Pediatric Board Review 2012

Front 1

What are the indications for hospitalization in PID?

Back 1

Indications for admission include pregnancy, surgical emergencies cannot be excluded, suspected pelvic/tubo-ovarian abscess, uncertain diagnosis, nausea/vomitin preclude oral therapy or failure to respond to oral agents in 24-48 hours.

Front 2

How do most patients who have tetrology of fallot present in the newborn period?

Back 2

Most do not have cyanosis, but have a harsh systolic murmur resulting from infundibular and pulmonary stenosis NOT the VSD.

Hint 2

Most patients who have TOF do not present with cyanosis in the newborn period, but rather come to medical attention because of a harsh systolic murmur. The murmur results from infundibular stenosis and pulmonary stenosis, not from the VSD. The second heart sound is single. Because the degree of pulmonary blood flow obstruction can vary among patients, the degree of systemic oxygen desaturation ranges from mild to severe. Children who have mild obstruction may appear "pink," and those who have severe pulmonary stenosis have significantly reduced pulmonary blood flow and an increase in right-to-left shunting across the VSD into the aorta, leading to more pronounced cyanosis. Furthermore, as pulmonary blood flow decreases with tight pulmonary stenosis, pulmonary venous return to the left atrium decreases, resulting in less highly saturated blood leaving the left ventricle and entering the aorta. Conversely, mild pulmonary stenosis is associated with more pulmonary blood flow, less right-to-left intracardiac shunting, and less systemic desaturation. In the mildest cases, there is left-to-right shunting across the VSD and near-normal or normal systemic saturation.

Front 3

How do most patients who have tetrology of fallot present in the newborn period?

Back 3

Most do not have cyanosis, but have a harsh systolic murmur resulting from infundibular and pulmonary stenosis NOT the VSD.

Hint 3

Most patients who have TOF do not present with cyanosis in the newborn period, but rather come to medical attention because of a harsh systolic murmur. The murmur results from infundibular stenosis and pulmonary stenosis, not from the VSD. The second heart sound is single. Because the degree of pulmonary blood flow obstruction can vary among patients, the degree of systemic oxygen desaturation ranges from mild to severe. Children who have mild obstruction may appear "pink," and those who have severe pulmonary stenosis have significantly reduced pulmonary blood flow and an increase in right-to-left shunting across the VSD into the aorta, leading to more pronounced cyanosis. Furthermore, as pulmonary blood flow decreases with tight pulmonary stenosis, pulmonary venous return to the left atrium decreases, resulting in less highly saturated blood leaving the left ventricle and entering the aorta. Conversely, mild pulmonary stenosis is associated with more pulmonary blood flow, less right-to-left intracardiac shunting, and less systemic desaturation. In the mildest cases, there is left-to-right shunting across the VSD and near-normal or normal systemic saturation.

Front 4

During what Tanner Stage does a girls peak height velocity occur?

Back 4

Tanner 2-3

Front 5

What presentation is marked by distress, crying, inconsolability, hyperpnea and increasing cyanosis?

Back 5

A tetralogy spell.

Front 6

What presentation is marked by distress, crying, inconsolability, hyperpnea and increasing cyanosis?

Back 6

A tetralogy spell.

Front 7

What percent of testicular function is preserved if surgery occurs within 6-12 hours of torsion?

Back 7

60-65%

Front 8

What typically triggers a tetralogy spell?

Back 8

They frequently occur in the morning or at times of dehydration (fever, GE etc). They can quickly lead to serious morbidity and mortality.

Hint 8

Treatment of cyanotic spells centers on increasing pulmonary blood flow, which is accomplished by several means. The first step is to alter the ratio of relative resistance of pulmonary and systemic beds. Increasing the systemic vascular resistance relative to the pulmonary vascular resistance decreases the right-to-left shunt at the VSD and can be accomplished by placing the patient in a knee-to-chest position or by squatting in older children. Pharmacologic augmentation of the systemic vascular resistance can be achieved with intravenous phenylephrine. Therapy also includes the use of sedation with morphine, which suppresses the sensation of suffocation and can relieve the patient's fear. The use of high-flow oxygen, which dilates pulmonary vasculature, constricts systemic vasculature and increases PO2 of pulmonary venous return, and generous intravascular fluid administration to increase preload are important therapies for the patient experiencing a tetralogy spell.

Front 9

What typically triggers a tetralogy spell?

Back 9

They frequently occur in the morning or at times of dehydration (fever, GE etc). They can quickly lead to serious morbidity and mortality.

Hint 9

Treatment of cyanotic spells centers on increasing pulmonary blood flow, which is accomplished by several means. The first step is to alter the ratio of relative resistance of pulmonary and systemic beds. Increasing the systemic vascular resistance relative to the pulmonary vascular resistance decreases the right-to-left shunt at the VSD and can be accomplished by placing the patient in a knee-to-chest position or by squatting in older children. Pharmacologic augmentation of the systemic vascular resistance can be achieved with intravenous phenylephrine. Therapy also includes the use of sedation with morphine, which suppresses the sensation of suffocation and can relieve the patient's fear. The use of high-flow oxygen, which dilates pulmonary vasculature, constricts systemic vasculature and increases PO2 of pulmonary venous return, and generous intravascular fluid administration to increase preload are important therapies for the patient experiencing a tetralogy spell.

Front 10

What percent of testicular function is preserved if surgery occurs within 12-24 hours of torsion?

Back 10

20-40%

Front 11

How do you treat a tetralogy spell?

Back 11

knee-to-chest position or squatting. Phenylephrine, morphine, high-flow oxygen and IV fluids.

Hint 11

Treatment of cyanotic spells centers on increasing pulmonary blood flow, which is accomplished by several means. The first step is to alter the ratio of relative resistance of pulmonary and systemic beds. Increasing the systemic vascular resistance relative to the pulmonary vascular resistance decreases the right-to-left shunt at the VSD and can be accomplished by placing the patient in a knee-to-chest position or by squatting in older children. Pharmacologic augmentation of the systemic vascular resistance can be achieved with intravenous phenylephrine. Therapy also includes the use of sedation with morphine, which suppresses the sensation of suffocation and can relieve the patient's fear. The use of high-flow oxygen, which dilates pulmonary vasculature, constricts systemic vasculature and increases PO2 of pulmonary venous return, and generous intravascular fluid administration to increase preload are important therapies for the patient experiencing a tetralogy spell.

Front 12

How do you treat a tetralogy spell?

Back 12

knee-to-chest position or squatting. Phenylephrine, morphine, high-flow oxygen and IV fluids.

Hint 12

Treatment of cyanotic spells centers on increasing pulmonary blood flow, which is accomplished by several means. The first step is to alter the ratio of relative resistance of pulmonary and systemic beds. Increasing the systemic vascular resistance relative to the pulmonary vascular resistance decreases the right-to-left shunt at the VSD and can be accomplished by placing the patient in a knee-to-chest position or by squatting in older children. Pharmacologic augmentation of the systemic vascular resistance can be achieved with intravenous phenylephrine. Therapy also includes the use of sedation with morphine, which suppresses the sensation of suffocation and can relieve the patient's fear. The use of high-flow oxygen, which dilates pulmonary vasculature, constricts systemic vasculature and increases PO2 of pulmonary venous return, and generous intravascular fluid administration to increase preload are important therapies for the patient experiencing a tetralogy spell.

Front 13

What percent of testicular function is preserved if surgery is delayed more than 24 hours of torsion?

Back 13

10-15%

Front 14

When does cyanotic heart disease present with clubbing?

Back 14

After a year of age.

Front 15

When does cyanotic heart disease present with clubbing?

Back 15

After a year of age.

Front 16

When can an athlete with a grade I concussion return to play?

Back 16

When they are asymptomatic at rest and with exertion.

Front 17

What is the most common form of cyanotic congenital heart disease?

Back 17

Tetralogy of Fallot (TOF) is the most common form of cyanotic congenital heart disease, with an incidence of approximately 0.2 in 1,000 live births and accounting for 9% of all congenital heart disease.

