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23. Sorry I do not have ans for it

24. C
Systemic lupus erythematosus (pronounced /sɪˈstɛmɪk ˈlupəs ˌɛrɪˌθiməˈtʰoʊsəs/ ( listen)), often abbreviated to SLE or lupus, is a systemic autoimmune disease (or autoimmune connective tissue disease) that can affect any part of the body. As occurs in other autoimmune diseases, the immune system attacks the body's cells and tissue, resulting in inflammation and tissue damage.[1] It is a Type III hypersensitivity reaction caused by antibody-immune complex formation.
SLE most often harms the heart, joints, skin, lungs, blood vessels, liver, kidneys, and nervous system. The course of the disease is unpredictable, with periods of illness (called flares) alternating with remissions. In SLE, the body's immune system produces antibodies against itself, particularly against proteins in the cell nucleus. SLE is triggered by environmental factors that are unknown. "All the key components of the immune system are involved in the underlying mechanisms [of SLE]" according to Rahman, and SLE is the prototypical autoimmune disease. The immune system must have a balance (homeostasis) between being sensitive enough to protect against infection, and being too sensitive and attacking the body's own proteins (autoimmunity). From an evolutionary perspective, according to Crow, the population must have enough genetic diversity to protect itself against a wide range of possible infection; some genetic combinations result in autoimmunity. The likely environmental triggers include ultraviolet light, drugs, and viruses. These stimuli cause the destruction of cells and expose their DNA, histones, and other proteins, particularly parts of the cell nucleus. Because of genetic variations in different components of the immune system, in some people the immune system attacks these nuclear-related proteins and produces antibodies against them. In the end, these antibody complexes damage blood vessels in critical areas of the body, such as the glomeruli of the kidney; these antibody attacks are the cause of SLE. Researchers are now identifying the individual genes, the proteins they produce, and their role in the immune system. Each protein is a link on the autoimmune chain, and researchers are trying to find drugs to break each of those links.[ http://en.wikipedia.org/wiki/Systemic_lu...thematosus
Renal
Painless hematuria or proteinuria may often be the only presenting renal symptom. Acute or chronic renal impairment may develop with lupus nephritis, leading to acute or end-stage renal failure. Because of early recognition and management of SLE, end-stage renal failure occurs in less than 5% of cases.
A histological hallmark of SLE is membranous glomerulonephritis with "wire loop" abnormalities.[16] This finding is due to immune complex deposition along the glomerular basement membrane, leading to a typical granular appearance in immunofluorescence testing.
Lupus nephritis is an inflammation of the kidney caused by systemic lupus erythematosus (SLE), a disease of the immune system. Apart from the kidneys, SLE can also damage the skin, joints, nervous system and virtually any organ or system in the body.
Histologically a wire-loop lesion will be present. The wire loop lesion is a glomerular capillary loop with subendothelial immune complex deposition that is circumferential around the loop.
http://en.wikipedia.org/wiki/Lupus_nephritis

25. E
Kwashiorkor (pronounced /kwɑːʃiˈɔrkər/) is an acute form of childhood protein-energy malnutrition characterized by edema, irritability, anorexia, ulcerating dermatoses, and an enlarged liver with fatty infiltrates. The presence of edema caused by poor nutrition defines kwashiorkor.[1] Kwashiorkor was thought to be caused by insufficient protein consumption but with sufficient calorie intake, distinguishing it from marasmus. More recently, micronutrient and antioxidant deficiencies have come to be recognized as contributory. Cases in the developed world are rare.
The defining sign of kwashiorkor in a malnourished child is pedal edema (swelling of the feet). Other signs include a distended abdomen, an enlarged liver with fatty infiltrates, thinning hair, loss of teeth, skin depigmentation and dermatitis. Children with kwashiorkor often develop irritability and anorexia.
http://en.wikipedia.org/wiki/Kwashiorkor
Marasmus is a form of severe protein-energy malnutrition characterized by energy deficiency.
A child with marasmus looks emaciated. Body weight may be reduced to less than 80% of the average weight that corresponds to the height .[citation needed] Marasmus occurrence increases prior to age 1, whereas kwashiorkor occurrence increases after 18 months. It can be distinguished from kwashiorkor in that kwashiorkor is protein wasting with the presence of edema.
The malnutrition associated with marasmus leads to extensive tissue and muscle wasting, as well as variable edema. Other common characteristics include dry skin, loose skin folds hanging over the glutei, axillae, etc. There is also drastic loss of adipose tissue from normal areas of fat deposits like buttocks and thighs. The afflicted are often fretful, irritable, and voraciously hungry. The word “marasmus” comes from a Greek word meaning starvation. Marasmus is generally known as the gradual wasting away of the body due to severe malnutrition or inadequate absorption of food. Marasmus is a form of severe protein deficiency and is one of the forms of protein-energy malfunction (PEM). It is a severe form of malnutrition caused by inadequate intake of proteins and calories.
http://en.wikipedia.org/wiki/Marasmus

