pediagenosis
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Wednesday, June 9, 2021

Anxiolytic Agents

Anxiolytic Agents

Anxiolytic Agents

Anxiolytic Agents


Two main categories of anxiolytics are benzodiazepines and mis­cellaneous (eg, buspirone, zolpidem, zaleplon). Subclassification of benzodiazepines is based on speed of onset or duration of action, metabolism, and adverse effects. Benzodiazepines cross the blood­brain barrier and bind to specific receptors on the GABAA complex; these receptors occur in many brain regions. The drugs do not bind to the same sites as does GABA but potentiate GABA action. Benzodiazepines are safer than barbitu­rates (largely obsolete); adverse effects include dependence, ataxia, and drowsiness. Diazepam, chlordiazepoxide, prazepam, and the prodrug clorazepate undergo hepatic metabolism to the intermediate oxazepam. Alprazolam, flurazepam, lorazepam, and triazolam directly undergo conjugation before excretion.

Clinical Anxiety

Clinical Anxiety

Clinical Anxiety

Clinical Anxiety


To experience anxiety is normal. However, clinical anxiety is tension or apprehension that is grossly disproportionate to an actual or perceived stimulus. The source of anxiety may not be apparent and indeed may not be external; an underlying biochemical defect and genetic predisposition are hypothesized. 

Resting Membrane and Action Potentials

Resting Membrane and Action Potentials

Resting Membrane and Action Potentials

Resting Membrane and Action Potentials


The CNS comprises many types of neurons. In general, myelinated neurons conduct impulses more rapidly than do nonmyelinated neurons. The magnitude of the electrical potential difference across the neuronal membrane in the resting state, termed the resting membrane potential, depends on the relative intracellular and extracellular concentrations of Na+ and Cl (higher on the outside) and K+ (higher on the inside). The cytoplasmic electrical potential is more negative than the extracellular fluid by approximately −70 mV. The potential difference is partly maintained by an Na+/K+ active transport exchange mechanism (ion pump).

BASAL CELL NEVUS SYNDROME

BASAL CELL NEVUS SYNDROME

BASAL CELL NEVUS SYNDROME

BASAL CELL NEVUS SYNDROME


Basal cell nevus syndrome (BCNS), also known as nevoid basal cell carcinoma syndrome or Gorlin syndrome, is an uncommon autosomal dominant genodermatosis caused by mutations in the patched-1 (PTCH1) gene on chromosome 9. Approximately 40% of cases represent new, spontaneous mutations. Affected individuals are predisposed to the development of multiple basal cell carcinomas (BCCs), often in the hundreds over their lifetime. The diagnosis of this syndrome is based on a number of established criteria.

AMYLOIDOSIS

AMYLOIDOSIS

AMYLOIDOSIS

AMYLOIDOSIS


The term amyloidosis refers to a heterogeneous group of diseases. Systemic and cutaneous forms of amyloidosis can occur and are caused by the deposition of one of many different amyloid proteins. The primary cutaneous forms are more frequently seen. They include nodular, lichen, and macular amyloidosis (also referred to as lichen or macular amyloidosis). The systemic form is a multisystem, life-threatening disorder that requires systemic therapy. Most systemic disease is caused by an abnormality in plasma cells; myeloma-associated amyloid is a distant second in incidence. In addition to amyloidosis of the skin, the central nervous system may be involved with amyloidosis, as it is in Alzheimer’s disease.

ADDISON’S DISEASE

ADDISON’S DISEASE

ADDISON’S DISEASE

ADDISON’S DISEASE


Addison’s disease (chronic primary adrenocortical insufficiency) occurs when the adrenal gland has lost most of its functional capacity. Addison’s disease can be caused by many different disease states that inhibit the functioning of the adrenal gland. The adrenal gland has a massive reserve capacity, and clinical manifestations of chronic adrenal insufficiency are not seen until the bilateral glands have lost at least 90% of their ability to produce adrenal hormones. Autoimmune destructive atrophy of the adrenal glands is the most common cause of Addison’s disease. Infectious processes can cause destruction of the adrenal gland, with tuberculosis one of the more common causes of chronic adrenal gland insufficiency. Most cases of acute adrenal gland destruction are caused by bacteria (i.e., meningococcal disease).

WILSON’S DISEASE

WILSON’S DISEASE

WILSON’S DISEASE

WILSON’S DISEASE


Wilson’s disease, also known as hepatolenticular degeneration, is a disorder caused by a defect in copper metabolism. The disease is rare, with a worldwide incidence of approximately 1 in 18,000. It is an autosomal recessive condition that is caused by a defect in the ATP7B gene, which is located on the long arm of chromosome 13. The product of this gene is responsible for the proper transport of copper. The main clinical findings relate to nervous system involvement and liver disease. Wilson’s disease has a variable phenotype depending on the specific genetic mutation. Cutaneous disease and ophthalmological disease are frequently seen.

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