Welcome to mousie’s page.
Contributor score: 210
Adding on, hoarseness + difficulty swallowing means something is pushing on the recurrent laryngeal.
Murmur in the second right intercostal space = AR, AS, or Pulm regurg --> AR associated with thoracic aortic aneurysm, or at minimum, you can infer it's a cardiac etiology
The dyspnea, dysphagia, stridor, and cough are pretty indicative of a mediastinal mass. So expansion of the aorta can cause compression of the esophagus, trachea, recurrent laryngeal nerve, etc. depending on the severity of it.
Also talked about under liquefactive necrosis on pg. 209 FA 2020
UW: 302 & 9989 are both great for representing/explaining this.
FA says, "euphoria, disinhibition, hyperactivity, distorted sensory and time perception, bruxism.
Lifethreatening effects include hypertension, tachycardia, hyperthermia, hyponatremia, serotonin syndrome."
So I think they wanted you to see Sinus Tachy and jump for MDMA. Idk why Ketamine couldn't also potentially be correct though.
I picked ketamine because it said no diaphoresis. But if you need to find a reason, I guess the half life of ketamine might rule it out. Remember from sketchy, ketamine is used for anaesthesia induction, so probably won't keep the HR and BP high for 8 hrs. In fact, its action is ~10-15 mins-ish iv.
Because the NBME is full of fuckers. The guy is probably dehydrated so he cant sweat anymore?
you wouldnt see tachycardia with ketamine. It causes cardiovascular depression but honestly i saw " all-night dance party" picked the mdma answer and moved on lol
Ketamine acts as a sympathomimetic but oh well. NBME hasn't caught on to ketamine as a drug of recreation :)
@usmleuser007 LSD doesn't cause HTN and ↑ HR.
@fulminant_life FALSE. KETAMINE CAUSES CARDIOVASCULAR STIMULATION.
Take a look at why the patient has pale and cold extremities.
"Mechanistic clinical studies indicate that the MDMA-induced elevations in body temperature in humans partially depend on the MDMA-induced release of norepinephrine and involve enhanced metabolic heat generation and cutaneous vasoconstriction, resulting in impaired heat dissipation."
@sbryant6 you're both saying the same thing. Ketamine has a direct negative inotropic effect on the heart, but it is also a sympathomimetic. You are both correct.
@drzed Can you please site that? As far as I understand ketamine has a sympathomimetic effect on the CV system --> increased chronotropy and BP. I also don't see how they're saying the same thing. One person said "stimulation" and the other said "depression"
People tend to drink a lot of water on MDMA. I just guessed the confusion was a result of hyponatremia (too much free water) but no idea if there's any data saying that people tend to become hyponatremic due to water over-consumption on MDMA lol.
"Despite possessing a direct negative cardiac inotropic effect, ketamine causes dose dependent direct stimulation of the CNS that leads to increased sympathetic nervous system outflow. Consequently, ketamine produces cardiovascular effects that resemble sympathetic nervous system stimulation. Ketamine is associated with increases in systemic and pulmonary blood pressures, heart rate, cardiac output, cardiac work, and myocardial oxygen requirements."(https://www.openanesthesia.org/systemic_effects_of_ketamine/)
LSD does cause HTN and tachycardia according to uworld! @d_holles
Caudal = Bottom of the SC = failure to close = spina bifida and Rostral = top of SC = failure to close = Anencephaly
I'm confused. In first Aid doesn't have meningomyelocele as failure of caudal or rostral pore to close. Is the answer Cadual because in this patient specifically, his condition takes place on L2-5 which is more caudally?
its a neural tube defect aka failure of neural tube closure
They are just asking about side effect of statins, not about treatment of hypothyroidism
Hypothyroidism is just a red herring.
statins cause both hepatotoxic and mypopathy so I want for hepatotoxic:( I thought usmle expects different stuff
Statins don't cause 'toxic hepatitis' they just cause a mild asymptomatic rise in LFTs that is reversible with discontinuation of the drug. The more worrisome side effect is of course, myopathy
statins cause both liver injury and myopathy in a dose related, so kidney failure increases their dose, which leads both liver and muscle risk elevated;
Pravastatin is said less liver concerns but the myopathy, so choose myopathy when renal failure.
VS: progressive unilateral hearing loss, doesn't affect Rinne Test, associated with NF2 and actor Mark Ruffalo
Otoslcerosis is (usually....) progressive bilateral hearing loss, BC > AC.
If BC > AC in BOTH ears, why does he have hearing loss in only one ear?
My logic was that he probably had otosclerosis in both ears and then something extra going on in his right ear that would make it worse than the left. I still don't understand why otosclerosis is the best answer here.
