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Comments ...

 +0  (nbme20#15)

Couldn't you also decrease the FIO2? Per FA, CPP also increases to hypoxia also decreases CPP when PO2 < 50 mmHg.

cienfuegos  Obviously not the BEST option in this scenario, but seems like it could work unless I'm missing something.




Subcomments ...

submitted by hungrybox(175),

Loperamide: Agonist at u-opioid receptors. Slows gut motility (remember, constipation is a common side effect for all opioids).

quiz yourself:

Q: Would a junkie want to use Loperamide?

A: No, it has poor CNS penetration (which is why it has a low addictive potential).

Q: Would a junkie rather have morphine or buprenorphine?

A: Morphine. Both are u-opioid agonists, but morphine is a full agonist while buprenorphine is only a partial agonist.

Q: What about morphine vs. codeine?

A: Trick question, both are partial agonists.

cienfuegos  Thanks for passing off the knowledge. Regarding the last part, aren't morphine and codeine full agonists? +  


submitted by sahusema(12),

I got tricked into picking the "acquired antibodies against P1A1". Human platelet Ag platelet antigen P1-1a, located on integrin β3, is the main target for responsible for neonatal thrombocytopenia.https://www.jimmunol.org/content/194/12/5751

cienfuegos  Same, except in my case I was the person who was tricked and who did the tricking though. Thx for the link. +  


submitted by neonem(227),

Sounds like a case of Li-Fraumeni syndrome - since p53 is a tumor suppressor for a bunch of cell types, mutations in this gene (as in LFS) result in a myriad of familial tumor types.

pparalpha  Li-Fraunemi syndrome = SBLA (sarcoma, breast, leukemia, adrenal gland syndrome) and occurs because of an autosomal dominant inherited mutation of p53 APC: linked to FAP (colorectal cancer) RET: linked to papillary thyroid cancer, MEN 2A, MEN 2B RB1: retinoblastoma +3  
privatejoker  The thing that threw me off was that the only connection in her FH to the above SBLA reference was the mention of a paternal cousin with adrenocortical carcinoma. The other two mentioned had brain cancers, which seem completely outside the scope of the above mnemonic. Then again, as mentioned elsewhere, I suppose the best policy on these is just to rule out the absolute wrong answers. I swear, the NBME is lying when they tell us to choose the "best" answer on some of these. What they actually mean in practice is for us to choose the least shitty. +2  
dbg  ^ this guy cracked the code. nbme ur doomed. +1  
cienfuegos  @privatejoker: I feel the pain. Quick FYI: UW includes brain in the associated tumors. +1  
hyperfukus  we can just make her thing SBBLA and hopefully never get this wrong again +  


submitted by ergogenic22(28),

why is protection of the choroid plexus, from intraventricular rupture secondary to germinal matrix hemorrhage not a possible answer?

whoissaad  yes same question, both retinopathy and intraventricular hemmorage can occur due to high oxygen levels.. +  
cienfuegos  I mistakenly chose choroid plexus too, based on wiki seems this is most common cause of IVH in term infants: IVH in the preterm brain usually arises from the germinal matrix whereas IVH in the term infants originates from the choroid plexus. However, it is particularly common in premature infants or those of very low birth weight... Most intraventricular hemorrhages occur in the first 72 hours after birth. The risk is increased with use of extracorporeal membrane oxygenation in preterm infants. https://en.wikipedia.org/wiki/Intraventricular_hemorrhage#Babies +  
burak  choroid plexus is different than germinal amtrix +  


submitted by neonem(227),

I think you can know that this is a thalamic stroke rather than cortical because a cortical stroke occurring only in the postcentral gyrus (primary sensory cortex) and involving the entire homunculus without affecting the nearby precentral gyrus (primary motor cortex) is very unlikely.

sahusema  Ya I think this question is trying to test your knowledge between a cortical lesion and a subcortical lesion. +  
cienfuegos  Central Stroke Syndrome: Neuropathic pain due to thalamic lesions. Initial paresthesias followed in weeks to months by allodynia (ordinarily painless stimuli cause pain) and dysesthesia on the contralateral side. Occurs in 10% of stroke patients. FA 2018 499 +  


submitted by beeip(56),

This has been a tough concept for me to get, but I think I'm finally there:

The stem is describing primary adrenal insufficiency, or Addison's.

