Mehl. bullet cases 8 CARDIO (UW dalies ner) Flashcards
Cardio Hy + pathologies resembling cardio path
M. Q will give a post-term birth at 42 or 43 weeks + meconium-stained fluid + echo of the neonate shows a R -> L shunt across the foramen ovale. Dx, mechanism?
Persistent fetal hypertension
Answer on USMLE will be “failure of pulmonary vasodilation.”
M. If they tell you a kid is born with normal APGAR scores but a week later becomes cyanotic and they ask why, the answer is??
“closure of ductus arteriosus.”
M. PDA Tx?
Indomethacin (NSAID) will close the PDA
M. you get tricuspid regurgitation, first though about the cause?
pulmonary hypertension or cor pulmonale
M. when neonate is exposed to too much oxygen at birth, usually while in ICU and/or on home oxygen, followed by development of fibrotic lung disease -> backs up to right heart.
Dx?
Bronchopulmonary dysplasia can cause cor pulmonale in infants on NBME.
M. Bicuspid valve can present with AS murmur in child or high schooler.
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M. The bounding pulses can be described on NBME as “brisk upstroke with precipitous downstroke.” In turn, they can just simply say, “the pulses are brisk,” meaning the systolic component is strong. Dx?
Aortic regurgitation.
M. I would say 4/5 times bounding pulses means AR. The other 1/5 will be PDA and AV fistulae (discussed below). Bounding pulses occur when blood quickly leaves the arterial circulation. In AR, the blood quickly collapses out of the aorta back into the LV. In PDA, it leaves the aorta and enters the ductus arteriosus; in AV fistulae, it leaves for a vein.
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M. Marfan and Ehlers-Danlos -> aortic dissection -> what valve dysfunction?
A. regurg
M. Peds shelf can give you random 2-year-old with robust decrescendo diastolic murmur = Dx?
Aortic regurgitation
Student says, “What’s causing it though?” Great question. It’s still what shelf will do. You could be aware that congenital bicuspid valve also can cause AR in peds, not just AS.
M. One 2CK NBME Q mentions patient with history of rheumatic heart disease who, years later, now has 4/6 rumbling diastolic murmur without an opening snap; Dx?
this is still mitral stenosis. Although opening snap is buzzy for MS, just be aware it’s not mandatory and that this Q exists on NBME.
M. MVP.
On 2CK forms, they want you to know about “mitral valve prolapse syndrome,” which is symptomatic MVP that presents as repeated episodes of “fleeting chest pain” on the left side in an otherwise healthy patient 20s-30s, sometimes starting in teenage years. They might say there is Hx of MI in the family, but this is MVPS, not MI. Answer on 2CK form is “no treatment necessary.”
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M. MVP. USMLE loves using MVP as a distractor in panic disorder questions, particularly on the 2CK Pysch CMS forms. They will give long paragraph about panic attack/disorder + also mention there’s a mid-systolic click; they’ll ask for cause of patient’s presentation -> answer = panic disorder, not MVP -> student is confused because they say mid-systolic click, but the MVP isn’t the cause of the patient’s presentation; the panic disorder is; MVP’s are usually incidental, benign, and asymptomatic.
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M. They’ll give you a 17-yr-old male who feels doom / like he’s going to die. Dx?
Panic attack
M. Panicattack - Sometimes they mention in stem Hx of MI in family as distraction.
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M. Panic attack Tx?
benzodiazepines
M. They can say patient has mid-systolic click and then they ask for cause of patient’s symptoms. Dx?
answer = panic disorder, not MVP.
Student gets confused, but MVP is almost always asymptomatic, where panic attack is clearly cause of the patient effusively hyperventilating.
M. Vasovagal syncope. how to Dx?
2CK wants you to know a tilt-table test can be used to diagnose, where a reproduction of symptoms can occur.
M. Will present as chest pain that worsens with palpation or when patient reaches over the head or behind the back. Dx?
M. Costochondritis.
M. They’ll say 3-year-old was having a tantrum followed by falling on the floor + appearing blue. Dx?
Breath-holding spell.
NBME 10. 200Q.
A 3-month-old boy is brought to the physician for evaluation of delayed growth. He was born at term following an uncomplicated pregnancy and delivery. There was no cyanosis at birth. His mother says that he feeds poorly and turns blue around the lips and fingers during feedings. He frequently cries and becomes restless, short of breath, and cyanotic. He is at the 20th percentile for length and 10th percentile for weight. During the examination, he has paroxysms of crying during which he becomes cyanotic; his color is normal at rest. A grade 3/6, systolic ejection murmur is heard at the left sternal border. Which of the following is the most likely diagnosis?
Tetralogy of Fallot
M. 7F + seizure-like episode + during episode, ECG shows P waves at 80bpm but not QRS complexes + normal sinus rhythm resumes after 20 seconds + patient fully alert after one minute; Dx?
on Peds NBME = Adam-Stokes attack -> not true seizure disorder as per EEG; arrythmia leads to hypoxia of brainstem -> seizure-like fits ensue.
