Glucagon potassium

Alprenolol HCl Bromelain Ciprofibrate Clortermine HCl Desonide Fenofibrate Flucloronide Flunisolide Fluocinonide Flurandrenolide Glucagon Gramicidin Hetacillin potassium I proniazid Kebuzone Methyltestosterone Niaprazine Probucol Relaxin Somatotropin Triamcinolone acetonide Acetonitrile... 

Diazoxide is a potassium channel opener with a rapid antihypertensive action after intravenous administration. Diazoxide causes hyperglycaemia which may underlie side-effects such as nausea and vomiting, cardiac dysrhythmia and ketosis. Diazoxide was used occasionally in the management of hypertensive emergencies, but it is now largely abandoned for this indication. Diazoxide is an alternative for glucagons in patients with hypogycaemia. 

The major action of sulfonylureas is to increase insulin release from the pancreas (Table 41-5). Two additional mechanisms of action have been proposed—a reduction of serum glucagon levels and closure of potassium channels in extra pancreatic tissue (which are of unknown but probably minimal significance). 

Insulin is an endogenous hormone produced by fi-cells of islets of Langerhans of the pancreas, which consist of two chains of amino acids. It is required to be administered by a parenteral routes as it is destroyed when given orally. Insulin is used for the control of IDDM and in the emergency management of diabetic ketoacidosis.30 Insulin promotes the intracellular uptake of potassium and is used in hyperkalemia. Baker et al.31 have used insulin and glucagon in the treatment of liver disorders. Recent evidence indicates that the effects of insulin with glucose and potassium in ischemic heart disease have proved beneficial.32 It also is used in acute myocardial infarction.32... 

Endocrine and metabolic Blood tests Serum concentrations of pituitary horrmones (TSH, LH, FSH, ACTH, growth hormone, prolactin, vasopressin) serum concentrations of other hormones (insulin parathyroid hormone, glucagon, calcitonin, vitamin D) and serum electrolyte concentrations (sodium, potassium, calcium, magnesium)... 

The glucagon/insulin ratio can rise under certain pathological conditions (i.e., insulin-dependent diabetes). A small percentage of diabetics develop ketoacidosis, a condition that results from the overproduction and underuhlization of ketone bodies. Increased concentrations of p hydmxybutyrate and acetoacetate, which are acids, can cause a drop in the pH of the blood. This acidification, known as acidosis, can impair the ablLity of the heart to contract and result in a loss of consciousness and coma, which, in rare cases, may be fatal. Diabetic ketoacidosis may manifest as abdominal pain, nausea, and vomiting. A subject may hyperventilate (breathe quickly and deeply) to correct acidosis, as described under Sodium, Potassium, and Water in Chapter 10. It is the responsibility of the clinician, when confronted with a subject whose breath smells of acetone or who is hyperventilating, to facilitate prompt treatment. 

After an overdose of detajmium bitartrate in a dose of 18 mg/kg, a 36-year-old woman developed ventricular flutter, which responded to treatment with lidocaine, defibrillation, glucagon, noradrenaline, and sodium chloride (17). Hjrpokalemia responded to intravenous potassium chloride. 

Its primary action is inhibiting the release of GH from the pituitary gland. Somatostatin al.so suppresses the release of both insulin and glucagon. It causes a decrease in both cAMP levels and adenylate cyclase activity. It also inhibits calcium ion influx into the pituitary cells and suppresses glucose-induced pancreatic insulin secretion by activating and deactivating potassium ion and calcium ion permeability, respcc-tively. The chemistry. SARs, and potential clinical applications have been reviewed.--- ... 

In muscle and adipose tissue, insulin promotes transport of glucose and other monosaccharides across cell membranes it al.so facilitates tran.sport of amino icids, potassium ion.s. nucleosides, and ionic phosphate. Insulin also activates certain enzymes—kinases and glycogen. synthetase in muscle und adipose tissue. In adipose tissue, insulin decreases the release of fatty acids induced by epinephrine or glucagon. cAMP promotes fatty acid release from adipose ti.ssue therefore. it is pos.sible that insulin decreases fatty acid release by reducing tissue levels of cAMP. Insulin also facilitates the incorporation of intracellular amino acids into protein. 

Miki T, Liss B, Minami K, Shiuchi T, Saraya A, et al. 2001. ATP-sensitive potassium channels in hypothalamic neurons play an essential role in the maintenance of glucose homeostasis by controlling glucagon release and food intake. Nat Neurosci 5 507-512. 

Outcomes following unintentional and supratherapeutic ingestions of a patient s own BB or CCB have been reviewed [37 ]. Out of 436 cases reviewed, symptoms developed in 44 (10.1%) and 32 (7.3%) cases were admitted due to the ingestion. Of those admitted, five (15.6%) received treatment (three intravenous fluids, one glucagon and one calcium). Only one death was recorded in a 90-year-old lady who ingested four doses of her daily medications diltiazem 240 mg, atenolol 50 mg, glyburide 5 mg, warfarin 2 mg, frusemide 40 mg, lisinopril 5 mg, potassium chloride 20 mg, Zaroxyln 5 mg and hydralazine 25 mg. She was reported to have died of shock after the family initiated a do-not-resuscitate directive. 

Fig. 3. Effect of intraportal injections of saline (5 exp.) and of glucagon on plasma potassium of normal anesthetized dogs (5 exp.) and of dogs pretreated with DHE (5 exp.). Initial concentrations 3.6-4.3 (av. 3.9) mEq.l.

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