Case Tirotoksikosis
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CASE REPORTNurhikmawati
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INTRODUCTION
It has long been recognized that thyroid diseasestates exert profound eects on the heart andcirculatory system
The close physiological relationship is armed bypredictable changes in cardiovascular functionacross the entire range of thyroid disease states
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INTRODUCTION
Thyrotoxicosis associated with a 50% decline insystemic vascular resistance
arterial resistance and venous tone venousreturn of blood to the heart
mean circulatory lling pressure
oxygen consumption in the periphery and metabolic demands blood supply and pumpingaction of the heart
atrial natriuretic peptide ! total proteinsynthesis "cardiac hypertrophy#
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PATIENT IDENTITY
$ame ! $n &
'edical (ecord ! )*+,0-
.ge ! // years old
.ddress ! 'aassar
.dmitted to hospital ! 1uly -,th/0--
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HISTORY TAKING
Chief complaint ! 2hortness of breath
Histor ta!in" !
It3s been felt since - day before admitted to the
hospital4 and worsening ) hours beforeadmission 2tarted with chest pain4 not radiated4and no cold sweat
pigastric pain "6#4 nausea "6#4 vomitting "6#4about ) times
7rination and defecation ! normal
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#EDICA$ HISTORY
8istory of 8yperthyroid "6#4 since / years
ago4 regularly on treatment "Thyrax4
maintate# 8istory of heart disease "9#
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PHYSICA$ E%A#INATION
:ital 2ign ! ;lood pressure ! -+0
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$A&ORATORY 'INDING
8b ! -+5 gr
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ADDITIONA$ E%A#INATION
>H !
9 2inus Tachycardia4 8( ! -50x
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ADDITIONA$ E%A#INATION chocardiography !
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/or!in" Dia"nosis
Thyroid 8eart isease
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Plannin"
Baboratorium examination ! 2HJTonsult to ndocrine and metabolic department
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'O$$O/ UP
2 ! 2hortness of breath "6#4 feels dicult to breath4 >hestpain "6#4 feels lie stabbed4 radiated to her bac
:ital 2ign ! ;lood pressure ! -)0
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'O$$O/ UP
B.;J(.TJ(I7'
-*
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'O$$O/ UP
B.;J(.TJ(I7'
/0
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'O$$O/ UP
B.;J(.TJ(I7'
/0
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'O$$O/ UP
B.;J(.TJ(I7'
/-
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'O$$O/ UP
B.;J(.TJ(I7'
/5
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ADDITIONA$ E%A#INATION
>T scan thoras with contrast !
;ronchopneumonia bilateral
>ardiomegaly
There3s no sign of .orta dissection
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/or!in" Dia"nosis
Thyroid 8eart isease
2usp 'yocarditis
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#ANAGE#ENT
J/ )9+ literl 0*% -0 dpm
'ethyprednisolone -/5 mg
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INTRODUCTION
.s early as -,0= 4 a persistent inAammatoryprocess following such an infection "eg4diphtheria# of the myocardium led to progressivecardiac damage and dysfunction
In -,)C4 the term myocarditiswas rst introducedas inAammation or degeneration of the heart bypostmortem
ndomyocardial biopsy in -*,0 allows thesampling of human myocardial tissue during life
and antemortem diagnosis of myocarditis
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INTRODUCTION
2tudies suggest that myocarditis is a ma1or causeof sudden"/0%#4 unexpected death in adults lessthan +0 years of age
&rospective and retrospective studies have
identied myocardial inAammation in - to *percent of routine postmortem examinations
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CAUSATION
. large variety of infections4 systemic diseases4drugs4 and toxins have been associated with thedevelopment of this disease
:iruses4 bacteria4 protozoa4 and even worms have
been implicated as infectious agents
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Pathophsiolo"
2everal mechanisms of myocardialdamage
"-# irect in1ury of myocytes by theinfectious agent"/# 'yocyte in1ury caused by a toxin suchas that
from Corynebacterium diphtheriae")# 'yocyte in1ury as a result of infection9 induced immune reaction orautoimmunity
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Pathophsiolo"
Triphasic disease process
Phase I( 0iral Infection an1 Replication
Phase 2( A,toimm,nit an1 in3,r
Phase 4( Dilate1 Car1iomopath
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Phase I( 0iral Infection an1Replication >oxsacievirus ;) causes an infectious phase4
which lasts C9-0 days4 and is characterized byactive viral replication
uring this phase initial myocyte in1ury taes
place4 causing the release of antigenicintracellular components such as myosin into thebloodstream
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Phase 2( A,toimm,nit an1in3,r
The local release of cytoines4 such asinterleuin9-4 interleuin9/4 interleuin9=4tumor necrosis factor "T$F#4 and nitric
oxide may play a role in determining the T9cell reaction and the subseNuent degree ofautoimmune perpetuation
These cytoines may also cause reversible
depression of myocardial contractilitywithout causing cell death
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Phase 2( A,toimm,nit an1in3,r Immune9mediated by >, lymphocytes and
autoantibodies against various myocytecomponents
.ntigenic mimicry4 the cross reactivity of
antibodies to both virus and myocardial proteins 'yocyte in1ury may be a direct result of >,
lymphocyte inltration
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Phase 4( Dilate1Car1iomopath
:iruses may also directly cause myocyteapoptosis
