Step 1 Complicated Concepts Thread

[TheSeanieB]

ASK AND ANSWER TOUGH QUESTIONS RELATED TO STEP 1.

Starting with me:
physiologic chloride shift - When CO2 diffuses into a RBC, it quickly converts with H2O to H+ and HCO3- so that CO2 will continue to passively diffuse into the RBC. The HCO3- is then excreted into the plasma by a Cl-/HCO3- exchanger. When the RBC enters the pulmonary capillaries, the process reverses. HCO3- is taken up by exchange for a Cl-. It combines with H+ to creates CO2 +H2O. The CO2 then diffuses out of the RBC and ultimately into the alveoli. This process allows for maximal CO2 excretion by a RBC.

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[JP2740]

Few Q's:

1. Uworld Q -> Renal artery stenosis >75%. What would increase? The answer was filtration fraction. I thought this would decrease both RPF and GFR, and the explanation said GFR can decrease. Confused.

2. Pox virus doesn't replicate in the nucleus because it has its own DNA dep RNA pol (per first aid).... so how does it replicate back into DNA?

3. What determines pulse pressure?

 

[Transformers]

Question on Congenital adrenal hyperplasia- 21hydroxylase...so UWORLD had a question on a boy who was growing (linear growth) at the 96th percentile and had hairy genitals...i idiotically picked the wrong answer (pituitary adenoma thinking it was growth hormone)...but heres my confusion (its about testosterone)....

I thought testosterone causes precocious puberty in males (i.e.- why would you grow more?I'm too fed up on the fact that high testosterone causes your epiphyseal growth plates to fuse early.

 

[sharklasers]

Few Q's:

1. Uworld Q -> Renal artery stenosis >75%. What would increase? The answer was filtration fraction. I thought this would decrease both RPF and GFR, and the explanation said GFR can decrease. Confused.

2. Pox virus doesn't replicate in the nucleus because it has its own DNA dep RNA pol (per first aid).... so how does it replicate back into DNA?

3. What determines pulse pressure?

1) (http://courses.washington.edu/conj/bess/gfr/gfr.htm halfway through the page)

Local autoregulation in renal vasculature (primarily the arterioles) helps maintain GFR. FF = GFR/RPF, so RPF would decrease but GFR would be maintained, FF will increase (would decrease if BP goes too low)

2) Good question, no idea lol. Maybe It also has a DNA dependent DNA polymerase?

3) PP = Systolic BP - Diastolic BP. That is literally all I know about pulse pressure, I'd like to know more about what determines systolic BP vs what determines diastolic BP

 

[sharklasers]

Question on Congenital adrenal hyperplasia- 21hydroxylase...so UWORLD had a question on a boy who was growing (linear growth) at the 96th percentile and had hairy genitals...i idiotically picked the wrong answer (pituitary adenoma thinking it was growth hormone)...but heres my confusion (its about testosterone)....

I thought testosterone causes precocious puberty in males (i.e.- why would you grow more?I'm too fed up on the fact that high testosterone causes your epiphyseal growth plates to fuse early.

maybe increased peripheral conversion of androgens to estrogen? estrogen causes you to grow more until some point, but then causes the growth plates to fuse early. growth hormone does not cause the growth plates to fuse early, which differentiates the two.

is that what you are asking? lol

 

[Transformers]

Nah its more about in a 4 year old...I guess the AGE does matter like if you area 4 year old, testosterone is growth-promoting and if you are say around puberty, testosterone would be growth inhibiting....I mean people with congenital adrenal hyperplasia don't end up being super tall right, I assume they have an early growth spurt but then the epiphyseal plates close really early.

 

[Transformers]

Is blood pressure normal in SIADH? Its interesting because Aldosterone is decreased and ANF is increased as a response (Aldosterone is the response to high volumes or BP) but in contrast...

