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+--- Thread: NBME 7 block 2 q 1 to 50 - maryam2009 (/showthread.php?tid=585303)
NBME 7 block 2 q 1 to 50 - maryam2009 - ArchivalUser - 05-11-2011
Welcome....,Please choose and answer the Qs in order. We are always looking for more volunteers. ... Any help would be appreciated .Thank you.
0 - ArchivalUser - 05-11-2011
1.AA
Caspase-9 is an initiator caspase, encoded by the CASP9 gene.
The aspartic acid specific protease caspase-9 has been linked to the mitochondrial death pathway. It is activated during programmed cell death (apoptosis). Induction of stress signaling pathways JNK/SAPK causes release of cytochrome c from mitochondria and activation of apaf-1 (apoptosome), which in turn cleaves the pro-enzyme of caspase-9 into the active form.
0 - ArchivalUser - 05-11-2011
2.AA
Primary symptoms of C. parvum infection are acute, watery, and non-bloody diarrhoea. C. parvum infection is of particular concern in immunocompromised patients, where diarrhea can reach 10–15L per day. Other symptoms may include anorexia, nausea/vomiting and abdominal pain.Infection is caused by ingestion of sporulated oocysts transmitted by the fecal-oral route
Entamoeba histolytica is an anaerobic parasitic protozoan.The active (trophozoite) stage exists only in the host and in fresh loose feces; cysts survive outside the host in water, in soils, and on foods, especially under moist conditions on the latter.
http://upload.wikimedia.org/wikipedia/commons/c/cf/Trophozoites_of_Entamoeba_histolytica_with_ingested_erythrocytes.JPG
http://en.wikipedia.org/wiki/File:Entamoeba_histolytica_life_cycle-en.svg
Giardia lamblia is a flagellated protozoan parasite that colonizes and reproduces in the small intestine, causing giardiasis. The giardia parasite attaches to the epithelium by a ventral adhesive disc, and reproduces via binary fission. Giardiasis does not spread via the bloodstream, nor does it spread to other parts of the gastro-intestinal tract, but remains confined to the lumen of the small intestine.
http://upload.wikimedia.org/wikipedia/commons/0/08/Giardia_lamblia_SEM_8698_lores.jpg
Giardia infection can occur through ingestion of dormant cysts in contaminated water, food, or by the faecal-oral route (through poor hygiene practices). The Giardia cyst can survive for weeks to months in cold water, and therefore can be present in contaminated wells and water systems, especially stagnant water sources such as naturally occurring ponds, storm water storage systems, and even clean-looking mountain streams.
http://en.wikipedia.org/wiki/File:Giardia_life_cycle_en.svg
Strongyloides stercoralis is a nematode that can parasitize humans. The adult parasitic stage lives in tunnels in the mucosa of the small intestine.Strongyloides stercoralis is a nematode that can parasitize humans. The adult parasitic stage lives in tunnels in the mucosa of the small intestine.
Many people infected are usually asymptomatic at first. Symptoms include dermatitis: swelling, itching, larva currens, and mild hemorrhage at the site where the skin has been penetrated. If the parasite reaches the lungs, the chest may feel as if it is burning, and wheezing and coughing may result, along with pneumonia-like symptoms (Löffler's syndrome). Eventually, the intestines could be invaded, leading to burning pain, tissue damage, sepsis, and ulcers. In severe cases, edema may result in obstruction of the intestinal tract as well as loss of peristaltic contractions.
Strongyloidiasis in immunocompetent individuals is usually an indolent disease. However, in immunocompromised individuals, strongyloidiasis can cause a hyperinfective syndrome (also called disseminated strongyloidiasis) due to the reproductive capacity of the parasite inside the host. This hyperinfective syndrome has a mortality rate of close to 90%.
http://en.wikipedia.org/wiki/File:Strongyloides_stercoraliz_larva.jpg
wikipedia
0 - ArchivalUser - 05-11-2011
3.BB
β2 microglobulin is a component of MHC class I molecules, which are present on all nucleated cells (excludes red blood cells).
Mice models deficient for the β2 microglobulin gene have been engineered. These mice demonstrate that β2 microglobulin is necessary for cell surface expression of MHC class I and stability of the peptide binding groove.
In fact, in the absence of β2 microglobulin, very limited amounts of MHC class I (classical and non-classical) molecules can be detected on the surface. In the absence of MHC class I, CD8 T cells cannot develop. (CD8 T cells are a subset of T cells involved in the development of acquired immunity.)Low levels of β2 microglobulin can indicate non-progression of HIV.
Levels of beta-2 microglobulin can be elevated in multiple myeloma and lymphoma,though in these cases primary amyloidosis (amyloid light chain) and secondary amyloidosis (Amyloid associated protein) are more common
0 - ArchivalUser - 05-11-2011
4.BB
Calcitriol , also called 1,25-dihydroxycholecalciferol or 1,25-dihydroxyvitamin D3, is the hormonally active form of vitamin D with three hydroxyl groups.
It increases the level of calcium (Ca2+) in the blood by
(1) increasing the uptake of calcium from the gut into the blood,
(2) decreasing the transfer of calcium from blood to the urine by the kidney, and
(3) increasing the release of calcium into the blood from bone.
Calcitriol is produced in the cells of the proximal tubule of the nephron in the kidneys by the action of 25-hydroxyvitamin D3 1-alpha-hydroxylase
0 - ArchivalUser - 05-11-2011
5.EE
consistent use of CSF-PCR for HSV serology established a diagnosis in the majority of acute aseptic meningitis patients.