Hint 17

The four components of TOF are right ventricular outflow/pulmonary stenosis, ventricular septal defect (VSD), overriding aorta, and right ventricular hypertrophy (Item C37). The primary lesion is underdevelopment of the pulmonary infundibulum, which has led some to refer to this disease as "monology of Fallot" because all aspects of the tetrad result from this lesion. The result of underdevelopment of the pulmonary infundibulum is deviation of the infundibular septum anteriorly and superiorly, bringing it into the right ventricular outflow tract. This leads to obstructed right ventricular outflow and the commonly seen underdevelopment of the pulmonary valve and pulmonary arteries caused by diminished blood flow through these structures. The underdeveloped pulmonary infundibulum also creates a VSD, which is almost universally large and of the malalignment type. The defect resulting from anterior malalignment of the infundibulum allows the aorta to "override" the ventricular septum. Finally, right ventricular hypertrophy results from exposure to systemic pressures (large VSD and pulmonary stenosis).

Front 18

What is the most common form of cyanotic congenital heart disease?

Back 18

Tetralogy of Fallot (TOF) is the most common form of cyanotic congenital heart disease, with an incidence of approximately 0.2 in 1,000 live births and accounting for 9% of all congenital heart disease.

Hint 18

The four components of TOF are right ventricular outflow/pulmonary stenosis, ventricular septal defect (VSD), overriding aorta, and right ventricular hypertrophy (Item C37). The primary lesion is underdevelopment of the pulmonary infundibulum, which has led some to refer to this disease as "monology of Fallot" because all aspects of the tetrad result from this lesion. The result of underdevelopment of the pulmonary infundibulum is deviation of the infundibular septum anteriorly and superiorly, bringing it into the right ventricular outflow tract. This leads to obstructed right ventricular outflow and the commonly seen underdevelopment of the pulmonary valve and pulmonary arteries caused by diminished blood flow through these structures. The underdeveloped pulmonary infundibulum also creates a VSD, which is almost universally large and of the malalignment type. The defect resulting from anterior malalignment of the infundibulum allows the aorta to "override" the ventricular septum. Finally, right ventricular hypertrophy results from exposure to systemic pressures (large VSD and pulmonary stenosis).

Front 19

When can an athlete with a grade II concussion return to play?

Back 19

1 week after they are asymptomatic at rest and with exertion.

Front 20

What genetic anomaly have features of punched-out scalp lesions, bilateral cleft lip and palate, polydactyly, holoprosencephaly, microcephaly and cardiac defects?

Back 20

Trisomy 13

Hint 20

The newborn described in the vignette has a 47,XX+13 karyotype consistent with trisomy 13. Her unusual features of "punched-out" scalp lesions (also known as "aplasia cutis"), bilateral cleft lip and palate, and polydactyly are present in at least 50% of newborns who have this diagnosis. Other common anomalies in affected individuals include holoprosencephaly (incomplete septation of the frontal lobes), microcephaly, and cardiac defects (80%). Trisomy 13 has a poor prognosis, with approximately 50% of affected individuals dying by 2 weeks of age and 90% dying by 1 year.

Front 21

What genetic anomaly have features of punched-out scalp lesions, bilateral cleft lip and palate, polydactyly, holoprosencephaly, microcephaly and cardiac defects?

Back 21

Trisomy 13

Hint 21

The newborn described in the vignette has a 47,XX+13 karyotype consistent with trisomy 13. Her unusual features of "punched-out" scalp lesions (also known as "aplasia cutis"), bilateral cleft lip and palate, and polydactyly are present in at least 50% of newborns who have this diagnosis. Other common anomalies in affected individuals include holoprosencephaly (incomplete septation of the frontal lobes), microcephaly, and cardiac defects (80%). Trisomy 13 has a poor prognosis, with approximately 50% of affected individuals dying by 2 weeks of age and 90% dying by 1 year.

Front 22

When can an athlete with a grade III concussion return to play?

Back 22

2 weeks after they are asymptomatic at rest and with exertion.

Front 23

What genetic anomaly have features of punched-out scalp lesions, bilateral cleft lip and palate, polydactyly, holoprosencephaly, microcephaly and cardiac defects?

Back 23

Trisomy 13

Hint 23

The newborn described in the vignette has a 47,XX+13 karyotype consistent with trisomy 13. Her unusual features of "punched-out" scalp lesions (also known as "aplasia cutis"), bilateral cleft lip and palate, and polydactyly are present in at least 50% of newborns who have this diagnosis. Other common anomalies in affected individuals include holoprosencephaly (incomplete septation of the frontal lobes), microcephaly, and cardiac defects (80%). Trisomy 13 has a poor prognosis, with approximately 50% of affected individuals dying by 2 weeks of age and 90% dying by 1 year.

Front 24

What genetic anomaly have features of punched-out scalp lesions, bilateral cleft lip and palate, polydactyly, holoprosencephaly, microcephaly and cardiac defects?

Back 24

Trisomy 13

Hint 24

The newborn described in the vignette has a 47,XX+13 karyotype consistent with trisomy 13. Her unusual features of "punched-out" scalp lesions (also known as "aplasia cutis"), bilateral cleft lip and palate, and polydactyly are present in at least 50% of newborns who have this diagnosis. Other common anomalies in affected individuals include holoprosencephaly (incomplete septation of the frontal lobes), microcephaly, and cardiac defects (80%). Trisomy 13 has a poor prognosis, with approximately 50% of affected individuals dying by 2 weeks of age and 90% dying by 1 year.

Front 25

What is the difference between grade I and grade II concussions?

Back 25

The length of time that patient is symptomatic. Less than 15 min in grade I and more than 15 min in grade II.

Front 26

If there is a negative T wave in lead V6 after 7 days of life, what cardiac problem should be suspected?

Back 26

LVH

Front 27

If there is a negative T wave in lead V6 after 7 days of life, what cardiac problem should be suspected?

Back 27

LVH

Front 28

What is the difference between grade II and grade III concussions?

Back 28

Loss of consciousness

Front 29

What is suspected if an adolescent or adult has right axis deviation, increased R voltage in V1 or S in V6 and rsR1 and V1.

Back 29

RVH

Front 30

What is suspected if an adolescent or adult has right axis deviation, increased R voltage in V1 or S in V6 and rsR1 and V1.

Back 30

RVH

Front 31

What type of thinking is prominent in late adolescents ?

Back 31

Cognition is complete

Front 32

What drug should never be given in any wide comples tachycardia in the emergency setting?

Back 32

Verapamil

30% with rapidy deteriorate

Front 33

What drug should never be given in any wide comples tachycardia in the emergency setting?

Back 33

Verapamil

30% with rapidy deteriorate

Front 34

What type of thinking is prominent in early adolescents ?

Back 34

Cognition is concrete

Front 35

What is often associated with a prominent U wave and a prolonged QT interval?

Back 35

Torsades de pointes

Front 36

What is often associated with a prominent U wave and a prolonged QT interval?

Back 36

Torsades de pointes

Front 37

What is the most important relationship for middle adolescents ?

Back 37

Peers

Front 38

What drugs can cause prolonged QT and torsades de pointes?

Back 38

Any Class Ia antiarrhythmics (procainamide etc), and tricyclic antidepressants.

Front 39

What drugs can cause prolonged QT and torsades de pointes?

Back 39

Any Class Ia antiarrhythmics (procainamide etc), and tricyclic antidepressants.

Front 40

What is the most important relationship for early adolescents ?

Back 40

Peers ( just starting )

Front 41

What is the treatment of torsades de pointes?

Back 41

Isopreterenol or overdrive pacing or Mag sulfate.

DO NOT GIVE CLASS Ia ANTIARRYTHMICS

Front 42

What is the treatment of torsades de pointes?

Back 42

Isopreterenol or overdrive pacing or Mag sulfate.

DO NOT GIVE CLASS Ia ANTIARRYTHMICS

Front 43

What is the most important relationship in a late adolescent ?

Back 43

Individual relationships

Front 44

Who do you need to avoid the use of verapamil with?

Back 44

Infants less than 1 year
A Fib with WPW
A Flutter
Wide Complex Tachycardia
Beta Blocker

Front 45

Who do you need to avoid the use of verapamil with?

Back 45

Infants less than 1 year
A Fib with WPW
A Flutter
Wide Complex Tachycardia
Beta Blocker

Front 46

What is a bigger concern at an adolescent visit, breast exam ortesticular exam ?

Back 46

Testicular exam because testicular caner does occur in adolescents while breast cancer is near zero

Front 47

When is it ok to use verapamil?

