Welcome to kevin’s page.
Contributor score: 17
Just to show why the other answers are wrong: Lidocaine - Blocks Na channels, Morphine Sulfate - mu opioid receptor blocker, Pentobarbitol - increased duration of GABA-A channel thus increased Cl thus decreased nerve firing, Potassium Chloride - replenish K, Tetrodotoxin - Blocks Na channels. Question shows Phrenic nerve trying to make the diaphram move with Ach release but fails because Tubocurarine is a competitive antagonist of Ach at the NMJ.
leukemia not lung, sorry
I was initially thinking it was rhinovirus too but in retrospect I think the wheezes etc make RSV more likely
The key demographic for RSV is infants (<2yo), so based on age alone RSV is what they're going for imo.
Signs of respiratory distress = bronchiolitis over rhinovirus
To add, LDH would be increased with many types of hemolytic anemia. Not be the best answer, not as specific
Penicillins and cephalosporins act as haptens, alpha-methyldopa causes direct Abs against self Ag on RBC. - Dr. Sattar
Cholecalciferol is synthesized from 7-dehydrocholesterol by UV, but yes, correct
Didn't know the products of it were considered hormones my bad i guess
I think part of it stems from the fact that this patients symptoms are occurring within the time-frame for adjustment disorder while SSD seems to have a longer timeline. Aside from that I find it difficult to see why SSD wasn't a possible answer.
To add to that, I inferred that the obsession with checking temp and with the tingling sensation were signs provided to him by the physicians of recurrence. He is anxious over his cancer recurring, and they are more specific than a variety of body complaints
In somatic symptom disorder, the motivation is unconscious. I think for the patient in this Q-stem, his motivation is conscious -- he wants to make sure that recurrence of cancer is not going "undetected".
@chillqd Same! Why not OCD? He's fearful that something bad might happen (=cancer relapse; obsession) and calling his doc (=compulsion)
great reasoning @hello, this was confusing me but that makes perfect sense
She's in her 90s, she would've likely presented with a platelet disorder decades ago. Given the vignette a normal aging process was most likely
Just adding support to the above explanation:
do all azoles or just itraconazole only requires an acidic environment to be absorbed?
just itraconazole and posaconazole
@chandlerbas, where did you find this information? I was looking over this on FA but they do not mention it and I would like a bit more information. Thanks!
haha no stress! the article above submitted by @necrotizingfasciitis does a descent job explaining it, however its not good enough, I looked into a bit more on uptodate but wasn't fruitful in my endeavours. goodluck!
How are we supposed to know this!! It is not in UWORLD or FA right?
Someone said it on here, since there was no CYP inducer of the answer choices, the only way to even think about an answer to this question was to just go with a less acidic environment from the PPI affecting absorption. It was simply the only reasonable answer choice, I don't think there's any way we were expected to know of this exact interaction prior
Golan pharm book states the exact same thing. Cannot be given to patients with acholrhydria.
i'm sorry guys it's bladder cancer blocking urine flow => reflux ureteral widening => reflux nephropathy.
Is the idea since that since the histology shows transitional cell cancer the most likely is smoking and that's the answer? The fact that this was unilateral really threw me off. Is it common to have unilateral carcinoma of the ureter (if that's what this case was, of the ureter) rather than bilateral?
I Choose F) vinyl chloride <- only liver angiosarcoma. :(
about many Carcinogen FA2019, 226pg.
Schistosoma haemaTobium: spine is on the Tip ("T" for Tip and haemaTobium) and Schistosoma manSoni has a spine on the Side ("S" for manSoni and Side)
FA 2019 pg. 192: Do not take tetracyclines with milk (Ca2+), antacids (eg. Ca2+ or Mg2+), or iron-containing preparations b/c divalent cations inhibit drugs' absorption in the gut
This is also why tetracyclines are teratogenic and should not be given to children because tetracyclines chelate with the calcium in the teeth and cause tooth discoloration and inhibit bone growth in the fetus/growing child (Source: SketchyPharm)
just remember fluoroquinolones also are prone to chelation. you know it's gonna pop up on the real one
But a low VD corresponds to high Plasma Binding Concentration(FA 233, 2019). That's my main confusion with this question.
