The effects of excess thyroid hormone: attempted compensatory TSH suppression, increase in both T4 and free T4, and normal TBG. Note that the question doesn’t even hinge on TBG and is also unlikely to on the real thing.

Splitting is an immature defense mechanism often employed by patients with borderline personality disorder. When splitting, a person fails to see others as capable of having both positive and negative qualities; at any given time, it’s all or nothing.

Stroke characterized by left hemiparesis and right CN12 palsy. Crossed findings mean a brainstem lesion. Right (ipsilateral) tongue, left-sided (contralateral) weakness means the exiting right hypoglossal nerve has been affected (within the right medulla). C is the pyramid where the corticospinal tract runs to control muscles (prior to the decussation). This is known as the medial medullary syndrome or Dejerine syndrome.

Air and fluid = hydropneumothorax. If that fluid is blood (s/p stabbing), it’s a hemopneumothorax. Lack of mediastinal shift indicates that it’s not under tension.

Maintenance dose formula is (Css × Cl × tau) ÷ F

where Css is steady-state target plasma conc. of drug, Cl is clearance, tau is dosage interval & F is bioavailability.

Neither dosage interval nor bioavailability is given, so ignoring those & plugging in the numbers (careful to convert units to mg/kg/day):

=(12 ug/mL × 1 mg/1000 ug) × (0.09 L/hr/kg × 1000 mL/1 L × 24 hr/1 day)
= 25.92 mg/kg/day

...which isn't any of the answer choices listed. They must have rounded 0.09 L/hr/kg to 0.1 L/hr/kg, and doing so gives exactly 28.8 mg/kg/day (choice C)

I thought of this as squamous cell carcinoma of the lung causing increased PTHrP and hypercalcemia.

How is this the answer if there is no family history of recurrent fractures? I thought osteogenesis imperfecta was autosomal dominant?

Was it just me, or did "age at onset in years" appear RIGHT above the number of patients, rather than the mean. Which confused me for a good 3 minutes.

Why no sweating? I mean I get Ecstasy is probably the drug of choice before an all night dance party (lol) but don't understand why there would be cold extremities and no sweating when is FA it says hyperthermia and rhabdo????

The way I thought about this question was that in MM there is a TON of antibodies being made, so the VDJ segment is being broken up/selected/rearranged many times and has been shortened to 1.5kb. As for the T Cells, that region isn’t being used (since there is no clonal expansion or selection) so it’s still got the full 6kb length untouched.

out of curiosity, how may people knew this? (dont be shy to say you did or didnt?)

My poverty education didn't ingrain this in me.

Hypopigmented lesions refer to Ash-leaf spots, CNS lesions likely hamartomas . TS also associated with seizures.

Patient has BPH. Give alpha one antagonist to reduce smooth muscle contraction and relieve difficulty urinating.

https://www.youtube.com/watch?v=4-DuvwoH2zQ if ur lazy like me, this is a good refresher video

I just knew that sperm need fructose, not sure what disease process this is though. He was pretty normal so 5a reducatase doesn't present like that. I wasn't sure if there was any odd use of the other answers. here is a link. Feel free to expand.

https://www.labce.com/spg27422_question.aspx

Fructose makes up 99% of the reducing sugar present in semen. This sugar is produced in the seminal vesicles. Diminished levels of fructose have been shown to parallel androgen deficiency and the testosterone level. Following testosterone therapy, the level of fructose increases. Although the fructose test is not part of a routine semen analysis, it is useful in cases of azoospermia (absence of sperm in semen). In azoospermia secondary to the absence of vesicles or if there is an obstruction, no fructose is present. In testicular azoospermia, fructose is present. When azoospermia and low semen volume exists, the fructose test should also be done, on a postejaculate urine sample to check for retrograde ejaculation. This occurs when the ejaculate goes into the bladder instead of out the urethra. The procedure for determining the amount of fructose in semen involves heating semen in a strong acid in the presence of resorcinol. Fructose gives a red color (Selivonoff reaction) and may be read in a photometer. The normal average is 315mg/dL fructose.

the infarct occurred 16 hrs ago, from 12-24hrs after the infarct there will be Red Neurons.

