Amebiasis is an intestinal infection caused by the protozoan Entamoeba histolytica. It is transmitted through the fecal-oral route and infects 50 million people annually. Symptoms range from mild diarrhea to severe dysentery. Rarely, the infection may spread to other organs and cause liver abscesses. Diagnosis involves microscopy of stool or biopsy samples to identify the protozoan trophozoites. Treatment consists of metronidazole or tinidazole to eliminate the intestinal infection, followed by other drugs like paromomycin or diloxanide furoate to clear cysts from the gut and prevent recurrence.
Jaundice – a detailed view by Rxvichu :) :)RxVichuZ
Hello friends...............me ,Vishnu.......back to u all with a MEGA PPT..........................
This PPT, is terminalized by me as "MEGA" , coz It comprises DETAILED VERSIONS OF :
1. ADULT JAUNDICE
2. NEONATAL JAUNDICE
Surely will prove to be a great resource knowledge for anyone who go through this....................but mistakes and errors are humane.............so do share ur feedbacks and reviews..............
Will be back soon with a new ppt....
Keep studying well
#rxvichu-roar4more!!!
:)
Hemostasis is the arrest of bleeding, whether it be by normal vasoconstriction (the vessel walls closing temporarily), by an abnormal obstruction (such as a plaque) or by coagulation or surgical means (such as ligation)
To know basic etiology of this disease and difference between duodenal ulcer and peptic ulcer as well as how we can approach if children having peptic ulcer disease. By conservative and surgical means
Jaundice – a detailed view by Rxvichu :) :)RxVichuZ
Hello friends...............me ,Vishnu.......back to u all with a MEGA PPT..........................
This PPT, is terminalized by me as "MEGA" , coz It comprises DETAILED VERSIONS OF :
1. ADULT JAUNDICE
2. NEONATAL JAUNDICE
Surely will prove to be a great resource knowledge for anyone who go through this....................but mistakes and errors are humane.............so do share ur feedbacks and reviews..............
Will be back soon with a new ppt....
Keep studying well
#rxvichu-roar4more!!!
:)
Hemostasis is the arrest of bleeding, whether it be by normal vasoconstriction (the vessel walls closing temporarily), by an abnormal obstruction (such as a plaque) or by coagulation or surgical means (such as ligation)
To know basic etiology of this disease and difference between duodenal ulcer and peptic ulcer as well as how we can approach if children having peptic ulcer disease. By conservative and surgical means
Hello Docs ! My name is Maharshika It's my small presentation on hemorrhagic syndromes, hemostasis and It's Disorder i hope you guys likes it. Please like it and share it and keep studying 🙂
Chronic glomerulonephritis is a kidney disorder caused by slow, cumulative damage and scarring of the tiny blood filters in the kidneys. These filters, known as glomeruli, remove waste products from the blood.
When your blood has too few platelets, mild
to serious bleeding can occur. Bleeding can occur inside your body (internal
bleeding) or underneath your skin or from the surface of your skin (external
bleeding).
A normal platelet count in adults ranges
from 150,000 to 450,000 platelets per microliter of blood. A platelet count of
less than 150,000 platelets per microliter is lower than normal. If your blood
platelet count falls below normal, you have thrombocytopenia.
However, the risk for serious bleeding
doesn't occur until the count becomes very low—less than 10,000 or 20,000
platelets per microliter. Mild bleeding sometimes occurs when the count is less
than 50,000 platelets per microliter.
Many factors can cause a low platelet
count, such as:
-- The body's bone marrow doesn't make enough
platelets.
-- The bone marrow makes enough platelets, but
the body destroys them or uses them up.
-- The spleen holds on to too many platelets.
The spleen is an organ that normally stores about one-third of the body's
platelets. It also helps your body fight infection and remove unwanted cell
material.
-- A combination of the above factors.
-- How long thrombocytopenia lasts depends on
its cause. It can last from days to years.
The treatment for this condition also
depends on its cause and severity. Mild thrombocytopenia often doesn't require
treatment. If the condition causes or puts you at risk for serious bleeding,
you may need medicines or blood or
platelet transfusions. Rarely, the spleen may need to be removed.
Hello Docs ! My name is Maharshika It's my small presentation on hemorrhagic syndromes, hemostasis and It's Disorder i hope you guys likes it. Please like it and share it and keep studying 🙂
Chronic glomerulonephritis is a kidney disorder caused by slow, cumulative damage and scarring of the tiny blood filters in the kidneys. These filters, known as glomeruli, remove waste products from the blood.
When your blood has too few platelets, mild
to serious bleeding can occur. Bleeding can occur inside your body (internal
bleeding) or underneath your skin or from the surface of your skin (external
bleeding).
A normal platelet count in adults ranges
from 150,000 to 450,000 platelets per microliter of blood. A platelet count of
less than 150,000 platelets per microliter is lower than normal. If your blood
platelet count falls below normal, you have thrombocytopenia.
However, the risk for serious bleeding
doesn't occur until the count becomes very low—less than 10,000 or 20,000
platelets per microliter. Mild bleeding sometimes occurs when the count is less
than 50,000 platelets per microliter.
