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Welcome to pakimd’s page.
Contributor score: 8


Comments ...

 +0  (nbme15#21)

partial seizures are focal seizures that are limited to one lobe of the brain and symptoms are according to what lobe of the brain is affected. since only motor symptoms are seen in one part of the body frontal motor cortex of that area of the body is the probable area of hyperactivity. now since there is a post ictal state (pt takes a few min to return to normal) and during the episode of seizure the pt. does not respond to questions (impaired awareness) followed by automatisms you know its complex and not simple partial. you know its not absence because even though pt's awareness is impaired during the seizure there is no post ictal state.

pakimd  there is no post ictal state in absence +

 +0  (nbme15#27)

empty can test isolates the supraspinatus tendon impingement between the acromion and humeral head and finds weakness of the supraspinatus muscle. it is performed by asking the pt. to abduct the arm in the scapular plane at 90 degrees with the arm extended with the the thumb point downwards and asked to abduct the shoulder against resistance. this will reproduced pain and indicate a positive empty can test and indicate supraspinatus tendinopathy

djeffs1  I just love "Abduction of the shoulder when the shoulder is abducted..." +1
pakimd  was just trying to say that the pt. is asked to resist the downward pressure applied by the examiner which will only occur when the pt. is asked to abduct/keep his arm elevated against resistance. no need to be nasty. we are all trying to help each other here. +
pakimd  you can just ask the pt. to resist downward pressure but too many times in clinical practice ive notced pts. getting confused so you specifically have to instruct them not to put their arm down when pressure is applied. that is why my answer (unintentionally) was phrased the way it was. +
djeffs1  @pakimd I got the question right, and i wasn't criticizing you. just pointing out a funny literary chiasmus in the actual question stem +1

 +0  (nbme15#36)

Anterior (or sternocostal) – Right ventricle.

Posterior (or base) – Left atrium.

Inferior (or diaphragmatic) – Left and right ventricles.

Right pulmonary – Right atrium.

Left pulmonary – Left ventricle.

both left and right ventricles are on the diaphragmatic surface. AV node is also affected. PDA supplies posterior 2/3rd walls of both right and left ventricles and the AV nodes so we know that PDA is affected. now we need to figure out the order of cath passage. question states left dominant circulation. so itll be left coronary -> LCX -> PDA (aka posterior interventricular since PDA supplies post. 1/3 of interventricular septum)

pakimd  FA pg 283 +

 +0  (nbme15#41)

loading dose= [target plasma conc. (at steady state) x vol of distribution / bioavailability] x weight

bioavailability is 100% if IV dose. so bioavailability is 1 (100/100= 1 which is 100%)

now loading dose is:

10 mg/L x 1.81 L/kg X 55 kg

(cut all the common units in numerator and denominator)

you get-- 10 mg x 1.81 x 55 = 995.5 mg ~ 1000 mg total loading dose


 +0  (nbme15#9)

@docinthehouse18 yes colon cancer spreads to distant organs via lymphatics e.g. to the lungs but the reason why the most common location of colon cancer metastasis is the liver is because of the unique anatomic situation with regards to portal venous system. so colon cancer spreads to the liver hematogenously via portal venous system but otherwise spreads to distant sites via lymphatics. the question asks the route of metastasis to the liver and tumor seeding of the abdominal cavity from the colonic tumor will not cause mets in liver. 4 carcinomas that spreads hematogenously only and only spreads via blood.

cheesetouch  4 hematogenously spreading cancers (pathoma ch3): RCC (renal vein) HCC (hepatic vein) Choriocarcinoma Follicular ca of the thyroid +




Subcomments ...