0 - ArchivalUser - 05-11-2011
6.CC
Esophageal varices are extremely dilated sub-mucosal veins in the lower esophagus. They are most often a consequence of portal hypertension, commonly due to cirrhosis; patients with esophageal varices have a strong tendency to develop bleeding.
The majority of blood from the esophagus is drained via the esophageal veins, which carry deoxygenated blood from the esophagus to the azygos vein, which in turn drains directly into the superior vena cava. These veins have no part in the development of esophageal varices.
The remaining blood from the esophagus is drained into the superficial veins lining the esophageal mucosa, which drain into the coronary vein (left gastric vein), which in turn drains directly into the portal vein. These superficial veins (normally only approximately 1mm in diameter) become distended up to 1–2 cm in diameter in association with portal hypertension.
http://upload.wikimedia.org/wikipedia/commons/b/b6/Esophageal_varices_-_wale.jpg
0 - ArchivalUser - 05-11-2011
7.EE
DIC leads to the formation of small blood clots inside the blood vessels throughout the body. As the small clots consume coagulation proteins and platelets, normal coagulation is disrupted and abnormal bleeding occurs from the skin (e.g. from sites where blood samples were taken), the gastrointestinal tract, the respiratory tract and surgical wounds. The small clots also disrupt normal blood flow to organs (such as the kidneys), which may malfunction as a result.
The activation of the coagulation cascade yields thrombin that converts fibrinogen to fibrin; the stable fibrin clot being the final product of hemostasis. The fibrinolytic system then functions to break down fibrinogen and fibrin. Activation of the fibrinolytic system generates plasmin (in the presence of thrombin), which is responsible for the lysis of fibrin clots. The breakdown of fibrinogen and fibrin results in polypeptides called fibrin degradation products (FDPs) or fibrin split products (FSPs). In a state of homeostasis, the presence of plasmin is critical, as it is the central proteolytic enzyme of coagulation and is also necessary for the breakdown of clots, or fibrinolysis.
0 - ArchivalUser - 05-11-2011
8.BB
p53 is a tumor suppressor protein that in humans is encoded by the TP53 gene. p53 is important in multicellular organisms, where it regulates the cell cycle and, thus, functions as a tumor suppressor that is involved in preventing cancer
p53 has many mechanisms of anticancer function, and plays a role in apoptosis, genomic stability, and inhibition of angiogenesis. In its anti-cancer role, p53 works through several mechanisms:
It can activate DNA repair proteins when DNA has sustained damage.
It can induce growth arrest by holding the cell cycle at the G1/S regulation point on DNA damage recognition (if it holds the cell here for long enough, the DNA repair proteins will have time to fix the damage and the cell will be allowed to continue the cell cycle).
It can initiate apoptosis, the programmed cell death, if DNA damage proves to be irreparable.
If the TP53 gene is damaged, tumor suppression is severely reduced. People who inherit only one functional copy of the TP53 gene will most likely develop tumors in early adulthood, a disease known as Li-Fraumeni syndrome. The TP53 gene can also be damaged in cells by mutagens (chemicals, radiation, or viruses), increasing the likelihood that the cell will begin decontrolled division. More than 50 percent of human tumors contain a mutation or deletion of the TP53 gene.
0 - ArchivalUser - 05-11-2011
9.A
9. A
The renin-angiotensin system (RAS) or the renin-angiotensin-aldosterone system (RAAS) is a hormone system that regulates blood pressure and water (fluid) balance.
When blood volume is low, juxtaglomerular cells in the kidneys secrete renin. Renin stimulates the production of angiotensin I, which is then converted to angiotensin II. Angiotensin II causes blood vessels to constrict, resulting in increased blood pressure. Angiotensin II also stimulates the secretion of the hormone aldosterone from the adrenal cortex. Aldosterone causes the tubules of the kidneys to increase the reabsorption of sodium and water into the blood. This increases the volume of fluid in the body, which also increases blood pressure.
If the renin-angiotensin-aldosterone system is too active, blood pressure will be too high. There are many drugs that interrupt different steps in this system to lower blood pressure. These drugs are one of the main ways to control high blood pressure (hypertension), heart failure, kidney failure, and harmful effects of diabetes.[2][3
Activation
The system can be activated when there is a loss of blood volume or a drop in blood pressure (such as in hemorrhage). Alternatively, a decrease in plasma NaCl concentration will stimulate the macula densa to release renin.
1. If the perfusion of the juxtaglomerular apparatus in the kidney's macula densa decreases, then the juxtaglomerular cells release the enzyme renin.
2. Renin cleaves a zymogen, an inactive peptide, called angiotensinogen, converting it into angiotensin I.
3. Angiotensin I is then converted to angiotensin II by angiotensin-converting enzyme (ACE)[4] which was thought to be found mainly in lung capillaries. However new evidence suggests the ACE is found in all blood vessel endothelial cells.[5]
4. Angiotensin II is the major bioactive product of the renin-angiotensin system, binding to receptors on intraglomerular mesangial cells, causing these cells to contract along with the blood vessels surrounding them and causing the release of aldosterone from the zona glomerulosa in the adrenal cortex. Angiotensin II acts as an endocrine, autocrine/paracrine, and intracrine hormone.
http://en.wikipedia.org/wiki/Renin-angiotensin_system