Tuberculosis management describes the techniques and procedures utilized in treating tuberculosis (TB). The medical standard for active TB is a short course treatment involving a combination of Isoniazid, Rifampicin (also known as Rifampin), Pyrazinamide, and Ethambutol for the first two months. During this initial period, Isoniazid is taken alongside Pyridoxal phosphate to obviate Peripheral neuropathy. Isoniazid is then taken coicident with Rifampicin alone for the remaining four months of treatment. A patient is considered free of all living TB bacteria after six months. Latent tuberculosis or Latent Tuberculosis Infection (LTBI) is treated with three to nine months of Isoniazid alone, this longterm treatment often risks the development of Hepatotoxicity. A combination of Isoniazid plus Rifampicin for a period of three to four months is shown to be an equallly effective method for treating LTBI, while mitigating risks to Hepatotoxicity. Treatment of LTBI is essential in preventing the spread of active TB. Drugs
First line
All first-line anti-tuberculous drug names have semistandardized three-letter and single-letter abbreviations:
ethambutol is EMB or E,
isoniazid is INH or H,
pyrazinamide is PZA or Z,
rifampicin is RMP or R,
streptomycin is SM or S.First-line anti-tuberculous drug names are often remembered with the mnemonic "RIPE," referring to the use of a rifamycin (like rifampin), isoniazid, pyrazinamide, and ethambutol. US practice uses abbreviations and names that are not internationally convened: rifampicin is called rifampin and abbreviated RIF; streptomycin is abbreviated STM.
Primary
Primary aldosteronism (hyporeninemic hyperaldosteronism) was previously thought to be most commonly caused by an adrenal adenoma, termed Conns syndrome. However, recent studies have shown that bilateral idiopathic adrenal hyperplasia is the cause in up to 70% of cases. Differentiating between the two is important, as this determines treatment. Also, see congenital adrenal hyperplasia. Adrenal carcinoma is an extremely rare cause of primary hyperaldosteronism.Two familial forms have been identified: type I (dexamethasone suppressible), and type II, which has been linked to the 7p22 gene.Features

Hypertension
Hypokalemia (e.g., may cause muscle weakness)
AlkalosisInvestigations

High serum aldosterone
Low serum renin
High-resolution CT abdomenManagement

Adrenal adenoma: surgery
Bilateral adrenocortical hyperplasia: aldosterone antagonist, e.g., spironolactone

Secondary
Secondary hyperaldosteronism (also hyperreninism, or hyperreninemic hyperaldosteronism) is due to overactivity of the renin–angiotensin–aldosterone system (RAAS).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 bodys 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. Likewise, fibromuscular dysplasia may cause stenosis of the renal artery, and therefore secondary hyperaldosteronism. Other causes can come from the tubules: low reabsorption of sodium (as seen in Bartter and Gitelman syndromes) will lead to hypovolemia/hypotension, which will activate the renin–angiotensin system (RAAS).Secondary hyperaldosteronism can also be caused by excessive ingestion of licorice or other members of the Glycyrrhiza genus of plants that contain the triterpenoid saponin glycoside known as glycyrrhizin.