Back 47

To control the ventricular response to A fib in a normal heart and is PSVT

BUT NEVER IN INFANTS!!!

Front 48

When is it ok to use verapamil?

Back 48

To control the ventricular response to A fib in a normal heart and is PSVT

BUT NEVER IN INFANTS!!!

Front 49

What type of thinking is prominent in middle adolescence?

Back 49

Cognition begins to mature

Front 50

What are the Class Ia antiarrythmics?

Back 50

Procainamide
Disopyramide
Quinidine

Front 51

What are the Class Ia antiarrythmics?

Back 51

Procainamide
Disopyramide
Quinidine

Front 52

What STD should be screened for in all asymptomatic sexually active females ?

Back 52

Chlamydia

Front 53

What are the Class Ib antiarrythmics?

Back 53

Lidocaine,
Tocainide
Mexiletine
Phenytoin

Front 54

What are the Class Ib antiarrythmics?

Back 54

Lidocaine,
Tocainide
Mexiletine
Phenytoin

Front 55

What is the mean age of adolescent smoking ?

Back 55

12 yrs

Front 56

What are the class Ic antiarrythmics?

Back 56

Flecainide and propafenone

Front 57

What are the class Ic antiarrythmics?

Back 57

Flecainide and propafenone

Front 58

What is the mean age of adolescent acohol consumption ?

Back 58

12.6 yrs

Front 59

What are the Class II antiarrythmics?

Back 59

beta-blockers

Front 60

What are the Class II antiarrythmics?

Back 60

beta-blockers

Front 61

Who is most likely to smoke boys or girls ? Drink ?

Back 61

Girls smoke more than boys
Boys drink twice as often as girls

Front 62

What drugs are Class III antiarrhythmics?

Back 62

Amiodarone
Bretylium
Sotalol
Dofetilide
Ibutilide

Front 63

What drugs are Class III antiarrhythmics?

Back 63

Amiodarone
Bretylium
Sotalol
Dofetilide
Ibutilide

Front 64

What percent of adolescents use marijuana? Cocaine ? Crack ?

Back 64

50% marijuana
10% cocaine
5% crack

Front 65

What drugs are Class IV antiarrythmics?

Back 65

Calcium Channel Blockers (verapamil, diltiazem etc)

Front 66

What drugs are Class IV antiarrythmics?

Back 66

Calcium Channel Blockers (verapamil, diltiazem etc)

Front 67

What is concerning for young kids / adolescents with depression ?

Back 67

The earlier a child is, the more severe and recurrent the depression is likely to be

Front 68

How do Class I antiarrythmics work?

Back 68

They decrease the upslope of the action potential by blocking Na2+ channels which slows conduction

Front 69

How do Class I antiarrythmics work?

Back 69

They decrease the upslope of the action potential by blocking Na2+ channels which slows conduction

Front 70

When is hospitalization appropriate for depression?

Back 70

- suicidal/ homicidal
- psychosis
- mania
-substance abuse
- not responding to outpatient therapy

Front 71

How do Class II antiarrythmics work?

Back 71

They decrease sympathethic activity (beta-blockers)

Front 72

How do Class II antiarrythmics work?

Back 72

They decrease sympathethic activity (beta-blockers)

Front 73

When is the peak incidence of anorexia nervosa ?

Back 73

Ages 14.5 and 18

Front 74

How do Class III antiarrythmics work?

Back 74

They prolong the action potential duration.

Front 75

How do Class III antiarrythmics work?

Back 75

They prolong the action potential duration.

Front 76

How is anorexia split between boys and girls ?

Back 76

Girls outnumber boys by 10:1

Front 77

How do Class IV antiarrythmics work?

Back 77

They block inward Ca2+ current

(verapamil and diltiazem)

Front 78

How do Class IV antiarrythmics work?

Back 78

They block inward Ca2+ current

(verapamil and diltiazem)

Front 79

What is the recommended daily intake of calcium and vitamin D ?

Back 79

Calcium 1,200 - 1,500
Vitamin D 400 IU

Front 80

How does adenosine work?

Back 80

It slows the conduction in the SA and AV node.

Front 81

How does adenosine work?

Back 81

It slows the conduction in the SA and AV node.

Front 82

What EKG chances occur with anerexia ?

Back 82

- ST depression on exercise stress testing
- prolonged QT intervals
- V tach
- Bradycardia

Front 83

If a patient develops dyspnea following adenosine, what is the treatment?

Back 83

A bronchodilator (terbutaline, albuterol etc)

Front 84

If a patient develops dyspnea following adenosine, what is the treatment?

Back 84

A bronchodilator (terbutaline, albuterol etc)

Front 85

When is the highest risk of heart faliure with anorexia nervosa ?

Back 85

The first 2 wks of treatment(refeeding)

Front 86

What are the major side effects of quinidine?

Back 86

Prolong QRS complex, prolong QT,torsades de pointe, diarrhea, ATP, "cinchonism"

Front 87

What are the major side effects of quinidine?

Back 87

Prolong QRS complex, prolong QT,torsades de pointe, diarrhea, ATP, "cinchonism"

Front 88

What three componenets are meant by the term "cinchonism"?

Back 88

hearing loss
tinnitus
psychosis

Front 89

What should daily wieght gain be limited to in treatment of anorexics ?

Back 89

0.2 - 0.4 kg/day

Front 90

What three componenets are meant by the term "cinchonism"?

Back 90

hearing loss
tinnitus
psychosis

Front 91

What are the major side effects of procainamide?

Back 91

It prolongs QT and QRS, can cause blood dyscrasias, agranulocytosis, neutropenia and thrombocytopenia. Also drug induced lupus and need caution in heart failure patients.

Front 92

What ECHO findings are consistent with anorexia ?

Back 92

Ventricular wall thickness MVP pencardial effusion

Front 93

What are the major side effects of procainamide?

Back 93

It prolongs QT and QRS, can cause blood dyscrasias, agranulocytosis, neutropenia and thrombocytopenia. Also drug induced lupus and need caution in heart failure patients.

Front 94

What are the major side effects of lidocaine?

Back 94

seizures

Front 95

When does menses return in anorexics ?

Back 95

After achieving 80% of ideal body wt

Front 96

What are the major side effects of lidocaine?

Back 96

seizures

Front 97

What are the major side effects of beta-blockers

Back 97

bradycardia and asthma exaccerbation

Front 98

Which is more common ; anorexia orbulemia ?

Back 98

Bulemia
2 - 5% of girls
W< 1% of boys

Front 99

What are the major side effects of beta-blockers

Back 99

bradycardia and asthma exaccerbation

Front 100

What are the major side effects with bretylium?

Back 100

transient hypertension, then postural hypotension

Front 101

What are classic findings of bulemia ?

Back 101

- edema
- bilateral painless parotid swelling
- calluses on the dorsum of fingers
- loss of tooth enamel
- possible hypoka and cardiac toxicity ( from ipecac )
- metabolic alkalosis and increase amylase

Front 102

What are the major side effects with bretylium?

Back 102

transient hypertension, then postural hypotension

Front 103

What are the major side effects of amiodarone

Back 103

corneal deposits, pulmonar fibrosis, gray skin, hyper/hypothyroidism, hepatic toxicity, sun sensitivity, death from pulmonary fibrosis.

Front 104

What is Russell sign(s) ?

Back 104

Calluses on the dorsum of fingers secondary to induced vomiting from bulemia

Front 105

What are the major side effects of amiodarone

Back 105

corneal deposits, pulmonar fibrosis, gray skin, hyper/hypothyroidism, hepatic toxicity, sun sensitivity, death from pulmonary fibrosis.

Front 106

What is the most effective antiarrythmic drug and why is it not generally used in pediatrics?

Back 106

Amiodarone - not usually used due to extremely high iodine content.

Front 107

Of the following, what is helpful to differentiate anorexia and bulemia
- metabolic alkalosis
- hypokalemia
- cardiac involvment
- elevated amylase
- enamel destruction

Back 107

Elevated amylase

Front 108

What is the most effective antiarrythmic drug and why is it not generally used in pediatrics?

Back 108

Amiodarone - not usually used due to extremely high iodine content.

Front 109

What adverse reaction is caused by Class I antiarrhythmics but not Class III drugs

Back 109

Hematologic changes

Front 110

What is the role ofSSRIs in bulemia ?

