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peds20 Flashcards

1
Q

def of CHF

A

inadequate ox delivery by the myocardium to meet the demands of the body

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2
Q

what do the kidneys do during CHF?

A

retain salt and water as an attempt to increase blood volume because the kidneys are being hypoperfused

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3
Q

catecholamines and CHF?

A

they are released to incr heart rate

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4
Q

how does incr pulm blood flow cause CHF?

A

it’s just not what your heart is made to do; examples are VSD, PDA, transp of great arteries, truncus arteriosus, and total anomalous pulm venous conneciton

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5
Q

what obstructive lesions cause CHF?

A

severe aortic, pulm, and mitral valve stenosis, coarctation of the aorta, interrupted aortic arch, and hypoplastic left heart syndrome

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6
Q

infectious cause of CHF?

A

viral myocarditis (common in older kids), endocarditis, pericarditis,

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7
Q

evidence of pulmonary congestion

A

tachypnea, cough, wheezing and rales

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8
Q

evidence of impaired myocardial performance

A

tachycardia, sweating, pale or ashen skin, diminished urine output, and enlarged cardiac sillohuette on cxr

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9
Q

hepatomegaly and peripheral edema are evidence of what?

A

systemic venous congestion

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10
Q

late manifestations of CHF

A

cyanosis and shock

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11
Q

three types of drugs used for CHG

A

cardiac glycosides, loop diuretics, inotropes

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12
Q

how do cardiac glycosides work?

A

increase calcium-induced calcium release and therefore the force of contraction

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13
Q

example of cardiac glycoside

A

digoxin

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14
Q

ethacrynic acid

A

loop diuretic

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15
Q

how do inotropes work?

A

increase heart contractility

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16
Q

examples of inoropes

A

dobutamine, dopamine

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17
Q

how do phosphodiesterase inhib help CHF?

A

improve contractility and reduce afterload

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18
Q

balloon valvuloplasty used for what?

A

critical aortic and pulm valve stenosis

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19
Q

what percent of kids have an innocent heart murmur?

A

50%

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20
Q

still’s murmur age, location, and characteristics

A

age 2-7 years; mid-left sternal border; grade 1-3 systolic vibratory or buzzing; loudest supine and louder with exercise

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21
Q

pulmonic systolic murmur (systolic ejection murmur)

A

any age; upper left sternal border; grade 1-2, peaks in early systole; blowing, high-pitched, loudest supine and louder with exercise

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22
Q

venous hum- age, location, and characteristics

A

any age, but esp school age; neck and below the clavicles; continuous murmur, heard only sitting or standing; disappears if supine; changes with compression of the jugular vein or with neck flex or extension

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23
Q

ostium primum

A

ASD in the lower portion of the atrial septum. Often associated with cleft or division in the ant mitral valve leaflet and cause mitral regurg

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24
Q

ostium primum more common in what population?

A

down syndrome

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25
Q

ostium secondum

A

ASD in the middle portion of the atral septum. Most common type of ASD

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26
Q

sinus venosus

A

ASD high in the septum near the junction of the right atrium and SVC. The right pulm vein drains anomalously into the right atrium or SVC instead of into the left atrium

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27
Q

symptoms of acyanotic heart disease

A

minimal; incr RV impulse, systolic ejection murmur (from excessive pulm blood flow)at mid and upper left sternal borders; mid-diastolic murmur and fixed split second heart sound

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28
Q

how does acyanotic heart disease cause mid-diastolic filling rumble

A

excessive blood flow through the tricuspid valve

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29
Q

how does acyanotic heart disease cause fixed-split heart sound?

A

excessive pulm blood flow causes the the normal variation in timing of aortic and pulm valve closure with resp to be absent

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30
Q

VSD murmur?