submitted by pakimd(8),

empty can test isolates the supraspinatus tendon impingement between the acromion and humeral head and finds weakness of the supraspinatus muscle. it is performed by asking the pt. to abduct the arm in the scapular plane at 90 degrees with the arm extended with the the thumb point downwards and asked to abduct the shoulder against resistance. this will reproduced pain and indicate a positive empty can test and indicate supraspinatus tendinopathy

djeffs1  I just love "Abduction of the shoulder when the shoulder is abducted..." +1  
pakimd  was just trying to say that the pt. is asked to resist the downward pressure applied by the examiner which will only occur when the pt. is asked to abduct/keep his arm elevated against resistance. no need to be nasty. we are all trying to help each other here. +  
pakimd  you can just ask the pt. to resist downward pressure but too many times in clinical practice ive notced pts. getting confused so you specifically have to instruct them not to put their arm down when pressure is applied. that is why my answer (unintentionally) was phrased the way it was. +  
djeffs1  @pakimd I got the question right, and i wasn't criticizing you. just pointing out a funny literary chiasmus in the actual question stem +1  


submitted by pakimd(8),

empty can test isolates the supraspinatus tendon impingement between the acromion and humeral head and finds weakness of the supraspinatus muscle. it is performed by asking the pt. to abduct the arm in the scapular plane at 90 degrees with the arm extended with the the thumb point downwards and asked to abduct the shoulder against resistance. this will reproduced pain and indicate a positive empty can test and indicate supraspinatus tendinopathy

djeffs1  I just love "Abduction of the shoulder when the shoulder is abducted..." +1  
pakimd  was just trying to say that the pt. is asked to resist the downward pressure applied by the examiner which will only occur when the pt. is asked to abduct/keep his arm elevated against resistance. no need to be nasty. we are all trying to help each other here. +  
pakimd  you can just ask the pt. to resist downward pressure but too many times in clinical practice ive notced pts. getting confused so you specifically have to instruct them not to put their arm down when pressure is applied. that is why my answer (unintentionally) was phrased the way it was. +  
djeffs1  @pakimd I got the question right, and i wasn't criticizing you. just pointing out a funny literary chiasmus in the actual question stem +1  


submitted by andro(169),

The uneven distribution of ADHD based on gender(more cases of ADHD among boys ) is a potential confounder , and so STRATIFICATION addresses this

pakimd  how is a disease more common in one age group a confounder? +  


submitted by pakimd(8),

partial seizures are focal seizures that are limited to one lobe of the brain and symptoms are according to what lobe of the brain is affected. since only motor symptoms are seen in one part of the body frontal motor cortex of that area of the body is the probable area of hyperactivity. now since there is a post ictal state (pt takes a few min to return to normal) and during the episode of seizure the pt. does not respond to questions (impaired awareness) followed by automatisms you know its complex and not simple partial. you know its not absence because even though pt's awareness is impaired during the seizure there is no post ictal state.

pakimd  there is no post ictal state in absence +  


submitted by cassdawg(924),

She has left homomynous hemianopia, which can be due to lesion of the contralateral optic tract or as in this case lesion to the contralateral occipital lobe. It is not mentioned explicitly but this causes macular sparing. (FA2020 p542 gives the visual field defects)

bbr  tricky tricky +1  
pontiacfever  Left homonymous hemianopia w/o macular sparing can also occur due to damage to parietal and temporal lobes. But occipital lobe damage is more common. +  
i_hate_it_here  <-- +  
pakimd  macular sparing will only occur if there is an infarct of the posterior coronary artery supplying the occipital lobe. this is because the macular region of the visual cortex has a double blood supply from the middle cerebral artery and the posterior cerebral artery. this woman has breast cancer hence the mets are probably directly to the occipital lobe causing left homonymous hemianopia WITHOUT macular sparing. FA pg 542 look at the illustration: it says number 3 (left homonymous hemianopia WITHOUT macular sparing) and 6 (if PCA infarct when there is left homonymous hemianopia WITH macular sparing) +1  


submitted by hungrybox(961),

Image from problem

Fluent speech, impaired comprehension β†’ Fluent aphasia β†’ Wernicke's area

Here are the others (as near as I could tell):

A: Broca's area β†’ "Broken Boca" β†’ would present with non-fluent speech with intact comprehension

B: ?

C, D: Motor cortex

E, F: Sensory cortex

G: ?

H: Wernicke's area


No idea what B or G are.

