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PATHOLOGY > VALVULAR HEART DISEASE, RHEUMATIC FEVER AND RHD > Flashcards

VALVULAR HEART DISEASE, RHEUMATIC FEVER AND RHD Flashcards

1
Q

STATE 5 CAUSE OF MITRAL REGURGITATION

A
  • IE
  • RHD
  • RUPTURE OF PAPILLARY MUSCLE
  • PAPILLARY MUSCLE DYSFUNCTION
  • MITRAP VALVE PROLAPSE
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2
Q

STATE 5 CAUSE AORTIC REGURGITATION

A
  • IE
  • RHD
  • MARFAN’S SYNDROME
  • RA
  • DEGENERATIVE AORTIC DILATION
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3
Q

STATE 1 CAUSE OF MITRAL STENOSIS

A

RHD

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4
Q

STATE 2 CAUSE OF AORTIC STENOSIS

A

RHD
CALCIFICATION OF CONGENITALLY DEFORMED VALVE

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5
Q

AORTIC STENOSIS WILL PRODUCE ___ MURMUR.

A

SYSTOLIC MURMUR

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6
Q

MITRAL STENOSIS WILL PRODUCE ___ MURMUR.

A

DIASTOLIC MURMUR

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7
Q

ACQUIRED VALVULAR HEART DISEASE IS DIVIDED INTO

A
  1. DEGENERATIVE VALVE DISEASE
  2. VALVULAR VEGETATIONS
  3. RHEUMATIC VALVULAR DISEASE
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8
Q

CATEGORIES UNDER DEGENERATIVE VALVE DISEASE

A
  1. CALCIFIED AORTIC STENOSIS
  2. MYXOMATOUS MITRAL VALVE
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9
Q

CATEGORIES UNDER VALVULAR VEGETATIONS

A

IE

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10
Q

CATEGORIES UNDER RHEUMATIC VALVULAR DISEASE

A
  1. ACUTE RF
  2. CHRONIC RHD
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11
Q

HOW DOES DEGENERATIVE VALVE DISEASE OCCUR?

A
  1. CALCIFICATION - ANULUS OR CUSPAL
  2. LOW NO OF FIBROBLAST AND MYOFIBROBLAST
  3. ALTERATION OF ECM
  4. CHANGES IN THE MMP
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12
Q

PATHOGENESIS OF CALCIFIC AORTIC STENOSIS

A
  1. AGE RELATED WITH WEAR AND TEAR
  2. CHRONIC INJURY DUE TO
    - HPT
    - HYPERLIPIDAEMIA
    - INFLAMMATION
    - ATHEROSCLERSIS
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13
Q

CM OF CAS

A
  • SYSTOLIC DIASTOLIC DYSFUNCTION
  • ANGINA
  • CHF
  • CONCENTRIC LV HYPERTROPHY
  • STENOSIS
  • ISCHAEMIA
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14
Q

MORPHOLOGY OF CAS

A
  • HEAP UP OF CALCIFIED MASS ON THE OUTFLOW OF THE CUSP
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15
Q

DEFINE MYXOMATOUS MITRAL VALVE

A

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

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16
Q

PATHOGENESIS OF MYXOMATOUS MITRAL VALVE

A

PRIMARY
- INTRINSIC DEFECT OF THE CT SYNTHESIS OR REMODELING -> MARFAN’S SYNDROME
- INJURY TO VALVE MYOFIBROBLAST DUE TO CHRONICALLY HAEMODYNAMIC FORCES

17
Q

CM OF MYXOMATOUS MITRAL VALVE

A
  • 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
18
Q

COMPLICATION OF MYXOMATOUS MITRAL VALVE

A
  • MITRAL REGURGITATION, CCF, IE, VENTRICULAR ARRHYTHMIA, SUDDEN CARDIAC DEATH, STROKE
19
Q

MORPHOLOGY OF MYXOMATOUS MITRAL VALVE

A
  • DILATED LA
  • PROMINENT HOODING WITH A PROLAPSE OF THE POSTERIOR CUSP INTO THE LEFT ATRIUM
20
Q

DEFINE IE

A

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

21
Q

CLASSIFICATION OF IE

A

ACUTE
SUB ACUTE

22
Q

DIFFERENCE BETWEEN ACUTE AND SUBACUTE IE

A

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

23
Q

CM OF IE

A
  1. ACUTE: FEVER, CHILLS, WEAKNESS
  2. SUBACUTE: AFEBRILE, FATIGUE, WEIGHT LOSS, FLULIKE SYNDROME
  3. MUMURS ON THE LEFT SIDE
  4. MICROEMBOLI, PETECHIAE, SPLINTER HEMORRHAGE, ROTH SPOT, OSLER NODE, JANEWAY LESION
24
Q

