nbme5 block 4 q1..to 50 - maryam2009

[ArchivalUser]

Welcome to everybody "Please choose and answer the Qs in order,Thank you"

[ArchivalUser]

1.AA

Aortic regurgitation is an immediate high pitched blowing diastolid murmur due to aortic root dilation ,bicuspid aortic valve,or rheumatic fever.

2.AA
sawtooth appearance of the flutter wave....rapid succession of identical back to back atrial depolarization wave


3.EE

About 60% of people with cystic fibrosis have a chronic respiratory infection caused by a bacteria called Pseudomonas aeruginosa that settles into the thick mucus trapped in the airways. Once it sets up house in the respiratory tract, Pseudomonas aeruginosa is hard to get rid of. Respiratory failure caused by the infection is often the ultimate cause of death in many people with CF.

4.CC

http://upload.wikimedia.org/wikipedia/co...sounds.png

http://www.youtube.com/watch?v=vL0s_nEkC8Q

5.DD

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,[4] 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:Giardi...cle_en.svg

A distinguishing characteristic of the cyst is four nuclei and a retracted cytoplasm.
treatment with metronidazole, tinidazole or nitazoxanide.

[ArchivalUser]

6.FF

Tetralogy of Fallot (TOF) is a congenital heart defect which is classically understood to involve four anatomical abnormalities (although only three of them are always present). It is the most common cyanotic heart defect, and the most common cause of blue baby syndrome.

http://en.wikipedia.org/wiki/File:Tetral...Fallot.svg
http://upload.wikimedia.org/wikipedia/co...se-133.jpg

The abnormal boot-like appearance of a heart with tetralogy of Fallot is easily visible via chest x-ray, and before more sophisticated techniques became available, this was the definitive method of diagnosis

[ArchivalUser]

7.DD

8.BB
Metabolic acidosis

9.CC

T3 is a lipid souluble hormone and it difusses through the cell membrane ,where it binds to its respective receptor inside the cell.

10.BB

Menopause ....Hormonal change .....>dec Estrogen and high level of FSH and inc. LH(no surge) and inc. of GnRH.

[ArchivalUser]

11.EE

TBG deficiency does not cause thyroid disease.
First, any decrease in TBG levels initially increases the concentration of the free hormone. Subsequently, the tendency to cause hyperthyroidism is counterbalanced by the tendency to shut off TSH secretion and hence decrease the TH secretory rate from the thyroid gland. Finally, the total TH concentration in the serum decreases until the concentration of the free hormone is restored to normal.

This equilibrium is achieved extremely rapidly and on a physicochemical level. If chronic, the decreased extrathyroidal pool of TH may lead to small, transient declines in circulating free TH levels, thus resulting in transient TSH stimulation of the thyroid. The latter mechanism may explain the moderate elevation in serum thyroglobulin levels observed in up to one third of patients with TBG deficiency.
Because TBG deficiency is not an acute process, a state of resultant hypothyroidism does not occur. Total T4 and T3 may be low in states of TBG deficiency, but the free T4, free T3, and TSH remain normal.

*** Thyroid function tests (TFTs) in patients with TBG deficiency show normal TSH and free T4, but low total T4 and, occasionally, low total T3 serum concentrations.

Thyroid binding protein deficiency states :

***Inherited causes include the following:

•TBG gene defects - Partial deficiency (X linked) and complete deficiency (X linked)
•Other genetic defects - Carbohydrate-deficient glycoprotein syndrome type 1 (CDG1), which is autosomal recessive.

***Acquired causes include the following:
•Hyperthyroidism
•Nephrotic syndrome
•Chronic renal failure
•Chronic liver disease
•Severe systemic illness (except human immunodeficiency virus/acquired immune deficiency syndrome [HIV/AIDS] and acute intermittent porphyria)[2]
•Malnutrition
•Acromegaly (in very rare cases only)[3, 4]
•Cushing syndrome
•Drugs (eg, androgens, glucocorticoids, L-asparaginase)

[ArchivalUser]

12.EE

In women, progesterone levels are relatively low during the preovulatory phase of the menstrual cycle, rise after ovulation, and are elevated during the luteal phase.