Finally!!!! Someone who ACTUALLY explains what the fuck bone conduction even is and teaches the whole topic. Here's the link for anyone else who struggled to find someone who takes time to explain this concept
I thought the elevated Estrogen and progesterone depress the function of Prolactin until delivery. I guess you needed to know that it decreases its function by downregulating receptors or something as opposed actually decreasing the prolactin production. I picked gonadotrophs. This was a fair question but I reasoned it out and arrived at the wrong conclusion.
Specifically, the estrogen is stimulating lactotrophs as progesterone is preventing the prolactin from actually working on the breasts. So it's the estrogen that is stimulating the lactotrophs to grow, and you would see the effects of this growth if it weren't for the progesterone preventing the action of prolactin (their secretory product) on the breasts.
why not somatotrophs. she's understress. wouldn't that increase the production of GH
First off, do yourself a favor and check this out - https://www.youtube.com/watch?v=NJYNf-Jcclo
The LDL receptor is found on peripheral tissues. It recognizes B100 on LDL, IDL, and VLDL (secreted from the liver). Therefore, an issue with that would cause an increase in those, but mainly LDL.
Since in this question we see that Triglycerides and Chylomicrons are elevated, that points towards a different problem. That problem is in the Lipoprotein Lipase receptor. This is the receptor that allows tissues to degrade TGs in Chylomicrons. So, if it's not working, you get increased TGs and Chylomicrons. Additionally, you get eruptive xanthomas, which are the yellow white papules the question refers to.
There is much easier way go to page 94 in first aid. This kid has Type 1 Hyper-Chylomicronemia which is I) Increased Chylomicrons, Increase TG and Increased Cholesterol.
It can be either Lipoprotein Lipase or Apolipoprotein CII Deficiency
The video sympathetikey referred to only mentions pancreatitis in type IV but according to page 94 of FA 2019 it is also present in type I Hyper-chylomicronemia which is what the question stem is referring to with the abdominal pain, vomiting and increased amylase activity
thats not the only difference in that video....
Pixorize has a set of videos on all the lipid disorders that made it a breeze to answer.
Pixorize is basically sketchy but for biochem and other basic science subjects.
Pancreatitis was a huge clue for me to think of hyperchylomicronemia
Also, when Meningococcal meningitis is treated ... close contacts are also treated prophylactically whereas the others typically are not. There's also a subunit vaccine for n. meningitis due to high infectivity rate especially in crowded establishments.
So, Cholera is also p2p but Mening is more likely?
Remember the fire sprinklers from Sketchy for M. Meningitis. as respiratory droplets are the easiest to transmit from person to person.
but the poop water comes from people so....
Respiratory dropplets is easier than fecal-oral tho
Can also reason that n. meningitidis is common in college students because they live in close quarters which suggests high rate of transmission even amongst immunocompetent individuals
I can see why fecal-oral can seem like person-to-person transmission. What helped me reason it was that in countries with lots of cases of cholera, the primary reason is lack of water sanitation. Even when you google cholera, you get pictures of people collecting dirty water and how the WHO is aiming to reduce cases of the disease by improving water sources. Therefore it's more of a systemic/environmental problem rather than the fact that one person accidentally touched another person's poopy parts and then transmitted it to their own mouth, making this less of a person-to-person thing, especially when compared to another answer choice such as Meningococcal meningitis.
To add, think of the water in cholera as a reservoir. The bug is going to hang out there between infecting another person. In meningitis it seems we are going from 1 persons saliva to another. Without much of a reservoir inbetween. (might be using the word reservoir incorrectly).
I knew it was MEN2B but forgot medullary ca of Thyroid is parafollicular/c cells which means Calcitonin, not T3/T4
AntiThyroglobulin: Hashimoto's (or other thyroiditis)
Dexamethasone suppression test: positive/suppressed in pituitary adenoma (acth secreting), negative/unresponsive in Adrenal hyperplasia/adenoma (suppressed by high dose) or ectopic acth (unresponsive to high dose)
Serum TSH test: for papillary or follicular ca, thyroid adenomas are usually cold but could also cause HyperT
TSHR antibodies: graves disease, hyperT
Fibromuscular dysplasia = middle aged female with HTN... Maybe it'll stick this time 🤯
This has to do with Intention-to-treat analysis. Essentially, when participants are non-adherent but the data shouldn't be lost. They just undergo another statistical model to account for their changes.
Here is a nice video
Where does the question mention "intention-to-treat"?