If it's high plasma binding, then it's low Vd. But, low VD doesn't necessarily require high plasma binding. Low Vd can simply be due to it being a large polar molecule
stimulates K+ efflux (hyperpolarization) and inhibits Ca2+ influx (no vesicle release)
FA 2019, 538page !!
i thought aspirin blocking off the TXA2 production would allow for vasodialation.
This was a UWorld question. I originally thought the same, it's just cilostazol does the vasodilation and inhibition of platelet activation most directly
b-endorphin - an endorphin and ACTH hormone (similar to ACTH, POMC) that can bind to the µ-opioid receptor
Enkephalin - a neurotransmitter involved in the indirect basal ganglia pathway (along with GABA); it can also bind to delta-opioid receptors
Morphine - an opioid agonist (used for pain relief)
Oxycodone - Another opioid agonist (~same potency as morphine)
enkephalin, endorphin, dynorphin are the bodies endogenous opioids
Isnt alkaline tide related to an increase in pH after meals? Your logic is on point but I'm not sure whether we can apply that concept here.
If you're already losing chloride through vomiting, why would you push chloride out into the stomach, which would further decrease serum chloride?
You can get contraction alkalosis from vomiting (decreased skin turgor). Therefore, the RAAS system would be activated.
concept can be applied here because we need to replete the Cl- in order to create HCl; the stomach doesn't care if Cl- is low in serum, only that Cl- is low in the parietal cells and so will pump out HCO3- in its expense
For the purposes of STEP 1 I don't think there is an antibiotic that would do that. If you wanted to really stretch the definition of enhanced cell permeability you could go with a polymixin which is essentially a detergent for bacterial membranes and can be used rarely for pseudomonas and other bacteria
It's permissive because without cortisol Epi wouldn't be able to attain its full effect
efferent dilates with an ACE-I due to loss of angiotensin mediated vasoconstriction
Axillary controls deltoid not musculocutaneous but otherwise yes
Just look at the arrows; the last one will be efferent since it flows from afferent to efferent
pg. 47 on FA got the good visuals!
COPII* proteins are needed to coat vesicles from the RER to Golgi. "Two(COPII) steps forward; one(COPI) step back."
Anterograde goes RER -> Golgi -> Lysosomes/Secretory Vesicles -> Plasma membrane
and I thought large lysosomes due to lack of enzymes to degrade
The size of the lysosome is not affected by the presence or absence of protein, but its function is compromised (eg. protein is getting stuck in the RER)
I hope this helps to whomever was lost like me
Null mutation: A mutation (a change) in a gene that leads to its not being transcribed into RNA and/or translated into a functional protein product. For example, a null mutation in a gene that usually encodes a specific enzyme leads to the production of a nonfunctional enzyme or no enzyme at all.
I think you made a typo: COPII (RER -> cis-Golgi); COPI (trans-golgi -> cis-golgi and cis-golgi -> RER), clathrin (endocytosis and trans-golgi -> lysosome)
So my thought process was if there is no COP signal then instead of going to Golgi it would be sent astray into cytoplasm, akin to how in I-cell Dx the enzymes get sent out of the cell since there is no trafficking signal (therefore I presumed large lysosome due to eating the aggregated protein). Are we saying without COP or Clathrin that the vesicle will simply stay put where it is? If I can get a reply before my exam (2 weeks) that'd be much appreciated
leukemia not lung, sorry
"Immediately following creation, arteriovenous fistula (AVF) is associated with an increase in cardiac output (CO), achieved predominantly through a reduction in systemic vascular resistance, increased myocardial contractility, and an increase in stroke volume (SV) and heart rate. Over the following week, circulating blood volume increases in conjunction with increases in atrial and brain natriuretic peptides. These alterations are associated with early increases in left ventricular (LV) filling pressure with the potential for resultant impact on atrial and ventricular chamber dimensions and function." (PMID: 25258554)
There's also another study by Epstein from the 1950s looking at the effects of AVF's effect on CO in men (PMID: 13052718). Apparently, the increase in resting CO is a big problem because it can lead to high-output cardiac failure (LVH).
