Specific codes in ICD-10 are unique alphanumeric designations used to identify and categorize diseases, disorders, and conditions. They consist of 3-5 characters, including both letters and numbers, that provide a high level of detail and specificity.
Language | Translation |
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English | Diabetes mellitus in pregnancy: Pre-existing diabetes mellitus, non-insulin-dependent |
French | Diabète sucré préexistant, non insulino-dépendant, au cours de la grossesse |
Level | Code | Title | |
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1 | XV | Pregnancy, childbirth and the puerperium | |
2 | O20-O29 | Other maternal disorders predominantly related to pregnancy | |
3 | O24 | Diabetes mellitus in pregnancy | |
4 | O24.1 | Diabetes mellitus in pregnancy: Pre-existing diabetes mellitus, non-insulin-dependent |
Active Ingredient | Description | |
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Dapagliflozin |
Dapagliflozin is a highly potent, selective and reversible inhibitor of SGLT2. SGLT2 is the predominant transporter responsible for reabsorption of glucose from the glomerular filtrate back into the circulation. Dapagliflozin improves both fasting and post-prandial plasma glucose levels by reducing renal glucose reabsorption leading to urinary glucose excretion. |
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Insulin (human) |
The blood glucose lowering effect of insulin is due to the facilitated uptake of glucose following binding of insulin to receptors on muscle and fat cells and to the simultaneous inhibition of glucose output from the liver. |
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Insulin aspart |
The blood glucose lowering effect of insulin aspart is due to the facilitated uptake of glucose following binding of insulin to receptors on muscle and fat cells and to the simultaneous inhibition of glucose output from the liver. Insulin aspart produces a more rapid onset of action compared to soluble human insulin, together with a lower glucose concentration, as assessed within the first four hours after a meal. Insulin aspart has a shorter duration of action compared to soluble human insulin after subcutaneous injection. |
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Insulin degludec |
Insulin degludec binds specifically to the human insulin receptor and results in the same pharmacological effects as human insulin. The blood glucose-lowering effect of insulin is due to the facilitated uptake of glucose following the binding of insulin to receptors on muscle and fat cells and to the simultaneous inhibition of glucose output from the liver. |
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Insulin detemir |
Insulin detemir is a soluble, long-acting insulin analogue with a prolonged duration of effect used as a basal insulin. |
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Insulin glargine |
Insulin glargine is a human insulin analogue designed to have a low solubility at neutral pH. After injection, the acidic solution is neutralised leading to formation of a precipitate from which small amounts of insulin glargine are continuously released. |
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Insulin glulisine |
Insulin glulisine is a recombinant human insulin analogue that is equipotent to regular human insulin. Insulin glulisine has a more rapid onset of action and a shorter duration of action than regular human insulin. |
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Liraglutide |
Liraglutide is a GLP-1 analogue with 97% sequence homology to human GLP-1 that binds to and activates the GLP-1 receptor. The GLP-1 receptor is the target for native GLP-1, an endogenous incretin hormone that potentiates glucose-dependent insulin secretion from the pancreatic beta cells. Unlike native GLP-1, liraglutide has a pharmacokinetic and pharmacodynamic profile in humans suitable for once daily administration. |
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Metformin |
Metformin is a biguanide with antihyperglycaemic effects, lowering both basal and postprandial plasma glucose. It does not stimulate insulin secretion and therefore does not produce hypoglycaemia. |
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Nateglinide |
Nateglinide is an amino acid (phenylalanine) derivative, which is chemically and pharmacologically distinct from other antidiabetic agents. Nateglinide is a rapid, short-acting oral insulin secretagogue. Its effect is dependent on functioning beta cells in the pancreas islets. |
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Repaglinide |
Repaglinide is a short-acting oral secretagogue. Repaglinide lowers the blood glucose levels acutely by stimulating the release of insulin from the pancreas, an effect dependent upon functioning β-cells in the pancreatic islets. |