can somebody answer this

[porcelain258]

how is alkalosis associated with tetany???

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[porcelain258]

hi guys
so i assume that nobody could answer the above question
i hav some more 4 u
1) transitional epithelium d/t cigarette smoking is seen in which of the foll conditions
a glomerulonephritis
b pyelonephritis
c carcinoma of the kidney
d polycystic kidney ds

2) most susceptible site in the nervous system for effects of acute ischemic anoxia are
a motor end plates
b sensory receptors
c synapses in autonomic ganglia
d synapses in cns

 

[dr.internationa]

Too alkaline condition of the blood (like in parathyroidectomy, gastric fistula, continous vomitting etc) can lead to tetany..
Hope this helps..

 

[porcelain258]

thanku dr international.....great waiting 4 the other 2 answers too

 

[Ibanez]

hi guys
so i assume that nobody could answer the above question
i hav some more 4 u
1) transitional epithelium d/t cigarette smoking is seen in which of the foll conditions
a glomerulonephritis
b pyelonephritis
c carcinoma of the kidney
d polycystic kidney ds

2) most susceptible site in the nervous system for effects of acute ischemic anoxia are
a motor end plates
b sensory receptors
c synapses in autonomic ganglia
d synapses in cns

Well the explanation for the first question regarding association of tetany with Alkalosis is not factual, and therefore, has a good reason. The reason is that Ca++ competes with H+ for binding plasma proteins.

Albumin is basic and "Attracts" H+. And in the condition of Alkalosis, there's a decrease in H+. So there's a decreased binding of plasma proteins by H+.

Plasma Proteins serve as excellent multi-dentate ligands for metal ions (Chelation). So in the absence of H+, Ca++ (a metal ion) binds to plasma proteins. This binding of Ca++ to plasma proteins decreases effective Ca++ in serum/blood. So there is a conditional HYPOCALCEMIA.

The Na+ Ca++ countertransport doesn't work since there is less of Ca++ outside the cell. So, now, Na+ remains inside the cell prolonging "DEPOLARIZATION" and thus "Action Potential Summation".

And, therefore, tetany as a result of alkalosis.


Now the MCQs...

A1. The answer is CA Kidney. I guess the keywords says it all... "Cigarette Smoking" "Transitional eptithelium"
I will never waste my time thinking about any other pathologies but Carcinomas.
By the way, what is meant by "d/t". Anyway the CA most likely is a Transtional cell CA.

Anyway the etiology of glomerulonephritis is Infectious/Hypersenstivity induced inflammation; pyleonephritis is Infectious (Acute)/ Obstruction induced inflammation; polycystic disease is hereditary (AD, I guess).

A2 Acute Anoxia

Hypoxemia/Anoxia decreases Oxidative phosphorylation; which decreases ATP formation; which decreases Na+ K+ pump activity; which decrease the gradient; which decreases nerve conduction.

Well brain is in the central compartment and blood will reach CNS before it reaches "relatively" peripheral sensory receptors or muscle end plates or autonomic ganglions.
And more so because of its functional requirement, it needs a constant supply of oxygen and glucose (/ketone bodies)...
And well you may have heard of Brain death Vs. Clinical Death... Brain can be dead but the heart-lung circulation can be maintained by a heart-lung machine. (Brain is the "first" to "die", "heart" follows...)

I'm almost sure about this second question, but let me know if I'm wrong (if you've the answer?). And I'm 400% sure about the other two.


Mayank.

 

[porcelain258]

well done boss! great concepts i must mention here......by the way have u done with ur exam or still preparing? ....pls let me knowwhich books r u following coz i m giving in july......and about the 2nd Q which u r doubtful i think its a good reason that anoxia first occurs in the cns synapses and later it follows the peripheral nervous system
thanks 4 the answers good luck....

 

[Ibanez]

well done boss! great concepts i must mention here......by the way have u done with ur exam or still preparing? ....pls let me knowwhich books r u following coz i m giving in july......and about the 2nd Q which u r doubtful i think its a good reason that anoxia first occurs in the cns synapses and later it follows the peripheral nervous system
thanks 4 the answers good luck....

