Step 1 Complicated Concepts Thread

I got a good one- Why does vitamin D treat psoriasis yet vitamin A does not?

dbeast said:

I got a good one- Why does vitamin D treat psoriasis yet vitamin A does not?

Click to expand...

Vitamin A derivatives are also used in the treatment of psoriasis. Acitretin, as its name implies, is a vitamin A derivative and used in the treatment of moderate-severe psoriasis.

Myxedema said:

Vitamin A derivatives are also used in the treatment of psoriasis. Acitretin, as its name implies, is a vitamin A derivative and used in the treatment of moderate-severe psoriasis.

Click to expand...

I agree, they both cause differentiation and limit proliferation as far as I know.

I have written that VZV spreads hematogenously before getting into ganglia. Is that also true for HSV or any other herpesvirus for that matter?

sharklasers said:

maybe entameoeba? needs iodaquinol (or something like that) for cysts, but -bendazoles work for everything else

don't know about gallbladder in particular though

Click to expand...

From Robbins Basic Pathology, 9th Edition:

In some world populations, parasitic cholangitis is a significant problem. Causative organisms include Fasciola hepatica or schistosomiasis in Latin America and the Near East, Clonorchis sinensis or Opisthorchis viverrini in the Far East, and cryptosporidiosis in persons with acquired immunodeficiency syndrome.

Click to expand...

Pinkleton said:

I have written that VZV spreads hematogenously before getting into ganglia. Is that also true for HSV or any other herpesvirus for that matter?

Click to expand...

No, HSV replicates in the skin or mucous membrane, then moves up the neuron via retrograde flow and becomes latent in trigeminal (HSV-1) and lumbar/sacral (HSV-2) ganglia. When it is reactivated, it moves back down the neuron and infects the skin again.
VZV, on the other hand, infects the mucosa, then -like you've said- spreads via the blood to the skin. Then using a similar process, it infects the sensory nerves and becomes latent in dorsal root ganglia. When it is reactivated, it moves back along the neuron and infects the skin supplied by that dorsal root ganglion. This is why reactivation of VZV is seen in a dermatomal pattern.

Myxedema said:

No, HSV replicates in the skin or mucous membrane, then moves up the neuron via retrograde flow and becomes latent in trigeminal (HSV-1) and lumbar/sacral (HSV-2) ganglia. When it is reactivated, it moves back down the neuron and infects the skin again.
VZV, on the other hand, infects the mucosa, then -like you've said- spreads via the blood to the skin. Then using a similar process, it infects the sensory nerves and becomes latent in dorsal root ganglia. When it is reactivated, it moves back along the neuron and infects the skin supplied by that dorsal root ganglion. This is why reactivation of VZV is seen in a dermatomal pattern.

Click to expand...

Well done, sir. Well done

What are the arterial blood gases like of someone with emphysema?

Since they are "pink puffers" which first aid says includes hyperventilation, do they have low O2, low CO2, and high pH?

as opposed to "blue bloaters" aka bronchitis which has low o2, high co2, low ph.

thanks!

Myxedema said:

No, HSV replicates in the skin or mucous membrane, then moves up the neuron via retrograde flow and becomes latent in trigeminal (HSV-1) and lumbar/sacral (HSV-2) ganglia. When it is reactivated, it moves back down the neuron and infects the skin again.
VZV, on the other hand, infects the mucosa, then -like you've said- spreads via the blood to the skin. Then using a similar process, it infects the sensory nerves and becomes latent in dorsal root ganglia. When it is reactivated, it moves back along the neuron and infects the skin supplied by that dorsal root ganglion. This is why reactivation of VZV is seen in a dermatomal pattern.

Click to expand...

this is an amazing explanation, thank you.

Do we need to know the internal capsule in more detail other than the fact that a lesion in the internal capsule can cause contralateral hemiparesis? And that this can happen due to an aneurysm in the lateral striate artery?

I'm not really sure about anterior limb vs genu vs posterior limb or what artery supplies each one.

