FURTHER TOXIN RELEASE
NEUTRALIZE TOXIN PRESENT IN THE BODY OUTSIDE CNS
MINIMIZE EFFECT OF TOXIN ALREADY PRESENT IN CNS
35. HOW CAN YOU PREVENT FURTHER TOXIN RELEASE?
WOUND
Debridement
Additional
Antibiotic cover
ANTIBIOTIC
METRONIDAZOLE
500mg IV 8h
ERYTHROMICIN, TETRACYCLIN ,
CLARITHROMICIN
36. How can we Neutralize toxin present in the body
outside the CNS?
HUMAN TETANUS
IMMUNOGLOBULIN Ig
IM:150 units /kg
Within 24 h
(3000-6000 IU)
IV: 5000-
10000IU
ANTI TETANUS HORSE
SERUM
IM : 1500-
10000IU
A/E
Anaphylaxis
37. How to Minimize the effects of the toxin already in
the CNS?
SEDATION
RESPIRATORY SUPPORT
CONTROL AUTONOMIC
DISTURBANCE
38. WHAT SEDATION CAN YOU GIVE TO THESE
PATIENTS?
• BENZODIAZIPINES
• DIAZEPAM 0.1mg/kg IV 4h
• MIDAZOLAM 0.1 mg/kg IV 4h OR Infusion 2-10 mg/H
• OPIOIDS
• MORPHINE 0.1mg/kg IV or IM 2-6h
• PETHIDINE 1 mg/kg IV or IM 2-6h
• COMBINATION
• BENZODIAZIPINES + MORPHINE
• 1-10 mg / h IV
40. WHAT MUSCLE RELAXANTS TO USE?
• 0.1 mg /kg IV
VECURONIUM
• 0.5 mg/ kg IV
ATRACURIUM
• Worsen autonomic instability
• Inhibiting catecholamine uptake
PANCURONIUM
41. What is the Treatment of autonomic dysfunction?
• Minimize autonomic instability
FLUID
• Presynaptic NMB, reduces catecholamine
release from nerves & adrenal medulla
• LOADING 5g in 20 min ,INFUSION 2g/h
• Therapeutic range of Mg 2-4 mmol/l
MAGNESIUM SULFATE
• ESMOLOL short acting
• Long acting are not recommended
BETA BLOCKERS
• CLONIDINE
• Inhibits norepinephrine from nerve endings
ALPHA 2 AGONIST
42. WHAT ICU CARE WILL YOU GIVE THESE
PATIENTS?
• Enteral feeding - nutrition
• Prevention of Respiratory Complication
• Semi recumbent position
• Suctioning
• Oral care
• Tracheostomy IF Ventilation > 8-10 days
• Pressure sore care
• Minimize thromboembolism
• Psychological support
44. • At 2 months of age
• 3 inj at ONE month interval
• BOOSTER 5 years of age
vaccination
• Maternal vaccination
• Transplacental transfer of
immunoglobulin
Neonatal
immunity
• Immunity is not long lasting
• 2 boosters 10 years apart
Revaccination