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flocculonodular is medial (central). but yes it'll have nystagmus and truncal ataxia
Lesions of the lateral regions (cerebellar hemisphere) of the cerebellum affect the lateral body (dysmetria, fall toward injured side).
Lesions of the medial region (vermis, floculonodular lobe) cause medial (truncal) ataxia.
Oversimplified but these rules help me answer most questions about the cerebellum.
the same girl shows up on so many NBME exams its not even funny. Its just like that poor kidney that's cut in half that shows up in all kidney questions.
I turned my brightness up and down 2 times to make sure it wasn't my brightness messing with the sclera. I'm declaring it, NBME stands for "Naturally Bad at Making Exams" .
$60 a pop and no competitors...That's what happen when there's a monopoly.
Actually they used their best software to generate images. You might have heard it before, it's called MS Paint. Quite legendary.
It feels like they cranked up the contrast and saturation on a normal eye to make it look "blue"...
everyone hates on nbme, but they're showing you a picture zoomed in of her eyes and she has a history of multiple fractures/bad wound healing at the age of 4, I feel like OI should at least be a consideration based on the overall clinical picture
Yeah I got it right, it's just funny that they don't use higher quality pictures for the exam
that is clearly a malar rash... oh wait nvm just pixellation
"Pick your **Big** **Foamie** **Zeibra** nose with your Sphinger"
Choose options with the letter I.
SpIngomyelin, Sphingomyelinase, bIgorgans (hepatomegaly etc), zeIbra bodies, Foam cells
how are we supposed to know that dipalmitoyl lecithin is the same thing as dipalmitorylphosphatidylcholine
FA 2019 page 647
Pulmonary surfactant is a complex mix of lecithins, the most important of which is dipalmitoylphosphatidylcholine (DPPC).
Also: Screening tests for fetal lung maturity: lecithin- sphingomyelin (L/S) ratio in amniotic fluid
(≥ 2 is healthy; < 1.5 predictive of NRDS)
Step pneumonia is the most common pathogenic organism in CGD, and the most common cause of pneumonia, otitis media, meningits, and sepsis. While CGD are at an increased risk of encapsulated E. coli infections, however, they are at MOST risk for S. pneumo. This is kind of just a memorization fact that you need to know about S. pneumo.
Sorry english is clearly not my shit, but you get the point
CGD is susceptible against catalase-positive organisms (FA 109), of which S. aureus is the one to look out for. It's not about encapsulated organisms, like I had it confused in my head.
You are completely right about E.Coli being encapsulated and is also a CAT+ organism and patients with CGD would have an increased risk of infection for both S. Aureus and E. Coli. How you narrow down the two is the most common infections are S. Aureus and Aspergillus (FA 109 like mentioned above) and also using the pneumonic "Cats Need PLACESS to Belch their Hairballs" (FA 128) Nocardia, Pseudomonas, Listeria, Aspergillus, Candida, E.Coli, Staphylococci, Serratia, B cepacia, H pylori
In early shock you have increased SVR due to vasoconstriction. This would cause increased flow to the kidney. I could be wrong but I think what makes that answer incorrect is NOT that RAAS hasn't been activated yet. It is what is causing vasoconstriction via Angiotensin II. What is possibly wrong about that answer is that it says via sympathetic stimulation. I do think it is a little vague between those two answers though. Because you can get sympathetic activation of the RAAS system causing vasoconstriction and blood shunted to vital organs such as the kidneys. Bottom line is you can't argue with weak pulse during hypovolemic shock.... so an obvious right answer. You could make a case for the increased blood flow to the kidney though.
@makinallkindzofgainz no need to dismiss the question... so pretentious
I was thinking lung cancer secreting SIADH, resulting in hyponatremia. But because the question asked specifically about the cause of the facial edema, I put hyponatremia (answer choice C). I was wondering how you guys were able to differentiate between C. hyponatremia and E. lung cancer? Thank you!
The first thing that crossed my mind was SVC syndrome from the cancer obstructing the R brachiocephalic vein preventing venous blood from returning to the heart (and staying in the facial area). Also I assume Hyponatremia would be equivalent to decreased body volume so there wouldn't be edema. FA Renal physiology section has a good chart on what happens during electrolyte imbalances (hypo and hyper)
I was thinking that hyponatremia would be more loss of osmotic pressure --> edema, but I definitely see the argument for a mass that's simply blocking blood flow. Thank you!
only thing affecting osmotic pressure is albumin, which would be more towards liver cirrhosis. The body will attempt to maintain a Na+ of 140 with various mechanisms, but doesn't contribute to osmotic pressure.
Additionally, AML is the only answer choice that has multiple blast forms (myeloblasts, promyelocytes, etc.). ALL is characterized by a single blast form (lymphoblasts).
CML has blasts too but they tend to favor mature forms.
You see numerous blast forms == AML, which is characterized by >20% blasts
The answer choices are all of lymphoid origin except for AML and Hodgkin Disease. We know Hodgkin Disease is a lymphoma (not leukemia) and would present with lymphadenoapthy. So the answer must be AML #testtakingstrategies
@atstillisafraud thanks for mentioning the merchlorethamine increasing risk for AML, i was trying to make a connection with the drugs but couldnt. Had to lean on the test taking skills just like key company
Procarbazine is alkylating as well.
@keycompany how did you know the phrase "multiple blast forms" meant literally different types of blasts and not just many blast cells were seen?
@keycompany, how did you know it had to be of myeloid origin?
Thanks for a good answer. This question made me feel like I was taking T21 pills
Thank you- I was really thinking this question had 2 correct answers... of course my dumbass picked Mast cells.
where do i find this info??
@ajss pg 112 of first aid 2019, under type I hypersensitivity. Immediate --> mast cells releasing histamine and tryptase, late--> eosinophils and leukotrienes recruited via chemokines
Wow, i missed the fact that the question is asking for the RESULT of the reaction, NOT the cause of the reaction. Mast cells cause the initial reaction, eosinophils would be the result of the eosinophils. *facepalm
Pathophys (as far as I understand it)...Mast cell degranulates, thus the phospholipid bilayer et. Al are left behind and needs to be degraded. Who comes in? Our good friend eosinophils, as they contain Major Basic Protein (responsible from breakdown of expired mast cell).
Note, you can tie this in to the delayed Leukotriene effects of an allergic rxn, as the bilayer is also broken down by arach. Acid.
(See this link to support my credibility https://images.app.goo.gl/3cUF3ZVc7qy8uxAi9)
who else looked up what T21 pills were
I guess F is the vagus nerve. Thanks to NBME I am also training to become a mind reader.
Thanks to the NBME I have crippling depression