PATHOGENESIS OF IE

A
  • SEEDING OF BACTERIA INTO THE CIRCULATION VIA
    1. DENTAL PROCEDURE
    2. INJECTION OF CONTAMINATED MATERIAL DIRECTLY BLOOD STREAM
    3. GUT, ORAL CAVITY, TRIVIAL INJURIES
25
Q

COMPLICATIONS OF IE

A
  • GLOMERULONEPHRITIS
  • RENAL FAILURE
  • SEPTICAEMIA
  • SYSTEMIC EMBOLISM
  • ARRHYTHMIA
26
Q

MORPHOLOGY OF IE

A

GROSS:
- IRREGULAR REDDISH TAN VEGETATIONS OVERLIE VALVE CUSPS THAT ARE BEING DESTROYED

MICROSCOPIC:
- VEGETATIONS
- NEUTROPHILS
- FIBRINS

27
Q

DEFINE RF

A

ACUTE, IMMUNOLOGICALLY MEDIATED, MULTISYSTEM INFLAMMATION DISEASE THAT OCCUR AFTER A FEW WEEKS EXPOSURE TO GRP A STREP.

28
Q

RF TYPICALLY APPEARS AFTER

A

10 DAYS TO 6 WEEKS AFTER EXPOSURE

29
Q

RF ALWAYS OCCUR IN

A

CHILDREN AGE 5 TO 15 YRS OLD

30
Q

PATHOGENESIS OF ACUTE RHEUMATIC FEVER.

A
  1. RESULTS FROM IMMUNOLOGICALLY MEDIATED RESPONSE
  2. IN WHICH THE AB WILL AGAINST THE GRP A STREP AKA M PROTEIN.
  3. AB WILL CROSS REACT WITH HOST AG AND FORMING AG- AB COMPLEX.
  4. 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
  5. FC RECEPTOR BEARING CELL WILL RELEASE MACROPHAGES AND NEUTROPHILS
  6. THEN THE ACTIVATED T CELL WILL. ALSO RELEASE CYTOKINE IN WHICH IT WILL STIMULATE THE ACTIVATION OF THE MACROPHAGES
  7. GENETIC SUSCEPTIBILITY MAY ALSO INFLUENCE THIS HYPERSENSITIVITY REACTION
  8. THE CHARACTERISTICS 2-3 WEEKS DELAY IN SYMPTOMS ONSET AFTER INFX IS DUE TO INCUBATION PERIOD.
31
Q

CM OF RF.

A
  1. MIGRATORY POLYARTHRITIS
  2. MYOCARDITIS
  3. ACUTE CARDITIS
  4. DEATH (1%)
32
Q

DIAGNOSIS OF RF.

A
  • 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

33
Q

MORPHOLOGY OF RF

A
  • HAVE ABUNDANT OF ASCHOFF BODIES IN WHICH CONTAINING A PROMINENT NUCLEI WITH WAVY CHROMATIN WHICH IS KNOWN AS ANITSCKOW CELLS
34
Q

IS THERE ASCHOFF BODIES SEEN IN RHD?

A

RARELY SEEN BCZ IT HAS BEEN REPLACED BY FIBROUS SCAR

35
Q

COMPLICATION OF RHD

A

CARDIAC HYPERTROPHY
CARDIAC DILATATION
CHF
ARRYTHMIA
TE
IE

36
Q

PROGNOSIS

A
  • LONG TERM
  • BETTER DO A SURGICAL REPAIR OR PROSTHETIC REPLACEMENT

PATHOLOGY (13 decks)

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