Rheumatic heart disease is caused by an autoimmune response following a streptococcal throat infection. It commonly affects the mitral and aortic valves, causing stenosis or regurgitation. Management involves antibiotics to prevent recurrent infections, surgery to repair or replace damaged valves, and medications for heart failure symptoms. Complications include atrial fibrillation, thromboembolism, and heart failure if left untreated. Regular antibiotic prophylaxis is important to prevent initial and recurrent infections that can exacerbate valve damage.
Acute Rheumatic Fever and Rheumatic Heart Disease, are two common conditions in children between 3-15 years of age following a Group B Streptococcal throat infection. We discuss these two conditions in the slides above, as well as their management.
Acute Rheumatic Fever and Rheumatic Heart Disease, are two common conditions in children between 3-15 years of age following a Group B Streptococcal throat infection. We discuss these two conditions in the slides above, as well as their management.
RHEUMATIC FEVER AND RHEUMATIC HEART DISEASEANILKUMAR BR
Rheumatic heart disease (RHD) is damage to one or more heart valves that remains after an episode of acute rheumatic fever (ARF) is resolved.
It is caused by an episode or recurrent episodes of ARF, where the heart has become inflamed.
The heart valves can remain stretched and/or scarred, and normal blood flow through damaged valves is interrupted.
Untreated, RHD causes heart failure and those affected are at risk of arrhythmias, stroke, endocarditis and complications of pregnancy.
These conditions cause progressive disability, reduce quality of life and can cause premature death in young adults.
Heart surgery can manage some of these problems and prolong life but does not cure RHD.
RHD is the a chronic condition characterized by scarring and deformity of the heart valves following rheumatic fever infection.
Rheumatic fever is an inflammatory disease that may affect many connective tissues of the body, especially those of the heart, joints, brain or skin. It usually starts out as a strep throat (streptococcal) infection.
RHEUMATIC FEVER AND RHEUMATIC HEART DISEASEANILKUMAR BR
Rheumatic heart disease (RHD) is damage to one or more heart valves that remains after an episode of acute rheumatic fever (ARF) is resolved.
It is caused by an episode or recurrent episodes of ARF, where the heart has become inflamed.
The heart valves can remain stretched and/or scarred, and normal blood flow through damaged valves is interrupted.
Untreated, RHD causes heart failure and those affected are at risk of arrhythmias, stroke, endocarditis and complications of pregnancy.
These conditions cause progressive disability, reduce quality of life and can cause premature death in young adults.
Heart surgery can manage some of these problems and prolong life but does not cure RHD.
RHD is the a chronic condition characterized by scarring and deformity of the heart valves following rheumatic fever infection.
Rheumatic fever is an inflammatory disease that may affect many connective tissues of the body, especially those of the heart, joints, brain or skin. It usually starts out as a strep throat (streptococcal) infection.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
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Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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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.
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.
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.
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
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
4. Introduction
• Acute rheumatic fever (ARF) is a delayed, nonsuppurative sequela of a pharyngeal infection with
the group A streptococcus (GAS).
• Following the initial pharyngitis, a latent period of two to three weeks occurs before the first signs
or symptoms of Acute Rheumatic Fever appear.
• In developing areas of the world, acute rheumatic fever and rheumatic heart disease are estimated
to affect nearly 20 million people and are the leading causes of cardiovascular death during the first
5 decades of life.
• Worldwide, there are 470,000 new cases of rheumatic fever and 233,000 deaths attributable to
rheumatic fever or rheumatic heart disease each year; most occur in developing countries and
among indigenous groups.
• The mean incidence of Acute Rheumatic Fever is 19 per 100,000.
5. Epidemiology
• Age 5 to 15 years are more susceptible.(average age of 10years)
• M=F although the prognosis is though to be worse in females
• Common in developing countries.
• Incidence more common in cold season
• Environmental factors :overcrowding, poor sanitation, poverty.
6. Aetiology
• Acute rheumatic fever is a systemic disease of childhood often that follows a group A beta
hemolytic streptococcal infection.
• Rheumatic fever is thought to result from an inflammatory autoimmune response.
• Rheumatic fever only develops in children and adolescents following group A beta-hemolytic
streptococcal pharyngitis, and only streptococcal infections of the pharynx initiate or reactivate
rheumatic fever.
• The proposed pathophysiology for development of rheumatic heart disease is as follows:
Cross-reactive antibodies bind to cardiac tissue facilitating infiltration of streptococcal-primed
CD4+ T cells
trigger an autoimmune reaction releasing inflammatory cytokines (including TNF-alpha and IFN-
gamma).
Because few IL-4–producing cells are present in valvular tissue, inflammation persists, leading to
valvular lesions.
