Hyperplasia

Hypertrophy is an increase in the size of the cells due to synthesis of more sub-cellular components. An increase in the size of the organ results. Take, for example, cardiac hypertrophy in response to increased workload. The increased load is often a result of some pathological condition such as heart valve incompetence or stenosis of an outflow path. Hypertrophy of the muscles of a body builder is another good example, in which the increased workload is due to continued weight training. 

Hyperplasia is an increase in the number of cells in a given organ or tissue, usually resulting in an increase in the size of the organ as well. Only certain differentiated 

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The growth of animals can be defined as an increase in mass of whole body, tissue(s), organ(s), or ceU(s) with time. This type of growth can be characterized by morphometric measurements eg, skeletal muscle or adipose tissue growth can be described by observing temporal changes in ceU number, ie, hyperplasia, and ceU size, ie, hypertrophy. Growth also includes developmental aspects of function and metaboHsm of cells and tissues from conception to maturity. 

Acute benzene poisoning results in CNS depression and is characterized by an initial euphoria followed by staggered gait, stupor, coma, and convulsions. Exposure to approximately 4000 ppm benzene results in complete loss of consciousness. Insomnia, agitation, headache, nausea, and drowsiness may persist for weeks after exposure (126). Continued inhalation of benzene to the point of euphoria has caused irreversible encephalopathy with tremulousness, emotional lability, and diffuse cerebral atrophy (125). In deaths arising from acute exposure, respiratory tract infection, hypo- and hyperplasia of sternal bone marrow, congested kidneys, and cerebral edema have been found at autopsy. 

Phenytoin s absorption is slow and variable yet almost complete absorption eventually occurs after po dosing. More than 90% of the dmg is bound to plasma protein. Peak plasma concentrations are achieved in 1.5—3 h. Therapeutic plasma concentrations are 10—20 lg/mL but using fixed po doses, steady-state levels are achieved in 7—10 days. Phenytoin is metabolized in the fiver to inactive metabolites. The plasma half-life is approximately 22 h. Phenytoin is excreted primarily in the urine as inactive metabolites and <5% as unchanged dmg. It is also eliminated in the feces and in breast milk (1,2). Prolonged po use of phenytoin may result in hirsutism, gingival hyperplasia, and hypersensitivity reactions evidenced by skin rashes, blood dyscrasias, etc... 

The effects of dmgs and adjuvants must be assessed, both in short-term administration and during chronic treatment. Local effects include changes in mucocihary clearance, cell damage, and irritation. Chronic erosion of the mucous membrane may lead to inflammation, hyperplasia, metaplasia, and deterioration of normal nasal function (76). 

As regards toxicity, pyrazole itself induced hyperplasia of the thyroid, hepatomegaly, atrophy of the testis, anemia and bone marrow depression in rats and mice (72E1198). The 4-methyl derivative is well tolerated and may be more useful than pyrazole for pharmacological and metabolic studies of inhibition of ethanol metabolism. It has been shown (79MI40404) that administration of pyrazole or ethanol to rats had only moderate effects on the liver, but combined treatment resulted in severe hepatotoxic effects with liver necrosis. The fact that pyrazole strongly intensified the toxic effects of ethanol is due to inhibition of the enzymes involved in alcohol oxidation (Section 4.04.4.1.1). 

N-Heterocycles as drugs for the treatment of benign prostatic hyperplasia 97JMC1293. 

Ornithine decarboxylase is a pyridoxal dependent enzyme. In its catalytic cycle, it normally converts ornithine (7) to putrisine by decarboxylation. If it starts the process with eflornithine instead, the key imine anion (11) produced by decarboxylation can either alkylate the enzyme directly by displacement of either fluorine atom or it can eject a fluorine atom to produce viny-logue 12 which can alkylate the enzyme by conjugate addidon. In either case, 13 results in which the active site of the enzyme is alkylated and unable to continue processing substrate. The net result is a downturn in the synthesis of cellular polyamine production and a decrease in growth rate. Eflornithine is described as being useful in the treatment of benign prostatic hyperplasia, as an antiprotozoal or an antineoplastic substance [3,4]. 

Srivatsa SS, Tsao P, Holmes DR et al (1997) Selective av(33 integrin blockade limits neointima hyperplasia and lumen stenosis in stented porcine coronary artery injury in Pig. Cardiovasc Res 36 408-428... 

Hyperplasia is the enlargement of an organ due to an increased number of cells. 

CYP21 catalyzes steroid C21 hydroxylation required for cortisol biosynthesis. Genetic defects in this gene cause congential adrenal hyperplasia. 

Analysis of ESRB 7 mice showed fewer and smaller litters than wild type mice as well as abnormal vascular function and hypertension. The reduction in fertility was attributed to reduced ovarian efficiency. Mutant females had normal breast development and lactated normally. Older mutant males displayed signs of prostate and bladder hyperplasia. s -2-deficient mice furthermore display diverse regulatory defects in the function of brain, lung, and white blood cells. The results indicated that ESRB is essential for normal ovulation efficiency but is not essential for lactation, female or male sexual differentiation, or fertility. 

In breast cancer patients, total PR status is measured for hormonal treatment. The presence of PR is associated with increased survival rates and hormonal responsiveness of mammary tumors. PR agonists are widely used in contraception, HRT, breast cancer, and endometrial hyperplasia. Antiprogestins such as RU486 are used for blocking ovulation and preventing implantation, and in addition they are in clinical testing for the induction of labor and to control various neoplastic transformations. 

TRPV5 and TRPV6, also known as the epithelial Ca2+ channel or ECaC (TRPV5) and Ca2+transporter 1 or Ca2+ transporter-like (TRPV6), are the only two Ca2+-selective TRP channels identified so far. They may function in vitamin D-dependent transcellular transport of Ca2+in kidney, intestine and placenta. TRPV6 is also expressed in pancreatic acinar cells, and in prostate cancer, but not in healthy prostate or in benign prostate hyperplasia. 

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