Rheumatic fever is an inflammatory disease that can occur 2-3 weeks after a streptococcal infection like strep throat. It is caused by an autoimmune reaction where antibodies created to fight streptococcus mistakenly attack heart, joints, brain and skin tissues. Treatment involves antibiotics to eliminate streptococcus, medications to reduce inflammation and symptoms, and preventing recurrent episodes through ongoing antibiotic prophylaxis. Complications can include long-term heart valve damage leading to mitral stenosis, regurgitation or heart failure if not properly treated.
Acute rheumatic fever-definition,pathophysiology,clinical presentation and ma...onlinefreelancer1
A detailed approach to ACUTE RHEUMATIC FEVER,based on Harrison Principles of internal medicine and Braunwald Textbook of Cardiology.Useful for post graduate seminars.
Acute rheumatic fever-definition,pathophysiology,clinical presentation and ma...onlinefreelancer1
A detailed approach to ACUTE RHEUMATIC FEVER,based on Harrison Principles of internal medicine and Braunwald Textbook of Cardiology.Useful for post graduate seminars.
Rheumatic fever is an acute inflammatory disease, due to cross reaction of antibodies against GAS M protein, which resembles the proteins of heart, joints, brain and other connective tissues
Rheumatic fever is an acute inflammatory disease, due to cross reaction of antibodies against GAS M protein, which resembles the proteins of heart, joints, brain and other connective tissues
Rheumatic fever (acute rheumatic fever) is a disease that can affect the heart, joints, brain, and skin.
Rheumatic fever can develop if strep throat and scarlet fever infections are not treated properly.
Early diagnosis of these infections and treatment with antibiotics is key to preventing rheumatic fever.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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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Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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.
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
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.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
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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
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
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NYSORA Guideline
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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.
1. Rheumatic fever is an inflammatory disease that occurs
following a Group A streptococcal infection, (such as
strep throat or scarlet fever). Believed to be caused by
antibody cross-reactivity that can involve the heart,
joints, skin, and brain, the illness typically develops two
to three weeks after a streptococcal infection. Acute
rheumatic fever commonly appears in children between
the ages of 5 and 15, with only 20% of first-time attacks
occurring in adults. The illness is so named because of its
similarity in presentation to rheumatism.
Pathophysiology- Rheumatic fever is a systemic disease
affecting the peri-arteriolar connective tissue and can
occur after an untreated Group A Beta hemolytic
streptococcal pharyngeal infection. It is believed to be
caused by antibody cross-reactivity. This cross-reactivity
is a Type II hypersensitivity reaction and is termed
molecular mimicry. Usually, self reactive B cells remain
anergic in the periphery without T cell co-stimulation.
During a Strep. infection, mature antigen presenting cells
such as B cells present the bacterial antigen to CD4-T
cells which differentiate into helper T2 cells. Helper T2
cells subsequently activate the B cells to become plasma
2. cells and induce the production of antibodies against the
cell wall of Streptococcus. However the antibodies may
also react against the myocardium and joints, producing
the symptoms of rheumatic fever.
Group A streptococcus pyogenes has a cell wall
composed of branched polymers which sometimes
contain M protein that are highly antigenic. The
antibodies which the immune system generates against
the M protein may cross react with cardiac myofiber
protein myosin,heart muscle glycogen and smooth
muscle cells of arteries, inducing cytokine release and
tissue destruction. However, the only proven cross
reaction is with perivascular connective tissue. This
inflammation occurs through direct attachment of
complement and Fc receptor-mediated recruitment of
neutrophils and macrophages. Characteristic Aschoff
bodies, composed of swollen eosinophilic collagen
surrounded by lymphocytes and macrophages can be
seen on light microscopy. The larger macrophages may
become Aschoff giant cells. Acute rheumatic valvular
lesions may also involve a cell-mediated immunity
3. reaction as these lesions predominantly contain T-helper
cells and macrophages.
In acute RF, these lesions can be found in any layer of the
heart and is hence called pancarditis. The inflammation
may cause a serofibrinous pericardial exudates described
as “bread-and-butter” pericarditis, which usually resolves
without sequelae. Involvement of the endocardium
typically results in fibrinoid necrosis and verrucae
formation along the lines of closure of the left-sided
heart valves. Warty projections arise from the
deposition, while subendothelial lesions may induce
irregular thickenings called MacCallum plaques.
Chronic rheumatic heart disease is characterized by
repeated inflammation with fibrinous resolution. The
cardinal anatomic changes of the valve include leaflet
thickening, commissural fusion and shortening and
thickening of the tendinous cords. Rheumatic heart
disease at autopsy with characteristic findings (thickened
mitral valve, thickened chordae tendineae,
hypertrophied left ventricular myocardium).