No, I 'm writing my Part 1 on 9th June... and I'm not even "a quarter" prepared for it

For the super-zuper accelerated preparation I'm sticking with the BRS physio/path (a lil Biochem as well) and Kaplan notes for DA, Micro, Biochem and Gross Anat; high yield for embryo, histo (plus the "indespensable" Decks and released papers). I'll also try give Mosby's NBDE part 1 Review a read before my exam plus questions from Rapid Review series and Clinical Vignettes.

I hope that this much should suffice. Anyway this attempt will be my first and last... I hope I don't disappoint myself

Good Luck,
Mayank.

PS Let me know if I answered that "second" question correctly... (check the answer if you've the annswer key)

 

[porcelain258]

hi mayank
I know 4 sure that u wont get disappointment in the exam .....r u seriously telling that u r not prepared and still u know so well .....well could u pls lemme know from where could i get the rapid review series and clinical vignettes 4 practicing more questions....... and about the second q i dont have the answer key but i think u r answer was correct .......still if somebody feels its wrong then correct it pls.......
Ill be in touch with u if i come across another doubts n all the best 4 ur preparation......
thanks

 

[Ibanez]

hi mayank
I know 4 sure that u wont get disappointment in the exam .....r u seriously telling that u r not prepared and still u know so well .....well could u pls lemme know from where could i get the rapid review series and clinical vignettes 4 practicing more questions....... and about the second q i dont have the answer key but i think u r answer was correct .......still if somebody feels its wrong then correct it pls.......
Ill be in touch with u if i come across another doubts n all the best 4 ur preparation......
thanks

Uh huh, sadly but that's the truth... I'm not prepared at all! Well Rapid Review (software on the lines of USMLE) series is under Mosby publication release. Try "Google" it if you want to buy (but I don't know if it will be helpful for a NBDE candidate). Or well if you can rationalize the use of open source (I personally do ) you can try search for torrents or google it for torrent.

Well I'll try answer your doubts...

Good Luck,
Mayank.

 

[impaction]

regarding cause of tetany due to hyperventilation

if the Ca+ compete with the H+ for attatching with albumin in blood plasma, then how is it possible in acidosis, that Ca+are still transported by albumin

the concept i read somewhere is that when there is hyperventilation, there results a net loss of H+ resulting in alkalosis, and this leads to excessive HCO3 ions. to these HCO3 ions Ca+ binds and thus making it unavailable ,
resulting in tetany

 

[Ibanez]

regarding cause of tetany due to hyperventilation

if the Ca+ compete with the H+ for attatching with albumin in blood plasma, then how is it possible in acidosis, that Ca+are still transported by albumin

the concept i read somewhere is that when there is hyperventilation, there results a net loss of H+ resulting in alkalosis, and this leads to excessive HCO3 ions. to these HCO3 ions Ca+ binds and thus making it unavailable ,
resulting in tetany

Listen its not that simple... or if you're not aware of primary active transport of ions/electrolytes? Diffusion? Secondary primary transport? . Its not that there's just a single transport channel. There are many things going on simultaneously... H+ PUMP; Na+ K+ Pump; Ca++ pump and theres' simple diffusion going on (eg. Na+ K+ channels, and secondary active transports (Na+ Ca++ counter; H+ K+ counter, Na+ H+ counter, Na+ HCO3- symport)

Its a cumulative/overall effect (that I mentioned!)

And there;s binding of Ca++ to plasma proteins during Acidosis but that is "decreased" (not much though but "it does" because Ca++ is mostly intracellular during Acidosis and there's a functional Ca++ pump- Active primary transport which will pump it out) and mostly because this decrease causes activation of PTH (and Vit D, but it takes time to act) which will correct the blood Ca++ deficit, anyway. PTH plus Primary Active transport.

Normally 40 % Ca++ is bound to plasma proteins... this increases in Alkalosis and decreases in Acidosis. Well the increase of binding causes symptoms of tetany and decrease in binding causes an increase in INTRA-CELLULAR calcium. This decrease is not of much importance in acute cases but chronic acidosis pateints may have symptoms of hypocalcemia. But its unlikely, however, in most cases due to renal compensation (Increased excretion of H+; Ca++ will come out of cell in blood).