Thanks!

sharklasers said:

Do we need to know the internal capsule in more detail other than the fact that a lesion in the internal capsule can cause contralateral hemiparesis? And that this can happen due to an aneurysm in the lateral striate artery?

I'm not really sure about anterior limb vs genu vs posterior limb or what artery supplies each one.

Thanks!

Click to expand...

Genu carries corticobulbar and posterior is pretty much everything else. I don't think anterior capsule is important for our purposes. Blood supply is MCA and ACA, not PCA

Very cold vs very hot weather. Effect on BMR? Do they both increase it?

sharklasers said:

What are the arterial blood gases like of someone with emphysema?

Since they are "pink puffers" which first aid says includes hyperventilation, do they have low O2, low CO2, and high pH?

as opposed to "blue bloaters" aka bronchitis which has low o2, high co2, low ph.

thanks!

Click to expand...

Whether it is "pink puffers" (emphysema) or "blue bloaters" (chronic bronchitis), the underlying pathologic mechanism is obstruction (hence the name COPD). Obstruction of airways (especially small ones) during expiration leads to air trapping. Because of this air trapping, residual volume increases at the expense of FVC. In addition, due to obstruction and destruction of alveolar walls in emphysema, gas exchange will be limited, resulting in hypoxemia and hypercapnia. Now, at this point, we can differentiate between pink puffers and blue bloaters.

- Some patients can overcome this hypoxemia and hypercapnia by hyperventilation. In these patients, the level of hypoxemia and hypercapnia will become less severe. Hence, they are called as "pink" (because hypoxemia is less severe) and "puffers" (because they compensate via hyperventilation). However, because of hyperventilation, the air trapping will become more pronounced in these patients. These patients tend to have a more pronounced emphysema rather than bronchitis.

- Other patients do not hyperventilate. Thus, their hypoxemia and hypercapnia will be more severe. Hence they are "blue" (because of hypoxemia). However, air trapping will not be as prominent in these patients. As to the "bloater" part, one way to remember it would be to imagine these patients as not spending enough effort to overcome their hypoxia and hypercapnia. As a result, they become "bloated" .

To sum it all up:

- Both pink puffers and blue bloaters can have hypoxemia (low pO2) and hypercapnia (high pCO2, which will manifest itself as low pH). However these will be less pronounced in pink puffers, because they can overcome them by hyperventilation at the expense of more air trapping.

wow another amazing explanation myxedema, thanks!

do you know why someone with bronchitis cannot compensate with hyperventilation while someone with emphysema would be able to?

sharklasers said:

wow another amazing explanation myxedema, thanks!

do you know why someone with bronchitis cannot compensate with hyperventilation while someone with emphysema would be able to?

Click to expand...

Airways are blocked in bronchitis-heavy COPD, so you can't get rid of air no matter how hard or fast you breath; in emphysema-heavy COPD, you have less alveoli but you have no trouble hyperventilating.

sharklasers said:

Do we need to know the internal capsule in more detail other than the fact that a lesion in the internal capsule can cause contralateral hemiparesis? And that this can happen due to an aneurysm in the lateral striate artery?

I'm not really sure about anterior limb vs genu vs posterior limb or what artery supplies each one.

Thanks!

Click to expand...

• Anterior limb: Supplied by medial striate branches of anterior cerebral artery
• Genu: Supplied by lenticulostriate branches of middle cerebral artery
• Posterior limb: Same as genu

Apart from the corticospinal tract as a whole, I think one important feature of internal capsule lesions is the potential to have pure sensory or motor problems of a limb. To understand it, we must describe the course of tracts within the posterior limb:

In the anterior part of the posterior limb, corticobulbar and corticospinal tracts travel within in a spatially organized way (fibers innervating face travel more anteriorly; legs --> more posteriorly). In the posterior part, thalamocortical fibers arising from VPL and VPM nuclei travel in a similar spatially organized fashion (face -> anterior, legs -> posterior).