Back 110

They are much more effective than in anorexia - Fluoxetine has the best results.

Front 111

What adverse reaction is caused by Class I antiarrhythmics but not Class III drugs

Back 111

Hematologic changes

Front 112

How often is pulmonary fibrosis fatal

Back 112

10% in general, but very rare in children

Front 113

How common is polymastia / polythelia in adolescent girls ?

Back 113

1 - 2%
Polymastia ( accessory breast tissue )
Polythelia ( accessory nipples )

Front 114

How often is pulmonary fibrosis fatal

Back 114

10% in general, but very rare in children

Front 115

What major side effects are caused by digoxin?

Back 115

arrhythmias - more likely if patient has low K+ or high Ca+2

Front 116

What is the most common breast mass in the adolescent ?
What is the txt and course?

Back 116

A solitary cyst
> 50% resolve in 2 - 3 mos
U/S if can not differentiate from solid mass

Front 117

What major side effects are caused by digoxin?

Back 117

arrhythmias - more likely if patient has low K+ or high Ca+2

Front 118

How do you monitor for toxicity of digoxin and quinidine?

Back 118

EKG

Front 119

When should a breast mass be referred for surgery ?

Back 119

Persistence of a mass over 3 menstrual cycles warrants referral to sugery for an aspiration

Front 120

How do you monitor for toxicity of digoxin and quinidine?

Back 120

EKG

Front 121

What cardiac anomaly is associated Noonan syndrome

Back 121

Pulmonic stenosis
Hypertrophic cardiomyopathy

Front 122

Why is mammography a poor choice for evaluation of a breast mass in an adolescent ?

Back 122

Because adolescents do not have enough breast fat to make a mammogram redable

Front 123

What cardiac anomaly is associated Noonan syndrome

Back 123

Pulmonic stenosis
Hypertrophic cardiomyopathy

Front 124

What cardiac anomaly is associated with Apert Syndrome

Back 124

VSD
Coarctation of Aorta

Front 125

What presents in adolescent females as a hard, fixed mass with overlaying skin changes, frequently under the nipple?

Back 125

Breast cancer - but it is extmeley rare with family history being extremeley important but only ~6% have breast cancer associated genes

Front 126

What cardiac anomaly is associated with Apert Syndrome

Back 126

VSD
Coarctation of Aorta

Front 127

What cardiac anomaly is associated Holt-Oram syndrome

Back 127

ASD
VSD

Front 128

What are the procedures of choice for evaluation of breast mass with concern of cancer ?

Back 128

Ultrasound and Biopsy

Front 129

What cardiac anomaly is associated Holt-Oram syndrome

Back 129

ASD
VSD

Front 130

What cardiac anomaly is associated with Alagille syndrome?

Back 130

Pulmonic stenosis

Front 131

What is the most common organism causing mastitis ?

Back 131

Staph aureus
Tx with anti staph abx, heat and analgesea

Front 132

What cardiac anomaly is associated with Alagille syndrome?

Back 132

Pulmonic stenosis

Front 133

What cardiac anomaly is associated with Ellis-van Creveld syndrome

Back 133

Single atrium

Front 134

When is it considered primary ammenorrhea ?

Back 134

1) 16 yrs of age
2) 14 yrs if breast development or stigmata of chromosomal abnormality such as Turners
3) Tanner Stage V for more than a year despite onset of thelarche 4 yrs prior

Front 135

What cardiac anomaly is associated with Ellis-van Creveld syndrome

Back 135

Single atrium

Front 136

What cardiac anomaly is associated with Cri-du-chat ssyndrome?

Back 136

VSD

Front 137

What are the three main groups of causes of amenorrhea ?

Back 137

Central ( hypothalamic or pitrutary ) Ovarian - or - Anatomic ( uterus, cervix, vagina )

Front 138

What cardiac anomaly is associated with Cri-du-chat ssyndrome?

Back 138

VSD

Front 139

What cardiac anomaly is associated with Turner syndrome?

Back 139

Bicuspid aortic valves
Coarctation of the aorta

Front 140

What is isolated GnRH deficienty and inability to smell caused by ?

Back 140

Kallmann Syndrome

Front 141

What cardiac anomaly is associated with Turner syndrome?

Back 141

Bicuspid aortic valves
Coarctation of the aorta

Front 142

What cardiac anomaly is associated with Trisomy 21?

Back 142

Endocardial cusion defect

Front 143

What is the most common pituitary cause of amenorthea in women who are of reproductive age ?

Back 143

Prolactin - secreting adenoma ( prolactinoma most commonly )

Front 144

What cardiac anomaly is associated with Trisomy 21?

Back 144

Endocardial cusion defect

Front 145

What cardiac anomaly is associated with Trisome 13?

Back 145

VSD

Front 146

Can secondary amennorthea be caused by/in Rokitansley Syndrome ?

Back 146

No but primary amenorthea can because it involes millerian agenesis with absence/hypoplasia of the vagia, cervix and/or uterus

Front 147

What cardiac anomaly is associated with Trisome 13?

Back 147

VSD

Front 148

What cardiac anomaly is associated with Trisomy 18?

Back 148

VSD

Front 149

What is the most common reason for 15-24 yr old outpatient visits ?

Back 149

Pregnancy

Front 150

What cardiac anomaly is associated with Trisomy 18?

Back 150

VSD

Front 151

What is the most common congenital heart lesion?

Back 151

VSD

Front 152

What is the most common reason for 10-14 yr old outpatient visits ?

Back 152

Health supervision visits

Front 153

What is the most common congenital heart lesion?

Back 153

VSD

Front 154

What is second most common congenital heart lesion?

Back 154

pulmonic stenosis

Front 155

What are the five most common reasons for hospitalizations in adolescents (10-12 yr old) ?

Back 155

1) pregnancy
2) mental disorders
3) injuries
4) digestive tract disorder
5) respuatiery tract diseases

Front 156

What is second most common congenital heart lesion?

Back 156

pulmonic stenosis

Front 157

What heart anomaly is associated with Lithium use in pregnancy.

Back 157

Prenatal exposure associated with Ebstein anomaly of the tricuspid valve.

Front 158

What are the two leading causes of adolescent morbidity and mentality ?

Back 158

Automobile and motorcycle accidents

Front 159

What heart anomaly is associated with Lithium use in pregnancy.

Back 159

Prenatal exposure associated with Ebstein anomaly of the tricuspid valve.

Front 160

What heart anomaly is associated with gestational diabetes?

Back 160

Temporary hypertrophic cardiomyopathy.

Front 161

What is the 2nd leading cause of death in adolescents, and the #1 cause of death in African-American adolescents ?

Back 161

Homicide

Front 162

What heart anomaly is associated with gestational diabetes?

Back 162

Temporary hypertrophic cardiomyopathy.

Front 163

When does the ductus arteriosus normally close?

Back 163

10-15 hours after birth, with complete closure up to three weeks of age normal.

Front 164

What is the number one cause of mortality for 24-44 yr old Hispanics and African-Americans ?

Back 164

HIV

Front 165

When does the ductus arteriosus normally close?

Back 165

10-15 hours after birth, with complete closure up to three weeks of age normal.

Front 166

How often do premature infants <1750 grams have a clinically apparent PDA?

Back 166

40-70% of the time.

Front 167

How long does pubescence last in girls? boys?

Back 167

4 yrs for girls
3 yrs for boy

Front 168

How often do premature infants <1750 grams have a clinically apparent PDA?

Back 168

40-70% of the time.

Front 169

What type of murmur does a PDA have?

Back 169

Continuous or machine-like

Front 170

What is the mean age for the onset of pubescece in girls? boys?

Back 170

Girls 9.7 yrs
Boys 11.4 yrs

Front 171

What type of murmur does a PDA have?

Back 171

Continuous or machine-like

Front 172

How often is indomethicin successful when used in a premature infant?

Back 172

80%

Front 173

What is the mean age for the beginning of menses?

Back 173

12.75 ( 10-16.5 )

Front 174

How often is indomethicin successful when used in a premature infant?

Back 174

80%

Front 175

What is the treatment to close a PDA?

Back 175

Indomethicin

Front 176

When does axillary hair occur ?

Back 176

Mid-puberty

Front 177

What is the treatment to close a PDA?

Back 177

Indomethicin

Front 178

What is the most common congenital heart defect?