They seem to be pretty obsessed with "intention-to-treat" it's been asked in one way or another in all the new NBMEs that I've done. (Haven't done 24 as yet)
They don't, intention-to-treat is just the best way to go about it @dr.xx
I agree with @notadoctor !!
i think if it were per protocol, both groups would be excluded, the ones that were inconsistent, the ones that dropped out, and the ones that switched. But answer choices only allow ITT or exclusion of one group.
Yes. Diarrhea is a side effect of misoprostol.
Probably a Strawberry Hemangioma since she's a baby
Can anyone explain what is option A?
bc, it's a benign "capillary" hemangioma, we can see "thin-walled blood vessels with narrow lumens filled with blood and separated by connective tissue". It sounds similar to "arterioles in a fibrous stroma" but it's capillary.
@meningitis I believe option A ("arterioles in a fibrous stroma") is describing an angiofibroma. The name angiofibroma already tells you that there is some component of fibrotic tissue involved, whereas in this case of strawberry hemangioma, the name tells you that it's more like pure blood vessels (capillaries in this case).
I picked impetigo because of the gold stippling... I guess I took that as honey crusted lesions. F*ck NBME.
Huffing gold spray paint. A la the chrome huffers in Mad Max
LOL I think that might be what they were going for here. Gold spray paint.
Anyone know what may be causing his weight loss and unwillingness to eat? I thought too much into it and put "mercury poisoning", since I thought the heavy metal's abdominal symptoms may have caused him to not want to eat. ¯_(ツ)_/¯
I'm not sure about the pathophysiology there... But I do know that inhalants are popular in places where there's extreme poverty. I spent some time abroad, and one of the patients was using inhalants to take the edge off the hunger, so that she could spend her money on food for her kids instead. She also worked on the streets so I guess it also made it easier to, you know...
I didn't know how to approach this either, but now this is my thought process: Patient has pain after eating. If it's not due to an ulcer (which is the only thing I could come up with because I didn't know what else it was talking about), why would eating cause pain? Well... eating causes increased GIT activity which means increased blood flow. As you pointed out, the patient has HTN and CAD, indicating likely extensive atherosclerosis. This is important because why would eating leading to increased blood flow cause pain, when usually it doesn't? Well... atherosclerosis in the heart leads to stable angina. This presentation sounds like a "stable angina" of the abdomen.
FA 2019 pg 248 pill-induced esophagitis : bisphosphonates, ferrous sulfate, NSAIDs, potassium chloroide, tetracyclines
The question describes how he had a strep infection 15 days ago, and now this is poststreptococcal glomeruloneprhitis, which can also be described as proliferative glomerulonephritis
The question would be too fair if it just said PSGN. Instead we need to smell our own farts first.
And they used terminology NOT found in FA
who said they were limited to FA?
FA uses the common nomenclature and the fact most of our other resources use the same nomenclature for this, I think we can agree that is is the accepted terms. If they're gonna decide not to use the nomenclature that most medical students are taught then they should provide their own study materials at that point for us to use. The test shouldn't be this convoluted for no reason.
Ok. They can use terminology whatever they want. But BUN-CR>20 is CLEARLY prerenal right?
Yes! Allergic/anaphylactic blood transfusion reaction is within minutes to 2-3 hours.
(pg 114 of the 2019 FA has a list of them ordered by time)
(also allergy / anaphylactic presents with more skin findings (urticaria, pruritus)
The time through me off too. I though ABO mismatch since it occured around an hour. I thought TRALI would take a little longer.
Guys anaphylactic reaction to whole blood doesnt occur much except for selective IgA defi. so look out for prev history of mucosal infection. And it can have all feature of type 1 HS inclding bronchospasm.
I saw hypotension and though anaphylaxis........ -.-
Chest Xray showed "bilateral diffuse airspace disease". This is much more indicative of TRALI than anaphylaxis which would have wheezing and possibly respiratory arrest but no actual damage to the lungs. Additionally there was no urticaria or pruritus one would expect to see with anaphylaxis.
My take on this----His respirations are high-22/min--that will cause c02 washout---so actually lung has high oxygen---pulmonary vasodilation. Dont know if its right.
My understanding is that the pulmonary circulation changes very little in terms of an acute MI. It is b/c pulmonary circulation has a lot more room to fill with blood much like the spleen in terms of blood accumulation. With higher volume of blood in pulmonary circulation, more blood vessels are able to be recruited specially the apex. With more recruited blood vessels = reduced pressure d/t circulation in parallel
haloperidol induced Parkinson's... ? adding a anticholinergic can counter these adverse effects of the antipsychotic .. ?
@mousie yeah it balances the dopamine-cholinergic imbalance caused by the antipsychotics
+So antipsychotics induce Extrapyramidal side effects which is drug induced Parkinson = low Dopamine High Ach, and you would treat this with anticholinergic (Benztropine).This is neurologic.
