[OS 213] LEC 10 Rheumatic Fever and RHD (B)

OS 213: Circulation and Respiration (CardiovascularModule) LEC 08: RHEUMATIC FEVER and Rheumatic Heart Disease Quiz 1 | Dr. Sanchez-Acosta | July 25, 2012 OUTLINE I. Rheumatic Fever and Rheumatic Heart Disease A. Rheumatic Fever B. Rheumatic Heart Disease C. Epidemiology: RF & RHD D. Risk Factors II. Rheumatic Fever A. Pathogenesis of Rheumatic Fever B. Etiology C. Lab Test for GAS Tonsillopharyngitis D. ARF: Age & Sex Distribution E. Pathology     F. Diagnosis: Jones Criteria 1992 G. Diagnosis: RF Modified Jones Criteria 1992 H. RF: Other Laboratory Exams I. Management III.Rheumatic Heart Disease A. Description B. Diagnosis C. Medical Management D. Disease Progression and Intervention E. Differentiating RF and RHD F. Management IV. Questions and Answers RHEUMATIC FEVER AND RHEUMATIC HEART DISEASE Rheumatic Fever Most common cause of acquired heart disease in children, adolescents and young adults worldwide Pathology: diffuse inflammation of connective tissues of heart, joints, brain, blood vessels & subcutaneous tissues Rheumatic process, when it heals, causes fibrosis of heart valves leading to rheumatic heart disease (RHD) as a sequelae and onset depends whether it was detected early or not or treated early or not Relationship with Group A β-hemolytic Streptococcus established Rheumatic Heart Disease  Chronic valvular heart disease as a sequelae of rheumatic fever (RF)  When recurrent RF causes scarring of the heart, it becomes Rheumatic Heart Disease (RHD) o Must have both the recurrence and the scarring to consider RHD as a sequelae of RF o Exactly when?  It depends on the patient  when in the continuum, did he/she sought intervention? does he/she take medication regularly, etc. Epidemiology: RF and RHD  Why?  they can afford a check-up because they have the money Risk Factors  Risk factors for RF o Poverty o Poor housing, overcrowded housing o Reduced access to health care  Risk factor for RHD o Recurrent episodes of RF RHEUMATIC FEVER Pathogenesis of Rheumatic Fever  Actual mechanism unknown  Postulate: o Autoimmune or hypersensitivity reaction to Group A Strep (GAS) produces pathogenic autoantibodies to cardiac tissues o Anti-streptococcal antibodies made by the infected host cross-react with host connective tissue (ie. cardiac, pulmonary, synovial, peritoneal) antigens and lead to end-organ damage by an immunologic mechanism. o It is believed to be caused by antibody crossreactivity. 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 Streptococcus infection, mature antigen presenting cells such as macrophages present the bacterial antigen to CD4T cells which differentiate into helper T 2 cells. Helper T2 cells subsequently activate the B cells to become plasma 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.  Myocardial Aschoff’s Body/Nodule – focal inflammatory lesions in the heart; swollen eosinophilic collagen surrounded by lymphocytes and Anitshkow; cells are large, elongated, with large nuclei; some are multinucleate. Table 1. Prevalence of RF and RHD in School Children Country Rate Developing countries 18.6 / 1000 Philippines 1971-1980 0.9 / 1000 1981-1990 0.6 / 1000 2010 0.5 / 1000 Developed countries USA 1971-1980 0.7 / 1000 Australia 1981-1990 12.3 / 1000 (because of aborigines) Factors in the Development of Rheumatic Fever  Philippines o In a study at the PGH (1986-1990), the peak incidence of RF and RHD is from 5-15 years old o Deaths from RF and RHD (Achutti & Achutti, 1992)  1% of cardiovascular death  200,000 cases/ year  Worldwide (World Heart Federation) o 15.6 million people affected worldwide o Almost 500,000 new cases each year o Approximately 350,000 deaths each year o Most occur in developing countries (for developed countries, this is already part of the grand rounds) o Skin infection only leads to AGN but never RF  Persistence of virulent strain GAS organism  Antibody response  Age: usually at ages 5-15 because of exposure to school grounds  Genetic or familial tendency: specific B cell alloantigen (D817) & HLA identified (not yet proven)  Socio-economic status o Poverty, overcrowded housing, reduced access to health care  still the most common risk factor JEREEL, SITTI, DAYAN  Site of GAS infection o Throat → rheumatic fever (RF), sometimes acute glomerulonephritis (AGN) o If the patient complains to you of tonsillitis, ask yourself whether it is a viral infection or not o Check for presence of exudates  No exudate does not mean no risk for RF  Exudate will usually appear after several days so reexamine the patient  If still no exudate, usually viral infection. If with exudate, consider risk for RF.  