Back 178

VSD and accounts for 25-30% of congenital heart lesions.

Front 179

How does the growth spurt of adolescents differ between boys and girls ?

Back 179

Boys - tanner 4 (~18)
Girls - tanner 2-3 (~16)

Front 180

What is the most common congenital heart defect?

Back 180

VSD and accounts for 25-30% of congenital heart lesions.

Front 181

Where is a VSD most common?

Back 181

< 1 year = muscular septum.

> 1 year = membranous

Front 182

Where is a VSD most common?

Back 182

< 1 year = muscular septum.

> 1 year = membranous

Front 183

What murmur is typically described as a harsh or high-pitched murmur that becomes apparent at 3-4 weeks of age?

Back 183

VSD

Front 184

What murmur is typically described as a harsh or high-pitched murmur that becomes apparent at 3-4 weeks of age?

Back 184

VSD

Front 185

When will the symptoms occur from volume overload secondary to a VSD with large L-to-R shunt?

Back 185

4-8 weeks of age

Front 186

When will the symptoms occur from volume overload secondary to a VSD with large L-to-R shunt?

Back 186

4-8 weeks of age

Front 187

When does an asymptomatic patient with a VSD murmur need referred to a cardiologist?

Back 187

At 1 year of age because if the murmur is still persistent then it is more likely membranous and less likely to close.

Front 188

When does an asymptomatic patient with a VSD murmur need referred to a cardiologist?

Back 188

At 1 year of age because if the murmur is still persistent then it is more likely membranous and less likely to close.

Front 189

What is the most common type of ASD?

Back 189

Ostium secundum defects are the most common form of ASD.

Front 190

What is the most common type of ASD?

Back 190

Ostium secundum defects are the most common form of ASD.

Front 191

ASDs are more common in ?Males or Females?

Back 191

Females 2:1

Front 192

ASDs are more common in ?Males or Females?

Back 192

Females 2:1

Front 193

At what age does pulmonary vascular disease with pulmonary hypertension occur in a patient with ASD?

Back 193

Age 20-30

Occurs about 5% of the time

Front 194

At what age does pulmonary vascular disease with pulmonary hypertension occur in a patient with ASD?

Back 194

Age 20-30

Occurs about 5% of the time

Front 195

What causes congenitally corrected trasposition of the great vesssles?

Back 195

The embryonic cardiac tube loops to the left instead of to the right.

Front 196

What causes congenitally corrected trasposition of the great vesssles?

Back 196

The embryonic cardiac tube loops to the left instead of to the right.

Front 197

What presents with a high-pitched early diastolic murmur that begins with the aortic component of the second heart sound.

Back 197

Aortic regurgitation

Front 198

What presents with a high-pitched early diastolic murmur that begins with the aortic component of the second heart sound.

Back 198

Aortic regurgitation

Front 199

What is a low-pitched, mid-diastolic murmur at the apex of the heart that it is associated with Rheumatic Fever?

Back 199

Austin Flint murmur

Front 200

What is a low-pitched, mid-diastolic murmur at the apex of the heart that it is associated with Rheumatic Fever?

Back 200

Austin Flint murmur

Front 201

What causes an Austin Flint murmur?

Back 201

the regurgitant aortic jet striking the anterior leaflet of the mitral valve

Front 202

What causes an Austin Flint murmur?

Back 202

the regurgitant aortic jet striking the anterior leaflet of the mitral valve

Front 203

What are the common causes of Aortic Regurgitation?

Back 203

Congenital aortic stenosis
Marfan syndrome
Rheumatic Fever
Infective endocarditis

Front 204

What are the common causes of Aortic Regurgitation?

Back 204

Congenital aortic stenosis
Marfan syndrome
Rheumatic Fever
Infective endocarditis

Front 205

What is the #1 cause of Aortic Regurgitation in the world (but not the US)?

Back 205

Rheumatic Fever

Front 206

What is the #1 cause of Aortic Regurgitation in the world (but not the US)?

Back 206

Rheumatic Fever

Front 207

What presents with an apical, high-pitched blowing systolic murmur?

Back 207

Mitral Regurgitation

Front 208

What presents with an apical, high-pitched blowing systolic murmur?

Back 208

Mitral Regurgitation

Front 209

What is the #1 cause of Mitral Regurgitation worldwide?

Back 209

Rheumatic Fever

Front 210

What is the #1 cause of Mitral Regurgitation worldwide?

Back 210

Rheumatic Fever

Front 211

What is the #1 cause of Mitral Regurgitation in the US?

Back 211

Mitral valve prolapse

Front 212

What is the #1 cause of Mitral Regurgitation in the US?

Back 212

Mitral valve prolapse

Front 213

What predisposes a patient to Mitral Valve Prolapse?

Back 213

Marfan's, Ehlers-Danlos syndrome or the mucopolysaccharidoses

Front 214

What predisposes a patient to Mitral Valve Prolapse?

Back 214

Marfan's, Ehlers-Danlos syndrome or the mucopolysaccharidoses

Front 215

What present with a late systolic crescendo murmur at the apex - almost always preceded by a click?

Back 215

MVP

Front 216

What present with a late systolic crescendo murmur at the apex - almost always preceded by a click?

Back 216

MVP

Front 217

What happens to a MVP murmur when the patient squats down?

Back 217

The murmur becomes softer, shorter and later in systole.

Front 218

What happens to a MVP murmur when the patient squats down?

Back 218

The murmur becomes softer, shorter and later in systole.

Front 219

When you only hear a murmur in the standing or sitting BUT NOT SQUATTING positions, what is the diagnosis?

Back 219

MVP

Front 220

When you only hear a murmur in the standing or sitting BUT NOT SQUATTING positions, what is the diagnosis?

Back 220

MVP

Front 221

What presents as an early low-pitched, decrescendo diatolic murmur that starts with the pulmonary component of the second heart rate sound?

Back 221

Pulmonary Regurgitation

Front 222

What presents as an early low-pitched, decrescendo diatolic murmur that starts with the pulmonary component of the second heart rate sound?

Back 222

Pulmonary Regurgitation

Front 223

What is the most common cause of pulmonary regurgitation?

Back 223

Post-operative complication for pulmonary stenosis or tetralogy of Fallot.

Front 224

What is the most common cause of pulmonary regurgitation?

Back 224

Post-operative complication for pulmonary stenosis or tetralogy of Fallot.

Front 225

What presents as a pansystolic murmur that is loudest along the lower left sternal border with radiation to the right?

Back 225

Tricuspid Regurgitation

Front 226

What presents as a pansystolic murmur that is loudest along the lower left sternal border with radiation to the right?

Back 226

Tricuspid Regurgitation

Front 227

What is the most common cardiac defect in children?

Back 227

VSD

Front 228

What is the most common cardiac defect in children?

Back 228

VSD

Front 229

What is the 2nd most common cardiac defect in children?

Back 229

Pulmonic Stenosis

Front 230

What is the 2nd most common cardiac defect in children?

Back 230

Pulmonic Stenosis

Front 231

How do you keep a ductus open?

Back 231

Prostaglandin E1

(PGE1)

Front 232

How do you keep a ductus open?

Back 232

Prostaglandin E1

(PGE1)

Front 233

What has EKG findings of RSR' in V1?

Back 233

ASD

Front 234

What has EKG findings of RSR' in V1?

Back 234

ASD

Front 235

What has EKG findings of peaked P waves in lead II, RVH and RAD?

Back 235

Pulmonic Stenosis

Front 236

What has EKG findings of peaked P waves in lead II, RVH and RAD?

Back 236

Pulmonic Stenosis

Front 237

What presents with a systolic ejection click along the left sternum followed by a crescendo-decrescendo murmur?

Back 237

Pulmonic Stenosis

Front 238

What presents with a systolic ejection click along the left sternum followed by a crescendo-decrescendo murmur?

Back 238

Pulmonic Stenosis

Front 239

Where is the murmur associated with Pulmonary Stenosis

Back 239

Left upper sternal border that radiates to below the left clavicle and often to the back.

Front 240

Where is the murmur associated with Pulmonary Stenosis

Back 240

Left upper sternal border that radiates to below the left clavicle and often to the back.

Front 241

When is treatment indicated for pulmonary stenosis?

Back 241

Right Ventricular Systolic pressure from over 50% of systemic to greater than systemic pressure or are symptomatic with exercise.