Here's a relevant image from Amboss

kahin  B-Frontal eye field? G-Parietal lobe +  
specialist_jello  G : Gerstmann syndome? angular gyrus? not sure +  
pakimd  G does look like angular gyrus since it is right above the wernicke area +  


submitted by pakimd(8),

Anterior (or sternocostal) – Right ventricle.

Posterior (or base) – Left atrium.

Inferior (or diaphragmatic) – Left and right ventricles.

Right pulmonary – Right atrium.

Left pulmonary – Left ventricle.

both left and right ventricles are on the diaphragmatic surface. AV node is also affected. PDA supplies posterior 2/3rd walls of both right and left ventricles and the AV nodes so we know that PDA is affected. now we need to figure out the order of cath passage. question states left dominant circulation. so itll be left coronary -> LCX -> PDA (aka posterior interventricular since PDA supplies post. 1/3 of interventricular septum)

pakimd  FA pg 283 +  


submitted by cassdawg(924),

The -navirs are protease inhibitors, so a mutation in protein processing would cause resistance.

radzio1  in FA p203 it literally says Protease Inhibitors act by inhibiting maturation and assembly. So thats what I picked. Why is protein processing more appropriate? +2  
radzio1  in FA p203 it literally says Protease Inhibitors act by inhibiting maturation and assembly. So thats what I picked. Why is protein processing more appropriate? +  
kaf  maybe packaging means sending out of the cell? +  
pakimd  on pg 203 of first aid it says protease inhibitors inhibit HIV-1 protease which cleaves polypeptide products of HIV mRNA into their functional parts; proteases are responsible for cleaving and processing proteins made from HIV RNA transcript into functional parts and protease inhibits this process by inhibiting proteases responsible for processing proteins that are made from HIV mRNA +  
pakimd  on pg 203 of first aid it says protease inhibitors inhibit HIV-1 protease which cleaves polypeptide products of HIV mRNA into their functional parts; proteases are responsible for cleaving and processing proteins made from HIV RNA transcript into functional parts and protease inhibits this process by inhibiting proteases responsible for processing proteins that are made from HIV mRNA +  
pakimd  protease inhibitors* inhibit proteases +  
pakimd  and then those functional proteins are assembled and packaged into virions to be released and infect other T cells +  
pakimd  if you look at the illustration on pg 201 of FA youll see that they say that protease inhibitors inhibit proteolytic processing +1  
cheesetouch  in a UW question I did, it said that protease inhibitors inhibit gag-pol cleavage, which would probably be considered a form of processing. gag -> p24 capsid and p17 matrix proteins pol -> reverse txase, aspartate protease, integrase pakimd makes a great point above about the img on 201. I think this is just kind of a crappy question LOL +  
whk123  [Check here the image says that, sketchy pharma mentioned regarding pol gene too in regard of navirs] (https://basicmedicalkey.com/wp-content/uploads/2017/02/image01621.jpeg) => Here it comes +  


submitted by cassdawg(924),

The -navirs are protease inhibitors, so a mutation in protein processing would cause resistance.

radzio1  in FA p203 it literally says Protease Inhibitors act by inhibiting maturation and assembly. So thats what I picked. Why is protein processing more appropriate? +2  
radzio1  in FA p203 it literally says Protease Inhibitors act by inhibiting maturation and assembly. So thats what I picked. Why is protein processing more appropriate? +  
kaf  maybe packaging means sending out of the cell? +  
pakimd  on pg 203 of first aid it says protease inhibitors inhibit HIV-1 protease which cleaves polypeptide products of HIV mRNA into their functional parts; proteases are responsible for cleaving and processing proteins made from HIV RNA transcript into functional parts and protease inhibits this process by inhibiting proteases responsible for processing proteins that are made from HIV mRNA +  
pakimd  on pg 203 of first aid it says protease inhibitors inhibit HIV-1 protease which cleaves polypeptide products of HIV mRNA into their functional parts; proteases are responsible for cleaving and processing proteins made from HIV RNA transcript into functional parts and protease inhibits this process by inhibiting proteases responsible for processing proteins that are made from HIV mRNA +  
pakimd  protease inhibitors* inhibit proteases +  
pakimd  and then those functional proteins are assembled and packaged into virions to be released and infect other T cells +  
pakimd  if you look at the illustration on pg 201 of FA youll see that they say that protease inhibitors inhibit proteolytic processing +1  
cheesetouch  in a UW question I did, it said that protease inhibitors inhibit gag-pol cleavage, which would probably be considered a form of processing. gag -> p24 capsid and p17 matrix proteins pol -> reverse txase, aspartate protease, integrase pakimd makes a great point above about the img on 201. I think this is just kind of a crappy question LOL +  
whk123  [Check here the image says that, sketchy pharma mentioned regarding pol gene too in regard of navirs] (https://basicmedicalkey.com/wp-content/uploads/2017/02/image01621.jpeg) => Here it comes +  