A

high pitched holosystolic murmur at LLSB and thrill at LLSB; as the size of the VSD decreases, the intensity of the murmur increases

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31
Q

PDA murmur

A

continuous “machinery like” murmur at ULSB; brisk pulses; diastolic rumble of blood across mitral st the apex;

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32
Q

phys exam fininds in coarctation of aorta

A

elevated BP in right arm, reduced BP in legs, delayed and dampened fem pulse; bruit left upper back

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33
Q

aortic stenosis murmur

A

ejection click; systolic ejection murmur at base with radiation to URSB, apex, suprasternal notch and carotids; thrill at URSB and suprasternal notch

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34
Q

murmur with pulm stenosis?

A

ejection click; systolic ejection murmur at ULSB

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35
Q

ECG findings in VSD

A

normal or mild LVH; RVH if pulm htn present

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36
Q

ecg findings in PDA

A

LVH; RVH if pulm htn present

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37
Q

ecg finding in coarctation of the aorta

A

normal or LVH

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38
Q

aortic stenosis findings on ECG

A

normal or LVH

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39
Q

pum stenosis finding on ecg

A

RVH

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40
Q

ASD finding on ecg?

A

right axis dev, rvh, and right atrial enlargement

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41
Q

small VSD prognosis?

A

may close spontaneously

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42
Q

what if VSD with 2:1 ul to systemic blood flow?

A

diastolic murmur of mitral turbulence (excess blood from lungs now passing through the mitral valve) heard at apex

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43
Q

eisenmenger syndrome

A

ehn PVR exceeds SVR and shunting shifts to R to L

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44
Q

ductus arteriosis

A

connects pulm art to aorta

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45
Q

management of PDA

A

indomethacin, can be closed surgically by coil embolization, thorascopic surgery, and ligation in a thoracotomy

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46
Q

coarctation of the aorta

A

narrowing of the aortic arch just below the origin of the left subclavian artery and typically at or just proximal to the ductus arteriosus

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47
Q

neonates with open PDA and coarctation

A

depend on R to L shuntthroug the PDA for perfusion of the lower thoracric and descending aorta; sx develop when the PDA closes

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48
Q

findings in older kids with coarctation of aorta

A

hypertension in right arm and bp reduced in lower extremities; radiofemoral delay

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49
Q

other findings in coarctation of the aorta

A

bicuspid aortic valve or aortic stenosis is present in half of kids (if either is present, you have systolic murmur); bruit through the coarctation may be heard at the LU back near the scapula

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50
Q

management of coarctation of the aorta

A

improve circulation to the lower body by IV prostaglandin E to open the DA, then inotropic meds; surgery but recurrence Is common so balloon angioplasty is the choice

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51
Q

aortic stenosis in the neonate may lead to what?

A

hypoplasia of the LV as a result of impaired fetal left ventricular development

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52
Q

initial management of aortic stenosis

A

balloon valvuloplasty, then surgery for aortic valve replacement (Russ procedure) after 5-10 yrs after palliative valvuloplasty bc of recurrent stenosis

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53
Q

ross procedure

A

aortic valve is replaced with the patient’s own pulm valve

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54
Q

most common cardiac causes of central cyanosis

A

the 5 Ts: tetrology of fallot, tranposiiton of the great arteries, tricuspid atresia, truncus arteriosis, and total anomalous pulm venous connection

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55
Q

100% oxygen challenge test suggest cyanotic CHD when?

A

when PaO2 fails to rise despite administration of 100% ox

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56
Q

tetrology of fallot

A

VSD, overriding aorta, pulm stenosis, and RV hypertrophy

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57
Q

most common cause of central cyanosis

A

tetrology of fallot

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58
Q

murmor in tetrology of flalot?

A

systolic ejectrion murmur representing the pulm stenosis

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59
Q

what kinds of activities bring on cyanosis in a kid with tetrology of fallot?

