+- USMLE Forum - Largest USMLE Community (https://www.usmleforum.com)
+-- Forum: USMLE Forum (https://www.usmleforum.com/forumdisplay.php?fid=1)
+--- Forum: Step 1 (https://www.usmleforum.com/forumdisplay.php?fid=2)
+--- Thread: NBME#3 block 2 Q1----------------------Q50 - maryam2009 (/showthread.php?tid=574726)
0 - ArchivalUser - 03-17-2011
thnak you, drona I was confused about the Q.11
0 - ArchivalUser - 03-17-2011
12. A, Enterobius vermicalis, treat with mebendazole or pyrantel
0 - ArchivalUser - 03-17-2011
12--AA
pic
http://en.wikipedia.org/wiki/File:Eggs_of_Enterobius_vermicularis_5229_lores.jpg
characteristic of autoinfection--
diagnosis by tape test -
0 - ArchivalUser - 03-17-2011
13--GG
Invasive Pathogens-- invade enterocytes
Low-volume diarrhea
Diarrhea with blood and leukocytes (i.e., dysentery)
Shigella spp.,
Campylobacter jejuni,
Entamoeba histolytica
Fecal smear for leukocytes: positive
Order stool culture and stool for ova and parasites
Shigella species-- No animal reservoirs -
Mucosal ulceration, pseudomembranous inflammation, dysentery
0 - ArchivalUser - 03-17-2011
9.D
to add more
Hyperaldosteronism, also aldosteronism,[ is a medical condition where too much aldosterone is produced by the adrenal glands, which can lead to lowered levels of potassium in the blood.
there are 2 types.....primary and secondary
Primary aldosteronism, also known as primary hyperaldosteronism, is characterized by the overproduction of the mineralocorticoid hormone aldosterone by the adrenal glands. when not a result of excessive renin secretion.
many causes, including adrenal hyperplasia and adrenal carcinoma. When it occurs due to a solitary aldosterone-secreting adrenal adenoma (a type of benign tumor), it is known as Conn's syndrome.Conn's syndrome is an Aldosterone-Producing Adenoma (APA).
Secondary hyperaldosteronism is due to overactivity of the renin-angiotensin system.
Secondary refers to an abnormality that indirectly results in pathology through a predictable physiologic pathway, i.e., a renin producing tumor leads to increased aldosterone, as the body's aldosterone production is normally regulated by renin levels.
Examples:
cardiac failure with edema
liver cirrhosis with ascites
nephrotic syndrome with edema
0 - ArchivalUser - 03-17-2011
one important difference we can say betn primar and secondary hyperaldosteronism is
in primary --low renin ;edema absent
sec..-----high renin and edema present.
0 - ArchivalUser - 03-17-2011
14--DD chags disease-American trypanosomiasis
vector rudivid bug or "the kissing bug".
The human disease occurs in two stages: an acute stage, which occurs shortly after an initial infection, and a chronic stage that develops over many years
Acute disease--
These can include fever, fatigue, body aches, headache, rash, loss of appetite, diarrhea, and vomiting. The signs on physical examination can include mild enlargement of the liver or spleen, swollen glands, and local swelling (a chagoma) where the parasite entered the body. The most recognized marker of acute Chagas disease is called ''Romaña's sign,'' which includes swelling of the eyelids on the side of the face near the bite wound or where the bug feces were deposited or accidentally rubbed into the eye.
chronic disease--
The symptomatic (determinate) chronic stage affects the nervous system, digestive system and heart. About two thirds of people with chronic symptoms have cardiac damage, including cardiomyopathy, which causes heart rhythm abnormalities and may result in sudden death. About one third of patients go on to develop digestive system damage, resulting in dilation of the digestive tract (megacolon and megaesophagus), accompanied by severe weight loss. Swallowing difficulties (secondary achalasia) may be the first symptom of digestive disturbances and may lead to malnutrition.
diag--
direct visualisation by giemsa stain-
http://en.wikipedia.org/wiki/File:Trypanosoma_cruzi_crithidia.jpeg
rx--Drugs of choice include azole or nitro derivatives such as benznidazol or nifurtimox.
0 - ArchivalUser - 03-17-2011
15--cc
The membrane attack complex, frequently referred to as the complement membrane attack complex and abbreviated to the MAC, is one of the methods used by the immune system to attack threats to the body. The membrane attack complex is closely related to the complement system, which exists to aid antibodies and other aspects of the immune system in clearing pathogens from one's body. The complementary system and the attack complex both involve many varieties of proteins that are found in the blood. The proteins bind to the membranes of pathogenic cells and form a circular pore that allows extracellular substances into the cell. When enough of these pores form, the integrity of the cell is severely compromised and cellular death is almost inevitable.
mech--
There are two primary stages through which the different proteins in the membrane attack complex act to destroy pathogenic cells. The first stage, usually referred to as initiation, involves the proteins C5, C6, and C7. Through a procedure involving the cleaving and binding of these proteins, the C7 protein is able to penetrate the pathogenic cell's membrane. Proteins C6 and C5 are bound to protein C7; this initiation stage and insertion into the membrane are necessary for the attack complex to proceed.
The second stage through which the membrane attack complex functions is referred to as the polymerization stage. The polymerization stage involves the proteins C8 and C9 and has the goal of actually forming the pore that will eventually destroy the pathogenic cell. C8 is able to insert itself into the pathogenic cell's membrane because of traits relating to the polarity of the molecules that make up the membrane and the protein. C8 is then able to induce many C9 proteins to form into a porous structure that penetrates the pathogenic cell's membrane. The structure is connected to the C5, C6, C7, and C8 proteins
ppl with MAC def prone for bacterial infe mainlyneissria gonorrhea - multiple attacks
0 - ArchivalUser - 03-17-2011
http://student.ccbcmd.edu/courses/bio141/lecguide/unit4/innate/u2fig27g.html
0 - ArchivalUser - 03-17-2011
http://student.ccbcmd.edu/courses/bio141/lecguide/unit4/innate/classical.html#classmac