Wernicke-Korsakoff syndrome. Don't have to be an alcoholic to get this, just usually is related to alcoholism / thiamine deficiency.

Needing "higher concentrations" of the B6 for enzyme activity is another way of saying Km is higher since more is required for 1/2 vmax activity. Increased Km values result in 1/Km being smaller (closer to 0 on the x-axis), which is demonstrated in answer choice B.

A "normal" enzyme activity in the presence of higher B6 concentrations means that Vmax is not changing, but Km is.

I think the concept they’re testing is the increased TBG levels in pregnancy, and not just hyperthyroidism in general.

When screening for hypo/hyperthyroidism, TSH levels are ALWAYS preferentially checked because they are more sensitive to minute differences in T3/T4. Often times TSH levels can demonstrate a change even when T3/T4 levels are in the subclinical range. The only exception to this would be in pregnancy (and I guess maybe liver failure? I doubt they would ask this though). High estrogen levels prevents the liver from breaking down TBG, leading to increased TBG levels in the serum. This binds to free T4, decreasing the amount of available free T4. As a compensatory mechanism, TSH levels are transiently increased and the RATE of T4 production is increased to replenish baseline free T4 levels. However the TOTAL amount of T4 is increased.

The question is asking how to confirm hyperthyroidism in a pregnant woman --> you need to check FREE T4 levels (because they should be normal due to compensatory response). You cannot check TSH (usually elevated in pregnancy to compensate for increased TBG), and you cannot check total T4 levels (will be increased). You got the answer right either way but I think this is a different reasoning worth considering, because they can ask this concept in other contexts of hyper-estrogenism, and if they listed “TSH” as an answer choice that would be incorrect.

The obliques do the opposite action of their name. Inferior oblique moves the eye UP and OUT (extortion, elevation, ABduction). Since the question says that there is a fracture involving the orbital floor, that automatically rules out D (medial rectus and inferior oblique), leaving the only logical answer to be the inferior rectus and inferior oblique. https://www.youtube.com/watch?v=lWKkHWWDIEI

lower quadrantanopia: parietal lesion

vs upper quadrantanopia = temporal lesion

This is a postpartum mood disturbance, a pretty common disorder that has to have an onset within 4 weeks of delivery to be termed as such. Postpartum blues is the most mild, with a 50-85% incidence rate (per FA 2018), usually resolves within 10 days and treatment is only supportive but need to follow-up to assess for possible postpartum depression. Postpartum depression = 10-15% rate, characterized by depressed affect, anxiety, poor concentration for greater than 2 weeks and needs to be treated w/ CBT + SSRI. I think the question is getting at screening for this and a potentially more problematic complication, postpartum psychosis.

this is a cervical spinal cord section. the cuneate fasciculus is intact (UE) vibration and proprioception, but the white section is the gracile fasciculus (LE) and is damaged. I think the lateral portion that is uneven is just natural/artifact.

Male internal genitalia -> Intact SRY , testes, and testosterone.

No female internal genitalia -> Presence of MIF (antimullerian hormone) and intact Sertoli cell function.

Female external genitalia -> No androgen present, which is required for male external genitalia formation.

Male internal genitalia -> Intact SRY , testes, and testosterone.

No female internal genitalia -> Presence of MIF (antimullerian hormone) and intact Sertoli cell function.

Female external genitalia -> No androgen present, which is required for male external genitalia formation.

Male internal genitalia -> Intact SRY , testes, and testosterone.

No female internal genitalia -> Presence of MIF (antimullerian hormone) and intact Sertoli cell function.

Female external genitalia -> No androgen present, which is required for male external genitalia formation.