A

things that decr SVR (exercise, vasodilation, volume depletion)or increase resistance through the RVOT (Crying, tachycardia)

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60
Q

Tet spells

A

sudden cyanosis and decr murmur intensity; caused by decr arterial ox sat, which increases resistance through the RVOT, resulting in incr R to L shunt

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61
Q

how does a kid deal with a tet spell?

A

squat; to incr venous return to the heart and incr SVR

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62
Q

management of tet of fallot?

A

surgical repair at 4-8 months old

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63
Q

some kids with tet of fallot who cannot undergo surgery right away get what?

A

palliative procedure to improve systemic saturation and encourage pulmonary growth; either modified Blalock-Taussig shunt or balloon pulm valvuloplasty

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64
Q

TGA

A

aorta arises from the RV and pulm art from the LV; in order to live, you must also have a VSD, ASD, PFO or PDA

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65
Q

physical exam in TGA

A

central cyanosis, single S2 and no murmur

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66
Q

management of TGA

A

initial management with PGE to improve ox sat by keeping the ductus patent; or emergent balloon atrial septostomy (rashkind procedure) that incr size of PFO or ASD

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67
Q

definitive repair of TGA

A

arterial switch operation; coronaries must also be incised and reimplanted

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68
Q

tricuspid atresia

A

plate of tissue on the floor of the right atrium; ASD or PFO is always present; whether or not a vsd is present determines the direction of blood flow

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69
Q

clinical signs of pulm atresia

A

single S2 (if intacts ventricular septum)

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70
Q

ECG finding in tricsupid atresia

A

left axis deviation, LVH, and right atrial enlargmenet

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71
Q

fontan procedure

A

flow from the IVC is directed into the pulm arteries; treatment for tricuspid atresia

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72
Q

glenn shunt

A

SVC is anastamosed to the right pulm artery

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73
Q

treatment for tricuspid atresia

A

glenn shunt and then fontan

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74
Q

truncus arteriosus

A

aorta and pulm artery originate from a common artery, the truncus; vsd is almost always present

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75
Q

pathophys of truncus

A

excessive blood flow to the lungs and CHF commonly develops; mixing of desat and sat blood occurs in the truncus so patients are mildly desat and sometimes cyanotic

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76
Q

murmur in truncus

A

systolic ejection mumur at the base from incr flow across the truncal vale; single S2; diastolic murmur across the mitral due to excessive pulm lood flow that returns to the LA

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77
Q

total anomalous pulm venous connection

A

pulm veins drain into the systemic venous side instead of the LA;

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78
Q

murmur in TAPVC

A

pulm murmur due to incr pulm blood flow

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79
Q

cardiomegaly with a snowman appearance

A

total anomalous pulm venous connection

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80
Q

most common cause of acquired heart disease in children in the US

A

kawasaki disease

81
Q

most common cause of acquired heart disease worldwide

A

acute rheumatic fever

82
Q

infective endocarditis

A

microbial infection of the endocardium (inside surface of the heart)

83
Q

most endocarditis occurs in who?

A

80% in kids with anatomic defects of the heart; 50% of cases occur after cardiac surgery

84
Q

bacteria that cause endocarditis

A

gram pos cocci (alpha hemolytic staph and strep)

85
Q

rare causes of endocarditis

A

gram net and funghi

86
Q

diagnosis of endocarditis

A

blood culture and ESR elevated

87
Q

splinter hemorrhages

A

linear hemorrhages beneath the nails, seen in endocarditis

88
Q

retinal hemorrhage

A

seen in endocarditis

89
Q

osler’s nodes

A

small, raised pink or blue swollen tender lesions on the palms, soles, or pads of the toes or fingers; sign of endocarditis

90
Q

janeway lesions

A

small erythematous hemorrhagic lesions on the palms or soles; sign of endocarditis

91
Q

roth’s spots

A

ound or oval white spots seen in the retina; sign of endocarditis

92
Q

rheumatoid factor

A

found in 50% of patients with endocarditis

93
Q

how to see vegetations?