submitted by cassdawg(924),

The -navirs are protease inhibitors, so a mutation in protein processing would cause resistance.

radzio1  in FA p203 it literally says Protease Inhibitors act by inhibiting maturation and assembly. So thats what I picked. Why is protein processing more appropriate? +2  
radzio1  in FA p203 it literally says Protease Inhibitors act by inhibiting maturation and assembly. So thats what I picked. Why is protein processing more appropriate? +  
kaf  maybe packaging means sending out of the cell? +  
pakimd  on pg 203 of first aid it says protease inhibitors inhibit HIV-1 protease which cleaves polypeptide products of HIV mRNA into their functional parts; proteases are responsible for cleaving and processing proteins made from HIV RNA transcript into functional parts and protease inhibits this process by inhibiting proteases responsible for processing proteins that are made from HIV mRNA +  
pakimd  on pg 203 of first aid it says protease inhibitors inhibit HIV-1 protease which cleaves polypeptide products of HIV mRNA into their functional parts; proteases are responsible for cleaving and processing proteins made from HIV RNA transcript into functional parts and protease inhibits this process by inhibiting proteases responsible for processing proteins that are made from HIV mRNA +  
pakimd  protease inhibitors* inhibit proteases +  
pakimd  and then those functional proteins are assembled and packaged into virions to be released and infect other T cells +  
pakimd  if you look at the illustration on pg 201 of FA youll see that they say that protease inhibitors inhibit proteolytic processing +1  
cheesetouch  in a UW question I did, it said that protease inhibitors inhibit gag-pol cleavage, which would probably be considered a form of processing. gag -> p24 capsid and p17 matrix proteins pol -> reverse txase, aspartate protease, integrase pakimd makes a great point above about the img on 201. I think this is just kind of a crappy question LOL +  
whk123  [Check here the image says that, sketchy pharma mentioned regarding pol gene too in regard of navirs] (https://basicmedicalkey.com/wp-content/uploads/2017/02/image01621.jpeg) => Here it comes +  


submitted by cassdawg(924),

The -navirs are protease inhibitors, so a mutation in protein processing would cause resistance.

radzio1  in FA p203 it literally says Protease Inhibitors act by inhibiting maturation and assembly. So thats what I picked. Why is protein processing more appropriate? +2  
radzio1  in FA p203 it literally says Protease Inhibitors act by inhibiting maturation and assembly. So thats what I picked. Why is protein processing more appropriate? +  
kaf  maybe packaging means sending out of the cell? +  
pakimd  on pg 203 of first aid it says protease inhibitors inhibit HIV-1 protease which cleaves polypeptide products of HIV mRNA into their functional parts; proteases are responsible for cleaving and processing proteins made from HIV RNA transcript into functional parts and protease inhibits this process by inhibiting proteases responsible for processing proteins that are made from HIV mRNA +  
pakimd  on pg 203 of first aid it says protease inhibitors inhibit HIV-1 protease which cleaves polypeptide products of HIV mRNA into their functional parts; proteases are responsible for cleaving and processing proteins made from HIV RNA transcript into functional parts and protease inhibits this process by inhibiting proteases responsible for processing proteins that are made from HIV mRNA +  
pakimd  protease inhibitors* inhibit proteases +  
pakimd  and then those functional proteins are assembled and packaged into virions to be released and infect other T cells +  
pakimd  if you look at the illustration on pg 201 of FA youll see that they say that protease inhibitors inhibit proteolytic processing +1  
cheesetouch  in a UW question I did, it said that protease inhibitors inhibit gag-pol cleavage, which would probably be considered a form of processing. gag -> p24 capsid and p17 matrix proteins pol -> reverse txase, aspartate protease, integrase pakimd makes a great point above about the img on 201. I think this is just kind of a crappy question LOL +  
whk123  [Check here the image says that, sketchy pharma mentioned regarding pol gene too in regard of navirs] (https://basicmedicalkey.com/wp-content/uploads/2017/02/image01621.jpeg) => Here it comes +  