In hyperaldosteronism, we do have an increase in BP (hypertension) because although ANP increases (aldosterone escape), ADH (which is our response to changes in osmolarity) doesn't really change I'm assuming

So while its wracking the subtle conclusions: normal sodium in hyperaldosteronism and normal volume (BP) in SIADH

 

[sharklasers]

Nah its more about in a 4 year old...I guess the AGE does matter like if you area 4 year old, testosterone is growth-promoting and if you are say around puberty, testosterone would be growth inhibiting....I mean people with congenital adrenal hyperplasia don't end up being super tall right, I assume they have an early growth spurt but then the epiphyseal plates close really early.

this 100% might just be me being brain dead... but i don't really understand what you are asking lol.

so if no one responds, maybe you can rephrase your question and i can give it a go again

 

[Transformers]

Ok one of the side effects of having too many androgens is the closure of epiphyseal growth plate (too many androgens) so I equate that with short height....in a disease like congenital adrenal hyperplasia, however, testosterone contributes to early rapid growth in a 4 year old...Im confused about how testosterone can basically do both functions and when having an excess can mean linear growth in one context (congenital adrenal hyperplasia in a 4 year old) vs. say a 14 yr old teen baseball player taking androgens (and possibly stunting his growth)

 

[sharklasers]

Ok one of the side effects of having too many androgens is the closure of epiphyseal growth plate (too many androgens) so I equate that with short height....in a disease like congenital adrenal hyperplasia, however, testosterone contributes to early rapid growth in a 4 year old...Im confused about how testosterone can basically do both functions and when having an excess can mean linear growth in one context (congenital adrenal hyperplasia in a 4 year old) vs. say a 14 yr old teen baseball player taking androgens (and possibly stunting his growth)

oh I get what you are asking now. unfortunately i do not have an answer lol.

as a side note, are you sure its androgens themselves? because i know for sure estrogens have that effect, and i figured androgens did via conversion to estrogens.

but you're right, i am curious about what changes physiologically that causes estrogen to go from increasing bone growth to prematurely closing the growth plate..

 

[blaqmamba]

OK not sure if this was already addressed but I'm having some issues with vitamin D

I know that it reabsorbs Ca & phos from the gut to help mineralize bone duh. And that it works at the kidney to reabsorb both as well

But why does FA say that it increases bone RESORPTION? If I'm not having a brain fart, I would assume that resorption means that it's taking Ca and phos OUT of bone?? Edit it's page 294 Endo section

And on this subject, does anyone know about specific receptor/binding sequences that take place at the level of the bone (ie rank/rankL) with regards to vitD

 

[Transformers]

Another question I have is about toxic radioactive iodide getting into your body...while the best treatment I think should be perchlorate anions (block the entry altogether)...UWorld favored Potassium Iodide (competitive inhibition) over PTU...wouldn't PTU be better since you can 100% shut the synthesis pathway down vs. competitive inhibition (i.e.- have the possibility of that even some radioactive iodine gets T3 and T4)... it was just a stretch, but whatever

 

[sharklasers]

Another question I have is about toxic radioactive iodide getting into your body...while the best treatment I think should be perchlorate anions (block the entry altogether)...UWorld favored Potassium Iodide (competitive inhibition) over PTU...wouldn't PTU be better since you can 100% shut the synthesis pathway down vs. competitive inhibition (i.e.- have the possibility of that even some radioactive iodine gets T3 and T4)... it was just a stretch, but whatever

I think radioactive iodide damages the thyroid directly, not by being turned into radioactive thyroid hormone.

So by blocking PTU, you still allow the radioactive iodine to enter the thyroid and damage the gland. That is why blocking it with KI is better, you prevent the damaging iodine from entering the thyroid.

 

[blaqmamba]

oh I get what you are asking now. unfortunately i do not have an answer lol.

as a side note, are you sure its androgens themselves? because i know for sure estrogens have that effect, and i figured androgens did via conversion to estrogens.

but you're right, i am curious about what changes physiologically that causes estrogen to go from increasing bone growth to prematurely closing the growth plate..