A

transesophageal echo is more sens than transthoracic echo

94
Q

management of endocarditis

A

IV anitbmicrobials fr 4-6 weeks; not a medical emergency, so therapy can be withheld until you do cultures

95
Q

who should get antibiotic prophylaxis for endocarditis for surgery?

A

al patients with structural heart disease except secundum ASD; all post-op cardiac surgery patients for 6 months; all post-op cardiac surgerypatients for an indefinite pd of time if any hemodynamic residua of the lesion remain

96
Q

pericarditis

A

inflamm of the pericardial space

97
Q

causes of pericarditis

A

infection, collagen vascular disease, uremia, and inflamm response after cardiac surgery

98
Q

most common cause of pericarditis in kids

A

viruses like coxsackievirus, echovirus, adenovirus, influenza, parainfluenza, and EBV

99
Q

purulent pericarditis

A

usually caused by bacterial infection like staph aureus and strep pneumo

100
Q

patients with purulent pericarditis have a high incidence of what?

A

constrictive pericarditis

101
Q

postpericardiotomy syndrome

A

occurs in up to 1/3 of patients whose pericardium has been opened for surgery; thought to be an autoimmune response to viral infx

102
Q

possible consequence of pericarditis

A

cardiac tamponade

103
Q

chest pain in pericardits?

A

most intense when supine and relieved when sitting upright

104
Q

physical exam findingsin pericarditis

A

friction rub, distant heart sounds if effusion is large, pulsus paradoxus, hepatomegaly

105
Q

rub

A

pericarditis or MI

106
Q

pulsus paradoxus

A

abnormally large decrease in systolic bp during inspir

107
Q

ecg in pericarditis MAY show

A

ST changes or low-voltage qrs complexes in patients with pericardial effusion

108
Q

treatment for bacterial or viral pericarditis?

A

antibiotics or steroids/aspirin

109
Q

myocarditis

A

common cause of sudden death in young athletes

110
Q

etiology of myocarditis

A

viruses, esp enterovirus like coxsackievirus; bacteria, fungi, protozoa, autoimmune disease, kawasaki disease

111
Q

bacteria that cause myocarditis

A

diptheria, strep pyogenes, staph aureus, tuberculosis

112
Q

symptoms of myocarditis

A

resting tachycardia and muffled heart sounds;

113
Q

labs in myocarditis

A

elevated ESR, creatinine kinase MB fraction, and CRP

114
Q

management of myocarditis

A

largely supportive; use of ionotropes, etc. as needed; heart transplant as last resort

115
Q

prognosis of myocarditis

A

variable; mortality 10-20% and is esp high in young infants and those with ventricular dysrhythmias

116
Q

most common cause of dilated cardiomyopathy

A

idiopathic

117
Q

other causes of cardiomopathy

A

viral myocarditis, mitochondrial abnormalities, carnitine def, nutritional def (selenium and thiamine), hypocalcemia, chronic tachydysrhythmia, anomalous origin of left coronary artery from the pulm artery (ALCAPA), meds (doxorubicin)

118
Q

eval of cardiomyopathy

A

viral serologies and serum carnitine

119
Q

ALCAPA can cause what?

A

infarction

120
Q

hypertrophic cardiomyopathy

A

LVH in the absence of any disease known to cause it; most typical finidng is asymm septal hypertrophy

121
Q

inheritance of hypertrophic cardiomyopathy

A

aut do n most cases

122
Q

most common cause of sudden death in athletes

A

hypertrophic cardiomyopathy

123
Q

phys exam findings for hypertrophic cardiomyopathy

A

harsh systolic ejection murmur at the apex that is accentuated with maneuvers that reduce LV volume like valsalva or standing (by reducing LV volume, they worsen the outflow obstruction)

124
Q

findings on ECG for hypertrophic cardiomyopathy

A

LVH, ST-seg and T wave changes, LAD and abnormally deep and wide Q waves in the inferior and lateral leads