Front 242

When is treatment indicated for pulmonary stenosis?

Back 242

Right Ventricular Systolic pressure from over 50% of systemic to greater than systemic pressure or are symptomatic with exercise.

Front 243

What cardiac defect is associated with congenital rubella syndrome, Williams syndrome, or Alagille syndrome (anteriohepatic dysplasia)?

Back 243

Peripheral branch Pulmonic Stenosis

Front 244

What cardiac defect is associated with congenital rubella syndrome, Williams syndrome, or Alagille syndrome (anteriohepatic dysplasia)?

Back 244

Peripheral branch Pulmonic Stenosis

Front 245

What is true in >85% of patients with congenital stenotic aortic valves?

Back 245

Bicuspid aortic valve.

Front 246

What is true in >85% of patients with congenital stenotic aortic valves?

Back 246

Bicuspid aortic valve.

Front 247

What has a "fish-mouth" appearance on ECHO?

Back 247

A bicuspid aordic valve

Front 248

What has a "fish-mouth" appearance on ECHO?

Back 248

A bicuspid aordic valve

Front 249

What has a "teardrop" appearance on ECHO?

Back 249

A monocuspid aortic valve

Front 250

What has a "teardrop" appearance on ECHO?

Back 250

A monocuspid aortic valve

Front 251

What is the common sequelae of congenital aortic stenosis?

Back 251

Progressively more stenosis as the valve opening becomes smaller and smaller.

Front 252

What is the common sequelae of congenital aortic stenosis?

Back 252

Progressively more stenosis as the valve opening becomes smaller and smaller.

Front 253

What presents with a crescendo-decrescendo, harsh-to-rough systolic murmur with a suprasternal notch thrill?

Back 253

Aortic Stenosis

Front 254

What presents with a crescendo-decrescendo, harsh-to-rough systolic murmur with a suprasternal notch thrill?

Back 254

Aortic Stenosis

Front 255

Where is the murmur of Aortic Stenosis heard best?

Back 255

Right upper sternal border with radiation to the surprasternal notch and neck with an apical ejection click.

Front 256

Where is the murmur of Aortic Stenosis heard best?

Back 256

Right upper sternal border with radiation to the surprasternal notch and neck with an apical ejection click.

Front 257

True or False? Physical findings, CXR and EKG are reliable in predicting the severity of the Aortic Stenosis?

Back 257

False

Front 258

True or False? Physical findings, CXR and EKG are reliable in predicting the severity of the Aortic Stenosis?

Back 258

False

Front 259

If a patient has Aortic Stenosis and becomes symptomatic with syncope or chest pain, what test is used to evaluate cardiac function?

Back 259

Cardiac cath.

Front 260

If a patient has Aortic Stenosis and becomes symptomatic with syncope or chest pain, what test is used to evaluate cardiac function?

Back 260

Cardiac cath.

Front 261

How do doppler gradient and gradient with direct catheterization correlate?

Back 261

Doppler of 70mm Hg correlates with > 50 mg peak-to-peak gradient on cath.

Front 262

How do doppler gradient and gradient with direct catheterization correlate?

Back 262

Doppler of 70mm Hg correlates with > 50 mg peak-to-peak gradient on cath.

Front 263

What is now considered the treatment of choice for aortic stenosis in children?

Back 263

Balloon valvoplasty - but about 40% will require repeat treatment within 10 years.

Front 264

What is now considered the treatment of choice for aortic stenosis in children?

Back 264

Balloon valvoplasty - but about 40% will require repeat treatment within 10 years.

Front 265

How often with patients who have undergone balloon valvoplasty require repeat treatmen within 10 years?

Back 265

40%

Front 266

How often with patients who have undergone balloon valvoplasty require repeat treatmen within 10 years?

Back 266

40%

Front 267

What procedure is the definitive surgical correction of Aortic Stenosis?

Back 267

The Ross Procedure

Front 268

What procedure is the definitive surgical correction of Aortic Stenosis?

Back 268

The Ross Procedure

Front 269

What is the Ross Procedure?

Back 269

Moving the pulmonary valve ring, with the valve intact, into the aortic annulus and placing a homogrraft aortic valve into the right ventricular outflow tract..

Front 270

What is the Ross Procedure?

Back 270

Moving the pulmonary valve ring, with the valve intact, into the aortic annulus and placing a homogrraft aortic valve into the right ventricular outflow tract..

Front 271

Is anticoagulation required after the Ross Procedure to correct Aortic Stenosis?

Back 271

No

Front 272

Is anticoagulation required after the Ross Procedure to correct Aortic Stenosis?

Back 272

No

Front 273

What is the primary risk with the Ross Procedure as treatment of Aortic Stenosis?

Back 273

The valve does not grow with the patient and requires surgical replacement in 10-15 years.

Front 274

What is the primary risk with the Ross Procedure as treatment of Aortic Stenosis?

Back 274

The valve does not grow with the patient and requires surgical replacement in 10-15 years.

Front 275

How is IHSS transmitted?

Back 275

Autosomal Dominant with variable expression.

Front 276

How is IHSS transmitted?

Back 276

Autosomal Dominant with variable expression.

Front 277

What type of shock is characterized by high cardiac output, very low systemic vascular resistance and low wedge pressure?

Back 277

Septic shock

Front 278

What type of shock is characterized by high cardiac output, very low systemic vascular resistance and low wedge pressure?

Back 278

Septic shock

Front 279

What type of shock is characterized by reduced cardiac output, high systemic vascular resistance and low wedge pressure?

Back 279

Hypovolemic shock

Front 280

What type of shock is characterized by reduced cardiac output, high systemic vascular resistance and low wedge pressure?

Back 280

Hypovolemic shock

Front 281

What type of shock is characterized by low cardiac output, high systemic vascular resistance and high wedge pressure?

Back 281

Cardiogenic shock

Front 282

What type of shock is characterized by low cardiac output, high systemic vascular resistance and high wedge pressure?

Back 282

Cardiogenic shock

Front 283

What type of shock is characterized by reduced cardiac output, high systemic vascular resistance and reduced wedge pressure?

Back 283

Obstructive shock

Front 284

What type of shock is characterized by reduced cardiac output, high systemic vascular resistance and reduced wedge pressure?

Back 284

Obstructive shock

Front 285

What murmurs get softer or with squating and louder with standing?

Back 285

MVP and IHSS

Front 286

What murmurs get softer or with squating and louder with standing?

Back 286

MVP and IHSS

Front 287

How is IHSS(or HOCM - hypertrophic, obstructive cardiomyopathy) inherited?

Back 287

Autosomal Dominant with variable expression. 50 % on chromosome 14

Front 288

How is IHSS(or HOCM - hypertrophic, obstructive cardiomyopathy) inherited?

Back 288

Autosomal Dominant with variable expression. 50 % on chromosome 14

Front 289

What is associated with a grade 3-4/6 crescendo-RUSB with a possible thrill BUT without a click and without a suprasternal notch murmur.

Back 289

IHSS

Front 290

What is associated with a grade 3-4/6 crescendo-RUSB with a possible thrill BUT without a click and without a suprasternal notch murmur.

Back 290

IHSS

Front 291

What has a characteristic EKG of LH, prominent septal Q waves and abnormal repolarization.

Back 291

IHSS

Front 292

What has a characteristic EKG of LH, prominent septal Q waves and abnormal repolarization.

Back 292

IHSS

Front 293

What cardiac anomaly is associated with Williams syndrome?

Back 293

Supravalvualar Aortic Stenosis

Front 294

What cardiac anomaly is associated with Williams syndrome?

Back 294

Supravalvualar Aortic Stenosis

Front 295

If there is a true interuption in the aortic arch what genetic anomaly should be checked for?

Back 295

DiGeorge syndrome (with FISH for 22q11 marker)

Front 296

If there is a true interuption in the aortic arch what genetic anomaly should be checked for?

Back 296

DiGeorge syndrome (with FISH for 22q11 marker)

Front 297

What presents with decreased pulses in the lower extremites and poor systemic output with CHF?

Back 297

Aortic hypoplasia/interruption

Front 298

What presents with decreased pulses in the lower extremites and poor systemic output with CHF?

Back 298

Aortic hypoplasia/interruption

Front 299

What is the first treatment of hypplastic or interuppted aortic arch?

