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she is also volume overloaded. more fluid leads to a decrease in Hematocrit.
I thought PTH increases 1-alpha-hydroxylase which increases levels of 1 ,25?
it's supposed to in the setting of proper kidney fxn
The decrease in GFR leads to decreased delivery of 25 dihydro vit D to the PCT and the decrease in functional renal mass limits production of 1a-hydroxylase. The increase in PO4 also stimulates FGF-23 from bone, which inhibits PO4 reabsorption and 1a-hydroxylase.
I literally got this wrong because I had the font zoomed in and assumed the 1 was on the line above like on uworld when it tries to squish the whole title in the same space x_X
Holy fuck they got me.
They boomed me. The fucking NBME boomed me.
Amen to the PSGN question. They got me on that one. lol
the psgn question is pinting to rapidly proliferating glomerulonephritis b/c the pt has developed acute renal failure within days of the insult
HOLY GOD MY BRAIN FILLED IN THE 1. i had to read this explanation 4 times to finally see 25-hydroxyvitamin D and not 1,25. F U NBME
this bs is prob why the question isnt on step 1 anymore
It’s just canker sores, they come and go. I think in herpes the gingivostomatitis really only happens when you first get infected. After that you just get recurrent cold sores.
Herpes zoster is not the same as herpes simplex virus.
you would see dermatome rash in zoster
cf) Just in case someone wanted to know the causative organism of aphthous ulcers
:The precise cause of canker sores remains unclear, though researchers suspect that a combination of factors contributes to outbreaks, even in the same person.
Unlike cold sores, canker sores are not associated with herpes virus infections.
Herpes Zoster doesnt cause gingivostomatitis. Herpengina can cause vesicular lesion in mouth but happens to children in summer season by entero virus
I'm wondering if this could be a mild case of Behcet syndrome without genital involvement
It sure can be Behcet or Pemphigus if the q provides us with more info. Canker sores just come and go for years with unclear mechanism. Also herpes zoster is shingles by VZV, not HSV1.
Most pictures on google show herpangina being present on the hard palate/throat, while aphthous ulcers are commonly on the lower lip. I think his lack of genital lesions are pointing us away from herpangina.
@sunshinesweetheart wucheria bancrofti shows microfilariae on blood smear. Filariasis in the name is referring to the microfilariae
This is correct. The patient doesn't have pneumonia, but sepsis from her UTI. Sepsis is a known cause of ARDS. ARDS can be due to extra-pulmonary tissue damage that leads to the release of inflammatory mediators, alveolar damage, pulmonary edema, and hyaline membrane formation. The hyaline membranes impair gas exchange and lead to hypoxia.
This makes sense, thanks!
I was able to break it down to diuretic or alcohol use and chose alcohol use under the assumption that the patient's serum Cl- levels were low (90; N = 95-105) since Cl- is also lost with vomiting. Im assuming that it was wrong for me to make the association between alcohol use and vomiting.
@dysdiadochokinesia I think we can rule out alcohol use by looking at our patient's history and demographic. A 16yo girl who is dieting and constantly studying probably isnt getting turnt because 1) alcohol has empty calories (defeats the point of dieting), 2) why would you try to study when you're drunk, 3) where will this 16yo in social isolation get alcohol
Sorry, hyponatremia* right?
I think that it's not ANP because ANP will cause a loss of Na but water will follow (they usually go together), whereas ADH will cause absorption of only water and will cause hyponatremia
except only thought this post getting the question wrong :")
Oops sorry the formatting is confusing: I think that it's not ANP because ANP will cause a loss of Na but water will follow (they usually go together), whereas ADH will cause absorption of only water and will cause hyponatremia.
@mantaray pretty sure you are right and that is the only way to get this question correct. Remembering that Na concentration really is a measure of water balance is key. If the pt is hyponatremic, that just means they have too much water in the blood, which is caused by ADH. If the patient was hypoVOLEMIC, that might mean they are losing too much Na.
This is illustrated by pts with SIADH. They are hyponatremic, but euvolemic, meaning that they have too much water (hyponatremia from the ADH) but their Na balance is ok (due to excretion of Na via ANP/BNP)
We need to be thinking about how heart failure is a condition with a low effective circulating volume. Our patient had an MI and now his heart cant keep up with the volume (low CO), leading to congestion. When congestion occurs, water is pushed into the interstitial spaces and isn't circulating in the arterial system. For that reason, the body ramps up the RAAS and ADH despite an actual increase in body water. This is a non-osmotic release of ADH. At this point plasma sodium levels are determined by relative intake and losses and hyponatremia is common in these patients because of that. Also, ANP and BNP don't hold a candle to the RAAS.