No idea for sure, but if the epiphyseal plate is growing early, it also stops early. So the bone grows at a faster RATE but for a shorter period of time, and then the cells of the epiphyseal plate ossify into bone and no longer divide (ie, plate closure)

 

[sharklasers]

OK not sure if this was already addressed but I'm having some issues with vitamin D

I know that it reabsorbs Ca & phos from the gut to help mineralize bone duh. And that it works at the kidney to reabsorb both as well

But why does FA say that it increases bone RESORPTION? If I'm not having a brain fart, I would assume that resorption means that it's taking Ca and phos OUT of bone?? Edit it's page 294 Endo section

And on this subject, does anyone know about specific receptor/binding sequences that take place at the level of the bone (ie rank/rankL) with regards to vitD

Vit D helps to increase blood levels of Ca and phos. It does by increasing aborption in the gut AND bone resorption. You are right, it does take Ca and phos out of the bone.

I know the above is true. The rest of this post is just going to be me theorizing the rest of your answer. With vitamin d deficiency, you have a defect in osteoblast activity because there is not enough calcium and phosphate to properly mineralize the bone. So vitamin d doesn't directly increase bone mineralization. It only increases calcium and phosphate which is necessary for osteoblasts to function normally.

 

[sharklasers]

No idea for sure, but if the epiphyseal plate is growing early, it also stops early. So the bone grows at a faster RATE but for a shorter period of time, and then the cells of the epiphyseal plate ossify into bone and no longer divide (ie, plate closure)

But I know growth hormone causes bone growth but does NOT cause an early closure of the growth plate. I think there must be something with estrogen in particular. I'm not sure exactly what it is, but I am like 95% sure it is not required of us to know (I am a bare minimum learner with certain things...)

 

[blaqmamba]

Vit D helps to increase blood levels of Ca and phos. It does by increasing aborption in the gut AND bone resorption. You are right, it does take Ca and phos out of the bone.

I know the above is true. The rest of this post is just going to be me theorizing the rest of your answer. With vitamin d deficiency, you have a defect in osteoblast activity because there is not enough calcium and phosphate to properly mineralize the bone. So vitamin d doesn't directly increase bone mineralization. It only increases calcium and phosphate which is necessary for osteoblasts to function normally.

so to further theorize....if you were able to give someone Ca & phos (IV for ex so no need for vitD to reabsorb it from the gut), then you wouldn't really need vitD to increase deposition of new bone?

Ah vitD/PTH - we know for sure we're going to be tested on it, but no idea how they're going to throw it at us...

But I know growth hormone causes bone growth but does NOT cause an early closure of the growth plate. I think there must be something with estrogen in particular. I'm not sure exactly what it is, but I am like 95% sure it is not required of us to know (I am a bare minimum learner with certain things...)

Haha yea this is probably one of those bare minimum things, but maybe it has to do with estrogen inhibiting IL-1 while I don't think GH has such an effect?

 

[xeroun]

so to further theorize....if you were able to give someone Ca & phos (IV for ex so no need for vitD to reabsorb it from the gut), then you wouldn't really need vitD to increase deposition of new bone?

Ah vitD/PTH - we know for sure we're going to be tested on it, but no idea how they're going to throw it at us...



Haha yea this is probably one of those bare minimum things, but maybe it has to do with estrogen inhibiting IL-1 while I don't think GH has such an effect?

I think Vit D acts almost like a steroid. It binds to a nuclear receptor that acts as a transcription factor. Trascription factor causes increase synthesis of RANKL from osteoblasts. RankL then binds to Rank receptor on Osteoclasts --> Bone resorption --> release of calcium and phos.

Vitamin D has been shown to regulate osteoblast function.
Level of Calcium in body also regulates Osteoblast function.
Soo maybe vitamin D causes bone mineralization by increasing calcium and stimulating osteoblast directly.

 

[sharklasers]

How can you tell between serosal inflammation and actual inflammation of the organ? I think I saw a picture where the outside of the appendix was red, and I couldn't tell if it was serosal or not. Thanks!

 

[hardee17]

Androgens don't cause direct epiphyseal closure, it's the aromatization to estrogens that does. Estrogens are obviously higher in females, that's part of why they are shorter than males.