Etiology- Acute rheumatic fever (ARF) has been linked
definitively with a preceding streptococcal infection,
4. usually of the upper respiratory tract. Evidence is very
strong that the M protein in certain streptococci
subtypes is responsible for antigenicity.
Clinical
History- Acute rheumatic fever (ARF) is associated with 2
distinct patterns of presentation.
The first pattern of presentation is sudden onset. It
typically begins as polyarthritis 2-6 weeks after
streptococcal pharyngitis and is usually characterized
by fever and toxicity.
If the initial abnormality is mild carditis, ARF may be
insidious or subclinical.
Age at onset influences the order of complications.
Younger children tend to develop carditis first, whereas
older patients tend to develop arthritis first.
Physical-Modified Jones criteria were first published in
1944 by T. Duckett Jones, MD.They have been
periodically revised by the American Heart Association in
collaboration with other groups. According to revised
Jones criteria, the diagnosis of rheumatic fever can be
made when two of the major criteria, or one major
5. criterion plus two minor criteria, are present along with
evidence of streptococcal infection. Exceptions are
chorea and indolent carditis, each of which by itself can
indicate rheumatic fever.
Major criteria
Migratory polyarthritis: a temporary migrating
inflammation of the large joints, usually starting in
the legs and migrating upwards.
Carditis: inflammation of the heart muscle which can
manifest as congestive heart failure with shortness
of breath, pericarditis with a rub, or a new heart
murmur.
Subcutaneous nodules: painless, firm collections of
collagen fibers over bones or tendons. They
commonly appear on the back of the wrist, the
outside elbow, and the front of the knees.
Erythema marginatum: a long lasting rash that
begins on the trunk or arms as macules and spreads
outward to form a snake like ring while clearing in
the middle. This rash never starts on the face and it
is made worse with heat.
6. Sydenham's chorea (St. Vitus' dance): a
characteristic series of rapid movements without
purpose of the face and arms. This can occur very
late in the disease.
Minor criteria
Fever
Arthralgia: Joint pain without swelling
Raised Erythrocyte sedimentation rate or C reactive
protein
Leukocytosis
ECG showing features of heart block, such as a
prolonged PR interval
Supporting evidence of Streptococcal infection:
elevated or rising Antistreptolysin O titre or DNAase.
Previous episode of rheumatic fever or inactive heart
disease
Other signs and symptomsAbdominal pain
Nose bleeds
Differential Diagnoses-
7. - Aortic Regurgitation
-Pediatrics, Scarlet Fever
- Atrial Fibrillation
-Acute
Pericarditis
- Endocarditis
- Reactive Arthritis
Huntington Chorea
- Rheumatoid Arthritis
- Lyme Disease
-Scarlet Fever
- Mitral Regurgitation
- Systemic Lupus
Erythematosus
Mitral Stenosis
- Myocarditis
-Pediatrics, Kawasaki Diseas
- Leukemia
-Juvenile rheumatoid
arthritis
DiagnosisLaboratory Studies
- No specific confirmatory laboratory tests exist for
acute rheumatic fever. However, several laboratory
findings indicate continuing rheumatic inflammation.
Some are part of the Jones minor criteria.
- Streptococcal antibody tests disclose preceding
streptococcal infection.
8. - The CDC has stated that a rapid antigen test in the
appropriate clinical setting is sufficient to make the
diagnosis of active GABHS infection and begin
treatment.
- Isolate group A streptococci via throat culture. A
significant percentage will result in a culture positive
for group A beta-hemolytic Streptococcus (GABHS).
However, a culture positive for GABHS does not
definitively prove active infection. Some patients are
carriers.
- Acute-phase reactants (eg, erythrocyte
sedimentation rate [ESR], C-reactive protein [CRP] in
serum and leukocytosis) may show an increase in
serum complement, mucoproteins, alpha-2, and
gamma globulins. Anemia is usually caused by
suppression of erythropoiesis.
- PR-interval prolongation is present in approximately
25% of all cases and is neither specific for nor
diagnostic of acute rheumatic fever.
- Although there are a few small studies that show the
contrary, troponins have not been shown to be
helpful in making the diagnosis because ischemia
and necrosis are not the major cardiac problems.
9. - Synovial fluid analysis may demonstrate an elevated
white blood cell count with no crystals or organisms.
- Differences exist among nations in terms of
diagnosing and treating GABHS pharyngitis. Most
North American, French, and Finnish guidelines
consider diagnosis of streptococcal infection
essential (with either rapid antigen detection or with
formal culture) and advise antibiotic therapy when
streptococci is detected. Several European
guidelines consider streptococcal infection a selflimited disease and do not recommend antibiotics.
Imaging Studies
- Echocardiography may be helpful in establishing
carditis. Some suggest it be performed in all
suspected cases.
- Chest radiography should be performed to
determine presence of cardiomegaly and congestive
heart failure.
