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@rainlad Protein C deficiency doesn't cause elevated PT and aPTT. I believe they're both normal and assays for the disease measure protein C activity.
Protein C is an anti-coagulant, so if you lack factor C, then you have MORE clotting factors. This means that the PT and PTT would not be prolonged.
this is exactly how I reasoned through it. Were we correct in our line of thinking? We'll never knooooow
But will you ever know on the real thing?
but will you ever know in real life? you may do the right thing (given time constraints, & information available), but outcome is bad; maybe you do the wrong thing, but the outcome is good (despite your decision). how to know the difference?
The bruit is basically just turbulent flow, which is most commonly caused by artery narrowing. I was just reading https://emedicine.medscape.com/article/463015-clinical on renal artery aneurysm and it looks like most of the hypertension is actually related to a pre aneurysm stenosis, so i think stenosis is the "better" answer, esp. since the pt has like every risk factor for stenosis.
To be honest I had not ever really thought about RAA for this case because bruit over RA has been drilled into my head as renal artery stenosis, but i apprecaite seeing how this is a super reasonable answer - just the stenosis is "more likely"
I think we're assuming that we eradicated the leukemia with the chemo. However at the same time a lot of normal stem cells were also killed off so we give GCSF to help recovery especially since they have an infection.
Short time course & tenderness was a tip for me.
Aka de Quervain's thyroiditis
I struggled between those two answer choices as well. I thought that the large needle shape right in the middle was a uric acid crystal which helped push me towards Uric Acid as my answer. I also took into account that she was older (even though STIs are rampant among the elderly) she didn't really seem to have any other symptoms or history of STI/gonorrhea. I figured with her age that she just wasn't able to excrete Uric Acid enough, and got a gout.
Something a pathologist told me one time was that they put the focus of the picture in the middle of the shot. So considering the uric acid-looking shape was right in the middle, I figured that's what they wanted us to focus on with the picture.
Hope this helps.
Ah gotcha! I guess I shouldn't have thought that the thing in the middle was an artifact lol... thank you!!
I believe it's because:
1) there is nothing given that would be risk factors for this woman to have N. gonorrhea
2) The thing in the middle is indeed an MSU crystal, just not under polarized light
3) apparently we get acute inflammation and increase in WBCs with crystal-induced arthropathies, per Table 11-2 on page 8 here (10 page document, top of page of interest will say p. 260) --> http://downloads.lww.com/wolterskluwer_vitalstream_com/sample-content/9781582558752_Mundt/samples/Chapter_11.pdf Also take a look at the pics on the previous page, left column for an example.
I got this wrong as well, but I definitely won't again! lol
i had the same problem, Whats about the fever?, could be present in gout?
I think this question mentioned the patient's temp was 100.4 which is consistent with mild fever in gout from inflammation.
This photo was wack though
The damage in gout is mediated by Neutrophils, so makes complete sense you see a bunch.
why not membrane receptor?
delF508 is a 3 base pair deletion of phenylalanine at amino acid position 508. Mutation causes impaired post-translational processing of CFTR (improper folding) which rough ER detects. Sends mutant misfolded CFTR to the proteasome for degradation, preventing it from reaching cell surface. So problem is not malfunctioning CFTR channels in the surface; problem is complete absence of CFTR on cell surface (since they keep getting misfolded and sent to proteasome to be trashed). Source of primary problem: error in protein structure
@Is3076 because the CFTR is a channel not a receptor.
FA 2019 p. 60
@a1913 is correct- as for @angelaq11, you can still have a receptor that also functions as a channel as they are not mutually exclusive. An example of this is the nAChR found on postsynaptic NMJ neurons. This is a non-selective, ligand-gated, ionotropic receptor that functions as a channel once its ligand (i.e., ACh) has bound to the active site to induce conformational change. Similarly on the same realm: CFTR is an ionotropic receptor that concurrently functions as a Cl- channel once its ligands (ie. 2 ATP) is bound to open the channel and enable Cl- flux.
This question in particular is asking for the underlying pathophysiologic mechanism for cystic fibrosis, which boils down to an issue with the primary structure of a protein resulting in its misfolding and subsequent sequestration/degradation.
There was a question about this in Uworld. for *stubborn* patients who are "not ready to quit" just yet you use the motivational approach. The technique acronym is OARS: Open ended questions, Affirmation, Reflect, Summarize.
Additionally the guy himself says "I know smoking is bad for me" Like he knows its bad, he doesnt care, but give him nicotine replacement and maybe he'll quit...
I didn't think nicotine replacement was a good answer choice b/c if he isn't ready to quit then why would he agree to use alternatives.
People who smoke and are addicted like the feel of the cigs and environmental ques. Using replacements would be more challenging. The second best answer choice would have been Rx.
why not detail the long-therm health effects of smoking?
@ titanesxvi: I assume because they always like the most "open ended" response.
If you start detailing the long term effects, the patient might interpret that as attempting to convince, and might resist or feel pressured. By having the patient elucidate what they consider pros and cons, you allow it to be an open discussion.