125
Q

management of hypertrophic cardiomyopathy

A

only treat patients w symptoms; beta blockers of CCBs reduce the LVOT obstruction; surgical myomectomy; antiarrhythmic medications; dual chamber pacing; participation in competitive sports prohibited

126
Q

restrictive cardiomyopathy

A

rigid ventricular walls that impair normal diastolic filling

127
Q

etiology of restrictive cardiomyopathy

A

amyloidosis,inherited infiltrative disorders like Fabry disease, Gaucher disease, hemosiderosis, hemochromatosis

128
Q

physical exam findings in restrictive cardiomyopahty

A

elevated central venous pressure leads to edema, hepatomegaly, and ascites

129
Q

management of restrictive cardiomyopathy

A

reduce CVP with diuretics and improve diastolic compliance with beta blockers and CCBs

130
Q

most common dysrhythmias of childhood

A

supraventricular tachy (most common), then heart block, and long QT syndrome

131
Q

AV re-entrant tachycardia

A

retrograde conduction through an accessory path leads to SVT

132
Q

AV node reentrant tachycardia

A

conduction abnormality occurs in diff pways within the AV node itself

133
Q

Wolf-Parkinson white syndrome

A

when anterograde conduction occures through a bypass tract between the atria and ventricles

134
Q

WPW associated with what?

A

sudden cardiac death

135
Q

WPW on ecg?

A

delta wave (upslope of QRS with a short PR)

136
Q

management of SVT

A

vagal maneuvers, IV adenosine, synchronized cardioversion, chronic med management, radiofrequency catheter ablation

137
Q

vagal manuever that helps convert SVT to sinus rhythm

A

ice pack on face

138
Q

primary med used to convert SVT to sinus rhythm

A

IV adenosine

139
Q

chronic medical management of SVT

A

digoxin or propanolol

140
Q

radiofrequency cathether ablation

A

used to destroy the accessory pway in SVT

141
Q

heart blcok

A

delayed or interrupted conduction of sinus or atrial impulses to the ventricles

142
Q

first degree heart block

A

prolongation of the PR interval

143
Q

second degree AV block

A

type 1 and type 2

144
Q

type 1 second degree AV block

A

aka wenkebach; progressive prolongation of the PR interval leading to failed AV conduction

145
Q

type 2 second degree AV block

A

abrupt failure of AV conduction without progressive prolongation of the PR interval

146
Q

third degree av block

A

complete block

147
Q

congenital third-degree block associated with what patient pop?

A

children born to mothers with SLE

148
Q

post-surgical AV block

A

as a result of cardiac surgery

149
Q

what infection may be associated with AV block?

A

bacterial endocarditis

150
Q

treatment of asymp AV block

A

cardiac pacemaker

151
Q

why is long QT bad?

A

increases the risk of lethal ventricular arrhythmias known as torsades de pointes

152
Q

different inheritance patterns of long qt syndrome

A

autosomal recessive is jervell-lang-nielsen syndrome; autosomal dom is romano-ward syndrome

153
Q

which cause of long qt is associated with congenital deafness

A

jervell-lange-nielson

154
Q

examples of drugs that prolong qt interval

A

phenothiazines, tricyclic antidepressants, erythromycin, tefenadine

155
Q

phenothiazine

A

antipsychotic

156
Q

terfenedine

A

antihistamine

157
Q

most common cause of chest painin kids

A

pericarditis

158
Q

rapid heart rate w absent p waves

A

superventricular tachycardia

159
Q

difference between vesicles and pustules

A

vesicles are fluid filled and pustules are purulent filled

160
Q

cyst

A

nodule filled with expressible material

161
Q

wheals

A

cutaneous elevations caused by dermal edema

162
Q

excoriations

A

linear erosions into the epidermis caused by fingernail scratches

163
Q

fissures

A

linear cracks into the dermis

164
Q

annular

A

configurated in a circle

165
Q

arcuate

A

in half circles

166
Q

distributions

A

generalized, acral (hands, feet, buttocks), confined to a dermatme

167
Q

how can we identify fungal hyphae

A

add 10% koh

168
Q

how do we identify scabies

A

examine under a microscope looking for mites, eggs, or feces

169
Q

absorption through the skin of a kid

A

same as through the skin of an adult except premature infants because they have a thinner stratum corneum

