This presentation on Adenovirus was prepared and presented by me and my classmate.This topic generally comes under subject of virology. Hope you will find it helpful. Thank you.
This presentation on Adenovirus was prepared and presented by me and my classmate.This topic generally comes under subject of virology. Hope you will find it helpful. Thank you.
Coronaviruses are a family of viruses that cause disease in animals. Seven, including the new virus, have made the jump to humans, but most just cause cold-like symptoms.
Two other coronaviruses – Middle East respiratory syndrome (Mers) and severe acute respiratory syndrome (Sars) – are much more severe,
Coronaviruses are a family of viruses that cause disease in animals. Seven, including the new virus, have made the jump to humans, but most just cause cold-like symptoms.
Two other coronaviruses – Middle East respiratory syndrome (Mers) and severe acute respiratory syndrome (Sars) – are much more severe,
This is about Leishmaniasis in humans and dogs delivered by Professor Dr. Mazhar Ayaz, Professor of Parasitology, Cholistan University of Veterinary and Animal
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Massive Splenomegaly By Dr Bashir Ahmed Dar Chinkipora Sopore Kashmir Associa...Prof Dr Bashir Ahmed Dar
Dr.Bashir Ahmed Dar Chinkipora Sopore Kashmir India,Associate Prof of medicine presently working in malaysia is a keen teacher, educator and takes pride in his clinical and research accomplishments. His interests include publishing articles related to health issues.Email drbashir123@gmail.com
Causes of Splenomegaly By Dr Bashir Ahmed Dar Chinkipora Sopore Kashmir Assoc...Prof Dr Bashir Ahmed Dar
Dr.Bashir Ahmed Dar Chinkipora Sopore Kashmir India,Associate Prof of medicine presently working in malaysia is a keen teacher, educator and takes pride in his clinical and research accomplishments. His interests include publishing articles related to health issues.Email drbashir123@gmail.com
: Parasitic water pollution in the Nile River (Schistosoma & Giardia lamblia)MenrvaSorial
Causative organism.
Geographical distribution.
Epidemiology & Risk factors.
Mode of Transmission.
Vector (if available).
Habitat.
Life cycle (including infective stage, Diagnostic stage, Final host, Intermediate host and Reservoir).
-According to your lab group assignment topic, you must mention at least two examples (Causative organisms) for the required type of parasitic infection and their prevalence in Egypt. -Then discuss briefly the mentioned examples covering all the following points:
As a pharmacist, how could you identify and confirm a patient with such disease?
(NB: Identification and confirmation include the signs and symptoms and the diagnostic tests in details)
What are the therapeutic options available (suggest a line of treatment).
How can we prevent & control such disease?
...Understand the Definition and the underlying pathology of endometriosis
...sites of endometriosis
....Theories of development of endometriosis
...the Clinical presentations and investigations
...Management options for endometriosis in patients presenting by pain and those presenting by infertility
....Understand the Definition of and the underlying pathology of adenomyosis.
.......the clinical presentation, diagnosis of adenomyosis.
....... management options (medical and surgical) for adenomyosis
Histology of group of immune cells that mediate the cellular immune response by processing and presenting antigens for recognition by certain lymphocytes such as T cells.
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
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.
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
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.
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.
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
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.
3. Schistosomes
It causes water-borne disease constituting an important public health problem
Dioecious, (sexes are separate) trematodes,
Which lead to schistosomiasis (bilharziasis)
Gynecophoric canal
It is estimated that over 100 milion people are infected
with S. haematobium, S. mansoni, and S. japonicum
The female resides in a groove in the male
5. Life cycle
Adult worm lives in the inferior mesenteric vein.
Habitat
Biomphalaria
Sexual cycle
Asexual cycle
6. Schistosoma Mansoni
Pathogenesis
Most of the pathologic findings are caused by the presence of eggs in the liver, spleen, or wall of
the gut or bladder.
Induce granulomas in liver
Hepatomegaly Portal hypertension
Splenomegaly
S. Mansoni eggs damage the wall of the distal colon
Evolved a remarkable process for evading the host defenses
Their surface becomes coated with host antigens
Stage of Invasion Stage of Migration Stage of Deposition
Dermatitis Pass into the portal circulation
Larva Adult
Granulomas
7. Schistosoma Mansoni
Clinical Findings
Most patients are asymptomatic, but chronic infections may become symptomatic.
The acute stage
The chronic stage
Begins shortly after cercarial penetration
Consists of itching and dermatitis followed 2 to 3 weeks later by fever, chills, diarrhea, lymphadenopathy,
and hepatosplenomegaly
Usually resolves spontaneously
Can cause significant morbidity and mortality
Gastrointestinal hemorrhage, hepatomegaly, and massive splenomegaly can develop
The most common cause of death is exsanguination from ruptured esophageal varices
8. Schistosoma Mansoni
Laboratory Diagnosis
Stool Microscopy
Serological Diagnosis
Rectal Biopsy
Imaging
Blood Examination
Detect hepatosplenomegaly and periportal fibrosis
May reveal eosionophilia, and increased levels of alkaline phosphatase
?
12. Leishmania donovani
Pathogenicity
L. donovani causes visceral leishmaniasis or kala-azar and Post Kala-azar Dermal Leishmaniasis
Reticuloendotheliosis resulting from the invasion of reticuloendothelial system
The parasitized macrophages disseminate the infection to all ? parts of the body
Spleen, liver, and bone marrow particularly
The amastigotes multiply enormously in the fixed macrophages to produce a ‘blockade’ of the
reticuloendothelial system
Incubation period of 2 weeks - 6 months
13. Leishmania donovani
Pathogenicity
Spleen:
The spleen is the most affected organ
Enlarged and the capsule is thickened
Soft and friable and cuts easily due to absence of fibrosis.