+Antipsychotics also produce non-neurologic, systemic anti-cholinergic effects like dry mouth, sedation, hypotension etc
MAGIC RACKS is a good mnemonic ive heard for 450 inhibitors
(macrolides, amiodarone, grapefruit, cimetidine, RITONAVIR, alcohol (chronic), cipro, ketoconazole, sulfa
Macrolides EXCEPT azithromycin -- they like to trick you with that one.
chronic alcohol induces 450, acute alcohol inhibits 450
The Boards and Beyond video of SC strokes was really helpful at explaining this if you are a video kind of person!
What pushed me away from pons was "dysarthric speech" which implied she still could speak to some degree.... which made me pick medulla.
I think FA may be misleading. Primarily it will effect the Pons because that is where the majority of the Basilar Artery is located. and I guess it could effect the other locations? but everywhere I have looked Locked-in syndrome is an issue with the Pons. But someone please continue to clarify, cause I was a bit tripped up at first with this question
Although FA says it can be pons, medulla, or lower midbrain, "locked-in" syndrome generally arises from BL pons lesions. Another way you can rule out medulla and midbrain in this question is the ocular movement findings. Since the patient has impaired horizontal gaze BL, you can conclude that the Abducens nuclei are involved on both sides. The abducens nuclei are located in the pons.
USMLE secrets also states that it is most commonly in the pons
Bates states that locked-in syndrome preserves consciousness but these patients have limited speaking ability
I was thinking along the lines of overhead motion - damage to the subacromial bursa which is between the acromion and the supraspinatus ... also its the most commonly injured rotator cuff m. so could have guessed this one right
Thanks for the explanation. I was scratching my head as to why this is correct, since supraspinatus only does 15 degrees of abduction, but you make a lot of sense.
why would injury to supraspinatus cause weakness with internal rotation though?
yeah coz of that i picked subscapularis
ya the whole question pointed to supraspinatus ...but last line internal rotation made me pick subscapularis
I went for Trapezius. That shoulder flexion thing was a big distraction. Silly me.
FA2019 pg. 438
Caudal = Bottom of the SC = failure to close = spina bifida and Rostral = top of SC = failure to close = Anencephaly
I'm confused. In first Aid doesn't have meningomyelocele as failure of caudal or rostral pore to close. Is the answer Cadual because in this patient specifically, his condition takes place on L2-5 which is more caudally?
its a neural tube defect aka failure of neural tube closure
My exact thinking also!
My thought as well but the answer says: "Binding of ligand to Nuclear transcription factor" and I thought to myself: "Estrogen Receptors aren't transcription factors.. they are receptors with Transcription Factor function that bind to the ER Element and recruit more Transcription Factors". Can anyone explain what I am missing? Am overthinking things?
You are overthinking it, Steroid hormones receptor is found intracellular in the cytoplasm then they are translocated to the nucleus where they regulate gene transcription. HOPE THIS HELPS
Could this be due to the PTEN gene being linked to endometrial hyperplasia?
The question stem says it's glandular hyperplasia "without" atypia
It's just due to increased levels of estrogen causing the hyperplasia
This is a bunch of scientific mumbo jumbo
Young child following URI with TCP is pretty classic ITP. Sometimes they throw in extra stuff on purpose, but I didn’t see much on the bone marrow aspirate either.
I was also thinking ITP but the bone marrow image kind of threw me off too, not sure what I'm supposed to see but still think ITP is best choice ...
It also almost threw me off, but then I remembered he had low platelet count and I guessed those multinucleated cells were Megakaryocytes (I looked for Megakaryocyte Bone Marrow Biopsy in google and they are the same).
Bone marrow shows increased megakaryocytes -> ITP
Hypotension can also cause pre renal azotemia with a FENa <1%.... How do you know this is ischemic ATN and not hypotension induced Prerenal Azotemia?
I had the same thought as you @mousie, but I think "azotemia" and low urine output push it more towards ATN (looking back; I got it wrong too). Plus, the initially MVC / muscle damage probably caused some tubule injury by itself.
This might help clarify why the pt. has ATN rather than pre renal azotemia.
The question did mention, though subtly, that the bleeding was controlled. That most likely indicates that his hypovolemia has been corrected. Developing azotemia 24 hrs after correction of hypovolemia is more suggestive of ATN (since he doesn't have hypovolemia anymore). I hope that helps and feel free to correct me, if I am wrong.
In addition to my earlier comment, I just noticed the question also explicitly mentioned that he was fully volume restored. Which is consistent with my earlier assumption!