Since posterior limb is supplied by lenticulostriate branches of MCA, blocking of these small branches can result in small infarcts ("lacunar"), which affect only a small, specific area within the posterior limb. For instance, strokes involving these branches of MCA can result in pure motor deficit of right leg (involving corticospinal tract) or pure sensory deficit of left face (involving thalamocortical fibers arising from VPM).

So... this brings up the question of would a pink puffer develop respiratory alkalosis from hyperventilation or respiratory acidosis from poor gas exchange?

Pinkleton said:

Very cold vs very hot weather. Effect on BMR? Do they both increase it?

Click to expand...

Cold weather should increase BMR, since cold ambient temperature will increase thermogenesis.

Myxedema said:

Whether it is "pink puffers" (emphysema) or "blue bloaters" (chronic bronchitis), the underlying pathologic mechanism is obstruction (hence the name COPD). Obstruction of airways (especially small ones) during expiration leads to air trapping. Because of this air trapping, residual volume increases at the expense of FVC. In addition, due to obstruction and destruction of alveolar walls in emphysema, gas exchange will be limited, resulting in hypoxemia and hypercapnia. Now, at this point, we can differentiate between pink puffers and blue bloaters.

- Some patients can overcome this hypoxemia and hypercapnia by hyperventilation. In these patients, the level of hypoxemia and hypercapnia will become less severe. Hence, they are called as "pink" (because hypoxemia is less severe) and "puffers" (because they compensate via hyperventilation). However, because of hyperventilation, the air trapping will become more pronounced in these patients. These patients tend to have a more pronounced emphysema rather than bronchitis.

- Other patients do not hyperventilate. Thus, their hypoxemia and hypercapnia will be more severe. Hence they are "blue" (because of hypoxemia). However, air trapping will not be as prominent in these patients. As to the "bloater" part, one way to remember it would be to imagine these patients as not spending enough effort to overcome their hypoxia and hypercapnia. As a result, they become "bloated" .

To sum it all up:

- Both pink puffers and blue bloaters can have hypoxemia (low pO2) and hypercapnia (high pCO2, which will manifest itself as low pH). However these will be less pronounced in pink puffers, because they can overcome them by hyperventilation at the expense of more air trapping.

Click to expand...

dude, you're amazing

Myxedema said:

Cold weather should increase BMR, since cold ambient temperature will increase thermogenesis.

Click to expand...

It for sure does, which explains the insane amount of calories that mountain climbers need to consume to stay at the same weight, even you factor out the expenditure from physical work.

dbeast said:

So... this brings up the question of would a pink puffer develop respiratory alkalosis from hyperventilation or respiratory acidosis from poor gas exchange?

Click to expand...

Both. Initially, hyperventilation would create respiratory alkalosis, since it would be adequate to blow off that excess CO2 with effort. As the disease progresses, hyperventilation may no longer be sufficient to overcome hypercapnia. As a result, respiratory acidosis will develop.

Myxedema said:

Both. Initially, hyperventilation would create respiratory alkalosis, since it would be adequate to blow off that excess CO2 with effort. As the disease progresses, hyperventilation may no longer be sufficient to overcome hypercapnia. As a result, respiratory acidosis will develop.

Click to expand...

Correct me if i'm thinking of something else, but does this tie into how O2 supplementation could be problematic? Because of their chronic respiratory acidosis, chemoreceptors become desensitized to CO2 levels and pH, but the driving factor behind respiration then becomes hypoxemia. The hypoxemia can easily be corrected on 100% O2, but then they have no respiratory drive and go into a dangerous and extreme respiratory acidosis.

I'm honestly not sure if this relates to chronic bronchitis or emphysema, and now that I'm trying to think about it I'm really not sure. I just remember learning about this scenario at some point and can't place it. If anyone can clarify my thoughts that would be appreciated!

CrouchingLiger said:

Correct me if i'm thinking of something else, but does this tie into how O2 supplementation could be problematic? Because of their chronic respiratory acidosis, chemoreceptors become desensitized to CO2 levels and pH, but the driving factor behind respiration then becomes hypoxemia. The hypoxemia can easily be corrected on 100% O2, but then they have no respiratory drive and go into a dangerous and extreme respiratory acidosis.