170
Q

hyperkeratosis

A

thickened skin

171
Q

keratolytis

A

salicylic acids, urea, alpha hydroxy acids, and retinoic acid

172
Q

destructive therapies (for warts, molluscum contagiosum)

A

high dose salicylic acid, podophyllin, 5-FU, cryotherapy, electrotherapy, and laser therapy

173
Q

only low dose corticosteroids should be used where?why?

A

face and groin because these areas have thinner skin

174
Q

local side effects of steroids

A

acne, hirsutism, folliculitis, striae (esp in axilla or groin), hyper- or hypopigmentation, atrophy, ecchymoses and telangiectasias, tachyphylaxis

175
Q

tacrolimus ointment

A

immunomodulator used for atopic dermatitis

176
Q

one to five percent sulfur

A

formulated with other meds, used for acne

177
Q

tar

A

used for eczema and psoriasis

178
Q

contact dermatitis

A

inflamm of the epidermis and superficial dermis secondary to direct contact with the skin by a sensitizing substance

179
Q

two types of contact dermatitis

A

allergic contact dermatitis and primary irritant contacst dermatitis

180
Q

allergic contact dermatitis

A

T cell mediated

181
Q

common causes of allergic dermatitis

A

poison ivy, oak or sumac; nickel containing jewelry and belt buckles; topical lotions and creams, perfumes, soap

182
Q

clincial features of allergic dermatitis

A

erythematous papules and vesicles

183
Q

treatment of allergic dermatitis

A

topical steroids

184
Q

primary irritiant contact dermatiits

A

substance irritates the skin (not an allergic reaction); reaction is dose-dependent unlike allergic dermatitis

185
Q

most common type of primary irritant dermatitis

A

diaper dermatitis

186
Q

secondary infection with what on diaper dermatitis?

A

candida albicans

187
Q

clinical features of diaper dermaitis

A

erythema with papules on the upper thighs, buttocks, and genitourinary area WITHOUT involvement of the inguinal creases

188
Q

involvement of the inguinal creases may suggest what

A

candida superinfection

189
Q

seborrheic dermaitits predominantly affects who?

A

infants and adolescnets

190
Q

seborrheic dermatitis

A

cause unknown maybe due to a yeast that lives in areas that overproduce sebum;

191
Q

clinical features of seborrheic dermatitis

A

red scales and crust in areas with high numbers of sebaceous glands (scalp, face, chest, groin); skin lesions may be greasy

192
Q

seborrheic capitus

A

aka cradle cap dermatitis limited to the scalp

193
Q

management of seborrheic dermatitis

A

low potency topical steroids, anti-fungals, sulfur, zinc, or salycilic acid shampoos

194
Q

ptyriasis rosea

A

uncommon before 5 years old but extremely common in late childhood and adolescence

195
Q

atopic dermaitits

A

aka eczema

196
Q

clinical features of pityriasis rosea

A

malaise/ache, then solitary large red lesion (herald patch) on the trunk or upper extremities present for 1-30 days; THEN oval red macules and papules erupt for 3-6 weeks from chin to midthigh in christmas tree distrib

197
Q

are pityriasis rosea lesions pruritic?

A

in about 50% of cases

198
Q

managemnet of pityriasis rosea

A

topical or systemic antihistamines; exposure to UV light may shorten the disease course

199
Q

psoriasis in kids?

A

way more common in adults

Peds (99 decks)

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