 

[hardee17]

How can you tell between serosal inflammation and actual inflammation of the organ? I think I saw a picture where the outside of the appendix was red, and I couldn't tell if it was serosal or not. Thanks!

The pain description should give it away:

inital--blockage--visceral pain
later---transmural--somatic pain

 

[sharklasers]

The pain description should give it away:

inital--blockage--visceral pain
later---transmural--somatic pain

thanks hardee!

i'm assuming that is with the inflammation of the appendix itself right?

with serosal, would it just be somatic pain? like rebound tenderness?

and is visceral pain the referred pain you would get in the umbilical area?

 

[CrouchingLiger]

Few Q's:

1. Uworld Q -> Renal artery stenosis >75%. What would increase? The answer was filtration fraction. I thought this would decrease both RPF and GFR, and the explanation said GFR can decrease. Confused.

2. Pox virus doesn't replicate in the nucleus because it has its own DNA dep RNA pol (per first aid).... so how does it replicate back into DNA?

3. What determines pulse pressure?

1) (http://courses.washington.edu/conj/bess/gfr/gfr.htm halfway through the page)

Local autoregulation in renal vasculature (primarily the arterioles) helps maintain GFR. FF = GFR/RPF, so RPF would decrease but GFR would be maintained, FF will increase (would decrease if BP goes too low)

2) Good question, no idea lol. Maybe It also has a DNA dependent DNA polymerase?

3) PP = Systolic BP - Diastolic BP. That is literally all I know about pulse pressure, I'd like to know more about what determines systolic BP vs what determines diastolic BP

1) FF is directly regulated by efferent arteriolar constriction with angiotensin 2. Anytime the RAAS system is activated, such as this person with renal artery stenosis (in response to low perfusion pressure), it will activate renin, etc. to maintain GFR.

2) They do this in a similar way as all RNA viruses actually, which also replicate in the cytoplasm for the most part. How do RNA viruses replicate their RNA? There's no RNA-dependent RNA polymerase in eukaryotic cells that they can use. They must code for their own RNA-dependent RNA polymerase, which can then replicate their genetic material. Pox virus has to make its own DNA-dependent DNA polymerase that it codes for (actually, it may be pre-formed within its envelope so that it can begin immediately upon infection; either way it still has to make more of that protein for its progeny). Pox virus also has to have its own DNA-dependent RNA polymerase to transcribe its genetic code, wheras other DNA viruses don't necessary need to since they can hijack the host's RNA Pol that are located in the nucleus.

3) Pulse pressure is determined by 2 specific things: stroke volume and arterial compliance. Higher stroke volumes means that there is a larger stroke volume since each beat has more blood pumped into the vasculature. Compliance of arteries is important because with each beat, normally the large arteries expand to handle the blood from the heart, and can then continue to perfuse the distal arteries during diastole. However, decreased arterial compliance is a normal process of aging, which is why the elderly often have increased pulse pressures, or can present with systolic-only hypertension.

 

[223556]

Ah, but which cells? Would epithelial cells share monoclonal G6PD? Would stromal cells? Or both?

Hmm....I was thinking that just the tumor of epithelial cells would be monoclonal since its a neoplasm. Right?

 

[MLT2MT2DO]

What's the difference between psuedo tumor cerebri and increased intracranial pressure where there is a preference in acetazolamide (in the latter) instead of mannitol?

 

[dbeast]

1) FF is directly regulated by efferent arteriolar constriction with angiotensin 2. Anytime the RAAS system is activated, such as this person with renal artery stenosis (in response to low perfusion pressure), it will activate renin, etc. to maintain GFR.

2) They do this in a similar way as all RNA viruses actually, which also replicate in the cytoplasm for the most part. How do RNA viruses replicate their RNA? There's no RNA-dependent RNA polymerase in eukaryotic cells that they can use. They must code for their own RNA-dependent RNA polymerase, which can then replicate their genetic material. Pox virus has to make its own DNA-dependent DNA polymerase that it codes for (actually, it may be pre-formed within its envelope so that it can begin immediately upon infection; either way it still has to make more of that protein for its progeny). Pox virus also has to have its own DNA-dependent RNA polymerase to transcribe its genetic code, wheras other DNA viruses don't necessary need to since they can hijack the host's RNA Pol that are located in the nucleus.

