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* NBME 7 block 1 q 1 to 50
  maryam2009 - 05/09/11 08:41
  Welcome....,Please choose and answer the Qs in order. We are always looking for more volunteers. ... Any help would be appreciated .Thank you.  
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* Re:NBME 7 block 1 q 1 to 50
  maryam2009 - 05/09/11 08:53

HMG-coA reductase inhibitors are more effective for bringing the LDL to normal level....
They inhibit cholestrol precursor,Mevalonate
reversible high level liver function test

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* Re:NBME 7 block 1 q 1 to 50
  maryam2009 - 05/09/11 08:59

Zafirlucast,Montelucast.....Leukoterine receptor blockers prevent bronchoconstriction
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* Re:NBME 7 block 1 q 1 to 50
  maryam2009 - 05/09/11 09:08

betwen B and C....I'll choose C bcause according to verbal recommendation ,sending a list of low sodium diet with patient that needs to follow it is more efficient.

if there is any other ideas,please add ,TY

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* Re:NBME 7 block 1 q 1 to 50
  usmle_guy - 05/09/11 09:39
  we have to inform the patient about what foods have high sodium...That's the correct answer for sure.  
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* Re:NBME 7 block 1 q 1 to 50
  maryam2009 - 05/09/11 09:43

the tumor shows a haphazard arrangement of somatic tissues representing derivatives of ecto...,meso.. and is a characteristic of germ cells.


Tricyclic antidepressant overdose....Tricyclics have a narrow therapeutic index, i.e., the therapeutic dose is close to the toxic dose.

The peripheral autonomic nervous system, central nervous system and the heart are the main systems that are affected following overdose.
Initial or mild symptoms typically develop within 2 hours and include tachycardia, drowsiness, a dry mouth, nausea and vomiting, urinary retention, confusion, agitation, and headache.
More severe complications include hypotension, cardiac rhythm disturbances, hallucinations, and seizures. Electrocardiogram (ECG) abnormalities are frequent and a wide variety of cardiac dysrhythmias can occur, the most common being sinus tachycardia and intraventricular conduction delay resulting in prolongation of the QRS complex and the PR/QT intervals.
Seizures, cardiac dysrhythmias, and apnea are the most important life threatening complications.[
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* Re:NBME 7 block 1 q 1 to 50
  maryam2009 - 05/09/11 10:11

Professional APCs are very efficient at internalizing antigen, either by phagocytosisThe acidic compartments of macrophages are also responsible for the degradation of ingested micro-organisms ) or by receptor-mediated endocytosis, and then displaying a fragment of the antigen, bound to a class II MHC molecule, on their membrane. The T cell recognizes and interacts with the antigen-class II MHC molecule complex on the membrane of the antigen-presenting cell.

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* Re:NBME 7 block 1 q 1 to 50
  god99 - 05/09/11 10:25
  7. D
Pyruvate carboxylase is a mitochondria enzime requiring biotin. It is activated by acetylCoA( from beta- oxidation. The product oxaloacetate(OAA), a citric acid cycle intermediate, cannot leave the mitochondria but is reduced to malate that can leave via a Malate shuffle. In the cytoplasm malate is reduced to (OAA).
Pyruvate carboxylase deficiency is an inherited disorder that causes lactic acid and other potentially toxic compounds to accumulate in the blood. High levels of these substances can damage the body's organs and tissues, particularly in the nervous system. Pyruvate carboxylase deficiency is a rare condition, with an estimated incidence of 1 in 250,000 births worldwide. This disorder appears to be much more common in some Algonkian Indian tribes in eastern Canada.
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* Re:NBME 7 block 1 q 1 to 50
  maryam2009 - 05/09/11 10:25

A deficiency of pyruvate carboxylase can cause lactic acidosis as a result of lactate build up. Normally, excess pyruvate is shunted into gluconeogenesis via conversion of pyruvate into oxaloacetate, but because of the enzyme deficiency, excess pyruvate is converted into lactate instead.
As a key role of gluconeogenesis is in the maintenance of blood sugar, deficiency of pyruvate carboxylase can also lead to hypoglycemia
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* Re:NBME 7 block 1 q 1 to 50
  maryam2009 - 05/09/11 10:36

I-cell disease is an autosomal recessive disorder caused by a deficiency of GlcNAc phosphotransferase, which phosphorylates mannose residues to mannose-6-phosphate on N-linked glycoproteins in the Golgi apparatus within the cell.

Without mannose-6-phosphate to target them to the lysosomes, the enzymes are transported from the Golgi to the extracellular space, resulting in large intracellular inclusions of molecules requiring lysosomal degradation in patients with the disease .

The Golgi apparatus is unable to target the lysosomal protein (which is normal) to the lysosome. Without proper functioning of N-acetylglucosamine-1-phosphotransferase, a build up of substances occurs when enzymes are unable to travel inside of the lysosome
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* Re:NBME 7 block 1 q 1 to 50
  god99 - 05/09/11 10:37
  8. A
I- Cell Disease: (Inclusion cell disease). Inherited lysosomal storage disorder; failure of addition to mannose 6 phosphate to lysosome proteins( enzime are secreted outside the cell instead of being targeted to the lysosme. Result in coarse facial future, clouded corneas, restricted join movement, and high plama levels of lysosomes. Often fatal childhood.
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