NBME 31. | Notion

Don’t open this file unless you’ve already taken the NBME.

The IDs at the top of each question are taken from elhusseinyusmleprep.com"

First Block.

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220935

Symptoms within minutes of starting a transfusion (headache, shortness of breath, hypotension) point to an acute hemolytic transfusion reaction.
Free hemoglobin in plasma and urine = intravascular hemolysis, a classic finding of ABO incompatibility.
ABO antibodies (IgM) are pre-formed and activate complement, causing rapid RBC lysis.
ABO reactions are the most severe and most common life-threatening transfusion reactions.
Delayed reactions (days–weeks) are usually due to non-ABO antigens, not immediate reactions like this one.

B. Duffy:

Duffy is a minor blood group antigen
Antibodies form after prior exposure (transfusion or pregnancy)
Causes delayed hemolysis (days to weeks later)
Does not cause immediate shock

C. Kell:

Kell is another minor RBC antigen
Antibodies are IgG, not IgM
Causes extravascular hemolysis (spleen/liver)
Reaction is delayed, not within minutes

D. MN:

MN antigens are clinically insignificant
Rarely cause transfusion reactions
Not tested as a cause of severe hemolysis

E. Rh:

Rh antibodies are IgG
Form only after exposure
Cause delayed hemolytic reactions or hemolytic disease of newborn
Not an immediate transfusion emergency

Reaction	Mechanism	Timing after transfusion	Key Findings	Coombs test	Classic vignette clue
Febrile Non-Hemolytic Transfusion Reaction (FNHTR)	Recipient preformed antibodies against donor leukocyte antigens → activation of donor WBCs → cytokine release	Within 1–2 hours	Fever, chills ONLY (no hemolysis)	Negative	Fever + chills shortly after transfusion, otherwise stable
Acute Hemolytic Transfusion Reaction (ABO mismatch)	Recipient anti-A / anti-B antibodies bind donor RBCs → complement activation → intravascular hemolysis	Minutes	Fever, chills, flank pain, hypotension, hemoglobinuria, ↑ LDH	Positive	“10 minutes after transfusion, impending sense of doom”
Delayed Hemolytic Transfusion Reaction	Recipient antibodies against minor RBC antigens (Rh, Kell, Duffy, Kidd) → extravascular hemolysis	Days to 1 week	Gradual ↓ Hb, ↑ unconjugated bilirubin	Positive	Post-op patient with falling Hb days later
TRALI (Transfusion-Related Acute Lung Injury)	Neutrophil priming in lungs + cytokines from transfused blood → non-cardiogenic pulmonary edema	< 6 hours	ARDS-like: hypoxia, bilateral crackles, normal heart	Negative	Acute respiratory failure shortly after transfusion
TACO (Transfusion-Associated Circulatory Overload)	Volume overload → ↑ hydrostatic pressure → cardiogenic pulmonary edema	> 6 hours OR anytime with heart disease	Pulmonary edema, crackles, JVD	Negative	Elderly / HF patient + SOB after multiple transfusions
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220946

Restenosis happens when smooth muscle cells proliferate and grow over the stent, narrowing the artery again.
Paclitaxel is an antiproliferative drug that inhibits cell division.
It works by stabilizing microtubules, preventing cells from completing mitosis.
This effect is strongest on vascular smooth muscle cells, not platelets or endothelium.
By stopping smooth muscle proliferation, paclitaxel reduces neointimal hyperplasia, preventing restenosis.

Drug-eluting stents (paclitaxel, sirolimus) = stop smooth muscle proliferation

Microtubule inhibitor drugs (they love giving one in q and ask which of these works similarly):
- Colchicine (gout)
- Vinca alkaloids (vincristine, vinblastine) – inhibit microtubule formation
- Taxanes (paclitaxel, docetaxel) – hyperstabilize microtubules
- Mebendazole/albendazole – anti-helminthics, inhibit tubulin polymerization
- Griseofulvin – antifungal, disrupts microtubules
A. Enhanced endothelial growth over the stent:

• Faster endothelial healing is helpful but not paclitaxel’s mechanism

• Paclitaxel actually slows cell growth

B. Increased adhesion of the stent to the atheromatous lesion:

• Mechanical attachment is not drug-mediated

• Has nothing to do with paclitaxel

C. Prevention of platelet adhesion to the stent:

• This is the role of antiplatelet drugs (e.g., aspirin, clopidogrel)

• Paclitaxel does not inhibit platelets

E. Stabilization of the cholesterol core:

• This is the role of statins, not paclitaxel

• Unrelated to stent drug coatings

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220950

The patient is 46,XY, so testes are present and testosterone is produced normally.
5α-reductase deficiency means testosterone cannot be converted to dihydrotestosterone (DHT).
DHT is required for development of external male genitalia and the prostate.
Internal male structures (from Wolffian ducts) develop normally because they depend on testosterone, not DHT.
Therefore, the structure most affected is the prostate, which will be hypoplastic or absent.

Testosterone → internal male organs

DHT → prostate + external genitalia

Androgen Insensitivity Syndrome (AIS)

The patient has a 46,XY karyotype with defective androgen receptors.

The testes are present, usually in the abdomen or inguinal canal.

Testosterone levels are normal or elevated due to intact testicular production.

The external genitalia are female because tissues cannot respond to androgens.

Müllerian structures are absent because Sertoli cells produce MIF.

The vagina ends in a blind pouch and secondary sexual hair is sparse or absent.

The condition commonly presents as primary amenorrhea.

Müllerian Inhibiting Factor (MIF) Deficiency

The patient has a 46,XY karyotype with normal testosterone production.

Sertoli cells fail to produce MIF.

Male external genitalia develop normally due to normal androgen action.

Müllerian structures such as the uterus and fallopian tubes are present.

The testes may be undescended and the condition is often found incidentally.

5-Alpha Reductase Deficiency </aside>

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