NBME 11 q--Need some medical geniu's help plz. - risenshine

[ArchivalUser]

Just few q:

My q1-

For this q, I was thinking it would be PDA since it says " I was told that she'd grow out of it." Isn't PDA the only one children grow out of as it closes on its own and not the VSD even when the LV/PulA pressure are high? Does VSD also closes on its own too?

I was thinking of from UW:

RA=5
RV=25/5
Pul A=25/10
LA=

[ArchivalUser]

ahhhhh.... it got cut off... this sucks...

From UW:
RA=5
RV=25/5
Pul A=25/10
LA less than 12
LV=130/10
Aorta=130/90

My q2-

what would be the pressure abnormality in ASD and PDA?



here's the NBME 11 q:-----------------------------------------------

A 5-year-old girl is brought to a new physician by her mother for an examination prior to attending kindergarten. Her mother says, "My daughter has a murmur, but I was told that she'd grow out of it." The patient has no history of major medical illness. She is at the 50th percentile for height and weight. A grade 2/6 systolic murmur is heard over the left sternal border. Cardiac catheterization shows:
Location Pressure (mm Hg) O2 Saturation
Aorta 105/60 98%
Vena cava 7/2 75%
Pulmonary artery 25/9 85%
Right atrium 4 75%
Left atrium 8 98%
Right ventricle 25/4 83%
Left ventricle 105/8 98%

The failure of which of the following during embryonic development best explains this patient's condition?

A-Closure of the ductus venosus

B-Closure of the foramen ovale

C-Development of the septum secundum

D-Fusion of the interventricular septum with endocardial cushions

E-Reabsorption of the septum primum

[ArchivalUser]

VSDs do close spontaneously in the first few years of life.
A PDA should not persist beyond the first few years of life unless there is an additional pathology.

So in this case, the murmur at the external border + closure in the first few years of life = VSD

[ArchivalUser]

*murmur at sternal border + closure in the first few years of life = VSD

[ArchivalUser]

Thank you... I didn't know that.

Do you know about this one?

A 65-y-old man undergoes an operation to remve an abdomminal mass. Histologic examination of the mass shows a large number of blood vessels. Further analysis shows an increased concentration of VEGF in the tumor. Which of the following most likely stimulated the production of VEGF in the mass of the patient.

A) Increased endostatin
B) Decreased endostatin
C) Decreased Pco2
D) Decreased Po2
E) Decreased thromboplastin
E) Increased Po2
F) Increased Pco2
G) Increased thrombospondin

[ArchivalUser]

DEC PO2

[ArchivalUser]

Cardio69, can you please explain why that would be it?

[ArchivalUser]

What stimulate VEGF expression? Agents/condition *hypoxia/dec PO2, cytokines, GFs many tgf, tgf, pdgf…
Q give all the story u just hv to glue it together
“tissue hypoxia” in tumor + some solid tumors overexp to survive and the dictator life and become immortal - > abnormal cause of angiogenesis and trigger this heparin binding glycoprotein (VEGF ) -> INC endothelial-> angiogenesis. VEGF transcription has control by HIF.

all my nice stories has something

[ArchivalUser]

Thank you very much, it's hard to get explanation for NBME unless some genius explains it.

I knew tumors such as cardiac rhabdomyoma ( I think this was it) m/c in Right atrium produced VEGF and that's how it grows. I didn't know it produced it in "tissue hypoxia" and by the ones you mentioned. Thank you so much....

What is HIF?

Also, I searched in other forums, some students were talking about endostatin and thromboplastin playing a role in it, but I have never came across these term before or maybe I did and missed it.
Can you please explain them too?