Features suggestive of viral etiology: conjunctivitis, coryza (inflammation of mucus membranes lining the nasal cavity), cough, diarrhea UPCM 2016 B: XVI, Walang Kapantay! 1 of 6 OS 213: Circulation and Respiration (Cardiovascular Module) LEC 08: RHEUMATIC FEVER and Rheumatic Heart Disease Quiz 1 | Dr.3%  Strep. should last for at least 5 days) o Arthralgia o Increased acute phase reactants: elevated erythrocyte sedimentation rate (ESR) and Creactive protein (CRP) o Prolonged PR interval via ECG test will cause 1 st degree AV block How to Use Jones Criteria  There is a high probability of RF when the patient has o 2 major manifestations. or focal interstitial inflammation  Fully developed: granulomatous structures consisting of fibrinoid change. there are less than 5 cases who are aged 2-3 years old Pathology Exudative degenerative inflammatory lesions o Transient manifestations o Responds to anti-inflammatory agents  Proliferative lesions o Aschoff’s nodules   Areas of inflammation of the connective tissue of the heart. Walang Kapantay! 2 of 6 . tonsillitis. Figure 1. it is just that the patients do not have the money to seek consult Rheumatic Fever: Attack Rate  Strep.Tender. or o 1 major and 2 minor manifestations plus supporting evidence of preceding GAS infection (always!) UPCM 2016 B: XVI.Nausea. tonsillitis treated penicillin = 0. 6 & 19 cross react with myosin  Enzymes o Streptolysin o Deoxyribonuclease o Fibrinolysin o Diphosphopyridine nucleotidase o Hyaluronidase o Valuable for confirmation of previous streptococcal infections in patients suspected of having acute RF (ARF) or post-streptococcal glomerulonephritis (PSGN) o Helpful in prospective epidemiological studies for distinguishing patients with acute infection from patients who are carriers o A positive anti-streptococcal antibody titers does not necessarily mean that RF is present. lymphocytic infiltration. the Diagnosis of GAS Tonsillopharyngitis o Clinical & Epidemiological Findings o Laboratory test/s – throat culture and/or Rapid Antigen ARF: Age and Distribution  Most common in ages 5-15 years old  Rare in children less than 5 years old  In the Philippines. vomiting. untreated = 3%  Known rheumatic patients with strep infection = 60% Etiology  Relationship with Group A β-hemolytic Streptococcus established  Inflammation of pharynx and tonsils – patchy discrete exudates  Good thing it’s still sensitive to penicillin  Cell wall (virulence factors) o M-protein o Induces antibodies o Serotypes 5. Streptococcal Tonsillopharyngitis.Sudden onset sore throat 4. occasional plasma cells and characteristically abnormal macrophages (may fuse to form multinucleated giant cells) surrounding necrotic cells  Diagnostic for RF  Done on biopsy but today in RP.Patient aged 5–15 years 3. not done anymore. Jones criteria must still be followed o cut-off: > 220 units  In summary. Sanchez-Acosta | July 25. SITTI. Note the presence of patchy discrete exudates (“nana”) and the beefy-red color of the pharynx and tonsils which are characteristic of bacterial (versus viral) tonsillopharyngitis. Clinical & Epidemiological Finding & Diagnosis of GAS Tonsillopharyngitis 1.History of exposure 2.Fever & Headache 5. enlarged anterior cervical nodes 8.Inflammation of pharynx and tonsils patchy discrete exudates 6. and abdominal pain Laboratory Test for GAS Tonsillopharyngitis  Throat swab and culture (gold standard) o Standard for documentation of GAS in upper respiratory tract & for confirmation of clinical diagnosis of acute strep pharyngitis o If done correctly – sensitivity of 90-95% o Disadvantage – there is delay (after about 48 hours) in obtaining the result  Rapid Antigen Detection Tests (RADT) – but this is very expensive so not done anymore  Anti-streptococcal Antibody Titers (done in PGH) o Can reflect past but not present immunologic events o No value in the diagnosis of acute pharyngitis JEREEL. DAYAN  Persists for many years Diagnosis: Jones Criteria 1992  Establish initial attack of acute rheumatic fever  Not intended o To establish diagnosis of inactive or chronic RHD o To measure rheumatic activity o To predict course or severity of disease  Previous RF or RHD not included as manifestation  Major Manifestations o Carditis – most common among hospitalized patients o Polyarthritis – most common manifestation overall (migratory) o Chorea o Erythema marginatum (least common) o Subcutaneous nodule  Minor Manifestations o Fever (high-grade. with regard to peak incidence. 