This document discusses identification and management of sepsis in the prehospital environment. It defines sepsis as an exaggerated immune response to infection that can lead to organ dysfunction. Early signs may be nonspecific but include fever, altered mental status, and fast heart rate and breathing. Prehospital treatment involves giving fluids and communicating the suspicion of sepsis to the receiving hospital. Maintaining oxygen levels and treating shock are priorities as sepsis can progress rapidly to organ failure. Monitoring end-tidal carbon dioxide and checking for lactacidosis provide valuable information.
Septic shock, updated presentation, including latest guidelines from Intensive care societies and how to approach to the diagnosis with few notes about Early Goal Directed Therapy and role of steroids
presentation on SIRS septic shock and multiorgan failure,and their corelation together in increasing morbidity and mortalitiy in shocked patient explaning pathophysiology clinical picture and how to manage
Septic shock, updated presentation, including latest guidelines from Intensive care societies and how to approach to the diagnosis with few notes about Early Goal Directed Therapy and role of steroids
presentation on SIRS septic shock and multiorgan failure,and their corelation together in increasing morbidity and mortalitiy in shocked patient explaning pathophysiology clinical picture and how to manage
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
CDSCO and Phamacovigilance {Regulatory body in India}NEHA GUPTA
The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
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
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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 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
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
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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
4. “Sepsis is caused when the body’s
immune system becomes
overactive in response to an
infection, causing inflammation
which can affect how well other
tissues and organs work.”
–National Institute for Health and Care Excellence Guidelines
5. Defining Sepsis
Sepsis is a syndrome
–A group of body dysfunctions found
together
–Dysfunctions that progress together in a
predictable way
–High mortality rate, variable clinical
presentations
7. Sepsis Spectrum
• HR>90
• RR>20
• T > 100.4 F
or < 96.8 F
• Abnormal
WBC count
• Low pCO2
SIRS
• 2 SIRS
criteria
• +
• Infection
Sepsis • Sepsis
• +
• -
Hypotensio
n
• -End organ
damage
• -Elevated
lactate
Severe
Sepsis
• Severe
sepsis and
persistent
signs of end
organ
dysfunction
• Mortality
50%
Septic
Shock
MORTALITY
8.
9. Normal Response to Infection
• Local infection
• Non-specific inflammatory response
• 3 phases
– Vasodilation - increased blood flow to site, infusion
of antibodies and cells to fight infection
– Vessel permeability - antibodies and cells exit
bloodstream and enter infected tissue
– Once infection is controlled, tissue repairs itself
10. Pathophysiology of
Sepsis
• Uncontrolled, exaggerated immune response
• Endothelium damage, cell mediator activation, disruption
of coagulation system homeostasis
• Vasodilation and capillary permeability
• Systemic inflammatory response
• End-organ damage, death
11.
12. SIRS
• Systemic Inflammatory Response
Syndrome
– A constellation of abnormal signs
– Many triggers, infection is most
common
– EMS uses a version of SIRS that doesn’t
rely on blood test results (WBC count,
ABG)
– Temp, HR, RR, glucose, mental status
13. Risk Factors for Sepsis
• Extremes of age (old and young)
– Can’t communicate, need careful assessment
– Patients with developmental delay
– Cerebral Palsy
• Recent surgery, invasive procedure,
illness, childbirth/pregnancy
termination/miscarriage
• Reduced immunity
15. Increased Risk for Sepsis
• Chemotherapy
• Post-organ transplant (bone marrow, solid
organ)
• Chronic steroid use
• Recent antibiotic use
• Indwelling catheters of any kind (dialysis,
Foley, IV, PICC, PEG tubes, etc)
16. Signs/Symptoms of Sepsis
• Symptoms of sepsis are often nonspecific and
include the following:
– Fever = most common (elderly patients often do
NOT mount a febrile response)
– Flu-like symptoms
– Chills/shaking (mistaken for seizure)
– Nausea/vomiting
– Mental status changes/fatigue/lethargy
Patient often does NOT
appear acutely ill
19. United Effort to Improve Survival from
Sepsis
• Research from past 20 years is saving lives
– Rapid identification, fluids, antibiotics
• Education to all physicians, nurses, technicians
• “Care bundles” monitored by Feds
• Sepsis alert teams in hospitals
• Chart review
• Administrative support at all levels
21. Identifying the Sepsis Patient
• Look for and ask about infection
– Did you look at all the skin???