I'm honestly not sure if this relates to chronic bronchitis or emphysema, and now that I'm trying to think about it I'm really not sure. I just remember learning about this scenario at some point and can't place it. If anyone can clarify my thoughts that would be appreciated!

Click to expand...

What you've written is true for any chronic hypercapnic state. That is indeed the classic explanation given to explain the rationale behind cautious O2 supplementation. However, this "hypoxic drive" theory is in fact incorrect. For those who are interested, there is a detailed explanation at the website below:

http://respiratorytherapycave.blogspot.com/2012/02/hypoxic-drive-theory-history-of-myth.html

CrouchingLiger said:

Correct me if i'm thinking of something else, but does this tie into how O2 supplementation could be problematic? Because of their chronic respiratory acidosis, chemoreceptors become desensitized to CO2 levels and pH, but the driving factor behind respiration then becomes hypoxemia. The hypoxemia can easily be corrected on 100% O2, but then they have no respiratory drive and go into a dangerous and extreme respiratory acidosis.

I'm honestly not sure if this relates to chronic bronchitis or emphysema, and now that I'm trying to think about it I'm really not sure. I just remember learning about this scenario at some point and can't place it. If anyone can clarify my thoughts that would be appreciated!

Click to expand...

Yep, that's the theory. Your respiratory centers in the medulla are sensitive to the PaCO2, so any change in PaCO2 (specifically H+) either stimulates or inhibits your respiratory drive.

In COPD, you get chronic respiratory acidosis, so your respiratory centers in the medulla are densitized. Now, your PaO2 sensors in the carotid and aortic bodies are the ones primary responsible for your respiratory drive. Since they only work under hypoxemic conditions (< 60 mmHg), giving oxygen to someone with COPD will suddenly inhibit the carotid/aortic bodies and their respiratory drive will be gone.

This is just a theory. I remember reading about another one where the mechanism was something like: giving O2 would dilate the pulmonary arteries that were previously constricted due to emphysema (low O2 = vasoconstriction), so essentially you get a shunt where your blood is shifted towards supplying the arteries that really don't undergo gas exchange.

Myxedema said:

What you've written is true for any chronic hypercapnic state. That is indeed the classic explanation given to explain the rationale behind cautious O2 supplementation. However, this "hypoxic drive" theory is in fact incorrect. For those who are interested, there is a detailed explanation at the website below:

http://respiratorytherapycave.blogspot.com/2012/02/hypoxic-drive-theory-history-of-myth.html

Click to expand...

Haha nice.

Myxedema said:

What you've written is true for any chronic hypercapnic state. That is indeed the classic explanation given to explain the rationale behind cautious O2 supplementation. However, this "hypoxic drive" theory is in fact incorrect. For those who are interested, there is a detailed explanation at the website below:

http://respiratorytherapycave.blogspot.com/2012/02/hypoxic-drive-theory-history-of-myth.html

Click to expand...

Woah. Mind = blown. After reading that article I'm questioning my whole existence haha. But that's definitely something to think about then, thanks for the insight!

Myxedema said:

What you've written is true for any chronic hypercapnic state. That is indeed the classic explanation given to explain the rationale behind cautious O2 supplementation. However, this "hypoxic drive" theory is in fact incorrect. For those who are interested, there is a detailed explanation at the website below:

http://respiratorytherapycave.blogspot.com/2012/02/hypoxic-drive-theory-history-of-myth.html

Click to expand...

wha?! holy ****.. you ruined my world

I remember reading somewhere that octreotide can be used for portal hypertension but don't remember the exact mechanism. I think it has to do with decreased glucagon, but im not sure. Anyone mind sharing?

sharklasers said:

I remember reading somewhere that octreotide can be used for portal hypertension but don't remember the exact mechanism. I think it has to do with decreased glucagon, but im not sure. Anyone mind sharing?

Click to expand...

