Shock can be best be defined as a complex
life threatening condition characterised by
inadequate blood supply to the tissues and cell
body .
[BRUNNER&SUDDARTH]
Shock can be best be defined as a complex
life threatening condition characterised by
inadequate blood supply to the tissues and cell
body .
[BRUNNER&SUDDARTH]
Fainting: Causes and Ways to Minimize RiskSummit Health
Fainting may cause physical injury, lead to hospitalization and be a sign of an underlying cardiac disorder. Our cardiac electrophysiologist will review the causes of fainting, tell who's at risk, and discuss methods to minimize the chances of fainting. Presentation by Summit Medical Group Cardiologist Roy Sauberman, MD FACC
Fainting: Causes and Ways to Minimize RiskSummit Health
Fainting may cause physical injury, lead to hospitalization and be a sign of an underlying cardiac disorder. Our cardiac electrophysiologist will review the causes of fainting, tell who's at risk, and discuss methods to minimize the chances of fainting. Presentation by Summit Medical Group Cardiologist Roy Sauberman, MD FACC
NEONATAL JAUNDICE IS MOST COMMON CAUSE OF MORBIDITY IN 1ST WEEK OF LIFE IT IS ALSO MOST COMMON CAUSE OF READMISSION AFTER DISCHARGE .THIS BEAUTIFUL SLIDE FOR NNJ.
neonatal sepsis is commonest cause of death in neonatal period,but it is preventable by prevention,timely recognition appropriate antibiotics and supportive care.
PNEUMONIA IS MAJOR CAUSE OF MORTALITY IN UNDER 5 YR OF AGE, IN THIS PPT I TRIED TO COVER ALL IMPORTANT FACTOR ABOUT PNEUMONIA, FOLLOW WHO PLAN FOR MANAGEMENT GOD WILL DO REST FOR BETTERMENT OF YOUR PT.
DIARRHOEA IS LEADING CAUSE OF MORTALITY IN INDIA AS WELL AS GLOBALLY .THIS IS NICE PPT BASED ON WHO GUIDELINES,DIARRHOEA IS EASY TO TREAT BUT STILL IT IS IS 2ND MOST COMMON CAUSE OF CHILDHOOD MORTALITY AFTER PNEUMONIA
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.
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.
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
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
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.
The Gram stain is a fundamental technique in microbiology used to classify bacteria based on their cell wall structure. It provides a quick and simple method to distinguish between Gram-positive and Gram-negative bacteria, which have different susceptibilities to antibiotics
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.
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
2. INTRODUCTION
•SEIZURE OCCUR BETWEEN 1) 6-60 MONTH,
• 2)>_38 *C (100.4*F)
•NOT DUE TO CNS INFECTION,METABOLIC
ABNORMALITIES,NO AFEBRILE SZ IN PAST
3. SIMPLE FEBRILE SZ- GTCS,<15MIN,NO RECURRENCE WITHIN
24 HR
COMLEX FEBRILE SZ- SZ 15MIN,FOCAL,RECURRENCE WITHIN
24 HR
SIMPLE FZ PLUS --- RECURRENT WITHIN 24 HR
FEBRILE STATUS EPILEPTICUS; FZ LASTING >30MIN
*FZ GENERALLY HV SHORT POST ICTAL PHASE
RECURRENCE RATE IS 30%AFTER FIRST EPISODE 50%AFTER 2
OR MORE EPISODE OR YOUNGER CHILD <1YE WITH FZ
4. R/F FOR FEBRILE SZ ;
MAJOR : <1YR,DURATION OF FEVER <24 HR,FEVER 38-
39*C
MINOR: F/H OF FZ,EPILEPSY,COMPLEX FEBILE SZ,DAY
CARE,BOYS,HYPONATREMUIA
GENETIC FACTOR:+ F/H SOME TIME AD (feb1,feb2 single
gene or polygenic)
5. R/F FOR OCCURANCE OF SUBSEQUENT EPILEPSY
