....> GueSs LOveR <...

tHE hisTOry Of guESs :...

....was FoundEd by gEorge,ArmaNds. pAul, and MauricE mArciaNo..der ar fOur bROTHerZ bOrn in QuarzAzate, MOrrocO.

In the 1990s, they also had a division called Guess Home, which featured youthful, upscale bedding collections (Guess was the first company to package each sheet, duvet and pillowcase pair in packaging actually made from sheeting material, which was a clever way to show what the pattern really looked like) as well as a number of innovative towel collections. By the end of the decade, sales dropped and Guess discontinued their home division.

GueSS,, da mOst PopuLAr bRAndEd dat I lyke so Much..

lEbih2 lagI i sKe bEli hanDbag tuk di jadiKAN mY cOllecTiOn..

...> dEr ar sOme cOllectiOn of HANdbags<...

daTz My new handBag.. ahaKzz.. juZ boUGHt frOm memBer..hiii.( aCTlly, xJAdi beli, dUk pK2 if xbeli rUgi sgt..)hahAA.. cOz gOt 50% dari harGa asaL..

wOww.. cAn u imagine dat?? sO cheaP!!!

,,,cAse sTUdy,,,,,

Tuan A, 45 Yearz Old, rasA xsedap didaDa dIsebelaH tenGAh staTS kAt ulu haTi kE ataS, rasAnyE sepErti TERBAKAR,PANAS, disErtai PELUH DINGIN(peluh sejuk) afTer makan malam.
hILang seteLah tiDur..1 jam afTer banGun tiDur, teRasa lagI Keluhan sePerti td dan diseRTai puSing kepaLA(penIng).

RPD: Ibu - HT (+)
Px - sakIT gastritiS siNce muDa
mErOkOk 2pak/haRi
TD : 100/60mm/Hg
NaDi: 60x/minIt
sUhU: 36 darjah celciuS
RR: 24x/miniT
ES+
ECG:Irama siNUs brAdikarDi 56x/miniT
ST Elevasi II,III, aVF, PVC,(ESV)

,,,...sO da Dx Is...???


#INfarK miokArd aKuT#
wHy..?
,,bCOz of paDA Ax n Pmx fIsik MengatAkan bahAwa.::.

Gx prODomaL unTuk IMA :
chESt disCOMforT
Rasa LemaH
kElelAhaN

NYeri dAda(saKIt dadA) ;
- bErvariaSi..sanGAt beraT iatu sakiT dadA selamA 20 minIt- bERjam-jAm, kualItas sakIT(Nyeri) dirASAakn sepErti MENEKAN(compreSSing), diRAmas( sQUeEzing/CrushIng/cONstriCtiNg), tErcekIk(chOkING),Berat (hEAvy paIN), Tajam(kNife lIke) atAu terbaKar(bUrniNg)
- lOkasi nYeri(sakiT) ;di rETRoSTErnaL, menJALar keDua dIndinG daDa trutaMa dAda kiri,ke bawAh ke bAHAGiaN mediaL lengAn meNimbULKAn rasa LengUH(PEgaL) pda prgeLANgan tanGAn dan jaRi.
-kadANG2 nyeri tersA di seKitar epigasTRiuM hinggA timbUL abdOMInal diSCOmfOrt

Gx penYerta:
mual, muntah, badaN LemaH, berDEbar-dEbara daN bErpelUh diNgiN

PMX fisIk;
ST Elevasi II,III,aVF ...........adalah Lead inferiOr xtensvE

pmX lab:
CK
CK-MB
SGOT
LDH
....

!!!uNtuk menEGAKkAN lagi DiagnoStik IMA ....!!!!
jika adA 2 faktoR dari faktoR berikUt ; sakiT dada yg speSifik
pErubAHAn ECG( gelmbg Q patologis, elevasi segm ST
PeningkataAN enzIm jantUng

miTRal STenOsiS

Mitral stenosis is characterized by restriction of blood flow from the left atrium (LA) to the left ventricle (LV) as a result of a narrowed mitral passage. It is an acquired valvular defect; it is usually a consequence of rheumatic heart disease, though cases of congenital mitral stenosis are occasionally encountered. Extensive mitral annular calcification (MAC) may result in mitral stenosis, particularly in the aged.

Mitral stenosis is seen more often in women than in men, and it generally develops at an earlier age in developing countries than in Western societies. In the latter, the incidence of rheumatic fever has declined precipitously over the past 4 decades.

Patients with mitral stenosis usually remain symptom-free for years. After the mitral orifice is reduced to one third of its normal size, symptoms typical of left-sided heart failure develop, such as dyspnea on exertion, orthopnea, and paroxysmal nocturnal dyspnea. Right ventricular (RV) failure gradually ensues, causing ascites and edema.Asymptomatic individuals with sinus rhythm on ECG need no treatment.

Symptoms of dyspnea and orthopnea improve with the use of diuretics. As symptoms worsen and pulmonary hypertension occurs, mechanical correction of the stenosis, rather than medical therapy, becomes necessary. These surgical options, which include valvuloplasty and mitral valve replacement, have changed the natural history of mitral stenosis, and terminally bedridden patients with mitral facies, cardiac cachexia, and end-stage congestive heart failure (CHF) are no longer encountered in everyday clinical practice.