I have no idea but I know it is used in esophageal varices in conjunction with banding..

http://en.wikipedia.org/wiki/Octreotide#Pharmacological_effects

"reduce portal vessel pressures in bleeding varices."

yeah there it is! how does it do that exactly??

because the wiki also says that it "causes vasoconstriction in blood vessels" which seems like it could make portal hypertension and thus the bleeding varices worse

sharklasers said:

I remember reading somewhere that octreotide can be used for portal hypertension but don't remember the exact mechanism. I think it has to do with decreased glucagon, but im not sure. Anyone mind sharing?

Click to expand...

I thought it just acted to decrease splanchnic bloodflow? Decrease splanchnic input, you decrease portal pressure?

Pons Asinorum said:

I thought it just acted to decrease splanchnic bloodflow? Decrease splanchnic input, you decrease portal pressure?

Click to expand...

I'm having strange block 9 flashbacks about this being the same reason why octreotide is the drug of choice for hepatorenal syndrome too...

dbeast said:

I'm having strange block 9 flashbacks about this being the same reason why octreotide is the drug of choice for hepatorenal syndrome too...

Click to expand...

Yes, speaking of things not in FA that do show up on block exams...

Pons Asinorum said:

I thought it just acted to decrease splanchnic bloodflow? Decrease splanchnic input, you decrease portal pressure?

Click to expand...

splanchnic vasodilation per wikipedia.

But why would you want less flow to the kidneys in this situation? That doesn't make sense at all.

sharklasers said:

"reduce portal vessel pressures in bleeding varices."

yeah there it is! how does it do that exactly??

because the wiki also says that it "causes vasoconstriction in blood vessels" which seems like it could make portal hypertension and thus the bleeding varices worse

Click to expand...

I think I looked it up once, maybe it was on UW. Octreotide inhibits the secretion of vasoactive intestinal peptide (a vasodilator), causing vasoconstriction at the varices which reduces bleeding.

Anybody know about the neuro deficits somebody will get after a transtentorial herniation? I seem to remember a question from uworld that the cranial nerve defect will be on the opposite side of the mass/bleed. Does that sound familiar to anyone?

This isn't really a complicated concept but does anyone know a good way to remember the sensory receptors in the skin, where they are, what they do, etc.

This seems to be something I always forget and can't find any way to remember it besides just memorizing but then I forget it in basically a day. Probably low yield for the exam but you never know what's going to show up.

dbeast said:

Anybody know about the neuro deficits somebody will get after a transtentorial herniation? I seem to remember a question from uworld that the cranial nerve defect will be on the opposite side of the mass/bleed. Does that sound familiar to anyone?

Click to expand...

Everyday typical CN3 palsy, ipsalateral side.

Opposite side of mass/bleed I could only guess because the hernia would be on the contralateral side? If you ask me it sounds like typical everyday UW "I'm going to trick your @$$" bullcrap.

MLT2MT2DO said:

Everyday typical CN3 palsy, ipsalateral side.

Opposite side of mass/bleed I could only guess because the hernia would be on the contralateral side? If you ask me it sounds like typical everyday UW "I'm going to trick your @$$" bullcrap.

Click to expand...

Two other findings with Uncal herniations (which is a subtype of transtentorial herniations) are iplisateral compression of the PCA (meaning contralateral homonomous hemianopia with macular sparing) and compression of the contralateral cruz cerebri (leading to ipsilateral paresis of both extremities). These aren't cranial nerve deficits, but still related. There aren't any contralateral cranial nerve deficits that I know of as you referred to in the original question, so maybe I'm missing something.

Also, the ipsilateral CN3 compression will lose the parasympathetics before motor functions (so early sign is a dilated pupil, then later will also be down and out).

223556 said:

splanchnic vasodilation per wikipedia.

But why would you want less flow to the kidneys in this situation? That doesn't make sense at all.

Click to expand...

Splanchnic blood flow doesn't affect RBF. Not connected. VIP doesn't affect the renal vasculature, IIRC.

sharklasers said:

Do we need to know the internal capsule in more detail other than the fact that a lesion in the internal capsule can cause contralateral hemiparesis? And that this can happen due to an aneurysm in the lateral striate artery?