• Look for and ask about risk factors for
infection
• Check a temperature accurately
– > 38°C (100.4°F)
– < 36°C (96°F) more dangerous
22. Identifying the Sepsis Patient
• Look for SIRS criteria in the vital
signs
• Look for shock/dehydration
• Check end-tidal CO2
23. Treating the Sepsis Patient
• Airway/breathing
– Get sats > 92%
– NRB, CPAP, invasive airway
• Circulation
– 2 large bore IV, consider IO
– 20 cc/kg NS bolus
– May repeat if lungs remain clear
24. Sepsis Alert
• Communicate your suspicion early!
• It doesn’t matter if accepting facility has a
formal sepsis alert response process
• Explicitly communicate abnormal vitals
(especially temp) just as you would in
trauma
25.
26.
27.
28.
29.
30.
31. Respiratory Component of Sepsis
• Mismatch of oxygen availability to
changing needs of organs (ie.
Increased oxygen demand)
• Keep sats ≥ 92 % (NRB, CPAP,
intubation)
• Respiratory failure can happen
quickly
• Acute Respiratory Distress Syndrome
32. Severe Sepsis/Septic Shock
A story of imbalance…
Oxygen
Consumption
Oxygen
Deliver
y
As sepsis progresses, circulatory abnormalities lead to an imbalance of
systemic oxygen delivery and demand, resulting in global tissue hypoxia.
Global tissue hypoxia is a key development preceding multi-organ failure and
death.
33. Sepsis Pitfalls
• Beta blockers block tachycardia
response
• Altered mentation not recognized as
“end-organ failure”
• Temperatures not checked
• EtCO2 not checked or recognized
• Discouragement due to hospital
response
34. EtCO2 and Lactate
• Low EtCO2 associated with high lactic
acid
• Low EtCO2 predicts mortality
• EtCO2 of 25 mmHg = lactate up to 6.1
mm/L
Editor's Notes
Reviewed and updates approved by Education Committee on July 16, 2020.
Sepsis is a complicated disease process that high a high mortality rate. Until the early 2000s, 50% of people would die. Over the past 15 years, we have learned more about the disease and enhanced therapy has greatly decreased mortality. Over 750,000 people in the US develop sepsis annually at a cost $22,100 per case or $16.7 billion per year.
"Sepsis is caused when the body’s immune system becomes overactive in response to an infection, causing inflammation which can affect how well other tissues and organs work. When sepsis is recognized early, people can be quickly given the right treatment. However, the signs and symptoms of sepsis can vary and may be subtle which can lead to it being missed if it is not considered early on."
The fundamental concept to keep in mind when discussing sepsis is that of “hemostasis,” the healthy balance of blood coagulation vs anti-coagulation. In times of normal health, our bodies produce clotting factors in the blood that are always on standby to clot whenever necessary. These factors are activated whenever the endothelium (the lining of organs and blood vessels) is disturbed or traumatized. Clotting factors are like a cache of highly unstable gun powder. Once activated, they can set off a dangerous chain-reaction of clotting everywhere. This potential is kept in check by anticoagulating factors also present in healthy blood.
In sepsis, infecting organisms cause direct trauma to endothelium, and the body also suppresses or depletes the supply of available anticoagulating fators. A perfect storm of intravascular coagulation occurs everywhere in the body, most notably in the most delicate microvascular system. This leads to hypoperfusion and clinical exam findings of “end-organ injury.” The endothelium continues to malfunction, resulting in loss of blood vessel wall motor tone, which leads to hypotension, as well as leaky blood vessels, which leads to edema in the lungs, brain, and soft tissues.