Although initially, hypotension causes prerenal azotemia, the volume correction pushes you away from prerenal azotemia. but they want you to remember that in hypovolemia, the kidneys are also becoming ischemic, and so development of azotemia 24 hours later is more indicative of intrarenal azotemia due to ATN
for anyone who wants to see it: FA 2019 pg591
i'm confused about one thing. if the tubules aren't working like they should, the bun:cr ratio falls right? doesn't that essentially mean azotemia reduces too?
Lets all take a moment to admire how shit this question is
"Bp 90/60.""Repeated episodes of hypotension in the OR" and still the answer is ATN
if this isn't a globe rupture than idk what is tbh
the air in the center of the globe made me think rupture too .....
There may be some global rupture, but impairment of one of the ocular muscles causing diplopia would still be the best explanation for this patient's double vision.
Globe rupture leads to entrapment of the IR muscle which causes diplopia. The question is asking what is causing his visual complaints, which is diplopia, not loss of vision.
So do these patients have h.Flu? What was the giveaway?
I chose Enveloped simply bc it said dies when heated, not sure if there where any other clues to narrow this down or make me feel more confident in my choice but I went with it anyway
I don't think they expected us to narrow down the answer to a specific virus. Enveloped viruses tend to be less stable (?) than the non-enveloped ones and don't survive as well under harsher environments (outside human's body, heat, etc.)
To add on, I also have no idea what virus this could be but the question stem does say "A previously unidentified virus is recovered from urine specimens" making me think that it's not something we're supposed to have know about, unless I'm totally understanding it wrong.
haha I picked this too bc she's 44.... isn't celiac something that would present much younger?? but I don't think IBS would cause an iron deficiency anemia is the hint they were trying to give us.
If it was IBS, they would have mentioned something about them having abdominal pain, different stool frequency, and then relief after defecation, me thinks.
I was between celiac sprue and IBS but what pushed me towards celiac's was a few things:
1. The Iron deficency anemia (I think that would be unlikely in IBS)
2. Steatorrhea (which would also be unlikley in IBS)
3. Osteopenia- I was think vitamin D deficency
4. Lack of a psychiatric history
IBS is a diagnosis of exclusion. If you haven't excluded Celiac (and this can't be excluded based on epidemiology alone), you can't diagnose IBS.
I think you may have confused it with IBD, IBS would not present like this.
I got this wrong but best I could come up with was this was about Bradford Hill Criteria for establishing causality. And of the 9 included, F has the most that are actually included in the information given to us. I chose D but I think since we don't know about other study results, we can't include it as directly answering the question about *this* study.
Someone double check me here:
A: biologic plausibility is a weak point in the criteria, according to the wiki. Also probably not true in regards to this study.
B: Sensitivity is not part of the criteria
C: " "
D: We don't know about consistency
E: " B "
Found this ... still confused about why A and D are wrong though... https://stats.stackexchange.com/questions/534/under-what-conditions-does-correlation-imply-causation
The three criteria for causality are: 1) empirical association (i.e. strength of association; a change in independent variable correlates or is associated with a change in dependent variable), 2) time order (i.e. temporal relationship; the independent variable must come before change in the dependent variable, or plainly stated, cause must come before effect). and 3) nonspuriousness (i.e. dose-response gradient; the relationship between 2 variables is due to a direct relationship between the two, not because of the actions of changes in a third variable... this can be evinced by a dose-dependent response).
The question clearly lead us to think about Osmotic pressure by talking about protein and urine. I wonder how many people used that line of reasoning (like myself)?
Great explanation, I chose lymphatic drainage for the same reasoning (similar Q on different bank)
My reasoning was much more simplistic (maybe too simple) but in my mind, systolic BP is determined by Cardiac Output and diastolic BP is determined by arterioles. Therefore, what comes before the capillary and regulates resistance? Arterioles. That's why I said that pre-capillary resistance.
the main difference between the 2 cases is that in this case the patient has high BP
So in kindergarten language the question is essentially asking how high pressure in the arterial system is NOT transmitted to the venous system (which is where EDEMA develops). But you know they have to add all this info to try confuse a basic principle and make you second guess yourself. (Got it wrong by the way) because of what @ferrero said of Qbank questions.
@ferrero what are you talking about? lymphatic drainage is the wrong answer...
ok never mind. i got it. hard to understand b/c it was a big block of text.
I think they may be talking about the myogenic compensatory mechanism: https://www.ncbi.nlm.nih.gov/books/NBK53445/figure/fig4.1/?report=objectonly
"Increased arterial or venous pressure also induces myogenic constriction of arterioles and precapillary sphincters, which raises arteriolar resistance (thereby minimizing the increase in capillary pressure) and reduces the microvascular surface area available for fluid exchange.