And I can go on and on... but the scope of a NBDE candidate isn't that deep.
Study the concept again, you might be mistaken.

Regards,
Mayank.

 

[impaction]

thanks mayank
so what type of Ca decreases in alkalosis?
is it free caclcium ions?
< as sometimes they ask the above que in MCQ>

 

[Ibanez]

thanks mayank
so what type of Ca decreases in alkalosis?
is it free caclcium ions?
< as sometimes they ask the above que in MCQ>

Yes it is the free Ca++ in the serum/blood that decreases in alkalosis. And the % Calcium bound to plasma proteins increases.


Regards,
Mayank.

 

[impaction]

Yes it is the free Ca++ in the serum/blood that decreases in alkalosis. And the % Calcium bound to plasma proteins increases.


Regards,
Mayank.

thanks mayank
but the maximum % of ca in blood plasma is the one who is bound to albumin < in normal conditions >

 

[Ibanez]

thanks mayank
but the maximum % of ca in blood plasma is the one who is bound to albumin < in normal conditions >

No, the % Ca bound to plasma protein is less than the free Ca++ under normal condition. (40% is plasma protein bound)

Free Ca++ is less than 60%, as some of the free Ca++ forms Ca3 (PO4)2, Ca Oxalate, Ca-other proteins, bicarbonate et cetra.

Mayank.

 

[parking2008]

Hey Hi Mayank,
I read ur replies in this thread. Great job Man I am also preparing for Part I and would like to discuss topic and preparation with u as it seems ur quite serious with ur studies and preparation and I would like to join ur company and blast the exam. What do u say ?? Plz let me know ur interest and can email me - [email protected] for contact information.
Waiting 4 ur reply
All the best.

 

[Ibanez]

Hey Hi Mayank,
I read ur replies in this thread. Great job Man I am also preparing for Part I and would like to discuss topic and preparation with u as it seems ur quite serious with ur studies and preparation and I would like to join ur company and blast the exam. What do u say ?? Plz let me know ur interest and can email me - [email protected] for contact information.
Waiting 4 ur reply
All the best.

Well its an illusion, I'm the laziest-direction-less-man-ever. Well you can join my caravan (there's only me though), but I'm unsure that you'll reach your destination. I can answer some technical questions, and that is all.

Good Luck and Best Regards,
Mayank.

 

[porcelain258]

hey mayank
how is it that urine urobilinogen rises in case of a hemolytic jaundice but falls in hepatocellular n obstructive jaundice coz i hav read that conjugated bilirubin converted by the liver into bile is converted by gut bacteria to urobilinogen .....but conjugated bilirubin is increased only in case of obstructive or hepatocellular jaundiceand not in hemolytic jaundice
thanks in advance

 

[Ibanez]

hey mayank
how is it that urine urobilinogen rises in case of a hemolytic jaundice but falls in hepatocellular n obstructive jaundice coz i hav read that conjugated bilirubin converted by the liver into bile is converted by gut bacteria to urobilinogen .....but conjugated bilirubin is increased only in case of obstructive or hepatocellular jaundiceand not in hemolytic jaundice
thanks in advance

Hey porcelain

In hemolytic jaundice, there is an increase in hemolysis; heme concentration; increased metabolism of heme; increased bilirubin (unconjugated; Water insoluble) in spleen.
This increased bilirubin is transported to the liver (bound to plasma proteins). In the liver unconjugated bilirubin is conjugated with Glucuronic acid.
Now this conjugated bilirubin (increased) is transported through hepatic duct to gall bladder, where it is released along with bile into small intestine.
In small intestine it is further metabolized into urobilinogen (and sterco-) and excreted through urine.

THERE'S AN INCREASE IN UROBILINOGEN IN THE URINE (and not conjugated bilirubin in urine). Liver Function is normal and there is no obstruction to passage of bilirubin/bile. So, it will be metabolized.