  • ACTH is being over-produced to stimulate the adrenals to produce cortisol, but they can't respond, either due to atrophy or destruction (TB, autoimmune: DR4, etc.)
  • The first 13 amino acids of ACTH can be cleaved to form α-MSH, which stimulates melanocytes, causing hyperpigmentation
jotajota94  Good job! Also, cortisol is involved in maintaining blood pressure. which was decreased in the patient. +3  
tinydoc  Decreased Na and increase K+ --- Hypoaldosteronisim Hypoglycemia, and hypotension --- Hypocortisolism so the adrenals arent working ---- adrenal Insufficiency the Hyperpigmentation comes from the increase ACTH as ACTH is from Proopiomelanocorticotropin. SO - increased ACTH also increases a -MSH ---> Hyper pigmentation. +5  
hungrybox  thank u for this answer +  
bilzcop  Ugh! I misread the question and chose ACTH :( +  
cienfuegos  @bilzcop: same +  
cienfuegos  @bilzcop: let's never do it again, k? +  
maxillarythirdmolar  Why does this patient have elevated BUN and creatinine?? +  


submitted by beeip(56),

This has been a tough concept for me to get, but I think I'm finally there:

The stem is describing primary adrenal insufficiency, or Addison's.

  • ACTH is being over-produced to stimulate the adrenals to produce cortisol, but they can't respond, either due to atrophy or destruction (TB, autoimmune: DR4, etc.)
  • The first 13 amino acids of ACTH can be cleaved to form α-MSH, which stimulates melanocytes, causing hyperpigmentation
jotajota94  Good job! Also, cortisol is involved in maintaining blood pressure. which was decreased in the patient. +3  
tinydoc  Decreased Na and increase K+ --- Hypoaldosteronisim Hypoglycemia, and hypotension --- Hypocortisolism so the adrenals arent working ---- adrenal Insufficiency the Hyperpigmentation comes from the increase ACTH as ACTH is from Proopiomelanocorticotropin. SO - increased ACTH also increases a -MSH ---> Hyper pigmentation. +5  
hungrybox  thank u for this answer +  
bilzcop  Ugh! I misread the question and chose ACTH :( +  
cienfuegos  @bilzcop: same +  
cienfuegos  @bilzcop: let's never do it again, k? +  
maxillarythirdmolar  Why does this patient have elevated BUN and creatinine?? +  


submitted by kentuckyfan(13),

I get why the mixed venous oxygen tension decreased. However,, isn't the systemic vascular resistance also decreased?

yb_26  no, decreased CO => peripheral vasoconstriction => SVR will be increased +2  
yssya1992  No SVR will increase due to RAAS and SAN thats why we decrease afterload in HF treatment ( ACEI, ARBs ) +2  
snafull  Wouldn't pulmonary vascular resistance also be decreased here due to pulmonary vasodilation in the setting of an MI? +  
cienfuegos  @snafull: my initial thought is that we would see pulmonary vasoconstriction because of the relatively low oxygen tension (that results from the low cardiac output). +1  


submitted by nala_ula(32),

In diabetic ketoacidosis, there is increased acid in the extracellular space. According to FA there is a transcellular shift due to decreased insulin that leads to more H+ entering the cell in exchange for K+. This leads to hyperkalemia with depleted intracellular stores of K+. There is also osmotic diuresis that leads to increased K+ loss in the urine and total body K+ depletion. The question asks that is most likely to decrease with insulin therapy: serum potassium concentration will decrease as K+ is now exchanged for H+ inside the cell.