M. 8M + low-pitched vibratory murmur heard throughout cardiac cycle + loudest at left upper sternal border when sitting + murmur disappears when supine and neck rotated; Dx?
answer on Peds NBME = venous hum
benign/innocent pediatric murmur that will disappear as child grows; caused by turbulent venous return in SVC and jugular veins.
M. Neonate with APGARs good at birth + 3-10 days later has BP 60/35 in upper extremities and unobtainable in lower extremities + O2 sats 98 mmHg but nails appear dusky + 3/6 holosystolic murmur at left sternal border; Q asks what’s responsible for current presentation?
Dx?
“closure of ductus arteriosus”
Dx = preductal coarctation (the type seen in neonates); CoA can be associated with tricuspid regurgitation and other cardiac abnormalities. Dusky nailbeds don’t equate to cyanosis if O2 sats are normal.
M. 7-day-old neonate + not cyanotic + 4/6 holosystolic murmur at left sternal border + murmur was not present (or soft) at birth; what best explains the current presentation?
“decreased pulmonary vascular resistance”; this is a VSD with L->R shunt; pulmonary vessels have gradually opened up over first week of life as ductus arteriosus closes; the decrease in pulmonary vascular resistance causes decr. right-heart pressure -> enables a favorable L->R pressure gradient for the VSD murmur to become more salient; lack of cyanosis means there is no R->L shunt + Eisenmenger wouldn’t occur till later in life anyway.
M. 5-day-old neonate + not cyanotic + 3/6 holosystolic murmur at left sternal border + murmur was not present (or soft) at birth; what best explains the child’s presentation at birth?
increased pulmonary vascular resistance”;
lungs still hadn’t opened up so VSD L->R pressure gradient was not yet conducive to salient murmur; Peds shelf asks both versions of this question (i.e., increased vs decreased pulmonary vascular resistance as answers).
M. 14F + Down syndrome + polycythemia + moderate cyanosis and digital clubbing + no murmur on cardio exam but loud S2 + echo shows large VSD and dilated main pulmonary artery; mechanism for polycythemia?
Dx?
Pulmonary artery hypertension”;
Dx is Eisenmenger (large VSD with reversal R->L); large VSDs may present without murmur; pulmonary vessels constrict to compensate for high preload from previous L->R VSD shunt; constriction leads to hypoxia and secondary polycythemia with high EPO; should also be noted that Down syndrome is associated with endocardial cushion defects (AVSD > VSD > ASD; Step 1).
M. Neonate + pulmonary valvular stenosis; Dx
Noonan syndrome; second most common syndrome associated with congenital heart disease after Down.
M. 2-month-old boy + not cyanotic + to-and-fro murmur; Dx?
“extracardiac left-to-right shunt”;
Dx = PDA.
M. Four ways PDA sounds on Peds shelf. 1
ontinuous, machinery-like murmur (easy; the one everyone knows).
M. Four ways PDA sounds on Peds shelf. 2
Pan-systolic-pan-diastolic (if it’s continuous, then it’s present throughout cardiac cycle).
M. Four ways PDA sounds on Peds shelf. 3 To-and-fro murmur.
(student says wtf?àHY; also on NBME 6 for 2CK, where the Q rides on
you specifically knowing the description).
M. Four ways PDA sounds on Peds shelf. 4 !!!!!!!!
!!!!!!!!!!Bounding pulses (normally refers to aortic regurg, but also a rare descriptor for PDA -> blood leaves aorta quickly L->R);
in this scenario, the Q will say there’s a continuous murmur with bounding pulses; in contrast, AR is a decrescendo holodiastolic murmur.
M. 2-month-old boy + fixed splitting of S2; Dx?
patent foramen ovale (ASD).
M. Heart problem in neonate of mom with SLE?
congenital third-degree heart-block.
M. Bicuspid aortic valve; most likely to cause which murmur?
aortic stenosis.
M. Mid-systolic (crescendo-decrescendo) murmur + gets worse with Valsalva? Dx
HOCM.
M. Mid-systolic (crescendo-decrescendo) murmur + no change or softens with Valsalva?
aortic stenosis.
M. Myxomatous degeneration of mitral valve?
mitral valve prolapse (MVP).
M. Mid-systolic click? Dx?
MVP
M. Marfan or Ehlers-Danlos syndrome; heart murmur(s)?
MVP or aortic regurg.
M. Late-peaking systolic murmur with ejection click?
another way they describe aortic stenosis.
M. 2-week-old girl + HR of 240 + QRS duration of 50ms + no P waves + awake and alert + ice pack to the
face does not change the HR; next best step?
Dx?
adenosine; Dx is paroxysmal supraventricular tachycardia (PSVT); complexes are needle-shaped (short QRS); in contrast, ventricular tachycardia has wide complexes (>120ms).
M. 10-month-old girl + sore throat for 2 days + fever 101F + S3 gallop heard on auscultation; what best explains these findings?
myocarditis (rheumatic fever);
should be noted that PSGN will take 1-2 weeks to occur after Group A Strep infection, but NBME has RF occurring as early as 2 days after the Strep pharyngitis; type II hypersensitivity via molecular mimicry with Group A Strep M protein (Step 1);
M. 10-month-old girl + sore throat for 2 days + fever 101F + S3 gallop heard on auscultation; Tx?
Tx with penicillin