In "mild" hepatic jaundice, there is disruption of cell junctions (inflammation). The conjugated bilirubin leaks from the hepatocytes into the blood and is excreted. So there is presence of conjugated bilirubin in the urine. And decreased concentration of conjugated bilirubin is transported to gall bladder and then to intestine for further metabolism (to urobilinogen; therefore U/B decreases.)

In Obstructive Jaundice, there is decrease in transportation of conjugated bilirubin to small intestine due to obstruction. This results in tissue accumulation of conjugated bilirubin which is absorbed into blood and excreted (Increase in Urine/Blood Bilirubin conc. and decrease in Urine U/B conc. )
To say, if you fail in 5th grade... Then you'll still be in 5th grade and not 6th.
If conjugated bilirubin fails to appear in intestine, it will still be conjugated bilirubin and not urobilinogen.

Decrease in plasma proteins, glucuronic acid, moderate/severe hepatitis etc will result in tissue accumulation of unconjugated bilirubin.

Mayank.

 

[porcelain258]

thanks mayank
in case of hepatocellular jaundice , liver wont be able to convert unconjugated bilirubin into conjugated bilirubin ...so wont there be an increase in unconjugated rather than conjugated bilirubin so how come a decrease in urine urobilinogen then?

 

[Ibanez]

thanks mayank
in case of hepatocellular jaundice , liver wont be able to convert unconjugated bilirubin into conjugated bilirubin ...so wont there be an increase in unconjugated rather than conjugated bilirubin so how come a decrease in urine urobilinogen then?

Well urobilinogen conc in urine is not a good marker in Hepatic Jaundice. U/B conc can present as increased/decreased/not affected.

What I mentioned was about the mild jaundice, in moderate to severe hepatitis there is decrease in conjugation of bilirubin (compromised liver function) and therefore a decrease in urobilinogen (because conjugated bilirubin is water soluble and not unconjugated; Unconjugated will not be metabolized and excreted in urine but will accumulate in tissues)

I'm not sure how it can increase in hepatic jaundice... but all I know (for sure) is that U/B is not a good marker for hepatic jaundice. Liver Function Test is clinically co-related to confirm Hepatic Jaundice.

I'm too lazy to find my medicine books... and I've biochem to finish.

Mayank.

 

[porcelain258]

thanks mayank
i really appreciate ur quick replies ....uve been a great help and a good learner......wish u all the best ......

 

[Ibanez]

thanks mayank
i really appreciate ur quick replies ....uve been a great help and a good learner......wish u all the best ......

You're welcome, Porcelain.
Its hard to digest facts, so conceptual understanding makes it easier for me... (most of the times; I, too, have my moments of *****-ism... )

Mayank.

 

[chato1234]

Well the explanation for the first question regarding association of tetany with Alkalosis is not factual, and therefore, has a good reason. The reason is that Ca++ competes with H+ for binding plasma proteins.

Albumin is basic and "Attracts" H+. And in the condition of Alkalosis, there's a decrease in H+. So there's a decreased binding of plasma proteins by H+.

Plasma Proteins serve as excellent multi-dentate ligands for metal ions (Chelation). So in the absence of H+, Ca++ (a metal ion) binds to plasma proteins. This binding of Ca++ to plasma proteins decreases effective Ca++ in serum/blood. So there is a conditional HYPOCALCEMIA. This is similar to Milk-Alkali Syndrome.

The Na+ Ca++ countertransport doesn't work since there is less of Ca++ outside the cell. So, now, Na+ remains inside the cell prolonging "DEPOLARIZATION" and thus "Action Potential Summation".

And, therefore, tetany as a result of alkalosis.


Now the MCQs...

A1. The answer is CA Kidney. I guess the keywords says it all... "Cigarette Smoking" "Transitional eptithelium"
I will never waste my time thinking about any other pathologies but Carcinomas.
By the way, what is meant by "d/t". Anyway the CA most likely is a Transtional cell CA.

Anyway the etiology of glomerulonephritis is Infectious/Hypersenstivity induced inflammation; pyleonephritis is Infectious (Acute)/ Obstruction induced inflammation; polycystic disease is hereditary (AD, I guess).