Causes of mitral stenosis

• Rheumatic heart disease
• MAC, degenerative
• Congenital conditions
  • Thickened chordae
  • Single papillary muscle
• Miscellaneous conditions
  • Carcinoid
  • Lupus
  • Rheumatoid arthritis
  • Mucopolysaccharidosis (Hurler syndrome)
  • Coxsackie infection
  • Amyloidosis
  • Methysergide

Differential diagnoses

• Atrial myxoma
• Ball-valve thrombus
• Cor triatriatum
• Submitral ring or web

Mitral stenosis with atrial fibrillation

Patients with mitral stenosis and atrial fibrillation frequently present with decompensated congestive heart failure (CHF). The rapid ventricular rate shortens the diastolic filling time to a period insufficient to allow the LA to empty. As a consequence, the LA pressure rises and the forward cardiac output decreases.

Congenital mitral stenosis

Symptoms of mitral stenosis usually appear within the first 2 years of life. Infants have delayed development and breathlessness, caused by heart failure. Cyanosis and pallor may be noted. The heart is enlarged as a result of dilatation and hypertrophy of the RV and LA. Rumbling apical diastolic murmur is usually audible, followed by a loud first sound. The OS is usually absent.

Preferred Examination

Echocardiography, especially Doppler echocardiography, is the procedure of choice for evaluating the degree of mitral stenosis; in most of the patients, echocardiography may be adequate for the planning of therapeutic interventions.

aOrta aneUrysM

,,,deFINitiOn,,,

an aortic aneurysm is a weakened and bulging area in the aorta, the major blood vessel that feeds blood to the body.

The aorta, about the thickness of a garden hose, runs from your heart through the center of your chest and abdomen. Because the aorta is the body's main supplier of blood, a ruptured aortic aneurysm can cause life-threatening bleeding. Although you may never have symptoms, finding out you have an aortic aneurysm can be frightening.

Most small and slow-growing aortic aneurysms don't rupture, but large, fast-growing aortic aneurysms may. Depending on the size and rate at which the aortic aneurysm is growing, treatment may vary from watchful waiting to emergency surgery.

Once an aortic aneurysm is found, doctors will closely monitor it so that surgery can be planned if it's necessary. Emergency surgery for a ruptured aneurysm can be risky.

,,sympTOmz,,

Aortic aneurysms often grow slowly and usually without symptoms, making them difficult to detect. Some aneurysms will never rupture. Many start small and stay small, although many expand over time.

Some aortic aneurysms enlarge slowly, increasing less than half an inch (1.2 centimeters) a year. Others expand at a faster rate, which increases the risk of rupture. How quickly an aortic aneurysm may grow is difficult to predict.

As an aortic aneurysm grows, some people may notice:

• A pulsating feeling near the navel, if the aneurysm occurs in the abdomen
• Tenderness or pain in the abdomen or chest
• Back pain

Aneurysms can develop anywhere along the aorta, but most occur in the abdomen and are called abdominal aortic aneurysms. Aneurysms that occur in the part of the aorta that's higher up in your chest are called thoracic aortic aneurysms.

When to see a doctor
You should see your doctor if you have any of the symptoms listed above.

Anyone age 60 and older who has risk factors for developing an aortic aneurysm should consider regular screening for the condition. Men ages 65 to 75 who have ever smoked should have a one-time screening for abdominal aortic aneurysm using abdominal ultrasound. Men age 60 and older with a family history of abdominal aortic aneurysm should also consider screening.

If you have a family history of aortic aneurysm, your doctor may recommend regular ultrasound exams to screen for aortic aneurysm

pENyakiT JanTUNg KoRonEr /COroNaRy artEry DiseAse

• penYakit janTUng KoronEr /CORonarY artEry diSeasE (PJK/ CAD) adalah sAlaH saTu penyAkit yANg sangat penTiNG keraNA diDerita oLEh jUtaaN orAng dan pEnyeBab kemaTIan uTama.
• tImbuLnya PJK diDAsari Oleh prOses arterosklerOSis yanG sangaT prOgrEsif yaiTu di mUlai sejaK MAsa kAnAK -kanAk hInggA dekad 3-4.

..fAktOr riSikO PJK..
MajOr rIsk ; HipeRKOLesterOLeMia( kuRangKan lar KolesterOl yeK!)

hiPERtensi

mErOkok
dIabetEs melliTus (kenCing mANis)
GeneTik

MinOr risK : leLAKi
obESitaS (geMUk)
stResS
Kurang eXCeRsice
mENOpauSe

..manEfestASi kLinIK PJK..

,silEnt mYOcARDIal iSchemIa
,AnginA pecToRIS

• aNgina pEctORis stAbil
• vAriant AngiNA (prINZmetaL aNGIna)

,iNFark mIOkaRD akUt
,dEkoMPensasI kOrdis
,arItmiA janTung
,suDDent DeatH
,sYncOpe (pengsan)

bARefOot iS bEst fOr aRthRItis kNeeS

#FleXIblE shOes aRe kINDer tO arthritIs knEes bUt nOthinG beatS gOin barEfOot (frOm RUSH UNIVERSITYMEDICAL COLLEGE IN CHICAGO) #:

• sTAbiliTy shOes r pOpulaR and mAny peOple wit OstEoarthrItis of da kNee enD up wEarinG thEm.
• peOple wit arthRitiC knEes SticK wit fLat,flexible,shOes.
• whEn tHere is lEss suRface tO Da shOes, Da fOot has a BettEr pRopriOcepTive senSe- meaNing iT noEz whEn it tOuches dA gRoUnd, cOmpare tO An insUlatEd fOot.
• dIz allOwz nOrmal NeuroMusculaR reflExes tO comE iN tO plAy anD pRotect thE resT Of the lEg froM da iMpact Of hiTTing da gROund.