Enteric fever is caused by infection of the intestines and intestinal lymphoid tissues by Salmonella typhi or Salmonella paratyphoid bacteria. It is spread through contaminated food, water, or flies carrying human excreta. Symptoms include sustained fever, abdominal pain, diarrhea or constipation. Complications can include intestinal perforation or hemorrhage. Diagnosis involves culture of stool or blood after 1 week of symptoms or a widal test detecting antibodies after 2 weeks. Treatment is usually with fluoroquinolones or third generation cephalosporins for 7-14 days. Prevention involves vaccination, water purification, hygiene and sanitation. Chronic carriers can harbor the bacteria long-term and
Brief Presentation on clinical examination of Cardio Vascular System with Report of Normal case
references:
macleod's clinical examination 13th edition
hutchinson clinical methods
Proper Case Presentation for Dengue Fever, Prevention, Treatment and everything else. Prepared by Dr Zain Khan, Doctor at Liaquat College of Medicine and Dentistry
Brief Presentation on clinical examination of Cardio Vascular System with Report of Normal case
references:
macleod's clinical examination 13th edition
hutchinson clinical methods
Proper Case Presentation for Dengue Fever, Prevention, Treatment and everything else. Prepared by Dr Zain Khan, Doctor at Liaquat College of Medicine and Dentistry
We will discuss briefly common tropical diseases found in INDIA. The presentation is basic for undergraduate students. we are covering dengue, malaria, chikungunya, and rickettsia in this presentation.
Typhoid fever, also known as enteric fever, is a potentially fatal multisystemic illness caused primarily by Salmonella enterica, subspecies enterica serovar typhi and, to a lesser extent, related serovars paratyphi A, B, and C.
The protean manifestations of typhoid fever make this disease a true diagnostic challenge. The classic presentation includes fever, malaise, diffuse abdominal pain, and constipation. Untreated, typhoid fever is a grueling illness that may progress to delirium, obtundation, intestinal hemorrhage, bowel perforation, and death within 1 month of onset. Survivors may be left with long-term or permanent neuropsychiatric complications.
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
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.
Antimicrobial stewardship to prevent antimicrobial resistanceGovindRankawat1
India is among the nations with the highest burden of bacterial infections.
India is one of the largest consumers of antibiotics worldwide.
India carries one of the largest burdens of drug‑resistant pathogens worldwide.
Highest burden of multidrug‑resistant tuberculosis,
Alarmingly high resistance among Gram‑negative and Gram‑positive bacteria even to newer antimicrobials such as carbapenems.
NDM‑1 ( New Delhi Metallo Beta lactamase 1, an enzyme which inactivates majority of Beta lactam antibiotics including carbapenems) was reported in 2008
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.
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
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.
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
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
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- 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
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
DISSERTATION on NEW DRUG DISCOVERY AND DEVELOPMENT STAGES OF DRUG DISCOVERYNEHA GUPTA
The process of drug discovery and development is a complex and multi-step endeavor aimed at bringing new pharmaceutical drugs to market. It begins with identifying and validating a biological target, such as a protein, gene, or RNA, that is associated with a disease. This step involves understanding the target's role in the disease and confirming that modulating it can have therapeutic effects. The next stage, hit identification, employs high-throughput screening (HTS) and other methods to find compounds that interact with the target. Computational techniques may also be used to identify potential hits from large compound libraries.
Following hit identification, the hits are optimized to improve their efficacy, selectivity, and pharmacokinetic properties, resulting in lead compounds. These leads undergo further refinement to enhance their potency, reduce toxicity, and improve drug-like characteristics, creating drug candidates suitable for preclinical testing. In the preclinical development phase, drug candidates are tested in vitro (in cell cultures) and in vivo (in animal models) to evaluate their safety, efficacy, pharmacokinetics, and pharmacodynamics. Toxicology studies are conducted to assess potential risks.
Before clinical trials can begin, an Investigational New Drug (IND) application must be submitted to regulatory authorities. This application includes data from preclinical studies and plans for clinical trials. Clinical development involves human trials in three phases: Phase I tests the drug's safety and dosage in a small group of healthy volunteers, Phase II assesses the drug's efficacy and side effects in a larger group of patients with the target disease, and Phase III confirms the drug's efficacy and monitors adverse reactions in a large population, often compared to existing treatments.
After successful clinical trials, a New Drug Application (NDA) is submitted to regulatory authorities for approval, including all data from preclinical and clinical studies, as well as proposed labeling and manufacturing information. Regulatory authorities then review the NDA to ensure the drug is safe, effective, and of high quality, potentially requiring additional studies. Finally, after a drug is approved and marketed, it undergoes post-marketing surveillance, which includes continuous monitoring for long-term safety and effectiveness, pharmacovigilance, and reporting of any adverse effects.
