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Welcome to pakimd’s page.
Contributor score: 11


Comments ...

 +0  (nbme16#45)

Women with PCOS have an increased LH:FSH ratio primarily 2:1. this results in increased activity of theca cells causing increased androgen production but because of low FSH there is decreased activity of granulosa cells causing decreased conversion of those androgens to estrogen. the excess androgens are then converted peripherally into estrone (estrogen) by aromatase present in tissues like adipose tissue. excess unopposed estrogen results in anovulatory cycles and endometrial hyperplasia (increasing the risk for endometrial cancer). excess testosterone results in alopecia and hirsutism. women with PCOS also exhibit a greater degree of insulin resistance than patients with the same BMI and visceral adiposity who do not have PCOS resulting in hyperinsulinemia (which causes acanthosis nigricans).


 +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 +2

 +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


 +2  (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 +1




Subcomments ...

submitted by cassdawg(1101),

Pelvic splanchnic nerves carry the parasympathetic fibers that are responsible for hindgut intestinal motility including voiding (image). [FA2020 p364].

Diabetes mellitus can cause nerve damage and gastroparesis, treated with metoclopromide (FA2020 p400).

pakimd  thank you for sharing the image +  


submitted by cassdawg(1101),

Sildenafil is a PDE5 inhibitor that runs the risk of causing hypotension in patients on nitrates due to the synergy of the mechanisms of action. [FA2020 p246]

Nitrates, like nitroglycerin, work by increasing NO production which in turn acts to increase cGMP in smooth muscle causing vasodilation. PDE5 inhibitors act by decreasing the breakdown of cGMP in smooth muscle, enhancing the action of NO to cause vasodilation. Thus, when combined there can be systemic vasodilation that leads to dangerous hypotension.

lee280  For some reason, I had two answers that I felt like both made absolute sense to me. As explained above, that totally came to my mind and I knew this was the case. When I thought about Metoprolol blocking B1 receptors in a patient with an ejection fraction of only 30%, I was thinking this could as well be a contraindication, not sure if it's an absolute one or relative. Now, am I right if I said that Beta-blockers are only contraindicated in acute decompensated HF? and can be used unless otherwise? Someone, please help me clarify this, so then this distinction can come clean in my thoughts. Thanks +2  
notyasupreme  I thought the same thing as you, I think we're just overthinking the most important thing - never give antihypertensive with Viagra lmfao. I totally thought too deep into it. +1  
topgunber  sildenafil does make sense, especially since hes on 2 vasodilators. I picked diltiazem because the pt has systolic heart failure. thought it was contra indicated to give CCB to systolic heart failure because you could further decrease contractility. Either way never give NTG and viagra +  
sexymexican888  Yeah @topgunber I also picked diltiazem.... I guess they were looking for "COMBINATION" rather than a specific contraindication +  
pakimd  @lee280 you are right in saying that beta blockers are only contraindicated in acute decompensated heart failure. this is because beta blockers, which would normally prevent the deleterious effects of neurohormones like norepinephrine on cardiac remodeling that occurs in HFrEF, will further impair cardiac output in decompensation. hope this helps :) +  


submitted by cassdawg(1101),

Polyarteritis nodosa is a medium vessel vasculitis associated with different stages of transmural inflammation with fibrinoid necrosis of vessels. [FA2020 p314]

Because this is a vasculitis that affects medium vessels, it can affect the arteries supplying the muscles and thus cause segmental ischemic necrosis from loss of blood supply.

radzio1  I thought that segmental is a key word for Burgers dz. +1  
radzio1  *Buerger +  
feochromocytoma  Beurger is characterized by segmental thrombosis with nerve involvement. +2  
cheesetouch  So he has both PAN and Buerger's? +  
pakimd  polyarteritis nodosa is characterized by segmental (different stages) of transmural inflammation with fibrinoid necrosis causing narrowing of vessel lumen and increased risk of thrombosis leading to tissue ischemia/infarction FA2020 pg314 +  
shieldmaiden  The problem in Buerger is segmental thrombosis while PAN is ischemia from immune complexes with hepatitis antigens and it is also segmental (a string of pearls) +  


submitted by bingcentipede(243),

Alocholics can get aspiration pneumonia, which involves aspiration of the normal oral flora (Klebsiella and anaerobes like Peptostreptococcus, Fusobacterium, Prevotella, Bacteroides). So this is normally part of the flora and can be aspirated in alcoholics.

iury_r1beiro  Hello, i think it is Streptococcus viridans; coccus in chains and normal oral flora. Alcoholics can get aspiration pneumonia, which can evolve to a pulmonary abscess. FA2020 p146. https://www.atsjournals.org/doi/pdf/10.1164/ajrccm.156.5.97-03006 +1  
pakimd  oral mucosa composed of aerobes e.g. streptococcus, klebsiella and anaerobes e.g. Peptostreptococcus, Fusobacterium, Prevotella, Bacteroides +  


submitted by utap2001(5),
  • Fur is a TRANSCRIPTION FACTOR that acts as a REPRESSOR to control the gene expression.

