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Rheumatic heart disease is caused by an untreated streptococcal infection which allows antibodies to cross-react with proteins in heart valves, causing inflammation and damage over time. This can lead to valvular stenosis or regurgitation as the valves thicken and do not open/close properly, forcing blood to backflow. Left untreated, the condition can progress to heart failure and death as the heart's ability to pump blood effectively is compromised.
Rheumatic heart disease is caused by an untreated streptococcal infection which allows antibodies to cross-react with proteins in heart valves, causing inflammation and damage over time. This can lead to valvular stenosis or regurgitation as the valves thicken and do not open/close properly, forcing blood to backflow. Left untreated, the condition can progress to heart failure and death as the heart's ability to pump blood effectively is compromised.
Rheumatic heart disease is caused by an untreated streptococcal infection which allows antibodies to cross-react with proteins in heart valves, causing inflammation and damage over time. This can lead to valvular stenosis or regurgitation as the valves thicken and do not open/close properly, forcing blood to backflow. Left untreated, the condition can progress to heart failure and death as the heart's ability to pump blood effectively is compromised.
> Cold and damp weather/climate (Group eta!hemolytic "treptococci# > Genetic "usceptiility > $mproper use of antiiotics/ > Gender (more women% &'(% are improper antiiotic therapy "treptococci gains entry through rea)s in affected than men% *'(# the s)in and mucous memranes > Pre+ious infections caused y G,-H" $n+ades the pharyn. $n+ades the tonsils $n+ades the s)in Pathogens gain entry in the loodstream Edema in the syno+ial /oints Pharyngitis/"trepthroat 0onsillitis $mpetigo Goes to the heart Pancarditis 1onocytes phagocyti2e the streptococci 1onocytes present pieces of the Endocardium 1yocardium Pericardium pathogens to Helper 0 cells Helper 0 cells acti+ate - cells and induce production of antiodies against the cell wall of streptococci ,ntiodies not only react against 31 proteins4% polymers found on the cell wall of G,-H"% ut also react (cross react# with cardiac cardiac myofier% syno+ial /oints and other connecti+e tissues Rheumatic Fe+er - lymphocytes produces immunogloulins and ,cti+ation of serum complement cascade Chemota.is of phagocytes of the immune response Rheumatic factors of the $gG and $g1 classes $nfiltration of acti+ated 0 cells Deposited in the tissues Pro+ides a arrier against diffusion of "yno+ial /oints Heart nutrients to the cartilage 5asodilation of lood +essels Formation of granulation tissues at the Production of e.cess syno+ial fluid in the syno+ial /oints syno+ial lining (,schoff -odies# "yno+ium cartilages is irritated and thic)ens Production of en2ymes that cause tissue damage c d a a e e a f g "yno+ial /oint cells use up all the nutrients 6nderlying one egins to disintegrate 7-C cannot enter as the +al+es of the heart do not actually recei+e any lood supply of their own Glucose le+el in the tissues drop E+ident /oint destruction "treptococci estalishes a hold on the +al+e "tar+ation and death of cartilage cells "treptococci attach and enmeshed in the protein% firin% and platelets 5egetate on the margins of the +al+e leaflets 0he leaflets gradually thic)en and shorten $nflamed margins of the +al+e leaflet ecome adherent and fuse along the commissures and the chordae tendinae fuse and erode Failure of the mitral +al+e to close completely 5al+ular "tenosis Reduced leaflet motion Difficulty of lood to lea+e from the left atrium to go tot the left +entricle 8structing the forward flow of lood Forcing lood to flow ac)ward through the mitral +al+e as the left +entricle contracts -ac) flow of lood into the pulmonary circulation
Pulmonary -P/ Pulmonary congestion
Distention of lood +essels in the pulmonary circulation 7hen pressure in the pulmonary +ein reaches 9:mmHg% the fluids egin to push from the Cardiac output pulmonary capillary memrane into the interstitial spaces surrounding the al+eoli themsel+es "ystemic -P Pulmonary edema Fluids accumulate in the pleural ca+ity Peripheral +asoconstriction occurs to systemic -P
Pleural Effusion
Pressure in the pulmonary capillaries
f Rheumatoid ,rthritis g 5al+ular Regurgitation Heart 1urmurs Rapid and wea) thready pulse 8rthopne a Paro.ysmal ;octurnal Dyspnea h i ) ) Rupture of pulmonary capillaries Fluid coats the al+eolar e.change space "mall amounts of lood lea) into the al+eoli $nterfering C89<89 e.change 89 saturation of the lood $schemia HR Di22iness and confusion 7ea)ness Easy fatigaility myocardial contractility Cardiac ,rrest Cardiac output -lood circulation ceases
Pericardium roughen Fluids accumulate in the pericardial space pressure in the pericardial space less lood enters the +entricles Forces the septum to end to the left +entricle "tro)e +olume "hoc) h Producti+e cough of lood spec)ed sputum i ,ngina pectoris 5entricular firillation Deat h d Friction ru / / c Rapid and wea) thready pulse ) Pulmonary +al+e stenosis/tricuspid +al+e stenosis 8utput of the right +entricle is less than the lood +olume recei+ed y the right atrium form the +ena ca+a Congestion of the systermic +enous circulation and cardiac output to the lungs -ac) pressure to the +ena ca+a =ess lood goes to the aorta/ systemic circulation Pressure in the +ena ca+a Distention of /ugular +eins ) Peripheral edema