cienfuegos  Additional UW fun facts regarding Potassium and DKA: use caution giving insulin and IV fluids to dehydrated hyperglycemic because i forces K in cells causing fast decrease of extracellular Potassium, thus give K supplementation even when serum K elevated +  


submitted by cr(1),

why not C?. It´s not supose that it improve the efectivity of insulin?

yb_26  thiazolidinediones (pioglitazone) increase insulin sensitivity (in muscles and liver) through activation of peroxisome proliferator-activated receptor-gamma (PPAR) I think they are asking about primarily mechanism of action, that's why it is E +  
cienfuegos  UW explanation regarding the genes upregulated 1. GLUT4: insulin responsive on adipocytes/skeletal increases G uptake 2. adiponectin: cytokine secreted by adipocytes increases # of insulin responsive adipocytes and stims FA oxidation 3. PPAR family also plays significant role in pathogenesis of metabolic syndrome +  


submitted by nosancuck(30),

Yo dis B got NO INTERNAL FEMALE ORGANS

Why dat!???

We be lookin at someone with an SRY from dere Y chromie! Dey be a Y chromie Homie so they be makin some Testis Determinin Factor which I be sure makes some nice lil ANTI MULLERIAN FACTOR so dey aint got that Female Internal Tract u know what i be sayin

And since wimminz is da DEFAULT they stil be gettin dose pussy lips and breastes

meningitis  The above explanation is correct (disregarding the hard to read and unprofessional dialect) but just in case anyone was wondering: chromatin-negative= Just a quick way of knowing it was a boy. The term applies to the nuclei of cells in normal males as well as those in individuals with certain chromosomal abnormalities +10  
yotsubato  Turner syndrome patients are also chromatin negative as well though.... +3  
sympathetikey  I didn't know a complication post-meningitis was lack of humor. +2  
sympathetikey  Ah, didn't read the last line. Yeah, that is taking it a bit far +1  
niboonsh  yall are haters. this is the first explanation that has ever made sense to me +2  
arkmoses  https://www.youtube.com/watch?v=yuXL-3eoB-o&t=77s Interesting syndrome watching this helped me to put it into real life perspective, interesting points they have no pubic hair/body hair, they apparently also dont smell, and breast size is usually increased... +  
whoissaad  How does chormatin-negative indicate a normal cell? Isn't chormatin just condensed DNA? +1  
cienfuegos  According to this paper most individuals with Turner Syndrome are chromatin negative: "One of the initial laboratory procedures used to confirm or rule out this diagnosis involves a sex chromatin determination from a buccal smear. Cells from the lining of the mouth are stained for the presence or absence of X-chromatin or Barr bodies, which represent a portion of an inactivated X chromosome. The typical Turner’s syndrome patient, who has 45 chromosomes and only one sex chromosome (an X), has no Barr bodies and is, therefore, X-chromatin negative. This abnormal X-chromatin negative finding in the majority of Turner’s syndrome females is similar to the result found in a normal male, who also has only one X chromosome, and differs from the X-chromatin positive condition observed in the normal female, who has two X chromosomes. Occasionally, the patient with features of Turner’s syndrome is found to be X-chromatin positive." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6233891/ +  
hyperfukus  i really hate haters this is awesome! +  


submitted by haliburton(74),

Bullous pemphigoid antigen must be hemidesmosome. FA: bulla are "bullow" the dermis (subepidermal blister). BP also yield "tense" bulla.

seagull  I love how this cant be straight forward. All the other proteins are either subunits of desmosomes or cytoskeletal components. Because I know molecular biology that well on top of the majority of medicine....FML +1  
cienfuegos  @seagull: excellent comment, literally loling right now +  
cienfuegos  or sobbing and threatening to hold my breath if they don't make it stop +  


submitted by haliburton(74),

Bullous pemphigoid antigen must be hemidesmosome. FA: bulla are "bullow" the dermis (subepidermal blister). BP also yield "tense" bulla.