I'm not really sure about anterior limb vs genu vs posterior limb or what artery supplies each one.

Thanks!

Click to expand...

Just came across this and I thought of your post... the chart in the middle of the page is pretty good:

http://en.wikipedia.org/wiki/Lacunar_stroke

I think I should get a joint degree from Wikipedia based on how much I've used it.

CrouchingLiger said:

Two other findings with Uncal herniations (which is a subtype of transtentorial herniations) are iplisateral compression of the PCA (meaning contralateral homonomous hemianopia with macular sparing) and compression of the contralateral cruz cerebri (leading to ipsilateral paresis of both extremities). These aren't cranial nerve deficits, but still related. There aren't any contralateral cranial nerve deficits that I know of as you referred to in the original question, so maybe I'm missing something.

Also, the ipsilateral CN3 compression will lose the parasympathetics before motor functions (so early sign is a dilated pupil, then later will also be down and out).

Click to expand...

I'd like to make a small correction. Transtentorial (uncal) herniation will result in contralateral spastic paralysis, not ipsilateral. This is because the herniation will affect the crus cerebi in the midbrain, whereas the decussation of the motor tract takes place in the medulla. However, ipsilateral hemiparesis can also be seen in further herniation. This is because displacement of brainstem laterally causes indentation of the opposite crus cerebri against the tentorial membrane. This indentation is also known as Kernohan's notch.

To sum it up:

- Compression of CN III: Dilation of pupil ipsilaterally.
- Compression of PCA: Homonymous hemianopia (often with macular sparing)
- Compression of brainstem:
Contralateral hemiparalysis
Ipsilateral hemiparalysis (if opposite crus cerebri becomes compresssed)
*Further compression can result in:
Cushing response (hypertension with bradycardia)
Respiratory failure (Cheyne-Stokes breathing)

Myxedema said:

I'd like to make a small correction. Transtentorial (uncal) herniation will result in contralateral spastic paralysis, not ipsilateral. This is because the herniation will affect the crus cerebi in the midbrain, whereas the decussation of the motor tract takes place in the medulla. However, ipsilateral hemiparesis can also be seen in further herniation. This is because displacement of brainstem laterally causes indentation of the opposite crus cerebri against the tentorial membrane. This indentation is also known as Kernohan's notch.

To sum it up:

- Compression of CN III: Dilation of pupil ipsilaterally.
- Compression of PCA: Homonymous hemianopia (often with macular sparing)
- Compression of brainstem:
Contralateral hemiparalysis
Ipsilateral hemiparalysis (if opposite crus cerebri becomes compresssed)
*Further compression can result in:
Cushing response (hypertension with bradycardia)
Respiratory failure (Cheyne-Stokes breathing)

Click to expand...

You're a boss, man. Thanks for this.

Myxedema said:

I'd like to make a small correction. Transtentorial (uncal) herniation will result in contralateral spastic paralysis, not ipsilateral. This is because the herniation will affect the crus cerebi in the midbrain, whereas the decussation of the motor tract takes place in the medulla. However, ipsilateral hemiparesis can also be seen in further herniation. This is because displacement of brainstem laterally causes indentation of the opposite crus cerebri against the tentorial membrane. This indentation is also known as Kernohan's notch.

To sum it up:

- Compression of CN III: Dilation of pupil ipsilaterally.
- Compression of PCA: Homonymous hemianopia (often with macular sparing)
- Compression of brainstem:
Contralateral hemiparalysis
Ipsilateral hemiparalysis (if opposite crus cerebri becomes compresssed)
*Further compression can result in:
Cushing response (hypertension with bradycardia)
Respiratory failure (Cheyne-Stokes breathing)

Click to expand...

That's what I was thinking of. Thanks for the correction!

pg. 293 FA2013

- it says low Mg causes increase in PTH but very low Mg leads to decreased PTH.

Can someone elaborate on this?

sharklasers said:

I remember reading somewhere that octreotide can be used for portal hypertension but don't remember the exact mechanism. I think it has to do with decreased glucagon, but im not sure. Anyone mind sharing?

