VALVULAR HEART DISEASE, RHEUMATIC FEVER AND RHD Flashcards
STATE 5 CAUSE OF MITRAL REGURGITATION
- IE
- RHD
- RUPTURE OF PAPILLARY MUSCLE
- PAPILLARY MUSCLE DYSFUNCTION
- MITRAP VALVE PROLAPSE
STATE 5 CAUSE AORTIC REGURGITATION
- IE
- RHD
- MARFAN’S SYNDROME
- RA
- DEGENERATIVE AORTIC DILATION
STATE 1 CAUSE OF MITRAL STENOSIS
RHD
STATE 2 CAUSE OF AORTIC STENOSIS
RHD
CALCIFICATION OF CONGENITALLY DEFORMED VALVE
AORTIC STENOSIS WILL PRODUCE ___ MURMUR.
SYSTOLIC MURMUR
MITRAL STENOSIS WILL PRODUCE ___ MURMUR.
DIASTOLIC MURMUR
ACQUIRED VALVULAR HEART DISEASE IS DIVIDED INTO
- DEGENERATIVE VALVE DISEASE
- VALVULAR VEGETATIONS
- RHEUMATIC VALVULAR DISEASE
CATEGORIES UNDER DEGENERATIVE VALVE DISEASE
- CALCIFIED AORTIC STENOSIS
- MYXOMATOUS MITRAL VALVE
CATEGORIES UNDER VALVULAR VEGETATIONS
IE
CATEGORIES UNDER RHEUMATIC VALVULAR DISEASE
- ACUTE RF
- CHRONIC RHD
HOW DOES DEGENERATIVE VALVE DISEASE OCCUR?
- CALCIFICATION - ANULUS OR CUSPAL
- LOW NO OF FIBROBLAST AND MYOFIBROBLAST
- ALTERATION OF ECM
- CHANGES IN THE MMP
PATHOGENESIS OF CALCIFIC AORTIC STENOSIS
- AGE RELATED WITH WEAR AND TEAR
- CHRONIC INJURY DUE TO
- HPT
- HYPERLIPIDAEMIA
- INFLAMMATION
- ATHEROSCLERSIS
CM OF CAS
- SYSTOLIC DIASTOLIC DYSFUNCTION
- ANGINA
- CHF
- CONCENTRIC LV HYPERTROPHY
- STENOSIS
- ISCHAEMIA
MORPHOLOGY OF CAS
- HEAP UP OF CALCIFIED MASS ON THE OUTFLOW OF THE CUSP
DEFINE MYXOMATOUS MITRAL VALVE
ONE OR BOTH MITRAL VALVES ARE AFFECTED IN WHICH THEY ARE FLOPPY AND PROLAPSE RESULTIN IN THE BALLONING OF THE POSTERIOR CUSP INTO THE LEFT ATRIUM DURING SYSTOLE
PATHOGENESIS OF MYXOMATOUS MITRAL VALVE
PRIMARY
- INTRINSIC DEFECT OF THE CT SYNTHESIS OR REMODELING -> MARFAN’S SYNDROME
- INJURY TO VALVE MYOFIBROBLAST DUE TO CHRONICALLY HAEMODYNAMIC FORCES
CM OF MYXOMATOUS MITRAL VALVE
- MOSTLT ASYMPTOMATIC
- INCIDENTAL FINDINGS ON PHYSICAL EXAMINATION: HEAR A MID- DIASTOLIC CLICK WITH OR WITHOUT MURMUR
- SOME CASES COME WITH DYSPNEA, PALPITATION, ATYPICAL CHEST PAIN
COMPLICATION OF MYXOMATOUS MITRAL VALVE
- MITRAL REGURGITATION, CCF, IE, VENTRICULAR ARRHYTHMIA, SUDDEN CARDIAC DEATH, STROKE
MORPHOLOGY OF MYXOMATOUS MITRAL VALVE
- DILATED LA
- PROMINENT HOODING WITH A PROLAPSE OF THE POSTERIOR CUSP INTO THE LEFT ATRIUM
DEFINE IE
SERIOUS INFX OF VALVULAR AND MURAL ENDOCARDIUM CHARACTERISED BY:
- BULKY
- FRABLE VEGETATIONS WHICH CONSIST OF NECROTIC DEBRIS, ORGANISMS AND
MAY INVOLVE AORTA, ANEURSYMAL SAC, OTHER BLOOD VESSELS PROTSTHETIC DEVICES
CLASSIFICATION OF IE
ACUTE
SUB ACUTE
DIFFERENCE BETWEEN ACUTE AND SUBACUTE IE
ACUTE
- < 6 WEEKS
- D/T S. AUREUS
- HIGHLY VIRULENCE
- THE VALVE ARE NORMAL BEFORE
