Bronchial secretions

Mechanism of Action A G1 ant ispasmodic and ant ichol inergic agent that inhibits the action of acetylcholine at postganglionic (muscarinic) receptor sites. Therapeutic Effect Decreases secretions (bronchial, salivary, sweat gland) and gastric juices and reduces motility of G1 and urinary tract. 

Meeran K (1989) Venepuncture causes rapid rise in plasma ACTH. Br J din Pract 1993 47 246-7 Raff H (1989) A new immunoradiometric assay for corticotropin evaluated in normal subjects and patients with Cushing s syndrome, din Chem 35 596-600 Raff H (1995) Intraoperative measurement of adrenocorticotropin (ACTH) during removal of ACTH-secreting bronchial carcinoid tumors. J Clin Endocrinol Metab 80 1036-9... 

In addition to tracheobronchial secretions, bronchial smooth muscle is stimulated by the muscarinic agonists. Asthmatic patients respond with intense bronchoconstriction, secretions, and a reduction in vital capacity. These actions form the basis of the methacholine challenge test used to diagnose airway hyperreactivity. 

Sandler, M., Scheuer, P. J. and Watt, P. J, 5-Hydroxy tryptophan-secreting bronchial carcinoid tumor. Lancet, 1961, p. 1067. 

Expectorants enhance the production of respiratory tract fluid and thus faciUtate the mobilisation and discharge of bronchial secretions. Historically, expectorants have been divided iato two classes based on specific mechanisms of action. Stimulant expectorants iacrease respiratory tract secretion by a direct effect on the bronchial secretory cells. Sedative expectorants act by gastric reflex stimulation. Many compounds classed as expectorants have been iaadequately studied and the mechanisms of action are not known with certainty. 

E. PucheUe, ed.. Rheology of Bronchial Secretions and Respiratory Functions, Masson and Co., Paris, 1973. 

These cascades of reactions need time in the range of seconds synaptic transmission through GPCRs is slow. All further postsynaptic changes depend on the type of postsynaptic cell. For example activation of 32-adrenoceptors causes in the heart an increase of the rate and force of contraction in skeletal muscle glycogenolysis and tremor in smooth muscle relaxation in bronchial glands secretion and in sympathetic nerve terminals an increase in transmitter release. 

Enflurane (Ethrane) is a volatile liquid anesthetic that is delivered by inhalation. Induction and recovery from anesthesia are rapid. Muscle relaxation for abdominal surgery is adequate, but greater relaxation may be necessary and may require the use of a skeletal muscle relaxant. Enflurane may produce mild stimulation of respiratory and bronchial secretions when used alone Hypotension may occur when anesthesia deepens. 

Drowsiness and sedation are common adverse reactions seen with the use of many of the antihistamines. Some antihistamines appear to cause more drowsiness and sedation than others. These dm may also have varying degrees of anticholinergic (cholinergic blocking) effects, which may result in dryness of the mouth, nose, and throat and a thickening of bronchial secretions. Several newer preparations (eg, loratadine) cause little, if any, drowsiness and fewer anticholinergic effects than some of the other antihistamines. Hiotosensitivity may occur with the use of the antihistamines. 

As part of the preadministration assessment, the nurse assesses the patient s blood pressure, pulse, and congestion before administering a decongestant. The nurse assesses lung sounds and bronchial secretions, which are noted in the patient s record. It is important to obtain a history of the use of these products, including die name of the product used and die frequency of use. 

Respiratory Effects. Pulmonary edema has been reported in humans who died of acute methyl parathion (Wofatox) intoxication (Fazekas 1971). Edema was foimd in a man who died 2 horn s after intoxication and in others who died as long as 9 days after exposure. Bronchoconstriction and h er-secretion of bronchial glands are primary muscarinic effects of methyl parathion. Pulmonary edema is not considered to be a primary effect of methyl parathion it is considered to be secondary to the neurologic effects of this compound on the heart and vascular smooth muscle. 

It has been known for many years that antimuscarinic drugs like hyoscine, which enter the brain, cause amnesia when used clinically, e.g. pre-operatively, to reduce bronchial secretions. In experimental studies in both humans and animals they disrupt both the acquisition and the performance of learned behaviour. Anti-cholinestrase drugs have the opposite effect. It is by no means certain, however, that the memory defects induced by antimuscarinics are identical to those seen in AzD. 

Approaches (1) and (2) depend on sufficient cholinergic function remaining to make its supplementation feasible, while all three methods suffer from the fact that not only does ACh have other central effects (e.g. in striatum), but also numerous peripheral parasympathomimetic ones, such as increased bronchial and gastric secretion or reduced heart rate. 

ACTH-secreting non-pituitary tumors (ectopic ACTH syndrome)—15% of cases of endogenous Cushing s syndrome usually from small cell lung carcinoma, bronchial carcinoids, pheochromocytoma, or thymus, pancreatic, ovarian, or thyroid tumor. The tumor is usually disseminated (difficult to localize). 

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