2012 o In the Philippines (and probably in other developing countries as well) we are capable of treating it.Presentation in winter or early spring 7. even without treatment. freely movable & transient  Extensor surface of elbows. not the face  Urticaria-like but is induced by heat (disappears when cold so cover with blanket to elicit) TYPES OF CARDITIS       Mild carditis o no cardiomegaly and no CHF o can be cured and the heart can revert back to its normal state Moderate carditis o mild cardiomegaly & CHF o commonly proceeds to severe carditis Severe carditis o cardiomegaly with severe pulmonary congestion or edema o may die on admission Echocarditis . Tricuspid and Pulmonic) in order of being affected the most  Cardiomegaly o not present in mild carditis  Resting tachycardia – know if the resting tachycardia is due to fever or carditis o Usually associated with fever o General rule in children: an increase of one degree Celsius in temperature corresponds to an increase of heart rate by 10 beats per minute  Pericardial friction rub o Once pericardial effusion is present. By the natural history of diseases.OS 213: Circulation and Respiration (Cardiovascular Module) LEC 08: RHEUMATIC FEVER and Rheumatic Heart Disease Quiz 1 | Dr. disappear in 1–2 wks.Echocardiographic abnormalities like MVP. firm. SITTI. usually occurs with fever Irregularly-shaped and map-like lesion Distinctive non-pruritic transient rash Pale centers with round or serpiginous (slowly progressing/creeping) margin  Blanches  Trunk & proximal extremities. Sanchez-Acosta | July 25. Major Manifestation 1: Rheumatoid Carditis  worst sequela and the only symptom that is not selflimiting  Valvulitis – means ‘leaky valves’ o Most common manifestation and the most severe o Almost always present o Primary valvular involvement o Pancarditis – involves all layers of the heart (like Kawasaki disease) o Mnemonic: MATP (Mitral. muscular incoordination & weakness. elbows. or AR in acute rheumatic fever in the absence of clinical carditis (valvular regurgitation) Mitral stenosis in children – most probably congenital because you need at least 5 years of RF in order to produce mitral stenosis Subclinical carditis o Cardiac involvement in the absence of valvulitis symptoms. chorea minor  Rheumatic involvement of basal ganglia & caudate nucleus  Purposeless & involuntary movement. MR. & wrists. The lesions spread outward to form a serpiginous ring with erythematous raised margins and central clearing. sudden flinging of arms. you cannot combine it with arthralgia as minor and carditis with prolonged PR interval o Exception to the rule: Chorea! WHY? Must have vasculitis to affect the brain which would take months to come up. deterioration of handwriting  “milk maid’s sign”  Delayed manifestation or self-limiting  Exception to the Jones criteria: when chorea is present without any other symptoms. ankles. no more sound o Usually seen in post-op patients or usually very early in a disease  Congestive heart failure o gallop rhythm (S3) o muffled heart sounds o arrhythmia o Edema in both L and R o For R: pulmonary edema  Rapid healing without sequelae o in contrast with Juvenile Rheumatoid Arthritis which is prolonged and can cause deformities  Usually resolves in <24 hrs when given aspirin Major Manifestation 3: Chorea  Sydenham’s chorea. Walang Kapantay! 3 of 6 . Vitus’ dance. Major Manifestation 5: Subcutaneous Nodules  Small. St. wrists exquisitely painful JEREEL. knees. painless. 