need help with your account or subscription? click here to email us (or see the contact page)
join telegramNEW! discord
jump to exam page:
search for anything ⋅ score predictor (โ€œpredict me!โ€)

NBME 21 Answers

nbme21/Block 1/Question#41 (reveal difficulty score)
A 35-year-old woman comes to the physician ...
Uroporphyrinogen decarboxylase ๐Ÿ” / ๐Ÿ“บ / ๐ŸŒณ / ๐Ÿ“–
tags:

 Login (or register) to see more


 +12  upvote downvote
submitted by โˆ—neonem(629)
get full access to all contentpick a username

This is a case of porphyria cutanea tarda. The way I remember this is that it's the only high-yield porphyria that has skin manifestations due to UV. I remember this by "After U (uroporphyrin), it's UV". Apparently it's also associated with Hepatitis C, which could be the reason why there's increased AST & ALT, or it could be due to toxic buildup of intermediates in heme synthesis.

get full access to all contentpick a username
meningitis  Why cant it be protoporphyrinogen oxidase? It was because of that reason (Increased AST and ALT) I thought it wasnt uroporphyrinogen decarb. My train of thought was: "wow, mitochondria are messed up.. there must be a lot of intermediates in there,therefore the Uroporph decarb must OK." +
arlenieeweenie  FA 2019 pg. 417, the later on the defect in the heme synthesis pathway is the one more associated with skin findings! Also according to this year's edition uroporphyrinogen synthase is now known as prophobilinogen deaminase +9
nobody  AMBOSS has estrogen therapy listed as a susceptibility factor for PCT. I could not find a link between elevated AST/ALT and estrogen therapy that would occur 15 years into treatment. +



 +3  upvote downvote
submitted by โˆ—h0odtime(54)
get full access to all contentpick a username

Heme Mnemonics

  • Sideroblastic Anemia - ALAS (Ends in S = Sideroblastic)
  • Lead Poisoning - ALAD & Ferrochelatase. (ALeAD, FerrocheLEADtase)
  • Cytoplasmic Intermediates: Purposefully (PBD) Hold 3Urine (UPD) Cups
  • Porphobilinogen PBD โ†’ Hydroxymethylbilane โ†’ Uroporphyrinogen 3 UPD โ†’ Copropohyrinogen 3
get full access to all contentpick a username



 +2  upvote downvote
submitted by โˆ—divya(75)
get full access to all contentpick a username

The porphyrinogens following PBG conversion into Uroporphryinogen 3 cause photosensitivity because ONLY these react with oxygen on excitation by UV light.

Therefore deficiency of any of the following enzymes -

uroporphyrinogen decarboxylase coproporphyrinogen oxidase, proporphyrinogen oxidase and ferrrochelatase can cause photosensitivity.

But between answer choices B & C, C is right because of it's association with Hep C, raised AST ALT as @neonem said.

get full access to all contentpick a username



 +0  upvote downvote
submitted by โˆ—nwinkelmann(366)
get full access to all contentpick a username

If you struggle with Biochem and haven't heard of Moof Universitry, I would highly recommend checking it out. The below information I got from this video: https://courses.moofuniversity.com/courses/take/medical-biochemistry-for-usmle-step-1-exam/lessons/4363869-porphyrias-porphyria-cutanea-tarda-pct and it's great.

Porphryia cutanea tarda = AD mutation of uroporphyrinogen decarboxylase, this is the MCC of porphyria, and it presents in 40s-50s.

Main symptom of photosensitivity leading to skin lesions/blisters/bullae due to skin porphyrinogens being oxidized by light to prophryins that damage the skin, and other skin findings of hypertrichosis/hyperpigmentation.

A key feature is possible liver problems due to associated precipitating factors. MCC precipitating factors = excessive EtOH and OCPs because of CYP450 inducers reducing serum heme levels to be utilized in the new CYP450 enzymes, thus stimulating ALA synthase due to decreased heme inhibition. Other precipitating factors include viral hepatitis, especially hepatitis C, and excess iron as in hemochromatosis. These can lead to elevated AST and ALT levels.

Another sign is dark "port-wine" colored urine which pink fluoresces under Wood light. Absent symptoms = abdominal pain and CNS problems because ALA and PBG do not accumulate. Accumulated products = uroporphyrin III, uroporphyrinogen III, uroporphyrin I, and uroporphyrinogen I.

Treatment = sun exposure avoidance, removal of precipitating factors, phlebotomy, chloroquine (which can bind and lead to excretion of accumulations). Prognosis = excellent.

get full access to all contentpick a username



 +0  upvote downvote
submitted by euphoria(1)
get full access to all contentpick a username

OCPs is associated with Porphyria cutanea tarda as well. in the stem the patient was on OCPs for 15 years.!

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1947755/

https://porphyria.eu/sv/content/hormonal-contraception

get full access to all contentpick a username



Must-See Comments from nbme21

nosancuck on Absorption atelectasis
assoplasty on Free T4
seagull on GM2
lnsetick on Apocrine
niboonsh on NMDA receptors are blocked by Mg2+ at the ...
drdoom on Deletion of a hydrophobic amino acid ...
hayayah on HCO3โˆ’ transported in the plasma
mcl on Aortic
notadoctor on Usual interstitial pneumonitis
madojo on Genital herpes
hungrybox on Obstruction of the bile duct
jambo2222 on Lung
hungrybox on Mismatch repair
hungrybox on Hydrochlorothiazide

search for anything NEW!