Back 299

PGE1 to keep the ductus open and stabilize for surgery.

Front 300

What is the first treatment of hypplastic or interuppted aortic arch?

Back 300

PGE1 to keep the ductus open and stabilize for surgery.

Front 301

How does coarctation of the aorta usually present?

Back 301

It is detected in an otherwise asymptomatic older child or young adult during a HTN or murmur workup.

Front 302

How does coarctation of the aorta usually present?

Back 302

It is detected in an otherwise asymptomatic older child or young adult during a HTN or murmur workup.

Front 303

How late can you use PGE1 to keep a ductus open?

Back 303

3-4 weeks.

Front 304

How late can you use PGE1 to keep a ductus open?

Back 304

3-4 weeks.

Front 305

What can present with epistaxis, claudication-like symptoms in the lower extremities with exercise and headaches?

Back 305

Coarctation

Front 306

What can present with epistaxis, claudication-like symptoms in the lower extremities with exercise and headaches?

Back 306

Coarctation

Front 307

What complications can occur in coarctation?

Back 307

Stroke secondary to berry aneurysm (low risk) and infective endocarditis (high risk)

Front 308

What complications can occur in coarctation?

Back 308

Stroke secondary to berry aneurysm (low risk) and infective endocarditis (high risk)

Front 309

What are the components fo Tetralogy of Fallot?

Back 309

Interventricular septal defect
Hypertrophic Right Ventricle
Overriding aorta
Pulmonic stenosis

Front 310

What are the components fo Tetralogy of Fallot?

Back 310

Interventricular septal defect
Hypertrophic Right Ventricle
Overriding aorta
Pulmonic stenosis

Front 311

What type of shunt does TOF have?

Back 311

Right to Left (hense the cyanosis)

Front 312

What type of shunt does TOF have?

Back 312

Right to Left (hense the cyanosis)

Front 313

If corrective surgery is not done at birth, what complications are associated with TOF?

Back 313

Brain abscess, cerebral thrombosis with hemiplegia and infective endocarditis.

Front 314

If corrective surgery is not done at birth, what complications are associated with TOF?

Back 314

Brain abscess, cerebral thrombosis with hemiplegia and infective endocarditis.

Front 315

What classic presentation appears on CXR with TOF?

Back 315

Boot-shaped heart

Front 316

What classic presentation appears on CXR with TOF?

Back 316

Boot-shaped heart

Front 317

What looks like a boot-shaped heart?

Back 317

Tetralogy of Fallot

Front 318

What looks like a boot-shaped heart?

Back 318

Tetralogy of Fallot

Front 319

What will help alleive a tet spell in an infant?

Back 319

Place the infant on it abdomen in a knee-chest position or holding the infant with the knees flexed on the abdomen.

Front 320

What will help alleive a tet spell in an infant?

Back 320

Place the infant on it abdomen in a knee-chest position or holding the infant with the knees flexed on the abdomen.

Front 321

If there is a prolonged tet spell, what may help?

Back 321

Morphine

Front 322

If there is a prolonged tet spell, what may help?

Back 322

Morphine

Front 323

What medication can help prevent tet spells?

Back 323

propranolol

Front 324

What medication can help prevent tet spells?

Back 324

propranolol

Front 325

What components make up the surgery for TOF?

Back 325

Close the VSD
Resect the subpulmonic muscle
Place RV outflow and main pulmonary artery patch to increase flow of outflow tract
Sometimes Pulmonary Valvulotomy

Front 326

What components make up the surgery for TOF?

Back 326

Close the VSD
Resect the subpulmonic muscle
Place RV outflow and main pulmonary artery patch to increase flow of outflow tract
Sometimes Pulmonary Valvulotomy

Front 327

What is common in post op tetralogy of Fallot?

Back 327

ventricular arrhythmias with recurring PS or severe PI

Front 328

What is common in post op tetralogy of Fallot?

Back 328

ventricular arrhythmias with recurring PS or severe PI

Front 329

What is the most common cardiac cause of cyanosis in the newborn during the first few days of life?

Back 329

Transposition (complete) of great vessels

Front 330

What is the most common cardiac cause of cyanosis in the newborn during the first few days of life?

Back 330

Transposition (complete) of great vessels

Front 331

What is the most common cardiac cause of cyanosis for all ages of children?

Back 331

Tetralogy of Fallot

Front 332

What is the most common cardiac cause of cyanosis for all ages of children?

Back 332

Tetralogy of Fallot

Front 333

What presents with a single, loud second heart sound with a 2-3/6 non-specific ejection murmur at the middle of the left sternal border?

Back 333

Complete Transposition of the Great Arteries

Front 334

What presents with a single, loud second heart sound with a 2-3/6 non-specific ejection murmur at the middle of the left sternal border?

Back 334

Complete Transposition of the Great Arteries

Front 335

When is corrective surgery done for TOF?

Back 335

6-12 months

Front 336

When is corrective surgery done for TOF?

Back 336

6-12 months

Front 337

When is corrective surgery done for Transposition?

Back 337

2-3 weeks

Front 338

When is corrective surgery done for Transposition?

Back 338

2-3 weeks

Front 339

What has the classic presentation of an egg-shaped heart on CXRi?

Back 339

Transposition

Front 340

What has the classic presentation of an egg-shaped heart on CXRi?

Back 340

Transposition

Front 341

What is operative survival of TOF adn Transposition?

Back 341

90-95%

Front 342

What is operative survival of TOF adn Transposition?

Back 342

90-95%

Front 343

What is associated with a round or apple-like heart on CXR?

Back 343

Tricuspid atresia

Front 344

What is associated with a round or apple-like heart on CXR?

Back 344

Tricuspid atresia

Front 345

How does Tricuspid atresia present?

Back 345

cyanosis within hours to days of birth due to the ductus closing.

Front 346

How does Tricuspid atresia present?

Back 346

cyanosis within hours to days of birth due to the ductus closing.

Front 347

Which common cyanotic heart disease is associated with LAD and LVH on EKG?

Back 347

Tricuspid Atresia

Front 348

Which common cyanotic heart disease is associated with LAD and LVH on EKG?

Back 348

Tricuspid Atresia

Front 349

Which common cyanotic heart disease is associated with RAD and RVH on EKG?

Back 349

Tetralogy of Fallot and Transposition of Great Arteries

Front 350

Which common cyanotic heart disease is associated with RAD and RVH on EKG?

Back 350

Tetralogy of Fallot and Transposition of Great Arteries

Front 351

What are the congenital heart defects that have LAD?

Back 351

Ostium primum ASD, Complete AV canal and Tricuspid atresia

Front 352

What are the congenital heart defects that have LAD?

Back 352

Ostium primum ASD, Complete AV canal and Tricuspid atresia

Front 353

What is Ebstein anomaly?

Back 353

when the posterior and septal leaftlets of the tricuspid valve are displaced downward and attached to the RV wall.

Front 354

What is Ebstein anomaly?

Back 354

when the posterior and septal leaftlets of the tricuspid valve are displaced downward and attached to the RV wall.

Front 355

What is classic on CXR with Ebstein anomaly?

Back 355

Huge RA on EKG and CXR

Front 356

What is classic on CXR with Ebstein anomaly?

Back 356

Huge RA on EKG and CXR

Front 357

What is associated with the development of Ebstein anomaly?

Back 357

maternal lithium use

Front 358

What is associated with the development of Ebstein anomaly?

Back 358

maternal lithium use

Front 359

What is associated with a snowman or figure eight appearance on CXR?

Back 359

Total anomalous pulmonary venous return with UNOBSTRUCTIVE pulmonary venous return (to the innominate vein.)

Front 360

What is associated with a snowman or figure eight appearance on CXR?

Back 360

Total anomalous pulmonary venous return with UNOBSTRUCTIVE pulmonary venous return (to the innominate vein.)

Front 361

What cardiac anomaly is associated with ground glass appearance on CXR?

Back 361

Total anomalous OBSTRUCTIVE pulmonary venous return

Front 362

What cardiac anomaly is associated with ground glass appearance on CXR?

Back 362

Total anomalous OBSTRUCTIVE pulmonary venous return

Front 363

When do patients with hypoplastic left heart present?

Back 363

They are acutely ill with signs of poor perfusion and CHF in the first days or weeks of life.