Click to expand...

I think the short answer should be this: the exact mechanism of action of octreotide regarding the treatment of esophageal varices is unknown. I very much doubt something which is still unclear would be asked in USMLE.

Long answer: Katzung and Goodman & Gilman list two mechanisms: (1) Inhibition of glucagon, and (2) Constriction of splanchnic vasculature. The second part can be linked to pathophysiology of portal hypertension, especially the type seen in cirrhosis. To understand that, we must review the pathogenesis of portal hypertension in cirrhosis.

One mechanism of portal hypertension is relatively easy to understand: Regenerative nodules and fibrotic bands press on sinusioids and central vein. However, this compression is not enough to explain the portal hypertension. The second mechanism of splanchnic vasodilation is a little long winded. Within the fibrotic bands, anastomoses between the portal and arterial circulations start to form. Keep in mind that these are not porto-caval (venous) anatomoses, but arterial-portal anastomoses. Bacterial products and components, especially bacterial DNA, normally enter the sinusoids via the portal system and processed by the Kupffer cells. However, because of these anastomoses, bacterial DNA bypasses the sinusoids and enter systemic circulation. Eventually, bacterial DNA finds its way into the vascular of bed of splanchnic circulation, where they cause the release of nitric oxide. This results in arterial vasodilation which results in increased arterial blood flow to the liver. Then this blood flows from high-pressure arterial system into the portal circulation via the anastomoses, resulting in increased portal venous blood flow. In summary: bacterial DNA bypasses sinusoids and enters systemic circulation --> Increased NO --> Arterial vasodilation --> Increased arterial flow to the liver --> Increased blood flow into the portal circulation. This whole process is an example of hyperdynamic circulation.

As a further note, this arteriolar vasodilation also results in reduced effective arterial blood volume. This decreased effective blood volume is one of the underlying mechanisms of hepatorenal and hepatopulmonary syndromes.

skyblue2000 said:

pg. 293 FA2013

- it says low Mg causes increase in PTH but very low Mg leads to decreased PTH.

Can someone elaborate on this?

Click to expand...

Like FA says, mild hypomagnesemia results in increased PTH, but severe chronic hypomagnesemia results in decreased PTH. This is one of the mechanisms why hypocalcemia can be seen in settings of hypomagnesemia.

Anybody have a list of all the diseases that start as a normally developing baby who regresses early in life? I know there's a few of them, and it seems like it'd be a pretty valuable clue for eliminating a bunch of answer choices. I can only think of Rett's syndrome off the top of my head, but I feel like some of the lysosomal storage diseases do this too?

Uworld question 1276 on cross sectional studies. Wtf is up with this? I thought it was to determine prevalence, but in this question they're related hypertension to some genetic defect?

Friends,

needed some help with 2 questions I came across:

#1. 40 year old male presents with easy fatigability, weakness, weight loss, anorexia, and left upper abdomen discomfort. His leukocyte count is 70 X 10^3/ mcl consisting of predominantly PMN's and metamyelocytes. There are occasional basophils, eosinophils, myelocytes and a few blast cells. The platelet count is elevated (>1000 X 10^3/ mcl)

He has:
A. ALL
B. AML
C. CML
D. Multiple Myeloma
E. Reactive thrombocytosis

The patient's condition will most likely:
A. Involve lymph node metastasis
B. Precipitate in Renal disease
C. resolve after therapy
D. Terminate in Blast crisis
E. Terminate in DIC

#2. A 56 year old male undergoes a bilateral orchiectomy after diagnosis of androgen sensitive carcinoma of the prostate. Androgen ablation therapy in this patient is designed to inhibit which of the following mechanisms of cell signaling?

A. Activation of tyrosine kinase activity within androgen receptor
B. Coupling of the transmembrane androgen receptor to G proteins
C. Generation of androgen activated cellular second messengers
D. Stimulation of activity of Ser/Thr kinases within prostate
E. Transcription factor activity of the androgen receptor.

thanks in advance!