seagull  I love how this cant be straight forward. All the other proteins are either subunits of desmosomes or cytoskeletal components. Because I know molecular biology that well on top of the majority of medicine....FML +1  
cienfuegos  @seagull: excellent comment, literally loling right now +  
cienfuegos  or sobbing and threatening to hold my breath if they don't make it stop +  


submitted by benzjonez(10),

Uworld Qid 1543 has a good explanation as to how pulmonary fibrosis increases the radial traction on the airway walls.

cienfuegos  I think this is it -pulmonary fibrosis increases elastic recoiland widens airway 2/2 increased outward force (radial traction) by fibrotic tissue thus decreasing airflow resistance thus supernormal expiratory flow rates (higher than nl following correction for lung volume) +  


submitted by est88(11),

Retroperitoneal structures: SAD PUCKER.

Only the descending colon is part of this.

meningitis  SAD PUCKER: Suprarenal (adrenal) glands [not shown] Aorta and IVC Duodenum (2nd through 4th parts) Pancreas (except tail) Ureters Colon (descending and ascending) Kidneys Esophagus (thoracic portion) Rectum (partially) +3  
cienfuegos  I find "SAID PUCKER" to be helpful because it includes IVC +  


submitted by hungrybox(175),

other answers:

inhibition of H2 receptors: (for GERD) prevent gastric acid secretion (cimetidine,

inhibition of phosphodiesterases (PDE):

  • theophylline (asthma) inhibits cAMP PDE
  • -nafils (dick pills) for ED inhibit cGMP PDE

β2 agonists: (for asthma) cause bronchodilation

  • albuterol (short acting - A for Acute)
  • salmeterol, formoterol (long acting - prophylaxis)

(idk lymphocyte membrane stabilization)

hungrybox  H2 blockers are the -tidines +1  
yotsubato  > dickpills lol +5  
temmy  hungrybox, you are a life saver +1  
cienfuegos  Via FA: take H2 before you dine, think "table for 2" to remember H2 +  


submitted by hayayah(330),

Note: The abducens n. is actually the nerve most likely to be damaged by an expanding internal carotid aneurysm in the cavernous sinus but they give you specific CN3 function in this question.

hungrybox  One pupil larger than the other indicates damage to the pupillary light reflex - afferent: CN II, efferent: CN III. +3  
cienfuegos  A little more info regarding other sxs (via UW): -cavernous carotid aneurysm: small usually asx, enlargement can cause u/l throbbing HA &/or CN deficits. VI most common thus ipsilateral lateral rectus weakness, can cause esotropia = inward eye deviation & horizontal diplopia worse when looking toward lesion -can also damage III, IV and V1/2 -can occasionally compress optic nerve or chiasm thus ipsilateral monoocular vision loss or non-specific visual acuity decrease +1  


submitted by haldol(3),

BP is low so obviously the body will want to respond by increasing sympathetics and decreasing parasympathetics. since the BP is low, there is less pressure against the wall of the carotid sinus -- meaning less stimulation and fewer impulses. fewer carotid impulses means fewer parasympathetics

pparalpha  Hyotension will lead to decreased arterial pressure and DECREASED stretch. This leads to decreased afferent barcreceptor firing (carotid sinus and aortic arch). This leads to an increase in efferent sympathetic firing and decreased efferent PNS stimulation. This leads to vasoconstriction, increased HR and increased BP. +  
sahusema  The way I remember this, carotid massage slows the heart. So baroreceptor stimulation (more impulses) increases parasympathetic output. +  
cienfuegos  FA 2018 pg 291 has helpful image/description +  


submitted by seagull(349),

Idiotypic means --- antibody against antibody. B cells don't have surface antibodies but mere synthesize them.