Front 364

When do patients with hypoplastic left heart present?

Back 364

They are acutely ill with signs of poor perfusion and CHF in the first days or weeks of life.

Front 365

Hypoplastic left heart accounts for what percent of all cardiac deaths in the first year of life?

Back 365

25%

Front 366

Hypoplastic left heart accounts for what percent of all cardiac deaths in the first year of life?

Back 366

25%

Front 367

What is the first surgical procedure for hypoplastic L heart?

Back 367

The Norwood Procedure - Cut main pulmonary artery and ligate the PDA. Use proximal artery to reconstruct the ascending aorta and aortic arch to establish output from the RV to the aorta

Front 368

What is the first surgical procedure for hypoplastic L heart?

Back 368

The Norwood Procedure - Cut main pulmonary artery and ligate the PDA. Use proximal artery to reconstruct the ascending aorta and aortic arch to establish output from the RV to the aorta

Front 369

What is the second surgical procedure for hypoplastic left heart?

Back 369

The Glenn procedure - SVC to PA shunt which is 4-6 months after initial procedure?

Front 370

What is the second surgical procedure for hypoplastic left heart?

Back 370

The Glenn procedure - SVC to PA shunt which is 4-6 months after initial procedure?

Front 371

What is the third procedure for hypoplastic L heart?

Back 371

The Fontan procedure - connects the IVC to PA

Front 372

What is the third procedure for hypoplastic L heart?

Back 372

The Fontan procedure - connects the IVC to PA

Front 373

What are the two possible surgical corrections for Hypoplastic Left Heart?

Back 373

The Norwood/Glenn and Fontan Procedures in sequence

Orthotopic heart transplant.

Front 374

What are the two possible surgical corrections for Hypoplastic Left Heart?

Back 374

The Norwood/Glenn and Fontan Procedures in sequence

Orthotopic heart transplant.

Front 375

What is the most common aortic arch abnormality?

Back 375

Aberrant right subclavian artery arising from the descending aorta.

Front 376

What is the most common aortic arch abnormality?

Back 376

Aberrant right subclavian artery arising from the descending aorta.

Front 377

What is the most common aortic arch abnormaity TO CAUSE SYMPTOMS?

Back 377

Double aortic arch (persistence of both right and left 4th arches)

Front 378

What is the most common aortic arch abnormaity TO CAUSE SYMPTOMS?

Back 378

Double aortic arch (persistence of both right and left 4th arches)

Front 379

If there is posterior indention/compression of the esophagus, what is the cause?

Back 379

Vascular rings cause posterior indention.

Front 380

If there is posterior indention/compression of the esophagus, what is the cause?

Back 380

Vascular rings cause posterior indention.

Front 381

If there is anterior indention/compression of the esophagus, what is the cause?

Back 381

Pulmonary slings cause anterior indentation.

Front 382

If there is anterior indention/compression of the esophagus, what is the cause?

Back 382

Pulmonary slings cause anterior indentation.

Front 383

What is the most common cause of sudden death in participating athletes?

Back 383

IHSS

Front 384

What is the most common cause of sudden death in participating athletes?

Back 384

IHSS

Front 385

What is the second most common cause of sudden death in participating athletes?

Back 385

coronary artery anomalies.

Front 386

What is the second most common cause of sudden death in participating athletes?

Back 386

coronary artery anomalies.

Front 387

What is pathognomonic for pericarditis?

Back 387

friction rub

Front 388

What is pathognomonic for pericarditis?

Back 388

friction rub

Front 389

What condition has a characteristic diffuse ST elevation in most or all leads?

Back 389

Pericarditis.

Front 390

What condition has a characteristic diffuse ST elevation in most or all leads?

Back 390

Pericarditis.

Front 391

What infections commonly cause Pericarditis?

Back 391

Coxsackie A and B, echovirus, adenovirus, histoplasmosis, coccidiodomycosis, staphylococci and pneumococci, and TB.

Front 392

What infections commonly cause Pericarditis?

Back 392

Coxsackie A and B, echovirus, adenovirus, histoplasmosis, coccidiodomycosis, staphylococci and pneumococci, and TB.

Front 393

What drugs are known to cause pericarditis?

Back 393

phenytoin, hydralazine and procainamide

Front 394

What drugs are known to cause pericarditis?

Back 394

phenytoin, hydralazine and procainamide

Front 395

What are the causes of pericardial effusions?

Back 395

The same as pericarditis - viruses, bacteria, fungal, and medications.

Front 396

What are the causes of pericardial effusions?

Back 396

The same as pericarditis - viruses, bacteria, fungal, and medications.

Front 397

What happens to cardiac parameters during cardiac tamponade?

Back 397

End diastolic pressure up,
Atrial pressure up,
Ventricular pressure up,
Cardiac output falls,
Heart rate up, BP down,
Narrow pulse pressure

Front 398

What happens to cardiac parameters during cardiac tamponade?

Back 398

End diastolic pressure up,
Atrial pressure up,
Ventricular pressure up,
Cardiac output falls,
Heart rate up, BP down,
Narrow pulse pressure

Front 399

What is it called when aortic pressure falls greater than 10-15 mmHg with inspiration/

Back 399

Pulses paradoxus

Front 400

What is it called when aortic pressure falls greater than 10-15 mmHg with inspiration/

Back 400

Pulses paradoxus

Front 401

JVD with no collapse during diastole and pulsus paradoxus is most likely?

Back 401

Cardiac tamponade

Front 402

JVD with no collapse during diastole and pulsus paradoxus is most likely?

Back 402

Cardiac tamponade

Front 403

If the diastolic pressure readings are all the same, it is most likely?

Back 403

Cardiac tamponade

Front 404

If the diastolic pressure readings are all the same, it is most likely?

Back 404

Cardiac tamponade

Front 405

Kussmaul sign is associated with what?

Back 405

Cardiac tamponade or constrictive pericarditis.

Front 406

Kussmaul sign is associated with what?

Back 406

Cardiac tamponade or constrictive pericarditis.

Front 407

What is Kussmaul sign?

Back 407

The jugular venous pressure rises with inspiration.

Front 408

What is Kussmaul sign?

Back 408

The jugular venous pressure rises with inspiration.

Front 409

What is Beck's triad?

Back 409

Rising JV pressure, dropping systolic BP and muffled heart sounds.

Front 410

What is Beck's triad?

Back 410

Rising JV pressure, dropping systolic BP and muffled heart sounds.

Front 411

Who now needs SBE prophylaxis for dental procedures?

Back 411

Prosthetic valve
History of endocarditis
Cardiac transplant recipients who develop cardiac vlvulopathy
CHD with unrepaired cyanotic heart disease, completely repaired with prosthetic material or device for 6 months post procedure.

Front 412

Who now needs SBE prophylaxis for dental procedures?

Back 412

Prosthetic valve
History of endocarditis
Cardiac transplant recipients who develop cardiac vlvulopathy
CHD with unrepaired cyanotic heart disease, completely repaired with prosthetic material or device for 6 months post procedure.

Front 413

SBE is indicated for what procedures?

Back 413

Dental work but not GU or GI procedures.

Front 414

SBE is indicated for what procedures?

Back 414

Dental work but not GU or GI procedures.

Front 415

What are Aschoff bodies associated with?

Back 415

That are pathognomonic for rheumatic fever.

Front 416

What are Aschoff bodies associated with?

Back 416

That are pathognomonic for rheumatic fever.

Front 417

What are the JONES criteria for Rheumatic Fever?

Back 417

Joint - polyarthritis
Carditis
Nodules - subcutaneous
Erythema marginatum
Sydenham's Chorea

Front 418

What are the JONES criteria for Rheumatic Fever?

Back 418

Joint - polyarthritis
Carditis
Nodules - subcutaneous
Erythema marginatum
Sydenham's Chorea

Front 419

What are the six factors that increase risk of coronary aneurysm in children with Kawasaki disease?

Back 419

1) <1 yr
2) male
3) cardiomegaly
4) arrythmias
5) fever > 16 days
6) recurrence of fever after 48 hours afebrile.

Front 420

What are the six factors that increase risk of coronary aneurysm in children with Kawasaki disease?

Back 420

1) <1 yr
2) male
3) cardiomegaly
4) arrythmias
5) fever > 16 days
6) recurrence of fever after 48 hours afebrile.