Progesterone levels tend to be < 2 ng/ml prior to ovulation, and > 5 ng/ml after ovulation. If pregnancy occurs, progesterone levels are initially maintained at luteal levels. With the onset of the luteal-placental shift in progesterone support of the pregnancy, levels start to rise further and may reach 100-200 ng/ml at term.

[ArchivalUser]

13.FF

***Primary (hyporeninemic hyperaldosteronism):
hypertension
hypokalemia (e.g. may cause muscle weakness)
alkalosis
high serum aldosterone
low serum renin

**Management

adrenal adenoma: surgery
bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone

***Secondary (hyperreninemic hyperaldosteronism)

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.

One cause is a juxtaglomerular cell tumor. Another is renal artery stenosis in which the reduced blood supply across the juxtaglomerular apparatus stimulates the production of renin. Also fibromuscular hyperplasia may cause secondary hyperaldosteronism.

[ArchivalUser]

14.CC

Human placental lactogen (HPL)—From the second month of pregnancy, the placenta releases large amounts of HPL. This hormone appears to be instrumental in breast, nipple, and areola growth before birth.

HPL is present only during pregnancy, with maternal serum levels rising in relation to the growth of the fetus and placenta. Maximum levels are reached near term, typically to 5–7 mg/L. Higher levels are noted in patients with multiple gestation.

Its structure and function is similar to that of human growth hormone. It modifies the metabolic state of the mother during pregnancy to facilitate the energy supply of the fetus. HPL has anti-insulin properties, therefore, raises maternal blood glucose levels, whilst decreasing maternal glucose utilization, which helps ensure adequate fetal nutrition .

[ArchivalUser]

15.CC

Zinc fingers are steroid hormone receptors and DNA binding domain that bind to a specific nucleotide sequence in the promoter or response element.

Tha activator proteins that bind response elements are often referred to as transcription factors.TF contain at least 2 recognizable domains,DNA-BINDING DOMAIN AND ACTIVATION DOMAIN.

DNA- BINDING DOMAIN:
Zinc fingers
Leucin zippers...cAMP dependent TF
Helix loop Helix
Helix-turn Helix

THE ACTIVATION DOMAINallows th TF to:
bind to other TF
interact with RNA polymerase II to stabilize the formation of the initiation complex
recruit chromatin-modifying proteins such as Histone acetylases or deacetylases

Kaplan 2010,pg 72-73

[ArchivalUser]

16.BB

Dilated cardiomyopathy due to
coronic alcoholic abuse
Beriberi
cocxackie B myocarditis
choronic toxicity
Chagas dis.
Doxorubicin toxicity
peripartum cardiomyopathy

http://upload.wikimedia.org/wikipedia/co..._lores.jpg

Finding S3 and dilated all four chambers of heart

17.DD

Pulmonary embolism (PE) is a blockage of the main artery of the lung or one of its branches by a substance that has travelled from elsewhere in the body through the bloodstream (embolism). Usually this is due to embolism of a thrombus (blood clot) from the deep veins in the legs, a process termed venous thromboembolism.

Treatment is typically with anticoagulant medication, including heparin and warfarin. Severe cases may require thrombolysis with drugs such as tissue plasminogen activator (tPA) or may require surgical intervention via pulmonary thrombectomy.

18.AA

Emphysema....centriacinar caused by smoking

The majority of all emphysema cases are caused by smoking tobacco,In some cases it may be due to alpha 1-antitrypsin deficiency....>panacinar.


19.BB

accumulation of metabolic products in heart tissue (lactic acid/bradykinin) which causes the pain during angina / MI.

posted by step1an

20.DD

Alveolar pO2 increases with increasing intensity of exercise, while arterial pO2 remains relatively unchanged. These relationships are shown below.

http://physiology.umc.edu/themodelingwor...hange.HTML

21.AA

normal appearing female with 46 XY......female external genitalia and rudimentary vagina ,uterus and uterine tubes absent,develope testes (often found in labia majora)
level of Test.,Estrogene,and LH are all HIGH