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Cardiovascular > 04.28 - Valve Disease 2 (Nichols) > Flashcards

04.28 - Valve Disease 2 (Nichols) Flashcards

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

A

VSD

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
Q

Murmur in PDA

A

Harsh, “machinery-like” murmur

26
Q

Once significant pulmonary HTN develops, the structural defects of congenital HD

A

are considered irreversible

27
Q

Ostium Primum ASD’s can be related to

A

Mitral and Tricuspid valve abnormalities

28
Q

Paradoxical embolus

A

Venous embolus that enters systemic circulation (thru patent septum or foramen ovale)

29
Q

Percent of VSDs that occur in isolation

A

20-30 (Most are associated with other malformations)

30
Q

Prevalence of Probe-patent Foramen Ovale

A

20%

31
Q

Pulmonary HTN in TOF

A

No, because Pulmonic Outflow Stenosis protects pulmonary vasculature

32
Q

Result of Left-to-Right Shunts

A

Increase pulmonary resistance –> RV Hypertrophy and eventually failure or shunt reversal

33
Q

Right-to-Left shunting in TOF also increases risk of

A

Infective Endocarditis and Systemic Embolization

34
Q

RV Failure in TOF

A

Rare, no Pulmonary HTN

35
Q

Sinus Venosus ASD’s are often accompanied by

A

Anomalous drainage of pulmonary veins into RA or SVC

36
Q

Site of approx 90% of VSD’s

A

Basal (membranous) region (last part of septum to develop)

37
Q

Size of chambers of TOF

A

Left side normal, RV hypertrophy

38
Q

Tiny (1-2mm) verrucous (wartlike) vegetations lined up on line of valve closure

A

Acute Rheumatic Valvulitis

39
Q

Top 3 Congenital Hart Malformations

A

VSD, ASD, Pulmonary Stenosis

40
Q

Typical sequelae of Cyanotic Heart Disease

A

Polycythemia; Hypertrophic Osteoarthropathy

41
Q

What is nuclear dust

A

Basophilic debris

42
Q

What leads to radiographically visible “notchin” of the ribs

A

Postductal Coarction without PDA

43
Q

What size are vegetations of Libman-Sacks Endocarditis

A

Intermediate (bigger than Acute Rheumatic, smaller than Infective Endocarditis)

44
Q

What type of defect is Ostium Secundum

A

ASD

45
Q

When are you most likely to Eisenmenger Syndrome

A

Children with congenital heart disease with septal defects, and chronic left-to-right sunts

46
Q

When do ASD’s become symptomatic

A

Adulthood

47
Q

When does Postductal Coarction without PDA present

A

Usually asymptomatic, and may remain unrecognized until adult

48
Q

When does Preductal Coarction with PDA usually present

A

Early in life, most infants don’t survive neonatal period

49
Q

When is survival possible in Transposition

A

Shunt such as VSD

50
Q

When will Paraxodical embolism occur

A

If right sided pressures increase: Pulmonary HTN or Valsalva

Cardiovascular (18 decks)

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