Many factors can cause a low platelet
count, such as:
-- The body's bone marrow doesn't make enough
platelets.
-- The bone marrow makes enough platelets, but
the body destroys them or uses them up.
-- The spleen holds on to too many platelets.
The spleen is an organ that normally stores about one-third of the body's
platelets. It also helps your body fight infection and remove unwanted cell
material.
-- A combination of the above factors.
-- How long thrombocytopenia lasts depends on
its cause. It can last from days to years.
The treatment for this condition also
depends on its cause and severity. Mild thrombocytopenia often doesn't require
treatment. If the condition causes or puts you at risk for serious bleeding,
you may need medicines or blood or
platelet transfusions. Rarely, the spleen may need to be removed.
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
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ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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.
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.
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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
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.
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
2. Amebiasis.
Definition:
Infection of the colon with entamoeba
histolytica, which is commonly
asymptomatic but may produce clinical
manifestations ranging from mild
diarrhoea to severe dysentery.
3. Aetiology.
It is caused by entamoeba histolytica.
E. dispar is a nonpathogenic protozoon
morphologically identical to E histolytica.
Previously reported asymptomatic
infections due to the so-called
nonpathogenic strains of E histolytica
now are recognized to be due to E.
dispar.
4. Transmission.
It is a natural infection of man, that may be
transmitted by direct contact from person
to person, through the faecal-oral route,
or indirectly by food, drink and
vegetables.
5. Epidemiology.
Amebiasis is the third leading parasitic
cause of death worldwide, surpassed
only by malaria and schistosomiasis. On
a global basis, amebiasis affects
approximately 50 million persons each
year, resulting in nearly 100,000 deaths.
6. Entamoeba life cycle
Cysts shed in faeces of carriers
Cysts transferred via contaminated food, water or
hands
Feacal-oral
Anal sex
Colonic irrigation
Excystation in the small bowel releasing
trophozoites
Cysts resistant to gastric acid but broken down by
trypsin releasing trophozoites
7. Entamoeba life cycle
Trophozoites migrate to the colon and
reproduce (forming cysts)
Within the colon trophozoites feed on
bacteria and feacal material
If trophozoites adhere and then penetrate
the mucosa clinical infection results
Hepatic infection if trophozoites enter
mesenteric venules
Trophozoites and cysts are passed in the
feaces
8. Pathology.
Trophozoites emerge from the cyst in
the small intestine and then pass on
the colon, where they multiply.
There is lysis and necrosis of the mucosa
by means of proteolytic enzymes
released by the trophozoites.
Rectosigmoidoscopy and colonoscopy
may show small mucosal ulcers
covered with yellowish exudates.
9. Cont. pathology.
The intervening mucosa appears normal.
Biopsy results and scrapings of ulcer
edge may locate trophozoites.
Primary intestinal flask-shaped (button
hole) necrotic ulcers occur in the
submucosa of the large intestine, most
commonly the cecal and
sigmoidorectal regions.
10. Cont. pathology.
Ulcers contain necrotic debris,
actively feeding trophozoites with
ingested erythrocytes, cytolyzed
cells and mucous.
polymorphonuclear leukocytes and
round inflammatory cells.
11. Cont. pathology
Hematogenous spread may result in
abscesses of the liver, spleen, lung
or brain. Hepatic amebiasis
(abscess, hepatitis) is the most
common and grave complication.
13. Clinical features
Asymptomatic
• Most common form of infestation
• “carriers”
These people almost never develop
symptoms but can spread disease
• Spontaneously clear disease within 12
months
• If detected on stool sample should be
treated
• Risk of infection 10%/year
14. Clinical features
Symptomatic
Amoebic colitis
• Subacute presentation (weeks)
Abdominal pain/ cramping/ distention
Diarrhoea (blood, mucus)
Fever (40%)
Tenesmus
Ameobic liver abscess
Most common extraintestinal manifestation
(10% of infected patients develop liver abscesses)
15. Clinical features.
Amebiasis is an intestinal infection in which
cysts are passed in the feces. Symptoms
can include fever, chills and diarrhea,
sometimes bloody or with mucus and often
with cramps. Some people may have only
mild abdominal discomfort or no symptoms
at all. Symptoms can start 2 or more weeks
after infection. Rarely, trophozoites (the
mobile amebas) may invade the liver, lung
or brain, or perforate the colon causing
septicemia.
18. Laboratory diagnosis.
By microscopy, the diagnosis is not confirmed
until active trophozoites containing RBCs are
demonstrated from the stools.
An iodine-stained cyst of the pathogen
Entamoeba hystolytica with 4 nuclei is
illustrated.
The harmless commensal Entamoeba coli has
larger cyts with 8 nuclei.
22. Cont. lab. diagnosis
The cyst of E histolytica averages
12 m, ranging from 5-20 m.
It has 1-4 nuclei that are
morphologically similar to the
nuclei of the trophozoite.