7. Pathogenesis
• Rheumatic fever develops in some children and adolescents following pharyngitis with group A
beta-hemolytic Streptococcus (ie, Streptococcus pyogenes).
• The organisms attach to the epithelial cells of the upper respiratory tract and produce a battery of
enzymes allowing them to damage and invade human tissues.
• After an incubation period of 2-4 days, the invading organisms elicit an acute inflammatory
response with 3-5 days of sore throat, fever, malaise, headache, and an elevated leukocyte count.
• In 0.3-3% of cases, infection leads to rheumatic fever several weeks after the sore throat has
resolved.
• Group A streptococci may be subserotyped by surface proteins on the cell wall of the organism.
The presence of the M protein is the most important virulence factor for group A streptococcal
infection in humans.
• Anti-M antibodies against the streptococcal infection may cross-react with components of heart
tissue (ie, sarcolemmal membranes, valve glycoproteins).
8. Pathogenesis
• Acute rheumatic heart disease often produces a pancarditis characterized by endocarditis,
myocarditis, and pericarditis.
• Endocarditis is manifested as valve insufficiency. The mitral valve is most commonly and severely
affected (65-70% of patients), and the aortic valve is second in frequency (25%).
• The tricuspid valve is deformed in only 10% of patients and is almost always associated with
mitral and aortic lesions. The pulmonary valve is rarely affected.
• Severe valve insufficiency during the acute phase may result in congestive heart failure and even
death (1% of patients).
• Chronic manifestations due to residual and progressive valve deformity occur in 9-39% of adults.
• Fusion occurs at the level of the valve commissures, cusps, chordal attachments, or any
combination of these resulting in stenosis or a combination of stenosis and insufficiency.
• Associated atrial fibrillation or left atrial thrombus formation from chronic mitral valve
involvement and atrial enlargement may be observed.
9. Clinical Presentation
• Previous Hx of throat infection or rheumatic fever.
• The Jones criteria require the presence of 2 major or 1 major and 2 minor criteria along with
evidence for recent streptococcal infection for the diagnosis of rheumatic fever.
• The major diagnostic criteria include: carditis, polyarthritis, chorea, subcutaneous nodules, and
erythema marginatum.
• The minor diagnostic criteria include: fever, arthralgia, prolonged PR interval on ECG, elevated
acute phase reactants (increased erythrocyte sedimentation rate [ESR]), presence of C-reactive
protein, and leukocytosis.
• After a diagnosis of rheumatic fever is made, symptoms consistent with heart failure eg difficulty
breathing, exercise intolerance, tachycardia, may be indications of carditis and rheumatic heart
disease.
11. Management
• supplemental oxygen, bed rest, and sodium and fluid restriction
• Diuretics which include furosemide and spironolactone.
• Digoxin (only after checking electrolytes and correcting hypokalemia).
• Afterload reduction ie using ACE inhibitor eg captopril
• Steroid therapy eg prednisone
• Junior Aspirin .
• Surgical intervention:
balloon mitral valvuloplasty
Open heart surgery-MV replacement
12. Complications
• Valve deformities, thromboembolism, cardiac hemolytic anemia, and atrial arrhythmias are the
most common cardiac manifestations of chronic rheumatic heart disease.
• Mitral stenosis occurs in 25% of patients with chronic rheumatic heart disease and in association
with mitral insufficiency in another 40%.
• Aortic stenosis from chronic rheumatic heart disease is typically associated with aortic
insufficiency.
• Thromboembolism occurs as a complication of mitral stenosis. It is more likely to occur when the
left atrium is dilated, cardiac output is decreased, and the patient is in atrial fibrillation
• Cardiac hemolytic anemia is related to disruption of the RBCs by a deformed valve. Increased
destruction and replacement of platelets also may occur.
• Atrial arrhythmias are typically related to a chronically enlarged left atrium (from a mitral valve
abnormality).
13. Mitral stenosis
• Mitral disease begins with the formation of tiny nodules located along the coapting portions of the
valve leaflets.
• The leaflets thicken with eventual deposition of fibrin on the cusps and loss of normal valve
morphology
• Disease progression results in a number of pathologic changes affecting the mitral valve apparatus,
which are diagnostic for rheumatic valve disease:
Fusion of the leaflet commissures
Thickening, fusion and shortening of the chordae tendineae
• In addition, there may superimposed thickening, fibrosis, and calcification of the leaflet cusps
• The net effect is a stenotic mitral valve with a symmetric, central oval-shaped orifice and a classic
pattern of "doming" of the leaflets in diastole due to fusion of the leaflet tips at the commissures
14. Mitral Stenosis
• The primary hemodynamic consequence of MS is :
a pressure gradient between the LA and LV in diastole.
elevated left atrial pressure is reflected backward, causing an ↑ in pulmonary venous, capillary,
and arterial pressures and resistance.