26. C
Primary polydipsia or psychogenic polydipsia is a special form of polydipsia.[1] It is usually associated with a patient's increasing fluid intake due to the sensation of having a dry mouth.
When the term "psychogenic polydipsia" is used, it implies that the condition is caused by mental disorders. However, the dry mouth is often due to phenothiazine medications used in some mental disorders, rather than the underlying condition
The patient drinks large amounts of water, which dilutes the extracellular fluid, decreasing its osmotic pressure. The body responds to this by decreasing the level of vasopressin (antidiuretic hormone), with a resultant increased production of urine (polyuria). This urine will have a low electrolyte concentration.
Clinical presentation
Patients have been known to seek fluids from any source possible.
In extreme episodes, the patient's kidneys will be unable to deal with the fluid overload, and weight gain will be noted.
Primary polydipsia can be life threatening as serum sodium is diluted to an extent that seizures and cardiac arrest can occur.
http://en.wikipedia.org/wiki/Primary_polydipsia

27. A
Kawasaki disease: Acute, self-limiting necrotizing vasculitis in infants/ children. Association with Asia ethnicity. Fever, conjuntivitis, changes in lips/ oral mucosa (“strawberry tongue”), lymphadenitis, desquamative skin rash. May develop coronary aneurysms.

28. D
In genetic medicine, a mosaic or mosaicism denotes the presence of two populations of cells with different genotypes in one individual who has developed from a single fertilized egg.[1] Mosaicism may result from a mutation during development which is propagated to only a subset of the adult cells.
Somatic mosaicism
Somatic mosaicism occurs when the somatic cells of the body are of more than one genotype. In the more common mosaics, different genotypes arise from only a single fertilized egg cell, due to mitotic errors at first cleavage.
Another form of somatic mosaicism is chimerism, where two or more genotypes arise from the fusion of more than one fertilized zygote in the early stages of embryonal development.
In rare cases, intersex conditions can be caused by mosaicism where some cells in the body have XX and others XY chromosomes.[2][3]
The most common form of mosaicism found through prenatal diagnosis involves trisomies. Although most forms of trisomy are due to problems in meiosis and affect all cells of the organism, there are cases where the trisomy occurs in only a selection of the cells. This may be caused by a nondisjunction event in an early mitosis, resulting in a loss of a chromosome from some trisomic cells.[4] Generally this leads to a milder phenotype than in non-mosaic patients with the same disorder.
An example of this is one of the milder forms of Klinefelter's syndrome, called 46/47 XY/XXY mosaic wherein some of the patient's cells contain XY chromosomes, and some contain XXY chromosomes. The 46/47 annotation indicates that the XY cells have the normal number of 46 total chromosomes, and the XXY cells have 47 total chromosomes.
Around 30% of Turner's syndrome cases demonstrate mosaicism, while complete monosomy (45 XO) occurs in about 50–60% of cases.
True mosaicism should not be mistaken for the phenomenon of X-inactivation, where all cells in an organism have the same genotype, but a different copy of the X chromosome is expressed in different cells, such as in calico cats.
http://en.wikipedia.org/wiki/Mosaic_(genetics)

*****
23.DD

It is a mathematic calculation...

She is asked to loss 2 pounds weight weekly...each pounds=3500 cal and brisk walking consums 500cal per hour
so........................................................... 2 pounds=7000cal
she needs to loss 1000 cal per day......if she walked 2 hours per day....she could lose 1000 calories
but between choices there is no 2 hours.so if she decreases 500 cal in her diet and gets 1 hour brisk walking then she will loss 1000 cal/day.......and 7000/week

29- pass
30-F The classic triad for congenital rubella syndrome is:

Sensorineural deafness (58% of patients)
Eye abnormalities—especially cataract and microphthalmia (43% of patients)
Congenital heart disease—especially patent ductus arteriosus (50% of patients)
Other manifestations of CRS may include:

Spleen, liver or bone marrow problems (some of which may disappear shortly after birth)
Mental retardation
Small head size (microcephaly)
Eye defects
Low birth weight
Thrombocytopenic purpura (presents as a characteristic blueberry muffin rash)
Hepatomegaly
Micrognathia
Children who have been exposed to rubella in the womb should also be watched closely as they age for any indication of the following:

Developmental delay
Autism spectrum disorders[1]
Schizophrenia[2]
Growth retardation
Learning disabilities
Diabetes
Glaucoma
Note:NO a congenital cytomegalovirus Generalized infection may occur in the infant, and can cause complications such as low birth weight, microcephaly, seizures, petechial rash similar to the "blueberry muffin" rash of congenital rubella syndrome, and moderate hepatosplenomegaly (with jaundice).

Maryam thanks for the explanation to Q # 23

31. C
Pityriasis or tiña versicolor caused by malassezia furfur. Degradation of lipids produces acids that damage melanocytes and cause hypopigmented patches. Occurs in hot humid weather.
Yeast clusters & and short curved septate hyphae KOH scaping shows “spaghetti and meatballs”.
Malassezia (formerly known as Pityrosporum) is a genus of fungi. Malassezia is naturally found on the skin surfaces of many animals, including humans. In occasional opportunistic infections, some species can cause hypopigmentation on the trunk and other locations in humans.
T: Topical Miconazole, selenium sulfide.

32. A
N. meningitidis:
Gram neg. kidney bean shaped diploccoci, large capsule; latex particule agluttination ( or Counter immunoelectrophoresis ( CIE) to identify N. meningitidis capsular antigen in CSF.
Reservorio: Human nasopharynx
Transmision: Respiratory droplets; oropharyngeal colonization, spread to meninges via blood stream.
Pathogenesis: Important virulent factor:
Polysacharide capsule: antiphagocytic, antigenic, 5 common serogrups : B is not strongly immunogenic( sialid acid), B strain is most common strain in US.
(Kaplan Microbiology book page 257)