Chlamydia trachomatis - NGU
5) Thorotrast is associated with TCC though. I guess cholangio would also make sense.
9) Did you mean Hodgkin's, not NHL? RS cells are Hodgkin's.
Chlamydia is more likely
And i would add tb in differential
& neisseria gono as well.
I think Neisseria would show up on Gram stain because it's not intracellular... Chlamydia from sexual abuse.
Right.
One last question from me (again remembered from that book I mentioned before):
A farmer from Indiana presents to you with a 1 cm coin shaped lesion on the upper lobe of his right lung that appears calcified on a routine follow-up xray. The lesion hasn't grown in the past one year based on his previous xrays. He doesn't abuse drugs, take alcohol or even smoke. How will you treat him?
Farmer has Histoplasmosis and needs to be treated with Amphoteracin B?
A 3-week-old infant has milk intolerance due to a defect in the enzymes that digest lactose. This enzyme is located at which of the following sites in enterocytes?
A) At the apical surfaces
B) At the basolateral surfaces
C) Within the Golgi complex
D) Within lysosomes
E) Within peroxisomes
I guess its A
As far as i remember only monosaccharides can enter enterocytes
I think Neisseria would show up on Gram stain because it's not intracellular... Chlamydia from sexual abuse.
How is sterile pyuria defined ? as non-stainable with ordinary gram stains or as culture negative ?
Pathoma states that it wouldn't show up on gram stain...
Then I think that's a mistake in pathoma although Gram stain isn't 100% sensitive or specific for gonorrhea, especially in women, which is maybe what Dr. Sattar meant
A male infant has low Apgar scores following birth by C-section at 30 weeks gestation. Increasing respiratory distress in the next hour requires intubation and positive pressure ventilation. Two months later, the infant is finally taken off the ventilator, but still does not oxygenate normally.
1. Why did the premature baby experience respiratory distress?
2. What laboratory test indicates neonatal lung maturity?
3. What are two chemical factors that contribute to this lung maturity? Why did the C-section contribute to a lack of one of those factors?
4. What is a chemical factor that inhibits fetal lung maturity (not revelent to this question stem)?
5. Why is the neonate not oxygenating normally even after recovering from the initial problem and being taken off the ventilator after two months? What is the pathophys behind this?
5 m/o male baby is brought in due to weakness, lethargy, and vomiting. Blood levels revealed hypoglycemia, increased levels of ammonia, and no ketone bodies.
1. What is the Dx?
2. Why is this condition normally asymptomatic in the first few months?
3. What else can you find in the blood that is very characteristic of the disease?
4. Treatment? Although this is steeping into the Step 2 boundaries I guess, we can skip it.
1. Low surfactant
2. Lecithin:Sphingomyelin ratio <2
3. Cortisol, Epinephrine? C-section = no stress on the baby, thus no release of Epi
4. Insulin (?)
5. Bronchopulmonary dysplasia. Prolonged intubation / ventilation with high pressures and high O2 concentration --> O2 free radicals that damage the lung tissue
Quite a confusing question to me. My D/Ds in the order of preference:
1. Carnitine Acyltranferease I deficiency
2. Acyl CoA Dehydrogenase deficiency
3. OTC deficiency (hypoglycemia due to general lethargy and refusal to feed)
Which one is it and why?
If it is 1 or 2, dicarboxylic acid increases causing acidosis. If 3, orotic acid is seen.
EDIT: I suspect the male baby portion is to point towards XLR OTC, and no ketone bodies is to r/o PKU, but the other parts of the question like hypoglycemia doesn't fit clearly. Also, all three can present even a few days after birth, if I am not wrong, and can also present late.
The male baby was a distractor you can say, I just stated the sex like most questions would.
1. MCAD Deficiency
2. Newborns are asymptomatic in the first few months due to the frequent feedings.
3. Increased levels of C8-C10 acyl carnitines in the blood is characteristic (builds up and then spills out into the bloodstream)
4. IV glucose, high carb/low fat diet (short chain FA), avoid fasting, etc.
The reason for increased ammonia in the blood is due to the low ATP levels, thus the urea cycle can't run.
No ketone bodies because there is no B-ox of the FA, thus no ketone bodies being generated during the period of "fasting" when the feeds aren't as frequent.
So #2 then. But why not #1?
A four year old boy is brought to the doctor due to a rash he developed on his face after playing outside with his friends. The rash appears erythematous, slightly scaly, and having a butterfly-shaped rash on the cheeks and nose. He has had multiple prior visits to the family physician due to pneumonia and middle ear infections. The boy is short for his age (also LBW upon delivery) and has some peculiar facial characteristics such as a small jaw and a long face.
What is the diagnosis?
Belongs to a category of what syndromes?
Higher predisposition to what?
Wiskott aldrich syndrome
Nothing comes to mind other than that
A four year old boy is brought to the doctor due to a rash he developed on his face after playing outside with his friends. The rash appears erythematous, slightly scaly, and having a butterfly-shaped rash on the cheeks and nose. He has had multiple prior visits to the family physician due to pneumonia and middle ear infections. The boy is short for his age (also LBW upon delivery) and has some peculiar facial characteristics such as a small jaw and a long face.
What is the diagnosis?
Belongs to a category of what syndromes?
Higher predisposition to what?