uring the autoimmune phase4 cytoine activatethe matrix metalloproteinases4 such as
gelatinase4 collagenases4 and elastases In later stages of immune activation4 cytoines
play a leading role in adverse remodeling andprogressive heart failure
>ardiomyopathy developed despite the absenceof viral
proliferation but was correlated with elevatedlevels of
cytoines such as T$F
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Clinical 'in1in"s
Smptoms an1 Si"ns9 &atients"5*%# freNuently present days to weesafter an acute febrile illness4 particularly a Au9liesyndrome
9 'yocarditis is most commonly asymptomatic4with no evidence of left ventricular dysfunction9 fever4 malaise4 fatigue4 arthralgias4 myalgias4and sin rash9>ardiac symptoms may result from systolic or
diastolic left ventricular dysfunction or fromtachyarrhythmias or bradyarrhythmias "dyspnea4fatigue4 decreased exercise tolerance4palpitations #
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Clinical 'in1in"s
Smptoms an1 Si"ns
9 >hest discomfort")5%# is a commonsymptom
and is typically pericardial in nature9 'yocarditis may present as suddendeath4 as a result of malignant ventricular
arrhythmias orcomplete heart bloc
92ystemic and pulmonary thromboembolihavealso been noted
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Clinical 'in1in"s
Phsical E5amination9Tachycardia4 hypotension4 fever and tachycardiamay be disproportionate to the degree of fever9;radycardia is seen rarely4 and a narrow pulse
pressure is occasionally detected9'urmurs of mitral or tricuspid regurgitation arecommon 4 2) and 2+ gallops may also be heard9istended nec veins4 pulmonary rales4 wheezes4gallops4 and peripheral edema may be detected
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Cate"or I( Clinical Smptoms
Clinical heart fail,re
'e7er
0iral pro1rome 'ati",e
Dspnea on e5ertion
Chest pain
Palpitations Presncope or sncope
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Cate"or II( E7i1ence of Car1iacStr,ct,ral-',nctional Pert,r9ation in the AbsenceofRe"ional Coronar Ischemia
Echocar1io"raph e7i1ence
Re"ional 8all motion a9normalities
Car1iac 1ilation
Re"ional car1iac hpertroph
Troponin release Hi"h sensiti7it ;
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Cate"or III( Car1iac #a"netic Resonance Ima"in"
Increase1 mocar1ial T2si"nal on in7ersion
reco7er se@,ence
Delae1 contrast enhancement follo8in"
"a1olini,m?DTPA inf,sion
Cate"or I0( #ocar1ial &iopsPatholo"ical or#olec,lar Analsis
K Patholo" Bn1in"s compati9le 8ith Dallas criteria
K Presence of 7iral "enome 9 polmerase chainreaction or in sit, h9ri1iation
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Dia"nostic St,1ies
Electrocar1io"raph
The most common abnormality is sinustachycardia
may show ventricular arrhythmias or heart
bloc4 or it may mimic the ndings in acutemyocardial infarction or pericarditis
(elations between these clinical and laboratoryndings
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Dia"nostic St,1ies
Chest ra1io"raph9'ild to moderate cardiomegaly fromdilatation of the left or right ventricular
cavity9The cardiac silhouette may also beglobular when a pericardial eusion ispresent
9 :enous congestion and pulmonaryedema may be seen in more severe cases
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Dia"nostic St,1ies
Echocar1io"raph
myocardial contractility 4 chambersizes 4valvular function
Beft ventricular systolic dysfunction4regional wall motion abnormalities 4global hypoinesis
B: may be normal in size or minimallyenlarged
'itral or tricuspid regurgitation
'ural thrombi in -5% of cases
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Dia"nostic St,1ies
- helpful in demonstrating abnormalities ofdiastolic lling that mimic restrictivecardiomyopathy and indistinguishingventricular dilatation from pericardial
eusion- monitor the course of the illness and to
evaluate therapy
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Dia"nostic St,1ies
#ocar1ial ima"in"9Hallium9=C imaging 9G active inAammation of themyocardium and pericardium9Indium9--- monoclonal antimyosin antibody imaging 9G detecting myocyte in1ury in patients
9>ontrast media9enhanced '(I 9Gdetecting myocardial inAammation
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Dia"nostic St,1ies
Car1iac catheteriation9 elevated left ventricular end9diastolic pressure4a depressed cardiac output4 and increasedventricular volumes
9 >oronary angiogram typically demonstratesnormal coronary arteries
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Dia"nostic St,1ies
En1omocar1ial 9iops9 gold standard for the diagnosis ofmyocarditis
9Dallascriteria"an inAammatory inltrate of the
myocardium 6in1ury to the ad1acent myocytes#9borderline myocarditis is made when the
inltrate is not accompanied by myocytein1ury
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Others test
levated erythrocyte sedimentation rate "2(# 4 mild tomoderate leuocytosis
>E9'; 4 >ardiac troponin9I
Jther laboratory analyses that may be useful include a'ono9spot test4 pstein9;arr virus titers4 hepatitis serology4
and urine and serum for cytomegalovirus ">':#
T i h i 1i
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Triphasic 1isease process=
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#ana"ement of mocar1itis
'anagement is dictated by clinical signsand symptoms
'.$O proposed therapies4 most have onlya theoretical basis 2ome have beentested in animal models
>onventional heart failure therapy iscurrently the only accepted therapy formyocarditis including .> inhibitors4angiotensin receptor blocing agents4diuretics4 P9blocers or amiodarone
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Diet an1 $ifestle
(estrict salt intae to /9)g of sodium perday
xercise especially during the acute phase
of >oxsacie virus ;) murine myocarditisenhances viral replication rate4 enhancesimmune mechanisms and increasesinAammatory lesions and necrosis(esumption of physical activity can taeplace within / months of the acutedisease
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T8.$E OJ7