2012 o GAS infection: through (1) antibody sensing and (2) streptococcal culture – gold standard o Note: manifestations should be two unrelated symptoms such as if you use polyarthritis as major criterion. Aortic. Pink-to-red non-pruritic macules or papules located on the trunk and proximal limbs but never on the face. automatically it is rheumatic in origin unless proven otherwise  can stand alone  also an exception: indolent carditis as RF in origin automatically  Affects adolescents. emotional lability & slurred speech. everything else might have disappeared at the time of consultation. o Controversy whether to include subclinical carditis in the modified Jones Criteria o “Although echocardiography is of established value in the evaluation & management of Figure 2. diagnosed with 2D echo. scalp & spinal areas (always palpate cardiac patient of rheumatic origin in scalp and spine)  Often seen with carditis Major Manifestation 2: Migratory Arthritis     Most frequent & benign but least specific Asymmetric & migratory Inflammation Larger joints: knees. DAYAN UPCM 2016 B: XVI. more common in women  Treat with penicillin Major Manifestation 4: Erythema Marginatum     Not easy to see. darting tongue. low voltages.2 M units every 21 days best choice because long acting. cost effective and due to good compliance.000 U for patients ≤ 27 kg Children: 250 mg 2-3x/day Adolescents/adults: 500 mg 2-3x/day 500 mg on first day Oral 5d 250 mg/d for the next 4 d Bonow et al. long-term prophylaxis because of scarring  if both are present. Nov 1998: 1486-1588ACC/AHA Guidelines for the Management of Patients WithValvular Heart Disease  Secondary Prophylaxis : prevents recurrences of RF o Penicillin (PCN) VK 250 mg twice daily o Benzathine PCN 1. Fever must be at least > 38oC  Arthralgia o Diagnostic:  ECG – PR interval is prolonged suggesting 1o AV block  Increased acute phase reactants: ESR & CRP are increased  Complete Blood Count (CBC) and Chest X-Ray (CXR) not specific to RF of RF: Other Laboratory Exams  CBC o Anemia (hemolysis and dilutional anemia due to heart failure) o Leukocytosis (inflammation. DAYAN Mod e IM Azithromycin  Notes minor manifestations o Clinical vs Diagnostic  Jones Criteria 1992.minimum of 5 years or until age 21 whichever is longer assuming no recurrence of the disease between 5-21 years. 2012 treatment of streptococcus = 10 days of penicillin to prevent initial attack o if patient already has RF upon consultation.000 U every 21 days for Filipinos (very important!!!!!!) (every 3 wk for high risk patients such as those with residual carditis) 250 mg 2x/day UPCM 2016 B: XVI.200.given only for 5 days o Duration of recurrence)  Primary prophylaxis : prevents 1st episode of RF 2o prophylaxis (or prevention of  Arthritis . Major and Minor Manifestations of RF According to the Jones Criteria Major Manifestations Minor Manifestations Carditis Fever Polyarthritis Arthralgia Sydenham’s Chorea Elevated acute phase reactants Erythema marginatum Prolonged PR Interval Subcutaneous nodules *PLUS supporting evidence of preceding GAS infection Estolate Ethylsuccinate  Clinical: Fever must last more than 5 days. No. still treat him/her with penicillin for 10 days because you do not know if strep is still active (treatment is always 10 days upon initial consult) o Table 3. add more 5 years from last onset. choose the long-term so treat carditis! Table 4.OS 213: Circulation and Respiration (Cardiovascular Module) LEC 08: RHEUMATIC FEVER and Rheumatic Heart Disease Quiz 1 | Dr. administered via the intramuscular route or depot because this makes the levels in the blood constant  for Filipinos: every 21 days because penicillin levels go down after 21 days  Short acting benzyl penicillin  Oral penicillin .200.2x a day for 10 days (important to stress compliance with the number of days the antibiotic is administered to ensure that the microorganism will be completely eradicated)  Azithromycin . If there is recurrence. 5. SITTI..at least 10 years assuming recurrence free & no residual heart disease or 21 whichever is longer  if RHD. ST-T wave changes  CXR o Normal (but may depend on severity of valvular lesion) o Cardiomegaly o Pulmonary congestion and edema Management  Prophylaxis  Anti-inflammatory agents Durati on Once Oral 10 d Oral 10 d 20-40 mg/kg/d Oral 10 d 2-4 x /day (max: 1g/d) Oral 10 d 40 mg/kg/d 2-4 x daily (max: 1g/d) Oral 10 d 600. Nodules are firm.000 U for patients ≤ 27 kg 1. Secondary Prevention of Rheumatic Fever Agent Benzathine Penicillin G Prophylaxis JEREEL. Sanchez-Acosta | July 25. Supporting Evidence Antecedent Group A Streptococcal Infection o Positive throat culture or rapid antigen test o Elevated or rising Streptococcal antibody titer For people allergic to Penicillin: Erythromycin Dose Penicillin V Dose 1.  