local names, definition, etiology,epidemiology lifecycle, pathogenesis, clinical findings, necropsy finding, diagnosis,treatment, control and prevention
local names, definition, etiology,epidemiology lifecycle, pathogenesis, clinical findings, necropsy finding, diagnosis,treatment, control and prevention
THESE SLIDES ARE PREPAREED TO UNDERSTAND CHILD HEALTH DISORDERS IN EASY WAY
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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
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.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
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.
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
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
2. Ascariasis – is a intestinal parasitic disease caused by
species of roundworm of the class Nematoda, and can
cause intestinal and lung damage.
• Ascaris lumbricoides, an intestinal roundworm, is
one of the most common helminthic human
infections worldwide.
• Highest prevalence in tropical and subtropical
regions, and areas with inadequate sanitation.
Ascariasis occurs in rural areas of the southeastern
United States.
3. Morphology
• A. lumbricoides is the largest
intestinal nematode of man.
• The female worms are larger
than the males and can
measure 40 cm in length and 6
mm in diameter.
• They are white or pink and are
tapered at both ends.
• The ova are oval, have a thick
shell, a mamillated outer coat.
4. EPIDEMIOLOGY
• It is estimated that more than 1.4 billion people are infected
with A. lumbricoides, representing 25 percent of the world
population. Transmission is enhanced by the fact that
individuals can be asymptomatically infected and can continue
to shed eggs for years, yet prior infection does not confer
protective immunity.
• The majority of people with ascariasis live in Asia (73 %),
Africa (12 %) and South America (8 %), where some
populations have infection rates as high as 95 %.
• Ascariasis is most common in children 2 to 10 years old, and
prevalence decreases over the age of 15 years. Infections tend
to cluster in families, and worm burden correlates with the
number of people living in a home.
• Ova can survive in the environment for prolonged periods and
prefer warm, shady, moist conditions under which they can
survive for up to 10 years.
5. • Transmission — Transmission occurs mainly via ingestion of
water or food (raw vegetables or fruit in particular)
contaminated with A. lumbricoides eggs and occasionally via
inhalation of contaminated dust. Children playing in
contaminated soil may acquire the parasite from their hands.
• Transplacental migration of larvae has also occasionally been
reported.
6. LIFE CYCLE
• Adult worms inhabit the lumen of the small intestine, usually in
the jejunum or ileum. They have a life span of 10 months to 2 years
and then are passed in the stool.
• The ova are passed out in the feces, and embryos develop into
infective second-stage larvae in the environment in 2 to 4 weeks
(depending upon environmental conditions).
• When ingested by humans, the ova hatch in the small intestine and
release larvae, which penetrate the intestinal wall and migrate
hematogenously or via lymphatics to the heart and lungs.
• Occasionally, larvae migrate to sites other than the lungs, including
to the kidney or brain.
7.
8. Life Cycle
• Adult worms (1) live in the lumen of the small intestine.A female may produce
approximately 200,000 eggs per day, which are passed with the feces
(2). Unfertilized eggs may be ingested but are not infective. Fertile eggs
embryonate and become infective after 18 days to several weeks (3), depending
on the environmental conditions (optimum: moist, warm, shaded soil).After
infective eggs are swallowed (4), the larvae hatch (5), invade the intestinal
mucosa, and are carried via the portal, then systemic circulation to the lungs
(6). The larvae mature further in the lungs (10 to 14 days), penetrate the
alveolar walls, ascend the bronchial tree to the throat, and are swallowed (7).
Upon reaching the small intestine, they develop into adult worms (1). Between 2
and 3 months are required from ingestion of the infective eggs to oviposition by
the adult female. Adult worms can live 1 to 2 years.
9. Pathophysiologic mechanisms include
• Direct tissue damage
• The immunologic response of the host to infection
with larvae, eggs or adult worms
• Obstruction of an orifice or the lumen of the
gastrointestinal tract by an aggregation of worms
• Nutritional sequelae of infection
10. CLINIC SYMPTOMS
• The majority of infections with A. lumbricoides are
asymptomatic.
• Clinical disease is largely restricted to individuals
with a high worm load.
• When symptoms do occur, they relate either to the
larval migration stage or to the adult worm
intestinal stage.
11. • The symptoms and complications of infection can be
classified into the following:
•
• 1. Pulmonary and hypersensitivity manifestations
• 2. Intestinal symptoms
• 3. Intestinal obstruction
• 4. Hepatobiliary and pancreatic symptoms
12. Pulmonary and hypersensitivity
manifestations
• Transient respiratory symptoms can occur
in sensitized hosts during the stage of
larval migration through the lungs.