This leads to pulmonary hyperetension.
With mild to moderate MS, these abnormalities are often only apparent with exercise or other
conditions that increase heart rate; they eventually are seen at rest as the severity of the stenosis
increases.
Thromboembolism occurs as a complication of mitral stenosis. It is more likely to occur when the
left atrium is dilated, cardiac output is decreased, and the patient is in atrial fibrillation
15. Mitral Stenosis-management
• Anti hypertensives-diuretics,digoxin,ACE inhibitors
• Patients who have thrombus formation -Steroid therapy eg prednisone or NSAIDs eg Junior Aspirin can
be used.
• Anticoagulants eg warfarin
• Mitral valvotomy indicated in:
symptomatic NYHA Functional Class II–IV patients with isolated MS
Mitral valve area is <1.5 cm2 .
• Mitral valvotomy can be carried out by two techniques:
PMBV percutaneous mitral balloon valvotomy
surgical valvotomy.
• Mitral Valve Replacement
16. Mitral Regurgitation
• The resistance to LV emptying (LV afterload) is reduced.
• The LV is decompressed into the LA during ejection, and with the reduction in LV size during
systole, there is a rapid decline in LV tension.
• This increase in LV volume is accompanied by a reduced forward CO
• The regurgitant volume varies directly with the LV systolic pressure and the size of the regurgitant
orifice; which is influenced by the extent of LV and mitral annular dilation.
• A modest reduction in ejection fraction (EF)ie <60% reflects significant dysfunction.
17. Mitral Regurgitation-Management
• Urgent stabilization.
• Antihypertensives-Diuretics, ACE inhibitors,Digoxin
• Anticoagulants-Aspirin, Warfarin should be provided once Atrial Fibrillation intervenes with a
target INR of 2–3.
• Surgery-mitral valve replacement
18. Aortic stenosis
• Outflow obstruction leads to an increase in left ventricular (LV) systolic pressure.
• To compensate , LV wall thickness increases by parallel replication of sarcomeres, producing
concentric hypertrophy.
• At this stage, the chamber is not dilated and ventricular function is preserved, although diastolic
compliance is reduced.
• Eventually, LV end-diastolic pressure (LVEDP) rises ,causing a corresponding increase in
pulmonary capillary arterial pressures and a decrease in cardiac output due to diastolic dysfunction.
• The contractility of the myocardium may also diminish, which leads to a decrease in cardiac output
due to systolic dysfunction.
19. Aortic Stenosis Management
• Severe AS (valve area <1 cm2), strenuous physical activity and competitive sports should be
avoided, even in the asymptomatic stage.
• Avoid dehydration and hypovolemia to protect against a significant reduction in CO.
• Antihypertensives - Diuretics and ACE inhibitors.
• Percutaneous Balloon aortic valvuloplasty.
• Aortic valve replacement.
20. Aortic Regurgitation
• Acute AR of significant severity leads to:
increased blood volume in the LV during diastole. The LV does not have sufficient time to dilate in
response to the sudden increase in volume.
LV end-diastolic pressure increases rapidly, causing an increase in pulmonary venous pressure.
• Chronic AR causes:
Gradual left ventricular volume overload
LV enlargement
eccentric hypertrophy.
The LV becomes larger and more compliant, with greater capacity to deliver a large stroke volume
that can compensate for the regurgitant volume
21. Aortic Regurgitation-Management
• Antihypertensives- diuretics and vasodilators
• Beta blockers are also best avoided so as not to reduce the CO further or slow the heart rate.
• Surgery is the treatment of choice-Aortic valve replacement.
22. Tricuspid regurgitation
• The pathophysiology of tricuspid regurgitation focuses on the structural incompetence of
the valve.
• Tricuspid valve insufficiency due to leaflet abnormalities may be secondary to
endocarditis or rheumatic heart disease.
• Ebstein anomaly is the most common congenital form of tricuspid regurgitation.
• Chronic RV volume overload results in right-sided congestive heart failure (CHF)
manifested by hepatic congestion, peripheral edema, and ascites.
• In severe TR, the CO is usually markedly reduced
• The mean RA and the RV end-diastolic pressures are often elevated.
• Systolic murmur best heard at the left lower sternal border
24. Prevention
• Primary prophylaxis (initial course of antibiotics administered to eradicate the streptococcal
infection.
• An injection of 0.6-1.2 million units of benzathine penicillin G intramuscularly every 4 weeks is
the recommended regimen for secondary prophylaxis upto 21 years of age.
• Prophylactic antibiotics 1 hour before surgical or dental procedures.