Cut section is red or chocolate in color
Liver:
The Kupffer cells and vascular endothelial cells are heavily parasitized, but hepatocytes are not affected
Liver function ?
The liver is enlarged
The sinusoidal capillaries are dilated and engorged ‘nutmeg’
appearance
14. Leishmania donovani
Pathogenicity
Bone marrow:
Heavily infiltrated with parasitized macrophages, which may crowd the hematopoietic tissues
Severe anemia with hemoglobin levels of 5–10 g/dL may occur in Kala-azar
WBCs ?
Secondary infections
Reduced activity
15. Leishmania donovani
Clinical Features of Kala-Azar
The onset is typically insidious. The clinical illness begins with fever
Splenomegaly
Hepatomegaly and lymphadenopathy
Skin becomes dry, rough, and darkly pigmented
Kala-azar
Cachexia with marked anemia
Epistaxis and bleeding from gums are common
Untreated patients die in about 2 years ?
16. Leishmania donovani
Post Kala-azar Dermal Leishmaniasis
About 3–10% cases of patients of visceral leishmaniasis in endemic areas develop PKD
PKDL is a nonulcerative lesion of skin. The lesions are of 3 types
Depigmented macules
Erythematous patches
Nodular lesion
17. Leishmania donovani
Laboratory Diagnosis
Diagnosis is usually made by detecting ? in a bone marrow, spleen, or lymph node biopsy
The organisms can also be cultured
Skin test
Serologic (indirect immunofluorescence) tests are
positive in mostpatients.
18. Laboratory diagnosis
Clinical significance
Main properties
Organism
Stool Microscopy
Rectal Biopsy
Serological Diagnosis
Imaging
Schistosomiasis disease (bilharziasis)
Trematodes
Sexes are separate
Schistosoma
Mansoni
Examination of bone marrow,
lymph node or splenic
aspirates, peripheral blood for
amastigotes
PCR
Kala-azar (visceral leishmaniasis)
Post Kala-azar Dermal Leishmaniasis
2 forms (amastigotes,
promastigotes)
Definitive host: Human
Vector: Female sandfly
(Phlebotomus species).
Leishmania
donovani
Summary
20. Reference
Warren E. Levinson (2014) Review of Medical Microbiology and Immunology, 13th edn., New
York, United States: McGraw-Hill Education - Europe.
Neal R. Chamberlain ( 2009) Medical Microbiology: The Big Picture, New York, United States:
McGraw-Hill Education - Europe.
Sougata Ghosh, C. K. Jayaram Paniker (2013) Paniker's Textbook of Medical Parasitology, 7th
edn., Philadelphia, PA 19106, USA: Jaypee Brothers Medical Publishers (P) Ltd., 2013..
Editor's Notes
The male worm is broader than the female
The male has 6 to 9 testes, and the male genital pore opens ventrally, immediately posterior to the ventral sucker.
Female has a single ovary located in the anterior portion of the body.
The skin is covered with many tubercles. Have 2 suckers oral and ventral
In the gravid female, the uterus contains very few eggs, usually 1–3 only. The prepatent period (the interval between cercarial penetration and beginning of egg laying) is 4–5 weeks.
The egg has a characteristic lateral spine, more near to the rounded posterior end. The eggs are non operculated and yellowish brown.
The epidemiology of schistosomiasis depends on the presence of the specific freshwater snails that serve as intermediate hosts.
Mesenteric veins of the connections of the small intestine to the posterior abdominal membranes lining the cavity provide an anatomic site for these organisms to colonize
Eggs may be emitted through either the bladder or through the intestine
Sexual cycle Definitive host
Asexual cycle Intermediate hosts
due both to digestion of tissue by proteolytic enzymes produced by the egg and to the host inflammatory response that forms granulomas in the venules
Schistosomes have evolved a remarkable process for evading the host defenses. There is evidence that their surface becomes coated with host antigens, thereby limiting
the ability of the immune system to recognize them as foreign.
Eosinophilia is seen in response to the migrating larvae
A mastigote form: Rounded form multiplies in macrophages and other phagocytic cells in internal organs, skin or mucocutaneous tissues.
Promastigote form: flagellated highly motile form of the parasite, found in sand fly vectors and in vitro cultures. It multiplies in the gut of the sand fly
characterised by the presence of an organelle with a large massed DNA called kinetoplast (hence the name).
Definitive host: Man, dog, and other mammals. reservoir of infection
Vector: Female sandfly (Phlebotomus species).
Infective form: Promastigote form present in midgut of female sandfly
. This leads to a marked proliferation and destruction of reticuloendothelial tissue in these organs.
the organs of the reticuloendothelial system (liver, spleen, and bone marrow)
The striking enlargement of the spleen is due to a combination of proliferating macrophages and sequestered blood cells. The marked increase in IgG is neither specific nor protective.
Blood cell production in the bone marrow is greatly depressed. the patient becomes anemic, leucopenic and thrombocytopenic with many a mastigotes in macrophages.
Most untreated patients die in about 2 years, due to some intercurrent disease such as dysentery, diarrhea, and tuberculosis
Patients who recovered from visceral Leishmaniasis are immune to reinfection.