A2 Acute Anoxia

Hypoxemia/Anoxia decreases Oxidative phosphorylation; which decreases ATP formation; which decreases Na+ K+ pump activity; which decrease the gradient; which decreases nerve conduction.

Well brain is in the central compartment and blood will reach CNS before it reaches "relatively" peripheral sensory receptors or muscle end plates or autonomic ganglions.
And more so because of its functional requirement, it needs a constant supply of oxygen and glucose (/ketone bodies)...
And well you may have heard of Brain death Vs. Clinical Death... Brain can be dead but the heart-lung circulation can be maintained by a heart-lung machine. (Brain is the "first" to "die", "heart" follows...)

I'm almost sure about this second question, but let me know if I'm wrong (if you've the answer?). And I'm 400% sure about the other two.


Mayank.

hey mayank,

You mentioned milk alkali syndrome..
Ingestion of over 2g of elemental calcium per day may lead to this disorder. When a large quantity of calcium is ingested and absorbed by the GI tract, hypercalcemia works to feedback on the parathyroid gland to inhibit production of PTH. This, in turn, leads to an increased absorption of bicarbonate in the kidney, establishing metabolic alkalosis.

Can you please explain why decrease in parathormone will lead to incresed absorption of bicarbonate in the kidney?

please help

 

[Ibanez]

hey mayank,

You mentioned milk alkali syndrome..
Ingestion of over 2g of elemental calcium per day may lead to this disorder. When a large quantity of calcium is ingested and absorbed by the GI tract, hypercalcemia works to feedback on the parathyroid gland to inhibit production of PTH. This, in turn, leads to an increased absorption of bicarbonate in the kidney, establishing metabolic alkalosis.

Can you please explain why decrease in parathormone will lead to incresed absorption of bicarbonate in the kidney?

please help

PTH has nothing to do with absorption of "BICARBONATE". In milk alkali syndrome, excess Ca++ ingestion is accompained by INGESTION OF BICARBONATE.

Both the % bound and free Ca++ increases resulting in HYPERCALCEMIA.

Hypercalcemia will result in stone formation and other metastatic calcifications.

HYPERCALCEMIA, also, worsens the alkalosis by driving H+ intracellularly through Ca+ channel(Ca++ H+ counter-transport).

And renal compensation of Alkalosis will drive the INCREASED EXCRETION OF CALCIUM; resulting in Calciuria. Calcium and bicarbonate reabsorption is coupled to Na+. So alkalosis will drive the excretion of bicarbonate and along with it Na+ and Ca++ as well.


Mayank.

PS There is no association of Milk Alkali Syndrome to above mechanism. I was wrong (a little)!

 

[chato1234]

PTH has nothing to do with absorption of "BICARBONATE". In milk alkali syndrome, excess Ca++ ingestion is accompained by INGESTION OF BICARBONATE.

Both the % bound and free Ca++ increases resulting in HYPERCALCEMIA.

Hypercalcemia will result in stone formation and other metastatic calcifications.

HYPERCALCEMIA, also, worsens the alkalosis by driving H+ intracellularly through Ca+ pump (Ca++ H+ ATPase).

And renal compensation of Alkalosis will drive the INCREASED EXCRETION OF CALCIUM; resulting in Calciuria. Calcium and bicarbonate reabsorption is coupled to Na+. So alkalosis will drive the excretion of bicarbonate and along with it Na+ and Ca++ as well.


Mayank.

PS There is no association of Milk Alkali Syndrome to above mechanism. I was wrong (a little)!

but hypercalemia means increase ca+ level in the blood stream that is unbound or free calcium.. increase in free calcium would lead to increase in bound calcium, beacause ca+ will compete with h+ to bind with plasma proteins..

 

[Ibanez]

but hypercalemia means increase ca+ level in the blood stream that is unbound or free calcium.. increase in free calcium would lead to increase in bound calcium, beacause ca+ will compete with h+ to bind with plasma proteins..

Too much Ca++ will result in saturation of BINDING SITES on plasma proteins. So both Free Ca++ and bound Ca increases. Never mind the "bound Ca", just remember ulitmately it will result in "Hypercalemia".