AFTER FZ
• SIMPLE FEBRILE SZ……….1%
• RECURRENT FZ…………...4%
• COMPLEX FZ(>15MIN,RECURRENT WITHIN 24 HR….6%
• FEVER <1HR BEFORE SZ…….11%
• FAMILY H/O EPILEPSY ….18%
• COMPLEX FEBRILE SZ (FOCAL)….29%
• NEURODEVELOPMENTAL ABNORMALITIES….33%
• *ANY TYPE OF EPILEPSY CAN BE PRECEDED EG GENERALISED EPILEPSY WITH
FEBRILE SZ PLUS GEFS+ ,SEVERE MYOCLONIC EPILEPSY OF INFANCY
(DRAVET SYNDROME)
6. • GEFS+ …….AD SYNDROME,EARLY CHILHOOD AND REMISSON IN
MID CHILDHOOD,CHARECTERISED BY MULTIPLE FZ+
SUBSEQUENT SEVERAL TYPE OF AFEBRILE SZ INCLUDING
GTCS,MYOCLONIC,ATONIC ETC
7. EVALUATION
FEBRILE SZ OFTEN OCCUR IN CONTEXT OF OTITIS
MEDIA,ROSEOLA,HHV6,HHV7
• HISTORY
• NEUROLOGICAL EXAMINATION
• MANAGEMENT OF ACUTE SZ
• DETERMINE R/F FOR OCCURANCE
8. COUNSIL PARENTS ABOUT RISK OF OCCURRENCE
,PROVIDE FIRST AID AND MANAGE FEVER
DETEMINE R/F FOR LATE EPILEPSY
A)LOW RISK NO THERAPY,INVESTIGATION NECESSARY
B)INTERMEDIATE AND HIGH RISK; CONSIDER
EEG,IMAGING,CONSIDER INTERMITTENT ORAL
DIAZEPAM,IN EXCEPTIONAL CASES THAT RECUR
CONTINOUS THERAPY
9. •LP
• <6M OR ILL LOOKING PT
6-12 M DEFICIT IN H.INFLUENZA AND
STREPTOCOCCUS PNEUNONIA IMMUNISATION
NON TRAUMATIC CSF RARELY SHOW
PLEOCYTOSIS AND CSF PROTEIN AND GLUCOSE
ARE USUAL NORMAL
10. EEG
SFZ AND OTHERWISE NEUROLOGICAL HEALTHY PT NOT REQUIRED
REQUIRED IN ONLY WHEN EPILEPSY IS HIGHLY SUSPECTED ,EEG
SHOW GENERALISED SLOWING WITHIN 72 HR OF FSE A/W
HIPPOCAMPAL INJURY
IF INDICATED DELAY AND REPEAT >2 WK BEFORE <2WK SHOW
NON SPECIAFIC SLOWING
INDICATED IN TYPE OF EPILEPSY RATHER THAN PREDICT ITS
OCCURANCE (FZ OR EPILEPSY)
EEG HELP IN DISTINGUISH BETWEEN ONGOING SZ ACTIVITY AND
A PROLONG POSTICTAL PERIOD.SOME TIME TERMED NON
EPILEPTIC TWILIGHT STATE
11. BLOOD STUDIES
• S.ELECTROLYTES,CA++,PHOSPHORUS,MG, CBC IS NOT
ROUTINELY INDIACTED IN WORKUP OF SIMPLE FEBRILE
SZ,BLOOD GLUCOSE IS INDICATEDIN PROLONG
FASTING,PROLONG POST ICTAL OBTUNDED
• IN CLINICALLY INDICATED (DEHYDRATION)DO S.ELECTROLYTE
• LOW NA+ IS A/W HIGH RISK OF OCCURANCE WITH 24 HR
12. NEUROIMAGING
• NOT INDICATED IN SIMPLE FEBRILE SZ
• IN COMPLEX FEBRILE SZ IT IS INDIVIDUALISED
(EEG+NEUROIMAGING) IF PT NEUROLOGICALLY ABNORMAL
• 11% COMPLEX FZ IS A/W U/L HIPPOCAMPUS SWELLING --
LATER HIPPOCAMPAL ATROPHY---TEMPORAL LOBE
EPILEPSY
13. TREATMENT
• ANTIPYRETICS DECREASE COMFORT BUT DO NOT REDUCE
RECURRENCE OF FEBRILE SZ
• AED IS NOT REQUIRED GENERALLY FOR ONE OR MORE SZ
• COUSELLING IS REQUIRED (RECURRENCE OF FEBRILE SZ AND
RECURRENCE OF EPILEPSY)
• IF SZ LAST FOR MORE THAN >5 MIN GIVE ACUTE T/T BY
DIAZEPAM,MIDAZOLAM,LORAZEPAM
• RECTAL DIAZEPAM CN BE GIVEN FR RECURRENCE SZ LASTING MORE
THAN 5 MIN (ALT BUCCAL OR NASAL MIDAZOLAM CAN BE USED)
14. • IV BENZODIAZEPAM,PHENOBARBITONE,PHENYTOIN,VALPORATE MAY
NEEDED FOR FEBRILE STATUS EPILEPTICUS
• FOR ANXIOUS PARENTS INTERMITTENT ORAL DIAZEPAM (.33MG/KG
EVERY 8 HRLY DURING FEVER OR RECTAL DIAZEPAM .5 MG/KG 8
HRLY CN BE USED INTERMITTENT
• NITRAZEPAM,CLOBAZAM,CLONAZEPAM(0.1MG/KG/DAY CN BE USED
• IN CONTINOUS PROPHYLAXIS PHENOBARBITONE 4-5MG/KG/DAY IN
1-2 DIVIDED DOSE OR VALPORATE 20-30MG/KG /DAY IN 2-3
DIVIDED DOSE CAN BE GIVEN
• CONTIONOUS PROPHYLAXIS GENERALLY NOT JUSTIFIED DUE (SE,LACK
OF LONG TERM BENEFIT)
• IRON DEFICIENCY IS ASSOCITED WITH INCREASED RISK OF FEBRILE
SEIZURE