3) Pulse pressure is determined by 2 specific things: stroke volume and arterial compliance. Higher stroke volumes means that there is a larger stroke volume since each beat has more blood pumped into the vasculature. Compliance of arteries is important because with each beat, normally the large arteries expand to handle the blood from the heart, and can then continue to perfuse the distal arteries during diastole. However, decreased arterial compliance is a normal process of aging, which is why the elderly often have increased pulse pressures, or can present with systolic-only hypertension.

These are great. For #1, I'd like to add that you can calculate this out (it sucks but I promise you'll get it right). Yes GFR and RPF will both drop, but RAAS activation will somewhat counteract the GFR decrease, so it's less profound than the decrease in RPF due to stenosis. Choose some imaginary values, plug it into the formula FF = GFR/RPF and you'll see that FF actually increases.

For #2, can anybody explain what "DNA-dependent" vs. "RNA dependent" means for me? I'd super appreciate it.

 

[CrouchingLiger]

For #2, can anybody explain what "DNA-dependent" vs. "RNA dependent" means for me? I'd super appreciate it.

In the simplest of terms, they are referring to what is being used as the template strand. In mRNA transcription, it is using the DNA as the template, so that would be a DNA-dependent RNA polymerase. Normally, there isn't any RNA-dependent synthesis of anything in eukaryotic cells. Two examples of when you will see RNA-dependent enzymes are in certain viral infections, as mentioned above, or during the construction of a cDNA library (mRNA strands are used as the template to create DNA of just the expressed protein, meaning it must use an RNA-dependent DNA polymerase).

 

[Ugen]

Myxedema is probably Dr. Goljan or Dr. Sattar secretly answering questions on the SDN boards.

Don't lie,
We're on to you.

 

[dbeast]

In the simplest of terms, they are referring to what is being used as the template strand. In mRNA transcription, it is using the DNA as the template, so that would be a DNA-dependent RNA polymerase. Normally, there isn't any RNA-dependent synthesis of anything in eukaryotic cells. Two examples of when you will see RNA-dependent enzymes are in certain viral infections, as mentioned above, or during the construction of a cDNA library (mRNA strands are used as the template to create DNA of just the expressed protein, meaning it must use an RNA-dependent DNA polymerase).

So does that mean something like hepatitis B has a DNA-dependent RNA polymerase or does it steal one from the host cell? Also, is the enzyme we know and love as "DNA polymerase" during replication technically "DNA-dependent DNA polymerase"?

 

[CrouchingLiger]

So does that mean something like hepatitis B has a DNA-dependent RNA polymerase or does it steal one from the host cell? Also, is the enzyme we know and love as "DNA polymerase" during replication technically "DNA-dependent DNA polymerase"?

Yes on the "DNA-dependent DNA polymerase." Just like the enzymes we always call "RNA polymerase I/II/III" are technically DNA-dependent RNA polymerase. I guess if its not specified, you can assume that the enzyme is DNA-dependent, because its much rarer to be making a nucleic acid strand using an RNA as a template.

Hep B is weird because it has a gapped DNA. However, I don't think that it interferes with transcription, so it should be able to use the host's DNA-dependent RNA polymerase. However, it definitely cannot use the hosts DNA polymerase because its DNA is gapped, so it has to make its own RNA-dependent DNA polymerase to replicate its genome. Most of the other DNA viruses (except pox virus) can use the hosts DNA polymerase.

 

[dbeast]

Yes on the "DNA-dependent DNA polymerase." Just like the enzymes we always call "RNA polymerase I/II/III" are technically DNA-dependent RNA polymerase. I guess if its not specified, you can assume that the enzyme is DNA-dependent, because its much rarer to be making a nucleic acid strand using an RNA as a template.