submitted by cassdawg(924),

The -navirs are protease inhibitors, so a mutation in protein processing would cause resistance.

radzio1  in FA p203 it literally says Protease Inhibitors act by inhibiting maturation and assembly. So thats what I picked. Why is protein processing more appropriate? +2  
radzio1  in FA p203 it literally says Protease Inhibitors act by inhibiting maturation and assembly. So thats what I picked. Why is protein processing more appropriate? +  
kaf  maybe packaging means sending out of the cell? +  
pakimd  on pg 203 of first aid it says protease inhibitors inhibit HIV-1 protease which cleaves polypeptide products of HIV mRNA into their functional parts; proteases are responsible for cleaving and processing proteins made from HIV RNA transcript into functional parts and protease inhibits this process by inhibiting proteases responsible for processing proteins that are made from HIV mRNA +  
pakimd  on pg 203 of first aid it says protease inhibitors inhibit HIV-1 protease which cleaves polypeptide products of HIV mRNA into their functional parts; proteases are responsible for cleaving and processing proteins made from HIV RNA transcript into functional parts and protease inhibits this process by inhibiting proteases responsible for processing proteins that are made from HIV mRNA +  
pakimd  protease inhibitors* inhibit proteases +  
pakimd  and then those functional proteins are assembled and packaged into virions to be released and infect other T cells +  
pakimd  if you look at the illustration on pg 201 of FA youll see that they say that protease inhibitors inhibit proteolytic processing +1  
cheesetouch  in a UW question I did, it said that protease inhibitors inhibit gag-pol cleavage, which would probably be considered a form of processing. gag -> p24 capsid and p17 matrix proteins pol -> reverse txase, aspartate protease, integrase pakimd makes a great point above about the img on 201. I think this is just kind of a crappy question LOL +  
whk123  [Check here the image says that, sketchy pharma mentioned regarding pol gene too in regard of navirs] (https://basicmedicalkey.com/wp-content/uploads/2017/02/image01621.jpeg) => Here it comes +  


submitted by cassdawg(924),

TL;DR: Even with Type I or II renal tubular acidosis the ammoniagenesis from glutamine is not impaired and thus is the main source of ammonia.

Here is my take: Based on her history and measured plasma values, this girl likely has one of the "low potassium" renal tubular acidoses, either Type I or Type II (see this chart for reasoning based on measured values or this image for fun colorful renal tubular acidosis and FA2020 p593)

Then, we are told that she has a defect in "ammoniagenesis". In the renal tubules, ammonia is generated in two primary ways: via direct conversion of glutamine to ammonia in the proximal tubule which is then secreted into the tubule, or by NH3 combining with with H+ in the collecting tubules (which I guess they are considering a separate ammoniagenesis pathway even though its all kinda related?). See this diagram or this diagram

Assuming our girl has Type I renal tubular acidosis, there will be decreased availability of hydrogen ions in the renal tubules to combine with NH3. Thus, the primary source of ammonia production in this patient will be glutamine (which is the major source of ammoniagenesis in a normal person anyways).

