Velopharyngeal incompetency occurs when the soft palate and the lateral/posterior pharyngeal walls fail to separate the oral cavity from the nasal cavity during speech. Although the definitions are similar, the etiologies correlated with each term differ slightly. However, in the field of medical professionals these terms are typically used interchangeably. References
Conley SF, Gosain AK, Marks SM, Larson DL (1997). "Identification and assessment of velopharyngeal inadequacy". Am J Otolaryngol. 18 (1): 38–46. doi:10.1016/S0196-0709(97)90047-8. PMID 9006676. Johns DF, Rohrich RJ, Awada M (2003). "Velopharyngeal incompetence: a guide for clinical evaluation". Plast. Reconstr. Surg. 112 (7): 1890–7, quiz 1898, 1982. doi:10.1097/01.PRS.0000091245.32905.D5. PMID 14663236. McWilliams, Betty Jane; Peterson-Falzone, Sally J.; Hardin-Jones, Mary A.; Karnell, Michael P. (2001). Cleft palate speech. St. Louis: Mosby. ISBN 0-8151-3153-4. Hardin-Jones, Mary A.; Peterson-Falzone, Sally J.; Judith Trost-Cardamone; Karnell, Michael P. (2005). The Clinicians Guide to Treating Cleft Palate Speech. St. Louis: Mosby-Year Book. ISBN 0-323-02526-9. Willging JP (1999). "Velopharyngeal insufficiency". Int. J. Pediatr. Otorhinolaryngol. 49 Suppl 1: S307–9. doi:10.1016/S0165-5876(99)00182-2. PMID 10577827. == External links ==
Trabecular bone loss in the lumbar spine precedes cortical bone loss in the femoral neck. Exhaustive list
Allergic: allergic or hypersensitivity reactions, anaphylactoid reaction, anaphylaxis, and urticaria.Cardiovascular: hypertension, congestive heart failure in susceptible patients, premature atherosclerotic disease, arrhythmias, and possible hyperlipidemia.Dermatologic: impaired wound healing, petechiae and ecchymoses, thinning of the skin, facial erythema, and increased sweating.Endocrine: Cushingoid features, growth suppression in children, secondary adrenocortical and pituitary unresponsiveness, menstrual irregularities, decreased carbohydrate intolerance, and latent diabetes mellitus. In patients with diabetes, increased requirements of insulin or oral hypoglycemic agents.Fluid and electrolyte disturbances: sodium retention, fluid retention, potassium loss, hypokalemic alkalosis, or congestive heart failure in susceptible patients.Gastrointestinal: peptic ulcer, pancreatitis, abdominal distention, and ulcerative esophagitis.Metabolic: protein catabolism which causes negative nitrogen balance.Musculoskeletal: muscle weakness, loss of muscle mass, steroid myopathy, osteoporosis, tendon rupture (especially Achilles), vertebral compression fractures, aseptic necrosis of femoral and humeral heads, and pathologic fracture of long bones.Neurological: increased intracranial pressure with papilledema, convulsions, vertigo, and headache.Ophthalmic: posterior sub-capsular cataracts, increased intraocular pressure, glaucoma, and exophthalmos. Withdrawal
Feedback of the exogenous glucocorticoids at the hypothalamic–pituitary–adrenal (HPA) axis inhibits the secretion of the corticotropin-releasing hormone (CRH) and the adrenocorticotropic hormone (ATCH) at the hypothalamus and pituitary glands, respectively. Prolonged suppression leads to inadequate responses to physical and emotional stresses, such as illness and trauma. Suppression of ATCH may result in adrenal hypoplasia or secondary adrenal gland atrophy within 6 weeks of methylprednisolone therapy, leaving a patient at risk for developing life-threatening adrenal insufficiency crisis.