Treatment- The goals of treatment for rheumatic fever
are to destroy any remaining group A streptococcal
10. bacteria, relieve symptoms, control inflammation and
prevent recurring episodes of rheumatic fever.
Antimicrobials- Because of the direct link between ARF
and group A beta-streptococcal infection, the first step in
treatment is the eradication of the organism.
-Penicillin G benzathine (Bicillin LA, Bicillin C-R)Interferes with synthesis of cell wall mucopeptide during
active multiplication, resulting in bactericidal activity
against susceptible bacteria. Adult- 2.4 million U IM once
-Penicillin G procaine (Crysticillin, Wycillin)- Long-acting
parenteral penicillin (IM only) indicated in the treatment
of moderately severe infections caused by penicillin G–
sensitive microorganisms.Some prefer 10-d therapy.
Administer by deep IM injection only into the upper
outer quadrant of the buttock. In infants and small
children, the midlateral aspect of the thigh may be the
best site for administration. Adult- 2.4 million U IM once.
- Penicillin VK (Beepen-VK, Betapen-VK, Robicillin VK,
Veetids), Amoxicillin- Inhibits the biosynthesis of the cellwall mucopeptide and is effective during the stage of
active multiplication. Inadequate concentrations may
11. produce only bacteriostatic effects. Penicillin VK is the
oral alternative for the treatment of rheumatic fever.
Some authors suggest that once-daily amoxicillin is as
effective and can be recommended as an alternative
because compliance is likely to be better. Adult- 500 mg
PO q6h for 10 d
- Erythromycin (EES, E-Mycin, Ery-Tab, Erythrocin)DOC(drug of choice) for patients allergic to penicillin;
inhibits RNA-dependent protein synthesis, possibly by
stimulating the dissociation of peptidyl tRNA from
ribosomes, which inhibits bacterial growth.
In children, age, weight, and severity of infection
determine the proper dosage. When bid dosing is
desired, one-half the daily dose may be administered
q12h. For more severe infections, the dose may be
doubled. Adult- 1 g/d PO divided bid for 10 d
-Azithromycin (Zithromax)- Acts by binding to 50S
ribosomal subunit of susceptible microorganisms and
blocks dissociation of peptidyl tRNA from ribosomes,
causing RNA-dependent protein synthesis to arrest.
12. Treats mild-to-moderate microbial infections. Adult- 500
mg on day 1 followed by 250 mg/d for 4 additional days.
Glucocorticoids- These agents possess antiinflammatory (ie, glucocorticoid) and salt-retaining (ie,
mineralocorticoid) properties. Glucocorticoids cause
profound and varied metabolic effects. In addition, these
agents modify the body's immune response to diverse
stimuli.
Prednisone (Deltasone, Sterapred)- Patients with carditis
require prednisone instead of aspirin. The goal is to
decrease myocardial inflammation. Some authors
suggest that carditis without associated cardiomegaly or
congestive heart failure be treated with aspirin instead of
glucocorticoids.
Glucocorticoids are useful in treatment of inflammatory
and autoimmune disorders. Adult- 60-80 mg/d PO
Neuroleptic agents- These agents may help to control
the chorea associated with ARF.
Haloperidol (Haldol)- A dopamine receptor blocker useful
in the treatment of irregular spasmodic movements of
13. limbs or facial muscles.
0.5-2 mg PO bid/tid
Adult-
Inotropic agents- Some believe that digoxin may be
helpful in congestive heart failure.
Digoxin (Lanoxin)- Cardiac glycoside with direct inotropic
effects and indirect effects on the cardiovascular system.
Effects on the myocardium involve a direct action on
cardiac muscle that increases myocardial systolic
contractions and indirect actions that result in increased
carotid sinus nerve activity and enhanced sympathetic
withdrawal for any given increase in mean arterial
pressure.
Adult- 0.125-0.375 mg PO qd
Anti-inflammatory agents- Reduce the inflammation
associated with the disease process. Joints and heart are
the targets of inflammation, but carditis is treated with
glucocorticoids as noted above.
Aspirin - Treats mild to moderate pain. Inhibits
prostaglandin synthesis, which prevents formation of
platelet-aggregating thromboxane A2.
Adult- 6-8 g/d PO for 2 mo or until ESR has returned to
normal
14. Naproxen (Anaprox, Naprelan, Naprosyn)- For relief of
mild to moderate pain; inhibits inflammatory reactions
and pain by decreasing activity of cyclooxygenase, which
is responsible for prostaglandin synthesis.
NSAIDs decrease intraglomerular pressure and decrease
proteinuria. Adult- 250-500 mg PO bid; may increase to
1.5 g/d for limited periods.
Complications-
Carditis
Mitral stenosis
Mitral regurgitation
Aortic stenosis
Congestive heart failure (CHF)