Further reasoning - Type I is impaired secretion of hydrogen ions into the lumen, so there will be less hydrogen ions available. She likely has type I because this is primarily treated with potassium citrate (both to buffer and to prevent renal stones which are a common complication). Even if she had Type II the increased excretion of bicarb would also buffer more H+ leaving less for ammoniagenesis in the NH3/H+ combination fashion.

Contrarily, Type 4 renal tubular acidosis (hyperkalemic) results in decreased synthesis of ammonia in the proximal tubules, which we know she does not have because of her low potassium.

cheesetouch  Cassie you're a god. Simple/stupid approach to make a good guess - if she cannot make ammonia in the kidney, main ammonia source probably from an exogenous form like amino acids -> Glutamine! +2  
pakimd  thank you @cassdawg, you're amazing! +  


submitted by ergogenic22(300),
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laccsis atyeinshma sagvir ip.erutc eosnsrW hwti e.us Sx cnileud apipil.od Irvemtpoemn tiwh h.CEA

losA dies nt,oe do'nt fucos no eth cnrngaepy tauts,s tub oenwm hwo era ni hte usappomtrt eordi aer at pryirtullaca ihhg irsk fo ndpgeveoli htasmiyaen rigsva

pakimd  why are answers unscrambled on here? +  


submitted by cassdawg(924),

Deoxyhemoglobin has a higher pKa than oxyhemaglobin and thus will accept hydrogen ions more readily. This is important in the ability to "carry" CO2 as the main mechanism of CO2 transport is actually conversion of CO2 to HCO3- (CO2 + H2O -> HCO3- + H+), thus deoxyhemaglobin carries the H+ while HCO3- is transported in the plasma to the lungs. Carbaminohemaglobin is actually only about 20% of the CO2 trasnport and CO2 dissolved as CO2 is 10%; trasnport as HCO3- is around 70% of the CO2 transport.

Here is another image of the process.

Another important aspect of the process to take note of that they like to ask about is the chloride shift. Chloride moves the opposite direction as HCO3- in the RBC. Thus at tissues where we are generating HCO3- from CO2 and need to pump it out of the cell, chloride moves into the cell.At the alveoli where we need to pump HCO3- back into the RBC to turn it into CO2, chloride moves out of the cell.

Other answers:

  • 2,3BPG will bind and stabilizes deoxyhemaglobin making it less attracted to oxygen, shifting the hemaglobin dissosiation curve right.
  • Deoxyhemaglobin has a higher capacity to form carbanimohemaglobin
  • Deoxyhemaglobin has a higher pKA than oxyhemaglobin (this is why it can accept hydrogen ions more readily)
  • Competition for binding site is not a major mechanism for the ability to carry CO2 as most CO2 is "carried" by conversion to HCO3-
  • Nitric oxide binding is not a mechanism of CO2 carry.
i_hate_it_here  <-- +  
pakimd  @cassdawg thank you for explaining so well along with explaining all the answer options. +  


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p + q = 1 p2 ^ + pq2 + 2^q = 1 if q^2 = 10/601 = .036000 neh t q = r(q2stq^) = .0052 v sleo ofr p ot gte p = 1 - r = 1 - .0052 = .5907 eth oyzoestehugr sracrrie = p2q = 1 - ^2p = 1 - 095. = 0.5 ^2q nca eb oprdpde cb/ is't mhcu rlleams tnha 2.^p e Th ldenetio is ensrilbsope ofr %08 fo teh mniat.tsuo 0.8 x 05. = 004. = 00/41 = 51/2

heerT imthg eb an aierse ywa to do hsti, tbu ti rkewdo ofr e.m

thechillhill  So apparently I don't know how to format very well. Sorry! +1  
pakimd  So because i couldnt spend more than a minute on this question and honestly didnt recall the Hardy-Weinberg equation this is how i solved it under a minute: so you know in a given population half of them will be carriers since its an autosomal recessive disease Aa Aa= AA aa Aa Aa so of that half 80% are due to deletion mutations and 20% are due point mutations by that logic 80% of half into 20% of half will give you 1/25 +1  
draykid  0.8 x 0.5 is 0.4 +  