- THE LESION ARE DISRUPTIVE, INVASIVE AND SUPPURATIVE
- IT FEATURES THE ACUTE SYSTEMIC INFLAMMATION
SUBACUTE
- > 6 WEEKS
- D/T S. VIRIDANS
- LESS VIRULENCE
- THE VALVE ARE ABNORMALS
- THE LESSION ARE LESS LIKELY TO BE DISRUPTIVE AND SUPPURATIVE
- SPLENOMEGALY, CLUBBING FINGERS AND PETECHIAE
CM OF IE
- ACUTE: FEVER, CHILLS, WEAKNESS
- SUBACUTE: AFEBRILE, FATIGUE, WEIGHT LOSS, FLULIKE SYNDROME
- MUMURS ON THE LEFT SIDE
- MICROEMBOLI, PETECHIAE, SPLINTER HEMORRHAGE, ROTH SPOT, OSLER NODE, JANEWAY LESION
PATHOGENESIS OF IE
- SEEDING OF BACTERIA INTO THE CIRCULATION VIA
1. DENTAL PROCEDURE
2. INJECTION OF CONTAMINATED MATERIAL DIRECTLY BLOOD STREAM
3. GUT, ORAL CAVITY, TRIVIAL INJURIES
COMPLICATIONS OF IE
- GLOMERULONEPHRITIS
- RENAL FAILURE
- SEPTICAEMIA
- SYSTEMIC EMBOLISM
- ARRHYTHMIA
MORPHOLOGY OF IE
GROSS:
- IRREGULAR REDDISH TAN VEGETATIONS OVERLIE VALVE CUSPS THAT ARE BEING DESTROYED
MICROSCOPIC:
- VEGETATIONS
- NEUTROPHILS
- FIBRINS
DEFINE RF
ACUTE, IMMUNOLOGICALLY MEDIATED, MULTISYSTEM INFLAMMATION DISEASE THAT OCCUR AFTER A FEW WEEKS EXPOSURE TO GRP A STREP.
RF TYPICALLY APPEARS AFTER
10 DAYS TO 6 WEEKS AFTER EXPOSURE
RF ALWAYS OCCUR IN
CHILDREN AGE 5 TO 15 YRS OLD
PATHOGENESIS OF ACUTE RHEUMATIC FEVER.
- RESULTS FROM IMMUNOLOGICALLY MEDIATED RESPONSE
- IN WHICH THE AB WILL AGAINST THE GRP A STREP AKA M PROTEIN.
- AB WILL CROSS REACT WITH HOST AG AND FORMING AG- AB COMPLEX.
- AFTER THE BINDING OF THE AB TO THE AG, IT WILL ACTIVATE THE COMPLEMENT IN WHICH IT WILL LEAD TO THE RECRUITMENT OF THE FC RECEPTOR BEARING CELL
- FC RECEPTOR BEARING CELL WILL RELEASE MACROPHAGES AND NEUTROPHILS
- THEN THE ACTIVATED T CELL WILL. ALSO RELEASE CYTOKINE IN WHICH IT WILL STIMULATE THE ACTIVATION OF THE MACROPHAGES
- GENETIC SUSCEPTIBILITY MAY ALSO INFLUENCE THIS HYPERSENSITIVITY REACTION
- THE CHARACTERISTICS 2-3 WEEKS DELAY IN SYMPTOMS ONSET AFTER INFX IS DUE TO INCUBATION PERIOD.
CM OF RF.
- MIGRATORY POLYARTHRITIS
- MYOCARDITIS
- ACUTE CARDITIS
- DEATH (1%)
DIAGNOSIS OF RF.
- EVIDENCE OF RECENT INFX WITH GRP A STREP.
- 2 MAJOR JONE CRITERIA
- 1 MAJOR + 2 MINOR JONES CRITERIA
MAJOR:
1. MIGRATORY POLYARTHRITIS
2. SYDENHAM CHOREA
3. PANCARDITIS
4. SUBCUTANEOUS NODULES
5. ERYTHEMA MARGINATUM
MINOR:
1. FEVER
2. ARHTRITIS
3. ELEVATED CRP
MORPHOLOGY OF RF
- HAVE ABUNDANT OF ASCHOFF BODIES IN WHICH CONTAINING A PROMINENT NUCLEI WITH WAVY CHROMATIN WHICH IS KNOWN AS ANITSCKOW CELLS
IS THERE ASCHOFF BODIES SEEN IN RHD?
RARELY SEEN BCZ IT HAS BEEN REPLACED BY FIBROUS SCAR
COMPLICATION OF RHD
CARDIAC HYPERTROPHY
CARDIAC DILATATION
CHF
ARRYTHMIA
TE
IE
PROGNOSIS
- LONG TERM
- BETTER DO A SURGICAL REPAIR OR PROSTHETIC REPLACEMENT