hungrybox  This is wrong. PLASMA cells (mature B cells, the ones found in multiple myeloma) secrete antibodies, but IMMATURE B cells have antibodies that haven't switched classes yet (IgM and IgD). +2  
hungrybox  To clarify - immature B cells have antibodies attached to their membrane. +  
seagull  I should have clarified that I was speaking about mature B cells. Thank You +1  
sahusema  So because MM has mature B cells, exogenous antibodies can't attach to them. Am I getting that right? +  
cienfuegos  What is an Anti-Idiotypic Antibody? As shown in figure 1, an anti-idiotypic (Anti-ID) antibody binds to the idiotype of another antibody, usually an antibody drug. An idiotype can be defined as the specific combination of idiotopes present within an antibodies complement determining regions (CDRs). A single idiotope, is a specific region within an antibodies Fv region which binds to the paratope (antigenic epitope binding site) of a different antibody. Therefore, and idiotope can be considered almost synonymous with an antigenic determinant of an antibody. https://www.genscript.com/antibody-news/what-is-an-anti-Idiotypic-antibody.html +  
cienfuegos  @sahusema: almost exactly correct, but it's important to note they are talking about idiotypic antibodies specifically because by definition these bind the "idiotype" of another antibody (see definition above) +  


submitted by seagull(349),

Idiotypic means --- antibody against antibody. B cells don't have surface antibodies but mere synthesize them.

hungrybox  This is wrong. PLASMA cells (mature B cells, the ones found in multiple myeloma) secrete antibodies, but IMMATURE B cells have antibodies that haven't switched classes yet (IgM and IgD). +2  
hungrybox  To clarify - immature B cells have antibodies attached to their membrane. +  
seagull  I should have clarified that I was speaking about mature B cells. Thank You +1  
sahusema  So because MM has mature B cells, exogenous antibodies can't attach to them. Am I getting that right? +  
cienfuegos  What is an Anti-Idiotypic Antibody? As shown in figure 1, an anti-idiotypic (Anti-ID) antibody binds to the idiotype of another antibody, usually an antibody drug. An idiotype can be defined as the specific combination of idiotopes present within an antibodies complement determining regions (CDRs). A single idiotope, is a specific region within an antibodies Fv region which binds to the paratope (antigenic epitope binding site) of a different antibody. Therefore, and idiotope can be considered almost synonymous with an antigenic determinant of an antibody. https://www.genscript.com/antibody-news/what-is-an-anti-Idiotypic-antibody.html +  
cienfuegos  @sahusema: almost exactly correct, but it's important to note they are talking about idiotypic antibodies specifically because by definition these bind the "idiotype" of another antibody (see definition above) +  


submitted by dr.xx(34),

Gastric varices are fed by the short gastric veins.

https://www.sciencedirect.com/science/article/pii/B9781437707748100764

cienfuegos  Add'l UW fun fact is differentiating from gastric varices 2/2 PHTN: Gastric varices: can also be seen w/ splenic vein throbmobis 2/2 chronic panceatitis, pancreatic cancer and abdominal tumors - gause gastric varices only in the fundus (remainder of stomach and esophagus usually not affected vs. PHTN: increased pressure in left gastric vens thus both gastric and esophageal varices) +  


submitted by liltr(8),

I choose MVP too, but this patient’s main symptom is cough only during exercise. This is more indicative of exercised associated asthma. You could see shortness of breath in MVP during exercise, but choosing MVP leaves the cough unaccounted for.

.ooo.   I agree! Also, At the end of the stem, the question is which of the following best explain the patients symptoms? Not physical exam findings. Since this patient is coming in with a chief complaint of SOB while playing sports exercise induced asthma is the best choice. Hopefully that helps. +3  
uslme123  I mean... couldn't increased BP during exercise worsen his MVP and give him SOB? +  
uslme123  (by causing slight regurg) +1  
yotsubato  "Lungs are clear to auscultation" +3  
sahusema  But wouldn't choosing exercise-induced asthma leave the murmur unaccounted for? +  
cienfuegos  I incorrectly chose malingering and am wondering if the fact that he presented (although it doesn't state who brought him in/confirmed his symptoms while exercising) makes this less likely despite the fact that he clearly states "I don't want to play anymore" which could be interpreted as a secondary gain? Also, regarding the MVP, I'm wondering if the fact that these are usually benign should have factored into our decision to rule it out? Thoughts? +  
cienfuegos  Just noticed that he has FHx, game changer. +  
kimcharito  clear lungs, they try to say no cardiogenic Pulm. edema, means is not due to MVP shortness of breath while doing sports and no shortness at rest makes me to think more asthma induced by exercise) +  


submitted by liltr(8),

I choose MVP too, but this patient’s main symptom is cough only during exercise. This is more indicative of exercised associated asthma. You could see shortness of breath in MVP during exercise, but choosing MVP leaves the cough unaccounted for.