Jesus big92 you went in on the research lmao u must be MSTP
big92 you are right. that is why pagets disease pagets have high output cardiac failure because of the av shunts.
what is "increase PL"
Some more UW info: incomplete fusion in up
to 25% of adults: remain
functionally closed until
RA > LA pressure (e.g.
valsalva), esp. concerning
if hypercoagulable (e.g.
stroke with buble study:
inj agitated nl saline and
look for bubbles in left
Are you very sure of this answer? because she is an adult and not a baby anymore so it can't be a patent foramen ovale.
has not closed basically
cienfuegos is spot on with his explanation @athenathefirst
Is it because it's MS? So for sure need a GABA agonist
Never heard of mecamylamine, just know UW and FA say Baclofen, GABA-B agonist for spasticity. It's not solely because it's MS, it's just the drug they want us to know for specifically spasticity
How were we supposed to know this? Thanks for the clarification. I picked cecum because FA says Crohn is usually the terminal ileum and colon, so I figured cecum would be the most likely vs the descending colon.
Yeah that's what I thought at first too. Figuring it was a tricky question, I went with descending colon because 1) ascending and descending are retroperitoneal, so we know the latter is for sure right, and 2) cecum has it's own name (ie it's different than the ascending colon), so it probably isn't retroperitoneal in that regard. You can remember ascending and descending are retroperitoneal by remembering the greater omentum wraps around the transverse colon and from anatomy lab that there's a mesoappendix, mesocecum, etc (peritoneal)
I think the key is in the answer phrasing, the answer mentioning H-bonds says "Disruption of H-bonds between collagen molecules"
Although collagen does undergo H-bonding to support the triple helix, this is done within the same collagen molecule.
Linking different collagen molecules occurs via the lysine - hydroxylysine links done in the ECM
this is the one comment that finally helped me understand why that was incorrect. thank you
(B) You get an increased BUN:Cr ratio because increased urea absorption at the proximal tubule (conservation of water), but you lose the same amount of Cr since none of it is reabsorbed; thus the ratio increases.
I may be wrong but I think more of the urea (BUN) would be absorbed in medullary collecting duct in this situation due to ADH; think I saw a question on this in uworld, could pop up
yeah I'm pretty sure schistocytes alone could give you ttp as answer
well that and pt/ptt being normal
yeah I'm pretty sure schistocytes alone could give you ttp as answer
well that and pt/ptt being normal
just for people who are taking exam this year, ewing is now understood to be mesenchymal stem cell neoplasm (uworld)
I actually thought that the posterior column findings were likely due to B12 deficiency - "subactue combined degeneration", due to malabsorption, as we see in this pt (. Turns out vitamin E can also cause symptoms which look like subacute combined degeneration: https://www.ncbi.nlm.nih.gov/pubmed/9012278, as does Copper (TIL): https://www.ncbi.nlm.nih.gov/pubmed/15249607
Vitamin E deficiency causes posterior column findings and hemolytic anemia :)
The way I think about it is that essentially, vitamin E is an anti-oxidant. Vitamin E deficiency = LOTS of oxidation, i.e. free radicals, which are toxic to most cells in the body (particularly myelination and RBCs). That's why it can be used with Alzheimer's patients.
Vitamin E presents like B12 deficiency but without megaloblastic anemia
B12 would also affect lateral corticospinal tracts, vit E doesn't to my knowledge (b12 deficiency would also present with hyperreflexia but E deficiency just romberg sign, loss of proprioception and touch, ataxia)
yeah, i’ve never heard of antiphospholipids increasing PT time ...
Not sure if that little detail was to throw us off. I think the point of the question was to ID antiphospholipid syndrome based on the clinical criteria (spontaneous abortion + thrombosis)
I actually went down a rabbit hole with this one recently - essentially in vitro findings =/= in vivo findings, clot-wise with anti-phospholipid antibodies.
No mention of lupus anticoagulant, anticardiolipin, or anti Beta 2 antibodies. FA mentios prolonged PTT but nothing on PT. What a piece of shit question. But thanks to the dudes above who explained it
UWorld mentioned "prolong aPTT (and sometimes PT)" in APS
@yb_26 Can u please tell the QID because the one I have seen it says, "Although patients often have prolonged ptt (because the antiphospholipid interferes with ptt test), pt is normal."
just to clarify, lupus anticoag is in antiphospholipid and presents with paradoxical increased ptt +/- pt despite increase risk thrombosis
saturday night palsy is radial nerve; only hint for axillary was arm abduction
The crutches would affect the radial nerve (FA p440).