For example, because vascular smooth muscle in arterial and arteriolar walls contracts when exposed to elevated intravascular pressures, this myogenic response increases precapillary resistance and protects capillaries from a concomitant rise in their intravascular pressure."
haha mine didn't either. But they usually leave out most high yield info so, to be expected I guess.
I didnt have physiology in my medical school. None, zip, zero, none. Nor did I have biochem. They said "you learned all this shit in undergrad, youll memorize it again for step 1 and forget it promptly" and then just moved on.
In the Caribbean thats 1 thing we were given... lots and lots of toilet paper
I also chose Gemfibrozil too because its the best TG lowering drug listed but I can see where there might be some red flags for this drug in the way they asked the question... 40 year old obese woman with some upper abdominal pain ..... HELLO GALL STONES which is a common adverse outcome of Fibrates.
Well I didn't wanna give a fat, forty, female, that smokes a fibrate. So a statin, for me, was the best next option.
Used same reasoning to choose statins. Fibrates are the main drug of choice for hypertriglyceridemia but given her symptoms, statins made more sense. Why do they do this to us...
what a tricky question! there are multiple factors should be taken in consideration.. she has triglyceridemia which put her in risk of pancreatitis, and most importantly atherosclerotic disease, and all of that would outweigh the risk of giving her gallstone.
Yeah I had statins selected initially because "statins are always the answer" but when I saw them stating first line "recently diagnosed with hyper TG" I figured this follow-up was purely to address that. So Fibrate is the best move.
Equation is Maintenance dose = (concentration at steady state) * (Clearance)
if you convert all the units to what it wanted them in (mg/kg/day) you'll get 25.92 like weird-in said above
I didn't think to round 0.09 to 0.1 of course so I guessed 2.5 assuming I must have done a conversion wrong and was off by a tenth .... BOO bad Q
He has heart failure which leads to a decrease in renal blood flow and prerenal azotemia. In prerenal azotemia BUN/Cr ratio is >= 20; Activation of the RAAS system due to the prerenal azotemia means that the spec grav is high at 1.025 and he is holding onto sodium so urinary sodium will be low (<20, FENa <1%).
Agree with above, HF and not taking meds would increase or activate RAAS = increase ATII and Aldosterone which leads to body retaining Na and H2O so the urine concentration of Na will be low and the urine will be very concentrated i.e. high SG. I didn't think about the BUN:Cr > 20 but this would have also narrowed it down!
thanks for this explanation!
can any one explain to me why not lens ?
@macrophage95 Lens are an interal part of the refractive power of the eye. Without the lens the image would not be formed on the retina, thus leading to visual loss
Do anyone know why not choroid?
@qfever, no choroid would also be more detrimental to vision since it supplies blood to the retina
That random zanki card with colobomas associated with a failure of the choroid fissure to close messed me up
Seems like the key to this question is in what is omitted from the question stem: there is no mention of vision loss. If we assume there is no vision loss, then we can eliminate things associated with visual acuity (weird to think of in 2 week old but whatever): C, D, E, F. Also, by @hayayah 's reasoning, we eliminate E & F. If you reconsider the "asymmetric left pupil" then the only likely answer between A & B is B, Iris because the iris' central opening forms the pupil. I mistakenly put A because I was thinking of the choroid fissure and I read the question incorrectly - but it's a poorly worded question IMO.
Key here is that it doesn't affect vision- the only thing would be the iris. All others are used in vision. Don't have to know what a coloboma actually is.
The extra section of that Zanki card specifically says that a coloboma "can be seen in the iris, retina, choroid, or optic disc." Don't you dare talk trash about Zanki!
I agree that it's confusing but I looked at it as a physical *obstruction* since it's impinging on the airway.... but yeah idk this is weird
Doesn't the trachea have cartilage rings so it wouldn't collapse which makes it seem less like a typical obstructive disorder? I'm really not sure why FVC would change because I don't see how total lung capacity or residual volume would change because those are static conditions where there is no airflow at all. I understand FEV1, peak expiratory flow, peak inspiratory flow etc.
Agree this is a really tough Q but I also think I really over thought it... I eliminated all with a normal Ratio bc something obstructing would obviously produce an obstructive pattern although I don't know why FVC would be decreased. I wasn't sure about both peak expiratory and inspiration flow being decreased can someone help me with this or tell me I'm totally overthinking again.. are they both decreased simply bc theres an obstruction ..?