2. Introduction
Fever (Caused) by Infection in Intestine
An Acute Generalized Infection of Intestinal
Lymphoid Tissues, RES , Gall Bladder
Typhoid – 90 % cases
Paratyphoid - 10 % cases
3. Historical Background
• Typhoid = Typhus ( Rickettsial ) like
• Typhos (Gk) = Smoke (cause), Cloudy (sensorium)
• Phytos (Gk) = Putrefaction (of food as cause)
• Identified as a separate identity by : Huxlam(1972),
Louis(1829), Gerhardt(1837), Shoenlein(1839),
Jenner(1850), Budd(1873), Gaffkey(1884)
4. The Organism
• Gram Negative, Nonacid fast, Noncapsulated,
Nonsporing bacilli
• A Very Diehard Organism Life Long Carriers
• Types :
– Salmonella typhi
– Salmonella paratyphoid A
– Salmonella paratyphoid B
– Salmonella paratyphoid C
5. The Organism – Antigenic Structure
• O – Cell Wall Polysaccharide – Heat Stable
• H – Flagellar – Heat Labile
• Vi – Surface – Virulence – Heat Labile
( Useful in Serodiagnoses e.g Widal Test)
6. Epidemiology
Occurs Exclusively in Humans
Spread – Contaminated Food, Milk, Water
- By Flies from Human Excreta to Food
- Poor Personal Hygiene
- Poor Sanitation
Age – Older Children, Young Adults
<5 Years = only 10 %
<2 Years = only 2 %
Gender - Equal
7. Epidemiology – Contd..
Areas – Underdeveloped, Poor
Annual Occurrence – Throughout the year
Peak Time – July to August (Summer/Early Rains)
Incubation Period – 1 to 2 weeks (3-60 days)
∞ Dose of Inoculation
Infectivity Period – Long (>2 to 3 m)
Carriers (5%) – 20-50 years; Females more
12. Peyer’s Patches
Liver and Gallbladder Spleen
Typhoid Fever
Bones and Bone marrow Solid Viscera
Heart and Major Vessels
Multi - Organ Effects
13. Clinical Features
• Fever :
– Acute Onset
– Continuous (+ Morning Remission )
– Moderate To High Grade
– Persisting since 6-7 Days
– Classic Step Ladder Pattern Not Seen in children
20. Agglutination (WIDAL) Test
• Agglutinins appear in blood by end of 1st week
• O agglutinin : Rises Rapidly ( 4 fold in 10-14 days )
Persists for months
Disappears in a year
• H agglutinin : Rises Slowly
Persists for years
• Hence, O agglutinin is important in recent infection
• Diagnostic levels: >1/80 or 1/160 or Rising Titres (7-10
days apart)
• H agglutinin indicates past infection/ immunization
21. False Positives and Negatives in Widal
Test
False Positives Immunization with Typhoid Vaccine
Repeated Sub clinical Infections
Past Clinical Infection
Healthy Carriers of S.typhi
Anamnestic Response
Patients of Cirrhosis and Hepatitis
False Negatives Too Early collection of blood sample
Patients on Antibiotics
5 to 10 % do not respond by antibody formation
22. Non Specific Lab Findings in Typhoid
Fever
• Mild Normochromic Anemia
• Mild Thrombocytopenia
• Leucopenia with Relative Lymphocytosis
• (Leucocytosis suggests either perforation or an incorrect diagnosis)
• Eosinopenia – Presence heralds recovery
• An Increased ESR
• Laboratory Evidence of Mild DIC
• Hyponatremia and Hypokalemia
• Elevation of Liver Enzymes
• Urine : Some Proteins and White Cells
• Stool : Leucocytes and Blood common
24. Treatment - General
• Tepid Sponging
• Paracetamol
• Adequate Water and Food intake
• Hospitalize if : Toxemic / Complications
• Needs Fluids/ Therapy by IV Route
25. Treatment - Medical
Before 1980s
• Chloaemphenicol 50-100 mg/kg/day/ O or IV in 4 doses x 14 days
• Ampicillin / Amoxycillin 100-200 mg/day/ O or IV in 4 doses x 14 days
• Trimethoprim – Sulphamethaxazole 10 mg of TMP/ kg/day/O or IV
in two divided doses x 14 days
After 1980s(MDRTF)
• Ciprofloxacin 20mg/kg/day/O or 15 mg/kg/day/IV in 2 doses x 7 days
• Ofloxacin 15mg/kg/day/O or 10 mg/kg/day/IV in 2 doses x 7 days
26. Treatment – Medical – Contd..
Presently
• Cefixime : 10-20 mg / kg/day/O in 2 doses x 7-10 days
• Cefuroxime : 30-40 mg/kg/day/O in 2-3 doses into 7-10 days
• Ceftriaxone : 80-100 mg/kg/day/IV in 2 doses x 7 days
• Cefotaxime : 200mg/kg/day/IV in two doses x 7 days
• Azithromycin : 10mg/kg/day/O single dose x 5 days
28. Prevention
• Maintain Personal Hygiene
• Safe Drinking water and food habits
• Public health measures for
– Disposal of Excreta
– Ban on sale of contaminated food
• Tracing & Treatment of Carriers
• Active immunization with vaccine
29. Carriers
• Convalescent carrier: Patients who continue to shed bacilli
in feces for 3 weeks to 3 months after cure
• Temporary carrier: Those who shed for 3 months to 1 year
• Chronic Carrier: Those who shed more than 1 year (2 – 4%
patients become chronic carrier)
• Healthy carrier / Intermittent carrier:
– Harbours infection without suffering from the disease
– Bacilli persists in gall bladder or kidney
• Treatment:
– Prolonged treatment with qunilones or Cephlosporins
– May require gall bladder removel
30. Typhoid Vaccines
Earlier:
– Parenteral killed whole cell vaccine (TAB/TA)
– To children above one year
– Three doses S/C at 4-6 weeks interval
– Booster every year
Later :
– Live oral attenuated Ty21a Vaccine
– To children above 6 years
– Total of 3 capsules on A/D
– Repeated every 3 years
Presently :
– Vi Polysacchride subunit vaccine IM single dose
– To children > 2 years, repeated every three years