 

[Ibanez]

but hypercalemia means increase ca+ level in the blood stream that is unbound or free calcium.. increase in free calcium would lead to increase in bound calcium, beacause ca+ will compete with h+ to bind with plasma proteins..

Too much Ca++ will result in saturation of BINDING SITES on plasma proteins. So both Free Ca++ and bound Ca increases. Never mind the "bound Ca", just remember ulitmately it will result in "Hypercalemia".

Mayank.

 

[SCDC]

how is alkalosis associated with tetany???

This has to be related to fall in Pco2 due to prolonged hyperventilation in severe panic attacks.
I read about that some where but cannot remember the details.

 

[Ibanez]

how is alkalosis associated with tetany???

This has to be related to fall in Pco2 due to prolonged hyperventilation in severe panic attacks.
I read about that some where but cannot remember the details.

Oh!
Yeah sure... I'm such an idiot! Plain and simple!
And wasted my time answering the Q...

Mayank.


PS "One man's theology is another man's belly laugh". Lazarus Long (Robert. A. Heinlein)

 

[SCDC]

Looks like you never heard of respiratory alkalosis caused by hyperventilation , especially at high altitudes.

yeah yeah i am heart broken, psss sarcasm

 

[Ibanez]

Looks like you never heard of respiratory alkalosis caused by hyperventilation , especially at high altitudes.

yeah yeah i am heart broken, psss sarcasm

Yeah sure!

Looks like your senses have failed you... If you, still, can manage to "read" my explanation above? Or you can have someone read-out-loud, you can "HEAR" (if assumed that you're not a hypocrite? And when you say "Looks like you never 'heard'..." ) ?

God have mercy on superficial-skim-read-ers! Science is not worth your SKIM-READ! Pssst Sarcasm? Heart Broken?

Well suit yourself...

Mayank.

PS All Apologies.
PSS If you're blind and/or deaf and/or dumb, that is.

 

[SCDC]

Yeah sure!

Looks like your senses have failed you... If you, still, can manage to "read" my explanation above? Or you can have someone read-out-loud, you can "HEAR" (if assumed that you're not a hypocrite? And when you say "Looks like you never 'heard'..." ) ?

God have mercy on superficial-skim-read-ers! Sciene is not worth your SKIM-READ! Pssst Sarcasm? Heart Broken?

Well suit yourself...

Mayank.

PS All Apologies.
PSS If you're blind and/or deaf and/or dumb, that is.


PSS go get a life

 

[SCDC]

if you are prepared to have a civilised conversation, we can discuss the subject at hand

If you want to persist on with the childish behaviour....

,

 

[Ibanez]

Looks like you never heard of respiratory alkalosis caused by hyperventilation , especially at high altitudes.

yeah yeah i am heart broken, psss sarcasm

I'm feeling bad, already. I know my behaviour was irrational and I'm sorry. But at the same time it was painful for me because I take-out-precious-time to answer Qs on SDN. It doesn't feel alright when someone comes "poke-ing-in" with "I-have-read-somewhere" and "sort-of-challenge-my-intellect".
Well suit yourself... If you're happy with Skim-read-ing, so be it!

I don't have anything against you!

Good Luck and Best Regards,
Mayank.

 

[SCDC]

Skim-read-ing,

I have to agree.

 

[SCDC]

I started preparing for the EE about a week or 2 back so right now i am skimming over the textbooks, will go in for detailed reading later onwards .
Any way i found your replies useful.
Many thanks for that.
And let us not hijack this thread any more.
Peace.

 

[Ibanez]

I started preparing for the EE about a week or 2 back so right now i am skimming over the textbooks, will go in for detailed reading later onwards .
Any way i found your replies useful.
Many thanks for that.
And let us not hijack this thread any more.
Peace.

You're welcome. And yeah, Truce!

 

[porcelain258]

for god sake guys i have started this thread with a purpose that we can all put in our doubts and clear them and not just stick to one question that is very well answered by a person with a very good reasoning .....and not to forget that the person who is answering is himself preparing 4 the exam just like all of u......how many of u can take out ur time to go to that minute details in clearing the fact .......so dont just keep on probing the same q again and again and move further as we all know that nobody will crack the nbde by doing research on one topic .....i m sure we all have lots of other stuff to study too
thanks

 

[NileBDS]

I agree. Let's stick to the original topic guys. No need to taint this nor any thread with personal feuds.

