Welcome to dentist’s page.
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I endorse clicking that link
Hahahahahahaha, that's a must click. Someone please buy it and let me know.
welcome, O great physician of the skull and oral cavity. we revere your intricate understandings of the face, jaw, maxilla and all their tiny and hidden foramina. teach us your ways.
He could have 4x the normal because of current PPI use. the point was that you'd get him off, wait for it to normalize, then check again to see if it's due to neoplasm or PPIs
I know Insulin cause shift K+ into cells due to closing of ATP-sensitive K channels (blocking K from leaving)? Does it increase K in the cells by another mechanism?
@dentist - Insulin stimulates the Na+-K+-ATPase pump, this drives K+ into the cell (Source: Amboss)
Another mechansim = acidosis causes hyperkalemia due to H+/K+ antiporters. H+ is high in blood so shifts into cells via this antiporter, which shifts K+ out. --potassium section of acid/base chapter in Costanzo physiology
and explains the flame hemorrhages (Goljan) caused by malignant HTN
FA 2020 pg 301*
The flame hemmorhages are also a good buzz word for recognizing he has hypertensive retinopathy 2e chronic, uncontrolled HTN. Pt's with hypertensive retinopathy can also present with "cotton wool spots" and "macular star". Pics on FA 2019, p. 299
i think C is type III
i think C is type III
In Type III HS, First C happens then then D happens
If you look at the picture you can see the epithelioid and giant cells. I only picked granuloma because I remember seeing a similar picture in Uworld.
granulation tissue is a part of the normal wound healing process, and happens within the first week.
I agree I looked at that grey blob and thought foreign body --> granuloma
The question asks "the most likely cause of the facial finding involving the lip in this patient..."
cleft lip = 'processes'
clef palate = 'shelves'
Don't let a dentist tell you whats up :(
did you get scabies from "burrows" and "night itching"
My question is where do you get scabies originally? I knew it was transmitted person-to-person, but thought it has to originate somewhere (a pet possibly?) so I went with pets. The internet only seems to say that you get scabies from another person with scabies, so the question remains: where do people contract scabies from?
@pg32 , long quote:
+ "Sarcoptes scabiei mites seek the source of stimuli originating from the host when they are off the host but in close proximity to it. This behavior may facilitate their finding a host if they are dislodged from it and contaminate the host environment. Thus, direct contact with an infested host may not be required for humans and other mammals to become infected with S. scabiei. In the case of human scabies, live mites in bedding, furniture, toys, and clothing can be a source of infection. Sarcoptes scabiei var. hominis have been recovered from laundry bins in a nursing home." + from here: https://parasitesandvectors.biomedcentral.com/articles/10.1186/s13071-017-2234-1
to summarize leafhouse: Fomites
FA 2020 p.161
"transmission through skin-to-skin contact (most common) or via
No, the constant studying is to trick you into thinking shes abusing amphetamines.Amphetamines decrease appetite so a lot of people abuse them for weight loss. That combined with increased concentration to study all day errrday.. #onehellofadrug
forgot to mention, another side effect of amphetamines would be increased BP due to the increased catecholamines..don't forget to keep an eye out for that
would amphetamines influence electrolytes at all?
This is where the timing of everything in the question trips me up. FA say PV mechanism is increase EPO (2019, p299)
Different types of Polycythemia have different effects on EPO levels. "Appropriate Absolute" and "Inappropriate Absolute" will both increase EPO levels (Inappropriate is caused by this EPO increase). Where as Polycythemia Vera has decreased EPO levels due to the negative feedback loop. FA2019 pg 425 hooks it up nicely.
Sorry, you narrowed it down to HOCM, MVP, and LA myoxma, but I only see LA myxoma as an answer choice. Wouldn't you have been able to stop right there?
@dentist, I appreciate this full answer b/c nwinkelmann is telling those of us that were wondering "how to ddx one from the other in case we need to"?
@dentist btw, HOCM is an answer choice (RVOT is part of HOCM)
@hello but since that's pseudo-aortic stenosis, it would present with a systolic murmur, correct?
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
you're right! heart rate is the only option under sympathetic control.
The cervical ganglion is a fusion of the last few cervical levels and the first thoracic level, so it is plausible.
I would say: "I understand why you are missing injections, but you're going to have a BAD TIME IF YOU KEEP MISSING INJECTIONS"
@dentist, I was searching for that answer as well, but it wasn't there so I picked C ahahaha
you would definitely do C as well. key word is "initial step"
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?
in cholera people to water => water to people
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).
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
How did you know that this wasnt oral hairy leukoplakia? just from the picture?
To piggyback off of @hpkrazydesi, you ruled out oral hairy leukoplakia because the patient was seeing the doctor for normal health maintenance, i.e. not immunocompromised, I'm assuming.
@nwinkelmann thats correct! my time to shine.
The v-fib/death is an attempt to throw you off. The simple way of asking this question would have been: "18 days after an MI, you should see____?"
i would use pathoma for this. it says 1-3 weeks after an MI you can see granulation tissue