Symptoms associated with the
pneumonitis, which are known as
Loffler's syndrome, tend to occur one to
two weeks after ingestion of the eggs. The
severity of symptoms tends to correlate
with larval burden, but pulmonary
symptoms are also less common in
countries with continuous transmission of
A. lumbricoides.
•
• Urticaria and other symptoms related to
hypersensitivity usually occur toward the
end of the period of migration through the
lungs.
13. INTESTINAL SYMPTOMS
• Heavy infections with Ascaris are frequently
believed to result in:
• Abdominal discomfort,
• Anorexia,
• Nausea
• Diarrhea.
14. Intestinal obstruction
• A mass of worms can obstruct the bowel lumen in heavy
Ascaris infection, leading to acute intestinal obstruction.
• The obstruction occurs most commonly at the ileocecal valve.
• Symptoms include colicky abdominal pain, vomiting and
constipation. Vomitus may contain worms. Approximately 85
percent of obstructions occur in children between the ages of
one and five years. Complications including volvulus, ileocecal
intussusception, gangrene, and intestinal perforation
occasionally result.
• The overall incidence of obstruction is approximately 1 in 500
children. In endemic areas, it has been shown that between five
and 35 percent of all cases of bowel obstruction are due to
ascariasis.
15. Hepatobiliary and pancreatic symptoms
Symptoms related to the migration of adult worms into the biliary
tree can cause:
• abdominal pain,
• biliary colic,
• acalculous cholecystitis,
• ascending cholangitis,
• obstructive jaundice, or bile duct perforation with peritonitis.
• Strictures of the biliary tree may occur.
• Hepatic abscesses can also result.
• The pancreatic duct may also be obstructed, leading to
pancreatitis, and the appendix resulting in appendicitis.
• High fever, diarrhea, spicy foods, anesthesia and other stresses
have all been associated with an increased likelihood of worm
migration.
16. Laboratory diagnostic
• Microscopy — Characteristic eggs
may be seen on direct examination of
feces or following concentration
techniques.
• Eosinophilia — (during the phase of
larval migration through the lungs).
Eosinophil levels are usually in the
range of 5 to 12 percent but can be as
high as 30 to 50 percent.
• Serum levels of IgG and IgE are also
often elevated during early infection.
17. • Plain film of the abdomen. The
mass of worms contrasts against the
gas in the bowel, typically
producing a "whirlpool" effect.
• Radiologic detection of adult
worms is sometimes made by
detecting elongated filling defects
following barium meal
examinations of the small bowel.
The worms also sometimes ingest
barium, in which case the
alimentary canal appears as a white
thread bisecting the length of the
worm's body.
• Radiographs will also show when
there is associated intestinal
obstruction.
18. • Ultrasound examinations can help to diagnose
hepatobiliary or pancreatic ascariasis.
• Computed tomographic (CT) scanning or magnetic
resonance imaging (MRI) may also be used to identify
worm(s) in the liver or bile ducts, but this is not usually
necessary. Imaging the worm in cross-section gives a
"bull's eye" appearance.
• Serology — Infected individuals make antibodies to A.
lumbricoides which can be detected.
19. TREATMENT
Choice of Drugs — A number of drugs can be used in the treatment of
ascariasis:
• * Pyrantel pamoate (11 mg/kg up to a maximum of 1 g) is effective in
eradicating adult worms.
• * Mebendazole (100 mg BID for 3 days or 500 mg as a single dose).
• * Albendazole — A single dose of albendazole (400 mg) is effective
in almost 100 percent of cases.
• Ivermectin — Ivermectin causes paralysis of adult worms and is
approximately as effective as other available therapies but is not
generally used.
• * Piperazine citrate — Piperazine citrate (50 to 75 mg/kg QD up to a
maximum of 3.5 g for 2 days) is used seldom because of the big
toxicity
• * Levamisole — Levamisole (150 mg for adults and 5 mg/kg for
children) is safe and is effective in 77 to 96 percent of cases of
ascariasis.
20. PREVENTION
• Good sanitation to prevent fecal contamination of soil
is required. Soil treatments have been attempted but
are generally not practical.
•
• Mass treatments with single dose mebendazole or
albendazole for all school-age children every three to
four months has been used in some communities.