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ncealrIotzao reqeiurs teh icdcia mntneoeirnv fo eht sohcamt to eb erb.dasbo Ozepmolrea nbiitsih hte +/H+K mppu of het t,mosach bhteeyr sicnadgeer the dcaytii of eth .tmscaoh So nhew eth pttiena eksat lepzoamerO nda rnztalaoIoce gor,hetet taczonaIolre on'tw be serdobab tino the .oybd hs'taT ywh ti hsa no fetcfe.

tIs' ormdeedcnme to ekta idiotcesanm at aeslt 2 oshru riorp ot gikant an tan.cadi

necrotizingfasciitis  Just adding support to the above explanation: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3671798/ +3  
pakimd  do all azoles or just itraconazole only requires an acidic environment to be absorbed? +2  
chandlerbas  just itraconazole and posaconazole +5  
lilyo  @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! +5  
chandlerbas  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! +  
haozhier  How are we supposed to know this!! It is not in UWORLD or FA right? +7  
kevin  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 +  
aoa05  Golan pharm book states the exact same thing. Cannot be given to patients with acholrhydria. +  


submitted by ergogenic22(300),
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iagng trsusle in adeneicsr tiaelrra sfsnfites (agcneh ni atxEr allrculCe artMmix omstciniopo - daceereds ,eatlnis isacdeern lngacloe )st;idnepooi HIS si ssrpoielebn orf 6-0%08 of NTH eascs ni tatsipne ;tg& .06 ,Aols ceresedda accpminleo as a uletrs of anggi sceaus esrcednai plseu esresrpu

rio19111  why not dev. of coronary atherosclerosis? +1  
pakimd  @rio19111 i think the Q stem is asking in absence of any lesions of blood vessels; the number and severity of which increase with age. So with normal aging SBP should increase in isolation which may then result in the development of coronary atherosclerosis- if that makes sense +1  
chandlerbas  aging causes decreased compliance in large arteries: (1) accumulation of collagen and calcium (2) degraded elastin and large arteries accumulation and it also may have something to do with lipofuschin +1  


submitted by thomas(0),
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Thye lelt uoy htta eht kdi sha no vcielc.la Tshi smean teh dtfeec is in amuoebmsrn iotasn,sofici TNO ohncldo,enadr os the galohotyp is NOT iogng to ivnoelv eth otahnerwcorhdve- clels. edcredase KLA is otcsenntsi ithw oetsoltbsa cefdet.

pakimd  isnt increased alk phos consistent with increased osteoblastic activity? +  
eacv  @pakimd Yes ! ALK phos is a measure of osteoblast work, if the are not working is LOW as in thix px. +  


submitted by hayayah(1056),
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A gib ngith eerh oto is ioictnng taht hte PLA si cdedarees. bOltsatose tatcyivi is marusede yb onbe A.PL I think ahtt asw the mnia focus here nda tno htta yuo eienyrlscas dnee to okwn the B1FAC eeng ntuotm.ia

sympathetikey  Exactly. That's the only way I got to the answer. +3  
pakimd  isnt increased alk phos consistent with increased osteoblastic activity? +  
champagnesupernova3  A defect with chondrocytes would cause an short limbs like in achondroplasia so those are ruled out +  
pg32  Exactly. Can also be helpful if you remember that the clavicles are formed by intramembranous ossification rather than endochondral; that allows you to rule out the chondroblast/cyte answer choices. +4  


submitted by rio19111(9),
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I hkint a olt of uyo mssdie hte tpino. heT arwnse is lortsiCo aescbue ti pelhs tananiim lobod sureersp veen ni teh tetsgin ehwer eh si ihea.snmulrod

rio19111  FA 2019, Pg. 329 +2  
pakimd  according to pathoma, cortisol is the hormone neccessary for life. in a condition like the one presented in the Q-stem the most important hormone will be cortisol. +2  
pontiacfever  Also Cortisol is generally a stress hormone. Starved body is generally understress--Cortisol +