  • if INCREASE IRON CONCENTRATION--> INCREASE Fur DNA binding = INCREASE the REPRESSOR function and the opposite action w/ [LOW IRON].

  • Fur helps in the BACTERIAL VIRULENCE FACTORS control.

https://en.wikipedia.org/wiki/Ferric_uptake_regulator_family

dentist  is getting this question correct contingent upon memorizing that fur is a transcription factor? +  
pakimd  @utap2001 can you explain how you figured that fur is a repressor and not a promoter? +  
pakimd  oh i just clicked on the link you posted. sorry +  
utap2001  It doesn't matter if Fur is suppressor or promoter. The question stem says " Ferric uptake regulation protein (Fur) binds tightly to DNA a short distance from the 5’end of the genes for these virulence factors." So it's function to modulate the transcription of DNA. +1  
drdoom  @dentist, utap2001 hits the key sentence of the stem. No one has ever heard of Fur, but the description of a protein that binds tightly to DNA, and does so nearby the start of a gene (5'), is unlikely to be anything other than a transcription factor. +  
drdoom  (Transcription of DNA is such a highly conserved and tightly regulated process that no protein other than a TF can willy-nilly bind to DNA in the manner described in the stem.) +  


submitted by utap2001(5),
  • Fur is a TRANSCRIPTION FACTOR that acts as a REPRESSOR to control the gene expression.

  • if INCREASE IRON CONCENTRATION--> INCREASE Fur DNA binding = INCREASE the REPRESSOR function and the opposite action w/ [LOW IRON].

  • Fur helps in the BACTERIAL VIRULENCE FACTORS control.

https://en.wikipedia.org/wiki/Ferric_uptake_regulator_family

dentist  is getting this question correct contingent upon memorizing that fur is a transcription factor? +  
pakimd  @utap2001 can you explain how you figured that fur is a repressor and not a promoter? +  
pakimd  oh i just clicked on the link you posted. sorry +  
utap2001  It doesn't matter if Fur is suppressor or promoter. The question stem says " Ferric uptake regulation protein (Fur) binds tightly to DNA a short distance from the 5’end of the genes for these virulence factors." So it's function to modulate the transcription of DNA. +1  
drdoom  @dentist, utap2001 hits the key sentence of the stem. No one has ever heard of Fur, but the description of a protein that binds tightly to DNA, and does so nearby the start of a gene (5'), is unlikely to be anything other than a transcription factor. +  
drdoom  (Transcription of DNA is such a highly conserved and tightly regulated process that no protein other than a TF can willy-nilly bind to DNA in the manner described in the stem.) +  


submitted by cassdawg(1101),

Prader-Willi syndrome occurs due to a defect in the paternal chromosome 15 which causes issue because of imprinting that occurs silencing the maternal chromosome. If there is not a functioning paternal allele, any maternal allele will be silenced leading to lack of a functional copy of the alleles and disease.

Imprinting is when certain alleles are expressed differently depending on which parent they are inherited from. Genes are silenced specific to either maternal or paternal origin, and therefore only one allele is expressed. If the NON-silenced gene is dysfunctional or absent, then there will not be expression of a functioning allele, and thus disease results.

The two primary disorders of imprinting are P rader-Willi (caused by dysfunctional Paternal chromosome 15) and Angel M an (caused by dysfunctional Maternal UBE3A on chromosome 15).

In this individual, he has Prader-Willi syndrome but does not have the customary deletion on the arm of chromosome 15. Remembering in Prader-Willi that the paternal chromosome is typically dysfunctional and the maternal genes are silenced, it can be assumed that in order to have the disorder he had two copies of the maternal chromosome and both were silenced, producing a functional deletion even though he does not have the actual deletion.