There are multiple infectious causes of sepsis. There are multiple triggers for SIRS. Once you identify SIRS, you must look for the trigger. Infection from any type of germ (bacteria, virus, fungi, etc) is possible. As shown in the Venn diagram above, conditions other than infection can result in SIRS (trauma, burns, pancreatitis, etc.).
SIRS is a constellation of associated abnormal vital signs that are not specific for any one disease. 60% of all ED patients happen to meet SIRS criteria, but they don’t all have infection. As a good rule of thumb, if your patient meets SIRS criteria for any reason, they are probably critically ill.
SIRS technically includes results rom blood work, such as white blood cell counts. We adapted SIRS for EMS use that does not rely on WBC results and uses glucose and mental status instead.
Sepsis occurs when the inflammatory processes of the body in response to an infection exceed the boundaries of the local environment. The immune response becomes more global, more generalized to all parts of the body. It becomes uncontrolled, unregulated, and self-sustaining (domino-effect). This generalized inflammation causes wide-spread cellular injury. Cells are unable to perform their functions efficiently, leading to organ dysfunction. Tissue ischemia (low blood flow) results from a mismatch in available oxygen to changing tissue oxygen needs. The body responds by secreting catecholamine (fight or flight) hormones like epinephrine to compensate. The body produces lactic acid as it uses epinephrine to help jump start energy production.
Mortality is high in septic patients with elevated lactic acid levels.
Different criteria of what constitutes organ dysfunction have been defined for each organ system. These criteria are used in many ways when treating sepsis, primarily in identifying the severity and progression of sepsis.
At many hospitals around the Valley, administrative leaders are educating all those that are in contact with these patients: docs, nurses, technicians. We are using posters, videos, lectures, placards to educate. In addition, some hospitals have formed sepsis alert teams to respond to all septic workups to assist with IV access, antibiotic and fluid administration, and perform audits to maintain compliance with care bundles. Some hospitals perform chart audits to assess compliance in the ED, ICU and floor.
Early identification of sepsis is important for many reasons. The time it takes to administer the correct antibiotics is one of the most important factors. Mortality increases by 7.6% for every hour that antibiotics are delayed.
Some hospitals recognized EMS-initiated sepsis alerts like stroke, STEMI, and trauma alerts, and others may not. IT WON’T MATTER TO YOU AS THE EMS PROVIDER! It may help save a life just because you explicitly communicate your concern for sepsis to the accepting facility! Early notification of the hospital will help trigger the process of more aggressive care. As they say, attitude is infectious. Your heightened tone of alarm gets attention from others and helps combat the systematic inertia that can doom a septic patient. “Load the boat! Get everybody on board!”
ARDS - Acute Respiratory Distress Syndrome is an acute condition characterized by bilateral pulmonary infiltrates and severe hypoxemia in the absence of evidence for cardiogenic pulmonary edema. It is the most severe form of acute lung injury (ALI), a form of diffuse alveolar injury. There are many causes (trauma, aspiration), but severe sepsis is the most common cause.
Severe shortness of breath — the main symptom of ARDS — usually develops within a few hours to a few days after the precipitating injury or infection.
Capnography, a well-known tool in EMS, provides valuable information not only about ventilation but perfusion as well. As long as the body is metabolizing glucose and oxygen, waste products will be eliminated into the bloodstream. They can only be released into the alveolus and exhaled in the breath if there’s normal perfusion of the lung with blood.
As perfusion decreases, so does the EtCO2. This results in elevation of the metabolic waste, which is comprised mainly of lactic acid. Therefore, EtCO2 level is inversely proportional to lactate levels. As we see lactate levels rise in septic patients, we see EtCO2 levels drop. EtCO2 readings of less than 25 mmHg in the clinical setting of shock are associated with significant increase in mortality. Patients with EtCO2 of 25 mmHg may have lactate levels as high as 6.1 mmol/L. Capnography can be monitored and helpful in assessing the impact of therapies designed to improve perfusion.
Remember, mortality is higher in septic patients with elevated lactic acid (and thus low EtCO2) levels.