24. Cont. Diagnosis.
Leukocytosis and mild anemia can occur.
Erythrocyte sedimentation rate generally is
elevated.
Liver function tests reveal elevated alkaline
phosphatase in 80% of patients, elevated
transaminases and reduced albumin.
Urinalysis may reveal proteinuria.
Rectosigmoidoscopy and colonoscopy may show
small mucosal ulcers covered with yellowish
exudates.
The intervening mucosa appears normal.
25. Drugs for treatment.
Five pharmaceuticals are briefly noted:
Asymptomatic intestinal infection may be
treated with iodoquinol, paromomycin or
diloxanide furoate.
Recommended drugs for treatment of
symptomatic intestinal disease and for
hepatic abscess are metronidazole and
tinidazole.
26. Cont. treatment.
Since these drugs may not eliminate the
cysts of the intestine, immediately follow
metronidazole and tinidazole with
iodoquinol, paromomycin or diloxanide
furoate.
27. Cont. treatment
1/ Metronidazole (Flagyl, Protostat). Kills
trophozoites of E. histolytica in intestine
and tissue.
Does not eradicate cysts from intestines.
Adult oral dose: 500-750 mg 3 times
per day for 10 day.
Elimination is accelerated by simultaneous
use of phenytoin and phenobarbital.
28. 2/Tinidazole (Fasigyn). 5-nitroimidazole
derivative with selective antimicrobial
activity against anaerobic bacteria and
protozoa. Adult oral dose: 600 mg bid or
800 mg 2 times a day for 5 days. Pediatric
dose 50-60 mg/kg for 5 days, not to
exceed 2 g/day.
Cont. treatment
29. 3/Paromomycin (Humatin). Amebicidal
aminoglycoside antibiotic that is poorly
absorbed. Active only against intestinal
form of amebiasis. Used to eradicate cysts
of E. histolytica following treatment with
metronidazole or tinidazole for an invasive
disease. Adult oral dose: 25-35 mg/kg/day
divided 3 times for 7 days. Pediatric dose:
Administer as in adults.
Cont. treatment
30. 4/Diloxanide furoate (Furamid, Entamizole,
Furamide). Luminal amebicide; acts primarily
in bowel lumen since it is poorly absorbed.
Used to eradicate cysts of E. histolytica after
treatment of invasive disease. Available
through US CDC Drug Service (404-639-
3670). Adult oral dose 500 mg 2 times a day
for 10 days. Pediatric dose 20 mg/kg/
divided twice a day for 10 days, not to
exceed 1500 mg/day.
Cont. treatment
31. 5/Iodoquinol (Yodoxin). Halogenated
hydroxyquinoline. Luminal amebicide; acts
primarily in bowel lumen since it is poorly
absorbed. Best tolerated when given with
meals. Since active only against intraluminal
form of amebiasis, used to eradicate cysts of E.
histolytica after treatment of invasive disease.
Adult oral dose 650 mg 2 times a day for 20
days. Pediatric dose: 30-40 mg/kg/day divided
2 times for 20 days; not to exceed 2 g/day.
Cont. treatment
34. Amoebic liver abscess
Trophozoites invade small vessels of the
bowel wall and reach liver via portal
circulation
Microembolization in the portal system
causes infarction and focal areas of necrosis
Amoeba cause lysis of neutrophils and the
edge of these lesions causing release of toxic
mediators and further hepatic necrosis
Usually multiple small lesions coalesce
forming the “amoebic liver abscess”
35. Amoebic liver abscess
Usually solitary lesion
Right lobe more common
80% of abscesses in right lobe
Right lobe larger in volume and
receives most of the blood from the
caecum – where trophozoites are
commonly found
36. Amoebic liver abscess
Presentation
Acute, <14d (more common)
May have preceding amoebic colitis (20-30%)
Fever, malaise, rigors, diaphoresis
RUQ pain:
Sharp, constant, relieved by lying on left side
Radiating to shoulder tips and scapulae
Pleuritic component
Hepatomegaly
chronic presentations
Weight loss and vague abdominal discomfort
Can present years after amoebic colitis
37. Amoebic liver abscess
Rare presentations
Pulmonary symptoms (20%)
Ameobic pulmonary abscess
Bronchopulmonary fistula
Cough, chest pain
Jaundice (5%)
Due to large or multiple abscesses and/ or
bacterial superinfection
Diarrhoea
38. Amoebic liver abscess
Examination findings
Common
• Febrile
• Tender hepatomegaly
• Often point tenderness
• Epigastric mass (left sided disease)
Uncommon
• Right lower lobe pneumonia
• Jaundice
• Severe sepsis - usually indicates secondary bacterial
infection
39. Amoebic liver abscess
Diagnosis
Aneamia, leukocytosis, eosinophilia
Ultrasound
CT scan
LFT’s
Jaundice, hypoalbuminaemia
Elevated AST (acute) and ALT (chronic)
Serology
Aspirate microscopy
Stool sample
Low sensitivity (only 30% of patients have concomitant
intestinal amoebiasis)
Response to metronidazole 750 t.i.d