Yea I got confused on this question. But I guess they wanted us to look at it as a obstructive disease . If this were the case all of those function tests would dec. ( See FA )
Because the obstruction is above the alveolar regions there is a decrease in air flow, not lung volumes, which would make this an obstructive pathology.
FVC here dec same way it dec in Obstructive lung disease. Read the concept of Equal pressure point of BnB. There he says in bronchitis we have onstructive pattern because inflammed airways gen more resistance. so EPP comes early. I guess here due to tracheal narrowing pressure inc downstream. which collapses smaller airway. result in air trapping.
I'm confused about the phosphate level in questions like these. Decreased calcitriol would decrease phosphate absorption while PTH decrease lowers phosphate excretion. I'm assuming that the PTH decrease has the greater effect with serum phosphate levels?
PTH = "Phosphate trashing hormone" if PTH is high Phosphate must be low - they are always opposite (unless d/t renal failure then Phosphate will be high - kidneys will be unable to get rid of phosphate)
So low Ca d/t low PTH does not effect 25 H. Vit D ... only 1,25 H Vit D (active Calcitriol)?
Clarification because I was confused: PTH stimulates kidney to produce 1,25-(OH)2 D3 (calcitriol) via 1α-hydroxylase in proximal convoluted tubule. Therefore, without parathyroid glands, low PTH, 25,D is not converted and therefore not down (normal or up). phosphate "trashed" by PTH as eloquently stated above.
Here the primary defect is high up from the parathyroid gland, there is decresed or no PTH which normally trashes phosphate but not in this case so serum PHOSPHATE INCREASES and the serum calcium is low because PTH should have prevented the urine calcium so there is calciuria and no resorption from bone-LOW CALCIUM, Vitamin-D is independent of PTH so stays NORMAL
Could you help me with understanding why this isn't a Type I HSR? I understand that ABO incompatibility is Type II HSR but I don't know how to tell the difference between a patient who is IgA deficient and having a Type I Reaction to an infusion vs ABO incompatibility ....
@mousie - https://imgur.com/QH5rCEX
Basically, think of Type 1 HS like a normal allergic reaction (itchy, wheezing, etc.). Whereas, with ABO incompatibility you get the question's presentation.
When it comes to Acute hemolytic transfusion reactions, they are Type II hypersensitivity and divided into Intravascular (ABO) and Extravascular (host Ab against foreign antigen on donor RBC). The differentiating factor between them is simple. Intravascular (ABO) will present with hemoglobinuria alongside all the other common symptoms (fever,hypotension, tachypnea etc.) Extravascular hemolysis will stand out with Jaundice as one of the presenting symptoms. Hope this helps!
Also just to add: Rh incompatibility causes a delayed hemolytic transfusion reaction, this reaction was immediate so it is indicative more of the ABO blood group incompatibility (FA2020 p114 has all the blood transfusion reactions)
Anion Gap: Na - (Cl + HCO3) = normally around 10-12
good to know. I keep looking up the urine values but all it said was "varies", then I threw my computer and yelled "does that vary Mother F****ers. I do feel better now.
glad I wasn't the only one who got very pissed off at the urine values
Usually the first thing I look at is whether or not the Cl- is high. Generally if the Cl- is high its going to be a normal gap
i think they gave you the urine values bc you can calculate the URINE anion gap which is (Na + K - Cl). In this case the Urine Anion Gap is positive (5). Boards and Beyond mentions that a positive UAG is due to Renal Tubular Acidosis Type 1 (inability of alpha intercalated cells to secrete hydrogen ions). just another approach to answer this q
Actually diarrhea is the "D" in "HARDASS"(reason why I was stuck between Chron's and RTA). Ended up getting it right with RTA..
So the reason this is not Crohn's disease is actually what BnB explains in Renal Tubular acidosis video. Anytime there is a Metabolic Acidosis with intact kidney secretion of H+, the URINARY Anion gap (Na+K-Cl) is NEGATIVE. This is because the excess NH4 that is secreted into urine is combined with Cl-. Therefore, in Crohn's disease and Type 2 Renal Tubular Acidosis, the urinary anion gap is NEGATIVE.
In this question, the urinary anion gap is POSITIVE so this would be an example of Type 1 RTA because the kidney can not excrete H+.
I got it right by chance, definitely did not understand it in this much detail when I was answering it lol
When ever I hear Rosettes I always think NE tumors ....
and I agree non smoking kind of RO small cell, squamous cell, or lg cell
I thought it was Hamartoma & pick chondrocyte! Can lung even have hamartoma? Pardon me it was the laast ques of whole nbme
@charcot_bouchard i thought the same. uworld gave a question on coin lesion in the lungs as classically hamartoma
From pathoma benign coin lesions such as bronchial hamartomas composed of lung tissue and cartilage are especially found in younger patients. So i guess because of the age and histology this would be less likely.