 

[Ibanez]

for god sake guys i have started this thread with a purpose that we can all put in our doubts and clear them and not just stick to one question that is very well answered by a person with a very good reasoning .....and not to forget that the person who is answering is himself preparing 4 the exam just like all of u......how many of u can take out ur time to go to that minute details in clearing the fact .......so dont just keep on probing the same q again and again and move further as we all know that nobody will crack the nbde by doing research on one topic .....i m sure we all have lots of other stuff to study too
thanks

Hey thanks for the back-up!
I think I may start answering on SDN, again, from now on...


Mayank.

 

[SCDC]

which of the statements best describe G-proteins?

1, Are important components of steroid-hormone signal transduction
2, Catabolise the reaction which produces diacyl glycerol
3, Are tightly bound to adenylate cyclase
4, usually inactivate protein kinase C
5,Are membrane proteins

And why?

 

[SCDC]

TYpes of inflammatory exudates?

 

[Ibanez]

which of the statements best describe G-proteins?

1, Are important components of steroid-hormone signal transduction
2, Catabolise the reaction which produces diacyl glycerol
3, Are tightly bound to adenylate cyclase
4, usually inactivate protein kinase C
5,Are membrane proteins

And why?

G proteins are MEMBRANE PROTEINS.

• steroid hormone signal transduction is through new protein synthesis, and are not related to G proteins/receptors. Steroid receptors are present as freely-floating-in-Cytosol.
• Diacylglycerol is produced by the action of Phospholipase C; and is not direct mechanism of action of G protiens. (G-Ca+2-IP3 Transduction)
• ARE NOT BOUND TO ADENYLATE CYCLASE; [Free floating in the cytoplasm; adenylate cyclase is released from golgi app into cytosol]
• Inactivation/activation of Protein kinase C is not a direct action of G proteins, but is mediated by Diacylglycerol (and Ca++). \G-Ca2+-IP3 Transduction.
• G proteins (almost all families) are plasma membrane proteins. (Inner surface? Well I'm almost sure)

I'm running out of time...

I'll answer next Q when I'm done with a good 8 hour sleep or may be when I'm done with my studies... And I'm majorily lacking on it.

Mayank.

 

[SCDC]

thanks

 

[SCDC]

Mandibular canine on right side is lost how will it affect the protrusive contacts on the left canine?
Answers welcome

 

[porcelain258]

which of the foll. has been shown to have a relationship to carcinoma of the cervix?
papovavirus
varicella zoster virus
herpes virus hominis type1
herpesvirus hominis type2
none of the above

the answer acc to the key is herpesvirus hoministype2
but i think the cancer of the cervix is due to papova (papillomavirus)
what do u think guys?

 

[Ibanez]

which of the foll. has been shown to have a relationship to carcinoma of the cervix?
papovavirus
varicella zoster virus
herpes virus hominis type1
herpesvirus hominis type2
none of the above

the answer acc to the key is herpesvirus hoministype2
but i think the cancer of the cervix is due to papova (papillomavirus)
what do u think guys?

HPV (papova-), 100% sure!

Herpesvirus hominis type 2 causes VD, at most.
Varciella zoster is an etio agent in Chicken Pox, Shingles/Herpes zoster.

Mayank.

PS Is it from a very old paper... Late 70s/ Early 80s?

 

[porcelain258]

thanks mayank and yes its from 80's released paperbut why did u ask that.....are there many wrong answers we can find in them....

 

[Ibanez]

thanks mayank and yes its from 80's released paperbut why did u ask that.....are there many wrong answers we can find in them....

Not many but few (like one Q on an avg.!)
I did all the DA released Qs a while ago, and found out around a dozen typos/mistake in the answer key. (Like 14-15 out of 1200-1300; not that bad but still each typo drove me crazy to the limit of pulling my hair and hitting my head hard on walls... )

Mayank.