NBME 7 block 3 q 1 to 50 - maryam2009

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It's true your right, Thanks.

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6 - AAA had it's origen than the renal artery, no Superior mesenteric bc it's origen is superior to the top of the kidneys

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7 E Kartagener syndrome, sinusitis, bronchiectasis, infertility, is Autosomal R, there is abnormal ciliary motion and impaired mucociliary clearence, reason for the clinical signs

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6. A

The Inferior Mesenteric Artery (IMA) branches off the anterior surface of the abdominal aorta below the renal artery branch points, and approximately midway between these and the aortic bifurcation (into the common iliac arteries). Supplies the large intestine from the left colic (or splenic) flexure to the upper part of the rectum, which includes the descending colon, the sigmoid colon, and part of the rectum. Proximally, its territory of distribution overlaps (forms a watershed) with the middle colic artery, and therefore the superior mesenteric artery. The SMA and IMA anastomose via the marginal artery of the colon (artery of Drummond). The territory of distribution of the IMA is more or less equivalent to the embryonic hindgut.
http://en.wikipedia.org/wiki/Inferior_mesenteric_artery

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8. B
Autoimmune Metaplastic Atrophic Gastritis (AMAG) is an inherited form of atrophic gastritis characterized by an immune response directed toward parietal cells and intrinsic factor.[1] The presence of serum antibodies to parietal cells and to intrinsic factor are characteristic findings. The autoimmune response subsequently leads to the destruction of parietal cells, which leads to profound hypochlorhydria (and elevated gastrin levels). The inadequate production of intrinsic factor also leads to vitamin B12 malabsorption and pernicious anemia. AMAG is typically confined to the gastric body and fundus.

9. D
Complement component 8 is a protein involved in the complement system. A hereditary deficiency of C8 can result in increased susceptibility to Neisseria infections, such as meningitis and gonorrhea.
Deficiency of C5-C8 leads to Neisseria bacteremia.

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10. C
The Urachus is the part of the allantoids duct between the bladder and the umbilicus.
The median umbilical ligament is a structure in human anatomy. It is a shrivelled piece of tissue that represents the remnant of the embryonic urachus.
It extends from the apex of the bladder to the umbilicus, on the deep surface of the anterior abdominal wall. It is unpaired.
It is covered by the median umbilical fold
Lateral to this structure are the medial umbilical ligament (which is a different structure, not to be confused) and the lateral umbilical ligament.

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11. A
Addison Disease: Chronic adrenal insufficiencydue to adrenal atrophy or destruction by disease (Autoimmmune, TB, metastasis). 1º deficiency of aldosterone and cortisol causing hypotension, and skin hyperpigmentation. (FA page 291)
Because primary hypocortisolism is manifested as a deficiency in glucocorticoid release from the adrenal cortex, increased ACTH will be released by the pituitary in order to trigger release of the absent glucocorticoid; it is because of this overstimulation of ACTH that bronzing of the skin occurs. In secondary or tertiary hypocortisolism, there is a deficiency of either CRH or ACTH release by the hypothalamus or pituitary gland, respectively. The former will manifest as no ACTH release while the latter will manifest as physiologic (normal) ACTH release; neither will cause an overproduction of ACTH. On examination, the following may be noticed:[2]
•Low blood pressure that falls further when standing (orthostatic hypotension)
•In long-standing Addison's Disease, the pinna of the ear may become calcified
•Most people with primary Addison's have darkening (hyperpigmentation) of the skin, including areas not exposed to the sun; characteristic sites are skin creases (e.g. of the hands), nipple, and the inside of the cheek (buccal mucosa), also old scars may darken. This occurs because melanocyte-stimulating hormone (MSH) and adrenocorticotropic hormone (ACTH) share the same precursor molecule, Pro-opiomelanocortin (POMC). After production in anterior pituitary gland, POMC gets cleaved into Gamma-MSH, ACTH and Beta-lipotropin. The subunit ACTH undergoes further cleavage to produce Alpha-MSH, the most important MSH for skin pigmentation. In secondary and tertiary forms of Addison's, skin darkening does not occur.
•Medical conditions such as type I diabetes, autoimmune thyroid disease (Hashimoto's thyroiditis and goiter) and vitiligo often occur together with Addison's (often in the setting of Autoimmune polyendocrine syndrome). Hence, symptoms and signs of any of the former conditions may also be present in the individual with Addison's.

http://en.wikipedia.org/wiki/Addison's_disease

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12. C
12. C
Ethanol (ethyl alcohol) and isopropanol (isopropyl alcohol) are alcohols that kill bacteria. Alcohols kill bacteria by first making the lipids that are part of the outer protective cell membrane of each bacterium cell more soluble in water so that the cell membrane begins to lose its structural integrity and fall apart. As the cell membrane disintegrates, alcohol can then enter the cell and denature proteins within each bacterium.

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13. C
Neisseria are fastidious Gram-negative cocci that require nutrient supplementation to grow in laboratory cultures. Specifically, they grow on chocolate agar with carbon dioxide
Infection of the genitals in females with N. gonorrhoeae can result in pelvic inflammatory disease if left untreated, which can result in infertility. Pelvic inflammatory disease results if N. gonorrhoeae travels into the pelvic peritoneum (via the cervix, endometrium and fallopian tubes). Infertility is caused by inflammation and scarring of the fallopian tube. Infertility is a risk to 10 to 20% of the females infected with N. gonorrhoeae.

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14. B
Varicella zoster virus (VZV) is one of eight herpes viruses known to infect humans (and other vertebrates). It commonly causes chicken-pox in children and Herpes zoster (shingles) in adults and rarely in children. Primary VZV infection results in chickenpox (varicella), which may rarely result in complications including encephalitis or pneumonia. Even when clinical symptoms of chickenpox have resolved, VZV remains dormant in the nervous system of the infected person (virus latency), in the trigeminal and dorsal root ganglia.[1] In about 10–20% of cases, VZV reactivates later in life producing a disease known as shingles. Serious complications of shingles include postherpetic neuralgia, zoster multiplex, myelitis, herpes ophthalmicus, or zoster sine herpete.
Herpes zoster (or simply zoster), commonly known as shingles and also known as zona, is a viral disease characterized by a painful skin rash with blisters in a limited area on one side of the body, often in a stripe. The initial infection with varicella zoster virus (VZV) causes the acute (short-lived) illness chickenpox which generally occurs in children and young people. Once an episode of chickenpox has resolved, the virus is not eliminated from the body but can go on to cause shingles—an illness with very different symptoms—often many years after the initial infection.
http://en.wikipedia.org/wiki/Herpes_zoster