FA P120-122. Immunosuppressants for RA are calcineurin inhibitor (cyclosporine and tacrolimus), 6MP, and TNFa inhibitors (adalimumab,infliximab, etanercept). It is important to distinguish that calcineurin inhibitors block t cell activation by preventing IL-2 transcription, not necessarily block IL-2 action. Sirolimus(rapamycin) blocks IL-2 action but it is used for kidney transplant rejection prophylaxis specifically.
in addition to the above responses, IL 1 antagonists (Anakinra) can be used to treat RA. Anakinra is a recombinant human IL 1 receptor anatagonist but less effective than other treatment modalities.
Prednisone is a glucocorticoid (which inhibits IL-2 synthesis) is already being used with no effect. So TNF-alpha is the next option.
DMARDs: methotrextate, sulfasalazine, hydroxychloroquine, leflunomide, TNF inhibitors, Anti- IL6 (Tocilizumab), JAK inhibitor (Tofacitinib), Rituximab.
You can use cyclosporine and tacrolimus to treat RA, but those aren't first line treatments. DMARDs are used the long term treatment of RA and methotrexate is often started first, and the other drugs are prescribed if methotrexate does not sufficiently control symptoms. None of the other choices listed are a part of DMARD therapy.
you can r/o SMA because as kidneys ascend they get stuck low in the INFERIOR MA (L3 level). So I guess there should be no problem w SMA
I think friability of vascular tissue would indicate in inflammatory process (the one I can think of is strawberry cervix) -- so i think that's why you can rule out choice C.
You can rule out multiple ureters with abnormal courses because the ureteral development relies on the ureteric bud. There will multiple ureters if the ureteric bud divides before it comes in contact with the metanephric blastema. Horseshoe kidneys are simply due to fusion of the lower poles and don't involve the embryonic tissues, so those two processes are not likely related.
Estrogen increases HDL. Testosterone is converted into estrogen. Why doesnt testosterone increase HDL. Why is my logic wrong?
The woman in this vignette has an increased androgen:estrogen ratio, so the effects of testosterone on lipid levels will be greater than those of estrogen on lipid levels. Boards and beyond also states that testosterone causes an increase LDL, decreased HDL, and increase in hematocrit, which is why males with primary hypogonadism can present with anemia and the use of anabolic steroids can present with erythrocytosis.
Nystatin does treat vaginal candidiasis but is TOPICAL.
Nystatin is NOT for esophageal candidiasis, Swish and spit, not swallow.
Me - picks Metronidazole -_-
@thotcandy...actually you can swish and swallow nystatin for esophageal infections (per Sketchy micro candida sketch)
I have seen that on the wards so I hope it works!
and my smartass picks amphp B
Please no one give a poor girl with a yeast infection amphoterrible
No hepatosplenomegaly, ascites, or edema through me off. We that being said, I shied away from cirrhosis. I thought that he showed signed of depression, so I went with the thyroid. But who's to say he isn't injection anabolic steroids?!
The principle is you can get liver dysfunction without having HSM, ascites, etc. Liver disease is on a progressive spectrum.
He likely has hepatitis B/C given his history of intravenous drug use. I believe both can have liver dysfunction but may or may not have ascites, whereas the type of damage we would expect from alcohol that would match this presentation would also show ascites.
For Ascities u need to have portal HTN. Thats a must. (unless exudative cause like Malignancy)
For anyone who needs it; the FA photo is kinda burned into my mind for these questions. NBME has some weird infatuation with this clinical presentation.. FA (2019) Pg: 383 "Cirrhosis and Portal HTN".
@paulkarr the problem was that the FA image was burned into my mind so without no ascites or edema threw me off of cirrhosis.
cirrhosis doesn't present hepatomegaly, instead, the liver could be shrunken.
Cirrhosis (most likely due to alcoholism in this patient) leads to an increase in sex hormone binding globulin, causing a relative increase in estrogen compared to androgens. Cirrhosis doesn't always have to present with ascites and adema. I agree with @catch-22 that liver disease is a spectrum. This patient does not have ascites because his liver is still able to produce enough albumin to maintain oncotic pressure in the blood.
Exactly!! it's an autosomal dominate disease!
Autosomal dominant diseases are variably expressive. Still, I think this was a badly written question (should have given us some family history).
Also, FA says that fractures may occur during the birthing process, which is what I believe they were going for. I don't believe these findings would be seen at birth with any of the other choices.
Yeah I thought I outsmarted NBME by selecting Rickets bc it said no family history ... guess I got played lol.
Could it be a sporadic cases? Spontaneous Mutation
This is a change in a gene that occurs without an obvious cause, in a family where there is no history of the particular gene mutation. OI is inherited as an autosomal dominant trait. Approximately 35% of cases have no family history and are called "sporadic" cases. In sporadic cases, OI is believed to result from a spontaneous new mutation.
Amboss says the severe subtypes (types II, III) of OI are usually due to a new (sporadic) mutation in COL1A1 or COL1A2, while patients with the mild forms (types I, IV) typically have a parent with the condition.