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Biomedical subjects

C A Kessler

Publications and source records attributed to C A Kessler.

5 recordsLinked to original sources
PubMed1992

An overview of endocrine function and dysfunction.

In more ways than is probably appreciated, critical care nurses deal with clinical situations that involve abnormalities in endocrine function. Endocrine emergencies frequently precipitate patient admissions to critical care units. More common, however, is the deleterious impact of critical illness and prescribed therapies on endocrine function. The manifestations of endocrine pathology are typically subtle and often go undetected until exacerbations and serious medical consequences ensue. To ensure prompt diagnosis and proper therapy, a general understanding of the endocrine function and hormone regulation is essential. It is also important that critical care nurses broaden their repertoire of assessment skills and become more attuned to the consequences of hormonal imbalance.

Biofeedback, Psychology↗
PubMed1992

Endocrinopathies of hyperfunction: Cushing's syndrome and aldosteronism.

Increased function of the adrenal cortex is a normal response in times of physiologic and psychologic stress. Adrenal cortical secretions (e.g., glucocorticoids, aldosterone) orchestrate a multitude of internal processes aimed at maintaining homeostasis and psychologic integrity. Many patients admitted to a critical care unit will manifest some increase, even minor, in adrenal function. However, excessive secretions of these hormones can have a lethal effect of fluid and electrolyte balance, energy metabolism, and immune function. Cushing's syndrome denotes a disorder characterized by increased circulating levels of glucocorticoids (primarily cortisol). An easily recognizable disorder, it may arise from pathology of the adrenal cortex or the anterior pituitary glands, ectopic secretions from a nonendocrine tumor, or from excessive doses of exogenously administered glucocorticoids. Cushing's syndrome is rarely an admitting diagnosis to critical care but is a disorder that can seriously affect recovery from coexisting illnesses if not treated. Aldosteronism, although rare, will often be diagnosed after admission to a critical care unit for management of troublesome hypertension, hypokalemia, congestive heart failure, and various dysrhythmias. Suspicion of the diagnosis should always arise when these manifestations occur, particularly when hypokalemia is refractory to potassium supplementation. Without timely diagnosis and treatment, these patients will succumb to lethal dysrhythmias.

Adrenocortical Hyperfunction↗
PubMed1992

Hyperglycemic emergencies.

Hyperglycemic emergencies are the most common endocrinopathies that require intensive care. It is estimated that between 10% and 15% of patients admitted to intensive care units experience complications of acute hyperglycemia. The common denominator of hyperglycemic emergencies is diabetes mellitus, a group of diseases in which, either because of beta-cell destruction of the pancreas or insulin receptor-site defects, there is a relative or absolute deficiency of insulin that results in hyperglycemia. In response to various precipitating factors, staggering hyperglycemia may develop in the form of diabetic ketoacidosis (DKA) or hyperglycemic hyperosmolar nonketotic syndrome (HHNK). The existence of DKA has been known since ancient times, and critical care nurses are familiar with the diagnosis. The more lethal disorder of HHNK was "rediscovered" in the 1950s and is occurring with greater frequency as clinical awareness of the condition grows and the elderly (who are at greatest risk for the disorder) populate critical care units in increasing numbers. Prevention is instrumental in abating deadly hyperglycemic emergencies. A positive outcome can be realized but only with timely diagnosis and prompt hormonal and fluid replacement.

Diabetes Mellitus, Type 1↗
PubMed1990

The chicken urokinase-type plasminogen activator gene.

The chicken urokinase-type plasminogen activator (uPA) cDNA and gene have been isolated and the complete nucleotide sequence of each established. cDNA sequence and Northern blot RNA analysis indicate that the chicken uPA mRNA is approximately 2500 nucleotides in size and contains a large 3'-noncoding region (998 nucleotides). The predicted amino acid sequence of the chicken uPA primary translation product (434 residues) suggests a domain architecture comparable to the mammalian uPA proteins with the form: (i) signal peptide, (ii) growth factor domain (GF), (iii) kringle domain (K), and (iv) serine protease domain (C). The overall sequence identity between the chicken and human proteins is 43.1%, with 56.3, 48.5, and 45.6% identity in the GF, K, and C domains, respectively. The chicken uPA gene is similar to the mammalian uPA genes in both size (8158 base pairs between transcription initiation and polyadenylation sites) and organization (11 exons). However, the sequence of the chicken uPA gene is similar to the mammalian uPA genes only within the protein-coding portions of exons. The transcription initiation site is flanked by a remarkably G/C-rich region (77% between nucleotides -1 and -300) which contains a TATA element and several potential transcription factor Spl-binding sites. The promoter region also contains several repeat elements, including two 11-nucleotide repeats that encompass six potential transcription factor AP-2-binding sites. This work provides a foundation for exploring the mechanism(s) by which protein-tyrosine kinase pp60v-src and protein kinase C modulate uPA gene transcription.

Amino Acid Sequence↗