Also because the patient states he already knows smoking hurts him in the long run so it may come off as lecturing on something he already knows. I view this as what is the least-judgmental way to facilitate the patient moving on to the next step of the stages of change model largely of their own volition.
i choose the option c which is initiate a pulmunary function test. why is that a wrong choice?
@usmlehulk - he's asymptomatic, knows it is not good for him in the long run, but is not quite ready to make a change. It is best to talk with him about the pros/cons of cessation so that maybe he will make the decision to quit smoking soon.
Ordering a pulmonary function test is not going to be useful. Let's say it's decreased. Ok, so what? It doesn't change management in this patient right now.
Think of it as motivational interviewing
Still don't like the answer given that the patient already stated that he knows that it can do him harm in the long run. It seems like overkill.
What does "fixed cardiac output" signify?
"fixed cardiac output" might mean that with the stenosis (ie. narrowed aortic valve) there is a limited or rather reduced cardiac output. Exercise would not increase cardiac output because the stenosis is caused by a mechanical (physical) rather than a biochemical process. Therefore, At any given moment the heart can not increase its output no matter how forcefully it contracts.
why not option A?arterial compression ?
@fallot4logy LVH does not lead to coronary artery compression. only reallyyyy rarely will pulmonary artery dilation cause coronary artery compression. plus that would cause angina but probably wouldnt decrease cerebral bloodflow to syncope. her murmur + LVH point us toward aortic stenosis which does cause those --> fixed CO
@fallot4logy LVH can cause coronary artery compression, but typically leading to coronary ischemia after exercise (i.e. stable angina in this patient). The question is asking what leads to her syncope. Syncope actually means her brain is lacking blood supply abruptly.
how do we rule out mitral valve prolapse in this case?
@rainlad murmurs at the right upper sternal border are aortic in nature. Mitral murmurs are heard at left 5th intercostal at the midaxillary line.
Also, nobody mentioned the "prominent left ventricular impulse". I kinda get thrown off by these. Anyone have thoughts? Google was telling me it is from a hypertrophied ventricle so I'm thinking her aortic stenosis causes the LV hypertrophy and an impulse. Is this the correct line of thinking?
I don't think so. I know that K+ levels decrease with laxative use, due to dehydration, which activates the RAAS, which increased aldosterone, which cause Na+ re-absorption and K+ wasting. Aldosterone also causes the alpha intercalated cells to secrete more H+ into the urine, which causes a serum alkalosis. Therefore, in order to correct that, bicarb re-absorption decreases in the kidneys, which brings the pH closer to normal. As far as Chloride, I guess that must be re-absorbed with Na+ due to it being negatively charged (?). That's the one thing I'm not sure about.
I think what they are getting at is that it is Diarrhea--> Non-anion gap metabolic acidosis (HARDASS). This would mean that HCO3- would be low and chloride would be high (in non-anion gap acidosis the chloride increases and that's why you don't have a gap).
Normally, stool's electrolyte content primarily consists of bicarb, potassium, and sodium. Since the colon reclaims sodium in exchange for potassium, the potassium content of stool is usually double that of sodium. Most of our bicarb loss in stool actually occurs through the loss of organic acid anions, i.e. bicarb that's been titrated by the organic acids formed by bacterial fermentation in the colon (e.g. lactic acid).
*Bottom line: our stool is alkaline, with mostly bicarb and potassium.*
Diarrhea is a cause of *NON-anion gap metabolic acidosis* due to bicarb loss in the stool. We aren't adding any acids to the mix -- we're simply losing anions -- which is why our anion gap remains normal. Potassium goes along for the ride and we end up with *hypokalemic* metabolic acidosis. And because we're losing anions, we want to compensate by *increasing retention of Cl-*.
**Anion gap = Na+ - [Cl- + HCO3-]**
another observation to support this: The patient's RR is 30/min, which demonstrates a compensatory respiratory alkalosis, in response to the non-anion gap metabolic acidosis
I think it's because we would expect to see some more proteinuria/albuminuria if the plasma oncotic pressure had increased to compensate
Yeah haha I had the same conundrum.
If she's breathing deep as she breathes fast, then oxygen is still reaching the alveoli , so arterial pO2 would not be effected.
lmao i'm so freaking dumb i thought she was having alcohol withdrawals because it was relieved by alcohol
Maybe Po2 is unaffected bc its perfusion (blood) limited not difusion limited (under normal circumstances).
PErioral tingling- due to transient hypocalcemia induced by resp alkalosis.
I believe CO2 diffuses ~20x faster than O2, so increases in her respiratory rate have more effect on her PCO2 than her PO2
adding onto Charcot_bouchards comment, I found this:
Respiratory alkalosis secondary to hyperventilation is probably the most common cause of acute ionised hypocalcaemia. Binding between calcium and protein is enhanced when serum pH increases, resulting in decreased ionised calcium. Respiratory alkalosis can induce secondary hypocalcaemia that may cause cardiac arrhythmias, conduction abnormalities and various somatic symptoms such as paraesthesia, PErioral numbness, hyperreflexia, convulsive disorders, muscle spasm and tetany.