Hep B is weird because it has a gapped DNA. However, I don't think that it interferes with transcription, so it should be able to use the host's DNA-dependent RNA polymerase. However, it definitely cannot use the hosts DNA polymerase because its DNA is gapped, so it has to make its own RNA-dependent DNA polymerase to replicate its genome. Most of the other DNA viruses (except pox virus) can use the hosts DNA polymerase.

Ok awesome, I felt like I had heard somewhere that Hep B was a special case. It must be because of that whole "partial circular" thing it has going on. I love micro so much.

 

[sharklasers]

What stimulates the adrenal gland to produce sex steroids? is it just ACTH?

 

[loveoforganic2]

So, a UW question says NSAID's can cause hyperkalemia via decreased renin and aldosterone secretion, and this is apparently true

http://pedneph.info/NewFiles/NSAID - Electrolyte complications.pdf

Now... how exactly do NSAID's decrease renin/aldosterone secretion when decreased PG's are going to lead to afferent arteriolar constriction?

 

[blaqmamba]

Anyone have a good link/description on how to get a hang on some of these EKGs?

 

[xeroun]

So, a UW question says NSAID's can cause hyperkalemia via decreased renin and aldosterone secretion, and this is apparently true

http://pedneph.info/NewFiles/NSAID - Electrolyte complications.pdf

Now... how exactly do NSAID's decrease renin/aldosterone secretion when decreased PG's are going to lead to afferent arteriolar constriction?

Hmm, never linked NSAIDs with hyperkalemia but it makes complete sense now that I think about it.

Renin release is not caused by Reduced Plasma flow.
Its caused by 1.Reduction in Blood Pressure; 2.Reduced Na delivery to Macula Densa; 3.Increased Sympathetic Stimulation.

NSAIDS block COX so no synthesis of Prostaglandins.
Prostaglandins are vasodilator --> Reduced BP. So their loss cause Vasoconstriction --> Increase BP--> No Renin

Normally when Macula Densa senses low Na it releases Prostaglandins (PGI2 and PGE2) made by its COX2 enzyme. This is also blocked by NSAIDS.

 

[loveoforganic2]

Hmm, never linked NSAIDs with hyperkalemia but it makes complete sense now that I think about it.

Renin release is not caused by Reduced Plasma flow.
Its caused by 1.Reduction in Blood Pressure; 2.Reduced Na delivery to Macula Densa; 3.Increased Sympathetic Stimulation.

NSAIDS block COX so now synthesis of Prostaglandins.
Prostaglandins are vasodilator --> Reduced BP. So their loss cause Vasoconstriction --> Increase BP--> No Renin

Normally when Macula Densa senses low Na it releases Prostaglandins (PGI2 and PGE2) made by its COX2 enzyme. This is also blocked by NSAIDS.

The renal vasculature has two regulatory systems - an intrinsic myogenic mechanism that responds to blood pressure and the JG apparatus that responds to alterations in sodium flow through the DCT. Sodium flow through the DCT is the direct monitor for the RAAS system, and its mediated by perfusion (and all the things that typically affect it - blood pressure, arteriolar radius, etc.)

 

[xeroun]

The renal vasculature has two regulatory systems - an intrinsic myogenic mechanism that responds to blood pressure and the JG apparatus that responds to alterations in sodium flow through the DCT. Sodium flow through the DCT is the direct monitor for the RAAS system, and its mediated by perfusion (and all the things that typically affect it - blood pressure, arteriolar radius, etc.)

Low Na delivery to the Macula Densa cells release Prostaglandins (PGI2 and PGE2). These Prostaglandins released by the Densa cells is responsible for renin release by the JG cells.
So by using NSAIDs to block COX2 and Prostaglandins synthesis the Macula Densa is not able to signal the JG cells to release Renin.

 

[loveoforganic2]

Low Na delivery to the Macula Densa cells release Prostaglandins (PGI2 and PGE2). These Prostaglandins released by the Densa cells is responsible for renin release by the JG cells.
So by using NSAIDs to block COX2 and Prostaglandins synthesis the Macula Densa is not able to signal the JG cells to release Renin.