Carditis . infection)  ECG o Sinus tachycardia o 1o AV block—prolonged PR interval o No chamber enlargement (as opposed to RHD) o Rarely 2o AV block. free from attachments to the overlying skin. ACC/AHA TASK FORCE REPORT JACC Vol. Primary Prophylaxis or Prevention of Rheumatic Fever Agent Benzathine Figure 3. 32. Walang Kapantay! Mode IM Oral 4 of 6 . non-tender. and they range from a few millimeters to 1-2cm Penicillin G Penicillin V RF Modified Jones Criteria 1992 Table 2. LAE. if there is. blood culture study) & urinalysis  ECG and CXR  Echocardiography: TTE (transthoracic). CRP. LVH o CXR . usually with MR  Prominent carotid pulse  Corrigan’s pulse  Natural History: CHF. ECGNormal. though not all do  ECG . dilated MV annulus. 2012 0. RVF Aortic Regurgitation  a diastolic blowing decrescendo murmur best heard at the left sternal border with the person sitting up and leaning forward in full expiration  ECG .  Once the mitral valve is damaged. SITTI. Sanchez-Acosta | July 25. increase in LV volume.normal. RVH. Small MVA (fishmouth commisure)  History of CHF. after surgery a 2007 World Health Federation b We start counting the duration of prophylaxis WHEN rheumatic fever is cured c For carditis. ESR.Normal. RVH  CXR . Anti-Strep Antibody Titers. TEE (transesophageal)   Mitral Regurgitation  a pansystolic murmur heard loudest at the apex and radiating laterally to the axilla. LAE. DAYAN  Why does it radiate to the axilla?  the left atrium is the most posterior chamber of the heart  Most common o ECG . chronic & severe lesions o o o o o dilated MPA if Medical Management  Anti-CHF UPCM 2016 B: XVI.Sulfadiazine OS 213: Circulation and Respiration (Cardiovascular Module) LEC 08: RHEUMATIC FEVER and Rheumatic Heart Disease Quiz 1 | Dr. diastolic rumble heard best at the apex with the bell of the stethoscope and with the person lying in the left lateral position. RVH AR: LVH TR: RAE.5 g once daily for patients ≤ 27 kg 1. then it’s most probably congenital Tricuspid regurgitation Tricuspid stenosis: rare (least common) Pulmonary regurgitation: related to pulmonary hypertension Pulmonary stenosis: very rare Summary of ECG and CXR  ECG Normal if lesions are mild MR: LAE. you start counting 10 years from the time the heart was cleared from carditis d In the Philippines. it’s forever damaged o In 10-30% of cases o Produces a thrill upon PE. aortic run-off  LV dilation decreased myocardial contractility  Rarely isolated (bicuspid aortic valve if isolated).LVH. Dilated aorta  Echocardiogram . the cut off age is 21 years Anti-inflammatory Agents  For 6-8 weeks o prednisone – 2 mg/kg/day o aspirin – 100 mg/kg/day  plus complete bed rest for at least 3 months for severe carditis (may even stop schooling)       RHEUMATIC HEART DISEASE Description Heart disease as a sequelae of chronic RF and its recurrences Heart valves are scarred due to healing process following ARF RHD is more likely to develop following ARF if o The initial episode of ARF was severe o The heart was affected with ARF o ARF occurred at a young age o There has been recurrent ARF 50% of people with RHD do not remember having ARF because some symptoms are self-limiting Valve Regurgitation suggests that heart valves o Are thickened and stick against the walls of the heart o Leakage (the blood flows backwards over the valve) Valve Stenosis suggests that heart valves o Become stiff o Do not allow blood to flow through easily (restricted forward flow) Diagnosis Clinical history and physical examination Blood examinations (CBC. when the patient is cured it can return to its normal state  When the aortic valve is damaged. soft S1 JEREEL. or Until age 25 years (whichever is longer) Continue for life Severe RHD. infective endocarditis o Ischemic AR less coronary perfusion during diastole Others      Aortic stenosis: not common. LAE.LVH.thickened leaflets with prolapsed  Heave indicative of volume overload  Fibrosis and contracture of the aortic valve  Regurgitation across incompetent valve. or Until age 21 years whichever is longer Minimum of 10 years after last ARF. RVH  Chest X-Ray o Pulmonary venous congestion. LVH MS: LAE. LAE. Table 5. Walang Kapantay! 