Explanation:

Explanation:

This woman has hypertension which is discovered in her pregnancy but has evidence of LVH on her ECG suggesting that this is longstanding.
Often, it takes at least two years of sustained hypertension to develop LVH, and although her pregnancy may have contributed to any deterioration, the LVH suggests may have contributed to any deterioration, the LVH suggests that it was pre-existent.
The cause for her hypertension may be secondary but her high BMT is suggestive of it being essential.

Explanation:

In this case the patient has features that would suggest polycystic ovary syndrome (PCOS) yet the 17OHP concentration is elevated and is compatible with non-classical congenital adrenal hyperplasia (CAH) yet just below the threshold of 33nmol/L confidently to make the diagnosis. Thus a short Synacthen test would be the most appropriate investigation with measurement of 17OHP. A rise in 17OHP above 33nmol/L suggests non classical CAH.

Explanation:

Explanation:

Typical antipsychotic medications include haloperidol, chlorpromazine and thioridazine. Their mechanism of action is they block the dopamine (D2) receptors. They treat positive symptoms like hallucination or delusions.
Atypical antipsychotics include risperdione and clozapine. They work by blocking both D2 and serotonin (5-HT) receptors. They treat both positive and negative symptoms.

Explanation:

Her symptoms are suggestive of postural hypotension, which together with hyperkalaemic (and hyponatraemia) acidosis would strongly indicate the presence of Addison´s disease. Cushing´s and Conn´s syndromes are associated with hypertension and hypokalaemia. Hypokalaemia is the most frequent complication of bulimia which may cause cardiac arrhythmias, fits and paraesthesia. Renal tubular acidosis (RTA) is due to inability of the renal tubules to maintain acid-base balance, causing a hyperchloraemia and a normal anion-gap. In type 1 (distal) RTA; there is hypokalaemic acidosis with low urinary ammonium production. Patients present with hyperventilation/acidosis and muscular weakness from hypokalaemia. In type 4 RTA (hyporeninaemic hypoaldosteronism), there is hyperkalaemic acidosis caused by chronic renal insufficiency from diabetes or tubulointerstitial disease.

Explanation:

Prolactin receptors are located on Leydig cells in the testes. Under normal conditions, prolactin synergizes with LH to stimulate testosterone production by Leydig cells. In males with hyperprolactinemia secondary to a pituitary tumor, elevated prolactin levels interfere with testosterone production. Excessive prolactin reduces the number of LH receptors and/or inhibits intracellular events stimulated by LH. Hyperprolactinemia may also decrease the pulsatile nature of LH secretion, also causing a decrease in testosterone production. Testosterone production is required for spermatogenesis, so elevated prolactin decreases sperm count and frequently causes infertility. An increase in FSH, LH, and LHRH would increase testosterone production rather than decrease it. LHRH is released from the hypothalamus and acts on the anterior pituitary to stimulate LH and FSH release. LH acts on the Leydig cells of the testes to increase testosterone production which acts on the Sertoli cells to facilitate spermatogenesis. An increase in testosterone would result in an increase in spermatogenesis and would not result in infertility.

Explanation:

While recent technological advances have led to earlier detection of breast cancer, this has not led to an absolute cure and a marked increase in survival. The major advance has been in demonstrating that lumpectomy with axillary node dissection offers about the same five-year survival as mastectomy The choice between these treatments should be determined on an individual treatment basis, with the psychological implications of mastectomy weighed against the fear of recurrence if the breast is not removed.

Explanation:

The patient´s ankle edema, shortness of breath, and relatively low blood pressure suggest the possibility of congestive heart failure which is confirmed by the cardiac enlargement and perihilar infiltrates seen on chest X-ray. The serum urea nitrogen is elevated while serum creatinine is normal, suggesting a prerenal cause for the azotemia.
Congestive heart failure with its resulting decreased blood pressure is a common cause of decreased renal perfusion leading to prerenal azotemia. Most disease processes that affect BUN and creatinine cause both to rise together. Exceptions are early congestive heart failure (in which the BUN can rise selectively) and processes that lead to increased urea synthesis, such as burns and prolonged high fever. Postrenal causes of azotemia are typically due to urinary tract obstruction distal to the kidney, and usually cause a rise in both urea and creatinine, with the rise in urea being larger than that in creatinine. Increased synthesis of urea is seen in severe burns and prolonged high fever. Renal glomerular disease severe enough to cause acute or chronic renal failure will cause urea and creatinine to rise together. Renal tubulointerstitial disease severe enough to cause renal failure will cause both urea and creatinine to rise. The creatinine may rise out of proportion to the urea, particularly in acute tubular necrosis.

Explanation:

The treatment of scoliosis is dependent on the age of the patient and curve progression. Premenarchal females have a greater chance of curve progression then females one to two years after menarche with similar curves. Curves of less than 25 degrees are observed and reevaluated every four to six months. The stage of pubertal development is important to note because a patient who has attained menarche will only have a small amount of additional growth; therefore, scoliosis will not progress.