That makes sense, thanks. When I searched to confirm that, there's actually an uptodate article if anyone wants it

http://www.uptodate.com/contents/nsaids-electrolyte-complications

 

[blaqmamba]

But what about the fact that the JG cells can secrete renin independent of the MD?

 

[MLT2MT2DO]

But what about the fact that the JG cells can secrete renin independent of the MD?

That's pressure induced

 

[sharklasers]

Can someone explain the table on FA2013 page 335? For those with other versions of first aid, it is the table in the GI section about different types of jaundice.

I understand the hyperbilirbinemia column. I don't really understand the difference between urine bilirubin and urine urobilinogen.

Thanks!

 

[dbeast]

Tomorrow's the big day, thank you all for the help these past few weeks!

 

[xeroun]

Can someone explain the table on FA2013 page 335? For those with other versions of first aid, it is the table in the GI section about different types of jaundice.

I understand the hyperbilirbinemia column. I don't really understand the difference between urine bilirubin and urine urobilinogen.

Thanks!

Urine Bilirubin in this table is really Conjugated/Direct Bilirubin. Remember Unconjugated Bilirubin is lipid soluble so you should not find it in urine. Conjugated on the other hand is water soluble.
Normally it should not be in urine because normally once conjugated in the liver its sent to Bile ducts and Gut to get converted to Urobilinogen by bacteria. 80% of Urobilinogen breaks down to Urobilin which gives color to stool. About 20%of Urobilinogen get recycled back mainly to liver (90% of 20%) and (10% of 20%) to Kidney. Urobilinogen breaks down to Urobilin which gives Color to Urine.

 

[xeroun]

Tomorrow's the big day, thank you all for the help these past few weeks!

Goodluck!!! Hope you Rock it.

 

[loveoforganic2]

What cell mediates abscess formation? I think Dr. Sattar says PMN's in his acute inflammation lecture, but it was under a series of bullet points about things macrophages mediate, and he was speaking quickly (so maybe he misspoke?). I know PMN's form the pus inside of them, but what mediates the fibrosis?

 

[TheSeanieB]

Can anyone point me to a link that has a list of biochemical enzymes with important information in table format?

 

[JP2740]

are psammoma bodies different from keratin pearls? I can't see a difference

 

[tiedyeddog]

are psammoma bodies different from keratin pearls? I can't see a difference

found this somewhere: Both do have a whorled appearance. A psammoma body has actual calcium in it, which stains blue and looks crunchy. A keratin pearl just has keratin in it, which stains pink and often looks just like the keratin on top of keratinized epithelium.

 

[loveoforganic2]

found this somewhere: Both do have a whorled appearance. A psammoma body has actual calcium in it, which stains blue and looks crunchy. A keratin pearl just has keratin in it, which stains pink and often looks just like the keratin on top of keratinized epithelium.

Yep, big big big difference (and HY). Disorganized epithelial growth in SCC leads to keratin pearls. Psammoma bodies are dystrophic calcifications associated with focal areas of necrosis in tumors with whorling morphology or papillary structure.

Pretty sure those details are right (the gist is at least)

 

[sharklasers]

Does the VPM get ipsilateral or contralateral face?

EDIT: nevermind, figured out it projects to the somatosensory cortex ipsilaterally, so loss of the left VPM would cause a defect in sensation from the right face

but brainstem lesions would cause loss of sensation to the face ipsilateraly right?

so its AFTER the brainstem when the fibers cross to the contralateral VPM?

 

[tiedyeddog]

Does the VPM get ipsilateral or contralateral face?

EDIT: nevermind, figured out it projects to the somatosensory cortex ipsilaterally, so loss of the left VPM would cause a defect in sensation from the right face

but brainstem lesions would cause loss of sensation to the face ipsilateraly right?

so its AFTER the brainstem when the fibers cross to the contralateral VPM?

VPM gets cotralateral. VPM gets medial leminiscus fibers, which are all contralateral fibers. The fibers cross in the pons, also where trigeminal nerve comes out.