5 of 6 . Duration of Secondary Prophylaxis Group ARF (no carditis) Mild-moderate carditis (or healed carditis) Duration of Secondary Prophylaxis Minimum of 5 years after last ARF. Strain pattern  CXR . Pulmonary congestion. pulmonary congestion o Echo .LAE.thickened valve. it cannot return to its original state.Thickened fixed leaflets.0 g once daily for patients ≥ 27 kg Oral For people allergic to penicillin and sulfadiazine: Erythromycin 250 mg twice daily Oral *High-risk patients include those with residual rheumatic carditis as well as patients from economically disadvantaged populations. Dilated MPA  Echo . LVH. LVH Mitral Stenosis  low-pitched. chest pain (in AR vs MR).normal. Anyway. haha.Valvuloplasty or valve replacement Remember: o If porcine valves used. hahaha. diuretics and ACE inhibitors. heehee. hahaha. with pulmonary artery hypertention (dilated vessels) PE No chronic heart disease Precordial bulge ECG No tachycardia. Wag kayong matakot. Wag masyadong malandi ah. pwede pa mag-apply. Hi Block A friends kung mababasa ninyo ‘to. usually in younger population can be initially asymptomatic but is actually chronic: usual in adults but not always CXR Valvular lesions Valvular lesions. Guys watch Bourne Legacy. SITTI. And syempre. Baka nagkaron kayo ng symptoms nung bata pero di nyo lang matandaan. Hoy Jim! Naiintindihan ko na hindi tayo mag-seatmate dahil busy ka. valve replacement o MS – Commisurotomy o AR . Good luck sa atin sa cardio. children rely more on breathing for survival) o MI in children mainly due to pulmonary congestion Disease Progression and Intervention Primary Prophylaxis END OF TRANSCRIPTION Ate Dayan:  Sitti: Hello everyone. need to be replaced later in life due to calcifications o If pediatrics patient. Summary of the Lecture (Important!) Differentiating RF and RHD Table 5.) Heya virGinnie! AlexeisCelina(block A ). don’t be paranoid. sobrang mababait kami.Valvuloplasty. Hala… Joke lang. Sinusuportahan kita dyan pero hinay-hinay lang ha! . Kayanin natin ang lahat ng transes!  Jones Criteria. β-blockers only if with arrythmia 2o prophylaxis Benzathine penicillin. hi 2016! helLU4 na! Sana okay pa tayong lahat. Nood nga pala kayo ng block screening ng Bourne Legacy by MSSR and RSO! woohoo! Hello sa Mangotukola! I miss y’all and our toxic days NOT.OS 213: Circulation and Respiration (Cardiovascular Module) LEC 08: RHEUMATIC FEVER and Rheumatic Heart Disease Quiz 1 | Dr. Sanchez-Acosta | July 25. hello Block B! Ang toxic ng cardio pero sana kayanin natin!  MSSR-IPPNW go! Kung interested kayo. DAYAN RF RHD History (not always useful) symptoms occur early. RSO and MSSR are selling tickets for the benefit of a very unfortunate elementary school and Unang Yakap Program  Jereel: Babawi ako sa greeting dahil nakalimutan ko sa first trans namin. kumusta ang mebendazole mo? haha. coffee shop review na! Oi Jer. Walang Kapantay! 6 of 6 . Watch out for RF. annular placation. hindi ko alam kung maganda. heart structures return to normal Valvular disease which is lifetime UPCM 2016 B: XVI.21 days Infective Endocarditis prophylaxis o antibiotics Anticoagulant (coumadin) so that there will be no thrombus Arrhythmia management Surgical o MR . promote lang dahil shinoot sa Manila. 2012       o ionotropes (dopamine). Ikaw na bahalang maghanap ng MTTh sched niya. Wala na kong kinikiliti. chamber enlargement Prognosis Px. Differences Between RF and RHD          Management Education (most important) o you really have to make them understand their situations especially the parents and unruly adolescents Adherence to secondary prophylaxis Regular clinical assessment and follow-up echocardiography Management of cardiac failure Management of atrial fibrillation Dental care and Infective endocarditis prophylaxis Family planning referral (for women) Vaccination Appropriate surgical intervention QUESTIONS AND ANSWERS  Indications for tonsillectomy o repeated acute tonsillitis with treatment for a year o obstructive apnea  We still don’t know yet if there is a genetic factor but there is a familial predisposition JEREEL. Umayos ka! hihi. 20 Prophylaxis Tertiary Prophylaxis Medication of Penicillin only Figure 4. Hello to my new seatmate Tato.  Hoy Clintaba! Wag kang mag-IPad forever. Hello bestie Allie!  Hello nga pala kay Niko! Nami-miss na kita. primary drug to give are diuretics because it will relieve pulmonary causes of RHD (remember.