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NBME 7 block 4 q 1 to 50 - maryam2009
#41
30.CC

Adison disease...

Metabolic acidosis (increased blood acidity), due to loss of the hormone aldosterone because sodium reabsorption in the distal tubule is linked with acid/hydrogen ion (H+) secretion. Low levels of aldosterone stimulation of the renal distal tubule leads to sodium wasting in the urine and H+ retention in the serum.
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#42
31.AA

Haemophilus influenzae type B....

The Hib conjugate vaccine is an inactivated vaccine. It is made by chemically bonding a polysaccharide (sugar) to a protein. This long chain of sugar molecules makes up the surface capsule of the bacterium.
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#43
32.EE

Absence seizures or petit mal epilepsy

There is a correlation between SLOW WAVE SLEEP (stage 3 and 4 aka delta sleep ) and abscence seizures ....one of the correlation is Slow-wave sleep as well as generalized absence seizures are characterized by the occurrence of synchronized oscillations in thalamocortical systems that spontaneously appear and disappear.

What are this synchronized oscillations ?

-Oscillations =Remember from highschool physics ...if u put a load to a spring it oscillates ....the same thing neurons oscillate (another term is repititive variation) ...which is called neural oscillation

Neural oscillation is rhythmic or repetitive neural activity in the central nervous system .And this can be due to rhythmic increases and decreases in action potential activity,which then produce rhythmic activation of synapses in target neurons.

This oscillations can be physiolgical or patholgical.

Pathological oscillations =Specific types of neural oscillations may also appear in pathological situations, such as Parkinson's disease or epilepsy. Interestingly, these pathological oscillations often consist of an aberrant version of a normal oscillation. For example, one of the best known types is the spike and wave oscillation(synchronized oscillation ) , which is typical of generalized or absence epileptic seizures, and which resembles normal sleep spindle oscillations.


posted by yeabiruh -

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#44
33) C

Blood supply to the testis primarily originates from the testicular artery, which arises from the aorta. Other sources of blood supply include the deferential artery, which supplies the epididymis and the vas deferens and the cremasteric artery supplies the peritesticular tissues.
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#45
33.CC

The testicular artery (the male gonadal artery, also called the internal spermatic arteries in older texts) is a branch of the abdominal aorta that supplies blood to the testis. It is a paired artery, with one for each of the testes.

It is the male equivalent of the ovarian artery.

http://en.wikipedia.org/wiki/File:Gray531.png

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#46
34.FF


I go with 60 % ...for the following reasons

1-Autosomal dominant diseases occurence is affected by many things ...among those is the number of trinucleotide repeats in the proband...also variable penetrance ...and etc.....
Which means AD diseases are not always shown up 100 %


2-Clearly the question gives us the trinucleotide repeat expansion peneterance figures

and for 15 Trinucleotide Repeat Expansion the risk is 60 % ....

posted by fitche -

......


Huntington's Disease is an AD disease which means that an affected individual TYPICALLY inherits a defective gene from an AFFECTED parent. If the parent has a trinucleotide repeat count that is normal (40 (full penetrance).

Back to the question. it can be any trinuc expansion disorder. But used Hunt. disease to illustrate some points. First, risk doesn't necessarily reflect that the parent has the disorder but the parent can be an unaffected carrier with trinuc expansions that will not result in full penetrance. Second, the graph is very important. It shows that individuals inheriting a gene with a trinuc expan. of 20 have a 100% risk of the disease (full penetrance), as well as those with CAG repeats of 9 or less have 0% risk. The curve represents reduced penetrance (where some individuals fail to exhibit the trait even though they carry the abnormal allele. As the number of CAG repeats increase there is an increase in the percentage of individuals at risk of the disease. This implies that penetrance is increasing up to point where it becomes full or complete (all individuals who have the abnormal allele will manifest (signs/symptoms) the disease. The answer that best fits the curve is 60%

posted by einst74 -
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#47
35.CC

Clostridium perfringens is a Gram-positive, rod-shaped, anaerobic, spore-forming bacterium of the genus Clostridium. C. perfringens is ever present in nature and can be found as a normal component of decaying vegetation, marine sediment, the intestinal tract of humans and other vertebrates, insects, and soil.

Clostridium perfringens is the most common bacterial agent for gas gangrene, which is necrosis, putrefaction of tissues, and gas production. It is caused primarily by Clostridium perfringens alpha toxin. The gases form bubbles in muscle (crepitus) and the characteristic smell in decomposing tissue

In the United Kingdom and United States, C. perfringens bacteria are the third-most-common cause of food-borne illness, with poorly prepared meat and poultry the main culprits in harboring the bacterium.The clostridium perfringens enterotoxin (CPE) mediating the disease is heat-labile (inactivated at 74 °C) and can be detected in contaminated food, if not heated properly, and feces .

Wikipedia

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#48
36) ddddd

graph A: LH
graph B: FSH
graph C: progesterone
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#49
37.CC

High sodium intake increases body weight , plasma volume,cardiac index , and stroke volume index.


In the body, sodium is processed by the kidneys. However, when a person eats too much sodium, the kidneys cannot process all of it. The excess sodium ends up in the bloodstream. Because the mineral retains water, the volume of blood in the body increases. As a result, the circulatory system has to work harder to pump the blood. Over time, this added strain on the system can result in heart disease and kidney failure

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#50
38 - D Patient had CHF, "LVF", allways if pulmonary edema LHF the main symptom the SOB
Can't get blood out of the heart b/c the LV fails, increassed the EDV because all the blood can not get out, then the pressure and volume will go back to the left atrium, back into the pulmonary vessels, increased the hydrostatic pressure and then PULMONARY EDEMA
What happen in the CHF?: Dicreased the cardia output regulated by RAA System like the Blood pressure, the renal perfusion is decreased then the renin increases---- renin convert angiotensinogen into angiotensin I. ACE found mainly in endotelial cells of pulmonary vessels, converts angiotensin I into angiotensin II. Angiotensin II has a potent effects to stimulate secretion of aldosterone and to cause arteriolar vasoconstriction. stimulates reabsorption of Na+ and ALSO Cause increased renal excretion of potassium affecting the plasma K_ concentration
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