.ooo.   I agree! Also, At the end of the stem, the question is which of the following best explain the patients symptoms? Not physical exam findings. Since this patient is coming in with a chief complaint of SOB while playing sports exercise induced asthma is the best choice. Hopefully that helps. +3  
uslme123  I mean... couldn't increased BP during exercise worsen his MVP and give him SOB? +  
uslme123  (by causing slight regurg) +1  
yotsubato  "Lungs are clear to auscultation" +3  
sahusema  But wouldn't choosing exercise-induced asthma leave the murmur unaccounted for? +  
cienfuegos  I incorrectly chose malingering and am wondering if the fact that he presented (although it doesn't state who brought him in/confirmed his symptoms while exercising) makes this less likely despite the fact that he clearly states "I don't want to play anymore" which could be interpreted as a secondary gain? Also, regarding the MVP, I'm wondering if the fact that these are usually benign should have factored into our decision to rule it out? Thoughts? +  
cienfuegos  Just noticed that he has FHx, game changer. +  
kimcharito  clear lungs, they try to say no cardiogenic Pulm. edema, means is not due to MVP shortness of breath while doing sports and no shortness at rest makes me to think more asthma induced by exercise) +  


submitted by yo(21),

I just knew that sperm need fructose, not sure what disease process this is though. He was pretty normal so 5a reducatase doesn't present like that. I wasn't sure if there was any odd use of the other answers. here is a link. Feel free to expand.

https://www.labce.com/spg27422_question.aspx

Fructose makes up 99% of the reducing sugar present in semen. This sugar is produced in the seminal vesicles. Diminished levels of fructose have been shown to parallel androgen deficiency and the testosterone level. Following testosterone therapy, the level of fructose increases. Although the fructose test is not part of a routine semen analysis, it is useful in cases of azoospermia (absence of sperm in semen). In azoospermia secondary to the absence of vesicles or if there is an obstruction, no fructose is present. In testicular azoospermia, fructose is present. When azoospermia and low semen volume exists, the fructose test should also be done, on a postejaculate urine sample to check for retrograde ejaculation. This occurs when the ejaculate goes into the bladder instead of out the urethra. The procedure for determining the amount of fructose in semen involves heating semen in a strong acid in the presence of resorcinol. Fructose gives a red color (Selivonoff reaction) and may be read in a photometer. The normal average is 315mg/dL fructose.

sam.l  Thank you for the explanation. I'm still confused about this answer. I was in between Zinc and fructose. Zinc deficiency also presents with anosmia (pg 71 First Aid 2019). Fructose is used for the movement. His hormones are normal. +1  
d_holles  Apparently diabetes, occlusion, and inflammation can result in ↓ fructose in sperm. Mauss et al, Fert Stert 25, 1974 https://www.fertstert.org/article/S0015-0282(16)40391-2/pdf +1  
cienfuegos  Thanks all for the info, quick note on the Zinc reply above @Sam.I: anosmia = lost sense of smell. +  
sam1  Great find yo! I believe this question was alluding to cystic fibrosis and the congenital absence of the vas deferens. Here is a link to a NEJM article about it below: https://www.nejm.org/doi/full/10.1056/NEJM196807112790203 +  
burak  zinc deficiency cause hypogonadism. there is no hypogonadism, sperms are damaged? +  


submitted by nerdy nik(2),

DVT that went to the brain. If it would have gone to the pulmonary artery she would have a PE, but it crossed the atria wall via a patent foramen ovale and went directly to the brain.

