04.28 - Valve Disease 2 (Nichols) Flashcards

(50 cards)

1
Q

4 Components of Tetrology of Fallot

A

PROVe: Pulmonic Stenosis, RV Hypertorphy, Overriding Aorta, Ventricular Septal Defect

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2
Q

6 Cyanotic Congenital Heart Defects

A

TOF, Transposition, Truncus Arteriosus, Total Anomalous Pulmonary Venous Return, Tricuspid Atresia, Hypoplastic Left Heart

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3
Q

90% of ASD’s are

A

Ostium Secundum Defects

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4
Q

ASD vs VSD: in which does Pulmonary HTN occur more quickly

A

VSD

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5
Q

ASD vs VSD: which has increased risk for infective endocarditis

A

VSD due to jet lesions

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6
Q

Clinical severity of TOF depends largely on

A

Degree Pulmonary Outflow Obstruction (if mild –> Condition is more benign)

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7
Q

Clubbing of the tips of fingers and toes, Polycythemia, Paradoxical Embolization

A

Severe systemic cyanosis (Right-to-Left Shunts)

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8
Q

Common congenital heart defect in females with Turner

A

Coarction of Aorta

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9
Q

Defect in lowest part of atrial septum

A

Ostium Primum ASD

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10
Q

Does Libman-Sacks Endocarditis often embolize?

A

No

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11
Q

Eisenmenger Syndrome

A

When a Left-to-Right shunt reverses do to increased Pulmonary hypertension

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12
Q

Harsh, “machinery-like” murmurs

A

PDA

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13
Q

In Calcific Aortic Stenosis, onset of symptoms =

A

Time for valve replacement

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14
Q

In more than half of cases, Coarction of Aorta is accompanied by

A

Bicuspid Aortic Valve

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15
Q

In whom is Libman-Sack Endocarditis most common

A

Young Black Females (same as SLE?)

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16
Q

Large, boot-shaped heart

A

Tetrology of Fallot

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17
Q

Location of Ostium Secundum vs Ostium Primum

A

Ostium Secundum is Fossa Ovalis, Primum is near AV valve

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18
Q

Marantic Endocarditis: common or rare

A

Common

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19
Q

Markedly enlarged intercostal and internal mammary arteries

A

Postductal Coarction without PDA

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20
Q

Midsystolic Click =

A

Mitral Valve Prolapse

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21
Q

Morphologic changes in Ostium Secundum ASD

A

RA and RV dilation, RV hypertrophy, Dilation of Pulmonary Artery (increased volume load)

22
Q

Most common cause of cyanotic congenital heart disease

A

Tet of Fallot

23
Q

Most common congenital cardiac anomaly at birth

24
Q

Most common defects to be first diagnosed in adults

A

ASD’s (VSD’s more common at birth, but many close spontaneously)

25
Murmur in PDA
Harsh, "machinery-like" murmur
26
Once significant pulmonary HTN develops, the structural defects of congenital HD
are considered irreversible
27
Ostium Primum ASD's can be related to
Mitral and Tricuspid valve abnormalities
28
Paradoxical embolus
Venous embolus that enters systemic circulation (thru patent septum or foramen ovale)
29
Percent of VSDs that occur in isolation
20-30 (Most are associated with other malformations)
30
Prevalence of Probe-patent Foramen Ovale
20%
31
Pulmonary HTN in TOF
No, because Pulmonic Outflow Stenosis protects pulmonary vasculature
32
Result of Left-to-Right Shunts
Increase pulmonary resistance --> RV Hypertrophy and eventually failure or shunt reversal
33
Right-to-Left shunting in TOF also increases risk of
Infective Endocarditis and Systemic Embolization
34
RV Failure in TOF
Rare, no Pulmonary HTN
35
Sinus Venosus ASD's are often accompanied by
Anomalous drainage of pulmonary veins into RA or SVC
36
Site of approx 90% of VSD's
Basal (membranous) region (last part of septum to develop)
37
Size of chambers of TOF
Left side normal, RV hypertrophy
38
Tiny (1-2mm) verrucous (wartlike) vegetations lined up on line of valve closure
Acute Rheumatic Valvulitis
39
Top 3 Congenital Hart Malformations
VSD, ASD, Pulmonary Stenosis
40
Typical sequelae of Cyanotic Heart Disease
Polycythemia; Hypertrophic Osteoarthropathy
41
What is nuclear dust
Basophilic debris
42
What leads to radiographically visible "notchin" of the ribs
Postductal Coarction without PDA
43
What size are vegetations of Libman-Sacks Endocarditis
Intermediate (bigger than Acute Rheumatic, smaller than Infective Endocarditis)
44
What type of defect is Ostium Secundum
ASD
45
When are you most likely to Eisenmenger Syndrome
Children with congenital heart disease with septal defects, and chronic left-to-right sunts
46
When do ASD's become symptomatic
Adulthood
47
When does Postductal Coarction without PDA present
Usually asymptomatic, and may remain unrecognized until adult
48
When does Preductal Coarction with PDA usually present
Early in life, most infants don't survive neonatal period
49
When is survival possible in Transposition
Shunt such as VSD
50
When will Paraxodical embolism occur
If right sided pressures increase: Pulmonary HTN or Valsalva