Another way of thinking of this is the genes that prevent Prader-Willi will always be silenced on maternal chromosomes, so even if he has normal maternal chromosomes he will have a lack of function and thus Prader-Willi syndrome unless he has a normal paternal chromosome.

pakimd  just to add to this. this is an example of uniparental disomy +  


submitted by pakimd(11),

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 +2  


submitted by pakimd(11),

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 +2  


submitted by andro(188),

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? +1  


submitted by pakimd(11),

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(1101),

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(1026),

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(11),

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(1101),

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(1101),

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(1101),

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(1101),

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(1101),

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(1101),

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! +3  
pakimd  thank you @cassdawg, you're amazing! +  


submitted by ergogenic22(320),
unscramble the site ⋅ remove ads ⋅ become a member ($39/month)

cslsaic mestnahiya rsigva ipetu.rc srWneos tihw e.us xS leicndu ipioa.lpd emItroenvmp hwit EAC.h

Aslo seid eotn, n'odt ofusc no eth regpcnany taus,st ubt mnewo who rae in teh tmprsouapt eiodr rae ta rtlclyurpiaa hihg ksri of dovienlgep imeyaansth asivgr

pakimd  why are answers unscrambled on here? +  


submitted by cassdawg(1101),

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  <-- +1  
pakimd  @cassdawg thank you for explaining so well along with explaining all the answer options. +  


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p + q = 1 2^p + q2p + 2q^ = 1 i f q^2 = 06110/ = .000306 eh nt q = ^2tsq()rq = .0502 esvlo rof p ot teg p = 1 - r = 1 - 0.520 = .0795 e th ostzreguhyeo reiracsr = 2qp = 1 - 2p^ = 1 - .509 = 5.0 2q^ nca eb ppdrdeo /bc sti' hcum rlslmea htan ^.p2 heT leondtei is sbnripesloe ofr 08% of het sitonutma. 80. x .05 = 0.04 = 00/14 = 15/2

reThe hmgti eb na esaeri yaw ot do ,iths btu ti rdewok ofr me.

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 +  
topgunber  hate this whole scramble thing: In one line: 2 * q * 80%. This is for diseased individuals (two q alleles).I = 1/1600 = q^2 The frequency of q = 1/40 Now carriers is 2 p q. P is close to one assuming HW eqm (p+q=1). There's an additional step in this question due to the two different mutations. so 2(q) = 1/20. 80% of these carriers are deletions so multiply 1/20 * 0.8 = 1/25 +  


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ooaacenrtzIl usqrieer eth ciadic vnenmrtieon fo het mcthosa to eb orbdsbe.a ramoelpzOe ithsinbi hte HK+/+ mpup of eth moc,hats reeyhtb agsnrdeeci het icdiaty fo het tmosahc. So wenh eth intetap tseka mzaoOeprle dan Inezocaroatl ohrgee,tt Incartoezaol now't be rbesaobd oint hte yd.bo a'tThs why it sah on tfecf.e

tI's mdecemerond ot take oescdmatiin at atlse 2 urhso irpor ot aitkgn an .iacadnt

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? +9  
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 +1  
aoa05  Golan pharm book states the exact same thing. Cannot be given to patients with acholrhydria. +  


submitted by ergogenic22(320),
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ggian tsursel in einecsrda eraitral ffssinets (nhcgea in rEtxa rcleCllau aMrimtx miocstpoino - drceesdea lnstia,e ecdrnisae aoenlcgl i;n)oostdeip HIS si bospniresle rof 0680%- of TNH scase ni stpentai ;tg& 60. sA,lo resedcead oclencmapi as a ltrues of gaign acssue eindeascr pulse eerpssru

rio19111  why not dev. of coronary atherosclerosis? +2  
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(2),
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Tehy ltel ouy ahtt teh kdi sah on .aeclcilv shiT manes eth etefcd is in bmreosmanu iof,iactisnso OTN ecdnh,randloo so teh agopohytl si NOT iggno ot vvenloi eth ohrvawrenhctoe-d l.cles decradees KAL is tnossnteic hitw otsoelstab f.eedtc

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. +1  


submitted by hayayah(1074),
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A ibg nghti heer too is nngiitco tath het APL is eaedd.scer oseOtabtls ciatiytv si ersdemau yb bneo .LAP I iknth hatt aws the mian csfou reeh nda tno htat ouy elianesrcys dene ot nwko hte FCAB1 neeg mtiouan.t

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. +6  


submitted by rio19111(10),
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I knhit a otl fo uyo dssmei eth .itopn Teh aerswn si olirtsoC cseeuab it plhes miniaatn dbool essrpeur vnee ni teh sgtiten wheer eh is deunlharosmi.

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 +