cienfuegos  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. OCP) -evaluate cryptogenic stroke with buble study: inj agitated nl saline and look for bubbles in left heart +  


submitted by hyoscyamine(19),

This is lateral medullary/PICA/Wallenberg syndrome. The woman has damage in the sympathetic chain (sensory syndromes are lateral according to the rule of 4s) resulting in Horner syndrome, spinothalamic tract (pain/temp which are also sensory), and CN IX and CN X dysfunction resulting in the dysphagia/dysarthria (helps us localize to the medulla).

nala_ula  Also, just to add, FA specifies that Nucleus ambiguus effects (dysphagia, hoarseness, decreased gag reflex) are specific to PICA lesions. +1  
cienfuegos  Thanks for the input. I have always found this topic to be tricky and just came across this article that helped me out a ton regarding the rule of 4's hoscyamine mentions above. https://rdcu.be/bLjOB +  


submitted by xxabi(78),

Broca’s aphasia: expressive (motor aphasia) with agrammatism (pts aware that they don’t make sense) - area A Wernicke’s aphasia: receptive (sensory) aphasia with impaired comprehension (pts lack insight)

breis  Why would B be incorrect? I realize Broca is "technically lower" but A seems too low to be causing weakness of the lower 2/3 of the face? Am I missing something? +  
shaeking  @breis B is incorrect because of the lower 2/3 of the face weakness. B isn't located on the motor cortex but in the premotor cortex, plus it isn't low enough for the lower two thirds of the face. https://thebrain.mcgill.ca/flash/a/a_06/a_06_cr/a_06_cr_mou/a_06_cr_mou.html https://www.sciencenews.org/blog/science-ticker/homunculus-reimagined +  
cienfuegos  @breis, per UW: "a/w r. hemiparesis (face & UE) bc close to primary motor cortex" +  


How would you know that it isn't wool sorters disease?

cienfuegos  FA 2018 137: inhalation of spores leads to flu-like symptoms that progress quickly to fever, pulmonary hemorrhage, mediastinitis and shock, with imaging possibly showing widened mediastinum +  


submitted by cienfuegos(4),

Couldn't you also decrease the FIO2? Per FA, CPP also increases to hypoxia also decreases CPP when PO2 < 50 mmHg.

cienfuegos  Obviously not the BEST option in this scenario, but seems like it could work unless I'm missing something. +  


Salivary secretion 1. At low flow = High concentration of potassium; low concentrations of sodium, bicarb, & chloride 2. at high flow = low concentration of potassium; high concentrations of sodium, bicarb, & chloride

sherry  That's exactly what I was thinking when I was taking the test. But I was sidetracked by same HCO3 level. Can somebody explain this part to me?? +  
charcot_bouchard  Because salivary duct removes Na & Cl while secrete K & Hco3 in lumen. In low flow rate HCO3 & K inc because duct is doing its thing for more time. At high flow rate K slightly dec (as cant be secrted as much) but HCO3 stays almost same. the reason is high flow indicates higher metabolism & higher bicarb production. +  
cienfuegos  Regarding the bicarb (via BRS Physiology, which explains flow rate as coming down to "contact time" where slow flow allows more reabsorption of NaCl): The only ion that does not “fit” this contact time explanation is HCO3−; HCO3− secretion is selectively stimulated when saliva secretion is stimulated. +1  


submitted by johnthurtjr(42),

While I can get on board with Adjustment Disorder, I don't see how this answer is any better than Somatic Symptom Disorder. From FA:

Variety of bodily complaints lasting months to years associated with excessive, persistent thoughts and anxiety about symptoms. May co-appear with illness.

SSD belongs in a group of disorders characterized by physical symptoms causing significant distress and impairment.

savdaddy  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. +  
chillqd  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 +  
hello  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". +3  
cienfuegos  I also had issues differentiating these two and ultimately went with SSD, but upon further review it seems that a key differentiating feature was the timeline. His somatic symptoms would have had to have been present for at least 6 months per the DSM criteria https://www.ncbi.nlm.nih.gov/books/NBK519704/table/ch3.t31/ +