Adding on to the answer above. I was stuck between the gonadotropin injections and clomiphene. But, clomiphene acts to increase activity of GnRH which then exerts its effects on the pituitary. The man in this question had his pituitary removed because of an adenoma. So, he needs the FSH and LH directly.
Removal of the pituitary would case a deficit in Gonadotropins (LH, FSH) and therefore nothing to simulate the testes to make sperm... replacing the T with a patch would not stimulate the testes to make sperm and if his axis was intact (although its not) this would further down regulate the production of sperm. I eliminated Clomiphene because if he dosent have T to induce negative influence on the hypothalamus he will have increased GnRH and further increasing it with Clomiphene would not correct the deficit in Gonadotropins.
Oh duh... that makes much more sense. Thanks! P.s. I thought clomiphene was more of a fertility drug for women, since it blocks negative feedback of estrogen on the hypothalamus/pituitary. But in men the system is under feedback due to testosterone, not estrogen.
83 might seem an uncommon age, but we don't know for sure her sexual history. She only recently (8 months ago) started showing some signs of mild cognitive impairment. She has all these results implying that she has syphilis, so the most likely answer is that she has syphilis, so we should speak to her privately about her sexual history. The tests don't necessarily means she got syphilis very recently, it's possible she's had syphilis for a while and never got treated.
I understand that she could possibly have syphilis but I also put repeat tests because I know there are a few things that can cause false positive VRDLs but if she also has a + RPR does this make a FP less likely? And also if she has mild cognitive impairment you still discuss with her not her daughter correct ...?
This definitely could be a false positive, but before we want to consider it to be a false positive, we should talk to the patient about it privately. Assuming that it's a false positive before asking the patient about it could delay treatment of her syphilis. There's a chance she didn't want to disclose her sexual history in front of her daughter or maybe she was embarrassed or didn't think it was important to mention.
And you're absolutely right, she only has mild cognitive impairment, so we most definitely should talk to the patient alone without her daughter first.
She has dementia. She doesn't have the capacity to determine her own care (23/20 MME). I feel the daughter should have the word on the care since Grandma likely doesn't have the capacity to understand her actions.
From what I remember, dementia is typically a combination of impaired memory *and* impaired thought processes. There is nothing to indicate that the patient has impaired thought processes, and the memory impairment is only mild. The patient can still reasonably said to be competent, and so her private information should be discussed with her alone.
Elder care homes or elderly communities actually have a high rate of STDs. Turns out, when you put a bunch of divorced/widowed adults together in a community they have sex.
Additionally, you should respect the privacy of a competent adult with "Mild memory" impairment. I know I could have mild memory impairment considering the crap I forget studying for step 1
also.... I think we can assume that "repeated tests" means repeat VRDL, not "additional tests to rule out false positives"
the entire point of this question is that when you see an STD in an unexpected demographic (children, elderly), THINK SEXUAL ABUSE
I thought it was ALS too (and I think it still could be?) but my thought process was that a lower motor neuron lesion would be the more specific answer.
Yeah makes sense, just threw me off cause ALS is both lower and upper motor neuron problems. Corticospinal tract would have been a better answer if they described more upper motor neuron symptoms, but as you said, they only describe lower motor neuron symptoms. Thanks!
Agree I thought ALS too but eliminated Peripheral nerves and LMN because I guess I thought they were the same thing ....??? Am I way off here or could someone maybe explain how they are different?
peripheral nerves would include motor & sensory, whereas LMN would be just motor
Also, a LMN damage wouldn't include both hand and LE unless it was somehow diffuse as in Guil-barre syndrome. It would likely be specific to part of a body. right???
No. if it was a peri nerve it would be limited to a particular muscle or muscles. but since its lower motor neuron it is affecting more diffusely. Like u need to take down only few Lumbo sacral neuron to get lower extremity weakness. but if it was sciatic or CFN (peri nerve) it would be specific & symptom include Sensory.
I think it's ALS too. The correct answer choice here seems more based on specific wording:
the answer choice "Corticospinal tract in the spinal cord" wouldn't explain the tongue symptoms, since tongue motor innervation doesn't involve the corticospinal tract or the spinal cord (it's corticobulbar tract). This is a situation of "BEST answer choice," not "only correct answer choice."
Cyclins help regulate cell cycle phases. They help with checkpoints before progression to the next phase of a cell cycle. Therefore the checkpoint before mitosis would be in G2 and probably where mitotic specific cyclins are synthesized